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Title: A System of Practical Medicine By American Authors, Vol. II
       General Diseases (Continued) and Diseases of the Digestive System

Author: Various

Editor: William Pepper
        Louis Starr

Release Date: April 3, 2014 [EBook #45313]

Language: English

Character set encoding: ASCII

*** START OF THIS PROJECT GUTENBERG EBOOK SYSTEM OF PRACTICAL MEDICINE, VOL II ***




Produced by Ron Swanson






A SYSTEM OF PRACTICAL MEDICINE BY AMERICAN AUTHORS.


EDITED BY WILLIAM PEPPER, M.D., LL.D., PROVOST AND PROFESSOR OF THE
THEORY AND PRACTICE OF MEDICINE AND OF CLINICAL MEDICINE IN THE
UNIVERSITY OF PENNSYLVANIA.

ASSISTED BY LOUIS STARR, M.D., CLINICAL PROFESSOR OF DISEASES OF
CHILDREN IN THE HOSPITAL OF THE UNIVERSITY OF PENNSYLVANIA.


VOLUME II. GENERAL DISEASES (CONTINUED) AND DISEASES OF THE DIGESTIVE
SYSTEM.




PHILADELPHIA: LEA BROTHERS & CO.

1885.




Entered according to Act of Congress, in the year 1885, by

LEA BROTHERS & CO.,

in the Office of the Librarian of Congress at Washington. All rights
reserved.

WESTCOTT & THOMSON, _Stereotypers and Electrotypers, Philada._

WILLIAM J. DORNAN, _Printer, Philada._




CONTENTS OF VOLUME II.


GENERAL DISEASES (CONTINUED).
                                                                  PAGE
RHEUMATISM. By R. PALMER HOWARD, M.D.  . . . . . . . . . . . . .    19

GOUT. By W. H. DRAPER, M.D.  . . . . . . . . . . . . . . . . . .   108

RACHITIS. By ABRAHAM JACOBI, M.D.  . . . . . . . . . . . . . . .   137

SCURVY. By PHILIP S. WALES, M.D. . . . . . . . . . . . . . . . .   167

PURPURA. By I. EDMONDSON ATKINSON, M.D.  . . . . . . . . . . . .   186

DIABETES MELLITUS. By JAMES TYSON, A.M., M.D.  . . . . . . . . .   195

SCROFULA. By JOHN S. LYNCH, M.D. . . . . . . . . . . . . . . . .   231

HEREDITARY SYPHILIS. By J. WILLIAM WHITE, M.D. . . . . . . . . .   254


DISEASES OF THE DIGESTIVE SYSTEM.

DISEASES OF THE MOUTH AND TONGUE. By J. SOLIS COHEN, M.D.  . . .   321

DISEASES OF THE TONSILS. By J. SOLIS COHEN, M.D. . . . . . . . .   379

DISEASES OF THE PHARYNX. By J. SOLIS COHEN, M.D. . . . . . . . .   390

DISEASES OF THE OESOPHAGUS. By J. SOLIS COHEN, M.D.  . . . . . .   409

FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH. By SAMUEL
  G. ARMOR, M.D., LL.D.  . . . . . . . . . . . . . . . . . . . .   436

SIMPLE ULCER OF THE STOMACH. By W. H. WELCH, M.D.  . . . . . . .   480

CANCER OF THE STOMACH. By W. H. WELCH, M.D.  . . . . . . . . . .   530

HEMORRHAGE FROM THE STOMACH. By W. H. WELCH, M.D.  . . . . . . .   580

DILATATION OF THE STOMACH. By W. H. WELCH, M.D.  . . . . . . . .   586

MINOR ORGANIC AFFECTIONS OF THE STOMACH (Cirrhosis; Hypertrophic
  Stenosis of Pylorus; Atrophy; Anomalies in the Form and the
  Position of the Stomach; Rupture; Gastromalacia). By W. H.
  WELCH, M.D.  . . . . . . . . . . . . . . . . . . . . . . . . .   611

INTESTINAL INDIGESTION. By W. W. JOHNSTON, M.D.  . . . . . . . .   620

CONSTIPATION. By W. W. JOHNSTON, M.D.  . . . . . . . . . . . . .   638

ENTERALGIA (INTESTINAL COLIC). By W. W. JOHNSTON, M.D. . . . . .   658

ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS,
  COLITIS, PROCTITIS). By W. W. JOHNSTON, M.D. . . . . . . . . .   667

CHRONIC INTESTINAL CATARRH. By W. W. JOHNSTON, M.D.  . . . . . .   699

CHOLERA MORBUS. By W. W. JOHNSTON, M.D.  . . . . . . . . . . . .   719

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER. By J. LEWIS
  SMITH, M.D.  . . . . . . . . . . . . . . . . . . . . . . . . .   726

PSEUDO-MEMBRANOUS ENTERITIS. By PHILIP S. WALES, M.D.  . . . . .   763

DYSENTERY. By JAMES T. WHITTAKER, A.M., M.D. . . . . . . . . . .   777

TYPHLITIS, PERITYPHLITIS, AND PARATYPHLITIS. By JAMES T.
  WHITTAKER, A.M., M.D.  . . . . . . . . . . . . . . . . . . . .   814

INTESTINAL ULCER. By JAMES T. WHITTAKER, A.M., M.D.  . . . . . .   823

HEMORRHAGE OF THE BOWELS. By JAMES T. WHITTAKER, A.M., M.D.  . .   830

INTESTINAL OBSTRUCTION. By HUNTER MCGUIRE, M.D.  . . . . . . . .   835

CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES. By I.
  EDMONSON ATKINSON, M.D.  . . . . . . . . . . . . . . . . . . .   868

DISEASES OF THE RECTUM AND ANUS. By THOMAS G. MORTON, M.D., and
  HENRY M. WETHERILL, JR., M.D., PH.G. . . . . . . . . . . . . .   877

INTESTINAL WORMS. By JOSEPH LEIDY, M.D., LL.D. . . . . . . . . .   930

DISEASES OF THE LIVER. By ROBERTS BARTHOLOW, A.M., M.D., LL.D. .   965

DISEASES OF THE PANCREAS. By LOUIS STARR, M.D. . . . . . . . . .  1112

PERITONITIS. By ALONZO CLARK, M.D., LL.D.  . . . . . . . . . . .  1132

DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA). By SAMUEL
  C. BUSEY, M.D. . . . . . . . . . . . . . . . . . . . . . . . .  1182


INDEX. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  1195




CONTRIBUTORS TO VOLUME II.


ARMOR, SAMUEL G., M.D., LL.D.,
  Brooklyn.

ATKINSON, I. EDMONDSON, M.D.,
  Professor of Pathology and Clinical Medicine and Clinical Professor
  of Dermatology in the University of Maryland, Baltimore.

BARTHOLOW, ROBERTS, A.M., M.D., LL.D.,
  Professor of Materia Medica, General Therapeutics, and Hygiene in
  the Jefferson Medical College, Philadelphia.

BUSEY, SAMUEL C., M.D.,
  An Attending Physician and Chairman of the Board of Hospital
  Administration of the Children's Hospital, Washington, D.C.

CLARK, ALONZO, M.D., LL.D.,
  Late Professor of Pathology and Practical Medicine in the College of
  Physicians and Surgeons, New York.

COHEN, J. SOLIS, M.D.,
  Professor in Diseases of the Throat and Chest in the Philadelphia
  Polyclinic; Physician to the German Hospital, Philadelphia.

DRAPER, W. H., M.D.,
  Attending Physician to the New York and Roosevelt Hospitals, New
  York.

HOWARD, R. PALMER, M.D.,
  Professor of Theory and Practice of Medicine in McGill University,
  Montreal; Consulting Physician to Montreal General Hospital, Canada.

JACOBI, ABRAHAM, M.D.,
  Clinical Professor of Diseases of Children in the College of
  Physicians and Surgeons, New York, etc.

JOHNSTON, W. W., M.D.,
  Professor of Theory and Practice of Medicine in the Columbian
  University, Washington.

LEIDY, JOSEPH, M.D., LL.D.,
  Professor of Anatomy in the University of Pennsylvania,
  Philadelphia.

LYNCH, JOHN S., M.D.,
  Professor of Principles and Practice of Medicine in the College of
  Physicians and Surgeons, Baltimore.

MORTON, THOMAS G., M.D.,
  Surgeon to the Pennsylvania Hospital, Philadelphia.

MCGUIRE, HUNTER, M.D.,
  Richmond, Va.

SMITH, J. LEWIS, M.D.,
  Clinical Professor of Diseases of Children in the Bellevue Hospital
  Medical College, New York.

STARR, LOUIS, M.D.,
  Clinical Professor of Diseases of Children in the Hospital of the
  University of Pennsylvania, Philadelphia.

TYSON, JAMES, A.M., M.D.,
  Professor of General Pathology and Morbid Anatomy in the University
  of Pennsylvania, Philadelphia.

WALES, PHILIP S., M.D.,
  Washington.

WELCH, WILLIAM H., M.D.,
  Professor of Pathology in Johns Hopkins University, Baltimore.

WETHERILL, HENRY M., JR., M.D.,
  Assistant Physician to the Pennsylvania Hospital for the Insane,
  Philadelphia.

WHITE, J. WILLIAM, M.D.,
  Surgeon to the Philadelphia Hospital; Assistant Surgeon to the
  University Hospital; Demonstrator of Surgery and Lecturer on
  Venereal Diseases and Operative Surgery in the University of
  Pennsylvania, Philadelphia.

WHITTAKER, JAMES T., M.D.,
  Professor of Theory and Practice of Medicine in the Medical College
  of Ohio, Cincinnati.




ILLUSTRATIONS TO VOLUME II.

FIGURE                                                            PAGE
 1. POSITION OF PUNCTURES IN DIABETIC AREA OF MEDULLA OBLONGATA
    NECESSARY TO PRODUCE GLYCOSURIA  . . . . . . . . . . . . . .   195

 2. THE LAST CERVICAL AND FIRST THORACIC GANGLIA, WITH CIRCLE OF
    VIEUSSENS, IN THE RABBIT, LEFT SIDE  . . . . . . . . . . . .   196

 3. DIAGRAM SHOWING COURSE OF THE VASO-MOTOR NERVES OF THE
    LIVER, ACCORDING TO CYON AND ALADOFF . . . . . . . . . . . .   197

 4. DIAGRAM SHOWING ANOTHER COURSE WHICH THE VASO-MOTOR NERVES
    OF THE LIVER MAY TAKE  . . . . . . . . . . . . . . . . . . .   197

 5. JOHNSON'S PICRO-SACCHARIMETER  . . . . . . . . . . . . . . .   214

 6. PEMPHIGUS BULLA FROM A NEW-BORN SYPHILITIC CHILD . . . . . .   276

 7. SECTION OF RETE MUCOSUM AND PAPILLAE FROM SAME CASE OF
    PEMPHIGUS AS FIG. 6  . . . . . . . . . . . . . . . . . . . .   276

 8. SECTION OF AN OLD GUMMA OF THE LIVER . . . . . . . . . . . .   284

 9. SYPHILITIC DACTYLITIS, FROM BUMSTEAD . . . . . . . . . . . .   292

10. THE SAME AS FIG. 9 . . . . . . . . . . . . . . . . . . . . .   292

11. SERRATIONS OF NORMAL INCISOR TEETH . . . . . . . . . . . . .   297

12. NOTCHING OF SYPHILITIC INCISOR TEETH . . . . . . . . . . . .   297

13. OIDIUM ALBICANS FROM THE MOUTH IN A CASE OF THRUSH . . . . .   331

14. CHRONIC INTUMESCENCE OF THE TONGUE (HARRIS)  . . . . . . . .   351

15. HYPERTROPHY OF TONGUE (HARRIS), BEFORE OPERATION AND AFTER .   352

16. GLOSSITIS (LISTON) . . . . . . . . . . . . . . . . . . . . .   361

17. INCISION FOR A CUSPID TOOTH (WHITE)  . . . . . . . . . . . .   378

18. INCISION FOR A MOLAR TOOTH (WHITE) . . . . . . . . . . . . .   378

19. FUSIFORM DILATATION OF OESOPHAGUS (LUSCHKA)  . . . . . . . .   433

20. and 21. FAUCHER'S TUBE FOR WASHING OUT THE STOMACH . . . . .   605

22. ROSENTHAL'S METHOD OF WASHING OUT THE STOMACH  . . . . . . .   606

23. ANTERIOR VIEW OF A STRANGLUATED INTESTINE AND STRICTURE  . .   842

24. POSTERIOR VIEW OF A STRANGULATED INTESTINE AND STRICTURE . .   842

25. APPEARANCE OF THE NATURAL RELATIONS OF THE DIVERTICULUM TO
    THE INTESTINE  . . . . . . . . . . . . . . . . . . . . . . .   843

26. SIMPLE INVAGINATION OF THE ILEUM . . . . . . . . . . . . . .   844

27. SIMPLE INVAGINATION, WITH OCCLUSION OF BOWEL, FROM
    INFLAMMATORY CHANGES . . . . . . . . . . . . . . . . . . . .   844




{17}

GENERAL DISEASES (_CONTINUED_).

FROM DERANGEMENTS OF THE NORMAL PROCESSES OF NUTRITION.


RHEUMATISM.    | PURPURA.
               |
GOUT.          | DIABETES MELLITUS.
               |
RACHITIS.      | SCROFULA.
               |
SCURVY.        | HEREDITARY SYPHILIS.




{19}

RHEUMATISM.

BY R. P. HOWARD, M.D.


Acute Articular Rheumatism.

SYNONYMS AND DEFINITION.--Acute Rheumatism, Acute Rheumatic
Polyarthritis, Rheumarthritis, Rheumatic Fever, Polyarthritis
Synovialis Acuta (Heuter).

Acute articular rheumatism is a general non-contagious, febrile
affection, attended with multiple inflammations, pre-eminently of the
large joints and very frequently of the heart, but also of many other
organs; these inflammations observing no order in their invasion,
succession, or localization, but when affecting the articulations
tending to be temporary, erratic, and non-suppurating; when involving
the internal organs proving more abiding, and often producing
suppuration in serous membranes. It is probably connected with a
diathesis--the arthritic--which may be inherited or acquired. It may
present such modifications of its ordinary characters as to justify
being called (2d) subacute articular rheumatism, and it may sometimes
pass into the (3d) chronic form.

ETIOLOGY.--There is a general consensus of opinion that acute articular
rheumatism belongs especially to temperate climates, and that it is
exceedingly rare in polar regions; but respecting its prevalence in the
tropics contradictory statements are made. Saint-Vel declares that it
is not a disease of hot climates; Rufz de Levison saw only four cases
of acute articular rheumatism, and not one of chorea, in Martinique
during twenty years' practice; while Pruner Bey says it is common in
Egypt, and Webb remarks the same for the East Indies. Even in temperate
climates, like those of the Isle of Wight, Guernsey, Cornwall, some
parts of Belgium (Hirsch), the disease is very rare--a circumstance not
to be satisfactorily explained at present.

Acute articular rheumatism is never absent; it occurs at all seasons of
the year, although subject to moderate variations depending mainly upon
atmospheric conditions. It is the general opinion that it prevails most
during the cold and variable months of spring, but this is not true of
every place, nor invariably of the same place. Indeed, Besnier,[1]
after a long and special observation of the disease in Paris, concludes
that there it is most frequent in summer and in spring. In Montreal,
during ten years, the largest number of cases of acute rheumatism
admitted to the General Hospital obtained in the spring months (March
to June {20} inclusive), when they averaged 51 a month; 33 was the
average for all the other months, except October and November, when
26-1/2 was the average. The statistics of Copenhagen, Berlin, and
Zurich show a minimum prevalence in summer or in summer and autumn.

[Footnote 1: _Dictionnaire Encyclopedique des Sciences Med._, Troisieme
Serie, t. iv.]

Occupations involving muscular fatigue or exposure to sudden and
extreme changes of temperature, especially during active bodily
exertion, predispose to acute articular rheumatism; hence its frequency
amongst cooks, maid-servants, washerwomen, smiths, coachmen, bakers,
soldiers, sailors, and laborers generally.

While no age is exempt from acute articular rheumatism, it is, par
excellence, an affection of early adult life, the largest number of
cases occurring between fifteen and twenty-five years of age, and the
next probably between twenty-five and thirty-five. A marked decline in
its frequency takes place after the age of thirty-five, and a still
greater after forty-five. It is not uncommon in children between five
and ten, and especially between ten and fifteen, but is very rare under
five, although now and then one meets with an example of the disease in
children three or four years of age. While the acute articular
affections observed in sucklings are, as a general rule, either
syphilitic or pyaemic, some authentic instances of rheumatic
polyarthritis are recorded. Kauchfuss's two cases among 15,000 infants
at the breast, Widerhofer's case, only twenty-three days old, Stager's,
four weeks old, and others, are cited by Senator.[2]

[Footnote 2: _Ziemssen's Cyclop. of Pract. Med._, xvi. 17.]

An analysis of 4908 cases of acute rheumatism admitted to St.
Bartholomew's Hospital, London,[3] during fifteen years, and of 456
treated in the Montreal General Hospital during ten years,[4] gives the
following percentages at given periods of life:

             London.                        Montreal.
  Under      10 years,  1.79 %  |  Under      15 years,  4.38 %
  From 10 to 15   "  ,  8.1  %  |  From 15 to 25   "  , 48.68 %
   "   15 to 25   "  , 41.8  %  |   "   25 to 35   "  , 25.87 %
   "   25 to 35   "  , 24.5  %  |   "   35 to 45   "  , 13.6  %
   "   35 to 45   "  , 14.2  %  |  Above      45   "  ,  7.4  %
  Above      45   "  ,  9.5  %  |

The close correspondence existing in the two tables for all the periods
of life above fifteen is very striking: the disparity between them
below the age of fifteen may, I believe, be explained by the
circumstance that the pauper population of Montreal is, when compared
with that of London, relatively very small, and by the further fact
that the practice of sending children into hospitals hardly obtains
here.

[Footnote 3: _St. Bartholomew's Hospital Reports_, xiv. 4.]

[Footnote 4: Dr. James Bell, in _Montreal General Hospital Reports_, i.
350.]

No doubt the above tables do not correctly represent the liability of
children to acute articular rheumatism, but they are probably a fair
statement of the relative frequency of the disease in the adult
hospital populations of London and Montreal. If primary attacks of the
disease only were tabulated, the influence of youth would be more
evident, for it is scarcely possible to find on record an authentic
instance of the disease showing itself for the first time after sixty.
Dr. Pye-Smith[5] has done {21} this in 365 cases, and the results prove
the great proclivity of very young persons to acute rheumatism: Between
five and ten years, 6 per cent. occurred; between eleven and twenty, 49
per cent.; from twenty-one to thirty, 32.3 per cent.; from thirty-one
to forty, 9.5 per cent.; from forty-one to fifty, 2.2 per cent.; and
from fifty-one to sixty-one, 1.1 per cent. The same author has also
shown that secondary attacks are most common in the young; so that
advancing age not only renders a first attack of the disease
improbable, but lessens the risk of a recurrence of it. The influence
of age upon acute rheumatism is further shown in the fact that the
disease is less severe, and less apt to invade the heart, in elderly
than in young persons.

[Footnote 5: _Guy's Hospital Reports_, 3d Series, xix. 317.]

The general opinion that sex exercises no direct influence beyond
exposing males more than females to some of the predisposing and
exciting causes of acute rheumatism is perhaps true if the statement be
confined to adults, to whom, indeed, most of the available statistics
apply; but it should be borne in mind that a larger proportion of men
than of women resort to hospitals, and there is some reason to believe
that in childhood the greater liability to the disease is on the part
of the female sex. Thus, the number of cases of rheumatism treated at
the Children's Hospital in London from 1852 to 1868 was 478, of whom
226 were males and 252 females.[6] Of Goodhardt's 44 cases of acute
rheumatism in children, 26 were girls and 18 were boys.[7] Of 57
examples of rheumatism in connection with chorea observed by Roger in
children under fourteen, 33 were girls and 24 were boys.[8]

[Footnote 6: Vide Dr. Tuckwell's "Contributions to the Pathology of
Chorea," in _St. Bartholomew's Hospital Reports_, v. 102.]

[Footnote 7: _Guy's Hospital Reports_, 3d Series, xxv. 106.]

[Footnote 8: _Arch. Gen._, vol. ii. 641, 1866, and vol. i. 54, 1867,
quoted by Tuckwell.]

That heredity predisposes to acute articular rheumatism is admitted by
nearly all modern authorities, even Senator, while speaking of it as "a
traditional belief," not venturing to deny it. The frequency of the
inherited predisposition Fuller placed at 34 per cent.; Beneke, quoted
by Homolle,[9] at 34.6 per cent; Pye-Smith at 23 per cent.[10] Such
predisposition favors the occurrence of the disease in early life, but
does not necessarily determine an attack of acute rheumatism in the
absence of the other predisposing or exciting causes. That the
inherited bias or mode of vital action or condition of tissue-health
may be so great as, per se, to induce an attack of the disease, is held
by some authorities. It is probable that not only acute articular
rheumatism in the parents, but simple chronic articular rheumatism and
those forms grouped under the epithet rheumatoid arthritis, may impart
a predisposition to the acute as well as to the chronic varieties of
articular disease just mentioned. But owing to the obscurity which
still surrounds the relations existing between acute articular
rheumatism and rheumatoid arthritis this point needs further
investigation. In what the inherited predisposition to acute articular
rheumatism consists we are ignorant; to say that it imparts to the
tissues or organs a disposition to react or act according to a fixed
morbid type, or that some of the nutritive processes are perverted by
it, is merely to state a theory, not to explain the nature of the
predisposition.

[Footnote 9: _Nouv. Dict. de Med. et de Chir._, t. 31, 557.]

[Footnote 10: _Guy's Hospital Reports_, 3d Series, xix. 320.]

No type of bodily conformation or temperament can be described that
{22} certainly indicates a proclivity to acute articular rheumatism;
nor is there any change in the constitution of the tissues or fluids of
the body by which the proclivity may be recognized. We infer the
existence of the inherited predisposition--the innate bias--when
rheumatism is found in the family history; when acute rheumatism or
cardiac disease, or chorea not produced by mental causes, occurs in
childhood; when the first attack of acute articular rheumatism is
succeeded by subsequent attacks; and especially when the intervals
between the attacks are short. Goodhardt has recently furnished
valuable, but not conclusive, evidence to prove that in children
obstinate headaches, night-terrors, severe anaemia, various
neuro-muscular derangements, such as torticollis, tetany, muscular
tremors, stammering, incontinence of urine, recurring attacks of
abdominal pain, with looseness of the bowels quickly succeeding a meal,
the cutaneous affection erythema nodosum, are indications of a
rheumatic bias or predisposition.[11]

[Footnote 11: _Guy's Hospital Reports_, 3d Series, xxv.]

There is some basis for the opinion that residence in damp, cold
dwellings predisposes somewhat to acute articular rheumatism, although
not at all to the same degree that it does to the chronic articular and
muscular forms. Chomel and Jaccoud especially have insisted that it
will gradually create a predisposition to the disease, even if it has
not been inherited. All pathologists agree that cold is the most
frequent exciting cause of acute articular rheumatism, and that it is
especially effective when applied while the body is perspiring freely
or is overheated or fatigued by exercise. There is no necessary ratio
between the degree of cold or its duration and the severity of the
resulting rheumatism. A slight chilling or a momentary exposure to a
current of cold air will in some act as powerfully and as certainly as
a prolonged immersion in cold water or a night spent sleeping on the
damp grass. This circumstance, together with the fact that cold applied
in the same way may also produce a pharyngitis or a bronchitis, a
pneumonia or a nephritis, etc., is held to indicate that the cold acts
according to individual predisposition; and Jaccoud, Flint, and others
maintain that unless a rheumatic proclivity exists cold will not
produce an attack of the disease under consideration. I doubt that we
are yet in a position to assert that absolutely, although the weight of
argument is in its favor. Let it suffice to say, that while a prolonged
residence in a cold, damp dwelling may gradually develop a
predisposition to rheumatism, a short exposure to cold will be likely
to induce an attack of rheumatism if the predisposition exist.

There are other influences which may be regarded as auxiliaries to cold
in exciting an attack, as they seem to increase the susceptibility of
the patient to its operation: they establish what has been felicitously
called a state of morbid opportunity. Such are all influences that
reduce the resisting powers of the organs and organism, as bodily
fatigue, mental exhaustion, the depressing passions, excessive venery,
prolonged lactation, losses of blood, etc. It is probably in such a
manner that local injuries (traumatism) sometimes appear to induce an
attack of rheumatism. A blow on a finger (Cotain), the extraction of a
tooth (Homolle), a hypodermic injection (ibid.), etc., may act
powerfully in some persons upon and through the nervous system, and by
lessening their resisting power {23} may favor the overt manifestation
of the rheumatic predisposition. But doubtless some such cases have
been examples of mere coincidence.

There are certain pathological and even physiological conditions during
or after which an inflammatory affection of one or several joints
closely resembling acute articular rheumatism more or less frequently
arises. Thus, during the early desquamating stage of scarlatina a mild
inflammation of the joints of the hands and feet, and frequently of the
large articulations as well, is very often seen, and it is attended
with profuse perspiration, with a condition of urine like that of
ordinary acute rheumatism, and occasionally with inflammation of the
heart or pleura. During convalescence from dysentery an affection of a
single or of several articulations resembling rheumatism has been
noticed, and the two affections have even alternated in the same
patient. That singular epidemic disease dengue is attended with a
polyarticular affection closely resembling acute articular rheumatism,
occasionally pursuing a protracted course, and not seldom leaving after
it a cardiac lesion. In haemophilia polyarticular and muscular
disorders frequently arise which closely resemble, and appear to be
sometimes identical with, ordinary acute articular and muscular
rheumatism. Gonorrhoea too is often associated with a febrile
polyarthritis, and rarely with an endocarditis at the same time. In the
puerperal state an inflammation of one or several articulations is not
unfrequently observed (puerperal rheumatism).

Respecting the real nature of these polyarticular inflammations very
much has to be made out; and it must suffice at present to say that
while many of them are of a pyaemic nature, as some examples of
puerperal and scarlatinal arthritis, in which pus forms in or about the
joints and in the serous cavities and viscera, some of them are no
doubt examples of genuine rheumatism occurring in persons of rheumatic
predisposition, which have either been induced by the lowering
influence of the disease upon which they have supervened, or by the
accidental coincidence of some of the other causes of acute rheumatism.
There remains, however, the ordinary form of scarlatinal arthritis,
which so closely resembles true acute articular rheumatism in its
symptoms, course, visceral complications, and morbid anatomy that it
cannot be said that the two affections are distinct and different. And
much the same appears to be true of the articular affection of dengue.
Yet so frequently does the articular affection accompany scarlatina and
dengue respectively that it cannot logically be referred to a
coexisting rheumatic predisposition, and must be a consequence of the
disturbing influences of the specific poison of those zymotic
affections per se.

PATHOLOGY.--The pathology of acute articular rheumatism is a very much
debated question, and is not at all satisfactorily known. Hence a mere
statement of the most prominent theories now held by different
pathologists will be given.[12]

[Footnote 12: The reader may consult with advantage Dr. Morris
Longstreth's fourth chapter in his recent excellent monograph upon
_Rheumatism, Gout, and some Allied Disorders_, New York, 1882.]

The latest modification of the lactic-acid theory of Prout is founded
upon the modern physiological teaching that during muscular exercise
sarcolactic acid and acid phosphate of potassium are formed, and carbon
dioxide set free, in the muscular tissue, and that cold, acting on {24}
the surface under such circumstances, may check the elimination of
these substances and cause their accumulation in the system. This view,
it is held, explains why the muscles and their associated organs, the
joints and tendons, suffer first and chiefly, because the morbific
influence is exerted upon them when exhausted by functional activity;
and it further accounts for the visceral manifestations and the
apparent excess of acid eliminated during the course of the disease.
The circumstance that in three cases of diabetes (Foster,[13]
Kuelz[14]) the administration of lactic acid appeared to induce
polyarticular rheumatism favors the idea that acid is the materies
morbi in rheumatism.

[Footnote 13: _Brit. Med, Jour._, ii. 1871.]

[Footnote 14: _Beitrage zur Path. und Therapie des Diabetes_, u. s. w.,
ii. 1875.]

Now it must be admitted that, as yet, no sufficient proof is
forthcoming that a considerable excess of lactic acid exists in the
fluids or solids of the body or in the excretions in rheumatism (it is
true the point has not been sufficiently investigated). On the other
hand, that acid has been found in the urine of rickets, and its excess
in the system is regarded by Heitzmann and Senator[15] as the cause of
the peculiar osteoplastic disturbances of that disease--an affection
altogether different from rheumatism. It is quite improbable that the
amount of sarcolactic acid produced by over-prolonged muscular
exertion, and whose elimination has been prevented by a chill or a
mental emotion, is sufficient to maintain the excessive acidity of the
urine and other fluids during a long rheumatic fever; and arguments can
be adduced favorable to the view that excessive formation of acid is an
effect rather than the cause of rheumatism: cases of that disease occur
in which neither excessive muscular exertion nor exposure to chill have
preceded the rheumatic outbreak. Lastly, lactic acid is not the only
principle retained when the functions of the skin are arrested by cold,
the usual exciting cause of rheumatism; why should not the retained
acetic, formic, butyric, and other acids, for example, play their role
in the production of the symptoms observed under such conditions?

[Footnote 15: _Ziemssen's Cyclop._, xvi. p. 177.]

The same objections apply to Latham's[16] hypothesis that
hyperoxidation of the muscular tissue is the starting-point of acute
rheumatism. He assumes, with other physiologists, the existence of a
nervous centre which inhibits the chemical changes that would take
place if the tissues were out of the body. If this centre be changed or
weakened, the muscle, instead of absorbing and fixing the oxygen and
giving out carbonic acid, disintegrates; lactic acid is formed, and,
passing into the blood, may be there oxidized and produce the pyrexia
of acute rheumatism. It need hardly be remarked that the existence of a
chemical inhibitory centre has yet to be proved, although much may be
advanced in its favor; and, secondly, the recent investigations of
Zuntz render it highly probable that in all febrile affections it is
the muscles chiefly, if not solely, which suffer increased oxidation,
and that this is due to increased innervation--views not easily
reconciled with Latham's theory.

[Footnote 16: _Brit. Med. Jour._, ii. 1880, p. 977.]

The nervous theory of rheumatism and of articular diseases originated
with Dr. J. K. Mitchell of Philadelphia[17] in 1831, and was afterward
elaborated by Froriep in 1843,[18] Scott Alison[19] in 1846, Constatt
in 1847,[20] {25} Gull in 1858, Weir Mitchell in 1864,[21] Charcot in
1872, and by very many others since. According to present physiological
doctrine, the exciting cause of rheumatism, cold, either acts directly
upon the vaso-motor or the trophic (?) nerves of the articulations, and
excites inflammation of them, or else it irritates the peripheral ends
of the centripetal nerves, and through these excites actively the
vaso-motor and trophic nerve-centres. The local lesions, on this
hypothesis, are of trophic origin; the fever is due to hyperactivity of
the centres supposed to control the chemical changes going on in the
tissues; the excessive perspiration to stimulation of the
sweat-centres; and so on. It is not held that a definite centric lesion
of the nervous system exists in rheumatism, analogous to the lesions
which in myelitis or locomotor ataxia develop the arthropathies of
those affections, but rather a functional disturbance. One of the
latest and ablest advocates of the neurosal theory of rheumatism in all
its forms (simple, rheumatoid, gonorrhoeal, urethral, etc.), Jonathan
Hutchinson, calls it "a catarrhal neurosis, the exposure of some tract
of skin or mucous membrane to cold or irritation acting as the incident
excitor influence."[22]

[Footnote 17: _Am. Jour. Med. Sci._, 1831; _ib._, 1833.]

[Footnote 18: _Die Rheumatische Schwiele_, Weimar, 1843.]

[Footnote 19: _Lancet_, 1846, i. 227.]

[Footnote 20: _Spec. Pathologie und Therapie_, 1847, ii. p. 609.]

[Footnote 21: Vide _Am. Jour. Med. Sciences_, April, 1875, vol. lxix.
339-348.]

[Footnote 22: _Trans. International Med. Congress_, 1881, ii. 93.]

In order that peripheral irritation shall thus induce inflammation of
the joints and the other affections of muscles, tendons, fasciae, etc.
which are called rheumatic, he holds with the French School that the
arthritic diathesis must exist, or that state of tissue-health which
involves a tendency to temporary inflammation of many joints or fibrous
structures at once, or to repeatedly recurrent attacks of inflammation
of one joint or fibrous structure. If I understand Mr. Hutchinson
correctly, he also holds that a nerve-tissue peculiarity exists which
renders persons liable to rheumatism. He does not indicate either the
cause or the nature of the nerve-tissue peculiarity. But modern
pathology teaches that the functional conditions of the nervous centres
known as neuroses, whether inherited or acquired, reveal themselves as
morbid manifestations of nerve-function on the part of special portions
of or the entire nervous system, and, as Dr. Dyce Duckworth has well
pointed out, these neuroses may be originated, when not inherited, in
various ways, as by excessive activity of the nervous system, by
prolonged or habitual excesses, etc. "Thus, undue mental labor,
gluttony, alcoholic intemperance, debauchery, and other indulged evil
propensities in the parent come to be developed into definite neurotic
taint and tendency in the offspring."

But is there nothing more in acute articular rheumatism than an
inflammation of certain structures, articular and visceral, lighted up
in an individual of a neuro-arthritic diathesis? What do we learn from
that closely-allied affection, gout, which involves especially the same
organs as rheumatism, and is held by many of the ablest pathologists to
belong to the same basic diathesis as it? Duckworth[23] has very ably
advocated a neurotic theory of gout, but it is admitted on all
hands--and by Duckworth himself--that in gout a large part of the
phenomena is due to perverted relations of uric acid and sodium and to
the presence of urate of soda in the blood. May we not from analogy, as
well as from other evidence, infer that in that so-called other
neurosis, rheumatism, a considerable part of the phenomena is due to
perversions of {26} the processes of assimilation and excretion, and to
the presence of some unknown intermediate product of destructive
metamorphosis--lactic or other acid? This is admitted by Maclagan and
strongly advocated by Senator; and in this way the pathology of the
disease may be said to embrace the humoral as well as the solidist
doctrines--the resulting theory being a neuro-humoral one. No doubt
pathological chemistry and clinical investigation will ere long make
important discoveries respecting the pathology of acute rheumatism
which shall maintain the close alliance believed to exist between that
affection and gout.

[Footnote 23: _Brain_, April, 1880.]

The miasmatic theory, so ably advocated by Maclagan,[24] assumes that
rheumatism is due to the entrance into the system from without of a
miasm closely allied to, but quite distinct from, malaria. His argument
on this topic is ingenious and elaborate, yet has not been favorably
received by pathologists. Opposed to it are the following amongst other
considerations: Heredity exercises a marked influence upon the
occurrence of rheumatism; unlike malarial disease, no climate or
locality is immune from rheumatism; the many indications that a
diathesis plays a chief role in rheumatism; the remarkable influence
exerted by cold and dampness in the etiology of the disease.

[Footnote 24: _Rheumatism: its Nature, Path., etc._, London, 1881, pp.
60-95.]

Heuter's[25] infective-germ theory, like the miasmatic, refers
rheumatism to a principle not generated in the system, but introduced
from without. A micrococcus enters the dilated orifices of the
sweat-glands, and, reaching the blood, first sets up an endocarditis,
and then capillary emboli produce the articular inflammations. This is
a reversal of what really happens, so far as the time of invasion of
the endocardium and the synovial membranes is concerned; and
Fleischauer's case, in which miliary abscesses were found in the heart,
lungs, and kidneys, was probably one of ulcerative endocarditis, which,
after all, is a rare complication of acute articular rheumatism.
Moreover, it is a gratuitous assertion to say that endocarditis exists
in all cases of the disease. If, however, Heuter were content to say
that acute articular rheumatism was produced by a specific germ, as
held by Recklinghausen and Klebs, which on entering the system acted
specially upon the joints and the fibro-serous tissues, as the poison
of small-pox does upon the skin, while at the same time it sets up
general disturbances of the entire economy as other zymotic poisons do,
there would be nothing opposed to general pathological laws. Even the
existence of a diathesis capable of favoring the action of the specific
germ would be analogous to the tuberculous diathesis, which favors the
action of the bacillus of tubercle; and cold, its ordinary exciting
cause, might be regarded simply as a condition which renders the system
more susceptible to the action of the germ, and the modus operandi of
cold in doing this might be variously explained.

[Footnote 25: _Klinik der Gelenkkrankheiten_, Leipzig, 1871.]

SYMPTOMS.--The disease has no uniform mode of invasion. (_a_) Very
frequently slight disorder of health, such as debility, pallor, failure
of appetite, unusual sensibility to atmospheric changes, grumbling
pains in the joints or limbs, or even in some muscle or fascia,
precedes by one or more days the fever and general disturbance. (_b_)
Not infrequently a mild rigor or repeated chilliness, accompanied or
soon followed by moderate or high fever, ushers in the illness, and in
from a few hours to one {27} or at most two days the characteristic
articular symptoms ensue. (_c_) In very rare cases febrile disturbance,
ushered in by chills, may be followed by inflammation of the endo- or
pericardium or pleura before the joints become affected.

Whatever the mode of invasion, the symptoms of the established disease
are well defined, and marked febrile disturbance, transient
inflammation of several of the larger articulations, excessive activity
of the cutaneous functions, and a great proclivity to inflammation of
the endo- and pericardium constitute the stereotyped features of the
disease.

As a very general rule, the temperature early in the disease promptly
attains its maximum of 102 degrees F. to 104 degrees F., yet the
surface does not feel very hot; the pulse ranges from 90 to 100 or 110,
and is regular, large, and often bounding; the tongue is moist, but
thickly coated with a white fur; there are marked thirst, impaired
appetite, and constipation; the stools are usually dark; the urine
scanty, high colored, very acid, of great density, and holding in
solution an excess of uric acid and urates, which are frequently
deposited when the urine cools. The general surface is covered with a
profuse sour-smelling perspiration, whose natural acid reaction, as a
general rule, is markedly increased; indeed, the naturally alkaline
saliva is also acid. Beyond a little wandering during sleep,
occasionally observed in irritable, nervous patients, there is very
rarely any delirium, and this notwithstanding that sleep is frequently
much disturbed by the pain in the joints and the excessive sweating.

If the local articular symptoms have not set in almost simultaneously
with the pyrexia, or even preceded it, they will follow it in from a
few to twenty-four or forty-eight hours. At first one or more joints,
usually the knees or ankles, become painful, sensitive to pressure,
hot, more or less swollen, and exhibiting a slight blush of redness or
none at all. The swelling may consist of a mere puffiness, due to
slight infiltration of the soft parts external to the joint, or of a
more or less considerable tumefaction, caused by effusion into the
synovial capsule. In the knees, elbows, shoulders, and hips the
swelling is usually confined to the articulations, and there is but
little redness of the integument, but in the wrists and ankles the
inflammatory process is often more severe, and may invade the whole
dorsum of the hand or foot, rendering the integument tense, tumid red,
and shining. Pitting of the swollen parts, although quite exceptional
in acute articular rheumatism, will exist under the conditions just
mentioned. The metacarpo-phalangeal articulations are likewise often a
good deal swollen and of a bright-red color.

The pain in the affected articulations varies from a trifling
uneasiness or dull ache to excruciating anguish; sometimes the pain is
felt only on moving or pressing the joint; pressure always aggravates
it; even the weight of the bed-clothes may be intolerable; and in
severe cases the slightest movement of the joint or a jar of the bed
produces great suffering. The pain, like the swelling, sometimes
extends beyond the affected joints to the tendinous sheaths, the
tendons, and muscles, and even to the nerves of the neighborhood.

It is a striking peculiarity of acute rheumatism that the inflammation
tends to invade fresh joints from day to day, the inflammation usually,
but not invariably, declining in those first affected; and sometimes
this retrocession of the inflammation in a joint is so sudden, and so
coincident {28} with the invasion of a different one, that it is often
regarded as a true metastasis. Exceptionally, however, one or several
joints remain painful and swollen, although this occurs chiefly in
subacute attacks. In this way most of the large joints may successively
suffer once, twice, or oftener during an attack of acute rheumatism.
And as the inflammation commonly lasts in each articulation from two to
four or more days, it is usual to have six or eight of the joints
affected by the end of the first week. While the ankles and knees,
wrists, elbows, and shoulders, are especially liable to be affected,
and with a frequency pretty closely corresponding to the above order,
the joints of the hands occasionally, and the hips even more
frequently, escape. The intervertebral and tempero-maxillary
articulations have very rarely suffered in the writer's experience.

If the ear be applied to the cardiac region in acute rheumarthritis,
another local inflammation than the articular will very frequently be
detected, which otherwise would probably be unrecognized, and yet it is
the most important feature of the disease. In the first or second, or
even as late as the fourth, week of the fever the signs of endocarditis
of the mitral valve, occasionally of the aortic, and sometimes of both,
will exist in an uncertain but large proportion of cases, or those of
pericarditis, but in a less proportion, will obtain. Indeed, the
cardiac inflammation may even precede the articular, and some believe
it may be the only local evidence of rheumatic fever. As a general
rule, the implication of the endo- or pericardium in acute
rheumarthritis gives rise to no marked symptoms or abrupt modification
of the clinical features of the case, and a careful physical
examination must be instituted to discover its existence. But the
recurrence of pain or tightness either in the precordial or sternal
region, of marked anxiety or pallor of the face, of sudden increase in
the weakness or frequency of the pulse, or of irregularity in its
rhythm, of restlessness or delirium, of oppression of breathing, or of
short, dry cough,--may indicate the invasion of the endo- or peri- or
myocardium, and a physical examination will be needed to detect the
cardiac disease and to exclude the presence of pleuritis, pneumonia, or
bronchitis. Sometimes, however, especially in severe cases, an
extensive pericarditis, with or without myocarditis, will produce grave
constitutional disturbance, in which sleeplessness, delirium, stupor,
generally associated with a very high temperature and marked
prostration, will, as it were, mask both the articular and the cardiac
affection.[26]

[Footnote 26: See Stanley's case, _Med.-Chir. Trans._, 1816, vol. vii.
323, and Andral's _Clinique Medicale_, t. i. 34.]

As regards the murmurs which arise in acute rheumatic endo- or
pericarditis, while they are usually present and quite typical, this is
not always so. The only alteration of the cardiac sounds may be at
first and for some time a loss of clearness and sharpness, passing into
a prolongation of the sound, which usually develops into a distinct
murmur, or the sounds may be simply muffled. In pericarditis limited to
that portion of the membrane which covers the great vessels no friction
murmur may be audible, or it may be heard and be with difficulty
distinguished from an endocardial murmur. On the other hand, a systolic
basic murmur not due to endo- or pericarditis frequently exists,
sometimes in the early, but usually in the later, stages of rheumatic
fever.

{29} Other local inflammations occasionally arise in the course of
acute rheumatism: pneumonia is one of the most frequent; left pleuritis
is not infrequent, and is doubtless often caused by the extension of a
pericarditis; but both pneumonia and pleurisy are occasionally double
in rheumatic fever. Severe bronchitis is observed now and then, and
very rarely peritonitis, and even meningitis. These several affections,
together with delirium, coma, convulsions, chorea, and hyperpyrexia,
which are likewise occasional incidents of the disease, will be
considered under the head of non-articular manifestations and
complications of acute articular rheumatism.[27]

[Footnote 27: See observations of W. S. Cheesman, M.D., _New York
Medical Record_, Feb. 25, 1882, 202.]

Some of the symptoms of acute articular rheumatism need individual
notice.

The temperature in acute articular rheumatism maintains no typical
course, and usually exhibits a series of exacerbations and remissions,
which correspond closely in time and degree with the period, duration,
and severity of the local inflammatory attacks. As a very general rule
in average cases, the temperature attains by the end of the first or
second day to 102 degrees F., and while the subsequent evening
exacerbations may reach 104 degrees, 104.4 degrees, or very rarely 105
degrees, yet in the great majority of cases the maximum temperature
does not exceed 103 degrees F., and in a very considerable number falls
short of 102 degrees. An analysis of one of Dr. Southey's tables[28]
shows that in 84 cases of acute rheumatism 1 attained the temperature
of 105.8 degrees; 8, that of 104 degrees to 105 degrees; 15, that of
103 degrees to 104 degrees; 32, that of 102 degrees to 103 degrees; 17,
that of 101 degrees to 102 degrees; 10, that of 100 degrees to 101
degrees; and 1, that of 99.8 degrees; that is, the temperature was
below 103 degrees in five-sevenths, and below 104 degrees in about
ten-twelfths, of the whole. In very mild cases, in which but a few
joints are inflamed, and only to a slight degree, the temperature may
not reach 100 degrees at any time, and there may be intervals of
complete apyrexia. On the other hand, in a few rare severe cases of
rheumatic fever, especially when complicated with pericarditis,
pneumonia, or delirium, or other disturbance of the cerebral functions,
the temperature attains to 106 degrees, 108 degrees,[29] 109.4
degrees,[30] 110.2 degrees,[31] or even 111 degrees,[32] or 112
degrees. Such cases are now spoken of as examples of rheumatic
hyperpyrexia.

[Footnote 28: _St. Bartholomew's Hospital Reports_, xiv. p. 12.]

[Footnote 29: Weber, _Clinical Society's Trans._, vol. v. p. 136.]

[Footnote 30: Th. Simon, quoted by Senator, _Ziemssen's Cyclop. of
Prac. Med._, xvi. p. 46.]

[Footnote 31: Murchison and Burdon-Sanderson, two cases, _Clinical
Society's Trans._, vol. i. pp. 32-34.]

[Footnote 32: Ringer, _Med. Times and Gaz._, vol. ii., 1867, p. 378.]

There is no rule about the mode of invasion of this high temperature.
It may ensue gradually or suddenly, the previous range having been low,
moderate, or high, steady or oscillating.

Defervescence in rheumatic fever takes place, as a very general rule,
gradually--_i.e._ by lysis--but exceptionally it is completed in
forty-eight or even twenty-four hours. An interesting observation,
which will be of much prognostic value if it be confirmed hereafter,
has been made by Reginald Southey,[33] to the effect "that a short
period of defervescence, or a sudden remission and an early remission,
betokens the relapsing form of the disease, and the likelihood of
frequent relapses, as well as of slow ultimate recovery, in the direct
ratio as this defervescence has been early and abrupt."

[Footnote 33: _St. Bartholomew's Hospital Reports_, xiv. p. 16.]

{30} The characters of the urine in acute rheumatism are tolerably
uniform, but far from constantly so. Its quantity in the majority of
cases is reduced, frequently not exceeding twenty-four ounces per diem,
and occasionally not exceeding fourteen. This is owing in some degree
to profuse sweating, but also, as in other febrile affections, to
retention of water. Its density is usually high--1020 to 1030, or even
1035--which is due chiefly to its concentration, and not, as has been
generally supposed, mainly to an increase in the total solids
excreted.[34] Its color is a very dark red or deep reddish-yellow,
partly from concentration; but it is yet not known whether the deep hue
is partly from increase of the normal pigments or of one of them
(urobilin),[35] or from the presence of some abnormal coloring matter.
Its reaction is generally highly acid, and continues so for many hours
after its discharge, unless in subacute cases, when it is occasionally
neutral or sometimes alkaline at the time of its escape, or becomes so
in a very short time afterward. It is commonly toward the decline of
the attack that the urine becomes neutral or alkaline. As a very
general rule, the amount of urea and of uric acid excreted during the
febrile stage exceeds what is physiological, and begins to decline when
convalescence commences; but this may be reversed (Parkes,[36]
Lede,[37] Marrot[38]). The sulphuric acid is notably increased
(Parkes), the chlorides often diminished and sometimes absent, and the
phosphoric acid very variable (Beneke, Brattler[39]), but usually
lessened (Marrot).

[Footnote 34: See _Guy's Hospital Reports_, 3d Series, vol. xii. 441.]

[Footnote 35: Jaffe, _Virchow's Archiv_, xlvii. 405, quoted in
_Ziemssen's Cyclopaed. Prac. Med._, xvi. 41.]

[Footnote 36: _On Urine_, p. 286.]

[Footnote 37: _Recherches sur l'Urine dans le Rheumatisme Artic.
Aigue_, Paris, 1879.]

[Footnote 38: _Contribution a l'Etude du Rheumatisme Artic., etc._,
Paris, 1879, 41.]

[Footnote 39: Quoted by Parkes, _op. cit._, 290.]

During convalescence the urine increases in quantity, while, as a
general rule, the urea and uric acid lessen relatively and absolutely,
and the chlorides resume their normal proportions to the other
ingredients. The reaction frequently becomes alkaline, and the specific
gravity falls considerably, although not always as soon as the
articular inflammation subsides. Temporary albuminuria occurs very
frequently in the febrile and occasionally in the declining stage, but
generally disappears when convalescence is completed. It obtained on
admission in 8 out of 43 cases lately reported by Dr. Greenhow.[40] A
more abiding albuminuria, due very rarely to acute parenchymatous
nephritis, may be met with (Johnson, Bartels, Hartmann, Corm). Blood,
even in considerable amounts, has also rarely appeared in the
urine,[41] sometimes in connection with embolic nephritis and
endocarditis, for such appear to have been the nature of Rayer's
nephrite rheumatismale.[42]

[Footnote 40: _Lancet_, 1882, i. 913.]

[Footnote 41: _Clinical Lectures_, R. B. Todd, edited by Beale, 1861,
p. 346.]

[Footnote 42: _Traite des Maladies Reins_. See also Dr. Weber, _Path.
Trans. of London_, xvi. p. 166.]

The saliva, which is normally alkaline, has usually a decidedly acid
reaction in acute articular rheumatism, and Dr. Bedford Fenwick states
that it always in this disease contains a great excess of the
sulpho-cyanides, and that these slowly and steadily diminish, till at
the end of the third week or so they become normal in amount.

A profuse, very acid, sour-smelling perspiration is one of the striking
symptoms occurring in the course of acute articular rheumatism, and
{31} until very lately it has been generally held to indicate an
excessive formation in, and elimination of acid from, the system,
either lactic acid or some of the acids normal to the perspiration, as
acetic, butyric, and formic. However, not only have chemists failed to
detect lactic acid in the perspiration of acute rheumatism, but late
research tends to show that the excessive acidity of the perspiration
in this disease is but very partially due to the perspiration itself,
and is chiefly owing to chemical changes taking place in the overheated
and macerated surface of the skin and its epidermis, and to the
retention of solid products accumulated on that surface. Besnier says
that if in acute articular rheumatism or other disease attended with
much perspiration the surface be kept well washed, the sweat will be
found in the greater number of cases at the moment of its secretion to
be nearly neutral as soon as actual diaphoresis occurs, more decidedly
acid when the perspiration is less abundant or begins to flow, and
exceptionally alkaline. Most physicians are aware that the profuse
perspiration of acute rheumatism is non-alleviating; it is not a real
critical discharge of noxious materials from the system, nor is it
followed by prompt reduction of the temperature and other symptoms. It
is but a symptom of the disease, and occurs especially in severe cases,
and when it continues long after the reduction of the temperature it is
a source of exhaustion, and may be checked with advantage.

The blood is deficient in red globules, Malassez finding in men from
2,850,000 to 3,700,000 per cubic millimeter instead of 4,500,000 to
5,000,000, and in women 2,300,000 to 2,570,000 instead of 3,500,000 to
4,000,000. The haemoglobin and the oxidizing power of the blood are
also considerably reduced; the fibrin is largely increased (6 to 10
parts in 1000 instead of 3); the albumen and albuminates are lessened,
the extractives increased; the proportion of urea is normal, and no
excess of uric acid is found in the blood. Instead of that fluid being
less alkaline than normal, Lepine and Conard have recently stated that
its alkalinity is increased in acute rheumatism, but constantly
diminished in chronic rheumatism,[43] and no excess of lactic acid has
been proved to exist in the blood in either acute or chronic
rheumatism. A condition of excessive coagulability of the fibrin,
independently of its excessive amount (inopexia), is an habitual
character of acute rheumatism; however, in very bad cases, especially
those attended with hyperpyrexia and grave cerebral symptoms, the blood
after death has been black and coagulated and the fluid in the serous
cavities has given an acid reaction. The above alterations in the blood
usually are proportionate to the intensity of the fever and the number
of the joints and viscera involved.

[Footnote 43: Lepine, "Note sur la determination de l'Alcalinite du
Sang," _Gaz. Med. de Paris_, 1878, 149; Conard, _Essai sur l'Alcalinite
du Sang dans l'Etat de Sante, etc._, These, Paris, 1878.]

The manifestations of acute articular rheumatism other than the
articular are various, and some of them, more especially those observed
in the heart, may be regarded as integral elements of the disease, for
they occur in a large proportion of the cases, often coincidentally
with the articular affection, and may even precede it, and probably may
be the sole local manifestation of acute rheumatism, although under the
last-mentioned circumstances it is difficult to prove the rheumatic
nature of the ailment.

The cardiac affections may be divided into inflammatory and {32}
non-inflammatory. The former consist of pericarditis, endocarditis, and
myocarditis; the latter embrace deposition of fibrin on the valves,
temporary incompetence of the mitral or tricuspid valves, and the
formation of thrombi in the cavities of the heart. For practical
purposes haemic murmurs may be included in the latter group.

No reliable conclusions can be drawn respecting the gross frequency of
recent cardiac affections in rheumatic fever, for not only do authors
differ widely on this point, but they do not all distinguish recent
from old disease, nor inflammatory from non-inflammatory affections,
nor haemic from organic murmurs. Nor does it appear probable, from the
published statistics, that these differences are owing to peculiarities
of country or race. The gross proportion of heart disease of recent
origin in acute and subacute articular rheumatism was in Fuller's[44]
cases 34.3 per cent.; in Peacock's,[45] 32.7 per cent.; in Sibson's[46]
(omitting his threatened or probable cases), 52.3 per cent.;[47] in
3552 St. Bartholomew's Hospital cases analyzed by Southey,[48] 29.8 per
cent.; in Bouilland's cases, quoted by Fuller,[49] 5.7 per cent.; in
Lebert's,[50] 23.6 per cent.; in Vogel's,[50] 50 per cent.; in
Wunderlich's,[50] 26.3 per cent. I am not aware of any analysis,
published in this country, of a large number of cases of rheumatism
with reference to cardiac complications, but Dr. Austin Flint,[51]
after quoting Sibson's percentage of cases of pericarditis, which was
(63 in 326 or) 19 to the 100, remarks, "I am sure that this proportion
is considerably higher than in my experience."

[Footnote 44: _On Rheumatism, Rheumatic Gout, etc._, 3d ed., p. 280.]

[Footnote 45: _St. Thomas's Hospital Reports_, vol. x. p. 19.]

[Footnote 46: Reynolds's _Syst. of Med._, Eng. ed., vol. iv. 186.]

[Footnote 47: Those familiar with the accuracy and diagnostic skill of
the lamented Sibson will not hesitate to add his 13 cases of very
probable endocarditis to his 170 positive cases of cardiac inflammation
in 325 examples of acute rheumatism, which will raise his percentage to
56.3.]

[Footnote 48: _Lib. cit._, vol. xiv. 6.]

[Footnote 49: _Lib. cit._, 264.]

[Footnote 50: See Senator in _Ziemssen's Cyclopaed. Pract. of Med._,
xvi. 49.]

[Footnote 51: _Pract. Med._, 5th ed., 314.]

The frequency of cardiac complications in rheumatism is influenced by
several circumstances. Some unexplained influence, such as is implied
in the terms epidemic and endemic constitution, appears to obtain.
Peacock found the proportion of cardiac complications in rheumatism to
range from 16 to 40 per cent. during the five years from 1872 to 1876,
and a similar variability is shown in Southey's statistical table[52]
covering the eleven years from 1867 to 1877. Be it observed that these
variations occurred in the same hospitals and under, it may be
presumed, very similar conditions of hygiene and therapeusis. Youth
predisposes to rheumatic inflammation of the heart, so that it may
still be said that the younger the patient the greater the proclivity.
Of Fuller's cases, 58 per cent. were under twenty-one, and the
liability diminished very markedly after thirty. Of Sibson's cases, 62
per cent. were under twenty-one. In infancy and early childhood the
liability is very great, and at those periods of life the heart, and
more especially the endocardium, rarely escapes; and the cardiac
inflammation often precedes by one or two days the articular. The
careful observations of Sibson confirm the spirit, but not the letter,
of Bouilland's original statement, and proves that the danger of heart
disease is greater in severe than in mild cases of acute rheumatism,
and that this is especially true of pericarditis. (It may be remarked
here, en parenthese, that the number of joints affected is {33} very
generally in proportion to the severity of the attacks.) However, the
mildest case of subacute rheumatism is not immune from cardiac
inflammation, and it has occasionally been observed even in primary
chronic rheumatism.[53] Occupations involving hard bodily labor or
fatigue, whether in indoor or outdoor service, render the heart very
obnoxious to rheumatic inflammation. Existing valvular disease, the
result of a previous attack of rheumatism, favors the occurrence of
endocarditis in that disease. Some authorities maintain that treatment
modifies the liability to rheumatic affection of the heart, and this
will be spoken of hereafter. The period of the rheumatic fever at which
cardiac inflammation sets in varies very much, but it may be
confidently stated that it occurs most frequently in the first and
second weeks, not infrequently in the third week, seldom in the fourth,
and very exceptionally after that, although it has happened in the
seventh. An analysis of Fuller's experience[54] in 22 cases of
rheumatic fever and 56 of endocarditis--a total of 78--shows that the
disease declared itself under the sixth day in 8; from the sixth to the
tenth in 29; from the tenth to the fifteenth in 17; from the fifteenth
to the twenty-fifth in 18; and after the twenty-fifth in 6. The
friction sound was audible in Sibson's 63 cases of rheumatic
pericarditis--from the third to the sixth day in 10, and before the
eleventh day in 30, or nearly one-half of the whole. That observer
concludes "that in a certain small proportion of the cases, amounting
to one-eighth of the whole," the cardiac inflammation took place at the
very commencement of the disease, and simultaneously with the invasion
of the joints.[55]

[Footnote 52: _Lib. cit._]

[Footnote 53: Raynaud, _Nouveau Dict. de Med. et de Chir._, t. viii.
367.]

[Footnote 54: _Lib. cit._, pp. 77-278.]

[Footnote 55: _Lib. cit._, p. 209. See also Dickinson in _Lancet_, i.,
1869, 254; Bauer in _Ziemssen's Cyclopaed._, vi. 557.]

Of the several forms of rheumatic cardiac inflammation, endocarditis is
the most frequent, and in a large proportion of cases it may exist
alone; pericarditis is also very often observed, but it seldom is found
per se, being in the vast majority of cases combined with endo- and
occasionally with myocarditis. It is generally the ordinary verrucose
endocarditis that obtains. The ulcerative form occurs sometimes, and
should be suspected if in a mild or protracted case of acute rheumatism
endocarditis sets in with, or is accompanied by, rigors, and the
general symptoms are of pyaemic or typhoid character or both, even
although an endocardial murmur is not present, for extensive vegetating
ulcerative endocarditis frequently exists without audible murmur. It is
remarkable, as Osler has shown,[56] how few instances of ulcerative
endocarditis developing during the course of acute rheumatism are
reported; and I would add that by no means all of these were examples
of first attacks, chronic valvular lesions, the consequence of former
illness, existing in many of them at the time of the final acute
attack. Southey's[57] patient, and both of Bristowe's,[58] had had
previous rheumatic seizures. However, Peabody's case,[59] one of Ross's
three cases,[60] and Pollock's[61] case appear to have been examples of
ulcerative {34} endocarditis occurring during a first attack of acute
articular rheumatism. The united and thickened condition of two
segments of the aortic valve in one of Ross's cases indicates
old-standing disease, although no history of former rheumatism is
given. Goodhardt[62] has lately insisted upon the tendency of
ulcerative endocarditis to appear in groups or epidemics, but the
evidence is not conclusive.

[Footnote 56: _Archives Medecine_, vol. v., 1881; _Trans. International
Med. Cong._, vol. i. 341.]

[Footnote 57: _Clin. Soc. Trans._, xiii. 227.]

[Footnote 58: _Brit. Med. Jour._, i., 1880, 798.]

[Footnote 59: _Medical Record N.Y._, 24th Sept., 1881, 361.]

[Footnote 60: _Canada Med. and Surg. Journ._, vol. xi., 1882, 1, and
_ib._, vol. ix., 1881, 673.]

[Footnote 61: _Lancet_, ii., 1882, 976.]

[Footnote 62: _Trans. Path. Soc. London_, xxxiii. 52.]

Space will not permit any detailed description of the symptoms and
signs of endo- or pericarditis: these will be found in their proper
places in this work, but a few observations are needed upon
myocarditis, which occasionally occurs in combination with rheumatic
pericarditis, and is a source of much more danger than the latter is,
per se. Dr. Maclagan[63] is almost the only authority who recognizes
the occurrence of rheumatic myocarditis independently of inflammation
of the membranes of the heart. He maintains that the rheumatic poison
probably and not infrequently acts directly on the cardiac muscle; in
which case the resulting inflammation is apt to be diffused over the
left ventricle and to produce grave symptoms, while in other instances
the inflammatory process begins in the fibrous rings which surround the
orifices of the heart (especially the mitral), extends to the substance
at the base of the heart, and is there localized. As in this latter
form the inflammation usually extends also to the valves, "any symptoms
to which the myocarditis gives rise are lost in the more obvious
indications of the valvulitis." However, this limited inflammation of
the myocardium is not dangerous. Dr. Maclagan asserts that the more
diffused and dangerous inflammation of the walls of the left ventricle,
while always difficult, and sometimes impossible, of diagnosis, can be
determined with tolerable certainty in some cases. In this view,
however, he has been preceded by Dr. Hayden,[64] who states that the
diagnosis of myocarditis is quite practicable irrespective of the
accompanying inflammation of the membranes of the heart.

[Footnote 63: _Rheumatism: its Nature, Pathology, and Successful
Treatment_, 1881.]

[Footnote 64: _Diseases of the Heart and Aorta_, 1875, 746.]

From the observations of the author just named, as well as of many
others, it may be inferred that acute diffused myocarditis of the left
ventricle exists in rheumatic fever when either with or without
coexisting pericarditis there are marked smallness, weakness, and
frequency of pulse, anguish or pain or great oppression at the
praecordia, severe dyspnoea, the respiration being gasping and
suspirious, feeble, rapid, and irregular action of the heart, great
weakness of the cardiac sounds, and almost extinction of the impulse,
evidence of deficient aeration of the blood combined with coldness of
surface, tendency to deliquium, and when these symptoms and signs
cannot be fairly attributed to extensive pericardial effusion or to
pulmonary disease, or to obstructed circulation in the heart consequent
upon endocarditis with intra-cardiac thrombosis or upon rupture of a
valve. It might, however, be impossible to exclude endocarditis
complicated with thrombosis, conditions which do occur in rheumatic
endocarditis, or a ruptured valve, which, although rarely, has been
occasionally observed. Grave cerebral symptoms, delirium, convulsions,
coma, though frequently present, are not peculiar to acute
myocarditis.[65] {35} Hence, even with the above group of clinical
facts, the diagnosis at best can be but probable. The disease, too, may
be latent, or, like Stanley's[66] celebrated case, produce disturbances
of the cerebral system rather than of the circulatory.

[Footnote 65: In illustration see case by Southey in which the symptoms
and signs agree very well with the above description, and yet, although
the heart's substance was of dirty-brown color and the striation of its
fibre lost, Southey did not believe these appearances due to carditis.
(_Clin. Trans._, xiii. p. 29.)]

[Footnote 66: _Med.-Chir. Trans._, vol. vii.]

Dr. Maclagan has advanced the opinion that a subacute myocarditis is
not of uncommon occurrence in acute articular rheumatism, and may be
unattended by endo- or pericarditis. Such a condition, he says, may be
diagnosed when early in the course of the case the heart's sounds
quickly become muffled rather than feeble. As he quotes but one
case[67] in which an autopsy revealed alterations in the walls of the
heart, and as endocarditis and a little effusion in the pericardium
coexisted, it is premature to accept the evidence as final, and the
great importance of the subject demands further investigation.

[Footnote 67: _Lib. cit._, p. 175.]

Admitting with Fuller the occasional deposition of fibrin upon the
valves and endocardium in rheumatic fever independently of
endocarditis, the murmur resulting therefrom could not be reliably
distinguished from that of inflammatory origin. It remains to speak
briefly of temporary incompetence of the mitral and tricuspid valves
and their dynamic murmurs, and of haemic murmurs. Occasionally, in
severe cases of rheumatic fever, more especially in the advanced stage,
there may be heard a systolic murmur of maximum intensity either in the
mitral area or over the body of the left ventricle, unaccompanied by
accentuation of the second sound, or, as a general rule, by evidence of
pulmonary obstruction. Such murmurs are apt to be intermittent, and as
they disappear on the return of health, they have been satisfactorily
referred to temporary weakness of the walls of the heart, so that the
auriculo-ventricular orifices are not sufficiently contracted during
the ventricular systole for their valves to close them, and
regurgitation follows. Yet, inasmuch as Stokes distinctly mentions the
absence of murmur in many cases of softening of the heart in typhus, it
is probable that an excessive weakness of the ventricular wall is
incompatible with the production of murmur, and that the presence of
murmur in such circumstances is evidence of some remaining power in the
heart.

Dr. D. West[68] has published some cases of acute dilatation of the
heart in rheumatic fever which strongly corroborate these views. The
murmur in one of them became appreciable only as the heart's sounds
increased in loudness and the dilatation lessened. One ended fatally,
and acute fatty degeneration of the heart's fibres was found in
patches.[69] I believe that some of these temporary mitral murmurs in
acute rheumatism depend upon a moderate degree of valvulitis quite
capable of complete resolution. Sibson[70] has lately stated that he
has met with the murmur of tricuspid regurgitation without a mitral
murmur in 13 out of 107 cases of rheumatic endocarditis, and with a
recent mitral murmur in 27 out of 50 {36} cases. "The tricuspid murmur
generally comes into play about the tenth or twelfth day of the primary
attack, along with symptoms of great general illness;" it appears
earlier, as a rule, in those cases in which it is associated with
mitral regurgitation than when it exists alone; it is of variable
duration, but usually short--from one to nineteen days or more. He
regards it as of non-inflammatory origin, and dependent upon
regurgitation due to the so-called safety-valve function of the
tricuspid valve; and when limited to the region of the right ventricle
he infers that it is usually the effect and the evidence of
endocarditis affecting the left side of the heart. These novel
statements are confirmed by the observations of Parrot, Balfour, and
William Russell,[71] which go to prove that tricuspid regurgitation
occurs frequently in the more advanced stages of debility. No other
authority than Sibson, however, insists upon its frequent occurrence in
acute rheumatism.

[Footnote 68: _Barth. Hosp. Repts._, xiv. 228.]

[Footnote 69: On this subject see Stokes, _Dis. Heart and Aorta_, pp.
423, 435, 502; Stark, _Archives generales de Med._, 1866; DaCosta,
_American Journal Med. Sci._, July, 1869; Hayden, _Dis. Heart and
Aorta_, 1875; Balfour, _Clin. Lects. on Heart and Aorta_, 1876; Cuming,
_Dublin Quart. Jour. Med. Sci._, May, 1869; Nixon, _ib._, June, 1873.
I. A. Fothergill has seen several cases in which such mitral murmurs
have followed sustained effort in boys, and have disappeared after a
time: _The Heart and its Diseases_, 2d ed., 1879, p. 177.]

[Footnote 70: Reynolds's _System. Med._, Eng. ed., vol. iv. 463.]

[Footnote 71: See _Brit. Med. Jour._, i. 1883, 1053.]

The anaemia which is so striking a symptom of rheumatic fever,
especially when several joints are severely inflamed, coexists very
frequently with a systolic basic murmur, which is most often louder
over the pulmonary artery (in second left intercostal space and more or
less to left of sternum) than over the aorta. The murmur may appear
early in the disease, but sets in most frequently when the disease is
subsiding. When thus appearing late in a case accompanied by
endocarditis and pulmonary congestion, it is of favorable omen and
indicates improvement in the thoracic affection. The growing opinion,
however, respecting so-called anaemic murmurs is, that they depend
chiefly upon regurgitation through the tricuspid orifice, although Dr.
W. Russell refers them to pressure of a distended left auricle upon the
pulmonary artery.[72]

[Footnote 72: _Ib._, 1065.]

Pulmonary affections in form of pleuritis, pneumonia, or bronchitis are
common complications of rheumatic fever. Adding Latham's,[73]
Fuller's,[74] Southey's,[75] Gull and Sutton's,[76] Pye-Smith's,[77]
and Peacock's[78] cases together, we have a total of 920 in which some
one or more of the above pulmonary affections obtained in 109
instances, or 11.8 per centum. A further analysis of Latham's and
Fuller's cases shows that it is especially when rheumatic fever is
complicated with cardiac disease that the lungs suffer; thus, pulmonary
affections obtained in 26.5 per cent. of cases complicated with heart
disease, and in only 7 per cent. of cases free from that disease. It is
more especially when pericarditis complicates rheumatic polyarthritis
that pulmonary affections occur. Thus, these were found in only 10.5
per cent. of cases of recent rheumatic endocarditis, in 58 per cent. of
cases of pericarditis, and in 71 per cent. of cases of
endo-pericarditis. The tendency which inflammation of the pericardium
has to extend to the pleura probably partially accounts for the more
frequent association of the pulmonary affections with rheumatic peri-
than with rheumatic endocarditis. (Sibson found pleuritic pain in the
side twice as frequent in pericarditis, usually accompanied with
endocarditis (31 in 63), as in simple endocarditis, 26 in 108.[79]) But
the greater severity of those cases of rheumatic fever complicated with
peri- or endo-pericarditis must also have a decided influence in
developing the pulmonary affections. {37} Pneumonia and pleuritis are
very frequently double in rheumatic fever, and are often latent,
requiring a careful physical examination for their detection. So
suddenly does the exudation take place in some cases of rheumatic
pneumonia that the first stage is not to be detected either by symptoms
or signs. On the other hand, in some cases the absence of the typical
signs of hepatization, the want of persistence in the physical signs,
and their rapid removal, and even in rare instances an obvious
alternation between the pulmonary and the articular symptoms, suggest
that the process often stops short of true hepatization, and partakes
rather of congestion and splenization, with or without pulmonary
apoplexy--a view which has been occasionally confirmed by the
autopsy.[80]

[Footnote 73: Latham's _Works_, Syd. Soc., i. 98 _et seq._]

[Footnote 74: _Lib. cit._, 317.]

[Footnote 75: _Bartholomew Hospital Reports_, xv. 14.]

[Footnote 76: _Guy's Hosp. Reports_, 3d Series, xi. 434.]

[Footnote 77: _Ib._ xix. 324.]

[Footnote 78: _St. Thomas's Hospital Reports_, x. 12-17.]

[Footnote 79: Reynolds's _System Med._, iv. 233.]

[Footnote 80: Vide Sturges, _Natural History and Relations of
Pneumonia_, 1876, pp. 70-78; T. Vasquez, These, _Des complications
Pleuro-pulmonaires du Rheumatisme Artic. Aigue_, Paris, 1878, pp.
25-31; M. Duveau, _Dictionnaire de Med. et de Chir._, t. xxviii. p.
443.]

Active general congestion of the lungs has occasionally been observed
in this disease, and has proved fatal in five minutes[81] and in an
hour and a half[82] from the invasion of the symptoms. The rheumatic
poison frequently excites pleuritis, some of the characters of which
are--the suddenness with which free effusion occurs; the promptness
with which it is removed, only perhaps to invade the other pleura, and
then to reappear in the cavity first affected; the diffusion of the
pain over the side and its persistence during the effusion; and its
frequent concurrence with pericarditis, and in children with
endocarditis; its little tendency to become chronic, and its marked
proclivity to become double. It is often latent and unattended with
pain. Sibson asserts that if in rheumatic pericarditis "pain over the
heart is increased or excited by pressure over the region of the organ,
it may with an approach to certainty be attributed to inflammation of
the pleura," etc. The product of the inflammation is commonly serous,
but occasionally purulent.

[Footnote 81: _These d'Aigue pleur._, 1866, par B. Ball.]

[Footnote 82: M. Aran, quoted by Vasquez, _lib. cit._, p. 14.]

The disturbances of the nervous system are amongst the most important
complications of acute rheumatism, and are due either to functional
disorder or very rarely to obvious organic lesions of the nerve-centres
or their membranes. The dominant functional disturbance may be
delirium, which is greatly the most frequent; or coma, which is rare;
or chorea, very frequently observed in children; or tetaniform
convulsions, which occur very seldom per se. As a rule, two or more of
these forms coexist or alternate with or succeed one another, and the
grouping, as well as the variety, of the symptoms may be greatly
diversified. In 127 observations there were 37 of delirium only, 7 of
convulsions, 17 of coma and convulsions, 54 of delirium, convulsions,
and coma, 3 of other varieties (Ollivier et R., cited by Besnier).

Rheumatic Delirium.--Either with or without subsidence of the articular
inflammation, about from the eighth to the fourteenth day of the
illness, but occasionally at its beginning, or sometimes on the eve of
apparent convalescence, the patient becomes restless, irritable,
excited, and talkative; sleep is wanting or disturbed; some excessive
discharge from the bowels or kidneys occasionally occurs; profuse
perspiration is usually present, and may continue, but frequently
lessens or altogether ceases; the skin becomes pungently hot, the
temperature generally--not always, however--rising rapidly toward a
hyperpyrexial point, and ranging from {38} 104 degrees to 111 degrees;
and transient severe headache and disturbances of special sense
sometimes obtain. At a later period, or from the outset in hyperacute
cases, flightiness of manner or incoherence in ideas is quickly
succeeded either by a low muttering delirium, twitchings of the
muscles, violent tetaniform movements and general tremors, and a
condition perhaps of coma-vigil, or by an active, noisy, even furious,
delirium. The articular pains are no longer complained of, and
sometimes the local signs of arthritis also quickly disappear; but
neither statement is uniformly true. The pulse becomes rapid;
prostration extreme; semi-consciousness or marked stupor gradually or
rapidly supervenes; the temperature continues to rise; the face,
previously pale or flushed, becomes cyanotic; and very frequently death
ensues, either by gradual asthenia or rapid collapse, often preceded by
profound coma or rarely by convulsions. Deep sleep often precedes
prompt recovery.

The duration of the nervous symptoms varies from one or two, or more
usually six or seven, hours in very severe cases, to three or four days
in moderate ones, or occasionally seven, eight, or sixteen[83] or
twenty-nine days[84] in unusually protracted cases. In the
last-mentioned, however, the delirium is not usually constant, and
frequently disappears as the temperature falls, and recurs when its
rises. Moreover, a rapid and extreme elevation of temperature is
frequently altogether wanting.

[Footnote 83: Southey's case, _Clin. Soc. Trans._, xiii. p. 25.
Sleeplessness preceded it for four days, and there was no
hyperpyrexia.]

[Footnote 84: Graham's case, _ib._, vi. p. 7. Delirium set in on the
seventh day of illness, and three days after invasion of joints.
Temperature 104.8 degrees early in disease; never exceeded 106 degrees,
probably owing to repeated use of cold baths. Temperature at death,
104.2 degrees.]

No real distinction can be established between these protracted cases
of rheumatic delirium and so-called rheumatic insanity, in which occur
prolonged melancholia, with stupor, mania, hallucinations, illusions,
etc., often associated with choreiform attacks. This variety may be of
short duration or continue until convalescence is established, or may
rarely persist after complete recovery from the articular affection.

Coma may occur in acute rheumatism without having been preceded or
followed by delirium or convulsions, although it is very rare; and,
like delirium, it may obtain without as well as with peri- or
endocarditis or hyperpyrexia. It usually proves very rapidly fatal. In
Priestly's case, an anaemic woman of twenty-seven, during a mild attack
of acute rheumatism, one night became restless; at 3 A.M. the pain
suddenly left the joints; apparent sleep proved to be profound coma,
and at 6 A.M. she was in articulo mortis.[85] Southey relates the
history of a girl of twenty who, without previous delirium or high
temperature, suddenly became unconscious, and died in half an hour.[86]
One of Wilson Fox's cases had become completely comatose, and was
apparently dying nine hours after the temperature had rapidly risen to
109.1 degrees, when she was restored to consciousness by a cold bath
and ice to her chest and spine.[87]

[Footnote 85: _Lancet_, ii., 1870, 467.]

[Footnote 86: _Clin. Soc. Trans._, xiii. p. 29.]

[Footnote 87: _The Treatment of Hyperpyrexia_, 1871, 4.]

Convulsions of epileptiform, choreiform, or tetaniform character
frequently succeed the delirium, but in exceptional cases they occur
independently of it, and may even prove fatal.

Besides the choreiform disturbances which occur in connection with
delirium, stupor, tremor, etc. in cerebral rheumatism, simple chorea is
{39} frequently observed as a complication or a sequence, or even as an
antecedent, of acute articular rheumatism, and they occasionally
alternate in the same patient and in the same family. Chorea is perhaps
most frequently seen in mild cases and in the declining and
convalescent stages of rheumatic fever, and, while very common in
childhood and adolescence (five to twenty), it is very rare later in
life.

Such are the chief functional disturbances of the brain met with in
rheumatic fever, and the post-mortem examination reveals in them either
quite normal naked-eye appearances, or more frequently, especially in
rapidly fatal cases, general congestion of the pia mater, and to a less
degree of the cerebral substance, or in more protracted cases a greater
or less increase of transparent or opalescent serum in the subarachnoid
space and ventricles. The serum may be slightly or deeply tinged with
blood. If the serous or sero-sanguinolent effusion be considerable, the
encephalic mass or portions of it may be anaemic. But besides these
conditions, which are also commonly observed in many other febrile
diseases, and which are probably only concomitants of the functional
disturbance arising in the advanced stage of acute articular
rheumatism, certain organic affections of the nervous centres or their
membranes occasionally occur in this disease, and are plainly the cause
of the cerebral disturbance observed during life. Cerebral meningitis,
although very rare as a complication of acute articular rheumatism,
except in certain hot climates, like that of Turkey,[88] does occur,
and lymph or pus is found, usually over the convexity of the brain, but
sometimes at the base and down the cord.[89] The symptoms of rheumatic
cerebral meningitis are very like those of rheumatic delirium;
vomiting, and even, but less frequently, pain in the head, may be
absent, while hyperpyrexia may coexist (Foster's case), although not
necessarily present. Should the pulse from being frequent become slow
and irregular, and any paralytic symptoms ensue, meningitis may be
suspected. In some of these cases the meningitis is a consequence of
ulcerative endocarditis and embolism of the cerebral vessels,[90] but
in others it obtains without endocarditis or any purulent formation
elsewhere than in the meninges, as there is probably a true rheumatic
localization like pericarditis. The articular inflammation may continue
after the invasion of the meningitis, or the latter may promptly follow
the disappearance of the former, as though a metastasis of morbid
action had taken place.[91] In many instances, according to Ollivier,
Ranvier, Behier, and others, although the macroscopic signs of
meningitis are absent, the microscope detects proof of its presence in
the existence of an increased number of vessels, fatty granulations on
their walls, proliferation of nuclei and capillary
extravasations--histological conditions identical with those found in
the mild degrees of rheumatic inflammation of the joints.

[Footnote 88: Senator, in _Ziemssen_, xvi. 50.]

[Footnote 89: Watson's _Prac. Physic_, 1872, Am. ed. vii. 335; Fyfe,
_Med. Gazette_, vol. xxix. 703; Fuller, _lib. cit._, 302; Leudet,
_Clin. Medicale_, 139; Dowse, _London Lancet_, ii. 1872, 9; Foster,
_ib._, ii. 1868, 115; Hicks, _New York Medical Record_, Nov., 1878,
404.]

[Footnote 90: That ulcerative endocarditis frequently produces
meningitis is illustrated by Osler's cases, 4 out of 7 of which were
complicated with purulent meningitis: _Transactions of International
Med. Congress_, 1881, i. 344.]

[Footnote 91: See a case reported by W. L. Ramsey in _New York Medical
Record_, i., 1881, p. 9.]

Embolism of the cerebral arteries, producing meningitis, or more
frequently softening of the cerebral substance or hemorrhage, or
proving {40} fatal before necrobiosis has time to set in, is an
occasional complication of acute articular rheumatism. A young lady,
while under my care suffering from her first attack of articular
rheumatism complicated with endocarditis, became suddenly hemiplegic
and aphasic, and died twelve hours later. In a girl of thirteen, the
subject of acute articular rheumatism complicated with ulcerative
endocarditis, right hemiplegia suddenly occurred, and at the autopsy
Bristowe found an embolon in the left middle cerebral artery and a
softened area in the left corpus striatum. Bradbury reports a primary
acute rheumatism with endocarditis, delirium, and coma, but without
paralysis, in which a plug was found in the right middle cerebral
artery, but the brain was quite healthy.[92]

[Footnote 92: _Lancet_, ii., 1870, 148; also a case in _Lancet_, i.,
1882, p. 605: in eighth week of subacute articular rheumatism;
embolism; right hemiplegia. Autopsy: large vegetations on valves;
obstruction in middle cerebral artery.]

Very much the same observations are applicable to the disturbances of
the spinal cord and its envelopes in rheumatic fever as have been made
in reference to those of the cerebrum and its coverings. They may exist
with or without any alteration of the cord or membranes to which they
can be reliably referred; that is to say, they may be simply functional
in the peculiar sense in which that word is now understood, or they may
be connected with obvious structural changes, and chiefly with those
indicating inflammation of the membranes or substance of the cord. The
spinal symptoms may precede the articular affection, but generally
appear after it. They sometimes closely resemble those of idiopathic
tetanus,[93] or of spinal meningitis, or of myelitis, or of
meningo-myelitis; and in the last case, along with severe rachialgia,
muscular rigidity, cutaneous and muscular hyperaesthesia, and neuralgic
pains, there will occur numbness and more or less paralysis of the
lower extremities,[94] bladder, and rectum (paraplegia). These spinal
disturbances may or may not be accompanied by hyperpyrexia, and when
simply functional they are usually less severe and persistent, have a
greater tendency to alternate with one another and with the articular
affection, and are more amenable to treatment, than when due to those
very rare complications of rheumatic fever, spinal meningitis or
meningo-myelitis. The inflammation may involve both the cerebral and
spinal membranes at the same time.

[Footnote 93: Bright's case, 2, _Med.-Chirurgical Transactions_, xxii.
4; Dr. E. C. Mann, _N.Y. Medical Record_, 1875, 38; Bouilland, _Traite
sur les Maladies du Coeur_, t. i. p. 33.]

[Footnote 94: Leudet, _lib. cit._, p. 139; Dowse, _Lancet_, i., 1872,
9.]

The causes of these disturbances of the nervous system, when not
attributable to appreciable lesions, such as congestion, inflammation,
hemorrhage, embolism, thrombosis, and softening, are not established.
The following appear to be reasonable conclusions from the facts at
present known:

The most constant condition, and without which these cerebral symptoms
very rarely arise, appears to be some susceptibility or vulnerability
of the nervous system, inherited or acquired, rendering it apt to be
disturbed by influences which less susceptible centres would
successfully resist. Trousseau, who has especially advocated this
view,[95] considered intemperance in the use of spirits to be a
frequent source of this nervous predisposition. Accepting this neurotic
predisposition as the factor generally present when acute articular
rheumatism is complicated {41} with disturbances of the nerve-centres,
we may inquire what are the circumstances in the disease capable of
developing into activity the predisposition.

[Footnote 95: _Clin.-Med._, Syd. ed., i. 513 _et seq._]

Unquestionably, the existence of acute pericarditis, or of
endocarditis, or of inflammation of the lungs or pleura, is one of
those conditions.

Probably hyperpyrexia acts in some cases as an exciting cause of the
nervous phenomena, for while the delirium preceded the hyperpyrexia in
6 cases, it accompanied it in 19 and followed it in 10;[96] and the
nervous symptoms disappear when the hyperthermia is removed by the
employment of cold, and recur with the return of high temperature. The
phenomena of sunstroke and heat-apoplexy prove that a high temperature
is capable of producing convulsions and coma. That these grave cerebral
disturbances are so infrequent in acute rheumatism (obtaining in about
3 or 4 per cent. only) is probably owing to the usual moderate range of
temperature and the rarity of hyperpyrexia in the disease. Still, while
hyperpyrexia is a disturber of cerebro-spinal function, too much
importance must not be attached to it, for not only does such
disturbance very frequently precede the hyperpyrexia, but there are
many facts indicating that the hyperpyrexia is itself very frequently,
like the delirium, tremor, and coma which precede or accompany it, but
a consequence of disorder, usually of a paralyzing kind, of the
nerve-centres. It has been met with in lesions of the pons, in tetanus,
in injuries of the cord, in some cases of non-inflammatory softening of
the brain and of cerebral hemorrhage; that is, in a class of affections
not belonging to the specific fevers, but to those directly disturbing
or destroying the functions of the nerve-centres. And cases of acute
rheumatism do rarely occur in which a very high temperature is not
accompanied by cerebral disturbances. Sibson quotes two such,[97] one
of which, with a temperature of 110.8 degrees, was only restless and
talked when asleep, and the other, with a temperature of 106.3 degrees,
presented only vomiting and dyspnoea. Cardiac inflammation was absent
in both. DaCosta relates one in his valuable paper upon cerebral
rheumatism in which, although the temperature was 110 degrees, no
cerebral symptoms nor cardiac affection existed.[98]

[Footnote 96: "Abstract Report upon Hyperpyrexia in Ac. Rheum.," _Brit.
Med. Jour._, 1882, p. 807.]

[Footnote 97: _Lib. cit._, p. 264.]

[Footnote 98: This essay contains a record of 11 cases of cerebral
rheumatism and several autopsies: _Am. Jour. Med. Sci._, 69, 1845, p.
36, case xi.]

The goodly number of instances lately published in which grave cerebral
symptoms have obtained in acute articular rheumatism at ordinary
febrile temperatures, while they prove that hyperthermia is not an
essential condition productive of such symptoms, require to be
explained. Some such, no doubt, have been instances of marked
predisposition, so that a moderate febrile temperature or some
complication sufficed to disturb the brain, as we see in typhoid and
other fevers, in pneumonia, etc. If there be a rheumatic poison--which
has not yet been proved--it may, in predisposed persons, produce the
cerebral symptoms. The argument[99] that such poison should produce
inflammation of the nervous centres if it acted directly on them is not
convincing. It need not necessarily produce similar alterations in
serous or synovial membranes and in nervous tissues. Many toxic agents
disturb, and even suspend, the {42} cerebro-spinal functions, and leave
no appreciable changes in them. Do these cases prove that there is
something peculiar to rheumatic fever which tends to disturb the
nervous centres? Hardly; for while such disturbance is comparatively
rare in that disease, it is observed frequently in many other febrile
affections, notably in typhus, scarlatina, and small-pox; and as in
these, so in rheumatic fever, it is more often observed in the severe
than in the mild cases, as though it were a part of the systemic
disturbance incident to the febrile affection and largely proportionate
to its severity.

[Footnote 99: Maclagan, _Rheumatism: Its Nature, Pathology, etc._,
1881, 287.]

Yet there is something special in acute rheumatism which perhaps has to
do with the occurrence as well as the severity of the cerebro-spinal
symptoms and of the hyperpyrexia; viz. the long duration and severity
of the pain, and the number and importance of the parts, in addition to
the articulations, which are one after the other or simultaneously
involved in severe inflammation--peri-, endo-, myocardium, lungs,
pleura, etc. Perhaps in no other acute febrile disease are so many
distinct and important organs involved in inflammation at the same time
or in rapid succession; and it is no wonder that the functions of the
nervous system should in consequence become greatly depressed,
exhausted, or disturbed.

The kidneys appear very rarely to suffer serious disease in acute
rheumatism, if we except embolism of their arteries due to
endocarditis; and it is very doubtful whether the rare instances[100]
in which an acute parenchymatous nephritis has been observed in acute
rheumatism can be referred to direct rheumatic inflammation, or not,
rather, to the operation of the exposure which induced the rheumatism.
Further investigation is needed to determine whether interstitial
nephritis is even very exceptionally an indirect consequence of
rheumatism, as Lancereaux admits.

[Footnote 100: See DaCosta's cases 1 and 2, _Cerebral Rheumatism, lib.
cit._; case 1 certainly favors the view that either the rheumatic
poison, if there be such, or the constitutional disturbance incident to
acute polyarticular rheumatism, may sometimes produce nephritis. See
also a case by A. Deroye, These, Doctorat, Paris, 1874, quoted by P.
Coubere in _Contribution a l'Etude des Complications Renales du
Rheumatisme Artic. Aigue_, Paris, 1877.]

The other complications, being of less importance, must be but barely
alluded to. A pharyngitis attended with severe dysphagia and high fever
occasionally precedes the other symptoms or occurs in the early stage
of the disease. Gastralgia, enteralgia, simple serous diarrhoea, and
dysentery also rarely occur in acute rheumatism. That they are
sometimes, at least, truly rheumatic appears probable from the
circumstance that they may precede, follow, or alternate with the
articular affection, and are all intensely painful. I have but once met
with acute peritonitis as a complication of acute rheumatism; the
immunity of this serous membrane from rheumatic inflammation is an
inexplicable anomaly in view of the proclivity of the pericardium and
pleura to that process. Cystitis and orchitis are rare.

Several cutaneous affections are not unfrequently observed in relation
with acute rheumatism. Besides sudamina and miliaria rubra, which are
very common as consequences of the excessive perspiration,[101] there
{43} are others which may be themselves rheumatic manifestations. Such
are especially erythema marginatum,[102] e. papulatum, and e. nodosum.
A well-marked urticaria frequently precedes acute rheumatism in a
friend of the writer's; it may occur during its course or soon after
the cessation of the pains. Scarlatiniform eruptions are occasionally
observed, and very rarely punctiform hemorrhages--peliosis rheumatica
or rheumatic purpura. The purpuric symptom may be accompanied by
erythema or urticaria, and may precede, accompany, or alternate with
other rheumatic manifestations. Unlike purpura variolosa and idiopathic
purpura haemorrhagica, this variety appears to be free from danger.

[Footnote 101: Dr. J. T. Metcalfe of New York many years ago showed me
a case of rheumatic fever in which the sweat-vesicles had run together,
forming, instead of the usual pearly globular vesicles, irregular flat
blebs, some of them equal in area to seven or nine primary vesicles,
filled with transparent fluid, and this fluid could be displaced by
pressure to adjacent parts, as though it lay simply under the
superficial epidermic layer. I have seen several similar cases since.]

[Footnote 102: Dr. Palmer relates a case complicated with erysipelas
and peritonitis in _Boston Med. and Surg. Journal_, 1868.]

Besides a slight local oedema affecting the malleoli, scrotum, eyelids,
etc., or accompanying the cutaneous eruptions just mentioned, a more
decided infiltration of the subcutaneous cellular tissue occasionally
exists in the vicinity of the inflamed joints and tendinous sheaths,
and more rarely extends to an entire limb, which may not only be
considerably enlarged and painful and resemble a milk leg, but may be
red, hot, and tender, and excite suspicion of phlegmonous erysipelas.
Phlebitis, although infinitely less frequent than in gout, has been
observed in acute articular rheumatism.[103] Jaccoud in 1871[104]
mentioned the exceptional occurrence of subcutaneous nodosities in
rheumatism, which he says Froriep first pointed out;[105] but Homolle
states that they had been previously mentioned by Sauvage and
Chomel.[106] Since then several independent observers have met with
this affection, and Drs. Thomas Barlow and Francis Warner of London
have lately written a short valuable paper upon the subject based upon
27 cases which they had separately or conjointly investigated. From
their paper the following account is chiefly derived:[107] These
nodules may vary in number from one to fifty, and in size from that of
a pin's head to the volume of an almond, and are quite subcutaneous,
firm and elastic, painless, and freely movable. They are not usually
attached to the skin, but to the tendons, deep fasciae, pericranium,
periosteum, etc.; the integument over them is free from heat, redness,
and infiltration, although exceptionally tenderness on pressure and
slight redness may exist over them. They are found most frequently on
the back of the elbow, the malleoli, and margins of the patella, but
occur occasionally on the extensor tendons of the hand and foot, the
scapular spine and iliac crest, the temporal ridge and superior
occipital curved line, the ear, etc. These nodules occur singly or in
clusters, and are often symmetrical; they are very rapidly developed in
crops or in succession, and last sometimes for a few hours, more
frequently from three or four days to four or five months, or even
eighteen to thirty months. The original formations may disappear, and
be succeeded by fresh ones; and sometimes, when no longer perceptible
by touch, they may be found post-mortem. Their development is
unattended by pyrexia, unless pleuritis, pericarditis, or other
condition coexist to which the pyrexia might {44} be referred. These
nodosities do not appear to suppurate or ossify or become infiltrated
with urate of soda, and histologically they resemble organizing
granulative tissue. As regards their pathological associations, Drs.
Barlow and Warner found evidences of rheumatism in 25 out of 27 cases;
a morbid condition of the heart existed in all of them, and chorea in
10 of them. Two of the conclusions formulated by the authors just
mentioned are of great importance: that these subcutaneous nodosities
"may be considered as in themselves indicative of rheumatism, even in
the absence of pain;" that, while unimportant in themselves, they are
"of serious import, because in several cases the associated heart
disease has been found actively progressive." Dr. Dyce Duckworth has
reported two cases in which these nodules occurred in adults, lasted
eighteen months in one, and were still present in the other case after
thirty months, and were attached to the skin and periosteum. In one of
them the nodules were very painful and ached more in cold weather, and
the patient had no history of rheumatism or of chorea, although her
mother and one sister had.[108] In Dr. Stephen Mackenzie's case the
woman was the subject of tertiary syphilis, and had no personal history
of rheumatism or chorea, and she was free from heart disease; but her
family history was not given.[109]

[Footnote 103: _Phlebite Rheumatismale Aigue_, Paris, 1869, par M.
Lelong. In _Revue de Med._, t. i. 492-499, 1881, a case by Dr.
Launois.]

[Footnote 104: _Pathologie Interne_, ii. 546, 1871.]

[Footnote 105: _Die Rheumatische Schwiele_, Weimar, 1843.]

[Footnote 106: _Lib. cit._, p. 628.]

[Footnote 107: _Trans. International Medical Congress_, London, vol.
iv. pp. 116-128, 1881. In this paper, and in an article by MM. E.
Troisier and L. Brock, to be found in _Revue de Medecine_, t. i.
297-308, 1881, are references to the authors who had written upon it.]

[Footnote 108: _Brit. Med. Journ._, i., 1883, 868.]

[Footnote 109: _Ibid._, i., 1883, 867.]

The course and duration of acute polyarticular rheumatism vary very
much, and are apparently influenced by several circumstances, such as
the severity or the mildness of the articular affection, as well as of
the constitutional disturbance; the presence or not of complications;
the state of health of the patient about the time of the attack, and,
probably, the existence or not of a proclivity to the disease; and
whether the disease present the continued or the relapsing type. As a
tolerably general rule, when the constitutional symptoms are acute, the
skin hot, the perspiration free and very acid, the urine of high
density, color, and acidity, and several of the articulations are
swollen and very painful--when no serious complication, and especially
no severe cardiac affection, exists, and when the patient is endowed
with a fair constitution and with organs not damaged by previous
disease, the course of the fever is tolerably short and continuous, and
the recovery more or less prompt. Amongst the most reliable evidences
of approaching recovery in such cases is the tongue becoming clean and
losing its red color and the urine increasing considerably in quantity,
but containing a large proportion of solid matter, as indicated by a
high density.

On the other hand, a large proportion of cases run a more irregular and
protracted course, and more or less marked relapses succeed real but
temporary improvements, the local disturbance affecting fresh joints or
reappearing in those previously attacked, and the general symptoms
resuming renewed activity. The duration of the active symptoms in these
cases is considerable, seldom under six weeks, and frequently occupying
seven, eight, or more. In these protracted cases the symptoms, as a
rule, are usually rather milder, the perspiration not as profuse or
sour, the urine of less density and acidity, the articulations less hot
and painful, than in the previously described group. Sometimes, indeed,
the perspiration and the urine are of neutral or even faintly alkaline
reaction. It is not only the unexplained tendency to relapse which
protracts these {45} cases, but sometimes in addition an established
proclivity to the disease--the rheumatic habit--or a condition of
previous unsound or frail health.

Such cases occasionally pass into the subacute form, or the mild
febrile symptoms gradually and finally decline, and the joints may
either remain tender, swollen, and stiff some time longer, or these
signs of recent inflammation may soon disappear and leave the
articulations merely weak.

Many cases of acute rheumatism embody several of the features of the
two groups just described, and no definite course or duration of acute
articular rheumatism can be accurately laid down.

The course and duration of acute polyarticular rheumatism have received
a good deal of attention of late years. But Dr. Austin Flint[110] was
one of the first to study the natural history of the disease
uninfluenced by active treatment, and he was followed in 1865,[111]
1866,[112] and 1869[113] by Sir William Gull and Dr. Sutton, who
treated a series of cases without medicine, unless mint-water be so
regarded. The mean duration of Flint's 13 cases from the date of attack
to convalescence, excluding one in which pericarditis and pneumonia
occurred, was a fraction under twenty-six days. It is unfortunate that
the number of cases was so small, and that 11 of the patients were
females, who appear to be especially subject to the milder and more
protracted attacks of the disease. A larger number, with an equal
proportion of the sexes, would probably have given a different result.

[Footnote 110: _American Journal of Med. Sciences_, July, 1863.]

[Footnote 111: _Ib._, vol. xii.]

[Footnote 112: _Medico-Chirurgical Transactions_, vol. lii.]

[Footnote 113: _Guy's Hospital Reports_, 2d Series, vol. xi.]

Gull and Sutton have published the natural histories of 62 cases--viz.
of 41 in their first series, of 8 more in their second, and of 13 more
in their third. The average duration of the acute symptoms was, in the
first series, 8.5 days, in the second, 9 days, and in the third, 10
days, giving an average of 9.1 days for the duration, after admission
to hospital, of the acute symptoms of acute polyarticular rheumatism
when there is no very severe cardiac disease. In their third paper,
based upon 13 new cases and 12 of those published in their two previous
communications, they conclude "that rheumatic fever uncomplicated with
any very severe heart affection tends to run its course in nineteen
days, calculating from the time the rheumatic symptoms first set in to
their termination."[114] Yet an analysis of the 23 of the 41 cases
contained in their first series[115] respecting which the duration of
the rheumatic symptoms before admission and from admission to complete
convalescence is given, shows that the period occupied from the setting
in of the rheumatic symptoms to convalescence was in the 13 male
subjects 25.8 days, and in the 10 female 42 days, or, including both
sexes, the average duration was 32.8 days--_i.e._ 6.8 days longer than
Flint's result.

[Footnote 114: _Med.-Chir. Trans._, lii. 82.]

[Footnote 115: _Guy's Hospital Reports_, xi. 435.]

As Gull and Sutton had especially pointed out the class that tends to
assume acute characters and recover more quickly than any other, and
the class that runs a protracted course and tends to relapse, it is
somewhat remarkable that they did not tabulate the cases belonging to
those classes separately, and show distinctly their differences in
duration and {46} modes of convalescence. This has been attempted by
Southey,[116] but, unfortunately, his conclusions, as will hereafter
appear, have not been confirmed by other observers.

[Footnote 116: _St. Bartholomew's Hospital Reports_, xiv., and _ib._,
xv.]

Finally, in this connection, after carefully weighing ten subjects of
acute articular rheumatism during their illness and until they had
regained their usual weight, A. Roussel[117] found that the time during
convalescence occupied in regaining the weight previously lost was
inversely proportional to the duration of the attack.

[Footnote 117: _Essai sur la Convalescence du Rheumatisme Artic.
Aigue_, Paris, 1881, 66.]


Subacute Articular Rheumatism.

Under this head Charcot, Besnier, and Homolle describe an affection
which corresponds closely with one variety of the disease commonly
called rheumatoid arthritis, but the writer employs the term with the
same significance as most modern English authors (Garrod, Sutton,
Flint, Maclagan). It is milder yet more enduring than the acute form,
but their symptoms are identical in kind. It is usually subacute from
the outset, although occasionally succeeding the acute type. The
febrile disturbance is but slight, rarely reaching 101 degrees, and the
perspiration is less abundant; there is less pain, heat, and tenderness
in the joints, and only a few of them are involved together; but
although the articular affection moves from joint to joint, it persists
for weeks or months in several of them or in one only, improving and
relapsing generally without apparent reason. However, it does not
seriously damage the articulations, and they ultimately quite recover.
Mild cardiac affections also occur, but less frequently, and the
serious disturbances of the cerebral and respiratory systems are very
seldom met with. The gradations between subacute articular rheumatism
and the acute form on the one hand, and the simple chronic form on the
other, are almost innumerable. Marked anaemia is as much a feature of
subacute as of acute articular rheumatism, and its victims are often of
unhealthy or asthenic constitution, and subject to recurring attacks of
the disease on but slight provocation. The return of warm weather often
relieves such cases.

THE MORBID ANATOMY OF ACUTE AND SUBACUTE ARTICULAR
RHEUMATISM.--Although opportunities of ascertaining the conditions of
the articulations in acute articular rheumatism are rare, yet it is now
established that the process is an inflammation involving chiefly the
synovial membrane, and to a less degree the cartilages, ligaments,
tendinous sheaths, and in some cases even the bones and periarticular
soft parts. The synovial membrane is more or less injected and reddened
diffusely or in patches, especially where it forms fringe-like folds
and at its line of union with the cartilage. It is somewhat thickened,
opaque, and devoid of its satin-like lustre, and in somewhat protracted
cases covered here and there with a thin, easily detached
neo-membranous formation. Within the articulations will be found from a
few drops to one or two ounces of a viscid, pale, citron- or
reddish-colored fluid, like synovia, but more fluid, and generally
turbid and containing transparent or semi-opaque gelatinous masses or
albumino-fibrinous flocculi. The {47} microscope reveals in the
effusion large detached spherical epithelial cells in various stages of
germination or of fatty degeneration, and a variable number of red
blood-corpuscles and pus-cells. Very exceptionally, the effusion is
mixed with more or less true pus. In two out of the eight fatal cases
reported by Fuller, in which the joints were examined, pus in moderate
quantity was found along with other products in some, but not in all,
of the inflamed articulations, and one of them was complicated with
erysipelas, the other with sloughs over both trochanters. In very
severe forms complicated with hemorrhagic tendencies the inflammatory
products have contained a large proportion of blood. Cornil et
Ranvier[118] insist that even in slight cases of rheumatic arthritis
the diarthrodial cartilage constantly suffers changes arising from
nutritive irritation and proliferation of the cartilage-cells. At first
the cartilage loses here and there some of its polished hyaline
appearance, and the microscope reveals a finely-striated condition of
its structure which gives it a velvety aspect. When the inflammation
has been more severe and of longer duration, so that the deeper layers
have been involved, the unaided eye will perceive local swellings in
which the natural elasticity and resistance of the cartilage are
impaired, and its surface is fissured or villous-like in appearance.
"In certain rare cases of mono-articular acute arthritis true
ulcerations of the cartilage are observed."

[Footnote 118: _Manual d'Histologie pathologique_, Paris, 1869, 406.]

The soft parts in the immediate vicinity of the inflamed joints may be
in some cases more or less congested and oedematous, and the tendinous
sheaths, and even the bursae mucosae, inflamed and distended with
inflammatory products like those in the articulations. Charcot,[119]
holding the opinion that arthritis deformans is but a chronic variety
of articular rheumatism, quotes Gurlt's statement that in acute
articular rheumatism "the medullary tissue of the ends of the bones
undergoes a great increase of vascularity, with proliferation of its
corpuscles," and remarks that Hasse and Kussmaul have also referred to
lesions of the bone and periosteum in that disease. But the condition
of the osseous parts of the joints in acute articular rheumatism can
hardly be said to be known, and it is premature to speak positively
respecting it.

[Footnote 119: _Clinical Lectures on Acute and Chronic Diseases_,
Sydenham Soc., 1881, p. 148.]

Finally, in subacute rheumatism the alterations in the synovial
membrane, and especially in the cartilages just described, are likely
to be more marked than in the acute form.

The DIAGNOSIS of acute polyarticular rheumatism is seldom difficult in
adults, but when acute rheumatism localizes itself in one joint or
occurs in infancy or early childhood, a diagnosis, especially an early
one, sometimes cannot be easily established. The considerations by
which acute polyarticular rheumatism may be distinguished from acute
gout, subacute rheumatoid arthritis, and gonorrhoeal rheumatism will be
given in connection with those topics.

Pyaemia has perhaps been confounded with acute articular rheumatism
more than any other disease, but the rheumatic affection, unlike the
pyaemic, is not necessarily connected with any pre-existing condition
capable of causing purulent infection of the blood or system, such as a
wound, fracture, abscess, or a local inflammation of bone, periosteum,
vein, pelvic organ, or a specific fever (variola, relapsing, typhoid,
{48} glanders, etc.); it does not present severe rigors, which recur at
irregular intervals and are attended with teeth-chattering and a high
temperature, 104 degrees to 105 degrees, rapidly attained; its type of
fever is not so intermittent or markedly remittent as that of pyaemia;
its profuse sweating continues although the temperature remains
febrile, but that of pyaemia coincides with the decline of the
temperature; unlike pyaemia, it only very rarely produces profound
constitutional disturbance of a typhoid character, and has no tendency
to run a rapidly fatal course in eight to ten days or in two or three
weeks; its visceral inflammations are chiefly cardiac, pleural, and
pulmonary, and tend to resolve; those of pyaemia are especially
pulmonary, pleural, and hepatic, although frequently cardiac also, and
generally produce suppuration and destruction of tissue. Multiple
subcutaneous abscesses and cutaneous blebs and pustules do not occur in
acute articular rheumatism, and its articular affection differs in many
respects from that of pyaemia; many more joints are involved; the
inflammation is erratic, very rarely fixed, and generally resolves
without damage to the articulation; the affected joint is usually
hotter, redder, more painful, and more sensitive, and the swelling is
less diffused, and its outline corresponds more accurately with that of
the synovial capsule. Sometimes acute articular rheumatism is
complicated with the phenomena of pyaemia, as when so-called ulcerative
endocarditis obtains.

The acute inflammations which are occasionally observed in one or
several articulations of newly-born infants are generally pyaemic. It
is only in the early stage of acute glanders that the severe muscular
and articular pains sometimes present in that very rare disease in man
might lead to its being confounded with acute articular rheumatism; but
the patient's occupation and history, the early and severe prostration,
the absence, as a rule, of redness and swelling around the painful
articulations, and, in some instances, the early appearance of pustules
and blebs on the skin and of abscesses in the deeper tissues, will
suggest the real nature of the case.

Acute periostitis frequently occurs in children in close proximity
either to one joint, or less frequently to more than one, and may
readily be confounded with acute articular rheumatism. But the
constitutional disturbance in acute periostitis is prompt and severe at
the outset; the swelling increases rapidly, is firmer than that of
arthritis, does not involve the joint proper and its capsule, but, like
the tenderness on pressure, exists above or below the articulations,
especially around the head of the bone; there are no visceral
complications, provided pyaemia has not supervened; the constitutional
symptoms early assume a typhoid character, and unless an early incision
be made a fatal issue soon ensues.

The enlarged ends of the long bones and the pains in the limbs of
rickets might lead to a suspicion of acute articular rheumatism, but
the early age of such children, the absence of pain and swelling in the
joints, the beaded condition of the sternal ends of the ribs, the late
dentition and locomotion, the peculiarly shaped head, and other
evidences of that affection, would prevent a careful observer from
making a mistake. Inherited syphilis in infants, like rickets, may
produce fusiform swelling and thickening at the ends of the long bones,
especially the humerus and femur, and sometimes pain in the joints on
movement; but at first the swelling {49} is confined to the epiphyseal
line, and only later extends to the joint; there is a pseudo-paralysis
of the limb, and but little pain or fever; bony osteophytes may often
be felt under the skin at the line of union of the epiphysis with the
shaft; the epiphysis often becomes separated from the shaft, and
suppuration may ensue around the bone and in the articulation;
sometimes adhesions and perforation of the integument take place,
allowing of the escape of disintegrating osseous and cartilaginous
tissue; and there will coexist either on the skin or mucous membrane
some of the ordinary evidences of inherited syphilis.[120] The acute
and subacute articular inflammations occasionally observed in cerebral
softening and hemorrhage, in injuries and inflammation of the spinal
cord and caries of the vertebrae, may be distinguished from acute and
subacute articular rheumatism by the following circumstances: the
existence of some one of these diseases of the brain or cord, the
articular affection being usually confined to the paralyzed limbs; its
invasion about the time of the setting in of the late rigidity, or even
still later; the absence of cardiac complications and the presence of
other trophic or neuro-paralytic lesions, such as acute sloughings,
rapid atrophy of the palsied muscles, cystitis, ammoniacal urine,
etc.[121]

[Footnote 120: Vide Parrot, _Archives de Physiol. Norm. et Path._, 1872
and 1876; R. W. Taylor, _Bone Syphilis in Children_, New York, 1875.]

[Footnote 121: See J. K. Mitchell, _Am. Jour. Med. Science_, vol.
viii., 1831, and _ib._, 1833; Scott Alison, _Lancet_, i., 1846, 276;
Brown-Sequard, _Lancet_, i., 1861; Gull, _Guy's Hosp. Repts._, 1858;
Charcot, _Archives de Physiologie_, t. i. p. 396, 1868, and many
others.]

Acute articular rheumatism in children presents peculiarities. It often
affects but one joint, and has little tendency to become general; the
joints of the lower extremity, ankle, and knee are most obnoxious; the
local signs of inflammation, redness, swelling, and pain, are feebly
developed, and the child may walk as if nothing were wrong; the disease
is usually subacute; the temperature rarely very high; the perspiration
not profuse; the urine not scanty, and not often loaded with lithic
acid. Cardiac and the other internal complications, except the
cerebral, are more frequent than in adults; endocarditis is especially
frequent, pericarditis and pleuritis not rare. It is almost exclusively
in childhood that acute articular rheumatism becomes associated with or
followed by chorea, and yet the delirium, coma, and convulsions
frequently observed during rheumatic fever in the adult are very rarely
seen in the child. Muscular rheumatism, however, in the form of
torticollis, frequently coexists, and so do erythema nodosum and the
subcutaneous fibrous nodules previously described.


Mono- or Uni-Articular Acute and Subacute Rheumatism.

It is very rarely indeed that acute rheumatism invades a single joint
to the exclusion of the rest; and it is perhaps impossible to be
certain that such an arthritis is rheumatic unless some of the other
symptoms or complications of articular rheumatism supervene, or unless
it have succeeded a polyarticular rheumatism, which it very rarely
does. Mono-articular rheumatism is very generally of the subacute type,
and unattended with fever from the outset, or only a moderate pyrexia
obtains for a few days; there is generally considerable effusion into
the joint, with {50} swelling, pain, and moderate local heat; visceral
complications very rarely arise, but the local inflammation persists
most obstinately for six or eight weeks or three or four months, and
often leaves the joint tender, stiffs, and weak for a long time or even
permanently. In both the acute and subacute forms, before concluding
that the uni-arthritis is rheumatic, we must exclude the probability of
its being traumatic, strumous, syphilitic, gonorrhoeal, neurotic, or,
above all, of the nature of rheumatoid arthritis, which many such cases
really are.

PROGNOSIS.--The disease is rarely directly fatal during the attack, yet
as the frequency of the complications varies unaccountably from time to
time, so the mortality may be exceptionally large or small for even
prolonged periods. It may be said that the average mortality ranges
between 1.16 and 4 per cent. in the experience of modern authors. The
average mortality in the Paris hospitals for four years (1868-69,
1872-73) Besnier fixes at 1.65 per cent.;[122] in St. Bartholomew's,
London, Southey found it for fifteen years (1861-75) to be 1.16 per
cent.;[123] Pye-Smith fixes the rate at 4 per cent. in 400 cases
treated in Guy's;[124] W. Carter gives 2.5 per cent. as the rate during
ten years at the Southern and Royal Southern Hospitals of
Liverpool.[125] The death-rate appears to vary remarkably with age, as
Southey's figures show:[126] under ten years, 3.40 per cent.; between
ten and fifteen, 1.5 per cent.; between fifteen and twenty-five, 1.4
per cent.; between twenty-five and thirty-five, 0.9 per cent.; between
thirty-five and forty-five, 0.8 per cent., the mortality declining very
greatly after the tenth, after the twenty-fifth, and after the
forty-fifth year of life.

[Footnote 122: _Dictionnaire Encyclopedique_, Troisieme serie, t. iv.,
p. 463.]

[Footnote 123: _Barth. Hospital Reports_, vol. xiv., p. 4.]

[Footnote 124: _Guy's Hospital Reports_, xix. p. 327.]

[Footnote 125: _The Liverpool Medico-Chirurgical Journal_, July, 1881,
p. 88.]

[Footnote 126: _Lib. cit._, p. 4.]

The danger of the case is usually proportionate to the youth of the
patient, the degree of the pyrexia, the number of the joints involved,
and the number and the character of the complications, the habits, and
previous health of the patient. A fatal issue is most frequently
observed in connection with hyperpyrexia alone, or in combination with
delirium or coma. A rapid rise of temperature and a temperature over
105 degrees, especially if cerebral disturbance coexist, indicate
danger; and so does arrested perspiration while the temperature is
high. In a much smaller number of cases death is due to some other
complication, especially to purulent pericarditis or to that combined
with pleuritis or pneumonia; in not a few cases the prior existence of
chronic valvular disease, with fibroid induration of liver and kidneys,
renders a fresh rheumatic endo- or pericarditis, occurring as part of
acute articular rheumatism, fatal. There is good if not conclusive
evidence that rather sudden death in acute articular rheumatism is
occasionally due either to diffuse myocarditis or to fatty degeneration
of the muscle of the heart. In Greenhow's 2 deaths out of 50 cases
treated by sodium salicylate the pericardium was universally adherent
and the heart's fibre fatty in one and pale and flabby in the other.
Sudden death in this disease is very rarely due to embolism of the
pulmonary artery or of the cerebral vessels, while ulcerative
endocarditis is very exceptionally one of the sources of a fatal
issue.[127] But although acute articular rheumatism rarely kills {51}
directly, it frequently lays the foundation of subsequent ill-health,
and ultimately proves fatal through organic disease of the heart and
its many consequences. However, it is an interesting circumstance that
while acute rheumatic inflammation is prone to damage the heart
permanently, it very rarely, quite exceptionally, impairs the structure
or functions of the articulations. It is almost solely the subacute
form that now and then becomes chronic or renders a joint for a long
time painful, swollen, and crippled in its movements. Whether acute
rheumatism, however intense per se, ever ends in destructive
suppuration and ulceration of a joint is doubted by some authorities,
notwithstanding the cases published by Fuller and others. No doubt some
of the cases were really pyaemic, or perhaps gonorrhoeal; and it must
be borne in mind that acute articular rheumatism occasionally develops
pyaemia, and then an arthritis might be considered rheumatic when truly
pyaemic. The question of acute rheumatic arthritis exciting a chronic
rheumatoid affection will arise hereafter.

[Footnote 127: See an article on the mortality among rheumatic risks by
A. Huntingdon, M.D., in _N.Y. Medical Record_, 1875, p. 195.]

TREATMENT.--Owing to our imperfect knowledge of the real nature of
acute articular rheumatism, its treatment is still largely either
empirical or intended to combat certain prominent symptoms or
complications of the disease. Of the various methods of treatment which
have been employed space will not permit a description; even of those
advocated by authorities of the present hour only very few will be
considered.

The method which is now unquestionably the favorite one in both Europe
and America, and which in its power of promptly relieving the articular
and muscular pains and reducing the fever of acute rheumatic
polyarthritis may without exaggeration be compared to that exercised by
quinia over the paroxysms of ague, is that in which salicylic acid or
salicylate of sodium is given in repeated and full doses. It was in
July, 1875,[128] that Buss first asserted that salicylic acid was a
specific for rheumatism, and in March, 1876,[129] Maclagan, after
having employed salicine from 1874, published his experience of it as a
valuable remedy in the treatment of acute rheumatism, its beneficial
action being "generally apparent within twenty-four, always within
forty-eight, hours of its administration in sufficient dose." Perhaps a
sufficient time has now elapsed to permit of a just opinion of the
power of these new remedies, the salicyl compounds, over acute
articular rheumatism. The facts presented at the discussion recently
held at the Medical Society of London[130] are sufficiently numerous
and authoritative to justify, at least provisionally, some definite
conclusions as to the remedial relations of the salicylates to acute
articular rheumatism.

[Footnote 128: "Die Antepyr. Wirkung der Salycylsaure," _Centralbl. f.
d. Medic. Wissenschr._, 1875, 276.]

[Footnote 129: _The Lancet_, March 4 and 11, 1876.]

[Footnote 130: _The Lancet_, Dec. 17, 24, 31, 1881; Jan. 7, 14, 28,
1882.]

1. The articular pain and the fever of acute rheumatic polyarthritis
are more or less speedily removed by the salicyl remedies (salicylic
acid, sodium salicylate, and salicine); the pains very frequently
persist after the temperature has become normal. Both symptoms were
removed by five days' use of such agents in 50 per cent., and by eleven
days' use in 80 per cent., of 355 cases treated at Guy's Hospital, and
tabulated by Fagge,[131] and by five days' use in 60 per cent., and by
eleven days' use {52} in 66 per cent., of the 60 severe cases treated
and severely criticised by Greenhow.[132]

[Footnote 131: _Ibid._, ii., 1881, 1031.]

[Footnote 132: _Clinical Society's Transactions_, vol. xiii., 1880. See
Dr. Fagge's table iv., _Lancet_, ii., 1881, 1032.]

Again, in 190 cases of acute and subacute rheumatism the average
duration, under salicyl remedies, of pyrexia was 5.5 days and of joint
disease, 5.3 days (Warner[133]); in 156 cases at St. George's Hospital
the average duration of pyrexia was 3.66 days, of pain 4 days
(Owen[134]); in 82 at the Middlesex the average duration of pyrexia was
5 days, of pain 5.6 days (Coupland[135]); and in 55 at the Westminster
the average duration of pyrexia was 7 days, of pain 7.25
days[136]--that is, a general average duration in the whole series for
the pain and pyrexia of 5.4 days.

[Footnote 133: _Ibid._, p. 1080.]

[Footnote 134: _Ibid._, p. 1081.]

[Footnote 135: _Ibid._, i., 1882, 10.]

[Footnote 136: _Ibid._, ii., 1881, p. 1080.]

Further, 36 per cent. of Fagge's cases and 58 per cent. of Greenhow's
were relieved of both the above symptoms on the fourth day; 24.8 per
cent. of Fagge's and 50 per cent. of Greenhow's on the third day; and
13.5 per cent. of Fagge's and 26.6 per cent. of Greenhow's on the
second day. In Clouston's 27 cases, treated in private, 66.6 per cent.
were free from pain and 59 per cent. from fever within three days, and
85.2 per cent. were devoid of pain and 72.7 per cent. of fever within
four days.[137] Finally, all who have had much experience of this
method of treating acute rheumatism will agree that the first or second
dose frequently relieves the articular pains like a charm, and the
local swelling then frequently subsides in from sixteen to forty-eight
hours.

[Footnote 137: _The Practitioner_, i., 1882.]

2. Relapses are more frequent--probably considerably more
frequent--under treatment by salicylates than under other methods.
Thus, the average of relapses in eight different tables of cases
treated by the salicyl remedies ranged from 16.6 per cent. to 35 per
cent., giving a general average of 26 per cent.;[138] while under other
methods in three different tables the average ranged from 5.4 per cent.
to 27.6 (this last under the full alkaline), giving a general average
of 16 per cent.[139] Relapses appeared to recur less frequently in
those cases which yielded to the salicylates within five days than in
those which took from six to eleven days to yield, in the ratio,
according to Fagge's figures, of 26.6 per cent. for the first, and 29.4
per cent. for the second day; and, according to Hood's, as 18.4 per
cent. to 24.4 per cent. There does not appear to be any regularity in
the order of occurrence or recurrence of relapses, nor is Southey's
definite statement that in "relapsing cases the temperature is nearly
or quite normal on the eighth evening, and a slight relapse occurs on
the thirteenth morning," borne out by the statistics produced at the
London Medical Society. Moreover, W. Carter's cases[140] have not
confirmed Southey's precise statement respecting the gradual remission
of the temperature on the eighth and ninth days of illness in the
continued or non-relapsing, uncomplicated forms. Irregularity and
inconstancy are the typical features of articular rheumatism. The
relapses under the treatment by the salicylates have been referred to
the premature disuse of those remedies, but they do occur
notwithstanding {53} the continued employment of them. It is a general
opinion that exposure to cold, errors in diet, and an early return to
work are frequent causes of relapse; and Broadbent refers the increased
liability to relapse under the salicyl compounds to the rapidity with
which those remedies relieve the acute symptoms of articular
rheumatism, in consequence of which sufficient care is not observed
either by the patients or their nurses, and they are exposed to some of
the above exciting causes of relapse. All the above causes do probably
play their part so long as the materies morbi (if that really exist
either as a chemical principle or as a germ) has not been wholly
eliminated or destroyed. Indeed, the short intervals which frequently
obtain between the primary invasion of the so-called relapses, and the
failure of the salicyl compounds to prevent peri- and endocarditis,
render it probable that what are commonly spoken of as relapses are not
due to a new infection, as in the case of the relapse of typhoid fever,
but to the recrudescences of a disease not yet terminated, but over
some of the manifestations of which--the articular inflammation and the
pyrexia--the salicylates exercise some control.

[Footnote 138: Fagge's, 26.2 per cent.; Greenhow's, 35; Warner's, 33.6;
Owen's, 30.2; Hood's, 18.8; Coupland's, 35.3; Broadbent's, 16.6;
Powell's, 18.7; total, 214 divided by 8 = 26 per cent.]

[Footnote 139: Hood's, 5.4; Warner's, 14.9; Owen's, 27.6; total, 47.9
divided by 3 = 16 per cent.]

[Footnote 140: _The Liverpool Med.-Chirurgical Journal_, July, 1881, p.
101.]

3. Authorities are generally agreed that the salicyl compounds do not
arrest or control rheumatic inflammation of the endo- or pericardium or
pleura, or subdue the pyrexia, if these complications in well-marked
degree exist; and there is strong evidence to show that they do not at
all constantly prevent the disease from involving those organs, even
after the articular affection has subsided under their use. Inestimable
as is the benefit conferred by these remedies in promptly relieving the
articular pain and fever, they do not secure the great desideratum in
the treatment of acute articular rheumatism--protection of the heart.

In 352 cases treated with salicylate of soda at the Westminster
Hospital, heart disease developed in 13.6 per cent.; in 267 treated
without the salicylate, heart disease developed in 14.2 per cent.
(Warner's cases).[141] In 350 cases treated with salicylates at Guy's,
heart complications obtained in 68 per cent., while in 850 treated
without them, the cardiac complications occurred in 58.8 per cent.
(Hood).[142] Gilbart-Smith collected a large number of cases from
several of the London hospitals, and analyzed them with the following
results: Of 1727 cases of acute rheumatism treated before the
introduction of the salicyl compounds, the proportion of cardiac
complications was 54.4 per cent.; in 1748 cases treated subsequently to
their introduction, the cardiac affections obtained in 63.4 per cent.;
and in 533 cases treated by the salicyl compounds, those affections
obtained in 68.4 per cent.[143]

[Footnote 141: _The Lancet_, ii., 1881, 1080.]

[Footnote 142: _Ibid._, ii., 1881, 1120.]

[Footnote 143: _Ibid._, i., 1882, 136.]

These facts certainly seem to prove that the salicyl compounds do not
prevent the occurrence of the visceral complications or manifestations
of acute articular rheumatism; and if space permitted instances might
be quoted from many authors in which either endo- or pericarditis or
pleuritis or pneumonia or other visceral manifestation had set in after
the patient had been taking the salicylates long enough to have
produced their usual physiological effects; some of these will be
mentioned under the next section.

It may be objected that in the above estimates sufficient attention has
not been paid to the period of the disease at which the treatment by
the {54} salicylates was begun, the time it was continued, the doses
given, the age of the patient, the severity and other characters of the
illness, such as whether acute or subacute, first or second attack,
complicated or not.

4. It must be admitted that there are a few facts which render it very
probable that the salicyl compounds do really reduce the frequency of
these complications, and thus give some protection to the heart in
rheumatism. Of Powell's 32 cases, 19 = 60 per cent. had heart disease
when admitted; and of the remaining 13, 6 = 46 per cent. developed
cardiac disease after admission and while under the salicylates.[144]
Of Dr. Jacobi's[145] 150 cases, 78 = 52 per cent. were admitted with
unsound hearts, and of the other 72, only 5 = 6.9 per cent. developed
cardiac disease after beginning salicylate treatment. Of Southey's 51
cases, 24 = 47 per cent. were admitted with diseased hearts; and of the
remaining 27, only 4 = 14.8 per cent. developed a cardiac affection
subsequent to beginning treatment by the salicylates.[146] Of the
Boston Hospital cases, 38 per cent. were affected with heart disease at
entrance, and only 4.76 per cent. afterward. No heart affection was
developed in any of Clouston's 27 private cases--a result he attributes
to the early period at which the remedies are given in private
practice. But the number is too small to permit of any conclusion being
drawn, and 4 of the cases were examples of recurrence of the disease at
short intervals (three and four weeks) in the same patient, in whom
there appears to have existed no proclivity to cardiac complication,
for he had had four attacks before he came under Clouston's care.
Moreover, his cases were mild, but 16 of them being acute, and of these
only 3 attaining a temperature of 103 degrees and upward. Finally,
Herman[147] estimates the percentage of heart affections that developed
after beginning the salicylates in the London Hospital at 18.7 per
cent., and after other treatment at 30 per cent. Omitting Clouston's,
the general average of the above results is, that in 49.2 per cent.
cardiac disease existed before the patients began the salicyl
treatment, and that in 18.2 per cent. it developed after that, while 30
per cent. of cardiac disease developed after other methods of treatment
were begun.

[Footnote 144: _Lancet_, i., 1882, 134.]

[Footnote 145: _St. Thomas's Hospital Reports_, New Series, viii. 252.]

[Footnote 146: _St. Bartholomew's Hospital Reports_, xvi. 10.]

[Footnote 147: Quoted by T. G. Smith, _Lancet_, i., 1882, 137.]

The subject is one beset with difficulties, and still needs
investigation. It is reasonable to infer that as the salicylates
promptly arrest the articular inflammation and allay the fever of
uncomplicated acute rheumarthritis, they will prevent the visceral
inflammations so apt to develop when the disease runs its course
uninfluenced by treatment; but experience has shown that they do not
control or arrest rheumatic inflammation of the heart or pleura or the
attending pyrexia, although capable of subduing the articular
inflammation and the pyrexia that accompanies it. The most eminent
therapeutists are divided on the subject. Maclagan, while admitting
that the salicyl compounds do not ward off cardiac complications, or
cure them when they exist, maintains that their existence is an
additional reason for giving those remedies freely and in large
doses.[148] Broadbent,[149] while believing in the protective influence
of the salicylates "when brought to bear upon the fever in the first
days of its existence," finds in the presence of any cardiac
inflammation a reason for at once discontinuing those remedies.
Flint[150] believes that rheumatic endo- and {55} pericarditis are more
common since the introduction of the salicyl treatment than when the
alkaline method was relied upon almost entirely, and advises[151] the
administration of alkalies with the salicylates to protect the heart.
Vulpian[152] thinks the protective power in question probable, but not
established; while the latest French authority, Homolle, is of opinion
that "cardiac affections are really less frequent in patients treated
by salicylate of sodium than in others."[153]

[Footnote 148: _Lib. cit._, pp. 266, 275.]

[Footnote 149: _Lancet_, i., 1882, 138.]

[Footnote 150: _New York Med. Record_, 1882, 66.]

[Footnote 151: _Pract. Med._, 5th ed., 1098.]

[Footnote 152: _Du Mode d'Action du Salicylate du Soude dans le
Traitement du Rheum. Artic. Aigue_, Paris, 1881, 11.]

[Footnote 153: _Nouveau Dict. de Med. et de Chir._, xxxi., 1882, 648.]

5. The occurrence of hyperpyrexia is not always prevented by the
salicyl remedies, even when they have produced their full physiological
effects. Fagge endeavors to explain away the two cases of hyperpyrexia
which occurred under Greenhow and the other two which happened amongst
the cases tabulated by himself, and remarks that if the temperature
should begin to fall under the use of salicylic acid, and then should
change its course and rapidly attain a dangerous height, that would
really show that the drug is sometimes incapable of preventing the
occurrence of hyperpyrexia. This actually happened in one of Powell's
two cases,[154] and the patient died suddenly at a temperature of 107
degrees. In Greenhow's first case the patient had been taking the
salicylate for four days, and was deaf and delirious when the
temperature became 105.8 degrees.[155] Finney reports a case in which
drachm iss of salicine were given daily for two days, and drachm ij on
the third day, when pericarditis set in, and on the fourth day
hyperpyrexia supervened.[156] Haviland Hall records an instance in
which the temperature fell from 103.5 degrees to 100.6 degrees after
twenty-grain doses of salicylate soda, every three hours, taken for two
days; on the third day the medicine was given every four hours; the
temperature rose in the evening to 103.4 degrees, and on the next day
it rose rapidly to 108.7 degrees, and the patient became delirious.
Patient recovered rapidly after two baths.[157]

[Footnote 154: _Lancet_, i., 1882, 135.]

[Footnote 155: _Clin. Soc. Trans._, xiii. 264.]

[Footnote 156: _Brit. Med. Journ._, ii., 1881, 932.]

[Footnote 157: _Lancet_, ii., 1881, 1082. See also two cases in _Med.
Times and Gaz._, ii., 1876, 383.]

Pericarditis is not always present when hyperpyrexia arises during the
administration of salicylic acid; it was absent in Powell's cases, is
not mentioned in Hall's, and did not ensue in one of Greenhow's until
two days after the temperature had reached 105.4 degrees F. However,
either pericarditis or pneumonia is very frequently present when the
temperature is excessive. It is generally admitted that the salicylates
do not control rheumatic hyperpyrexia once it exists.

6. Notwithstanding the prompt removal of the pain and reduction of the
fever by the salicyl compounds, the average duration of acute articular
rheumatism is not very considerably lessened by those remedies. Thus,
of Hood's[158] 350 cases treated by salicylates the average duration of
the illness was 35.95 days as against 38.75 under other methods. The
average time spent in bed by Warner's 342 cases was 19.5 days under the
salicylates, and by 352 patients under other remedies 23.5 days. Both
estimates show a curtailment of the duration of the disease by the new
treatment of three to four days only; which is not a very material
improvement.

[Footnote 158: Calculation from Dr. Hood's Tables 1 and 1_a_, _Lancet_,
ii., 1881, 1119.]

{56} 7. Nor do the salicylates materially alter the time spent in
hospital by rheumatic patients; some evidence indicates that they
actually prolong that period. The following are the average residences
in hospital under the salicylates, according to several recent authors,
and they are remarkably uniform with two exceptions: Coupland, 36 days;
Warner, 34.9; Hall, 34; Southey, 32.5; Broadbent, 31.2; Powell, 31;
Finlay and Lucas, 29.7;[159] Owen, 23; Brown, 21.9;[160] or a general
average of 30.4 days for the salicyl remedies. Under full alkaline
treatment: Owen, 26 days; Dickinson, 25;[161] Fuller, 22.2;[162]
Blakes, 24;[163] or a general average of 24.3 days for full alkaline
treatment. And if to these we add Finlay and Lucas's results, 27.7
days, under but two to three drachms of alkaline salts in the
twenty-four hours--a quantity only the fourth of that given under the
full alkaline method--the general average residence in hospital under
alkaline treatment was but 25.4 days; that is, five less than under the
salicylate.

[Footnote 159: _Lancet_, ii., 1879, 420.]

[Footnote 160: _Boston Med. and Surg. Journ._, Feb., 1877. The four
cases excluded by the reports are included in this calculation, that it
may more fairly be compared with other reports.]

[Footnote 161: _Lancet_, i., 1869.]

[Footnote 162: _The Practitioner_, i., 1869, p. 137.]

[Footnote 163: _Boston City Hospital Reports_, 1st Series.]

These several estimates of the time spent in hospital under the
salicylates, with the exception of Owen's and Brown's, correspond
closely with that of the time spent by Gull's and Sutton's patients
under mint-water--32.8 days--although the general average of them falls
short of the latter by 2.4 days.

The following table (iii.) of Hood's[164] shows that under the
salicylate method 45.7 per cent. remained in hospital beyond forty
days, and 39 per cent. under other methods, and that about 50 per cent.
more were discharged within twenty days under the other methods than
under the salicylate:

  350 cases treated with salicylates:
                        Days.
  Under 10.   Under 20.      Under 30.     Under 40.     Ill longer.
  3 = 0.84%.  31 = 8.88%.    76 = 21.7%.   84 = 24%.     160 = 45.7%.

  850 without salicylates:
                        Days.
  Under 10.   Under 20.      Under 30.     Under 40.     Ill longer.
  12 = 1.4%.  105 = 12.35%.  175 = 20.1%.  182 = 21.4%.  331 = 39%.

[Footnote 164: _The Lancet_, ii., 1881, 1120.]

These statistics favor Greenhow's opinion that patients treated with
salicylate of sodium regain their strength slowly, and are long in
becoming able to resume their ordinary occupations. Some allowance,
however, must be made for the precautions against relapse under
salicylates observed in hospitals since the great tendency thereto has
been recognized.

8. Certain unpleasant or toxic effects are produced by salicylic acid
and salicylate of sodium; such are nausea, vomiting, abdominal pain,
frontal headache, tinnitus, incomplete deafness, vertigo, tremor,
quickened respiration, very rarely amblyopia and even temporary
amaurosis, and not unfrequently delirium. A feeling of prostration and
general misery is not uncommon. These phenomena of salicylism are in
great measure proportionate to the dose employed, but they have
followed moderate {57} doses, owing sometimes to idiosyncrasy, and
perhaps frequently to retarded elimination consequent upon previous
disease of the kidneys or disturbance of their function by the
salicylic acid or its salt. Those agents are usually completely
excreted in forty-eight hours, but in one of Powell's[165] cases
elimination was not completed before the fifth day, and not before the
eighth in Byanow's case.[166] Possibly uraemia may in some cases cause
the delirium.[167] The delirium, which may be violent or not, is often
preceded by dryness of the tongue, restlessness, and rapid breathing.
Impurities in the acid may account for the inconstancy with which
delirium has been noticed by different observers. While but 2 instances
in 82 cases were met with by Coupland, 3 out of 90 cases by Broadbent,
and 3 out of 109 by Brown,[168] Charles Barrows[169] encountered 8
instances in 28 cases. In one of these a boy of eleven became delirious
in eighteen hours, having taken 10 grs. of salicylate of sodium every
three hours. In another instance the drug had been in full use for five
days before the delirium manifested itself. These phenomena of
salicylism rapidly disappear when the medicine is stopped, and delirium
has not always recurred on its resumption. They are less frequent in
children, in whom elimination by the kidneys takes place very rapidly
and a marked tolerance of salicyl compounds exists. Occasionally more
serious effects appear to be produced by the salicylates, owing to
their direct action on the heart, impairing its power, as evidenced by
feeble impulse and sounds, increased frequency of the pulse, and
diminution of the arterial pressure.[170] But, notwithstanding the very
large number of cases of acute rheumatism that have been treated by the
salicyl compounds, very few clear instances of their toxic action on
the heart have been recorded, and even in some of these there were
other conditions present that may have played some part, perhaps a
chief part, in the production of cardiac failure. In Greenhow's
case[171] the autopsy revealed a dilated fatty heart and slightly
granular kidneys, and the cardiac failure coincided with a fall of
temperature to 97 degrees F. Goodhardt's[172] patient died in nine
hours after beginning the salicylic acid, of which she took but one
drachm, in divided doses, every three hours. The pulse rose rapidly to
160; she was restless and moaning, but died quietly and suddenly.
Recent pericarditis, with one or two points of fatty degeneration of
the heart's substance, and sound kidneys were found. The reporter of
the case inclines to the opinion that the acid produced sudden collapse
and cardiac failure, while Bristowe referred them to the rheumatic
poison itself. I have not been able to refer to Hoppe Seyler's
paper,[173] in which he relates that having given 5 grammes of
salicylic acid to a child of seven and a half years affected with
articular rheumatism, shortly afterward there occurred deafness,
agitation, profuse sweating, dyspnoea, and finally fatal collapse. The
condition of the heart and kidneys before and after death is not given.
Weber {58} published[174] an instance in which 15-gr. doses of salicin
given to a woman of twenty-seven produced in thirty-four hours a rapid
fall of temperature from 103 degrees to 96 degrees F., accompanied by
delirium and serious but not fatal collapse. It is well to remember
that a similar failure of cardiac power is occasionally observed in
other fevers when rapid defervescence occurs, although the salicyl
compounds have not been taken; and it is certainly necessary to give
these remedies cautiously, and often to administer alcohol with them,
when the heart's action is at all enfeebled by protracted pyrexia and
pain, or by disease (inflammatory or degenerative) of its substance or
envelope. Indeed, if severe cardiac inflammation obtain in rheumatism,
the remedies are powerless and perhaps unsafe. The sudden reduction of
the temperature when much exhaustion obtains, even in the hyperpyrexia
of rheumatic and other fevers, whether by salicylic acid or quinia or
the cold bath, may be attended with fatal collapse of the heart.

[Footnote 165: _Lancet_, i., 1882, 135.]

[Footnote 166: Quoted by Wood in his _Therapeutics and Mat. Med._,
1880, from _Centralb. fur Chir._, 1877, 809.]

[Footnote 167: See DaCosta's observations in _Am. Med. Journal_, vol.
lxix., and Ackland's in _B. Med. Journal_, i., 1881, 337.]

[Footnote 168: _Boston Med. and Surg. Journal_.]

[Footnote 169: _N.Y. Med. Record_, April 29, 1882, 456.]

[Footnote 170: Kohler, _Centralb. f. Med. Wissensch._, 1876, and
Dunowsky, _Arbeiter Pharm. Labor._, Moskau, i. p. 190, quoted by H. C.
Wood, _Therapeutics, Mat. Med., etc._, 3d ed., p. 639.]

[Footnote 171: _Clin. Soc. Trans._, xiii. p. 266, c. iii.]

[Footnote 172: _Ibid._, p. 123.]

[Footnote 173: Quoted by D. Seille, These, _De la Med. Salicylee dans
le Rheumatism_, Paris, 1879, p. 54.]

[Footnote 174: _Clin. Soc. Trans._, x. p. 70, 1877.]

Instead of the frequent weak pulse above mentioned, I have many times
found salicylate of sodium render the pulse very slow, labored, and
compressible in typhoid fever, and generally at the same time the
temperature has been considerably reduced below what it had been.

A temporary albuminuria is not infrequent; excluding mere traces, it
obtained in 52 per cent. of cases treated by the salicylates alone or
in conjunction with full doses of alkali, and in but 25 per cent. of
those in which full doses of alkali, with or without quinia, were
employed.[175]

[Footnote 175: Isambard Owen, _Lancet_, ii., 1881, p. 1081.]

Very rarely haematuria and even nephritis have occurred. The active
principle is chiefly eliminated by the kidneys, which may account for a
local irritating influence upon those organs.

Salicine is much preferred by Maclagan to salicylic acid and to
salicylate of sodium, on the grounds that it is a bitter tonic and
produces less debility and more rapid convalescence than those agents,
and that it never produces delirium nor depresses the heart's action.
Ringer[176] and Charteris[177] state that they have never seen
salicine, even in large doses, cause delirium; and Prof. Gairdner has
not found it produce any unfavorable symptoms.[178] On the other hand,
Greenhow[179] found that marked depression of the heart's power ensued
in 4 out of 10 cases whilst the patients were taking salicine, and
entirely subsided after it was discontinued. Further careful and
extended observation is needed before the relative value of salicine
and salicylate of sodium can be reliably stated. It is probable that
the salt is more active and prompt than the bitter principle; and this,
with the greater cheapness of the former, may perhaps account for the
more general employment in hospitals of the salicylate than of
salicine. The latter, moreover, is often tolerated when the former is
not.

[Footnote 176: _Handbook Therapeutics_, 8th ed., 1880, 587.]

[Footnote 177: _Brit. Med. Jour._, i., 1881, 229.]

[Footnote 178: _Lancet_, i., 1882, in table giving experience of
British hospitals, prepared by Maclagan.]

[Footnote 179: _Trans. Path. Soc._, xiii. 262.]

As regards the doses of these agents required in acute rheumatic
arthritis, practitioners are not agreed; Maclagan, Stricker, Fagge,
Broadbent, Ringer, Flint, See, recommend large doses at short intervals
at the outset, with the view of getting the patient rapidly under the
influence of the drug. Maclagan gives salicine scruple i-ij at first
hourly, then every two hours {59} as the acute symptoms begin to
decline; after the second day he allows 20 to 30 grs. every four hours
for two or three days; "and for a week or ten days more that quantity
should be taken three times a day." Stricker, Fagge, Broadbent, and See
recommend about 20 to 30 grs. of salicylate of sodium every hour or two
for six doses (= drachm ij-iij in the day), and Ringer would employ 10
grs. hourly, and if in twenty-four hours this dose has not either
modified the disease or produced its characteristic symptoms, he would
increase it to 15 and then to 20 grains hourly. On the other hand,
Owen's[180] results show practically no difference in the duration of
pain and pyrexia and in the average duration of illness from the
commencement, whether drachm iij or drachm ij or drachm iss were given
every twenty-four hours; and C. G. Young[181] found that 10 to 15 grs.
every one, two, or three hours are sufficient.

[Footnote 180: _Lancet_, ii., 1881.]

[Footnote 181: _Dub. Journ. Med. Sci._, Sept., 1880, 193.]

Indeed, exceptionally good and exceptionally indifferent results are
reported under similar doses. No such good results are reported as
those of the Boston City Hospital under doses of drachm ij to drachm iv
per diem, the average residence in hospital being only eighteen days if
four cases which became chronic are excluded, or 21.9 days if they are
included.

The plan in vogue at our hospital here and in my own private practice
is to give about 15 grains every two or three hours, according to the
severity of the case and until the articular pain and pyrexia are
relieved. After the pain and pyrexia have yielded, the remedy should be
continued in smaller doses, say 10 to 15 grs., three or four times a
day, according to the severity of the case, for eight to ten days
longer, to prevent relapse, and during this period exposure, exercise,
and dietetic excesses must be carefully guarded against.

The salicine may be given dissolved in milk or enclosed in wafers; the
salicylate of soda, in a solution of any aromatic water, to which
extract of liquorice or syrup of lemon and a few drops of spirits of
chloroform may be added. The French add a little rum to flavor the
mixture. Should severe cardiac inflammation exist, and, even although
not severe, should there exist signs of failure of cardiac power,
salicylates and salicine had better be avoided. If the secretion of
urine diminish considerably under their use, or haematuria supervene,
or organic disease of the kidneys exist, they must be employed
cautiously, and may require prompt suspension. If marked debility
exist, stimulants, especially the alcoholic, should be combined with
them.

The oil of wintergreen has recently been well spoken of by F. P.
Kinnicutt of St. Luke's Hospital, New York,[182] as a substitute for
salicylate sodium. It is itself a methyl salicylate 90 per cent., plus
terebene 10 per cent. Its officinal name is oleum gaultheria, and it is
given in doses of minim x-xv every two hours except during sleep, and
in severe cases of articular rheumatism during the twenty-four hours,
either by floating the oil upon a wineglass of water or milk or in
capsules or upon lumps of white sugar. It resembles in its influence
upon acute rheumatism very closely the sodium salicylate, for which it
may perhaps be substituted, and Kinnicutt maintains that it is quite as
effectual, pleasanter to take, and free from the intoxicating
properties of the salt and the salicylic acid. It requires to be
continued during convalescence just like the salicylate.

[Footnote 182: _Med. Record of New York_, Nov., 1882, 505.]

{60} The alkalies--in this country at least--were the favorite remedies
in the treatment of acute articular rheumatism before the powers of
salicine and salicylic acid became generally known, and there are still
authorities who maintain their excellence, if not their superiority
over the salicylates, in protecting the heart against the recurrence of
rheumatic inflammation (Flint, Dickinson, Sinclair, Stille).

Under the term the alkaline treatment unfortunately are included two
distinct methods of administering the salts composed of potash and soda
and the vegetable acids, carbonic, tartaric, citric, etc.--viz.: that
in which about half a drachm of one of these salts is given three or
four times a day; and the other known as Fuller's method, in which
large doses are prescribed, so that from an ounce to an ounce and a
half is given in the first twenty-four hours, with the view of rapidly
rendering the urine alkaline, and if possible the perspiration also;
for I have frequently produced the former effect in less than twelve
hours, yet have found the perspiration still redden litmus on the
second, and even the third, day and later. A disregard of the essential
differences existing between these two methods of employing alkalies in
acute rheumatism may partially account for the differences of opinion
existing as to the value of the alkaline treatment, and for the
differences in the statistical results thereof published by various
observers--a remark applicable to other methods and statistics also.
Fuller commonly ordered every three or four hours bicarb. sodium drachm
iss and acetate of potassium drachm ss dissolved in ounce iij of water
and rendered effervescing at the moment of administration by the
addition of an ounce of lemon-juice or drachm ss of citric acid. As
soon as the urine presents an alkaline reaction--which is usually the
case in twelve to twenty-four hours--the quantity of the alkali is
reduced by one-half, or to about 8 drachms, during the succeeding
twenty-four hours, and provided the urine continues alkaline to 3
drachms on the third day. On the fourth day and subsequently only a
scruple to half a drachm of alkali is given three times a day,
sufficient to keep the urine alkaline, and to each dose are added 3
grains of quinia dissolved in lemon-juice; and this combination is
continued till convalescence sets in. An aperient pill is given
whenever needed, but is administered "only under conditions of extreme
nervous irritation." The method is not an exclusively alkaline one.

Space will not allow of a lengthened analysis of the statistics that
have been published on this subject, and I will give only some of the
more important statistical results. While, as we have seen, the average
duration of pyrexia and articular pain under salicylate treatment is
about 5.4 days, under moderate alkaline treatment, according to the
recent statistics of Finlay and Lucas,[183] the average duration of
pyrexia was 10.3 days and of articular pain 12.2 days, and of Owen[184]
6.5 days for the first and 8 days for the second, or a general average
for the pain and pyrexia together of 9.25 days, or about 3.85 days
longer than under the salicylate treatment. Nor can it be said even of
the full alkaline plan that the first or second dose frequently
relieves the articular pains like a charm. On the other hand, it has
been already shown that the average time spent in hospital was five
days less under the full alkaline than under the salicylate treatment.

[Footnote 183: _Lancet_, ii. 1879, 420.]

[Footnote 184: _Ibid._, ii., 1881, 1081.]

As regards the relative power of the salicylates and of full alkaline
{61} treatment in protecting the heart, the following analysis and
calculation deserve attention. The percentage of cases in which cardiac
disease set in after the salicylate treatment began was, according to
Powell, 18.75; according to Haviland Hall, 37.1; according to Finlay
and Lucas, 11.60; Southey, 8; Brown, 4.76; Jacobi, 3.35, or a general
average of 14 per cent.; whereas cardiac disease developed after the
alkaline treatment had commenced in 13.6 per centum according to
Blake;[185] in 10.7 per cent. according to Dickinson;[186] in 7 per
cent. according to Owen; in 6.6 per cent. according to Finlay and
Lucas; and in 2 per cent. according to Fuller; making a general average
of only 7.8 per cent.

[Footnote 185: _Med. and Surg. Reports of Boston City Hospital_, 1st
Series, 1870.]

[Footnote 186: This percentage is obtained by adding together all the
cases treated by alkalies given by Dickinson in his IX., X., XI., and
XII. tables. Their total was 65 cases in which the heart was affected
seven times. In table IX. from drachm ii-iv of alkaline salts were
given daily, and in table X. about drachm iij daily.--_Lancet_, i.,
1869.]

Judging from these statistics, it is not improbable that a combination
of sodium salicylate, with full doses of bicarbonate of sodium or
chlorate of potassium, will give better results in the treatment of
acute rheumatism than either of those classes of remedies singly.
Indeed, Flint and others have advised such combinations, and Bedford
Fenwick has recently stated, as a result of his experience in 30 cases,
that if, after giving a free purge, followed by scruple doses of sodium
salicylate hourly for six hours, that salt be stopped, and in twelve
hours afterward half-drachm doses of citrate of potassium be
administered every four or six hours until the saliva becomes alkaline,
relapses will be extremely rare, and that this is the safest and most
successful method of treating acute and subacute articular
rheumatism.[187]

[Footnote 187: _Lancet_, i., 1882.]

Having spoken somewhat fully upon the remedies of which I have most
personal experience, and which have the largest number of advocates at
the present time, and having advised the combination of these remedies,
I shall only glance at some of the other remedies or methods of
treating the disease still more or less employed.

Quinia, given in divided doses to the extent of 15 to 30 grains in the
day, is still highly thought of in France in the early stages, during
the course of and on the occurrence of relapses, in acute (especially
febrile poly-) articular rheumatism. It is claimed by Briquet,
Monneret,[188] Legroux, and others that although not a specific for the
disease it moderates the general disturbance, diminishes the local
affections, and even retards the development or lessens the gravity of
the cerebral symptoms--that, although it does not control the cardiac
inflammations, it is not contraindicated by them. The only recent
English authority who has strongly advocated full doses of quinia in
this disease is Garrod,[189] but he mixed the drug, in five-grain
doses, with half a drachm of bicarbonate of potassium, a little
mucilage, and spirits of chloroform, and gave it every four hours until
the fever and articular affection had completely abated. Sufficient
facts have not been published to permit of the formation of a reliable
judgment as to the actual or the comparative value of either the simple
quinia or the quino-alkaline treatment of acute and subacute articular
rheumatism. There can be no doubt as to the value of quinia to meet
certain conditions incident to the disease, such as debility, lingering
{62} convalescence, periodical relapse, excessive perspiration, failure
of appetite, and perhaps, in some instances, high temperature. Barclay
has found quinia of much service when depression has followed the long
continuance of the alkaline treatment and is attended with alkaline
urine and a deposit of the earthy phosphates.[190] It may be given by
the rectum if not tolerated by the stomach or if the alkalines are
being taken.

[Footnote 188: _La Goutte et le Rheumatisme_, Paris, 1857.]

[Footnote 189: Reynolds's _Syst. Med._, 1870, p. 951.]

[Footnote 190: _St. George's Hospital Reports_, vol. vi. p. 111 _et
seq._]

Greenhow[191] has treated 43 cases with iodide of potassium and
quinine, and says that his experience of this method contrasts
favorably with that of salicine and salicylate of soda. However,
pneumonia supervened in 3 cases while under treatment; cardiac
inflammation arose in 6 cases (= 14 per cent.) after admission; single
relapses of short duration occurred in 21 per cent.; and, excluding two
cases in which the treatment was soon discontinued and 7 very mild
cases, the remaining 34 cases were on the average each thirty-six days
in hospital. Under this method relapses were less frequent (21 per
cent. instead of 26 per cent.), and stay in hospital longer (36 instead
of 30.4 days), than under that by the salicylates; but the number of
cases treated is too small to base a final opinion upon. He prescribed
5 grains each of iodide of potassium and carbonate of ammonia three or
four times a day, and 2 grains of quinia with three of extract of
hyoscyamus in pill as often. This method, in principle at least,
resembles that recommended by DaCosta, who administers in uncomplicated
cases bromide of ammonium in 15- to 20-grain doses every three hours,
and as soon as the acute symptoms have disappeared follows it by quinia
in fair doses. It has not come into general use in this country,
although its eminent proposer published his cases in 1869.[192]

[Footnote 191: _The Lancet_, i., 1882, 913.]

[Footnote 192: _Pennsylvania Hospital Reports_, vol. ii., 1869; _New
York Medical Record_, September, 1874, p. 481.]

Notwithstanding the encomiums passed upon propylamine--or, more
correctly, trimethylamine--as a remedy for acute and chronic rheumatism
by Awenarius of St. Petersburg in 1856, by Gaston of Indiana in 1872,
by Dujardin-Beaumetz in 1873, and Peltier in 1874 (both of France), and
Spencer of England in 1875, it has not been much employed, especially
since the salicylates have attracted attention. It appears that in a
considerable proportion of cases the articular pains have subsided in
two or three days under its employment, and then the temperature has
declined, but the visceral complications have not been prevented. From
4 to 8 minims of trimethylamine in an ounce of peppermint-water, with a
drachm of syrup of ginger, may be given every hour or two, the
intervals to be increased as the pains diminish. When pain has quite
ceased the drug may be stopped and quinia given its place. It merits
further study in this disease,[193] and Dr. Shapter of the Exeter
Hospital has very recently stated that he is so convinced or the value
of propylamine that salicylic acid has not fully commended itself[194]
to him. Senator has recently recommended benzoic acid or its sodium
salt in large doses (about ounce ss in the day) in those cases of acute
rheumatic arthritis in which {63} the salicylates have failed, although
he admits that it scarcely rivals them.[195] His 22 patients were
relieved in 4.4 days as the average, and no complications occurred in
any of them. Benzoic acid is said not to produce the nausea,
depression, or unpleasant head phenomena of salicylic acid, to which it
is closely related in chemical composition.

[Footnote 193: On this subject see Farier-Lagrange's _Essai sur la
Trimethylamine_, Strasbourg, 1870; _Journal de Med. et de Chirurgie_,
1873, No. 2; _Medico-Chir. Rev._, i., 1873, 497; _Lancet_, ii., 1875,
675; _The Practitioner_, London, i., 1875; _Le Progres Medicale_, Jan.
10, 1874; _ibid._, Aug. 9, 1879.]

[Footnote 194: _The Brit. Med. Jour._, 1881, p. 1012. See also Tyson,
_Philadelphia Med. Times_, 1879, vol. x. 359.]

[Footnote 195: _Centralb. f. d. Med. Wiss._, 1st May, 1880, quoted in
_Practitioner_, Sept., 1880. See also McEwan's experience, _Brit. Med.
Journ._, i., 1881, 336; F. A. Flint, M.D., _N.Y. Med. Gazette_, 1880.]

Space will not permit of any notice of lemon-juice, perchloride of
iron, the mineral acids, or the blistering treatment. Of this last my
experience enables me to say that it frequently relieves the pains
promptly, but does not at all always protect the heart. In my opinion
it deserves an extended employment in conjunction with early and full
doses of the sodium salicylate. As Andrews has not by any communication
made since the publication of his paper in 1874[196] maintained the
value of the treatment of the disease by an exclusively non-nitrogenous
diet of arrowroot, and as he had then treated but eight cases in that
way, it is hardly necessary to consider it as a method of treatment.

[Footnote 196: _St. Barth. Hospital Reports_, vol. x. 359.]

Having spoken of the treatment of the general disease acute articular
rheumatism, it remains to speak of the treatment of its visceral
manifestations and of some of its more important incidental symptoms
and complications. As the treatment of the various forms of cardiac
inflammation will be given in extenso in the articles specially devoted
to those topics, I will be very brief in my notice of them.

In every case of rheumatic fever it is our primary duty to employ those
measures as early and deftly as possible which in the present state of
knowledge appear to promptly relieve the pyrexia and articular
symptoms, and lessen the tendency to, but do not altogether prevent,
the visceral complications. Such measures have been already said to be
the administration of the salicylates and alkaline salts together in
full doses, and the observance of certain dietetic and hygienic details
to be given hereafter. If, notwithstanding, peri- or endocarditis, or
both, supervene, as it frequently happens, what is to be done? I reply
that even in pericarditis active interference is seldom necessary; the
general treatment previously employed may be continued in the hope that
it may mitigate the cardiac inflammation by reducing the pyrexia and
subduing the polyarthritis, even although it be incapable of directly
controlling the pericardial inflammation. If the pain in pericarditis
be really severe and the heart's action much disturbed, a dozen leeches
may be applied over the heart, and be followed by anodyne fomentations
or hot poultices applied, as Lauder Brunton advised, over several
layers of flannel interposed between the skin and them. Leeching,
however, is seldom needed, a hypodermic injection of morphia generally
sufficing to relieve the pain. Should these measures not relieve the
pain and allay the cardiac excitement, small and repeated doses of
chloral, which Balfour observes "is not more useful as a sedative than
as an antiphlogistic," may be given. If there be, as so frequently
happens, but little pain or cardiac disturbance, there being only a
friction sound revealing the inflammation, the hot poultices or anodyne
fomentations, or even covering the front of the chest with wadding or a
belladonna plaster, which I prefer, will suffice. Should pericardial
effusion ensue, the diet must be improved, and if much {64} debility
exists, the salicylate and alkalies should be stopped, and wine may be
given along with quinine alone or with pretty full doses of muriate of
iron. As the strength returns absorption commonly takes place; but if
it is delayed, either the iodide of potassium or the infusion of
digitalis may be employed along with the quinia; or, if no special
contraindication exist, a pill containing a grain each of blue mass,
digitalis, squill, and quinia may be given three times a day and its
effects carefully watched. Much difference of opinion obtains as to the
value of flying blisters on the praecordia. Although not often
required, they appear to be more useful than iodine applications. In
those comparatively rare instances in which the effusion is abundant
and remains unabsorbed, either because it is largely sero-purulent or
purulent, it is proper to aspirate the pericardial sac, which should
certainly be done if marked signs of cardiac oppression and failure
coexist. Having once hesitated to aspirate in recent rheumatic
pericarditis with copious effusion in a lad, and found a large amount
of pus in the sac after death, I would warn against hesitancy under
such circumstances. Careful employment of the instrument can hardly do
harm if even no large amount of effusion exist.

Active treatment is quite uncalled for, as a rule, in acute rheumatic
endocarditis unattended by pericarditis. If the valvulitis occur
notwithstanding the employment of the anti-rheumatic remedies, it is
very doubtful if we have any others capable of directly controlling
that inflammation. Inasmuch, however, as, owing to the inflamed surface
being in constant contact with the fluid, many of our remedies may be
applied directly to the diseased part, it is well neither to be
dogmatic on the point nor to abandon hope that agents may yet be found
that will prove directly useful. While carefully treating the rheumatic
fever, the main indications remaining to be filled appear to be to
quiet the cardiac excitement and secure as much rest to the inflamed
valves as possible. The alkaline salts, salicine, and the salicylate of
sodium do usually greatly reduce the frequency of the heart, and, pro
tanto, secure rest. The tincture of aconite given hourly, so as to
slacken the heart's speed, is useful in the sthenic stage of endo- and
of pericarditis; and the benefit of absolute rest of the body in bed
and of the joints in splints during the entire course of rheumatic
fever, in preventing cardiac inflammations and in treating them, has
been shown by Sibson.[197] When signs and symptoms of cardiac weakness
arise, whether from the pressure of pericardial effusion or from
myocarditis or any other cause, the employment of salicylates,
alkalies, aconite, and chloral should be at once stopped and alcoholic
stimulants and tonics (strychnia, quinia, iron) and good food should be
freely administered. The most valuable point made of late in the
therapeutics of acute inflammations of the valves is Fothergill's
development of Sibson's principle--viz. that "general quietude for
weeks after an attack of acute endocarditis is indicated," as the
cell-growth in the valve may not be quite over in a less time,[198] and
the work of repair, we may add, not completed. The same principle is
specially applicable in myocarditis.

[Footnote 197: Reynolds's _System of Med._, vol. iv. p. 527, Eng. ed.]

[Footnote 198: _Diseases of Heart, with their Treatment_, 2d Series,
1879, 149.]

The disturbances of the nervous system were divided into those {65}
dependent upon gross organic alterations of the nervous centres and
their envelopes, and those not so related, but which we commonly speak
of as functional. Were it possible generally--which it is not--to
diagnosticate rheumatic meningitis from the merely functional form of
so-called cerebral rheumatism, then its treatment would resolve itself
into a vigorous use of the anti-rheumatic remedies, salicylates,
alkalies, etc., and the active employment of ice and leeches to the
scalp, purgatives, full doses of the iodide and bromide of potassium,
ergot, etc. If, together with the symptoms of that often obscure and
comparatively rare complication of rheumatic fever, ulcerative
endocarditis, there occurred severe headache, delirium, or paralysis,
we might find great difficulty in determining the cause of the cerebral
disturbance, and would naturally vary our measures according as we
suspected meningitis, embolism, or simple functional disturbance, and
the treatment adapted to these several conditions will be found under
their respective heads in this work.

Coming now to the functional disturbances of the nervous centres, which
are the ordinary forms met with in acute articular rheumatism, they may
be divided, for therapeutical reasons, into two groups: (1) Those
unattended by hyperpyrexia, and (2) those preceded, accompanied, or
followed by hyperpyrexia.

(1) When any sign of disturbance of the nervous system, delirium,
restlessness, taciturnity or talkativeness, insomnia or somnolence,
deafness, tremulousness, vacancy, stupor, or what not, occurs in
rheumatism with but a moderate temperature, 101 degrees to 103 degrees,
while we anxiously watch the temperature from hour to hour, prepared to
combat any tendency to hyperthermia the moment it is discovered, we
endeavor to control the cerebral disturbance as in other febrile
affections, but with greater diligence, knowing that in this disease
these nervous symptoms very often precede hyperpyrexia. We persist with
the salicylates to reduce the rheumatic element of the affection,
employ remedies to control the cardiac or pulmonary inflammations which
are so frequent in such circumstances, sustain the general powers by
food, wine, and quinia, if, as frequently happens, there are evidences
of failing strength, and meet any other special indication that may
arise. For example, we procure sleep and allay motor and mental
excitement by opium or chloral and by evaporating lotions or the
ice-cap to the head. We reduce temperature, allay restlessness,
preserve the strength, and promote sleep by lightening the bed-clothes,
drying frequently the entire surface of the body if it is perspiring
freely, or by sponging it with tepid water hourly if dry and hot. We
act on the kidneys, bowels, and if necessary the skin, if from the
scantiness of the urine or other evidence we suspect uraemia. Should
these means fail and the delirium and other symptoms which occur in
cerebral rheumatism continue, and especially should they be severe, it
would be, in the writer's opinion, proper to employ the methods that
are now resorted to when hyperpyrexia accompanies those symptoms; for
patients suffering from cerebro-spinal disturbance or rheumatic fever,
although unattended by hyperthermia, do die if those symptoms continue.
Moreover, the hyperthermia may at any moment supervene; it is itself
perhaps as much a nervous disturbance as delirium, and apt to succeed
the latter. It was in these very cases in which the delirium preceded
the hyperpyrexia that the London committee to be presently mentioned
found the highest {66} mortality. If along with these nervous symptoms
the articular pain or the sweating disappear suddenly, or if the pulse
suddenly increase in frequency without demonstrable increase of cardiac
mischief, there is reason to anticipate the supervention of
hyperpyrexia.

(2) When the cerebro-spinal disturbance of rheumatic fever is followed,
preceded, or accompanied by hyperpyrexia, there is one indication for
treatment which dominates all others, and that is the prompt reduction
of the hyperthermia. The terrible danger of this condition in rheumatic
fever is known to all persons who have had much experience of the
disease. Wilson Fox in 1871 had not known a case recover after a
temperature of 106 degrees unless under the use of cold, yet that is
not an alarming temperature in intermittent or relapsing fever, and is
often recovered from in typhoid fever. Thanks to Wilson Fox,[199]
Meding,[200] H. Thompson,[201] H. Weber,[202] I. Andrew,[203] Maurice
Raynaud,[204] Black,[205] Fereol,[206] and many others since, it has
been established that when the hyperthermia is removed by external cold
the nervous disturbances also usually at once disappear or lessen very
much. And thus we are brought to the treatment of the hyperpyrexia of
acute articular rheumatism. On this important topic it will be most
satisfactory and convincing to give some of the conclusions arrived at
respecting hyperpyrexia in acute rheumatism by a committee of the
Clinical Society of London.[207] I will condense some of them.

[Footnote 199: _Treatment of Hyperpyrexia_, 1871, and _Lancet_, ii.,
1871.]

[Footnote 200: _Archiv fur Heilkunde_, 1870, xi. 467.]

[Footnote 201: _Brit. Med. Jour._, ii., 1872; _Lancet_, ii., 1872; and
_Clinical Lectures_, 1880.]

[Footnote 202: _Clin. Soc. Transactions_, v. 136.]

[Footnote 203: _St. Bartholomew's Hosp. Repts._, x. 337.]

[Footnote 204: _Journal de Therap._, No. 22, 1874.]

[Footnote 205: _Gaz. Hebdomad. de Med. Sci._, 1875.]

[Footnote 206: _Soc. Med. des Hopitaux_, 8 Juin, 1877.]

[Footnote 207: _Brit. Med. Jour._, i. 82, 807.]

1. "Cases of hyperpyrexia in acute rheumatism prevail at certain
periods;" "such excess corresponds in a certain degree, but not in
actual proportion, to a similar excessive prevalence of acute
rheumatism generally. The largest number of cases of hyperpyrexia arise
in the spring and summer months, whereas rheumatism is relatively more
common in the autumn and winter." 2. "Whilst very little difference
obtains between the two sexes in regard to proclivity to rheumatism,
the proportion of males to females exhibiting hyperpyrexial
manifestations is 1.8 to 1." (3 omitted.) 4. "The cases of hyperpyrexia
preponderate in first attacks of rheumatic fever." 5. "Hyperpyrexia is
not necessarily accompanied by any visceral complications, but may
itself be fatal. The complications with which it is most frequently
associated are pericarditis and pneumonia." 6. "The mortality of these
cases is very considerable, hyperpyrexia being one of the chief causes
of death in acute rheumatism." 7. "Although present in a certain number
of cases, and these of much value from their prodromal significance,
neither the abrupt disappearance of articular affection, nor the
similarly abrupt cessation of sweating, is an invariable antecedent of
the hyperpyrexial outburst." (8, 9, 10 omitted.) 11. "The post-mortem
examinations in a certain proportion elicited no distinct visceral
lesions, and when present the lesions were not necessarily extensive."
12. "The prompt and early application of cold to the surface is a most
valuable mode of treatment of hyperpyrexia. The chances of its efficacy
are greater the earlier it is had recourse to. The temperature cannot
safely be allowed to rise above 105 degrees F. Failing the most {67}
certain measure--viz. the cold bath--cold may be applied in various
ways: by the application of ice, by cold affusions, ice-bags, wet
sheets, and iced injections."

Whatever differences of opinion may obtain as to the value of cold in
the treatment of the hyperthermia of typhoid fever, there is a
tolerable consensus of opinion that it is our most reliable and
promptest resource in those formidable cases of rheumatic fever
attended with hyperpyrexia, both when alarming delirium and coma
coexist and when they are absent.[208] Space will not allow of details
here in the employment of cold to reduce hyperpyrexia--a subject
discussed elsewhere in this work. Suffice it to say, that besides the
cold bath (70 degrees or 60 degrees) which the committee regards as the
most certain, the tepid bath (96 degrees to 86 degrees) is employed by
Fox and regarded as the best by Andrews; it may be cooled down to 70
degrees by adding ice or cold water to it (Ziemssen). The cold wet
sheet-pack is still thought much of, like the last, in old and feeble
people. Kibbie's method deserves more attention than it has received.
He pours tepid water (95 degrees to 80 degrees) over the patient's
body, covered from the axillae to the thighs with a wet sheet and laid
upon a cot, through the open canvas of which the water passes and is
caught on a rubber cloth beneath the cot, and conveyed into a bucket at
the foot of the bed.

[Footnote 208: The powerful depressing effects of high temperature on
the human body, and the remarkable opposite influences of a cool
temperature, have been personally experienced by the writer in the last
three days. For two or three days the weather has been very hot, and he
has experienced the usual feeling of exhaustion, incapacity for thought
and action. After a thunderstorm last evening the temperature fell 25
degrees, and this morning, twelve hours later, he feels vigorous,
refreshed, and capable of intellectual and physical labor. The change
is remarkable.]

The existence of polyarthritis, of peri- or endocarditis, of pneumonia
or pleurisy, does not contraindicate the cold bathing. If much weakness
of the heart obtains, it is well to give some wine or brandy before
employing the bath, and perhaps while in it, and the patient should not
be kept in the bath until the temperature reaches the norm, for it
continues to fall for some time after his removal from the bath. If the
temperature fall rapidly 2 degrees to 3 degrees in five or six minutes,
remove the patient from it as soon as the temperature recedes to 102
degrees or 101 degrees F. If it fall very slowly, the bath may be
continued till the temperature declines to 99.5 degrees, when he should
be taken out. Should marked symptoms of exhaustion or of cyanosis
arise, the bathing should be at once stopped. After it has been found
necessary to employ cold in this way, the thermometer should be used
every hour, and if the temperature tend to rise rapidly again, the
diligent application of a succession of towels wrung out of iced water
and applied to the body and limbs, or of Kibbie's method, may suffice;
but should they not, and a temperature of 103 degrees or 104 degrees be
rapidly attained again, the cold or tepid bath should be at once
resumed. In severe cases of this kind a liberal administration of
alcohol and liquid food is generally needed, and it is well to try
antipyretic doses of quinia by mouth or rectum, although they are
usually very disappointing in these cases. It is admitted that cold
baths have in a few rare instances caused congestion of the mucous
membrane, pneumonia, pleurisy, and even fatal syncope. This is a reason
for the exercise of care and constant oversight on the part of the
physician, but hardly an excuse for permitting a person to die in
rheumatic hyperpyrexia without affording {68} him at least the chance
of recovery by the use of the cold or tepid bath.

If delirium and deafness supervene during the employment of the
salicylates, it is prudent to suspend their use and take the
temperature every couple of hours, as one cannot feel confident that
hyperpyrexia may not be impending. Both Caton and Carter have found
that the addition of bromohydric acid to the sodium salicylate
mitigated or controlled the tinnitus and deafness produced by full
doses of that salt.

SUMMARY OF TREATMENT OF ACUTE RHEUMATIC POLYARTHRITIS.--As a general
rule, commence at once with a combination of sodium salicylate, say 10
grains, and citrate of potass. gr. xv, every hour for twelve doses,
after which give the citrate alone every two hours during the rest of
the day. Repeat these medicines in the same way daily until the
temperature and pain have subsided, when only half the above quantities
of the drugs are to be given every twenty-four hours for about a week
longer, after which three 15-gr. doses of the salicylate, with a like
quantity of the citrate, are to be administered every day for another
week or ten days, to prevent relapses. It is in this third week that
quinia is most likely to be required, and as a general rule it may be
given with benefit at this period in doses of 2 grains three times a
day between the doses of the salicylate. Should the above dose of
salicylate not relieve the pains sensibly in twenty-four hours,
increase next day the hourly dose to 15 or 20 grains; and if this free
administration of the medicine afford no relief after four or five
days' use, substitute for the salicylate salt the benzoate of ammonia
in 15- to 20-grain doses hourly, continuing the citrate of potassium
and conducting the treatment in the manner first advised. Should the
benzoate likewise fail after four or five days' trial, omit it, and
employ the full alkaline method together with the quinia, of which
about 10 to 15 grains may be given in the day between the doses of the
alkaline salt.

For the local treatment no uniform method is invariably applicable. In
many cases simply painting the joints with iodine daily, or enveloping
them in cotton wool, with or without the addition of belladonna or
laudanum, and securing it by the smooth and gentle pressure of a
flannel roller, proves sufficient. Hot linseed poultices containing a
teaspoonful of nitre or of carbonate of soda often afford relief, and
so does Fuller's lotion, applied to the articulations by means of
spongio-piline, or lint covered with oiled silk. It consists of liq.
opii. sed. fl. ounce j, potass. carb. drachm iv to drachm vj,
glycerinum fl. ounce ij, aqua fl. ounce ix. It must be plentifully
applied. If the articular affection be very severe and not relieved by
the above measures, absolute immobility of the joints, secured by means
of starch and plaster-of-Paris bandages, has been shown to be very
useful, relieving the pain, shortening the duration of the local and
the general disturbance, and protecting neighboring joints from
invasion.[209]

[Footnote 209: See Heubner in _Archiv der Heilkunde_, vol. xii., and
Oehme in _ibid._, vol. xiv., and a striking case in _St. Barth. Hosp.
Reports_, 1876, p. 174, by R. Bridges, M.D.]

We have little experience in this country of ice continuously applied
to the joints until all the symptoms of acute rheumatism have
disappeared (Esmarch and Stromeyer).

Circlets of blistering fluid applied above all the affected joints {69}
simultaneously, as practised especially by Herbert Davies,[210] often
afford prompt relief to the pain, but they do not invariably protect
the heart, in my experience.

[Footnote 210: _London Hospital Reports_, vol. i., 1864, 292.]

The hygienic and dietetic management of acute articular rheumatism
demands careful attention. While the room should be well supplied with
fresh air and sunlight, it should be kept at a uniform temperature and
free from draughts. Feather and other very soft beds should be
prohibited. Many authorities put the patient between heavy blankets,
which I regard as a mistake. The bed-clothing should be light and just
sufficient to keep the patient agreeably warm; the night-gown may be of
thin flannel and the sheets of cotton. The excess of perspiration
should be removed by gentle rubbing with a warm towel at regular
intervals, and the sheets should be changed frequently before they
become almost saturated with the perspiration. Fatigue and exposure of
the patient's person when taking food, attending to his natural calls,
or having his personal or bed-clothing changed should be specially
guarded against.

The diet in the early actively febrile stage should consist of panada,
corn-meal or oat-meal gruel, milk, and barley-water, or even pure milk.
Where persons will not take milk the various thin animal broths to
which good barley-water or arrowroot or well-boiled rice has been
added, jellies, sago and other starchy puddings, may be allowed.
Suitable drinks are--plain water, Seltzer and Apollinaris water,
carbonic-acid water, lemonade. This low, unstimulating diet should be
observed until all fever and articular inflammation have subsided, the
tongue become clean, and the visceral inflammations declined, and a
return to solid food, and especially to animal food, should be made
cautiously. Eggs are to be regarded as of very doubtful safety in this
disease. As a very general rule, ales, wines, and the stronger
alcoholic liquids are objectionable, but they may be required under the
same conditions as in other fevers. Should the salicylates depress the
heart, old wine or whiskey may be given with advantage.

During convalescence the patient should not be permitted to leave his
bed for several days after complete removal of the fever and articular
pain, and for the first four days he should occupy a sofa or
easy-chair. Premature walking may induce relapse. An occasional
alkaline or sulphur bath, if cautiously taken, sometimes appears to
complete the recovery. If endocarditis have existed, a longer rest is
desirable, more especially in severe cases, in order that the
reparative process going on in the lately inflamed valves may not be in
the least disturbed.


Chronic Articular Rheumatism,

synonymous with rheumarthritis chronica, rheumatisme articulaire
chronique simple (Besnier), polyarthritis synovialis chronica (Heuter),
is defined here as a chronic idiopathic inflammation of one or a few
articulations, which is more prone to become fixed than the acute form,
and which, notwithstanding its protracted duration, produces no
profound structural alterations in the joints.

ETIOLOGY.--It may be the direct sequel of a single attack or more {70}
commonly of several attacks, of acute, or more especially of subacute,
articular rheumatism. But it is generally a primary affection,
occurring in persons who have not had either acute or subacute
rheumarthritis, yet owning the same causation as these, and
occasionally in its course exhibiting acute or subacute symptoms. The
specially predisposing conditions are inheritance; repeated attacks of
subacute or acute articular rheumatism, which in accordance with
general laws impair the resisting power of the affected joints;
prolonged residence or employment in cold, damp, or wet rooms or
localities; repeated exposure to bleak, cold currents of air or to
frequent wettings of the body or lower limbs. For these reasons it is
most common amongst the poor, who are especially exposed to the
influences just mentioned; and amongst them cellar-men and sailors,
washerwomen and maid-servants, are very liable to the disease. It is
chiefly an affection of advanced life, or at least of mid-age, and is
rare in youth. The first attacks, and especially exacerbations, are apt
to be induced by the direct action of a draught of cold air or by
unusual exposure to cold and damp air, especially when the body has
been fatigued or overheated. In many cases no distinct exciting cause
can be traced.

The morbid anatomy of simple chronic articular rheumatism will vary
with the severity and duration of the disease. The alterations are such
as chronic inflammation of a non-suppurative character might be
expected to produce in the joints by one who had learned those
characteristic of acute rheumarthritis. In the simple chronic form the
proliferating process involves chiefly the synovial membrane, the
capsular and other ligaments, and the periarticular tissues; to a less
degree the cartilages, and to a much less degree, and exceptionally,
the osseous surfaces. The synovial membrane is thickened, slightly
injected, and its fringes hypertrophied and more vascular than
normally. Little fluid usually exists in the joint unless during an
exacerbation, when a moderate amount of thin, cloudy serum may be
present; generally only a trace of thick, turbid fluid, containing
oil-globules, and in severe cases debris of the cartilages, but no pus,
is found. The fibrous capsule and ligaments become thickened, dense,
and stiffened by hyperplasia; and sometimes the adjacent tendons and
their sheaths, the fasciae and aponeuroses, undergo similar
alterations, so that the movements of the joints become seriously
interfered with. In some cases this irritative hyperplasia specially
involves these periarticular fibrous structures, and these, undergoing
retraction, produce marked deviations, subluxations, and deformities of
the articulations very like those observed in rheumatoid arthritis,
although the osseous components of the joints are unaffected. Jaccoud
gave to such cases the title of chronic fibrous rheumatism.[211] It is
worth noting that Jaccoud's, Charcot's,[212] and Rinquet's[213] cases
of so-called "chronic fibrous rheumatism" developed out of acute
articular rheumatism, while Besnier's was primarily chronic. In simple
chronic rheumatism, if protracted, the cartilages also proliferate,
lose their semi-transparency and polish, and become opaque and white;
they are often rough and traversed by fissures, and occasionally
present erosions; and these erosions {71} are either naked or covered
with a layer of newly-formed connective tissue, which may occasionally
produce fibrous adhesions between the articular surfaces. Points of
calcification occur in the cartilages and tendons in very chronic
cases. Instances are observed in which the bones exhibit, to a slight
degree, the alterations found in rheumatoid arthritis, and are probably
transitional between the two affections. The muscles which move the
affected articulations in severe cases are often atrophied, and the
wasting imparts to the joints an appearance of considerable
enlargement.

[Footnote 211: Vide Jaccoud, _Clin. Med. de la Charite_, 23e Lecon,
Paris, 1867.]

[Footnote 212: Besnier, _Dictionnaire Encycloped., etc._, t. iv., p.
680 _et seq._]

[Footnote 213: _Du Rheum. Artic. Chronique, etc._, par Martial Rinquet,
These, Paris, 1879, pp. 28-33.]

SYMPTOMS AND COURSE.--Simple chronic articular rheumatism presents many
varieties. In the milder forms the patient experiences trifling or
severe pain in one, or less frequently in two or more, joints, more
especially in the knee or shoulder, or both, attended with want of
power in the member or with stiffness in the affected articulation. The
pain frequently is likewise felt in the soft parts, muscular and
tendinous, near the joints, and is usually increased by active or
passive movement; it is not always accompanied by tenderness, and
rarely with local elevation of temperature or swelling. The wearying
aching in the joint is of an abiding character, but is very liable to
exacerbations, especially at night; and these come on just before
atmospheric changes, such as a considerable fall of temperature, the
approach of rain, variations in the direction of the wind, etc., and
they usually continue as long as the weather remains cold and wet. A
very common symptom is a creaking or a grating which may be felt and
heard during the movements of the joint.

The above symptoms may rarely prove more or less constant by night and
day for years, but far more frequently, at least at first, they last an
indefinite period and disappear to recur again and again, especially in
the cold and changeable seasons of the year. Although in the earlier
attacks, and often for a long time, no alteration of structure is
perceptible in the painful joints, yet in some instances slight
effusion into the articulation may be observed during the
exacerbations, or the capsule and ligaments may at length become
slightly thickened, or the muscles may waste and produce an apparent
enlargement of the joint; and this prominence of the articular surfaces
may be increased by retraction of the tendons and aponeuroses--a
condition which causes real deformities (deviations, subluxations,
etc.) of the articulation and impairs more or less its movements. In
very chronic cases a fibrous ankylosis may be established.

These last-mentioned conditions often entail great and long-continued
suffering, and may even cause some anaemia and general debility; but
very frequently the general health and vigor continue good,
notwithstanding the permanent impairment of the functions of one or
several of the large articulations, and the liability to exacerbations
often amounting to attacks of subacute rheumarthritis from changes in
the weather, fatigue, or exposure.

Besides the above varieties may be mentioned a not infrequent one
consisting of a series of attacks of subacute articular rheumatism
recurring at short intervals, involving the same joints, and attended
with slight elevation of temperature, febrile urine, perspiration, and
moderate local evidences of synovitis, heat, pain, tenderness,
swelling, and effusion into the affected joints. This is an obstinate
variety, and is often associated with rheumatic pain in the muscles and
fibrous tissues of the affected member.

{72} Simple chronic articular rheumatism, like the acute form, is most
apt to affect the larger articulations, knees, shoulders, etc., but it
frequently also involves the smaller ones of the hands and feet.
Although usually polyarticular, it is prone to become fixed in a single
joint, but even then it may attack several other articulations, and may
migrate from one to another without damaging any.

The course of the disease is usually one of deterioration during
persistent or recurring attacks, and in many cases the intervals of
relief become shorter and less marked; the joints become weaker and
stiffer; and although the pain may not increase and the general health
may not be seriously impaired, yet the patients may continue for many
years or the rest of their lives severe sufferers, unable to work, and
often hardly able to walk even with the aid of a stick. Occasionally,
after several years of pain and weakness, a sudden or slow improvement
may set in and the patient become free from pain and lameness, and only
experience some stiffness in the movements of the joints after several
hours of rest, and slight thickening of the ligaments and capsule of
one or more articulations. The duration of the disease is indefinite;
the danger to life trifling.

The complications of simple chronic articular rheumatism are held by
many, and especially by those who regard the disease as constitutional
or diathetic, to be the same as those of the acute form, and that they
may precede, follow, alternate, or occur simultaneously with the
articular affection. All admit that they are observed much less
frequently in the former than in the latter. Other pathologists either
deny the occurrence of the visceral complications (Senator, Flint) or
do not mention them (Niemeyer). It is not denied that cardiac disease
may be found in chronic articular rheumatism which has succeeded the
acute form, and which may then be referred to the acute attack. The
tissue-changes then set up may not have produced at the time the
murmurs indicative of endocarditis, but these tissue-changes may have
ultimately roughened the endocardium, puckered a valve, or shortened
its cords, so that cases of chronic articular rheumatism having a
history of an acute attack cannot be safely included when inquiring
into the influence of the chronic form upon the heart or other internal
organ. Attention has not been sufficiently given to ascertain the
frequency of the occurrence of these complications in primary chronic
articular rheumatism, and reliable evidence is not at hand. It is not
unlikely that the chronic form may slowly develop cardiac changes, as
the acute form rapidly does; but when the advanced age of the persons
most liable to chronic rheumatism is borne in mind, it must be admitted
that valvular and arterial lesions (endarteritis) are observed at such
periods of life independently of rheumatism, and referable to such
causes as repeated muscular effort, strain, chronic Bright's disease,
senile degeneration, etc. Somewhat similar observations are applicable
to the attacks of asthma, of subacute bronchitis, of neuralgia, and of
dyspepsia, which are frequently complained of by sufferers from simple
chronic rheumarthritis. Such affections are common in elderly people in
cold and damp climates; they may be mere complications rather than
manifestations of rheumatism, or outcomes of the confinement and its
attendant evils incident to chronic articular rheumatism, as is
probably the relationship of the dyspepsia. There is {73} no doubt of
the frequent coexistence of muscular rheumatism with this variety.

DIAGNOSIS.--Simple chronic articular rheumatism may be confounded with
rheumatoid arthritis, with the articular affections of locomotor ataxia
and other spinal diseases, with chronic articular gout, with syphilitic
and with strumous disease of the joints. The reader may consult the
observations made on four of these affections in connection with the
diagnosis of rheumatoid arthritis. A few additional remarks are called
for in distinguishing chronic articular rheumatism from chronic
articular gout, which is often a very difficult problem. Both are apt
to be asymmetrical in distribution, to have paroxysmal exacerbations,
to recur frequently without damaging the articulations, to have been
preceded by acute attacks of their respective affections, and to be
uncomplicated by endo- or pericarditis. But chronic rheumarthritis has
no special tendency to attack the great toe; it is more persistent than
gouty arthritis; it does not, even when of long standing, produce the
peculiar deformities of the articulations or the visible chalk-like
deposits in the ears or fingers observed in chronic gout. The etiology
of the two diseases is dissimilar. There is no special liability to
interstitial nephritis in articular rheumatism, nor is urate of soda
present in the blood in that disease.

In chronic strumous or tubercular disease of a joint the youth, the
personal and family history, and sometimes the evident defective
nutrition, of the patient; the moderate degree of local pain compared
with the considerable progressive and uniform enlargement of the joint;
the evident marked thickening of the synovial membrane, either early or
late according as the disease has originated in the synovial membrane
or in the bones; the continuous course, without marked remissions or
exacerbations, of the disease; the rarity with which more than one
joint is affected; and the tendency to suppuration, ulceration, marked
deformity, and final destruction of the joint,--will prevent the
disease from being mistaken for chronic rheumatism.

The PROGNOSIS in simple chronic rheumarthritis is unfavorable as
regards complete recovery, and it is chiefly while comparatively
recent, and when the sufferer can be removed from the conditions
productive of the disease, that permanent improvement, and sometimes
cure, may be expected. As a rule, the disease once established recurs.
It does not, however, endanger life.

TREATMENT.--All are agreed that hygienic treatment constitutes an
essential, if not the most valuable, part of the curative and
palliative management of chronic rheumarthritis. A dry and uniform
climate is the most suitable, and there is much evidence in favor of a
dry and warm rather than a dry and cold climate. Protection of the body
against cold and damp by means of flannel next the skin, sufficient
clothing, residence in dry and warm houses, etc., is of prime
importance. In fact, all the known or suspected causes of the disease
should be as far as possible removed.

The direct treatment of the disease resolves itself into general and
local, and is essentially the same as that recommended for rheumatoid
arthritis, to which subject the reader is referred. A few observations
only need be made here. Although, like everything else in chronic
rheumarthritis, it often fails, no single remedy has in the writer's
{74} experience afforded so much relief to the pain and stiffness of
the joints as the sodium salicylate; and he cites with pleasure the
confirmatory testimony of J. T. Eskridge of Philadelphia,[214] of whose
28 cases 75 per cent. were decidedly benefited. Jacob of Leeds also
reports some benefit in 75 per cent. out of 87 cases treated by the
same agent.[215] It must be given in full doses, and be persevered
with. Salicylate of quinia should be tried if there be much debility or
if the sodium salt fail. Propylamine or trimethylamine is deserving of
further trial in this disease. From 100 to 200 grains are given in the
day in peppermint-water. Iodide of potassium, cod-liver oil, arsenic,
iodide of iron, and quinia are all and several remedies from which more
or less benefit is derived in chronic articular rheumatism. The
combination of iodide of potassium with guiaiac resin--gr. ij-iij of
each three times a day in syrup and cinnamon-water--is sometimes very
useful. The writer has no experience of the bromide of lithium
(Bartholow). When the skin is habitually dry and harsh a dose of
pilocarpine every other night for a few times will often prove very
useful.

[Footnote 214: _Phila. Med. Times_, vol. ix. pp. 75-77, 1878, and _The
Medical Bulletin_, Phila., July, 1879, pp. 44-48.]

[Footnote 215: _Brit. Med. Jour._, ii., 1879, 171.]

Cod-liver oil, iron, quinia, etc., the various forms of baths and
mineral waters, electricity, and the several local measures recommended
for the treatment of rheumatoid arthritis, are all occasionally very
useful in, and constitute the appropriate treatment of, simple chronic
articular rheumatism. The dietetic management of the two affections
should be the same.


Muscular Rheumatism.

SYNONYMS.--Myalgia rheumatica or myopathia; _Fr._ Rheumatisme
musculaire; _Ger._ Muskelrheumatismus.

DEFINITION.--The affections included under this term are certain
painful disorders of fibro-muscular structures. They are commonly found
in persons the subjects of the rheumatic diathesis, and are
characterized by pain and often spasm, and sometimes a slight degree of
fever. No doubt as our knowledge increases so many attacks connected
with painful states of muscles and fasciae are eliminated from the
somewhat uncertain group of muscular rheumatism. True inflammation is
not believed to exist, and pathological investigation has rarely shown
any morbid changes in the affected parts. The symptoms, therefore, have
been attributed to some temporary hyperaemia, slight serous exudation,
or neuralgic state of the sensory nerve-filaments. The strongest
support is given to this statement from the absence of any marked
tenderness in such affected muscles as can be sufficiently examined. In
certain cases, undistinguishable clinically, it is quite probable that
a periarthritis is in reality the principal factor in the case. In
others, again, a subacute rheumatism affecting a joint seems to spread
to the adjoining tendinous sheaths, and thus secondarily to attack the
muscles themselves, the affection of which may ultimately remain the
only condition present.

ETIOLOGY.--Muscular rheumatism is a very common affection. All ages are
liable to its occurrence, but the part affected varies with the time
{75} of life, children and young adults being much more subject to
torticollis, and older persons to lumbago and general rheumatism of the
limbs. Amongst hospital patients the disease prevails more amongst men
than women, owing doubtless to the greater exposure of the former to
the cold; but amongst other classes the same difference is not seen. It
is observed in all countries, but according to some writers it is
unusually frequent in tropical climates, although there acute
rheumatism is very uncommon. The causes of muscular rheumatism are
mainly exposure to cold and strain or fatigue of muscles. If these two
conditions coexist--_e.g._ standing in a draught of cold air or lying
on the ground when fatigued--the chances of the affection coming are
greatly enhanced. Strain, a twist of the body, or a false step can
actively start an attack of this kind, and by the sufferers themselves
it is constantly attributed to this cause. The part played by this
element is difficult to determine, a very slight strain being often
followed by great pain and distress from the subsequent rheumatic
affection. Some individuals are specially prone to attacks, the
slightest current of air, change of clothing, etc. being sufficient to
determine its occurrence. These persons are often found to have
suffered from rheumatism in some other form, and thus in them we must
consider that the rheumatic diathesis furnishes the reason for their
unusual susceptibility. It only remains to mention the fact that a
disposition to gout seems to favor the development of muscular
rheumatism. In gouty families, therefore, it has been observed to be
common.

SYMPTOMS.--In all cases pain is the prominent, and in many cases the
only, symptom present. In all except the more aggravated attacks pain
is felt only when the affected part is disturbed. In such when complete
rest or fixed immobility is maintained there is comfort, or at most a
somewhat dull, uneasy sensation, but when any contraction of the
muscles in question is produced, whether voluntary or otherwise, severe
often excruciating pain is at once experienced, often giving rise to a
sudden cry or causing the features to be contracted in a grimace. The
suffering ceases almost at once when the muscular contraction is
relaxed. In more aggravated attacks the pain is more severe, and
besides persists, though to a less degree, even when there is no
contraction. In rare cases when the maximum degree has been attained
there is continuous pain, but the affected muscles are persistently
maintained in a relaxed condition by means of true spasm in the
surrounding muscles. Slow passive movement affects the subject of
muscular rheumatism, and may often be accomplished with a little
management without causing pain. If, at the same time, these muscles be
handled by pinching and slight pressure, it will be found that they are
very sensitive to the touch. When some tenderness does exist, it is
slight and is not located in the district of the lower nerve-trunks.
Pressure even sometimes allays pain. The constant effort to avoid pain
gives rise to a feeling and appearance of stiffness, and thus
characteristic attitudes and positions of the head, trunk, or limbs are
voluntarily and persistently maintained. There is no spasm of the
affected muscles; the distortion is the result of stiff contraction of
the associated muscles, which thus forcibly fix the faulty one and hold
it in a state of relaxation. Cramp or spasmodic contraction of a single
muscle of a painful character does, however, sometimes occur in
rheumatic subjects, and much resembles the condition above described.
In {76} the same persons also muscular rheumatism may occur in a much
more fugitive or erratic form, frequently being nothing more than a
slightly painful condition of some group of muscles which have in some
way been exposed to cold. This may last but a short time, and either
spontaneously disappear or be readily removed by exercise or friction.
Muscular rheumatism is generally confined to one muscle or a single
group of muscles. Those most liable to it are the very superficial and
those easily exposed to cold (_e.g._ the deltoid and trapezius),
powerful muscles often subjected to violent strain (_e.g._ the lumbar
muscles), and those aiding in the formation of the parietes of the
great cavities.

This affection very commonly exists without any constitutional
disturbances, but sometimes there are present the symptoms of
pyrexia--slight elevation of temperature and temporary disorder of the
digestive organs--loss of appetite, constipation, and general malaise.

The acute forms generally last but a few days, terminating by gradual
subsidence and final disappearance of the pain. The fugitive kind,
already alluded to, may, however, be present more or less during
several weeks.

DIAGNOSIS.--Errors of diagnosis between muscular rheumatism and a
variety of other disorders are common. Laymen especially are only too
apt to attribute pain felt in muscles at once to rheumatism of these
muscles--a term which is badly abused. Some of these errors are of no
great interest, but others are of the highest importance, for they may
cause the onset of a serious disease to be overlooked. The principal
affections to be borne in mind with reference to diagnosis are the
following: organic diseases of the spinal cord (notably tabes
dorsalis), causing peripheral pains as an early symptom; functional
disorder of the same part, as hysteria or spinal irritation;
intra-thoracic inflammation; the onset of an exanthem; the pains
produced by the chronic poisoning of lead and mercury; neuralgia;
painful spasm of muscle from deep-seated inflammation or suppuration.
It is sufficient to indicate these various sources of fallacy, which,
if remembered, can generally be guarded against by a consideration of
the special features characteristic of each one.

TREATMENT.--The indications for the treatment are mainly two--viz. to
relieve the pain and to counteract the diathetic condition generally
present. The relief of the pain is accomplished in various ways,
according to the seat of the trouble. In severe cases it is proper to
resort to the hypodermic use of morphia, to which may be advantageously
added some atropia. When the pain is seated in large muscles, the
injection will produce better results if thrown not merely under the
skin, but into the substance of the muscle. Sometimes perfect rest in
bed is necessary to secure the required immobility; in other cases this
can better be secured by plaster or firm bandages. Soothing anodynes
are extremely useful locally, and counter-irritants also may be used
with benefit. Liniments give us a convenient form of application. The
best are those containing a considerable proportion of chloroform with
either aconite or belladonna, or both. The repeated application of
tincture of iodine often gives great relief. Galvanism sometimes proves
a rapid cure. Continuous heat is nearly always grateful, and may be
applied either in the dry form or by means of soft warm linseed
poultices with or without a {77} percentage of mustard. When these are
discontinued, care should be taken to protect the affected muscles from
cold by keeping them enveloped in flannel or woollen coverings.

Whilst these local measures are being adopted the constitutional
disorder should also receive attention. A diaphoretic action should be
set up. For this purpose the hot-air or Turkish bath at the outset
would seem to be sometimes really abortive. Of medicinal means amongst
the most reliable are liquor ammonii acetatis and Dover's powder.
Pilocarpine occasionally proves useful. The fixed alkaline salts are
also sometimes beneficial, such as the acetate and citrate of potassium
and, at a later stage, the iodide of potassium. In a certain number of
cases of muscular rheumatism the sodium salicylate acts promptly and
well. This drug will succeed well in proportion as the evidence of the
rheumatic constitution is well marked, as shown by the tendency on
other occasions to attacks of acute articular rheumatism.

Persons who are subject to muscular rheumatism should be made to wear
warm clothing, avoid draughts, guard against strains and twists, and in
other respects to be careful of their general hygiene. Obstinately
recurring cases will very often receive benefit from a visit to some of
the natural springs known to possess antirheumatic qualities.

The chief varieties of muscular rheumatism, divided according to the
locality affected, require some separate description.

1. Lumbago, or myalgia lumbalis, is that common form which attacks the
lumbar muscles and the strong aponeurotic structures in connection with
these. It is more frequently than any other form attributed to some
effort of lifting or sudden twist of the trunk, but in many cases it
owes its origin directly to exposure to cold. The pain comes on
suddenly and renders the person helpless, the body, if he is able to go
about, being held stiffly to prevent any movement or bending; if
severe, he is absolutely compelled to observe complete rest in bed. The
muscles, when handled, appear slightly sore, but no local point of
acute tenderness can be found. This fact, with the characteristic
shrinking from any movement, distinguishes lumbago from neuralgia and
from abscess. Pain in the loins, more or less severe, is such a
frequent accompaniment of disorder of several organs and parts that
careful examination should always be instituted lest some serious
organic disease with lumbar pain as a symptom be mistaken for a simple
lumbago. The most important of these are perinephritis, lumbar abscess,
spinal disease, abdominal abscess, and disease of the rectum and
uterus.

2. Pleurodynia, myalgia pectoralis or intercostalis. Here the affected
muscles are the intercostals, and in some cases the pectorals as well.
Spasmodic pain is felt in one or other side of the chest, and is
especially aggravated by the movements of respiration; it is rendered
intense by the efforts of coughing or sneezing. Pleurodynia may be
confounded with pleurisy, the distinguishing features being the absence
of fever and the friction sound of pleurisy. Intercostal neuralgia is
sometimes with difficulty known from pleurodynia, but in the former the
pain is more circumscribed, more paroxysmal, and more easily aggravated
by pressure than in pleurodynia, and when severe there are tender
points in the course of the nerve a little outside of the middle line
posteriorly (dorsal point) and anteriorly (sternal point). Now and then
the hyperaesthetic {78} areas become anaesthetic, and even patches of
herpes may form in the course of the nerve, when doubt can no longer
remain. From periostitis of a rib pleurodynia may be known by the fact
that in the one the tenderness is marked in the intercostal space, and
in the other in the rib itself. Pleurodynia is a frequent accompaniment
of thoracic affections, causing cough, the frequent paroxysms of
coughing tending to induce a painful state of the overworked muscles.
The pain, which may be very great, can often be controlled by fixing
the chest with imbricated plaster or a firm bandage. Dry cups sometimes
answer very well; if more active measures are necessary, then
hypodermic injections of morphia must be resorted to.

3. Torticollis, myalgia cervicalis, stiff neck or wry neck, caput
obstipum. This term includes those cases of rheumatic idiopathic
affection of one or more of the muscles of the side and nape of the
neck, which fixes the head firmly in the median line or else in a
twisted fashion, with the face turned toward the sound side. The
disease can be recognized at a glance by the peculiar manner in which a
person will turn his whole body round instead of rotating his head
alone. It is much more common in children than in adults. The
sterno-mastoid is the muscle chiefly affected, but any of the muscles
of the neck may become rheumatic in the same way, and frequently
several of them suffer at the same time. The most important point at
the outset of an attack of wry neck is to determine whether we have to
do with a true rheumatic (idiopathic) disorder, or whether the muscular
stiffness is secondary to some spinal or vertebral lesion. The
diagnosis is usually founded upon the suddenness of the onset, the
absence of other symptoms of nerve disease, and the rapid course of the
case, terminating in a cure in a few days. There is nothing special in
the treatment of torticollis beyond what has been already said under
the general heading.

Other forms of muscular rheumatism which have received special names
and have been separately described are the following: myalgia
scapularis or omalgia, when the surroundings of the shoulder are
affected; myalgia cephalica or cephalodynia, an affection of the
occipito-frontalis; and abdominal rheumatism, when the external muscles
of the abdomen are involved.


Rheumatoid Arthritis.

SYNONYMS.--Nodosity of the joints (Haygarth); Chronic rheumatic
arthritis, or rheumatic gout (Adams); Arthritis, rheumatismo
superveniens (Musgrove); Goutte asthenique primitive; Arthritis
pauperum; A. sicca; Usure des cartilages articulaires (Cruveilhier);
Arthrite chronique (Lute); Progressive chronic articular rheumatism;
General and partial chronic osteo-arthritis;[216] Arthritis deformans.

[Footnote 216: _Nomenclature of Diseases R. C. Physicians_, London.]

Neither my space nor time will permit of a history of this disease; it
must suffice to say that Sydenham in 1766-69 appears to have first
tersely described it and distinguished it from gout; that in 1800,
Landre-Beauvais in his inaugural thesis made some observations upon the
disease under the title of primary asthenic gout; that in 1804,
Heberden, and {79} more especially Haygarth, in 1805, pointed out some
of the more striking clinical features of this disease, and
distinguished it from both gout and chronic rheumatism under the title
nodosity of the joints. The latter author, in the work mentioned,
claims to have written a paper upon the subject twenty-six years
previously, although it was not published; and to him belongs the merit
of having so described the disease as to have given it a place in
nosology. Incidental allusions were made to the affection in 1813 by
Chomel, in 1818 by Brodie, and by Aston-Key in 1835; in 1833, Lobstein,
and about the same time Cruveilhier, pointed out some of the more
striking characters of the morbid anatomy of the affection. But it is
to Adams of Dublin that we are indebted for the most complete account
of the anatomy and of many of the clinical features of the
disease--first in a paper read before the British Association in 1836,
next in his article on "The Abnormal Conditions of the Elbow, Hand,
Hip, etc.,"[217] and finally in his able monogram "On Rheumatic Gout"
in 1857. The contributions to this subject since that date have been
very numerous as well as valuable from the leading countries of Europe,
and I must not here attempt to assign to each investigator his proper
portion of the work.

[Footnote 217: Todd's _Cyclop. of Anat. and Phys._ (1836-39).]

It may be here remarked that Landre-Beauvais and Haygarth described
more particularly that form of the disease which, beginning in the
small joints of the extremities, tends to extend to the larger joints
in a centripetal way, and to involve many of them--peculiarities which
have given rise to the epithets progressive polyarticular chronic
rheumatism, peripheral arthritis deformans, and which is the form of
the disease usually described by physicians as rheumatic gout,
rheumatoid arthritis, nodular rheumatism, and by the other names just
mentioned. On the other hand, Key, Colles, Adams in his earlier paper,
and R. W. Smith described the disease as it affects the larger joints,
hip, shoulder, or knee, to one or two only of which it may be confined;
and as this variety is frequently observed in elderly persons, and in
them often involves the hip, it is often spoken of as senile arthritis,
malum senile articulorum, morbus coxe senilis, mono-articular arthritis
deformans, partial chronic rheumatism, and has been described by
surgeons rather than by physicians. However, even when beginning in the
hip or shoulder, the disease is apt to involve several of the
intervertebral articulations, and not unfrequently to extend to other
joints than the one first affected, and even to the peripheral joints.
Its progressive and general nature is thus evidenced, whether it invade
from the beginning a single large joint or several symmetrical small
articulations. Finally, on this topic Charcot has insisted that
Heberden's nodi digitorum contributes a special form of the disease
under consideration, and proposes to call it Heberden's rheumatism or
nodosities.[218]

[Footnote 218: _Lectures on Senile Diseases_, Syd. ed., 1881, p. 137.]

Rheumatoid arthritis presents the clinical varieties or groupings of
phenomena just mentioned, at times quite distinctly appreciable from
one another, but sometimes more or less blended, yet even then
manifesting in their periods of invasion and early stages an adhesion
to all of these typical groupings. Charcot has especially dwelt upon
these: 1st, the general or polyarticular and progressive form; 2d, the
partial or oligo- or mono-articular form; 3d, Heberden's nodosities.

{80} 1st. The symptoms and clinical history of general or polyarticular
and progressive rheumatoid arthritis. This is the most common form of
so-called chronic rheumatic arthritis, the classical rheumatic gout, or
rheumatisme noueux, and it may declare itself, as Garrod and Fuller
pointed out, very rarely in an active or acute form, or, as it usually
does, in a chronic and insidious form.

The acute form of rheumatoid arthritis closely resembles the milder
varieties of acute articular rheumatism or the best marked examples of
the subacute form of that disease. But it presents the following
particulars, by which it may generally perhaps, but not always, be
distinguished: while the temperature, the thirst, the furring of the
tongue, the frequency of the pulse, the articular pains and tenderness,
etc., are less developed than in acute articular rheumatism, there is
wanting the profuse and continued perspiration, the early involvement
of the endo- or pericardium in the inflammation, and the prompt
prostration of the strength so commonly witnessed in that disease. On
the other hand, while the rheumatoid affection may involve the larger
joints--knees, ankles, elbows, and wrists--it almost certainly
implicates the smaller joints of the fingers, and often of the toes.
There is apt to be greater effusion into the synovial capsules
(McLeod's capsular rheumatism) and into the synovial sheaths and bursae
about the affected joints than in ordinary acute or subacute
rheumatism; further, the inflammation does not migrate from joint to
joint, but obstinately persists in several of them, and more especially
in the wrist and in the metacarpo-phalangeal joints of the index and
middle finger, perhaps also in the ankles and in the
metatarso-phalangeal articulation of the great toe. Instead of
disappearing in four to six weeks, the articular inflammation
continues, although the pain may abate very much, and the capsules of
the joints continue swollen and rather tense. The muscles of the
extremities waste, and are the seat of painful reflex spasms which
interfere with the movements of the joints; and although the patient is
capable of moving about, and is free from all febrile disturbance, one
or several of his joints remain permanently swollen, painful, and
crippled. Perfect restoration of all the affected joints seldom if ever
occurs. In common with other observers, I have met with this acute form
most frequently in young women twenty to thirty years of age--several
times in connection with recent delivery or rapid child-bearing, or
lactation; once after what was regarded by the medical attendant as an
attack of acute rheumatism occurring not long after labor. It has been
observed in children, and is not uncommon after forty. These patients
usually suffer in their general health--become weak, pale, depressed in
spirits, and lose flesh. In several cases of this form marked intervals
of improvement have occurred; the local disease has ceased to progress,
and tolerable comfort has been experienced, perhaps, till pregnancy,
delivery, or lactation again determined a fresh outbreak of the
disease. Sometimes, however, this acute form steadily advances, and in
a year or two establishes changes in the cartilaginous and osseous
structure of the affected joints. Such a case I met in a lady of
twenty-one who had had a good deal of anxiety as a mathematical
teacher, and whose illness set in during vacation while at the seaside.
It proved obstinately progressive for several years, until several of
the larger joints, as well as the smaller, were badly crippled.

{81} The primary chronic form is much the more frequent, although
between it and the acute variety there are many intermediate grades.
For weeks or months the patient may experience numbness or formication
and rheumatic pains in the limbs, perhaps with a sense of stiffness in
the joints, especially felt after rest or the day after unusual
fatigue. Then one or more joints--most frequently the
metacarpo-phalangeal of the fingers--become painful, swollen, tender
when touched, and inordinately hot; these symptoms may subside under
rest or treatment, and after weeks or months recur, either without
known cause or from exposure, fatigue, or some impairment of the
health. Usually, the original joint is again affected, but frequently
one or two more of the same on the other hand suffer likewise. More or
less complete remissions of the pain and local inflammation now tend to
take place from time to time and alternate with exacerbations or fresh
attacks of the local disturbance, and the disease extends, as it were,
centripetally and more or less symmetrically to the wrists, then to the
elbows, and then to the shoulders, or from the toes to the ankles and
thence to the knees--although there is no invariable sequence of this
kind--and next to the hands; the knees are specially liable to
invasion. Of Haygarth's 34 cases, in 2 the knees alone suffered, and
"in all or nearly all the rest the hands, chiefly the fingers, were
probably affected." In Charcot's 45 cases the debut took place in the
small joints of the hands and feet 29 times; in the hands, feet, and
one large articulation, 7 times; in one large joint, and later in the
fingers, 9 times. Even in this primary chronic form there is usually in
the earlier stages some effusion into the joints; the soft parts of the
articulation are thickened and swollen; obscure fluctuation in the
smaller and very distinct fluctuation in the larger joints may be felt.
The pain may be severe, especially at night, and during the
exacerbations of the disease it varies greatly in its degree and
persistency. The position and shape of the joints are altered, partly
by spasmodic retraction of the muscles, and more or less by the
effusion into the capsules and adjacent bursae and sheaths, and the
thickening of the soft parts covering the articulations. As the disease
progresses further deformities ensue from the growth of new bone around
the heads of the bones, the absorption of the articular cartilage, the
development of masses of cartilage in the hypertrophied synovial
processes and beneath the synovial membrane at the margin of the bones;
the relaxation of the articular ligaments; and the displacements and
subluxations of the unshapely bones composing the joint. The great
wasting of the muscles of the member affected has some share in
producing its unnatural appearance. In the advanced stage there is more
or less abiding pain, soreness, and stiffness in the affected
articulations, violent cramps are experienced in the course of the
adjacent muscles, and pains either along the nerves or vaguely down the
limbs. Crackings or creakings are to be heard, and grating is to be
felt during the movements of the joints; these movements become more
and more restricted, so that an immobility almost equal to that of true
bony ankylosis is established, this result seldom occurring except
amongst the carpal, tarsal, tibio-tarsal, and the vertebral
articulations. Interlocking of the osteophites formed on and around the
articular surfaces, and in other cases union of these surfaces by the
interposition of newly-formed fibrous tissue, produce a spurious
ankylosis {82} destructive of the articular functions. In the very
advanced stages the feet, ankles, and legs are often considerably
enlarged and the integument thickened by a chronic oedematous
infiltration, or the bones and soft parts are atrophied and the
integument is pale, smooth, and attenuated, resembling parchment or the
condition seen in certain stages of scleroderma and tightly drawn over
the wasted rigid fingers. This primary chronic form is especially apt
to progress steadily for many years, the joints earliest affected
becoming gradually more distorted and crippled, and fresh joints
becoming invaded until there may hardly remain a single sound
articulation in the limbs, or even in the body; and at length the
patient may be unable to feed himself or masticate or raise his chin
from his sternum or rotate his head or stand.

The deformities of the several joints, being largely the result of
muscular contraction, observe certain general types, which, however,
are not peculiar to the disease, but occur in various affections of the
nerve-centres, involving paralysis or spasm or both. Charcot has
carefully described those met with in the hands, and I must refer to
his masterly article upon chronic articular rheumatism for his account
of them.

(1) It must suffice to say here that the predominant features of the
hand in chronic rheumatoid arthritis are the following: The first
phalanx of the fingers is either flexed upon the metacarpus or
extended, and the terminal phalanx in like manner is either markedly
flexed or extended upon the second, or these two phalanges are
maintained in a straight line, while the first phalanx is, as usual,
decidedly flexed upon the metacarpus.[219] In all these varieties the
hand is pronated; there is a great tendency to deviation of the fingers
toward the ulnar border of the hand, although sometimes the deformed
fingers stand out, not unlike a bunch of parsnips. The thumb escapes
longer than the other fingers, and its metacarpo-phalangeal joint is
usually flexed, rarely extended.

[Footnote 219: _Lectures on Senile Diseases_, Syd. ed., trans. 1881.
Figs. 1 and 2, Pl. II., on the hand, give good illustrations of these
deformities.]

(2) The great toe, enlarged at the metacarpo-phalangeal articulation,
is usually drawn to the outer border of the foot, across and above, but
rarely below, the other toes, and the foot is usually abducted and
flattened, the prominent internal border resting on the ground. The
wrist, elbow, and knee-joints are generally flexed; the distal ends of
the ulna and radius, more or less enlarged, project backward; the
semi-flexed tibia is drawn backward on the femur and rotated outward,
thus rendering the internal condyle of the femur prominent and
displacing the patella toward the external condyle, and foreign bodies
may frequently be felt in the enlarged knee- and elbow-joints. Finally,
the extremities of the affected bones will, as a rule, be found
enlarged and misshapen, and nodosities, rims, tips, ridges, and
stalactiform growths of new bone may be felt on them.[220]

[Footnote 220: Figs. 12 to 18 and 22 in Adams's _Treatise on Rheumatic
Gout_ are nice illustrations of these deformities.]

The general condition in this chronic form varies in different
individuals, and there is no characteristic disturbance of the
functions, such as obtains in chronic gout. There is no elevation of
temperature, unless to a slight degree during an active crisis of the
disease; the tongue may be clean, the pulse tranquil, the appetite and
digestion satisfactory, and {83} the urine normal or perhaps pale and
of low density. Fuller, however, says that "more generally the
complexion is sallow and the skin sluggish, and evidence of mischief is
furnished by yellowishness of the conjunctivae, constipation of the
bowels, a pale and unhealthy character of the dejections, excessive
flatulence after meals, turbidity of the urine, and fulness of the
pulse." My own experience hardly harmonizes with this, and I have seen
many persons suffering for years from the general and partial form in
the enjoyment of excellent general health. Should, however, the disease
develop in a person the subject of menorrhagia or other uterine
disorder, or of repeated child-bearing, or after prolonged mental
anxiety, some disturbance of the general health fairly referable to
such disturbing conditions may be certainly looked for. In the advanced
stages the prolonged suffering and confinement often induce anaemia,
dyspepsia, and failing health.

More numerous and exhaustive analyses of the perspiration, urine, and
blood in the disease are needed. There is no uniform condition of the
skin; general perspirations, chiefly at night, often obtain, but I know
of no authoritative report as to the chemical reaction of the sweat in
this disease; Garrod[221] and Charcot[222] vouch for an absence of uric
acid in the blood, while Marrot[223] found both this acid and the urea
below the normal quantity in the urine, although the acid increased
notably under baths of high temperature.

[Footnote 221: Reynolds's _Syst. Med._, i. 918.]

[Footnote 222: _Loc. cit._, p. 190.]

[Footnote 223: _Contribution a l'Etude des Rheum. Artic., Examen de
l'Urine et du Sang_, Paris, 1879, p. 42.]

Certain affections other than the articular have been occasionally
observed in persons suffering from rheumatoid arthritis, but many even
of those authors who regard the disease as a form of rheumatism speak
of these affections as coincidences, and not as essential
manifestations of the disease. Charcot and Besnier, however, maintain
the latter to be their true relation to the articular affection which
they regard as chronic rheumatism. The two authors just named allege
that all the visceral localizations that occur in acute articular
rheumatism may obtain in the nodular form, but that such localizations
are infinitely less frequent and serious than in the acute, subacute,
or simple chronic forms of articular rheumatism--that endo- and
pericarditis undoubtedly do occur in nodular rheumatism, and appear
especially where there is an exacerbation of the disease and where
there is some approach to the acute state.[224] As Charcot has adduced
these cardiac affections in proof of the rheumatic nature of rheumatoid
arthritis, it is deserving of mention that he had personally met with
but two instances of endocarditis and five of pericarditis, four of the
latter having been discovered not during life, but in nine autopsies,
and that he cites only eight other cases of endo- or pericarditis which
had been either published or reported to him. He admits too that there
had generally been in these cases, at some former period, an attack of
acute rheumatism. Besnier, Homolle, Malherbe, Vidal, and Colombel, in
their articles upon the disease under consideration, do not cite a
single case in which they have seen cardiac disease in rheumatoid
arthritis. On the other hand, McLeod, Garrod, Fuller, Flint, Senator,
and Pye-Smith either deny or ignore the occurrence of cardiac disease
as a manifestation or complication of this disease. My personal {84}
experience coincides with that of those authorities last cited, except
in one instance, and that is open to the objection that the patient's
father had had acute articular rheumatism, the mother was the subject
of chronic deforming arthritis, and the patient had experienced during
many winters an affection which began in the smaller joints and
permanently damaged them; when first seen by me he had chronic disease
of the aortic valves. He may have had true articular rheumatism as well
as rheumatoid arthritis. His father had experienced the one, his mother
the other. If those instances be excluded in which a former attack of
acute rheumatism might be adduced in explanation of the supervention of
cardiac disease, but few cases will remain to suggest that rheumatoid
arthritis may develop endo- or pericarditis; and when it is borne in
mind that in several ways the cardiac affections may have arisen as
mere coincidences of the rheumatoid affection, it is well to wait for
further evidence before accepting as proved the occurrence of cardiac
affections as local manifestations of rheumatoid arthritis. Garrod's
observation is still pertinent: "The form of the disease in which acute
cardiac inflammation has occurred may be rather that of true articular
rheumatism of a very subacute character."

[Footnote 224: _Loc. cit._, 172-175; Besnier, _loc. cit._, 699.]

Nor is the evidence at all satisfactory in favor of any special
tendency to the following affections, much less of their being local
manifestations of rheumatoid arthritis: viz. pleuritis (McLeod,
Fuller), asthma (Charcot), chronic laryngitis (Garrod), grave cerebral
or spinal disturbances (McLeod, Fuller, Vidal), paralysis agitans,
locomotor ataxia, sciatica, trifacial neuralgia, and albuminous
nephritis.[225]

[Footnote 225: To mention only some of the many sources of cardiac
disease other than rheumatism may be adduced scarlet and other fevers,
extension of inflammation from the pleura or lung and other sources of
local irritation, powerful or oft-repeated muscular efforts, Bright's
disease, senile degeneration, etc.]

Among the more frequent complications may be mentioned migraine,
certain cutaneous affections, more especially psoriasis, prurigo,
lichen, and some diseases of the eye, chiefly iritis, which is apt to
be relapsing, and sometimes episcleritis. It is remarkable that iritis
very seldom occurs as a complication of acute articular rheumatism.

The so-called rheumatic nodules occur also in chronic rheumatoid
arthritis. It is not yet established that they are peculiar to
rheumatism and to rheumatoid arthritis. Dr. Stephen Mackenzie has seen
them in one instance in tertiary syphilis, the patient not having had
arthritis, rheumatism, or chorea.

2d. The partial or oligo-articular form of rheumatoid arthritis, like
the general or polyarticular variety, is usually a primarily chronic
affection, insidious in its invasion and slow in its progress. It is
chiefly observed in old persons, especially men (senile arthritis),
affects frequently a single joint, and chiefly the hip, but
occasionally the knee, shoulder, or spinal column, either as a
consequence of special injury or of the wear and tear of life, or
exposure to cold and wet, or even of what seemed to be simple acute or
subacute articular rheumatism or gonorrhoeal rheumatism. When not the
result of injury, two or three joints may suffer, both hips or knees,
or hip and some of the vertebrae, hip, knee, and ankle of the same
limb, and so on. Even in those cases in which the disease for a long
time is confined to a single joint and may have been caused by an
injury,[226] other joints, finally, are apt to become {85} affected,
often in a symmetrical order. So that it may seem almost general, or at
least polyarticular, just as the converse sometimes happens in the
general rheumatoid arthritis of long standing, where the disease
becomes greatly aggravated in one articulation and produces great
deformity and destruction of it, the others remaining as they were.

[Footnote 226: See Ord's case, II., _Brit. Med. Journal_, i., 1880,
158.]

The symptoms of this partial chronic form are very much those of the
general form already described, but there is usually in the early
stages less heat, tenderness, and swelling of the affected joint; the
pain is less acute, but more abiding, and, with the exception of more
or less stiffness or impeded movement in the joint, it may be the only
sign of disease present, so that at this stage of the affection it may
be taken for simple chronic articular rheumatism. But the disease
persists; the voluntary movements become more painful and difficult;
slight exercise of the joint is followed promptly by fatigue and
aggravation of the pain, and yet the articular surfaces may be pressed
together, and flexion and extension be practised, without causing much
suffering. Slowly and continuously alterations take place in the
affected articulation; with but little heat or redness it enlarges
steadily, the soft parts becoming infiltrated and thickened, or
effusion taking place into the capsule; the articular surfaces become
irregularly depressed by the growth of osteo-cartilaginous rings,
osseous nodosities, and stalactiform processes upon them, and these
irregularities, together with one or several loose bodies, may be felt
in the joint. The enlargement of the articulation becomes more
apparent, owing to the wasting of the muscles of the limb; its
movements become more and more restricted and difficult, although
perhaps not more painful, and are attended with creakings and gratings
perceptible to the ear and hand; and at last nearly all movement of the
joint may be prevented by the alterations in the shape of the
epiphyses, or by the interlocking of the osseous outgrowths, or in rare
cases by actual union of the bones. This form constitutes, par
excellence, arthritis deformans. In many instances there is little
effusion throughout the process, notwithstanding the grave deformity in
progress; hence the term dry arthritis. Even the partial form is
sometimes more active in its invasion, as when it very rarely succeeds
acute or subacute articular or gonorrhoeal rheumatism, or, more
frequently, follows an injury.

The duration of the partial form is usually very protracted; it may be
ten or twenty years. Exacerbations of the disease occur from time to
time, in the intervals of which the patient may be free from pain,
although the affected joints are seriously crippled.

The affection is not in itself fatal; the patient may attain an
advanced age and die of some intercurrent disease, such as dysentery,
pneumonia, cerebral hemorrhage, or other affection incident to old age.

A description of the features presented by partial rheumatoid arthritis
affecting the hip (morbus coxa senilis), the shoulder, and other joints
rather appertains to works on surgery, and only a glance at the
evidences of the disease in the vertebral column (spondylitis
deformans) will here be given. When the cervical vertebrae are
implicated the power of rotating the head from side to side is usually
preserved and is attended with a crackling noise, while the rest of the
cervical region is stiff and the head cannot be bent forward; when the
dorsal or lumbar vertebrae suffer the back becomes bent, the patient
stoops greatly and cannot stand {86} erect, and his body is shortened
and more or less twisted. A careful examination will discover not only
the great rigidity of the spine, and as it were fusion en masse of its
joints, but in these persons the bony outgrowths may be felt.
Occasionally the alteration in the vertebrae by compressing the cord or
its membranes, or the spinal nerves and ganglia, may produce neuralgic
pains in the cervical, dorsal, lumbar, or sciatic nerves, wasting of
the muscles, more or less paralysis, and even vasomotor disturbances.

3d. Heberden's nodosities are certainly sometimes the effect of
rheumatoid arthritis, implicating chiefly, often solely, the distal
joints of the fingers, where it slowly forms two little hard nodules
about the size of dried peas upon the side of the articulations. These
are notably enlarged and their movements impaired, but pain is seldom
experienced, and were it not for deviation of the end of the finger to
one side or the knob-like excrescences upon the joints--appearances
which much disfigure the hand--patients would not speak of the
affection. In many cases these alterations likewise involve, but in a
minimum degree, the first phalangeal articulations, and less frequently
the metacarpo-phalangeal, and even some of the larger joints--the
wrist, knee, or hip, etc. Like the other varieties of rheumatoid
arthritis, this form occasionally has a more active invasion than is
above mentioned, and may be attended by local pain, heat, and redness,
or such symptoms may occur as exacerbations of the chronic disease.

Gout may precede these nodosities, or, as in the case of
Charcot's,[227] the latter may precede the former by several years.
Finally, Charcot remarks that Heberden's nodosities are "often
accompanied by asthma, migraine, neuralgia, especially of the sciatic
nerve, and muscular rheumatism, and that these manifestations may
alternate with the exacerbations of the disease."

[Footnote 227: _Loc. cit._, 198.]

MORBID ANATOMY.--Every component tissue of the articulations exhibits
signs of a chronic inflammatory process. In the chronic form affecting
the larger joints the synovial membrane is found more or less
congested, opaque, and thickened; at the point of its reflection upon
the bones its fringes are thickened and injected and their villosities
greatly increased in number, length, and thickness, and in extreme
instances have been aptly compared to the wool on a sheep's back. The
cartilage-cells normally existing in the synovial fringes likewise
proliferate and develop into cartilaginous growths, many of which
become infiltrated with lime salts, or even ossified, and in this way
originate some of the foreign bodies, pedunculated or sessile, which
are found in the joints. These may be attached to the synovial fringes,
or imbedded in the membrane itself, or set free by rupture of their
pedicles. In some examples these neoplasms resemble in size small
melon-seeds; in others they form irregular masses, many of which are as
large as hazel-nuts.

At the outset there is frequently an increase of synovial fluid, richer
in mucine than natural, which lessens considerably in the later stages
and becomes a turbid, viscid fluid of a dirty white or reddish-yellow
color, containing no pus, but degenerating epithelium and fragments of
villosities and cartilage. In many cases, more especially of the
partial {87} form, very little effusion into the articulations takes
place (arthrite seche).

The inflammatory irritation excites proliferating and degenerating
processes in the cells and basis-substance of the cartilage covering
the bones, and the changes described in connection with acute rheumatic
arthritis ensue. Those parts of the cartilage covering the bones which
suffer pressure in locomotion fibrillate on their surface, and either
undergo mucous degeneration, resulting in ulceration and complete
absorption, or are thinned and worn away by attrition. In either way
the ends of the bones become laid bare. Those portions of the cartilage
at the periphery of the joints which escape compression in the erect
posture likewise proliferate, but, according to Cornil and Ranvier, in
consequence of being covered by the synovial membrane the proliferating
elements are retained in situ, instead of escaping into the articular
cavity, and develop into actual cartilage, and may ultimately ossify.
In this way irregular masses of cartilage (enchondromata) and bone
(osteophytes) form around the heads of the bones, enlarging them
considerably, altering their shape, encroaching upon the articular
cavity as well as extending up the shafts of the bones, and displacing
the capsules of the articulations. Similar productions of cartilage
sometimes form in the thickened capsules and ligaments, especially in
very protracted cases, or these parts become infiltrated with lime
salts.

While these processes are going on at the periphery and the centre of
the cartilages, in its deeper layers the proliferating cells are
undergoing ossification and rendering the ends of the bones very dense
and compact, so that under the attrition to which they are exposed by
the articular movements they acquire the smoothness, polish, and white
aspect of ivory (eburnated). It is probable that the articular ends of
the bones participate in this proliferation and development of bone,
which increases their compactness and is followed by eburnation. That
the bone itself does sometimes play a part in the hyperostosis which is
in progress is shown by an increase of an inch in the length of the
right ramus of the maxilla over that of the left in Adams's first
plate.[228] Forster's[229] and Ziegler's[230] later investigations
confirm this view. Nor is the periosteum exempted from the
proliferating process which may have long existed in the several
articular tissues, as is shown by the considerable enlargement of the
diameter of the shaft of the long bones and by the osteophytes which
form on the exterior of the vertebrae and often unite several of them
together by a series of osseous splints, interfering with the mobility
of the spine. Notwithstanding this development of cartilage and bone
upon the exterior of the articular extremities, the interior,
especially in old people or in very chronic examples of the general
form of the disease, or rarely in the partial form, undergoes
degeneration and atrophy. The spongy substance becomes rarefied,
thinned, and friable (osteoporosis), so that it has been easily cut or
crushed, and it is frequently loaded with fat. True ankylosis of the
diseased joints is rare, except in the very small articulations when
kept at rest; even under this condition fibrous ankylosis is not of
frequent occurrence.

[Footnote 228: _Illustrations of the Effects of Rheumatic Gout_,
London, 1857.]

[Footnote 229: Forster, _Handbuch der Path. Anat._, p. 1000.]

[Footnote 230: _Virchow's Archiv_, 1877.]

Finally, the interarticular fibro-cartilages and ligaments and the long
{88} tendon of the biceps degenerate and are absorbed. The muscles in
protracted cases suffer simple atrophy, but are sometimes the seat of
an interstitial accumulation of fat. Thus far, no lesions of the nerves
supplying the diseased joints nor of the spinal cord have been
discovered.

ETIOLOGY.--The causation of rheumatoid arthritis is involved in much
obscurity--in part, because sufficient attention has not been paid to
its clinical varieties. We will examine first the general progressive
form which is the more common.

In women it prevails during the child-bearing period. It is probably
oftenest developed between twenty and thirty, and continues to occur
frequently up to the period of the menopause, fifty, after which it
develops comparatively seldom. Of Ord's 33 cases, 10 were between
twenty and thirty years; 11 between thirty and forty; 9 between forty
and fifty; and 3 between fifty and sixty.[231] Children are not exempt.
E. C. Seguin saw three children of the same family suffering from the
disease at ages from two and a half to four years.[232] Moncorvo[233]
met with an example at two years and a half, Laborde at four, and
Charcot at ten. It occasionally begins in both sexes after sixty.

[Footnote 231: _Brit. Med. Jour._, 1880, 156.]

[Footnote 232: _The Med. Record_, London, 1877, 797.]

[Footnote 233: _Du Rheumatisme Chronique Noueux des Enfans_, Paris,
1880.]

It is pre-eminently a disease of females up at least to fifty; after
that it is not infrequent in men, and is then often only partial, at
least at first. The most frequent progressive form, however, does often
occur even in boys.

It is probably more frequently observed in cold and damp climates than
in those of opposite qualities, for cold is regarded as its most common
cause. However, it is met with in India and other hot climates. Besnier
asserts it is almost unknown in the tropics, but new investigations are
needed on this point.

Direct hereditary predisposition exercises but little influence,
according to Garrod, and we certainly often see the disease confined to
a single member of a large family, although Seguin saw three young
children of one family affected with it, their parents being free from
any disease. Trastour three times saw the children of women who were
afflicted with nodular rheumatism already suffering from articular
rheumatism; and Charcot once saw the grandmother, the mother, and the
granddaughter successively attacked. At present I have a patient whose
mother at fifty-five and maternal grandmother at sixty became subjects
of a crippling polyarticular affection; another of my patients informed
me that his mother and a young sister were like himself victims of the
disease. This direct transmission appears to be rare, judging from my
own experience and from the few instances of it mentioned by writers.
But very many authorities maintain that simple acute and chronic
rheumatism and gout in the parents predispose to rheumatoid arthritis
in the offspring (Charcot, Trastour, Besnier). Now, the facts given in
support of this opinion are not numerous. Trastour found that out of 45
cases of nodular rheumatism the father or mother were rheumatic in 10
instances, but the form of the rheumatic affection is not stated.
Charcot, Besnier, and Homolle, although believers in the doctrine, do
not cite an example in proof. However, in Pye-Smith's 27 cases of
osteo-arthritis, five stated that rheumatism had occurred in their
families. Thus, two fathers {89} had had rheumatic fever, and one was
rheumatic, and two sisters of different families had had rheumatic
fever. Besides, the father of a sixth and the grandmother of a seventh
had had gout.[234]

[Footnote 234: _Guy's Hospital Reports_, 3d Series, xix. 348.]

The evidence in favor of the doctrine that true articular rheumatism
transmits an hereditary tendency to rheumatoid arthritis does not
appear to be conclusive, although it is highly thought of by those who
regard the latter disease as a variety of rheumatism. Some
considerations of an opposing character deserve mention. Acute
articular rheumatism has very rarely passed continuously into
rheumatoid arthritis, and very rarely has been followed at short
interval by that disease; and in such exceptional cases the antecedent
affection may have been really the acute form of rheumatoid arthritis,
which closely resembles acute articular rheumatism. Trastour,[235]
Vidal,[236] Charcot,[237] and others admit that acute rheumatism can
hardly be placed amongst the antecedents of the rheumatoid affection.
Garrod[238] with some others states that now and then acute rheumatism
acts as an exciting cause of it, which appears to have been Fuller's
view;[239] he had repeatedly known it to commence apparently as a
sequel of acute rheumatism. However, Ord met with a case in which the
lesions of rheumatoid arthritis were present in a typical form in a
patient who had mitral disease as a result of acute rheumatism, the
arthritis having begun as a continuation of the acute attack.[240]

[Footnote 235: _These de Paris_, 1853, p. 41.]

[Footnote 236: _Ibid._, 1855, p. 9.]

[Footnote 237: _Lecons Cliniques_, p. 214.]

[Footnote 238: Reynolds's _Syst. Med._, 1870, i. 920.]

[Footnote 239: _Lib. cit._, 333.]

[Footnote 240: _Brit. Med. Jour._, 1880, i., 158.]

That so common an affection as articular rheumatism should occur in the
family or personal history of a patient the subject of the rheumatoid
arthritis is not improbable; nasal catarrh and many other very common
diseases must be frequent antecedents of the rheumatoid affection, yet
are not causes of it. Much the same remarks apply to the view that gout
in the parents may transmit a tendency to rheumatoid arthritis in the
offspring. The experience of English physicians in this matter is
hardly reliable, owing to the great prevalence of gout in England. In
Canada and many parts of the United States, however, while gout is a
rare disease, rheumatoid arthritis is a common one, and the writer has
not found an intimate relationship to obtain between the two
affections. It is not intended to deny that when the children of
rheumatic or gouty parents fail in health owing to their inherited
constitutional disease, they become liable to rheumatoid arthritis, for
feeble health predisposes to that affection.

Finally, many of the difficulties connected with this subject are
reasonably met by Hutchinson's[241] doctrine that there exists a state
of tissue-health which is transmissible by inheritance, which involves
liability to inflammations of joints and fibrous structures, and upon
this arthritic diathesis as a foundation may be built up, under the
influence of special causes, a tendency to gout, rheumatism, or any one
of their various modifications or combinations.

[Footnote 241: _Trans. International Med. Congress_, ii. 95; Gueneau de
Mussy's chap., "De la Diathese Arthritique," _Clin. Med._, 1874, t. i.
317-338.]

Hutchinson has demonstrated that gout is often followed by rheumatoid
arthritis, the lesions characteristic of both affections coexisting in
the same joint. Charcot and Cornil had previously observed the same
{90} thing.[242] Acute and perhaps chronic rheumarthritis have
sometimes preceded rheumatoid arthritis. If a predisposition, inherited
or acquired, to rheumatoid arthritis exist, the occurrence of gouty or
rheumatic irritation in the joints may suffice to induce the peculiar
form of disturbance characteristic of the rheumatoid affection, just as
injuries sometimes develop the partial form.

[Footnote 242: _Memoires de la Societe de Biologie_, 1864.]

There is a group of conditions affecting the sexual functions and
organs of women which appear to be specially connected with the general
peripheral form of rheumatoid arthritis. The disease follows pregnancy,
and specially frequent pregnancies, protracted lactation, and various
disorders of menstruation. The latter influence obtained in ten out of
eleven instances of the disease met with in girls under eighteen by
Fuller.[243] The frequency of the disease about the period of the
menopause has been already mentioned. Todd noticed its coincidence with
dysmenorrhoea. Ord in an able and original paper[244] has lately dwelt
upon ovario-uterine disorder or irritation as a frequent active cause
of the disease, having in his opinion met with 33 instances of the
kind. The relationship between these various conditions of the
functions and organs of generation and rheumatoid arthritis cannot be
regarded as settled. Garrod supposed that such conditions, by causing
debility, predisposed to the articular disease. Todd, an ardent
humoralist, held the nexus between the two to be unhealthy secretions
of the uterus, leading to blood impurity; while Ord has ably defended
Remak's view that a direct influence of the nervous system is the real
link of relationship. It seems necessary to remark that mere
coincidence may play a large role in the explanation of many of these
cases. In 17 at least of Ord's 33 cases the conditions stated by that
author cannot safely be adduced as anything more; and it is probable
that they would be found present in much the same proportion in any
other chronic painful disease of women.

[Footnote 243: _Loc. cit._, 335.]

[Footnote 244: _Brit. Med. Jour._, i., 1880, 151-153.]

Scrofula and phthisis are regarded by Charcot, Cornil, and Garrod as
frequent antecedents of rheumatoid arthritis: the first had several
times seen white swelling in youth, followed by nodular rheumatism in
later life;[245] and Fuller found that 23 out of 119 victims of
rheumatic gout had lost a parent or one or more brothers and sisters by
consumption.[246] Chlorosis has several times preceded rheumatoid
arthritis. When the prevalence of scrofula, phthisis, and chlorosis is
borne in mind, it will not appear strange that they should frequently
be found amongst the antecedents of rheumatoid arthritis, without
inferring any other relationship between them. Gonorrhoeal rheumatism
has also occasionally preceded rheumatoid arthritis, but Ord and
Hutchinson are probably correct in regarding that affection as a
variety of rheumatoid arthritis.[247]

[Footnote 245: _Loc. cit._, p. 208, foot-note.]

[Footnote 246: _Loc. cit._, p. 334, foot-note.]

[Footnote 247: _Trans. International Med. Congress_, vol. ii. p. 92;
_Brit. Med. Jour._, 1881, p. 158.]

Cold, especially when prolonged and associated with dampness, is
commonly held to be the most common cause of general rheumatoid
arthritis. A protracted residence in low, damp dwellings, deprived of
the sun's rays and of a free circulation of air, is a condition thought
most favorable to the provocation of this disease, perhaps years after
the condition has been done away with.

{91} Poverty and all that it implies are at least frequent antecedents
of the disease (hence one of its epithets, arthritis pauperum), as are
other debilitating influences, such as night-watching, insufficient
food, mental worry, grief, anxiety, etc. Be it remembered, however,
that the disease is frequently observed in the well-to-do, who live in
dry climates and warm houses, are well fed, and want for nothing; so
that the external conditions first mentioned are not essential causes
of the disease, and many of them may act merely as adjuvants.

Direct injury of a joint from a blow, a fracture, a whitlow, etc. may
sometimes induce a local rheumatoid arthritis, which may subsequently
become multiple and involve several articulations more or less
symmetrically.[248]

[Footnote 248: Vide Charcot's and Ord's cases, _loc. cit._]

The partial form presents some peculiarities of causation--thus: it
occurs chiefly in advanced life (senile arthritis), much less
frequently in middle life, very exceptionally in the very young. Men
are much more liable to it than women. It is chiefly this variety which
follows injuries, blows, dislocations, pressure, etc., and the disease
may then be limited to the injured joint and be monoarticular, or it
may extend and become polyarticular, or rarely, as in Ord's case, even
general. This monoarticular form appears to be sometimes induced by
other local irritations of the articular structures than those
following traumatic influences; and as foreign growths in joints and
gouty irritation may respectively induce the lesions indicative of
rheumatoid arthritis, so, it is probable, may simple chronic
rheumatism; and this may be the true relationship existing between
these several affections. It is doubtful at present whether purely
local irritation or injury of a joint can originate the alterations
belonging to rheumatoid arthritis--that is, in the absence of all
predisposition to that disease or of the arthritic diathesis. Cold and
dampness are generally admitted to be causes of the partial form, but
the evidence on this point is not altogether satisfactory. It may be
that chronic articular rheumatism is induced by the prolonged operation
of damp cold, and that the prolonged rheumatic irritation, aggravated
by constant use of the joint and by occasional violence, ultimately
superinduces the profounder alterations characteristic of arthritis
deformans. It appears highly probable that if the predisposition exist,
any long-abiding irritation of a joint, whether the result of violence
or disease, may ultimately originate the alterations of the cartilages
and bones which obtain in rheumatoid arthritis.

As regards the etiology of Heberden's nodosities, and their relation to
other affections of the joints, the following summary must suffice:
They obtain chiefly in advanced life, but do occur rarely in the young;
they are probably somewhat more frequent in women than in men; although
more frequently seen in the upper classes, the poor are not exempt from
them, no doubt because they are specially exposed to slight but
oft-recurring injuries of their digits, such traumatism being an
exciting cause of the disease, especially when confined to a single
joint. The affection is sometimes hereditary; both it and the general
or the partial forms of rheumatoid arthritis may coexist in the same
family and even in the same person. The alterations in the joints are
identical with those found in the general variety of rheumatoid
arthritis, and exist without {92} deposits of urate of soda (Charcot).
It resembles the general form of the disease just mentioned in its
tendency to involve many symmetrical articulations at the same time,
and the partial form in the rarity with which it extends beyond the
joints first attacked. While Heberden's nodosities, as Haygarth taught,
do occur independently of gout and the gouty habit, I believe with
Begbie[249] and Duckworth[250] that in some persons they are evidences
of gout or the gouty diathesis.

[Footnote 249: _Contributions to Practical Med._, 1802, p. 29.]

[Footnote 250: "On Unequivocal Gouty Diseases," _St. Bartholomew's
Hospital Reports_, vol. xvi., 1880, p. 190.]

Quite recently a woman aged forty-eight consulted me with these
nodosities beginning upon the last joint of the fingers, while she was
the subject of vesico-renal irritation and was passing free uric acid
in the urine. Hutchinson has twice seen them in combination with a
peculiar insidious and painless inflammation of the iris and vitreous
body, which occurs in the children of the gouty, yet such children have
no deposits of lithates in their joints, nor any lithiasis, nor acute
paroxysms of true gout, and he considers that "the last joint arthritis
is to be regarded as in part gouty, and in part a kind of articular
chilblain."[251]

[Footnote 251: _Trans. International Med. Cong._, ii. p. 96.]

Lastly, in some instances they are no doubt the hybrid offspring of an
inherited tendency to both gout and rheumatoid arthritis.

No more important principle in pathology exists than has been of late
years insisted upon, especially by Jonathan Hutchinson and in his
recent lecture by Sir James Paget[252]--to wit, that "by inherited
dispositions, accumulating and combining or converging in definite
proportions, new diseases may be developed and old ones be variously
modified."

[Footnote 252: _Lancet_, ii., 1882, 1017-1021.]

The pathogenesis of rheumatoid arthritis is the subject of differences
of opinion very like those existing in regard to acute articular
rheumatism. The weight of evidence is in favor of its diathetic
relationship to rheumatism; and the doctrine of an arthritic diathesis
and of the operation of the causes of the disease through the nervous
system appears to be specially applicable to it, with less difficulty
than to acute rheumatism, and the probability of a specific germ being
its true cause is very remote. What seems to be necessary in addition
to the preceding is, that the causes shall be more persisting and
oft-recurring, so as to maintain a prolonged local irritation of the
articular tissues, or that the neuro-arthritic diathesis shall be
highly developed. Under these conditions the prolonged or oft-repeated
application of cold and damp to the peripheral nerves, severe or
oft-repeated slight injuries to joints, urethral or ovario-uterine
irritation, chronic gout or rheumatism, or even, exceptionally, an
attack of the acute form of these diseases, may originate rheumatoid
arthritis; and all wearing influences, such as anaemia, excessive
menstruation, prolonged lactation, innutrition, failing health, mental
anxiety, or shock, etc., act as adjuvants in the development,
aggravation, and maintenance of the articular disease.

DIAGNOSIS.--It is perhaps not possible to distinguish with certainty
either the acute or the chronic form of rheumatoid arthritis from
subacute or chronic rheumarthritis respectively before the
characteristic deformities of the former affections have appeared.
Acute rheumatoid arthritis, which is comparatively rare, may be said to
exist, rather than subacute {93} articular rheumatism, if the disease
affect early and chiefly the smaller joints of the hands and feet alone
or along with some of the larger articulations, especially the
sterno-clavicular or the temporo-maxillary; if the effusion into the
joints be abundant; if inflammation persist in the articulations first
involved, notwithstanding the invasion of other joints; if the heart
escape; if the patient be a female who is constitutionally delicate, or
has borne children rapidly, or is the subject of disordered
menstruation, or has been attacked soon after childbirth or during
lactation;--finally, if, on cessation of the attack, one or more of the
joints remain swollen and permanently enlarged and impaired in
function. The coexistence of iritis, or a history of a previous attack
of that disease not attributable to syphilis or gout, would strengthen
the above view.

Precisely the same considerations serve to distinguish chronic general
or polyarticular rheumatoid arthritis from chronic articular
rheumatism, with the following qualifications: endo- or pericarditis is
not of frequent occurrence in chronic rheumatism, so that this
distinction is not available, and chronic rheumarthritis of long
standing does sometimes impair the movements of the joints, and even
produce slight alterations in them. However, it does not, as a rule,
involve so many joints as rheumatoid arthritis; it is less symmetrical
in its distribution, and much less prone to implicate the
sterno-clavicular, the temporo-maxillary, or the vertebral
articulations. Nor does it cause removal of the articular cartilage,
enlargement of the heads of the bones, and the formation of osteophytes
around them, and of loose bodies in the articulations, together with
marked deformities and luxations of the joints. A history of a remote
or recent attack of acute rheumarthritis or of chorea, or the presence
of chronic valvular disease, would strongly indicate the simple
rheumatic nature of the case.

The partial form of rheumatoid arthritis can with even less certainty
than the general be distinguished from chronic articular rheumatism
before the characteristic alterations of the joints have been
developed, more especially as it is sometimes a consequence of gouty
irritation and probably of chronic rheumatism. Chronic arthritis
following a traumatic cause, and persisting obstinately in the injured
joint is probably rheumatoid, if not strumous, gouty, or periarthritic.

But before definitely deciding it will be prudent to await the
development of some of the characteristic alterations of structure
appertaining to rheumatoid arthritis. An affection of the shoulder
frequently occurs which resembles in many respects rheumatoid
arthritis, and has been well described by Simon Duplay[253] and W.
Pepper.[254] It usually follows an injury, such as contusion, sprain,
etc., of the joint, but may be spontaneous; it is unattended by
swelling or deformity. Its early symptoms are pain on pressure of the
shoulder a little below the outer border of the acromion, and
especially behind it and at the coracoid process, also about the
insertion of the deltoid and below the acromion during movements of the
joint, especially when the arm is raised from the side or rotated
inwardly; early restriction of these movements, which increases till a
fibrous ankylosis becomes established and scapula and humerus move
together as one piece, motion between those bones no longer existing,
and forcible attempts to produce it giving great pain, and sometimes
producing {94} crepitus in or about the articulation; sometimes early
numbness and pain down the member to the hand in the course of the
ulnar, internal cutaneous, or the radial nerve; vicious and painful
semiflexion of the elbow; after a time wasting of the group of muscles
which move the shoulder-joint. Although usually monoarticular and of
traumatic origin, I have seen it affect first one and then the other
shoulder in the absence of any known injury, and beginning like a
neuritis or a neuralgia of the scapulo-humeral nerves. Duplay, however,
regards it as a periarthritis. It may be distinguished from the
rheumatoid arthritis by the absence of effusion into or enlargement of
the articulation, and of deformity of the bones; by the early
restriction of the movements and the rapid development of adhesions
which fix the articulation; and by the curability of the disease.

[Footnote 253: _Archives Generales de Med._, Nov., 1872, pp. 512-542.]

[Footnote 254: _Archives of Med._, Oct., 1880.]

The articular affection of locomotor ataxia sometimes closely resembles
monoarticular rheumatoid arthritis,[255] but may be distinguished by
its sudden invasion, often without pain or fever; the prompt
development of a general and often enormous tumefaction of the entire
member, with copious effusion into the joint; the early destruction of
the articular cartilages, the rapid wearing away of the heads of the
bones, and the proneness to spontaneous fracture of their brittle
shafts; the prompt absorption of the articular effusion, followed by a
relaxed state of the ligaments and a facility of dislocation; the early
occurrence of the articular affection, when motor inco-ordination is
scarcely developed, and its frequent association with the crises of
ataxia or the presence of some of the other symptoms of that disease.
The importance of these facts will be especially evident in those
examples of ataxic articular disease in which, at an advanced stage,
eburnation and deformity of the articular surfaces, with the formation
of loose bodies and osteophytes, are observed, just as they are in
arthritis deformans.

[Footnote 255: Charcot's _Lectures on Diseases of the Nervous System_,
Syd. Soc., 1877; _Archives de Physiologie_, t. i., p. 161, 1868;
_ibid._, xi., 1869.]

Articular disease closely allied to what occurs in locomotor ataxia is
now and then observed in the early stages of progressive muscular
atrophy,[256] but while the large joints, more particularly the knee
and the shoulder, suffer in the former affection, the phalangeal
chiefly and the larger articulations more rarely are attacked in the
latter. Of course the peculiar symptoms of progressive muscular atrophy
coexisting with those of the articular affection would serve to
distinguish the latter from rheumatoid arthritis.

[Footnote 256: Remak, _Allgem. Med. Central. Zeitung_, March, 1862;
Rosenthal, _Clinical Treatise on Diseases of the Nervous System_,
translated by L. Putzel, M.D., 1879, p. 286.]

It is often very difficult to say whether a given case is one of
chronic rheumatoid arthritis or of chronic gout; and there is no doubt
that in England, where gout prevails, it is not unfrequently associated
with rheumatoid arthritis, sometimes preceding and even causing it,
much more often following it, for the one does not exclude the other.

While rheumatoid arthritis most frequently begins in the hand, and is
usually symmetrical and bilateral, gout commonly begins in the lower
extremities, and especially in the metatarsal joint of the great toe,
and of one foot only. Chronic gout is far more frequently preceded by
attacks of acute gout than chronic rheumatoid arthritis is by the acute
form of that affection; a history of inherited predisposition, of
indulgence in the {95} use of wine, ale, porter, and of animal food, of
deficient bodily exercise, with perhaps great mental occupation or
anxiety, of recurring gouty dyspepsia or of a tendency to lithiasis,
would indicate gout, while the absence of these and a history of
frequent exposure to cold and wet, of injury to the joint, of previous
exhausting disease or drain, of impaired health, debility, or poverty,
would strongly imply rheumatoid arthritis. Gout is especially observed
in males over thirty, and very rarely in children; general rheumatoid
arthritis is chiefly a disease of females during menstrual life, and
occasionally occurs in children of either sex.

The partial form is, like gout, chiefly a disease of men, but occurs
generally at a more advanced age than gout. Even chronic gout is more
or less paroxysmal, with distinct intermissions; chronic rheumatoid
arthritis is more or less abiding and progressive, with only remissions
in its course and severity; the former is frequently associated with
chronic renal disease, the latter is not. The urate-of-soda deposits
about the articulations in gout appear as more or less round or ovoid
swellings in the close vicinity of the joints, but not observing their
exact level or their general form; softish when recent, they never
acquire a bony hardness, and are nearly always capable of slight
lateral movement. The skin covering them is frequently stretched and
glossy, and may exhibit white spots of urate of soda. The articular
nodosities in chronic rheumatoid arthritis are actual osseous
enlargements of, or outgrowths from, the articular surfaces, forming
part of them, immovable and conserving more or less their form. The
integument covering the nodosities is not glossy or dotted with
chalk-like specks. The several types of deformity of the fingers
previously described, and mainly produced in rheumatoid arthritis by
muscular contractions and altered shape of the articular surfaces, are
not seen in gout. Finally, if chalk-like concretions are visible in the
ears, joints, or finger-ends, or if the blood contain uric acid, gout
is present. While rheumatoid arthritis and chronic gout occasionally
coexist in the same patient in England, in Canada, where the latter
disease is comparatively rare and the former quite common, the writer
does not remember to have observed such coexistence.

Besides the acute syphilitic disease of the joints already alluded to
as occurring in children (inherited), a chronic arthritis is observed
in the adult amongst the very late lesions of syphilis. It is usually
monoarticular, affects the larger joints, especially the knee, and may
originate either in the synovial membrane or in the bone and
periosteum. In syphilitic synovitis the history of the case, the
existence occasionally of soft gummy tumors in the periarticular
tissues and of hydrarthrosis, the trivial degree of pain and
tenderness, the insidious invasion and chronic course of the affection,
and its prompt relief by antisyphilitic remedies, will indicate the
nature of the case.

When it originates in the bone and periosteum, although the invasion
may be prompt and the pain at first severe, the latter usually
moderates greatly and becomes nocturnal, and the articular surfaces
present localized rather than general enlargement (hyperostosis); nodes
often coexist; effusion is moderate, unless the synovial membrane is
also involved, and full doses of iodide of potassium will soon afford
relief.

PROGNOSIS.--In the polyarticular form the course varies much more than
is commonly believed, and the disease must not be regarded as
necessarily {96} progressive and incurable. When it occurs in young
persons, and in children more especially, although it may suffer
exacerbations and remissions for a few years, yet arrest of the disease
and recovery of the functions of the joints, sometimes with very little
deformity, now and then take place under suitable management. Quite
recently a man of thirty-two consulted me about a vesical affection who
from the age of eight had suffered every winter for twenty years from
rheumatoid arthritis in his hands and feet, and finally in the knees.
Yet when seen by me he had been free from pain in his joints for three
years, and, although they were somewhat deformed, their movements were
remarkably free and painless.

Several of my younger patients while bearing children rapidly and
nursing them have had the disease in their hands or hands and wrists;
exacerbations have recurred during subsequent lactations, and yet the
disease has either become arrested or progressed very slowly and at
long intervals. It is admitted, however, that these are all exceptional
cases, and that the tendency both of polyarticular and of the
monoarticular forms is to progress, and, either steadily or at
intervals and by recurring attacks, to permanently deform the joints
and impair their movements. Even under these circumstances, however,
the patients may suffer little pain unless when forcible movements of
the articulations are attempted.

On the other hand, while the disease cannot be regarded as curable
under the employment of drugs, very much can frequently be done,
especially in the polyarticular form, to relieve the suffering and to
retard, if not arrest, the progress of the disease, and even to restore
sometimes very considerably the functions of the joints. Neither of
these forms of rheumatoid arthritis can be said to be dangerous to
life, and they often exist ten or twenty years and more without
seriously injuring the general health. Heberden's nodosities are
incurable, but they are little more than deformities.

TREATMENT.--The treatment of rheumatoid arthritis is, as a rule,
disappointing, and perhaps no affection requires more perseverence and
self-reliance on the part of the physician or more hopeful resolution
on that of the patient. Our first duty is to make an exhaustive search
as to the probable cause of the disease, as its removal is an important
step in the treatment of the affection, although such search is
frequently futile, and many of the alleged causes may, after all, be
mere antecedents or coincidences. However, inasmuch as the pathology of
the disease is very obscure, any abnormal condition of organ or
function that may be discovered should receive strict and prompt
attention, lest it should, either through disturbed innervation or
malassimilation or impaired nutrition or defective excretion, be the
predisposing or exciting cause of the disease. In women the most
careful inquiry should be made into the state of the ovario-uterine
organs and functions, and the least departure from their norm should be
at once treated. Deficient, excessive, or painful menstruation,
leucorrhoea, ovarian irritations, or pain, even displacements of the
uterus or ovary, should be corrected as soon as possible. Repeated
pregnancy and prolonged lactation, recurring mental anxiety and
physical fatigue, defects of diet, want of food, of sunlight, and of
good air, residence in damp dwellings, occupations involving exposure
to cold and wet, are conditions supplying important indications which
too often are {97} beyond the control of the physician, although they
peremptorily require his attention. The general form is often met with
in anaemic persons and in those of impaired health and vigor, and
probably very rarely occurs under opposite circumstances; and there is
a consensus of opinion that a lowering system of treatment is
contraindicated in rheumatoid arthritis.

Having efficiently set about correcting or removing these various
predisposing or determining causes of the disease, we next direct our
care to the disease itself. The remedies which had been found most
useful in rheumatoid arthritis before the introduction of salicylic
acid were cod-liver oil, quinia, iodine, iron, arsenic, and various
mineral waters, employed either externally or internally, usually in
both ways. Judging from my own late experience and from the results
obtained by See[257] and other French physicians, as communicated by
Jules Compagnon,[258] sodium salicylate, given in sufficient doses,
promises to be more generally useful in the more acute forms or in the
actively inflammatory periods and exacerbations of the disease than any
of those agents. Including See's cases, Compagnon has related 17
examples of rheumatoid arthritis, most of them of the general
progressive form, in which great improvement as regards pain,
stiffness, swelling, and even deformity, followed promptly the
employment of that salt, even after the failure of other remedies. It
proved signally useful recently in a rebellious chronic case of my own.
Pollock has lately published an instance in which 5 grains of
salicylate of quinia three times a day were in three or four days
followed by great relief.[259] The testimony already given of Dr. J. T.
Eskridge as to the great value of this salt in chronic rheumatism will
be held by some to be corroborative of its value in rheumatoid
arthritis. It is hardly necessary to say that it often fails in this
intractable disease, but it has frequently relieved the pain and
swelling and arrested the progress of it, at least for the time, even
when alkalies, iodine, arsenic, baths, etc. had failed.

[Footnote 257: _Bulletin de l'Academie de Med._, Paris, t. v., 2d
Serie, 1877.]

[Footnote 258: _De l'Utilite du Salicylate de Soude dans le Traitement
du Rheumatisme_, par Jules Compagnon, Paris, 1880.]

[Footnote 259: _The Lancet_, ii., 1882, 141.]

It is probable that less than 45 grains per diem of the sodium salt is
of little value in even the most chronic forms, and that the quantity
requires to be increased in proportion as the febrile symptoms are
active, so that a drachm and a half or two drachms may need to be
administered in the day to some persons. It should be given in divided
doses at intervals of two hours, and, what is of primary importance, it
should be continued for a long time, even after much improvement has
resulted, and should be resorted to from time to time, especially
during recurrences of the pain, heat, or swelling. It is of
consequence, especially in elderly patients, to ascertain that the
medicine is being promptly eliminated by the kidneys and to watch its
effect upon the heart. The administration along with it of a little old
rye whiskey or brandy will sometimes be necessary in feeble people. In
those rather common cases in which the skin is inactive and perhaps
harsh the salicylate often improves that important organ of oxidation
and elimination, and should it not do so the addition of the ammonium
carbonate may be tried, especially in feeble persons with weak hearts.

{98} Moreover, the other drugs which sometimes prove serviceable in
this disease may be given at the same time or alternately with the
salicylate, or instead of it if it is not found to be of use or is not
tolerated. In chronic cases a prolonged course of cod-liver oil, alone
or along with malt extract, often seems to be of real service,
especially when nutrition is much impaired or when the patient is the
subject of acquired or inherited struma. Iodide of potassium, in
combination with quinia or other tonic, will often prove signally
useful in chronic cases unaccompanied by pyrexia, in which the pains
are worst at night. It should be first tried in moderate doses (5 to 8
grains), and be continued for a long time with occasional
intermissions, and before discarding it from disappointment--which
often arises--15- to 20-grain doses may be given tentatively for a
short period. Milk or coffee or Vichy water are good vehicles for its
administration. Whether free iodine in the form of the tincture, so
highly spoken of by Lasegue,[260] acts as well or better than the
iodide of potassium is doubtful. He gave it at meals, in doses
progressively increased from 10 drops to 5 or 6 grammes twice a day, in
sherry or sweetened water, and persevered with it for a long period.
Garrod has had many restorations to health in severe forms of this
disease from the persevering employment of the syrup of the iodide of
iron. The iron in these preparations may deserve as much commendation
as the iodine, for it has often proved signally useful in this disease,
not alone on account of the anaemia which so frequently attends it, but
through its beneficial influence upon the nutritive functions and the
circulation.

[Footnote 260: _Arch. Gen. de Med._, 1856.]

The usual rules regulating the employment of iron are to be observed,
and the condition of the digestive organs will demand special attention
during its employment. Although the influence of arsenic upon
rheumatoid arthritis is not uniform, yet as it sometimes proves really
useful[261] it should be tried. Like iron, it may prove beneficial in
several ways--by improving the quality of the blood, promoting the
circulation in the superficial layers of the skin, or exerting some
influence upon either the nerve-centres or perhaps upon the vaso-motor
nerves of the cutaneous or articular tissues. The last-mentioned
suggestion is favored by the circumstance noted by Charcot--viz. that
the first effects of arsenic in nodular rheumatism are often
intensification of the articular pains, and sometimes the production of
redness and swelling where they did not exist before. That author found
arsenic without effect or injurious in very inveterate cases and when
the disease had appeared at an advanced age. Five to ten minims of
Fowler's solution, or of the solution of the arseniate of sodium, which
is perhaps less irritating than the former, should be given immediately
after meals, and its effects upon the gastric and hepatic functions
carefully watched. De Mussy has highly recommended arsenical baths
(drachm ss-ij of arseniate of soda to 30 gallons of water), but as the
arsenic is not absorbed by the unbroken skin, any improvement which may
follow its employment is probably owing to the temperature of the bath
or the bath itself.

[Footnote 261: As to the value of arsenic in rheumatoid arthritis, see
Bardsley's _Medical Reports_, London, 1807; Begbie, _Edin. Med. and
Surg. Jour._, 1858; Fuller, _lib. cit._, p. 362; Garrod, _lib. cit._,
3d ed., p. 534; Gueneau de Mussy, _Bull. de Therapeutique_, t. lxvii.,
1864, p. 24; Charcot, _lib. cit._, p. 222.]

A similar remark has been made respecting the value of the various {99}
thermal mineral baths, natural and artificial, so much employed in this
disease.[262] It is neither the nature nor proportion of their mineral
ingredients, but the degree of temperature, which constitutes the
essential point in the action of a bath. This, if true, explains the
almost equal reputation of the many varieties of thermal mineral
springs in the treatment of rheumatoid arthritis and chronic
rheumatism. It is this that permits the physician to promise the poor
patient as much benefit from the employment of hot baths of simple
water as of those of New Zealand, Plombieres, or Arkansas.

[Footnote 262: Vide Niemeyer, _Text-Book Pract. Med._, N.Y., 1867, p.
488; _Traitement du Rheum. par les bains a haute temperature_, par Ch.
Aug. Bouther, Paris, 1878.]

The time for a resort to hot baths in rheumatoid arthritis is when the
very violent pains have subsided sufficiently to allow of their
employment; and while they may be hopefully used in the most chronic
and advanced cases, the earlier they are employed the more curative
they are. The temperature of these hot baths need not, as a rule,
exceed 95 to 100 degrees F., although some authorities approve of
raising the temperature to 110 degrees or 112 degrees while the patient
is in the water. A series of twenty to thirty such baths, taken every
second day for ten to twenty minutes, is sufficient for one trial, and
often effects very great improvement in the disease. The aggravation or
return of pain in the joints which often follows the employment of warm
baths will cease after the fifth or sixth bath. Garrod's experience of
the Turkish bath is not favorable; it very often does much mischief by
causing debility, and its excessive use has induced rheumatoid
arthritis in persons previously free from the disease.

Now, while it may be true that simple hot-water baths employed at home
are as good as mineral thermal baths taken at their source, it is
generally admitted that it is best to send persons who can afford the
expense to the springs themselves, where they may drink the waters as
well as employ them externally, and at the same time secure all the
advantages arising from change of habits, scene, and climate, from
restriction to a proper diet, and from the systematic employment of the
waters and baths under the direction of persons experienced in their
administration, etc. No reliable rules can be laid down for the
selection of the mineral waters best adapted to each case: the stronger
alkaline waters perhaps had better be used with great care, such as
those of Carlsbad, Vichy, Mont Dore, Weisbaden, and after a course of
thermal mineral baths at such places as Aix-les-Bains, Wildbad, Bath,
Aix-la-Chapelle, etc., Garrod advises resort to some place where the
air is bracing and the waters tonic or chalybeate, as Buxton, Spa,
Schwalbach, or St. Moritz. In this country good results are often
obtained at the Hot Springs of Arkansas and the Hot Sulphur and the
Lithia Springs of Virginia. The use internally and in the form of hot
baths of the mineral springs of Saratoga, of Michigan, of the Licks of
Kentucky, and of California, of St. Leon and St. Catherine's (Canada),
is frequently very beneficial. In the selection of the mineral waters
to be drunk, and of the temperature and other qualities of the baths to
be employed, careful attention must be paid to the condition of the
functions of the skin, liver, kidneys, and nervous system; but space
cannot be afforded here for the consideration of this extensive topic.
Moreover, it occasionally happens that after failure of {100} sulphur
or alkaline baths some other form may succeed, as the vapor or hot-air,
or tepid or very hot-water bath. If decided benefit follow the first
series of baths, recourse should be had from time to time to a fresh
series, even for several years, in obstinate cases. Mud and peat baths
are much valued in Germany, although they do not always agree with
weakly or aged people.

The local treatment is of equal importance with the general, and it is
not unfrequently more effective in restoring the functions of the
articulations. In that rare variety, acute rheumatoid arthritis,
attended with much pain and heat in the joints, perfect rest in bed is
called for, together with other measures adapted to subdue the
inflammation and allay the pain. Compresses wet with warm water,
rendered anodyne by the addition of laudanum or belladonna, or both,
and covered with oiled silk, suit some cases--light linseed poultices,
applied moderately warm and extending considerably beyond the limits of
the articulation and covered with gutta-percha or oiled silk, in
others. As the pain and local heat subside, the tincture of iodine may
be applied extensively, or blistering-fluid over limited areas above
and below the affected joints, but not on them until the inflammation
has very much abated and is becoming chronic. These simple methods
should be employed assiduously and be aided by appliances to secure
actual rest of the inflamed joints. In the chronic variety complete
rest is not needed unless during the acute exacerbations, but the
movements should be at first somewhat restrained and be regulated by
the effects produced. But the severe pain experienced during the
movements must be borne; it will subside promptly. Decided increase of
pain and heat in the part, lasting many hours, would indicate more
reserve in the use of the joints. It is frequently very difficult to
determine when and to what extent movement may be permitted in this
disease. No fixed rule can be laid down of universal application, but
it may be stated that in proportion as the local disease becomes
indolent and inactive may pressure and active movements of the joints
be resorted to, for they then have a beneficial influence in preventing
stiffness, contraction, and deformity. Indeed, in my opinion it is not
wise to delay these movements long even in subacute cases. The editor
of this work has especially insisted upon the importance of systematic
daily movements of the affected joints as the most essential part of
the treatment,[263] "combined with thorough massage of all the muscles
whose functional activity is impeded and impaired."

[Footnote 263: "Some Practical Remarks on Chronic Rheumatism," by Wm.
Pepper, M.D., _Archives of Medicine_, Oct., 1880.]

The abiding chronic inflammation indicated by local heat, swelling, and
inflammation of the affected tissues may be variously treated. The
joints may be thoroughly fomented with tolerably hot water or by means
of the local vapor bath for half an hour, morning and night, and then
be gently rubbed for ten or fifteen minutes with iodine or weak
mercurial ointment or with the compound camphor or acetic turpentine
liniment, or, if these are too stimulating, with some bland oil, such
as cod-liver or neats' foot or cocoa oil, after which should be applied
hot-water compresses or linseed poultices or a wrap of soft cotton wool
covered with oiled silk and secured by an elastic, moderately tight
roller. If these means prove inefficient and the inflammatory process
grow more {101} indolent, counter-irritants may be conjoined with or
substituted for them. Small fly blisters or strong iodine paint may be
applied close to the joints, or the ordinary iodine tincture may be
brushed over them, or the above ointments or liniments and one of the
bland oils may be more forcibly rubbed in. The prolonged rubbing of
these stiff, swollen joints with oil is not valued as much as it
deserves.

Compression of the thickened tissues by means of a thick envelope of
cotton wool and thin flannel or rubber bandage sometimes acts very
well, probably by reducing the amount of blood and interfering with
cell-growth or promoting cell-degeneration. Hot sand-baths to the
affected joints are sometimes useful.

These several measures should be perseveringly applied, and in
proportion as chronicity prevails the active and passive movements of
the articulations and massage of the muscles and adjacent tissues
should be daily and efficiently practised.

Electricity will often be found an important adjuvant in this as well
as in an earlier stage, not only in improving the nutrition of the
muscles, but in promoting absorption, allaying pain, and subduing
excitability of the peripheral structures, removing muscular
contractions, and probably modifying the local inflammatory processes.
It appears also in some cases to improve the general health. The
constant current is generally the most useful, and should have an
intensity of about ten to fifteen milliamperes, and be applied daily
for ten or fifteen minutes. The positive pole, terminating in a large
flat moistened sponge, is applied to the spinal origin of the brachial
or lumbar plexus, according as the superior or inferior members suffer,
while the negative pole is immersed in a vessel of warm salt water in
which the hands or feet are placed. Some apply the negative electrode
to the joints and the positive to the limb higher up.[264] The faradic
current may also be employed on account of its action upon the muscles
and small vessels. In the advanced stage attended with marked
thickening of the articular and periarticular tissues, with
contractions of the muscles and greater or less impairment of movement,
the above measures are still our chief resources; but they may be
employed more vigorously. We have little fear now of lighting up
inflammation; we indeed desire to excite a more active circulation in
the part with a view of removing the congested state of the capillaries
and venules, so favorable to the development of fibroid growths. In
this stage especially vigorous active and passive movements of the
affected joints, and massage of the muscles which move them, and
gymnastics, are imperatively needed, and it is sometimes almost
marvellous what an amount of mobility and usefulness may thereby be
restored to apparently helplessly crippled and deformed articulations
and members. Persons who have not walked for years are frequently so
much improved as to be able to leave their sofa or bed, and with or
without crutches or mechanical aids walk about, while their abiding
pains depart, and this notwithstanding the permanent deformity of the
articular surfaces. (For the various mechanical appliances that are
sometimes necessary in this advanced stage works upon surgery may be
consulted.)

[Footnote 264: Homolle, _lib. cit._, p. 710.]

The hygienic measures to be observed are probably very much the {102}
same as those indicated in the article upon simple chronic articular
rheumatism--some of them at least--and are such as may be inferred from
a review of the exciting causes of rheumatoid arthritis. Be it
remembered also that acute and chronic articular rheumatism appear
amongst the causes of that disease. We are hardly justified in
promising arrest of the disease on removal to a warm, dry, and even
climate; yet wealthy patients need not be dissuaded from trying the
experiment. The use of flannel underclothing and the employment of
tepid or even moderately cool baths, followed by the use of the
flesh-brush or rough towel, are important means of protecting persons
predisposed to this disease. The ordinary hygienic laws adapted to
maintain a healthy state of all the functions, mental as well as
physical, are to be observed, for in this disease the influence of the
mind over the body is shown by the frequency with which rheumatoid
arthritis follows closely upon mental shocks, worry, etc.

The diet, it is generally admitted, should be of a nutritious
character, yet plain and digestible, and, unless specially required to
meet certain indications, should not include heavy wines or fermented
liquors. However, Garrod affirms that uncomplicated rheumatoid
arthritis is not aggravated by the use of porter, ale, or sound wines;
and his rule is to give sufficient of these alcoholic beverages to
support the tone of the whole system, but not enough to excite the
circulation and thereby produce subsequent reaction.

Finally, the above system of treatment must be persisted in year by
year with the object of securing arrest when cure has not been
effected.


Gonorrhoeal Rheumatism, or Gonorrhoeal Arthritis.

SYNONYMS.--Arthrite ou Arthropathie blennorrhagique,
Tripper-rheumatismus, Gonocele, Urethral Rheumatism, Urethral
Synovitis.

ETIOLOGY.--As its name implies, the cause, par excellence, of the
disease is gonorrhoea, as was perhaps first indicated by Selle[265] and
Swediaur,[266] although, no doubt, an affection apparently identical is
rarely observed associated with non-contagious urethral discharge and
with the urethral irritation incident to catheterism and to stricture.
I have seen it associated with a simple mucous urethral discharge in a
man of gouty habit, married and free from the suspicion of specific
infection. Such discharge has been attributed to gouty irritation, to
dietetic and venereal excesses, and to the contact of non-specific
vaginal secretion; and such origin is well established. More than one
observer has noticed a susceptibility to urethritis on the part of
persons who have had gonorrhoeal rheumatism. A gouty taint is
undoubtedly often present in urethral rheumatism. These non-gonorrhoeal
cases require more close investigation than they have received.[267]
Fournier has not met with them.[268]

[Footnote 265: Chr. Th. Selle, _Medicina Clinica, oder Handbuch der
Medicin_, Berlin, 1781.]

[Footnote 266: Swediaur, _London Med. Gaz._, 1781.]

[Footnote 267: See Elliotson, "Non-contagious Urethral Rheum.," _Med.
Times_, i. 60, p. 613.]

[Footnote 268: Fournier, _Nouv. Dict. de Med. et de Chir._, t. v. p.
228.]

The stage of the gonorrhoea at which the articular affection may appear
varies very much. It frequently sets in from the sixth to the sixteenth
day of the discharge; it is common enough between the third and sixth
or twelfth weeks, and may be delayed as late as the twelfth month.
There {103} is no constant relation between the severity of the
urethral inflammation and the frequency with which, or the time at
which, the articular symptoms arise; and these, once established,
appear to be largely independent of the state of the urethra. On the
advent of the joint affection the discharge usually continues as it
was, although it often abates somewhat. Fresh attacks of gonorrhoea,
even when very mild, often develop new invasions of the articular
affection, as though an idiosyncrasy existed.

While the ordinary exciting causes of simple acute articular rheumatism
are not necessary to the production of gonorrhoeal rheumatism, they do
now and then act as adjuvants. Such are cold, fatigue, and injuries of
the joints, and a severe acute arthritis is not infrequently developed
during gonorrhoea under such circumstances. Other predisposing
influences probably exist, the absence of which in some measure
explains the infrequency of gonorrhoeal rheumatism as compared with the
prevalence of gonorrhoea. Besnier holds that constitutional rheumatism,
the arthritic habit, or l'heredite arthritique, is not infrequently
present in the victims of gonorrhoeal rheumatism as a predisposition;
Nolen[269] found an inherited rheumatic predisposition in 6 out of 88
cases, and that 4 others had had rheumatism before contracting
gonorrhoea; and Hutchinson maintains that it is the existence of the
arthritic diathesis which enables urethral inflammation to produce
gonorrhoeal rheumatism. He says: "From statistics that I have carefully
collected I have no hesitation in believing that the predisposing cause
of it usually is the inheritance of arthritic tendencies;" and adds,
"Very often the subject of gonorrhoeal rheumatism will give a family
history of gout." However, the disease often occurs in the absence of
any discoverable tendency, hereditary or acquired, to simple articular
rheumatism. On the other hand, persons have had one or several attacks
of gonorrhoea previously that did not give rise to rheumatism. Nolen's
table of 88 cases contains 12 instances of this kind. It is probable
that by reducing the resisting force of the organism, scrofula, the
so-called lymphatic diathesis, anaemia, and debility favor the
development of the disease.

[Footnote 269: "Rheumatismus gonorrhoicus," _Deutsches Archiv fur klin.
Med._, Bd. xxxii., 1883.]

Gonorrhoeal rheumatism, like gonorrhoea, is proportionally as well as
actually much more frequent in men than in women (111 men, 7 women,
Nolen); and the greater proclivity of the former has been attributed to
the greater delicacy, sensibility, and complexity of the structures
involved in them than in women by gonorrhoea.

MORBID ANATOMY.--The lesions of gonorrhoeal rheumatism in the early
stage resemble closely those of acute articular rheumatism; and it is
probable, for opportunities of ascertaining by actual dissection are
very rare, that the synovial membrane chiefly suffers. In more advanced
stages the joints contain serous fluid in which fibrinous flakes and
numerous leucocytes are found; the cartilages may be eroded and
softened; and in some protracted cases even the bones may participate
in the inflammation, and the changes found in polyarticular rheumatoid
arthritis may be developed. Ultimately fibrous adhesions, resulting in
ankylosis, may occur. Suppuration very rarely takes place, and it is
probable that in such cases pyaemia is added to gonorrhoeal arthritis.

{104} SYMPTOMS.--Gonorrhoeal rheumatism may attack any of the joints;
it most commonly invades the larger at first, more especially the knee;
the ankle is next in order of frequency, and then succeeds the
shoulder, closely followed by the smaller joints of the hands and feet,
which are very seldom affected primarily and antecedently to the larger
joints. The temporo-maxillary, the sacro-iliac, the sterno-clavicular,
the intervertebral, do not escape gonorrhoeal rheumatism more than they
do rheumatoid or pyaemic arthritis.[270] The disease most frequently
invades several joints simultaneously or successively, but, soon
declining in many of them, it finally becomes localized in a few or
rarely in a single articulation. It is monoarticular from the first in
about 20 per cent. of cases, especially in the knees.

[Footnote 270: Vide Fournier, _Nouv. Dict. de Med. et de Chir. Prat._,
t. v. p. 230: in 119 cases, knee, 83; ankle, 32; fingers and toes, 23;
hip, 16; wrist, 14; shoulder, 12; elbow, 11; temp.-maxillary, 6; etc.]

Gonorrhoeal rheumatism presents several clinical forms: First,
Arthralgic: pains of greater or less severity, sometimes increased by
movement, but unaccompanied by redness or swelling, affect one or
frequently several joints; they wander from joint to joint, are liable
to exacerbations, and sometimes resist treatment. This form occurs
either in a chronic state in the course of an old gonorrhoea, and
without other rheumatic symptoms, or as an acute affection along with
other rheumatic symptoms, as in the second form. Second: Rheumatic: in
this the symptoms are almost identical with those of subacute articular
rheumatism or the more active forms of polyarticular rheumatoid
arthritis. Several joints are usually implicated, perhaps suddenly,
either quite spontaneously or after chill, exertion, or strain, or
rheumatic-like pains having been felt for two or three days in the
soles, ankles, or loins, the painful joints become moderately swollen,
tender, and hot; pyrexia supervenes with its early chilliness, malaise,
and anorexia; the temperature is not high; the profuse acid sweating
and the very acid, high-colored urine of acute articular rheumatism are
not observed or but transiently and to a very slight degree. In a few
days the moderate febrile disturbance subsides, but the local
inflammation persists, and extends to other joints, without promptly
leaving those first invaded; while lingering in all it often fixes
itself in one or more joints, and is apt to produce a copious and
rebellious intra-articular effusion. Still, it very rarely involves as
many articulations as primary acute rheumatism. The periarticular
tissues usually are more involved than in subacute or even chronic
primary articular rheumatism. Hence the considerable swelling from
oedema on the back of the hand or foot, around the knee, behind the
elbow, and the copious effusion into the adjoining bursae and tendinous
sheaths, and in the case more especially of the small joints of the
fingers and toes the fusiform enlargement and deformities resulting
from periostitis of the articular extremities. The pain, deformity,
pseudo-ankylosis, etc. produced by these periarticular processes are
very persistent and rebellious, and, although they do usually disappear
at last, occasionally the inflammatory irritation extends to the
cartilaginous and osseous structures, and rheumatoid arthritis with its
permanent deformities results. It is perhaps chiefly in this
polyarticular form of gonorrhoeal rheumatism that cerebral, spinal,
cardiac, pleural, and ocular complications most frequently occur. {105}
In the Third form, or Acute Gonorrhoeal Arthritis, after two or three
days of pain wandering from joint to joint, a single articulation
suddenly, and frequently about the middle of the night, becomes the
seat of atrocious and abiding pain, followed in a few hours by very
considerable swelling of the articulation, not due chiefly to articular
effusion, but to periarticular oedema and enlargement of the bones. The
pain and tenderness are most severe at the line of junction of the
articular surface; the swelling begins at that point, and extends
widely, especially over the dorsal aspects of the wrists and elbows,
the joints most liable to this form, although any articulation may
suffer. The joint is also hot, it may be pale, but is usually more or
less red, and occasionally presents the appearances of severe
phlegmonous inflammation, and excites a sensation of
pseudo-fluctuation.[271] The affection may resolve, or fibrous
ankylosis may ensue, or very rarely suppurative destruction of the
articulation may occur, although such issue has been denied (by
Fournier, Rollet, Voelker). It is remarkable that, like the other forms
of gonorrhoeal rheumatism, the acute inflammatory form is not
accompanied by a general febrile disturbance at all proportionate to
the severity of the local disease. A Fourth form occurs as a Chronic
Hydrarthrosis. Although occasionally accompanying the polyarticular
variety, it is frequently observed independently, and is then often
monoarticular, and affects especially the knee; however, both knees
sometimes are involved. The ankle- and elbow-joints suffer much less
commonly than the knee. The effusion into the articulation takes place
insidiously, although rapidly producing considerable enlargement of and
fluctuation in the joint, without local heat, redness, or tenderness,
and often with but little or no pain or pyrexia. It is not as often
associated with inflammation of the tendinous sheaths and bursae or of
the eye as the polyarticular form, but it is apt to be very slow in
resolving, and may last for two or three months, a year, or several
years, and in scrofulous patients may degenerate into white swelling.
The formation of pus in the joint is very rare. It occurred twice in 96
cases tabulated by Nolen; hydrarthrosis obtained 12 times; and serous
synovitis 64 times; chronic rheumatism or arthritis deformans 5 times;
tumor albus once.[272] A Fifth form of gonorrhoeal rheumatism, like
other varieties of so-called secondary rheumatism, involves
predominantly the tendons and tendinous sheaths, the bursae and
periosteum, sometimes without, but far more frequently in association
with, affection of the joints. Pain, sometimes severe and increased by
movement and pressure and aggravated at night, with local swelling and
tenderness, are the symptoms. In their fixity and persistence, their
tendency to relapse, and their chronic course these periarticular
affections resemble gonorrhoeal inflammation of the joints. Gonorrhoeal
bursitis is often severe enough to resemble phlegmon, but it does not
end in suppuration; it is most common in the bursae covering the
patella, the olecranon, and especially in that under the tendo Achillis
and the deep one covering the inferior tuberosity of the os calcis; but
any of the bursae may suffer from gonorrhoeal rheumatism. The
periosteum in the vicinity of the affected articulation and over the
most prominent parts of the bones is sometimes the seat of small
circumscribed firm nodes which {106} are painful and tender, and may
either resolve rapidly or very slowly (Fournier).

[Footnote 271: _De l'Arthrite aigue d'origine blennorrhagique_, par le
Dr. Andre Felix Bieur, Paris, 1881.]

[Footnote 272: _Loc. cit._, p. 133.]

Along chiefly with the third form of gonorrhoeal rheumatism, or
independently, the various muscles and nerves may be the seat of
myalgia and neuralgia. The sciatic nerve is specially liable. In the
same form are often met those ocular affections observed not
infrequently in rheumatoid arthritis and very rarely in acute articular
rheumatism--viz. conjunctivitis and iritis. Aqua capsulitis is more
common than the others, according to Fournier. The ocular affections
may precede, accompany, or alternate with the articular, and, not being
due to direct introduction of the urethral contagium into the eye, are
regarded as manifestations or localizations of gonorrhoeal rheumatism.
The varieties of erythema sometimes present in primary acute articular
rheumatism have been observed in gonorrhoeal rheumatism.

Much difference of opinion obtains as to whether inflammations of the
heart, lungs, and serous membranes occur as manifestations or
localizations of true gonorrhoeal rheumatism. Even those who, like
Besnier, contend for the rheumatic nature of gonorrhoeal rheumatism
admit that they are quite exceptional in that affection. Endocarditis
is probably more frequent than pericarditis, and the aortic are more
liable than the other valves to suffer. Gonorrhoeal endocarditis has
been observed without the articular affection, although it is
especially when several joints are involved and the pyrexia is well
marked in gonorrhoeal rheumatism that the above visceral complications
occur. While admitting that Morel,[273] Marty,[274] Pfuhl,[275] and
others have reported what appear to have been authentic cases of
gonorrhoeal endocarditis, I would remark that it must be almost
impossible at times to distinguish a polyarticular acute gonorrhoeal
rheumatism from ordinary acute articular rheumatism, and that in other
instances the possibility of pyaemia developing in gonorrhoea, and
producing both the articular and the visceral lesions, or the latter
only, cannot be denied. And the same remarks are applicable to the
cerebral and spinal disturbances that Vidart and others have recorded
as occurring in gonorrhoeal rheumatism.

[Footnote 273: _Rev. des Sciences Med._]

[Footnote 274: _Archives generales de Med._, Dec., 1876.]

[Footnote 275: _Deutsche Zeitschrift fur pract. Med._, No. 50, 1878.]

The course, termination, duration, and prognosis need not be insisted
upon after what has gone before. The duration is very variable. Many
recover in four to eight weeks, many not for three to six months and
longer; relapses are of frequent occurrence; complete and tolerably
prompt recovery is not uncommon in first attacks and in young and
healthy subjects; rebellious persistency, and even deformity, with
impairment of the articular movements, and not infrequently even
fibrous ankylosis of one or many joints, sometimes including the
vertebral, may be observed. Indeed, the most formidable examples of
spondylitis are associated with gonorrhoeal rheumatism as its exciting
cause.[276] These unfavorable issues are most apt to follow repeated
attacks in unhealthy and especially scrofulous persons. Both rheumatoid
arthritis and strumous articular disease have appeared as sequels of
gonorrhoeal rheumatism. Life is not endangered, except in very rare
instances in which cardiac or cerebral {107} complications obtain; and
to stiffened enlarged joints the functions may often be restored by
efficient treatment.

[Footnote 276: Brodfurst cites two such cases: Reynolds's _System of
Med._, i. 980. So does Nolen in an elaborate article upon rheumatismus
gonorrhoicus in _Deutsches Archiv fur klin. Med._, Bd. xxxii., 1883. I
had not seen it before this paper was written.]

DIAGNOSIS.--In some instances no doubt what appears to be ordinary
gonorrhoeal rheumatism, owing to the coexistence of urethral discharge
and articular inflammation, is really pyaemic arthritis. The
intermediate link in the causation may be suppuration in the prostate
or its veins or in the testicle or the penis or in its dorsal vein, or
the urethral pus may undergo changes and become septic and be absorbed.
In other instances it is highly probable that true primary acute
articular rheumatism sometimes occurs coincidentally with gonorrhoea.
If in addition to the presence or recent existence of gonorrhoea the
case present several of the following features, gonorrhoeal rheumatism
may be said to exist: moderate or mild pyrexia and articular pain; the
number of joints attacked being few, with a tendency to concentration
in one, either from the first or secondarily; no migration from one
joint to another; no delitescence, but marked chronicity and indolence,
with a tendency to hydrarthrosis and to implication of the synovial
sheaths and bursae; an absence of cardiac complications; the frequent
and often early coincidence of special ophthalmic affections.

TREATMENT.--The patient should be confined to bed, so as to secure rest
to the inflamed articulations, and when severe arthritis (third form)
exists an efficient splint is peremptorily required, and its
application is often followed by prompt relief to the pain. It should
be retained until not only all pain, but all tenderness on pressing the
articulation, has disappeared. In short, the principles and details of
local treatment suited to gonorrhoeal rheumatism are the same as those
recommended for rheumatoid arthritis, which it so closely resembles;
and the reader is referred to that article for information. Although
there is a greater proclivity to copious effusion into the joints in
gonorrhoeal rheumatism than in rheumatoid arthritis, there is less to
those deeper lesions which affect the bones, and complete recovery is
usually more certain and more prompt in the former than in the latter.
Measures to prevent stiffness and even ankylosis of the articulations
are often an urgent indication. In the general treatment, also, almost
the same remedies are indicated as have been recommended for rheumatoid
arthritis. The salicylate of sodium, given freely, is sometimes
signally useful, more especially when several joints are acutely
inflamed. In the more chronic stages, when much articular effusion
exists, a prolonged course of potassium iodide is occasionally
beneficial. The local measures, however, simultaneously employed,
doubtless co-operate efficiently. Iron and quinia will frequently be
demanded by general debility, anaemia, and impaired nutrition; and the
same may be said of cod-liver oil, extract of malt, etc. The
circumstances under which the various baths are likely to be useful
have been mentioned in connection with the treatment of rheumatoid
arthritis.

The gonorrhoea should be treated in the same way that it ought to be if
no arthritis existed. The rest, the moderate diet, and even the
salicylate of sodium, favor its removal, but the frequent employment of
mild astringent injections should not be omitted.




{108}

GOUT.

BY W. H. DRAPER, M.D.


DEFINITION.--Gout, as a disease, in the traditional acceptation of the
term, is a specific arthritis, characterized by the deposit of the
salts of uric acid in the affected joints. Gout, as a diathesis, is a
blood crasis in which there is an accumulation in the blood serum of
the uric acid salts, the consequence either of the increased formation
or of the defective excretion of these products of proteid
metamorphosis. The manifold irritations of the different tissues, and
the accompanying subjective and objective symptoms provoked by this
dyscrasia, are termed gouty.

SYNONYMS.--(_a_) _Eng._, Gout; _Lat._, Gutta; _Fr._, Goutte; _Sp._,
Gota; _Ger._, Gicht--derived from the nomenclature of humoral pathology
and descriptive of the distillation (goutte a goutte) of the poisonous
humor into the joints--arthritis uratica. (_b_) Gouty diathesis;
constitutional gout; irregular gout.

CLASSIFICATION.--(_a_) Gout as a specific form of articular
inflammation is classified according to its location--cheiragra,
onagra, podagra, gonagra, etc. (_b_) Gout as a constitutional disease
is classified, 1st, according to the structures affected--_e.g._
articular gout; tegumentary gout, embracing mucous as well as cutaneous
affections of gouty origin; nervous gout; parenchymatous or visceral
gout; 2d, according to the degree of the inflammatory process--acute,
subacute, and chronic; 3d, according to certain irregularities
manifested in the development and progress of gouty lesions as
metastatic, retrocedent, and suppressed gout. This classification of
constitutional gout is based upon the well-recognized clinical
observation in the history of gouty persons and gouty families, that
the characteristic lesions of the joint-structures are often correlated
with lesions of the skin, mucous and serous membranes, vessels, nerves,
and parenchymatous organs, which are marked by the same blood dyscrasia
that exists in articular gout, and which are most successfully treated
by the same measures which experience has suggested in the management
of the arthritic disease.

Musgrave in his work[1] treats of a great number of varieties of gout,
as follows: De arthritide anomala; de colica arthritica; de diarrhoea
arthritica; de dysenteria arthritica; de abscesse intestinorum
arthritica; de melancholia arthritica; de syncope arthritica; de
calculo renum arthritico; de asthmate arthritico; de catarrho, tussi,
et peripneumonia arthritica; de phthise arthritica; de angina
arthritica; de capito dolore et {109} vertigine arthritica; de
apoplexia arthritica; de paralysi arthritica; de doloribus in corpore
vagis, fixis; de ophthalmia, de erysipelate et achoribus arthriticis;
etc.

[Footnote 1: _De Arthritide Anomala, sive Interna, Dissertatio_,
Geneva, 1715.]

HISTORY.--The records of medicine furnish simple evidence of the
prevalence of gout in all ancient as well as in modern civilized
communities. Its origin in the perversion of physiological functions
was as clearly recognized by the prophets of the old testament of the
medical art as it is by the founders of the gospel of modern science.
The refined processes of animal chemistry have simply revealed the
materies morbi which was foreshadowed in the "peccant matters" of the
humoralists, which were supposed to be distilled into the joints and
other structures, provoking inflammation and tophous deposits. This is
the most notable and interesting fact in the history of gout, that it
has from the earliest times been regarded as a specific form of
arthritis and dependent upon the circulation in the blood of peccant
matter. It was not, however, until the latter part of the eighteenth
century, when Murray Forbes, and a few years later Wollaston, called
attention to the fact that uric acid was the chief ingredient in
urinary calculi and in tophous deposits, that our knowledge of the
pathology of gout may be said to have had its beginning. The
demonstration by Garrod, in 1848, of the presence of lithate of soda in
the blood of gouty persons, also marks an era in the history of the
pathology of gout.

While the humoralistic theory of gout has prevailed almost to the
exclusion of all others, it is historically interesting to note that
the views of the solidists, as represented by Cullen, who maintained
that "gout was an affection of the nervous system in which the primary
moving powers of the whole system are lodged," have been recently
revived and are attracting considerable attention.

ETIOLOGY: PREDISPOSING CAUSES.--Heredity may be regarded as the most
prominent of the predisposing causes of gout. Statistics of arthritic
gout show this tendency in a varying but always large proportion of
cases. Scudamore observed it in nearly 60 per cent. of his cases;
Garrod, in 50 per cent. of his hospital cases and, in a much larger
proportion, in his private practice; Gairdner found it in 140 out of
156 cases. If all the manifestations of the gouty vice were taken into
consideration in determining the influence of heredity, it would
doubtless be shown in a still larger percentage of cases.

It is generally supposed that there is a greater frequency of
inheritance from the male ancestors and in the male descendants. This
may be explained by the fact that men are more exposed to the other
predisposing and to the exciting causes of gout. My own experience
leads me to suspect that if we took into consideration the irregular
manifestations of this morbid inheritance, we should find it as
frequently in the female, both in the ascending and descending line; of
the greater frequency of acute articular gout, however, in the male,
there can be no question. While it is true that acute attacks are
comparatively rare in women, both before and after the menopause, it is
undeniable that the subacute and chronic forms of gouty arthritis are
by no means rare in them, both before and after the cessation of
menstruation. The Hippocratic proposition that women enjoy immunity
from gout by reason of the menstrual flux can hardly be entitled to
much consideration in view {110} of the fact that they are commonly
less exposed to the exciting causes of the disease, and that when they
subject themselves to the same vicious habits which entail the disease
in men they suffer like men.

Statistics as to the age at which articular gout is most often
developed show that the larger proportion of cases occurs in the decade
from thirty or forty. It is rare before twenty, and the frequency
diminishes rapidly after sixty. Some well-authenticated cases have been
observed before puberty in children in whom the hereditary taint was
strongly developed. Gairdner claims to have seen several cases in
infants at the breast. Trousseau saw a case in a boy aged six, and
Garrod in a youth of sixteen. At the other extreme Garrod reports a
first attack at the age of eighty, and another in the ninetieth year.
The cases at the extremes of age are certainly rare, and other causes
of arthritic inflammation might easily be invoked to explain them. It
is a significant fact that the largest proportion of attacks of acute
articular gout occurs after the period of complete development is ended
and before the period of degenerative changes has begun, when the
necessities of growth have ceased and food is required only for the
nutrition of the tissues, the maintenance of vital energies, and the
demands of work.

Much stress was laid by the earlier writers on the effect of
temperament as a predisposing cause of gout. The vague ideas involved
in the classification of mankind according to temperament may be said
to have lost their influence in the scientific conceptions of modern
pathology. Gout is observed in persons exhibiting the most diverse
peculiarities in physical conformation and physical disposition. The
true interpretation of the facts in regard to the relations of
temperament to gout, so far as those relations exist, would seem to be
that the conditions which give rise to gout are responsible also for
the physical and moral idiosyncrasies of gouty subjects.

A vicious hygiene may be regarded as one of the chief predisposing
causes of gout. The disease is essentially one of advanced
civilization, and is alike the product of the luxury and the misery
which a high civilization entails. It is a common error to suppose that
gout is the consequence only of luxurious living. If the essential
cause of the disease is the circulation of imperfectly oxidized plasma,
then there are two ways in which this defective oxidation may be
brought about: either there is an excess of food ingested beyond the
capacity of the individual, under the most favorable conditions, to
consume, or the conditions of oxidation may be so impaired that the
complete combustion of even a moderate supply of food is impossible.
Perfect oxidation requires an even balance between the amount of food
ingested and the oxygen inhaled. A consideration of this axiom explains
several circumstances in the history of gout. As has been remarked, the
disease is rare during the period of growth and development, when the
processes of nutrition are active and the consumption of food in
excessive quantities is rendered possible by the large demands for the
needs of the growing body and for the development of active energy. It
is common in adult life when the processes of nutrition are less
active, when growth is complete, and when the supply of food must be
regulated according to the amount of energy to be developed. It must
also be observed that while the disease is most frequently caused by
excesses in the consumption of {111} food, it is also often the
consequence of an insufficient supply of pure air; hence we find it
often among those who cannot be accused of gluttony, but whose
occupations or poverty compel them to live and work in a vitiated
atmosphere.

The influence of alcoholic liquors in the production of gouty dyscrasia
is generally acknowledged. There seems to be a striking difference,
however, in the effects of the distilled and fermented preparations of
alcohol in this respect. Gout is certainly more prevalent in countries
where large amounts of fermented liquors are used than in those where
distilled spirits are chiefly consumed. The disease is more prevalent,
for example, in England than in Scotland or Ireland, especially among
the lower classes; it is said also that it is rare in Russia and
Poland, where spirits are more exclusively used. There is a difference
also in the predisposing influence of the different varieties of
fermented liquors in the production of gouty dyscrasia. The heavier
wines, sherry, madeira, and port, are known to be more mischievous in
this respect than the lighter wines of France and Germany, though there
is abundant clinical evidence of the fact that even these wines, and
especially the richer clarets. Burgundies, and Rhine wines, frequently
give rise to acute gout and the gouty habit. There can be no question
as to the pernicious effects of the malt liquors as gout-producers. The
great frequency of gouty diseases particularly among the lower classes
who consume these beverages in large quantities is undeniable. This is
true especially of the stronger English and Scotch ales, and to a less
degree of the lighter English, American, and German beers. The effect
of cider and perry as gout-producers is also well recognized. It has
been observed in certain districts of England where cider is largely
consumed, and, though acute articular gout is said not to be a common
disease in New England, where cider has always been much used, there
can be no question that it often leads to the development of the
irregular forms of gout. As one of the forms of fermented alcoholic
beverages containing, in its fresh state especially, a large amount of
sugar, it favors the production of the acid dyspepsia which is a common
antecedent in the formation of a gouty dyscrasia.

In 1854, Garrod called attention to the fact that a considerable
proportion of the gouty patients in hospital practice--at least 30 per
cent.--was represented by painters and other workers in lead. This
statement has since been confirmed by other observers, and the
association of the characteristic symptoms of this form of metallic
poisoning, such as the blue line on the gums, colic, and the different
forms of paralysis, with both articular and visceral gout, especially
the contracted kidney, is certainly frequent. The relation, however, of
saturnine poisoning to gout in this association is not easy to
determine, Garrod himself pointing out that while the women in the
lead-works frequently had the colic, they but rarely had gout. The
difference in susceptibility of different individuals to all forms of
metallic poisoning is well recognized. It is more strikingly observed
perhaps in mercurial and arsenical poisoning than in that of lead. It
is well known that the internal use of lead as an astringent in cases
of hemorrhage and intestinal catarrh is occasionally, though very
rarely, followed by the evidences of lead-poisoning. This difference in
susceptibility is perhaps explicable on the theory that persons
inclined to gout have less power in eliminating the {112} metal than
those who are not gouty, so that it is possible that plumbism is the
effect rather than the cause of gout, as has been commonly supposed.

Tanquerel des Planches found none of those changes in the kidneys as
the result of plumbism such as are frequently met with in gout, and
Rosenstein, who was able to produce saturnine epilepsy in dogs, found
no renal changes to have occurred. Charcot and Gombault in recent
experiments of feeding guinea-pigs with lead found changes in the
kidneys similar to those produced by tying the ureters.

EXCITING CAUSES.--Paroxysms of acute or subacute gouty inflammation of
the joints, skin, or mucous membranes, as well as the neuroses of gouty
origin, are excited by a variety of causes: errors in diet, both as to
quantity and as to specific articles; excesses in the use of fermented
liquors--even moderate indulgence, in persons with strong gouty
tendencies--are perhaps the most common exciting causes. Sudden changes
in temperature, and especially sudden changes in barometrical pressure,
sometimes excite and often aggravate the sufferings of gouty persons.
Blows, contusions, and mechanical strain frequently determine arthritic
attacks; the large proportion of paroxysms affecting the
metatarso-phalangeal joint of the great toe is explained by the fact
that this joint is more exposed than any other to strain and injury.
Finally, nervous exhaustion, from any cause, from overwork or sexual
excesses, from grief, anger, or shock, may provoke any of the
inflammatory or neurotic consequences of this disease.

PATHOLOGY.--It would be impossible in the limits of this article to
review the many theories that have prevailed in regard to the pathology
of gout, or even to discuss fully those that may be said to divide
professional opinion at the present day. Since the discovery, by
Garrod, of the salts of uric acid in the blood-serum of gouty patients,
the humoral pathology of gout has certainly had the largest number of
adherents.

The lithaemic pathology may be said to be based primarily upon the
chemical theory of digestion or food-transformation. This theory
proceeds upon the idea that every atom of albuminous or carbonaceous
food that enters the body, whether it goes to the construction of
tissue or is destined for the direct conversion of potential into
active energy, is finally eliminated, for the most part, as urea,
carbonic acid, and water. This transformation, of course, is supposed
to be effected by a process of oxidation, but neither the exact mode of
transformation nor the share which the different organs and tissues
take in its accomplishment can be said to be certainly known. Recent
investigations seem to indicate that the liver is chiefly concerned,
not only in the metamorphosis of the carbohydrates, but also in the
formation of urea, so that the arrest in the conversion of starches and
sugars which results in glycosuria, and the check in the metabolism of
the proteids which give rise to lithaemia, may both have their origin
in hepatic derangement. The not infrequent association of glycosuria
and lithaemia in the same patient, and the frequent alternation of gout
and saccharine diabetes in gouty families, are significant facts in
support of the common origin of these diseases.

The purely chemical theory of gout and diabetes, that they are diseases
of suboxidation--a theory most ably advocated by Bence Jones[2]--has
{113} much to commend it from the valuable suggestions which it affords
in the clinical management of these maladies; but it must be
acknowledged that while a defective oxidation seems to be an essential
factor in the production of gout and diabetes, it is impossible to
reduce the process to the simplicity of a chemical equation. It cannot
be claimed that the complex chain of transformations which organic
chemistry has demonstrated in the destructive metamorphosis of albumen
and starch in the laboratory is represented in the vital chemistry of
the body. All that can be said in the present state of knowledge is,
that the metabolism of food is in its nature a chemical analysis,
modified and regulated by vital force, and resulting in the building up
of tissues and in the conversion of potential into active energy.
Imperfect blood-elaboration must depend upon much besides a disturbance
of the balance between the amount of food ingested and the oxygen
inhaled, though this must unquestionably be an important factor in its
production. Heredity and the mysterious influence of the nervous system
complicate the problem of the malnutrition which leads to gout, in such
a way that while the general proposition may be maintained that gout is
a disease in which suboxidation occurs, it is not possible to affirm
whether suboxidation is the essence of the disease or only one of its
phenomena.

[Footnote 2: _Lectures on Some of the Applications of Chemistry and
Mechanics to Pathology and Therapeutics_, H. Bence Jones, London,
1867.]

It is probable, however, that the pathogenesis of the gouty dyscrasia
involves a much more complex process than the simple accumulation of
uric acid salts in the blood. Uric acid, like urea, is one of the
normal results of the metamorphosis of the albuminous foods and
tissues. In birds and reptiles it takes the place of urea as the final
issue of this metabolism. It has been supposed, as one atom of uric
acid can be split by oxidation into two atoms of urea and one of
mesoxalic acid, that uric acid was the penultimate of urea, the result
of a lower degree of oxidation. It is by no means certain, however,
that it is a necessary antecedent of urea. In birds, who consume by
their rapid breathing an enormous proportion of oxygen, as well as in
the slow-breathing reptilia, the nitrogenous excrements are in the form
of urates; and under such divergent conditions it is impossible to
explain the variations in the proteid metabolism by varying degrees of
oxidation. The only reason that can be assigned for the elimination of
the nitrogenous waste in some animals in the form of urea and in others
in that of urates is the teleological one that the urea is destined for
a fluid and the urates for a solid excretion.

But apart from these physiological objections to the theory that uric
acid is necessarily the offending substance in gout, it is well known
that uric acid salts accumulate in the blood in febrile diseases, in
disorders of digestion, and in anaemia--notably in splenic anaemia--and
do not produce either the symptoms or lesions of gout. Todd maintained
that gout might occur without an excess of uric acid in the blood; and
it is certain that in the atonic and irregular forms of the disease
uric acid may not be found in excess in the blood or appear in excess
in the urine. Another significant circumstance in the history of gouty
persons tending to show that uric acid may be, after all, only an
epiphenomenon in the disease, and not its exciting cause, is that the
power of digesting farinaceous and saccharine foods in this disease is
markedly diminished. To such a degree is this true that sufferers from
the gouty dyscrasia are most {114} promptly relieved of their symptoms
of primary indigestion by restricting their diet very largely to
albuminous foods; and not only does such a diet diminish the dyspeptic
symptoms, but I am persuaded by a considerable experience that it is
one of the surest prophylactics against the recurrence of gouty
lesions. It is well known that the fermented preparations of alcohol
are among the most frequent exciting causes of acute gout, and cases
are by no means infrequent in which indulgence in sweet foods and in
fruits will provoke many of the well-recognized local lesions of the
disease.

The explanation of this anomaly in the uric acid pathology of gout may
possibly be found in the suggestion of Garrod, that the deposition of
the urates is caused by their insolubility, and, as this insolubility
is increased by the diminished alkalinity of the serum, that the
evolution of the acids in the digestion of the carbohydrates so
diminishes the normal alkaline state of the blood that the uric acid
salts are more readily precipitated. But even if we accept this
explanation, the fact remains that as efficient factors in the
production of the gouty diathesis the carbonaceous foods may play as
large and perhaps a larger part than the albuminous foods. It would
seem, therefore, in view of the conflicting evidence in regard to the
theory of the uric acid origin of gout, that the chemical pathology of
this dyscrasia is still involved in considerable obscurity.

The recent advances in neuropathology have revived of late years the
views of Cullen on the pathology of gout. Dyce Duckworth[3] has lately
advocated the theory that gout is a trophoneurosis. This theory grows
out of the recognition of the protean manifestations of this disease,
and especially of the neurotic element which is so prominently
developed in its evolution. The frequency of purely nervous symptoms in
gouty persons is a fact which is daily brought to the notice of those
who have much opportunity to study the disease. These symptoms may be
said to affect all the functions of the nervous system; among these we
may mention psychical disturbances, such as hypochondriasis and
hysteria; derangements of sensation, such as neuralgias and
dysaesthesias of every variety; and spasms of voluntary and involuntary
muscles, such as cramps, grinding of the teeth, asthma, and vesical
tenesmus. Another fact which arrests attention in the history of gouty
persons is the frequency with which purely nervous influences determine
attacks of gout; the effect of nervous exhaustion, whether provoked by
overwork or mental anxiety, or the more explosive discharges of
nerve-force in rage and great emotional excitement of any kind, is well
recognized as a frequent precursor of gouty lesions. The influence of
certain diseases of the nervous centres also, such as cerebro-spinal
meningitis, Pott's disease, and tabes dorsalis, in determining
arthropathies and lesions of the skin and mucous membranes, furnishes a
striking analogical argument in favor of the possible nervous origin of
the lesions in gout. The recognition of these facts, however, does not
necessarily militate against the commonly accepted humoral pathology of
gout. The healthy action of the nervous centres must depend primarily
upon a normal nutrition, and a normal nutrition depends on healthy
blood-elaboration. That perverted innervation may be an important
factor {115} in the development of malnutrition through the accident of
inheritance is doubtless true, but in the acquired disease it seems
more probable that the lithaemic condition is the primary source of
disturbed innervation. It may be that gouty lesions are determined as
reflex phenomena through the medium of the trophic centres--if such
centres there be--rather than by the direct irritation of the affected
tissues by the gouty blood; and it is not unreasonable to suppose that
nervous exhaustion from any cause may produce in these centres greater
reflex excitability.[4]

[Footnote 3: _Brit. Med. Jour._, March 26, 1881.]

[Footnote 4: Edward Liveing, in his work _On Megrim, Sick Headache, and
Some Allied Disorders_, p. 404, thus expresses his conviction as to the
neurotic theory of gout: "The view which is commonly entertained is,
that the excessive generation or retention of uric acid in the system,
which is regarded as the fundamental fact in the pathology of gout,
exerts a toxic influence upon the nervous centres, while the particular
character of the disorder is determined by the territory involved. This
limited operation of a cause so general in its nature is a real
obstacle to this view; on the other hand, there is much in the history
of gout--its hereditary character, limitation to particular ages and
sexes, periodicity, explosive character, sudden translations, and
remarkable metamorphic relations with nervous disorders--which seems to
stamp the malady as a pure neurosis; and even the fit itself, with its
sudden nocturnal invasion, the late Dr. Todd was accustomed to compare
to one of epilepsy or of asthma."]

PATHOLOGICAL ANATOMY.--Blood-Changes.--Garrod's demonstration of the
excess of uric acid in the blood of gouty persons constitutes the chief
recognized haemic change in this disease. That this is a constant
change, and one that is essential to the existence of gout, cannot be
said to be proved. The presence of uric acid in the blood is not always
productive of gout, since it has often been found in the blood of
healthy persons, and its temporary excess during pyrexia, and
especially in the fevers and other morbid states in which spleen is
congested, has already been noted. The excess of uric acid, however, in
gouty blood may reach, according to Garrod, as much as 0.11 grain in
1000 grains of serum. It is probable that other excrementitious
substances exist in the blood in gout which bear a closer etiological
relation to this disease than uric acid, but they have not been
demonstrated. The other blood-changes which are noted by Garrod--the
diminished specific gravity of the serum from loss of albumen, the
diminished alkalinity, and the increase of the fibrin in the
inflammatory forms of the disease--are probably inconstant. In chronic
gout the objective signs of anaemia which are often present would
indicate a marked diminution in the red blood-corpuscles.

The tissues which are the chief seat of gouty lesions are the
connective tissues. In the evolution of the disease the joints, where
the connective tissue is most dense and the least vascular, suffer
earliest; at a later period the connective tissue of the blood-vessels,
nerves, and viscera becomes subject to gouty changes.

According to Garrod, the exudations in articular gout are rich in the
urates of soda, lime, magnesia, and ammonia; they also contain some
phosphate of lime and traces of organic matter. The watery portion is
absorbed and the salts are deposited in crystalline forms. The location
of these deposits varies: they are found on the synovial surfaces, in
the cartilage-cells, and in the intercellular substance; in the
tendons, ligaments, and bursae, and in the subcutaneous connective
tissue. The urate of soda occurs not on the free surface of the
cartilage, and replacing {116} the latter, as was formerly generally
supposed, but as an infiltration into the substance of that tissue; and
Garrod found that there is always a thin layer of unaffected cartilage
lying between the deposit and the free articular surface--an
observation which has been confirmed by Budd and quite recently by
Ebstein.[5]

[Footnote 5: W. Ebstein, _Die Natur und Behandlung der Gicht_,
Wiesbaden, 1882.]

Very important are the recent investigations of the latter. After
making numerous observations on the cartilages and other affected
tissues of gouty subjects, besides studying the disease artificially
produced in fowls, he has shown that those portions of cartilage and
other tissues in which the deposit occurs are in a state of necrosis,
as is evident from the fact that when the urates are dissolved out by
warm water the area in which the deposit occurred, though apparently
normal to the eye, refuses to be stained with aniline dyes, and lies
plainly visible as a light spot in the midst of stained tissue. Since
the work of Weigert we know that this is a sure sign of that peculiar
form of death of a tissue to which the name of coagulation necrosis has
been given. Ebstein regards this necrosis as primary and the deposition
of the uratic salt as secondary. According to him, the urates
circulating in the blood give rise to necrosis in parts where the
circulation is sluggish (as the articular cartilages, the ears, and the
extremities generally), and where, consequently, they remain a greater
length of time in contact with the tissues. The necrotic portion has,
however, an acid reaction, which causes a deposition, from the soluble
neutral salt, of an acid urate in a crystalline form. Ebstein claims
that this necrotic area, in which there is deposited a crystalline
urate of soda, and around which there is a secondary inflammatory zone,
is characteristic solely of gout. "I have never seen," he says, "in
gout a crystalline deposit of urates occurring in normal tissue."

In addition to these so-called specific changes we find a hyperplasia
of the connective tissue in the fibrous structures of the affected
joints. The thickening thus induced, with the contraction of the new
tissue and the atrophic changes resulting from pressure and disuse, are
the causes of the deformities, subluxations, and impaired movements of
gouty joints. Occasionally, the local irritation provoked by the
pressure of the tophous deposits results in abscesses from which a
mixture of pus and pasty urates may be discharged. These abscesses in
feeble and anaemic subjects are sometimes difficult to heal. More
frequently the skin undergoes gradual absorption and the chalk-like
deposits are exposed.

The frequency with which the metatarso-phalangeal joint of the great
toes is affected in gouty persons has always been noted. In Scudamore's
tables the proportion of the first attacks in this joint was 72 per
cent., and in 66 per cent. one or both great joints were affected to
the exclusion of other joints. This frequency is due to the fact that
this joint is the most vulnerable one in the body, bearing as it does
the weight of the body and being exposed to most frequent shock. The
phalangeal joints of the hands and the wrist-joints are also often the
seat of acute gout, though these joints are more frequently affected by
the subacute form of the disease. The larger joints may also be the
seat of true gouty inflammation; indeed, no joint, not even the
intervertebral, can be said to enjoy immunity, and the hip and shoulder
are occasionally attacked to {117} the exclusion of others. The
cartilages of the ear and the arytenoid cartilages are sometimes the
seat of gouty deposits.

The great frequency of arterial sclerosis, and the subsequent fatty and
chalky metamorphosis in persons who have suffered from chronic gout,
are well recognized. Next to syphilis, gout seems to be the most common
cause of these arterial changes. The influence of these lesions in the
arteries and capillaries in determining cardiac hypertrophy and
cerebral hemorrhage is often seen in the accidents which terminate the
lives of gouty patients.

In the heart a gouty endocarditis is of not uncommon occurrence,
according to Ebstein, who cites Lancereaux as having found uric acid in
concretions on the valves. Garrod, however, after examining a number of
cases in which cardiac disease existed with gout, states that in his
opinion the valvular changes are not due to a gouty deposit, he never
having been able to demonstrate the presence of uric acid in them.

Some years ago Sir James Paget called attention to the frequency of
adhesive phlebitis as a gouty lesion. This is observed in connection
with articular gout, but may also occur independently of joint-lesion.
It is observed most frequently in the lower limbs, is generally
symmetrical, and shows a disposition to metastasis.

Neuritis and sclerotic lesions of the nerve-centres are not uncommon in
the history of acquired and inherited gout. The neuralgias and other
temporary dysaesthesias which constitute a considerable category in the
symptoms of gouty persons are doubtless due to transient central and
peripheral lesions.

The so-called gouty kidney is the most striking illustration of the
effect of the gouty dyscrasia in the production of a characteristic
visceral lesion. The changes which occur in the kidney as a result of
gout are--a contraction of the organ, the result of interstitial
inflammatory processes, and a deposition of uratic salts, occurring
mainly in the papillary portion. The views as to the exact locality
where these deposits occur still differ considerably. Garrod is of
opinion that it occurs in the fibrous interstitial tissue. Virchow, on
the other hand, regards the lumen of the tubuli as the seat of the
deposit, and in this he is supported by Charcot and Cornil and Ranvier,
Lancereaux and Wagner. Dickinson inclines to the view of Garrod, and
believes that it is the deposition of the urates in the interstitial
tissue which gives rise to the chronic inflammation which results in
cirrhosis of the kidney--the granular kidney of gout. Ebstein seems to
think that the interstitial connective tissue, having previously
undergone a state of necrosis, as in cartilage and other connective
tissues, is the seat of the deposit. As in cartilage, he regards this
necrotic state as typical of gouty deposits. About the necrotic area in
which the deposit has occurred a secondary inflammation takes place,
leading ultimately to contraction of the new fibrous tissue formed. He
calls attention to the fact that (1) the kidneys may be perfectly sound
in gout; (2) the kidneys may be the seat of chronic interstitial
inflammatory changes, with cirrhosis, without any urate deposits of any
kind being demonstrable; (3) there may be chronic interstitial
nephritis, with crystallized urates in the urinary tubules.

As regards changes in the liver, few satisfactory accounts exist. {118}
Portal originally called attention to the fact that in gout and
rheumatism indurations of the liver caused by the deposit of a
phosphatic earth occurred, and Charcot has recently referred to the
fact. Ebstein cites a case in which in a gouty patient he was able to
make a diagnosis of moderate hypertrophic hepatic cirrhosis, but so far
he had not been able to confirm it by post-mortem examination.[6]

[Footnote 6: Gout in Animals.--Of the occurrence of gout in animals not
many reliable reports exist; Ebstein has collected a few. Thus, he
cites a case where in an old hunting-dog uratic concretions were found
in the articular ligaments and in the periosteum of the epiphyses of
many joints, but especially those connecting the ribs with their
cartilages. In the toes of falcons and of parrots kept in confinement
deposits of urates have been observed, and in an alligator dying in
captivity deposits were found in the muscles as well as the joints
which consisted of free uric acid together with sodium urate.

Experimentally, Ebstein was able to produce gouty lesions having all
the characteristics of those occurring spontaneously in man by
injecting subcutaneously small quantities of the neutral chromate of
potash into the blood of cocks for a considerable period of time. By
this method changes in the epithelial elements of the kidney were
produced, preventing the elimination of the urates from the blood and
causing their consequent accumulation in the system. He obtained in
this way typical deposits of urates in the joints, tendons, muscular
sheaths, heart, and other organs, while the birds emaciated and finally
died. But these experiments, which are extremely valuable and
interesting, still need confirmation.

The experiment of tying the ureters of fowls is an old one. Galvani who
was perhaps the first to perform it, employed it in his investigations
on the kidney, and since then Zalesky, Pawlinoff, Von Schroeder,
Colosanti, and others have made use of it in their experimented studies
on the site of origin of uric acid. As a result of this operation
deposits of urates occur in various organs. Ebstein, however, does not
regard them as analogous to the gouty deposit in human beings, as they
lack the feature of necrosis, which, as mentioned above, he considers
as alone characteristic of the true gouty lesion.]

SYMPTOMATOLOGY.--The development of true gouty lesions, whether of the
acute or subacute form, is usually preceded by a period, more or less
protracted, in which characteristic derangements of the health present
themselves. These derangements may be conveniently classified as
disturbances of primary digestion and as manifestations of
malnutrition.

The disturbances of primary digestion are repeated attacks of flatulent
dyspepsia, with pyrosis, colicky pains, alternate constipation and
diarrhoea, and a scanty, high-colored, and heavy urine with uratic
sediments. This dyspepsia may be accompanied with a variety of reflex
nervous symptoms, such as pain in the nape of the neck and occiput,
insomnia, palpitation, sighing respiration, singultus, and nausea.
These symptoms are commonly described as due to biliousness, and are
provoked by excesses in diet, and not unfrequently by moderate
indulgence in certain common articles of food, such as sweets, fruits,
farinaceous foods, and the fermented preparations of alcohol.

Derangements of nutrition are shown by a disposition to erythematous
and catarrhal affections of the skin and mucous membranes, to
affections of the sebaceous glands, and to premature falling of the
hair. There is often a more or less marked tendency to obesity.
Accompanying these derangements there may be a loss of energy, both
physical and mental, manifesting itself in indolence and fatigue on
slight exertion, in irritability of temper, with diminished
intellectual activity and hypochondriasis. Neither the primary
indigestion nor the nutritive derangements invariably precede the
development of acute gouty lesions, nor are they necessarily followed
when they exist by the articular signs {119} of gout; but they are so
commonly associated with the evolution of what are regarded as the
specific lesions of gout that they may fairly be described as
constituting its prodromal period.

ACUTE ARTICULAR GOUT.--A typical attack of acute gout is usually
sudden. It seizes its victim without warning, and often rouses him from
sleep with a vicious agonizing pain in the joint assailed. Examination
will reveal a slight redness, heat, and puffiness of the part affected
altogether disproportioned to the intensity of the pain; the tenderness
is exquisite, and the torture is often aggravated by the occurrence of
reflex spasms of neighboring muscles. There is usually moderate fever,
and if the surface be exposed there may be a chill. Sleep is impossible
and the restlessness uncontrollable. As the morning advances slight
perspiration occurs, and sleep may become possible. With the abatement
of pain there is coincident increase in the signs of inflammation: the
joint swells, the skin becomes red and oedematous around the joint, and
the superficial veins are distended. But, though the pain subsides with
the occurrence of swelling, and usually in proportion to its degree,
the tenderness and pain on any attempt to move the joint continue to be
extreme. The day is passed in comparative ease, but the evening
generally brings an exacerbation of pain and fever, and the night
another paroxysm of agony--not as severe as the first, but severe
enough to make the daylight a benison. The progress of the disease
after the second day, provided it is confined to one joint, is usually
marked by a steady and regular decline in the severity of the symptoms.
If the attack is confined to a single joint, a week may elapse before
the inflammatory signs subside, and it may be a fortnight before
pressure can be borne or the mobility of the joint is restored.
Occasionally the sufferings of an acute attack of gout may be
protracted by successive seizures for several weeks. The fever during
the attack is distinctly remittent, the evening exacerbation rarely
exceeding 103 degrees F.

The urinary symptoms before, during, and after an acute paroxysm of
gout are interesting and important in their bearing upon the uric-acid
theory of the disease. Garrod's statements upon this point are
generally accepted, and have been confirmed by other observers. He says
that previous to the attack the amount of uric acid in the urine is
below the average--that during the paroxysm the proportion grows
smaller, and only rises to the normal standard with the termination of
the seizure. The reaction of the urine is strongly acid during the
paroxysm. This is due probably to the increased excretion of acid
phosphates. The quantity of the urine is generally diminished, the
specific gravity increased, and the color deepened.

Attacks of acute gout are generally followed by improved health and
capacity for physical and mental work and enjoyment. The blood seems to
be purified, the processes of digestion and assimilation are once more
normally performed, the equilibrium of the nervous centres is restored,
and the evolution of all the vital energies proceeds with ease and
vigor. This state of well-being may continue for a year or two years,
or even a longer period, after the first attack, the immunity varying
according to the intensity of the inheritance or the habits of life.
The subsequent attacks are apt to occur at increasingly shorter
intervals, and, as a rule, the acuteness of them tends to diminish.
Gradually the dyscrasia becomes more {120} profound, and the
constitutional symptoms and structural changes which belong to the
atonic and irregular forms of the disease are developed.

ATONIC GOUT.--Though subacute, irregular, or atonic gout is often the
sequence of repeated attacks of the acute disease, it is not
necessarily preceded by them, nor is acute gout invariably followed by
a marked gouty dyscrasia. It is not uncommon for a well-characterized
gouty habit to exist, manifesting itself by many and varied gouty
phenomena, without the occurrence of any acute lesions, and repeated
attacks of acute articular gout may occur without the development of
the progressive impairment of health and the tissue-changes which
distinguish the chronic malady. The recognition of this fact is
important, inasmuch as the occurrence of acute gout is commonly
regarded as an essential element in the diagnosis of the gouty
dyscrasia. Acute articular attacks, as already noted, are very rare in
women, in whom the subacute and irregular forms of the disease are by
no means infrequent. So far as acute articular gout is of value in the
diagnosis of the constitutional vice, it is perhaps as significant if
established in the history of a near relative as in the individual in
whom the disease is suspected.

The general symptoms of atonic gout--or, as it may more properly be
called, the gouty dyscrasia--are similar to those which sometimes
precede the development of the acute form. The difference lies in their
persistence, in the subacute character of the local lesions, and in the
absence of the relief to the constitutional symptoms which follows
acute attacks.

The dyspeptic symptoms are perhaps the most pronounced and uniform in
the history of the evolution of chronic gout. These symptoms have been
already described, but the fact which seems especially to distinguish
them is that they are chiefly provoked by the acid fermentation of the
carbohydric elements of the food, the sugar and starches, and
especially by the fermented preparations of alcohol; the ability to
digest these articles of diet appears to be deficient in the gouty
dyspeptic.

The changes in the urine in the gouty dyscrasia are especially
important. In the formative stages of the gouty vice the amount of
urine may not vary much from the normal quantity, but the proportion of
solid constituents, especially of the urea, is increased, so that the
specific gravity may rise to 1.030 or 1.035. The acid reaction is
intensified by the excess of the acid urates and phosphates upon which
the normal acidity depends. Sometimes crystalline deposits of uric
acid, urates, and oxalates take place in the tubuli of the kidney and
in the bladder, and lead to the nephritic and vesical irritations which
are often the source of much inconvenience and pain. Where the urine is
free from these crystalline constituents as it comes from the bladder
it may deposit them within a few hours after its passage. At a later
stage in the development of the gouty dyscrasia the quantity and
quality of the urine undergo marked changes. The quantity is increased;
the color is pale, partly in consequence of dilution and partly through
a diminution in the amount of coloring-matter. The quantity may be so
considerable as to constitute a polyuria. The reaction is neutral or
only feebly acid; crystalline sediments of uric acid and calcium
oxalate may occasionally appear, and the specific gravity may be so low
as to indicate not only a relative but an absolute diminution in the
daily excretion of urinary solids. Traces of albumen and of sugar are
not infrequently observed.

{121} The articular symptoms of chronic gout are subacute. They affect
the joints, as a rule, which are most exposed to strain and injury, and
hence are most common in the hands and feet, but they may involve the
knee and the hips, the elbow and the shoulder, and even the
intervertebral joints. The pain is less severe, because the tension is
never so considerable; the tenderness is often a source of great
discomfort; the swelling varies with the acuteness of the inflammatory
process, the joints being more or less permanently enlarged by
hypertrophic changes affecting the articular structures and by tophous
deposits. The deformities are increased by ankylosis, by contractions,
by absorption of the cartilages, by partial luxations, and by the
atrophy of disused muscles. Crepitations are often observed in the
affected joints. Exacerbations of the local symptoms are often provoked
by movements, by imprudence in diet, by changes in temperature or in
barometric and hygrometric conditions, and not infrequently by
psychical disturbances.

The frequency with which tegumentary affections, mucous as well as
cutaneous, are observed as correlative phenomena of arthritic lesions
in gouty persons and in gouty families justifies the inference that the
same lithaemic vice which determines articular inflammations is often
responsible for derangements of nutrition in the skin and mucous
membranes. The French school of dermatology, which has always
maintained the humoral origin of many cutaneous diseases, has long
recognized the arthritic nature of a large class of affections of the
skin. Bazin[7] has given the most precise description of the
arthritides, as he terms them. He insists upon certain functional
derangements of the skin as characteristic of the gouty diathesis, such
as excessive perspiration, especially in certain regions, as the head,
the axillae, the hands and feet, and the sexual organs, and also
affections of the sebaceous glands, causing the different forms of
seborrhoea and the premature falling of the hair. He notes the
liability in gouty persons to certain neurotic affections, such as
pruritus, general or localized, about the arms and genital organs.
Erythematous affections, especially urticaria, erythema nodosum, and
the fugitive erythema which occurs about the face, causing sudden and
evanescent swelling of the eyelids, cheeks, lips, and even the tongue
and soft palate, are recognized by him and other observers as arthritic
in their origin. Among the erythemata which are observed in gouty
persons the peliosis rheumatica should be mentioned.

[Footnote 7: _Affections generiques de la Peau_, Paris, 1862.]

The more persistent inflammatory lesions of the skin, such as eczema
and psoriasis, which are characterized by long-continued hyperaemia
with hyperplasia, are now recognized as among the possible
transformations of gout. They are certainly often observed alternating
with arthritic lesions, and associated with all the characteristic
derangements of nutrition which belong to the gouty habit. The
frequency of the various forms of acne, the inflammatory, as well as
those which result from excessive function of the glands, in persons
having a strong gouty inheritance, is recognized by many
dermatologists. I have noticed these lesions especially in young women
belonging to gouty families. They are generally accompanied by marked
dyspeptic symptoms, and not infrequently by neurotic derangements.

Garrod, in a paper read at the International Medical Congress in 1881
{122} on "Eczema and Albuminuria in Relation to Gout," affirms that
each year strengthens his conviction that gout and eczema are most
closely allied. Since his attention was first called to this relation
in 1860, he has found a gradually increasing percentage of eczema in
the cases of gout that have come under his observation. Dividing all
the cases from 1860 to 1881 into ten groups, he found the percentage
rose from 10 in the first group to 47 in the tenth. He accounts for
this rapid increase in the percentage in the fact that in the first few
years the eczema was only observed when it was very patent; during the
past two or three years he has had made more careful inquiries as to
the presence of eczema or other skin eruption in every case of gout,
and by these means has frequently discovered its presence when it might
otherwise have been overlooked. Garrod believes that eczema is the
special skin-lesion of gouty subjects, and does not regard psoriasis as
having anything more than an accidental connection with gout. He admits
that the latter is often associated with rheumatoid arthritis. It must
be remembered, however, that Garrod does not admit that gout ever
exists without lithatic deposits.

In regard to the location of gouty eczema, it appears to affect by
preference the more tender and vascular regions of the skin. The
eyelids, ears, the scalp, and back of the neck, the fingers and toes,
particularly the dorsal and lateral surfaces, and in old people the
legs, are especially liable to be attacked. The subjective symptoms of
gouty eczema are often the source of great suffering; the burning and
itching are sometimes intolerable. This is especially true of persons
of highly neurotic constitution.

It is not possible to affirm that there are lesions of the mucous
membranes which are strictly analogous in their transient character to
the erythematous affections of the skin, but it is not unreasonable to
suppose that many of the temporary disturbances of indigestion to which
gouty patients are subject are caused by an evanescent hyperaemia
corresponding to the vaso-motor derangements which are observed in the
external integument. In regard, however, to the more persistent
catarrhal lesions, there can be no question as to their analogy with
those which affect the skin. The continuity of these lesions at the
orifices of the mucous tracts, and the frequent association of external
eczemas with catarrhs of mucous membranes, are facts of common
experience. Greenhow[8] of London first called attention to the
frequency with which chronic bronchitis is associated with the gouty
dyscrasia. In an analysis of 96 cases of chronic bronchitis he elicited
the fact that in 34 out of the 96 a distinct gouty history attached
either to the patients themselves or to some of their immediate
relatives. In 14 of the cases the patients were subject to attacks of
acute regular gout as well as to bronchitis. He also noted the
association in a number of cases of bronchitis and psoriasis with
gravel and gout. My own experience confirms these observations, and
also the alternations of catarrhal and parenchymatous tonsillitis, of
pharyngeal and laryngeal catarrh, and of asthma and chronic bronchitis,
with the more common manifestations of regular and irregular gout.

[Footnote 8: _On Chronic Bronchitis_, E. Headlam Greenhow, M.D.,
London, 1869.]

The occurrence of subacute gastro-duodenal and intestinal catarrhs
{123} with hemorrhoidal complications is even more common that the
catarrhal affections of the respiratory tract. The lesion, in fact,
which gives rise to the manifold dyspeptic symptoms in gouty subjects
is doubtless a catarrhal one.

The genito-urinary tract exhibits also the tendency to catarrhal
affections in sufferers from the gouty dyscrasia. It is certain that
gouty persons are especially liable to vesical catarrh, and it is
generally admitted that rheumatic and gouty persons are particularly
susceptible to gonorrhoea. My own experience leads me to suspect that
chronic urethral discharge resulting from acute urethritis is more
common in rheumatic persons than in those not having this taint. The
etiological relations of gonorrhoeal rheumatism and kerato-iritis are
still involved in obscurity, though I am inclined to believe that a
careful examination of the personal and family history in cases of
these diseases would establish the opinion that has been maintained as
to their gouty origin.

The presence of albumen in the urine of persons suffering from acute
gout is occasionally observed. Under these circumstances it is
transient, and has probably no more significance than is usually
attached to this symptom in the course of any acute febrile disease. In
chronic gout it is by no means infrequently observed as a more or less
persistent symptom. It is associated under these circumstances with a
copious discharge of urine of pale color and low density, and with the
general signs of what Rayer first described as the nephrite goutteuse.

The importance of this symptom is very great when we consider the
insidious development of this form of disease and the difficulty of its
early diagnosis. Recent investigations point to the value of the
changes in the urine in the progress of the gouty dyscrasia as bearing
upon this question. It has already been noted that in the early history
of gouty persons the urine is often scanty, high-colored, excessively
acid, of high specific gravity, occasionally albuminous and saccharine,
and frequently depositing sediments of urates and calcium oxalate.
McBride of New York[9] has recently called attention to this condition
of the urine and its association with high arterial tension as the
functional stage of the granular kidney--as the stage, that is to say,
during which the necessity of eliminating large amounts of imperfectly
oxidized nitrogenous material maintains a constant state of renal
hyperaemia, which finally induces the changes in the tubular and
intertubular structures which constitute the anatomical features of
this form of disease.

[Footnote 9: _The Early Diagnosis of Chronic Bright's Disease_, T. A.
McBride, M.D., New York, 1882.]

The occasional presence of sugar in the urine of gouty persons has
already been noted. I have repeatedly observed this symptom in the
urine of gouty dyspepsia. It occurs more commonly in obese subjects,
and is usually intermittent and easily controlled by dietetic
restrictions. In these cases it is not necessarily associated with a
very large amount of urine. In chronic gout and in connection with the
granular kidney a more serious form of glycosuria is occasionally
observed. Under these circumstances it increases largely the polyuria
which is characteristic of gouty nephritis, and is sometimes overlooked
because it occurs in a urine of a low density, often not more than
1.010. It is not controlled by diet {124} to the same extent that it is
in the cases previously described, and is in my experience a prognostic
sign of bad import.

Some of the most distressing symptoms to which gouty persons are
especially liable are those connected with the passage of gravel from
the kidney to the bladder. Where gravel alone passes, it may cause
little uneasiness, and the fact is only recognized through the
discovery of blood in the urine in connection with uric acid or calcium
oxalate crystals. When, however, the sand forms concretions in the
pelvis of the kidney, their dislodgment and passage through the ureter
are accompanied by the well-known agonies of renal colic.

Dysuria is a symptom from which gouty persons often experience much
inconvenience and suffering. It is usually associated with extremely
acid urine of high density containing crystalline sediments. It may
manifest itself only in frequent and painful micturition, or it may be
associated with such a degree of vesical tenesmus as to cause retention
and necessitate the use of the catheter.

DIAGNOSIS.--If the term gout be restricted to that form of arthritis in
which an excess of urates is found in the blood with tophous deposits
in the affected joints, the cartilages of the ear and nose, and in the
subcutaneous connective tissue, then the diagnosis of this disease is a
simple one. It is a disease with a pathognomonic sign. But if the
pathology of gout consists rather in a more complex morbid condition of
the blood, of which an excess of urates in the serum is only one of a
number of phenomena, and not necessarily the sole and essential cause
of the local lesions, then the question of diagnosis involves a
consideration of all the correlated morbid conditions which are so
frequently associated in gouty persons and gouty families as to justify
the inference that they have a common origin in a perverted nutrition,
the essential nature of which is imperfectly understood.

The very existence of the terms gouty rheumatism and rheumatic gout
which are in common use shows that what is regarded by many excellent
authorities as the confounding of distinct entities must have some
foundation in clinical experience. If we consider gout, in its
strictest pathological sense, acute inflammatory rheumatism, rheumatoid
arthritis, or gouty rheumatism, and senile arthritis or the arthritis
deformans and gonorrhoeal rheumatism as separate and distinct diseases,
we shall find ourselves compelled to ignore certain common clinical
facts which indicate a bond of union between them. Heredity, for
example, is common to them all, and more than this, there appears to be
a tendency to a differentiation of the taint in families. It is well
known, for instance, that the children of gouty parents are especially
liable to acute rheumatism, and acute rheumatism in youth is often
followed by gout in later years. It is also a fact of common experience
that while the men in gouty families are the victims of true gout, the
women are apt to be the subjects of rheumatoid arthritis. The arthritis
deformans which develops with the degenerations of advancing years is
not infrequently associated with a family history of genuine gout.
Gonorrhoeal rheumatism also, according to the experience of many
trustworthy observers, often recognizes an inheritance to gouty
lesions. But it is not alone in heredity and the differentiation of the
type of the disease in families that the unity of these affections
displays itself. The same disturbances of digestion which {125}
characterize the history of true gout are observed in those who are
liable to acute rheumatism, to rheumatoid arthritis, and to arthritis
deformans. It is true that excesses in food and fermented liquors do
not determine, as in gout, attacks of acute rheumatism nor of the
chronic forms of arthritis, for these latter diseases are commonly due
to causes operating upon the nervous system, as exposure to cold and
dampness or to physical or emotional shock of some kind; still, there
is in the subjects of these diseases a more or less marked tendency to
the same dyspeptic disorders, and especially to the diminished capacity
in digesting the carbohydrates, which the subjects of true gout
exhibit. In the diagnosis of gout, therefore, it would seem that the
question of differentiating this disease from those which simulate it
is not one in which we are called upon to distinguish one morbid entity
from another, as typhus from typhoid fever or syphilis from cancer, but
rather to determine, first, the presence of a recognized constitutional
vice; and, secondly, to differentiate the variety of the lesions by
which this vice manifests itself.

In the diagnosis of the gouty dyscrasia the first point to determine is
that of heredity. This requires a careful inquiry into collateral as
well as direct descent, and does not necessarily involve the discovery
of arthritic diseases in the ancestors, though these are doubtless the
most striking and trustworthy proofs; but the tradition in the family
of persistent dyspepsia, or what is commonly called biliousness, of
chronic catarrhal affections of the skin and mucous membranes, and of
the chronic forms of renal disease, are significant indications of this
dyscrasia. In the personal history the evidences of the lithaemic
tendency, as indicated by the characteristic dyspeptic symptoms which
have been described, and especially by the feeble capacity for the
digestion of carbohydrates, are of great diagnostic value.

The diagnosis of gouty joint-lesions, whether acute or chronic, depends
partly upon the determination of the gouty dyscrasia, and partly upon
the differential distinctions which separate gouty inflammations from
acute rheumatism, rheumatoid arthritis, and from the arthropathies
which result from traumatism and from lesions of nerves and
nerve-centres.

Gouty arthritis may be distinguished from acute rheumatism by the fact
that it is more often hereditary--that it occurs in older subjects,
attacking generally the smaller joints, and, as a rule, in the acute
form, localizing itself in one or two joints. It is also noteworthy
that the constitutional symptoms are not as severe as in rheumatism.
Gout deforms the joints, while acute rheumatism leaves no traces of the
inflammatory process. In addition to these distinctions there is,
according to Garrod, the crucial test of an excess of urates in the
blood-serum.

From rheumatoid arthritis or rheumatic gout, gout in its acute and
regular form is distinguished by the more acute local and
constitutional symptoms. Gout is periodical in its attacks, while
rheumatoid arthritis is progressive. It attacks the smaller joints or
those most exposed to strain, while rheumatoid arthritis occurs in the
large as well as the small joints, and appears to be more independent
of traumatism as an exciting cause. Gout is more common in men,
rheumatoid arthritis in women. According to Garrod and other excellent
authorities, deposits of urates are never found in the joints in
rheumatoid arthritis, and there is no excess {126} of urates in the
blood. This statement is denied by Hutchinson. Ulcerations of
cartilages, contractions of tendons, atrophies of muscles with
subluxations of joints, are more common in rheumatoid arthritis than in
gout.

While these local distinctions are undeniable, it is proper to observe
that in rheumatoid arthritis the constitutional symptoms of the gouty
dyscrasia, especially the dyspeptic derangements and the nervous
disturbances, are often well marked; and it should also be noted that
the principal distinction, the absence of urates in the blood and in
the diseased joints, is one that is based on the exclusive theory that
uric acid is the materies morbi of true gout. If, as is still
maintained by some excellent authorities, uric acid is not essential to
gout, then it must be confessed that the other distinctions are purely
lesional, and that the common constitutional symptoms suggest that
these diseases are divergent branches of a single trunk.

Gouty arthritis is not always easily distinguishable from traumatic
inflammation of the joints, inasmuch as traumatism plays so important a
part as an exciting cause of gouty attacks. The history of previous
seizures and the presence of predisposing causes of gout are the points
upon which the determination of the gouty nature of the inflammation
would depend. A termination in suppuration would exclude the idea of
the gouty nature of an arthritis.

With the arthropathies of purely nervous origin, such as occur in
paralyzed limbs, in Pott's disease, and in tabes dorsalis, gout can
hardly be confounded, although the arthritic complications in these
diseases have been used to illustrate the neurotic theory of both gout
and rheumatism.

The diagnosis of irregular gout--_i.e._ of gouty affections of the skin
and mucous membranes, of the structures of the eye, and of the
parenchymatous organs--must be based more upon the hereditary history
and upon the correlated phenomena recognized in the personal history
than upon any specific character in the lesions themselves. In the
gouty form of nephritis there are, it is true, in the urinary symptoms,
in the anaemia, in the arterial fibrosis, and in the cardiac
hypertrophy, diagnostic signs of great value.

PROGNOSIS.--Acute, regular, articular gout is probably never a fatal
disease where it occurs in a robust person without visceral
complications. In rare instances the first attack may never be
repeated, or only two or three attacks may occur in the course of a
long life. In the majority of instances, however, frequent repetitions
are the rule, the intervals between the attacks growing progressively
shorter; occasionally repeated seizures go on through a long life, the
attacks becoming milder with advancing years, and, save the crippling
effects of the disease, the patient may enjoy in the intervals a fair
degree of health. This, however, is the exception. With the increased
frequency of the arthritic attacks the signs of the constitutional vice
become more marked. The dyspeptic disorders become more persistent and
rebellious to treatment, various transformations of the disease
manifest themselves, and tissue-changes make insidious and inevitable
progress. When this stage of the gouty disease is reached, the
prognosis becomes more grave because of the complications and accidents
to which the sufferer is liable. These complications and accidents are
the result of the nervous, vascular, and visceral lesions which have
been {127} described. Vaso-motor instability gives rise to a great
variety of painful functional derangements resulting from serious
cerebral, pulmonary, gastric, and renal congestions. Glycosuria is not
an uncommon complication in chronic gout, and seriously affects the
question of prognosis. Arterial degenerations may cause thrombotic
accidents, and the formation of miliary aneurisms in the brain may
determine a fatal issue by softening or hemorrhage. Anginal attacks due
to cardiac muscular degeneration may also imperil life.

The principal visceral lesion which leads directly or indirectly to a
fatal issue in gout is that of the kidney. This involves danger either
through the induction of a hopeless anaemia and its consequences in
dropsical effusions, or by determining inflammatory accidents of the
gravest nature.

That gout shortens life in the majority of cases is unquestionable--a
fact which is sufficiently attested by the care with which
life-insurance companies exclude risks in which a well-pronounced
inherited tendency or existing manifestation of the disease can be
substantiated.

The prognosis varies of course with the rapidity with which the
constitutional dyscrasia is developed, and this rapidity will depend on
the intensity of the inheritance and the mode of life. Some gouty
subjects escape the vascular and visceral complications of the disease
for a long period, although crippled and deformed by its articular
ravages, and attain advanced age; others may succumb in comparative
youth to its most profound lesions. It is a happy circumstance that
under wise hygienic management and judicious medication acquired gout
may be checked in its progress, and even a strong inherited tendency
may be largely controlled.

TREATMENT.--A logical consideration of the treatment of gout embraces,
first, the treatment of the constitutional vice, based, as far as
possible, on the nature and causes of the disease; and, secondly, the
treatment of the lesions which the disease determines. If we regard the
accumulation in the blood-serum of the salts of uric acid as the
essential cause of the gouty lesions, then the origin of the
constitutional vice is in the conditions which bring about this
accumulation. As we have urged, none of the theories of the production
of the lithaemic state harmonize all its phenomena. It is impossible to
represent the complex processes of nutrition by chemical formulae, and
equally impossible to divorce chemical reactions from a share in their
production. We can trace the metabolism of the azotized and
carbonaceous foods through many changes to their ultimate
disintegration into urea, carbonic acid, and water, but we do not know
all the steps by which this conversion is effected, nor the organs or
tissues in which it is accomplished. We may reasonably assume that the
agent through which the potential energy of the food is evolved is
oxygen, and that the process of nutrition is hence partly, at least, a
process of oxidation. This chemical view of the digestion and
assimilation of food may be said to be the rational basis of the
treatment of the lithaemic state. To control the accumulation of
azotized matters in the blood, and to secure their thorough combustion
and conversion into urea, carbonic acid, and water are the recognized
aims of the treatment of the vice upon which gout depends.

DIET.--The prevention of the accumulation of azotized matters in the
{128} blood involves, first, a consideration of the question of the
diet appropriate to the gouty dyscrasia. The almost uniform counsel
upon this point of all the authorities from Sydenham to the present
time is, that albuminous foods should be sparingly allowed in the diet
of the gouty patient, and that vegetable foods, especially the
farinaceous, should constitute the principal aliment. This counsel is
based upon the theory that uric acid is the offending substance, and,
this being the outcome of a nitrogenous diet, the nitrogenous element
in diet must be reduced. My own observation has led me to believe that
while this may be a legitimate deduction from the uric-acid theory of
gout, it is not supported by the results of clinical experience. If
there is one signal peculiarity in the digestive derangements of gouty
persons, it is their limited power to digest the carbohydrates, the
sugars and starches. In whatever form these foods are used, they are
more commonly the source of the dyspeptic troubles of sufferers from
gout than the albuminous foods. They provoke the acid and flatulent
dyspepsia which so generally precedes the explosion of the gouty
paroxysm; and it must have attracted the attention of every observer
who has studied the dyspeptic disorders of sufferers from inherited
gout, who have sought to control their unhappy heritage by abstemious
habits, that these disorders are especially provoked by over-indulgence
in saccharine and amylaceous foods.

It is not possible to explain satisfactorily why the lithaemic
condition should be induced by the carbonaceous aliments, but we
believe there can be no question as to the fact. If, as modern
physiological investigations tend to show, the liver is the organ in
which urea as well as glycogen is formed, it may be that the overtaxing
of its functions manifests itself more readily in the conversion of the
albuminous than in that of the carbonaceous foods; or it is possible
that the carbonaceous foods are destined chiefly for the evolution of
mechanical energy, and that when this destiny is not fulfilled through
indolence and imperfect oxygen-supply, they escape complete combustion,
and so vitiate the blood. But whatever may be the cause of this
anomaly, the clinical fact remains that in gouty persons the conversion
of the azotized foods is more complete with a minimum of carbohydrates
than it is with an excess of them--in other words, that one of the best
means of avoiding an accumulation of lithates in the blood is to
diminish the carbohydrates rather than the azotized foods.

The diet which a considerable experience has led me to adopt in the
treatment of the gouty dyscrasia is very similar to that which
glycosuria requires. The exclusion of the carbohydrates is of course
not so strict. Abstinence from all the fermented preparations of
alcohol is perhaps the most important restriction, on account of the
unfermented dextrin and sugar which they contain. This restriction
accords with the common experience respecting the part which wine and
beer play as predisposing causes of the gouty disease and as occasional
exciting causes of gouty lesions.

Next to the fermented liquors, the use of saccharine food in the diet
of gouty persons needs to be restricted. This limitation also is one
which common experience confirms. Sweet foods cannot be said to be as
provocative of the dyspeptic derangements of the lithaemic subjects as
wine and beer, but they are certainly often responsible for the
formation of {129} the dyscrasia and for perpetuating many most
distressing ailments. Their more or less strict prohibition may
constitute the essential point of treatment not only in controlling the
progress of the constitutional vice, but in subduing some of the most
rebellious lesions. It is important to observe that this prohibition
sometimes involves abstinence from sweet and subacid fruits, in the raw
as well as in the preserved state. Paroxysms of articular gout have
been known to follow indulgence in strawberries, apples, watermelons,
and grapes, and the cutaneous and mucous irritations which follow even
the most moderate use of these fruits in some gouty persons are
certainly not uncommon.

Next in order to the saccharine foods as the source of indigestion in
gouty persons come the amylaceous aliments. These constitute,
necessarily, so large an element in ordinary diet that the limitation
of them in the dietary of gouty persons applies, in the majority of
cases, only to their excessive use. This excessive use, however, is
often observed. There is a popular prejudice in favor of this class of
foods, and a corresponding prejudice against the too free indulgence in
animal foods. The purely starchy aliments, such as potatoes and the
preparations of corn and rice, and even those which contain a
considerable portion of gluten, like wheat, oatmeal, and barley, often
provoke in gouty subjects a great deal of mischievous and painful
indigestion. This feeble capacity for the digestion of farinaceous
foods is most frequently observed in the children of gouty parents, and
especially in persons inclined to obesity, and in those whose
occupations are sedentary and whose lives are passed for the most part
in-doors, and they are least common in those whom necessity or pleasure
leads to much active muscular exercise in the open air.

The fats are as a rule easily digested by gouty dyspeptics. This is a
fortunate circumstance, for the reason that in the anaemia which is
frequently one of the consequences of chronic gout the fatty foods are
of inestimable value. In cases of persistent and rebellious lithaemia
an exclusively milk diet constitutes a precious resource.

The succulent vegetables, such as tomatoes, cucumbers, cauliflower,
cabbage, and the different varieties of salads, constitute for the
gouty as well as the diabetic subject agreeable and wholesome additions
to a diet from which the starchy and saccharine vegetables have to be
largely excluded.

The quantity of food proper for gouty persons to consume can only be
determined in individual cases by the age, the habits, and the
occupation. It is fair to assume that in adults, in whom there is no
longer any provision to be made for growth, the daily quantity of food
must be regulated according to the amount of energy which is expended.
In this energy must be reckoned the amount necessary for the
maintenance of animal heat and the other vital functions, and the
amount which is necessary for the operation of every variety of nervous
force. In other words, the potential energy latent in the food must
correspond to the active energy exhibited in the daily evolution of
vital, intellectual, and mechanical work. The more nearly this balance
is maintained the more closely the physiological standard of health is
preserved. That an excess of food is a most frequent cause of the gouty
dyscrasia among the well-to-do classes is undeniable, and it is
possible that regulation of the quantity according to the rule above
mentioned {130} may, after all, be the most important point in the
management of many gouty patients. It may be, also, that the reason why
the withdrawal of the carbohydrates produces its good effects upon
these patients is that we thereby exclude a large amount of
force-producing foods which do mischief because they are imperfectly
consumed.

EXERCISE.--Next in importance to diet as a hygienic regulation in the
management of gouty patients is enforced exercise. The axiom of
Abernethy, "to live on a shilling a day, and earn it," comprises the
philosophy of the true relations of food to work, and of both to the
highest development of physical health. Exercise is to be enforced not
simply as a means of securing an active respiration, and thereby an
abundant supply of oxygen, but also as a means of converting the
potential energy of the food consumed into vital energy. The essential
condition, moreover, of healthy nutrition in every organ and in every
tissue is the maintenance of a vigorous functional activity. Over-use
is not more productive of tissue-degeneration than disuse. Hence the
question of exercise in its largest sense involves not only muscular
work, but work of all kinds, which tends to promote a healthy activity
of the psychical as well as the physical functions. Muscular exercise
in the open air has a special value for the victims of this gouty
dyscrasia by equalizing the circulation, quickening the respiratory
movements, and stimulating the elimination of effete matters from the
skin and lungs, but mental work and wholesome diversions are not less
important as antagonizing the evil effects of indolence and
over-feeding, which are among the common predisposing causes of
acquired gout. In persons who are incapacitated by neuraesthenia or by
excessive corpulence, the result of long indulgence in indolent and
luxurious habits, it may be necessary to resort to passive exercise by
rubbing, massage, and electrical excitation in order to secure the good
effects of voluntary work.

BATHING.--Another hygienic regulation of great value in the treatment
of gouty dyscrasia is the promotion by bathing and friction of the
eliminative function of the skin. Daily sponging with cold water, where
it is not contraindicated by a feeble circulation and a slow reaction
from the shock, is a practice to be commended. Where, for the reasons
mentioned, it is not practicable, tepid baths and frictions may be
substituted. In cases where the arthritic lesions are progressive and
advanced much benefit may be derived from hot baths. It is doubtful
whether the thermal alkaline and sulphur spas owe their renown in the
treatment of chronic gout so much to the mineral ingredients of their
springs as to their high temperature. The Russian and Turkish baths
furnish most efficient means for increasing the functional activity of
the skin, but they often have a depressing effect on the action of the
heart, producing faintness and dyspnoea, and should always be advised
with caution.

CLIMATE.--In rebellious forms of the gouty dyscrasia a warm climate is
unquestionably a hygienic condition of great value. The geographical
distribution of gout, which shows that the disease is much less common
in warm than in temperate and cold climates, while it may not perhaps
be wholly explained by temperature alone, is very certainly largely due
to it. The possibility of out-door life and the increased functional
activity of the skin which warm climates favor are circumstances more
or less antagonistic to the development of the gouty diathesis.

{131} MEDICINAL TREATMENT.--The objects to be aimed at in medicinal
treatment of the gouty dyscrasia are--

1st, the improvement of the primary digestion.

2d, the relief of the gastro-intestinal catarrh, which is the cause of
the direct and reflex dyspeptic symptoms which belong to this
diathesis.

3d, the augmentation of food-oxidation, so as to secure its thorough
combustion.

4th, the promotion of the elimination of the waste products of
nutrition.

1. The improvement of primary digestion--or, as it has been aptly
called, exterior digestion--often requires very strict attention beyond
the proper selection of alimentary substances. The distressing symptoms
that indicate primary gastric and intestinal indigestion are certainly
often relieved by the rigid exclusion of certain articles of diet, but
in many cases it is necessary to assist the preparatory processes which
are essential to perfect food-absorption by artificial methods based
upon the knowledge derived from physiological experiment. To no one is
the knowledge of these methods more largely due than to Roberts of
Manchester. Preparations of pepsin and pancreatin, by which the
proteids and starches are peptonized and the fats emulsified, are often
of inestimable value in the treatment of gouty dyspepsia. Pancreatin,
especially, which by means of its trypsin, diastase, and emulsive
ferment possesses the threefold property of aiding the digestion of the
azotized, amylaceous, and fatty elements of food, is certainly the most
valuable of the artificial means for augmenting the efficiency of
primary digestion.

2. The relief of the gastro-intestinal catarrh in gouty dyspeptics may
often be accomplished solely by dietetic restrictions and by the aid
which may be given to primary digestion. It is often necessary,
however, to direct some special medication toward the relief of the
catarrhal lesion. The circumstances which demand this special
medication are the existence of portal congestion, the result of
functional derangement, or of chronic atrophy of the liver, or of
chronic diffuse or interstitial nephritis, or of cardiac disease. The
hydragogues, such as calomel, podophyllin, colocynth, and other
vegetable cathartics, with the salts of sodium and magnesium,
constitute the most common and efficient means of relieving portal
congestion, whether it arise from temporary functional derangement or
from organic disease. The renown of some of the more famous mineral
springs in relieving the miseries of gouty sufferers is due mainly to
the relief of portal congestion and the washing away of the catarrhal
mucus which obstructs the process of primary food transformation and
absorption. This is especially true of the sulphate of sodium waters,
like those of Carlsbad, Marienbad, Friedrichshall, Pullna, and Hunyadi
Janos. While the value of these waters in chronic gout is
unquestionable where their use is properly regulated, there is good
reason to believe that their long-continued employment is often harmful
by relaxing the mucous membrane, and thereby tending to aggravate the
condition they are given to relieve. This is markedly true of their use
in weak and anaemic persons. For these the milder magnesian waters,
such as those of Kissengen, Hombourg, Wiesbaden, and Saratoga, are to
be preferred.

3. The augmentation of food-oxidation may be accomplished in a large
degree by regulation of the diet and by out-door exercise. The {132}
regulation of the diet according to the occupation and habits of life
is a point of primary importance in securing proper blood-elaboration.
My experience leads me to believe that the evil consequences of in-door
occupations and sedentary habits are most common in those who live upon
a diet composed largely of starchy and saccharine foods, and that a
diet in which animal foods and fats predominate is best suited to
indoor workers, whether they be engaged in mechanical or intellectual
labor.

The medicines which help to promote the oxidation of the food-elements,
especially the carbohydrates, are alkalies and iron. Clinical
observation establishes this fact as strongly in the treatment of gout
as in that of glycosuria. The relative power of the salts of potassium
and sodium in augmenting oxidation is not clearly determined. The salts
of sodium appear to be most useful in aiding the process of primary
digestion, and the potassium salts in improving the process of
sanguification. It is well known that potash predominates in the
corpuscles and soda in the serum of the blood. The efficacy of the
combinations of iron with the salts of potassium, as in Blaud's pills
and in the citrate and tartrate of iron and potassium, in the treatment
of anaemia, is well known. In the most renowned ferruginous springs,
however, such as those of Schwalbach, Spa, Pyrmont, and St. Moritz, the
iron is combined with salts of sodium, calcium, and magnesium. It would
appear, therefore, that the increased energy of iron in augmenting
haematosis, when combined with alkalies, is not relatively greater with
potash than with either of the other alkaline bases.

4. The promotion of the elimination of the waste products of nutrition
is to be accomplished by remedies which act as solvents of uric acid
and as diuretics. As solvents of uric acid the salts of lithia and
potash have been shown to be superior to those of soda. The urate of
lithia is the most soluble of the uric-acid salts, and the low chemical
equivalent of the metal lithium makes the neutralizing power of the
oxide much greater than that of equal proportions of the other
alkalies. It is used in the forms of carbonate and citrate, and is
generally combined with potash and soda. It exists in some of the
mineral springs of Europe and of this country, but in such minute
proportion as probably to be of little value. In administering the
salts of potash and soda it is generally admitted that the carbonates
and the neutral salts of the organic acids are to be preferred to
solutions of the caustic alkalies. They have less power in neutralizing
the acid of the gastric juice, and enter the circulation as neutral
salts, where they are decomposed into alkaline carbonates by the
oxidation of the organic acids, increasing the alkalinity of the serum
and acting as diuretics. The combinations of the alkalies with sulphur,
with iodine, and with mineral acids, as in the alkaline springs, are
frequently used in the treatment of gouty lesions of the subacute
variety. The sulphur salts probably owe their chief value to their
alkaline bases when they are used internally; and in sulphuretted
baths, as before remarked, the good effects are probably due to the
high temperature at which the bath is usually administered.

The salts of iodine are generally supposed to have a special action in
removing the consequences of chronic fibrous inflammation in gout and
rheumatism. They often disturb the digestion and provoke troublesome
irritations of the skin and mucous membranes. In removing the sclerotic
{133} effects of gouty inflammation they do not exhibit the same
sorbefacient power which they show in their action upon the granulation
tissue of syphilitic origin. It must be admitted, however, that in
certain catarrhal affections of a gouty nature the iodides of potassium
and sodium are almost specific in their good effects. In the
pharyngeal, laryngeal, and bronchial catarrhs from which some gouty
persons suffer, where there is a dryness and irritability of the mucous
membrane, the administration of these salts produces the most prompt
and beneficial result. As solvents of uric acid they do not appear to
equal the salts of the organic acids.

As to the mode of administering salines in the treatment of the gouty
dyscrasia, it is hardly necessary to observe that it must vary with the
effect desired. As antacids in acid dyspepsia they should be given soon
after meals, and for this purpose the salts of soda are to be
preferred, for the reason that they not only neutralize excessive
acidity, but they increase the efficiency of the peptonizing process.
Where it is desired to introduce these salts into the circulation for
their solvent action, as diuretics or to assist the process of
sanguification, they should be given three or four hours after meals
and largely diluted with water.

Before concluding the consideration of the treatment of the gouty
dyscrasia it should be remarked that the ability of water as a solvent,
as a means of stimulating tissue-changes and eliminating waste, is not
generally estimated at its true value. The use of copious libations of
hot water in the treatment of gout, recommended by Cadet de Vaux in
1825, has been revived from time to time, and is at present attracting
considerable attention.

TREATMENT OF ACUTE ARTICULAR GOUT.--There are three distinct methods of
managing an attack of acute gout--the antiphlogistic, the expectant,
and the abortive.

The antiphlogistic method, in the strict application of the term, is
practically obsolete. Bloodletting, both general and local, brisk
catharsis and diaphoresis, with low diet, were formerly advocated as
the natural and imperative antagonists of gout as well as of all other
acute inflammatory affections. Carried to its extreme degree, this
method was deprecated by Sydenham and his disciples as tending often to
prolong the attack and precipitate the manifestations of atonic gout.
The natural reaction from the vigorous antiphlogistic practice was what
has been termed the expectant method.

The expectant method may be said to be founded upon the aphorism of
Mead that "gout is the cure of gout." The discovery of the salts of
uric acid in the blood-serum and in the affected tissues gave a
scientific basis to the humoral pathology of gout and led to the
formulation of definite principles in the application of the expectant
method of treatment. These principles are the prevention of the further
accumulation of the urates in the blood and the promotion of their
oxidation and elimination. The first principle involves restriction to
a rigid diet during the attack, excluding albuminous foods and the
fermented preparations of alcohol, and allowing only milk and
farinaceous gruels. The oxidation of the urates is encouraged by the
administration of alkalies and by an abundant supply of air, the
inhalation of oxygen even having been recommended. The elimination of
the urates is accomplished chiefly {134} by diuretics and moderate
catharsis. The local treatment commonly used with this medication
consists in the application of alkaline and anodyne fomentations or of
dry flannel or cotton. Local bloodletting and blistering are now rarely
commended. Under this treatment the intensity of the inflammatory
process is abated, the suffering is allayed, but the progress and
duration of the disease are not materially modified. The recovery,
however, is satisfactory, and it is claimed that the chances of early
recurrence of the attack are diminished. This method has many
advocates, though it cannot be said to represent the common practice of
the present day. It is becoming traditional, and may be said to be
gradually giving place to the specific or abortive method.

The abortive method consists in cutting short the attack by the
administration of colchicum, veratria, or the salicin compounds.

The value of colchicum in joint affections is a tradition of the
earliest records of medicine. It shares its curative effects in acute
gout with veratria, and, though the active principle of the meadow
saffron and the veratrum album are not isomeric, their effects are
similar. They constitute the basis of the famous nostrums so
extensively patronized by sufferers from gout. Colchicum is the active
agent in the eau medicinale de Husson, in Wilson's and Reynolds's
specifics, and in the pills of Lartigue and Blair, while veratria is
supposed to be that of Laville's remedy. The action of these substances
is not understood. The physiological action of colchicum is that of a
local irritant and a cardiac depressant of great energy. It purges
violently when given in large doses, causes nausea and vomiting, and
may produce collapse. In therapeutical doses in a gouty paroxysm it
acts as a diuretic and an antipyretic, and allays, sometimes in a most
magical manner, the objective and subjective symptoms of the disease.
As simple purging by other cathartics does not abort the gouty seizure,
the value of colchicum cannot be ascribed to its purging effect, and,
besides, purging is by no means necessary to its efficiency. Nor can
its utility be ascribed to its diuretic property. There is some
question in regard to its claims as a diuretic, and there seems to be
no doubt that it often does good where this effect is not observed. Its
influence upon the heart does not explain its marvellous action upon
the local process, for the same influence obtained by other drugs has
no such result. We are driven, therefore, to the conclusion that
colchicum has a specific action in gout as certain and as inexplicable
as that of quinia in malarial fever, or iodide of potassium in
constitutional syphilis. For those who accept the theory that gout is a
tropho-neurosis the therapeutical action of colchicum is a strong
confirmation of its neurotic origin, for the reasons that colchicum has
no influence upon arthritic lesions which are not gouty, and that its
physiological effects point to its action on the nervous system.

It is useless, however, to speculate on the way in which colchicum and
allied substances affect gouty inflammation; the practical question to
be determined is: Are they the best and safest remedies to control it?
Upon this point there is a wide diversity of opinion. The objections to
the colchicum treatment are based upon humoral pathology, and upon the
idea that the attack is an effort of nature to cast out the poison and
purify the blood. Colchicum, it is claimed, arrests this process; the
poison is retained, diffuses itself through the tissues, and lays the
{135} foundation of vascular and visceral lesions. It shortens the
intervals between the attacks, and tempts the patient to continued
indulgence in the habits which perpetuate and exaggerate the disease.
The advocates of the abortive treatment, on the other hand, claim that
these arguments have no real force as applied to its therapeutical
value. The cure accomplished is, to all appearances, complete, and the
patient is saved the suffering and exhaustion which result from the
expectant method. The fact that he is so easily and speedily cured, and
that he resumes his vicious habits and suffers recurring attacks in
consequence, proves only that the treatment lacks the quality of moral
discipline which belongs to prolonged suffering and the penance of
vigorous medication. It is an acknowledged fact that the great majority
of sufferers from acute gout decide sooner or later in favor of the
abortive treatment; and as professional opinion has heretofore
generally advocated the expectant or eliminative treatment, they
commonly resort to the use of some one of the quack remedies which
contain colchicum or veratria.

In view of the present uncertainty of our knowledge of the true
pathology of the acute gouty arthritis, as to whether it is a
tropho-neurosis or the result of the local irritation caused by the
salts of uric acid, the specific treatment seems to be justified by a
regard for the comfort of the patient and as a means of protecting him
against falling into the reckless use of quack remedies. A speedy
relief of the acute symptoms, followed by the treatment appropriate to
the gouty habit, would seem to be the most rational and safest mode of
managing the acute articular attacks of gout.

The selection of the preparation of colchicum in the treatment of an
acute paroxysm is a matter of individual experience and preference. The
acetous extract and the wine of the seeds are most commonly used, and
many practitioners are not scrupulous in prescribing the proprietary
preparations of Reynolds, Laville, and Blair. The wine of colchicum may
be given in doses varying from 20 to 40 minims, alone or combined with
Epsom salts in drachm doses, with small quantities of opium, every six
or eight hours. Under this medication the pain, tenderness, and
swelling rapidly abate, and sometimes with an abruptness that is
magical. As soon as the acute symptoms subside, the colchicum should be
continued in smaller and less frequent doses until the fever and local
tenderness subside. The use of quinia with small doses of colocynth
after the colchicum has been discontinued helps to re-establish the
strength and regulate the digestive functions. The patient should
always be warned against the possible demoralizing effects of a speedy
recovery from a serious disease. Recurrence after the colchicum
treatment is certainly more common than after the expectant method, but
this should not be ascribed so much to a defective cure as to the
temptation which the antidote offers to trifling with the poison. The
accidents which have been ascribed to colchicum through its causing
heart-failure are probably to be explained by its injudicious
administration in large doses where acute gout is complicated with
cardiac or renal degeneration.

Next in importance and value to colchicum in the abortive treatment of
gout are salicin, salicylic acid, the sodium salicylate, and the oil of
wintergreen. Unlike colchicum, which has no marked effect upon acute
rheumatism, these medicines appear to act with similar energy on {136}
gout and rheumatism. The rapidity and the almost uniform way with which
they allay the inflammatory symptoms in rheumatic fever are well known;
their value as specific remedies in both acute and subacute gout is not
so generally appreciated. Whether the specific action of colchicum in
gout differentiates this disease from rheumatism, or whether the
similar action of the salicin compounds indicates that these diseases
are allied in their etiology, are questions yet to be solved. The good
effects of salicin and the sodium salicylate in many of the forms of
irregular gout, and notably in the dyspeptic disorders and the
erythematous tegumentary lesions, are especially worthy of notice. In
acute attacks of articular gout the salicylic acid or the sodium
salicylate, in 15 or 20 grain doses repeated every three or four hours,
will often cut short the attack, and will very certainly allay within
twenty-four hours the acuteness of the symptoms. As in rheumatism, the
medicine should be continued in smaller doses after the acute symptoms
have subsided for several days, the tendency to relapse being marked if
the drug be discontinued too soon. In subacute articular gout and in
the irregular forms of the disease, where the medicine has to be
continued for some time, salicin and the oil of wintergreen are to be
preferred to salicylic acid and the sodium salicylate. They are less
liable to disturb the stomach and to produce toxic effects.

It is unnecessary to describe the treatment of the different forms of
irregular gout, inasmuch as the general principles described in the
treatment of the gouty dyscrasia involve the most important
considerations in the management of these affections.




{137}

RACHITIS.[1]

BY A. JACOBI, M.D.

[Footnote 1: There is a difference of opinion as to the correct
spelling of this word, and strong reasons exist to regard the form
_rhachitis_ as the proper one. It is true that this spelling of the
word has been remarked upon as unorthographical by many, mostly modern,
authors. Even Virchow writes "Rachitis," claiming that Glisson took the
term from "the then popular _rickets_." This is a mistake, as H.
Rohlffs points out (_Deutsches Arch. f. Gesch. d. Med._, 1883, p. 294).
Rachitis is a Greek word, and was used in the classical time of
Hellenism. It has, however, seemed best to preserve here the usual
spelling, rachitis, which has become sanctioned by general usage.]


DEFINITION.--Rachitis is a general nutritive disorder, almost always of
long duration, usually with an introductory stage of weeks or months
and a course mostly extending over months or years. Its beginning is
mostly gradual, its final recovery slow. It is complicated with or
dependent on disorders of the digestive or respiratory apparatuses,
which are preceded by a disposition probably created by an undue width
of the arteries. It exhibits amongst its prominent symptoms muscular
debility; perspiration; anomalies of the subcutaneous tissue, which is
either very much infiltrated with fat or deprived of it; disturbances
of the intellectual and moral functions, and of those of the large
thoracic and abdominal viscera and lymphatic glands; changes in the
latter may outlive all others. Its most perceptible symptom, however,
consists in an inflammatory disease of the primordial cartilage of the
epiphyses, a copious deposit in that region and also under the
periosteum of the bones; curvature of the diaphyses, and, while
absorption remains intact, softening and retarded ossification of the
bone. Without these affections of the osseous system the diagnosis of
rachitis is not complete.

ETIOLOGY AND PATHOLOGY.--The nature of rachitis has been considered to
be inflammatory by F. A. Walter.[2] Renard looked for that inflammation
in the periosteum. Guerin emphasizes the vascular increase in
periosteum, bone, and marrow; Trousseau and Lasegue the congestive
character of the local tumefaction, besides fever and pain. Virchow
also[3] inclines to the opinion that the rachitical process is of an
inflammatory nature, though it be impossible to state the exact cause
of the process. Still, he claims that we are no better off in regard to
other inflammations of unknown character--for instance, those of the
skin--and that we have to look for a future increase of our knowledge
of such constitutional predisposition of the organism and of such
specific qualities of the blood as will produce the local irritation of
the osseous tissue in rachitis. Last, and mainly, it is Kassowitz who
seeks the {138} essence of the rachitical process in a chronic
inflammation originating in the points of apposition of the growing
bones of the foetus or infant. During the chronic inflammation
blood-vessels are formed in large numbers, and a morbid congestion
takes place in all blood-vessels, but mainly in those of the localities
in which new bone is forming; thus in the chondro-epiphyses, in the
perichondrium and periosteum, and the sutural substances. Faulty
introduction or elimination of lime has nothing to do with this
process. It cannot be deposited in the current of a copious
circulation; in fact, it is not deposited in the immediate neighborhood
of blood-vessels to any extent. Even in otherwise normal bone
hyperaemia produced by the experimenter softens the bone, which was
fully formed before. If the relative percentage of lime were of any
account in the etiology of rachitis, the periosteal and cartilaginous
proliferations would find no explanation. But why is it that this
peculiar process takes place at an early age only? and in the bone
only? Kassowitz urges the fact that the growth of the bone differs in
this from the development of all other tissues: that the latter grow
uniformly through their whole mass; that the circulation in them is
more uniform and carries material through and into every particle
simultaneously, while in the bones the only places in which the whole
circulation can contribute to their growth--the few blood-vessels
distributed in the interior not adding to their growth at all--are the
periosteum and the places of apposition between epiphysis and
diaphysis. Every morbid irritation, whether resulting from bad air,
habitation, and food, or from either chronic or acute ailment, acts on
the whole mass of other tissues and organs, but in the bones only on
the growing ends or surface.

[Footnote 2: _Anatom. Museum_, Berlin, 1796, vol. ii.]

[Footnote 3: _Arch. f. Path. Anat._, vol. v.]

The results of the pathologists and experimenters are confirmed by
chemical analyses. Fat has been generally found somewhat increased in
the rachitical bones, and water largely so; chondrin is diminished
according to Marchand and Lehmann, but was found unaltered in the later
analyses of A. Baginsky. The latter found, after having deprived the
bone of fat, the organic and inorganic material to be in a proportion
of 100 to 563 in the normal, and of 100 to 160 in the rachitical
osseous tissue; and in 100 parts of dry bone, Gorup-Besanez found in
the

                       Ossein. Phosphoric Acid. Lime. Manganese Oxide.
  Healthy adult         34           26          34        0.3
  Infant of six months  34.9         27          35        0.5
  Rachitical femur      72            7           9        0.3
      "      tibia      60           12.9        17        0.3

Defective calcification of the forming bone is one of the principal
characteristics of rachitis. In it lime cannot either enter into the
composition of the osseous tissue or remain in it. Its elimination must
take place either through the kidneys or the intestinal tract. In the
feces Ad. Baginsky, and many before him, have found an abnormal
quantity. In regard to the urine, modern investigations do not agree
with former analyses. Thus, Baginsky concludes that there is no
increase of lime in the urine of rachitical as compared with that of
healthy children; Seemann found even a diminution of the percentage of
lime. Amongst modern writers only Rehn found an occasional increase of
lime in the urine of rachitis.

{139} In regard to the elimination of phosphoric acid, the analyses of
different periods do not agree any better. The conclusions of previous
researches, pointing to a quadruple elimination of phosphoric acid in
the urine of rachitis, are refuted by Seemann, who found no increase,
and by Baginsky, according to whose researches the phosphoric acid of
the healthy urine compares with that of rachitical urine as 40:12-37.

As far as the elimination of nitrogen is concerned, there appears to be
but little difference between normal and rachitical urine. Chlorine was
found to be diminished in rachitis by Baginsky. Lehmann and Von Gorup
found lactic acid several times. Several times albumen was met with; in
a case of Ritchie's, blood; in one of Von Gorup's, fat.[4]

[Footnote 4: E. Salkowski und W. Leube, _Die Lehre vom Harn_, 1882, p.
536.]

The etiology of rachitis must be studied from two points of view. It
has its predisposition and its direct and proximate causes. The former
has been studied by F. W. Beneke[5] upon an anatomical basis. He finds
that the arteries of rachitical patients are large all through the
body. This is so particularly in the carotids; it seems probable that
the changes taking place in the head are due to this anomaly in the
size of the arteries. Three cases in which the width of the arteries of
the neck was unusually large terminated fatally--one by hydrocephalus,
one with a very large skull, and one suddenly. This width of the
arteries is most marked, under ordinary circumstances, from the second
to the fourth year; that is, the exact time in which (except the cases
of early rachitis) the rachitical process is at its height. It is
considered by Beneke to be the cause of the local increase of vascular
irritation, particularly in the epiphyses with their retarded
circulation; and also of the increase of nutritive development which is
so often noticed during recovery from rachitis; and, finally, of the
many pulmonary complications of an inflammatory nature.

[Footnote 5: _Die Anatomischen Grundlagen der Constitutions Anomalien
des Menschen_, 1878, p. 75, etc.]

There is another interesting consideration in regard to the effect of
wide arteries on the relations between the blood and tissues. A great
many more blood-cells are required to fill the arteries when wide than
when narrow. Now, the formation of blood-cells is hindered by any
disease of the digestive and blood-preparing organs, so that the
tissues are liable to show the relative increase in the percentage of
water, which is uniformly confirmed for rachitis by the biochemists.

The pulmonary artery of the healthy infant is larger than the aorta by
not more than four millimeters. In the majority of cases of rachitis
examined by Beneke this difference in size was very much more favorable
to the pulmonary artery; it is abnormally large in rachitis. This
anatomical fact is suggestive of the pathological processes so
frequently found in the lungs and in the neighboring lymphatic and
large abdominal glands. For, while the amount of blood introduced into
the lungs through its wide artery is unusually large, particularly so
in a chest which is contracted in consequence of the rachitical process
in the bones, the exit from the lungs is relatively impeded. Not only,
however, the narrowness of the chest is a cause of this disproportion.
For even in rather normal chests the lungs of rachitical children are
relatively small.

The liver of almost all rachitical children is large. In but one-half
{140} of the cases this enlargement is accompanied with a large heart.
In pure cases of scrofula, on the contrary, Beneke found a small heart,
rather narrow arteries, and usually a small liver, the size of the
lungs offering but few anomalies.

The spleen also is large in the majority of cases. Its size is not
dependent on the large size of the liver or the small size of the
lungs. For these conditions are found in the majority of cases only,
not in all of them, and the large spleen is not always found with a
large liver and small lungs. The variability of the anatomical
conditions permits of various degrees of combination; so that varying
combinations of rachitis with other constitutional disorders may
correspond with the different sizes of the principal organs. After all,
as there is a great deal of independence of these organs, as to size,
of each other, the conclusion is justified that those differences are
not the result of the disease, but that they are congenital and stand
in some causal relation with it.

The kidneys are large in the majority of cases, like the spleen and
liver, while the lungs are small. This disproportion is apt to result
in a hyperaemic condition of all the organs of the abdominal cavity,
and especially of the kidneys. To what extent this undue amount of
volume interferes with, or increases, renal secretion, it is difficult
to say. The amount of urine secreted by rachitical children is about
normal, though, as already stated, the percentage of lime in it is
rather diminished, contrary to the opinions held formerly.

For the direct cause of rachitis Glisson looked to the inequality of
nutrition by the arterial blood, and for that of the curvature of the
long bones to their superabundant vascularization. He found the disease
mainly amongst the well-to-do classes, not unlike a modern American
writer, who declares infantile paralysis to be the result of the
nervousness of the better classes of the American people! John Mayow
(1761) held a disturbance of the innervation responsible; Zeviani (in
the same year), improper food in general, and particularly prolonged
lactation; and Selle (1791), a peculiar diathesis (acrimonia
rachitica). About that time a defective nutrition with abnormal
function of the lymph-ducts was looked upon as the cause of rachitis by
many--by others, an undue production of acid, and the softening of the
osseous tissue thereby. This result was attributed by some to the
influence of milk (Veirac, De Krzowitz). Attention was directed at an
early time to phosphoric acid and lime, with the view that variations
in the elimination of these substances might explain the occurrence of
rachitis. A large quantity of both was found in some urines (Malfatti);
a superabundance of phosphoric acid was presumed to prevail in the
whole system (Wendt, Fourcroy); while symptoms resembling rachitis were
found in animals fed upon small doses of phosphoric acid by Caspari
(1824). Chossat fed young animals on food deprived of lime, and claimed
to produce softening of the bones and death, a result which was denied
by Friedleben. Guerin claimed to produce rachitis by feeding young
animals on meat in place of their mother's milk, a result equally
denied by Tripier, who, like Friedleben, found the bones under such
circumstances more liable to fractures, but not rachitical. Wildt and
Weiske found the bones uninfluenced by withholding lime from food;
Forster, however, and Roloff claimed to notice a marked influence, and
the latter {141} stated that animals, after having been rendered sick
by depriving them of lime, recovered when they were again supplied with
it. Wegner, in his numerous experiments with phosphorus, found that in
growing animals it increases the growth and firmness of both long and
flat bones; after the growth of the animal has been completed it
renders epiphyses and vertebrae denser. There is no change, however, in
the relative chemical composition of those parts. He found at the same
time that results similar to those caused by the administration of
phosphorus were obtained when food deprived of its phosphate of lime
was given. But he met with no rachitical changes proper during these
several procedures. Teissier having found an increase in the urine of
rachitis after the administration of lactic acid, and lactic acid
having been frequently found in the urine of rachitical patients by
Ragsky, Morehead, Simon, and Lehmann, C. Heitzmann fed with lactic acid
both carnivorous and herbivorous animals, found the cortical layer of
the bones softened and the medullary substance hyperaemic, and claimed
to produce rachitis in the former and osteomalacia in the latter. Both
of these assertions were denied by Tripier and Toussaint, who insist
upon Heitzmann's having selected animals which have a peculiar
disposition to suffer from rachitis. Again, Milne Edwards and
Boussaingault found the bones softened when they withdrew both
phosphoric acid and lime from the food, without restoring the bone's
consistency by administering powdered bone. But, lately, Ad. Baginsky
states that he produced rachitis by withholding lime, and increased the
effect by introducing lactic acid. By so doing, however, he changed
only the relation of the mineral to the organic substances, without
interfering with the normal proportions to each other of the
constituents of the ashes. Beneke, finding oxalic acid in the urine in
many cases of rachitis, attributes to it the want of calcification in
rachitis, and Senator suggests that what impedes the deposition of bone
might be formic, acetic, and lactic acids, which are also found in the
young osseous tissue.[6]

[Footnote 6: L. Furth, _Path u. Ther. d. Rachitis_, Wiener Klinik,
1882.]

Of these statements many are uniform, others contradictory. Thus far,
they are not convincing except in one way--viz. that both withholding
and introducing certain ingredients, mainly lime, influence the growth
of the bone considerably. This may prove nothing else but that lime is
of paramount importance in the building up of bone, and that bone in
the period of rapid development is amenable to a great many influences.

It is in the period of rapid development that rachitis is observed.
Thus it occurs in every stage of intra-uterine and infant life. It is
met with in the foetus in very early intra-uterine life; it is found as
a congenital affection, continuing to develop after birth when it has
originated in the latter half of foetal existence; there is, thirdly,
the rachitis of early infancy; and, lastly, that of advanced infancy
and childhood. Of 624 cases of rachitis enumerated by A. Baginsky,
there were 256 less than a year old, 313 in the second, and 63 in the
third year. After this time rachitis is rare, as far as the active
symptoms of the disease are concerned. But still, a retarded form of
rachitis (r. tardiva) has been described by some authors. It is said to
occur about puberty, and to exhibit local changes in the bones of
genuine rachitical character, but to be wanting in all the other
symptoms required for the diagnosis of general rachitis. Such cases
have been described {142} by C. Lucas.[7] He found it complicated, now
and then, with albuminuria. The occurrence of the latter at that time
of life had been referred to by Moxon.[8] The principal symptoms
described by Lucas are scoliosis, talipes valgus, and genu valgum. The
epiphyses were slightly thickened; there were pain in the limbs,
languor, and pallor. In some of the cases there were also rachitical
deformities dating from infancy. He believes rachitis of adolescence to
exhibit more symptoms belonging to relaxation of the ligaments than to
softening of the bones.

[Footnote 7: _Lancet_, June 9, 1883.]

[Footnote 8: _Guy's Hosp. Rep._, 1878.]

A case of rachitis of undoubtedly congenital nature has been reported
by Chiari. There were but twelve teeth. There were no other alveoli,
nor was there any intimation of the formation of alveoli in the shape
of the jaw, which resembled very much the usual senile form of
retrograde metamorphosis.

Twenty years ago I described the lesions in part of a rachitical
cranium removed from an infant who lived up to her eleventh day. She
was born at full term with hernia of the brain, about one-sixth of
which protruded through the small fontanel. Only the cranium could be
studied with regard to rachitis, and but small portions of the frontal
and the anterior half of the parietal bones surrounding the large
fontanel could be removed. In these few square inches of bone there
were between twenty-five and thirty openings of the usual craniotabic
nature, nothing but a transparent membrane being left. The bony edges
of these thin portions were partly sloping off gradually, partly very
steeply, and somewhat thickened. They were distributed over the whole
part of the skull removed; some were found in the immediate
neighborhood of the points of ossification. No recent deposits of soft
rachitical bone had taken place under the periosteum. Thus, evidently,
the process was of rather an early date of intra-uterine life, and had
at birth run the full course of its usual development without having
had an opportunity to terminate in the restitution of the normal
bone.[9]

[Footnote 9: _Amer. Jour. Obst._, Nov., 1870.]

In a case reported by Dr. F. A. Burrall[10] the infant (female) was
cyanosed at birth, and had a small head and feeble general development.
The respiration was shrill and piping from birth, as though from
congenital laryngismus; in a few days it became raucous. The
post-mortem examination proved the larynx normal, with no obstructive
growths. She was pigeon-breasted, and the last phalanx of her right
finger wanting.

[Footnote 10: _Trans. N.Y. Path. Soc._, vol. i. p. 81.]

In the meeting of June 27, 1883, of the Societe de Chirurgie of Paris,
Gueniot presented a newly-born baby with well-pronounced rachitis of
the extremities which had healed at the time of birth. The bones had
recovered their firmness, and the characteristic deformities remained.
In the meeting of December 19th he could report that the child had
exhibited neither symptoms of rachitis nor of syphilis since. In regard
to the latter, a very rigorous examination of the baby's whole family,
made by Gueniot and Fournier, resulted in the existence of no trace of
syphilis.[11]

[Footnote 11: _Rev. Mens. des Mal. de l'Enfance_, Janv., 1884.]

Kassowitz has examined many still-born infants, and also children dying
at an early age, at the foundling hospital of Vienna. In a large
majority of the cases he found rachitical changes in the ends of the
bones. In {143} many of those who lived several weeks he found rachitis
developed to such an extent that the presumption of its intra-uterine
origin became conclusive. Here nothing is left but the conclusion that
the cause of congenital rachitis has to be looked for in the condition
of the maternal blood.

Thus, the foetal and congenital occurrence of rachitis cannot be
doubted. Both forms are represented in literature. Neither requires the
presence of rachitis in one or both of the parents. But the cause of
the intra-uterine disease has not been found. Perhaps a disease of the
mother with considerable nutritive disorders or a defective placentar
supply may be found responsible. The foetal form runs its course long
before the normal termination of pregnancy; the congenital may have run
its full course at birth or complete it afterward. The bones are found
of characteristic nature, the diaphyses suffering more than the
epiphyses; even a rachitical pelvis has been met with by Fischer. Early
foetal rachitis is probably dependent upon a defective development of
the very first cartilaginous deposits and the first osseous nuclei;
thus, many of the congenital synostoses find a ready explanation.
Besides these, abnormal circulation is accounted for. For periosteal
proliferation at that early period contracts the foramina carrying the
blood-vessels, and, while interfering with the size of the bones, the
foramen magnum also. Thus, a certain class of cretinism appears to be
due to foetal rachitis, mainly of the base of the cranium, which
results in early ossification of the synchondroses, particularly of the
sphenoid bone. But lately I have seen a case of this description,
which, however, had not terminated at the time of birth. For after
birth the rachitical process developed further, and in addition to the
rachitical deformity of the base of the cranium there were afterward
thickening of the epiphyses, pigeon breast, and thoracic grooving and
flattening.

Rachitis is found in city and country, less on mountains than in
valleys. Still, it is met with at elevations of two thousand feet. In
the tropical regions it is almost unknown. Why it should have been
considered quite a new disease in England but a few centuries ago, or
whether it did not exist before that time, it is difficult to say. It
is certain, however, that deformities have been described in antiquity
which we are accustomed to attribute to rachitis.

As the disease is one that occurs during the period of rapid growth,
and is a developmental disease, everything that interferes with normal
growth and development is apt to change physiological functions into
pathological conditions and to produce rachitis. In the pregnant mother
her ill-nutrition and the defective cell-material used in the building
up of the embryo and foetus, or a defective placenta, may come in for
the explanation of foetal and congenital rachitis, although the case of
Klein's, who reports twins, of which one was normal and one rachitic,
is rather difficult to explain on that basis only. Even rachitis of
early infancy is not easily accounted for otherwise, for its first
symptoms show themselves at a very early period; thus constipation,
adiposity, and afterward craniotabes and thoracic grooving.

The common form, and that which is the usual subject of the text-books
and monographs, has, however, in most cases a well-marked preparatory
stage in the shape of diseases or ailments reducing sanguification
{144} and nutrition. Some cases are ushered in by, or follow the course
of, acute exanthems or acute gastric disorders or the presence of
entozoa. A larger number appear to result from insufficient oxygenation
resulting from lung diseases, with a long chronic ailment following the
acute stage. Even acute pneumonia, with its direct influence on general
nutrition, stands often for the proximate cause of rachitis. Bad air
alone, even swamp air, does not appear to be a sufficient cause. When
it seems so, it is complicated with the main cause of rachitis; that
is, bad, insufficient, improper food, with its immediate result--viz.
intestinal catarrh. Cow's milk, particularly when acid, starchy food
administered too early or in too large quantity or too exclusively,
early weaning followed by improper artificial food, insufficient
mother's milk or such as is either too thin or too caseinous, lactation
protracted beyond the normal limit,--may all alike be causes of
intestinal disturbances and rachitis.

Is rachitis hereditary? A number of women who were rachitical
themselves have been known to have rachitical children. But it has been
said that the process runs its full course during infancy, and that
therefore a direct inheritance of rachitis from mother to child is an
impossibility. Still, we must not forget that the consecutive
conditions of the parents may, or will, influence the general condition
of the infant and result in similar disturbances. No rule, however,
exists. Dyscrasic parents may have healthy children, and healthy
parents sickly or dyscrasic ones. But the probability is greater that
diseased children should come from dyscrasic parents than from healthy
ones. Tuberculosis in the parents has frequently been accused of being
the cause of rachitis in the infant--not directly, but in consequence
of general impairment of the tissues. Gout has also been accused of
being the cause of rachitis, but it is a peculiar fact that the poor
have but little gout and a great deal of rachitis. In all of these
cases it is better to look upon rachitis as only one of the forms of
general mal-nutrition, and to speak of inheritance of the disposition
rather than of the disease. Thus it was that about the end of the
eighteenth century Portal spoke of scrofulous, syphilitic, scorbutic,
rheumatic, arthritic, and exanthematic rachitis. Particularly has
syphilis been accused of being the main cause of rachitis by some, and
even the only cause by others. Thus it was looked upon by Boerhaave. In
modern times Parrot maintained, from 1872 up to the time of his death,
which occurred recently, that every case of rachitis is of syphilitic
origin. As his proof he relied mainly on the condition of the teeth and
the bones. But those appearances in the teeth, the thin and ragged
edges, the friability and the grooving, either horizontal or vertical,
which have been considered characteristic of syphilis by Hutchinson and
others, have no such dignity, and moreover they are not observed in the
temporary teeth at all, but in the permanent only; the rachitical
softening of the bones also is not found in syphilis at all.
Particularly are there no curvatures in syphilis and no infractions. It
is true that marasmus is found in both rachitis and syphilis, but it is
met with in all sorts of diseases. The changes in the bones of syphilis
are found at birth; in rachitis they usually develop in later months.
When a baby is syphilitic and rachitic at the same time, the syphilis
may last very much longer than the rachitis, which meanwhile has
healed. The internal organs in rachitis do not exhibit any such {145}
changes as are known to occur in very many cases of syphilis. No
gummata are ever found in rachitis, and the interstitial inflammation
of the internal organs in syphilis is not met with to the same degree
in rachitis. What Parrot claimed as a desquamative syphilide of the
tongue--that is, red insulated spots, denuded of their epithelium,
small in the beginning, later extending backward and increasing in
size--is by no means always syphilitic, but is found in a great many
cases where there is no suspicion of syphilis. It is mainly Kassowitz
and Bouchut who have taken the stand against Parrot. The former, taking
rachitis for a peculiar inflammatory process, admits that syphilis can
be one of the causes. The latter directs attention mainly to the fact
that by changing food in certain ways rachitis may be produced in dogs,
but that they cannot be made syphilitic. There is no doubt, however,
that syphilis may give rise to rachitis by its general influence on
nutrition, and in this fact lies the key to the connection of great
nutritive disorders with each other. Syphilis will undoubtedly change
nutrition to such an extent as to result in rachitis. Rachitis will
affect the glands; the caseous and suppurative degeneration of the
glands will lead to metastatic processes, to acute tuberculosis, and so
on.

Malaria been claimed as the main cause of rachitis by Z.
Oppenheimer,[12] or, rather, rachitis is presumed by him to be the form
in which malaria makes its appearance in young infants. After disposing
of other alleged causes of rachitis, none of which is proved to give
rise to every case, and referring to the anatomical belief that the
peculiar hyperaemia and inflammation of rachitical bones is created by
the embryonic condition of the growing osseous tissue, he points to the
prodromi, amongst which he emphasizes chronic diarrhoea and the
nocturnal crying. The latter, with its perspiration and subsequent
sleep, he claims as evidence of malaria, and as a substitute for the
intermittent neuralgia of adults, the more so as he believes he finds
the spleen tumefied. The persistent diarrhoea of these infants is said
to be paroxysmal--to take place in the morning, contrary to what is
seen in the usual form of intestinal catarrh; the discharges are said
to be serous, not tinged with bile; the appetite to be good through the
rest of the day; the weight of the body not to be lessened, but anaemia
to develop gradually, and fever to occur occasionally. In other cases
infants have cold hands and feet and blue lips toward evening; the skin
is pale, the spleen enlarged; otherwise there are perhaps no symptoms,
but the infants try to get uncovered, and have an increase of
temperature of from 1 degree to nearly 3 degrees F., and a perspiring
head in the morning. After a while the rachitical symptoms belonging to
the bones and the general system become apparent. After all of the
author's ingenious and emphatic assertions and deductions, it becomes
evident that malaria--in the severe forms in which it has been found by
Arnstein, Browicz, and Henck to cause bone diseases--may give rise to
rachitis, but it is also clear that he tries to prove too much. The
long series of attempts at proving that every form and case of rachitis
depends upon a single and uniform cause have proved futile. The
physiological hyperaemia of the bones and the rapid growth of all the
infant tissues are shaped into the complex ailment which we call
rachitis by more than a single disease or a single nutritive
disturbance.

[Footnote 12: _D. Arch. f. klin. Med._, xxx., 1881.]

{146} SYMPTOMS.--Before entering upon a more accurate and elaborate
enumeration of the symptoms of rachitis, I mean to dwell upon peculiar
differences which take place according to the age in which the disease
makes its appearance. Very young babies--that is, infants of a month or
two--develop rachitis in such a manner that many cases are overlooked
until it is too late to relieve them in time. This occurrence takes
place when there are no prominent causes, such as diarrhoea or other
nutritive disorders, nor any premonitory symptoms. Such infants appear
to be perfectly well; they have the average weight, and even more; they
have plenty of adipose tissue, and look well. The only anomaly appears
to be an undue degree of paleness. Without pain or flatulency they are
constipated. This constipation is not congenital, as it always is when
the colon is unusually long even for an infant, and when the sigmoid
flexure is of double or even treble length, but makes its first
appearance about the end of the first or the beginning of the second
month. It is relieved only when the increasing muscular power of the
intestine results in more effective peristalsis. The second symptom is
the thoracic groove, to which I shall allude later, and a gradual
thickening of the costo-cartilaginous junctures, with or without
periosteal pain on pressure. About the same time the cranial softening,
craniotabes, with its hyperaemia and perspiration of the entire scalp,
and baldness, and the first symptoms of maxillary rachitis, become
perceptible. During all this time the epiphysial swellings and the
diaphysial curvatures develop but very slowly; but at a very early time
chronic bronchial catarrh, with a loose cough, begins to be
troublesome. When rachitis begins at a late period--say, about the
sixth or eighth month--the aspect of the case is different. The infant
has suffered before either from bronchitis and broncho-pneumonia, or in
most cases from indigestion and intestinal catarrh. There is some
degree of emaciation; the skin does not fit the limbs, as it were--is
loose, thin, flabby, and rather dry. The tendency to diarrhoea
continues to prevail. The epiphyses, particularly of the lower
extremities, are thickened at an early time, curvatures of the tibiae
become apparent, and all the rest of the bones participate in the
process, with the exception, sometimes, of those of the head.

The head, however, is liable to exhibit symptoms of rachitis at a very
early period of life. It is large, or appears to be so,[13] mostly for
the reason that the face is proportionately small. The forehead is
large, the frontal protuberances very prominent, as are also those of
the parietal bones. Thus, the head is more or less square. Dilated
veins are visible in and through the pale skin; there is but little
hair, on the occiput less than on the rest of the head. Sometimes the
occiput is quite bald, the hair having been rubbed off on the pillow.
The scalp feels warm, except during perspiration. The latter is very
copious, particularly on the occiput--to such an extent, indeed, that
the pillow is drenched--and will remain so for months. The sebaceous
follicles are often still larger and more numerous than they normally
are at that age, and seborrhoea is {147} often, though not always, met
with. The sutures are wide, sometimes one or two centimeters; the
posterior fontanel remains open; the large anterior fontanel is very
large, being sometimes several inches long and wide. The pulse is felt
very distinctly through it. The systolic cerebral murmur, which was
first found by Fisher of Boston in 1833, and considered to be a
positive symptom of rachitis (which certainly it is not, as it is found
in almost every healthy baby with a patent fontanel), is very audible.
The fontanel and sutures remain open for a long period. Instead of
closing, as they do normally at the fourteenth or fifteenth month, the
former ossifies about the end of the second or third year, or later.
Gerhardt reports a case in which it persisted to the ninth year. The
cranial bones appear to be thin, and give way under the pressure of the
finger. Ordinarily, it is true, the cranial bones of every baby, even
if perfectly healthy, are movable under pressure, but they are so only
along the sutures, where they may retain this mobility, in some
instances, a long time. Indeed, it appears that sometimes about the
middle of the first year the occipital bone becomes thinned out in
apparently quite healthy children. Moreover, even in the skulls of
infants who were taken to be in good health small defects in the bones
were found (Friedleben), with no uncomfortable symptoms at all.
Therefore it is rather difficult to draw the exact boundary-line
between the healthy and the morbid condition; thus it is possible that
some of those cases which exhibited apparently morbid local changes
without morbid symptoms may not have been diseased after all. In those,
however, in which rachitis is really developed in the cranium a
peculiar condition is found. In the posterior half or third of the
parietal bones, either the right or the left side being more marked,
there are in the tissue of the bone distinct spots in which the osseous
material is not only thinned out, but has entirely disappeared. In
fact, the bone is perforated, the edges of the holes being rather
steep, sometimes slightly thickened, and the scalp separated from the
brain only by a thin, transparent membrane, the remnant of the
periosteum. These holes can be easily found through the integument. The
finger, though ever so gently pressing down upon it, moves the cranium,
if any be left, before it; the bone feels like paper, and the sensation
as if it could be easily broken through is quite distinct and
embarrassing. Such perforations are usually quite numerous; from five
to twenty or more can often be counted. They are surrounded by normally
hard bone, and thereby can be recognized from the flexible part of the
cranium extending along the sagittal and lambdoid sutures. Where these
results of rachitical softening, craniotabes, are most prominent--that
is, on the part on which the infant is mostly reclining--the bone is
flattened, and may remain so for life, though in the majority of cases
the asymmetry will disappear. The flattening and perforations result
from the same causes--viz. softening of the bones and pressure upon the
bone between the pillow outside and the brain inside. With it go, hand
in hand, thick rachitical deposits under the hyperaemic periosteum of
other portions of the skull. Where craniotabes is largely developed on
the occipital portion, the frontal and the parietal bones (in their
anterior halves) are usually thus thickened. A cross-section with a
knife will reveal a diameter of the new osteoid material between the
periosteum and bone of one-half to one centimeter in thickness. It is
very hyperaemic--even more so than the bone itself, {148} which, when
cut into, exhibits an unusual amount of blood. Sometimes the deposits
are still larger, and are apt to change the appearance and weight of
the skull considerably after recovery has taken place and eburnation
and sclerosis have taken the place of the normal osseous tissue.

[Footnote 13: Bootius (1649), quoted by Haller (_Bibl. Med. pract._,
1779): "Infantibus caput grandescit, reliquum corpus contabescit, ossa
in articulis tument, dextrum hypochondrium tumore aequali prominet; hoc
malum multis millibus infantum molestum est" ("The infant head grows
large, the rest of the body emaciates, the articular bones swell, the
right hypochondrium is raised by a uniform tumor; this malady is a sore
affection in many thousands of infants").]

Such a case of rachitical cranial sclerosis I have described in the
_Amer. Med. Monthly_ of 1861. It was, however, by no means a mate of
the case related by E. Huschke. The latter skull was that of a girl of
seventeen years, and weighed 4117 grammes instead of the normal weight
of 600 grammes. The medullary (Havers') canaliculi were large and very
numerous on the surface, narrow and very few in the interior of the
sclerotic bones, and the osseous canaliculi were more spherical and
irregular in site and shape. The chemical composition was also
abnormal, phosphate of lime being 65.59, carbonate of lime 11.12,
sulphate of magnesia 1.14, cartilage and fat (very little), etc. 22.15
per cent. No fluorate of lime was found. Most of the bones were
exceedingly hard, but fragile when tried in small pieces; very white
inside, yellowish on the surface, the latter color being the remnant of
extravasated blood or other pigmentous matter. Another skull, in
Huschke's possession, and moderately sclerotic, weighed (lower jaw
excluded) 1075 grammes; a third, in the museum of the University of
Jena, is that of a young baboon,[14] in which all the bones covering
the hemispheres had become sclerotic.

[Footnote 14: Baboons suffer from rachitis very extensively. In the
_Transactions of the Pathological Society of London_ (xxxiv., 1883, pp.
310, 312) I. B. Sutton gives the description of two baboons, one of
which was six months, the other one year and six months old, when they
died. The careful description of the specimens exhibited leaves no
doubt as to the rachitical nature of the changes in both the periosteum
and the tissue of all the bones of the body.]

Of undoubted total cranio-sclerosis Huschke reports but ten
cases--those of Malpighi (1697), Cuvier (1822), Ribalt (1828), J.
Forster and Bojanus (1826), Ilg (1822), Kilian (1822), Otto (1822),
Vrolik (1848), Albers (1851), Huschke (1858). The disease does not
affect the auditory bones, the condyles of the maxillary and occipital
bones, nor the styloid process of the temporal bone. It is recognizable
in the posterior part of the cranium and basis cranii, but affects
mostly the bones of the face and the frontal, parietal, and cribroid
bones. Thus, the disease takes its origin in the anterior portion of
the skull, particularly in the superior maxilla, and proceeds upward
and backward, terminating in the basis cranii in the neighborhood of
the infundibulum and appendices. But two of all the cases were observed
during life. In all the disease was traced back to early life. The
chemical composition of the bones was greatly changed in all. Instead
of the normal proportion of earthy to organic material = 2.1 (or
1.5):1, it was from 3.5 to 4.4:1. Particularly the carbonate of lime
was greatly increased.

The brain and its meninges participate, in many respects, in the
changes worked by rachitis, and mainly in the abnormal vascularization
of the bones. They are very much congested, and succulent. A section
through the brain shows a great many large and small blood-points. This
hyperaemia may give rise to over-nutrition, which assumes the character
of real hypertrophy of the brain. When that hyperaemia, however,
becomes excessive, effusion will take place into the cavities, the
tissue of the arachnoid, and the substance of the cerebrum, which
latter looks {149} peculiarly brilliant, elastic, and sometimes white,
in consequence of the blood-vessels being emptied by the pressure on
the part of the enlarged mass of the cerebrum upon the blood-vessels.
Thus, instead of cerebral hyperaemia there may be anaemia. Every form
of hydrocephalus may follow the rachitical process. Afterward, when the
craniotabes has healed, the secondary effusions will generally also
disappear, but not a few cases of hydrocephalus may be traced to
rachitis occurring during the first half year of life. When that
occurs, the intellectual faculties may suffer, while, on the contrary,
complete recovery not infrequently exhibits an unusual degree of mental
development, for the same reason which improves the chances of the
development of the bone. The degrees of physiological and pathological
nutrition and over-nutrition are very variable in their nature and
results.

This condition of the cranial contents is not the only one brought
about by rachitis. The softness of the cranial bones permits a direct
pressure on the brain. The side on which the infant for the most part
reposes gets flattened, and the brain is also compressed. The skull
consequently bulges out in the opposite direction. This anomaly, as
stated above, is sometimes visible through life, though in the large
majority of cases after recovery from rachitis has taken place this
asymmetry will gradually disappear. Before that can occur, however, the
infant is liable to suffer from the rachitical changes. Convulsions are
by no means rare. Vogel has, however, been able to produce an attack of
convulsions by pressing upon the softened spots of the cranium.
Permanent or temporary contractures of the fingers and toes I have seen
in several instances. Gerhardt looks upon rachitis as one of the causes
of tetany.

A frequent symptom of the cerebral changes which take place during, and
in consequence of, craniotabes is the crowing inspiration, or
laryngismus stridulus, of infants. It may be mild or severe. The mild
form is very frequent, and consists in the occurrence of a shrill
inspiratory sound while the baby is either quite placid or excited or
crying. It is frequently overlooked entirely, is usually overcome after
a number of months, and gives rise to serious trouble in but very few
instances. The severe form is of a different nature. While the baby is
awake or asleep, without any premonitory symptoms, while playing or
crying, placid or excited, all at once respiration will cease. This
will take place, usually, after expiration. The limbs are hanging down,
as it were lifeless, the face turns pale, then purple, and slight
convulsive twitching may set in for ten or twenty seconds. There
appears to be a complete paralysis, and death from apnoea seems to be
imminent. All at once, a long, deep crowing inspiration will be heard,
respiration will commence again, and the whole terrible attack is
overcome. It may return a number of times every day, or sometimes not
for several days, during a period of many weeks or several months. The
attacks which set in after inspiration are apt to be more dangerous. In
such an one, but also in the other kind which sets in after the
expiratory movement, death may occur suddenly, or the attack may be
followed by a convulsion which may terminate fatally like any other
eclamptic seizure. In this manner it is that the majority of cases of
rachitis perish which terminate fatally during the active progress of
the morbid process. In this connection, however, it may be well to add
that craniotabes is not the only cause of laryngismus, particularly
when the {150} latter is found in the second year of life, or even
later. But almost every case, without any exception, which is observed
during the first eight or nine months is due to that very cause; and a
good many cases occurring later, when the craniotabic bones have become
normal, arise from the effects, either meningeal or encephalic, of the
rachitic process. Still, complications of craniotabes with a large size
of the thymus gland may occur, and enlargements of the tracheal and
bronchial lymphatic glands are quite frequent, as we shall see
below.[15]

[Footnote 15: Z. Oppenheimer prefers the name rachitic asthma in place
of laryngismus, and suggests an explanation of the symptoms from a
strictly anatomical point of view. If not correct, it is at all events
interesting, as everything this ingenious writer proposes. He points to
the ligament situated between the spinae intrajugulares of the temporal
and occipital bones, which, as long as it is of normal consistency,
separates the jugular vein from the pneumogastric nerve. As it is
covered with periosteum and dura, it is apt to ossify, and forms an
osseous partition in the foramen jugulare, which participates in all
the changes taking place in the periosteum. As this becomes softened
and succulent, so will the ligament, either on both sides or on either.
Its influence on the neighborhood depends on its size or succulence (as
also on the difference in width of the foramen jugulare or lacerum,
which corresponds with the difference in size of the transverse
sinuses). The irritation of the pneumogastric is perhaps easily
explained thereby, but in very exceptional cases only the accessory
nerve would be affected. As, however, the latter controls the
sterno-cleido mastoid and trapezius, and also the laryngeal muscles,
and is apt to provoke cardiac paralysis during diastole, the occurrence
of sudden death would be best accounted for.]

While the size of the cranium is normal, or sometimes more than normal,
the face undergoes some changes which result in absolute or relative
diminution of size. These depend mostly on a reduction in the volume of
the jaws. Glisson knew of it, and therefore looked for the cause of
rachitis in the process of dentition. Now, both maxillae are liable to
become rachitical at an early date, as early indeed as the bones of the
cranium. Rachitical deposits and softening take place in them very
generally. The lower maxilla is flat anteriorly, it loses its rounded
outline, is shorter in longitudinal direction, while the rami are thick
and clumsy; the whole bone is shorter than normal, and sometimes
asymmetric. Its changed appearance is greatly due to the effect the
muscles, with their powerful insertions, produce on the softened bone;
mainly the masseter, also the mylohyoid, which draws the lateral
portions inward, and the geniohyoid, which pulls at the central
portion. Of the latter, the lower portion is drawn out, the inner and
the alveolar part inward. Thus, the teeth, mainly the incisors, of the
lower jaw are turned inward to such an extent that, as those of the
upper look outward, the two rows of teeth do not touch but cover each
other. Besides, the periosteal proliferation around the alveoli is
excessive, sometimes so much so as not only to crowd the teeth into
irregular positions, but even to absorb and annihilate alveolar
processes in the course of the morbid changes. The cases in which the
number of teeth are actually diminished by rachitis are not at all
rare. In the superior maxilla the last-described anomaly is also
observed. Periosteal thickening is mainly noticed about the
intermaxillary bone--sometimes to such an extent that above and behind
it a considerable impression takes place. The shape of the upper jaw is
more spherical than normal, and the cheek-bones become very prominent.

The belief that maxillary rachitis is now and then met without any
other symptom of rachitis I do not share. What I said of craniotabes is
also valid in regard to this form.

{151} Irregular teething is a constant companion of maxillary rachitis,
but is also present where the latter is not well, or not at all,
marked. As a rule, the first teeth protrude late, about the ninth or
tenth or twelfth month. That the first year and more should elapse
without any tooth is of frequent occurrence in rachitis. Cases in which
the first teeth do not come before the second year is completed are not
very uncommon; in some there are none even when the child is much
older. In most cases the retardation of dentition goes hand in hand
with very marked retardation in the development of the rest of the
bones and in the closure of the cranial fontanel. But not in every case
of rachitis is there a retardation in the process of teething. In some
a few teeth appear at the regular period (at the completion of the
seventh or eighth month), or even at a very early age (in the fourth or
fifth month); after which there is an interruption in the protrusion of
teeth for an indefinite period. Evidently, the period in which rachitis
is developed exerts its influence on the teething process. When it
exists at a very early age, it will retard teething until recovery
takes place. Still, it is possible that a moderate amount of periosteal
and osteal hyperaemia and over-irritation matures the teeth abnormally.
In all those cases, however, in which rachitis does not occur before
the second half of the first year, the first teeth will appear at the
normal time, and a long period will follow in which no teeth at all
will make their appearance. Then, again, when the whole process comes
to a standstill, and recovery takes place with solidification of the
bones, and even eburnation, the teeth will come in rapid succession.
Whether they will, as is frequent, decay almost as soon as formed, or
whether they will be unusually hard, solid, and yellowish, depends on
the stage of the disease in which they made their appearance, and on
the complications aggravating the case. Of very grave import in this
respect are digestive disorders before and during the course of the
disease.

The vertebral column suffers also. In the normal infant it is straight,
but in the rachitic it exhibits a kyphotic deformity very soon. When
such a baby of three or six months is sitting up, the middle portion of
the back is protruding, as in Pott's disease. In almost every case,
however, this kyphosis is but apparent and the result of muscular
debility. In order to arrive at a diagnosis at once, it is sufficient
to place the patient on his face and support the head, and raise the
lower extremities and pelvis in the air. If the kyphosis is but
functional, the prominence disappears at once. By nothing can the
muscular insufficiency of early rachitis be better demonstrated than by
this little experiment. But actual deformity is also found in rachitis.
It softens both the vertebrae and intervertebral cartilages, and either
their anterior or posterior portion may be irregularly developed, and
be either too high or too low. Besides, the articulating surfaces are
sometimes too convex. Thus the causes of both kyphosis and scoliosis
are amply furnished, and complications of the two are quite frequent,
and the deformities resulting therefrom quite formidable. Scoliosis is
mostly to the left; kyphosis generally complicated with lordosis, and
sometimes the vertebral column exhibits a spiral shape.

The ribs of the convex half are prominent and divergent, those of the
concave side flattened and parallel. The two halves of the chest are
therefore very unequal indeed. Muscular traction, atmospheric pressure,
{152} the elastic traction of the lungs, the presence of pulmonary
complications, and the pressure from below on the part of the enlarged
viscera of the abdominal cavity, come also in for a considerable share
in the completion of the deformity.

The ribs and the sternum aggravate it considerably. Even without any
affection of the vertebral column they suffer seriously from the
general affection. The manubrium is thickened and drawn inward, the
ensiform process protuberant, the sternum often swelled and painful to
the touch. The ribs are sensitive to the touch on one or both sides.
The child cries when taken up or when fearing to be taken up. The
costo-cartilaginous junctures are thickened, mainly so from the fourth
to the eighth ribs. The insertion of the diaphragm becomes soon
perceptible by a deep groove around the chest. The anterior portion of
the ribs is flattened, posteriorly they are inserted at acute angles.
Thus the intrathoracic space becomes narrow, the sternum with the
costal cartilages is pressed forward (pigeon breast, pectus carinatum),
the thorax is deprived of its elliptical shape and becomes triangular,
the dorsal aspect being flattened, and the distance between the
vertebral column and the sternum increased. Below the diaphragmatic
groove the thorax expands, the liver and other abdominal organs
crowding the ribs outward. All sorts of changes are experienced by the
ribs in these conditions. Parts of them are flattened, parts undergo
infraction, parts are even concave; they are bent and twisted, now and
then to such an extent as to turn the concave side out, the convex
surface in. In addition to all this, the scapula is big and clumsy and
protuberant, the clavicle considerably bent and frequently infracted,
and not rarely covered with genuine callus.

That the respiratory and circulatory organs must suffer from such
anomalies, though they be not excessive, is certain. The heart is
crowded by the flattening of the ribs and the contraction of the
thoracic cavity. Its beat is visible over a large surface, and its
percussion dulness is extended over its normal space, though no
enlargement have taken place. This, however, is very apt to occur after
some time by overexertion. The latter is increased by the condition of
the respiratory organs. The ribs being flexible, the chest contracted
and compressed, the diaphragm raised, the respiratory muscles feeble,
respiration is insufficient, even without the presence of any further
complications; thus dyspnoea and a certain amount of cyanosis are
frequently met with in consequence of the anatomical changes only. In
addition to this, there is from the beginning a tendency to catarrhal
and inflammatory conditions. Even without any deformity the rachitical
process is accompanied from an early time with bronchial and tracheal
catarrh. A chronic cough in an infant, with very little or no fever,
disappearing and returning, mostly with copious secretion--which,
however, is swallowed as soon as it reaches the pharynx--rouses the
suspicion of general rachitis. It is often complicated with extensive
dulness over the manubrium sterni, due (to rachitical thickening of
this bone and) mostly to the persistence of a large size of the thymus
gland; and also with enlargement of the bronchial and tracheal glands,
the latter of which are often accessible to recognition by percussion.
They are to be looked upon as a frequent occurrence in rachitis, though
no associated diseases leading to their enlargement have been noticed.
They and the chronic tracheo-bronchial {153} catarrh are closely
dependent upon each other. They are each other's both cause and effect.
Neither of them, however, remain uncomplicated. Catarrh grows into
broncho-pneumonia, with frequent returns. Atelectasis, interstitial
pneumonia, dilatation of bronchi, and pulmonary consumption are often
traceable to such apparently slight catarrhs, which, when not
recognized as depending on their constitutional cause, cannot be
removed. Nor are the cases of miliary tuberculosis, resulting from
caseous degeneration of rachitical glands, very exceptional.

The anatomical changes in the abdominal viscera may be due to the
preparatory diseases or the complications of rachitis; but, at all
events, the abdomen yields a number of changes visible through the
whole duration of rachitis. It is very large; its size is due to the
contraction of the thoracic cavity and the downward pressure of the
chest-wall upon the contents of the abdominal cavity. It is also due to
the changes wrought by rachitis in the pelvis. Softening of bones and
synchondroses, torsion, the weight of the trunk, and the pressure of
the femora from below produce the change of the pelvis so well known
and much feared in the parturient female. The promontory and sacrum are
pushed in, the arcus pubis is large, the pelvis asymmetric; the small
pelvis is contracted, the large pelvis broader. Thus, the small pelvis
has no room for viscera, which, then, are crowded upward. The digestive
disorders which gave rise to, or formed the first stage of, rachitis
result in the accumulation of gas; the scrobiculus cordis is greatly
expanded. The liver[16] is large, congested, and in fatty degeneration.
The latter is the more frequent the more a certain degree of fatty
condition is a normal attribute of every infant liver. When the liver
is found but small in post-mortem examination, it is so because of the
general anaemia and emaciation. Sometimes it is amyloid, as are also
the spleen (mostly hyperplastic only), the kidneys, and the arteries of
the intestines in many instances.

[Footnote 16: Dr. Norman Moore presented a cast and drawing to the
Pathological Society of London (_Trans._, vol. xxxiv., 1883, p. 185)
showing how considerable may be the digressions of the diaphragm and
local pressure upon the liver in a case of rickets. Three large beads
caused as many projections from the under side of the diaphragm, and
corresponded with local thickenings of the capsule of the liver,
probably produced by the continued pressure through the diaphragm of
the beads, which were on the seventh, eighth, and ninth ribs, and the
largest of which was equal in size to a hazel-nut.]

The alimentary tract is the seat of many changes recognizable during
life. The tonsils are often large. The tongue is seldom coated to an
unusual degree. On it are found little islands, red, marginated,
deprived of epithelium. They will increase in size and number and
extend backward. They will heal and reappear. They are by no means
syphilitic, as Parrot would have it, and correspond exactly with the
erosions near the solitary glands and those of Lieberkuhn in the
intestinal part, which mean nothing else but a nutritive disorder of
the epithelia, and give rise to nothing worse than incompetency of
absorption in that locality and abnormal secretion. The stomach is in a
condition of chronic catarrh, sometimes dilated. Acid dyspepsia is
frequent. Anorexia and bulimia will alternate. Feces contain an
abnormally large amount of lime. Diarrhoea and constipation will follow
each other in short intervals. The former owes its origin to faulty
ingesta or chronic catarrh; the latter, sometimes to improper food, but
more generally to muscular insufficiency. {154} This condition has not
been estimated at its proper value. Besides myself,[17] nobody but Bohn
has paid the attention to it which it deserves. Here, again, I have to
insist that rachitis is a disease of the whole system, and not
exclusively of the bones. Indeed, the muscular system is amongst the
first to suffer. In the same way in which the voluntary muscles are not
competent to raise and support the head or to allow a baby to sit up
without a functional kyphosis, the involuntary muscles of the intestine
are too feeble for normal peristalsis. The infant of a month or two
months of age may have had normal and sufficiently numerous
evacuations; gradually, however, constipation sets in; the feces become
dry, but are perhaps not much changed otherwise. If no other cause be
apparent, the suspicion of rachitical constipation is justified.
Seldom, however, after it has lasted some time--and only after some
time has elapsed relief will be sought--it will remain alone. Other
symptoms of rachitis will turn up and the case be easily recognized.
This constipation is an early symptom, as early as thoracic grooving or
craniotabes. Very often it precedes both--is, in fact, the very first
symptom--and ought therefore be known and recognized in time.

[Footnote 17: _Jour. Obst., etc._, Aug., 1869.]

The kidneys have been mentioned above. They are often found rather
large. Though the fact has been alluded to before, I will here again
state that it has always been the general impression that the amount of
lime eliminated in the urine of rachitic children is excessive. The
reverse of that is true. Seemann and Lander have proved beyond dispute
that in most stages of rachitis there is less than the normal amount of
lime in the urine. Thus, the theory that lime is eliminated by an
excess of acids in the blood is proven to be incorrect. But it is a
fact that the rachitical bone contains a proportionately small amount
of lime. The conclusion is, then, that its introduction must have been
diminished. On the other hand, every article of food contains a large
amount of lime, which might be introduced into the circulation if
digestion be not at fault. The fact is, that a large amount of lime
introduced is not utilized, and is eliminated with the feces.

In connection with these facts the following will be found very
interesting. It has been found by Bunge that when potassium, with the
exception of chloride of potassium, meets chloride of sodium, the two
will exchange their acids, so as to form chloride of potassium and
phosphate of sodium. They will be found in the blood also, will be
eliminated as such, and result in a comparative absence of chloride of
sodium from the serum of the blood. Now, comparative absence of
chloride of sodium diminishes the possibility of the development of
hydrochloric acid. Thus, it is not a surplus of acid, but a lack of
hydrochloric acid, which results from such chemical combinations. If
such be the case, calcium salts are not absorbed sufficiently. Thus,
they will appear in the feces, and not even be absorbed in the
intestines, because of the alkalinity of the intestinal secretion, by
which the lime cannot be dissolved. The more lime, then, is introduced
under these circumstances, the greater the incumbrance to digestion.

The correct proportion between chlorine, phosphorus, potassium, and
sodium is certainly exhibited in woman's milk. There is lime enough in
even the poorest article of that kind. But indigestion brought on by
{155} woman's milk in a disordered condition or by any other cause will
prevent the absorption of lime when a superabundance of phosphorus and
potassium disturbs the formation of hydrochloric acid. In these cases
not only the development of the bones, but also that of the muscles, is
disturbed. The latter is of great importance in regard to circulation,
because a large part of the circulation depends on the pressure on the
part of the muscular fibres exerted on the small blood-vessels. These
facts have been the reason why I insist upon the addition of chloride
of sodium to the food of infants and children, particularly those who
are fed on cow's milk; for cow's milk and vegetables contain a relative
superabundance of potassium compared with sodium. Even adults will find
cow's milk very much more digestible by adding table-salt to it.

The extremities begin to suffer at a later period than the ribs and
cranium. The opinion of Guerin, that the rachitical process begins in
the lower extremities and ascends gradually, is erroneous. It cannot
even be stated that the lower extremities are affected sooner than the
upper. There is no regularity at all; it is not even necessary that all
the osseous tissue should fall sick. But this can be taken as a fact,
that hands and feet, and particularly the phalanges, are the latest to
undergo the rachitical change. First in the line of morbid alteration
of the bones are the epiphyses, mainly of the tibia, fibula, radius,
and ulna. Their integument appears to be thin; now and then the
cutaneous veins are dilated. The periosteum of the diaphysis becomes
thick, softened, and painful to the touch and pressure, its compact
layer thin, the medullary space large, the whole bone flexible, at the
same time that the ligamentous apparatus of the joint becomes softened
and flabby. At this time babies are greatly admired and applauded for
the facility with which they introduce their feet into their mouths.
For at the same time the bones begin to curve under the influence of
the flexor muscles, which are always stronger, as they do in later
months under the weight of the body when the child begins to walk. The
curvature is not always a mere arching, but sometimes the result of
infraction (green-stick fracture), a complete fracture not being
accomplished because both of the softness of the osseous tissue and the
resistance on the part of the thickened and softened periosteum. Both
the legs and forearm bend on the external side, the resulting concavity
looking inward. The humerus bends in a direction opposite to that of
the forearm; the thigh, usually outward and forward.

The attempts at locomotion are often the causes of quite preposterous
anomalies; creeping, sliding, walking, turn the extremities in such
unexpected directions that talipes valgus, genu valgum, and now and
then double curvatures, are the results. These, however, may not always
be very marked, but there is one change in the rachitical bone which is
constant--viz. the impairment of longitudinal growth. In every case the
diaphyses remain abnormally short, and the proportion of the several
parts of the body are thereby disturbed. Chiari measured parts of the
skeleton of a rachitical woman of twenty-six years who was nine years
old before she could walk. Her height was 116 centimeters, the length
of the lower extremities 42, femur 23, tibia 15, fibula 20, humerus 16,
right radius 12.5, left radius 11, right ulna 15, left ulna 14
centimeters. In a second case the parts of the skeleton were measured
after they had {156} been extended with great care. The right arm from
the acromion to the middle finger (incl.) was 39 centimeters, the left
38; the right lower extremity from the trochanter to large toe (incl.)
39, the left 41.

The skin participates in the general nutritive disorder. It is soft and
flabby. In those infants who become rachitical gradually while proving
their malnutrition by the accumulation of large quantities of fat, it
exhibits a certain degree of consistency. When rachitis develops in the
second half of the first year or later, with the general emaciation the
skin appears very thin, flabby, unelastic. The veins are generally
large. Complications with eczema and impetigo are very frequent; where
they are found the glandular swellings of the neck and below are still
more marked than in uncomplicated cases. Circumscribed alopecia is
sometimes found (not to speak of the extensive baldness of the
occiput). It is not attended with or depending on the microsporon
Audouini, but the result of a tropho-neurosis. In the hair Rindfleisch
found fat-globules between its inferior and central third. Then it
would break, the axial evolution would cease, and the end become
bulbous by the new formation of cells.


Acute Rachitis.

There is a form of rachitis which may be, and has been, called multiple
epiphysitis or multiple periostitis of the articular ends of the long
bones. The changes which in the usual form of rachitis require months
to develop take place in a very short time. Not infrequently the
children were quite well before they were taken with this peculiar
affection. Cases have been known to occur between the fourth and
twenty-fourth months of life, and to last from two to six weeks, or
just as many months. They have been known to get well, or a few of them
terminate fatally. They are accompanied with fever and rapid pulse,
perspiration, now and then with diarrhoea, with eager or reduced
appetites. At the same time the epiphyses swell very rapidly, and are
painful. The same is true of the diaphyses and the flat bones of the
head. Many authors do not recognize this form as an independent
variety. Some call it an acute initial stage of certain cases of
rachitis, as they are not infrequently found in infants which exhibit a
very rapid growth. Some have taken it as an independent disease,
developed on the basis of a constitutional disposition; some look upon
it as a very intense acute form of rachitis; others, as an intense
growth of the osseous tissue only. Others call it an inflammation of
the bone. Some refer it to hereditary syphilis, and a few to the
influence of malaria. That the disease is epiphysitis and periostitis
there is no doubt. I do not hesitate to claim it as rachitis, for
epiphysitis and periostitis of early age not of rachitical basis are
not apt to run such a favorable course as this form frequently does.
The cases complicated with subperiosteal hemorrhages are claimed as
scurvy by Th. Barlow.

The differences of opinion would probably not have been so great if
every author had seen all the cases of the other observers. It will not
do to judge of unobserved cases by the light shed by a single case
under one's own observation. I have seen cases of acute rachitis which
were {157} the initial stages of general rachitis, and have observed
those of local or multiple epiphysitis, mainly after infectious fevers,
which were diagnosticated as such. They are, however, very uncommon.
But even without a preceding infectious fever, such as scarlatina or
more frequently typhoid fever, there are unexplained cases of rachitis
and deformity. Thus, R. Barwell had some before the Pathological
Society of London,[18] which are positive proofs that some forms of
ostitis may occur and result in the most formidable deformities without
being rachitical. A girl of seventeen years was perfectly well formed
up to the age of two and a half or three years. After that time the
deformities began to develop, and did not change after she was
thirteen, at which time the author saw her the first time.

  Her left humerus measured 7-3/4 inches from shoulder to elbow;
    distance 6-1/4
  Her right humerus measured 7-1/2 inches from shoulder to elbow;
    distance 4-1/4
  Her left tibia measured 10 inches from knee to ankle; distance 7-1/4
  Her right tibia measured 9-1/2 inches from knee to ankle;
    distance 4-1/2

Her bones were always very brittle. When she was between nine and
thirteen she broke her arms four times and her lower limbs on several
occasions. A male patient of twenty-two years, who was born healthy and
well formed, continued thus until five years of age, when he was
attacked with a fever, after which his bones became soft and bent.
Osteotomy was performed on him, and the femora were found to be mere
thin shells of bones surrounding cavities containing great quantities
of medulla, which flowed out of the wound as oil; five ounces were
discharged at once. In both cases there appeared to be a hypertrophy of
the medulla at the expense of the bone-substance--a condition which
Barwell proposes to call eccentric atrophy. "While these subjects are
still youthful very little bone-earth is deposited, or at least remains
in the very thin layer of osseous tissue that subsists. The
relationship between infantile ostitis and extreme development of the
intraosseous fat, though well known, is still occult; neither should we
lose sight of the possibility that the softening process of ostitis may
be due to a fatty acid. Now, fatty ostitis usually occurs in epiphyses.
In these cases the shafts were affected."

[Footnote 18: _Trans._, xxxiv., 1883, pp. 203-208.]

PROGNOSIS.--The course and the prognosis of rachitis are, as a rule,
favorable, but they change according to the degree and locality of the
affection and the age of the patient. Generally there is neither fever
nor rapid exhaustion. But the process lasts for months and even years.
In favorable cases, when recovery takes place the teeth will grow
faster, the bones become firmer, the epiphyses will diminish in
relative size, the bowels become regular. But the length of the bones
is, and remains, reduced, and the head remains large as compared with
the length of the body. Not only are the bones of normal firmness, but
the compact substance undergoes a process of hardening called
eburnation by Guerin. The internal organs also become very active,
perhaps because the total amount of blood has to supply only a body
less extended in length. Nor does the brain suffer after complete
recovery has taken place. On the contrary, it appears that the somewhat
more than normal vascular dilatation, which under unfavorable
circumstances leads to effusion, is {158} frequently apt to nourish the
organ of intellect up to a higher standard. In all cases of rachitis,
however, the curvatures of the extremities will not disappear
altogether, while mild ones, it is true, are hardly recognizable in
advanced age. Curvature of the ribs and of the vertebral column,
however, will remain, and interfere with the expansion and the normal
functions of the lungs and heart. In regard to the lungs, it appears
that in many cases they do not find sufficient space to expand. As far
as the heart is concerned, it touches the flattened, no longer
elliptic, chest-wall over a larger surface, and is very apt to give
rise to the suspicion of enlargement in consequence of extended dulness
on percussion. The rachitic pelvis is well known to the obstetrician
for the difficulties it gives rise to during parturition.

Thus, the prognosis would, as a general thing, be sufficiently
favorable if it were not for the number of complications or severe
symptoms. The chronic catarrh of the lungs accompanying rachitis, the
enlargement of the tracheal and bronchial glands and the lymphatic
glands in general, are apt to lead to inflammatory disease of the
lungs, which, after having returned several times, leads to
infiltration of the lungs with caseous deposits, and not infrequently
results in phthisis. The nervous symptoms accompanying craniotabes may
prove very dangerous. Spasm of the larynx and laryngismus stridulus may
prove fatal in a single attack by suffocation, or general convulsion
may set in during an attack of laryngismus or without it, in which the
child may perish. Therefore the prognosis in every case of laryngismus
and in every case of craniotabes has to be very guarded. It is my rule
to wait from six to eight weeks before giving expression to a decided
prognosis, because during that time medicinal and dietetic treatment
will probably have resulted in such an improvement of the symptoms and
condition as to render the prognosis more favorable. Under no
circumstances, however, ought we to lose sight of the fact that, though
rachitis may disappear, the causes leading to it may still linger on.
Defective nutrition, diseases of the lungs, and intestinal affections
which gave rise to or accompanied rachitis will complicate the
prognosis, though rachitis itself, as far as the bones were concerned,
be no longer in existence.

TREATMENT.--To meet the cause of a disease by preventive measures is
the main object and duty of the physician. He thus either obviates a
malady or relieves and shortens it. Now, if the original disposition to
rachitis, as has been suggested, is to be looked for in early
intra-uterine life, when the blood-vessels begin to form and to
develop, we know of no treatment directed to the pregnant woman or
uterus which promises any favorable result. But the more we recognize
an anatomical cause of the chronic disorder, the more we can appreciate
the influence upon the child of previous rachitis in the mother, and
are justified in emphasizing the necessity on the part of the woman to
be healthy when she gets married, and to remain so while she is
pregnant. After the child is born the most frequent cause of rachitis
is found within the diet or the digestion of the patient. To attend to
the former is in almost every instance equal to preventing disorders of
the latter; for most of the digestive disturbances during infancy and
childhood are the direct consequences of errors in diet. It is,
however, impossible to write an essay on infant diet in connection with
our subject. I have elaborated the subject in my {159} _Infant Diet_
(2d ed. 1876), in the first volume of Buck's _Hygiene_, and of C.
Gerhardt's _Handbuch d. Kinderk._ (2d ed. 1882). Still, the importance
of the subject requires that some points should be given, be they ever
so aphoristic.

The best food for an infant, under ordinary circumstances, is the milk
of its mother. The best substitute for the mother is a wet-nurse.
Woman's milk ought not to be dispensed with when there is the slightest
opportunity to obtain it, particularly when the family history is not
good and nutritive disorders are known to exist, or to have existed, in
any of its members. When it cannot be had, artificial food must take
its place, and it is in the selection of it where most mistakes are
constantly made. This much is certain, that without animal's milk no
infant can or ought to be brought up; as ass's milk can be had only
exceptionally, and dog's milk, which has been said to cure rachitis, is
still less available, the milk of either goat or cow must be utilized.
The former ought not to be selected if the latter is within reach,
mainly for the reason that it contains, besides other objectionable
features which it possesses in common with cow's milk, an enormous
percentage of fat. Cow's milk differs in this from woman's milk, that
it contains more fat, more casein, more potassium, and less sugar than
the latter, and that its very casein is not only different in quantity,
but also in chemical properties. Even the reaction of the two milks is
not the same, woman's milk being always alkaline, cow's milk often
either neutral or amphoteric, and liable to acidulate within a short
time. Thus, the dilution of cow's milk with water alone yields no
equivalent at all of woman's milk, though the dilution be large enough
to reduce the amount of casein in the mixture to the requisite
percentage of one, and one only, in a hundred. The addition of sugar
(loaf-sugar) and of table-salt, and sometimes alkali (bicarbonate of
sodium or lime-water, according to special circumstances), is the least
that can be insisted upon. Besides, the cow's milk must be boiled to
prevent its turning sour too rapidly, and this process may be repeated
to advantage several times in the course of the day. Instead of water,
some glutinous substance must be used for the purpose of diluting cow's
milk. As its casein coagulates in hard, bulky curds, while woman's milk
coagulates in small and soft flakes, some substance ought to be
selected which keeps its casein in suspension and prevents it from
curdling in firm and large masses. Such substances are gum-arabic,
gelatin, and the farinacea. Of the latter, all such must be avoided
which contain a large percentage of amylum. The younger the baby, the
less is it in a fit condition to digest starch; thus arrowroot, rice,
and potatoes ought to be shunned. The very best of all farinacea to be
used in diluting cow's milk are barley and oatmeal. A thin decoction of
either contains a great deal of both nutritious and glutinous elements,
the former to be employed under ordinary circumstances, the latter to
take its place where there is, on the part of the baby, an unusual
tendency to constipation. The decoction may be made of from one to
three teaspoonfuls of either in a pint of water; boil with a little
salt, and stir, from twelve to twenty minutes, and strain through a
coarse cloth. It ought to be thin and transparent. Then mix with cow's
milk in different proportions according to the age of the baby. Four
parts of the decoction, quite thin, and one of milk (always with
loaf-sugar), for a newly-born, equal parts for an infant of six months,
{160} and gradual changes between these two periods, will be found
satisfactory. Whenever there is a prevalence of curd in the passage the
percentage in the food of cow's milk must be reduced, and now and then
such medicinal correctives resorted to as will improve a disturbed
digestion. Care ought to be taken lest for the newly-born or quite
young the preparations of barley offered for sale contain too much
starch. The whiter they are, the more unfit for the use of the very
young, for the centre of the grain contains the white and soft amylum
in preference to the nitrogenous substances which are found near the
husk. Thus, it is safest to grind, on one's own coffee-grinder, the
whole barley, but little deprived of its husk, and thus secure the most
nutritious part of the grain, which is thrown out by the manufacturer
of the ornamental and tidy packages offered for sale. But very few
cases will ever occur in which the mixtures I recommend will not be
tolerated. In a few of them, in very young infants, the composition
recommended by Meigs[19] has proved successful. It consists of three
parts of a solution of milk-sugar (drachm xvij-3/4 in pint j of water),
two parts of cream, two of lime-water, and one part of milk. For each
feeding he recommends three tablespoonfuls of the sugar solution, two
of lime-water, two of cream, and one of milk: mix and warm. The baby
may take all of it, or one-half, or three-fourths.

[Footnote 19: In _Med. News_, Nov. 28, 1882.]

The recommendations given above are based on a long experience, and the
simplicity, cheapness, and facility of preparation of the articles. The
substitutes offered for sale under the title of infant foods are in
part worthless, all of them expensive when compared with the simple
articles recommended by me, and not recognizable as to their uniformity
and compounds. But no matter how appropriate my mixture may be, it is
always for the young infant to be considered as a makeshift. It is to
be used as a representative of mother's milk only when this cannot be
had. Therefore it is better to alternate with breast-milk when this is
secreted in but an insufficient quantity. Some good breast-milk is
better than none at all; but with this proviso, that it _is_ good.
There are some milks either too watery or too dense and white. The
former will produce diarrhoea, the latter hard and dense curd. The
former may be improved by feeding and strengthening an anaemic and
overworked mother; the latter, by giving the baby, before each nursing,
a tablespoonful of a mixture of barley-water and lime-water, or, when
it produces constipation, lime-water and thoroughly sweetened
oatmeal-water. The cases in which breast-milk, such as can be had, is
not digested by the infant are rare, but they will occur. In them the
proper substitute will yield a better result than mother's milk; for
mother's milk will not always be a boon, and must then be dispensed
with. Particularly is this so when it is too old. Weaning ought to take
place when the first group or the first two groups of teeth have made
their appearance. After that time mother's milk is no longer the proper
food, and instead of preventing indigestion and sickness it is a
frequent cause of them and of rachitis. Instead of muscle, it will then
give fat, and the large fontanels and big head, the paleness of the
rotund cheeks, the flabbiness of the soft abdomen and thighs, will tell
the story of rachitical disease slowly engendered by the persistent
employment of an improper article of food. I cannot insist too often on
this, that rachitis may develop with increasing weight, {161} and that
the use of the scales alone is no means of ascertaining the healthy
condition of a baby. As much harm, therefore, can be done by weaning
too late as by so doing too early or too abruptly.

At that early age we treat of here, digestive disorders are more
frequently the results of improper diet than of a primary gastric
disturbance. But when the latter is once established it furnishes its
own indications. A frequent occurrence, together with a general gastric
catarrh, is the presence of fat acids in the stomach, such as an
improper amount of lactic, acetic, butyric, etc. acids. Before
digestion can be anything like normal they must be neutralized. For
that purpose calcined magnesia, carbonate and bicarbonate of sodium,
prepared chalk, and lime-water have been found useful. The latter, as
it contains but a trifle of lime, in order to neutralize must be given
in larger doses than is usually done; a tablespoonful contains but a
quarter of a grain of lime. And all of the alkalies must not be given
in the food only, but also between meals. For when given in the former
way alone it neutralizes the abnormal and injurious acids, together
with the normal digestive secretion, the lactic and muriatic. Not
infrequently, when the infants have suffered for some time, general
anaemia will set in, and result in diminishing the normal secretions of
the mucous membranes (and glands). In those cases which do not produce
their own gastric juice in sufficient quantity or quality pepsin and
muriatic acid may be given to advantage. In these cases the plan
suggested by me is particularly favorable--viz. to add a fair amount of
chloride of sodium (one-half to one drachm daily) to the infant's food.
Also that of I. Rudisch referred to by me previously,[20] who mixes one
part of dilute muriatic acid with two hundred and fifty of water and
five hundred of milk, and then boils (one-half teaspoonful of dil. mur.
acid, one pint of water, one quart of milk). Again, there are the cases
in which wine and the bitter tinctures, which are known to increase the
secretion of gastric juice, render valuable service. The addition of
bismuth to any of the proposed plans is quite welcome. As a
disinfectant and a mild cover on sore and eroded mucous membranes it
has an equally good effect.

[Footnote 20: _Am. Jour. Obstet._, July, 1879.]

Under the head of roborants we subsume such substances, either dietetic
or remedial, which are known or believed to add to the ingredients of
the organism in a form not requiring a great deal of change. Rachitical
infants require them at an early period. Meat-soups, mainly of beef,
and of mutton in complications with diarrhoea, ought to be given at
once when the diagnosis of rachitis becomes clear or probable. Any mode
of preparation will prove beneficial; the best way, however, is to
utilize the method used by Liebig in making what he called beef-tea. A
quarter of a pound of beef or more, tender and lean, cut up finely, is
mixed with a cup or a tumbler of water and from five to seven drops of
dilute muriatic acid. Allow it to stand two hours and macerate, while
stirring up now and then. This beef-tea can be much improved upon by
boiling it a few minutes. It may be given by itself or mixed with
sweetened and salted barley-water or the usual mess of barley-water and
milk which the infant has been taking before. Older infants,
particularly those suffering from diarrhoea, take a teaspoonful of raw
beef, cut very fine, several times a day. It ought not to be forgotten,
however, {162} that the danger of developing taenia medio-canellata
from eating raw beef is rather great. Peptonized beef preparations are
valuable in urgent cases.

Iron must not be given during any attack of catarrhal or inflammatory
fever. The carbonate (cum saccharo) combines very well with bismuth; a
grain three times a day, or less, will answer well. The citrate of iron
and quinine (a few grains daily) can be given a long time in
succession. The syrup of the iodide of iron (three times a day as many
drops as the baby has months up to eight or ten), in sweetened water or
in sherry or malaga, or in cod-liver oil, acts very favorably when the
case is, as so frequently, complicated with glandular swelling.

Cod-liver oil, one-half to one teaspoonful or more, three times a day,
is a trusted roborant in rachitis, and will remain so. Animal oils are
so much more homogeneous to the animal mucous membrane than vegetable
oil that they have but little of the purgative effect observed when the
latter are given. The former are readily absorbed, and thus permit the
nitrogenous ingesta to remain in store for the formation of new tissue,
but still affect the intestinal canal sufficiently to counteract
constipation. As the latter is an early symptom in a peculiarly
dangerous form of rachitis, cod-liver oil ought to be given in time (in
craniotabes). Diarrhoea is but seldom produced by it; if so, the
addition of a grain or two of bismuth or a few doses of phosphate of
lime (one to four grains each) daily, may suffice to render the
movements more normal. There are but few cases which will not tolerate
cod-liver oil at all. The pure cod-liver oil--no mixtures, no
emulsions--ought to be given; the large quantities of lime added to it
in the nostrums of the wholesale apothecaries embarrass digestion and
bring on distressing cases of constipation. These mixtures have been
prepared and are eulogized on the plea of their furnishing to the bones
the wanting phosphate of lime. The bones, however, as we have seen
before, are not grateful enough to accept the service offered. But only
a certain amount of phosphate of lime is useful in rachitis and in
digestive disturbances. In small doses it neutralizes acids like other
alkalies; its phosphoric acid combines with sodium very easily, and
gives rise to the formation of glyco-phosphoric acid, which is of very
great importance in the digestive qualities of the upper portion of the
small intestines.

Plain malt extracts will be well tolerated by some older children. The
preparations which are mixed with a goodly part of the pharmacopoeia by
generous manufacturers are to be condemned.

Craniotabes requires some special care in regard to the head. The
pillow ought to be soft, but not hot; no feather pillow is permitted.
The copious perspiration of the scalp requires that it should be kept
cool, the perspiration wiped off frequently to avoid its condensing
into water, and the flattening side of the head may be imbedded in a
pillow with a corresponding depression. Copious perspiration indicates
the frequent washing with vinegar and water (1:5-6). The muscular
debility commands great caution. The baby must not be carried on the
arm, but on a pillow which supports both back and head, or in a little
carriage. No sitting must be allowed until the back will no longer bend
to an unusual degree. No walking must be encouraged at any time. The
patients will walk when their time has come. The bones are so fragile
that great care {163} is needed sometimes not to fracture or to infract
them and to avoid periosteal pain in lifting. The skin must undergo
some training by gradually accustoming the little patient to cool
water. It can be readily, but gradually, reduced to 70 degrees for a
bath at any season. The addition of rock- or table-salt to the bath is
a welcome stimulant. And fresh air ought to be granted freely.

Laryngismus stridulus shares the indications for treatment furnished by
craniotabes. The general treatment remains the same. Prominent symptoms
and complications ought to be treated besides; constipation requires
the more attention the more convulsive attacks of any description may
arise from reflex action. The general nervous irritability may be
relieved by bromide of potassium, sodium, or ammonium. One gramme daily
(15 grains) of either, in three doses, is well tolerated for a long
period. When there are symptoms of an imminent convulsion, or to soothe
the convulsibility which may break out any moment, chloral hydrate,
eight or ten grains in from one hour to four hours, two grains in a
dose, will be convenient. If the stomach refuses or is to be spared,
from four to eight grains may be given in an enema of warm water. A
severe attack of convulsions ought to be checked with inhalations of
chloroform. When a warm bath is to be had, care should be taken that
the child be not tossed about. Hold the baby in a small sheet or a
large napkin, and immerge it thus into the water, raising the head and
cooling it with cold cloths or an ice-bag. Genuine attacks of
laryngismus with well-developed stages--the first paralytic, the second
spasmodic--give but little time for any treatment. The proposition to
apply the electrical current is well meant, but the attack has passed
by, or terminated fatally, or resulted in a general convulsion, before
the apparatus can possibly be in operation. I can imagine, however,
that a Leyden flask kept ready might be used to advantage during the
stage of apnoea for the purpose of bringing on inspiration. Sprinkling
with cold water, beating with a wet towel, shaking by the shoulders,
may certainly contribute to awake respiratory movements. The advice to
wait quietly until the attack has passed by is more easily given than
carried out. Marshall Hall's direction to perform tracheotomy will, I
hope, soon be forgotten.

Nothing is more gratefully appreciated by the little patients than air.
May it never be forgotten that night-air is better than foul air, and
that furnace-air means air greatly modified by injurious additions.
More than twenty years ago I was in occasional attendance upon a male
baby--now a medical man of some promise--with craniotabes and a number
of general convulsions. No treatment would remove, or even relieve, the
attacks, until, without the physician's advice, the father took the
baby into the street in the hardest winter weather. After the first
long absence from his furnace the baby was well of his convulsions, and
the physicians profited by their involuntary experience.

In the same way that salt-bathing is beneficial, so is sea-air. A
summer at the seaside is a great blessing to rachitical children.
Sea-baths have been arranged for them in France (Berx-sur-mer), in
Italy (San Ilario di Nervi, Viarreggio, Livorno, Volti, Fano), in
England (Margate), in Germany (German Sea, by Prof. Beneke), and for
some little time past in the neighborhood of our own large cities.

{164} Complications command great attention in rachitis, particularly
where there is danger from the affection of the nerve-centres, for the
slightest irritation in some distant part of the body may give rise to
an outbreak. Thus, in craniotabes it is desirable to watch even the
gums. Not sharing the etiological superstition which attributes so many
diseases of infancy to dentition, I still know that a slight irritation
of the gums may suffice to exhaust the slim resisting power of the
infant. If there be local swelling and congestion of the gums over a
growing tooth, it may become necessary, or at least advisable, to
lance. An otitis which under ordinary circumstances would give rise to
no symptoms at all besides some inconvenience or slight pain will prove
the source of great danger in a rachitical (craniotabic) infant. The
chronic bronchial catarrh and frequent broncho-pneumonia of such
patients require early attention, for they and the neighboring
lymphatic glands stand too much in the relation of a vicious circle of
cause and effect.

Rachitical constipation, depending on incompetency of the intestinal
muscle, must not be treated with purgative medicines. Now and then,
when a great deal of abnormal acid is formed in the stomach, calcined
magnesia, a grain or two given before each meal, will control that
disorder and at the same time keep the bowels open. But, as a rule,
every purgative after it has taken effect will leave the intestinal
muscular layer less fitted to perform its functions than before. Its
place may be taken by a daily enema of tepid water. Further indications
are--such a change in the food as will contribute to keep the bowels
moist and slippery, but principally such a modification of food and
such medical treatment as are known to prove beneficial when all the
symptoms of rachitis are fully developed. When the cause of the
infant's rachitis can be traced back to the mother or to an
insufficient quality of her milk, she must give way to a wet-nurse, or
the nurse must be changed for similar reasons. When neither mother nor
wet-nurse prove competent, or either be dangerous, artificial food will
take their place to advantage in the manner I have stated above.
Beef-soup or beef-peptone is to be added to the baby's food daily. Of
the two best farinacea, barley- and oat-meal, the latter is preferable
as an addition to cow's milk, because of its greatly laxative effect.
The percentage of cow's milk in the food ought to be more carefully
watched than in other conditions. Pure cow's milk or cow's milk mixed
with water only is borne worse in no other condition. Half a drachm or
more of table-salt and a few drachms of sugar ought to be added to the
daily mess. The general indications require the administration of iron,
which has no constipating effect in this ailment. Particularly is that
the case with the iodide of iron. Cod-liver oil, in three
half-teaspoonful or teaspoonful doses daily, acts very satisfactorily
both for its general rachitical and for its local effect on the mucous
membranes. Now and then massage, repeated many times a day a few
minutes each time, practised with the palm of the hand only, or gentle
friction, with the dry or oiled hand, of the abdominal surface, will
prove effective in bringing about peristalsis and strengthening the
intestinal muscle. An obstinate case may also require two daily doses
of one one-hundred-and-fiftieth or one one-hundred-and-twentieth of a
grain of strychnia for the same purpose, or such other improvements on
the above detailed plan as the judgment of the attending physician may
direct. At all events, the diagnosis of {165} any case, and the
appreciation of the cause of any ailment, are, to a well-balanced and
educated mind, of infinitely greater value than any number of specified
rules and prescriptions.[21]

[Footnote 21: _Jour. Obstetr._, Aug., 1869.]

It is not impossible that phosphorus, in substance, not in any of its
compounds, may prove of great utility in the treatment of rachitis.
Minimal doses of phosphorus render the newly-formed tissue at the
points of apposition of the bones more compact in a very brief time.
The new formation of blood-vessels in the osteogenous tissue gets
retarded by it. Larger doses of phosphorus, however, increase
vascularization, and osseous tissue is either less rapidly formed or
even softened. When the doses are still larger, vascularization and
softening may rise to such a point as to separate the epiphysis from
the diaphysis. Thus the administration of the drug results in an
irritation which, according to the doses employed, may give rise either
to normal condensation or to inflammatory disintegration. This
experience, arrived at by Wegner in a great many experiments made on
animals, Kassowitz has confirmed. For its therapeutic effect he tried
phosphorus in 560 cases of rachitis. Employing doses of one-half
milligramme (one one-hundred-and-twentieth of a grain) several times
daily (less will suffice), he soon found the skull to become harder,
the fontanel smaller, the softening of the bones of the thorax and
extremities to disappear, and all the other symptoms of rachitis to
improve. This result was obtained though no particular change in the
feeding of the patients was resorted to. To what extent this experience
will be verified by others we shall soon learn. My own is already
sufficiently extensive to base upon it a strong recommendation of the
plan of treatment I have detailed. My therapeutical results in other
diseases of the bones also encourage me to believe that phosphorus will
accomplish much in the treatment of rachitis. Ever since Wegner's
publications--viz. these thirteen or fourteen years--I have utilized
phosphorus in cases of chronic and subacute inflammations of the bones,
mainly of the vertebral column and the ankle-joint and tarsus. After
having taught the method for many years in my clinic and otherwise, I
made a brief communication on the subject to the Medical Society of the
State of New York.[22] Since that time, again, I have followed the same
plan in many cases of the same description, and feel sure that the
prognosis in this serious class of bone diseases has become more
favorable and recovery speedier. Infants of a year or more were given a
dose of one-eightieth or one one-hundredth of a grain of phosphorus
daily. One grain, dissolved in an ounce of oil or cod-liver oil, is a
convenient mixture, four or six drops of which may be administered
daily in two or three doses.

[Footnote 22: _Trans._, 1880.]

From what I have seen of phosphorus in bone disease, and what is thus
far known by experience in rachitis, it appears to me that it will be
of decided advantage in that form of acute rachitis which is apt to
destroy rapidly with the symptoms of acute epiphysitis, rapid pulse,
diarrhoea, rapid diminution of strength, and scorbutic gum. In the few
cases I have seen these last years it appeared to me to act
satisfactorily, together with immobilization of the whole body.

Rachitical curvatures are very apt to become less marked while growth
is increasing and the limbs extending. But many of them are so marked
{166} that they remain for life. Many of these might have been
benefited by timely orthopaedic interference. That the application of
Sayre's jacket is indicated in every form and stage of spondylitis,
though it be not equally valuable in all forms, goes without saying;
and that infractions ought to be straightened and supported by splints
when observed and when practicable, is self-evident. But, as a rule,
while the chronic rachitical process is developing in the long bones
the use of mechanical apparatuses is of doubtful merit; they ought not
to be resorted to before the healing has at least commenced. Nor is it
advisable to postpone mechanical interference so long that eburnation
of the bones has time to take place. Surgical operations for the
purpose of removing the curvature are of different nature according to
the different types to be treated. Mere straightening of the curvatures
is indicated, and successful with children under two years.
Osteoklasy--that is, fracturing of the curvature while the periosteum
is left intact--is successful in children of three (or four, according
to Volkmann) years. The fracture does not injure the periosteum, and is
always transverse. In later years osteotomy has proved successful to an
almost unexpected degree, and is one of the happiest achievements of
modern surgery.

Partly as a preventive, partly as a curative measure, Gramba of Turin
and Pini of Milan point to well-directed gymnastics as a requisite in
the treatment of rachitis. For older children they have established
schools in which systematic exercises are brought to bear on chronic
deformities.




{167}

SCURVY.

BY PHILIP S. WALES, M.D.


SYNONYMS.--_French_, Scorbut; _Spanish_, Escorbuto; _Italian_,
Scorbuto, are the various terms in the Romance languages used to
designate this disease, derived from the Middle-Latin word scorbutus,
which is evidently an offspring of one of the early Gotho-Teutonic
dialects, perhaps of the Low German word Scharbunk, Danish Scorbuck, or
the Old Dutch Scheurbuyck, from _scheren_, to separate or tear, and
_bunk_, the belly. These terms originally denoted rupture of the belly,
and afterward scurvy, or scorvy, as it is found in the English dialect.
It has also been traced to the Sclavonic word scorb, disease. The first
is now believed to be the true etymology.

DEFINITION.--Scurvy is an acquired condition of the body whose
essential feature is a perversion of nutrition, which gradually arises
from prolonged employment of food deficient in succulent or fresh
vegetable matter, and progresses uniformly to a fatal issue, in a
longer or shorter time, if the dietetic errors remain uncorrected. This
condition becomes manifest by a change in the complexion to a dull
yellowish or earthy tint, lassitude, marked decrease in the muscular
power, depression of spirits and mental hebetude, breathlessness on the
slightest exertion, minute flecks at the roots of the hairs, especially
those of the legs; and, later, hemorrhagic effusion into the skin,
forming blotches and spots of varying sizes and aspects, which may
finally slough and lead to obstinate ulceration; sponginess of the
gums, which bleed easily and break down into a detritus that impresses
a malodorous taint upon the breath; ecchymotic staining of mucous and
serous surfaces, and, in advanced stages of the disease, effusions of
bloody serum or of blood into the cavities and tissues of the body.

HISTORY.--Obscure passages in certain of the ancient medical classics
(Hippocrates, Celsus) and historical works (Pliny, Strabo) have been
considered as descriptive of scurvy, but the earliest trustworthy
accounts are to be found in the writings of the thirteenth century.
Jacob de Vitry describes an epidemic which occurred among the troops of
Count Saarbrucken besieging Damietta in 1218, and Sire de Joinville
another epidemic among the troops of Louis IX. lying before the same
town in 1249. On both occasions the sufferings of the men were
inexpressible and the mortality fearful. The disease was directly
traceable to defective supplies of fresh vegetable food, aided by
exposure to wet and cold weather, fatigue, and mental depression.

{168} The almost total neglect of horticulture in Europe during the
Middle Ages, especially in its more sterile northern portions, the
habitual diet of salted, smoked, and dried flesh and fish, and the
prolonged spells of cold and damp weather of this region, were
conditions most favorable to the development of scurvy, and these
regions were the very first in which its devastating effects were early
observed and recorded. In the first half of the fifteenth century it
prevailed epidemically in the north of Europe and almost everywhere
endemically, more especially in the countries bordering on the Baltic
and North Seas, although the largest and richest cities were frequently
afflicted in the severest manner in consequence of imperfect
food-supplies and the wretched sanitary conditions under which the
inhabitants lived (Fabricius). The long voyages and imperfect diet of
crews of ships furnished a large quota of harrowing nautical
experiences with the scurvy, commencing with Vasco da Gama's voyage to
India in 1497, and running up to 1812. In this interval it was all but
universal on long voyages, both on single ships and in fleets, in the
mercantile marine and in the navy.

In 1798, through the better insight into the causes of the disease, and
especially through the exertions of Dr. James Lind in ameliorating the
dietary of British sailors, it was practically stamped out of the navy
or restricted to isolated occurrences. The influence of the success
thus achieved was not lost upon the navies of other nations nor upon
the growing fleets engaged in commerce, as the disease has become less
and less frequent, constituting at present but a very trifling
proportion of the diseases incident to seafaring people. This
remarkable result is in part attributable to the fact that the chief
maritime nations have enacted beneficent laws intended to compel the
owners and masters of merchant vessels to observe certain sanitary and
hygienic measures that protect the crews from scurvy. The number of
cases returned in the English navy for 1881, in an aggregate of 52,487
cases of all diseases, was 4; in the Prussian navy, 3 in 8659; in the
Austrian navy, 27 in 8096; in the U.S. navy, none in 13,387. Thus, in a
grand total of all diseases in the chief naval services of the world of
82,629 there were only 34 cases of scurvy--a ratio of .41 per 1000. In
the mercantile marine 62 cases occurred in 32,613 cases of all
diseases, of which 43 were on the Pacific coast: this gives a ratio of
1.9 per 1000. Altogether, the 115,242 cases produced only 96 of
scurvy--a ratio of .83 per 1000. The difference in favor of the naval
over the marine service is accounted for by the greater attention paid
to the health and comfort of the men in the former.

The U.S. steamer Jeannette spent two winters in the Arctic region, and
had a single case of scurvy. The U.S. steamer Rodgers was wrecked, and
the crew, during its sojourn of six months among the Siberian tribes,
suffered severely.

The operations of armies in recent times have not furnished the
frightful mortality which, from neglect of sanitary precautions,
formerly afflicted them. During the rebellion of 1861-64, out of
807,000 cases there were but 47,000 of scurvy, or 5.8 per cent., with a
death-rate of 16 per cent. The French army[1] of 103,770 men during the
Crimean struggle had 27,000 cases of scurvy, or 26.0 per cent., with a
death-rate of 1.5 per {169} cent. In the Bulgarian campaign of 1877-78,
in an army of 300,000 strong, there were, according to Pirigoff,[2]
87,989 cases of disease, of which 4234, or 4.8 per cent., were
frankly-expressed cases of scurvy. This gave a proportion of only 1.4
per cent. of the entire force--a result entirely due to the
maintenance, both before and during the war, of a high standard of
health.

[Footnote 1: Scrive, _Relation Medico-Chirurgicale de la Campagne de
l'Orient_, Paris, 1857.]

[Footnote 2: _Krieg Sanitats-Wesen_, Leipzig, 1882.]

ETIOLOGY.--Perhaps no disease has furnished a more fertile field for
etiological conjectures than scurvy. The father of medicine ranked the
disease in one place among those presenting enlarged spleens, and in
another with the twisted bowels. He recognized a putrescence of the
humors as the underlying factor--a theory that held sway until the
beginning of the nineteenth century. The disease attracted wide
attention in the seventeenth and eighteenth centuries from its frequent
epidemic and endemic occurrence in various parts of the north of
Europe, and was believed to be restricted to cold and particularly wet
districts--a view that has been long since abandoned with a better
knowledge of its habitats. It has been encountered alike in high
latitudes north and south, amidst sterile wastes covered with eternal
snows and ice, in the temperate zones and in the burning plains of the
equatorial regions of America and Africa.

Sex has no predisposing influence, and the fact that more males than
females are affected during an epidemic simply indicates that the
former are more exposed to the ordinary determining causes. During the
siege of Paris, according to the tables of Lasegue and Legroux, there
was a very large excess of male cases, and Hayem's figures show only 6
women in 26 cases.

Scurvy has been observed at all ages from infancy to advanced periods
of life; it is believed by certain writers that adolescence is less
predisposed than adult age.

The epidemic feature of the disease led many to the opinion that it was
contagious--a view that retained its hold for many years. It was also
considered to be of a miasmatic character, which, with the previous
feature, seemed to assimilate it in nature with typhus fever and other
diseases of the miasmatic contagious group. This view had a vigorous
advocate in Villemin, who in 1874 read a lengthy paper before the Royal
Academy of Medicine in its support. His arguments were specious,
inconclusive, and inaccurate, the weight both of facts and authority
being decisively against his view. Its occurrence among members of the
same family led a few to regard it as hereditary, and it was thought to
be transmissible from the mother to the recently-born as well as to
nursing infants. The depressing influence of certain emotions, fear,
anxiety, and nostalgia, upon the functions of nutrition has, as might
have been anticipated, been noted as contributing indirectly to the
manifestation of epidemics of scurvy in the presence of the essential
determining dietetic causes.

Scurvy cannot be regarded, as Lheridon-Cremorne[3] has argued, as the
last term of nostalgia, the other alleged causes being secondary; nor
as the immediate result of mental depression, as Gueit[4] believed from
his experience in the ship Henry IV. during his service on the blockade
in the Black {170} Sea in 1858, because the disease first invaded those
laboring under nostalgia. The currency of such opinions may be readily
explained by the fact that ordinarily depressing mental influences
occur under the same conditions as those associated with scurvy--viz.
during sieges, after defeat, in prisons, and in workhouses; and,
further, the mental phenomena ordinarily occur as prodromes of the
disease long before the pathognomonic phenomena present themselves. Out
of these facts grew the mistake of regarding the mental change as
causative instead of consecutive. Murray went farther and regarded
mental despondency as at once cause and effect, and long ago scurvy was
compared to hypochondriacal diseases.[5] It may be concluded from the
recorded epidemics that no degree of mental exhilaration could ward off
the disease in presence of the determining causes, nor any degree of
mental despondency induce it with proper alimentation.

[Footnote 3: _These de Paris_.]

[Footnote 4: _These de Montpellier_, 1858.]

[Footnote 5: Dolee, 1684.]

The various qualities or changes in the atmosphere were regarded
individually or collectively at various times as the determining
causes. It was supposed that the air might become impregnated with
putrid exhalations from various sources, as the holds of ships, or
rendered impure by the vapors of the sea. The foul air of crowded
habitations, vessels, or cities was appealed to, or the common cause
was sought either in its temperature or humidity, or in both. The
earlier observers gave prominence to cold as a determining cause of
scurvy, and especially when combined with dampness, and hence its
frequency in the north of Holland, Brabant, Belgium, Russia, and
Germany. This was the current view in the seventeenth century. On the
other hand, with equal confidence the disease has been supposed to be
determined by excessively high temperatures, and its occurrence in
India, South Africa, and the equatorial regions has been alleged in
support.

Personal habits have been in the eyes of earlier observers an
all-sufficient cause, and thus excessive exertion attended with fatigue
and exhaustion has been considered the cause of several severe
outbreaks on shore and at sea. In contrast with this opinion we find
the English physicians placing great stress upon indolent habits and
lack of exercise as a predisposing if not a powerfully determining
cause.

The use of tobacco was inveighed against by Maynwaring and Harvey as a
powerfully morbific cause, while to the lack of the same narcotic its
occurrence was ascribed by Van der Mye. More recently it has been
referred by Fabre[6] to vaso-motor disturbance due to a miasm.

[Footnote 6: _Des Relations Pathogeniques des Troubles Nerveux, etc._,
Paris, 1880.]

In the drink and food, however, most observers have sought the exciting
causes of scurvy. Instances have been reported where the disease seems
to have depended upon the use of impure water, etc. The imagination has
been tortured to seek in some quality or sort of food the specific
origin of scurvy. With regard to quantity, it may be stated that in
severe famines scurvy may or may not occur according as the food,
though scant, is in due proportions of animal and vegetable, though it
is true that the ordinary conditions of a famine preclude the
procurement of succulent vegetables. The quality of the food has
nothing further to do with the production of scurvy than by impairing
the general health, for it has often happened that putrid food has been
long used without scorbutic symptoms arising. The kind of food is
equally {171} innocent, although various special articles have been
charged with specific activity. The frequency of scurvy in Brabant was
attributed by Ronseus to the use of aquatic birds; Sherwin and Nitsch
assigned the same peculiarity to a free use of fish; and Henry Ellis to
the too free use of spirits. Even the generally widespread and
much-esteemed article of diet sugar was in disrepute with Willis. The
too free use of salted meats has been often accused of causing the
trouble. The fat rising on water in which salt provisions were boiled
was considered by Cook and Vancouver to be of particular pernicious
effect, and even the copper vessels in which they were cooked were
condemned by Travis as able to communicate the scorbutic poison to the
food. To the milk of animals browsing on verdure upon which pernicious
dew had fallen was referred an epidemic which occurred in Silesia in
1591. Diseased potatoes were considered sufficient to determine scurvy
in Ireland and Scotland by O'Brien.

The scurvy occurring on land was deemed to be different from that
occurring at sea, and its frequency afloat brought into unmerited
disrepute the sailor's salt diet, and its saline materials were even
considered the chief offending cause. This idea was rejected by
numerous observers, who assigned as the chief causative role in scurvy
deficiency in vegetable food, especially of the fresh, succulent
variety. The particular constituent of this sort of food, so powerful
in warding off scurvy and of curing it when prevention has failed, has
baffled discovery. Dr. Aldridge attributed it to mineral elements
generally. Dr. Garrod singled out the potassic salts as the particular
one to which the specific action must be attributed; but neither of
these views has gained in credit. From all the facts, both positive and
negative, we may reasonably assume that the essential dietetic error
leading to the development of scurvy, in the immense majority if not in
all cases, consists in a deficiency in the variety of food; that is to
say, there is not the requisite proportion of animal matter with a
diversity of vegetable substances. No single natural order contains
plants that supply all the elements essential to the nutrition of the
body and the right composition of the blood. The graminaceous and
leguminous articles of food, for instance, are numerous, but not
various; they all afford the same or analogous albuminous elements,
which have about the same nutrient value as the corresponding
substances in animal food, and hence health and vigor cannot be
sustained on a diet of flesh, combined with wheat, rice, and oatmeal or
with beans and peas, or with all of them together. Outbreaks of scurvy
have occurred on shipboard, where the ration is made up principally of
these articles; as in Anson's ship, when supplied with an abundance of
fresh animal, farinaceous, and leguminous foods. It is clear,
therefore, that in order to obtain a variety of materials required in
nutrition, we must resort to several of the natural groups, those
particularly which comprise the succulent vegetables and fruits.

MORBID ANATOMY.--The bodies of persons dead of scurvy are, in most
cases, much emaciated, because the quantity as well as the quality of
the food has usually been defective. When the food-supply is abundant
and only lacking in the elements indispensable in warding off scurvy,
the bodily weight is not noticeably decreased, although the
characteristic tissue-changes of scurvy are present. This was
noticeable in the cases recorded by Trotter of negro slaves dying of
scurvy while their bodies {172} presented a fat and sleek appearance.
Rigor mortis usually sets in early, and chemical decomposition invades
the tissues speedily. The skin presents the discolorations and
blotchings observed during life. The subcutaneous connective tissues
are soaked with serous exudations, especially in the lower extremities,
and in various localities are infiltrated with bloody or fibrinous
extravasations. The same changes occasionally affect the muscles, the
infiltration occurring beneath the fibrous sheaths and into the
intermuscular spaces, and the fibres are more or less torn. These
effusions occur most frequently about the knees, the elbows, and the
pterygoid muscles of the jaw.

The bones are sometimes necrosed by the mechanical influence of copious
effusion beneath the periosteum, forming nodes of varying sizes and
obstructing the supply of blood. The joints are occupied by serous or
bloody transudations; their synovial investment is destroyed in part,
so that the cartilage is exposed; and the latter not infrequently is
softened, and even separated from the subjacent osseous connections.
Sometimes the morbid changes occurring in the joints are the results of
disease in the subcutaneous connective tissues surrounding them.

The muscular system presents marked changes. The muscles undergo fatty
degeneration in a remarkable degree. The changes begin first in the
lumbar muscles, the fibres losing their striations and sarcolemma, and
finally being replaced by granular and fatty matter.

The brain has been found in rare instances the seat of softening and
infiltration, and the ventricles may contain serous or bloody fluid.
Similar effusions have also been noted in the arachnoid. Most
frequently, however, the brain and its membranes present an anaemic
appearance, there is less blood than natural in the vessels, and the
tissues are pale. Very often no changes whatever are observed.

The heart is smaller than normal, relaxed, and flabby, its fibres
easily broken, and a cut surface presents the yellowish aspect of fatty
degeneration in certain parts, with occasional extravasations located
in the cardiac walls. The valves of the heart are relaxed and illy
adapted to accurate closure. In certain recent cases soft coagula or
dark fluid blood, and in others firmly coagulated blood, are found in
the cavities; in those which have been prolonged the blood is more
likely to be found fluid and the coagula diffluent. The endocardium is
often blotched to a greater or less extent by sanguineous imbibition.
The pericardium often contains serum, and in the worst cases is
inflamed, lacerable, and contains bloody effusions. The inner surface
of the great vessels at the base of the heart is stained by imbibition.

The respiratory organs are variously affected. The mucous membrane
lining the nose, larynx, and trachea is generally pale and flecked with
extravasations of a dark-red color; more or less frothy fluid, tinged
with blood, is present in these passages, and occasionally oedema of
the glottis is encountered. The lungs are, as a rule, infiltrated with
a bloody serosity, particularly in those cases with renal complication,
or with a fibrinous or bloody exudation. The posterior portions of the
lobes often present evidences of hypostatic congestion, or even of
gangrene, and in the latter case the tissue is easily friable and emits
a disagreeable odor. Their surfaces are mottled with superficial
discolored patches of varying size and outline. The lungs may, on the
other hand, be found pale, {173} with empty collapsed vessels and with
little or no effusion. The pleural cavities commonly contain a serous
fluid, or, in rare cases, a copious effusion of blood. Traces of
inflammation and discoloration by sanguineous staining are traceable on
the pleural surfaces.

The digestive organs furnish strongly marked lesions. The mouth
presents the most constant scorbutic feature, a stomatitis in which the
gums are infiltrated, spongy, livid, and the seat of fatty
degeneration; the teeth are loosened or have already fallen out. The
stomach and small intestines are thin-walled, and the mucous membrane
is often softened, and in places ulcerated; similar changes have been
noted in the solitary glands. Follicular ulceration of the large
intestine occurs, with softening and infiltration of the mucous
membrane. Hemorrhagic effusions into the mucous membrane, forming
stippling, flecks, or patches, occur in various degrees along the whole
extent of the alimentary canal. The pancreas is occasionally found
softened and containing hemorrhagic effusions.

The kidneys are, as a rule, found in the normal condition in cases in
which albumen has been observed in the urine. Occasionally they are
engorged, with infarction of the cortical substance, and the mucous
lining softened and thickened and covered with blood-tinged mucus, or
they may present various degrees of parenchymatous degeneration. The
ureters and bladder sometimes present ecchymotic spots, and the
contained urine is mingled with blood.

The liver is always more or less altered by fatty degeneration, and at
times replete with blood and softened, and its surface ecchymotic. The
spleen is occasionally greatly enlarged, and its tissues very
lacerable, laden with blood, and infarcted.

PATHOLOGY.--The essential character of scurvy consists in perverted
nutrition, in which the blood undergoes such peculiar and profound
changes that its fitness for the maintenance and renewal of the various
tissues and organs is impaired; hence the nervous depression, loss of
muscular power and tonicity of tissues, and the transudation of the
blood or of its constituent parts.

The processes of secondary assimilation are chiefly at fault, leading
to the blood-changes, and through these to the textural lesions.
Primary assimilation remains intact, as the bodily weight is little
altered as long as the food is in sufficient quantity. This loss of
nutritive balance between the blood and tissue is due to the absence of
certain elements furnished by fresh vegetable matter. What these are,
and how their absence acts in inducing this disturbance, have not yet
been determined; we only know that the mysterious harmony of the vital,
chemical, and physical relations which exist between the blood and
tissues in health is deranged by their absence.

Endless explanatory surmises and assumptions have been proffered. The
earlier explanations involve either the Galenical theory of
putrefaction of the fluids and humors, a breaking down of the
blood-corpuscles, or the later chemical theories of superabundance or
absence of certain salts, sulphur, etc., and hence there were an acid
scurvy, an alkaline scurvy, a muriatic scurvy, etc.

The frequent effusions of blood in scurvy led Andral to suspect that
the chief peculiarity in scorbutic blood was the decrease of fibrin;
which was {174} in perfect accord with a theory that he had formed that
this change was the uniform cause of passive hemorrhage. Magendie had
already given experimental support to this conjecture by inducing in
animals phenomena analogous to those of scurvy by the injection into
the veins of defibrinated blood or of alkaline solutions. Andral[7]
believed his views confirmed when in 1841 he analyzed on two occasions
the blood of scorbutic patients and found the fibrin reduced to 1.6
parts per 1000. Similar results were obtained by Eckstein and Fremy. On
the other hand, the blood was analyzed by Busk, about the same time, in
three well-marked cases of scurvy that occurred on the Dreadnaught
hospital-ship, and in all of them the fibrin was in excess of the
normal amount, the least being 4.5 and the greatest 6.5 parts per 1000.
In perfect accord with Busk's results were the analyses of the blood of
five scorbutic females, communicated in a note to the Academy of
Sciences in 1847 by Becquerel and Rodier. In no case was the fibrin
diminished, but in some it was sensibly increased. In a subsequent case
Andral found that the fibrin, instead of being less, exceeded the
physiological mean, reaching 4.4 parts, and he concluded that a
diminution of this element was not a necessary and common occurrence,
but only an effect--a result of prior morbid modifications, and a
consequence which was produced more or less frequently according to the
severity and duration of the disease. Parmentier and Deyeux found the
blood of three scorbutics to resemble inflammatory blood in respect to
fibrin, while Frick obtained in one analysis 7.6 parts of fibrin and
Leven 4.3 parts.

[Footnote 7: _Essai d'hematologie pathologique_.]

In mild cases of scurvy neither the color, the alkalinity, nor the
coagulability of the blood differs from that of blood in health, though
Wood alleges that the clot is loose and cotton-like, and Canstatt that
its coagulability, in consequence of the large proportion of saline
matters, is diminished. In Busk's cases the separation of the clot and
serum was as perfect, and took place as rapidly, as in healthy blood,
and in two of them the blood was both buffed and cupped, as it was also
in Leven's cases. In two of the most severe of Becquerel's cases the
blood coagulated firmly, and in a slight case the clot was dark and
loose. The albumen of the blood shows no marked change as regards its
quantity. The five analyses of Becquerel and Rodier showed the average
amount of organic matters of the serum to be 64.3 parts in 1000, the
smallest being 56.2 and the largest 69.2 parts. 1000 parts of the serum
of the same cases gave an average of 72.1 parts of organic matter.
Frick's single case gave 87.045 parts per 1000, and the average of
Busk's was 78.2 parts, while Chotin and Bouvier obtained only 62.3
parts. The last-mentioned writers have recorded a fact in connection
with the physical characters of scorbutic blood that deserves notice:
the blood in one case did not coagulate at the usual temperature (about
158 degrees F.), but required a temperature some degrees higher for
that purpose. The red corpuscles in all the foregoing cases were
notably diminished, the largest amount given being 117.078 parts per
1000, while the lowest was 47.8 parts. In Andral's second case the
globules had decreased to 44.4 parts per 1000, the lowest amount yet
recorded.

The alkalinity of the blood seems not to be changed, although Chotin
and Bouvier noticed a slight increase. The saline constituents do not
{175} vary greatly from the normal standard. The average amount in the
cases of Becquerel and Rodier and Busk was 8.1 per 1000, the smallest
being 5.5 parts and the largest 11.5. In Ritchie's two analyses the
proportion of saline matters is given as 6.44 and 6.82 parts per 1000.
Opitz and Schneider have found less than the physiological mean. In
Frick's case the amount was 8.8, the iron being 0.721 parts per 1000,
and 0.782 to 127 parts of globules; lime 0.110, chlorides 6.846, and
phosphates 1.116 parts per 1000. The iron was in excess of that in the
normal blood, but in Becquerel's cases the mean was 0.381--less than
the normal. The proportion of iron in Duchet's cases was respectively
0.393, 0.402, and 0.476 parts, giving a mean of 0.423 parts per 1000,
which nearly approximates the normal. Garrod in one analysis of the
blood found a deficiency of the potassium salts, upon which he erected
his well-known theory of the etiology of the disease. It is an
interesting fact that in the physiological state the quantity of sodium
chloride is not subject to variation, any excess introduced with the
food being thrown off by the kidneys. The quantity in the urine bears a
relation to the amount introduced as food, but the proportion in the
blood is constant.

The quantity of water in the blood has been found to be increased in
all the analyses which have been made. Chotin and Bouvier estimated
water and loss at 831.1; in Frick's case it was 791.69 parts per 1000;
and in Becquerel's five cases it was put at 807.7, 810.9, 811, 813.7,
and 854.0 parts per 1000, respectively. In Busk's three cases the
lowest amount was 835.9 and the highest 849.9 parts per 1000. The
specific gravity of the defibrinated blood was in all cases low in
comparison with the normal standard (1057), the average in Becquerel
and Rodier's cases being 1047.2, the lowest 1083.3, and the highest
1051.7. In the single observation of Chotin and Bouvier it was 1060.
The specific gravity of the serum was also less than normal (1027), the
average of four of Becquerel's analyses giving 1023.8, the lowest
1020.8, and the highest 1025.5. Busk gives 1025 in one case and 1028 in
another.

The results of the most recent analyses, those of Chalvet, are shown in
the following table, in which scorbutic blood is contrasted with that
of a healthy, robust female:

                                      Scorbutic blood.  Healthy blood.
  Water                                    848.492         772.225
  Solid matters                            151.508         220.775
  Dry clot                                 140.194         209.000
  Albumen                                   72.304          68.717
  Fibrin                                     4.342           2.162
  Globules                                  63.548         138.121
  Extractive matter--by absolute alcohol    10.312           8.013
                     by ether                1.002           1.300
  Ashes of clot                              3.000           5.691
  Peroxide of iron of globules               1.060           2.259
  Potassium of globules                      0.329           0.625

From the conflicting statements of various observers the following
conclusions may be drawn: that in scorbutic blood water is in excess;
that there is, on the one hand, a marked increase of the fibrin, and in
a less degree of the albumen and extractive matters, while on the other
hand there is a marked decrease of the globules and in a less degree of
the mineral matters. On the authority of Chalvet it may be also stated
{176} that demineralization of the muscular tissue is a notable
chemical feature in scurvy.

So far, microscopic examination has been entirely negative. Hayem[8]
found no appreciable alteration from healthy blood, and in this view
Leven[9] concurs; while Laboulbene[10] notes the occurrence of an
unusual number of white globules.

[Footnote 8: _Mem. de la Societe de Biologie_.]

[Footnote 9: _Communication to the Academie des Sciences_, 1871.]

[Footnote 10: _Epidemie de Scorbut_.]

Petrone Luigi[11] injected scorbutic blood into the connective tissue
of rabbits. In three instances the animals died, presenting on the ears
distinct evidences of the formation of petechial extravasations. The
viscera revealed everywhere bloody effusions of larger or smaller size.
The spleen was enlarged and its parenchyma and capsule distended. In
the blood were found oval, shining, spontaneously-moving corpuscles,
which he regarded as the bearers of the specific poison of scurvy.

[Footnote 11: _Annali Univers. di Med. c. Chir._, 10, 1880.]

SYMPTOMS.--The symptoms of scurvy are insidiously and usually slowly
developed under the influence of the efficient causes, and the disease
runs a chronic course, often extending over five or six months,
especially in cases in which the hygienic surroundings of the patient
have been imperfectly or not at all rectified. In light cases the
course is much shorter. A gradual alteration of the nutritive processes
first occurs, until what might be called a scorbutic cachexia is
established in a period varying from a few weeks to several months. The
initial symptoms consist in the skin losing its color and tone and
assuming a yellowish or earthy hue: it is relaxed, dry, unperspiring,
and rough; in the legs particularly this roughness is very marked, and
the skin, when rubbed, sheds an abundance of furfuraceous scales. The
cutaneous follicles, markedly on the extensor aspect of the lower
extremities, are prominent, similar in appearance and feel to the
condition known as goose-flesh. Rouppe[12] calls this the signum primum
pathognomonicum. Dark-red or brownish flecks, of a circular outline and
of varying but small size, not unlike flea-bites, appear on the face
and limbs. The cutaneous circulation is feeble and the superficial
warmth less than natural; slight depression of the atmospheric
temperature produces a sensation of chilliness, and the feet and hands
are cold. On assuming the erect posture the patient complains of
headache and dizziness. The muscles are relaxed and soft to the feel,
and a corresponding loss of vigor and strength is experienced by the
patient, who is indisposed to exert himself in the performance of his
customary duties and seeks repose and freedom from feelings of fatigue
and languor in recumbency. This prostration is occasionally so extreme
that the slightest efforts in attempting to stand or walk are attended
with rapid action of the heart, accelerated respiratory movements, and
a sense of suffocation and breathlessness. The general circulation is
impaired; the heart acts feebly; the arteries are contracted; and the
pulse is slow, small, and compressible.

[Footnote 12: _De morbis navigantium_.]

The mental powers are equally impaired. The face wears a haggard
appearance and depressed expression; gloomy forebodings of evil and
disinclination to turn the attention to the usual mental pursuits are
markedly present--a disinclination that may subsequently merge into
complete apathy or indifference to passing events, or even into
somnolency.

{177} Pains in the legs, joints, and loins are early manifestations:
they closely resemble those of rheumatism, for which they are often
mistaken. The pains are not exacerbated at night, but, on the contrary,
are often more severe by day. Not unfrequently lancinating pains in the
muscles of the chest are complained of. The sleep is not disturbed
until the disease has made some advance, when it becomes broken and is
no longer refreshing.

The appetite is usually unimpaired in the early periods of the disease,
and even throughout its course the condition of the mouth alone
prevents the patient from indulging his desire for food, even, as is
occasionally noticed, to voracity. There may be a yearning for certain
articles of diet, principally those of an acid character; but, on the
other hand, some cases present exactly the reverse condition--a disgust
for food in general or for particular varieties; or the appetite may be
vacillating, at one time craving and at another repelling nourishment.
There is no noticeable change in the normal thirst, except on the
occurrence of febrile complications, when it is increased. The gums do
not, at this stage of the disease, present the livid, swollen
appearance of fully-developed scurvy, but, on the contrary, are
generally paler than usual, with a slight tumid or everted line on
their free margins, and are slightly tender on pressure. The breath is
commonly offensive, and the patient complains of a bad taste in the
mouth. The tongue is flabby and large, though clean and pale, and the
bowels are inclined to be sluggish.

This preliminary stage is followed, after varying intervals of time, by
certain local phenomena which are quite characteristic of the disease.
There is a marked tendency to extravasation of blood into the tissues,
either causelessly or upon the infliction of slight injuries or wounds.
Fibrinous exudations occur sooner or later into the gums, which become
darkened in color, inflamed, swollen, spongy, and bleed upon the
slightest touch or even spontaneously, and finally separate from the
teeth. These results are due, in part, to the considerable amount of
pressure to which these parts are subject in mastication, and it is a
conspicuous fact that the gums of edentulous jaws remain free from
these changes. In a few cases the gums are but slightly altered,
perhaps oedematous only or pitting upon pressure, or they become the
site of bloody extravasations. In severer examples, in later stages of
the disease, these various alterations progress to an extreme degree,
and the extravasation is so voluminous that the gums present great,
fungous, lacerable excrescences, which may finally break down into a
suppurating, brownish, and very fetid mass, communicating to the breath
an odor of a most offensive character. In certain epidemics of scurvy,
notably in that of Florence described by Cipriani, the lesions of the
gums were absent. The rest of the mucous membrane of the mouth remains
unaltered, or at most slightly ecchymotic. Samson and Charpentier[13]
in a large number of cases saw this but once, and in one of Leven's[14]
cases the fungous growth invaded the palatal mucous membrane, extending
to the anterior pillars of the fauces. The salivary glands are enlarged
and swollen; the tongue is imprinted with the form of the teeth, while
the latter become encrusted with tartar and more or less concealed by
the exuberant gums, or, becoming gradually loosened from the alveoli,
finally drop out. The morbid process may extend to the bone itself, and
necrosis and extensive {178} exfoliation follow. Mastication is more or
less painful, and often impossible, so that the patient is reduced to
the necessity of prolonging life by the use of fluid or semi-solid
food. Under the influence of appropriate treatment it is remarkable how
rapidly (in from two to four weeks) these marked changes recede and the
parts resume their normal condition, yet it occasionally occurs that
permanent, callous thickening of the gums results.

[Footnote 13: _Etude sur le Scorbut_, 1871.]

[Footnote 14: _Une epidemie de Scorbut_, p. 28, 1872.]

In the progress of the disease effusions of blood under the skin are of
early occurrence. They are at first located in the superficial stratum
of the cutis or just beneath the epidermis, especially around the roots
of the hair, and present themselves as roundish, bluish-red flecks,
varying in size from that of a pin's head to that of a split pea, not
effaceable by pressure with the tip of the finger, but slightly, if at
all, elevated above the surface, and enduring for weeks together. The
nutrition of the hair-follicles is impaired, so that the hairs are
often either lost, broken, or distorted. These petechiae fade in color
with progressive improvement in the case, and finally disappear,
leaving brownish-yellow discolorations. They first appear on the
extremities, particularly the lower limbs, then on the face, and lastly
on the trunk. At a later period extravasations of a larger size and
more irregular form occur in the deeper layers of the derma. They vary
in size from that of a finger-nail to blotches two or three inches in
diameter; at first reddish in color and subsequently of a bluish red.
When recession occurs under appropriate treatment, the color passes
through various shades of violet, blue, green, and yellow, as in
ordinary traumatic ecchymosis. Outpourings of blood also occur into the
subcutaneous connective tissue, notably that of the legs, and in
localities where connective tissue is particularly abundant and loose,
as in the ham and axilla. The dispersion of blood in this tissue may be
so considerable as to cause the legs from the knees down to present a
uniform dark-blue coloration that in form may not inaptly be compared
to a stocking. The upper extremities also suffer, usually on their
inner side from the armpit down, the extravasation rarely reaching,
however, to the hand. These extravasations may take place after the
infliction of very slight injuries, as from blows or the pressure of
hard bodies, or even from the mechanical effects of prolonged
dependency of the limbs, as in riding on horseback. Extravasations of a
similar nature are occasionally present in the connective tissues of
the muscles themselves or between them, giving rise to swellings of
various forms and dimensions. Nearly always along with the sanguineous
effusions there is more or less oedema, usually beginning at the ankles
and gradually extending upward; in some cases there are puffiness of
the face and general anasarca, so that deep pits remain on pressure.

This profound impairment of nutrition of the skin continuing, in the
worst cases blood is effused beneath the cuticle, forming blebs of
varying size, which finally break and leave superficial ulcerated
surfaces, that ultimately become covered with flabby, exuberant
granulations, pouring out a purulent often offensive sanies and
bleeding upon the slightest touch.

In some cases the ulceration begins in the petechiae at the hair-roots,
and a number of these, running together, form a large ulcer. The
destruction of tissue by ulceration is disposed to spread more widely
and deeply, and is often of a most intractable character. Old
cicatrices {179} are the first tissues in these cases to take on the
ulcerative action. Certain muscles, chiefly those of the legs, and
notably the gastrocnemii, the abdominal and pectoral muscles, the psoas
magnus, and pterygoids, may become the seat of fibrinous
extravasations, which finally change, by lapse of time, into hard, firm
tumors, impairing the functions of those parts and leading to
contractions of the limbs.

The symptoms in certain epidemics of extraordinary severity have
displayed alterations in still deeper structures. Effusions occur
between the periosteum and the bone, forming painful, hard, and
resisting nodes of varying dimensions, especially along the course of
the tibiae, upon the scapulae, and upon the maxillae. In young persons
the epiphyses are separated from the shaft of the long bones, and in
other cases the ribs become necrosed and disarticulated from the
sternum, producing a creaking noise during respiratory movements, as
related by Poupart.[15] This occurs mostly on one side and about the
middle of the series, yet it has been noted to occur on both sides, so
that the sternum and attached cartilages, deprived of support, were
perceptibly sunken. Oserctzkowski[16] reports two fatal cases of scurvy
attended with spontaneous fracture of the ribs. There was extravasation
into and beneath the periosteum, and subsequent destruction of the
continuity of the bone. In one case the ribs on both sides were
affected, so that the anterior wall of the thorax sunk in and
embarrassed the respiration, which was chiefly maintained by the
diaphragm. Inflammation of the lungs succeeded, and the patient died in
agony.

[Footnote 15: _Memoires de l'Academie des Sciences_, p. 237, 1699, and
_Philosophical Transactions_, vol. xv.]

[Footnote 16: _Wratsel_, No. 51, 1881.]

Recently-repaired fractures have been known to recur under the
influence of scurvy from the destruction of the callus.[17]

[Footnote 17: Anson's _Voyage Around the World_, edited by Walter.]

The articulations as well as the bones in very severe cases of scurvy
present evidences of disease, consisting in periostitic effusions which
involve the surrounding soft parts, producing impairment of motion,
enlargement, and false ankylosis, and even destroying the normal
anatomical relation of the osseous surfaces, so as to determine
deformities. These changes are usually attended with severe pain, and
most commonly occur in the ankle-, knee-, shoulder-, and hip-joints,
and disappear tardily, requiring perhaps months for their recession, if
indeed this takes place at all.

The symptoms manifested by the circulatory organs are prominent from an
early period of the disease. The pulsations of the heart are slower,
feebler, irregular, and often intermittent; its impulse is decreased or
becomes quite imperceptible; and when the associated anaemia has
progressed to a certain extent a systolic murmur may be audible. The
arterial and venous channels are of diminished calibre; the pulse
becomes soft, of less volume, and tardier; and a venous murmur may
sometimes be heard in the cervical veins. The remarkable nutritive
changes in the capillary walls in part account for the numerous
hemorrhages which occur both by rhexis and diapedesis. The most
frequent is epistaxis; the slightest blows, sneezing, or blowing the
nose will often determine it, or it may occur spontaneously, and in
severer cases with such profuseness as to threaten impending
dissolution, requiring nothing less than timeous introduction of the
tampon to rescue the victim. Hemorrhage from the {180} lungs is of rare
occurrence, and when it does happen is rather indicative of
pre-existing pulmonary disease, such as phthisis, or of the approach of
a complication, such as infarction or gangrene, than a constituent
feature of scurvy. Haematemesis is less uncommon, but is by no means
frequent; the blood ejected from the stomach is usually small in
quantity, but in isolated examples the bleeding is profuse, producing
great exhaustion and a sense of cardiac depression which preludes
speedy death. Hemorrhage from the bowels is also an ill-omened feature,
completely blanching the patient and presaging early exhaustion and
death. Blood may also appear as a product of a complicating dysentery
which determines abundant, offensive discharges that may run on for
several weeks before the patient is finally exhausted. Haematuria
sometimes occurs, especially in broken-down and cachectic subjects and
in an advanced stage of scurvy. All of these forms of hemorrhagic
effusion, now mentioned as localized in the mucous membranes, are to be
deprecated as exercising a pernicious influence, seriously aggravating
ordinary cases and fatally jeopardizing the issue of severe ones.

Effusive and inflammatory complications are also encountered in the
serous structures, and usually in cases of great severity, though they
occasionally present themselves when the more common localized
phenomena of scurvy are not particularly prominent. These complications
may be marked by a gradual accession, or they may rapidly arise and
involve the patient, just before in apparent security, in the greatest
peril. These incursions are almost always attended by febrile
exacerbations and the usual grouping of clinical characters denotive of
the same pathological conditions arising under ordinary circumstances.
The local complications may either affect the pleura or pericardium, or
both. In Karairajew's[18] 60 autopsic examinations pericardial
effusions were noticed in 30, pleural in 30, pericardial and pleural in
6, peritoneal in 7, and arachnoidal in only 1. The exudations are
sero-sanguinolent or fibrinous in character, and sometimes reach the
inordinate quantity of four or five pounds, occasioning the patient the
utmost distress and embarrassing the respiratory and circulatory
functions. Although these augment in a high degree the risk to life,
yet under prompt and appropriate treatment recovery may take place and
the effusions vanish with surprising rapidity.

[Footnote 18: Himmelstiern, _Beobachtungen uber den Scorbut_, S. 50,
Berlin, 1843.]

Hemorrhagic extravasation into the nervous centres is a very rare
occurrence. It has not been as yet recorded as having occurred in the
brain-substance itself, but has in several instances been noted between
the meninges, producing headache, dizziness, vertigo, and sometimes
somnolence, delirium, and coma. Opitz[19] relates an interesting case
in which convulsions suddenly occurred with unconsciousness, followed
by hemiplegia of the left side of the body and the corresponding side
of the face. After twenty-four hours consciousness returned and the
paralysis disappeared. There were, however, headache and hyperaesthesia
of the upper extremities present; twelve days later these also receded,
and the patient finally recovered. The same author records paralysis as
occurring in one case from extravasation into the spinal meninges.
Samson observed an instance in which a fibrinous effusion formed upon
the sciatic nerve, with consequent pain.

[Footnote 19: _Prag. Vierteljahrschrift_, S. 153, 1861.]

{181} In the circulatory system symptoms always of threatening and
often of fatal import may arise: embolism may occur at various points,
particularly in the lungs and spleen, occasioning hemorrhagic
infarctions, which have undoubtedly been the occasion of the sudden
deaths sometimes observed in scorbutic cases not apparently of a very
dangerous form nor attended with an excessive degree of exhaustion.

The urinary system supplies no prominent symptoms; the statements as to
the condition of the kidneys and the composition of the urine are
contradictory. The urine not infrequently contains albumen,
particularly in severe cases, but this is by no means indicative of
corresponding changes in the renal structure: on the contrary, this may
be found after death to be apparently free from disease.

The conclusions that would seem to be authorized by the statements of
various authorities are that the quantity of urine passed is decreased,
as well as that of the urea, while the amounts of the albuminoid and
mineral matters are increased.

Physical examination will reveal the frequent occurrence of enlargement
of the spleen, independent of malarial influences, and Krebel has
encountered one case in which the liver was involved in inflammation.

Some derangement of the visual organs is present in many cases. Foltz,
in the epidemic on the Raritan, reported four cases of nyctalopia and
two of hemeralopia, and other affections of the eye, such as
conjunctivitis, induration and irritation of the ciliary margins of the
lids, with a copious and acrimonious discharge, these conditions being
obviously due to the scorbutic diathesis. Medical Director J. Y.
Taylor, U.S. Navy, in a private communication to me states that
hemeralopia was a frequent premonitory symptom of scurvy that occurred
in the U.S. sloop-of-war Decatur in 1854 during a laborious and tedious
passage of three months through the Straits of Magellan. The men were
overworked and much exposed to cold and wet, and part of the time were
on diminished rations. The hemeralopia was at first erroneously
attributed to the reflection from the snow and glaciers--a species of
snow-blindness--but other phenomena speedily appeared in a majority of
the causes: a subacute inflammation, with considerable pain and
swelling of the small joints, especially those of the toes; sore and
tender gums, although only a few progressed so far as to exhibit
sponginess or bleeding; and debility, depression, anxiety, and
insomnia. In a few cases the blindness was so complete as to render
their subjects almost helpless after sunset. This was the most
pronounced and remarkable symptom and the one most complained of. These
incipient scorbutic symptoms were promptly arrested by the free use of
wild celery (Apium graveolens), which was found growing abundantly in
sheltered places. The short rations were also supplemented
advantageously by mussels (Mytilus edulis) whenever they could be
obtained. A few weeks later the crew appeared to be in ordinary health.

Hemorrhage may occur under the conjunctiva, raising it into small
pouches; into the anterior chamber, causing iritis and adhesions; and,
finally, into the choroid and vitreous humor, exciting a general
inflammation of the entire organ.

Dulness of hearing and buzzing in the ears have also been signalized as
occasional symptoms of scurvy.

{182} The phenomena of fever are always absent during the course of
uncomplicated scurvy, the temperature of the mouth sometimes falling as
low as 92 degrees F., and being always one or two degrees lower than
normal. It is only in the later periods of the disease, when
pathological processes most often supervene in the internal organs,
that an elevated temperature and the other ordinary symptoms of fever
are manifested. The lowered vital resistance of scorbutic subjects
particularly disposes them to the incursions of fevers, especially
those of malarial and typhoid types: hence in the low, marshy districts
of Northern Europe and in sections of country afflicted by famine and
overcrowded dwellings these complications are very common.

DIAGNOSIS.--Little or no difficulty will be encountered in
discriminating scurvy from other diseases under the circumstances that
usually surround its development and prevalence. These circumstances
are altogether peculiar and characteristic, and involve the absence of
succulent vegetable food as the prime factor, and exposure to cold,
fatigue, mental despondency, or other depressing influences as
accessory in its production. This combination of causes has been
usually witnessed in all the outbreaks of scurvy in camps, besieged
towns, on shipboard, particularly on ships in Arctic service.

Sporadic cases may escape immediate identification in the absence of
some of these circumstances, but a close attention to the symptoms will
surely lead to a correct conclusion. The scorbutic cachexia denoted by
the sallow or earthy hue of the skin; the spongy gums; the
discoloration of the surface; pains in the limbs and joints; the sense
of weariness, and, later, the exhaustion, dyspnoea on the slightest
exertion; the bloody and fibrinous effusions into the connective
tissues and muscles about the joints, and into the pleurae,
pericardium, and peritoneum; the stiffness and contraction of the
legs,--furnish a complexus of phenomena not met with in any other
disease than scurvy. The discoloration of the skin in purpura,
leucocythaemia, anaemia, chlorosis, and haematophilia, or other
conditions involving hemorrhagic extravasation, are easily
discriminated from those of scurvy when taken in connection with the
other symptoms and the history of those diseases. In the beginning of
scurvy the pains in the back and limbs might divert the attention to
rheumatism, but an examination at this early stage will, in all
likelihood, disclose the peculiar gingival and cutaneous lesions of
scurvy.

The rapid improvement of scorbutic cases under a fruit and vegetable
diet is also a noticeable feature not witnessed in any of the foregoing
diseases.

PROGNOSIS.--The prognosis of scurvy is always favorable in the early
stages, and even in the very worst recovery occurs under improved
hygienic surroundings with remarkable promptness and certainty. It must
not be overlooked, however, that sudden death may occur in seemingly
light cases from failure of the heart's action or from embolism. There
is a ready disposition to the recurrence of the disease under slight
causes, and it may so impair the health as to lead to the development
of other fatal maladies. The gravity of the case is to be gauged not so
much by its seeming severity as by the accessibility of proper
food-supplies, for without these the worst results may be expected.
Where the case is embarrassed with complications of the respiratory and
circulatory {183} organs, involvement of the bones, and intercurrent
diseases, the outlook becomes correspondingly grave.

Throughout the world, in recent times, greater areas of territory are
devoted to agriculture and horticulture, and the products are
distributed over wide extents of country by the increased facilities of
communication by the highways and railroads, so that it would now be
impossible for an epidemic of scurvy to devastate a region of country
so provided as it did a century ago, or might do and has done in
regions of country where tillage is neglected and communications are
cut off by an absence of roads from more productive centres, as in
Southern and Eastern Russia.

Hygienic improvements that have almost stamped out scurvy on shore have
also done good service for mariners, and thousands of ships now cross
the ocean on long cruises with perfect security from the disease. In
the naval services of the world, as has been already shown, the disease
is rarely encountered, and it is greatly diminished in the merchant
marine, from which, it is hoped, in a few years, by a more rigid
enforcement of existing laws for the protection of sailors, it may also
entirely disappear. Even in exceptionally long and arduous cruises, as
in the Arctic regions, the disease may be arrested, as was the case
with the Jeannette, which was drifted about, locked up in ice, for
sixteen months, yet only a single case of scurvy appeared.

It is of the first importance to enlist a healthy crew for long
voyages, free from previous syphilitic, scorbutic, or other
constitutional taint; then, by observing proper hygienic precautions,
to maintain their health. One of the prime factors in securing this
result is a suitable dietary. The improved methods of preserving food
afford facilities for storing up adequate quantities of both kinds,
animal and vegetable, to last the cruise. To economize these stores it
will be well to start with a stock of live animals and recent
vegetables, such as can be now had in almost any quantity in any
considerable maritime city, and not until these are consumed are the
canned and preserved supplies to be opened. All the ordinary meats, as
beef, mutton, veal, and lamb; most vegetable products, as asparagus,
beans, peas, potatoes, and a great variety of fruits, as peaches,
plums, berries, etc., are obtainable at moderate expense, and should
form an integral portion of the ration. Eggs can be easily preserved so
as to keep for months by simply packing them in plaster or in salt, and
they furnish a valuable and acceptable article of diet. Among articles
of great nutritive value milk takes high rank, and it can be preserved
sweet and pure indefinitely. Sauer-kraut is an antiscorbutic of
considerable virtue, and should not be overlooked in laying in stores
for a distant cruise. Cheese and oatmeal will be found useful additions
to the ordinary ration.

It may be proper to state in the event of the occurrence of scurvy and
the exhaustion of the fresh vegetable stores that various
quickly-growing vegetables, such as mustard, radishes, turnips, and
cresses, could be cultivated on shipboard if seeds are provided.

With such a varied dietary, comprehended in the above enumeration, it
would be impossible for scurvy to invade the ship's company, especially
when aided by other wholesome agencies, as cleanliness, well-ventilated
and dry sleeping rooms, and clothing adapted to the weather. The
antiscorbutic virtues of lime-juice were known long ago, being
mentioned by {184} Albertus in 1593, but it was not until many years
later that it became an integral part of the English navy-ration. The
law requires it to be carried on board all merchant vessels, and to be
served out ten days after the crew has been living on salt rations. The
juice keeps well if properly prepared and preserved from contact with
air, especially when fortified with a small quantity of alcohol, the
usual strength being about 10 per cent. It should be carried in vessels
containing just enough to furnish a few days' rations to the whole
crew, by which plan only a small amount need be exposed to the
decomposing influence of the air. The juice can be reduced by
evaporation to a very small bulk. This method was adopted in supplying
the Arctic cruiser Rodgers.[20] The juice was reduced to a paste, each
pound of which represented one gallon of the solution of the ordinary
strength. It has also been used in the form of lozenges and biscuit. It
may be stated that great reliance has been placed upon malt, the acid
wines, and cider as good antiscorbutics.

[Footnote 20: _Report of the Surgeon-General of the Navy for 1880_.]

In connection with the food-supplies it is proper to mention those
influences of a depressing character which have a tendency to favor the
development of scurvy. The first is dampness in the sleeping apartments
of the men. This should be prevented by ventilation, drying stoves, and
taking care that no wet garments are permitted to remain in the
apartments. They should be taken off immediately and hung outside to
dry, and under no circumstances should the men be permitted to sleep in
them, as is sometimes done.

Exposure to cold is unavoidable under certain conditions, and the men
should then be protected by proper clothing adapted to the weather.
Protracted fatigue is a third favoring circumstance, and the crew
should be spared all the strain of hard work possible, especially in
high latitudes. The apartments should also be kept well ventilated and
scrupulously clean; and, lastly, depressing mental emotions, which are
so apt to arise from exposure to danger and want, should be dispelled
by cheering assurances, constant occupation, and whatever amusements
can be had. These are the chief influences which are to be considered
in adopting measures to prevent the occurrence of scurvy in
communities, armies, on shipboard, or in persons confined in houses of
detention.

The therapeusis of scurvy presents no intricate problems for solution.
Its origin in dietetic errors is admitted by almost common consent, and
it is surprising with what rapidity patients apparently beyond hope of
recovery gather health and strength with a change in the character of
the food. This is indispensable in the treatment, as drugs have little
or no curative influence without it; and, therefore, the first object
should be to supply the patient with lemon-juice or acescent fruits and
fresh vegetables, as garlic, mustard, cresses, sorrel, nasturtium,
taraxacum among the wild plants, and potatoes, onions, turnips, beets,
radishes, etc. among the domesticated plants. And in conjunction with
these fresh meats, in the form of soups if the solids cannot be
masticated, may be used with advantage. Ordinarily, the dietetic
treatment alone will suffice to re-establish the health. Should,
however, convalescence be delayed, the vegetable bitters with the
mineral acids and ferruginous tonics and quinia will furnish useful
adjuvants. These are the standard remedies; others have been
recommended at various times, as the juice {185} of the maguey, a
Mexican plant, potassium nitrate alone or combined with vinegar,
tincture of cantharides, etc.

Attention will often be required to the various scorbutic
complications, especially stomatitis, which is always a source of
discomfort and suffering. One of the best local applications for this
is pencilling the parts with a solution of nitrate of silver, which
often affords marked relief. Mouth-washes, composed of solutions of
chlorinated lime, potassium permanganate, carbolic acid, are beneficial
by suppressing foul odors, exercising local stimulative action upon the
gums, and promoting healing. Should ulceration attack the legs, as is
often the case, the application of mild astringents and stimulative
ointments will be all that is required. The parts should, of course, be
kept clean and protected from irritation by protective dressings.

Hemorrhages from the nose, gums, stomach, bowels, or into the serous
cavities should be treated upon the general principles applicable to
their character, as the local use of cold, astringents, and the
internal administration of haemostatic agents--lead acetate, ergot,
tincture of iron, and other remedies, vegetable and mineral, of this
class. In desperate cases effusions into the chest, threatening death
by interfering with the respiratory and circulatory organs, may render
operation necessary as the last resort for their removal.

During the treatment it is important to obviate any sudden or severe
strain upon the heart by premature movements or exercises, as this is
fraught with danger.




{186}

PURPURA.

BY I. E. ATKINSON, M.D.


It has been customary with authors to describe under the general
heading Purpura a number of affections presenting as a common symptom
the extravasation of blood into the tissues, more especially of the
skin and mucous membranes, quite irrespective of etiological or
pathological considerations. Thus, the tiny ecchymoses caused by the
bites of fleas have been denominated purpura pulicosa; the larger
bruises resulting from external violence, purpura traumatica; the
extravasations occurring in the course of scurvy, purpura scorbutica;
those encountered in malignant small-pox, purpura variolosa; and so on.
These affections, differing widely in nature, possess as a common
symptom the escape of blood from the vessels into the tissues. It is
evident, therefore, that in the sense often employed the term purpura
is used to describe a symptom or symptoms common to a variety of
non-related maladies.

If there be a peculiar morbid process having for its constant and
characteristic symptom the spontaneous escape of the blood from the
blood-vessels, it is plain that interstitial hemorrhage from external
violence or from the action of a definite poison circulating in the
blood and disorganizing it and its containing vessels, as in
phosphorus-poisoning, or from the influence of certain zymotic
diseases, should not be designated by the title properly belonging to a
substantive malady. The question, therefore, is: Are there groups of
symptoms indicating morbid action of definite character, but of varying
intensity, to which the name purpura may with propriety be applied?

In the present light of pathological science it is impossible to answer
this question in the affirmative without considerable qualification. It
must be confessed that we do not possess a knowledge of any definite
chain of morbid processes constituting a distinct disease that may be
designated as purpura. And yet we are able to recognize a set of
symptoms varying greatly in intensity, from the most trivial petechial
eruption to profuse and fatal hemorrhages, accompanied by a train of
manifestations which we are unable to connect with any of the causes
already spoken of, and which, indeed, depend upon no fixed exciting
cause with which we are acquainted. It may be eventually proven that
purpura, even as we understand it, is merely a set of phenomena due to
widely-differing influences acting upon the blood and blood-vessels,
and that the term will disappear from our nomenclature as indicating a
disease, but will be preserved as denoting a symptom. For the present,
{187} purpura is understood to be a group of symptoms characterized by
the effusion of blood into the tissues of the body, or upon its free
surfaces, or into its serous cavities, which seem to arise
spontaneously, and for which we are unable to assign a definite cause.
With this view of the nature of purpura it becomes necessary to exclude
from present consideration blood-extravasations from internal or
external violence, the action of the specific principles of contagious
or infectious fevers, the dyscrasia of scurvy, the influence of
poisonous substances, and, in a word, any of those affections of which
the escape of blood from the vessels constitutes an epi-phenomenon.

Purpura may be conveniently considered as presenting three varieties:
1, purpura simplex; 2, purpura haemorrhagica; 3, purpura rheumatica.

These three forms of the disease are not distinguished by
sharply-outlined differences, but merge the one into the other, now
one, now another set of symptoms predominating. To these may be added,
likewise for convenience, three sub-varieties--purpura urticans,
purpura papulosa, and purpura nervosa. The difference between these
forms of purpura should not be considered as of more than clinical
import. Whatever variations present themselves may with probable
propriety be ascribed to complicating influences.

PURPURA SIMPLEX.--This is the mildest form of purpura, and may in many
cases readily escape observation. It may begin abruptly, in the midst
of health, without the slightest subjective symptom, or the
extravasations may be preceded for several days by some discomfort,
aching of limbs, sluggishness, anorexia, even a small amount of fever.
The eruption usually appears first upon the lower extremities,
preferably the flexor surfaces of the thighs (Duhring), but frequently
upon the legs. It extends from these points to the upper extremities
and trunk, usually sparing the face. The lesions vary in size from that
of a pin-head to that of a fingernail (petechiae), or they may be
linear (vibices). They remain discrete, and do not increase in size
throughout their course. Each spot of hemorrhage will endure for from
one to two weeks. At first the lesions are of a livid red color, and
declare their extra-vascular nature by remaining unaltered when
subjected to pressure. The color of these spots changes, as in ordinary
ecchymosis, in consequence of the metamorphoses of the haematin
preparatory to its final absorption, from crimson to purple, to blue,
to green, to yellow, and finally fades away. When recent, the spots
appear sharply outlined, with sometimes a faint encircling zone of
hyperaemia, but as they become older their margins grow indistinct.
While the early lesions slowly disappear, others continue to develop,
and the affection may thus be protracted for weeks. At times the
petechiae appear in crops, recurring every few days, the patient at one
time apparently nearly well, at another time worse than ever. Finally,
the symptoms definitely disappear, to return no more, or they pass into
those of other forms of purpura. During the course of purpura simplex
the blood-vessels of the skin alone are affected, the deeper tissues
and mucous membranes probably remaining unchanged.

Throughout the attack the general health may--usually does--remain
good. As an occasional symptom there will be observed a few vesicles or
blebs, containing blood, upon the skin. The extent of the general
eruption may vary from a few scattered petechiae to a copious and
startling {188} number of purpuric spots. The maintenance of the
upright position tends to perpetuate the evolution of the lesions.

In elderly persons purpura simplex is sometimes observed, and has been
described by many writers as purpura senilis. Hillier, following
Bateman, describes it as occurring in old women "upon the outside of
the forearms in successive dark, purple blotches of an irregular form
and various magnitude."[1] Aged men as well as women are liable to the
affection, which may quite as well appear upon the lower extremities of
either sex. It is altogether likely, however, that in such cases
degenerations of the vascular walls alone may cause the extravasations.

[Footnote 1: Reynolds's _System of Medicine_, vol. i. p. 792.]

PURPURA HAEMORRHAGICA (MORBUS MACULOSUS WERLHOFII).--In this form of
purpura there are added to the symptoms of purpura simplex hemorrhages
into and from the various mucous tracts, the nasal, faucial,
pharyngeal, gastric, intestinal, renal, uterine, rarely the pulmonary
mucous membranes, and exceptionally into the various serous membranes
and cavities. It may begin abruptly, in the midst of apparently
vigorous health, or after premonitory symptoms extending over several
days, vague sensations of discomfort--headache, pains, anorexia,
indisposition to exertion, and the like--or it may occur as a
transition from other forms of purpura. Usually there is no fever.

The hemorrhagic spots upon the skin appear much as in purpura simplex,
though the lesions are larger, acquiring the size of coins or even of
the palm of the hand. Spots soon appear upon the visible mucous
membranes, and free hemorrhages occur; indeed, the latter may be the
first symptom observed. Epistaxis is of most common occurrence, but
bleeding from the mouth, stomach, and intestines almost as frequently
results. The gums are almost constantly affected, and upon inspection
these may be found covered with blackish scabs, upon removal of which
the mucous membrane will be found pale and not swollen--an important
point in diagnosticating this affection from scurvy. Vesicles and blebs
filled with blood form both on the skin and mucous membranes. They
quickly rupture and discharge their contents. Bleeding from the stomach
and intestines is revealed--in the former case by the vomiting of a
brownish material resembling coffee-grounds; in the latter case by the
passage of black, tar-like evacuations. Pulmonary hemorrhage is to be
distinguished from haematemesis by the frothy and arterial character of
the blood. Haematuria may proceed from any part of the urinary tract.
Bleeding from several parts may occur at the same time, and may be very
copious.

In the mucous membranes extravasations of greater or less extent may
occur, as in the derma. Into the serous membranes they may take place
with or without effusion into serous cavities. It is only, however, in
cases that will almost certainly end fatally that the effusions into
these cavities are encountered. Hemorrhages into the substance of the
lungs, into the brain and other viscera, as well as into the tissues
generally, are occasionally observed.

At the outset of these bleedings the general health of the patient may
appear unimpaired, and if they be few in number and moderate in extent
but slight evidences of debility may be shown throughout the attack;
but it is often the case that the loss of blood is excessive and long
continued, and symptoms of profound anaemia supervene. The {189}
patient becomes greatly exhausted; intense pallor is developed, shortly
followed by general oedema. Attacks of syncope appear, and in fatal
cases--which are not common--death results from asthenia. This result
may occur after a few days from the profuseness of the hemorrhage;
usually, however, only after several weeks. Throughout the attack the
cutaneous lesions continue to develop, either irregularly or in
successive outbreaks, scattered over the general surface, involving the
face less frequently than other parts. These spots undergo the
color-changes peculiar to extravasated blood, and may be seen in all
the stages of involution in the same patient. Fever, usually absent
throughout the attack, may appear at the height of the affection, but
does not run high. Local inflammations are exceedingly rare. In
favorable cases recovery follows the gradual mitigation and
disappearance of the symptoms, but relapses frequently occur, and
convalescence may be retarded for months.

PURPURA RHEUMATICA (PELIOSIS RHEUMATICA).--Schoenlein in 1829 described
as peliosis rheumatica an affection in which the symptoms of purpura
simplex were associated with pain and often with effusion into the
joints, especially those of the knee and ankle. He considered it as an
independent malady. This opinion has been shared by Fuchs, Hebra,
Kaposi, Neumann, and many others. Kaposi[2] regards it as related to
erythema nodosum, with which affection, indeed, it possesses some
features in common. It probably, however, constitutes a complication of
ordinary purpura. That it is not primarily rheumatic is shown by the
almost invariable absence of many of the symptoms characteristic of
rheumatism; that it cannot be an independent affection appears from its
intimate relations with other forms of purpura.

[Footnote 2: _Hautkrankheiten_, 1880, p. 277.]

Purpura rheumatica commonly begins with malaise, anorexia, debility,
sometimes with mild fever. The patient is soon attacked with pains, of
a more or less acute character, in the joints, especially the knees and
ankles. There may be some effusion into the joint and cutaneous oedema.
After a few days the nature of the complaint will be revealed by an
eruption of petechiae, first near the painful joints, but soon
extending, involving in many cases even the head and trunk. The
eruption may be at first slightly elevated and surrounded by a fine
halo of hyperaemic injection.

The pains usually subside upon the appearance of the eruption, and the
malady may be completed after a single outbreak. More commonly new
joint-pains are experienced, fresh crops of petechiae appear, and the
trouble may be prolonged for weeks, even months, the patient meanwhile
suffering not very greatly in general health. The lesions may be
cutaneous only; rarely bleeding from mucous surfaces will occur
(Scheby-Buch). Albuminuria may be present (Kaposi). An annual type is
said by Kaposi, Neumann, and others to be sometimes observed, the
spring and autumn being the usual seasons for the outbreaks. This is
supposed to indicate a relationship with erythema nodosum and
multiforme. Cardiac murmurs have been detected in the course of purpura
rheumatica,[3] but these were probably anaemic or antedated the
purpuric symptoms. Purpura rheumatica never seems to result in endo- or
pericarditis.

[Footnote 3: Kinnicutt, _Archives of Dermatology_, i. p. 193; Molliere,
_Ann. de Dermatol._, v. p. 44.]

SUB-VARIETIES.--Henoch[4] and Couty[5] have described a form of {190}
purpura mostly observed in children, in whom rheumatoid pains occur
along with colic and vomiting of greenish or bilious matter, tenesmus,
and sometimes with loss of blood from the bowels. The disease may be
protracted throughout months by relapses. Cutaneous oedema frequently
occurs. Couty regards it as a form whose peculiarities justify its
assignment to a position of its own. The cause of the associated train
of symptoms is supposed (Couty) to reside in the sympathetic system,
and the name purpura nervosa is proposed for it. So many features of
ordinary purpura are manifested in these cases that it seems better to
consider them as examples of ordinary purpura complicated with
gastro-intestinal derangement. It has been suggested that the nausea,
vomiting, and abdominal pains may result from extravasation of blood
into the peritoneal tissue.[6]

[Footnote 4: _Berl. Klin. Wochenschr._, 51, 1874.]

[Footnote 5: _Gaz. Hebd._, 36 _et seq._, 1876.]

[Footnote 6: Immermann, _Ziemssen's Cyclopaed._, vol. xvii. p. 265.]

In the course of purpura there is frequently observed, more especially
in purpura simplex, a wheal-like arrangement of the eruption--such,
indeed, as occurs in urticaria. The term purpura urticans has been
given to this sub-variety, which may or may not be accompanied by
itching. Scheby-Buch has suggested that the urticaria may, with more
propriety, be attributed to the gastric disturbances that so often
accompany the forms of purpura presenting it.[7] The wheals are usually
seen upon the lower extremities, but may appear elsewhere. A
considerable degree of oedema may be present, particularly in lax
tissue, such as that of the scrotum, eyelids, etc.

[Footnote 7: _Deutsche Arch. f. Klin. Med._, B. xiv. p. 490.]

Purpura papulosa (lichen lividus, Willan) is a form of purpura where,
in the midst of ecchymoses, livid papules appear. These probably depend
upon a large amount of hemorrhage occurring within a limited space,
most often surrounding the orifices of hair-follicles, because these
are supplied with a capillary network that comes directly from the
deeper layer.[8] They are formed most abundantly on the legs of
scrofulous, cachectic persons who have purpura. Care must be taken to
distinguish this form of purpura from erythema multiforme and erythema
nodosum, where blood is usually extravasated secondarily into the
tissues. Those cases only where the purpura is primary should be
recognized as purpura papulosa.

[Footnote 8: Hebra, _Skin Diseases_, New Syd. Soc. Transact., ii. p.
425.]

The purpuric effusion appears to act as an irritant upon the tissues,
and to excite inflammation. Gangrene of the mucous coat of the
intestines has resulted from extensive hemorrhagic extravasations, and
from a similar cause cutaneous gangrene has been known. These
complications, however, are rare.

ETIOLOGY.--The immediate causes of purpura are quite unknown. Both
sexes and persons of every age are affected by it. While it is most
often seen in debilitated subjects, those in vigorous health possess no
immunity. It has often been observed during convalescence from other
maladies. It cannot be said that those who are miserably clothed, fed,
and lodged are especially predisposed to attacks of purpura. Between
purpura and haemophilia, etiologically, there are many points of
difference. Purpura is not hereditary, nor is there a purpuric
diathesis in the strict sense of the term. Some persons, indeed, seem
to possess a {191} predisposition to the disease, and some authors
claim for purpura rheumatica a distinct annual type. This, however, is
not at all certain.

Recently it has been claimed that purpura haemorrhagica depends upon
the presence of a minute organism in the blood. Petrone[9] injected
blood drawn from patients with this disease under the skin of rabbits,
producing widely-distributed hemorrhages. In the blood of these
individuals and of the injected rabbits micrococci and bacilli were
detected. Watson Cheyne[10] also describes a plugging of the
capillaries with bacilli. These were 1/7700 of an inch in length and
1/20000 of an inch in diameter, and were arranged in colonies. In
another case there were found micrococci arranged in chains. These
swarmed in the capillaries and some larger vessels, and sometimes
completely blocked them. Although an origin in infection has thus been
claimed for purpura haemorrhagica, the fact that more than one variety
of micro-organism was observed cannot fail to excite suspicion of,
possibly, erroneous observation.

[Footnote 9: _Lo Sperimentale_, 51, 1883.]

[Footnote 10: _Lancet_, i., 1884, 344.]

PATHOLOGY.--In the foregoing description those extravasations of blood
due to simple mechanical violence, as from flea-bite, and sudden
increase of blood-pressure, as in the effort of coughing in whooping
cough, also from the deleterious influence exerted upon the
blood-vessels and blood by certain drugs, the specific fevers, Bright's
disease, and the like, have been excluded. Only those have been
considered where the effusion of blood seemed to occur spontaneously,
and the symptoms to result from some peculiar but not understood morbid
process. The hemorrhage is but a symptom; the process by which it is
brought about depends upon some change in the blood or blood-vessels.
We do not know what these subtle changes are. The blood of purpuric
patients has been carefully examined, but, with the exception above
mentioned, no definite changes have been discovered. Immermann[11]
found during the first stage of the disease the blood-corpuscles
perfectly normal in appearance, the white corpuscles subsequently
slightly exceeding the red in number--a simple result of copious
hemorrhage. No stated chemical changes in the blood are known in
purpura, nor is it known how the blood escapes from the vessels. It
undoubtedly escapes through alterations in the vascular wall, but it is
also true that red blood-corpuscles, as well as the pale ones, may find
their way in considerable numbers through the unruptured wall of the
vessels, per diapedesin, as was first suggested by Velpeau, but
definitely determined by Stricker. The causes of this migration are
obscure. Immermann[12] asserts that a fatty degeneration of the
vascular tissues and of the muscles takes place. This, however, is
manifestly a result of the loss of blood, and not its cause. Dr. Wilson
Fox[13] found extensive albuminoid disease of the muscles and
capillaries of the skin; but the albuminoid degeneration involved
several organs of a patient with syphilis, and the purpura was
certainly secondary to the morbid conditions. Rigal and Cornil[14]
think that the hemorrhages are a result either of sympathetic
irritation or of diminished action of the vaso-motor centre. It is
indeed altogether likely that the cause will ultimately be found to
reside in the vaso-motor system.

[Footnote 11: _Ziemssen's Cyclop._, xvii. p. 258.]

[Footnote 12: _Loc. cit._]

[Footnote 13: _Brit. and Foreign Med.-Chir. Review_, Oct., 1865.]

[Footnote 14: _L'Union Med._, 5, 6, 7, 1880.]

{192} DIAGNOSIS.--The affection bearing the closest resemblance to
spontaneous purpura is scurvy; indeed, its supposed relationship to
this disease has given purpura one of its synonyms, land scurvy. The
two affections, however, are probably without the slightest
relationship. They possess in common the hemorrhagic symptoms, both in
the tissues and from free surfaces, but the resemblance does not extend
much beyond this. Scurvy depends upon deprivation of fresh vegetable
food and the use of unsuitable and insufficient food generally, and
upon bad hygienic surroundings. Purpura may--frequently does--appear in
broken-down constitutions, but it equally attacks the strong and
vigorous, while the character of food exerts no special influence on
its production. Scurvy only follows long-continued privations and as a
culmination of a train of distressing symptoms. Purpura appears in the
midst of health, or after brief premonition, or during convalescence
from totally unrelated diseases. In scurvy there is a decided tendency
toward ulceration, which is absent in purpura. In scurvy the mouth and
gums inflame and ulcerate, the latter becoming swollen, spongy, and of
a bluish-red color. In purpura, ulceration of the buccal mucous
membrane does not occur, and the gums are pale and intact. The curative
influence of fresh vegetables, lime-juice, etc. in the treatment of
scurvy is not observed in purpura. It has been claimed that purpura is
but a mild degree of scurvy: this cannot be so, for we may have a mild
scurvy or a severe, even fatal, purpura.

The hemorrhagic diathesis, or haemophilia, presents points of analogy
with purpura. Here, however, is found the almost constant history of
heredity and the implication only of persons of the male sex. The
disposition to bleed at all times upon the receipt of the smallest
injury is quite unlike the suddenly-developed and transitory
hemorrhages of purpura, which are also more generally distributed.

With the secondary hemorrhagic effusions and ecchymoses that occur in
conditions of profound alterations of the blood and blood-vessels in
cases of malignant small-pox, scarlatina, typhus fever, etc., and in
some cases of poisoning, as from phosphorus, spontaneous purpura
presents identities, but the history of the complaint and the condition
of the patient will prevent error. A knowledge of the circumstances
will serve to distinguish purpura simplex from the petechiae and small
ecchymoses produced by fleas, by diminished atmospheric pressure, by
coughing, in the course of Bright's disease, etc.

Purpura rheumatica presents, as has been shown, many points of
resemblance to erythema multiforme and erythema nodosum. The mild
fever, the joint-pains, the extravasations of the latter affections,
are much like the symptoms of this form of purpura. The nodular,
inflamed, tender condition of the lesions, their location--frequently
upon the extensor surfaces of the extremities--their course and
duration, usually serve to identify erythema nodosum, while with
erythema multiforme it is usually not difficult to observe its
essentially inflammatory character. Scheby-Buch has shown the
difficulties often opposed to the differentiation of purpuric lesions
and ecchymoses due to violence.[15] Where the petechial eruption of
purpura simplex is well marked, where the internal hemorrhages of
purpura haemorrhagica are copious, the inquiries of the observer will
usually lead him to correct conclusions. Where the {193} ecchymoses are
larger and upon exposed parts of the body, the diagnosis from the
lesions alone becomes impossible, and due consideration of all
concomitant circumstances is essential. It should be remembered that in
purpura very slight violence may call forth extensive ecchymosis. This
circumstance has important medico-legal bearings.

[Footnote 15: _Viertelj. f. Dermatol. und Syph._, 1879, p. 99.]

PROGNOSIS.--Purpura usually terminates favorably. Its course runs from
two to six weeks, rarely longer. Relapses and remissions are frequent.
Purpura simplex is of very little gravity, and need excite little
apprehension. Purpura rheumatica almost always ends in recovery; fatal
terminations, however, have been known. Purpura haemorrhagica is of
much more serious import. Even here, however, though the patient may
fall into profound debility from loss of blood, recovery is the rule,
the symptoms gradually diminishing in severity until health becomes
re-established. In fatal cases death ensues after prolonged and profuse
losses of blood. Purpura may subside after a single outbreak or many
relapses, and recrudescences may occur extending through months.
Anaemia may persist long after the disappearance of purpuric symptoms.
A tendency to purpura may be shown at irregular intervals for years,
and even throughout life.

TREATMENT.--Very mild cases of purpura simplex require no treatment,
not even confinement within doors. The patient is often first made
aware of his disease by accident; doubtless it frequently escapes
detection altogether. It has been observed that purpura often appears
upon the lower limbs of convalescents from other diseases when they
first essay the upright position. Relapses of purpura also frequently
appear as the patient leaves his bed. We have here an important
indication for treatment--viz. the maintenance of the recumbent posture
in cases of any degree of severity. Fresh vegetables and vegetable
acids do not have the same happy influence as in scurvy. It is
manifestly important that appropriate food should be administered in
sufficient quantity, both to improve the general health and to repair
the exhausting losses of blood. Milk is an exceedingly valuable article
of diet in these cases, being but little apt to irritate the mucous
membrane of the alimentary canal.

The patient should be guarded against violence. Injuries that may be of
no consequence to healthy persons may excite in the purpuric profuse
hemorrhage, free or interstitial. Violent emotions and physical efforts
should be avoided, as in stimulating the heart's action a condition of
increased blood-pressure ensues that may readily result in
extravasation.

There are no remedies that exert a specific influence over purpura, and
yet quite a number have enjoyed, and still enjoy, high reputation in
controlling the symptoms. Probably the most frequently employed remedy
against purpura is sulphuric acid, preferably the aromatic sulphuric
acid, in doses of from 15 to 20 drops, diluted well with water and
administered every third or fourth hour. It is certainly an agent of
value, though some authors maintain that it has no efficacy
(Immermann). Acetate of lead undoubtedly exercises an influence over
the course of the disease. More recently, ergot has been employed. Its
use has been highly extolled by Buckley and others. Very large doses
may be given. The hypodermic use of ergotin has been followed by
results most gratifying to those employing it. Oil of turpentine has
enjoyed considerable reputation. A remedy that undoubtedly has a good
effect is iron, both as {194} exercising a controlling action over the
bleeding and as assisting to repair the resulting anaemia. The tincture
of the chloride is the most suitable preparation, and may be given in
large doses (from minim xx to fluidrachm ss), well diluted, every
fourth hour. Care must be exercised to avoid irritating the digestive
organs with it. Formerly, venesection was employed to prevent the
occurrence of hemorrhage, but its efficacy in this direction is at
least doubtful, and cannot but help to intensify the disastrous
consequences of severe and protracted attacks.

The various complications that may arise, as well as the general
results of purpura, must be treated symptomatically. For the mucous
membranes astringent washes should be used, and in favorable situations
the tampon may sometimes be employed with profit. In purpura rheumatica
the arthritic pains will be alleviated by anodyne liniments and
plasters, and the often accompanying abdominal pains and colic by
anodynes internally administered. Haematemesis, haematuria, etc. must
be treated upon general principles. The results of profuse hemorrhage
must be combated with stimulants. Transfusion of blood has been
proposed and practised for the extreme anaemia that sometimes occurs,
but without encouraging results. If necessary, the bowels may be kept
free by mild aperients. In severe cases rest in bed should be rigidly
enforced until after the establishment of convalescence. Quinia, iron,
and nux vomica are indicated above all other remedies for the anaemia
resulting from an attack of purpura.




{195}

DIABETES MELLITUS.

BY JAMES TYSON, A.M., M.D.


Diabetes mellitus is a term applied to a group of symptoms more or less
complex, of which the most conspicuous is an increased flow of
saccharine urine--whence the symptomatic title. It is associated with a
derangement of the sugar-assimilating office of the liver, as the
result of which an abnormally large quantity of glucose is passed into
the hepatic vein and thence into the systemic blood, from which it is
secreted by the kidneys. The condition is sometimes associated with
alterations in the nervous system, at others with changes in the liver
or pancreas, while at others, still, it is impossible to discover any
structural alterations accompanying it.

[Illustration: FIG. 1. To show the position of the punctures required
to produce glycosuria, the lobes of the cerebellum are separated. Below
are seen the restiform bodies, the divergence of which circumscribes
the apex of the calamus scriptorius and the fourth ventricle. The
puncture _p'_ produces glycosuria; the puncture _p_, glycosuria with
polyuria; and a puncture a little higher up than _p_, albuminuria.]

PATHOLOGY AND PATHOGENESIS.--Notwithstanding that this disease has been
recognized for two centuries and a half, that abundant opportunity has
been furnished for its post-mortem investigation, and that experimental
physiology has contributed much information bearing upon the subject,
its pathology is still undetermined. Experiment has, however, rendered
it very likely that all cases of essential glycosuria--that is, all
cases in which saccharine urine is not the direct result of
over-ingestion of sugar or sugar-producing food--are accompanied by a
hyperaemia of the liver. This hyperaemia, with its consequent
glycosuria, can be induced by puncturing or irritating the so-called
diabetic area[1] in the medulla oblongata. This area corresponds with
the vaso-motor centre, and with the roots of the pneumogastric or vagus
nerve in the floor of the fourth ventricle; whence it was at first
inferred that this nerve is the excitor nerve of glycosuria. It was
soon ascertained, however, that when the pneumogastric was cut,
glycosuria ensued only when the central end was stimulated, while {196}
stimulation of the peripheral portion was without effect. Whence it
became evident that this nerve is not the excitor, but the sensory
nerve concerned in glycogenesis.

[Footnote 1: The diabetic area, as marked out by Eckhard, and which
corresponds with the vaso-motor area, as defined by Owsjannikow
(_Ludwig's Arbeiten_, 1871, p. 21), is bounded by a line drawn four or
five mm. above the nib of the calamus scriptorius, and another about
four mm. higher up.]

It was also learned in the course of continued experiment that
glycosuria resulted upon transverse section of the medulla oblongata,
of the spinal cord above the second dorsal vertebra, of the filaments
of the sympathetic accompanying the vertebral artery, upon destruction
or extirpation of the superior cervical ganglion, and sometimes, but
not always, after division of the sympathetic in the chest (Pavy); also
after section or careful extirpation of the last cervical ganglion,
section of the two nerve-filaments passing from the lower cervical to
the upper thoracic ganglion around the subclavian artery, forming thus
the annulus of Vieussens,[2] and after section or removal of the upper
thoracic ganglion.

[Footnote 2: Cyon and Aladoff, reprint from the _Melanges biolgiques_
and _Bulletin de l'Academie Imperiale de Petersbourg_, vol. xiii. p.
91; cited by Dr. Brunton in the Lectures named in note on p. 198; also
_British Medical Journal_, Dec. 23, 1871, p. 731.]

[Illustration: FIG. 2. The last cervical and first thoracic ganglia,
with circle of Vieussens, in the rabbit, left side. (Somewhat
diagrammatic, many of the various branches being omitted.)

_Trach._, trachea; _Ca._, carotid artery; _n. vag._, the vagus trunk;
_n. rec._, the recurrent laryngeal; _sym._, the cervical sympathetic
nerve ending in the inferior cervical ganglia, _gl. cerv. inf._ Two
roots of the ganglion are shown--_rad._, the lower of the two
accompanying the vertebral artery, _A. vert._, and being the one
generally possessing accelerator properties; _gl. thor. pr._, the first
thoracic ganglion. Its two branches, communicating with the cervical
ganglion, surround the subclavian artery, forming the annulus of
Vieussens. _sym. thor._, the thoracic sympathetic chain; _n. dep._,
depressor nerve. This is joined in its course by a branch from the
lower cervical ganglion, there being a small ganglion at their
junction, from which proceed nerves to form a plexus over the arch of
the aorta. It is this branch from the lower cervical ganglion which
possesses accelerator properties, hence the course of the accelerator
fibre is indicated in the figure by the arrows. (Modified from Foster's
_Physiology_.)]

All these operations paralyze the vaso-motor nerves by which, in
health, the blood-vessels of the liver are kept in a state of tonic
contraction; hence these vessels dilate when the nerves are cut. From
the facts named we also learn the path of the glycogenic influence,
which must be from the medulla oblongata into the spinal cord, thence
by the filaments of the {197} sympathetic which accompany the vertebral
artery into the lower cervical ganglion; thence through the annulus of
Vieussens into the first dorsal ganglion; and thence through the
prevertebral cord of the sympathetic, and branches not precisely
determined, to the hepatic blood-vessels as shown by the dotted line in
Fig. 3.

[Illustration: FIG. 3. Diagram showing the course of the vaso-motor
nerves of the liver, according to Cyon and Aladoff. These nerves are
indicated by the dotted line which accompanies them: _a_, vaso-motor
centre; _b_, trunk of the vagus; _c_, passage of the hepatic vaso-motor
nerves from the cord along the vertebral artery; _d_, fibres going on
each side of the subclavian artery and forming the annulus of
Vieussens; _e_, first dorsal ganglion; _f_, ganglionated cord of the
sympathetic; _g_, the spinal cord; _h_, the splanchnic nerves; _i_,
coeliac ganglion, from which vaso-motor nerves pass to the hepatic and
intestinal vessels; _k_, the lungs, to which fibres of the vagus are
seen distributed; _l_, the liver; _m_, the intestine; _n_, the arch of
the aorta.]

I say, by branches of the sympathetic not precisely determined, because
our power to produce artificial diabetes fails below the first thoracic
ganglion; for section of the sympathetic between the tenth and twelfth
ribs, and of the splanchnics, is not followed by glycosuria, although
the vaso-motor nerves to the liver are known to pass through them.

According to Eckhard,[3] the phenomena of artificial glycosuria are
irritative and not paralytic. This view he believes sustained by his
own experiments, according to which if the splanchnics, through which
{198} the vaso-motor nerves of the liver pass, are cut prior to the
diabetic puncture, not only does this operation fail to produce
glycosuria, but it even renders ineffectual the puncture itself as well
as the section higher up. But Cyon and Aladoff remind us that it is not
mere dilatation of the hepatic vessels, but increased velocity in the
movement of the blood, which deranges the sugar-assimilating function
and causes glucose to appear in the urine. The vaso-motor nerves of the
intestinal blood-vessels also pass through the lower part of the
sympathetic and the splanchnics, and section of the latter must cause
these blood-vessels to dilate. Now, in rabbits, in which this
experiment is usually performed, the digestive canal is very long, and
the blood-vessels so capacious that when dilated they hold as much
blood as all the rest of the vascular system together, so that when the
lower sympathetic and splanchnics are cut, so much blood goes into the
intestines that the increased velocity required in the blood-vessels of
the liver to produce glycosuria is impossible. But if the vessels of
the liver be first dilated by puncturing the floor of the fourth
ventricle, section of the sympathetic or of the splanchnics may then be
made without arresting the formation of sugar; whence it would appear
that the glycogenic influence may still pass through the lower
sympathetic and splanchnics.

[Footnote 3: _Beitrage zur Anat. und Physiologie_, iv., 1859, p. 1;
vii., 1873.]

In view of the fact that Eckhard[4] has failed to confirm the results
of Cyon and Aladoff, but has traced the glycogenic influence down the
spinal cord as far as the fourth dorsal vertebra in rabbits, and even a
little lower, and that Schiff[5] has shown that diabetes sometimes
results after section of the anterior columns of the cord between the
medulla and the fourth cervical vertebra, Dr. Brunton[6] suggests that
the vaso-motor nerves of the liver may not always leave the spinal cord
to join the sympathetic by the branches accompanying the vertebral
artery, but sometimes pass farther down the cord, leaving it by the
communicating branches to some of the dorsal ganglia, as indicated in
Fig. 4.

[Footnote 4: _Beitrage zur Anat. u. Physiologie_, viii., 1877, p. 79.]

[Footnote 5: _Untersuchungen uber Zuckerbildung in der Leber_, 1859, S.
108.]

[Footnote 6: _Lectures on the Pathology and Treatment of Diabetes
Mellitus_; reprinted from the _British Medical Journal_, 1874, p. 12.]

[Illustration: FIG. 4. Diagram showing another course which the
vaso-motor nerves of the liver may take. The letters indicate the same
parts as in Fig. 3. The hepatic vaso-motor nerves are here represented
as passing lower down the cord than in Fig. 3, and leaving it by
communicating branches to the second dorsal ganglion. It is possible
that they may sometimes leave by the branches to the first, and
sometimes by those going to a lower, ganglion. In such cases any
irritation to the third or one of the other cervical ganglia may cause
diabetes by being conveyed along the vertebral artery and up the cord,
as indicated by the dark line, to the vaso-motor centre, where it may
cause reflex inhibition in the same way as any irritation to the
vagus.]

It is evident that an agency involving any part of this tract in such a
way as to paralyze the vaso-motor nerves of the liver is capable of
producing glycosuria. Such cause may operate upon the central ganglia
whence the nerves emanate, as the vicinity of the oblongata and upper
parts of the spinal cord or the coeliac ganglion and its branches,
including those to the pancreas. Or the irritation may be peripheral
and its effects reflex. We have seen that irritation of the central end
of the cut vagus will produce glycosuria. Any irritation, therefore,
involving the peripheral distribution of this nerve may produce it.
Hence embarrassed respiration, whether due to disease of the
respiratory passages, strangulation, or inhalation of irrespirable
gases and anaesthetics, produces glycosuria in dogs and rabbits; and
this symptom has been known to attend these conditions in the human
subject. So, too, glycosuria may be produced by such substances as
woorara, strychnia, morphia, and phosphoric acid, introduced into the
blood and irritating the terminal filaments of the pneumogastrics, or
it may be brought about secondarily through the embarrassed respiration
these drugs produce. Such peripheral {199} irritation may reside also
in the stomach, intestines, liver, or any organ to which the
pneumogastric is distributed.

It is not unlikely that irritation of the extremities of sensory nerves
other than the pneumogastric may become the cause of reflex glycosuria.
Even puncture of the floor of the fourth ventricle itself may be reflex
in its operation, the roots of the pneumogastric being thus irritated.
The effect of the irritation conveyed to the glycogenic centre is to
inhibit the usual tonic influence of the vaso-motor nerve upon the
vessel walls. Among the experimental irritations, in addition to
puncture of the floor of the fourth ventricle, which produce glycosuria
by reflex action, are injuries of the cerebral lobes and cerebellum,
optic thalami, cerebral peduncles, pons varolii, middle cerebellar
peduncles, and even of the sciatic nerve and brachial plexus; whence it
may be inferred that pathological irritation in the same situations may
result in a glycosuria, which is temporary or permanent according as
the irritation is temporary or permanent.

Finally, there is no reason why an inhibitory reflex action should not
originate in the sympathetic itself. When we remember that this nerve
is both sensory and motor in function, and that the inhibitory
influence to which the heart's action is subject is accomplished
through the sympathetic as a sensory nerve and the pneumogastric as a
motor, there is no reason why similar results may not be brought about
by the sympathetic alone. This being the case, we need not ascribe
glycogenic phenomena to irritation in Eckhard's sense--that is, to a
direct stimulant action of the irritant upon the vaso-motor nerves of
the liver--but may suppose a sensory influence to ascend one set of
sympathetic filaments and an inhibitory influence to descend through
another.

Dr. Pavy has recently put forward some chemical theories which explain
the action of the hyperaemia in producing glycosuria, but they do not
account for the hyperaemia itself. In healthy digestion the
carbohydrates (starch and sugar) are converted, not into glucose, but
into maltose, C_{12}H_{22}O_{11}, dextrin being intermediate in
composition. Maltose is absorbed and assimilated, converted into
glycogen. So, too, when glucose is ingested as such, it is converted by
the glucose ferment into maltose in the stomach and intestines. For the
proper production of maltose and its assimilation a good venous blood,
producing a maltose-forming ferment, is necessary. In diabetes, in
consequence of the dilatation of the arteries of the chylopoetic
viscera, the blood enters the liver too little deoxygenated, and a
glucose-forming ferment is produced. The glucose thus formed is not
assimilable, but passes off into the circulation and the urine.

MORBID ANATOMY.--Such are some of the facts bearing upon the pathology
of diabetes mellitus. Throwing out the milder type of cases, in which
glycosuria is the result of an over-ingestion of saccharine and
sugar-producing food--and these can scarcely be called instances of
essential diabetes--it is evident that glycosuria may be produced in a
variety of ways operating through the nervous system; and accordingly
we may infer that there is scarcely an organ in close relation with the
sympathetic system derangement of which is not capable of producing it.
Among these we would naturally expect to find conspicuous alterations
in the nervous centres, and yet I have never found changes in these
centres after death. At the same time, others have noted meningitis,
tubercular {200} and traumatic, apoplectic effusions, and tumors of the
brain, especially in the neighborhood of the medulla oblongata. The
alterations in the nerve-centres described by Dickinson as the
essential morbid anatomy of diabetes I have looked for in vain. These
changes are described as a cribriform or porous condition of the white
nervous matter, said to be visible to the naked eye. The spaces thus
produced are partially occupied by dilated blood-vessels, which, in
turn, are surrounded by dilated perivascular sheaths and broken-down
nervous matter, into which extravasations of blood have taken place, as
evidenced by the presence of pigment-granules. The changes are found in
the white matter of the convolutions of the brain, but fewer and larger
in the central portions. The corpora striata, optic thalami, pons,
medulla, and cerebellum are favorite seats for the largest and most
striking holes. In rapidly-fatal cases the cavities are sometimes
filled with a translucent, gelatinous substance, containing, besides
vascular elements, the globular products of nervous disintegration. In
the more chronic forms of the disease, as it occurs in elderly persons,
the excavations are usually empty, although the elements of nervous
decay are still to be found fringing the margins or collected as an
irregular sheath upon the dilated or shrunken artery. There are changes
in the cord similar to those in the brain, but less decided. But the
most striking alteration in the cord, according to Dickinson, although
not always present, is dilatation of the central canal, which in the
dorsal and lumbar regions is sometimes expanded to many times its
normal diameter, and forms a conspicuous object immediately after the
cord is divided.

These alterations have eluded the vigilance of other pathologists who
have sought for them in well-determined cases of diabetes mellitus,
while they have been found, on the other hand, in the nervous centres
when no diabetes was present. In the recent discussion on diabetes at
the Pathological Society of London, Douglas Powell[7] seemed to be the
only one who was convinced that most of Dickinson's specimens were
examples of positive lesions.

[Footnote 7: _London Lancet_, May 5, 1883, p. 776.]

A hyaloid thickening of the blood-vessels of the brain has been noted
by Stephen Mackenzie[8] and Seymour Taylor[9] in some cases, and
miliary aneurisms of the retina in one.

[Footnote 8: Discussion on Diabetes, Path. Soc. of London, _London
Lancet_, April 7, 1883, p. 593.]

[Footnote 9: Ibid., _Lancet_, May 5, 1883, p. 774.]

Of other organs, one of the most frequently found diseased is the
pancreas, and, according to Senator, it is fair to assume that disease
of the pancreas is present in about one-half of all cases of diabetes.
As the result of increased experience, I am inclined to attach much
more importance to pancreatic disease as a cause of diabetes than I did
a few years ago. Among the changes found is a pseudo-hypertrophy, which
consists chiefly in a hyperplasia of the connective tissue, fatty
degeneration of the gland-cells, and atrophy of the glandular
structure; cancerous disease; calculous concretions in the ducts with
or without obstruction; and cystic dilatation.

Facts bearing upon the relation of pancreatic disease to diabetes have
been accumulating since Cowley first discovered calculi in the pancreas
of a diabetic, and Bright pancreatic cancer in a similar case. Since
then {201} instances have multiplied to such extent that it would be
unprofitable to enumerate them. But in 1877, Lancereaux[10]
communicated to the French Academy of Medicine specimens of profound
lesion of the pancreas from cases dying of diabetes mellitus. This, he
alleged, constitutes a special and distinctive variety of diabetes,
characterized by sudden onset, emaciation, polydipsia, polyphagia, and
peculiar alvine dejections. More recently, Depierre[11] has confirmed
these observations, apparently establishing this variety of diabetes
mellitus, of which a very rapid course--six months to three years--and
the habitual presence of diarrhoea are characteristic; while the
presence of greasy or creamy stools, and the appearance in them of
undigested nitrogenous substances, may aid in the diagnosis. Precisely
such a case, running the same rapid course--less than one year--with
emaciation, uncontrollable diarrhoea, creamy stools, jaundice, and
pancreatic disease, came under the writer's care in 1882. At the
autopsy the pancreas was found enlarged, and numerous gritty particles
were disseminated through it.

[Footnote 10: "Notes et reflexions a propos de deux cas de diabete
sucre avec alteration du pancreas," _Bull. Acad. de Med._, Paris, 1877,
2d Serie, vi. 1215-1240.]

[Footnote 11: _Med. News and Abstract_, vol. xxxix., June, 1881, p.
344, from _Jour. de Med. et de Chir. pratiques_, Dec, 1880.]

Supposing such pancreatic disease to be primary, it is evident that it
must operate through the coeliac plexus, which, with its ganglion, is
gradually encroached upon. On the other hand, it is also possible that
the disease of the coeliac plexus may be primary, and the coexisting
pancreatic disease and diabetes mellitus both secondarily dependent
upon it. This can only be settled by more careful study of the coeliac
plexus after death from diabetes, but up to the present time facts
would seem to support the view of primary pancreatic disease.

The liver is frequently enlarged--sometimes but slightly, at others
decidedly. It has been known to reach three times the size of the
normal organ. Again, it may be darker and harder--hyperaemic. By minute
examination the acini are found enlarged, the capillaries dilated and
distended; the liver-cells are enlarged, distinctly nucleated, rounded,
and indistinct as to their outline, appearing to fuse into each other.
A weak solution of iodine strikes a wine-red color, which, according to
Rindfleisch, is confined to the nucleus, but, according to Senator, may
extend to the whole cell. This reaction Klebs ascribes to post-mortem
changes in the glycogenic substance. They are more striking in the
portal or peripheral zone of the lobule, while the intermediate or
hepatic artery zone is often fatty, and the central part, surrounded by
the rootlets of the hepatic vein, is nearly normal. Stockvis and
Frerichs ascribe the enlargement of the liver partially to a new
formation of liver-cells--in other words, to a true hypertrophy. At
other times the organ has been found reduced in size.

Dickinson, Trousseau, and Budd describe an overgrowth of connective
tissue, as well as of the cells of the liver, producing a hypertrophic
cirrhosis.

According to Beale, Frerichs, and Folwarczny, the fat which is found in
small proportion in the liver-cells in health is often diminished, and
even absent, and quantitative[12] analysis by the last-named observer
{202} confirms this view. Such diminution may be the forerunner of an
atrophy of liver-cells which has been noted, and which, as the disease
continues, leads to the atrophy referred to as occasionally present. On
the other hand, intense fatty degeneration of the entire organ, similar
to that found in phosphorus-poisoning, has been met by Gamgee,
associated with a lipaemic state of the blood and symptoms of acute
acetonaemia.

[Footnote 12: Folwarczny, "Leberanalysen bei Diabetes Mellitus,"
_Wiener Zeitschr._, N. F., 1859, ii. 6.]

The kidneys, in cases which have continued some time, are apt to be
hyperaemic and enlarged, although primarily they are uninvolved. It
would seem that the long-continued hyperaemia which is a necessary
condition of the copious secretion of urine, results, sooner or later,
in an over-nutrition of the renal epithelium, a widening of the
tubules, and consequent enlargement of the whole organ. The changes are
mainly of a parenchymatous or catarrhal rather than an interstitial
nature, the epithelium being disposed to shed. These changes may reach
a more advanced stage of cellular degeneration, and may be attended by
albuminuria. The cells may become very large, present a yellowish-brown
color, their nuclei indistinct and non-responsive to ordinary staining
solutions, but may take a red stain with a weak solution of iodine,
similar to that described in the case of the liver-cells. Mackenzie
describes a hyaline degeneration of the intima of the arterioles and a
skeleton condition of the epithelium of the collecting tubes.[13] There
may also be a catarrh of the pelves of the kidneys and ureters, due to
irritation of the saccharine urine.

[Footnote 13: _Loc. cit._]

Atrophy of the testes has been noted by Romberg and Seegen in young
men, and recently Hofmeier[14] has reported the case of a young
diabetic woman, aged twenty, who came under observation for pruritus
vulvae, in whom the uterus was found small, scarcely 5 cm. (2 inches)
long, and the ovaries very much atrophied. As this young woman had no
other ailment, the atrophy was ascribed to the diabetes.

[Footnote 14: _Berliner klin. Wochenschr._, 1883, No. 42.]

Among the most constant secondary lesions is the aggregate of changes
known as those of pulmonary phthisis. But a few years ago, when our
ideas on this subject were more definite than they are to-day, and when
it was thought we had three distinct varieties of phthisis--the
tubercular, the catarrhal, and the fibroid--the phthisis of diabetes
was regarded as typically catarrhal.[15] At the present time, however,
when the tendency at least is to regard all phthisis as tubercular,
diabetic phthisis must be consigned to the same category. At the same
time, if the tubercle bacillus is to be regarded as the essential
criterion of tuberculosis, it must be stated that the diabetic patient
is subject to two different lung processes--at least if the
observations of Riegel of Giessen[16] are to be regarded as correct. In
two cases of diabetic phthisis studied at his clinic, the sputum of one
contained numerous bacilli, while the other, although the case
presented the most distinct signs of infiltration of the apex, and
although more than fifty preparations were investigated, revealed none.
The sputum was also said to present some unusual physical characters.
So far as I know, no autopsies of cases showing these clinical
differences have been reported, although there have been found in
diabetes, distinct from the usual cheesy foci, fibroid changes with
small smooth-walled cavities. In such cases {203} tubercle bacilli
would be absent, while the physical signs of consolidation would be
present.

[Footnote 15: See the writer's work on _Bright's Disease and Diabetes_,
Philada., 1881, p. 256.]

[Footnote 16: _Medical News_, Philada., May 19, 1883, from
_Centralblatt f. klin. Med._, Mar. 31, 1883.]

As a part of the phthisical process in diabetes, cavities of various
sizes are found and gangrene of the lungs has been observed.

ETIOLOGY.--The problem of the etiology of diabetes mellitus is as
unsatisfactorily solved as is that of its pathogenesis. Certainly, a
majority of cases of diabetes cannot be accounted for. A certain number
may be ascribed to nervous shock, emotion, or mental anxiety; a few to
overwork; some to injury and disease of the nervous system; others to
abuses in eating and drinking. Among the injuries said to have caused
diabetes are blows upon the skull and concussions communicated to the
brain, spinal cord, or vaso-motor centres through other parts of the
body. Hereditation is held responsible for a certain number of cases.
Malarial and continued fevers, gout, rheumatism, cold, and sexual
indulgence have all been charged with producing diabetes.

Diabetes mellitus is most common in adult life, although Dickinson
reports a case at six years which was fatal, Bence Jones a case aged
three and a half, and Roberts another three years old; and in the
reports of the Registrar-General of England for the years 1851-60 ten
deaths under the age of one and thirty-two under the age of three are
included. This statement, in view of the experience of the difficulties
of diagnosis in children so young, seems almost incredible. I have
never myself met a case in a child under twelve years. At this age I
have known two, of which one, a boy, passed from under my notice, while
the second, a girl, recovered completely. The disease is most common
between the ages of thirty and sixty. The oldest patient I have ever
had died of the disease at seventy-two years, having been under my
observation for three and a half years.

It is decidedly more frequent in men than in women, carefully prepared
statistics of deaths in Philadelphia during the eleven years from 1870
to 1880, inclusive, giving a total of 206 deaths, of which 124, or
three-fifths, were males, and 82, or two-fifths, females. This is the
experience of all.

My own experience has been singular and interesting. Up to April, 1881,
I had never met a case in a woman. Of 18 cases outside of hospital
practice which I have noted since that date, 9 were men and 9 women.
But I still do not recall an instance of a woman in hospital practice,
although I have constantly cases among men.

Not much that is accurate can be said of the geographical distribution
of the disease. It seems to be more common in England and Scotland than
in this country, at least if the statistics of New York and
Philadelphia are considered. In the former city, statistics extending
over three and a fourth years show that out of 1379 deaths, 1 was
caused by diabetes; in Philadelphia, in eleven years, 1 out of 875; in
England and Wales, according to Dickinson from observations extending
over ten years, 1 out of 632; and in Scotland, 1 out of 916. According
to the same authority, the disease is more prevalent in the
agricultural counties of England, and of these the cooler ones,
Norfolk, Suffolk, Berkshire, and Huntingdon. According to Senator, it
is more common in Normandy in France; rare, statistically, in Holland,
Russia, Brazil, and the West Indies, while it is common in India,
especially in Ceylon, and relatively very frequent in modern times in
Wurtemberg and Thuringia. Seegen says it is more {204} frequent among
Jews than among Christians, but I have never seen a case in a Hebrew.

SYMPTOMS, COURSE, AND DURATION.--The earliest symptom commonly noted by
the diabetic is a frequency of micturition and the passage of larger
amounts of urine than is natural. Coincident with or immediately
succeeding this is an undue thirst and dryness of the mouth, which soon
becomes the most annoying symptom the patient has, the freest draughts
of water giving but partial or temporary relief. To this succeeds
dryness, and sometimes itching, of the skin and absence of
perspiration. A good appetite with fair digestion accompanies this
stage of the disease, but notwithstanding this the patient loses in
weight. If a male, his attention is sometimes called to his urine by
the white spot left after the evaporation of a drop of urine on his
boot or clothing or by the stiffness of his linen due to the same
cause. To these symptoms are sometimes added an intolerable itching of
the end of the urethra in males and of the vulva in females, probably
due to the irritation caused by the saccharine urine in passing over
and drying upon these parts.

As the disease progresses muscular weakness supervenes. This, however,
comes on at varying periods after the incipient symptoms make their
appearance. Sexual inclination grows less. The muscular weakness
gradually increases, if the disease is not checked, until the patient
can barely walk: he totters in his gait, and reminds one of a case of
Duchenne's disease. Even before this he sometimes gives up and goes to
bed. Often harassing cough ensues, adding its exhausting effect to that
of the essential disease. Percussion and auscultation discover
consolidation at one apex or over larger areas of the lungs. Dyspepsia
and indigestion replace the good appetite which attended the onset of
the symptoms, and all efforts to increase the latter are unavailing.
The heart begins to flag, and its action is irregular. It finally
ceases to act, and the patient dies suddenly, sometimes unexpectedly.
Or coma may supervene before death. This coma, known as diabetic coma,
is generally ascribed to the accumulation of acetone or
acetone-producing substance in the blood. It is supposed to be a
product of the decomposition of the sugar in the blood, and the
phenomena resulting from its presence are known as those of
acetonaemia. Some further account of it will be given in the section on
changes in the urine. It is sometimes recognizable by a fruity odor of
the breath, which may even pervade the atmosphere of the room in which
the patient lies, and may be recognized on entering. It has been
compared to the odor of a room in which apples have been kept, again to
sour beer, and again to chloroform.

During all this time the thirst and discomfort arising therefrom,
continue, although it sometimes happens that toward the end the
quantity of urine and its contained sugar diminish and the urine
becomes darker in hue.

Such is the course of a typical case of diabetes mellitus. Other
symptoms, less conspicuous, are a lowered temperature of the body, from
1 degree to 2-1/2 degrees F. or even more; cataract, dilatation of the
retinal vessels, intraocular lipaemia, functional derangements of
vision, including amblyopia, presbyopia, and loss of accommodating
power; and occasionally total blindness from atrophy of the retina may
be present. I have known almost total blindness to appear very early in
the disease, and {205} subsequently to disappear. Derangements of the
other special senses, as impairment of hearing, roaring in the ears,
and disorders of smell and taste, also occur. Boils and carbuncles are
occasional symptoms; although usually late in occurrence, the former
are said to be sometimes the first symptoms recognized. Numerous skin
affections may occur. Ulcerated surfaces are slow to heal, and gangrene
supervenes sometimes spontaneously, but more often as the result of
some trifling injury. It may start from a blister produced by
cantharides, although such instances are scarcely frequent enough to
justify interference with treatment demanding blisters. More frequently
surgical operations do badly. Allied to this tendency is a spongy state
of the gums, with recession and excavation, resulting, in asthenic
cases, in absorption of the alveolar processes and falling out of the
teeth. Eczema of the labia and vicinity in females, and a similar
irritation about the meatus urinarius in males, are annoying symptoms.
A purulent-looking discharge has been seen issuing from the urethra, in
which the spores of penicilium glaucum have been recognized by the
microscope.

The term diabetic coma is applied to a form of coma which is apt to
occur late in the disease, indeed most frequently to terminate it;
while it is also used to indicate a train of nervous symptoms of which
coma is the terminal one. To this train of symptoms the word
acetonaemia is also applied, and should alone be used, while the term
diabetic coma should be restricted to the terminal symptom. The coma,
as well as the previous nervous symptoms, is considered due to the
accumulation in the blood of a product of the decomposition of sugar,
formerly believed to be acetone, but now thought to be an
acetone-producing substance, probably aceto-acetic acid. It is likely
that in all cases of diabetes a small quantity of this substance exists
in the blood, from which it is separated by the kidneys and lungs,
while it is only when these channels are insufficient for its removal
that it accumulates and produces the symptoms described.

Usually, the coma comes on gradually, deepening until it terminates in
death. In other instances it is preceded by various symptoms, including
dizziness, drowsiness, cephalalgia, delirium, mania, muscular pains,
gastric and intestinal symptoms, including epigastric pain,
vomiting--sometimes of blood--and even purging; also dyspnoea, with
short, panting respiration like that of an animal with both vagi cut,
and a fluctuating pulse-rate which continues until coma is established,
after which it remains rapid and small. Both the breath and urine may
exhale the peculiar odor of acetone, or it may be absent, and the urine
strikes the peculiar burgundy-red reaction with perchloride of iron to
be again referred to.

These symptoms may be sudden in their occurrence, whence acute
acetonaemia, or they may ensue slowly. Ralfe,[17] who has studied the
subject of acetonaemia very thoroughly, has called attention to the
parallelism between the phenomena of acute acetonaemia and those of
acute yellow atrophy of the liver and of phosphorus-poisoning. The
sudden, sharp epigastric pain, with gastric disturbance and vomiting,
often of blood; the peculiar panting dyspnoea referred to; the short,
{206} noisy delirium, followed almost suddenly by deep coma; the fall
in temperature as the nervous symptoms develop; the irregular, and
finally rapid, pulse,--are all symptoms common to the two conditions.

[Footnote 17: _Clinical Chemistry_, 1883, p. 98; also Discussion on
Diabetes before Pathological Society of London, _Lancet_, April 7,
1883, p. 592.]

Although acknowledged to be a grave complication, and the most frequent
cause of death in diabetes,[18] yet it does not follow that a fatal
termination is inevitable when diabetic coma sets in. I have now a
patient, a woman, who considers herself in perfect health, but in whom
there remains a trifling glycosuria, who at one time was supposed to be
dying of diabetic coma.

[Footnote 18: Of 400 cases of diabetes which passed under the
observation of Frerichs, the majority died of acetonaemia (Frerich's
"Ueber den plotzlichen Tod und uber das Coma bei Diabetes," _Zeitschr.
fur klin. Med._, 1883, vi. 3-53). Of 53 persons dying of diabetes at
Guy's Hospital, London, during the last ten years, 33 died comatose
(Dr. Fred. Taylor, Discussion on Diabetes, Pathological Society of
London, _Lancet_, May 5, 1883). In my own experience acetonaemia has
not been so frequent a cause of death as phthisis, acute pneumonia, and
heart-failure.]

Crampy pains in the legs and facial paralysis are among the nervous
symptoms sometimes present, and the term diabetic neuralgia has been
applied to a special form of neuralgia peculiar to this disease. It is
characterized by its acuteness, stubbornness, and symmetry. Its
favorite seats are the inferior dental nerves and the sciatics.
Greisinger referred to the frequency of sciatica in 1859, Braun again
in 1868, and others still later; but Worms in 1881 established the
close relation between the two conditions and the features described.
Most recently (1884), Cornillon[19] collected 22 cases of diabetic
neuralgia, and has further elaborated the study. Believing that
diabetes affects particularly those persons who have had serious
attacks of rheumatism and gout, he is inclined to think the neuralgia
as much due to uricaemia as to hyperglycosuria, and that these
conditions cause, not neuritis, but transitory lesions in the
nerve-centres, but whether in the membranes or gray or white matter is
undetermined.

[Footnote 19: "Des nevralgies diabetiques," _Revue de Medecine_, 1884,
iv. 213-230.]

That the phenomena of acetonaemia are those of a toxic agent or agents
in the blood derived from the sugar there present is generally
conceded, although Sanders and Hamilton,[20] after a study of the
clinical histories and the result of autopsies in several cases, are
disposed to ascribe diabetic coma to slow carbonic-acid poisoning due
to fat embolism of the pulmonary vessels. So far as I know, these
conclusions have not been reached by any other observers. R. H.
Fitz[21] and Louis Starr[22] have each reported cases of diabetic coma
with lipaemia, carefully studied with this point in view, without
finding any facts to sustain the carbonic-acid theory.

[Footnote 20: _Edinburgh Med. Journal_, July, 1872.]

[Footnote 21: "Diabetic Coma; its relations to Acetonaemia and Fat
Embolism," _Boston Medical and Surgical Journal_, vol. cvi. p. 24, Feb.
10, 1881.]

[Footnote 22: "Lipaemia and Fat Embolism in Diabetes Mellitus," _New
York Medical Record_, vol. xvii., 1880, p. 477.]

Alterations in the Blood.--The blood of diabetics is variously charged
with sugar, which may be in such quantity as to impart a viscidity and
higher specific gravity to the plasma, which has reached 1033, the
normal being 1028. On the other hand, analyses have sometimes failed to
discover sugar in the blood after death, the result, probably, of the
tendency of the sugar to rapid disintegration. Alcohol and acetone, or
{207} acetone-producing substance (aceto-acetic acid), are occasionally
present as the products of such decomposition, to which are ascribed
the symptoms of acetonaemia already discussed.

The presence of fat in the blood of diabetics was noted by the earliest
students of the disease. It is sometimes sufficient in amount to
produce a milky appearance of the serum, while the analyses of Simon
revealed a quantity of 2 to 2.4 per cent., the normal being 1.6 to 1.9
per cent. The fat thus present is said to be sometimes sufficient to
cause fat embolism in the capillaries of the lungs, and cases of this
condition have been reported by Sanders and Hamilton,[23] Louis
Starr,[24] and Rickards.[25] Ralfe ascribes the lactescent appearance
of the blood to the action of the aceto-acetic acid, since acetic will
give a milky appearance when agitated with a dilute and slightly
alkaline mixture of fatty matter at 100 degrees, and the injection of
acids into the blood of animals leads to the increase of fatty matter
in the blood and fatty infiltration of tissues.

[Footnote 23: _Loc. cit._]

[Footnote 24: _Loc. cit._]

[Footnote 25: _Birmingham Med. Review_, Jan., 1882.]

It must be admitted that the mode in which this lipaemic state of the
blood is brought about is imperfectly understood, and whether it be by
some chemical agency of the kind described by Ralfe, or by rapid
absorption of the subcutaneous fat, or from an imperfect oxidation of
absorbed fat, is undetermined. Possibly all may contribute.

Albert G. Heyl[26] has described an altered appearance of the retinal
vessels recognizable by the ophthalmoscope, which he ascribes to the
fatty blood-plasma at the periphery of the blood-current, the normal
plasma being invisible on account of its transparency.

[Footnote 26: For a detailed description of this appearance, with a
colored lithograph depicting it, see the author's work on _Bright's
Disease and Diabetes_, p. 262.]

The red blood-discs are diminished and their ratio to the white
corpuscles altered. In a count by F. P. Henry, in Louis Starr's case,
the number of red discs was 4,205,000 to a cubic millimeter, the normal
being at least 5,000,000; the white were 50,000 to a cubic millimeter,
or 1 white to 84 red, instead of 1 to 350 or 500.

Changes in the Urine.--The most important changes in the urine are its
increase in quantity and the presence of sugar. The variations in the
former are extreme, being from an amount which but slightly exceeds the
normal to as much as 50 pints (23.65 liters) in twenty-four hours, and
even more. The quantity is of course limited by the fluid ingested, and
although it may exceed this amount for a day or more, it cannot do so
for any length of time. It is generally a little less. The more usual
quantity in the twenty-four hours is from 70 to 100 ounces (210 to 300
cc.).

The quantity of sugar varies greatly in different cases and at
different times in the same case. The maximum quantity reported by
Dickinson was 50 ounces, or 1500 grammes, in twenty-four hours. The
proportion may reach as much as 15 per cent., but the more usual
amounts are from 1 to 8 per cent., or from 5 to 50 grains (.324 to 3.24
grams) to the fluidounce, or from 300 to 4000 grains (19.44 to 260
grams) in the twenty-four hours.

It is important to know that intercurrent febrile disease may produce a
decided diminution in the daily quantity of urine, and of the sugar
contained in it. A similar decrease, and even disappearance, is said to
take place sometimes toward the fatal termination of a case.

{208} The effect of exercise upon the sugar secretion is not uniform.
Bouchardat and Kuelz have noted a diminution, and even disappearance,
of sugar from urine as its result, and it is reasonable to suppose that
judicious exercise is at least without harmful effect, while it is
certain too that muscular exercise, if excessive, will increase
glycosuria.

Changes in diet of course modify the secretion of sugar, starches and
saccharine foods increasing it, while nitrogenous and oily foods
diminish it. So, too, the urine secreted on rising in the morning has
almost always less sugar in it than that passed on retiring; and it is
not rare to find no sugar in urine passed on rising, when that passed
on retiring at night may contain a small amount of sugar--from 1/4 to 1
per cent. On the other hand, I have found a small amount of sugar in
the morning urine when the evening urine contained none. Anxiety and
excitement both increase the proportion of sugar.

Inosite, or muscle-sugar, is sometimes associated in urine with
diabetic sugar, and occasionally replaces it. So, too, in experiments
upon animals puncture of the fourth ventricle is sometimes followed by
inosuria instead of glycosuria, and in corresponding organic disease of
the brain the same thing is observed. The substitution of grape-sugar
by inosite in the course of diabetes is considered by Laboulbene[27] a
favorable change.

[Footnote 27: "Note sur l'Inosurie, succedant au diabete glycosurique,
et paraissant avoir une action favorable," _L'Union Medicale_, Oct. 14,
1883.]

As would be expected, the specific gravity of saccharine urine is
usually high--most frequently from 1025 to 1040--and Bouchardat noted a
specific gravity of 1074 in one instance. On the other hand, I have
found sugar easily detectable in urine with a specific gravity as low
as 1010. Pavy records an instance of the same specific gravity, and
Dickinson one in which the specific gravity was as low as 1008. It is
to be remembered that the sugar is rapidly destroyed when fermentation
sets in. A coincident diminution in the urea and other solids of the
urine will reduce the specific gravity of a saccharine urine otherwise
heavier.

The depth of color of diabetic urine is inversely as the quantity
passed. Hence, when this is very large the urine is pale, and even
almost colorless, but it may still contain considerable amounts of
sugar and possess a decided color, quite as deep as that of urine
passed in smaller quantity. When exposed to the air, diabetic urine
becomes rapidly turbid from the growth of fungi, including the yeast
fungus and penicilium glaucum.

The odor of diabetic urine just passed is usually in no way peculiar,
but as fermentation progresses an acetous odor is developed, which is
ascribed to acetic acid. At other times the odor is quite peculiar,
being spoken of as vinous or compared to that of sour beer, stale
fruit, alcohol, chloroform, or, as by one of my patients, to
sweetbrier.

Diabetic urine has almost invariably an acid reaction, which becomes
more decided as fermentation progresses. As a consequence of this
increased acidity, and sometimes independent of fermentation-changes,
the urine deposits a sediment of uric acid, but with this exception
diabetic urine is generally free from sediment. Diabetic patients on a
meat diet sometimes have a good deal of uric acid from this source.

Albuminuria may coexist with glycosuria, but is not generally found
until late in the disease, after changes in the kidney begin to make
their {209} appearance, unless, as may happen, glycosuria supervenes
upon primary renal disease.

Alcohol and acetone, or an acetone-yielding substance--aceto-acetic
acid--are sometimes found in diabetic urine. They are products of the
breaking up of sugar, but chemists do not explicitly agree as to the
exact method in which acetone originates in the organism. First
recognized in the distillate of urine and blood of a diabetic patient
by Petters[28] through its physical properties, odor, combustibility,
etc., rather than by actual isolation, it was further investigated by
Kaulich,[29] Gerhardt,[30] Rupstein,[31] and Markownikoff,[32] who
obtained it in an impure state from urine; by Deichmuller and
Tollens,[33] whose isolated substance was pure, and finally most
recently by Jaksch[34] and Penzoldt.[35] The former found it not only
in diabetic urine, but also in that of fever, and even of carcinoma.
The latter found it by the indigo test in but 18 out of 22 diabetics,
and by the iodoform test, either decidedly or feebly, in 20 out of 20;
in 3 out of 11 cases of typhoid fever, in 6 out of 7 cases of
pneumonia, in none of 6 cases of phthisis, in 1 out of 3 cases of
measles, and in 1 case of cerebro-spinal meningitis. Finally, v. Jaksch
has been led to believe, from his extensive investigations, that
acetone is a constant and normal product of tissue-change, although
Penzoldt considers such conclusion scarcely justified.

[Footnote 28: _Prager Vierteljahrschrift_, xiv. 3, 1857, S. 88.]

[Footnote 29: _Ibid._, xvii. 3, 1860, S. 59.]

[Footnote 30: _Wiener Med. Presse_, No. 28, 1865.]

[Footnote 31: _Centralbl. fur d. med. Wiss._, No. 55, 1874.]

[Footnote 32: _Liebig's Annalen_, Bd. 182, S. 362.]

[Footnote 33: _Ibid._, Bd. 209, S. 25.]

[Footnote 34: _Zeitschrift fur physiol. Chemie_, vi. 6.]

[Footnote 35: "Beitrage zur Lehre von der Acetonurie und von verwandten
Erscheinungen," _Deutsch. Archiv fur klin. Med._, xxxiv., 2 Oct., 1883,
S. 127.]

Gerhardt early discovered a substance in the urine of diabetics and
habitual drinkers which struck a deep-red reaction with chloride of
iron. This he considered was the source of acetone, and was probably
ethyl diacetate or diacetic ether, which by decomposition yields equal
molecules of acetone and alcohol; thus:

  C_{4}H_{5}O_{3}C_{2}H_{5} + H_{2}O = C_{3}H_{6}O + CO_{2} +
                                                          C_{2}H_{6}O.

  Ethyl diacetate.            Water.     Acetone.            Alcohol.

This view is still held by some, but others, in view of the recent
discovery of Deichmuller and Tollens,[36] that diabetic urine when
distilled yields decidedly more acetone than alcohol, have suggested
that the substance is derived from aceto-acetic acid.

[Footnote 36: _Loc. cit._]

The first test suggested for acetone was Gerhardt's chloride-of-iron
test. A solution of chloride of iron added to urine containing acetone
strikes a burgundy-red color. But this reaction occurs with so many
substances that it cannot be considered entirely reliable. Ralfe's
modification of Lieben's iodoform test[37] is made as follows: About a
fluidrachm (3.7 c.c.) of liquor potassae, containing 20 grains (1.2
grams) of iodide of potassium, is placed in a test-tube and boiled; a
drachm (3.7 c.c.) of the suspected urine is then carefully floated upon
the surface. When the urine comes in contact with the hot alkaline
solution a ring of phosphates is formed, and after a few minutes, if
acetone or its allies are present, the ring will become yellow and
studded with yellow dots of iodoform, which, in turn, will sink through
the ring of phosphates and deposit itself at the bottom of the
test-tube. A number of other substances {210} produce the iodoform
reaction, but only one of these, lactic acid, is likely to be met in
urine.

[Footnote 37: _Clinical Chemistry_, Philadelphia, 1884, p. 100.]

The perspiration, saliva, exudations, and effusions in diabetic cases
have all been found, at times, to contain sugar.

DURATION.--Diabetes is a disease of which the duration is measured by
months and years, and although cases are reported in which death
supervened in from six days to six weeks after the recognition of the
disease, it is evident that such periods do not necessarily measure its
actual duration. The disease may have existed some time before coming
under observation. On the other hand, a case is reported by Lebert
which lasted eighteen years; another, under the successive observation
of Prout and Bence Jones, sixteen years; and a third, under Bence Jones
and Dickinson, fifteen years. The younger the patient the shorter
usually is the course run and the earlier the fatal termination. Yet I
have known a girl of twelve recover completely. After middle age the
disease is usually so easily controlled by suitable dietetic measures,
if the patient is willing to submit to them, that its duration is only
limited by that of an ordinary life, while carelessness in this respect
is apt to be followed by early grave consequences.

COMPLICATIONS.--The almost sole complication of diabetes mellitus is
the tubercular phthisis which so often terminates it. Indeed, it is
doubtful whether this complication should not be regarded as a
consequence, as should also the boils, gangrenous processes, and
ophthalmic conditions which have been mentioned under Symptomatology.
Jaundice has occurred three times in my experience up to the present
time. Senator says that when not an accidental complication due to a
catarrh of the duodenum it may result from compression of the biliary
capillaries by the overloaded blood-vessels and enlarged gland-cells of
the liver. In one of my cases, in which jaundice appeared to be the
initial symptom, but which disappeared some months before death, the
autopsy revealed atrophy of the liver. It is well known that pancreatic
disease, especially cancer, is apt to be accompanied by jaundice, and
as pancreatic disease is often at the bottom of diabetes, it will
similarly account for the jaundice, while the presence of jaundice may
also suggest a pancreatic diabetes.

DIAGNOSIS, INCLUDING THE TESTS FOR SUGAR IN THE URINE.--The diagnosis
of diabetes mellitus, the disease being once suspected, is easy. The
passage of large amounts of pale urine of high specific gravity, the
presence of thirst, dryness of the mouth, fauces, and skin, and
progressive emaciation even while the appetite is good, can scarcely be
misinterpreted. In the urine from such a case the application of any of
the tests for sugar will produce prompt response. The urine is not
always so much increased as to attract attention, while its color is
also sometimes but slightly changed; but the symptoms of thirst and
dryness or clamminess of the mouth are seldom wanting. On the other
hand, the discovery of a glycosuria without these symptoms is, as a
rule, accidental. It is a question how far such degrees of glycosuria
as do not produce the usual symptoms of diabetes in an appreciable
degree are signs of positive disease. At the same time, its detection
is important, in that there is always danger of the simple glycosuria
becoming a diabetes--a danger which its recognition and suitable
treatment may avert. Accordingly, the urine of all persons having
unusual appetites without evident cause, {211} and of those who are
fond of eating and drinking, should be tested for sugar. This should
also be done for those who have passed through severe mental or
physical strain, have suffered shock or concussion of the nervous
system, blows upon the abdomen, etc.

Testing for Sugar.--Under the head of Diagnosis I prefer to include the
testing for sugar, which requires some detailed consideration. Unless
it be that the indigo test recently revived by George Oliver of London
prove more delicate, that form of cupric test known as Fehling's
solution is, with suitable precautions, all things considered, the most
satisfactory for general use.

Fehling's volumetric solution, suitable for both qualitative and
quantitative purposes, is made as follows: Dissolve 34.639 grams of
pure crystallized cupric sulphate in about 200 cubic centimeters of
distilled water; 173 grams of chemically pure crystallized neutral
sodio-potassic tartrate and 80 grams of potassium hydrate in 500 or 600
c.c. of distilled water. To the latter add the copper solution slowly,
and dilute the clear mixed fluid to 1 liter. One cubic centimeter of
this solution will be decolorized by 0.005 grm. of sugar, or 200 grains
will be decolorized by 1 grain of sugar. Or the copper may be dissolved
in 1 liter of water, and the tartrate and potassium hydrate in another,
and a cubic centimeter of each mixed at the moment they are to be used.

For qualitative testing, put a cubic centimeter of Fehling's solution
into a test-tube (or if the copper and the alkaline sodio-potassium
tartrate solutions are kept separate, a cubic centimeter of each), and
dilute with distilled water to 5 c.c. Boil, and if, after the lapse of
a couple of minutes, the solution remain unchanged, it is fit for
testing. If it becomes turbid or a red sediment falls, it is spoiled,
and a new solution should be obtained.[38] A cubic centimeter of the
suspected urine is then measured out and added drop by drop to the
solution kept hot. If there is much sugar, the first drop will throw
down a yellow precipitate of suboxide of copper, which becomes rapidly
red. If no reaction takes place after adding the entire cubic
centimeter of urine, the addition should be continued until 4 c.c. are
added, when, if, after the mixture has cooled, there be no response, it
may be concluded that the urine is free from sugar. By operating with a
cubic centimeter of the test-fluid and the same quantity of urine or
multiples thereof, we may roughly estimate the proportion of sugar.
Thus, if the cubic centimeter of undiluted urine just decolorizes the
cubic centimeter of Fehling's solution, sugar is present in the
proportion of one-half of 1 per cent.; or if a half cubic centimeter of
the urine removes all the color, the quantity is 1 per cent. If the
urine is highly charged with sugar, it may be diluted, and the degree
of dilution being remembered, a rough quantitative estimation may be
similarly made.

[Footnote 38: Should this not be possible, a little more soda may be
added and the fluid filtered, when it is again ready for use.]

If the urine contains very minute quantities of sugar, the reaction is
less satisfactory. The copper is reduced, but the suboxide is so small
in quantity that it is obscured by the excess of copper solution, and a
mixture results which is greenish or greenish-yellow or yellow or
milky, and on standing a small yellow sediment falls to the bottom.
Now, it dare not be said that it is sugar which produces such reaction.
It may be {212} sugar, but it may also be uric acid. Uric acid is
really more frequently a source of error than is commonly supposed. I
have myself seen the reaction due to it so vivid that I did not suspect
it could be due to any reducing agent excepting sugar; but, noting the
next day a copious sediment of uric acid which had fallen during the
night, a testing of the supernatant fluid then revealed no reaction
whatever. Such a urine, after being treated by the lead process to get
rid of the uric acid, fails also to respond. But this process is very
tedious,[39] and cannot be conveniently carried out by the busy
practitioner. The same thing is, however, accomplished by treating the
urine with hydrochloric acid, which in twenty-four hours precipitates
all of the uric acid. Simple precipitation by lead acetate solution and
filtration does not answer, because all of the uric acid is not thus
removed. Other substances, as hippuric acid, urates, hypoxanthin, etc.,
are said to act similarly, but they produce no practical interference
with the test. On the other hand, a small amount of sugar may be
present and yet fail to show the reaction, because the cuprous oxide is
held in solution by certain substances. Such are ammonia and
nitrogenous matters, including albumen, creatinin, pepsin, peptones,
urinary coloring matters, etc. The latter probably produce their effect
through the ammonia which is given off while heating them in the
presence of an alkali. Hence all albumen should be precipitated and
filtered out of urines suspected to contain sugar, and the heat applied
should not be too great. Finally, excess of glucose will also hold in
solution cuprous oxide, so that the suspected urine should not be added
in too large a quantity at a time, but rather drop by drop.

[Footnote 39: The details of this process will be found in the writer's
work on the _Practical Examination of Urine_, 5th ed., 1883, p. 63.]

But qualitative testing is not sufficient during the treatment of a
case of diabetes. The percentage of sugar and the quantity discharged
in twenty-four hours should be determined occasionally. The process is
done as follows: Place 10 cubic centimeters of Fehling's solution in a
porcelain capsule, and dilute it with 40 c.c. of distilled water. Fill
a Mohr's burette with the urine, which, if it contain more than 1 per
cent. of sugar, should be diluted with nine times its bulk of distilled
water. Slowly heat the contents of the capsule to boiling, and then
allow a little of the diluted urine to run in from the burette;
continue the cautious addition of urine and the gentle heating until
the blue color is completely removed from the Fehling's solution. To
determine the exact moment at which this takes place requires a little
experience, but its recognition is facilitated by carefully tilting the
capsule after each addition and stirring, so that its clear white
surface may be seen through the edge of the fluid and contrasted with
the latter. The number of cubic centimeters of urine used should now be
read off from the burette, the number of c.c. of undiluted urine
calculated therefrom, and each c.c. multiplied by .005 grm. The result
indicates the quantity of sugar in grams in the urine employed, whence
the percentage of sugar is determined, and also the twenty-four hours'
quantity, the amount of urine passed in that period being known.

The Fermentation Test.--A very simple and easy method of determining
the proportion of sugar is by Roberts's fermentation method, which,
although not so precise as the volumetric process, is still {213}
sufficiently so for clinical purposes. A small piece of German yeast or
a teaspoonful of liquid yeast is added to about four ounces (120 c.c.)
of the urine, which is kept lightly stopped, at a temperature of 20
degrees to 30 degrees C. (68 degrees to 80 degrees F.), for about
twelve hours; at the end of this time the sugar will have been
converted into alcohol and carbonic acid. The latter will have passed
off, and the urine lost in weight because of the destruction of sugar;
while the difference between the specific gravity before and after the
fermentation indicates the number of grains of sugar per fluidounce.
Thus, suppose the specific gravity before fermentation to have been
1040, and afterward 1025; there will have been 15 grains of sugar to
the fluidounce, whence, again, the twenty-four hours' quantity can be
calculated. If the metric system is used, each degree of specific
gravity lost will correspond to .2196 grams of sugar in every 100 c.c.
of urine.

The specific gravity of the fermented urine should be compared with
that of the urine soon after it is passed, because saccharine urine
under suitable circumstances undergoes fermentation without the
addition of yeast; and, the specific gravity being thus lowered
spontaneously, the reduction in the urine fermented by yeast would
appear less than it actually is. At the same time, care should be taken
that the urine is of the same temperature when the specific gravity is
taken before and after fermentation.

The Picric Acid and Potash Test.--Although attention was called in 1865
by C. D. Braun,[40] a German chemist, to a reaction between grape-sugar
and picric acid, as the result of which the latter is converted into
picramic acid, very little attention seems to have been paid to this
announcement. Quite ignorant of it, George Johnson rediscovered this
reaction in 1882, and published it in 1883.[41] It is applicable to
both qualitative and quantitative purposes. In order to make use of it,
a standard comparison-solution is made as follows: Take 1 fluidrachm of
a solution of grape-sugar, 1 grain to the fluidounce; mix it in a long
test-tube with half a drachm of liquor potassae (U. S. P. or B. P.) and
ten minims of a saturated solution of picric acid; dilute the mixture
to 4 fluidrachms with distilled water, to facilitate which a tube used
for the purpose may be marked at 4 fluidrachms. Raise the mixture to
the boiling-point, and continue the boiling for sixty seconds, to
ensure complete reaction between the sugar and picric acid. During the
boiling the pale-yellow color of the liquid is changed to a vivid
claret-red. Cool the liquid by cautiously immersing the tube in cold
water, and if it is not then at the level of the 4-drachm mark, raise
it to this by adding distilled water. The standard color thus obtained
is that which results from the decomposition of picric acid by a grain
of sugar to the ounce, four times diluted, or by a solution of sugar
containing one-quarter of a grain per ounce. But the picramic solution
rapidly becomes pale on exposure, so it becomes necessary to make a
more permanent solution to use as a standard. This may be accomplished
by combining liquor ferri perchloridi drachm j, liquor ammonii acetatis
drachms iv, acidum aceticum (glacial) drachms iv, and water enough to
make ounces iiss. The color of this is identical with that of the
picric acid reduced by a one-grain solution diluted four times, and,
{214} according to Johnson, it will retain its color unchanged for at
least six months. At the same time, whenever a new solution is made it
should be compared with that of the one-quarter grain per ounce
solution of sugar, boiled with picric acid and potash.

[Footnote 40: "Ueber die Umwandlung der Pikrinsaure in Pikramminsaure,
und Ueber die Nachweisung der Traubenzucker," _Zeitschrift fur Chemie_,
1865.]

[Footnote 41: _British Medical Journal_, March, 1883.]

For qualitative testing Johnson directs: To a drachm of urine in a
test-tube add a few drops, enough to give a distinct yellow color, of a
saturated solution of picric acid. Add about 10 drops of liquor
potassae and boil. If sugar is present, the mixture becomes promptly
red in hue.

[Illustration: FIG. 5. _Johnson's Picro-Saccharimeter_.

The shading of the side tube indicates the ferric-acetate standard. The
darker shading at the bottom of the graduated tube shows the saccharine
fluid, darkened by boiling with picric acid and potash, and occupying
ten divisions between dilution.]

The quantitative estimation is based upon an accurate approximation, by
dilution, of the color of the tested fluid with that of the standard
solution. Johnson recommends the picro-saccharimeter figured in the
text. This is a stoppered tube twelve inches long and three-quarters of
an inch in diameter, graduated into ten, and each of these again into
ten other equal divisions. By the side of this tube, and held in
position by an S-shaped band of metal, is a stoppered tube of equal
diameter and about six inches long, containing the standard solution
corresponding to the reaction of the one grain of grape-sugar with
picric acid and potash diluted four times.

It has been found that ten minims of a cold saturated solution of
picric acid are rather more than sufficient for decomposition by one
drachm of a solution of grape-sugar in the proportion of one grain to
the ounce. A drachm of the solution will therefore contain one-eighth
of a grain of sugar, which is the strength of the solution used in
making the standard-color liquid. In making the analysis, while the
quantity of liquor potassae used is always the same and the dilution is
always to four drachms, the picric acid must be added in proportion to
the amount of sugar present, so that if the urine contains as much as
six grains to the fluidounce, sixty drops or a fluidrachm of the
picric-acid solution would have to be used; and when the proportion of
sugar is higher than this, the urine should be diluted with distilled
water five or ten times before commencing the analysis, and the degree
of dilution remembered in the computation.

If, now, a drachm of a solution of grape-sugar, containing two grains
to the ounce, be mixed with the same quantity of liquor potassae and
picric acid and increased by the addition of distilled water to four
drachms in the boiling tube, and boiled as before for sixty seconds,
the result will be a mixture of much darker color than will be produced
by the one-grain solution; but if the dark liquid be diluted with its
own volume of water, the color will be the same as that of the
one-grain solution or the standard.

It is plain, then, that if a given quantity of the dark saccharine
fluid produced by boiling--say, enough to cover ten divisions of the
graduated tube, as shown in the figure--has to have added to it an
equal bulk of distilled water in order to produce {215} the color of
the standard solution, the tested fluid will be of the strength of two
grains to the ounce; if three times, three grains; and so on; while
fractional additions, as indicated by the graduated markings, would
show fractional additions to the proportion of sugar.[42]

[Footnote 42: A more exact comparison of the saccharine liquid with the
standard is made by pouring into a flat-bottomed colorless tube six
inches long and an inch in diameter as much of the standard solution as
will form a column about an inch in height, and an exactly equal column
of the saccharine fluid in a precisely similar tube. The operator then
looks down through the two tubes at once, one being held in each hand,
upon the surface of a white porcelain slab or piece of white paper. In
this way slight differences of tint are easily recognized; and if the
liquid to be analyzed is found darker than the standard, it is returned
to the graduated tube and diluted until the two liquids are found to be
identical in color, when the final reading is made.]

The presence of albumen, even in considerable amount, has but little
effect upon the test, nor does the coloring matter of normal urine,
according to Johnson; but he says there is a coloring matter associated
with ser-albumen in albuminous urine, and with egg-albumen as well,
which has a reducing action on picric acid. This is partly separated by
filtering off the precipitated albumen, and entirely removed by
repeated filtration through animal charcoal. So, too, the albumen
removed by coagulation and filtration, if thoroughly washed, does not
give any red reaction if boiled with picric acid and potash diluted in
the same proportion as when testing for sugar. Neither do any other
unoxidized sulphur compounds found in urine decompose the picric acid
and render the test fallacious.

Johnson and his son, G. Stillingfleet Johnson, claim that the
picric-acid test is as accurate as any other, and that it is even more
accurate than either Fehling's or Pavy's process, because the picric
acid is not acted upon by uric acid or urates, which do reduce the
oxide of copper. The method of analysis by the picro-saccharimeter,
they claim, is at least as speedy and as easy as any other. The
materials and apparatus required are easily prepared, inexpensive, and
not, like Fehling's copper solution, liable to undergo rapid changes.

But while Johnson claims that neither coloring matters of normal urine
nor uric acid reduce the picric acid, he admits that he has tested with
picric acid and potash a large number of specimens of normal urine with
the almost uniform result of a depth of color indicating the proportion
of .6 of a grain of sugar to the fluidounce, the indication varying
between the limits of .5 to .7 grain. The ammonio-cupric method used at
the same time gave results of from .7 to .9 grain to the fluidounce, or
an excess of .1 to .3 grain. Now, if my own views, the grounds for
which are announced elsewhere,[43] are correct, strictly normal urine
contains no sugar, and any reducing action upon oxide of copper is due
to uric acid, either picric acid is reduced to a degree by uric acid or
by some other constituent of normal urine. This, in the light of
Oliver's[44] recent investigations, may be kreatinin. For he has shown
that kreatinin strikes in a few seconds a red color with the cold
alkaline picric solution, which is quickened by heat. From this it
would seem that the exact value of the picric-acid test has as yet to
be determined.

[Footnote 43: Tyson, _Practical Examination of Urine_, 4th ed.,
Philadelphia, 1884.]

[Footnote 44: _On Bedside Urine-Testing, including Qualitative Albumen
and Sugar_, by Geo. Oliver, M.D., London, Member of the Royal College
of Physicians of Lond., etc., 2d ed., London, 1884.]

{216} The Indigo-Carmine Test.--The fact that indigotine, the coloring
matter of commercial indigo, is converted into indigo when heated with
an alkali in the presence of glucose and certain carbohydrates, has
recently been applied by George Oliver of London in the construction of
a test-paper. Carmine of indigo is the sulph-indigotate of sodium, an
intensely blue salt, soluble in 120 parts of water. Sulph-indigotic
acid is made by heating indigo with sulphuric acid, and when combined
with a base, sodium, produces indigo-carmine. When sodium carbonate is
mixed with a solution of indigo-carmine, the latter is precipitated in
a minute state of division, but is redissolved on heating, when there
results a greenish-blue solution. A freshly-made mixture of the indigo
solution and sodium carbonate furnishes a fluid not unlike Fehling's
solution, which gives the reaction to be described with glucose.
Unfortunately, such a mixture will not keep, and the reagent would be
useless but for the happy idea of Oliver of making the test-paper. In
doing this bibulous paper is immersed in a solution of indigo-carmine
with carbonate of sodium.[45] The paper is then cut into strips an inch
long and one-quarter of an inch wide.

[Footnote 45: No more precise directions than this are given by Oliver,
either in his papers in the _Lancet_ for 1883 or in his little book
just published, _On Bedside Urine-Testing_. The sugar test-papers, as
well as the entire series of albumen test-papers, suggested by Oliver,
are now made by Parke, Davis & Co. of New York, and by Wilson & Son,
Harrogate, London.]

Mode of Testing.--One of the test-papers and a sodium carbonate
paper[46] are dropped into a half-inch test-tube, and water added until
the upper end is just covered; a column of fluid one inch in height and
half an inch in diameter will thus be produced, so that the solution of
carmine obtained on boiling will always acquire the same concentration.
Heat is now applied, the tube being gently shaken, and boiling kept up
for a second or two. A beautiful blue solution will result. The
test-paper may now be removed or allowed to remain.

[Footnote 46: Test-papers of the same size, charged with a saturated
solution of sodium carbonate.]

Not more than one drop of the suspected urine is let fall into the tube
from a pipette held in an upright position. Drops of equal size are
thus secured. The contents of the tube are again freely boiled for a
few seconds, after which the tube should be raised an inch or more from
the flame and held without shaking, while the solution is kept quite
hot, but not boiling, for exactly one minute. If glucose be present in
abnormal amount, the soft rich blue will be seen first of all to darken
into violet; then, according to the quantity of sugar, there will
appear in succession, purple, red, reddish-yellow, and finally
straw-yellow. When the last-named color has been developed the
slightest shaking of the tube will cause red streaks to fall from the
surface and mingle with the pale yellowness of the solution, while
further agitation will cause the return of purple and violet and the
restoration of the original blue.

The time required for the commencement of the reaction after the
boiling of the test liquid is in inverse proportion to the amount of
glucose present. When the latter is large, over 20 grains to the ounce,
it will be but a few seconds; but when small, 2 or 3 grains, from
thirty to sixty seconds may elapse. If the urine do not contain more
than the normal amount of sugar[47]--_i.e._ under half a grain to the
ounce--the color of the solution {217} at the end of the heating for
one minute will be unchanged. The test is available by artificial light
as well as by daylight.

[Footnote 47: It will be noted from this that Oliver accepts the view
that there is a small amount of sugar in normal urine.]

Precautions.--1. Care should be taken during the testing not to shake
the tube or to permit free ebullition. 2. While keeping the contents of
the tube hot, the latter should not be held up between the eye and the
sky, for then the early color-changes will probably escape observation.
The tube should be kept below the eye-level and its contents viewed by
the reflected light of some bright object, such as a sheet of white
paper propped up an inch or two beyond the tube as a background. 3.
Oliver is not aware that the presence of earthy carbonates will prevent
the carmine reaction, but as a precautionary measure he suggests the
use of a soda-paper whenever the water is exceptionally hard. 4. The
acids of the urine rob the carmine-paper of much alkali, so that the
addition of more than a certain number of drops of urine--varying of
course with the degree of acidity--will at first retard and then
prevent the reaction. The addition of the soda-paper will prevent any
such interference, although Oliver says that by invariably submitting
only one drop of saccharine urine to the test-paper, and keeping up the
heating for not less than two minutes, he has never failed to obtain
the characteristic reaction without using a soda-paper. It is well to
remember, however, that an excessively acid urine may thus interfere,
and that the soda-paper will prevent it. 5. The blue color of the
carmine is discharged by caustic alkali--liquor potassae or sodae. The
only chance of being misled by this reaction lies in using an
imperfectly cleansed test-tube which may have contained Fehling's
solution or the alkaline picric solution. The caustic alkali converts
the blue carmine into a green solution, which, on heating, disappears;
nor does it return by again shaking the contents of the tube.

Critical comparison of this test with Fehling's solution and picric
acid by Oliver has shown that of sixty-four substances experimented
upon, normal and abnormal constituents of urine or medicines which
after ingestion are eliminated in the urine, Fehling's was reduced by
fifteen, picric acid by eleven, and indigo-carmine by eight. The only
substances producing the characteristic play of colors with
indigo-carmine test-papers reacted with both picric acid and Fehling's
solution. They were unoxidized phosphorus, ammonium sulphide,
milk-sugar, dextrin, inosit, gallic acid, tannic acid, and iron
sulphate. Both the carmine and picric acid were reduced by inosit,
which merely turned Fehling's solution green. On the other hand, uric
acid and urates, which reduce Fehling's solution, do not react with the
carmine test, while kreatinin, which reacts with picric acid also, does
not respond to the carmine. Albumen, if abundant, interferes with
Fehling, but not with the indigo-carmine.

Detection of Inosit.--It has been said that inosit sometimes
accompanies, and even substitutes, grape-sugar in the course of
diabetes. It has been mentioned that it does not reduce Fehling's
solution, but turns it olive-green. It reduces the carmine and alkaline
picric acid solution, and is therefore not recognizable by these. The
methods recommended for its recognition in the books are troublesome,
and as its presence in the absence of sugar indicates a favorable
change, it is not likely that a more precise recognition than is
furnished by the olive-green reaction will be needed for clinical
purposes.

PROGNOSIS.--The prognosis in diabetes depends upon the organ whose
{218} involvement is responsible for the symptoms, upon the stage at
which the condition comes under observation, and upon the age of the
patient. It has appeared to me that the cases of diabetes depending
upon pancreatic disease are the most intractable, that their progress
is scarcely checked by treatment, and that they are comparatively
rapidly fatal in their termination. In the others, where the symptom is
one of a central nervous lesion, it has always seemed to me to be of
secondary importance that the glycosuria is itself less marked, that it
is unattended by the other distinctive symptoms of diabetes, and that
its issue is that of the nervous malady.

Again, it is well known that the later in life diabetes occurs the more
amenable it is to treatment, and that if a proper diabetic diet be
adhered to by the patient his life need scarcely be shortened. On the
other hand, diabetes mellitus is a disease in which the expectant plan
is dangerous. If it does not improve it usually gets worse; and many a
patient has fallen a victim to his own indifference and indisposition
to adhere to a regimen under which he could have lived his natural term
of life. This is especially the case when the disease appears after
middle life.

If, on the other hand, the condition becomes thoroughly established
before twenty-five years of age, it is less amenable to treatment; but
even in such cases a promptly vigorous treatment is sometimes followed
by recovery. I have already mentioned the case of a child twelve years
old in which complete recovery took place.

If tubercular phthisis supervenes, recovery is not to be expected,
while intercurrent disease, as pneumonia, which is rather prone to
occur, is very much more serious and apt to terminate fatally.

TREATMENT.--The treatment of the aggregate of symptoms known as
diabetes mellitus is conveniently divided into the dietetic, the
medicinal, and the hygienic, of which the first is by far the most
important. The efficiency of this treatment depends upon the successful
elimination from the diet of all articles containing grape-sugar,
cane-sugar, beetroot-sugar, and starch, it being universally recognized
that in the early stages of the disease these foods are the sole source
of the glucose in the urine. The normal assimilative action of the
liver, by which the carbohydrates are first stored up as glycogen, and
then gradually given out as glucose or maltose to be oxidized, being
deranged, such foods not only become useless as aliments, but if
continued seem to aggravate the glycosuria, and the excretion of sugar
steadily increases. There is, therefore, a double reason for excluding
them from the food. This is easiest accomplished by an exclusive milk
diet. The exclusive milk treatment of diabetes was suggested by A.
Scott Donkin in 1868. That he is correct in his assertion that in the
early stages of diabetes lactin or sugar of milk is quite assimilable,
and does not in the slightest degree contribute to the production of
glycosuria, I cannot doubt; that it is in this respect even superior to
casein, as claimed by Donkin, I am not prepared to state from actual
knowledge; but that casein itself resists the sugar-forming progress
immeasurably greater than any other albuminous substance, so that in
all but the most sure and advanced or complicated cases its arrest is
complete, I am also satisfied. Certain it is that in a large number of
diabetics the use of a pure skim-milk regimen results in a total
disappearance of the sugar from the urine. That in a certain proportion
of these cases a {219} gradual substitution of the articles of a mixed
diet may be resumed without a return of the symptoms is also true. In
other more confirmed cases the use of skim-milk results in a decided
reduction in the amount of sugar, with an abatement of other symptoms,
which continues as long as the diet is rigidly observed. In still other
cases, while the skim-milk treatment makes a decided impression upon
the quantity of sugar, it still remains present in considerable amount,
while the disease progresses gradually to an unfavorable issue. These
three classes of cases represent, ordinarily, different stages of the
disease, so that it may be said that as a rule cases recognized
sufficiently early may be successfully treated with skim-milk, although
it may occasionally happen that cases pursue a downward course from the
very beginning despite all treatment. Yet I have never seen a case
which, when taken in hand when a few grains of sugar only to the ounce
were present, failed to yield to this treatment.

As to the method of administration, my practice with adults is to give
eight ounces (an ordinary tumblerful) every two hours, beginning at
seven or eight o'clock in the morning, and continuing to the same hour
in the evening. Sometimes it is well to begin with half as much at
first, but rapidly to increase to the required amount. This method
ensures the ingestion of three to four quarts daily--a quantity
generally sufficient to maintain the body-weight of an adult person of
average size and taking moderate exercise, although a slight reduction
may take place at first. But if the individual is very active or of
large size, it will not be found sufficient. In such event the quantity
must be increased as demanded by a feeling of unsatisfied hunger. I
have known fourteen pints to be taken in twenty-four hours. But when
the quantity becomes thus large, the inconvenience in ingesting it is
very great, and it is much more convenient to coagulate the casein of a
part of the milk and use the curd thus obtained, while the second part
is drunk. Curd may be seasoned with salt to make it more palatable, and
should be thoroughly masticated before it is swallowed.

The milk should not be taken too cold, especially if the amount
ingested is large, else it is likely to reduce the temperature of the
stomach below the point necessary for gastric digestion. The
temperature should not be less than 60 degrees F., nor much over 100
degrees. Something depends upon the idiosyncrasies of the patient,
which must be the guide as to temperatures intermediate between those
named.

The chief advantage of the skim-milk over the unskimmed is simply that
it is more easy of digestion. Many persons who cannot take unskimmed
milk for any length of time without its deranging the digestion, or, as
is commonly said, making them bilious, can take with impunity milk from
which the cream is removed. Although Salomon[48] claims to have shown
that glycogen is produced in the liver of rabbits fed upon pure olive
oil, it is at least probable that fat is among the last of the
substances undergoing this conversion, and in ordinary cases of
diabetes it is rather its indigestible nature which renders it prudent
to remove from milk the greater proportion of fat by skimming it off.

[Footnote 48: _Virchow's Archiv_, Bd. 61, Heft 3, 1874, 18.]

Still more easily assimilable is the peptonized milk, in which the
casein is at least partially digested, and it should be employed where
there is any {220} difficulty in the way of using the ordinary milks.
Either skimmed or unskimmed milk may be used for peptonizing, the
latter peptonized being quite as easy of digestion as the former
unpeptonized. I have found the extractum pancreatis of Fairchild
Brothers & Foster most successful in the peptonizing of milk, and
according to the following directions: Into a clean quart bottle put 5
grains of extractum pancreatis, 15 of bicarbonate of sodium, and a gill
of cool water; shake, and add a pint of fresh cool milk. Place the
bottle in a pitcher of hot water or set the bottle aside in a warm
place, usually for three-quarters of an hour. When the milk has
acquired a slightly bitter taste, it has been completely
peptonized--that is, the casein has been completely converted into
peptone. After the process is complete the milk must be immediately put
on ice.

It is not always necessary to completely peptonize the milk, and if the
bitter taste is unpleasant the process may be stopped short of this by
putting the milk on ice, the degree of digestion depending upon the
length of time the milk is kept warm.

While I am confident that the promptest and most effectual method of
eliminating sugar from the urine is by a milk diet, it occasionally
happens that a patient cannot or will not submit to so strict a
regimen. In other instances, again, it is not necessary to resort to
it, because a less restricted diet answers every purpose.

A suitable diabetic diet would also be obtained by eliminating from the
bill of fare all saccharine and amylaceous and other sugar-producing
substances. Such a diet is, strictly speaking, impossible. For, apart
from the fact just mentioned that even fats, as well as albuminous
substances to a degree, are capable of producing glycogen, the monotony
of a pure meat diet soon becomes unbearable, to say nothing of other
derangements it may produce. Fortunately, it is not necessary that such
an exclusive diet should be maintained, for certain saccharine foods
seem capable of resisting the conversion into sugar more than others.
Sugar of milk, or lactin, has already been mentioned as one of these,
and to it may be added the sugar of some fruits, and probably also
inosit or muscle-sugar, mannite or sugar of manna, and inulin, a
starchy principle abundant in Iceland moss. It is found also that there
are many vegetable substances containing small quantities of sugar and
sugar-producing principles which may be used with impunity in at least
the milder forms of diabetes. This being the case, a bill of fare for
diabetics may be constructed quite liberal enough to satisfy the palate
of most reasonable persons by whom it is attainable.

FOOD AND DRINK ADMISSIBLE.--Shell-fish.--Oysters and clams, raw and
cooked in any way, without the addition of flour.

Fish of all kinds, fresh or salted, including lobsters, crabs,
sardines, and other fish in oil.

Meats of every variety except livers, including beef, mutton, chipped
dried beef, tripe, ham, tongue, bacon, and sausages; also poultry and
game of all kinds, with which, however, sweetened jellies and sauces
should not be used.

Soup.--All made without flour, rice, vermicelli, or other starchy
substances, or without the vegetables named below as inadmissible.
Animal soups not thickened with flour, beef-tea, and broths.

Vegetables.--Cabbage, cauliflower, brussels-sprouts, broccoli, green
{221} string-beans, the green ends of asparagus, spinach, dandelion,
mushrooms, lettuce, endive, coldslaw, olives, cucumbers fresh or
pickled, radishes, young onions, water-cresses, mustard and cress,
turnip-tops, celery-tops, or any other green vegetables.

Fruits.--Cranberries, plums, cherries, gooseberries, red currants,
strawberries, apples, without sugar. Or they may be stewed with the
addition of bicarbonate of sodium instead of sugar. (See below.)

Bread and cakes made of gluten, bran, or almond flour, or inulin, with
or without eggs and butter. Griddle-cakes, pancakes, biscuit,
porridges, etc. made of these flours. Where especial stringency is
required these should be altogether omitted.

Eggs in any quantity and prepared in all possible ways, without sugar
or ordinary flours.

Nuts.--All except chestnuts, including almonds, walnuts, Brazil-nuts,
hazel-nuts, filberts, pecan-nuts, butternuts, cocoanuts.

Condiments.--Salt, vinegar, and pepper in moderate quantities.

Jellies.--None except those unsweetened. They may be made of
calf's-foot or gelatin and flavored with wine.

Drinks.--Coffee, tea, and cocoa-nibs, with milk or cream, but without
sugar; also milk, cream, soda- (carbonated) water, and all mineral
waters freely; acid wines, including claret, Rhine, and still Moselle
wines, very dry sherry; unsweetened brandy, whiskey, and gin. No malt
liquors, except those ales and beers which have been long bottled, and
in which the sugar has all been converted into carbonic acid and
alcohol.

Vegetables to be especially Avoided.--Potatoes, white and sweet, rice,
beets, carrots, turnips, parsnips, peas, and beans; all vegetables
containing starch or sugar in any quantity.

The following list, including essentially the same articles, but
arranged in the shape of a true bill of fare, by Austin Flint, Jr.,[49]
will be found very convenient:

BILL OF FARE FOR DIABETES.--Breakfast.--Oysters stewed, without flour;
clams stewed, without flour. Beefsteak, beefsteak with fried onions,
broiled chicken, mutton or lamb chops; kidneys, broiled, stewed, or
devilled; tripe, pigs' feet, game, ham, bacon, devilled turkey or
chicken, sausage, corned-beef hash without potato, minced beef, turkey,
chicken, or game with poached eggs. All kinds of fish, fish-roe,
fish-balls, without potato. Eggs cooked in any way except with flour or
sugar, scrambled eggs with chipped smoked beef, picked salt codfish
with eggs, omelets plain or with ham, with smoked beef, kidneys,
asparagus-points, fine herbs, parsley, truffles, or mushrooms.
Radishes, cucumbers, water-cresses, butter, pot-cheese. Tea or coffee,
with a little cream and no sugar. (Glycerin may be used instead of
sugar if desired.) Light red wine for those who are in the habit of
taking wine at breakfast.

Lunch or Tea.--Oysters or clams cooked in any way except with flour;
chicken, lobster, or any kind of salad except potato; fish of all
kinds; chops, steaks, ham, tongue, eggs, crabs, or any kind of meat;
head-cheese. Red wine, dry sherry, or Bass's ale.

{222} Dinner.--Raw oysters, raw clams.

Soups.--Consomme of beef, of veal, of chicken, or of turtle; consomme
with asparagus-points; consomme with okra, ox-tail, turtle, terrapin,
oyster, or clam, without flour; chowder, without potatoes, mock turtle,
mullagatawny, tomato, gumbo filet.

Fish, etc.--All kinds of fish, lobsters, oysters, clams, terrapin,
shrimps, crawfish, hard-shell crabs, soft-shell crabs, (No sauces
containing flour.)

Relishes.--Pickles, radishes, celery, sardines, anchovies, olives.

Meats.--All kinds of meat cooked in any way except with flour; all
kinds of poultry without dressings containing bread or flour; calf's
head, kidneys, sweetbreads, lamb-fries, ham, tongue; all kinds of game;
veal, fowl, sweetbreads, etc., with curry, but not thickened with
flour. (No liver.)

Vegetables.--Truffles, lettuce, romaine, chicory, endive, cucumbers,
spinach, sorrel, beet-tops, cauliflower, cabbage, brussels-sprouts,
dandelions, tomatoes, radishes, oyster-plant, celery, onions,
string-beans, water-cresses, asparagus, artichoke, Jerusalem
artichokes, parsley, mushrooms, all kinds of herbs.

Substitutes for Sweets.--Peaches preserved in brandy without sugar;
wine-jelly without sugar, gelee au kirsch without sugar, omelette au
rhum without sugar; omelette a la vanille without sugar; gelee au rhum
without sugar; gelee au cafe without sugar.

Miscellaneous.--Butter, cheese of all kinds, eggs cooked in all ways
except with flour or sugar, sauces without sugar or flour. Almonds,
hazel-nuts, walnuts, cocoanuts. Tea or coffee with a little cream and
without sugar. (Glycerin may be used instead of sugar if desired.)
Moderately palatable ice-creams and wine-jellies may be made, sweetened
with pure glycerin; but although these may be quite satisfactory for a
time, they soon become distasteful.

Alcoholic Beverages.--Claret, burgundy, dry sherry, Bass's ale or
bitter beer. (No sweet wines.)

Prohibited.--Ordinary bread; cake, etc. made with flour or sugar;
desserts made with flour or sugar; vegetables, except those mentioned
above; sweet fruits.

[Footnote 49: "On the Treatment of Diabetes Mellitus," a paper read
before the American Medical Association at its meeting in Washington,
May, 1884, and published in the _Journal_ of the association July 12,
1884. I have so far modified the bill of fare as to permit the use of
milk, which Flint excludes.]

One of the foods the omission of which is most illy borne by the
diabetic, however great his previous indifference to it, is wheaten
bread, while the substitutes which have been at different times
suggested for it very imperfectly supply its place. Perhaps the best
known of these is the bread made of gluten flour. It was suggested by
Bouchardat in 1841, and is made by washing the ordinary wheat flour to
free it from starch.[50]

[Footnote 50: The Health Food Company, of 74 Fourth Avenue, N.Y.,
prepare a gluten flour by first removing the five bran-coats,
pulverizing the cleaned berry by the cold-blast process, stirring the
powder into iced water, and precipitating the gluten, cellulose, and
mineral matters, siphoning off the water holding in suspension the
starch, and drying out the precipitate. In this manner the salts of the
wheat are retained. A purified gluten made by the Health Food Company
is deprived of the cellulose walls of the cells in which the gluten
granules are held. Directions for making gluten bread and cakes of
various kinds are furnished by the company on application.]

Gluten flour, however prepared, contains some starch, as indeed it must
if bread is to be made out of it; and I confess to having been a good
deal disappointed in its use. I have known the sugar absent in a {223}
selected diet to return when gluten bread was permitted, and again
disappear on its withdrawal. Of course gluten flour contains less
starch than the ordinary wheat flour, and there may be cases where the
starch in the former can be assimilated when the quantity in the latter
cannot be. The gluten may be made into porridge.[51]

[Footnote 51: Gluten porridge is made by stirring the gluten into
boiling water until thick enough, and then keeping up the boiling
process for fifteen minutes. A little salt and butter are added at the
close to improve the flavor, and it may be eaten with milk or cream.]

A method of getting rid of the starch and sugar in bread, suggested by
Liebig and tried by Vogel, consists in converting the starch into sugar
by the action of diastase and dissolving out the sugar thus produced.
This is accomplished by treating thin slices of bread with an infusion
of malt. The bread is then washed, dried, and slightly toasted.

Another substitute for wheaten flour is the bran flour whence the
starch is removed by washing.[52] The bran itself, according to
Parkes,[53] sometimes contains as much as 15 per cent. of nitrogenous
matter, 3.5 per cent. of fats, and 5.7 per cent. of salts. It is
therefore not wholly innutritious, although the salts are washed out in
removing the starch. It is considered especially useful when there is
constipation, the slightly irritant properties of the bran aiding in
maintaining a proper peristalsis and action of the bowels. These
irritant properties are, however, inversely as the degree of
comminution. The bran flour may be made with milk and eggs into a
variety of cakes, of which the best known are those made according to
Camplin's directions.[54]

[Footnote 52: A very carefully prepared bran flour, as well as a
wheat-gluten flour, is prepared by John W. Sheddon, pharmacist, corner
of Broadway and Thirty-fourth street, New York City.]

[Footnote 53: _Practical Hygiene_, 5th ed., Philadelphia, 1878, p.
222.]

[Footnote 54: The following are Camplin's directions for making biscuit
of bran flour: To one quarter of a pound of flour add three or four
fresh eggs, one and a half ounces of butter, and half a pint of milk;
mix the eggs with a little of the milk, and warm the butter with the
other portion; then stir the whole together well; add a little nutmeg
or ginger or other agreeable flavoring, and bake in small forms or
patterns. The cake, when baked, should be about the thickness of an
ordinary captain's biscuit. The pans must be well buttered. Bake in
rather a quick oven for half an hour. These cakes or biscuits may be
eaten by the diabetic with meat or cheese for breakfast, dinner, or
supper; at tea they require rather a free allowance of butter, or they
may be eaten with curd or any soft cheese.]

Where extreme restriction of diet is not required the ordinary bran
bread of the bakers may be used. The unbolted flour of which this is
made of course contains the starchy principles, but in consequence of
the retention of the bran the proportion of starch is less. The
cold-blast flour of the Health Food Company is said to contain the
nutritious, but not the innutritious, parts of the bran.[55]

[Footnote 55: It is made by pulverizing the carefully cleaned wheat by
a compressed, cold air blast, which strikes the wheat and dashes it to
atoms.]

The almond food suggested by Pavy is another substitute for bread. The
almond is composed of 54 per cent. of oil, 24 per cent. of nitrogenized
matter known as emulsin, 6 per cent. of sugar, and 3 per cent. of gum,
but no starch enters into its composition. Theoretically, therefore,
the food should be everything that can be desired if the gum and sugar
can be removed. The latter is done by treating the powdered almonds
with boiling water slightly acidulated with tartaric acid, or soaking
the almonds in a boiling acidulated liquid which may form a part of the
process for blanching. The boiling and acid are necessary to
precipitate {224} the emulsin, which would otherwise emulsify the oil
of the almond. Pavy speaks well of biscuit made of almond flour and
eggs, which he says go very well with a little sherry or other wine,
although he admits they are found too rich by some for ordinary
consumption. One person only under my observation has used the almond
food, and found it unpalatable.

Seegen recommends an almond food made as follows: Beat a quarter of a
pound of blanched sweet almonds in a stone mortar for about
three-quarters of an hour, making the flour as fine as possible; put
the flour thus obtained into a linen bag, which is then immersed for an
hour and a quarter in boiling water acidulated with a few drops of
vinegar. The mass is thoroughly mixed with three ounces of butter and
two eggs; the yolks of three eggs and a little salt are added, and the
whole is to be stirred briskly for a long time. A fine froth made by
beating the white of the three eggs is added. The whole paste is now
put into a form smeared with melted butter and baked by a gentle fire.

Biscuits made of inulin, the starchy principle largely contained in
Iceland moss, were suggested by Kuelz. Although a starch, it is one of
the assimilable ones alluded to, of which small quantities at least may
be taken as food without appearing in the urine as sugar. The biscuits
are made with the addition of milk, eggs, and salt, and are
inexpensive.

To some persons sugar is almost as imperative a necessity as bread,
although to many it is not a very great sacrifice to omit it from
ordinary cooking, if not from tea and coffee. For the latter it is just
as well to dispense with sugar altogether. But where patients feel that
they must have some substitute for sugar, glycerin has been suggested
for this purpose, at least for sweetening tea and coffee. But Pavy has
noted[56] that under the use of glycerin the urine increased from three
and three and three-fourth pints to between five and six pints, and the
sugar from 1100 grains to 3000 grains per diem, in the course of three
days. Its withdrawal was followed by a prompt fall in both the urine
and sugar, a return to it by a second increase, and subsequent
withdrawal by another decline. Along with the increase of urine and
sugar came also more thirst and discomfort. An examination of the
chemical composition of glycerin would seem to confirm these results of
experience. Glycerin is represented by C_{3}H_{8}O_{3}, sugar by
C_{6}H_{12}O_{3}, and glycogen by C_{6}H_{10}O_{5}; whence it is
evident that a conversion of glycerin into sugar may take place in the
liver. These facts seem to show conclusively that glycerin is no
suitable substitute for sugar. I therefore do not use it.

[Footnote 56: _On Diabetes_, London, 1869, p. 259.]

From what has been said it may be inferred that sugar of milk, mannite,
and laevulose, or fruit-sugar, are admissible where sugar is demanded.
They may be tried, but the urine should be carefully examined under
their use, and if glycosuria occur or be increased they should be
promptly omitted.

Almost every purpose of sugar in the cooking of acid vegetables is
served by bicarbonate of sodium or potassium. As much bicarbonate of
potassium to the pound as will lie upon a quarter of a dollar will
neutralize the acidity of most fruits which require a large amount of
sugar to mask this property. In this manner cranberries, plums,
cherries, gooseberries, red currants, strawberries, apples, peaches,
and indeed {225} all fruits to which sugar is usually added in the
cooking, become available to the diabetic.

In the matter of drinks, where the patient is not on a skim-milk diet,
which usually affords as much liquid as is required by the economy,
little restraint need be placed upon the consumption of water, which is
demanded to replace that secreted with the sugar. Instead of water,
Apollinaris water, Vichy, or the ordinary carbonated water may be used
if preferred, and to many they are much more refreshing by reason of
the carbonic acid they hold in suspension. Apollinaris water is
particularly so, and one of my patients, who recovered completely under
a suitable selected diet with which this mineral water was permitted,
insists that it was that which cured her.

Where a simple selected diet is adopted, tea and coffee without sugar
are usually permitted. The propriety of the substitutes for sugar
already referred to must be determined by circumstances.

Of distilled and fermented liquors, moderate quantities of whiskey and
brandy, dry sherry and madeira, the acid German and French wines--in
fact, any non-saccharine wines--may be permitted. A medical friend who
reports himself about cured of diabetes writes me that he has consumed
eighty gallons of Rhine wine since he began to adhere closely to a
diabetic diet. On the other hand, the free use of the stronger
alcoholic drinks has been charged with causing diabetes, and I have
known such use to produce a recurrence of sugar. No malt liquors,
except those in which the sugar has been completely converted into
carbonic acid and alcohol, should be used. Bass's ale may be allowed
where no especial stringency is required.

HYGIENIC TREATMENT.--The patient should be surrounded by the most
favorable hygienic influences. He should sleep in well-ventilated
rooms; pass much time in the open air; bathe regularly, but not in
water that is very cold, and especially the body should not be long
submerged in cold water, as the liver must share the general internal
hyperaemia incident to prolonged cooling of the skin, and increased
glycosuria may result. I have known sugar to reappear after a prolonged
drenching of the skin of patients overtaken by a rainstorm. Perhaps the
most suitable time for the hot or tepid bath is on retiring in winter,
but in summer it may be taken on rising. Thorough friction of the
entire body should be practised after the bath or independently of it.
An ounce or two of sodium carbonate may be added to it with advantage,
as it softens the skin and facilitates the removal of the effete
epithelium. The bowels should be kept regularly open, as the effect of
their confinement is to produce torpor and congestion of the liver.

Certain natural mineral waters have always enjoyed a reputation for the
cure of diabetes, and notably those of Vichy and Carlsbad. The former
is an alkaline water with a slight laxative tendency, and the latter a
decided aperient alkaline-saline water; and it is not unlikely that
they owe a part of their good effects to an action upon the liver and
upper bowel. This seems the more likely because Carlsbad, which enjoys
the highest reputation, contains a far larger proportion of chlorides
and sulphates, which are purgative. Vichy water contains 35 grains of
carbonates to the pint, and Carlsbad 11, but the latter contains twice
the proportion of chlorides, or 8 grains to the pint, and ten times as
much sodium {226} sulphate, or 19 grains to the pint. They may be used
as adjuvants to the treatment, a pint of Vichy or half as much Carlsbad
in the morning. Being imported waters, they are comparatively
expensive, and I know of no American waters which closely approach them
in composition.

Of American waters, the Saratoga Vichy contains twice as much chlorides
as the Carlsbad, 17.7 grains to the pint, but no sulphates. It contains
about the same amount of carbonates as Vichy. It is therefore a
saline-alkaline water, and may be expected to serve the purposes of
Vichy and some of those of Carlsbad, for which it may be substituted.
Most of the American mineral waters vaunted as useful in diabetes will
be found, on comparison with these waters, to be chemically
indifferent, and therefore about as useful as so much ordinary
spring-water. Of the Crab Orchard Springs in Kentucky, the Sowder's
spring contains 25 grains of sulphate of sodium and magnesium and 7
grains of sodium chloride to the pint, therefore about the same
proportion of the two substances combined as Carlsbad; yet I am not
aware that these waters have any reputation in diabetes. The waters of
Bedford Springs, Pennsylvania, also approximate them in the proportion
of sulphates of sodium and magnesium.

Other Saratoga waters have an undoubted action on the liver through
their chlorides, and may be used in lieu of the European waters above
referred to, and of the Saratoga Vichy, when these cannot be obtained;
such are the Geyser spring, which contains 70 grains of chlorides to
the pint, and the Hathorn, containing 63 grains.

MEDICINAL TREATMENT.--While the dietetic treatment, and especially the
skim-milk treatment, of diabetes mellitus is much to be preferred for
its results over an exclusively medicinal treatment, and is of itself
sufficient to control, if not to cure, a large number of cases, yet
instances arise in which it is insufficient to complete the removal of
sugar from the urine, and there are others in which it is impossible
for various causes to carry out such treatment.

In my book on _Bright's Disease and Diabetes_, published three years
ago, I gave the preference of drugs to ergot; but since then extended
opportunities have convinced me that codeia is a far more efficient
remedy. Repeated comparative trials of this drug in the wards of the
Philadelphia Hospital and elsewhere have satisfied me of this. The
trials have been made while the patients were upon a mixed diet, which
I hold to be the only fair way of arriving at a knowledge of the true
value of a drug in the disease. Codeia was first suggested by Pavy in
lieu of opium and morphia, which had long been used, his reason being
that it did not produce the same narcotic effect. Favorable reports
upon its use have been made by Foster, Image, Brunton, R. Shingleton
Smith, Cavafy, Austin Flint, Sr., Harvey L. Byrd, and others. It may be
given in pill or solution. One should begin with 1/4 of a grain three
times a day, increasing 1/4 of a grain daily until the sugar disappears
or the remedy ceases to have any effect, or until drowsiness is
produced. Thus gradually increasing, I have reached as high as 47
grains in a day. Cavafy has given 15 grains three times daily.

Opium--which is said to have been used by Aetius for this disease--or
morphia might be used if codeia cannot be obtained, but they are less
efficient, more dangerous, and more apt to produce the troublesome
{227} symptom of constipation. MacGregor[57] gave in one case 60 grains
of opium, and in another 90 grains, in the twenty-four hours.

[Footnote 57: _London Medical Gazette_, 1837.]

While I have seen the most striking results upon the quantity both of
sugar and urine during the administration of codeia, and at the same
time have noted a gain in flesh and strength, I cannot say that I have
ever seen a case totally recover under its use. Such cases are,
however, reported by others. I have always used it in the very worst
cases, where dietetic measures had also failed to remove the sugar. As
to the mode of action of codeine, we can only speculate. It may be said
that it quiets the irritation of the vaso-motor centre, whence result
the glycosuria and other symptoms of diabetes.

Next to codeine in efficiency, of drugs, is ergot. The favorable
results of its use are more easily explained by its physiological
action--contraction upon the muscular walls of blood-vessels--than
those of codeine, but it is not so efficient a remedy. It may be used
by beginning with half a drachm, and increasing to a drachm, four times
a day. Larger doses than this, as much as half an ounce four times a
day, have been given, but the stomach rarely permits their continuation
for any length of time.

Bromide of potassium, an old remedy for diabetes, has recently been
revived and much lauded by the French physicians, but I have never
found any results from its use. I can understand, however, how in
certain cases of nervous origin it may be useful.

Comparatively recently, Clemens of Frankfort-on-the-Main has
recommended the use of what he terms brom-arsen or bromide of arsenic.
The dose is one-forty-eighth of a grain three times a day, gradually
increased by this same amount until one-sixth or one-fifth of a grain
is given daily.[58] Clemens, however, unites with its use a dietetic
treatment. I have used it in connection with an unselected diet, and
have not found the results claimed by Clemens. It is, however, both
tonic and sedative, and as such is to be recommended in conjunction
with other measures.

[Footnote 58: The late Mr. R. F. Fairthorne, with Mr. James T. Shinn,
apothecary, cor. Broad and Spruce streets, Philadelphia, prepared for
me a solution of bromide of arsenic in the following manner: 77 grains
of metallic arsenic in powder are added in small portions to 240 grains
of bromine, the latter being placed in a long test-tube immersed in
ice-water to control the otherwise violent reaction. One hundred grains
of the tribromide thus obtained are dissolved in sufficient distilled
water to make ten fluidounces. One minim will then contain
one-forty-eighth of a grain.]

Arsenic itself has some reputation in the treatment of diabetes, based
upon the observation of Salkowsky that glycogen diminishes in the
livers of animals poisoned with arsenic. It is at least a good adjuvant
tonic. Leube gave it in diabetes in doses of one-third of a grain three
times a day.

Strychnia is also very useful as a tonic, and may be used either alone
or in the shape of the sulphate, or combined with arsenic and iron, or
it may be given, perhaps preferably, in solution in combination with an
acid. Given in combination with phosphoric acid, I believe it the most
valuable tonic available in this disease.

To supply the phosphates, in which gluten bread is deficient, as well
as for their tonic effect, the various preparations of phosphates are
useful. {228} The well-known compound syrup of the phosphates, or
Parrish's chemical food, may be considered a type of these
preparations. Every fluidrachm, which is a dose, contains 2-1/2 grains
of calcium phosphate, 1 grain of ferric phosphate, with fractions of a
grain of sodium and potassium phosphate with free phosphoric acid.
Similar is the solution of phosphates and phosphoric acid[59] known in
this country as solution of phosphoric acid with iron, or the latter
may be omitted.

[Footnote 59: Rx. Calcii phosphat. gr. iij;
                  Magnesii   "     gr. ss;
                  Potassii   "     gr. iv;
                  Ferri      "     gr. ss;
                  Ac. phosphoric   minim vj;
                  Aquae q. s. ad.  fluidrachm i, which is a dose.]

Iodide of potassium has been used in some cases with satisfactory
results, and may be expected to be useful where syphilitic disease of
the nervous system is suspected.

Seegen has seen sugar disappear from the urine under a dosage of 20 to
30 drops of tincture of iodine daily, but the sugar reappeared after
the remedy was discontinued.

Lactic acid was recommended by Cantani on theoretical grounds as a
substitute for sugar. He supposes that in health the sugar ingested is
converted by the liver into lactic acid, and he would furnish the
latter already formed, and thus spare the liver this function. Senator
also favors the use of this acid for a similar purpose, but reasons
that in health sugar is converted into lactic acid in the small
intestine, while in diabetes this conversion is interfered with. Hence,
too, it should be given fully formed. Patients under its use are said
to gain in weight and to become stronger, while it is not claimed that
it alone diminishes the glycosuria; this must be brought about by a
selected diet. The lactic acid is simply an important force-producer
not otherwise obtainable, because sugar fails to undergo its usual
conversion. Cantani recommends that from 75 to 150 grains of the acid
should be taken daily in from 8 to 10 fluidounces of water. Diarrhoea
and pains in the joints are said to follow the use of large quantities
of the drug, but these again disappear on its omission. My experience
is limited to a single case, which recovered while taking 30 drops
three times a day in conjunction with Carlsbad water and a pill of
iron, quinia, and arsenic.

Senator suggested that the fatty acids--oleic, palmitic, stearic, and
butyric--be used on the same principle that lactic acid is given, that
their force-producing power may be availed of. To this end he
prescribed, with partially satisfactory results, soap in pills
containing 2-1/3 grains each, of which four were taken daily.

Cod-liver oil is especially suitable as a food where debility is to be
combated. Even those who claim that fats are convertible into sugar in
the liver admit that it is only in the most advanced stages of diabetes
that such conversion takes place. Cod-liver oil, therefore, in common
with other fats, may form part of a diabetic diet, and is especially
indicated where phthisis is present, as it so often is, in the latter
stages of the disease, or indeed whenever a good tonic is indicated.

In 1882, Moleschott[60] suggested the use of iodoform in diabetes. He
reported the effect of its use in five cases, giving .1 to .3 grm. (1.5
to {229} 4.5 grs.) in pill with extract of lactucarium and cumarin, the
purpose of the latter being to disguise the odor. His formula was as
follows: Iodoform, 1 gram (15 grs.); ext. lactuc. sat., .1 gram (15
grs.); cumarin, .1 gram (1.5 grs.), to be made into twenty pills. In
one case the sugar disappeared in twelve days; in the second, at the
end of six months; in the third case it had diminished from 14.4 to 1.6
grams in three months; in the fourth, from 28 grams to 1.6 in four
months; and in the fifth case, from 9.2 to 6.1 grams.

[Footnote 60: _Wiener Med. Wochenschr._, Nos. 17, 18, 19.]

The use of the remedy in Moleschott's hands produced no unpleasant
results, but Drasch,[61] who used the same treatment after Moleschott's
method in three cases, with the effect of diminishing the thirst, the
quantity of urine, and the proportion of sugar, found excessive itching
of the skin, diminished appetite, and diarrhoea to result in such
degree as to demand its disuse in the majority of cases. Iodoform has
been used by the Italian physicians De Renzi,[62] Bozzolo,[63] and
Silvestrini,[64] and by Sara E. Post[65] of New York, with varying but
generally favorable results, except in Silvestrini's case. These
results included diminution in thirst, quantity of sugar and urea, with
increase in weight. The drug deserves a trial in doses of from 1 to 2
grams (15 to 30 grains) a day, but due regard should be had to possible
toxic effects; and to this end the administration should be interrupted
at the end of one or two weeks, and the interruption continued for a
like period. It may be given in pill or in capsule, and in divided
doses or in a single dose at bedtime. The latter course is recommended
by Post, and is said to avoid eructations and anorexia. Theories of its
action based upon experimental use of poisonous doses ascribe its
effect to a primary stimulating and ultimately fatally degenerative
effect upon the protoplasm of cells, and especially those of the liver
and nervous system.

[Footnote 61: _Wiener Med. Presse_, 1882, xxiii. 1487.]

[Footnote 62: "Tre Storie di Diabete." _Gior. internaz. d. sc. med._,
Nap., 1882, N. S. iv. 913-917.]

[Footnote 63: "Sur l'action du iodoforme dans la diabete sucre," _Arch.
ital. de biol._, Turin, Feb., 1883, iii. 317-321.]

[Footnote 64: "Iodoforme dans le diabete," _La France Med._, October,
1883, ii. 567.]

[Footnote 65: _Archives of Medicine_, April, 1884, p. 116.]

Transfusion of blood has been recommended by Dieulafoy,[66] and is
approved of by Ralfe,[67] especially to combat the symptoms of
acetonaemia, which, if due to a toxic agent, as seems most likely,
should be met by altering the percentage composition of the blood with
relation to the toxic agent.

[Footnote 66: "Etude sur la Transfusion du Sang dans le diabete sucre,"
_Bulletin et Mem. Soc. Med. de Hop. de Paris_, 1884, 4, S. 1, 38, 41.]

[Footnote 67: "Discussion before the Path. Soc. of London," _Lancet_,
Apr. 7, 1883, p. 592.]

Diabetic neuralgia yields generally to the treatment of the disease in
general correspondingly to the reduction in the quantity of sugar, and
at times to salicylate of sodium, while it does not respond to morphia
or other remedies for ordinary neuralgia.

The alkalies, which attained some reputation after Mialhe claimed for
them the power of destroying sugar in the blood and of neutralizing the
fatty acids which were thought to accumulate there in consequence of
the deficient action of the skin, are not often used at the present
day. Potassium carbonate was the favorite preparation, and in the hands
of Pavy its use seems to have been followed by good results. He gave it
in 10, 15, and 20 grain doses in combination with aromatic spirit of
{230} ammonia. Sodium bicarbonate was less satisfactory, as were also
potassium acetate, potassium citrate, and Rochelle salts. These were
given in doses of from four drachms to an ounce daily. In Germany, too,
the alkaline treatment has been used to some extent.

As is the case with so many diseases which are incurable by any special
treatment, a large number of remedies have at different times been
suggested for diabetes, mostly on a foundation which does not admit of
close analysis. One of these was the nitrate of uranium, suggested by
Dale of Lemont, Pennsylvania, who gave it in doses of 1 grain three
times daily, increased to 3 if necessary, in pill, powder, or solution,
by aid of a few drops of nitric acid. He appears, however, to have used
it in connection with a selected diet. I have tried it both with and
without a selected diet; in the latter case there was no effect, and in
the former there was none which the diet alone would not have produced.

Sodium phosphate, salicylic acid, salicylate of sodium, have all been
used, it is claimed, with good results, and the late Dr. Dougherty of
Newark, New Jersey, used with apparent advantage a mixture into which
all of these, together with sodium carbonate, entered, made up with
glycerin, tincture of cardamom, and water, the doses being 2-1/2,
2-1/2, 4-1/2, and 8-1/2 grains respectively. Moleschott has also
obtained good results with salicylic acid.




{231}

SCROFULA.

BY JOHN S. LYNCH, M.D.


SYNONYMS.--Scrophula, Scrofulosis, Morbus scrophulosus, Struma, King's
evil, The evil, Quince, Cruels and Crewels (Scotice).

DEFINITION.--A morbid condition of the system manifested by a peculiar
liability to certain forms of nutritive disorders of the skin, mucous
membranes, joints, bones, organs of special sense, and especially the
lymphatic glands.

There is probably no disease of which it is more difficult to give an
exact and satisfactory definition than scrofula. The general tendency
of medical opinion within the last few decades has been to narrow the
significance of the term, and even to restrict it to those slow and
indolent inflammations and over-growths of lymphatic tissue which end
in caseation and finally imperfect suppuration. Formerly almost every
deviation from healthy functional activity in the young, as well as
every disorder of nutrition which could not be assigned to any definite
cause, was called struma; and thus, as Heule well remarks,[1] "Scrofula
became the receptacle into which one vaguely casts all the ailments
which afflict children under fourteen years, and of which we do not
know the cause."

[Footnote 1: _Handbuch der Rationellen Pathologie_.]

Before hereditary syphilis was understood all its manifestations were
classed as scrofulous, and at least one eminent authority in the United
States[2] has expressed the opinion that scrofula is only a
manifestation of the syphilitic poison in the second or third
generation. Rickets, chronic hydrocephalus, favus, lice, and worms
(Lugol), diabetes (Carmichael), and even scirrhus and cancer (R.
Hamilton), have all been classed as scrofulous diseases. Then there is
a large class of unhealthy persons whose morbid state can be no more
definitely expressed than by saying that they are "delicate" or of
"feeble health" or of "frail constitution," and by some all these are
included under the term scrofulous. But as knowledge advances, and
pathological knowledge as well as diagnostic acumen becomes larger and
keener, many of these affections and morbid conditions can be
eliminated from scrofula and assigned their true pathological and
nosological position.

[Footnote 2: S. D. Gross, _Transactions American Medical Association_,
1878.]

To many who have been educated in the more modern schools of medical
thought, therefore, our definition will appear much too broad, while to
others it may appear too narrow.

Scrofula is essentially and purely a diathetic, not a cachectic,
disease. {232} It is true that what may be called the manifestations or
lesions of the disease are often excited by some preceding dyscrasia,
and also that the long persistence of these lesions may excite a
cachectic condition which we might call the scrofulous cachexia; still,
as many children suffer from the lesions of scrofula who have never
exhibited any evidence of a precedent dyscrasia, but on the contrary
appear to be in perfect health, and many others, on the other hand,
show unmistakable evidence of ill-health and are decidedly dyscrasic,
yet are never attacked by scrofula, it is believed that every subject
of scrofula becomes so not because of any pre-existing dyscrasia or
cachexia, but because of some peculiar condition of the system--innate
or acquired--which constitutes a diathesis.

"The hypothesis," says Niemeyer,[3] "that scrofula depends upon a
faulty composition of the blood (dyscrasia), and that the lesions found
in scrofulous persons were due to a deposit in the tissues of a matter
circulated by the blood and called a scrofulous material, is almost
universally abandoned."

[Footnote 3: _Textbook of Practical Medicine_, vol. ii.]

But while insisting upon the peculiar and, so to say, specific origin
of the disease in some special condition of the system, without which
it will never exist, it is admitted that the lesions of scrofula do not
differ essentially from other similar lesions of the same tissues of a
non-scrofulous origin. They are mostly of an inflammatory nature, and
are only to be distinguished by the often trivial character of their
exciting causes--often, indeed, by the total absence of any known
exciting cause--and by their tediousness and intractability.

ETIOLOGY.--We believe, as already stated above, that the essential
cause of scrofula is some peculiarity in the constitution of the
tissues of the scrofulous subject; and we think it highly probable that
H. F. Formad of Philadelphia has pointed out what constitutes this
peculiarity. He declares--and the correctness of his observation has
been abundantly verified--that microscopic examination of the tissues
of certain animals characterized by their extreme aptness to be
affected by scrofula and tuberculosis, as well as of children known to
have been scrofulous or tuberculous, discloses the fact that the
lymph-spaces in these subjects are always more numerous, larger, and
more crowded with cells than in non-scrofulous subjects. The tissues of
the scrofulous are therefore coarser, less compact and solid, and there
is a greater tendency to undue cell-growth, than in the non-scrofulous.
And these are precisely the characteristics which they present
clinically, and such as we might have, a priori, expected to find.

This peculiarity of anatomical structure is in a large number of cases
undoubtedly inherited from the parents, but while heredity plays, as is
well known, an important part in the etiology of struma, it is not the
essential factor. Bad hygienic surroundings, overcrowding, and
consequent want of fresh air, improper food, consisting of a too great
proportion of starch, during the early months or years of life, will
cause the growing tissues to assume the peculiar anatomical arrangement
alluded to above. "A coarse diet, containing but little nourishment in
comparison with its bulk, is especially held in evil repute. The
earlier this injudicious feeding of an infant commences, so much the
greater danger that it will become scrofulous; hence the children fed
on pap furnish a very important contingent to the army of scrofulous
persons."[4] The {233} well-known fact that few children at the breast
suffer from scrofulous lesions, but that a large number do so within
the first two or three years after weaning, certainly tells in favor of
the belief that too much starch and an insufficiency of animal food
favor, if they do not actually produce, that faulty nutrition and
construction of tissues which we believe lies at the foundation of the
scrofulous diathesis. Independent, however, of improper food and the
other predisposing causes mentioned, it is quite probable that faulty
nutrition caused by accidental disease of the digestive or assimilative
organs during infancy may create a predisposition. How else can we
account for those not very rare cases in which from parents perfectly
free from any scrofulous taint a large family of children may be
reared, of which only one will suffer from any scrofulous lesions? Two
such instances have been brought to my notice, and as the children in
these cases lived upon a farm on the water-side, and enjoyed an
abundance of pure air and salt-water bathing, and were certainly not
stinted in food of proper quality, it is difficult to account for the
acquired diathesis except upon the hypothesis above. Among the general
predisposing causes of scrofula in addition to the special ones I have
mentioned may be added--

[Footnote 4: Niemeyer, _loc. cit._]

1. Locality and Climate.--It has long been believed that scrofula is
more common in the temperate zone than in the extreme north or in the
tropics. While this is probably true, it must be stated that a
sufficient amount of reliable statistics bearing upon this point have
not yet been collected to prove the fact beyond cavil. That we should
find that the disease prevails more extensively in cold and damp
situations than in warmer and drier ones is to be expected, since the
former conditions involve a greater confinement within dwellings, and
consequently a diminished supply of fresh air, which, as we have seen,
constitutes one of the predisposing causes of scrofula. Moreover, it is
in these situations we would encounter a greater number of catarrhs,
which, as we shall see, are known to be among the most active of the
exciting causes of the glandular affections of scrofula.

2. Season.--For the same reason we find that a large number of cases of
scrofula make their appearance in the early spring months, the results
of catarrh contracted during the previous winter or of the sudden
changes of temperature which accompany the transition of winter to
summer.

3. Age.--Scrofula is essentially a disease of early life, but not
exclusively so. As the diathesis can only be acquired directly from the
parent, or fortuitously by malnutrition during the period of active
growth, it follows that it becomes established, if at all, before the
age of twenty years. And as the predisposition seems to be quite strong
in most cases, and as the exciting causes are more apt to be applied
during the earlier years of life, it is not surprising that a very
large majority of the cases occur between the ages of three and fifteen
years. A few, however, escape during childhood, and only suffer from it
between twenty and thirty, while a small number only develop the
disease in old age. Rindfleisch mentions the period between twenty and
thirty as a common one for the development of hereditary scrofula; and
senile scrofula was first pointed out by Sir James Paget.[5] In all
these cases of deferred {234} manifestation of the scrofulous
diathesis--and they are not very numerous--it is to be presumed that
they have escaped the most active of the exciting causes of the
disease. Indeed, it is natural that a person having inherited the
predisposition should be more sedulously guarded--at first by his
parents, and afterward by himself--against the exciting causes of
scrofula during infancy and adolescence.

[Footnote 5: _Clinical Lectures and Essays_, London, 1875.]

4. Sex.--There is no reason to believe that sex plays any part in the
predisposition to this disease. Both sexes seem to be affected in about
equal proportions, but from the statistics bearing upon this point it
does seem to have some influence in determining the variety of its
lesions. Thus, females seem to be more frequently affected with
glandular disease, while males suffer from diseases of the joints in
the form of coxalgia, white swelling of the knee, and Pott's disease.

5. Condition in Life: Social Position.--If what we have said about the
predisposing influence of improper or insufficient food, overcrowding,
etc. be true, it will naturally be inferred that a large proportion of
the cases of scrofula will be found in the lower strata of society; and
this is true. Especially in cities, where the disease prevails most
extensively, we always find that the denizens of narrow streets, lanes,
and alleys furnish the largest contingent to the deaths as well as the
deformities from scrofula. It is here that the poor congregate to avail
themselves of the cheaper rents, and here will be found combined all
those predisposing causes which may be briefly summed up in one
word--poverty. It is true that cases of scrofula are quite numerous in
the country, and in a note to Sir Thomas Watson's _Practice of Physic_
(1851) D. Francis Condie quotes from a work on _The Nature and Causes
of Scrofula_, by Phillips, statistics which showed a greater
preponderance of deaths from scrofula in a given number of the rural
population than a nearly equal urban one. But at the time these
statistics were gathered in England (and perhaps now) it is probable
that there was a comparatively greater number of abjectly poor people
among the rural population than in London, where was congregated such a
large number of small tradesmen, artisans, and laborers, who, though
not well-to-do, were better paid, and consequently lived better, than
the agricultural laborers. Of course, a certain number of cases of
scrofula are found in the United States, and perhaps in all other
countries, among the children of the wealthy. These, however, are
almost invariably caused either by direct transmission from parents or
by some accidental injury to the digestive and assimilative organs in
early childhood, as we have already pointed out. When it is remembered
that in the constantly changing fortunes which are so frequently
witnessed in this age of excessive activities, and that in the grand
opportunities for obtaining wealth furnished by the liberal
institutions and rapidly-growing industries of the United States the
descendant of the pauper of the last generation may be the millionaire
of the present, it is not surprising that so many who are now wealthy
may possess the strumous diathesis as an inheritance from their parents
or grandparents, and which they in turn transmit to their offspring.

6. Consanguineous Marriage.--It has long been a popular belief that the
offspring of parents closely related by blood are more apt to be
scrofulous than when no such relation has existed. Indeed, not only
scrofula, but numerous other diseases, deformities, and imperfections
have been {235} ascribed to such unions. Idiocy or feeble-mindedness
has also been especially accredited to the production of such
marriages. But a thorough investigation of this point in England some
years ago demonstrated positively that no more idiotic, feeble-minded,
or insane children are born of such marriages than of an equal number
of marriages contracted between persons not related by blood to each
other. There is, however, this amount of truth in the popular belief:
if persons closely related to each other possess the scrofulous
diathesis, there will be a greater probability--almost certainty--that
the diathesis will be transmitted to their offspring. If one parent
only is tainted with scrofula, and the other is entirely free from it,
there is a possibility--even a probability--that some or all of the
children may escape.

7. Complexion and Temperament.--It has been stated by some observers
that scrofula occurred principally in the fair-haired, and with equal
positiveness by others that it was in the dark-haired that the disease
found the most of its victims. Such statistics as have been furnished,
however, upon this subject seem to show that there is no connection
whatever between scrofula and complexion. It will generally be found
that whenever in any country or locality more cases of scrofula occur
in persons of one or the other of the complexions, it is only because
that particular complexion is the predominant type among the
inhabitants of that locality.

8. Race and Nationality.--While it would seem that no race or nation is
entirely free from struma, yet there are certainly in the United States
two peoples who furnish an enormously disproportionate number of
scrofulous cases: these are the Irish and Jews. Among the first of
these both scrofula and tuberculosis abound with exceeding frequency,
while among the latter it is scrofula alone which seems to predominate.
The last, however, are not exempt from tuberculosis, but only exhibit
about an equal predisposition to it with their fellow-citizens. It is
not difficult to explain the special predisposition of these peoples to
scrofula when their past history is taken into account in connection
with what has been said about the bad influence of food and
surroundings in producing the scrofulous diathesis. The principal food
of the Irish peasantry--oppressed and ground into poverty by their
Anglo-Saxon conquerors for hundreds of years--have been bread and
potatoes, often potatoes alone. It cannot be surprising, therefore,
that Irish children fed upon this diet and reared in ill-ventilated
hovels should develop the scrofulous diathesis in legions. The Jews,
too, oppressed by all nations through ages, have been during many
generations reared in poverty and squalor. Even those of them who in
not very remote times had acquired by thrift the means of securing both
the comforts and luxuries of life dared not live according to their
means, lest a show of wealth should attract the unpleasant, often
fatal, attention of their rapacious and unscrupulous Christian or
Mohammedan neighbors. This condition, this mode of life, has existed
among them for many hundreds of years, and has so intensified the
strumous diathesis among them that almost the whole race may be said to
be patently or latently scrofulous. The negro or African race, however,
as observed by the writer in the Southern States of the American Union,
do not seem to have developed any special predisposition to struma,
notwithstanding their servile condition. This, at first sight, would
seem to {236} be contrary to our expectation based on what has been
said about Jews and Irishmen. But as my remark has been predicated only
on observation of the African in the Southern States, where the climate
is not favorable for the development of scrofula, the fact is not so
surprising. Besides, the food of these people consisted largely of
bacon or pork, fish, milk, and the succulent fruits and vegetables,
with a moderate quantity of corn bread, and very rarely potatoes. As
the rude cabins in which they dwelt were usually constructed of unhewn
logs and covered with rough boards, and cost almost nothing except
labor, overcrowding was unknown and ventilation always perfect. The
waiter practised medicine fourteen years in Wilcox county (S. W.),
Alabama, containing a population in 1870 of 28,377, of whom 21,610 were
colored, and during this time saw only two cases of genuine scrofula
and one of tuberculosis among the colored population.

Pork as an article of food has often been accused of producing a
tendency to scrofula, but evidently with great injustice, for we have
seen that the Jews, who never eat it, are almost universally
scrofulous, while the Southern negroes, whose staple animal food it
was, were conspicuously free from it.

9. Acquired Scrofula.--Although in perhaps a majority of all scrofulous
cases the diathesis has been inherited from the parents, the fact
cannot be too strongly emphasized that in a large number of cases the
disease may be developed de novo, independent of such heredity. To
scrofula developed from the influence of bad ventilation and
overcrowding, absence of sunlight, insufficient, bad, or unsuitable
food, cold and damp, imperfect clothing--in short, all those conditions
associated with poverty, squalor, and ignorance--Grancher has well
applied the term la scrofula a miseria. And it is only by a clear
comprehension that scrofula may be, and often is, developed under these
conditions that the medical profession in general, and municipal health
authorities in particular, may be induced to teach and enforce upon the
poor both the knowledge and the practice which may prevent it. Even in
the open country, where there is at least no lack of pure air and
light, the lesson can be enforced with equal profit; for the children
of the farm-laborer are likely to be imperfectly and improperly fed,
and lodged in apartments at night that in the matter of foul air and
filth could not be well surpassed in the purlieus of the dirtiest and
most overcrowded city.

EXCITING CAUSES.--The actual exciting causes of scrofula when the
diathesis already exists are too numerous to be mentioned in detail.
Indeed, almost any trivial injury or inflammation, any disease which
has produced a temporary cachexia, may rouse into activity the perhaps
hitherto latent tendency. How often do we see a slight blow upon the
knee-joint produce a white swelling which lames for life the heretofore
healthy and active boy or girl! A fall upon the hip which was almost
unnoticed at the time excites a coxalgia which either destroys life or
renders the child for life a cripple; or a slight jar of the spine
induces a disease of the vertebrae which, if recovered from at all,
produces a terrible deformity. A slight eczema of the face or scalp or
a catarrh of the mouth or throat will excite that slow and generally
painless enlargement and induration of a neighboring lymphatic gland
which always ends in its caseation and final destruction by
suppuration. A slight injury to the {237} periosteum may excite a
destructive caries or necrosis of the underlying bone, and a temporary
catarrh of the intestines a tabes mesenterica with all its fatal
consequences.

Speaking generally, it may be said that anything that produces a local
disorder of nutrition or impairs the health generally of a person
predisposed to scrofula is sufficient to bring about some
manifestations of the disease. They are especially apt to follow the
eruptive fevers. Measles and scarlatina are very commonly arousers of
the scrofulous process, not only by the temporary impairment of health
which follows them, but also through the catarrhs which are usually
present in both diseases. Vaccination has often been accused of
imparting scrofula; and, although this is untrue, since scrofula cannot
be imparted in the sense of transference from one person to another,
there can be no doubt that the predisposition may be roused into
activity by the slight impairment of health associated with vaccination
or by the slight injury inflicted at the point of introduction of the
vaccinal virus. In some cases the disease has manifested itself for the
first time during pregnancy or lactation, and there is no doubt that in
cases where the disease has existed in childhood these conditions often
cause it to reappear. In conclusion, it must be said that many cases
apparently occur spontaneously--"the disease came on of itself"--or if
there are any exciting causes they were so trivial as to have escaped
notice altogether.

Finally, it must be remembered that the eczemas, catarrhs, ophthalmias,
otitis, chilblains, erysipelas, and numerous other local disorders of
nutrition which are often the causes of graver manifestations of the
disease, are themselves very prone to run a peculiar course
characterized by chronicity and intractableness; and many regard these
disorders as themselves manifestations of scrofula. Indeed, Virchow,
basing his argument upon the fact "that scrofulous enlargement of the
lymphatic glands of the neck often follows upon certain diseases
affecting the throat, such as mumps, diphtheria, and scarlet fever,
maintains that scrofulous proliferation of these glands, like ordinary
inflammatory hyperplasia of the same organs, is always secondary to
some peculiar process going on at the mucous surface or other part
which is in direct relation with them by means of the lymphatic
vessels; that scrofulous disease of the glands of the neck is traceable
to some inflammatory condition of the throat, fauces, or contiguous
parts; of the bronchial and mediastinal glands, to pulmonary or
bronchial inflammation; and of the mesenteric and retro-peritoneal
glands, to similar conditions of the alimentary canal. But he considers
that there may be some special element or quality in the primary
inflammation, and a tendency in its products to undergo rapid decay
similar to that which characterizes the morbid products of the diseased
lymphatic glands, but that generally they are not recognizable, from
the fact that in this case the cells are mostly developed at a free
surface, and are speedily shed from it." He admits, however, "that
there may be some special aptitude or weakness, congenital or acquired,
in the lymphatic glands of certain persons, or of certain parts of
them, which makes their inflammations, induced by indifferent causes,
assume the scrofulous character."[6] From the last of these
propositions no one will be likely to dissent, but that there is "some
specific quality or {238} element in the primary inflammation," etc.
few will be inclined to agree. There is nothing peculiar in the
eczemas, ophthalmias, catarrhs, etc. spoken of, except that they occur
in persons possessing the scrofulous diathesis; and it is this alone
that gives them their special characters, if there are any. In other
words, we cannot say that these disorders occur in certain children
because they are scrofulous, but that they are specially intractable on
account of the scrofulous diathesis upon which they are engrafted.
Millions of children have catarrh and ophthalmia (indeed, few escape
these disorders throughout the first ten or twelve years of life) who
never show any other evidence of the scrofulous taint; and nearly all
have measles and scarlatina, but it is only the scrofulous who usually
suffer severely from the secondary effects of these diseases. But they
do not have measles or scarlatina because they are scrofulous, and we
can with no more justice say that they have catarrhs or other
inflammations because they are so. We do not believe, therefore, that
strumous children have cutaneous and catarrhal inflammations simply
because they are strumous; and if we speak of scrofulous catarrh or
ophthalmia or eczema, we use the terms in the same sense as when we
would speak of a scrofulous measle, scarlatina, or whooping cough.

[Footnote 6: _The Theory and Practice of Medicine_, by Jno. Syer
Bristowe, M.D., 1879, pp. 80, 81.]

Although we have few reliable statistics bearing upon the question, it
can scarcely be doubted, judged by the results of casual observation,
that scrofula is much less frequent in America than in Europe, and that
in the latter there is less of it than formerly. The cheapness of land
in America has prevented that excessive overcrowding that exists in the
older and more densely populated countries, and the abundance and
cheapness of animal food has prevented that excessive feeding on bread
and potatoes which constitutes such an important factor in the
production of the scrofulous diathesis in some other countries.

PATHOLOGY AND MORBID ANATOMY.--The most important and central
anatomical and pathological facts both in the causation and progressive
development of struma, according to the writer's views, are--

1st. That faulty anatomical--or rather histological--construction of
the tissues of the scrofulous individual already alluded to as having
been first brought to the notice of the profession by Formad of
Philadelphia, which consist of an unusually large number of
lymph-spaces (which are also unusually large), and consequently an
excessive number of lymph-vessels and lymph-glands.

2d. Excessive production of rudimentary lymphoid cells, and probably
also of lymphatic tissue.

3d. Diminished and insufficient number of the capillary blood-vessels;
and, as a necessary consequence of these,

4th. Diminished nutritive activity of all those processes, both
physiological and pathological, which depend upon a full supply of
nutritive blood.

The most striking feature in all scrofulous inflammation is excessive
cell-growth, but these cells show little tendency to differentiation
and organization, probably for two reasons: 1st, because they are
derived from the blood-vessels principally, and not from proliferation
of the proper connective-tissue cells of the part; and 2d, because they
are insufficiently supplied with nutrition from the scanty
blood-vascular {239} network, and this supply is too rapidly absorbed
into the lymph-spaces, and is carried off by the too numerous
lymph-vessels. The cells, therefore, speedily perish, undergo partial
or imperfect fatty degeneration, and finally caseation, unless the
process is going on at a free surface, in which case, of course, they
are shed and thus gotten rid of.

Virchow some time ago called attention to the predominant cellular
character of the scrofulous exudation and the low vitality of the cells
which compose it. Rindfleisch declares that the fresh scrofulous
exudations contain relatively large cells with glistening protoplasm,
and that the white blood-corpuscles have a tendency in scrofulous
persons to grow larger on their way through the connective tissue. He
adds that they swell up by the imbibition of albuminous substances, and
by this very swelling die and slowly degenerate.

It seems to the writer, however, that it is probable that herein lies
the reason why swelling and apparent hyperplasia of the lymphatic
glands in the neighborhood of a local inflammation occurring in a
scrofulous person always takes place. The swollen cells become arrested
at the first gland they reach, and block the channels through the
gland. Successive additions of cells continue to block these channels,
and finally the passage of lymph through the gland becomes impossible,
and then begins that secondary increase of the lymph-cells in the gland
resulting from their inflammatory proliferation.

"In scrofulous inflammation," say Cornil and Ranvier,[7] "there is a
remarkable tendency to permanent infiltration of the affected tissue.
In simple inflammation (_i.e._ inflammation in non-scrofulous persons)
the infiltration is a temporary condition which terminates in
suppuration, in organization, or in resolution." Now, the several steps
in this process of resolution are--contraction of the distended
blood-vessels, thus cutting off the excessive supply of blood which has
caused the exudation and cell-proliferation; fatty degeneration of the
new cell-formation; liquefaction of this fat by union with the alkaline
blood-plasma, converting it into a dialyzable (saponaceous) liquid
which can now be readily absorbed by the veins. In scrofulous
infiltration the cells are speedily attacked by fatty degeneration
(which seems to be strictly a physiological process), but instead of
becoming liquefied, it (the fat) remains, slowly dries and hardens, and
finally becomes converted into the so-called cheesy mass or cheesy
infiltration. It does not liquefy, because it does not receive a
sufficiently abundant supply of the alkaline blood-plasma from the
scanty blood-vessels, and that which is supplied too rapidly flows into
the numerous large lymph-spaces and is carried off by the
lymph-vessels. In the case of the infiltrated gland the supply of this
plasma is cut off in both directions. The passage of lymph through the
gland is blocked, when, of course, none can then reach it through the
lymph-vessel leading to it, while the swelling of the gland itself from
accumulated cells compresses the neighboring nutrient vessels and cuts
off the supply from this direction also. Hence the speedy death, fatty
degeneration, and caseation (not liquefaction) of the cells.

[Footnote 7: Ed. 1880, p. 114.]

"The newly-formed material not only interrupts the lymph-passages of
the gland, but also compresses the blood-capillaries in such manner
that the circulation completely stagnates. It is impossible by any
{240} method of injection to penetrate into the most swollen parts of
the gland. With the supply of blood the nutrition also self-evidently
ceases; the gland falls into caseous degeneration. Where this enters in
the gray mass first becomes opaque, then whitish-yellow,
non-transparent, dry, friable. If the whole gland has passed into the
caseous condition, it appears upon a section as a fresh potato, only
not quite so moist, but just as homogenously yellowish-white."[8]

[Footnote 8: Rindfleisch, _Textbook of Pathological Histology_, 1870,
p. 202.]

The subsequent fate of these glands seems to depend somewhat upon their
situation. In the mesenteric and bronchial glands almost always the
caseous mass is attacked by calcareous infiltration, and finally dries
into a solid chalky concretion. The writer counted seven of these
chalky masses around the primary bronchi of a boy about fifteen years
old whose body was brought into a dissecting-room in Baltimore City.
But the more common result of the caseous process in the glands of the
neck is softening. "The caseous depot melts from within outward into a
whitish-yellow, whey-like fluid, which holds a fatty granular detritus
suspended in smaller or larger fragments. If all the caseous material
has softened, the neighborhood of the gland is wont to inflame; this
inflammation facilitates the way for the scrofulous pus outward. This
is evacuated, and we have the scrofulous ulcer, with its overhanging,
bluish, hyperaemic, flabby edges. At length this opening also closes,
and a drawn-in, radiated cicatrix marks the place where the evacuation
took place."[9]

[Footnote 9: _Ibid._, _loc. cit._]

But it must be borne in mind that all so-called scrofulous hyperplasias
of lymphatic glands do not run this destructive course. Undoubtedly, in
a few cases there remains a sufficient nutritive supply to carry on the
liquefactive process which normally follows fatty degeneration, and
thus resolution of the affected gland takes place. We are, however, of
the opinion that Virchow was mistaken when he asserted that complete
resolution of the cheesy material could take place; and from what we
know of the dangerous and usually fatal consequences of the absorption
of this cheesy detritus, Rindfleisch is certainly in error in
describing this as the most desirable possibility of decomposition.

We have heretofore purposely avoided any mention of tubercle or
tuberculosis as a part of the scrofulous process. In the views of many
physicians the relations between the two processes are so close that to
them tuberculosis and scrofulosis mean one and the same thing. While
medical opinion as to the true meaning of the word tubercle was so
discordant and unsettled, while so many products of diverse
pathological processes were included in that term, and while many,
following the view of Burdon-Sanderson of England, believed that
tubercle always takes its origin in small, even microscopic,
collections of lymphatic tissue, such a belief in the identity of the
two processes was not only possible, but reasonable. But since, by very
many good authorities, the term tubercle is now limited to the miliary
or submiliary tubercle, since numerous inoculation experiments have
shown that tuberculosis can be induced in non-scrofulous animals, and
Koch of Germany has proved that there exists in decaying tubercle a
peculiar and distinctive bacillus which even when cultivated out of the
body of a tuberculous person will excite tuberculosis also if
inoculated upon a non-scrofulous animal,--a belief in the identity of
the two diseases seems to be no longer tenable. Certainly, it {241}
would seem that to Sanderson's view that tubercle always takes its
origin in lymphatic tissue it is only necessary to reply that the
subjects of miliary tuberculosis do not more frequently than those
suffering from other non-scrofulous diseases present those larger
glandular hyperplasiae which are so distinctly characteristic of
scrofula, and to which many persons limit the term scrofulosis. It may
be said, perhaps, that the converse of this is not true, and that
scrofulous persons are more frequently attacked by miliary tuberculosis
than an equal number of non-scrofulous persons. But the extreme
susceptibility or liability of the scrofulous to be attacked by
numerous and even diverse morbid processes, and the profound cachexias
and dyscrasias which the scrofulous processes engender, amply account
for the apparent susceptibility of the scrofulous to be attacked by
miliary tuberculosis. The strumous are more susceptible to the exciting
causes of tuberculosis undoubtedly, but perhaps the same may be said in
regard to measles, scarlatina, and the various other exanthemata. It is
undoubtedly true also that among the lower animals (and probably also
in the higher ones) the introduction into the circulation of the
semi-purulent fluid resulting from the breaking down of a cheesy
scrofulous gland will produce that peculiar (perhaps specific)
dyscrasia which results in miliary tuberculosis. But as it has also
been abundantly proved that a similar fluid derived from a cheesy
pneumonia, or from the inflammatory products of any other disease which
have undergone the cheesy degeneration, will also excite tuberculosis,
the fact does not seem to tell in favor of the identity of, or even of
any close relationship between, the two processes. Still, as the
scrofulous more frequently than other people are the subjects of this
cheesy process, it is not surprising that they should more frequently
be poisoned by the entrance into their blood of the cheesy detritus.

We do not deem it necessary to adduce all the evidence or to state
authorities upon this subject, but we think we are justified in stating
the following doctrine in regard to the relation of scrofula to
tuberculosis as best supported by facts and by the consensus of medical
opinion:

Scrofula is a purely diathetic disease inherent in the individual.

Tuberculosis is a cachectic (possibly a purely dyscratic) one, not
inherent in the individual, but always caused by some morbid influence
from without. Tuberculosis may therefore occur in the non-scrofulous as
well as in the scrofulous.

But the scrofulous are more likely than others to have
tuberculosis--1st, because of their greater susceptibility to all
morbid influences; 2d, because the scrofulous processes are apt to
produce some cachectic condition which is always a condition precedent
to tuberculosis; and, lastly, because the products of decay resulting
from scrofulous processes may enter the circulation and directly
produce the tuberculous dyscrasia. These remarks of course apply only
to primary tuberculosis.

But while we thus deny anything else than a purely incidental relation
of scrofula to tuberculosis, we believe that there exists the very
strongest possible relationship of scrofula to pulmonary consumption.
We think we are justified in stating that fully 95 per cent. of all
cases of pulmonary consumption are of inflammatory origin, and of that
variety miscalled catarrhal pneumonia. Broncho-pneumonia or
catarrho-pneumonia more exactly describes the process. It begins as a
catarrh, {242} sometimes in the nasal passages or post-nasal fossae,
sometimes in the pharynx, but most frequently in the trachea and large
bronchial tubes, and sometimes rapidly, but oftener more slowly,
travels downward and invades the lining membrane of the air-sacs, which
soon become packed with cells derived partly from emigration of
leucocytes, partly from proliferation of the epithelium lining the
sacs. These cells soon undergo the cheesy degeneration, and, finally
breaking up, as in the case of the scrofulous gland, cause the
formation of vomicae attended with the familiar signs of pulmonary
consumption. Every step in this process is attended with that abundant
cell-production, and the process itself is marked by that inveteracy
and intractableness, which always characterize scrofulous
inflammations, or rather inflammations in the scrofulous. Occurring as
they most frequently do in young adults, these cases are often mistaken
for pulmonary tuberculosis; and as post-mortem examination generally
reveals a more or less abundant secondary tubercular eruption caused by
absorption of infective material from the centres of cheesy
degeneration and softening, the diagnosis is claimed to be confirmed.
But they are for the most part, nevertheless, cases of genuine
scrofulous inflammation of the bronchial membrane and lining membrane
of the alveoli, and should be called scrofulous pneumonia. It is true
that Mr. Phillips, Mr. Kiener, Villemin, Grancher, Mr. Treves, and
others have collected numerous statistics which would show that
comparatively few of those who had died of pulmonary phthisis bore any
evidence of previous scrofulous disorder. But as the principal evidence
relied upon to prove this fact was an absence of scars resulting from
suppurating glands, their statistics are inconclusive. Besides, it is a
well-known fact that there is a decided antagonism between scrofulous
diseases of all kinds, and a patient who has one severe or well-marked
manifestation of scrofula is not likely to develop another strumous
disease at the same time. The records of the Margate Infirmary for
Scrofula show this fact very strongly, and numerous writers--among whom
may be mentioned Holmes, Birch-Hirschfeld, Walsh, Mr. Treves, and
others--strongly express the same opinion. Indeed, some of them go so
far as to maintain that one form of the scrofulous manifestation
confers protection against others. The question may perhaps be more
clearly stated by saying that the scrofulous, like the non-scrofulous,
have their special predispositions and indispositions to certain morbid
affections, and while one scrofulous child may be specially predisposed
to affections of the bones, joints, skin, or other tissues, it may have
no predisposition whatever to affections of the lungs or lymphatic
glands, etc. This difference in vulnerability or invulnerability of
certain tissues or organs in individuals, whether scrofulous or not, is
so distinctly recognized as a controlling factor in determining the
special form of disease resulting from a given irritant that its
discussion is entirely unnecessary. It is argued against the identity
of scrofula and pulmonary consumption that the commoner manifestations
of the former occur in childhood for the most part, while consumption
is a disease of adult life. But this is readily accounted for by the
different morbid tendencies and exposures in the two periods of life.
"Scrofula tends to appear in early life on account of the unusual
activity of the lymphatic system at that period, and phthisis somewhat
later--at a time, indeed, when the lungs are in more active use, when
{243} sedentary and perhaps unhealthy pursuits are assumed in exchange
for the liberty of childhood, when the modifying influences of puberty
are active, and the structural responsibilities of adult life press
heavily on an organization never other perhaps than frail.... I would,
on the contrary, assert that scrofula and phthisis are as much
manifestations of the same morbid change as acute bubo, acute orchitis,
and acute pneumonia are outcomes of one single process--acute
inflammation."[10]

[Footnote 10: _Scrofula and its Gland Diseases_, by Frederick Treves,
F.R.C.S., Eng.; New York, 1882, p. 62.]

It is entirely unnecessary--and indeed it would be too tedious--to
describe the anatomical appearances of the almost innumerable lesions
met with in the scrofulous. Holding as we do that scrofula is not a
disease per se, but merely a condition resulting from malnutrition and
consequent faulty construction of the tissues during the early years of
childhood, no peculiar or distinct anatomical lesion can be ascribed to
it; and yet every lesion of nutrition as well as of function may have
certain specific characteristics impressed upon it by the scrofulous
diathesis. These may be briefly summed up as great slowness in
evolution, intractableness, incurability, and chronicity of all
pathological processes, and in all inflammatory processes abundant
cell-production and tendency to caseation.

SYMPTOMS, COURSE, DURATION, AND TERMINATIONS.--A great deal of fine
writing has been expended in describing the physiognomy of scrofula,
and for ages writers exercised their descriptive powers upon the type
of face and form supposed to be indicative of the disease. It is almost
needless to say that much of this has been evolved from the
imaginations of the writers, while many of these descriptions are not
pictures of those liable to suffer from scrofulous processes, but of
those who are already the subjects of these, and are simply types, not
of the scrofulous diathesis, but only of the scrofulous cachexia. Many
of these pictures, too, were drawn not from the scrofulous, but the
tuberculous patient, because they were considered identical. Scrofula
is not confined to the dark or the fair, the dull or vivacious, nor
even to the weak and puny or the strong and robust; but all these may
have this faulty and often fatal construction. Nor do we believe that
scrofulous children are either more brilliant or more stupid than other
children. At most we can only say that the scrofulous habit is marked
by a deficiency of blood and a bad nutritive state of the more
important and more highly organized tissues. In some an abundance of
fat is found, giving to the individual a certain amount of plumpness,
which might be thought to be inconsistent with a state of bad health;
in others there is an imperfect development not only of the
subcutaneous fat, but of the skin and muscles also, so that they appear
tender and delicate. In the first of these conditions there is supposed
to be an indolent state of the processes of constructive and
destructive assimilation; in the second, an unnatural activity of these
processes. These differences have led to a classification of scrofula
into the phlegmatic or torpid and the sanguine or erethistic forms,
which Canstatt has thus described: "An unusually large head, coarse
features, a thick chin, a swollen abdomen, enlarged cervical glands,
and flabby, spongy flesh." The erethistic form is said to possess "a
skin of remarkable whiteness, with a tendency to redden easily, and
through which the {244} rose-pink or bluish subcutaneous veins are
visible, a deep redness of the cheeks and lips, blueness of the thin
and transparent sclerotica, which imparts a swimming and languishing
look to the eyes. The muscles of such persons are thin and soft, and
their weight is light in proportion to their stature, indicating a
slightness of their bones. The teeth are handsome and of a bluish
lustre, though long and narrow; the hair is soft."[11] Although this
description may be characterized as diagrammatic, since it describes
rather the extremes and not the mean of the general appearance of the
scrofulous, and numerous cases will be met with that cannot be assigned
to either of the above categories, yet as quite a large number of cases
will be seen that obviously belong to one or the other of these types,
and as, moreover, we shall see that by this classification we shall
obtain valuable data for therapeutic indications, it may be well to
preserve this division of the scrofulous into the lymphatic and
sanguine types.

[Footnote 11: Niemeyer's _Text-book of Practical Med._, vol. ii. p.
741.]

The leading points in the physiognomies of each of these types were
admirably shown in the composite photographs exhibited by Dr. Mohamed
at the last International Congress in England. By some special process
a composite photograph of many faces was, as it were, condensed into a
single picture, in which all that is common remains, all that is
individual disappears. And although Mohamed's pictures were all of
phthisical patients, it must be admitted that the two types of coarse
struma and sanguine struma were strikingly illustrated, and were very
suggestive of Canstatt's descriptions as given above. But it must be
borne in mind that a large number of the strumous belong strictly to
neither of these types, but rather to a medium between the two. "Such a
type would include what is known as pretty struma. The general features
of the individuals so termed belong to the so-called phlegmatic type,
but the coarseness of the features is toned down; the lips would be
called full, not tumid; and a coarse flabbiness would subside into a
pretty, plump condition of the body. The limbs, if not actually
graceful, are at least prettily rounded. The skin may not be thin and
fine, but it is soft, white, and clear. The general expression is not
absolutely apathetic, but would be termed gentle and eminently
feminine. Excellent representations of this type of pretty struma were
also shown in the photographic series above mentioned."[12]

[Footnote 12: Treves, _Scrofula and its Gland Diseases_, p. 84.]

This matter of physiognomy of the scrofulous has this much at least of
practical importance--viz. that to the sanguine or erethistic type
belong those cases that show distinct heredity, while the phlegmatic or
torpid is usually the type assumed in the acquired forms. While there
are doubtless numerous exceptions, it will generally be found that
scrofula in the rich assumes the first, and in the poor the second, of
these forms. It has been asserted that the erethistic form is more apt
to develop tuberculosis or phthisis; and to a certain extent this is
doubtless true, but the torpid are by no means exempt from this grave
accident. The first are undeniably more liable to the more severe and
fatal forms of the disease, which run a more rapid course and are less
amenable to treatment, while in the second phthisis is more apt to be
chronic and incomplete recoveries are by no means rare. The first form
is said to {245} be more frequent in women, while the second is more
frequent in males; and this accords with my own observation and
experience.

There are certain features more or less peculiar to scrofula, besides
those appertaining to the general physiognomy already discussed, which
it may be well to call attention to, since these may aid us in
detecting the scrofulous diathesis even before the grosser
manifestations have declared themselves.

Allusion has already been made to the defective blood-vascular
capillary network in the scrofulous as a necessary consequence of the
excessive predominance of lymph-spaces and lymphatic vessels. Indeed,
there can scarcely be a doubt that the slowness of evolution of various
pathological processes, their chronicity, and the absence of tendency
to resolution and cure of inflammatory lesions, so prominent a feature
in all scrofulous manifestations, is due to this very condition. It is
especially in the coarser type of struma that these defects in the
circulation are most conspicuous. In these the pulse is often below the
average, soft, and wanting in vigor. The cheeks and limbs often assume
a bluish and mottled aspect, due perhaps to a tendency to stagnation of
the blood in exposed parts. The extremities appear swollen as if from
cold, and in the winter generally appear chapped. They are particularly
liable to chilblains, which persist far into the summer and often take
on a very unhealthy action. This last feature is so common as to
constitute an important symptom in scrofula. These defects in the
circulation also probably explain the frequent catarrhs and eczemas
with which such persons are affected, and account also for their
intractableness as well as the unwholesome character of their wounds.

For the same reason (deficient circulation) the temperature is
generally found to be a little lower in the coarsely strumous than in
healthy children, and even in their fevers a very high temperature is
rarely met with. Acute sthenic inflammations are rarely seen, and hence
these persons seldom have acute croupous pneumonias; it is rather the
catarrhal variety, and of this the subacute and chronic forms, which
they suffer from.

Opinions are completely at variance as to the influence of the
scrofulous habit in delaying or hastening menstruation. Lugol referred
to the frequency of dysmenorrhoea among the strumous, and there is no
doubt that the scrofulous as a rule often suffer from suppressed or
scanty menstruation. But it is improbable that the diathesis exerts any
influence whatever in determining the period of puberty in either sex.

We have already stated our belief that the strumous are neither more
intelligent nor stupid mentally than other people. An exception ought
perhaps to be made to this in the case of the exaggerated type of the
coarsely strumous. In these extreme cases we must confess that we have
generally found associated great slowness and dulness of the mental
faculties. If great intelligence and precocity are sometimes met with,
it is only in the erethistic or pretty struma, who, because it is the
delicate one of the family, is petted, has more notice taken of it, and
afforded every facility for the development of the points that make up
the precocious infant. The prettiness of these children, moreover,
attracts more attention to them than to other children or than the bulk
of the sickly would receive.

In young scrofulous children we often observe a considerable amount
{246} of close-lying downy hair upon the forehead, more abundant upon
the sides of the forehead. Upon the arms and back from the occiput to
below the shoulders also a like condition is often seen. Later the
eyelashes appear thicker and longer, and the eyebrows more abundant,
coarser, and longer, than in the non-scrofulous. The color of these is
also apt to be darker than the rest of the hair.

Constantine Paul, as quoted by Treves, has drawn attention to certain
changes in the ears, after they have been pierced for earrings, that he
considers to be diagnostic of scrofula. The mere weight of the earring
seems to cause the puncture to slowly ulcerate, and the ring thus cuts
its way out, either leaving behind it a linear scar or a slit in the
lobule. If the lobule be repaired the ring may cut its way out again,
and this may occur three or four times. These changes seem not so
frequently to be observed in England and America, and may be due in
part to the fact that earrings of greater weight, and more frequently
of base metal, are worn in France than in the countries named. But
still, from what has been said concerning the histology and minute
anatomy of the scrofulous, and the consequent less resistance of the
tissues, this cutting-out process by earrings is just what we would be
led to expect in strumous persons.

The thick upper lip is never absent from the older descriptions of the
physiognomy of the strumous. This is almost invariably present in the
coarse type of struma, and seldom absent even in the erethistic. It is
not always due to irritation from acrid discharges from the nose, as is
maintained by Treves, though doubtless the eczematous and herpetic
eruptions are often caused and maintained by these discharges, and
these may in time cause and increase this thickening.

The teeth in scrofula show nothing that is distinctive, though there is
undoubtedly a tendency to early decay. As this tendency to decay is,
however, so common in many persons who have at least shown no other
evidences of the scrofulous diathesis, no positive conclusions can be
drawn from this fact.

Clubbed fingers, too, so common in persons who have become cachectic
from the long persistence of scrofulous disorders, are not
characteristic. Clubbed fingers and incurvated nails will generally be
found in persons suffering from any disease characterized by slow
wasting. They are seen in phthisis of all varieties, as well as in
cancer, heart disease, aneurism, Bright's disease, empyema. They
therefore have no significance as far as struma is concerned.

GENERAL MANIFESTATIONS OF SCROFULA.--As, according to our view, there
is no such disease per se as scrofula, but simply a diathesis which
impresses its own malign influence upon every other disease with which
the strumous individual may happen to be afflicted, increasing perhaps
the general predisposition to be injuriously affected by all morbific
influences, or impairing the powers of resistance to these, and
especially intensifying any special predisposition which age, sex,
personal peculiarities, occupation, habits, mode of life, or heredity
may have created, we cannot describe any morbid processes as
specifically scrofulous. At most, we can only say that struma is more
apt to impress its malign influence upon certain diseases or upon
inflammations and injuries of certain tissues, that some diseases in
the scrofulous are more apt to be {247} attended by certain
complications and followed by certain sequelae, and that all of these
are characterized by chronicity and incurability, by slowness of
evolution of pathological processes, and, in the case of inflammations,
by a tendency to profuse cell-production and to rapid caseation. Thus,
measles is apt to be complicated with or followed by otorrhoea, chronic
bronchitis, caseation of bronchial glands, phthisis, and even
tuberculosis; scarlatina by otitis, hyperplasia of the tonsils,
caseation or suppuration of the submaxillary and other lymphatic glands
about the neck, and by chronic catarrh of the renal mucous membranes,
causing dropsy and finally death; eczemas about the face or catarrhs of
the mouth and throat by hyperplasiae and caseation of lymphatic glands
in the neighborhood. Boils and other subcutaneous inflammations of the
areolar tissue, so common in childhood and adolescence, do not run
their usual rapid course, ending in suppurations and cicatrization, but
become in the one case the scrofulous gumma, degenerating into the
scrofulous ulcer, or if more deeply seated become a cold abscess. A
single injury of a joint, whether mechanical or rheumatic, will
"sometimes take the form of a simple hydrarthrosis, sometimes that of a
so-called tumor albus, while at others it assumes the nature of a
malignant arthrocace, accompanied by suppuration, caries of the
articular surfaces, burrowing of pus, and the establishment of
fistulae."[13] A slight injury inflicted in the sports of childhood and
soon forgotten--the prick of a pin perhaps--is followed by a disease
sometimes beginning in the periosteum, sometimes in the bone itself,
and presenting at one time the character of periostitis and ostitis,
and at another that of caries or necrosis, or of the two combined.

[Footnote 13: Niemeyer, _loc. cit._]

"As long as the existence of cheesy masses," says Niemeyer, "was
regarded as characteristic of the tuberculous nature of a disease, it
was of course necessary to ascribe many of the inflammations of the
joints and bones of scrofulous persons to a complication of scrofulosis
with tuberculosis."[14]

[Footnote 14: It is a well-established fact, however, that true miliary
tubercles are often found in the neighborhood of bone and joint
affections in the scrofulous, as well as in lupus, in cold abscess, and
in softening caseous glands, which last are considered by many as
specifically scrofulous diseases. It is suggested that an explanation
of this may be found in the probable fact that caseous pus may be
capable not only of producing a general tuberculosis when carried by
veins or lymphatics into the blood, but that it may also set up a local
tuberculosis by a morbid influence exerted upon the neighboring
lymphatics and blood-vessels with which it may come in contact. We are
aware that Wilson Fox (according to the _Medical Times and Gazette_),
captivated by the theory of Koch, has recently recanted his belief in
the inoculability of tuberculosis with anything except tubercle. But we
are afraid that Dr. Fox (who we believe was one among the first to
confirm Ferdinand Cohn's experiments in producing tuberculosis in
rabbits and guinea-pigs by inoculating them with caseous pus) is
suffering from that most active and virulent of all contagions, the
contagion of popular belief. Just now a belief in specific bacilli and
micrococci may be said to be riding upon the crest of a very high wave
of popularity, and we are afraid that many of those who are rushing
forward to mount this wave also will ultimately find themselves
stranded upon that shore which has been strewn with so many wrecks in
the past.]

A simple bronchitis, possessing nothing specific in its origin at
least, will persist and extend to the lobuli of the lung and excite a
catarrho-pneumonia which ends in consumption and death; a simple
intestinal catarrh will result in inflammation and caseation of the
mesenteric glands--a tabes mesenterica; or a simple dysentery,
persisting in spite of the most {248} approved treatment, causes
proliferation and caseation of the endothelial cells of the follicles,
terminating in that obstinate and intractable follicular ulceration
which wastes the strength and wears out the life of the little patient.

A simple conjunctivitis of the globe often will be followed by
ulceration of the cornea, giving rise to intense photophobia, and leave
behind it opacities of that organ which remain a perpetual evidence of
the scrofulous diathesis, if they do not shut out for ever the light
from the eye. Or if it is the palpebral conjunctiva that is affected,
the meibomian glands and follicles of the ciliae become involved,
destroying the lashes and leaving the lids raw and everted or
inverted--a perpetual deformity. In short, there is no conceivable
disease or injury occurring in what we may call the intensely
scrofulous that does not have impressed upon it some one or more of the
malign characteristics which we have spoken of as indicative of the
scrofulous diathesis. But it is not probable that there is ever any
special disorder or lesion which can be said to be caused exclusively
by scrofula; or, in other words, there is no such disease as a
specifically scrofulous one. Lupus, cold abscess, and particularly
caseous glands, are especially attributed to struma, because they are
often thought to make their appearance independent of any assignable
cause; but as boils, eczema, impetigo, and numerous other affections of
the skin and areolar tissue affect children who are not scrofulous, and
equally independent of any known causes, the argument is not
conclusive. Besides, all these affections occur sometimes in the
non-scrofulous; and even caseation of a single inflamed gland quite
often occurs in children who are weak or in ill-health, but who show no
other evidences at that or at any other time of the scrofulous habit.

DIAGNOSIS.--The only affection likely to be mistaken for scrofula is
congenital or acquired syphilis in its later manifestations. In this
disease we see the same tendency to increased cell-production, the same
tedious, slow, and intractable inflammations and ulcerations, which are
characteristic of scrofula. And this apparent similarity has induced
many persons to believe that scrofula is nothing else than syphilis in
the second or third generations. But in congenital syphilis the lesions
usually make their appearance soon after birth or are present at birth,
and long before even hereditary scrofula begins to show its malign
influence. In most cases, too, a history of syphilis can be obtained,
and even when this is not obtainable a few inunctions or fumigations
with mercury, in connection with a few large doses of iodide of
potassium, will very quickly decide the question of diagnosis for us.

In the case of lupus, in which Erichsen admits there is no means of
positively distinguishing the syphilitic from the so-called scrofulous
varieties, the diagnosis is more difficult. But as this disease appears
later in life than the more ordinary scrofulous manifestations--when,
therefore, a history of syphilis can generally be obtained if there is
one, and when there would almost certainly be also a history of
scrofula if it existed--it would seem that the diagnosis even in this
case cannot be so difficult. Diagnosis here, however, is of little
consequence, since the treatment recommended for both forms is the
same.

PROGNOSIS.--This of course depends upon the nature of the special
lesion. The simpler lesions incident to childhood, such as glandular
{249} hyperplasiae, catarrhs, eczemas, impetigoes, etc., usually do
well under appropriate treatment and proper hygienic conditions.
Diseases of joints, bones, mesenteric glands, etc. often terminate
fatally or result in serious deformities and permanent impairment of
function. Not infrequently diseases of the bones and articulations,
attended with profuse and protracted suppuration, cause amyloid
degeneration of the liver, kidneys, spleen, or other glandular organs,
and, as a consequence, death. Catarrho-pneumonia in a scrofulous
subject almost invariably causes phthisis sooner or later. Occasionally
the caseated cellular exudation in the air-sacs remains quiescent for
months, and even years, the patient remaining quite well except for a
harassing cough during the winter months; but sooner or later the
caseous mass will soften, the symptoms of active consumption ensue,
with fever and wasting, and death closes the scene. Far more
frequently, however, softening and suppuration follow swiftly upon the
caseous degeneration, and the whole process occupies a period of only a
few months. Tuberculosis especially runs a rapid course in these
subjects, and while a few perhaps only develop tuberculosis of the
lungs--in which case the duration of the disease may be a little
longer--in by far the larger number there is a generalization of the
tubercular process which puts a speedy end to their existence.

TREATMENT.--This may be most profitably discussed under two
heads--prophylactic and therapeutic.

Prophylactic.--Scrofulous persons who are closely related by blood
should be earnestly advised not to intermarry. We have so often seen
the deplorable results upon offspring of such marriages that we cannot
too strongly urge this upon the profession. Such persons should be
frankly and clearly told what are most likely to be the consequences of
such marriage, and all possible moral influences should be exerted to
prevent them. The canons of the Church wisely interdict such marriages,
but, unfortunately, its ministers seldom attempt to enforce them, or if
they do their efforts are made ineffectual by the facility with which
the marriage-rite can be obtained from civil officers in most of the
States of the American Union. The medical profession can do more than
any other class to diffuse knowledge and create a correct public
opinion upon this subject, but, unfortunately, it too often neglects
this important mission.

The children of scrofulous parents should be nursed (at the breast)
longer than other children, so as to ensure an abundance of animal food
during the first two years of life. Some advise scrofulous mothers not
to nurse their children, lest they should imbibe the scrofulous taint
through the milk. This fear is entirely groundless. We know of no
reason why such a mother should not nurse her offspring, unless it be
that it injures her. The child receives its scrofulous inheritance not
through the mother's milk, but from the ovarian or spermatic cell. Milk
can convey no disease or diathesis except on account of its deficiency
in nutritive properties. If, therefore, there is any special reason why
the mother should not nurse her infant on her own account, it may be
well to turn it over to a healthy wet-nurse; but the temptation to give
an infant raised on the bottle starchy foods prematurely is too strong
generally to be resisted. The numerous infant foods advertised consist
principally of starch, and young infants would infallibly starve on any
or all of them {250} if their venders did not always direct that they
should be taken with a large quantity of cow's milk. If the
circumstances of the parents do not enable them to obtain a wet-nurse,
then good cow's milk constitutes the best food for infants until they
have cut their canine and anterior molar teeth. The custom of weaning
infants at a certain age in every case is a pernicious one. Some
infants are as well developed as to their digestive organs at fifteen
months as others are at thirty, and the eruption of the teeth may
generally be taken as a safe guide as to that question. A moderate
amount of food containing starch after the period indicated may be
allowed, but always with a preponderance of animal food. It is not so
much the starch that acts injuriously upon the nutrition of children as
the excess of that substance; and if the food contains but little
nutrition in proportion to its bulk, it is so much the worse. Even milk
containing too little casein and fat in proportion to the watery
elements may be perhaps quite as injurious as potatoes. And hence if
the mother's milk should be poor in these elements, it ought to be
supplemented with cod-liver oil or other animal fat in small doses.

A practice existed among the Southern slaves (and to some extent also
among the whites) before emancipation which at first I was inclined to
condemn until I saw the excellent effects resulting from it. Within an
hour or so after birth a piece of fat salt pork or bacon was placed
between the child's lips, and it was permitted to suck this at all
times when not nursing. Tied to its wrist by a short string, so as to
prevent swallowing it, this piece of pork furnished both nutrition and
amusement to the infant for many hours while the mother was at work in
field or garden. The children throve well on it, and thus treated we
found them to be as well developed at twelve months as most other
children were at twenty. It was doubtless due in part to this practice
that there was so little scrofula among them.

An abundance of pure air is also a valuable factor in preventing the
establishment of the strumous diathesis. Strict regard, therefore,
should be had to ventilation, and overcrowding should if possible be
avoided. Children over twelve months of age should not even be
permitted to sleep with their parents, but should have in cold weather
a crib, cradle, or other bed to themselves; and in warm weather they
should be put to sleep in a net hammock, which is now so cheap as to be
within the means of almost everybody. This will not only secure to them
a better supply of air, but it will also prevent them from suffering so
much from the heat, which is so potent a factor in the production of
cholera infantum.

Bathing in proper season is also useful as a prophylactic. Sea-bathing
especially has long enjoyed great credit as a remedy for scrofula, but
we think this is often resorted to too soon and practised at improper
times. In warm countries a bath of cold water may be taken every day in
the year, but it should be given at the warmest hour of the day, not
early in the morning. In all climates due regard should be had to the
powers of resistance to cold and the promptness of reaction after the
bath. If children remain cold and pale for a long time after the cold
bath, the practice should be discontinued and tepid water substituted.
In colder climates tepid bathing should be practised once or twice a
day during the winter, and in summer a little lower temperature may be
used. Bathing children under three or four years in the sea at any time
is pernicious, {251} both because the temperature is too low and on
account of the fright which it always causes in these young children.
After four years a child will take to the water almost as instinctively
as a young duck.

Therapeutic.--Almost all of the so-called scrofulous manifestations
belong to the surgeon, dermatologist, or oculist and aurist, and we
shall therefore say nothing about the special and local treatment of
these manifestations, but refer the reader to works upon these several
departments of medicine. But as little success will be had in the
treatment of these special disorders unless due regard is had to the
general condition, and unless the local treatment is supplemented by
constitutional measures, we shall briefly give some directions for this
constitutional treatment of the scrofulous individual.

It is important in determining upon the proper treatment in any given
case to bear in mind the division of the scrofulous into the two types
of torpid or lymphatic and sanguine or erethistic already described. It
is true that in many cases it is not easy to determine to which class a
patient belongs, and many possessing some of the characteristics of
both certainly cannot be referred to either. Still, in many cases the
discrimination is easy, and then furnishes very clear and valuable
indications as to treatment. Iodine (and its preparations) has since
the time of Lugol, who first brought it into prominent notice, been
regarded as a useful remedy in scrofula. But burnt sponge (spongia
usta), which contained the iodides of sodium and potassium, had been
used to dissipate goitrous and scrofulous swellings many hundreds of
years before the time of Lugol. It is a valuable remedy in certain
cases, and if it is falling into disuse it is probably for the want of
proper discrimination in the selection of cases. In all cases in which
there seems to be an abundant production of fat, and therefore in
nearly all the cases of coarse struma where there is an indolent
process of assimilation and disassimilation, iodine and its
preparations will be found useful. Indeed, in the form of syrup of
iodide of iron we have rarely failed with it to cause strumous
enlargements of glands to disappear when the remedy was used soon after
their first appearance. Of course, neither iodine nor any other
medicine can have any effect in removing these enlargements after the
glands have become caseous. While good results may be obtained with the
syrup in all forms of scrofula, it is unquestionably in the sanguine
and neutral types that it is most useful. It should be given in doses
of 10 to 30 drops to children under five years of age, and to older
ones 1/2 to 1 fluidrachm three or four times a day may be administered.
We have given the latter dose to children four or five years of age for
a long time, with the best effect upon their scrofulous manifestations,
and without any injury whatever to their digestive organs.

In the torpid types preparations stronger in iodine should be used.
Here Lugol's solution or iodide of potassium or sodium will be found
very useful, either alone or in connection with the iron preparation
above mentioned. Indeed, as in these cases it seems to be
disassimilation that appears to be specially faulty, even very small
doses of mercury in the form of bichloride or biniodide will be found
useful. Donovan's solution may be prescribed in these cases along with
the active preparations of iodine with good effect, or if the arsenic
in that preparation is objectionable, one-fiftieth of a grain of
bichloride or biniodide of {252} mercury may be substituted. The
mercurial should not, however, be continued longer than one or at most
two weeks at a time, after which it should be suspended and the iodine
continued.

Cod-liver oil, which is too indiscriminately prescribed in all cases,
will be found to be of little use in the lymphatic types, if indeed it
is not actually injurious; but in those cases with pale, thin skin,
with deficient development of fat, and with small muscles--in short,
those in which emaciation or delicacy is prominent--it is a most
valuable remedy. It is almost surprising to see how rapidly
ulcerations, caries, eczemas, catarrhs, etc. occurring in this class of
subjects will disappear under the use of this medicine alone.

The hypophosphites and lactophosphates are also useful in this class of
cases, especially where there is disease of bone or joints, in
connection with the cod-liver oil. We have long been in the habit of
using the following formula, which we have found very useful:

  Rx. Pulv. Acaciae,                 drachm ij;
      Ol. Amygdal. amar.,            gtt. vj;
      Syr. Calcii hypophosphit.,
        vel Syr. Calcii lactophos.,  fluidounce iv;
      Ol. Morrhuae,                  fluidounce iv;
        Ft. mist.

S. Teaspoonful to tablespoonful three times a day according to age.
Syrup of iodide of iron may be added if desirable, though we prefer to
give this by itself.

Gentle exercise, passive or active, pure air, well-ventilated sleeping
apartments, a generous diet--in which wholesome animal food should
predominate--and bathing are of course as necessary and as useful in
the treatment as in the prevention of the scrofulous diathesis.

Alkalies should be given in all cases in which we are trying to
dissipate enlarged lymphatic glands, for the reason that caseation of
these glands occurs because of insufficient alkalinity of the blood to
effect reduction of fat, and because also the strumous almost always
suffer from excessive acidity of the gastric and other secretions. When
the iodides of potash or soda or the hypophosphites of lime and soda
are given, the additional administration of alkalies may not be
necessary; but if not, bicarbonate of sodium or potassium (which have
long enjoyed a good reputation in the treatment of struma) should be
added to the other remedies.

Since the appearance of Niemeyer's _Handbook of Clinical Medicine_ the
proper treatment of scrofulous glands that have undergone the caseous
degeneration has been a moot question. Some recommend the ablation of
these glands by the knife, some advise spooning out the caseous matter
through a small opening, while others prefer to await the natural
process of softening and the discharge of the caseous matter by
suppuration. There can be no question that the removal of these glands
by the knife, when this can be done without serious risk, will leave
behind a less unsightly scar, and will be attended with less fever and
consequent deterioration of the general health, than usually attends
suppuration. Spooning out the caseous matter will perhaps leave no
extensive cicatrix, but we can never be sure that by this operation we
have removed all the caseous matter, and it must certainly be more
painful than the knife. Mothers will generally object to either of
these {253} operations, and as the risks of infection by absorption of
the caseous pus during the suppurating process do not seem to be very
great, it is perhaps best to leave these glands to nature, unless the
vitality of the patient is so low as to give reasonable ground for fear
that the child may succumb to the effects of the natural process. If
any surgical interference is deemed necessary, we are decidedly in
favor of removing the caseous gland entire by the knife.




{254}

HEREDITARY SYPHILIS.

BY J. WILLIAM WHITE, M.D.


About a half century ago Mr. Abraham Colles, who had just resigned the
professorship of the Theory and Practice of Surgery in the Royal
College of Surgeons in Ireland, the duties of which, in the opinion of
the college, he had discharged for thirty-two years in an "exemplary
and efficient manner," wrote the following introductory paragraph to
his remarkable chapter on "Syphilis in Infants:" "Perhaps there is not
in the entire range of surgical diseases any one the contemplation of
which is more calculated to arrest our attention or to excite our
interest than syphilis infantum."

Although it was not then, and is not at the present day, strictly
relegated to the domain of surgery, hereditary syphilis, like its
parent disease, was generally treated of by the practitioner of that
branch of medicine. And yet in the great majority of instances the
management of such cases, especially as regards their family relations,
the relations of husband and wife, the management of the latter during
pregnancy, the delivery and subsequent care of the child, the necessary
attention to the safety of other members of the family--in fact, all of
the most weighty responsibility--falls upon the ordinary medical
attendant. It is therefore in every way proper that the condition
should receive some notice in a system of general medicine.

A proper presentation of the subject of hereditary syphilis involves a
consideration of the vexed question as to the mode by which the disease
is conveyed from parent to offspring. That it may be so transmitted has
been generally believed since the doctrine was first announced by
Torella at the end of the fifteenth century; and the facts in its
support are so numerous and convincing that, in spite of a few
distinguished opponents--among whom John Hunter was the most
conspicuous[1]--it has been unhesitatingly accepted by the profession
down to the present day. As regards the manner of transmission,
however, controversy has been and still is rife. Opposing theories have
been constructed and ardently supported, differing radically as to
essential points, often resting upon exceptional or anomalous, and
still oftener upon imperfectly observed, cases.[2]

[Footnote 1: _Works of John Hunter_, vol. ii. p. 383.]

[Footnote 2: Parrot, in a clinical lecture on syphilitic abortion (_Le
Progres Medicale_, Nov. 3, 1877, p. 798), says: "The infection of
children was known, but its true origin was not suspected. The belief
of Gaspard Torella (1498) and Matthioli (1536) that it came from the
nurses through the milk was generally accepted."

{255} According to Diday, Paracelsus (1529) was the first to plainly
state the heredity of syphilis: "Fit morbus hereditarius et transit a
patre ad filium."

Others attribute the original announcement to Augier Ferrier (1553),
and it seems certain that he was first to specify the three modes of
infection of the product of conception: "La semence du pere, celle de
la mere, et la contamination de la mere durant la grossesse."

Fallopius in a posthumous treatise on the Mal Francais (1566) adds the
authority of his name to this view: "Praeterea videbitis puerulos
nascentes ex foemina infecta, ut ferant peccata parentum, qui vedentur
semi cocti."

Ambroise Pare also acquiesced in the theory, saying, "Souvent on voir
sortir les petits enfants hors le ventre de leur mere, ayant ceste
maladie, et tost apres avoir plusieurs pustules sur leur corps;
lesquels etant ainsi infectes, baillent la verolle a autant de
nourrices qui les allaictent."

Subsequently, Mauriceau, Boerhaave, and Astruc sustained the same view,
which, with the single exception of Hunter, had no prominent
antagonist.

It was not, however, until the eighteenth century that it was described
with any attempt at detail or exactness by Rosenstein, and his essay is
loaded with errors. It was in the foundling hospitals of Paris at the
end of the last century, in the wards of Salpetriere and Bicetre, and
in the hospitals of Vaugirard and in the Capucin convents of the Rue
Saint Jacques, where pregnant women and nurses attacked with syphilis
were admitted, that methodical and trustworthy observations were made
(1780-1810) by Colombier, Despenieres, Doublet, Mahon, Cullerier, and
Bertin. Since then the history of the disease has been the history of
syphilis itself.]

A full consideration of these, or even a recapitulation of the
respective arguments pro and con, would far exceed the limits allotted
to the present article, and we will confine ourselves simply to stating
the questions which most nearly concern the practical physician, and
the conclusions which the accumulated observation and experience of the
profession seem to justify. The points bearing upon the general subject
of hereditary syphilis which exercise an important influence upon
advice or opinions of the utmost gravity as regards the happiness and
well-being of the individual or family may be enumerated as follows:

1. Is syphilis in all its stages transmissible (_a_) to the wife or
husband, (_b_) to the offspring? Or, in other words, is it ever proper
to consent to the marriage of a person who has had syphilis? If so,
under what circumstances?

2. By what means or through what channels can the disease of the
parents reach the child?

3. What are the pathology and symptoms of hereditary syphilis?

4. What is the treatment--(_a_) prophylactic, applied to the parents,
and (_b_) curative? We may now take these up seriatim.

No more important questions can be submitted to a medical man than
those pertaining to the marriage of syphilitics. Involving as it does
the welfare of many individuals, modifying or fixing the conditions or
circumstances of one or more lives, his opinion should be exceptionally
definite and well grounded. The responsibility of advising or
consenting to the marriage of a person who has once had syphilis is
undoubtedly great; the responsibility of prohibiting it is, however, no
less so. Matrimony is the natural condition for the majority of people.
Enforced celibacy, especially in males, brings with it not infrequently
a long train of attendant evils, moral and physical. It will not do to
assume that professional duty is properly discharged by telling all
patients to be on the safe side and to remain single for fear of
inoculating wife or offspring, unless it can be clearly shown that
there is a definite and unavoidable risk in every case, which continues
throughout life.[3]

[Footnote 3: "The surgeon who, on account of past syphilis, forbids
marriage to an otherwise {256} eligible man must remember that he
forbids it at the same time to some woman, who, possibly, if well
informed as to her risks, would willingly encounter them.... Respecting
a malady so common as syphilis, while it is often our duty to warn, it
is also not unfrequently our duty to encourage" (Mr. Hutchinson,
preface to the English translation of Fournier's _Syphilis and
Marriage_, p. vii.)]

There are two distinct methods of arriving at an answer to the question
under discussion: first, by considering the probabilities in regard to
the essential nature of syphilis; and, second, by carefully weighing
the clinical evidence in the matter. It seems evident that belief in
any particular theory of syphilis assigning it to this or that class of
disease must have an important influence in determining the opinion
which is held as to its curability, or at least as to its indefinite
transmissibility.

If the late symptoms, the so-called tertiary outbreaks of the disease,
are held to be evidences of the presence in the system of the specific
virus, which has simply remained for a long period, perhaps for many
years, latent or quiescent, and which is thus again manifesting its
power; if syphilis is believed, accordingly, to be a practically
unlimited disease, conforming to no known law as regards its duration,
corresponding to no other infectious or contagious malady in having a
period of termination--more or less delayed perhaps, or more or less
indefinite, but still invariably present--at which time either the
particular poison or the susceptibility of the system to its influence
has become exhausted;--if tertiary syphilis, in other words, is
regarded as simply a continuance or recurrence of the disease,
differing in no essential respect, except as to the particular tissues
involved, from the same disease in its early stages, it is difficult to
see how marriage can ever be conscientiously recommended to a person
who has once contracted it.

It is unfortunately true that in no given instance is it safe to assure
a patient of further complete immunity from the disease. In any case,
however mild in its course or under whatever treatment, there is always
an element of doubt as to the development of subsequent symptoms. The
probability of their appearance may be reduced to a minimum, the
character of the case and the thoroughness of the treatment may both
seem to give assurance that a cure has been completed, and yet both
patient and physician may be mortified and annoyed by an outbreak of
tertiary lesions. This, I think, would be admitted by every one of
large experience with the disease, and indeed furnishes the chief
argument to those who deny or are sceptical as to its curability. If,
then, it were impossible to predict with any sort of certainty that the
contagious and highly transmissible stage of syphilis would terminate
during the life of the individual, it would manifestly be unwise to
permit marriage, with its risk of inoculating the innocent partner and
the consequent double risk to the offspring.

If, however, syphilis is, as taught by Mr. Hutchinson,[4] one of the
exanthemata, having, like them, a period of outbreak, a period of
efflorescence or eruption, and a period of subsidence, and followed,
like them, by certain non-contagious sequelae, which we call the
tertiary symptoms, but which are merely relapses or degenerations of
parts affected during the secondary stage, it becomes evident that the
risk of transmission to wife or husband or children _after the lapse of
a certain interval_ becomes greatly reduced or almost nil. No one
thinks of forbidding marriage on {257} account of a previous attack of
small-pox or scarlet fever or typhoid fever, even although there are
unpleasant consequences which sometimes follow these diseases.

[Footnote 4: _The London Lancet_, Feb. 5, 1876; Reynolds's _System of
Medicine_, Am. ed., p. 423.]

Or if another and still more plausible theory of syphilis is adopted,
and we look on the tertiary period as one of contraction or
obliteration of lymphatics due to long-continued irritation by the new
cell-growths of the secondary stage, which from the very onset affect
those vessels, our views will be materially modified. During the
primary period, then, when the new cells, which either constitute the
poison of syphilis or are its carriers, are accumulating at the site of
original inoculation, constituting the induration of the chancre, or
are slowly finding their way into the general system through the
lymphatic vessels, proliferating in their walls and thickening and
hardening them, or during the secondary period, when they are rapidly
multiplying in all the tissues of the body, the risk of inoculation or
transmission would be manifestly great. When, however, by destructive
metamorphosis and degeneration, either with or without the aid of
drugs, they have been eliminated from the body, the contagious element
disappears with them; and although here and there throughout the body
some important lymphatic trunk may have undergone irreparable injury,
and may have been contracted or obliterated, permitting of the
accumulation of waste products until the node or gumma or tubercle
which we call a tertiary symptom makes its appearance, yet the disease
has lost much of its terror, and has become dangerous only to the
patient himself.[5]

[Footnote 5: _Clinical Lectures on the Physiological Pathology and
Treatment of Syphilis_, by F. N. Otis, M.D.; _Syphilis_, by V. Cornil,
Am. ed., 1882, pp. 17-27.]

These theories are only alluded to by way of elucidation of the
statement that belief in one or the other of them has an important
bearing on the relation of syphilis to marriage, and because, whichever
is thought to be the most plausible, they equally lessen or altogether
do away with a certain proportion of the danger formerly thought to
surround the marriage of a syphilitic even after a most protracted
interval. It is not necessary to accept either the one or the other
implicitly. The essential point is the recognition of the fact that
modern syphilographers, as a rule, regard the tertiary or late symptoms
as indicative of damage done during the active period--as relapses or
sequelae, and not as fresh outbreaks, of a highly contagious and
transmissible disease. Their time of appearance, their entire want of
symmetry, their non-contagiousness, their non-inoculability, all favor
this view, and we may now see what evidence corroborative of it may be
obtained from clinical facts.

It will be necessary, in the first place, to admit that there seems to
be but little doubt in the minds of most syphilographers that in rare
instances syphilitic children have been born to parents who had long
passed the limits of the secondary period. At least the great majority
of writers upon this subject speak confidently of the exceptional
occurrence of such cases, and assert that syphilis may be transmitted
during any of its stages.[6] If, however, we come to look for positive
evidence in this respect, we will find very little that is entirely
satisfactory. Cases are reported, to be sure, in which eight, ten,
twelve, or even fifteen or twenty, years after the primary sore,
syphilitic patients have become the parents {258} of children who
showed unmistakable indications of the disease. When we examine the
history of the cases, we find usually that many important points are
omitted without which it is impossible to be certain of its true
character. Were both parents originally infected? If not, has a recent
case of syphilis occurred in the one who at first escaped? If they were
both diseased originally, has either been subsequently re-infected?--a
much more frequent accident than has been commonly supposed.[7] On
applying these tests to the cases in question it will be found that few
if any of them are thoroughly convincing. Kassowitz's observations,[8]
made, it must be remembered, upon persons with whom no mercurial
treatment had been employed, seemed to show that the average limit of
transmissibility was about ten years, after which time healthy children
began to be born. His observations were, however, incomplete in many
respects, and, like all such investigations, are of course open to the
suspicion of intentional deception on the part of the patients.[9] Even
these cases, however, show unequivocally, as do all which have ever
been recorded, the steady diminution of the transmissive power under
the influence of time alone.

[Footnote 6: Belhomme et Martin, _Traite de la Syphilis_, p. 413.]

[Footnote 7: Cornil, _op. cit._, p. 20.]

[Footnote 8: _Die Vererbung der Syphilis_, Wien, 1876.]

[Footnote 9: See also Hutchinson, _British and Foreign Med.-Chir.
Rev._, Oct., 1877.]

I have said that the majority of writers seem to have no doubt of the
long continuance of this transmissive power in rare cases. There are,
however, a few notable exceptions. Fournier, whose immense experience
and acuteness of observation entitle his opinion to the utmost
consideration, says that in cases of paternal heredity the duration of
the force of transmission never exceeds at the maximum three or four
years.[10] In no case of the many hundreds he has observed has he known
a syphilitic father to infect a child--the mother being healthy--at a
later period than the one mentioned. And he is equally positive that
the gradual diminution and final extinction of the syphilitic reaction
of the parents upon the children is a veritable pathological law,
"absolutely demonstrated."[11]

[Footnote 10: _Syphilis and Marriage_, Am. ed., p. 87.]

[Footnote 11: _Op. cit._, p. 88. Of course when both parents are
diseased a somewhat longer period of activity is to be expected for the
poison.]

M. Mireur, a careful and accurate observer, records[12] a striking
instance in which in the history of a couple, both syphilitic and
untreated, eight pregnancies occurred. The first resulted in abortion
at fifth month; the second, in abortion at seventh month; the third, in
a stillbirth; the fourth, a syphilitic child dying in one month; the
fifth, in a syphilitic child dying in forty-five days; the sixth,
seventh, and eighth, in living, healthy children. To me the most
interesting fact in the whole relation is that during a portion of the
time, and immediately after the last three pregnancies, which resulted
in the birth of healthy children, both husband and wife manifested
grave tertiary syphilitic symptoms--gummata, tubercles, ulcers, etc.
This is direct evidence of the strongest kind in favor of the view that
syphilis ceases to be transmissible by heredity at the end of a certain
period, as we know that it ceases to be contagious or inoculable.

[Footnote 12: _Essai sur l'Heredite de la Syphilis_, These de Paris,
1867, p. 91.]

M. Ricord long ago,[13] and even before him Astruc and Doublet,[14] had
{259} promulgated the same theory, Ricord asserting that in the
tertiary stages the only effect of the disease upon the children was so
to modify their organization and temperament as to expose them to
developments of a scrofulous character--a view of the relation between
syphilis and struma which has been so ably supported in our own day by
Professor Gross.

[Footnote 13: _Traite pratique des Maladies veneriennes_ Paris, 1838,
p. 644.]

[Footnote 14: Legendre, _Nouvelles Recherches sur les Syphilides_, 1841
(quoted by Belhomme et Martin).]

M. Bazin also[15] denies absolutely that tertiary syphilis is any more
transmissible than it is communicable in other ways, although he fails
to give his reasons for this belief.

[Footnote 15: _Lecons sur les Syphilides_, 1859, p. 35.]

Hill and Cooper state[16] that the transmissive power continues as long
as the secondary eruptions are present, but usually ceases when the
tertiary stage is reached.

[Footnote 16: _Syphilis and Local Contagious Disorders_, London, 1881,
p. 62.]

Van Buren and Keyes[17] believe that fathers with tertiary syphilis
certainly, as a rule, procreate non-syphilitic children; and in
speaking of the fact that when the mother has syphilis the child is
generally infected, they except the later tertiary stages.

[Footnote 17: _Genito-urinary Disease and Syphilis_, 1874, p. 521.]

Bumstead[18] and Taylor say that without mercurial treatment the danger
of transmitting the disease to offspring usually persists up to the
fourth year of syphilitic contagion.

[Footnote 18: _Venereal Diseases_, 1879, p. 739.]

Mr. Lane says:[19] "It is certainly the rule that when the parents have
fully reached the tertiary stage the children born to them are free
from all signs of syphilis."

[Footnote 19: _Lectures on Syphilis_, London, 1881, p. 65.]

Mr. Hutchinson says:[20] "It is almost an acknowledged law that parents
in the late tertiary stages do not transmit taint."

[Footnote 20: _The Med. Press and Circular_, Aug. 2, 1882, p. 85.]

It will be seen from the foregoing extracts, which might be greatly
multiplied,[21] that there is a strong tendency on the part of many
authors to limit more or less strictly the period of transmissibility
of syphilis even when the disease is allowed to progress without
treatment. As to the facts that it becomes milder with time, both in
parents and offspring, that it ceases to be conveyed from husband to
wife or vice versa, that with each succeeding year after the
termination of the secondary period the chances of escape of the
product of conception increase in a rapidly augmenting ratio,--there is
no difference of opinion whatever. Neither is it seriously disputed
that the length of time during which the disease remains active, as
well as the degree of its activity, may be markedly and beneficially
influenced by the administration of mercurial treatment. Under proper
medication patients who have rashly or disobediently married in the
height of the secondary period have been enabled to escape the danger
of transmission either to spouse or offspring--have, in fact, had
children born healthy and who never subsequently manifested any
symptoms of the disease.

[Footnote 21: M. Diday, _Traite de la Syphilis des Nouveau-nes_, Paris,
1854, p. 183; M. Bertin, _Traite de la Maladie venerienne chez les
Nouveau-nes_, Paris, 1870, p. 142; M. Bazin, _op. cit._, p. 164; M.
Roger, _L'Union Medicale_, 1865, t. i. p. 147 (quoted by Fournier).]

I may add that my own experience seems to confirm the views which have
thus been set forth. I have notes of all my cases occurring in private
practice in a large city--some of them, I regret to say, among personal
friends or acquaintances, some of them in our own profession--and have
repeatedly {260} given permission to men to marry or to resume marital
relations after three years or three years and a half of mild mercurial
treatment, to which during the last six months or a year had been added
iodide of potassium. In many instances healthy children have been born:
in none, so far as I know, has the wife or mother been directly
infected. There have been a few doubtful cases in which premature
deliveries or stillbirths have occurred, but in nearly every such
instance there seemed to be other and entirely competent causes for the
accident; and in none of them, as I learned from the father or from the
obstetrician in attendance, were the children the subjects of
unmistakable syphilitic symptoms.

As to the exact time at which it is safe to permit marriage, and as to
the proper treatment before and after that event, it is hardly possible
in an essay like this to enter into many details. Yet so much is
involved in the answer to our first question that it may not be
altogether out of place here to indicate briefly the views of the
writer as to general methods of treatment. This is the more proper
because in every case of suspected syphilis in a new-born child, in
every case of threatened or actual abortion or miscarriage in the wife
of a man who has at some time in his life had syphilis, these questions
will present themselves, and the answers to them will greatly influence
not only the diagnosis and prognosis, but even the treatment, of such
cases.

1. In the first place, then, the diagnosis of syphilis should have been
assured. No venereal sore can with certainty be pronounced to be
syphilitic before the occurrence of general constitutional symptoms,
either the early cutaneous eruptions or at least the general glandular
involvement. Treatment begun prior to these developments leaves the
whole case open to the suspicion of mistaken diagnosis.[22]

[Footnote 22: "It is unsafe to predict confidently that any venereal
ulcer, even a soft sore attended with suppurating bubo, will entail no
further consequences. There is a strong probability that an indurated
sore will prove infecting; and there is a probability, though not
nearly so strong, that a soft suppurating sore will not; but exceptions
to both these general rules will be met with, and there is really no
absolute proof of the infecting nature of any given sore but the fact
of infection itself" (_Lectures on Syphilis_, James S. Lane, London,
1881, p. 23).]

2. The drug which should at once be begun when the character of the
case is fully recognized is mercury in one of its various forms. It may
be given by the mouth, by inunction, by vaporization, by hypodermic
injection, according to the preferences of the physician or patient;
but, however administered, it should be given in sufficient
quantity--_i.e._ in each case the full physiological dose of that
particular patient should be employed. To ascertain this the amount
used should have been gradually increased until commencing symptoms of
salivation are produced, when it should be diminished about one-half.

3. The quantity which has been thus determined should be given
continuously, or stopping only for the management of intercurrent
complications, for at least eighteen months. If during this time new
syphilitic symptoms make their appearance, the dose should be
temporarily raised until they have vanished, when it should be brought
down again to the original amount.

4. At the end of eighteen months or two years small doses of iodide of
potassium should be added to the mercurial, and this mixed treatment
should be persevered in for six months or a year longer, or should be
{261} still further prolonged if during that time any evidence of
syphilis is seen.

5. At the end, then, of from two to three years, if no symptom has been
seen for six months or a year, treatment may be stopped and the patient
kept under observation for a year; and if during that time no symptom
develops he may consider himself as in all probability cured. Any
course of treatment less thorough than this should be set down as
insufficient to afford any reasonable presumption of further immunity
from the disease.

There is evidence to prove, on the other hand, that this plan of
treatment, rigidly carried out, results in the majority of cases in
curing the disease, or at any rate in putting the patient in such
condition that he may with safety marry and may expect to have healthy
children.

To recapitulate: Syphilis after a certain period, not extending much
over four years where the disease is allowed to run its own course, and
probably much reduced by treatment, ceases to be a contagious disease;
and at about the same time or some time after loses, in the majority of
cases, its capability of being transmitted.

As there are probably exceptions to the rule that this power of
transmission disappears spontaneously within any specified time, it is
never safe to trust altogether to the unaided efforts of nature, but a
vigorous and sufficient specific treatment must be employed.

Given, however, the lapse of a sufficient time--say from three to four
years as a minimum--the history of a proper and continuous plan of
treatment, and the absence for a year or more of any specific symptoms
whatever, and the risks of marriage are so reduced as probably to
warrant a careful physician in permitting it.[23] And conversely, of
course--and this constitutes the reason for introducing the foregoing
matter into a paper on hereditary syphilis--in any doubtful case where
such a history can be elicited, and where all these precautions have
been observed, it is improbable that any taint of syphilis has been
transmitted.

[Footnote 23: This refers, of course, to an ordinary case of syphilis.
If the symptoms have been unusually grave, if the deeper tissues or the
viscera have been seriously involved, if cerebral or spinal
complications have occurred, the situation is of course much more
grave, and no step should be taken without the most thoughtful
deliberation. The work of Fournier already alluded to (_Syphilis and
Marriage_) furnishes an admirable guide under these circumstances.

Mr. Frederick Lowndes, surgeon to the Liverpool Dock Hospital
(_Lancet_, July 8, 1882), says: "Each case must be judged on its own
merits. When the constitution is good, and there has been sufficient
specific treatment, marriage may be permitted within a much shorter
period than M. Fournier suggests, and with safety. Syphilis alone and
syphilis combined with scrofula are two very different foes to contend
with, and if our patient be of a scrofulous temperament a delay even
longer than M. Fournier's may be desirable."

He quotes Dr. Thomas Edward Beatty in an address at the annual meeting
of the British Medical Association at Leeds in 1869: "Mercury given to
the man when first diseased would, I firmly believe, have prevented
this terrible calamity--_i.e._ the syphilitic infection of the wife;
and I would now humbly suggest to all who undertake the treatment of
venereal disease that if they have a certainty that their patients will
remain celibate all their lives, they may heal up their sores and
dispel their eruptions and sore throats in any manner they like, but
that they have no right to expose the pure, innocent, high-minded
females of society to contamination by marrying men treated without
mercury."]

Beyond this in positiveness of assertion it is not safe to go. There
may be exceptions to these as to most other hygienic or therapeutic
rules, but they will surely be of excessive rarity.

{262} Before considering the methods by which syphilis can reach the
child from one or the other of its parents, it may be well to mention
the modes in which they can infect each other.

The father can derive syphilis from the mother only in the usual
way--_i.e._ by contagion through a breach of surface permitting of the
direct absorption of the poison, the development of the disease being
attended by the usual phenomena--chancre, lymphatic enlargement, skin
eruptions, etc. The woman may--and in the vast majority of cases
does--acquire the disease from the husband in a similar manner. But
there seems to be good reason for believing that she may also become
infected through the medium of the child, who receives its syphilis
directly from the father, the mother up to the time of conception
having escaped contagion. More than this, it appears to be highly
probable[24] that no woman ever bears a syphilitic child and remains
herself absolutely free from the disease.

[Footnote 24: The strongest argument against the theory that every
woman who has had a syphilitic child has herself been infected lies in
the existence of cases like the following, several of which have been
observed: The wife of a man having active but untreated syphilis gives
birth to one or two syphilitic children, she herself developing no
symptoms. Later, the husband is placed on mercurial treatment. She then
conceives and gives birth to a healthy child. He stops treatment, and
she again bears a syphilitic child, which on his resuming his mercurial
course is followed by another healthy infant. Such cases certainly
indicate that the syphilis of the mother, if any exists, is incapable
of transmission to the child, as the effect of the treatment of the
father is too direct and unvarying to admit of doubt.]

The existence of this form of infection--syphilis by conception--has
been vehemently denied by many authors[25]--by some on the theoretical
grounds that as the essential elements or carriers of the syphilitic
virus have been shown to be cells or protoplasmic particles, and as,
after conception, the embryo is supplied with serum, but not with cells
of any kind, it is impossible that syphilis can be conveyed either to
or from it;[26] by others on reported observations of numerous cases in
which mothers who have been delivered of syphilitic children have shown
no evidences of the disease.

[Footnote 25: Kassowitz, Von Baerensprung, Bidenkap, and others.]

[Footnote 26: Bumstead and Taylor, _op. cit._, p. 742.]

It would appear, however, that, setting aside arguments based on
theoretical considerations, the weight of clinical evidence is
altogether in favor of the frequent, if not the invariable,
contamination of the mother through the medium of the foetus. No
physician of large experience in this class of cases can fail to have
seen some in which the husband, having had syphilis and having married
after an insufficient interval or an imperfect course of treatment, has
infected his wife with the disease, although at the time no
discoverable symptom is to be found upon his body--no abrasion, sore,
mucous patch, no lesion of continuity or suspicious point of any
description. An equally careful inspection of the woman will also in
such cases be attended by negative results--no initial lesion, no spot
of induration, no adenopathy being at all discoverable--and yet she
will be found with unmistakable evidences of constitutional
syphilis.[27] There is a clue to all such cases which will immediately
resolve the difficulty. In every instance, providing that no mistake
has {263} been made and that both husband and wife are really free--the
one from any contagious lesion, the other from any evidence of a
present or previous primary sore--it will be found that pregnancy has
occurred; that the woman has either been delivered of a syphilitic
child or has had an abortion or miscarriage at some time before the
outbreak of the symptoms of syphilis. Although I am firmly convinced
that this is a statement of facts based upon careful clinical
observation, and although this view has received the unqualified
endorsement of no less an authority than Fournier,[28] it is yet
strongly combated by many excellent authorities. They say in reply to
the above arguments that the reported cases are open to just criticism,
that trifling and unnoticed lesions of the father--chafes or abrasions
almost microscopic--suffice to transmit it on his part; while as an
explanation of the supposed absence of the primary lesion in the mother
they plead the well-known difficulty of discovering it in women under
any circumstances.

[Footnote 27: For a typical case see _Colles's Works_, New Sydenham
Society, London, 1881, p. 253. From that date to this hundreds of such
cases have been observed, and it would be idle to refer to them.]

[Footnote 28: _Op. cit._, pp. 26-30. He confesses to complete ignorance
as to the precise method by which this contagion takes place, whether
by poisoning of the fecundated ovule at the moment of conception (the
theory of Von Baerensprung) or by exchanges of the utero-placental
circulation, and regards the various hypotheses upon these points as
without practical value.]

Another argument, however, which seems to me to be unanswerable lies in
the application to the case in question of the well-known "law of
Colles," which from the date of its first enunciation by its
distinguished expounder in 1837 down to the present day has been found
to be absolutely without exception. I know of no other statement in
reference to disease which is at once so sweeping and comprehensive in
its bearings and so completely substantiated by clinical experience. It
may be given in his own words: "One fact well deserving our attention
is this: that a child born of a mother who is without obvious venereal
symptoms, and which, without being exposed to any infection subsequent
to its birth, shows this disease when a few weeks old,--this child will
infect the most healthy nurse, whether she suckle it or merely handle
and dress it; and yet this child is never known to infect its own
mother, even though she suckle it while it has venereal ulcers of the
lips and tongue."[29]

[Footnote 29: _The Works of Abraham Colles_, edited by Robert
McDonnell, the New Sydenham Society, London, 1881, chap. xiii. p. 287.]

As to the absolute and unvarying truth of this law there is no excuse
for a shadow of doubt. To quote Mr. Hutchinson: "It has received the
assent of every authority who has written on the subject since it was
announced. It has attracted attention both at home and abroad, and I am
not aware that a single exception to it has been recorded.[30] We have
all of us seen chancres on the nipples of wet-nurses. They are, indeed,
not very infrequent. We have, however, none of us seen such on those of
the mothers of infected children. Let us remember that it is very
unusual to put a syphilitic infant out to wet-nurse--a thing which no
prudent physician would ever permit--and that, probably, for one so
nursed a hundred are suckled by their mothers, and we can appreciate
the weight which this entire absence of proof that mothers ever suffer
{264} bears. It amounts, I think, to all but proof that they are
absolutely insusceptible."[31]

[Footnote 30: The cases of Cazenave (1847), Cocchi (1858), Muller
(1861), Ranke (1878), Guibout (1879), Scarenzio (1880), and Zingales
(1882), are defective in important particulars, the first two so much
so as to render them valueless. Ranke's case is by far the strongest
yet recorded, but lacks fulness and rests upon his unsupported
testimony. (See Hill and Cooper, _op. cit._, p. 55, and _Nouveau Dict.
de Med. et de Chir._, vol. xxxiv. p. 687.)]

[Footnote 31: Dr. J. N. Hyde suggests (_Archives of Dermatology_,
April, 1878, p. 103) that "the full weight of Colles's law is to be
estimated in connection with the question whether the child whose
hereditary syphilis is derived from the mother exclusively is capable
of infecting its healthy father; and if no instance of this latter can
be adduced a higher law becomes defined--viz. that the child whose
hereditary syphilis is transmitted by one parent only is incapable of
infecting either." He explains this hypothetical immunity, in which he
seems to believe, by saying that "it is probably due to the fact that
the syphilis-bearing cell-element cannot readily be implanted upon the
soil from which it sprang--a fact illustrated by the infecundity of
consanguineous marriages and the non-auto-inoculability in general of
the primary lesion of syphilis." When, however, we exclude the large
number of cases in which the father is already syphilitic, and remember
that in the others the contact between him and the child is slight,
infrequent, and fleeting--being usually limited to an occasional kiss
or caress--it does not seem strange that no instances of such infection
have been reported; nor does the fact seem at all worthy of being made
the foundation of a general law.]

There can be but one rational explanation of these facts--viz. that the
mothers who have thus acquired an immunity have done so by first
acquiring the disease. It may, in those cases where no secondary
symptoms appear, be in a modified form, due, as suggested by Mr.
Hutchinson, to some heteromorphism or alternation of generations on the
part of a specific fungus, or to the excessively small quantity of the
poison which finds its way from child to mother, or to some other
obscure cause with which we need not now concern ourselves. It is, at
any rate, no more mysterious than the protective influence of vaccine
in small-pox, and when one is rationally explained doubtless the other
will be found to be closely allied in its mode of action. The fact
which interests us at present is that it is in the highest degree
improbable that anything but some form of syphilis itself could afford
this entire protection, and that it is not in the least unreasonable,
but, on the contrary, logical and consistent with all the known facts,
to suppose that while in some cases no observable symptoms might be
produced, in others where the cause was the same, but more active, or
the powers of resistance less, the usual constitutional phenomena would
be developed.

We may conclude, then, that the husband may infect his wife--(1) In the
usual manner or by direct contagion; (2) through the medium of the
child, or at any rate by the production of conception.

The theory upheld by Von Baerensprung, that the syphilis of the mother
is imparted to her at the moment of impregnation, the disease being
impressed upon the fecundated ovule, does not materially conflict with
the above views, conception being in either case the essential factor,
but in the latter instance the intervention of the foetus itself not
being necessary. It has to support it the clinical fact that in those
cases where syphilis appears during pregnancy the outbreak of symptoms
occurs at about the ninth or tenth week after the date of conception,
or a period which closely corresponds to that of the appearance of
general symptoms after exposure to ordinary contagion--allowing about
three weeks for the so-called incubation of the chancre and six weeks
for the secondary incubation.[32]

[Footnote 32: This has been shown not only by Von Baerensprung (_Die
Hereditare Syphilis_), but also by Diday, whose observations were
intended to prove the possibility of syphilis being derived from the
child by the mother--"choc en retour." In 24 cases the period at which
the first eruption appeared in the mother averaged sixty-five days
after conception; only once did the first signs appear after the fourth
month of pregnancy.]

{265} It may also be said to be rendered probable by the following line
of argument:

Colles's law, which is without exception, demonstrates that every woman
who has had a syphilitic child has been herself infected, even if she
has had no observable symptoms;[33]

Cases are recorded, however, in which a woman having given birth to one
or more syphilitic children, and therefore herself syphilitic, bears
healthy ones in consequence of specific treatment administered to the
father before and during the period of conception, she remaining
untreated;[34]

The determining cause, therefore, of the syphilis of the child is not
the syphilis of the mother, but the condition of the fecundating germ
of the father; and, as a corollary,

The determining cause of the syphilis of mothers in whom the disease
follows conception is not by infection from the foetus through the
utero-placental circulation[35] or otherwise, but is the diseased male
procreative cell which becomes blended with the female ovule.[36]

[Footnote 33: It is obviously no explanation of the law of Colles to
say that "it would seem to indicate that the escape of the mother is
due to some occult, undiscernible change in her system" (Bumstead and
Taylor, _op. cit._, p. 745).]

[Footnote 34: See foot-note, p. 262.]

[Footnote 35: On account of the absence of cellular elements in the
fluid interchanged.]

[Footnote 36: An elaborate paper by Fraenkel (_Archiv fur
Gynaekologie_, 1873, vol. v. p. 1), based on twenty-one cases of
childbirth, was written to prove by the condition of the placenta that
direct infection of the child by the father was possible without the
participation of the mother, and that when the latter became infected
it was through the medium of the child (_choc en retour_). In fourteen
of his cases the specific change in the placenta began in the foetal
portion or affected it exclusively. These cases, however, as analyzed
by Hill and Cooper (_op. cit._, p. 57), are altogether defective in
important particulars. Of course to sustain his theory there should be
indubitable evidence that the fathers were syphilitic, and that the
mothers were not so. So far from this being the case, but one of the
fathers was known to be syphilitic, while two of the mothers had
evidences of constitutional syphilis at the date of childbirth, and
nine others had markedly suspicious histories. The lesions of the
placenta which are thought to be syphilitic consist in the development
of papular or gummatous growths which give rise secondarily to
inflammatory troubles affecting either the placenta itself or the
placenta and the uterine mucous membrane.]

If the premises are admitted the conclusions seem irresistibly to
follow.

There is no proof whatever that the semen of a syphilitic man is
contagious or can transmit the disease in any but the way above
discussed. On the contrary, it has been shown experimentally[37] that
it is entirely innocuous and non-inoculable.

[Footnote 37: Mireur, _Annales de Derm. et Syph._, 1876, p. 77.]

All other theories as to methods of contagion are so entirely
hypothetical and unsupported by trustworthy evidence that we can afford
to disregard them.

We may now consider the ways by which syphilis reaches the child, and
they may be broadly classified into--

1. By descent from the father.

2. By descent from the mother.

3. By direct infection.

As a matter of course, the influence of the father upon the child, so
far as regards heredity, ceases at the moment of conception; or, to be
more exact, no subsequent condition of the male parent, no development
or acquirement of disease, can exert any further effect. That the
existence of active syphilis in the father may result in the
transmission of the malady to the child can hardly be doubted. To be
sure, there are numerous {266} examples of cases where both wife and
child have escaped though the husband showed at the time of conception
very active secondary lesions. These, however, are exceptions, and do
not in the least invalidate the rule that it is possible for a father
to hand the disease directly to his child. There is no other possible
interpretation of the cases already alluded to in which successive
pregnancies in the same woman alternately resulted in healthy or in
syphilitic children according as the father was or was not kept under
specific treatment. Other arguments might be advanced, but that seems
to me conclusive.

The relative effect of paternal as compared with maternal influence may
be considered after we have described the latter.

Descent from the mother may occur theoretically in consequence of--

1. Infection of the mother previous to conception.

2. Infection of the mother at the moment of conception.

3. Infection of the mother during the period of utero-gestation.

As to the first of these methods of transmitting the disease there is
little if any difference of opinion. Even those who claim the most for
paternal influence[38] include among the conditions which may give rise
to syphilis in the child disease of the ovule, and it may be stated as
incontrovertible that recent or active syphilis in the mother at the
time of conception will almost certainly be followed by syphilis in the
child. As a rule, women who have borne syphilitic children, even when
they do not give unmistakable evidence of the disease, fail in health,
become anaemic, and often develop glandular or osseous swellings which,
according to Zeissl,[39] are only relieved by antisyphilitic treatment.
The bearing of Colles's law upon the alleged immunity in many instances
of the mothers of syphilitic children has already been shown (p. 264);
and there is other evidence, not perhaps so conclusive, but strongly
corroborative, of the same view--viz. that their escape is only
apparent, and that syphilis, either latent or active, always affects
such mothers.[40] There can be no manner of doubt that in every
instance at or about the time of childbirth there are not to be found
pathognomonic lesions of syphilis, nor do such lesions always make
their appearance in cases where the period of observation is a short
one; but it is claimed with much show of truth that prolonged and
patient inspection of such patients will in time result in the
discovery of some symptom which betrays the presence of the disease.

[Footnote 38: Bumstead and Taylor, _op. cit._, p. 745. Hutchinson in
Reynolds's _System of Medicine_, Am. ed., vol. i. p. 431: "In a large
proportion of the cases met with in practice the taint is derived from
the father only." (On this point see foot-note to p. 270.) If there
were any doubt as to the fact that syphilis in the mother only may be
transmitted to the child, it would be removed by the cases of Bardicet
and others mentioned in _Nouv. Dict. de Med. et Chir._, vol. xxxiv. p.
688. In these cases nurses who had contracted the disease from their
sucklings subsequently became pregnant (without having infected their
husbands) and gave birth to syphilitic children.]

[Footnote 39: _Jahrbuch_, vol. ii. p. 303, 1872.]

[Footnote 40: Zeissl, Sigmund, Oewre, Flindt, Woodman, and others are
quoted by Hill and Cooper to this effect. Woodman, for other purposes,
gave the histories of 200 cases of infantile syphilis. In all of these
the mothers had suffered from typical secondary lesions.]

The cases in which treatment of the father has resulted in healthy
children, whereas without treatment he procreated only syphilitic
children, the mother being without either symptom or treatment, have
been urged as evidence of the direct descent of syphilis from the
father to the child without the intervention or participation of the
mother. Doubt {267} has been thrown upon them by those who uphold the
contrary view;[41] but after looking into them carefully I am
constrained to admit that some of them, notably those of Kassowitz[42]
and R. W. Taylor,[43] are convincing of the facts--(1) that treatment
of the father controlled the condition of the child, and (2) that there
was no evidence that the mother had syphilis. But we have seen that the
only proof of the universal infection of mothers of syphilitic children
is the law of Colles, and that in many cases the disease is for a long
time latent or unrecognizable. Let us admit that this was the condition
in the cases in question; it does not at all follow, necessarily, that
because the mother has latent or hidden syphilis she must infect her
child. Every case even of active syphilis in the parents is not handed
down to the children, a certain proportion of whom escape even when
both parents are in the height of the secondary stage at the time of
conception.[44] But the activity of the disease in the children, and
even more the likelihood of its reaching them, are in direct proportion
to its activity in the parents.[45] A mother, therefore, who under the
influence of active syphilis in her husband has given birth to two or
three syphilitic children, and has herself shown no symptoms of the
disease, may nevertheless have it in the latent form and have no strong
tendency to transmit it. Consequently, treatment of the father will
result in the procreation of healthy children, because it removes the
active and efficient cause of their infection. To take any other view
of these cases is to assume that every syphilitic parent must hand down
the disease to the children--an assumption which is not in consonance
with numerous well-attested clinical facts.

[Footnote 41: Hill and Cooper, _op. cit._, pp. 52, 53.]

[Footnote 42: "Die Vererbung der Syphilis," _Stricker's Med. Jahrb._,
1875, p. 391.]

[Footnote 43: _Archives of Clinical Surgery_, New York, Sept., 1876.]

[Footnote 44: Fournier, _op. cit._, pp. 35-37.]

[Footnote 45: Hutchinson, _op. cit._, p. 431.]

Leaving this interesting question, however, we may consider the other
methods by which syphilis descends from the mother to the child, having
seen already that it is beyond doubt that it may be handed down by
disease of the ovule due to syphilis acquired previous to conception,
and having seen that there is a high degree of probability that the
mother herself rarely, if ever, escapes the disease. The second method,
or that in which the mother becomes syphilitic at the moment of
conception, has already been sufficiently discussed. It is really,
strictly speaking, an example of paternal heredity, as the resulting
germ is syphilitic--not because the ovule of the mother was infected,
but on account of the disease of the spermatozoid of the father.

There remains for consideration the influence upon the child of a
syphilis acquired by the mother during some period of utero-gestation.
That under these circumstances the child can become infected has been
and is still absolutely denied by some very respectable
authorities.[46] All that is {268} necessary for proof of its
occurrence is, however, (1) freedom of both parents from syphilis at
the time of conception, or, in other words, syphilis must have been
acquired by both--not alone by the mother--after the beginning of
pregnancy; (2) that the syphilis of the child be unmistakably
pre-natal--that is, not acquired by some accident during or after
birth.

[Footnote 46: Bumstead and Taylor, _op. cit._, pp. 742, 744. They base
their denial, first, on the physiological fact (?) that no interchange
of cellular elements between mother and father is possible, and next on
the absence of satisfactory evidence of the occurrence of infection
during pregnancy. Zeissl's case seems sufficient answer to the last
assertion, and there is strong evidence that the first is without good
foundation. "The placenta is penetrated by the virus, and does not play
the part of a filter for the elementary particles of matter which, so
far as we know, represent the true active contagion of the disease. In
the absence of direct experiments, which it would be almost impossible
to institute, we may argue from the facts known to exist in certain
acute infectious diseases in which there are very interesting points of
resemblance.

"It has been known for a long time that small-pox occurring in the
mother may be transmitted to the product of conception enclosed in the
uterus, and it is supposed that the virulent particles traverse the
walls of the maternal vessels in order to penetrate the circulating
apparatus of the foetus. But what is only a supposition in the case of
small-pox seems to have been actually demonstrated in symptomatic
charbon (Arloing, Cornevin, and Thomas), bacteridian charbon, and
recurrent fever, in which the poisonous element is easily recognized.
The recent experiences of Strauss and Chamberland (1882) have shown
that the foetus participates in the 'infection charbonneux' of the
mother. Albrecht has shown (1880) the presence of numerous spirochoetae
in the blood of the heart of a child born at seven months of a woman
with a second attack of relapsing fever. It may be supposed, therefore,
though not demonstrated, that the transmission of syphilis takes place
by the same method as that of relapsing typhus or of charbon" (_Nouveau
Dict. de Med. et de Chir._, pp. 682, 683).]

The following case,[47] reported by a most accurate observer, seems to
combine both these requisites. Zeissl the younger reports that O. X.,
thirty-six years old, never having had syphilis, left his wife, to whom
he had been married two years, to go a journey on July 15, 1877. The
wife was then in the second month of her first pregnancy. On July 24th
O. X. had extra-marital intercourse. About twenty-one days after this
coitus he observed a small lump on the inner surface of the foreskin,
and on Aug. 22d he consulted Zeissl the elder. On Sept. 23d a
maculo-papular eruption of the skin with erythema faucium appeared.
Under treatment these symptoms completely disappeared. On Oct. 29th he
went home to fetch his wife to Vienna for her lying-in, and had
intercourse with her soon after his return, notwithstanding Zeissl's
strict prohibition. At the beginning of December a hard sore developed
on the left nympha of the wife, who was then in the seventh calendar
month of her pregnancy. At the end of December a maculo-papular
eruption spread over the body and was treated with mercury. On Feb. 14,
1878, a well-grown and apparently healthy female child was born at full
term. When eleven days old[48] a pustulo-scaly eruption came out on the
child's soles and toes, and soon afterward a maculo-papular eruption
over the body generally. A few days later the child died. No
post-mortem examination was permitted. In July, 1878, the wife had
iritis, and after that gummata on the leg. She miscarried in July,
1878, at the third month, and again in February, 1879, at the second
month.

[Footnote 47: Quoted by Hill and Cooper, _op. cit._, p. 60.]

[Footnote 48: Of course much too early for constitutional symptoms if
the disease had been acquired during or after birth.]

There seems to be no reasonable escape, after reading this carefully,
from the conclusion that in some manner the poison of syphilis found
its way from the mother to the child. The old idea that the latter was
directly infected in utero from the semen of the father is altogether
without foundation. Other cases equally satisfactory and complete have
been reported, and, unless the intelligence or the truthfulness of the
observers be impugned, establish without doubt the possibility of
infection during utero-gestation.

In the above case the contagion of the mother occurred in the seventh
{269} month of pregnancy; and this, I believe, is as late as it has
ever been known to be communicated to the child. The exact date at
which it becomes impossible so to transmit it is unknown, but as a
general rule it may be said that the earlier a mother is infected
during gestation the less likely is it that the child will escape.
Treatment of the mother--as of the father in cases where he is at
fault--very greatly modifies the whole problem and adds immensely to
the chances that the child will not be infected.

Direct infection of the child during birth could not properly come
under the head of hereditary syphilis. There is no possible reason why,
when the mother has contagious lesions of the genitals, acquired too
late to infect the child in utero, this should not occur, but as a
matter of fact no such case has ever been recorded. One explanation of
this circumstance may be found in the protective covering of vernix and
mucus which coats the infant's body and lessens greatly the risk of
absorption. This hardly accounts satisfactorily, however, for the
entire absence of such cases from medical literature, and it is fair to
suppose that in all but those cases in which the primary sore is
acquired during the last month of gestation--which for obvious reasons
are excessively rare--the infant acquires some immunity which protects
it from its mother, and is similar to that which, under Colles's law,
operates in her favor. In other words, even though apparently free from
syphilis at birth--a not uncommon event, as we shall see--it has a
latent or modified syphilis which protects it from contagion.

We may now briefly restate the conclusions at which we have thus far
arrived:

1. After a certain interval, not less than four years, and after
thorough specific treatment, a person who has contracted a syphilis not
especially severe or malignant in its type may be permitted to marry.
The assent to marriage will then be based on a belief in the curability
of syphilis or the cessation of its contagiousness, its inoculability,
and, in the vast majority of cases, its transmissive power at the end
of the secondary stage.

2. It may be inherited from either parent or from both, and the
probability that this will occur increases in a direct ratio with the
nearness of the time of conception to the date of their infection with
the disease. The severity of the inherited disease in the child
increases in the same proportion.

3. It is undoubted that, the father being healthy and the mother
syphilitic, the child may, and in all probability will, have the
disease.[49]

[Footnote 49: Dr. Sturgis, who disbelieves altogether in the
possibility of paternal heredity, concludes, after examining the
subject carefully, that (1) a mother begets non-syphilitic children as
long as she is not infected, even though the father is syphilitic; and
(2) the moment she is diseased the children are inevitably so (Paper on
"The Etiology of Hereditary Syphilis," _New York Medical Journal_,
July, 1871). This doctrine was previously supported by M. Cullerier,
whose views gave rise to the remarks of M. Voillemier (quoted by
Fournier) that if they were accepted "the father would be only the
accidental occasion of a child; one would be, in reality, the child of
his mother only." Cullerier's cases are invalidated by the fact that
the syphilitic fathers who had healthy children had been subjected to
mercurial treatment (_Mem. de la Societe de Chirurgie_, Paris, 1854,
quoted by Taylor in _Archives of Clin. Surg._, vol. i. p. 83). The
theory is a very old one. Vassal has sustained this idea as long ago as
the end of the last century. Kostum (1804), and after him Hufeland,
were of the same opinion. Cullerier (1857) wrote: "In order that a
child acquire syphilis hereditarily it is necessary that the mother is
or has been {270} syphilitic." Notta, Follin, Charrier, Mireur (1867),
and Langlebert (1873) support this theory more or less earnestly. Oewre
wrote (1873): "Paternal influence is nil as regards hereditary
syphilis." Isseff (1879) wrote: "Where a man suffers or has suffered
from syphilis he cannot transmit the disease to his descendants without
infecting his wife; that is to say, in fewer words, there is no
infection from the father." Sigmund says: "The heredity of syphilis is
derived in its last analysis from the mother" (_Nouveau Dict. de Med.
et Chir._, vol. xxxiv. p. 689).]

4. It is probable, but less so,[50] that, the mother being healthy and
the father syphilitic, the child will be infected.

[Footnote 50: This refers simply to the comparative probability of
infection, and does not conflict with the statistical fact expressed by
Hutchinson (Reynolds's _System of Medicine_, vol. i. p. 431) in his
words: "In the large proportion of cases met with in practice the taint
is derived from the father only." This numerical predominance of
paternal influence is very readily explained. There are many more
syphilitic men than syphilitic women, and especially among the couples
who contract fertile marriages the number of women who are infected
before becoming mothers is inconsiderable. On the other hand, it
frequently happens that men who have had syphilis, but have been
without symptoms for a longer or shorter interval, marry and transmit
to a series of children a disease which has ceased to be directly
contagious to their wives, the transmissive power continuing after the
possibility of ordinary contagion has disappeared. As in the majority
of such women the disease is latent, and may be only displayed in their
immunity from infection, it becomes evident that, history and symptoms
both being wanting on their part, the conditions justify the assertion
of Mr. Hutchinson. (See _Nouveau Dict. de Medecine et Chirurgie_, p.
684.)

That assertion (quoted above) has, however, been thought by several
writers to indicate his belief in the escape of the mother. That I have
not misinterpreted him is evident from the following extract from an
article on "The Transmission of Syphilis," written by him (_Brit. and
For. Med.-Chir. Rev._, Oct., 1877): "I take it for granted (although I
know that there are still some who doubt) that it is possible for a
father to transmit the taint, the mother being at the time of
conception wholly free. I believe, indeed, that in practice this is by
far the most common way in which syphilis is transmitted. Whether in
these cases it is correct to speak of the inheritance being paternal
only is, as we have just seen, another matter, since it is possible
that in every instance the mother derives an infection from the father,
and may thus in turn influence it."]

5. It is highly probable, though it can hardly be considered as proven,
that in all cases where a child becomes syphilitic through paternal
influence the mother is also the subject of syphilis, which may,
however, assume a latent form, the only evidence of its presence in a
few cases being the protection which it affords against contagion
through the medium of the child.

6. Syphilis may be transmitted from mother to child even when it is
acquired by the former as late as the seventh month of utero-gestation.

Since writing the above the thirty-fourth volume of the _Nouveau
Dictionnaire de Medecine et de Chirurgie_ has been published. In the
article on syphilis seventeen pages are devoted to the question of
heredity, which is reviewed in a most thorough manner and finally
summed up as follows (p. 698):

"The most definite views which we possess on the subject of the
hereditary transmission of syphilis may be thus expressed:

"Children may be infected by heredity, not only when the two parents
are syphilitic, but also when only one, either the father or mother, is
diseased at the time of conception.

"When both parents are diseased at that time there is more certainty
that the child will be infected, and infected gravely, than if only one
of them has the pox.

"The hereditary disease is not always fatal, even when both progenitors
have actual specific symptoms. The more recent the disease of the
parents the greater the chances of their transmitting the disease and
of its assuming {271} a serious form. There is no proof that inherited
syphilis is more grave when derived from the father than when coming
from the mother.

"It is altogether exceptional for the mother, healthy at the moment of
conception, not to participate in the disease transmitted by the father
to the child. If she escapes direct contagion--which is rare when the
disease of the father is active--she undergoes a species of infection
from contact with the contaminated foetus.

"Syphilis by conception, which is thus transmitted from the foetus to
the mother, may present the usual characters and evolutions of the
acquired disease; frequently, also, it is latent, and is betrayed only
by the existence of immunity from further contagion on the part of the
mother. It may finally manifest itself by tertiary symptoms or by
systemic troubles without specific characters.[51]

"The power of transmitting syphilis hereditarily decreases
spontaneously as the disease of the parent becomes older. The influence
of treatment is no less certain than that of time. When the two
progenitors are at the moment of conception free from syphilis, the
foetus may still be infected if the mother acquire the disease during
her pregnancy."

[Footnote 51: "This form of syphilis shows itself in the mother in
three ways:

"1st. By the usual signs of syphilis by contagion, with the exception
of the primary sore, appearing about the sixty-fifth day after
conception.

"2d. Appearing at a later date as secondary or even as tertiary
symptoms, and preceded merely by a little disturbance of the general
health, unhealthy appearance of skin, falling of hair, etc., but
nothing truly specific.

"3d. Showing itself some years afterward in a tertiary form, having in
the mean while given no indication of its existence save only in the
protection it afforded against contagion from the child" (_Nouveau
Dict. de Med. et Chir._, vol. xxxiv. p. 696).]

       *       *       *       *       *

Syphilis of the placenta is of especial interest in its relation to the
abortions and stillbirths so frequent in syphilis. Until the elaborate
paper of Fraenkel upon this subject (see foot-note, p. 265) almost
nothing was known about it. He describes[52] the macroscopic changes as
consisting of increased size and weight of the placenta, closer and
firmer texture of the placental tissue, the presence of old and recent
extravasations of blood in all stages, opacity and thickening of the
decidual covering and of the amnion and chorion, which are in places
adherent to each other. Microscopically, it was found that the
placental villi were filled with small nucleated cells, which were
especially abundant in the centre of the villous spaces along the axis
where the vessels usually take their course. The ends of the villi were
enlarged with knob-like processes.

[Footnote 52: I condense here from the translation of Fraenkel's paper,
which constitutes the bulk of chap. xxvii. of Bumstead and Taylor's
excellent work.]

Fraenkel's explanation of these changes is as follows: Under the
influence of syphilis[53] cell-proliferation begins in the villi, which
are, normally, only sparingly supplied with cells. These new cells
excite proliferation of the cells of the connective-tissue stroma and
of the epithelium. This proceeds to such an extent that it leads to
compression of the vessels,[54] interfering with the circulation, and
finally obliterates them. The {272} vascular spaces into which the
villi dip become filled up and narrowed, and often disappear. In this
way, and also by reason of the thickening of the epithelium, the
interchange between the maternal and foetal blood is interfered with,
and at last is prevented.

[Footnote 53: Fraenkel took as his criterion of syphilis the presence
of the osteo-chondritis described by Wegner (see p. 286).]

[Footnote 54: "Hennig was the first who called attention to the
intimate relation of the cell-growths to the vessels. The obliteration
or compression of numerous vessels of the villi interferes with the
mutual interchange of gases between the maternal and foetal blood,
causing fatty degeneration of the villi and, if the process is
extensive, the death of the foetus" (article "Syphilis," _Ziemssen's
Cyclopaedia_, vol. iii. p. 237).]

If this process is spread over the whole placenta, the foetus perishes
before it is complete. If it is limited to circumscribed areas, it may
continue to live for a shorter or longer period.

These observations require to be repeated and confirmed, but they have
served to open up a most interesting branch of syphilitic pathology.

Syphilis in the parents will manifest itself in the children in one of
several ways, which are determined chiefly by two factors--viz. first,
the length of the interval between the infection of the parent and the
date of conception; and, second, the thoroughness of the treatment of
the parents during that interval. To these may be added as subsidiary,
but still of definite importance, a third, the type of disease which
has affected the father or mother, whether mild or severe, benign or
malignant.

From what has already been said in reference to the question of
marriage, it will be at once understood that the danger to the
offspring in untreated cases, and in those where conception has
occurred during the early secondary period of the disease, is of the
most extreme gravity.[55] In such cases the usual result of pregnancy
is abortion at from the first to the fifth or sixth month,[56] the
foetus sometimes exhibiting the evidences of the disease in the shape
of large bullae upon the palms and soles, or in the presence of
characteristic visceral lesions, but quite as often showing nothing
distinctive. It has generally undergone more or less maceration, and
the skin, which is readily detachable, is of a congested, purplish
color.

[Footnote 55: According to Kassowitz, in women who are not treated all
pregnancies occurring within the first three years of their infection
terminate either in abortion or in the birth of children who survive
for only a few weeks or months.

Weber (quoted by Parrot, _Le Progres Medicale_, Nov. 24, 1877, p. 882)
treated thirty-five pregnant women by mercurial inunction, and they all
went to full term under normal conditions. Among those treated with
mercury and iodide of potassium, but who, by reason of intolerance of
the former drug, took chiefly the latter, 20 per cent. aborted; when
the mixed treatment was carried out regularly 15 per cent. aborted; and
when only iodide of potassium was given 36 per cent. aborted. His
studies were made on 109 syphilitic pregnant women. Parrot himself says
(_ibid._) that "abortion occurs in about one-third of all syphilitic
women. Syphilis should always be suspected when this accident occurs
several times successively." "The date of abortion depends on the age
of the syphilis of the woman. It is most to be feared during the
evolution of secondary symptoms, particularly when they are grave.
There is more probability that it will occur when infection has
preceded pregnancy than when it occurs during its course. Nothing is so
much to be feared as contamination of the ovule. The nearer the date of
infection of the mother approaches to full term, the fewer the chances
of abortion. It is not likely to occur even when the mother is infected
at five months."]

[Footnote 56: Many observers think that abortion results directly from
the death of the foetus. Babington (notes to Hunter's _Treatise on
Venereal_), Trousseau, and Von Baerensprung were of this opinion.]

Dr. Cory thinks that in many cases it is possible that the effect of
syphilis may be to effect so early an abortion that the case is simply
regarded as one of delayed menstruation or of menorrhagia. Such a
conception would, however, be competent to infect the mother, and might
seem to explain cases otherwise involved in obscurity.[57] At least
one-third {273} of all syphilitic children are dead born.[58] As time
goes on, however, and the intensity of the parental disease is
lessened, or in cases where appropriate treatment has been applied,
either the abortion occurs at a later period of pregnancy or the
children are brought alive into the world. Even then, however, and
although at birth they may show no evidences of the disease, their
chance of escape is but small. One-fourth of them die within the first
six months. If they survive that period, the chances for life are
slightly in their favor, but those for health or freedom from deformity
and disease are still overwhelmingly against them.

[Footnote 57: As, for instance, when a woman married to a syphilitic
man, but without issue, remarries a man with no history of syphilis,
and yet gives birth to a syphilitic child. In such a case there would
be no history of direct infection and none of pregnancy, the only two
modes by which she could have contracted the disease, and the
father--the second husband--might be unjustly suspected.]

[Footnote 58: Kassowitz, _op. cit._]

The course of inherited syphilis differs strikingly from that of the
acquired disease. It will hardly be necessary to do more than remind
the reader of the ordinary stages of the latter affection--the primary,
which includes the period of the chancre and of lymphatic engorgement,
lasting about sixty to seventy days; the secondary, or exanthematic,
characterized by copious cutaneous eruptions and extensive involvement
of mucous surfaces, lasting from one to three years; the
intermediate,[59] or the stage of latency and relapses, lasting for a
very variable period, from three to ten years, but under proper
treatment very much reduced or altogether abolished; and finally, the
tertiary period, beginning four or five years after contagion,
extending indefinitely throughout life, but often in cases properly
treated absent altogether.

[Footnote 59: So designated by Mr. Hutchinson, and for clinical
purposes a very valuable addition to the periods of syphilis. He
describes it as follows: The patient may be either wholly free from
symptoms and in good health, or he may remain pale and rather feeble,
and liable from time to time to slight returns of eruption on the skin,
sores on the mucous membranes, condylomata, etc. He is protected as
regards fresh contagion, and should he beget children they are almost
certain to suffer. The relapses during this stage are usually easy to
be distinguished from true secondary symptoms. There is little or no
febrile disturbance, the rash is not copious, and often not
symmetrical. Acute iritis, retinitis, etc. never occur for the first
time, though they may do so in the form of relapses.]

For purposes of description and of contrast we may similarly divide the
whole period of evolution of a case of inherited syphilis,[60] omitting
the primary stage, which has never been found to exist in true cases of
hereditary syphilis. Of course in congenital or infantile syphilis, in
which by direct contagion, either from the mother or from any one else,
the disease was acquired by the child, the course would not differ
materially from that observed in the adult. But as this stage in all
probability corresponds to the period during which the poison is
already finding its way into the system through the lymphatics, of
course it is not found in the child who is infected from the moment of
conception or who receives the poison from the mother directly into the
circulation.[61] For from one to three weeks the infants often show no
symptoms of the disease. In 158 cases collected by Diday, 86 manifested
symptoms of the disease before the expiration of the first month, and
60 of the remainder before the end of the third month.[62] When to
these are added the {274} statistics of Roger, we find that of a total
of 172 cases, 159 showed syphilitic symptoms before the end of the
third month.[63] When the symptoms are present at birth, they consist
largely in a general withered, atrophied, weazened appearance of the
child; a hoarse cry, due to swelling, with subacute inflammation, or
even ulceration, of the laryngeal mucous membrane; a coryza,[64] due to
a similar condition of the Schneiderian membrane; and certain cutaneous
eruptions, the most common of which at this early date is the large
vesicular or bullous eruption known as syphilitic pemphigus.

[Footnote 60: The idea that the character of the symptoms which first
appeared depended upon and corresponded with the stage of the disease
in the parent has now, I believe, no supporters. It was once thought,
at least by some syphilographers, that if the parents were in the
tertiary stage at the time of conception the child would develop
tertiary symptoms, omitting the other stages.]

[Footnote 61: If chancre were the first symptom of constitutional
syphilis, why should it not appear in cases of hereditary syphilis?]

[Footnote 62: _Infantile Syphilis_, p. 101]

[Footnote 63: About 1823, from 16,000 to 17,000 children were admitted
annually to the wards devoted to foundlings at Lyons. Cliet, recording
his experience with this disease, says that syphilis is one of the most
common of their maladies, but that "it exceedingly seldom shows itself
at birth by evident signs" (_Compte-Rendu Med. Chir. des Observations a
l'Hopital general de la Charite de Lyon_, 1823). Cristoferi, physician
to the foundling hospital at Bologna, says that syphilis generally
manifests itself between the ages of one and three months. Never once,
he states, was a newly-born infant admitted with the disease
unquestionably developed (_Gazette Medica di Milano_, 1844). Trousseau
says that it "rarely appears before the second week, and very
exceptionally after the eighth month" (_Lectures on Clin. Med._, vol.
iv. p. 331, London, 1871, ed. of New Sydenham Society).]

[Footnote 64: Usually appears later, but exceptionally at birth.]

Pemphigus.--With regard to the specific or non-specific character of
this eruption there has been much difference of opinion, and, as it is
often the earliest distinctive expression of syphilis, a diagnosis of
which could hardly be founded on the general appearance of the child,
or even on the hoarse cry and the coryza, it becomes important to have
definite ideas upon the subject. Nearly a century ago (in 1794) it was
denied[65] that this eruption was a manifestation of venereal disease;
and this view has been supported by many able and accurate observers
down to the present day. In 1851 a discussion upon the subject took
place in the French Academy of Medicine, which elicited the opinions of
the majority of those members who were entitled to speak with authority
in the matter, and which has since been referred to by most writers.
Cazeaux upheld the non-syphilitic hypothesis on the ground (1st) that
the so-called syphilitic pemphigus of children does not differ from the
simple pemphigus of adults, presenting none of the physical characters
which distinguish the specific cutaneous eruptions; (2d) that it
appears at birth or immediately after, while the symptoms of hereditary
syphilis generally show themselves later;[66] and (3d) that at that
time there had been seen no cases of pemphigus at the Lourcine
Hospital, where so many syphilitic children were born.[67] In this view
he was supported by Trousseau, Lasegue, Gibert, Bazin, and other
obstetricians and syphilographers of note.[68]

[Footnote 65: Ariander, _Memoires de Med. et d'Accouch._, quoted by
Diday.]

[Footnote 66: This is now known to be an unreliable distinction,
expressing perhaps a general rule, but one with so many exceptions as
to render it void of diagnostic significance.]

[Footnote 67: This may have been true at that time, but has certainly
not continued to be so. Cornil says: "We often see at the Lourcine
children born prematurely or at the full term with pemphigus, either
fully developed at the moment of birth or appearing a few days
afterward, and who commonly die with syphilitic cachexia, the sad
heritage derived from their maternal parents."]

[Footnote 68: Pemphigus may indeed be a specific affection, but no
characteristic sign has been discovered sufficient to distinguish it
from the ordinary form of pemphigus. "On the other hand, there is no
inconsistency in admitting that syphilis, which so deeply impairs the
constitution of the parent, may act like any other common cause and
excite non-specific pemphigus; for an infant is badly lodged and poorly
nourished in the womb of an enfeebled mother, apart from the influence
of the virus" (Ricord, note to _John Hunter's Works_, 1853).]

On the other hand, Dubois claimed a specific character for the
affection {275} on the ground (1st) of the fact that in the majority of
cases there was a syphilitic history in the parents; and (2d) that the
eruption often coexists with well-known syphilitic lesions. This was
supported by Cazenave, Danyan, Bouchut, Vidal, Ollivier, and
others.[69] Diday, who devotes several pages of his interesting work on
_Infantile Syphilis_ to this subject, regards the eruption as simply a
manifestation of a cachexia produced by syphilis,[70] founding this
opinion on (1st) the absence of specific characters in the eruption;
and (2d) that syphilitic pemphigus is a rare affection in the adult, if
it occurs at all, so that to recognize it in the child would be to make
a single exception to the general rule that "all the syphilitic
eruptions of new-born children have their equivalents in those of
adults." He explained the two cases which were then (1858) recorded of
cures of pemphigus by mercury[71] by saying that it was the treatment
of the diathesis, not of the disease, which caused the improvement. He
acknowledges, however, the very frequent association of pemphigus in
the child with syphilis in the parent, and says that it springs from
the latter affection, "specially, but not specifically"--a rather
wire-drawn distinction.[72]

[Footnote 69: Jullien (_op. cit._, p. 1005), after considering the
opposing views as to the character of this eruption, says: "We have no
hesitation in declaring ourselves in accord with Roger, Ollivier,
Ranvier, Parrot, and others, and in distinctly separating from the
specific affection the rare eruption known as simple pemphigus,
sometimes epidemic, occasionally febrile, and appearing most frequently
about three months after birth. We consider likewise that an evidence
of congenital syphilis which is by no means doubtful is found in the
bullous eruption seen at birth or within the first two weeks,
comparatively frequent, and involving by preference the palms and
soles. This opinion is based upon (1st) its appearance in children
whose parents are known to be syphilitic; (2d) its association with
syphilitic lesions of the lungs, liver, kidneys, thymus gland, etc.;
(3d) its partial disappearance under mercurial treatment, and its
reappearance when that treatment is discontinued."]

[Footnote 70: _Op. cit._, pp. 70-77.]

[Footnote 71: Depaul, _Gaz. Med. de Paris_, 1851, p. 472, and Galligo,
_Gaz. Med. Toscana_, 1852, p. 123.]

[Footnote 72: Trousseau (_Clinical Lecture on Syphilis in Infants_),
after detailing a case in which there was some doubt as to the
existence of hereditary syphilis in a child born alive, and in which
case the previous pregnancy had resulted in a stillborn child at seven
months, the body of the latter having been preserved in alcohol and
exhibiting numerous traces of pemphigus, says: "So far as I was
concerned, this demonstration did not amount to more than the
establishing of a probability, and several physicians who participated
in this indecision finally accepted a compromise. They considered that
maternal syphilis had determined a sort of cachexia in the foetus which
had led to an eruption of bullae which was not specific. By accepting
this too-facile hypothesis you will imprudently open a door which you
will with difficulty be able to close."]

As these differences of opinion have been perpetuated to the present
day, it has seemed to me proper to make this reference to their
history, although I am strongly convinced that the progress of clinical
and pathological knowledge enables us now to assert that although, as
an exception, bullae may be due to a profound cachexia not dependent on
syphilis, yet that in the large majority of cases they are specific in
their character.

The argument which always seemed to me the strongest, the fact that a
similar eruption is almost--or quite--unknown in the adult, has been
removed by the observations of Cornil, who has shown that it belongs
properly with the papular rather than with the bullous eruptions, and
should be classed with the roseola and papules of early syphilis--just
where, from its clinical history, we should expect to find it. The
raising of the epidermic layers is due chiefly to their delicacy, their
slight resistance, and their previous immersion in the amniotic
fluid--_i.e._ to {276} conditions which are peculiar to the skin
shortly after birth.[73] He founds these very important opinions upon
the autopsy of a child stillborn a little before full term, the mother
being in the height of secondary syphilis. The child presented
characteristic bullae on the soles and palms. After hardening these
were found to consist of the two layers of epidermis placed one above
the other. Fig. 6 represents a bulla about one centimeter in diameter
which was situated on the plantar surface of the great toe.

[Footnote 73: Cornil, _op. cit._, p. 203.]

[Illustration: FIG. 6. Pemphigus bulla from a new-born syphilitic
child. The superficial epidermic layer _e_ is elevated by a fluid
exuded between it and the rete mucosum. The rete mucosum, _c_, is also
partly raised, so that there exists a space filled with fluid between
it and the papillae, _p_. The epithelial prolongations and the ducts of
the sudorific glands _m_, placed between the papillae, and which run
between them into the derm, are broken and suspended from the rete
mucosum. _d_. Derm. _a_. Fibrous and muscular layers. _t_. Tendons and
fibrous tissue. _o_. Cartilage of ossification of the first phalanx.
_v_. Vessels. X 8.]

[Illustration: FIG. 7. Section of the rete mucosum and papillae from
the same case of pemphigus as Fig. 6. _o_. Orifice of a sudorific
gland. _m_. Cells of the rete mucosum, some of which are excavated,
_c_. _p_. Papillae. _v_. Their vessels. _n_. Prolongations of the rete
mucosum between the papillae. X 200.]

If, then, we find an infant at birth or immediately after[74]
presenting on the soles, the palms, the fingers and toes, or on the
limbs, an eruption consisting of blebs more or less perfectly distended
with a liquid which may be clear, cloudy, or bloody, circular or oval
in shape, sometimes irregular, seated on inflamed, reddish skin, and
surrounded by trifling areolae, we may strongly suspect the presence of
syphilis in an active and most menacing form. And this suspicion
becomes a certainty if, in combination with such an eruption, the
general cutaneous surface is yellowish or muddy in hue, is hard, dry,
wrinkled, without elasticity or softness--owing to the absence of
subcutaneous fat--and, for the same reason, is furrowed and wrinkled
about the face, imparting an appearance of senility; if the child has a
hoarse cry, a discharge from the {277} nostrils; and, of course, if
there are at the same time other and unmistakable syphilodermata. This
eruption is specially important, however, because upon the recognition
of its specific character in cases of stillbirth, or in those in which
the child survives only a few days--not long enough for the development
of further symptoms--will depend the opinion as to the cause of death,
which, whether expressed or not, will determine the future treatment of
both parents during the interval and of the mother during the next
pregnancy.

[Footnote 74: Non-syphilitic pemphigus is said to be never present at
birth, nor until the child has become considerably exhausted by wasting
from some defect of nutrition. It therefore does not appear until it is
several weeks old. It then attacks the trunk in preference to the palms
and soles.]

We may now consider the other symptoms of the secondary period in the
child.

Coryza is one of the most characteristic, and at the same time one of
the most important, of these in its influence on the health of the
child. It is due to the same condition of the mucous membrane lining
the nasal fossae as manifests itself simultaneously or soon afterward
on the skin in the shape of erythema, roseola, or papules; in other
words, it is a hyperaemia with papillary infiltration. Now, on the skin
this condition, except in so far as it indicates the presence of a
grave constitutional disease, is of no special importance. In the
nostrils of a sucking infant, already debilitated and impoverished by
the anaemia of syphilis, and depending upon its nutrition for the
continuance of the miserable flickering life which was its original
endowment, the same condition assumes the gravest significance.

The excessive supply of blood to the parts induces a catarrhal
condition which shows itself in a thin, watery discharge, which, as the
child during sucking is compelled to breathe through the nose, is
rapidly dried into crusts. These become adherent, fill up and lessen
the channel for the passage of air, and in so doing add to the rapidity
and force of the respiration through the nose, and thus increase the
tendency to the deposit of these crusts. The peculiar nasal, noisy
respiration of the child has given the affection the popular name of
snuffles. As the child can no longer breathe, or can breathe only with
great difficulty, while sucking, it takes the breast only to drop it
again immediately on account of impending suffocation.[75] As the
disease progresses ulceration occurs beneath the crusts, and often
involves the entire thickness of the delicate mucous and periosteal
layers underlying the thin bones of the nose; perforation of these
bones results, sometimes with caries to such an extent as to cause an
entire loss of the nasal septum, with flattening of the nose--a symptom
comparable to one which sometimes occurs in the tertiary period of
adults, but produced, as we have seen, by other causes. In adults
syphilitic caries and necrosis are usually due to lesions seated
primarily in the osseous or subperiosteal tissues; in the child, at
least in this instance, these tissues are involved secondarily.

[Footnote 75: For an admirable description of the mechanism of this and
other symptoms of coryza see Diday, _op. cit._, pp. 78-83.]

Erythema, or roseola as it is differently called, is apt to present
itself about the second or third week[76] after birth. As in the adult,
it begins upon the abdomen in the form of little oval, circular, or
irregular spots, dull red in color and disappearing upon pressure.
Later the color becomes deeper, the eruption extends to the trunk and
limbs, and, as exudation and cell-proliferation succeed to simple
capillary stains, it {278} ceases to disappear when pressed upon. It is
often moist, owing to the thinness of the epidermis, sometimes
excoriated. Occasionally it is confluent, and covers large areas with
an almost unbroken sheet of deep-red color.

[Footnote 76: Bassereau gives an instance of its occurrence within
three days.]

The diagnosis in the early stage is often difficult on account of the
resemblance to the simple erythema of infancy. As the disease
progresses, however, maculae form here and there; the cell-infiltration
involves the papillae, several of which coalesce, forming flat papules;
the nutrition of the superficial layers of the epiderm is interfered
with, especially where it is thick, as on the palms and soles, and the
eruption in those regions becomes scaly, and then the diagnosis is not
difficult.

Papules and Mucous Patches.--In the ordinary evolution of the disease
the next manifestation is usually the development of papules upon the
general cutaneous surface and of mucous patches on the tongue, lips,
and cheeks--probably also on other mucous membranes not exposed to
examination. The papules are apt, for the reason already mentioned--the
thinness and moisture of the skin--to be of the broad, flat kind,
especially, as in the adult, in those regions where the elements of
warmth and friction are superadded to the moisture, as in the folds of
the skin about the genitalia, the neck, the flexures of the joints,
etc. They are then moist, covered with a grayish secretion or a thin
crust, and are in reality mucous patches. Occasionally they take on a
little hypertrophy and develop condylomatous excrescences which closely
resemble the simple acute condylomata of infants. In syphilis, however,
the growth springs from a previously existing papule, which is not apt
to be solitary, there being others in the neighborhood which will
probably establish the diagnosis. The syphilitic condylomata also have
a peculiar fetid discharge, resembling that of mucous patches and more
or less characteristic.[77]

[Footnote 77: Van Harlingen, article "Syphilis" in the _International
Encyclopaedia of Surgery_, vol. ii. p. 560.]

Mucous patches in the infant are among the most important of the early
syphilitic lesions--not to the child itself, because they do not
materially affect its health, save in those exceptional instances where
they are accompanied by a marked degree of stomatitis, and thus
interfere with its nursing. Their importance is due to the fact that
they are almost constantly present, and they are thus by far the most
frequent vehicle of contagion from the child to its nurse or to others
with whom it may come in contact. At times they do not differ
materially from the same lesion occurring in the adult, but lose much
sooner their epithelial investment (on account of the delicacy and
comparatively slight attachment of the epithelium at this stage), and
they then appear as oval or irregular red, slightly depressed spots,
distinct or coalescing, ulcerating or oftener covered by a false
membrane. They especially affect the angles of the mouth and the sides
and dorsum of the tongue; and indeed their disposition to select the
former situation constitutes a diagnostic difference between them and
non-specific stomatitis which is to be found in the sulci between the
gums and cheeks and on the gums themselves--locations rarely invaded by
mucous patches.[78] When the latter are ulcerating or are concealed by
diphtheritic membrane, and are situated on the tongue, they may be
mistaken for either simple or parasitic stomatitis. The {279} diagnosis
can often be made by the presence of other syphilitic symptoms--coryza,
erythema, and especially papules. In their absence, however, it must be
remembered that in simple stomatitis, the inflammation not being
limited to special areas, the whole tongue is apt to be involved or a
much larger portion of the buccal mucous membrane; and as there is no
marked tendency to cell-proliferation in these cases, the accompanying
exudation is apt to be serous or watery and to result in
vesiculation--a condition never seen in syphilitic stomatitis. In the
parasitic disease, too, the inflammation is less localized, there is
more swelling and congestion, and the false membrane is said to be of a
whiter color.

[Footnote 78: Bumstead and Taylor, _op. cit._, p. 750.]

No child that has even been suspected of having a taint of hereditary
syphilis should be permitted to nurse at the breast of any one but the
mother, to share its cup or nursing-bottle with other children, to
receive the caresses of relatives or friends; and in this last
restriction we would include the father, even if the suggestion[79] be
true, that in the case of syphilitic children the protection from
contagion probably extends to the male as well as the female parent.
Paternity is sometimes a more doubtful problem than would seem
probable, and even if the father were protected the husband might not
be. The mucous patches, if any are found to exist, should be actively
treated both locally and constitutionally, and during their
demonstrable presence a most rigorous quarantine should be observed.

[Footnote 79: Hyde, _op. cit._ See p. 264.]

Syphilitic condylomata are due to hypertrophic changes in the papules,
which under the influence of heat and moisture in certain regions
coalesce and become more elevated. They vary in size from an eighth of
an inch to a quarter or even a half of an inch in diameter. Their
surface is flat and covered by a crust or by an offensive secretion.
They are found most commonly about the anus or at the angles of the
mouth.

Pustular Syphilides.--A little later in the secondary period, usually
at about the sixth week, but sometimes much earlier, the papules become
transformed into pustules, the change taking place slowly, so that if
examined at any time after it has begun the child will present an
eruption which is markedly polymorphic, showing here and there
yellowish or reddish-yellow maculae left after the absorption of the
cell-element of certain papules, at other places beefy-red papules at
the height of their development, or papules crowned by a ring of
desiccated and desquamating epidermic scales, and in still other
regions pustules in various stages of formation. Or the various
formative stages of the pustules may be passed through so quickly that
the eruption will be almost entirely pustular, few if any unmodified
papules being discovered. The pustules may remain distended with pus
for a considerable time, after which they may wither and slowly
disappear or may rupture and leave ulcerated surfaces. A number of
these ulcers sometimes run together and make extensive patches covered
with thick, dark-colored crusts. These patches may resemble areas of
impetigo or of impetiginous eczema, but in those affections the crusts
are usually thinner and of a lighter color, and the skin beneath them
is generally on a level with the surrounding surface, bright red and
glazed; while under the crusts of the syphilide will be found a more or
less depressed or excavated ulcer, often covered with pus. The
diagnosis may indeed often be made by gently detaching and {280}
raising one of the crusts and noting the character of the surface
beneath. The erosion under the crusts of eczema heals over more readily
and without leaving a cicatrix.

A so-called furuncular eruption[80] is said to appear at variable
periods between the sixth month and the third year, but does not appear
to me to be clearly differentiated from the large pustular syphilides
with thickened and elevated bases on the one hand, or the ulcerating
tubercular eruption on the other.[81] They are all so rare in
hereditary syphilis, at any rate, as to have little clinical
importance.

[Footnote 80: Bumstead and Taylor, _op. cit._, p. 750.]

[Footnote 81: The distinction between the two forms is usually manifest
if the development of the lesions has been observed; but even this
fails in regard to the tubercular eruption. They both occur at the same
period; they both begin similarly, the furuncles as "small nodules in
the corium," the tubercles as "deeply-seated papules or nodules;" they
both run on to ulceration and pursue a chronic course (Van Harlingen,
_op. cit._, p. 561).]

Iritis.--Another symptom of the secondary period, but of later
development and of rarer occurrence than the syphilodermata which have
been described, is iritis. In spite of its rarity this is extremely
important, because it is frequently overlooked until it has reached
such a stage that occlusion of the pupil results, and also because when
it is recognized it constitutes an almost pathognomonic sign of
syphilis.[82] This statement may now be made unhesitatingly, although
for many years it was contended that iritis, and even the still more
characteristic symptom keratitis, were only associated with syphilis as
coincidences, the constitutional disease, when hereditary, having no
causative relation to the local condition.

[Footnote 82: "When primary iritis occurs in syphilis in young children
it is almost always due to syphilis" (Soelberg Wells, _Treatise on
Diseases of the Eye_, Philada., 1873, p. 173).]

To Mr. Hutchinson belongs the credit of having first clearly developed
the specific character of this trouble,[83] which, on account of the
mildness of the attendant symptoms, is often overlooked. The sclerotic
zone of congestion so marked in the adult, and therefore so valuable a
diagnostic sign to the general practitioner, is very slight, sometimes
absent; and as a consequence the attention of neither parent nor
physician is attracted to the condition until in the more serious cases
it has done irreparable mischief. In milder cases, particularly where
the child is under mercurial treatment for concomitant symptoms of
syphilis, it may run its course and escape notice altogether;[84] and
it is possible that owing to this fact the rarity of the affection has
been overestimated. It is also possible that in such cases changes
occurring at this time may in some instances lay the foundation for
some of the deeper-seated ocular troubles of later life.

[Footnote 83: _Med. Times and Gazette_, 1860, July 14; _Ophthalmic
Hospital Reports_, vol. i. pp. 191, 226; _A Clinical Memoir on Certain
Diseases of the Eye and Ear consequent on Inherited Syphilis_, London,
1863. In the introduction to this volume Mr. Hutchinson states that
acute iritis dependent on hereditary syphilis was first described in
connection with its true cause by Mr. Lawrence, but, as from the date
of that gentleman's first case (1830) up to 1863 but six cases had been
recorded, the announcement had made but little impression on the
profession.]

[Footnote 84: "In the cases of this form of iritis which are seen in
ordinary eye-practice much damage has often been done by occlusion of
the pupil and deeper mischief. Probably many of the slighter cases
escape the notice of the parents and are not brought to the surgeon"
(Mr. Edward Nettleship. See Hill and Cooper, p. 271).]

If, however, attention has been attracted to the eyes, the diagnosis is
not usually difficult. The pupil is irregular, especially under
atropia; {281} there are streaks of lymph, dulness, swelling, change of
color, and on very careful inspection a faint pink zone may be seen in
the sclerotic. The conjunctiva and cornea are generally clear.

Mr. Hutchinson's analysis of the twenty-three cases reported by him is
still of interest as furnishing reliable data for prognosis. The
average age at the time the iritis commenced was five months and a
half. The oldest was sixteen months at the time of the outbreak, the
youngest six weeks. In twelve cases but one eye suffered; in eleven
both were affected. In seven cases (ten eyes) the cure was complete; in
two or three other cases very slender adhesions remained; in twelve
cases, in nearly all of which the patients came under care only at a
late period of the disease, one pupil was permanently occluded by
organized false membrane. In nearly all, coincident symptoms of
syphilis of the skin or mucous membranes were present. Of the thirteen
cases in which alone a history of the family is recorded, the affected
infant was the only living child of his parents in twelve instances. In
the only case in the whole series in which it is stated that there were
other living children the mother had lost four infants out of seven
live births.

The prognosis depends on the stage at which they come under treatment.
The lymph if recent, no matter in what quantity, will probably be
absorbed under mercurial treatment, which will often be of great
benefit even in those cases in which a certain amount of organization
has occurred.[85]

[Footnote 85: It will not be uninteresting, perhaps, to append the
aphorisms regarding iritis in infants which Mr. Hutchinson at that time
enunciated: 1. The subjects of infantile iritis are much more
frequently of the female than the male sex. 2. The age of five months
is the period of life at or about which syphilitic infants are most
liable to suffer from iritis. 3. Syphilitic iritis in infants is often
symmetrical, but quite as frequently not so. (In his article in
Reynolds's _System of Medicine_, written in 1866, three years later,
but revised in 1870, he describes it as "usually symmetrical," vol. i.
p. 444.) 4. Iritis, as it occurs in infants, is seldom complicated, and
is attended by but few of the more severe symptoms which characterize
the disease in the adult. 5. Notwithstanding the absence of phenomena
of acute inflammation, the effusion of lymph and the danger of
occlusion of the pupil are usually very great. 6. Mercurial treatment
is most signally efficacious in curing the disease, and, if recent, in
procuring the complete absorption of the effused lymph. 7. Mercurial
treatment previously adopted does not prevent the occurrence of this
form of iritis. 8. The subjects of infantile iritis, though often puny
and cachectic, are also often apparently in good condition. 9. Infants
suffering from iritis should always show one or other of the
well-recognized symptoms of hereditary taint. 10. Most of those who
suffer from syphilitic iritis are infants born within a short period of
the date of the primary disease in their parents.]

We have now a group of symptoms characteristic of the secondary period
of syphilis, or that extending from birth, or much more commonly from
the age of three or four weeks to about the end of the first year. The
syphilitic child during this time has several or all of the following
symptoms: Coryza with snuffles; an erythematous, papular, or pustular
eruption on the skin; mucous patches on the lips, tongue, cheeks, etc.;
a marked tendency to general wasting; a hoarse cry or cough; senility
of aspect; iritis. The majority of syphilitic children born alive die
during this stage.

Before its termination, sometimes even at birth, other lesions have
been noticed (especially those affecting the liver), which, however,
may better be described in connection with the special organ or organs
involved.

Succeeding this stage--_i.e._ beginning in about a year or eighteen
{282} months--comes an intermediate period, which extends to second
dentition, to puberty, or even much later, and which is characterized
rather negatively--that is, by the absence of symptoms--than otherwise.
The evidence of the general diathesis will of course be present in the
shape possibly of malnutrition, stunted growth, or retarded
development, perhaps shown in the weazened or withered face, the sunken
nose, the pallor of the skin, the premature loss of the upper incisor
teeth or the malformation of the others if they have erupted.

There is but little tendency to recurrence or relapse of any of the
secondary symptoms; and in certain cases, not a very small proportion,
in which these symptoms have been light and have been well and
thoroughly treated, this stage extends throughout life; or, in other
words, as is frequently the case with the adult who has followed a
proper course of treatment, the disease appears to terminate with the
secondary stage. In other cases, however, it recurs, and the symptoms
which it then presents may be taken up in connection with the different
organs or tissues involved.

Syphilis of the ear is for obvious reasons not often discoverable until
the patient has reached an age at which interference with the function
of hearing becomes a noticeable phenomena. The only symptom likely to
attract attention during the stage of inherited syphilis which we are
now considering is a catarrh of the middle ear, which may have for its
starting-point some inflammation, ulceration, or mucous patch of the
pharynx, causing a temporary or permanent occlusion of the orifices of
the Eustachian tubes.[86] This may lead to perforation of the membrana
tympani, purulent infiltration of the mastoid cells, etc., and when
accompanied by an otorrhoea which attracts attention to the ear will be
easily discovered by the physician. These cases are, however,
exceptional, otorrhoea only being present in nine out of Hutchinson and
Jackson's[87] one hundred cases of inherited syphilis, and consequently
but little is known about the frequency or gravity of lesions of the
auditory apparatus in the secondary stage of this form of syphilis.[88]
The changes which occur later on are chiefly those which involve either
the nerves themselves or their distribution in the labyrinth.

[Footnote 86: Baumler, _Ziemssen's Cyclopaedia_, vol. iii. p. 226.]

[Footnote 87: Hutchinson and Hughlings Jackson, _Med. Times and Gaz._,
Nov. 23, 1861.]

[Footnote 88: Schwartze (quoted by Hill and Cooper) found also that
otorrhoea was a rare complication in deafness from syphilis.]

The affections of the middle ear and Eustachian tube are said to be
contemporaneous with the keratitis which appears in the neighborhood of
puberty,[89] while those of the nerve are somewhat later in point of
time, and are almost always conjoined with retinitis, choroiditis, and
optic neuritis. As usual when investigating or describing any subject
relating to syphilis, Mr. Hutchinson's opinion and observation must be
detailed. In 1863 he wrote[90] that it was only recently that he had
thought of specially investigating the disorders of hearing in
reference to hereditary taint, having had his attention called to a
peculiar form of deafness, usually symmetrical, passing rapidly through
its different stages and {283} unaccompanied by any marked degree of
pain or any external disease. He then reported eighteen cases of which
he had notes. The oldest of these patients was twenty-seven, the
youngest eight--the average time of development of the deafness from
twelve to fifteen. Although the membrana tympani was in no instance
quite normal, in none were there found adequate changes to account for
the deafness. In all the Eustachian tubes were pervious. In nearly all
the disease was symmetrical. This fact, together with the absence of
discoverable lesions of the external or middle ear, seems to point
conclusively to disease of the nerves themselves, or at least to a
central cause.[91] He adds: "With regard to the prognosis of
heredito-syphilitic deafness, I believe that it is very unfavorable.
When the disease was progressive I have rarely witnessed any permanent
improvement or arrest. In most it has gone on to total loss of hearing,
and this in several instances in spite of the cautious use of specific
remedies almost from the beginning. From six months to a year would
appear to be the usual time required for the completion of the process
and the entire abolition of the function."[92]

[Footnote 89: Purves, _Guy's Hospital Reports_, 1875, p. 564;
Pritchard, _British Medical Journal_, April 21, 1877.]

[Footnote 90: _Clinical Memoirs on Certain Diseases of the Eye and Ear
consequent on Inherited Syphilis_, London, 1863, pp. 182, 183.]

[Footnote 91: In the _Lancet_ for Jan. 16, 1875, he reports a case of
total deafness in a young woman of seventeen which had come on in ten
months without pain or otorrhoea. He believes the disease of the organ
of hearing to be parallel with those cases of choroiditis disseminata
or of optic neuritis in which blindness is produced without pain or any
external evidence of inflammation, and which are distinctly and
positively associated with inherited syphilis.]

[Footnote 92: Mr. Hinton, in his edition of Toynbee's work on _Diseases
of the Ear_, states that at Guy's Hospital, of his aural patients, one
in twenty is affected with deafness due to heredito-syphilis; that it
usually makes its appearance between the tenth and sixteenth years; and
that the great majority of the cases which he has seen have been
females. He adds: "Patients suffering from this disease may, as a rule,
at least when young, be at once distinguished by the amount of deafness
which they exhibit. I know no other affection except fever which in a
person under twenty brings on a deafness so rapidly and so nearly
complete. In the course of a few weeks a girl previously hearing well
will, without pain or known cause, become unable to distinguish words."
In one of Dalby's cases total deafness came on in three weeks, previous
to which hearing was normal. According to Pierce, the deafness is most
apt to manifest itself between eleven and eighteen years of age.
Troeltsch says that "l'audition du diapason par le vertex" is lost at
an early date after the beginning of the disease, and that there are
also often concomitant affections of the nose and pharynx.]

Dalby[93] is said to regard syphilis as, next to scarlatina, the most
fruitful cause of deaf-mutism as it occurs in children born with good
hearing powers. "The patient usually becomes deaf in early
childhood--after he begins to talk--or between this period and
puberty."[94]

[Footnote 93: _The Lancet_, Jan. 22, 1876.]

[Footnote 94: Bumstead, _op. cit._, p. 734.]

Syphilis of the Liver.--In 1852, Gubler published an account of the
general appearances in syphilitic disease of the liver in new-born
children, which was distinguished especially by increase in size and
weight. This increase depended, as might be expected in this
stage--that of general cell-proliferation--upon a proliferation of
cells from the connective tissue between the acini, or from the
adventitia of the interlobular vessels, this growth becoming
transformed into connective tissue.[95] The change is quite analogous
to what is taking place at the same time in the skin, the mucous
membranes, and other tissues. Wilks has also described[96] a form of
syphilitic disease of the liver which corresponds to that of Gubler,
and in which the whole organ is infiltrated by a new fibrous tissue,
producing a uniform and general hardening.

[Footnote 95: Baumler, _op. cit._, p. 186.]

[Footnote 96: _Trans. Path. Soc._, vol. xvii., 1866.]

{284} [Illustration: FIG. 8. Section of an old gumma of the liver. _a_,
_a_. Central caseous tissue of the gumma. _v'_, _v'_. Its vessels. _l_.
Boundary between the central portion and fibrous zone; this line of
demarcation is marked in places by an opening or cleft. _t_, _t_.
Connective tissue of the fibrous zone which entirely surrounds the
central part. _v_, _v_. Small vessels of this zone. _c_. An arteriole
of the fibrous zone. _f_, _f_. Quite large biliary vessels included in
the fibrous zone. _t'_. Fasciculi of connective-tissue fibres running
parallel with the surface of the caseous part. At _b_ and _d_ the
fasciculi of fibres of the fibrous zone penetrate into the central
caseous part. _e_, _e_. Tissue of hepatic cells interrupted by bands of
fibrous tissue, _m_, _m_. X 12.]

As described by Gubler,[97] the liver in such children is
hypertrophied; hard, resistant to pressure, so that it cannot be
indented; elastic, so that it rebounds; creaks, but does not bleed,
when it is cut into, and presents the yellow color and the
semi-transparence of flint. There are seen on a yellowish ground a
number of small white granulations like grains of wheat, which a
histological examination shows to be formed by an accumulation of
embryonic cells in the spaces which separate the hepatic acini.
Injections reveal the fact that the vascular network has become almost
impenetrable, the capillaries obliterated, the larger vessels
diminished in calibre. Fibro-plastic matter is found throughout the
organ in large quantity. In consequence of these conditions--the
compression of the hepatic cells and the destruction of the
vessels--the secretion of bile is stopped, and the gall-bladder is
found after death to contain a pale-yellow liquid consisting of bile
mixed with an excess of mucus. This form of hepatitis has thus far been
observed almost exclusively in infants. Cornil {285} says[98] that he
has had frequent occasion to examine such cases of hepatic syphilis,
and describes them as follows: "The hepatic acini, in the normal state,
are in contact except at the prismatic spaces which are formed by their
union--spaces in which the capsule of Glisson forms an envelope to the
afferent portal vessels of the lobuli. It is in these spaces that the
round lymph-cells form and collect into small nodules representing
microscopic gummata. The cells at the centre of the new formation are
sometimes granular. This neoplasm is seated about the ramifications of
the portal veins, which in consequence also present thickened walls
with newly-formed cells in their external tissues. The small granules
above mentioned are not always visible to the naked eye, and in their
places are only seen, about the perilobular capillaries of the portal
vein, an excessive number of embryonic cells." In addition to this
interstitial sclerosis or interstitial infiltrating hepatitis there is
an inflammation of the liver depending upon the presence of
gummata--gummous hepatitis--which occurs in two forms: one in which
very small and very numerous nodules are present, situated along the
course of the fibrous seams, the prolongation of the capsule, and
another in which there are two or three large circumscribed tumors.
This form of hepatitis is always accompanied by the interstitial form,
although the latter may be only slightly developed.[99] The gummata,
though not infrequently found in the liver of new-born children, are
more likely to develop later, at from about the eighth to the twelfth
year.

[Footnote 97: _Memoires sur une nouvelle Affection de Foie_, and _Gaz.
Med. de Paris_, 1852.]

[Footnote 98: _Op. cit._, Am. ed., p. 370.]

[Footnote 99: It does not differ essentially, either pathologically or
clinically, from the same lesion in adults.]

Rochebonne[100] describes the following symptoms of syphilitic
hepatitis in infants: A deep wine-colored venous stain and oedema of
the lower extremities, often accompanied by pemphigus; ascites due to
mechanical obstruction of the circulation, as in cirrhosis; a more or
less pronounced chloro-anaemic appearance of the face; and the presence
in the urine of albumen and haemato-globulin. Vomiting may occur, and
constipation alternating with diarrhoea has been observed. Icterus,
symptomatic of the affection, has not been observed.

[Footnote 100: Quoted by Bumstead and Taylor, p. 758.]

Baumler says:[101] Implication of the peritoneal coating of the liver
may be recognized by the pain in the hepatic region. In new-born
children--unless, possibly, there may be some enlargement of the
liver--the only local symptoms, often, are those due to
peritonitis--screaming, drawing up of the legs, vomiting. In those
cases it is not rare for the peritonitis to become diffuse.[102]

[Footnote 101: _Op. cit._, p. 194.]

[Footnote 102: In an article on "Inherited Syphilis" in the _British
and For. Medico-Chirurgical Review_, 1875, p. 28, it is said: "Of the
liver the lesion consists in enlargement and induration of the organ in
whole or in part, due to the development of fibro-plastic material
between the cells of the acini, with obliteration of the vessels and
interference with the secretion of bile. This condition is generally
doubtful during uterine life, and is rapidly fatal. The symptoms are
vomiting, diarrhoea, and tympanitis, but, strange to say, no jaundice.
The enlarged and indurated organ may be felt by palpation. It is
probably in this connection that the peritonitis described by Simpson
as occurring in inherited syphilis is found."]

Hill says:[103] "The symptoms are mainly those of functional
derangement of the organ, with alteration of its bulk."

[Footnote 103: _Op. cit._, p. 163.]

Hutchinson[104] has described cases in which in young persons the
subjects {286} of hereditary syphilis there has been great hepatic
enlargement which has subsequently wholly disappeared. He finds it
difficult to believe that there is any kind of gummous growth in such
cases, and feels obliged rather to fall back upon the hypothesis of
mere vascular turgescence. In one such case the liver occasionally was
so large as to be visible as the patient lay on his back in bed.[105]

[Footnote 104: _Path. Transactions_, 1877, p. 309.]

[Footnote 105: Illustrative cases of this condition may be found in the
_Med. Times and Gazette_, Dec. 22, 1877.]

It seems much more likely that the enlargement is due to an
exceptionally active cell-proliferation, which does not, however, go on
to organization, but may be just as susceptible of absorption and
resolution as are the papules or maculae of the skin. A portion of the
enlargement may be due to a passive congestion caused by the presence
of this cell-accumulation.[106]

[Footnote 106: Barlow (_Path. Trans._, 1877, p. 355) has suggested that
the engorgement is only a preliminary stage of the fibrous thickening,
and may disappear either with or without leaving permanent contractions
or adhesions in its wake.]

As to the diagnosis of hepatic syphilis in infants, I am disposed to
agree with Cornil, who says:[107] "The symptoms are null, or they are
identical with those of local and general troubles so often observed in
children who have poor or insufficient nourishment. The only physical
sign which properly belongs to hepatic syphilis is, when it exists at
all, increase in the size of the liver."

[Footnote 107: _Op. cit._]

Syphilis of the Bones.--Until the publication in 1870 of the researches
of S. Wegner,[108] an assistant of Prof. Virchow, diseases of the
osseous system due to hereditary syphilis were either ignored or denied
by the various writers upon this subject.[109] Valleix, Bargione,
Ranvier, and Gueniot had indeed recorded cases of bone disease
occurring at the points of junction between the epiphyses and diaphyses
and in the costal cartilages, but it remained for Wegner first fully to
describe the pathological changes which occurred there, and to
differentiate them from those due to rickets or scrofula. His memoirs
recognized three stages of alteration in the long bones:[110] 1st.
While in the normal state the boundary of the hyaline cartilage is
distinctly marked by a line which indicates the direct transformation
of the cartilaginous tissue into a spongy tissue, the unaided eye being
unable to distinguish a spongio-calcareous layer, in new-born
syphilitic children, on the contrary, the bones are seen to have a
spongio-calcareous layer interposed between the bone and cartilage,
measuring two millimeters in thickness. This is a zone of calcifying
cartilaginous material more extensive than in the normal state. 2d.
These same changes become more distinct and more extensive. The
unnaturally thick layer of calcareous material continues to grow. There
is proliferation of the cartilaginous trabeculae, abundant
calcification of the cartilage, too early and irregular ossification of
the intercellular substance {287} of the cartilage, and at the same
time an arrest of the normal formation of bone which should be going on
from the epiphysial cartilage. 3d. There is now added, by extension of
these processes, a thickening of the perichondrium and periosteum at
the extremities of the long bones and at the junction of the ribs with
the costal cartilages. In consequence of the interference with
nutrition occasioned by these changes atrophy and fatty degeneration of
the cartilage-cells occur, and they form between the epiphysis and
diaphysis a necrosed mass which irritates the living bone. This causes
osteo-myelitis, which frequently results in a separation of the
epiphyses. Occasionally pus is produced in such quantity as to
perforate the periosteum, escape into the surrounding tissues, and
become superficial. He terms the entire process an osteo-chondritis.

[Footnote 108: _Virchow's Archiv_, 1870, B. 50, S. 305: "Ueber
hereditare knochen Syphilis bei jungen Kindern."]

[Footnote 109: Diday says: "Affections of the bones are so rare in
children with inherited syphilis that the annals of medicine scarcely
offer five or six well-authenticated cases of caries or periostitis"
(_op. cit._, p. 83). Referring to this statement, Mr. Hutchinson
remarks: "So different has been my own experience from this that I may
say that we are scarcely ever without a severe example of it in the
wards of the London Hospital" (_Illustrations of Clinical Surgery_,
London, 1875, p. 47).]

[Footnote 110: Cornil, _op. cit._, p. 282 _et seq._]

Waldeyer and Kohner,[111] after examining twelve cases, confirm in the
main these investigations of Wegner, but interpret the changes as
arising rather from the formation of a gummous tissue between the
epiphysis and diaphysis than from an osteo-chondritis. The tissue-death
which occurs later, the atrophy of the cells, etc., they compare with
the same modifications observed in syphilomata.

[Footnote 111: "Beitrage zur Kenntwiss der hereditare knochen
Syphilis," _Virchow's Archiv_, B. 55, S. 367.]

Parrot[112] in a number of exceedingly valuable papers has repeated and
greatly extended these observations. He places especial importance upon
the formation of osteophytes, which, he says, in the first stage
envelop the diaphyses of the long bones, especially at their inferior
extremities. In the succeeding stage the new bony layers are more
porous; a gelatinous degeneration affects the epiphysial cartilage and
the spongy bones at a point where they are in contact; the epiphyses
tend to separate from the diaphyses. This solution of continuity
results in a characteristic pseudo-paralysis, with curvatures, abnormal
twistings, and preternatural mobility of the bones, with loss of the
power of locomotion. Then the osteophytes increase in size by the
formation of several layers, thus enlarging the inferior extremities of
the long bones. He describes the general process as consisting, first,
of a periosteo-genesis--a formation of osseous tissue from the
periosteum; next of a chondro-calcosis--a calcareous incrustation of
cartilage; and finally of a gelatiniform degeneration and softening of
the bone, with diaphyso-epiphysial disjunction.[113]

[Footnote 112: _Societe de Biologie_, June 1, 1872; _Societe
anatomique_, 1873, p. 92; _Archives de Physiologie_, 1876, vol. iii.
pp. 138, 139; _Revue mensuelle de Medecine et de Chirurgie_, 1877;
_Pathological Trans._, 1871, vol. xxx. p. 339, etc., etc.]

[Footnote 113: Cornil (_op. cit._) coincides in the main with this
description.]

Taylor[114] sums up the results of his observations as follows: "In the
first stage we have a simple hyperplasia of cells with irregular
deposition of lime salts; in the second, an intensification of this
condition; and in the third, a new element--namely, the abnormal
proliferation of all the elements of the tissues, with an infiltration
of granulation-tissue into the medullary spaces following the
vessels."[115]

[Footnote 114: _Syphilitic Lesions of the Osseous System in Infants and
Young Children_, New York, 1875, p. 134.]

[Footnote 115: Verraguth (_Archiv fur Path. Anat._) describes the first
step as an excessive formation of vessels in the cartilage and a
corresponding overgrowth of the cellular elements. This becomes
inflammatory, and constitutes a primary syphilitic chondritis, the
changes in the medulla of the bone being degenerative and secondary to
the affection of the cartilage. Still other observers have described
the process, each with minor modifications; but as they are of no
clinical importance, it does not seem worth while to quote them.]

{288} We see, then, that, setting aside minor points of difference,
these observers all coincide in describing this condition as one
essentially of the nature of syphilitic bone troubles with which we are
familiar in the acquired form of the disease, consisting primarily and
throughout of an unnatural accumulation of cell-elements, which in the
later stages by their pressure produce various degenerations of
surrounding structures, and which, as they occur during the process of
bone-formation, are accompanied by irregular and abnormal deposition of
lime salts. They especially affect the regions mentioned--the junctions
of the epiphyses and diaphyses--because at that time those points are
the seat of great physiological activity. Syphilis, indeed, throughout
its entire course is notably subject to similar influences, as one
example of which I may instance the preference displayed by the
periostitis which results in nodes or in caries for the subcutaneous
bones, the tibia, clavicle, cranium, etc.; or, in other words, for
those which are subject to frequent traumatisms--trifling, perhaps, but
sufficient to determine a slight hyperaemia, which is followed by
abnormal cell-proliferation or accumulation.

The symptoms which obtain in this condition of syphilitic
osteo-chondritis are as follows: The child may be attacked during
intra-uterine life, and in that event the osseous lesions will probably
be coincident with other syphilomata and with placental disease of
sufficient gravity to destroy life.[116] If the child is born alive,
the first development of the disease will probably be noticed as a
swelling at the diaphyso-epiphysial junction of one of the long bones,
which in the emaciated subjects of hereditary syphilis is often
visible, and can always be discovered by palpation. The bones most
frequently attacked are the humerus, radius and ulna, tibia and femur,
but the clavicle, ribs, sternum, and bones of the metatarsus and
metacarpus are also often involved, and much more rarely the frontal
and parietal. The more pronounced the syphilis of the parents, or the
nearer the date of conception to the time at which their infection
occurred, the more probable is it that several bones will be affected,
and the more unfavorable the prognosis as respects the life of the
child. Indeed, it has been noticed that "in stillborn infants and in
those dying soon after birth the majority, or even all, of the long
bones are affected."[117]

[Footnote 116: Pollnow found osteo-chondritis in 35 out of 50
syphilitic foetuses (_Der Hydrops Sanguinolentes foetus_, Berlin, 1874,
quoted by Hill and Cooper, _op. cit._, p. 352).]

[Footnote 117: Bumstead and Taylor, _op. cit._, p. 767.]

The swelling is found to consist of a ring or collar which more or less
completely surrounds the bone, is apt to be smooth rather than
irregular, and when two bones situated near to each other are
simultaneously affected may conjoin them. This condition persists
during the first stage of pathologists, and passes with greater or less
rapidity into the second stage, in which the swelling, the
cell-proliferation, reaches its height. This may take, in cases
uninfluenced by treatment, several weeks or even months. Under the use
of mercurials and iodide of potassium they usually subside rapidly.
During this second stage, however, owing to the proximity of the
swellings to the joints, a moderate amount of synovitis is often
present. This affects chiefly the elbow and the knee, but may appear in
any joint. It is also readily influenced by specific treatment and
well-regulated pressure.

{289} When the third stage is reached, or that of the formation of
granulation-tissue, with degenerative changes of the cartilages and of
the bones themselves, deformity often becomes more marked. There are
unnatural curves or angles in the bones, with more or less complete
separation at the point of junction. Where many bones are affected in
this way, the resulting deformity is extreme and the patient may be
absolutely powerless, a condition of pseudo-paralysis supervening in
which the limbs lie motionless or swing about like the arms or legs of
a doll when the child is carried.

When the swelling does not undergo absorption, the superjacent tissues
sometimes become involved, abscesses form and make their appearance
externally, extensive necrosis of the shaft of the affected bone takes
place, and the little patient usually dies of hectic, pyaemia, or
exhaustion. When the cranial bones are involved, the disease is apt to
limit itself chiefly to the stage of osteophytic formation, the
immovability of the bones probably favoring the organization of the new
cell-growth rather than the production in it of inflammatory changes.
The growths are met with chiefly in older children than those affected
with the form of osteo-chondritis just described; they affect the
periphery of the liver, and are found most usually around the anterior
fontanel, and later on the parietal and frontal eminences. The sutures
are sometimes completely soldered together.[118] The osteophytes vary
in thickness from a quarter of an inch to an inch, or are even
larger.[119]

[Footnote 118: In a case reported by Barlow it was not possible at the
autopsy to discover the point of union (_Path. Transactions_, 1879, p.
339).]

[Footnote 119: These conditions may all result in a child the subject
of acquired syphilis, but are apt to be milder, to involve fewer bones,
and to yield more readily to treatment. This would of course be
expected, inasmuch as the same difference in favor of the acquired
form, as compared with that which is inherited, extends to all the
lesions. As Diday succinctly expresses it: "In the one case the poison
vitiates only the elements of nutrition; in the other it vitiates at
the same time those of formation and those of nutrition." It would
exceed the limits of the present article to describe acquired syphilis
in children.]

The most important differential diagnosis to be made in these cases is
between the rachitis of young children and the form of syphilis in
question. Much difference of opinion still exists as to the relation
between these diseases, syphilis being claimed, on the one hand, as
having in the majority of cases a definite causative influence, while,
on the other, the existence of this relation is denied. When we come to
contrast the pathology of the two diseases, we can readily understand
why they should be confounded, the minuter changes which occur being
essentially the same--viz. cell-proliferation and accumulation, with
subsequent inflammatory changes, associated with irregular deposits of
lime salts.

Compare, for example, the description of the pathology of bone diseases
in inherited syphilis already given (pp. 287, 288) with the following
terse summary of the changes which take place in rickets in cases where
no suspicion of syphilis exists, either ancestral or acquired: "The
changes are more distinctly noticed at the epiphyses than in the
diaphyses. Instead of the regular stages and distinct boundaries
observed in the normal development of bone, there is a singular
disorderly commingling of the exaggerated cartilage-proliferation and
transition substance, with calcification. The cartilage-cells,
stimulated to excessive multiplication, are transformed, some into
bone-corpuscles, some into medullary cells, {290} and others into
connective-tissue forms. The same process is in active operation in the
deep periosteal layers, the material accumulating to such a degree as
to add much to the thickness of the shaft."[120]

[Footnote 120: Agnew's _Surgery_, vol. i. p. 1030.]

The points of resemblance are manifest, just as they are between a
syphilitic and a variolous pustule, but they end in both cases when we
come to study the evolution of the phenomena either from an anatomical
or from a clinical standpoint. They may be expressed as follows in
tabular form:

  OSSEOUS LESIONS DUE TO INHERITED |       RICKETS.
          SYPHILIS.                |
                                   |
  The swellings, particularly those| Rarely appear before six months,
  of the long bones, show          | generally still later.
  themselves at or soon after      |
  birth.                           |
                                   |
  A history of syphilis or evidence| No such history necessarily.
  of existing syphilis in one or   |
  both parents.                    |
                                   |
  Preceded or accompanied by       | No such prodromata.
  snuffles, coryza, and cutaneous  |
  and mucous lesions.              |
                                   |
  No such prodromata in most cases.| Pallor, restlessness, sweating,
                                   | nausea, diarrhoea, etc.
                                   | constitute a combination of
                                   | symptoms which often precede the
                                   | bone disease.
                                   |
  Cachexia absent or moderate.     | Cachexia marked.
                                   |
  Physiognomical peculiarities of  | Not present as a group.
  syphilis present.[121]           |
                                   |
  Circumscribed tumors on frontal  | Cranial bones thickened in spots,
  and parietal bones, rarely on    | usually upon the occiput.
  occiput.                         |
                                   |
  Ribs not markedly affected.      | All or nearly all involved.
                                   |
  Swellings on long bones or       | Extremities symmetrically
  extremities irregular.           | enlarged.
                                   |
  Disease of ribs, when existent,  | Nearly always so.
  not ordinarily coincident with   |
  that of other bones.             |
                                   |
  Fontanels close at usual period. | Closure delayed.
                                   |
  Other syphilitic symptoms        | Syphilitic symptoms absent.
  present; enlargement of          |
  phalanges, metatarsal bones, etc.|
                                   |
  Often accompanied by sinuses,    | Little external or surrounding
  synovitis, abscesses, cutaneous  | involvement.
  ulcers, etc.                     |
                                   |
  Generally disappears by          | Usually leaves some bending of
  resolution, without leaving any  | shaft and distortion of the
  permanent change.                | neighboring joint.
                                   |
  Mortality among children in whom | Much less.
  many bones are involved is very  |
  great.                           |
                                   |
  Specific treatment useful.       | Of no benefit.
                                   |
  In the first stage there is an   | This is less marked. There is
  exuberant calcification of the   | formed, instead, a soft and
  ossifying cartilage, causing     | non-calcified osteoid tissue.
  necrosis of the new-formed tissue|
  and a consecutive inflammation,  |
  which terminates in the          |
  separation of the epiphyses.[122]|

[Footnote 121: See p. 313.]

[Footnote 122: This table is founded on one which I added to the
translation of Cornil made by Dr. Simes and myself, and is compiled
chiefly from the excellent work of Dr. Taylor already alluded to.]

The diagnosis of the bone lesions of hereditary exostosis can readily
be recognized in a short time by noting the fact that they are
stationary, {291} even if their later appearance, larger size, the
absence of syphilitic history or symptoms, and the resistance to
specific treatment left us in doubt.

The diagnosis from accidental separation of the epiphysis, or from
fractures, may be made from the history of the case.

In cases of separation of the epiphysis, complicated with suppuration,
sinuses, etc., the trouble may be mistaken for a similar condition due
to non-specific inflammation. In all the recorded instances, however,
the latter has occurred much later in life, is attended with much more
acute inflammatory symptoms, lymphangitis, etc., and is of course
without concomitant symptoms of syphilis. In both these cases there is
a decided osteo-periostitis, and as so much depends on the early and
vigorous use of specific treatment, it may be worth while to contrast
the two forms of the disease.

  SYPHILITIC OSTEO-PERIOSTITIS.    | NON-SPECIFIC OSTEO-PERIOSTITIS.
                                   |
  Occurs in infants under three    | No instance of its occurrence in
  months of age.                   | children under one year of age.
                                   |
  History of syphilis in child and | No history of syphilis; sometimes
  its parents.                     | a history of traumatism.
                                   |
  Implication of other bones.      | Usually confined to one bone.
                                   |
  Coincident with the development  | Coexists with the ossification of
  of the shaft of the bone.        | the epiphyses.
                                   |
  Other lesions of syphilis: nodes,| No such symptoms.
  skin eruptions, etc.             |
                                   |
  All the local symptoms           | Pain, redness, and swelling very
  comparatively mild.              | marked.
                                   |
  Disease sharply localized.       | Involves neighboring parts.
                                   |
  Lymphatics of limb unaffected.   | Lymphangitis present.
                                   |
  Beneficial effect of specific    | No such effect.
  treatment if employed early.[123]|

[Footnote 123: Cornil, _op. cit._, p. 274.]

Syphilitic dactylitis in the inherited variety of the disease, as in
the acquired, consists of two varieties. The one of these which usually
appears earlier involves chiefly the periosteum and the fibrous and
integumentary structures surrounding a joint, usually a metacarpo- or
metatarso-phalangeal articulation, involving a phalanx, and is
characterized by slow, almost painless, swelling and discoloration of
the affected member. (Fig. 9.) This is due to a gummous infiltration
which, after absorption under proper treatment, leaves the toe or
finger temporarily stiff, but not permanently disabled.

The second form is a specific osteo-myelitis, with periostitis, coming
on later, and often destroying the bone or the articulation involved.
(Fig. 10.)

[Illustration: FIG. 9. FIG. 10. From Bumstead on _Venereal Diseases_,
illustrating Syphilitic Dactylitis.]

The absence of acute inflammatory symptoms in the first variety
distinguishes it from paronychia, whitlow, and gout. Rheumatoid
arthritis begins in the joints, is associated with other symptoms;
deformity of the fingers comes early in the disease, and there is a
teno-synovitis with contraction.

The second variety might be taken for enchondroma or exostosis, but
these growths increase much more slowly, involve only a limited portion
of the bone, are of greater density, and are much more strictly
circumscribed.

As a rule, especially in cases which are recognized early and treated
{292} actively, the prognosis is good. Iodide of potassium should be
used in combination with mercury.

Syphilis of the Teeth.--Syphilis of the teeth has its chief interest to
the general practitioner from its very important bearing on diagnosis.
As manifesting itself at an age when the child is not apt to present
the active and unmistakable cutaneous and mucous lesions of the
disease, and when, consequently, its recognition is often extremely
difficult, this diagnostic importance is greatly increased.

The teeth of the first dentition, although exhibiting the usual signs
of interference with nutrition in their irregular development, opaque
and chalky enamel deficient in quantity and unevenly distributed, soft
and friable dentine, incongruity of size individually and relatively,
and proneness to decay, do not often display any distinctive evidence
of syphilis. {293} The same conditions may, and often do, depend on
other causes, and are commonly associated with various cachexiae--the
strumous, gouty, rheumatic, rachitic, etc.--and even with other
slighter ailments tending to produce imperfect assimilation and
malnutrition.

In the permanent teeth, likewise, the same condition may be due to the
same causes. Stomatitis, however produced--by mercury, by
gastro-intestinal derangements, by local irritation of any kind--is apt
to result in imperfectly organized dental structures. Mercurial teeth,
for example, are usually irregularly aligned, horizontally seamed,
honeycombed, craggy, malformed, of an unhealthy dirty yellow color,
separated too widely, and deficient in enamel.[124] The diseases of
childhood, especially the eruptive fevers, eclampsia, typhoid fever,
etc., by temporarily arresting or greatly interfering with nutrition
during the developmental period of the teeth, often cause horizontal
furrows across their crowns, which are, of course, persistent
throughout life, and mark indelibly the influence of such disorders on
all the formative processes.

[Footnote 124: The latter defect is particularly noticeable on the
cusps of the sixth-year molars. (See note on "Syphilis of the Teeth,"
by Dr. James W. White, in Am. ed. of Cornil, pp. 287-290.) The
discussion as to the effect of mercury in producing the condition of
the teeth known as honeycombed is still going on, but the evidence
seems to point clearly to a direct connection with the administration
of mercury in infancy, either for syphilis or in excessive doses as a
purge, or in some of the teething powders, which often consist of
calomel and opium. Mr. Hutchinson, at a meeting of the Odontological
Society (see _Proceedings_ for 1877, p. 249), gave an interesting
description of the way in which the supposition was arrived at.
Lamellar cataract is a disease which affects the eyes of children who
have suffered from convulsions: it was noticed that in cases of that
form of catarrh there were also honeycombed teeth, and it was thought
that the convulsions, the cataract, and the honeycombed teeth were all
due to the same unknown cause. At last a few exceptions were
found--patients with cataract, but with good teeth, and then some who
had had convulsions only, and yet had honeycombed teeth; lastly, it was
noticed that most of the patients had been treated with mercury. So it
came to be recognized that the honeycombed teeth were only accidentally
associated with the cataract, and that they were, in fact, the result
of the mercury which had been given to cure the convulsions. The same
gentleman figures a case of this disease in his _Illustrations of
Clinical Surgery_ (London, 1875), and thus describes it (p. 55): "The
present state of his permanent teeth is so characteristic as to deserve
more detailed description. The change about to be mentioned affects all
the incisors, canines, and first molars of both upper and lower jaws,
the bicuspid being scarcely implicated at all; the second molars are
also quite healthy. In the first molars the alterations consist of
deficiency of enamel on the upper surface of the crown and the presence
of spines of uncovered dentine. In the case of the incisors a
considerable portion of the crown of each tooth is totally devoid of
enamel, and its dentine is also deficient to some extent, so that the
teeth are thin, sharp-edged, and of a dirty yellowish color. The
transition from the enamel-covered to the diseased part occurs suddenly
in a horizontal line at some little distance from the crown of each
tooth; the position of this line or step being in each tooth nearly at
the same distance from the gum. The general effect when all the teeth
are seen together is as if a string had been tied around them when soft
and the distal part had withered."]

None of these conditions, however, are in the least degree
characteristic of syphilis, the special expression of which in the
mouth is to be found only in the permanent upper median incisors. For
the recognition and description of the peculiarities of these teeth in
the subjects of inherited syphilis we are indebted, as we are for so
much else of inestimable value in the study of the disease, to Mr.
Hutchinson. In 1863, in a memoir on _Syphilitic Diseases of the Eye and
Ear_, he wrote as follows[125] {294} concerning the symptoms which, in
a suspected case, would aid in determining the diagnosis: "By far the
most reliable amongst the objective symptoms is the state of the
permanent teeth if the patient be of age to show them. Although the
temporary teeth often, indeed usually, present some peculiarities in
syphilitic children of which a trained observer may avail himself, yet
they show nothing which is pathognomonic, and nothing which I dare
describe as worthy of general reliance.[126] _The central upper
incisors of the second set are the test teeth_, and the surgeon not
thoroughly conversant with the various and very common forms of dental
malformation will avoid much risk of error if he restricts his
attention to this pair. In syphilitic patients these teeth are usually
short and narrow, with a broad vertical notch in their edges and their
corners rounded off. Horizontal notches or furrows are often seen, but
they, as a rule, have nothing to do with syphilis. If the question be
put, Are teeth of the type described pathognomonic of syphilis? I
answer unreservedly that when well characterized I believe they are. I
have met with many cases in which the type in question was so slightly
marked that it served only to suggest suspicion, and by no means to
remove doubt; but I have never seen it well characterized without
having reason to believe that the inference to which it pointed was
well founded."

[Footnote 125: Chapter on "The Means of Recognition of the Subjects of
Hereditary Syphilis during the Tertiary Stage," p. 204. Before this,
however, he had called attention to the same peculiarities in a paper
on "The Means of Recognizing the Subjects of Inherited Syphilis in
Adult Life," _Medical Times and Gazette_, London, Sept. 11, 1858, p.
265.]

[Footnote 126: So far as I know, the only recorded instances by
reliable observers of the temporary teeth presenting the peculiar
characteristics of syphilis are as follows: In the _Transactions_ of
the Odontological Society of Great Britain, vol. ix., 1877, p. 258, Mr.
Oakley Coles described a case--without, unfortunately, giving
details--in which the "peg-shaped temporary teeth were very
characteristic of syphilis." Mr. Coles's abilities are well known, and
the fact that at the previous meeting the society had been addressed by
Mr. Hutchinson on this very subject would seem to indicate that he was
quite familiar with the importance of his statement.

M. Fournier calls attention (_Archives de Derm. et Syph._, Sept. 25,
1883) to a cast (No. 48) to be found in the collection of M. Parrot in
the museum of the Foundling Hospital at Paris. This displays the
dentition of a child twenty-seven months old, in which the two upper
median incisors are typical Hutchinson teeth. M. Fournier adds that
later researches show unmistakably that the temporary teeth may be
affected by hereditary syphilis in the same manner as those of the
second dentition, although not more than one case of the former is
recognized to fifteen or twenty of the latter. He thinks, however, that
this proportion would be greatly modified if in the autopsies of young
children the alveoli were opened to examine the embryonic teeth. M.
Parrot by this means claims to have often discovered lesions of the
milk teeth.]

As a matter of course, so positive a statement in a matter of such
gravity and importance excited considerable criticism, and the views of
Mr. Hutchinson have never been without earnest and often able
opponents; but it is safe to say that time has only served to place
them on a surer foundation and to enhance their value in the eyes of
the profession. That they have undergone no material change in the mind
of their distinguished author is shown by his expressions of opinion
during the debate on syphilis in the London Pathological Society in
1876,[127] and still later by the following memoranda which he gives as
a guide in diagnosis:[128]

"1. No special peculiarities are to be looked for in the first set of
teeth.

"2. There can be no more serious blunder than to imagine that bad teeth
in proportion to their badness of form are to be suspected of syphilis.

{295} "3. The upper central incisors are the only teeth which are
positively characteristic. The others may afford corroborative
testimony, but are not to be relied upon alone.

"4. The chief peculiarity is a general dwarfing of the tooth, which is
both too short and too narrow, and, from its sides slanting together,
presents a tendency to become pointed. This tendency to pointing is
always defeated by the cutting off of the end, the truncation being
usually effected in a line curved upward, so as to produce a single
shallow notch. At the bottom of this notch the enamel is deficient and
the dentine exposed, but there is no irregular pitting, as in
stomatitis teeth.

"5. The malformations are unusually symmetrical and affect pairs of
teeth. The two central incisors resemble each other, and the two
laterals are also alike. If any defect passes horizontally across all
the incisors at the same level, and affects them all alike, it is
probably not due to syphilis.

"6. In syphilis the lateral incisors usually show little or no
malformation.

"7. The occurrence of the peculiarities due to syphilis and those due
to mercury in the same mouth are exceedingly common."

[Footnote 127: _London Lancet_, 1876, pp. 56 and 535.]

[Footnote 128: _Illustrations of Clinical Surgery_, fasciculus xi.,
London, 1878.]

The great importance of the subject seems to me to justify one more
quotation, as showing the opinion at a very recent date of men well
qualified to judge of the correctness or inaccuracy of these
statements. Mr. C. Macnamara and Dr. Thomas Barlow[129] say: "The
characters of the teeth are so valuable when present that it is
important to have them clearly noted--the more so that, in spite of Mr.
Hutchinson's clear description, they have been much misrepresented. It
may be pointed out--(1) That only the upper median permanent incisors
are characteristic, and sometimes only one of them is typical, of the
disease; (2) that these teeth are generally a little apart, instead of
being in apposition, and are more or less dwarfed; (3) that in a
typical specimen the width of the cutting edge is narrower than the
width of the tooth as it emerges from the gum; (4) that a typical
syphilitic tooth presents a single notch, not a serrated margin; and
that occasionally, if the notch has not been actually scooped out,
there is a little lunula-shaped area which may readily become a notch;
(5) finally, that although such teeth, when present, are absolutely
pathognomonic, the existence of normal permanent upper median incisors
by no means excludes the existence of hereditary syphilis."

[Footnote 129: On behalf of the Collective Investigation Committee, who
have issued a circular designed to elicit information as to the effect
of syphilis on the civil population of Great Britain. This circular has
been sent to physicians, and contains queries as to various points
relating to the symptoms of inherited syphilis; among others as to the
existence in any given case of "notched, dwarfed upper median
incisors," which, with or without other symptoms, would establish the
diagnosis of that case. The observations above quoted are explanatory
of this question (_The British Medical Journal_, Dec. 16, 1882).]

I believe this may fairly be taken to represent the general belief at
the present day among those best qualified to pronounce upon the merits
of the case; and I may say that it is unqualifiedly my own opinion,
arrived at after some experience and considerable investigation into
the literature of the subject. It is not uncommon, however, to hear
doubts expressed as to the value of this sign in the diagnosis of
syphilis, and at intervals articles are written or papers read to prove
that it is not of the uniform and distinctively conclusive significance
that has been attributed to it.[130]

[Footnote 130: "I cannot say more in favor of the diagnostic values of
these teeth than that, when {296} present in typical form, they have a
certain weight in favor of the existence of hereditary syphilis in the
given subject" (Van Harlingen, article "Syphilis" in _Internat. Encyc.
of Surgery_, vol. ii. p. 565). "It has been the custom from time to
time since Mr. Hutchinson made his observation to question the validity
of his views, both as to the fact of interstitial keratitis being due
to hereditary syphilis, and as to the diagnostic values of the
so-called characteristic teeth. Thus, it has been asserted, not only in
England, but on the Continent, and especially in Germany, that the
disease may be the result of malnutrition in scrofulous and rickety
subjects; and it has been maintained that the malformation of the teeth
is the simple arrest of development in a perverted constitution from
other causes than syphilis" (Bumstead and Taylor, _op. cit._, p. 701).
Garretson says (_Oral Surgery_, p. 316): "Observations will be found to
greatly vary concerning the existence of any constancy in phenomenal
expressions of the teeth in this relation."

M. Magitot, who has for some years been supposed to pay especial
attention to this subject, has recently written an elaborate paper
(_Gazette des Hopitaux_, Sept. 29, Oct. 4, 11, and 18, 1881) to prove
(1st) that dental erosions, as he calls them, are not due to syphilis;
and (2d) that they are due to, or are almost invariably associated
with, infantile convulsions. He has collected a number of interesting
facts, but a very careful study of his article and inspection of his
diagrams have convinced me that he does not recognize at all the
special peculiarities of the Hutchinson teeth, but includes under his
title of "erosion" a variety of widely-differing conditions. He has
altogether misinterpreted Mr. Hutchinson's views as stated in his
_Memoirs on Certain Diseases of the Eye and Ear due to Inherited
Syphilis_, and represents him as at that time (1863) believing that the
cause of the change in the incisors was a mercurial stomatitis. The
quotation on p. 294 sufficiently refutes this absurdity. Of course the
paper as an argument against the syphilitic origin of these teeth is
without the slightest value.]

Corroborative evidence--which, to my mind, is very strong as coming
from men whose opportunities for observation of dental peculiarities
are almost unlimited--is found in the writings of those gentlemen who
have devoted themselves to dental and oral surgery exclusively. Mr.
Henry Moon[131] says:[132] "My observations on this subject extend over
some twelve years, and include some hundreds of cases; and although, in
some details as to the manner of causation, I may differ from the view
published by Mr. Hutchinson (before knowledge on tooth-development was
advanced as it is at present), yet I must coincide entirely with his
general conclusions." "The question really is this: Is there one
peculiar conformation of the teeth due to inherited syphilis and not
produced by any other cause? The evidence in favor of an affirmative
answer to this question appears to me to be so strong that I think the
onus of disproof rests with the sceptics."[133] These views were
coincided in by the majority of the gentlemen to whom they were
addressed, all of them dentists and surgeons of experience and repute,
and who included men so well known to the profession as Mr. Oakley
Coles, Mr. Samuel Cartwright, Mr. Charles Tomes, and others.

[Footnote 131: Author of the section on "Surgery of the Teeth"
incorporated in Bryant's _Surgery_.]

[Footnote 132: _Proceedings of the Odontological Society of Great
Britain_, vol. ix., 1877, pp. 238, 239. In the same journal for 1875,
vol. vii. p. 17, Langdon Down says that whenever he has discovered
syphilitic teeth he has "never failed to find confirmatory evidence of
the syphilitic history of the case."]

[Footnote 133: He says elsewhere (Bryant's _Surgery_, 3d Am. ed., p.
429) that the most characteristic change in these teeth is "the
lessened breadth of the cutting edge as compared with that of the neck,
the vertical groove on their anterior face being often absent, and the
notch on their cutting edge not being an absolutely constant feature,
and being also subject to obliteration through wear."]

It may be considered as well established, then, that these peculiar
teeth--stunted, abnormally narrow at the cutting edge, crescentically
rounded with the convexity upward, and the surface inclined upward and
forward instead of backward as in normal teeth, widely separated, but
converging at their lower edges--are pathognomonic of hereditary
syphilis.[134] They are {297} often described as pegged, having been
likened to a row of pegs stuck in the gums. This appearance is due to
the fact that they are shortened, often projecting not more than half
the normal distance from the gum, and are also widely separated; which
abnormalities often affect the adjoining teeth as well, and sometimes
the entire dentine. It has been asserted that other specific
peculiarities are to be found associated with those of the incisors,
and Mr. Moon describes as characteristic, and figures[135] small
dome-shaped first molars with suppressed angles and absence of enamel
from the masticatory surfaces. He believes also that when the upper
incisors are typical it is exceedingly rare for the lower incisors to
be altogether unaffected.

[Footnote 134: Mr. Hutchinson stated in 1877 that in spite of the fact
that many years previously he had challenged any one to bring forward a
patient with well-marked syphilitic teeth in whose history no evidence
of syphilis could be found, none had come.]

[Footnote 135: _Proc. of Odont. Soc. of Great Brit._, vol. ix. pp. 241,
242; Bryant's _Surgery_, Am. ed., p. 429.]

[Illustration: FIG. 11. Serrations of Normal Incisors.]

[Illustration: FIG. 12. Syphilitic Incisors.]

A mistake which I know, from observation, to be frequently made is the
confusing of the normal serrations of the cutting edges of
recently-erupted normal incisors with the peculiar crescentic edges of
the syphilitic teeth. It seems worth while to call especial attention
to this, on account of the unpleasant consequences which often follow
injudicious questioning based on such supposed syphilitic phenomena.
Indeed, the space which has been devoted to this subject of syphilis of
the teeth is well warranted, I am sure, by the fact that not only do
diagnosis, prognosis, and treatment in cases of great severity, and in
both children and parents, often depend upon a recognition of these
peculiarities, but that in addition to the clinical and therapeutic
problems there are others the solution of which is dependent upon the
same knowledge on the part of the practitioner, and which may involve
reputation, marital relations, and personal honor and happiness.

The approximate cause of these peculiarities in the incisors can hardly
be said to have been demonstrated. Mr. Hutchinson thought at one
time[136] that they were due to a stomatitis or an alveolar
periostitis, but he has since changed his mind as to that point,
believing now[137] that the syphilitic tooth is the result of an arrest
of development in the central or first-formed portion of the dentine.
The incisors being made up of these lobes or denticles, and dwarfing of
the middle one taking place, the two lateral ones fall together. This
accounts at once for the small size of the tooth, its shape of an
inverted truncated cone, and its crescentic edge.[138] If it were due
to stomatitis, it would be more likely to be equally {298} distributed,
syphilis in its late manifestations being notably unsymmetrical; there
would be no rational explanation of the involvement of one or two teeth
while those on either side so frequently escaped; if it were mercurial
stomatitis, the enamel too would be involved, as is not usually the
case in the syphilitic teeth. It is possible that the central incisors
are chiefly affected because they, with the first molars--also affected
according to Mr. Moon--and the lower incisors--not infrequently
involved--are the first-formed teeth.

[Footnote 136: "The physiognomonical, dental, and other peculiarities
by which we recognize the subject of inherited taint when advanced
beyond the period of infancy are all of them the direct consequences of
special inflammations from which the patient has suffered at former
periods; _e.g._ the synechiae and lustreless iris of iritis; the
malformed teeth of periostitis of the alveolus and dental sacs; the
protuberant forehead of hydrocephalus; the flattened nose of snuffles;
the pale, earthy, opaque skin of cutaneous inflammation and eruption"
(_Aphorisms respecting Constitutional Syphilis_, 1863).]

[Footnote 137: _Proc. of Odont. Soc. of Great Britain_, vol. ix., p.
248. See also _ibid._, pp. 241, 242, remarks of Mr. Moon; also _Monthly
Review of Dental Surgery_, June 15, 1877.]

[Footnote 138: The denticle theory of formation is not necessarily
opposed by the fact that there is only a single undivided pulp-cavity
in these incisors. Instances of the separate formation of processes of
dentinal pulp while others are being used and worn away, all of them
finally to unite in a common pulp-chamber, have been observed in lower
animals, as in the molar of the elephant.]

The most elaborate article upon syphilitic teeth which has appeared
since Mr. Hutchinson's original memoir is one by Fournier,[139] in
which, after a very broad and comprehensive consideration of the
subject, he arrives at the following conclusions: The hereditary
influence of syphilis shows itself in the dental system in two ways,
very unequal in point of diagnostic value--viz. first, by a retardation
of evolution; second, by the arrest of growth and modifications of
structure. The phenomena belonging to the second class may be grouped
as follows: First, _dental erosion_. This is due to imperfect formation
of the tooth, the result of a temporary stoppage in its development;
but as it produces an appearance like that of worm-eaten wood, it has
been called erosion, though in so far as the word conveys the idea of
the wearing of a surface which has been previously normal, it is
incorrect. The tooth affected with syphilitic erosion has never been
normal. The different forms of erosion can be subdivided into groups
according as they affect the face or the free edge or grinding surface
of the tooth. Of those involving the face there are four types:
Erosions _en cupule_, consisting of small excavations or cups in the
surface of the crown; erosions _en facettes_, in which the surface
presents a series of small planes, as though they had been filed;
erosions _en sillon_ when there is a linear excavation in the crown of
the tooth in the shape of a transverse groove; and erosions _en nappe_,
in which the whole surface is discolored, disorganized, and
honeycombed.

[Footnote 139: _Archives de Derm. et Syph._, Sept. 25, Oct. 2, Oct. 9,
1883. A translation made by the writer may be found in the _Dental
Cosmos_ for January and February, 1884.]

A second group of erosions affects the free edge of the tooth, and
includes the Hutchinson teeth, with several less important varieties.
Dental erosions are multiple, symmetrical, maintain the same level on
the crowns of corresponding teeth, and are situated at different
heights on the crowns of teeth of different classes. It is evident,
therefore, that they are the result of a morbid influence of a general
character. There are three theories as to their etiology: (_a_) that
they have no relation to syphilis,[140] but are always connected with
infantile eclampsia; (_b_) that they are exclusively the result of
hereditary syphilitic influence; and (_c_) that they are simply
ordinary lesions originating from syphilis with marked frequency, and
even in one form--the Hutchinson tooth--appearing to originate only
from it. This latter view is the one adopted by Fournier himself.
Continuing to group the symptoms due to arrest of growth and
modification of structure, we have, second, _microdontism_, or dwarfing
and stunting of the teeth--pegged teeth; third, _dental amorphism_, in
{299} which the teeth are strangely distorted or even transformed in
type; fourth, _dental vulnerability_, or extreme susceptibility to all
traumatic or disintegrating influences.

[Footnote 140: M. Magitot, _Treatise on the Anomalies of the Dental
System_, Paris, 1877; _Clinical Studies on Erosion of the Teeth
considered as a Retrospective Sign of Infantile Convulsions_, Paris,
1881; Castanie, Paris, 1879, Thesis No. 384; Rattier, Paris, 1879,
Thesis 569; and others.]

Interstitial Keratitis.--The frequency of this form of diffuse
inflammation of the cornea, and the diagnostic significance which has
been so positively attributed to it--and has been as positively
denied--render it of special interest to the general practitioner, who
is almost certain to meet with occasional cases, and should be prepared
to recognize its possible relation with other, and often graver,
conditions.

It begins, commonly, as a slight, diffused haziness situated in the
substance of the cornea itself, usually not far from the centre, and at
first affecting only one eye. This depends at this stage on the
presence of a number of little distinct dots of inflammation, limited
to circumscribed, almost microscopic, areas, but later, in a few days,
these coalesce, and at the end of a few weeks the whole cornea will
probably have become nearly or quite opaque, looking like ground glass.
There is no ulceration, and but little congestion as compared with that
seen in other inflammatory diseases of the eye, although in the
majority of cases there is a fulness of the ciliary vessels and a
little photophobia with pains around the orbit. This condition may
persist for one or two months, after which the other cornea is nearly
always attacked,[141] and is similarly affected, although the disease
is apt to pass through its different stages rather faster than in the
first eye.

[Footnote 141: In 91 out of 102 cases in Mr. Hutchinson's series--in 6,
the left alone; in 5, the right alone (_op. cit._, p. 123).]

When the height of the disease is reached the corneae are nearly
opaque, a bare perception of light remaining, so that the patient is
just aware of the difference between its presence and absolute
darkness. Then the cornea which was first involved begins to clear;
this is soon followed by improvement in the other one, which in the
course of a year or two results in a return to fairly good sight,
although in most cases there remain a slight haziness and an abnormal
expansion of the cornea.

This favorable result is much influenced by the character of the case,
which is sometimes very mild from the outset, and by the thoroughness
of the treatment. It is sometimes complicated with iritis,
kerato-iritis, cyclitis, posterior choroiditis, secondary glaucoma,
etc., in which cases of course the prognosis is most unfavorable. Even
in ordinary cases it should be guarded in respect to perfect
restoration of function, as clearing of the corneae may reveal
adhesions from iritis or spots of choroiditis disseminata, which could
not, of course, have been previously detected. In very mild cases,
however, without much evidence of involvement of the other tunics, and
which have been submitted to treatment early, it is not uncommon for
the cornea to regain almost perfect transparency.

The diagnosis of this condition may generally be made with ease. The
ground-glass appearance in the earlier stages and the dull pink or
salmon color in the more vascular stage are very characteristic. The
vascularity differs from that attending other chronic forms of
keratitis, granular lids, etc., in which the vessels are large and
superficial, in that in the syphilitic keratitis they are much deeper
and very closely interwoven, so that the effect is almost that of an
ecchymosis. In other cases both eyes are not so apt to be affected, nor
is the tendency to spontaneous cure {300} so marked. The absence of
ulceration and the very slight degree of accompanying sclerotic or
ciliary congestion are also valuable features.

The conditions which Mr. Hutchinson has known to be most frequently
mistaken for it[142] are certain forms of inflammation following
small-pox and very superficial ulcers in a healing stage, together with
cases of vascular conjunctiva.

[Footnote 142: _Op. cit._, p. 128.]

There is also said[143] to be some difficulty in distinguishing it from
a form of non-syphilitic relapsing cyclitis with corneal opacities and
iritis. This, however, is a disease of adults, often limited to one
eye, with a strong tendency to relapse, the opacities being more
abruptly defined and limited to the region near the circumference.

[Footnote 143: Edward Nettleship in Hill and Cooper, _op. cit._, p.
267.]

The chief point of interest, however, in the diagnosis of interstitial
keratitis is its association with other symptoms of syphilis, upon
which, for the general practitioner at least, the diagnosis will
usually depend.[144] Mr. Hutchinson's conclusions, drawn from an
analysis of 102 cases of interstitial keratitis, bear strongly upon
this point, and are as follows:[145] A large proportion of all cases
occur in patients between the ages of eight and fifteen, the disease
being comparatively rare in early childhood, and still more so after
adult age has been reached. He never saw it begin after the age of
twenty-six. The patients presented the physiognomical peculiarities of
inherited syphilis (see p. 313). In more than half the cases the
previous history, especially as regards infancy, was one of hereditary
syphilis, and in many instances there was a clear history of infantile
syphilis in brothers or sisters. In half the cases no questions were
asked as to the existence of venereal disease in the parents prior to
the birth of the child. In 29 out of the other half such disease was
freely admitted. All the patients had lost in early life nearly half
their brothers and sisters. Omitting miscarriages and premature births,
it was found that 77 mothers had borne 547 children, of whom only 284
remained alive--an excessive rate of mortality. It appeared in the
large proportion of cases in the eldest children in their respective
families--a circumstance to be expected in view of the usual behavior
of hereditary syphilis in families. Undoubted syphilitic lesions, such
as nodes, ulceration of the palate, etc., are not infrequently
associated with the keratitis.

[Footnote 144: "To those who have not had opportunities for observation
at an ophthalmic hospital I would recommend that the diagnosis should
be held to be doubtful if the patient does not present the
peculiarities of teeth and physiognomy which I have described, since we
find that the latter are the almost invariable concomitants of the true
disease" (Mr. Hutchinson, _op. cit._, p. 128).]

[Footnote 145: _Op. cit._, pp. 109-129.]

Examination of large numbers of cases has, I believe, established the
general accuracy of these statements; and although there is still much
difference of opinion as to the exact relation between syphilis and
this form of keratitis--whether, for example, it is a symptom of
syphilis itself or of a cachexia frequently produced by syphilis, but
often by other systemic diseases affecting nutrition--yet, on the
whole, so far as I am able to judge of the question outside of its
purely technical and ophthalmological relations, I think the weight of
modern authority is chiefly on the side of a distinct and practically
invariable relation of cause and effect between inherited syphilis and
the corneal inflammation.

{301} Mr. James Dixon,[146] for example, proposes to call the disease
syphilitic keratitis, and says it is met with exclusively as a sequel
of an inherited taint. He adds: "We may meet with some syphilitic
keratitis in patients with healthy physiognomy and deformed teeth, or,
still more rarely, in those with faultless teeth and the syphilitic
cast of features; but to find the true form of keratitis in connection
with both good teeth and good complexion is, I think, next to
impossible." Many other ophthalmologists express themselves to the same
effect more or less strongly. Nettleship,[147] Noyes,[148]
Forster,[149] Macnamara,[150] De Wecker,[151] and Carter[152] may be
mentioned as having ranged themselves upon this side. On the other hand
we have Schweiger,[153] Maunther,[154] Saemisch,[155] Soelberg
Wells,[156] and others who are not convinced that syphilis is the sole
nor even, in the opinion of some of them, the principal cause of this
disease.

[Footnote 146: Article on "Diseases of the Eye," Holmes's _System of
Surgery_, Am. ed., vol. ii. p. 71.]

[Footnote 147: _Op. cit._]

[Footnote 148: _Text-book of Ophthalmology_.]

[Footnote 149: _Handbuch der gesam. Augenheilkunde_, vol. vii. p. 186,
1876.]

[Footnote 150: _Op. cit._]

[Footnote 151: _Ocular Therapeutics_, trans. of Forbes, 1879, p. 124.]

[Footnote 152: He even asserts the converse to be true, which is going
beyond what I believe can be established in regard to the invariable
connection between the two diseases. He says: "The subjects of what we
call simply inherited syphilis are liable--nay, are almost sure--to
suffer from a peculiar form of interstitial keratitis."]

[Footnote 153: "Hutchinson's view, that this form of keratitis is to be
regarded as the direct consequence of congenital syphilis, has not been
generally accepted in Germany" (_Handbook of Ophthalmology_, p. 298).]

[Footnote 154: Zeissl's _Jahrbuch der Syphilis_, 1875, p. 288.]

[Footnote 155: Graefe and S.'s _Handbuch d. Augenheilkunde_, 1875, vol.
iv. p. 264.]

[Footnote 156: _Diseases of the Eye_, p. 138.]

Probably the conclusions of Jullien[157] most nearly express the views
of those who do not accept in its entirety the syphilitic theory of the
disease. He concludes--(1st) that interstitial keratitis coincides
frequently, but not invariably, with syphilitic derangement of the
dental apparatus; (2) that it is associated with a feeble constitution
and with malnutrition, and is thus produced indirectly by scrofula,
rheumatism, or syphilis, each of which by its debilitating influence
may give rise to a diathesis which favors such morbid developments.

[Footnote 157: _Op. cit._, p. 1013.]

As a specimen of the evidence which is produced by observers other than
Mr. Hutchinson--who, as he himself observes, may be suspected of "that
bias which almost necessarily warps more or less the judgment of one
who supposes himself to have noted something new"[158]--the statistics
of Forster,[159] who apparently takes an unbiassed view of the
question, may be noted: In a total of 214 cases of interstitial
keratitis evidence of hereditary syphilis other than the corneal
disease was noted in 146 (68 per cent.). This number was made up as
follows: _a_, evidence of syphilis in parent, 17; _b_, evidence of
hereditary syphilis in other members of the family, 14; _c_, evidence
in the patient other than keratitis, 115; characteristic teeth, 69;
evidences in physiognomy, bones, skin, palate, or choroid, 46. In the
remaining 68 cases (32 per cent.), though inheritance of syphilis was
not proved, there was, almost without exception, strong suspicion of
that disease apart from the keratitis.

[Footnote 158: _Op. cit._, Preface, p. x.]

[Footnote 159: Graefe and Saemisch's _Handbuch_, vii., Part I.]

The condition of the permanent central upper incisors was noted in 138
of the cases; of these they were typical in 73 (53 per cent.);
suspicious in 34 (24 per cent.); normal in 31 (23 per cent.). In 15
cases {302} the permanent teeth had not been cut, and in the remaining
61 the state of the teeth was not recorded.[160]

[Footnote 160: Note by Mr. Nettleship, Hill and Cooper, _op. cit._, pp.
263, 264.]

This seems to me such direct and such unequivocal clinical evidence
that it is safe to say, as of the question of syphilitic teeth, that
the burden of disproof rests with the doubters, and that we may venture
the assertion that interstitial, diffuse, or parenchymatous keratitis
is a symptom of inherited syphilis, and that the unmistakable presence
of the former disease is sufficient proof of the existence of the
latter.

Syphilis of the Nerve-Centres and Nerves.--Until a comparatively recent
period our only guide to the course and progress of the nerve diseases
of inherited syphilis was to be found in analogy. We knew, for
instance, that in acquired syphilis three forms of cerebral disease
could be recognized in a general way--one characterized by sudden
attack of paralysis, in which the lesion was usually thrombosis from
specific endo-arteritis; one in which the symptoms of brain tumor were
present, and in which gummata were the cause of the difficulty; and one
in which pain, headache, and various functional or convulsive
disturbances--chorea, epilepsy, paralysis of single nerves, etc.--were
the customary phenomena, and in which periosteal, meningeal, or
neuroglial thickenings constituted the pathological basis. The last two
are often intermingled both symptomatically and histologically.

Heubner[161] divides cerebral syphilis into three groups, two of which
very closely resemble those I have described. In one, however, he
includes both the general physical disturbances, incomplete paralysis,
and final coma characteristic of tumor and the epileptiform attacks so
often due to peripheral or meningeal irritation. This combination is
explained by the results of his autopsies, which disclosed in 26 cases
in which these symptoms were conjoined a gummous growth in the pia
mater of the convexity of one of the cerebral hemispheres, either
limited and superficial or involving more or less of the cortex and
forming a distinct tumor. The epileptiform attacks were present in 19
out of these 26 cases, while in 20 other cases where the growth was
limited to the white substance at the base of the brain they were
present only twice. This second form is the apoplectic, followed by
general hemiplegia, and depending on disease of the cerebral arteries.
His third division is a very ill-defined one, depends much for its
limitations upon subjective symptoms, and is of no special interest as
applied to the subject of inherited syphilis.

[Footnote 161: _Ziemssen_, vol. xii.]

Althaus[162] also makes three divisions, two of which are as follows:
(1) Cerebral tumor--a gumma either hard or soft. There are then
nocturnal headache, sleeplessness, epileptiform attacks, the various
phenomena produced by involvement of the cerebral nerves, etc. (2)
Disease of the arteries, apoplexy, or softening, followed by
hemiplegia.

[Footnote 162: _Medical Times and Gazette_, Nov. 10, 1877.]

Hutchinson makes a similar division of lesions and symptoms,[163] and
the observations of Jaksch, Wilks, and Hughlings Jackson more or less
closely coincide with this general classification.

[Footnote 163: _Ibid._, Feb. 17, 1877.]

Now, in spite of certain striking differences--more apparent than real,
however--between inherited and acquired syphilis as regards cause,
{303} duration of stages, etc., the essential pathological changes are
the same. When syphilis in its later periods attacks the brain or
spinal cord or nerve-trunks or vessels of a foetus, it proceeds just as
in the adult, the same characteristic accumulation of cells taking
place and setting up an arteritis or a meningitis, thickening the
sheaths of nerves, or constituting a pericranial node or a gumma
according to their number and their situation. We would accordingly
expect to find in subjects of inherited syphilis manifestations closely
allied to those observed in the adult; and the observations of
Barlow,[164] Graefe,[165] Jackson,[166] Heubner,[167] Dowse,[168] and
Hutchinson,[169] though comparatively few in number, have already
demonstrated the correctness of this supposition.

[Footnote 164: _Trans. of Path. Soc. of London_, vol. xxviii., 1877.]

[Footnote 165: _Archiv fur Ophthalmologie_, Bd. 1, Ab. i.]

[Footnote 166: _Journal of Mental Science_, Jan., 1875.]

[Footnote 167: _Ziemssen_, vol. xii.]

[Footnote 168: _Syphilis of the Brain and Spinal Cord_, London, 1879,
chapter on "Hered. Syph.," p. 67.]

[Footnote 169: _Med. Times and Gazette_ (? Feb. 17, 1877).]

We find, thus, that in these patients meningitis, growths, and arterial
disease constitute the three clinical divisions of the disease which
have thus far been distinctly differentiated, and the reported cases,
with or without autopsy, fall naturally into these classes.

These cases are naturally few, and to make them absolutely reliable it
is necessary to have unmistakable evidence of hereditary syphilis in
some other form and the demonstration of syphilitic lesions at an
autopsy. The case of Dowse, however,[170] includes these requirements.
A child twelve years of age, of syphilitic parents, with a history of
coryza, sore eyes, and a tubercular syphilide, was attacked with
epilepsy, diplopia, facial paralysis, etc., and finally died. At the
autopsy three gummatous growths of the surface of the brain were found,
and the vessels of the base were found to have undergone the special
changes described by Heubner. Their lumen was in some places nearly
occluded by an accumulation of spindle-shaped cells between the tunica
fenestra and the epithelial lining; and interspersed with them, but
particularly in the muscular and adventitious coats, were to be seen
enormous quantities of round cells which in many parts seemed actually
to replace the normal structures. Dowse's other cases are not at all
conclusive in their clinical histories; even the diagnosis was not
established by autopsy.

[Footnote 170: _Op cit._, pp. 71-75.]

Barlow's two cases were both very young children, and are extremely
convincing.[171] A child four months old, with snuffles, serpiginous
ulcers, etc., and with a syphilitic father, had epileptiform attacks,
followed by laryngismus, carpo-pedal contraction, and changes in the
choroid. She died aged about fifteen months, and the autopsy disclosed
thickening of the pia mater, evidently not tubercular, and changes in
the arteries, which in the gradual narrowing of the lumen of the
vessel, the absence of ulceration or disintegration or calcification,
and the continuity and extent of the cell-proliferation are as
different as possible from ordinary atheroma, but correspond precisely
with the description of Heubner's cases, which were undoubtedly the
subjects of acquired syphilis.

[Footnote 171: _Transactions of the Pathological Society of London_,
1877, vol. xxviii. pp. 287-291.]

In the second case the symptoms were associated chiefly with the
cranial nerves. These were nystagmus, paresis of facial muscles,
laryngeal spasms, etc. He died at the age of fifteen months. The
vessels of the base were extensively diseased as in the other case, and
the fourth, {304} fifth, sixth, seventh, and eighth pairs of nerves
were smaller by a new growth of a gummatous nature which had produced
almost entire atrophy of the nerve-cylinders. There were cicatrices of
the liver and spleen. Cases in which the diagnosis rested upon the
history, upon the co-existence of undoubted syphilitic symptoms, and
upon improvement under specific treatment are by no means rare.

Berkely Hill reports[172] a typical case of syphilitic epilepsy. A girl
aged nine was the first child of the family that had lived, two having
previously been born dead. She presented characteristic teeth, traces
of choroiditis, and, while under treatment, suffered from both
keratitis and iritis. Her first fit was when she was four years of age,
and the attacks had recurred frequently since that time. The convulsion
was confined to the left side. The left arm was very weak, the weakness
having come on gradually, and being especially great in the extensors
of the wrist. Under specific treatment the attacks ceased entirely. In
this case there was certainly organic disease, probably a gumma on the
surface of the right hemisphere.

[Footnote 172: _Op. cit._, p. 253.]

Other cases reported by the same author, numerous instances of nervous
troubles in inherited syphilis reported by Hughlings Jackson,[173]
Fournier,[174] Henoch,[175] and Hutchinson,[176] warrant the statement,
then, that the nervous diseases of inherited syphilis fall into the
same general category as those of the acquired disease; that they may
appear at any age, from three or four months to that of puberty; that
they depend for their production upon a cell-proliferation which,
according to its locality, results in the development of new growths,
the production of localized meningeal inflammations, or the obstruction
and inflammation of arteries; and that the symptoms are those usually
associated with such pathological changes, the diagnosis of syphilis
depending chiefly on the history and the presence of other specific
phenomena.

[Footnote 173: _Journal of Mental Science_, Jan. 8, 1875; _Transactions
of St. Andrew's Med. Graduates' Ass._, vol. i., 1868.]

[Footnote 174: _Annales des Derm. et Syph._]

[Footnote 175: _Nouveau Dict. de Med. et Chirurgie_, p. 885.]

[Footnote 176: _Op. cit._]

The prognosis is more unfavorable than in similar cases in acquired
syphilis, the meningeal and vascular lesions being the most frequent
and showing themselves very obstinate even under careful treatment.
Spinal troubles, chorea, and idiocy have been attributed to inherited
syphilis, but must occur with great rarity.

Hill[177] reports a case of a child aged five years who had been
hemiplegic since he was two and a half years old, and who developed
paralysis of the flexors of the ankle in each leg.

[Footnote 177: _Op. cit._, p. 254.]

Keyes reports a case of a boy five years of age, with nodes on tibiae
and other signs of inherited syphilis, who had two attacks of
paraplegia.

Hill reports a case of imbecility associated with inherited syphilis,
but there is no evidence that it was other than a coincidence.

Fletcher Beach found not more than 1 per cent. of syphilitic children
in the Dareult Asylum, and Mr. Mercier could only trace syphilis in 5
out of 220 female idiots, probably imbecile from birth.[178]

[Footnote 178: _Ibid._, p. 255.]

Hughlings Jackson only found 1 case of inherited syphilis among 80
{305} cases of chorea. The most carefully recorded cases of the latter
affection associated with hereditary syphilis are two reported by
Alison.[179]

[Footnote 179: _American Journal of the Medical Sciences_, July, 1877.]

Syphilis of the Spleen.--Disease of this organ in inherited syphilis is
especially important from two points of view. It is a valuable aid to
diagnosis, and by its size and the degree of persistence of the
swelling gives an approximate indication of the severity of the case.

Attention was first called to the frequency and importance of
enlargement of the spleen in early hereditary syphilis by Gee in a
paper read before the Royal Medical and Chirurgical Society in
1867.[180] He gave the histories of thirteen children in support of the
statement that such enlargement occurred in almost one-fourth of all
cases of hereditary syphilis, sometimes with, sometimes without,
enlargement of the liver and lymphatic glands. According to him, the
degree of splenic enlargement may be taken as a sort of index of the
severity of the cachexia; the majority of cases with great enlargement
die, but sometimes such children survive, the spleen gradually
diminishing in size as the health improves--not diminishing, however,
pari passu with such improvement, but remaining for a long time "a
monument of past cachexia."

[Footnote 180: _British Medical Journal_, 1867, vol. i. p. 435.]

Barlow,[181] ten years later, thought Gee had rather understated the
proportion of cases in which splenic enlargement occurs, he having
found it in 22 out of 28 children with definite hereditary syphilis.
Birch-Hirschfeld, Eisenschitz, and Tepel[182] corroborate these
observations, finding that the enlargement is almost invariable and
that the spleen is often double its normal size.

[Footnote 181: _Trans. of Path. Soc. of London_, Jan. 20, 1877.]

[Footnote 182: Quoted by Hill and Cooper, _op. cit._, pp. 164, 165.]

Mr. W. J. Tyson has reported[183] a cure of a child born of syphilitic
parents, in whom, at two years of age, the spleen extended downward
three and a half inches, reaching the crest of the ilium and
approaching closely to the umbilicus. The liver was not enlarged; the
urine was not albuminous. He ordered mercury with chalk, one grain
every morning and evening, and one grain of iodide of potassium, with
ten minims of syrup of iodide of iron to an ounce of water, three times
a day. Sixteen months later the spleen had become imperceptible, and
three years afterward the child was in excellent health.

[Footnote 183: _The Lancet_, Oct. 23, 1880.]

The diminution of the liver under treatment appears to take place
before there is any diminution in the size of the spleen.[184] This
persistence of the latter renders it, as has been stated, a valuable
diagnostic sign. In the paper already quoted from,[185] Macnamara and
Barlow allude to this as follows: Enlargement of the liver, although it
ought to be noted because it is often present in hereditary syphilis,
has but little value as a confirmatory symptom--first, because the
liver is proportionally large in infancy, and it is difficult to state
the limit of what is actually normal; and, secondly, because other
causes besides congenital syphilis lead to its enlargement.

[Footnote 184: Barlow, _British Medical Journal_, Jan. 20, 1877.]

[Footnote 185: _British Medical Journal_, Dec. 16, 1882.]

With regard to enlargement of the spleen the case is different. Gee's
observation, that in the early stage of infantile syphilis some
enlargement of the spleen occurs in a large number of cases, has been
abundantly {306} confirmed. Although with the subsidence of the other
symptoms this enlargement often disappears, so that on post-mortem
examination two or three months after there may be no trace of it, yet
in a few cases it persists, and indeed sometimes increases, so as to be
considerable when the other signs have quite vanished. The importance
of this sign is greatest when noted early; as, for example, when the
child is from two to three months old, for at that period the
enlargement of the spleen due to rickets can hardly come into question.

The condition of the spleen during this period of enlargement seems to
be simply that of hyperaemia, or at the most of hyperplasia, Gee's,
Barlow's, and Birch-Hirschfeld's autopsies showing no evidence of new
growth or of amyloid or other changes.[186]

[Footnote 186: Parrot reports (_Le Mouvement med._, Paris, Nov. 23,
1872) two forms of splenic disease produced by inherited syphilis: 1. A
simple hypertrophy, which he thinks is secondary to diffuse
infiltration of the liver, obstructing the portal circulation and
causing the spleen to act as a reservoir; 2. An inflammatory condition
resulting in the formation of false membranes around the capsule. His
explanation of the first condition is unsatisfactory, because there are
numerous cases in which the spleen is enlarged without any involvement
of the liver. His other observations have never been confirmed.]

The cause seems to me to be in all probability the well-known effect of
syphilis on the glandular system in general, and the lymphatic system
in particular, to which I believe the spleen is now generally assigned.
The analogy between this slow, persistent, painless enlargement
preceding the cutaneous symptoms,[187] unaccompanied by inflammatory
symptoms, unattended by any breaking down of tissue, subsiding slowly
but evenly under specific treatment, and the behavior of the buboes of
acquired syphilis, is certainly very striking.[188]

[Footnote 187: Eisenschitz, _Wiener med. Wochenschrift_, Nos. 48 and
49.]

[Footnote 188: A similar enlargement occurs, but much more rarely, in
the secondary period of acquired syphilis. Weaver noted it in 3 out of
79 soldiers suffering from early syphilis. Wilks and Moxon report cases
in which the average weight was 19 oz.]

In most cases of hereditary syphilis there are evidences of disturbance
of the gastro-intestinal tract. Vomiting, diarrhoea, colic, anorexia,
and emaciation are well-known, but of course not at all characteristic,
symptoms.

It has been supposed that the mucous membrane of the entire tract was
probably, during the early period at least, and coincidently with the
cutaneous eruption, in a condition of hyperaemia and irritation
comparable to that of the skin.[189] Whether this be so, or whether it
is due to associated involvement of the glandular apparatus, has not
yet been determined.

[Footnote 189: "There is surely no a priori probability that a blood
disease so severe as syphilis should produce lesions on the skin, in
the mouth, and in the eye only--that it should, in fact, affect all the
visible parts and avoid all the concealed ones" (Mr. Hutchinson, _The
Lancet_, Feb. 6, 1876).]

Forster[190] has found fibroid degeneration of Peyer's patches in a
syphilitic infant who died six days after birth, the glandular
structure having been replaced by elevated grayish-red masses of
nuclei, cells, and connective-tissue fibre. Ulcers of the intestines
have been described, but appear to have had no specific characters.

[Footnote 190: Quoted by Bumstead and Taylor, _op. cit._, p. 757. His
observations were confirmed by Eberth, Roth, and Oser.]

The pancreas has been most extensively studied by Birch-Hirschfeld, who
examined seventy-three syphilitic foetuses. In thirteen of them he
{307} found enlargement of the pancreas with increased weight and
density, proliferation of connective tissue, and in some cases
compression--almost obliteration--of the lobules, with atrophy and
fatty degeneration of their epithelium.[191]

[Footnote 191: Klebs discovered a gumma in the pancreas of a
six-months' foetus.]

The peritoneum has been described by Simpson, Von Baerensprung, and
others as occasionally invaded in early hereditary syphilis. There
seems to be no evidence that it is ever directly affected, the cases in
which death occurs from peritonitis being due usually to trouble
connected with the liver or spleen.

Syphilis of the lung, originally described by Depaul and Virchow, has
been carefully studied also by Forster, Robin, Lorain, and Cornil, from
whose description[192] of the pathology of the condition I condense the
following: In the syphilitic foetus born before term, in the syphilitic
child born dead at full term, and in the syphilitic children who live a
few days, there are found at the autopsy, in the lungs, nodules or
tumors, usually superficial, sometimes deep, hard, isolated or in
groups, pink, gray, or red in color, with scattered whitish or
yellowish points. Their size varies from a pea to a small walnut. They
represent a portion of the lung more or less considerable in a state of
special lobular hepatization. Sometimes a whole lobe is involved. The
affected portion is very dense and covered with thickened inflamed
pleura. The lesions are those of chronic pneumonia. The interlobular
connective tissue enters into proliferation and presents a large
quantity of embryonal cells; the alveolar walls are thick, while the
narrow alveoli are livid, and even filled by epithelial cells, which
are of the pavement form in contact with the walls, round in the centre
of the alveoli. As the process progresses the epithelial cells become
fatty, degenerated, and subsequently broken down and absorbed, while
the embryonal interalveolar tissue rapidly organizes into fibrous
tissue. Thus results a small fibrous tumor, in which a gumma may
ultimately develop.[193]

[Footnote 192: _Syphilis_, trans. of Simes and White, Philada., 1882,
p. 404.]

[Footnote 193: Cornil and Ranvier's _Path. Histology_, Am. ed., 1880.]

It is impossible to confound this syphilitic pneumonia with
tuberculosis. The granulations of tubercle are never congenital.

The fact that in syphilitic interstitial hyperplasia the change begins
in the interlobular connective tissue and around the interlobular
vessels, at first consisting of small spindle-shaped and roundish cells
which quickly develop into connective tissue, and the fact that
blood-vessels are freely produced among the fibres of this new tissue,
seemed, in the estimation of those pathologists who took part in the
discussion on visceral syphilis in 1877, to constitute its most
distinctive feature.[194]

[Footnote 194: _Trans. of Lond. Path. Soc._, vol. xxviii.--views of
Green, Jones, Greenfield, Moxon, and others.]

Gummata in the lungs of children suffering from inherited syphilis have
been described by a number of writers. They appear likewise to begin in
the walls of the blood-vessels or the bronchioles. They differ from
tubercular nodules in being few in number--not more than half a dozen
usually--and are generally confined to one lung.

The condition of the arteries in the few cases in which they have been
noticed as affected by inherited syphilis was precisely similar to that
found by Heubner in the arteries of adults.[195]

[Footnote 195: See Cornil, _op. cit._, p. 305.]

{308} The symptoms are very variable; new-born children often die
asphyxiated in a few days. If they live longer, the disease develops
into a more generalized broncho-pneumonia.

Syphilis of the Larynx.--The hoarse cry of the new-born infant so
characteristic of hereditary syphilis depends upon the presence of
hyperaemia, of mucous patches, or even of extensive ulceration. I am
inclined to think that the first is the more common, as if it were
otherwise cases of death from oedema glottidis or other forms of
laryngeal obstruction would be oftener met with. When ulceration does
exist it is generally, but not invariably, secondary to pharyngeal
ulcers.[196]

[Footnote 196: See synopsis of six cases of George M. Lefferts,
reported in Bumstead and Taylor, _op. cit._, p. 754.]

Bronchial catarrh, giving rise to cough, and sometimes to considerable
embarrassment of respiration, is a not infrequent complication of
laryngeal syphilis.[197]

[Footnote 197: Schnitzler, _Die Lungen Syphilis, etc._, 1880, S. 41.]

Later troubles of the larynx in connection with inherited syphilis have
not yet been carefully enough studied to warrant us in drawing any
distinction between them and the usual symptoms seen in the acquired
disease.

Syphilis of the testicles has been studied by Henoch,[198] Cornil,[199]
Parrot,[200] Hutinel,[201] North,[202] Bryant,[203] and others. It is
found to consist of a true interstitial orchitis, very closely
resembling that seen in the syphilitic testicles of adults. Hutinel's
investigations, based on ten cases, showed the testicles slightly
enlarged and harder than normal, the scrotum pendent, the epididymis
normal, the tension of the tunica vaginalis and tunica albuginea
slight. The basis of the lesion is in a collection of small round
embryonal cells resembling lymph-cells, arranged in the connective
tissue around the arterioles which come from the tunica albuginea. This
may be accompanied by a more or less marked diffused interstitial
orchitis, or there may be only a thickening from the new formation of
small round cells on the connective tissues of the testicles. Cornil
found the seminal ducts separated by numerous round or fusiform cells.
The disease usually occurs at from two months to three years of age;
both testicles are generally involved, and are enlarged, hard,
inelastic, and frequently nodulated. Mercurial treatment generally
causes a marked improvement unless the inflammation has already
resulted in the development of a new fibroid formation, in which case
it would be likely to remain unaffected by any form of treatment.
Inunctions with diluted mercurial ointment, iodoform, etc. are useful
adjuvants.

[Footnote 198: _Schmidt's Jahrbuch_, 178, No. 4.]

[Footnote 199: _Op. cit._, p. 420.]

[Footnote 200: _Rev. mens. de Med. et de Chir._, Paris, Feb., 1878.]

[Footnote 201: _Ibid._]

[Footnote 202: _Med. Times and Gaz._, Lond., 1862, vol. i. p. 403.]

[Footnote 203: _Ibid._, Dec., 1863.]

The kidneys are not infrequently involved in inherited syphilis. Parrot
reports the pathological change to consist of a proliferation of small
round cells in the intertubular connective tissue, followed by
contraction, obliteration of the tubules, and degeneration of their
epithelium.

Bradley has reported[204] the case of a child aged four months in whom
a well-marked syphilitic eruption and an attack of acute Bright's
disease were coincident. Mercurial treatment for three weeks cured
both.

[Footnote 204: _British Med. Journ._, Feb. 4, 1876.]

Coupland has reported two cases of parenchymatous nephritis associated
with inherited syphilis, but advances no proof that it was not an
accident. {309} Gummata have been from time to time found in the
kidneys of very young children who have died from their effects and
from other visceral lesions due to syphilis.[205] Cases of enlargement,
of fibroid, fatty, and gelatinous degenerations of the suprarenal
capsules, have been recorded.

[Footnote 205: See discussion in Clinical Soc. of London, Jan., 1880;
"Remarks on Visceral, and especially on Renal, Syphilis," by
Barthelemy, _Annales de Derm. et Syph._, April, 1881.]

The thymus gland is occasionally found in syphilis to have undergone
alterations claimed by Dubois, Depaul, and others to be syphilitic in
their nature, but ascribed by Parrot simply to degenerative changes due
to malnutrition. The gland does not appear to undergo any marked
alteration in size, color, or consistency, but is found after death to
contain a small quantity of purulent matter.

The tendency of syphilis is certainly not, as a rule, to the formation
of pus. Nearly all the lesions we have studied with the exception of
breaking-down gummata have consisted in various forms of
cell-proliferation or accumulation, and not in the formation of
abscesses, and it is not probable that this is an exception. I doubt
very much the syphilitic character of these changes.[206]

[Footnote 206: Lancereaux believed that it was due to the breaking down
of a gummy deposit, but that seems to be entirely hypothetical, none
having been discovered. Weisflag (quoted by Bumstead) arrives at the
following conclusions after studying the lesion and the literature of
the subject: 1. This thymus abscess does exist. 2. When associated with
other signs of congenital syphilis it indicates that the father or
mother of an infant suffers or has suffered from syphilis. 3. It is
possible, but not proved, that this affection may exist in children in
whom there are no symptoms of syphilis, but its existence renders the
diagnosis of hereditary syphilis probable, even if the disease of the
parent is not proved. 4. Such is the great similarity in the appearance
of pus and of the secretion of the thymus that they cannot always be
distinguished.]

THE DIAGNOSIS AND PROGNOSIS OF INHERITED SYPHILIS.--In reviewing the
general course of a case of inherited syphilis it seems evident that
the differences between it and the acquired disease which have been so
much dwelt upon are apparent rather than real.[207] The primary stage
is of course missing, and on any theory of the essential nature of
syphilis this is readily comprehensible. Whether the chancre is the
first symptom of a constitutional disease, or, as I believe to be the
case, is the simple accumulation at the point of original inoculation
of the cells which constitute the syphilitic virus--or are at any rate
its carriers--it would naturally be in the first case undiscoverable,
in the second nonexistent.

[Footnote 207: "That the noteworthy differences between
chancre-syphilis and the inherited disease are to be interpreted by
considerations of the tissues of the growing child and the adult, is
made very probable by what is observed when a mother near the end of
pregnancy becomes infected with primary disease. In such a case the
foetus nearly full grown acquires the disease, without a chancre,
directly from the maternal blood. It is acquisition, not inheritance,
for at the date of conception both the paternal and maternal elements
were free from taint, and during the first six, seven, or even eight
months of intra-uterine life the foetus remained healthy. Yet, as I
have proved elsewhere by citation of cases, syphilis obtained in this
peculiar method resembles exactly that which comes by true inheritance,
and not that which follows a chancre. This important fact goes, with
many others, in support of the belief that the poison of syphilis
remains identical, however obtained, and that the differences which are
so patent in its manifestations are due to differences in the state of
its recipient" (Mr. Hutchinson, article on "Transmission of Syphilis,"
_Brit. and For. Med.-Chir. Rev._, Oct., 1877, p. 475).

"It is not true that the diversity of symptoms presented by infants
authorizes us to admit a congenital and an hereditary syphilis.
Whatever the mode of infection, it is impossible to make this
distinction" (Ricord, note to _John Hunter's Works_, 1883).]

The secondary stage, characterized in the acquired form chiefly by
{310} lymphatic engorgement and symmetrical, widely-spread, polymorphic
cutaneous and mucous eruptions, and pathologically by a marked tendency
to the proliferation of certain new small round nucleated cells, upon
the presence of which depend all the manifestations of the disease, is
in inherited syphilis strictly analogous. Eruptions of the same
character make their appearance, differing only in minor points, as in
a greater tendency to become moist or ulcerated, due to the more
delicate texture of the infantile epidermis. To the same cause must be
assigned the macroscopic peculiarities of the only syphiloderm said to
be peculiar to infantile syphilis--pemphigus--which has been shown,
however, to have a papular basis, and in that way to conform to all the
other secondary eruptions.

The lymphatic engorgement either exists in the infant as in the adult
or has its analogue in the enlargement of the spleen and
liver--especially the former, which is almost as constant a phenomenon
as is general glandular enlargement in acquired syphilis. The same
pathological changes occur, the same infiltration of cells producing,
according to their situation, papular, pustular, or mucous patches, or
inflammation of such structures as the iris, choroid, or retina.

The tertiary stage, except in the fact that its phenomena may appear
unusually early and may be commingled with those of the secondary
period,[208] does not widely differ in the hereditary from that of the
acquired disease. It affects the same tissues, results in the same
pathological formations, and is preceded by the same period of latency
or quiescence of variable duration. There is no reliable evidence with
which I am familiar to show that in this stage inherited syphilis is
either contagious or transmissible--another point of close resemblance
between the two varieties under consideration.

[Footnote 208: This is by no means unknown even in the acquired form;
frequent examples of it have been recorded, and it can be readily
explained either on the theory of relapses in parts previously diseased
(Hutchinson), or on that of obliteration of lymphatic trunks and
accumulation of nutritive waste (Otis).]

In considering the question of diagnosis, therefore, we have an
excellent guide in the fact that the disease conforms in most respects
to the general laws of acquired syphilis, and that our knowledge of the
latter affection will be a valuable aid to recognition of the former.

The chief elements of diagnosis and prognosis of inherited syphilis in
its various stages may then be summarized as follows:

A history of syphilis in either parent is important just in proportion
to the shortness of the interval between the time of infection and the
date of conception. In other words, the shorter that interval the more
likely (_a_) that the child will have syphilis, (_b_) that it will have
it in a severe or fatal form. If the mother has been syphilitic and the
father healthy--which is rare--it is perhaps more likely that the child
will be diseased than when the reverse is the case. If both parents
were syphilitic at or before the time of conception, the probability
that the disease will be transmitted, and in a severe form, is much
increased. There is no evidence to show that inheritance from one
parent results in a graver variety of the disease than when it is
derived from the other.

A history of abortion or miscarriage on the part of the mother should
have weight in the determination of any given case, and if such
accidents {311} have been very frequent their diagnostic importance is
greatly increased. The loss of elder brothers or sisters and the causes
of death, with the precedent symptoms, should be carefully inquired
into. The nearer either of these occurrences--abortion or death of
elder children, if there is a fair presumption that they were due to
syphilis--has been to the birth of the patient in question, the greater
the likelihood that the latter has been infected.

Upon examining the product of abortion or stillbirth the most easily
observable symptoms will be those of the skin. Maceration and elevation
of the epidermis into bullae are in themselves hardly characteristic,
though they may--especially the latter--be regarded as suspicious. If
the cutaneous lesions are, however, distinctly papular or pustular or
ulcerative, or if the bullae have all the characteristics of syphilitic
pemphigus, the diagnosis is assured.[209]

[Footnote 209: "It is probable that very early abortions are less rare
than statistics indicate, but are often unsuspected."

"It is impossible to demonstrate the existence of syphilitic lesions in
foetuses expelled during the first months of pregnancy. Later, the
signs which have the greatest value are the lesions of the epiphyses of
the long bones. When the foetus has nearly arrived at full term, and is
not macerated, visceral and cutaneous lesions may be observed.
According to Mewis, the skin eruptions cannot be seen before the eighth
month, and are only recognizable on foetuses whose death has been very
recent or who are born living. Pulmonary lesions may be determined at
the end of the sixth month. Those of the pancreas are met with in about
half the foetuses which perish a little before or a little after birth.
The lesions of the liver, the spleen, and the bones may be recognized
even in macerated foetuses, this frequency increasing from month to
month" (_Nouv. Dict. de Med. et Chir._, vol. xxxiv. p. 864).]

The most distinctive symptom--one which may really be considered as
pathognomonic, is, however, the inflammation of the diaphyso-epiphysial
articulations, with or without their disjunction. Distinct enlargement
of the spleen or liver, and arachnitis with hydrocephalus, are valuable
diagnostic points, and the presence of gummata--not very
infrequent--would of course be conclusive.

At birth the syphilitic child may be small, stunted, emaciated,
weazened, senile in appearance; this would properly give rise to
suspicion, but may be associated with any disorder of nutrition on the
part of child or mother. It may also disclose cutaneous or mucous
eruptions evidently specific in character. The most common of these at
this early date is the bullous eruption affecting the palms and soles,
sometimes distributed over the whole body, and, as it indicates a
feeble resistance of the tissues to the tendency to exudation and
cell-growth, is usually a precursor of an early and fatal termination.
In any event, marked symptoms at time of birth render the prognosis
highly unfavorable.

It is quite as common, however--perhaps more so--for the subject of
hereditary syphilis to give no evidence of the disease at birth, but
even to appear healthy and well-nourished. In such cases the first
symptoms of the disease appear, on an average, in from six weeks to two
or three months, and consist principally of coryza (snuffles),
hoarseness of voice, and syphilodermata. The latter may be macular,
papular, pustular, or bullous. They are usually polymorphous, irregular
in shape, dark coppery-red in color, with sometimes a glazed or
crusted, but oftener a moist or ulcerating, surface, with a strong
tendency to coalesce into large patches, or to form irregular
serpiginous ulcers, or to take on hypertrophic growth {312} and develop
into condylomata. Eruptions which are squamous and are situated about
the mouth and chin and on the body, the legs, or the soles of the feet,
though exceptional, are of more value than those on the nates, where
the results of irritation from urine and feces may closely simulate
syphilodermata.

Mucous patches on the tongue, cheeks, tonsils, and pharynx are common,
often extending to the larynx, increasing the hoarseness, and to the
nasal cavities, aggravating the snuffles. Both of these occurrences, by
interfering with the respiration of the child and rendering its nursing
interrupted and insufficient, greatly add to the gravity of the case.
Enlargement of the spleen (common), enlargement of the liver (less so),
and iritis (rare), may be mentioned among the phenomena of this stage,
often associated with the skin eruptions.

About the time of the subsidence of the rash there may be developed the
specific inflammation at the junction of epiphyses and diaphyses which
produces a swelling of the long bones near their ends. The child will
be noticed to cry a little when, for example, the wrist or elbow on one
side is washed, and not to use these joints as much as the
corresponding ones on the other side. The parts are not hot, only
slightly tender, and as yet there is but little swelling. Later, the
droop and the disuse of the affected limb become more noticeable and
simulate infantile paralysis. There is, however, no wasting, no
alteration of reaction by faradism, no real loss of power, so that the
term pseudo-paralysis is an appropriate one. In a week or two similar
symptoms will occur in the bone on the opposite side, and finally the
ends of all the long bones may be affected; ordinarily the elbows,
wrists, knees, and shoulders are the joints involved. Suppuration is
rare, disjunction of the epiphysis from the diaphysis common. Recovery
is apt to take place spontaneously within a month. The associated
changes are chiefly endosteal at the junction of the shaft with the
epiphysis, but there is also a little periostitis or perichondritis,
which is the principal cause of the external swelling. Moderate
deformity may ensue.[210]

[Footnote 210: For the diagnosis from rickets see p. 290.]

Similar changes occurring in the cranial bones give rise to what has
been called the natiform skull. During the first year it is very common
for syphilitic children to develop a number of lenticular swellings on
the cranium, which appear symmetrically around the anterior fontanel,
but at a little distance from it; _i.e._ one on each frontal and one on
each parietal bone. These are said to be "bossed." They are at first
circumscribed, and in a child nine or ten months old often measure
three-quarters of an inch to an inch in diameter. They are at first
circular, afterward more irregular, and finally tend to organize,
becoming diffused and massive and causing a permanent thickening of the
skull.

These symptoms which have been described are the prominent ones
occurring during the first six or eight or twelve months of life. If
they do not manifest themselves before the eighth month, it is highly
probable, even in a case with a syphilitic parental history, that the
child will either escape altogether or that the secondary stage has
been very slight and altogether intra-uterine and unattended with
noticeable phenomena. If during this first year the child's cachexia is
marked, if there are any intercurrent diseases, if the symptoms show
themselves early, if the nasal or laryngeal affection is severe, if the
eruptions are markedly bullar or {313} pustular or ulcerative, if the
enlargement of the spleen is great or the osseous lesions precocious or
grave, and if, especially, there is any intermingling of tertiary
symptoms, gummata, nodes, etc.,--the prognosis will be unfavorable.

From adolescence on through adult life the diagnosis of inherited
syphilis will depend on the following points: First, of course, the
history of parental or of infantile syphilis, or of both. Then a group
of physical and physiognomical peculiarities, which are not definitely
characteristic, and are of little value when taken separately, but are
of considerable importance when all or a majority are present in any
given case. These are low stature or puny development proportionate to
the severity of the intra-uterine and infantile symptoms; a pasty,
leaden, or earthy complexion,[211] a relic of previous syphilodermata,
probably also a result of malnutrition; a prominent forehead, bulging
in the middle line at and within the frontal eminence, and due either
to thickening of the skull or to a previous arachnitis and
hydrocephalus before the ossification of the fontanels; a flat, sunken
bridge to the nose, due to the coryza of infancy extending to the
periosteum of the delicate nasal bones, and either interfering with
their nutrition or partially destroying them; dryness and thinness of
the hair, with brittleness and splitting of the nails; synechiae and
dulness of the iris (rare); ulcerations of the hard palate;[212] and
periosteal thickenings or enlargements of the shafts of the long bones
near the ends, or slight angular deformity, results of the
osteo-chondritis of infancy.

[Footnote 211: Trousseau (_Clinical Lectures_, vol. ii. p. 588,
Philada., 1873), after calling attention to this peculiar hue of the
face, says: "It not unfrequently happens that the physician, taught by
long familiarity with this appearance, will almost at once diagnose
syphilis after having simply seen the child's face, although the
peculiar hue can be but vaguely described in words. The visage presents
a special shade of bistre; it looks as if it had been lightly smeared
with coffee-grounds or a very dilute aqueous solution of soot. There is
neither the pallor, the icteric hue, nor the straw-yellow tinge of skin
seen in other cachectic affections; the tinge is not nearly so deep,
but is almost like that of the countenance of a recently-delivered
woman, and either does not extend at all, or only partially, to the
rest of the body. I know no disease except syphilis in which a child's
skin has this peculiar color; and consequently, when it is well marked,
it has more diagnostic value than any other symptom."]

[Footnote 212: Mr. Oakley Coles reports (_Proc. of Path. Society of
Great Britain_, vol. vii. p. 5) several cases of inherited syphilis in
which there was wide separation of the jaws in the median line. In one
family one member had typical teeth and wide separation; three others
had the same separation, but not the characteristic teeth. It was
suggested that in such cases the teeth were in size far below the
average, and that the condition was that often observed where the jaws
are in development in excess of the teeth which they contain. I. E.
Atkinson details some interesting cases of this lesion in late
hereditary syphilis, and attributes to it considerable diagnostic
importance (_American Journal of the Medical Sciences_, New Series,
vol. lxxvii., Jan., 1879, p. 71).]

A much more valuable group of symptoms, however, are the following,
which are mentioned in the order of their importance, any one of the
first three being almost or quite conclusive:

Dwarfed permanent median upper incisors, broader at the top than at the
cutting edge, which is crescentically notched, separated by an undue
interval and converging toward each other.

Evidence of past or present interstitial keratitis--a dusky and thin
sclerotic in the ciliary region and slight clouds here and there in the
corneal substance, there being no scars on its surface--or of
disseminated choroiditis; patches of absorption especially around the
periphery.

{314} A radiating series of narrow cicatricial scars extending right
across the mucous membrane of the lips, or a network of linear
cicatrices on the upper lip and around the nostrils, as well as at the
corners of the mouth and on the lower lip.

Periosteal nodes on one or many of the long bones; sudden, symmetrical,
and complete deafness, without otorrhoea and unattended by pain or
other subjective symptoms.[213]

[Footnote 213: In a few instances there has been noticed an arrest of
sexual development; in one case of Hughlings Jackson's there was such
an entire absence of all sexual characteristics that it was supposed
that the ovaries had been destroyed by syphilitic inflammation in early
life.]

Late or tardy hereditary syphilis is rarely dangerous to life. The
prognosis is almost unvaryingly favorable unless some grave visceral
complication, such as interstitial pneumonia, gummata of the brain,
liver, or kidney, or meningeal and periosteal inflammation within the
cranium, should occur.

TREATMENT.--The prophylactic treatment, or that directed to the health
and sexual relations of the parents previous to conception, has already
been sufficiently considered. That of the mother during pregnancy,
after having conceived from a syphilitic husband, or having had
antecedent syphilis, or having contracted it by direct contagion
subsequent to impregnation, is simply that of acquired syphilis in
either adult or child. Mercury in its full physiological dose is the
drug indicated. It may not be amiss to combine with it iodide of
potassium in moderate doses, but the practice of employing the latter
to the exclusion of the former is both theoretically and clinically
unsound. Care should especially be taken to give it in such a manner,
either by inunction or vaporization or so guarded with opium, that it
will not produce any irritating effect on the intestinal canal, the
sympathy between which and the uterus may, in the event of a strong
purgative action being set up, lead to an abortion.[214]

[Footnote 214: "In respect to prophylaxis as applied to infants, all
chances of infection should be entirely removed whenever constitutional
symptoms exist or the nature of the primary symptoms renders them
probable. Our caution should be carried still farther, and in the
absence of all appreciable symptoms we should assure ourselves by the
antecedents, so far as possible, that the parents are not under the
influence of a syphilitic diathesis; in which case they may give birth
to infected infants until appropriate treatment shields the latter from
infection. With still stronger reasons, when the mother during
pregnancy is affected with primary syphilitic symptoms of such a
character as to give rise to secondary symptoms, or if the latter
already exist, we should hasten to cope with them, and, far from
regarding pregnancy as a contra-indication to treatment, should
recollect that it generally prevents the disease in the infant, and
when skilfully administered obviates the frequent abortions which
syphilis excites. When primary symptoms have been contracted by the
mother a short time before delivery, since the infant may be infected
in its passage into the world, the same course should be followed with
it as with a person who has just exposed himself to an impure
connection" (Ricord, note on prophylaxis of venereal disease appended
to his edition of John Hunter's _Treatise on Venereal_, Philada., 1853,
p. 481).]

As we have seen that the pathology, the stages, and the general course
of hereditary syphilis are all closely related to or identical with the
same phenomena in the acquired disease, and so know that they both
depend upon the same ultimate cause, whatever that may be--a virus, a
fungus, or a degraded cell--it follows that the same principles should
govern us in the treatment of the one as in that of the other.

We know from clinical experience that mercury exercises an almost {315}
controlling influence over the secondary manifestations of acquired
syphilis, whether by acting as a true antidote or as a tonic, or by
virtue of its property of hastening destructive metamorphosis and
thereby facilitating the absorption or elimination of new cell-growths.
We know also that iodide of potassium, probably by virtue of its
powerful stimulating influence on the lymphatic system, has an equal
power over the tertiary growths, which by their pressure upon or
situation in important tissues or organs may be so destructive. There
is no reason, therefore, by analogy why these drugs should not,
comparatively speaking, be equally beneficial in hereditary syphilis;
and such is, indeed, found to be the case. In the latter affection,
however, there are two elements which should modify the treatment
somewhat, and must be taken into consideration. These are--1st. The
existence of a more or less profound cachexia influencing all the
nutritive and formative processes, and in itself, entirely apart from
any definite specific involvement of vital organs, threatening life.
2d. The not infrequent occurrence during the secondary period of
symptoms--notably gummata--belonging to the tertiary stage.

The first indication is met by making the treatment from first to last
not only antisyphilitic, but also supporting or even stimulating; and
with this object in view especial attention should be paid to
nutrition. It may be stated, axiomatically, that for every reason,
whenever it is within the bounds of possibility, the nurse of a
syphilitic child should be its mother. To her it is harmless--to every
other woman, not already syphilized, it is in the highest degree
dangerous. Space will not permit me here to discuss the medico-legal
aspect of the interesting question as to relations between such
children and the outside world, especially as represented in their
nurses. It will suffice to say that it is criminal and legally
punishable to induce any healthy woman to act as wet-nurse to a
syphilitic child unless she does so with a full knowledge of the risks
she runs in undertaking that function. In the rare cases where with
such information she still consents to suckle the child a written
statement of the facts of the case should be signed by her, with the
proper legal formalities, for the protection of the physician and the
family.

If the mother has died or on account of ill-health is unable to nurse
her child, and if no wet-nurse willing to enter the above agreement can
be obtained, the possibility and propriety of obtaining one who has
already had syphilis must next be considered. This idea to many parents
seems revolting, but will naturally be less so to those who have
themselves had the disease, and is, besides, so almost vitally
important to the child that no hesitation should be felt about making
the suggestion. If it is accepted, and if there is any opportunity for
making a selection, it may be said that the more robust the present
condition of such a nurse, and the more remote the date of her
syphilis, the better will be the chances of the child.

If neither mother nor wet-nurse can be had to suckle the child, it must
be fed by cow's, goat's, or ass's milk or by artificial alimentation;
but its prospect of life will be greatly, immeasurably, reduced. In
addition to careful feeding a little careful tonic treatment should
from the first be employed in conjunction with the specific remedies,
iodide of iron, cod-liver oil, and preparations of the phosphates being
the most useful drugs.

The existence of the second condition, which, as I have stated,
exercises a modifying influence upon treatment--the early appearance of
tertiary {316} symptoms--is probably due in many cases at least to an
overwhelming of the lymphatic system by the new cell-growth, which not
only greatly increases the amount of material to be transported by the
lymphatics, but at the same time, by invading their walls and
diminishing their lumen, greatly cripples them. Accumulations of
nutritive matter and of these new cells then take place, forming the
characteristic new growths or deposits which we call gummata. This
leads us to combine with the mercury from the beginning, at least in
all cases where bony or periosteal involvement, suppuration, or the
existence of gummata points to this condition, small doses of iodide of
potassium or of some other soluble and easily decomposed iodine salt.

The principle of treatment being thus recognized, the routine procedure
may be thus described: Give mercury as soon as the diagnosis of
syphilis is assured--preferably by inunction. Sir Benjamin Brodie's
opinion, expressed many years ago, still represents that of the
profession:[215] "I have tried different ways of treating such cases. I
have given the child gray powder internally and given mercury to the
wet-nurse. But mercury exhibited to a child by the mouth generally
gripes and purges, seldom doing any good, and given to the wet-nurse it
does not answer very well, and certainly is a very cruel practice.[216]
The mode in which I have treated cases for some years past has been
this: I have spread mercurial ointment, made in the proportion of a
drachm to an ounce, over a flannel roller and bound it around the child
once a day. The child kicks about, and, the cuticle being thin, the
mercury is absorbed. It does not either gripe or purge, nor does it
make the gums sore, but it cures the disease. I have adopted this
practice in a great many cases with signal success. Very few children
recover in whom mercury is given internally, but I have not seen a case
where this method of treatment has failed."

[Footnote 215: _Clinical Lectures on Surgery_, Philada., 1846, p. 230.]

[Footnote 216: This, the so-called indirect method, is altogether
unreliable, and should only be employed as a forlorn hope in those
cases where in every other way mercury sets up gastro-intestinal
irritation.]

When, for any reason, as irritation of the skin, this cannot be
employed, probably the best form of giving mercury by the mouth is in
the following formula:

  Rx. Hydrarg. cum Creta, gr. j to vj.
      Sacch. alb.         gr. xij.
  In M. ft. chart No. xij.

S. One powder three times a day, to be taken soon after nursing.

Iodide of potassium may be given separately in a syrupy solution in
doses of a half-grain to a grain, or if there are any marked tertiary
symptoms even in much larger doses, three or four times daily.[217]
{317} Treatment should, of course, be continued long after the
disappearance of syphilitic symptoms, and it would probably be well to
continue the mixed treatment intermittently until after puberty.

[Footnote 217: Wm. Campbell of Edinburgh was in the habit of commencing
with doses of a quarter of a grain of calomel and two grains of creta
praeparata, once daily for the first ten days. He afterward
progressively increased the calomel to a quarter of a grain twice each
day. Sir John Rose Cormack says (_Clinical Studies_, vol. ii. pp. 423,
424, London, 1876) that an infant six weeks old will generally bear
these doses well. In cases where they do not, he was in the habit of
ordering a solution of half a grain of the bichloride in three ounces
of distilled water and one ounce of syrup--one to two teaspoonfuls
every six, eight, or twelve hours. When he used mercurial "swabbing" he
employed from one to four drachms of unguent, hydrargyri to the ounce
of lard. He alternated this treatment with short courses of the syrup
of the iodide of iron, and continued the treatment up to the period of
dentition. He says he has generally obtained excellent results by these
methods.]

With the treatment of special symptoms the general practitioner has
little concern. The cases of visceral syphilis in very young children
are generally fatal. Those that recover do so in response to the active
use of the above remedies. Later, the prognosis is more favorable, the
treatment the same. Of course moist eruptions should be dusted with
some astringent or absorbent powder; mucous patches should be
cauterized; and great attention should be paid to avoidance of sources
of cutaneous irritation--frequent changing of diapers, etc.--but the
general methods are the same as in the adult.




{319}

DISEASES OF THE DIGESTIVE SYSTEM.

  DISEASES OF THE MOUTH AND TONGUE.
  DISEASES OF THE TONSILS.
  DISEASES OF THE PHARYNX.
  DISEASES OF THE OESOPHAGUS.
  FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH.
  SIMPLE ULCER OF THE STOMACH.
  CANCER OF THE STOMACH.
  HEMORRHAGE FROM THE STOMACH.
  DILATATION OF THE STOMACH.
  MINOR ORGANIC AFFECTIONS OF THE STOMACH.
  INTESTINAL INDIGESTION.
  CONSTIPATION.
  ENTERALGIA (INTESTINAL COLIC).
  ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS, COLITIS,
    PROCTITIS).
  CHRONIC INTESTINAL CATARRH.
  CHOLERA MORBUS.
  INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER.
  PSEUDO-MEMBRANOUS ENTERITIS.
  DYSENTERY.
  TYPHLITIS, PERITYPHLITIS, AND PARATYPHLITIS.
  INTESTINAL ULCER.
  HEMORRHAGE OF THE BOWELS.
  INTESTINAL OBSTRUCTION.
  CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES.
  DISEASES OF THE RECTUM AND ANUS.
  INTESTINAL WORMS.
  DISEASES OF THE LIVER.
  DISEASES OF THE PANCREAS.
  PERITONITIS.
  DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA).




{321}

DISEASES OF THE MOUTH AND TONGUE.

BY J. SOLIS COHEN, M.D.


Stomatitis.

DEFINITION.--Inflammation of the interior of the mouth.

The term Stomatitis is used to designate inflammatory affections of the
mucous membranes of the structures of the interior of the mouth,
including thus the mucous membrane of the lips, gums, tongue, cheek,
palate, and anatomical adnexes. Inflammatory affections of the mucous
membrane of the palate, palatine folds, and tonsils are usually
described more particularly under the heads of angina, sore throat, and
tonsillitis.

Stomatitis occurs idiopathically, deuteropathically, and traumatically.

Several varieties of stomatitis occur, sufficiently characteristic to
require separate description: viz. erythematous or catarrhal, aphthous
or vesicular, folliculous or glandular, pseudo-membranous or
diphtheritic, ulcerous, gangrenous, cryptogamous or parasitic, and
toxic.


Stomatitis Catarrhalis.

Simple, superficial, erythematous, or catarrhal stomatitis; pultaceous
stomatitis.

DEFINITION.--A simple inflammation or erythema, general or partial, of
the mucous membrane of the interior of the mouth.

It occurs both in adults and in children, and may be primary or
secondary, acute or chronic. In adults and adolescents it accompanies
catarrhal and ulcerous affections of the throat, and is described,
therefore, to a certain extent, in connection with these affections.

SYNONYMS.--Ordinary or common diffuse Inflammation of the mouth;
Erythema of the mouth; Oral catarrh.

ETIOLOGY.--In many cases of catarrhal stomatitis, both in adults and in
children, the affection is of obscure origin and the cause eludes
detection. In the great majority of instances the cause lies in some
irritation of the alimentary tract, whether local or at a distance.

The local causes, which are by far the more frequent, include every
variety of topical irritation to which the oral mucous membrane is in
itself liable or to which it may be subjected. Thus, irritating foreign
substances taken into the mouth; unduly heated, unduly iced, or unduly
spiced food and drink; the excessive use or abuse of tobacco and of
stimulants; contact of acrid and corrosive acid and alkaline mixtures;
{322} the constitutional action of certain medicines, particularly
mercury, but likewise bromine, iodine, arsenic, antimony, and, to a
slighter extent, other medicinal substances also; inspiration of
irritating dust, gases, vapors, steam, and smoke; even hare-lip, cleft
palate, and congenital or acquired deformities of the mouth
generally,--may all be included in this category.

In the newly-born a special hyperaemia of the mucous membrane has been
cited (Billard) as the cause.

Morbid dentition is the most frequent local cause of catarrhal
stomatitis in children, but it is an occasional cause in adults
likewise. Hence it is frequent from the sixth to the thirtieth month of
life; again, between the ages of six and fifteen years, the period of
second dentition; and likewise between the eighteenth and twenty-second
years, the period for the eruption of the last molars. Deformed,
carious, and broken teeth, improper dentistry, wounds and ulcerations
of the gums, negligence in cleansing the teeth,--all these contribute
their quota as exciting causes. Nurslings occasionally contract the
affection from the sore nipples of their nurses. In some instances they
acquire it by protracted sucking at an exhausted breast. Protracted
crying, from whatever cause, sometimes induces catarrhal stomatitis,
not only in nursing children, but in older ones. Prolonged or too
frequent use of the voice, whether in talking, reading, singing, or
shouting, may be the exciting cause.

Distant irritations of the alimentary tract, exciting catarrhal
stomatitis, include stomachic and intestinal derangements of all sorts.
Poor food and lack of hygiene on the one hand, and over-feeding, excess
of spices, alcohol, and tobacco on the other, are not infrequent
exciting causes. Undue excitement, excessive mental emotion,
unrestrained passion, deranged menstruation, normal and abnormal
pregnancy and lactation, sometimes incite the affection. Slight colds
from cold feet or wet clothing give rise to catarrhal stomatitis. It
likewise presents as an extension from coryza, sore throat, glossitis,
tonsillitis, pharyngitis, and laryngitis.

Deuteropathic or secondary catarrhal stomatitis occurs in various
febrile diseases, especially the acute exanthemata--measles, scarlet
fever, small-pox; in syphilis, in pulmonary tuberculosis, and in
long-continued chronic pneumonia.

Infantile stomatitis is most frequent between the ages of two and
twelve months; the stomatitis of adolescents at the periods of
dentition; and that of adults when local sources of irritation
predominate.

SYMPTOMATOLOGY.--The symptoms in catarrhal stomatitis vary in severity
with the intensity and extent of the inflammatory processes.

In the infant the subjective symptoms usually commence with
restlessness, fretfulness, and crying. Unwillingness to nurse or
inability to do so soon becomes manifest. The child may seize the
nipple eagerly with a firm grasp of the lips, but at the first suction
lets it drop away with a cry of pain and disappointment. The cause of
the pain is made evident on inspection and palpation of the interior of
the mouth. The parts are dry, glazed, hot, and tender. So hot is the
mouth at times that its heat, conveyed to the nipple in suckling, is
sometimes the first intimation of the existence of the malady. Similar
conditions often prompt an older {323} child to refuse the teaspoon.
This sensitiveness is observed in the tongue and on the inner surface
of the cheeks. It increases during movements of the tongue and jaw.
Deglutition becomes painful, especially when the food tendered is
rather hot or rather cold. There is a grayish-white accumulation of
partially detached epithelium on the tongue, sometimes in longitudinal
strips, sometimes in a continuous layer. Should the stomatitis be due
to dentition, the affected gums will be swollen, hot, and painful.
There is usually an augmentation of the secretions in the mouth.
Sometimes they flow from the mouth in great quantity, inflaming the
lips. These secretions acquire an increased viscidity, so that they
become adherent in clammy masses to the tongue, the gums, and the lips.
Taste thus becomes impaired, while decomposition of these masses in
situ imparts fetor to the breath; the odor being especially pronounced
when the child awakens from a night's sleep, the secretions having
accumulated meanwhile more rapidly than they could be discharged. When
the secretions of the mouth are not excessive there may be merely a
faint mawkish odor to the breath, sweetish in some instances, sour in
others. Loss of appetite is usual. Diarrhoea sometimes exists to a
moderate degree, attended at times by gaseous distension of the
intestines.

In severe cases dependent on morbid dentition swelling of the
submaxillary glands and infiltration of the connective tissue may take
place. More or less pyrexia becomes evident. In some instances
convulsions supervene; either directly from cerebral hyperaemia, or in
reflex manner from irritation of the sensitive gingival nerves.

In the adult impairment of taste is one of the earliest subjective
symptoms. This symptom is usually accompanied or else closely followed
by peculiar viscid and sticky sensations about the tongue, gums, and
palate--sensations that excite vermicular motions of the lips and
tongue to get rid of the foreign material by expectoration or by
deglutition. The taste is usually a bitter one, and the viscid
sensations are usually due to accumulations of desquamated epithelium
upon the tongue and other structures. An unpleasant odor is sometimes
exhaled, the result of decomposition of the excessive secretions.

In the chronic form of the affection, especially as it occurs in the
adult, the alterations of taste, the saburral coatings of the tongue,
and the fetor of the breath are more marked than in the acute form.

The mucus accumulating during sleep often awakens the patient in
efforts at hawking and spitting to detach and expectorate it. These
movements are occasionally so violent as to provoke emesis. The
disagreeable odor from the mouth is almost continuous.

In uncomplicated cases there is no loss of appetite or impairment of
digestion. The presence of these symptoms is presumptively indicative
of gastric disease, usually ulcerous or carcinomatous.

The course of the disease varies according to the causes which have
given rise to it. When these subside, the stomatitis soon ceases; when
they are irremediable, the stomatitis remains incurable. No special
period can be mentioned, therefore, for its duration. It terminates,
when cured, in complete restoration of the parts to their normal
condition. There are no special complications or sequelae.

PATHOLOGY AND MORBID ANATOMY.--The hyperaemia of the {324} tissues,
physiological during the entire process of dentition, is readily
provoked into a pathological hyperaemia. Whatever the origin, however,
acute catarrhal stomatitis begins, usually, with congestion and
tumefaction of the oral mucous membrane. The congestion is sometimes
preceded by pallor, as though anaemia from constriction of the
capillaries were the initial step in the phenomena. The congestion and
swelling are more rarely diffuse than circumscribed; _i.e._ confined to
certain portions of the tissues, especially the gums, which become
swollen and painful to contact. The surface is dry and glistening, and
the secretion diminished. The mucous membrane is raised in patches here
and there where the submucous tissues are the most lax. These patches,
irregular in size and configuration, are seen on the tips and edges of
the tongue, on the inner surface of the cheeks, at the gingival
junctions of the jaws, around the dental margins of the gums, about the
angle of the mouth, and on the palate. Sometimes the patches
coalesce--to such an extent in rare instances as to cover the entire
mucous membrane even of the palate and the gums. Their margins are
bright red, their centres yellowish. These elevated patches are due to
local accumulation of new-formed cellular elements, perhaps determined
by the distribution of capillaries or lymphatics. Intensification of
the inflammatory process around or upon them, giving rise to a more
abundant cell-proliferation, sometimes occurs; the results presenting
macroscopically in ridges or welts of a vivid red, surrounding the
patches or traversing them.

The tongue undergoes engorgement, and becomes increased in bulk;
exhibiting dentated facets along its edges and around its tip, due to
the pressure sustained from the adjoining teeth. Opposite the lines of
junction of the two rows of teeth the impression is double. The
dividing lines separating the facets project a little, and are
opalescent, grayish, or whitish, owing to increased proliferation of
epithelium. Similar dentate impressions from a like cause may be seen
on the inner surfaces of the cheeks.

The hyperaemia of the parts is soon followed by excessive production of
new cellular elements, rendering the now increased secretions turbid;
so that the surfaces of the tongue and cheeks become moist again, and
covered with a grayish-white, pultaceous form of desquamated
epithelium, but slightly adherent, and therefore readily detached by
movements of the tongue, lips, and cheeks. In some instances the
epithelium becomes raised into minute vesicles, and chiefly on the
edges of the tongue, thus presenting a sort of lingual herpes.
Excoriations, and even shallow ulcerations, may follow.

Isolated lesions occur. There may be congestion of the palate without
tumefaction, its epithelium undergoing detachment in shreds. The
congested patches at the dental margins of the gums may become overlaid
by opalescent masses of desquamated epithelium, followed by their
actual ulceration, and even by detachment of the teeth.

In children the lips may be swollen and excoriated or surrounded by an
eruption of herpes. Profuse salivation may occur in a child a few
months old when the affection becomes protracted. Febrile movement is
rare before the fifth or sixth month.

In chronic stomatitis the tumefaction is usually greater, with
distension of the capillaries and hypertrophy of some of the mucous
follicles, {325} especially those upon the cheeks and palate. There is
also hypertrophy of the lingual papillae, especially those at the tip
of the tongue. Adherent to the gums and the tongue is a yellowish
tenacious mucus, composed of squamous epithelia, fat-globules,
bacteria, and the usual debris of disorganization. The saliva is
secreted in unusual quantities, and sometimes dribbles more or less
continuously.

DIAGNOSIS.--Recognition of the conditions described under the head of
Pathology and Morbid Anatomy, in the presence of the symptoms described
under Symptomatology, renders the diagnosis easy.

Chronic stomatitis may be mistaken for mere indication of gastric
catarrh, which is likewise attended with loss of appetite, fetor of
breath, and coating of the tongue.

PROGNOSIS.--The prognosis is favorable in almost every instance,
recovery being almost universal in the acute form. Stomatitis of
dentition subsides with the physiological completion of that process;
stomatitis of exanthematic origin ceases with the evolution of the
eruptive disorder. In the chronic form ultimate recovery will depend
upon the permanency of the existing cause and the extent of the
inflammatory new formations.

TREATMENT.--The first indication, as a matter of course, is to obviate
the cause, whatever that may be. This, when practicable, usually
suffices to bring the malady promptly to a favorable termination.

Intestinal disturbances, whether causative or incidental, must be duly
corrected, and the administration of a saline purge is almost always
desirable. In addition, resort is made to frequent ablutions with fresh
water, warm or tepid, in sprays, gargles, or washes, as may be most
convenient or practicable. Emollients (gum-water, barley-water,
quinceseed-water), astringents (alum, tannin), and detergents (borax,
sodium bicarbonate), may be added, with opiates to relieve pain if need
be.

Frequent or continuous suction of fragments of ice usually affords
prompt relief to local pain and heat. The anaesthetic properties of
salicylic acid have been utilized,[1] one part to two hundred and fifty
of water containing sufficient alcohol for its solution.

[Footnote 1: Berthold, cited by Ringer, _Handbook of Therapeutics_,
10th ed., London, 1883, p. 612.]


Aphthous Stomatitis.

DEFINITION.--Inflammation of the mucous membrane of the interior of the
mouth, characterized by small superficial ulcers. These ulcers are
irregularly circular or oval, are not depressed below the general
surface of the mucous membrane, and support a creamy sebum or
exudation. They occupy positions known to be normally supplied with
mucous glands.

The classical description of this affection includes the initial
eruption of vesicles or groups of vesicles which rupture within a day
or two of their appearance, leaving, upon discharge of their contents,
the little superficial characteristic ulcers. Modern investigation,
however, casts some doubt upon the vesicular character of the initial
lesion, and renders it extremely probable that the reiterated
expression of this opinion has {326} been a simple deference by writer
after writer to the descriptions given by his predecessors. This
subject will receive further elucidation more appropriately in
describing the pathology and morbid anatomy of the disease.

Aphthous stomatitis may be either idiopathic or symptomatic, discrete
or confluent. It is often recurrent, and is sometimes epidemic.

SYNONYMS.--Aphthae; Vesicular stomatitis; Follicular stomatitis
(Billard); Canker sore mouth.

ETIOLOGY.--Aphthous stomatitis occurs at all ages, and is most
prevalent during summer heat. In children it is most frequent from the
period of the commencement of dentition to the completion of the
eruption of the temporary teeth. It is infrequent during the fourth
year of life, and is rare after the fifth. It is most apt to appear in
pale, delicate, and scrofulous children, especially in such as are
predisposed to catarrhal and cutaneous diseases (Billard, Barthez and
Rilliet). Sometimes it seems to be hereditary (Barthez). Some
individuals are subject to frequent recurrences. Poor food,
insufficient clothing, want of due ventilation, lack of cleanliness,
and similar deprivations act as predisposing causes. Hence the disease
is apt to occur in the crowded wards of hospitals and asylums for
children.

Anything that exhausts the physical forces of the adult, such as
excessive heat, overwork, anxiety, hardship and privation as in
shipwreck, and the drains of menstruation, pregnancy, and lactation,
excessive sexual intercourse, etc., may predispose to the disease.

Long-continued debility from severe constitutional maladies, with
chronic febrile conditions, such as chronic phthisis, chronic syphilis,
chronic enteritis, chronic gastritis, and from diabetes and carcinoma,
likewise acts as a predisposing cause, giving rise, during the final
stages of the systemic disease, to symptomatic aphthae, often of the
confluent variety. Aphthous stomatitis sometimes accompanies certain of
the continued fevers, exanthematous and non-exanthematous.

As exciting causes the following may be cited: gingivitis, from morbid
dentition in children, and from neglect of the teeth, dental caries,
and dental necrosis in adults; tobacco-smoking; the local contact of
acrid substances in food or otherwise; acute gastro-intestinal disorder
from improper or tainted food. Excessive humidity of the atmosphere is
assigned as a prominent exciting cause of the disease in some
countries. This is especially the case in Holland, where it often
exists epidemically. The confluent form at these times is said to
attack parturient women principally (Ketslaer). Inundations, not only
in Holland, but in Hayti, Porto Rico, and in the United States, are
sometimes followed by an endemic of aphthous stomatitis. It is believed
that the emanations from decayed animal and vegetable matters left
ashore on the reflux of the water, produce the morbid conditions which
constitute the predisposing cause under such circumstances.

The use of certain drugs--preparations of antimony, for
example--sometimes produces a vesicular stomatitis sufficiently
analogous to aphthae to be mentioned in this connection, and only to be
distinguished therefrom by the history of the case.

PATHOLOGY AND MORBID ANATOMY.--As has been intimated, the morbid
anatomy of aphthae has long been described as a series of initial {327}
vesicles[2] upon the buccal, labial, gingival, or lingual mucous
membrane. Their variance from analogous cutaneous vesicles--herpes, for
instance--is attributed to anatomical differences in the constitution
of the mucous membrane and the skin. The rarity of their detection has
been accounted for by the rapid maceration of the epithelium.

[Footnote 2: Tardieu, Hardy and Behier, Barthez and Rilliet, Meigs and
Pepper, and many others.]

The general opinion at present, however, is that the apparent vesicle
is an inflamed mucous follicle.[3] Some observers contend that it is an
inflammation of the mucous membrane pure and simple (Taupin); others
consider it an inflammation, sometimes in a follicle, sometimes in the
mucous membrane (Grisolle); others, a fibrinous exudation in the
uppermost layer of the mucous membrane (Henoch). Some have described it
as the analogue of a miliary eruption (Van Swieten, Sauvage, Willan and
Bateman); others, of herpes (Gubler, Simonet, Hardy and Behier);
others, of ecthyma (Trousseau) and of acne (Worms).

[Footnote 3: Bichat, Callisen and Plenck, Billard, Worms, and others.]

The vesicle of the primary stage, though generally vouched for, is
rarely seen by the practitioner, so rapid is the metamorphosis into the
aphthous ulcer. Its very existence is positively denied by several
authorities (Vogel, Henoch), and Vogel states that he has never, even
upon the most careful examination, discovered a real vesicle upon the
mucous membrane of the mouth--one which, upon puncture, discharged thin
fluid contents and then collapsed.

Beginning in a few instances, only, in a simple stomatitis, the initial
anatomical lesion presents as a red, hemispherical elevation of
epithelium one to two millimeters in diameter, and barely perceptible
to the touch of the finger, though described by the patient as
positively appreciable to the touch of the tongue. Believed to have
been transparent or semi-transparent at first, its summit is usually
opaque when first seen by the medical attendant, appearing as a little
white papule. Billard describes a central dark spot or depression--the
orifice of the duct of the inflamed follicle, as he considers it. Worms
and others, however, who likewise attribute the little tumor to an
inflamed follicle, have failed to recognize any such central
depression. There may be but four or five of these papules; rarely are
there more than twenty. Diffuse inflammation between them is rare. A
few new papules are seen on the second day, perhaps a few fresh ones on
the third day. Eventually, contiguous desquamations coalesce into an
irregular excoriated or ulcerated surface. These appearances and
processes may be summed up as hyperaemia, increased cell-proliferation
into circumscribed portions of the mucous structures, with distension
of the epithelium (dropsical degeneration?), rupture, and ulceration.

This is the stage at which the local lesion usually comes under
professional notice as a superficial circular or ovoidal ulceration or
patch, with irregularly rounded edges and an undermined border of
shreddy epithelium. It is level with the surface or but slightly
tumefied, and is usually surrounded by an inflammatory areola that
gives it a slightly excavated aspect. Sometimes this is a narrow red
rim, and sometimes it is a delicate radiating arborescence of several
millimeters. Adjacent ulcerations coalesce and produce irregularly
elongated losses of substance. The floor {328} of the ulcer is covered
with an adherent semi-opaque or opaque lardaceous mass, sometimes
grayish-white, sometimes creamy or yellowish-white when unadmixed with
other matters; the color depending more or less upon the number of
oil-globules present, the result of fatty degeneration of the
epithelium.

For a few days, three to five or more, the surface of the ulcer
increases slightly by detachment of its ragged edges, eventually
leaving a clean-cut sore, gradually reddening in color, with an
inflammatory margin indicative of the reparative process. Repair
steadily progresses by the reproduction of healthy epithelium from
periphery to centre, so that within a day or two the size of the ulcer
becomes diminished to that of a pinhead; and this is promptly covered
over, leaving a red spot to mark its site, until, in a few days more,
the color fades in its turn, and no trace of the lesion remains. The
period of ulceration is prolonged to one or more weeks in some
subjects, chiefly those of depraved constitution.

It was the uniform configuration of the initial lesions, their
invariable seat, and the central depression which he detected, that led
Billard to the opinion that the so-called eruption or vesicle was an
inflamed mucous follicle. This view was further supported by the fact
that the disease does not occur in the new-born subject, in whom the
lymphatic glands and follicles of the digestive tract are barely
developed, while it does occur after the fifth or sixth month of life,
up to which time these structures are growing rapidly, and thus
predisposing the infant to this peculiar disease by reason of the
physiological nutritive hyperaemia.

Discrete aphthae are found principally in the sides of the frenum and
on the tip and sides of the tongue; on the internal face of the lips,
the lower lip particularly, near their junction with the gums; on the
internal face of the cheeks, far back, near the ramus of the jaw; upon
the sides of the gums, externally and internally; on the summit of the
gums of edentulous children (Billard); exceptionally upon the soft
palate; in rare instances upon the pharynx.

Confluent aphthae appear in the same localities as are mentioned above,
and are much more frequent in the pharynx and oesophagus than are
discrete aphthae. They are said to be found occasionally in the stomach
and in the intestinal canal.

In the confluent form of the disease the aphthae are much more
numerous, and the individual ulcerations run into each other;
coalescing into elongated ulcers, especially upon the lower lip and at
the tip of the tongue.

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--The discrete form of the affection is rarely attended by
constitutional disturbance of any gravity, and such disturbance, slight
as it may be, is much more frequent in children than in adults. The
local manifestation gradually wanes from periphery to centre in from
eight to ten days, the patches changing in color from grayish to
yellow, becoming translucent, and losing their red areola, until
nothing but dark-red spots remain to mark their site. These spots fade
in time, removing all trace of lesion.

Aphthous stomatitis of secondary origin attends conditions of serious
constitutional disturbance--circumstances under which it is incidental
and not causal.

The confluent form, unless exceedingly mild, is attended by symptoms
{329} of gastric or intestinal derangement--viz. coated tongue, thirst,
salivation, acid or acrid eructations, nausea, perhaps vomiting,
indigestion, and constipation or diarrhoea, as may be. The vomiting in
these instances is usually attributed to the presence of aphthae in the
oesophagus and stomach, and the diarrhoea to their presence in the
intestines.

Severer cases present, in addition, febrile phenomena, restlessness,
loss of appetite, and unhealthy fecal discharges.

The constitutional symptoms precede the local manifestations in some
instances by a number of days.

Confluent epidemic aphthous stomatitis, as it occurs in parturient
women, is described (Guersant) as commencing with rigors, headache, and
fever. The local symptoms are very severe. Pustules form upon the
palate and pharynx. Deglutition becomes painful and difficult. Vomiting
and painful diarrhoea occur, indicating extension of the disease to the
stomach and the intestines. Typhoid conditions may supervene, and
continue as long as three weeks, even terminating fatally.

The earliest local symptoms consist in some degree of discomfort and
heat, to which severe smarting becomes added at the period of
ulceration. The little sores, no matter how minute they may be, are
exceedingly painful to the touch, even to the contact of the tongue.
Mastication thus becomes painful, and even impracticable, in the adult;
and suction at the breast or the bottle difficult and painful in the
infant. The mouth of the infant is so hot that its heat is imparted to
the nipple of the nurse, whose sensations in nursing sometimes furnish
the earliest indication of the disease. Indeed, the heat of the child's
mouth at this time, and the acridity of the buccal secretions, are
often sufficient to irritate and inflame the nipple, and even to
produce superficial excoriation. The general mucous secretions of the
mouth are usually augmented. Hypersalivation is much less frequent.

The course of the disease is mild as a rule. The chief inconvenience is
the difficulty in alimentation consequent on the pain in mastication
and in swallowing.

The duration of the affection in idiopathic cases varies, as the rule,
from four to seven days, counting from the first appearance of the
local lesion to the complete repair of the succeeding ulceration.
Individual cases are often more protracted. Successive crops of aphthae
may prolong the disease for many days. In confluent aphthae the course
is slower and the disease less amenable to treatment; ulceration often
continuing longer than a week, and recovery requiring twelve or fifteen
days. The duration in consecutive cases varies with the nature of the
underlying malady. In individuals seriously debilitated by protracted
constitutional disease, as in the subjects of phthisis, the affection
may continue, with intermissions and exacerbations, as long as the
patient lives. The termination of the individual ulcerations is in
repair.

There are no special complications. The accompanying stomatitis is
usually a gingivitis simply, and is apt to be circumscribed when more
extensive.

There are no sequelae. Sometimes labial herpes or similar ulcerations
follow, which are likewise sore and painful.

DIAGNOSIS.--The isolated patches of the discrete form are usually
sufficiently characteristic to establish the diagnosis.

{330} In children the gums are usually seen to be congested, swollen,
moist, and glistening. Sometimes they are even sanious. This condition
is deemed of great importance in cases of small, solitary aphthae
concealed in the sinus between gums and lips (Rilliet).

Confluent aphthae may be mistaken for ulcerative or ulcero-membranous
stomatitis, especially when the emanations from a coated tongue exhale
a disagreeable or fetorous odor.

From thrush--with which it is most frequently confounded--it is to be
discriminated by the absence, upon naked-eye inspection, of the
peculiar curdy-like exudations to be described under the appropriate
section, and under microscopic inspection by the lack of the peculiar
thrush-fungus (Oidium albicans).

PROGNOSIS.--Recovery is usually prompt in discrete cases, but relapses
are not infrequent. In confluent cases recovery is dependent upon the
character of the constitutional disorder by which the local disease has
been caused or with which it is associated, and is therefore much
slower.

The disease is grave in certain epidemic confluent forms, such as are
described as occurring in Holland and elsewhere under conditions
alluded to. Parturient women under such circumstances occasionally
succumb to the typhoid condition into which they are thrown. When
following measles there is some danger of laryngitis, and the case
becomes grave. Oedema of the larynx is sometimes produced.

TREATMENT.--Very simple treatment suffices in the discrete form of the
disease. A mild antacid, or even an emetic, may be indicated when there
is gastric derangement or disturbance; or a mild laxative when the
patient is costive. Castor oil, rhubarb, or magnesia may be given,
followed, if need be, by an astringent if diarrhoea should occur. A
little opium may be administered if requisite. The diet should be quite
simple and unirritating. Cold milk is often the very best diet,
especially while the mouth remains quite sore.

Topical treatment in the milder cases may be limited to simple
ablutions, by rinsing or by spray, with water, cold or tepid as may be
most agreeable to the patient. A little opium may be added when the
parts are painful or tender. In severer cases an antiseptic wash may be
substituted, as the sodium sulphite or hyposulphite, thirty grains to
the ounce, creasote-water, or the like.

Demulcent washes of elm, sassafras-pith, or flaxseed are often more
soothing than simple water. Pellets of ice from time to time are quite
refreshing and agreeable. Occasional topical use of borax or alum,
applied several times a day by means of a hair pencil, soft cotton wad,
or the like, is often useful, care being taken to touch the sores
lightly, and not to rub them. If the course toward repair is retarded,
the parts may be touched lightly with silver nitrate in stick or in
strong solution (60 grains), or washed more freely, two or three times
a day, with a weaker solution, five or ten grains to the ounce of
distilled water. Cupric sulphate, ten grains to the ounce, zinc
sulphate, twenty grains to the ounce, mercuric chloride, one grain to
the ounce, or potassium chlorate, twenty grains to the ounce, may be
used as local applications, repeated at intervals of four or five
hours. Iodoform has been highly recommended of late.

{331} The confluent variety requires constitutional treatment adapted
to the underlying malady. Nutritious diet is often demanded, together
with tonics, such as iron and quinia, or even stimulants, wine or
brandy. Topically, cauterization with silver nitrate is more apt to be
indicated, and to be indicated more promptly than in the discrete form.
Potassium chlorate in doses of one or more grains may often be given
with advantage, at intervals of from four to two hours.


Stomatitis Parasitica.

DEFINITION.--An exudative inflammation of the interior of the mouth,
due to the development upon the mucous membrane of a parasitic
vegetable confervoid growth, the Oidium albicans (Robin).

SYNONYMS.--Stomatitis cremosa; Stomatitis pseudo-membranosa; Thrush;
Muguet of the French; Schwammchen of the Germans.

HISTORY.--Thrush was long regarded as a pseudo-membranous variety of
stomatitis, and was likewise confounded with other varieties of
stomatitis, especially aphthae, its differentiation from which will be
rendered apparent by a study of its etiology and morbid anatomy.

The microscopic researches of Berg[4] of Stockholm upon the minute
structure of the supposed pseudo-membrane developed the fact that it
was largely composed of certain cryptogams. This growth was named
Oidium albicans by Prof. Ch. Robin,[5] by whom it had been subjected to
minute study.

[Footnote 4: _Ueber die Schwammchen bei Kindern_, 1842--Van der Busch's
translation from the Swedish, Bremen, 1848.]

[Footnote 5: _Histoire naturelle des Vegetaux parasites_, Paris, 1853.]

Later observers consider the oidia in general simply transitional forms
in the life-history of fungi otherwise classified. According to
Grawitz, the O. albicans is a stage of the Mycoderma vini, his
experiments having shown that on cultivation the filaments germinate
like Torula and Mycoderma, and that the latter can be grown in the
epithelium of the mucous membrane.[6]

[Footnote 6: Ziegler, _A Text-book of Pathological Anatomy and
Pathogenesis_, translated by Macalister, vol. i. p. 319, London, 1883.]

[Illustration: FIG. 13. Oidium albicans, from the Mouth in a case of
Thrush (Kuchenmeister). _a_, fragment of a separated thrush-layer
implanted in a mass of epithelium; _b_, spores; _d_, thallus-threads
with partition walls; _e_, free end of a thallus somewhat swollen; _f_,
thallus with constriction, without partition walls.]

ETIOLOGY.--Thrush is usually a symptomatic disease, secondary to an
{332} acid condition of the fluids of the mouth. Athrepsia (Parrot,
Meigs and Pepper), or innutrition, is the presumable predisposing
cause. Negligence in maintaining cleanliness of the mouth and of the
articles which are placed in it is regarded as the main exciting cause.
It occurs both in the adult and in the infant, but it is much more
frequent in infancy and in early childhood. It is most frequently
encountered in asylums and hospitals for children, being often
transmitted from child to child by the nurse or by means of the
feeding-bottle. The poor health of the child seeming less accountable
for the disease than the unsanitary condition of the wards, buildings,
and surroundings, it is consequently much less frequent in private than
in public practice. It is more frequent in the first two weeks of life
than later. Seux observed it within the first eight days in 394 cases
out of 402 (Simon). It is much more frequent during summer than at any
other season, more than half the cases (Valleix) occurring at that
portion of the year.

In senile subjects, in adults, and in children more than two years of
age it is cachectic, and observed chiefly toward the close of some
fatal and exhausting disease, such as diabetes, carcinoma,
tuberculosis, chronic pneumonia, enteric fever, puerperal fever,
erysipelas, chronic entero-colitis and recto-colitis, and
pseudo-membranous sore throat. It is sometimes observed in the early
stage of enteric fever.

Meigs and Pepper, apparently following Parrot, deem the central cause
to lie in a certain failure of nutrition under which the general
vitality slowly ebbs away. They are inclined[7] to recognize a causal
factor in a deficiency in the supply of water in much of the artificial
food administered to young subjects. The normal acidity of the fluids
of the mouth of the newly-born (Guillot, Seux) is not sufficiently
counteracted until saliva becomes abundant. Premature weaning,
entailing, as it often does, the use of improper foods, renders the
child liable to gastro-intestinal disorders. To this add want of care
of the bottle and nipples, of the teaspoon or pap-boat, and of the
mouth itself, and the conditions are fulfilled in fermentations of
remnants of milk taking place without and within, which produce the
acid condition of the fluids and secretions of the mouth said always to
accompany and precede the development of the disease (Gubler).

[Footnote 7: _A Practical Treatise on the Diseases of Children_, 7th
ed., Philada., 1882.]

The theory of contagiousness seems established (Guillot, Berg, Gubler,
Robin, Trousseau). This has been further demonstrated by experiments
upon sheep (Delafeud), in which thrush has been implanted whenever the
animals were unhealthy, but not otherwise.

PATHOLOGY AND MORBID ANATOMY.--The mucous membrane of the mouth within
a few hours after its invasion by thrush is seen to be covered to some
extent by minute masses of a granular curdy substance adherent to the
tissues, which often bleed slightly when the substance is forcibly
removed.

In children much reduced by inanition or severe disease, much of the
deposit soon coalesces into a membraniform product, grayish or
yellowish from rarefaction by the air, or even brownish from admixture
of blood. By the same time the general congestion of the mucous
membrane will have subsided into the pallor of anaemia. Though
tolerably adherent when fresh, the deposit when older often becomes
loosened {333} spontaneously, so that it may be removed by the finger
in large flakes without producing any hemorrhage whatever.

The characteristic masses present both as delicate roundish flakes,
isolated, not larger than a pinhead, and as confluent patches several
times as large and more irregular in outline. These masses under
microscopic inspection are seen to be composed of the filaments and
spores of a confervoid parasitic plant, the Oidium albicans, enclosing
altered epithelia in various conditions. This parasitic growth does not
become developed upon healthy mucous membrane with normal secretory
products. Acidity of the fluids and exuberance of epithelium are the
requisites for its production, whatever be the cause. The acidity of
the fluids irritates the mucous membrane upon which they lie. This
irritation induces abnormal proliferation of epithelium, upon which the
spores of the cryptogam then germinate. Dissociated epithelial cells
become proliferated at the surface of the mucous membrane, between
which and upon which both free and agglutinated spores accumulate. From
these spores sprout out simple and ramified filaments in compartments
containing moving granular elements. (For the minute detailed anatomy
of these filaments and spores the reader is best referred to Robin's
work on _Vegetable Parasites_.)

It may suffice here to mention that the filaments are sharply-defined
tubercles, slightly amber-tinted, of a mean diameter of between four
and three millimeters, simple while immature and branched when fully
developed. These tubules are filled with link-like groups of elongated
cells in compartments, giving them an appearance of regular
constriction at the junctions of adjoining groups of cells. Surrounding
these tubules are groups of spheroid or slightly ovoid spores from five
to four millimeters in diameter. Each spore contains one or two
granules and a quantity of fine dust. This cryptogamic growth is
developed in the proliferated cells of epithelium. The filaments in
their further growth separate the epithelia, and even penetrate them.
Thence they penetrate the mucous membrane and the submucosa (Parrot).

The mucous membrane beneath the growth is red, smooth, and glistening.
Papillae are sometimes prominent. It is not excoriated unless the
growth has been removed with some violence, when, as noted, it may
bleed slightly. Duguet and Damaschino have recently encountered cases
associated with a special ulceration of one of the palatine folds; the
former in enteric fever, the latter in a primitive case. The growth is
quickly reproduced after removal--even within a few minutes when the
secretions are very acid.

The glossal mucous membrane is usually the tissue first involved, the
specks being more numerous at the tip and edges of the tongue than at
its central portion. The glands at the base of the tongue may become
invaded. From the tongue extension takes place to the lips, the cheeks,
the gums, and the palate, hard and soft. The growth is especially
prolific in the folds between lips and gums and between cheeks and
gums. Sometimes the parts mentioned become involved successively
without actual extension. In several recently reported instances
occurring during enteric fever,[8] the affection began on the soft
palate, tonsils, and pharynx, and then progressed anteriorly toward the
tongue, the cheeks, and the lips.

[Footnote 8: Duguet, _Soc. Med. des. Hop._, Mai 11, 1883; _Rev. mens._,
Juin 1, 1883, p. 187.]

{334} But there is no limitation of the disease to these structures.
The growth may cover the entire mucous membrane of the mouth. From the
mouth it may reach the lateral walls of the pharynx, and in rare
instances the posterior wall of the pharynx. The product is said to be
more adherent on the pharynx (Reubold) than in the mouth. From the
pharynx it may reach the epiglottis, and even the larynx (Lelut), in
which organ it has been seen upon the vocal bands (Parrot). It has
never been observed in the posterior nares or at the pharyngeal orifice
of the Eustachian tube. It flourishes best, therefore, upon squamous
epithelium. In infants much reduced, Parrot has seen ulceration in the
neighborhood of the pterygoid apophyses, but attributable to the
cachectic state of the child, and not to the disease in the mouth.

In many cases--in as large a proportion as two-thirds, according to
some observers--the oesophagus becomes invaded, either in irregular
longitudinal strips or in rings, in all instances (Simon) terminating a
little above the cardia. In exceptional cases the entire mucous surface
of the oesophagus may be covered with the product (Seux). It has been
seen in the stomach (Lelut, Valleix), and is even said to be developed
there (Parrot), presenting as little yellow projections, isolated or
contiguous, from the size of millet-seeds to that of peas, and usually
located along the curvatures, especially the smaller curvature and
cardia (Simon).

In instances still more rare it is found in the intestinal canal
(Seux), even at the anus (Bouchut, Robin), and thence upon the
genitalia. In a child thirteen days old, Parrot found it in the
pulmonary parenchyma at the summit of the right lung, where it had
probably been drawn by efforts of inspiration.

The nipple of the nurse often becomes covered with the growth (Gubler,
Robin, Trousseau, Simon).

SYMPTOMATOLOGY.--In infants the earliest symptom is distress during
nursing, the nipple being seized repeatedly, and as frequently released
with cries of pain and disappointment. This cry is hoarse when the
vocal bands are involved.

The constitutional symptoms depend upon the underlying malady, and may
of course vary with its character. Thus we may have the symptoms of
simple diarrhoea, gastro-enteritis, or entero-colitis on the one hand,
and of tuberculosis and other diseases elsewhere enumerated on the
other. Cachectic children, especially in asylum and hospital practice,
lose flesh, and their skins become harsh, dry, and inelastic from loss
of fluids (Meigs and Pepper). The genitalia, the anus, and the adjacent
parts become eroded by the acridity of the discharges, and then become
covered with the growth.

The disease rarely lasts longer than eight days in strong children that
can be well cared for. It may continue indefinitely, on the other hand,
in cachectic children; that is to say, for several months or until the
patient succumbs, as may be. Death occurs usually from the causal
disease, and not as a result of the morbid condition of the mouth.

DIAGNOSIS.--In the Infant.--Examination of its mouth to detect the
cause of the child's inability to nurse reveals congestion of the
mucous membrane, intense and often livid in severe cases. It is first
noticed at the extremity of the tongue. When the congestion is general
it is darkest in the tongue. This livid congestion may extend over the
entire {335} visible mucous membrane, save upon the hard palate, where
it is tightly adherent to the periosteum, and upon the gums, where it
is rendered tense by the approach of erupting teeth. The papillae at
the tip and sides of the tongue are very prominent. Sometimes the organ
is quite dry, even sanious, while it is painful to the touch. The
reaction of the secretions of the mouth is acid instead of alkaline,
and the parts are hot and very sensitive.

Two or three days later the circular milky-white or curdy spots or
slightly prominent and irregularly-shaped flakes or patches may be seen
on the upper surface of the tongue toward the tip and inside the lips
and the cheeks, especially in the grooves connecting gums and lips and
gums and cheeks. The surrounding mucous membrane is unaltered in mild
cases, and there is no evidence of other local disorder or of any
constitutional involvement. In severe cases the entire mucous membrane
is dry and deeply congested.

The affection can be positively discriminated from all others by
microscopic examination of the deposit, which reveals the presence of
the cryptogam described.

TREATMENT.--In infants, artificial nourishment, whether with milk of
the lower animals or prepared food of whatever composition, should be
given up, if possible, and a wet-nurse be supplied. If this procedure
be impracticable, the least objectionable mode of preparation of cow's
milk should be employed (and this will vary with the practice of the
physician), and the utmost circumspection should be maintained in
securing the cleanliness of the vessels in which it is prepared, the
bottle from which it is given, and the nipple which is placed in the
child's mouth. Should the sugar and casein in the milk appear to keep
up the disease, weak soups may be substituted for the milk diet until
it has subsided. Weiderhofer advises artificial nourishment, by way of
a funnel inserted in the nasal passages, in case the child should
refuse to swallow. Deglutition is excited in a reflex manner when the
milk or other fluid reaches the pharynx.[9]

[Footnote 9: _Journ. de Med. Bordeaux_, Juin 10, 1883.]

The local treatment should consist in careful removal of the patches
from time to time--say every two or three hours--with a moistened soft
rag. This must be done without roughness of manipulation. In addition
to this, the parts may be washed or painted every hour or so with an
alkaline solution for the purpose of neutralizing the acidity of the
fluids of the mouth. For this purpose borax is most generally used, in
the proportion of twenty grains to the ounce of water or the half ounce
of glycerin. Sodium bicarbonate or sodium salicylate may be substituted
for the sodium borate. The use of honey in connection with the drug is
calculated to promote acidity by fermentation of its glucose, and is
therefore, theoretically, contraindicated.

Adults may use washes, gargles, or sprays of solutions of sodium borate
or of sodium bicarbonate.

The constitutional treatment in each case must be adapted to the nature
of the underlying malady which has favored the local disease, with
resort in addition to the use of quinia, iron, wine, spirit, and
beef-essence. The hygienic surroundings should be made as sanitary as
possible.


{336} Stomatitis Ulcerosa.

DEFINITION.--Inflammation of the interior of the mouth, usually
unilateral, eventuating in multiple ulcerations of the mucous membrane.

SYNONYMS.--Fetid stomatitis, Phlegmonous stomatitis, Putrid sore mouth,
Stomacace, are synonymous terms for idiopathic ulcerous stomatitis.
Ulcero-membranous stomatitis, Mercurial stomatitis (Vogel), are
synonymous terms for the deuteropathic variety of the disease.

ETIOLOGY.--The principal predisposing cause of the disease is to be
found in ochlesis; the contaminating atmosphere of crowded dwellings
and apartments insufficiently ventilated; uncleanliness; insufficiency
of proper clothing; unhealthy food, and the like. It prevails
epidemically in crowded tenements, schools, prisons, asylums, and
hospitals; in garrisons and in camps; in transports and men-of-war. It
is often propagated by contagion, but whether by infection or actual
inoculation seems undetermined. Measles is an active predisposing
cause. Feeble individuals are the most liable to the disease. It occurs
at all ages. In civil life it is most frequent between the ages of four
and ten years. Sometimes more girls are affected than boys (Meigs), and
sometimes it is the more prevalent among boys (Squarrey). Autumn is the
season of greatest prevalence.

Carious teeth, fracture and necrosis of the jaw (Meigs), and protracted
catarrhal stomatitis are among the chief exciting causes. Irregular
dentition is sometimes the exciting cause; and this may occur at the
first and second dentition or at the period of eruption of the last
molars.

PATHOLOGY.--The anatomical lesion is the destructive inflammation of
portions of the mucous membrane of the mouth, leaving ulceration on
detachment of the eschars. It usually commences as a gingivitis. At two
periods of life--namely, from the fourth to the eighth year of life,
and from the eighteenth to the twenty-fifth year--it is apt to be
ulcero-membranous, a condition asserted to be altogether exceptional at
other periods (Chauffard).

A diffuse fibro-purulent infiltration of the lymph-spaces of the mucosa
is regarded as the first step in the pathological process. This
infiltration is sufficiently abundant to compress the capillary vessels
of the tissues, and thus arrest the circulation (Cornil et Ranvier).
All those localized portions of mucous membrane from which the
circulation is cut off perish and are discharged in fragments. The
ulcers thus left are grayish, granular, and sanious, with thin,
irregularly dentated borders a little undermined, through which pus can
be expressed on pressure. The usual cryptogams of the oral cavity, in
various stages of development, are in great abundance in the grayish
detritus, which likewise contains altered red and white
blood-corpuscles.

According to some observers (Caffort, Bergeron), the first evidence of
the disease is an intensely congested erythematous patch, upon which
one or more pustules present, point, and rupture promptly, leaving the
characteristic ulcerations.

For some indeterminate reason, the ulcerations are mostly unilateral,
and occur much the more frequently on the left side. The principal
{337} primal points of ulceration are upon the external borders of the
gums, more frequently those of the lower jaw, and upon the
corresponding surface of the cheek and lip--the cheek much oftener than
the lip. Thence ulceration may extend to the tongue, less frequently to
the palate. The ulcerative process follows the outline of the gums,
baring the bases of the teeth to a variable extent, so that they seem
elongated. On the cheek the patch of inflammation is generally oval,
the longest diameter being antero-posterior, and the most frequent
position is opposite to the last molar.

Each ulcer is surrounded by an intensely red areola, beyond which the
tissues are succulent and tumid from collateral inflammatory oedema,
often giving the ulcers an appearance of great depth; but when the
detritus is discharged they are seen to have been superficial.
Detachment of the necrosed segments of mucous membrane takes place by
gradual exfoliation from periphery to centre. Sometimes detachment
occurs in mass, usually in consequence of friction or suction. The
ulcers, gingival and buccal, bleed easily when disturbed. They may
remain separate, or may coalesce by confluence of interposing
ulcerations extending across the furrow between gum and cheek or lip.
The adjoining side of the tongue sometimes undergoes similar ulceration
from behind forward, inoculated, most likely, by contact with adjoining
ulceration. In rare instances, neglected cases most probably, the
ulceration may extend to the palatine folds, the tonsils, and the soft
palate.

SYMPTOMATOLOGY.--The affection usually begins without any
constitutional symptoms. Young infants sometimes present slight febrile
symptoms, with impairment of appetite and general languor. Fetid
breath, salivation, and difficulty in deglutition are usually the first
manifestations of the disease to attract attention. The mouth will be
found to be hot, painful, and sensitive to the contact of food. Infants
often refuse food altogether, though usually they can be coaxed to take
liquid aliment. Larger children and adults complain of scalding
sensations. They find mastication painful, and cannot chew at all on
the affected side. The salivation is excessive, the saliva bloody and
often extremely fetid. When swallowed, this fetid saliva causes
diarrhoea. The cheeks sometimes become swollen, and the submaxillary
connective tissue oedematous. Adenitis takes place in the submaxillary,
retro-maxillary, and sublingual glands of the affected side. Sometimes
the other side becomes affected likewise, but to a less extent. The
glands do not suppurate, but the adenitis may remain as a chronic
manifestation in scrofulous subjects.

The disease, left to itself, will often continue for a number of weeks,
or even months as may be, unmodified even by intercurrent maladies
(Bergeron). Long continuance may result in partial or complete
disruption of the teeth, or in local gangrene, or even in necrosis of
the alveoli (Damaschino). Properly managed, the ulcers become cleansed
of their detritus, and within a few days heal by granulation, their
position long remaining marked by delicate red cicatrices upon a hard
and thickened substratum. Repeated recurrences are sometimes observed.

DIAGNOSIS.--The appearances of the gums and adjoining structures
described under the head of Pathology establish the diagnosis. The
usually unilateral manifestation and the peculiar fetid odor
distinguish it from severe forms of catarrhal stomatitis. From cancrum
oris it is {338} distinguished by the absence of induration of the skin
of the cheek over the swollen membrane, and by the succulence and
diffuseness of the tumefaction. From mercurial stomatitis it is
discriminated by the history, and by the absence of the peculiar
manifestations to be discussed under the head of that disease.

PROGNOSIS.--The prognosis is good, the disease being susceptible of
cure in from eight to ten days in ordinary cases. When due nutrition is
prevented by the pain in mastication and deglutition, and in
much-reduced subjects, the disease may continue for several weeks. It
is in these cases that detachment of the teeth takes place, with
periostitis and necrosis of the alveoli. Protracted suppuration and
failure in nutrition may lead to a fatal result, but such a termination
is uncommon.

TREATMENT.--Fresh air, unirritating and easily digestible food, the
best hygienic surroundings practicable, attention to secretions from
skin and bowels by moderate and judicious use of ablutions,
diaphoretics, and laxatives, with the internal administration of
cinchona or its derivatives, with iron and cod-liver oil, comprise the
indications for constitutional treatment.

Locally, demulcent mouth-washes are called for, containing astringents,
detergents, or antiseptics. Acidulated washes are more agreeable in
some instances. For antiseptic purposes, however, sprays and douches
may be used of solutions of potassium permanganate, boric acid,
carbolic acid, or salicylic acid. Gargles of potassium chlorate, ten or
twenty grains to the ounce, are highly recommended, as well as the
internal administration of the same salt in doses of from two to five
grains three times a day for children, and of ten to twenty grains for
adults.

If the sores are slow to heal, the ulcerated surfaces may be touched
once or twice daily with some astringent, such as solution of silver
nitrate (ten grains to the ounce), or, if that be objectionable, with
alum, tincture of iodine, or iodoform.

Prompt extraction of loose teeth and of loose fragments of necrosed
bone is requisite.


Stomatitis Gangrenosa.

DEFINITION.--A non-contagious, deuteropathic inflammation of the
interior of the mouth, almost invariably unilateral, and characterized
by a peculiar gangrenous destruction of all the tissues of the cheek
from within outward.

SYNONYMS.--Gangrenous stomatitis; Gangrena oris; Grangrenopsis; Cancrum
oris; Stomato-necrosis; Necrosis infantilis; Gangrene of the mouth;
Gangrenous erosion of the cheek; Noma; Buccal anthrax; Aquatic cancer;
Water cancer; Scorbutic cancer; Sloughing phagedaena of the mouth.

HISTORY.--The most important work upon the subject was published in
1828, from the pen of Dr. A. L. Richter,[10] whose accurate historical
account of the disease was in great part reproduced, with additions
thereto, by Barthez and Rilliet in their _Treatise on the Diseases of
Infants_, Paris, 1843, and quoted by nearly all subsequent writers on
the {339} theme. From these records it appears that the first accurate
description of the affection was given in 1620 by Dr. Battus, a Dutch
physician, in his _Manual of Surgery_. The term aquatic cancer,
_water-kanker_, bestowed on it by van de Voorde, has been generally
followed by the physicians of Holland, although van Swieten (1699)
properly designated it as gangrene. J. van Lil termed it noma, as well
as stomacace and water-kanker, and cited a number of Dutch physicians
who had observed its epidemic prevalence. The majority of more recent
observers, however, deny its epidemic character.

[Footnote 10: _Der Wasserkrebs der Kinder_, Berlin, 1828; further,
_Beitrag zur Lehre vom Wasserkrebs_, Berlin, 1832; _Bemerkungen uber
den Brand der Kinder_, Berlin, 1834.]

Of Swedish writers, Lund described it as gangrene of the mouth; Leutin,
under the name of ulocace. In England, Boot was the first to write of
gangrene of the mouth, and was followed by Underwood, Symmonds,
Pearson, S. Cooper, West, and others.

In France it has received great attention. Berthe[11] described it as
gangrenous scorbutis of the gums; Sauvages (1816) as necrosis
infantilis. Baron in 1816 published[12] a short but excellent account
of a gangrenous affection of the mouth peculiar to children; and Isnard
presented in 1818 his inaugural thesis on a gangrenous affection
peculiar to children, in which he described, simultaneously, gangrene
of the mouth and gangrene of the vulva. Then followed Rey, Destrees
(1821), Billard (1833), Murdoch, Taupin (1839), and others, until we
reach the admirable description by Barthez et Rilliet, from which the
present historical record has been chiefly abstracted.

[Footnote 11: _Memoires de l'Academie royale de Chirurgie_, Paris,
1774, t. v. p. 381.]

[Footnote 12: _Bulletins de la Faculte de Medecine de Paris_, 1816, t.
v. p. 161.]

German physicians likewise have largely studied the subject. De Hilden,
A. G. Richter, C. F. Fischer, Seibert, and many others preceded A. L.
Richter, whose important contribution to the literature and description
of the disease has been so highly extolled by Barthez and Rilliet.

In America the disease has been best described by Coates, Gerhard, and
Meigs and Pepper, all of Philadelphia.

(For extensive bibliographies the following sources should be consulted
in addition to those cited: J. Tourdes, _Du Noma ou du Sphacele de la
Bouche chez les Enfants_, These, Strasbourg, 1848: A. Le Dentu,
_Nouveau Dictionnaire de Medecine et de Chirurgie pratique_, article
"Face," Paris, 1871.)

ETIOLOGY.--Almost exclusively a disease of childhood, gangrenous
stomatitis is exceedingly rare in private practice, and very infrequent
at the present day even in hospital and dispensary practice. Lack of
hygienic essentials of various kinds, impoverishment, long illnesses,
and debilitating maladies in general are the predisposing causes. It is
sometimes endemic in hospitals and public institutions, but rarely, if
at all, epidemic. It is not generally deemed contagious, though so
considered by some writers. It appears to have been more frequent in
Holland than elsewhere, to be more frequent in Europe generally than in
the United States, and now much less frequent in the United States than
formerly. To recognition of the predisposing causes and to their
abolition and avoidance may probably be attributed its diminished
frequency all over the world. Though attacking children only as a rule,
it has been observed in adults (Barthez et Rilliet, Tourdes, Vogel).
Nurslings are not liable to the disease. Though occurring occasionally
earlier in life, the greatest period of prevalence is {340} from the
third to the fifth or sixth year of age, and thence, with diminishing
frequency, to the twelfth and thirteenth years. It is probably equally
frequent in the two sexes, though the majority of authors have
described it as more frequent in females.

Healthy children are not attacked. Even in delicate children it is so
rarely idiopathic that this character is utterly denied it by many
observers. The disease which it follows, or with which it becomes
associated, may be acute or chronic. According to most writers, it
occurs with greatest frequency after measles. It follows scarlatina and
variola much less often. It is observed likewise after whooping cough,
typhus fever, malarial fever, entero-colitis, pneumonitis, and
tuberculosis. Excessive administration of mercury has been recognized
as an exciting cause, some cases of mercurial stomatitis progressing to
gangrene.

According to Barthez et Rilliet, acute pulmonary diseases, and
especially pneumonia, are the most frequent concomitant affections, and
are usually consecutive.

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--The disease usually becoming manifested during other
disease, acute or chronic, or during convalescence therefrom, there are
no special constitutional symptoms indicating its onset. Hence
considerable progress may be made before its detection. The earliest
local characteristic symptom distinguishing gangrenous stomatitis is a
tense tumefaction of one cheek, usually in proximity to the mouth. The
lower lip is generally involved, thus rendering it a matter of
difficulty to open the mouth. This tumefaction in some instances
progresses over the entire side of the face up to the nose, the lower
eyelid, and even out to the ear in one direction, and down to the chin,
and even to the neck, in the other. Before the parts become swollen
externally, ulceration will have taken place to some extent in the
mucous membrane, but usually without having attracted special
attention, the subjective symptoms having been slight. A gangrenous
odor from the mouth, however, is almost always constant. Its presence,
therefore, should lead to careful investigation as to its seat and
cause. The gums opposite the internal ulcer become similarly affected
in most instances, and undergo destruction, so that the teeth may
become denuded and loosened, and even detached, exposing their alveoli.
The bodies of the maxillary bones suffer in addition in some instances,
and undergo partial necrosis and exfoliation.

It is maintained (Loschner, Henoch) that in some instances there is no
involvement of the mucous membrane until the ulcerative process has
reached it from the exterior.

The tumefied portions of the check and lip are pale, hard, unctuous,
and glistening. They are rarely very painful, and often painless. On
palpation a hard and rounded nodule one or two centimeters in diameter
can be detected deep in the central portion of the swollen cheek.

From the third to the sixth day a small, black, dry eschar, circular or
oval, becomes formed at the most prominent and most livid portion of
the swelling, whether cheek or lip. This gradually extends in
circumference for a few days or for a fortnight, sometimes taking in
almost the entire side of the face or even extending down to the neck.
As it enlarges the tissues around become circumscribed with a zone
intensely red. The internal eschar extends equally with the external
one. Eventually, the {341} eschar separates, in part or in whole, and
becomes detached, leaving a hole in the cheek through which are seen
the loosened teeth and their denuded and blackened sockets.

During this time the patient's strength remains tolerably well
maintained, as a rule, until the gangrene has become well advanced.
Intelligence usually remains good. Many children sit up in bed and
manifest interest in their surroundings. Others lie indifferent to
efforts made for their amusement. Some exhibit insomnia and delirium.
The pulse is small and moderately frequent, rarely exceeding 120 beats
to the minute until near the fatal close, when it often becomes
imperceptible. Appetite is often well preserved, unless pneumonia or
other complications supervene, but thirst is often intense, even though
the tongue remain moist. The desire for food sometimes continues until
within a few hours of death. Toward the last the skin becomes dry and
cold, diarrhoea sets in, emaciation proceeds rapidly, collapse ensues
and death.

Death usually occurs during the second week, often before the complete
detachment of the eschar--in many instances by pneumonia, pulmonary
gangrene, or entero-colitis. Some die in collapse, which is sometimes
preceded by convulsions. When the eschars have become detached,
suppuration exhausts the forces of the patient, and death takes place
by asthenia.

The complication most frequent is pneumonia, and the next
entero-colitis. Gangrene of the lungs, of the palate, pharynx, or
oesophagus, of the anus, and of the vulva, may supervene. Hemorrhage
from the facial artery or its branches has been noted as an exceptional
mode of death (Hueber), the rule being that the arteries in the
gangrenous area become plugged by thrombi, and thus prevent hemorrhage.

Recovery may take place before the local disease has penetrated the
cheek--indeed, while the mucous membrane alone is involved. In recent
instances, however, the disease does not subside until after the loss
of considerable portions of the cheek, and the child recovers with
great deformity, not only from loss of tissue in the cheek and nose,
but from adhesions between the jaws and the cheek.

PATHOLOGY AND MORBID ANATOMY.--Gangrenous stomatitis always involves
the cheek, almost always that portion in proximity to the mouth. It is
almost invariably unilateral. Either side seems to be equally liable.
Both sides suffer only, it is contended, when the gangrene is limited
in extent, confined to the mucous membrane, and occupies the sides of
the frenums of the lips (Barthez et Rilliet). It usually if not
invariably begins in the mucous membrane, as a phlyctenular
inflammation, which undergoes ulceration, followed by gangrene,
immediately or not for several days, and then becomes covered with a
more or less brownish-gray eschar. The ulceration of the mucous
membrane is occasionally preceded by an oedematous condition of the
cheek externally, similar to that sometimes observed in ordinary
ulcerous stomatitis; but this is not the characteristic circumscribed,
tense infiltration observed later. This ulceration is situated most
frequently opposite the junction of the upper and lower teeth.
Sometimes it proceeds from the gingivo-buccal sulcus of the lower jaw,
sometimes from the alveolar border of the gums. It extends in all
directions, and often reaches the lower lip. From three to sixteen days
may be consumed in these extensions. The {342} surrounding mucous
membrane becomes oedematous. The ulceration soon becomes followed by
gangrene, sometimes within twenty-four hours, sometimes not for two or
three days, and exceptionally not for several days. The ulcerated
surfaces bleed readily, change from gray to black, and become covered
with a semi-liquid or liquid putrescent detritus. They are sometimes
surrounded by a projecting livid areola, which soon becomes gangrenous
in its turn. The shreds of mortified membrane, though clinging a while
to the sound tissues, are easily detached, and often drop spontaneously
into the mouth. Meanwhile, there is abundant salivation, the products
of which pour from the mouth, at first sanguinolent, and subsequently
dark and putrescent and mixed with detritus of the tissues. Large
portions of the gums, and even of the mucous membrane of the palate,
may undergo destruction within a few (three to six) days. The
gangrenous destruction of the gums soon exposes the teeth, which become
loose and are sometimes spontaneously detached. Thence the periosteum
and bone become implicated and undergo partial denudation and necrosis,
and portions of necrosed bone become detached if the patient survives.
The characteristic implication of the exterior of the cheek becomes
manifest from the first to the third day, but occasionally not until a
day or two later. A hard, circumscribed swelling of the cheek or cheek
and lip occurs, sometimes preceded, as already intimated, by general
oedematous infiltration. The surface is tense and unctuous, often
discolored. In its central portion is an especially hard nucleus, one
to two centimeters or more in diameter. Gangrene often takes place at
this point from within outward at a period varying from the third to
the seventh day or later. The skin becomes livid, then black; a pustule
is formed at the summit of the swelling, which bursts and discloses a
blackened gangrenous eschar from less than a line in thickness to the
entire thickness of the cheek beneath. The area of gangrene gradually
extends. The dead tissues become detached, and a perforation is left
right through the cheek, through which are discharged saliva and
detritus. Meanwhile, the submaxillary glands become swollen and the
surrounding connective tissue becomes oedematous. In some instances,
however, no change is noticeable in these glands.

Examinations after death have shown that thrombosis exists for some
distance around the gangrenous mass. Hence the rarity of hemorrhage
during the detachment of the eschar.

DIAGNOSIS.--In the early stage of the disease the main point of
differential diagnosis rests in the locality of the primitive lesion,
the mucous membrane of the inside of one cheek. Subsequently there is
the gangrenous odor from the mouth; the rapid peripheric extension of
the local lesion, which acquires a peculiar grayish-black color; its
rapid extension toward the exterior of the cheek or lip; the
tumefaction of the cheek, discolored, greasy, hard, surrounded by
oedematous infiltration, and presenting a central nodule of especial
hardness; then the profuse salivation, soon sanguinolent, subsequently
purulent and mingled with detritus of the mortified tissues. Finally,
the eschar on the exterior of the swollen cheek or lip leaves no doubt
as to the character of the lesion. From malignant pustule it is
distinguished by not beginning on the exterior, as that lesion always
does (Baron).

PROGNOSIS.--The prognosis is bad unless the lesion be quite limited
{343} and complications absent. At least three-fourths of those
attacked perish; according to some authorities fully five-sixths die.
The objective symptoms of the local disease are much more important in
estimating the prognosis than are the constitutional manifestations,
the vigor of the patient, and the hygienic surroundings, although, as a
matter of course, the better these latter the more favorable the
prognosis. Prognosis would be more favorable in private practice than
in hospital or asylum service.

TREATMENT.--Active treatment is required, both locally and
constitutionally. Local treatment is of paramount importance, and alone
capable of arresting the extension of the process of mortification. The
topical measure in greatest repute is energetic cauterization with the
most powerful agents, chemical and mechanical--hydrochloric acid,
nitric acid, acid solution of mercuric nitrate, and the actual cautery,
whether hot iron, thermo-, or electric cautery. The application of
acids is usually made with a firm wad or piece of sponge upon a stick
or quill, care being taken to protect the healthy tissues as far as
practicable with a spoon or spatula. After the application the mouth is
to be thoroughly syringed with water to remove or dilute the
superfluous acid. Hydrochloric acid has been preferred by most
observers.

As these cauterizations must be energetic to prove effective,
anaesthesia ought to be induced. Should ether be employed for this
purpose, hydrochloric acid or the acid solution of mercuric nitrate
would be selected of course.

In the early stages these agents are to be applied to the inside of the
cheek, so as to destroy all the tissue diseased, if practicable, and
expose a healthy surface for granulation. Should the exterior of the
cheek become implicated before cauterization has been performed or in
spite of it, it is customary to destroy the tissues from the exterior,
including a zone of apparently healthy surrounding tissue. As the
gangrene extends, the cauterization is to be repeated twice daily or
even more frequently. After cauterization the parts are dressed with
antiseptic lotions, and antiseptic injections or douches are to be used
frequently during day and night to wash out the mouth and keep it as
clear as possible from detritus.

Meigs and Pepper report beneficial results from the topical use of
undiluted carbolic acid, followed by a solution of the same, one part
in fifty of water, frequently employed as a mouth-wash. The progress of
the sloughing was checked and the putridity of the unseparated dead
tissue completely destroyed in the two cases mentioned by them, one of
which recovered quickly without perforation of the cheek. Gerhard
preferred undiluted tincture of the chloride of iron; Condie, cupric
sulphate, thirty grains to the ounce. Bismuth subnitrate has recently
been lauded as a topical remedial agent.[13]

[Footnote 13: Maguire, _Medical Record N.Y._, Feb. 3, 1883.]

The mouth should be frequently cleansed by syringing, douching,
spraying, or washing with disinfectant solutions, such as chlorinated
soda liquor, one part to ten; carbolic acid, one to twenty. Lemon-juice
is sometimes an agreeable application, as in some other varieties of
stomatitis. Constitutionally, tonic and supporting treatment is
demanded, even in those instances where the appetite is well maintained
and the {344} general health apparently well conserved. Soups, milk,
semi-solid food, egg-nog, egg and wine, wine whey, milk punch,
finely-minced meat, should be administered as freely as the state of
the digestive functions will permit. If necessary, resort should be had
to nutritive enemata. Quinia and tincture of chloride of iron are the
medicines indicated. When sufficient alcohol cannot be given with the
food, it should be freely exhibited in the most available form by the
mouth or by the rectum. The apartment should be well ventilated, the
linen frequently changed, the discharges promptly removed.


Toxic Stomatitis.

DEFINITION.--An inflammation of the interior of the mouth due to
poisoning, especially by drugs, and chiefly by mercury, copper, and
phosphorus.


Mercurial Stomatitis.

DEFINITION.--An inflammation of the mucous membrane of the mouth,
eventually ulcerating, the result of systemic poisoning by the
absorption of mercury.

SYNONYMS.--Stomatitis mercurialis; Mercurial ptyalism, Ptyalismus
mercurialis; Mercurial salivation, Salivatio mercurialis.

ETIOLOGY--Predisposing and Exciting Causes.--Special vulnerability to
the toxic influence of mercury, and special proclivity to inflammatory
affections of the mouth and the organs contained therein, are the
predisposing causes of mercurial stomatitis. The exciting cause is the
absorption of mercury into the tissues of the organism. The
susceptibility of healthy adults is much greater than that of healthy
children. The susceptibility of adults varies very greatly.
Constitutions deteriorated by prolonged disease, undue exposure, and
the like are much more promptly influenced in consequence. Tuberculous
subjects do not bear mercury well.

Idiosyncratic susceptibility to toxaemia by mercurial preparations is
now and then encountered in practice, and instances have been
published[14] in which fatal results have ensued, after prolonged
suffering, from the incautious administration of a single moderate dose
of a mercurial drug.

[Footnote 14: For example, see in Watson's _Practice of Physic_ a case
of furious salivation following one administration of two grains of
calomel as a purgative, the patient dying at the end of two years, worn
out by the effects of the mercury and having lost portions of the
jaw-bone by necrosis.]

Until comparatively recent years the most common cause of mercurial
poisoning was the excessive employment of mercurial medicines, whether
by ingestion, inunction, or vapor bath. Topical cauterization with acid
solution of mercuric nitrate is likewise an infrequent, and usually an
accidental, cause of the affection. Elimination of the mercury by way
of the mucous glands of mouth and the salivary glands proper excites
the stomatitis in these instances. An entirely different series of
cases occur in artisans exposed to handling the metal and its
preparations or to breathing its vapor or its dust. In these instances
the poison may gain {345} entrance into the absorbent system by the
skin, the mucous membranes of the nose, mouth, and throat, the stomach,
or the lungs. No matter what care may be exercised in cleansing the
hands, it is often impossible to prevent occasional transference of the
noxious material from fingers to throat, or to thoroughly free the
finger-tips under the nails. The avocations entailing the risks of
mercurial stomatitis comprise quicksilver-mining, ore-separating,
barometer- and thermometer-making, gilding, hat-making, manufacturing
of chemicals, and exhausting the globes employed in certain forms of
electric illumination.[15] The slow absorption of mercury into the
bodies of artisans induces in addition serious constitutional nervous
disturbances--tremors, palsy, etc.

[Footnote 15: _Med. and Surg. Reporter_, Philada., Dec. 30, 1883, p.
734.]

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--The principal subjective symptoms of mercurial stomatitis
are--characteristic fetor of the breath, sore gums and mouth,
continuous nauseous metallic brassy or coppery taste, and profuse
salivation.

At first the mouth feels parched and painful, the gums tender, the
teeth, the lower incisors especially, set on edge. Soon the gums become
swollen, and when touched with the tongue seem to have receded from the
necks of the teeth, which thereby appear to be longer than usual. The
gums feel quite sore when pressed upon with the finger or when put on
the stretch by clashing the rows of teeth against each other. This sort
of soreness is often watched for in the therapeutic administration of
mercurials purposely given to "touch the gums," as an indication that
the system is under the influence of the drug. It is, therefore, one of
the earliest indications of mercurial poisoning, but if not sought for
it may elude attention until after the mouth has become sore a little
later. The pain in the mouth is augmented by efforts of mastication and
expectoration, and may be associated with pains at the angle of the
lower jaw or extending along the domain of the third or of the third
and second divisions of the distribution of the fifth cerebral nerve.
Mastication of solid food is often unendurable. Constitutional
manifestations become evident about this time in increased heat of
skin, acceleration of pulse, furred tongue, dry mouth, great thirst,
and loss of appetite. The dryness of the mouth does not last long, but
is soon followed by hypersalivation, one of the characteristic
phenomena of the disorder. The saliva secreted, often acid in reaction,
varies greatly in quantity, which is usually proportionate to the
severity of the case. It is secreted night and day, sometimes to the
amount of several pints in the twenty-four hours--in moderately severe
cases to the amount of from one to two pints in that space of time. It
is limpid or grayish, mawkish or somewhat fetid, and reacts readily to
the simplest tests for mercury. The salivation is almost continuous,
sometimes quite so. The patient soon becomes unable to endure the
fatigue of constant expectoration, and the fluid then dribbles from his
mouth or runs off in an unimpeded slobber. When excessive, the
patient's strength becomes rapidly exhausted--in part by impoverishment
of the fluids, in great measure from the lack of refreshing sleep.

Meanwhile, the local inflammatory process extends from the gums to the
floor of the mouth and to the lips, and thence to the tongue and the
{346} cheeks. The salivary glands are in a state of inflammation
likewise, but rather in consequence of direct irritation in the
elimination of the poison through their channels than by extension of
the stomatitis along their ducts. The lymphatic glands of the lower jaw
become engorged and tender. Mastication, deglutition, and articulation
all become impeded mechanically by tumefaction of the tissues.

In some instances the glossitis is so great that the tongue protrudes,
thereby impeding respiration and even threatening suffocation. In some
cases oedema of the larynx has been noted, threatening suffocation from
that cause. Should the inflammatory process extend along the pharynx to
the Eustachian tubes, deafness and pains in the ears will become
additional symptoms.

The subsequent progress of unarrested mercurial stomatitis is that of
ulcerous stomatitis.

Should gangrene of the mucous membrane take place, there will be great
fetor from the mouth, and some danger of hemorrhage on detachment of
the sloughs should the process be taking place in the direction of
vessels of some calibre. Necrosis of the inferior maxilla entails
continuance of the disagreeable local symptoms until the discharge in
fragments or in mass of the dead portions of bone.

In the earlier stages of the attack the constitutional symptoms may be
sthenic. Fever, cephalalgia, and the usual concomitants of pyrexia,
however, soon give way to the opposite condition of asthenia. Exhausted
by the excessive salivation, and unable to repair waste by eating or
sleeping, the sufferer soon passes into a condition of hopeless
cachexia. Those who survive remain cachectic and feeble for a long
time--some of them disfigured for life by various cicatrices between
cheeks and jaw, by loss of teeth or of portions of the jaw-bone.

The duration of mercurial stomatitis varies with the susceptibility of
the patient, the intensity of the toxaemia, and the character of the
treatment. Mild cases may get well in a week or two; severe cases may
continue for weeks, and even months; extreme cases have persisted for
years. Even moderate cases occasionally resist treatment for weeks.

Under the improved therapeutics of the present day mercurial stomatitis
almost always terminates in recovery, especially if it receive early
and prompt attention. Neglected or improperly managed, it may terminate
in serious losses of tissue in gums, cheeks, teeth, and bone, leaving
the parts much deformed and the patient in a permanently enfeebled
condition.

Erysipelas, metastatic abscesses, inflammations, pyaemia, or
colliquative diarrhoea may be mentioned as complications which may
prove sufficiently serious to produce death, independently of the
virulence of the primary stomatitis.

PATHOLOGY AND MORBID ANATOMY.--Mercurial stomatitis is an ulcerative
process attended with an excessive flow of saliva containing mercury.
It has a tendency to terminate in destruction and exfoliation of the
mucous membrane of the gums and other tissues attacked, and eventually
in necrosis of the jaw-bone. The detritus is found, microscopically, to
consist of granular masses of broken-down tissue, swarming with
bacteria and micrococci, and containing some blood-cells and many
pus-cells. In some instances micrococci have been detected in the
blood.

The disease usually begins in the gums of the lower incisors, and {347}
extends backward, often being confined to one side of the jaw. The
gums, first swollen and then livid, become separated from the necks of
the teeth. Their edges undergo ulceration. The ulcers are surrounded by
fungous margins, pale or red, which bleed on the slightest contact, and
some become covered with grayish-yellow detritus. The ulceration
extends in depth, destroying the supports of the teeth, so that they
become loosened and even detached. The inflammatory process extends to
the lips, the cheek, and the tongue, which undergo tumefaction and
exhibit the impressions of the teeth in grayish opalescent lines or
festoons of thickened epithelium at the points of pressure. The
glossitis may become intense. It is almost always present, to some
extent, as a superficial or mucous glossitis. Occasionally acute
oedematous glossitis has ensued, and such cases sometimes terminate
fatally. Ulceration takes place in these structures similar to that
which has taken place in the gums. If not arrested, gangrenous
destruction ensues, not only in these tissues, but beneath them. Thus,
the teeth become loosened, and even detached; the jaw-bones themselves
may become bared, necrosed, and in part exfoliated; and the cheeks
undergo partial destruction by gangrene. Sometimes the inflammation
descends to the larynx, and this may produce oedematous infiltration of
the loose connective tissue of that structure. Sometimes it mounts the
pharynx and reaches the orifices of the Eustachian tubes. The salivary
glands become swollen and discharge great quantities of fluid, as
detailed under Symptomatology. The retro-maxillary and submaxillary
lymphatic glands become enlarged by inflammatory action.

DIAGNOSIS.--In the earliest stages the inflammation of the gums in
mercurial stomatitis cannot be distinguished from that which takes
place in other forms of ulcerative stomatitis. The fetor of the breath,
however, the profuse salivation, and the chemical reaction of the
saliva, together with the history of exposure to mercury, soon place
the nature of the case beyond doubt. Similar results following
poisonings by copper salts and by phosphorus are differentiated by the
history of the special exposure.

PROGNOSIS.--In mild cases the prognosis is favorable, provided further
exposure to the cause can be avoided. This holds good almost invariably
in cases due to over-medication with mercurials, but is far less
applicable to cases in artisans, the result of prolonged exposure to
the poisonous influences of mercury and its slow absorption. On the
whole, the affection is much less serious than formerly, both because
it can, in great measure, be guarded against by proper prophylaxis in
risky vocations, and because its treatment has been made much more
efficient. In severe cases serious results may ensue despite the most
judicious treatment, and convalescence is usually very slow, weeks
often elapsing before solid food can be chewed without pain or without
injury to the gums.

When death ensues, it may be by asthenia, erysipelas, pneumonia,
pyaemia, or colliquative diarrhoea.

TREATMENT.--Mercurial stomatitis may sometimes be prevented by the
administration of potassium chlorate during exposure. Mild cases
following the administration of mercurials often subside upon mere
withdrawal of the drug. Should spontaneous subsidence not take place,
the administration of potassium chlorate every few hours, in doses of
{348} from thirty to sixty grains or more in the twenty-four hours,
soon effects amelioration, which promptly terminates in recovery. The
characteristic fetor often ceases within twelve hours' use of this
drug. Should the inflammatory manifestations be severe, a few leeches
applied beneath the edge of the lower jaw, followed by a poultice
enveloping the neck to promote further flow of blood, often affords
prompt relief (Watson). Lead acetate (ten grains to the ounce of water)
and iodine (half a fluidrachm of the compound tincture to the ounce of
water) are useful as gargles and washes. When the result of slow
poisoning, elimination of the mercury by sulphur vapor baths and the
administration of small doses of potassium iodide are recommended.

Cauterization of the ulcerated surfaces is sometimes serviceable,
silver nitrate or hydrochloric acid (Ricord), or chromic acid 1:5
(Butlin, Canquil), being used for the purpose.

Opium in decided doses is indicated for the relief of pain. It may be
added with advantage to detergent and disinfective mouth-washes
(potassium chlorate, sodium borate, creasote-water, saponified emulsion
of coal-tar, tincture of cinchona, tincture of myrrh, etc.), the use of
which should form an important part of the treatment. Watson highly
recommended a wash of gargle of brandy and water, 1:4 or 5. In severe
cases difficulty is encountered in maintaining effective alimentation.
When mastication is not impracticable, soft-boiled egg and
finely-chopped raw beef may be given. When the patient cannot chew at
all, resort is confined to milk, soups, and the juice of beef.
Nourishing enemata should be administered, as in all affections where
it becomes impracticable to sustain the patient by way of the mouth.
Tonics and stimulants are indicated to avoid debility from the
excessive salivation and its sequelae--quinia, coffee, wine, and
alcohol, the first, if required, by hypodermatic injection, all of them
by enema if necessary.

Glossitis and oedema of the larynx may require the surgical procedures
often necessary when they occur under other circumstances.

Other forms of toxic stomatitis hardly require special elucidation.


Abnormalities and Vices of Conformation of the Tongue.

Apart from the anomalies presented in monsters, there are a few
congenital abnormalities of the tongue with which it becomes the
accoucheur at least to be familiar, as their presence may interfere
materially with the nutrition of the infant, whether nursed or
spoon-fed.

CONGENITAL DEFICIENCY OF THE TONGUE.--A considerable portion of the
tongue may be wanting anteriorly, comprising, in some instances, the
entire free portion of the organ. The stump then presents as a single
or a bifid protuberance of variable size. In some instances
considerable power of movement exists, and even conservation of taste.
Suction and deglutition are both practicable. When the child grows it
can speak, though with a certain amount of difficulty. A few cases are
on record, however, of ability to speak without any evidence of a
tongue above the floor of the mouth.

An instance of lateral deficiency has been observed by Chollet,[16] the
{349} deficient half being represented merely by the two layers of the
lingual mucous membrane, without any intervening muscular substance.

[Footnote 16: Demarquay, _Dict. de Med. et de Chir. prat._, xx. p.
130.]

BIFID TONGUE, separate investment of the two sides, has been
occasionally observed in connection with similar arrest of development
in the lower jaw and other organs.


Ankyloglossia.

DEFINITION.--An abnormal attachment or adhesion of some portion of the
tongue to some portion of the surrounding structures of the mouth.

SYNONYM.--Tongue-tie.

PATHOLOGY AND MORBID ANATOMY.--The ordinary form of tongue-tie consists
in an abnormal development of the frenum of the tongue, the anterior
vertical portion of the duplicature of mucous membrane which connects
the lower surface of the raphe of the tongue with the floor of the
mouth. The tongue cannot be extended beyond the lips. Suction is
interfered with in some cases. If not remedied spontaneously or by
surgical interference, mastication and articulation may become
seriously impeded.

Other forms of ankyloglossia, congenital and acquired, possess special
interest from surgical points of view mainly.

DIAGNOSIS.--Inspection and digital exploration readily reveal the
nature of the restriction in the movements of the tongue and the size
of the frenum.

PROGNOSIS.--The prognosis is good, the difficulty being susceptible of
relief by division of a portion of the constricting frenum. Accidents
have been reported following the operation, the occasional occurrence
of which should be borne in mind. These are hemorrhage, which is not
dangerous except in the prolonged absence of some one competent to
restrain it should it be extreme; and retroversion of the tongue, an
accident which has been known to prove fatal by occluding the orifice
of the larynx (Petit).

TREATMENT.--Slight cases rarely need operation; but when the movements
of the tongue are restricted by a very short and deep frenum its
division becomes necessary. The operation is usually performed with
scissors, the ranine arteries being protected by means of a fissured
plate of metal (Petit), such as has long been used as a handle to the
ordinary grooved director of the physician's pocket-case. The cut
should be more extensive in the lateral directions of the fold than
antero-posteriorly. After-treatment is rarely necessary, unless
annoying hemorrhage is produced by movements of suction. Compression
between the fingers, maintained for a number of minutes, suffices to
restrain the hemorrhage in most instances. When this fails, recourse
may be had to cauterization with the point of a heated iron or some
other form of actual cautery.


Macroglossia.

DEFINITION.--Hypertrophy of the tongue.

SYNONYMS.--Megaloglossia, Glossoptosis, Prolapsus linguae, Lingua {350}
propendula, Chronic prolapse of the tongue, Chronic intumescence of the
tongue.

HISTORY.--This rare affection has been long known, the first cases on
record being in the works of Galen. Other cases have been recorded by
Celsus and Avicenna. Among more modern recorders may be mentioned
Scaliger (1570), Bartholin (1680), Benedict and Pencer; among recent
recorders, Lassus,[17] Percy,[18] Harris,[19] Humphrey,[20]
Gayraud,[21] W. Fairlie Clarke,[22] Bryant,[23] and the French
dictionaries in present process of publication; to all of which the
reader is referred for bibliographic, descriptive, and illustrative
details.

[Footnote 17: _Memoire de l'Institut National_, 18--, an VI. t. i.]

[Footnote 18: _Dict. Sci. Med._, t. xxvii.]

[Footnote 19: _Am. Journ. Med. Sci._, vol. vii., 1830, p. 17; vol. xx.,
1837, p. 15--both illustrated.]

[Footnote 20: _Trans. Med.-Chir. Soc. London_, 1853, p. 113.]

[Footnote 21: _These de Montpellier_, No. 68, 1865.]

[Footnote 22: _Diseases of the Tongue_, London, 1873.]

[Footnote 23: "Surgical Affections of the Tongue," _Guy's Hosp.
Reports_, 1883, p. 102 _et seq._]

ETIOLOGY.--This affection is usually congenital, at least to a certain
extent, and augments with the growth of the child. It has been
attributed, on apparently insufficient grounds, to injury received
during parturition. It is probably intra-uterine in origin. Though
encountered in both sexes, the majority of recorded cases have been in
females. In summing up these observations, it appears that the
affection often attracts little or no attention until dentition is in
progress. The hypertrophy begins to augment rapidly during the second
or third year of age, or a year or two later in some cases.

The gradual increase of the congenital deformity during infancy has
been attributed to hypernutrition from local irritation produced by
habits of sucking on the organ, induced, in some subjects, by forcible
efforts at suction from a short nipple. Similarly, the rapid
augmentation of volume noted as occurring during the period of
dentition or a little later has been attributed to hypernutrition
excited by irritation suffered by the protruding organ from the lower
row of teeth. Cases commencing at this age have been supposed to be due
exclusively to tongue-sucking. In some instances, due to this cause
apparently, the deformity is associated with idiocy (Lawson[24]).
Convulsions, epileptic seizures, and whooping cough have been regarded
by some writers as occasional causes of the deformity. Indeed, idiocy
and cretinism are not infrequent co-associates with the deformity
(Parrot[25]). It has been observed likewise in anencephalous monsters
(Brissot, _idem_).

[Footnote 24: _Trans. Clin. Soc. London_, vol. v. p. 158.]

[Footnote 25: _Gaz. Med. Paris_, Dec. 10 and 17, 1881; _Lond. Med.
Record_, Mar. 15, 1882, p. 113.]

SYMPTOMS, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--The prominent symptom of macroglossia is the enlarged tongue
protruding beyond the mouth. The resemblance of the protruding tongue
of a child with macroglossia to the tongue hanging from the mouth of a
calf gave rise to the name lingua vitulina by which it has sometimes
been designated. In some instances, where the enlargement is but
moderate, the organ can be retained within the mouth. When bilateral,
the enlargement may be symmetrical, or may interest one side of the
tongue more than the other. When the enlargement is confined to the
free portion of the tongue, it interferes little with respiration and
with movements of suction. When occupying the base of the organ, it may
seriously embarrass respiration, and even produce suffocation in {351}
some instances (Clarke). The mouth being maintained open, saliva
dribbles away constantly except during alimentation. Thirst is often
very great in consequence of this, and of the desiccation of the tongue
and of the walls of the mouth by the unmodified air to which they are
continuously exposed. The tongue is usually free from pain.

In some subjects, although the tongue, left to itself, protruded
considerably, it has been found quite practicable to maintain it within
the cavity of the mouth by means of bandages or other appliances
secured to the back and top of the head. These bandages are removed
from time to time to give relief from the restraint and to permit food
and drink to be taken. Systematic compression, indeed, has been induced
in this way in some instances, and has produced considerable diminution
in the size of the organ--sufficient to maintain its concealment
without the aid of an appliance. When the tongue cannot be retained
within the mouth the patient becomes unable to close the jaws. Hence
saliva dribbles constantly, save when food or drink is being taken. The
protruded portion of the tongue undergoes a livid discoloration,
sometimes diffuse, sometimes disseminated. Though sometimes remaining
comparatively soft in texture, it usually becomes hard, dry, rough,
fissured, ulcerated and sanious, covered with desiccating layers of
mucus and epithelium, and marked by indentations made by the edges of
the teeth, which sometimes seem almost to strangle it. Mastication,
deglutition, and articulation often become very difficult, and
respiration also, but less frequently. The lower lip becomes much
everted. The larynx and hyoid bone become drawn upward and forward by
the weight of the organ. The configuration of the lower jaw undergoes
considerable change, and the teeth become pressed out of position.
Dislocation of the jaw from this cause has been noticed (Chalk[26]).

[Footnote 26: _Trans. Path. Soc. London_, vol. viii. p. 305.]

These symptoms undergo aggravation with the growth of the subject, and,
while presenting general features of resemblance in all cases, vary
considerably in individual instances. Great difficulty is encountered,
as a rule, in taking food, and mastication has to be performed very
slowly. In some instances mastication can be performed satisfactorily
by the molars, owing to a compensatory curvature of the lower jaw, even
though the anterior portions of the jaw may remain permanently
separated (Harris). Some patients get along by using their fingers to
push the bolus far {352} enough back to permit of its deglutition. Some
have used a cup with a long tube slightly curved to convey fluids to
the back part of the mouth for a similar purpose. Some have been
systematically fed by means of a catheter passed through a nasal
passage and thus on into the oesophagus. The difficulties in nourishing
patients reduce some of them to extreme emaciation.

Notwithstanding all these drawbacks, quite a number of cases are on
record where the patients have reached well into adult life before
being submitted to radical measures for relief. One patient is recorded
as having reached the age of eighty, having worn for some sixty-five
years a silver shield to conceal her deformity (Clarke).

PATHOLOGY AND PATHOLOGICAL ANATOMY.--The hypertrophy may involve all
the structures of the tongue, but usually implicates the muscular
tissue especially (Sedillot, Paget, Bouisson). In a case published by
W. Fairlie Clarke it was found on microscopic examination that the
papillae as well as the mucous and submucous tissues were somewhat
enlarged and thickened, while the bundles of muscular fibre were
slightly coarser than natural. Maas reports a unilateral case of
macroglossia in a male child two months of age associated with
hyperdevelopment of the entire left side of the body.[27] In some
instances the blood-vessels and lymphatics are chiefly involved
(Virchow, Billroth, Maas), two cases of which have been described by
Virchow as cavernous lymphatic tumors.

[Footnote 27: _Arch. klin. Chir._, p. 413, Bd. xiii. Heft 3.]

Hilliard reports[28] a congenital case from vicious growth, removed at
fourteen months of age. Microscopic sections showed the large lacunae
filled with corpuscles, blood-pigment in different stages of
degeneration, {353} and the papillae much hypertrophied. Winiwarter[29]
reports a congenital macroglossia associated with congenital cysts of
the neck.

[Footnote 28: _Brit. Med. Journ._, Nov. 26, 1870, p. 591.]

[Footnote 29: _Arch. klin. Chir._, 1874, Bd. xvi. Heft 3.]

Sometimes there is very little true muscular hypertrophy, as in a case
quoted by Bryant which was presented to the Pathological Society of
London in 1872 by M. H. Arnott. In this specimen the epithelial
covering was very thick and the papillae enlarged. The blood-vessels
were larger than usual, and there were large irregular spaces,
thin-walled and filled with blood or clear fluid. "A few vesicular
bodies which may have been enlarged lymphatics were also
present"--probably cross-sections of lymphatic vessels.

The size that may be attained even in young children seems incredible,
three and four inches protruding from the mouth in some instances. The
free portion is more bulky than the intra-oral portion. One case
reported "as thick as an arm" probably refers to the arm of the child.
As a rule, both sides of the tongue are involved; exceptionally, the
affection is unilateral.

In most instances the hypertrophy occupied the free portion of the
tongue chiefly, the base of the organ having been implicated in but a
few.

[Illustration: FIG. 14. Chronic Intumescence of the Tongue (Harris).]

[Illustration: FIG. 15. Hypertrophy of the Tongue (Harris), before
operation and after. A, odontolith.]

DIAGNOSIS.--The presence of the tongue outside of the mouth speaks for
itself (Figs. 14 and 15). The age of the patient, usually a young
child, the history of the case if it present in the adult, suffice to
differentiate macroglossia from the tumefaction of glossitis on the one
hand and from certain protruding tumors and malignant diseases on the
other. Hypertrophy of the tongue following chronic glossitis,
syphilitic or non-specific, must not be confounded with the congenital
or idiopathic affection under consideration.

PROGNOSIS.--The prognosis is good as to relief from the deformity,
provided the patient is submitted to surgical interference, and the
prognosis of the operation depends upon the procedure selected.
Sometimes additional operations are requisite to remedy the defects the
lower jaw has sustained by prolonged depression. In comparatively young
adults restoration of its position, configuration, and function seems
likely to result spontaneously after the protruding portion of the
tongue has been removed.

TREATMENT.--It has been maintained (Lassus) that the hypertrophy can be
overcome by systematic compression of the tongue, by leeching the
tongue, bandaging or strapping it, and forcibly maintaining it in the
mouth by suitable retentive appliances. While it has been admitted that
this plan may prove successful in cases of moderate enlargement of but
few years' duration and unaccompanied with change in the shape of the
lower jaw, the experience of more recent observers has been recorded as
unfavorable, at least in pronounced cases. Clanny[30] succeeded in this
way with a child five years of age whose tongue protruded three inches.
This plan is said to be very painful and irritating. It requires close
watching on account of the difficulty of respiration which may ensue
from thus blocking up the pharynx. It has been advised as a useful and
sometimes an essential preliminary (Syme) to a radical procedure
consisting in the excision of a V-shaped segment. This latter operation
(Boyer) has been successfully performed by Howe, Harris, Humphry, Syme,
and others. {354} Frederici[31] extended the incisions to the very base
of the tongue. It has been performed both with knife and with scissors,
the cut surfaces being united with sutures after ligation or torsion of
the bleeding vessels. Re-enlargement ensued in one of Syme's cases
operated upon in this way,[32] and likewise in a case of Gies,[33]
requiring subsequent excision of the exuberant portions. Operations
with the ligature, though sometimes successful (Fergusson,[34]
Hodgson[35]), may be followed by fatal septicaemia during the slough
(Liston[36]), or, failing to strangulate the tongue sufficiently, may
require the application of the knife, after all, to affect the
separation (Harris[37]).

[Footnote 30: _Edinb. Med. and Surg. Journ._, 1805, vol. i., cited by
Clarke.]

[Footnote 31: _Arch. gen. de Med._, 1844; _Edinb. Med. and Surg.
Journ._, p. 528, vol. lxiv., 1845.]

[Footnote 32: _Edinb. Med. Journ._, 1857, vol. ii. p. 1057.]

[Footnote 33: _Arch. klin. Chir._, 1873, p. 640.]

[Footnote 34: _Practical Surgery_, London, 5th ed., p. 518.]

[Footnote 35: _Trans. Med.-Chir. Soc. London_, 1858, p. 129.]

[Footnote 36: _Elements of Surgery_, p. 334, Philada., 1842.]

[Footnote 37: _Am. Journ. Med. Sci._, vol. vii. p. 17.]

Excision with the incandescent loop of the galvano-cautery seems to be
the most suitable procedure. Valerani[38] operated in this manner
without the loss of a drop of blood upon a congenital macroglossia in a
child seven months of age. Maas[39] operated in this way on a child two
months of age. Fairlie Clarke, who removed a congenital macroglossia
with the ecraseur in a child five months of age, recommends operation
before dentition begins[40]--an opinion which appears to be justified
by the belief that the pressure of the teeth contributes to the
subsequent rapid enlargement of the organ. Nevertheless, the operation
may be undertaken at any age. Several of those already cited were
performed upon adults, and Stephen O'Sullivan[41] excised the
hypertrophied tongue of a female sixty-five years of age.

[Footnote 38: _Giornale della Reale Accademia di Turino_, fasc. 1518;
_London Med. Record_, Sept. 15, 1876, p. 408.]

[Footnote 39: _Loc. cit._]

[Footnote 40: _Lancet_, March 30, 1872, p. 432.]

[Footnote 41: _Dublin Journ. Med. Sci._, Aug., 1875, p. 178.]

Ignipuncture with the thermo-cautery of Paquelin has been successfully
used of late by Helferich and by von Bruns of Tubingen.[42] In the
latter instance the subject was five years of age. Fourteen punctures
were made from above downward at intervals of about one centimeter, and
five were made transversely. Not a drop of blood was lost. On the third
day secondary hemorrhage occurred from the intercommunication of three
of the punctures; this was restrained by ferric chloride, and the case
went on to a favorable conclusion. Surgical procedures must constitute
our sole therapeutic reliance. The temporary subsidence of enlargement
under the influence of mercury and the iodides seems sure to be
followed, sooner or later, by reproduction of the deformity. It is
therefore a waste of time to attempt cures by medication.

[Footnote 42: _Centbl. f. Chir._; _Med. Times and Gaz._, Sept. 23,
1883.]


Glossitis.

DEFINITION.--Inflammation of the tongue.

The term glossitis is usually applied to inflammation of the tissues of
the tongue as a whole (parenchymatous glossitis), and not to those
superficial inflammations which exist associated with the different
varieties of {355} stomatitis and with other affections, and which
implicate the mucous membrane and its glands and papillae only
(superficial glossitis). Superficial glossitis, however, sometimes
terminates in parenchymatous glossitis. Papillae and glands are usually
affected together in superficial glossitis. When the inflammation
predominates in the papillae the disease is often designated as
papillary glossitis; when in the glands, it is often termed follicular
glossitis. Superficial glossitis, again, is sometimes manifested by the
eruption of vesicles on the tongue, under which circumstance it is
often denominated vesicular glossitis, sometimes herpetic glossitis.
Glossitis is sometimes restricted to a portion of the tongue
(circumscribed glossitis), and it sometimes involves the whole of the
tongue (diffuse glossitis). Either form may be unilateral
(hemiglossitis), though both forms are more frequently bilateral.
Either form may be acute or chronic.


Superficial Glossitis.

DEFINITION.--An inflammation of the mucous membrane of the tongue,
usually involving likewise both papillae and glands.

SYNONYMS.--Catarrhal glossitis, Angina lingualis. Varieties: Papillary,
follicular, vesicular (herpetic and eczematous), psoriatic, ichthyotic.

ETIOLOGY.--Predisposing and Exciting Causes.--It is rarely idiopathic,
is most frequently deuteropathic, and sometimes traumatic. Superficial
deuteropathic glossitis usually occurs in connection with gastric and
gastro-enteric affections. It occurs likewise in association with
stomatitis, tonsillitis, pharyngitis, many febrile affections,
scorbutus, tuberculosis, syphilis, so-called psoriasis and ichthyosis
of the tongue, carcinoma of the tongue, and the various neoplasms of
the organ. Irregular and sharp-cornered or jagged teeth often induce
traumatic superficial glossitis. Pungent vapors, such as those of
chloride of ammonium, so much used of late years in the treatment of
nasal catarrhs, sometimes produce a superficial traumatic glossitis,
usually localized on the superior surface of the anterior portion of
the tongue. Tobacco-smoking, especially from a short-stemmed pipe, will
likewise produce it occasionally at the point where the concentrated
smoke strikes the organ. Attempts to drink liquids too hot, too acrid,
or too caustic may be mentioned as other occasional causes. Nervous
irritation, such as of the chorda-tympani nerve, is attributed as a
causal influence of unilateral vesicular glossitis, herpetic or
otherwise, and as a probable factor in other varieties of unilateral
glossitis. Eczema of the tongue may ensue as a sequel of prolonged
cutaneous eczema (De Mussy[43]).

[Footnote 43: _Gaz. hebd._, June 22, 1883; _Med. News_, Aug. 11, 1883,
p. 151.]

PATHOLOGY AND MORBID ANATOMY.--Superficial glossitis, as indicated,
involves the mucous membrane, glands, papillae, and epithelium. It is
hardly necessary to dwell upon the pathological conditions of the
lingual mucous membrane and its epithelium in gastro-intestinal and
febrile disorders, as these are described in connection with the
various diseases. Ordinarily, the epithelium increases in thickness,
and when detached, spontaneously or otherwise, exposes a red and
swollen membrane with erect papillae. Sometimes the condensed
stratified layer of epithelium becomes dry and very hard. Under some
illy-defined {356} conditions, the papillae of the tongue undergo great
hypertrophy. The filiform papillae become elongated to several times
their normal length, and feel and look like so many hairs on the
tongue. Like many other lingual affections, this is often unilateral.
It is quite marked in some cases of influenza and other febrile
disorders, producing great annoyance in the mouth. It occurs likewise
in gastro-intestinal disorders and in disorders of the mouth and teeth.
It is evidently a deuteropathic phenomenon. In other cases the glands
of the tongue, especially at its base, become involved, forming the
follicular glossitis of some writers. In another class of cases, most
frequently syphilitic or at least quasi-syphilitic, one or more whitish
circumscribed patches are seen on the tongue, resembling such as are
left after superficial cauterization with nitrate of silver. This
condition is described as psoriasis linguae. It is due to condensation
of layers of epithelium, which may become detached in a few days in
mass or in fragments, leaving the denuded mucous membrane red and the
papillae erect and somewhat swollen.

When psoriasis of the tongue has existed for a long time, a further
change, and a more permanent one, takes place in the papillae and
epithelium. This condition has been denominated ichthyosis linguae.
Superficial ulceration takes place at the psoriatic patches, and the
repair eventually excites such a proliferation of epithelium that it
becomes quite horny to the sight and to the touch. It spreads over a
much larger extent of surface than the original psoriasis, but, like
it, leaves the unaffected portions of the tongue in an apparently
normal condition. Both affections are usually bilateral, and the
patches or series of patches most frequently symmetrical or engaging
analogous vascular territory upon the two sides.

In a case reported by Mr. Hulke[44] portions of the horny substance
were habitually sliced off with a razor. Microscopic examination
"showed colossal papillae; the indurated portion of the mass was
altogether epithelial, the lower cells being clear, transparent, and
natural, the middle ones granular, and the superficial layer felted
together into a dense opaque mass" (Clarke).

[Footnote 44: _Medical Times_, Nov. 30, 1861, p. 556.]

Both of these affections are liable in about one-third of the cases to
terminate in epithelioma. Although the opinion generally entertained
classes all cases of psoriasis and ichthyosis linguae in the category
of syphilitic affections, there is reason to doubt its accuracy.
Sangster[45] has drawn up a tabular statement of 44 cases, of which 1
only occurred in a female; 23 occurred in smokers, 12 being inveterate
smokers. In but 12 instances (8-1/3 per cent.) was there positive proof
or strong evidence of syphilis; 30 per cent. of the whole number
eventuated in epithelioma.

[Footnote 45: _Med. Times and Gaz._, London, April 8, 1882, p. 370.]

Vesicular glossitis, usually unilateral and most frequently
right-sided, has been described by Paget,[46] Stoker,[47] Barker,[48]
Hill,[49] and De Mussy,[50] and doubtless by others.

[Footnote 46: _Lancet_, March 11, 1865; Clarke, _op. cit._, p. 88.]

[Footnote 47: _Dub. Journ. Med. Sci._, May 1, 1876, p. 401,
illustrated.]

[Footnote 48: _Lancet_, Nov. 22, 1879, p. 764.]

[Footnote 49: _Brit. Med. Journ._, Oct. 7, 1882, p. 683.]

[Footnote 50: _Gaz. hebd._, June 22, 1883; _Med. News_, Aug. 11, 1883,
p. 151.]

{357} SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS,
AND SEQUELAE.--Dryness of the tongue, stiffness, heat, and pain--the
latter especially during movements of the organ in deglutition and in
articulation--are the prominent subjective symptoms of acute
superficial glossitis. There are rarely any marked symptoms of febrile
disturbance unless the disorder is about to undergo extension into
parenchymatous glossitis.

DIAGNOSIS.--Redness of the tongue, prominence of the papillae, slight
enlargement, perhaps bearing impressions made by the teeth, and pain or
sense of impediment on movement, are the main diagnostic features of
superficial glossitis.

Vesicles indicate the vesicular variety of superficial glossitis;
irregular whitish patches, the psoriatic variety; and hard, horny
patches with intervening fissures, the ichthyotic variety. A
superficial circumscribed glossitis attending the local ulcerations of
syphilis, tubercle, and epithelioma is differentiated by the clinical
history of the case.

TREATMENT.--In ordinary cases the treatment described under catarrhal
stomatitis suffices, so far as local measures are concerned. The
gastritis or gastro-enteritis requires appropriate attention, as does
any systemic malady under which the patient may be laboring. Demulcent
and astringent lotions may be applied by douche, spray, or gargle.
Local applications of weak solutions of iodine have been recommended.
In cases of considerable severity, and especially when there is reason
to expect extension into the deeper tissues, superficial scarification
of the dorsum of the tongue is advisable.

Ulcers are perhaps best treated locally by touching the edges daily
with the pencil of sulphate of copper. Any imperfect teeth in their
immediate vicinity to which the ulceration may be attributable should
be extracted or put in repair. De Mussy's case of eczema was cured
after five months' daily use of a large quantity of water-cress.


Glossitis Parasitica.

DEFINITION.--An inflammation of the tongue said to be due to parasitic
vegetation.

SYNONYMS.--Nigrities, Glossophytia, Black tongue.

Under the term black tongue two different affections have been
described, the one an epidemic erysipelatous disorder to be mentioned
under parenchymatous glossitis, and the other, now to be mentioned, a
peculiar black pigmentation due to parasitic disease seated upon and
around the hypertrophied filiform papillae. The ordinary parasitic
vegetations found upon the tongue do not produce the affection in
question.

HISTORY.--First described by H. Hyde Salter,[51] and then by Eulenburg,
it has been made the subject of observation by Raynaud,[52] Fereol and
others,[53] Lanceraux,[54] Dessois,[55] Hirz,[56] Pasquier,[57]
Moure,[58] and a few {358} others. Outside of French literature, little
had been written of it until very recently.

[Footnote 51: Article "Tongue," _Encyclopedia of Anatomy and
Physiology_, London, 1849-52, vol. iv. pp. 1159, 1160.]

[Footnote 52: _Gaz. hebd._, 1869, No. 14, p. 221.]

[Footnote 53: _Gaz. des Hop._, June 29, 1875.]

[Footnote 54: _Union Med._, March 20, 1877.]

[Footnote 55: _De la Langue noire [Glossophytie]_, Paris, 1878, 8vo, p.
38, illustrated.]

[Footnote 56: _Gaz. Med._, Strasbourg, 1879.]

[Footnote 57: _Bull. Med. du Nord_, 1883.]

[Footnote 58: _Revue mensuelle de Laryngologie, etc._, Sept., 1883, p.
276.]

ETIOLOGY.--The affection appears to be due to some fault of nutrition,
but the cause has not been determined. The fluids of the mouth always
exhibit an acid reaction. It has been seen chiefly in dyspeptics and
hypochondriacs, and has seemed in one instance (Moure) to have followed
the use of chlorate-of-potash lozenges. A case has been recorded by
Solomon Solis Cohen[59] in a negro child the subject of congenital
syphilis. Mr. George Stoker[60] and G. Y. Broatch[61] have each
reported a case of long duration occurring in a painter.

[Footnote 59: _The Polyclinic_, Philada., July, 1884, p. 10.]

[Footnote 60: _Brit. Med. Journ._, March 29, 1884, p. 602--said to be
first case recorded in England.]

[Footnote 61: _Ibid._, April 19, 1884.]

PATHOLOGY AND MORBID ANATOMY.--The disease is characterized by a
grayish-black or fully black discoloration on the upper surface of the
tongue, which gives it an aspect which recalls the normal appearance of
the tongue of the parrot and the giraffe, and an occasional appearance
of the organ in the ox, sheep, dog, cat, and some other animals. The
filiform papillae are enormously elongated, so that they closely
resemble hairs, and they are described by some writers as lying upon
the surface of the tongue in confusion like that of a field of wheat
thrown down by the wind. The individual papillae are surrounded with a
parasitic vegetable growth. Raynaud compared the microscopic spores in
his case to the microphyte of tinea tonsurans or that of herpes
circinatus. According to Malassez, they do not differ from those found
in the saburral tongue of the dyspeptic, and he considers that their
development is favored by their very arrest by the hypertrophied
papillae. Nevertheless, the subjects of this disease are not all
dyspeptics by any means. Dessois made culture-efforts to reproduce the
disease upon his own tongue, but failed to inoculate it. For detailed
description of the disease we cannot do better than refer the
interested reader to Dessois' monograph, from whose observations,
chiefly, it appears that the discoloration begins at the central
portion of the tongue, increases gradually in extent and intensity for
three or four days, and then gradually disappears by desquamation. The
tongue is very dry while the affection is at its height. Close
examination of the parts and microscopic inspection of papillae removed
for the purpose are said to show that the spores of the cryptogam are
first developed at the base of the papillae, separating them from each
other. The irritation produced by the parasite causes longitudinal
hypertrophy of the papilla, and the continued growth of the parasite
produces a muff-like envelopment of the papilla; the spores at the same
time becoming insinuated between the most superficial epithelial cells
and dislocating them, so that they maintain their position around the
axis of the papilla only by means of the intervening parasitic masses.
The papilla continues to elongate and the cryptogam to increase, until
finally it invades nearly the entire length of the papilla. This entire
parasitic mass soon becomes detached, carrying with it the epithelial
cells under which it has become insinuated, and leaves the papilla
naked, save for a few cells remaining attached by their superior
borders. In the case observed by my brother, as in Mr. Stoker's and
Broatch's cases, microscopical examination of the black filaments
showed them to be composed of closely-packed epithelial cells,
overlapping one another, stained {359} brown, and decreasing in
intensity of color from the apex toward the base of the filament. In
some cells the nucleus was darker, and in others lighter, than the
surrounding protoplasm. The cryptogam, therefore, cannot always be
detected. Indeed, there seems reason to believe that the affection may
not be parasitic,[62] although the prominence given to this feature by
French writers apparently warrants its being so considered. There may
be two kinds of black tongue--one non-parasitic.

[Footnote 62: Hutchinson, _The Medical Press_, p. 20, July 11, 1883.]

SYMPTOMS.--There are no special subjective symptoms. The objective
symptoms are the peculiar dark or black discoloration of the upper
surface of the tongue and the excessively elongated filiform papillae.

DIAGNOSIS.--The chief diagnostic feature is the black discoloration of
the tongue which has given the name black tongue to the disease.
Discrimination is requisite from discoloration by food or medicine.

PROGNOSIS.--This is favorable, the condition subsiding under treatment,
and sometimes spontaneously, though liable to recurrence. In some
instances the condition becomes chronic.

TREATMENT.--The indication is to endeavor to favor desquamation of the
papilla by means of potassium chloride or sodium borate, and to
administer alkalines, so as to render the saliva alkaline and
unfavorable for the development of the parasite. It is recommended, in
addition, to scrape the tongue with a spatula, and to douche it with a
spray of mercuric chloride, 1:500. Attention to the general health is
requisite, especially in dyspeptics and hypochondriacs. In the case of
the negro child above alluded to the discoloration of the tongue
finally disappeared under the systemic use of potassium iodide, without
topical treatment, although repeated recurrences took place at varying
intervals.


Parenchymatous Glossitis.

DEFINITION.--An inflammation of the tongue involving its substance as
well as the mucous membrane.

SYNONYMS.--Idiopathic glossitis. Interstitial glossitis. Erectile
glossitis (Salter), Glossomegistus (Sauvages), Paraglossia.

HISTORY.--Albeit a comparatively infrequent disease, especially at the
present day, numerous cases and collections of cases are on record from
very early times; and the affection seems to have attracted the
attention of medical writers ever since. Hippocrates, Galen, Aretaeus,
Celsus, Aetius, Avicenna, Forestus, Riviere, Schenkins, Sauvages,
Vogel, van Swieten, are referred to by more modern writers as having
described the disease. Louis, De la Malle, Lassus, J. P. Frank, Jn.
Frank, Fleming,[63] Clarke, and Bryant may be cited as the most
prominent recent observers.

[Footnote 63: _Dublin Journ. Med. Sci._, 1850, vol. x.]

ETIOLOGY.--Predisposing and Exciting Causes.--Glossitis is sometimes
idiopathic, sometimes deuteropathic, and sometimes traumatic. Impaired
health from over-fatigue or from exhaustive disease may be regarded as
a predisposing cause in the presence of the causes which more
frequently give rise to traumatic glossitis. Sudden or prolonged
exposure to atmospheric changes, to cold and moisture, as when working
in damp and wet localities, is often the apparent determining cause in
{360} both the idiopathic and deuteropathic varieties. In many
instances occurring in this way it is found that the tongue has long
been subjected to mechanical irritation from jagged teeth.

Idiopathic glossitis occurs at all ages, but has been supposed by some
observers to be more frequent in scrofulous subjects. It occurs in the
apparently healthy only after severe exposure to wet and cold, and in
convalescents from acute febrile diseases usually after some moderate
exposure to a draught of air or change of temperature. It appears to be
more imminent after influenza (Moller, Smee, Graves, Salter) than after
other febrile disorders. It has occasionally been caused by chewing
acrid plants, some of them food-plants, some of them medicinal. In the
list have been included celery, bilberries, Daphne mezereum and Daphne
laureola, aconite, and tobacco. It has been known to follow the eating
of shellfish (Watson, Salter).

Deuteropathic glossitis has occurred during the course of scarlatina,
variola, epidemic erysipelas (black tongue), scorbutus, enteric fever,
glanders, septicaemia from various causes, rheumatism, diffuse
inflammation of the connective tissue of the cervico-mental region,
herpes, syphilis, ptyalism, mercurial and other varieties of toxaemic
stomatitis, tonsillitis, pharyngitis, gastritis, and epithelioma of the
tongue. It appears to be occasionally endemic (Fleming[64]), and is
occasionally epidemic (Reil[65]). In the United States it prevailed
extensively during an epidemic of erysipelas that overran the country
from 1842 to 1846, inclusive, and was frequently reported in the
American medical journals of that period under the name of black
tongue. In some localities more than half the cases terminated fatally,
sometimes within two or three days, more frequently about the eighth or
tenth day, and occasionally still later. Traumatic glossitis arises
from a number of causes. Among these may be mentioned the irritation of
jagged edges of broken and carious teeth; wounds from firearms and
other weapons; wounds from splinters of toothpicks, spiculae of bone,
broken pipe-stems, pins, needles, nails, slate-pencils, and other
pointed things inadvertently placed in the mouth; wounds from the teeth
during epileptic seizures and other convulsive paroxysms; contact of
the tongue with cold iron in cold weather; the inspiration of very hot
air, as in burning buildings; burns, scalds, scalding beverages; acrid
and corrosive substances introduced by design or accident; incautious
use of tobacco in bulk, and of ammonia; incautious cauterization;
concealed calculi in the tongue; concealed bulbs of teeth; rupture of
the lingual frenum; the bites and stings of venomous insects, as the
wasp, the hornet, and the bee. For many years writers have referred to
a case reported by Dupont to the Parisian Academy of Medicine which
followed a young man's attempt to win a wager that he would bite into
the body of a living toad, and to two fatal cases reported by Ambrose
Pare from drinking a vinous infusion of sage which was subsequently
found to have been impregnated with the saliva of the toad.

[Footnote 64: _Dub. Journ. Med. Sci._, 1850, vol. x. p. 88.]

[Footnote 65: _Memorabilia Clinica_ (_Dict. Sciences med._), vol.
xviii.]

SYMPTOMS, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--In acute parenchymatous glossitis the local symptoms often
appear quite suddenly, usually unilaterally, even when they become
bilateral subsequently, and they increase in severity with great
rapidity. {361} These symptoms are, at first, distinct sensations of
heat and tumefaction in the tongue, quickly followed by stiffness and
considerable impediment in its movements, as though it were numb and
weighted down. In cases where the glossitis is an extension from
tonsillitis, these sensations begin in the root of the organ. They
commence at the root likewise, in most instances following exposure to
severe cold and moisture. In other instances the extremity of the organ
is affected first. In cases resulting from local injury the symptoms
commence at the injured portion. The local symptoms are sometimes
preceded by rigor, followed by fever, cephalalgia, and pains in the
neck and occiput. Examined at this time, the tongue is seen to be
swollen and studded with indentations due to the pressure sustained
from the teeth. At first the surface is punctated and red; subsequently
it becomes brownish or decidedly brown. Although the organ may remain
moist for several hours, it eventually becomes excessively dry, and
supports a thick adhesive coating of mucus and epithelium.

[Illustration: FIG. 16. Glossitis (Liston).]

In a few hours, sometimes as few as two or three, the entire organ may
become involved in the inflammation, enlarging to such an extent as to
keep the lower jaw depressed, to fill almost the entire oral cavity or
to quite fill it, and to project like a tumor beyond the teeth and the
lips (Fig. 16). In exceptional cases the enlargement of the tongue has
been so great as to produce dislocation of the lower jaw. The soft
palate is lifted up and the epiglottis often pressed down. The latter
condition has been known to threaten suffocation. In this condition the
patient cannot breathe through the mouth, widely as it may be forced
open, and has great difficulty in breathing through the nose.
Respiration is therefore laborious. Articulation is impeded or
impossible, and deglutition difficult or impracticable. The tumefaction
and congestion are often continuous into the floor of the mouth and the
parts adjacent. The sublingual and submaxillary glands often become
swollen, tense, and painful; and the entire neck is sometimes swollen
to such a degree as to exert injurious pressure on the jugular veins.
The tongue is very hard to the touch, almost or quite immovable, and is
the seat of burning heat and pain. The pain often extends from the root
of the tongue along the glosso-pharyngeal folds into the pharynx, and
thence by way of the Eustachian tubes into the ears, the folds just
named being very much upon the stretch. When the tongue protrudes far
out of the mouth it becomes excessively dry, fissured, sanious, and
excoriated, or even ulcerated at points where it is subjected to the
pressure of the teeth. It is covered with dark viscid secretions, which
often extend beyond it and over the entire aperture of the mouth. The
epithelial coating often undergoes desquamation, and then the organ
becomes exquisitely sensitive to the contact of food, water, or even
the air. This desquamation is sometimes in mass, in sheets peeling off
like a pseudo-membrane. The general symptoms vary in individual cases.
As a rule, the face is turgid and its expression anxious; the
conjunctiva suffused, respiration impeded, and sleep disturbed or
impracticable. Saliva dribbles externally, often in considerable
quantity. The {362} odor from the mouth becomes quite fetid from
decomposition of the retained products of secretion. Thirst is usually
intense, though immoderate only in some cases. Cough is more or less
constant and quite exhausting. This and the dribbling of saliva
contribute with the dyspnoea to prevent sleep. Pyrexia is often
intense. The pulse is strong and quick at first, 100-120 per minute,
and there is often marked throbbing of the temporal and carotid
arteries. The skin is hot and dry at first, but cold sweat subsequently
accumulates upon the face and neck as the dyspnoea increases. The
bowels are constipated. The urine is scanty and high colored. The
impediment to the return of blood to the heart from the head causes
cerebral congestion, drowsiness, and even threatens asphyxia. In other
cases there is intense cephalalgia, nervous irritability, restlessness,
and even delirium.

The symptoms sometimes reach their acme in rather less than forty-eight
hours, and then gradually subside. More frequently they continue on
into the third or fourth day. Occasionally they are protracted as long
as the fifth or sixth or even the eighth day, rarely longer. Resolution
occasionally takes place within twenty-four hours, however (van
Swieten), though more frequently occurring from the fifth to the
seventh day. In some instances remittance or intermittence has been
noted, the cause therefor not being apparent, although attributed to
malaria.

Resolution of the inflammatory process is usually indicated by the
gradual return of moisture on the tongue and progressive detumescence
of the organ, accompanied by subsidence of the redness, heat, and pain.
Increased secretion of saliva, general perspiration, or diuresis
sometimes marks the cessation of the pyrexia.

Should the process be going to terminate in suppuration, the local
distress increases, markedly about the end of the week. The pains
become lancinating, and associated with throbbing of the lingual
blood-vessels. The swelling becomes prominent and softer at some one
point, although the sense of fluctuation is not very perceptible on
palpation, and finally the abscess bursts through the surface, unless
previously incised, and discharges a fetid pus. Suppuration always
involves a prolonged duration of the attack.

In rare instances glossitis terminates in gangrene of the tongue,
circumscribed or diffuse. This result is indicated by adynamic symptoms
on the part of the constitution, and by the livid appearance of the
parts undergoing mortification. The hemorrhage following extensive
sloughs from gangrene has been fatal in some instances.

Fleming[66] calls prominent attention to a complication of glossitis,
of which he alludes to several examples. This is "an inflammation,
circumscribed or diffused, originating in the loose areolar tissue
between the genio-hyo-glossi muscles, and first manifesting itself by a
train of symptoms identical with those of ordinary glossitis, but soon
characterized by peculiar features." These features comprise fulness
under the chin like that dubbed double chin, pressure upon which,
especially near the hyoid bone, being very painful; and suppuration,
which, circumscribed or diffuse, burrows most freely toward the base of
the tongue.

[Footnote 66: _Loc. cit._, p. 91.]

Chronic induration of the tongue sometimes remains unilateral, although
the acute disease has not been unilateral.

{363} PATHOLOGY AND MORBID ANATOMY.--It has been advanced that in
idiopathic glossitis from cold the engorgement of the vessels is
probably a consequence of vaso-dilator influence of the
glosso-pharyngeal nerve for the base of the organ, and of the
chorda-tympani for the anterior portion. An instance of herpetic
glossitis from probable irritation of the chorda-tympani nerve by an
aural polypus (Berkely Hill[67]) seems to lend some force to this
opinion. However engendered, there is a rapid distension of the organ
by blood, followed by infiltration of fibrin and serum into the
intermuscular connective tissue and into the planes of the connective
tissue separating the muscular fasciculi. In some instances
degeneration of muscular fibre has been observed. There is great
increase in the thickness of the coats of epithelium, beneath which the
mucous membrane is red and its papillae erect. This coating sometimes
peels off like a false membrane. In cases extending from tonsillitis
the base of the tongue suffers most.

[Footnote 67: _Brit. Med. Journ._, Oct. 7, 1882, p. 683.]

The disease usually terminates by resolution, although a slight amount
of hypertrophy, unilateral or bilateral, sometimes persists, and
occasionally to a marked degree (Wells). In instances much less
frequent suppuration ensues, usually in debilitated subjects or in
cases due to traumatism or in cases inefficiently treated. The
suppurative process is usually circumscribed and unilateral, and the
abscess points most frequently just beneath the side of the tongue;
sometimes, however, the pointing takes place at the dorsum, sometimes
at the tip. The pressure of the teeth seems to be the provocative cause
of the disposition to point at the edge of the tongue. The pus is
usually quite fetid. Sometimes the abscess is gangrenous.

Gangrene is an infrequent result of glossitis. The pressure of the
teeth, strangulating the organ at the oral outlet, seems to occasion
the failure of nutrition in instances where it occurs. The losses are
ordinarily insignificant, though appearing quite extensive while the
tongue remains swollen. Sometimes large portions drop off, and fatal
hemorrhage has resulted (Frank) in consequence. From the nature of the
organ the parts separate more readily than in almost any other
instance. Gangrenous abscess, ensuing even from very slight causes,
such as a wound with the head of a barleycorn (Ranking[68]), sometimes
proves fatal.

[Footnote 68: _Provincial Med. and Surg. Journ._, 1844.]

In those cases of diffuse inflammation of the interconnective tissue of
the genio-hyo-glossi muscles Fleming states that the
suppuration--which, whether circumscribed or diffuse, burrows toward
the root of the tongue--absolutely dissects its extrinsic muscles and
destroys their functions; ultimately injuring the periosteum and laying
bare the inside of the inferior maxilla in the vicinity of their
attachments. When an incision is made to the parts through the
integument, the muscles will be found on palpation flabby and detached,
and their interstices filled with purulent matter, sometimes very
fetid.

DIAGNOSIS.--These is no difficulty in the diagnosis, except in the
early stage of such examples as are attributed to metastatic gout and
rheumatism. The subsidence of the peculiar pains elsewhere, and the
onset of pain in the tongue, would lead to the inference that a
glossitis of this kind {364} was in progress. The acuteness of the
tumefaction would distinguish it from hypertrophy of the tongue on the
one hand, and from the tumefaction attending malignant disease on the
other.

Cystoma of the tongue has sometimes been mistaken for abscess due to
glossitis; but even here the history of the case should serve in most
instances as a satisfactory factor for the differential diagnosis.

PROGNOSIS.--The prognosis depends upon the gravity of the local
symptoms and the activity of the treatment. A case left to itself will
be likely to terminate fatally within five or six days. Death, indeed,
has been known to take place within forty-eight hours, even in cases
submitted to treatment. On the whole, however, the prognosis should be
regarded as favorable in the absence of specially lethal complications.
Even suppuration adds little gravity to the prognosis, the structure of
the organ being but little favorable to accumulations of purulent
material. Should an abscess become gangrenous, however, the prognosis
becomes grave at once, as it in the presence of gangrene from pressure
or other cause. Should the patient survive losses by gangrene, there
may be permanent impairment in articulation.

TREATMENT.--Superficial glossitis, as a rule, merely requires active
purgation, with the topical use of cold emollient mouth-washes
containing mucilage of slippery elm, quince-seed, or the like, to which
detergents, such as alum and borax, may be advantageously added in the
proportion of five grains to the ounce. In cases resisting this mild
treatment topical applications of glycerite of tannin twice or thrice a
day are often serviceable.

Parenchymatous glossitis demands the most active antiphlogistic
treatment. If the case be seen at an early stage of the process, before
the tumefaction of the tongue has become so great as to fill the mouth
and interfere with swallowing, a saline purge--say salts and
senna--containing some tartar emetic can be advantageously administered
to begin with. Following this, tartar emetic may be continued in small
doses every two or three hours, associated with small doses of tincture
of aconite-root (minim j-iij), according to the condition of the pulse
and the effect of medication. Should this treatment fail to produce
prompt amelioration in the local symptoms, or should the tongue be
considerably swollen when the case comes under care, free leeching
should be applied from the hyoid bone to the angle of the jaw on each
side, including the region of the hyoid bone (fifteen to twenty-five
Spanish leeches). This should be followed by emollient cataplasms,
reaching from ear to ear, to favor continuous hemorrhagic oozings from
the leech-bites. The internal antiphlogistic treatment is indicated
just the same, and if not administrable by the mouth may be
administered by the bowel; the nauseant and depressent effects of the
tartar emetic and aconite being maintained by hypodermatic injection.
Leeching the inflamed tongue itself is said to be often prompter in
producing detumescence of the organ than leeching exteriorly, but the
leech-bites are apt to add to the local irritation; besides which, the
mouth is so filled by the swollen tongue as to leave little more than
the tip accessible to the leeches without danger of losing control of
them. Venesection from the arm, the jugular vein, or from vessels
elsewhere is no longer much in vogue, it being doubtful whether general
venesection is more useful than local bleedings. Debility, whether
presenting originally or as the result of withdrawal of blood and other
{365} antiphlogistic measures, may be met by the systematic use of
tincture of chloride of iron and of quinia.

Severe cases demand one or more longitudinal incisions on each side of
the raphe of the tongue, deep enough to reach nearly halfway into the
substance of the organ and carried from base to tip. Cases are on
record in which the patients themselves had in their despair cut into
their tongues in order to obtain relief from their local sufferings,
and had in this way rescued their own lives by the means most
appropriate for the purpose (Camerarius, Lusitanus[69]). When the mouth
is filled by the tongue, it is necessary to insert the knife on the
flat until the base of the tongue is reached, and then to turn it and
make the cuts as indicated. Copious bleeding usually follows these
incisions, often followed by marked diminution in the volume of the
organ. Deep as these cuts appear when made, they become quite shallow
before the organ has shrunk to its normal volume. Bleeding from the
ranular veins, recommended by some practitioners in preference to
incisions into the organ, is often impracticable on account of the
tumefaction preventing access to them.

[Footnote 69: _Dict. Sciences med._, vol. xviii.]

If severe hemorrhage takes place from divided vessels, the vessels may
be subjected to torsion, which is the preferable mode of management, or
to searing with some form of the incandescent cautery (hot iron,
electric cautery, Paquelin's thermo-cautery). Astringent and chemical
styptics are of little use. The method of searing is open to the
objection that secondary hemorrhage may ensue on detachment of the
eschars, but this accident is not likely to happen under circumstances
at all favorable.

In localized or circumscribed glossitis the incision to be made should
interest the swollen portion only.

Should the tongue swell again, the incisions may be repeated. Whether
the tongue require incision or not, it is good treatment to have the
patient inhale vapor from hot vinegar, alcohol, or cologne spirits to
render the parts more comfortable. Washes of weak detergent solutions
containing potassium nitrate, sodium borate, or ammonium chloride may
be used by syringe or spray to cleanse the parts and promote detachment
of the epithelial coatings on the tongue and interior of the mouth, the
accumulations of which are sometimes matters of great annoyance. The
drug last mentioned exerts in addition a special action on the
inflammatory process which is often quite serviceable. I have seen good
results follow the prolonged use of sprays of an aqueous solution of
ammonium chloride (Stuver), one drachm to the ounce, from the
steam-spray apparatus, continued for fifteen to twenty minutes at a
time and repeated every two or three hours.

In many instances the patient is unable to take food by the mouth. The
best plan under such circumstances is to pass a catheter into the
stomach through the larger of the two nasal passages, and retain it in
position unless its presence interferes too much with respiration. Milk
and stimulus can then be poured into the stomach from time to time with
the aid of a funnel passed into the outer opening of the tube, which
should be kept corked during the intervals when retained in position.
This failing or impracticable, it will be necessary to nourish the
patient with enemata.

On the appearance of abscess the same should be freely laid open. In
cases of hesitation, the true nature of the presumable abscess can be
{366} determined beforehand with the exploring-needle. The pus from an
abscess of this kind is rarely copious and is usually fetid. It would
be good practice to distend the sac after discharge of pus by injecting
into it a solution of carbolic acid.

In resisting or advanced cases of suppurative inflammation of the
planes of connective tissue between the muscles at the lower portion of
the root of the tongue, Fleming recommends a free incision under the
chin in the middle line, through skin and fasciae and on through the
raphe of the muscles themselves.

In cases of gangrene, washes, douches, or sprays of carbolic acid,
chlorinated soda, hydrogen peroxide, or potassium permanganate are
indicated to relieve fetor; while the most supporting treatment by
mouth or otherwise is requisite on general principles.


Chronic Glossitis.

Chronic glossitis, like acute glossitis, may be superficial or
parenchymatous.


Chronic Superficial Glossitis.

Superficial chronic glossitis is usually confined to the papillae of
the tongue, territories of which, so to speak, are mapped out on the
surface of the tongue, separated by furrows reaching to the basement
mucous membrane. In pronounced cases the dividing furrows are quite
deep, giving the organ a mamelonnated appearance, and they penetrate
into the mucous membrane (dissecting glossitis, Wunderlich), which
becomes subjected to great irritation by the retention of articles of
food in the fissures. Demarquay[70] has recorded a case of this kind in
which, to relieve the intense sufferings with which the patient had
been plagued for a number of years, he had been forced to amputate the
anterior half of the organ--an operation which succeeded thoroughly.

[Footnote 70: _Loc. cit._, p. 142.]

In another group of cases the surface of the swollen tongue is mapped
out in small ovoid patches, smooth, red, and glossy, from which the
papillae have become separated without regeneration. Sometimes chronic
glossitis presents as an aphthous inflammation. Sometimes superficial
ulcers occur upon the dorsum of the tongue, irritable, indolent, and
indurated.

ETIOLOGY.--Chronic superficial glossitis is in rare instances a sequel
of the acute form of the disease. Usually, however, it is encountered
as a chronic affection from the outset, so to speak, generally as a
result of long-continued irritation in connection with dyspepsia and
other gastric and gastro-intestinal disorders. It is frequently
encountered in subjects of chronic alcoholism.

The superficial ulcerations often occur at the sides of the organ,
usually in some of the depressions formed by the contact of the teeth.

SYMPTOMATOLOGY.--The symptoms are those due to a consciousness that the
tongue is too large, with occasional pain in taking acid and succulent
food.

{367} PATHOLOGY.--The pathology does not differ from that of chronic
inflammations elsewhere. The apparent obliteration of the papillae in
some cases is due to a filling up of the intervening furrows by
permanent deposit of new-formed cells. The excoriations and superficial
ulcerations are most frequently due to disturbance of nutrition by
pressure.

DIAGNOSIS.--The affection may be confounded with syphilitic disease of
the tongue or with papillary epithelioma, but the history of the case,
the resistance to antisyphilitic treatment, and the negative results
from microscopic examination of fragments of tissue removed for the
purpose, serve to establish the diagnosis in cases of doubt. It must
not be forgotten, however, that many cases of epithelioma begin in
chronic glossitis, non-specific as well as syphilitic.

PROGNOSIS.--Though not threatening to life, the prognosis of the
disease itself is bad. It resists treatment, being, in fact, a
complication of some obstinate or intractable gastric or
gastro-intestinal disorder, or an evidence of constitutional dyscrasia.
Cure may be expected in recent cases, following cure of the dyspepsia
or other malady upon which the chronic glossitis may be dependent.

TREATMENT.--Care to cleanse the tongue by washes, douches, or wet
cloths after each meal, in order to remove particles of food which may
have become impacted in the anfractuosities of the organ, is important
in order to avoid additional sources of irritation.

Astringents and caustics of various kinds have been extensively
employed, carefully applied to the floors of the fissures, but it is
very rarely that any benefit ensues. Demarquay[71] reports good results
in one case of dissecting papillary glossitis from biweekly
applications of equal parts of chromic acid and water. Butlin reports
good results from chromic acid (1:10).

[Footnote 71: _Loc. cit._, p. 143.]

Careful attention to the gastro-intestinal functions, and a thorough
change of diet, such as the adoption of the milk cure and the like,
with due attention to bathing and outdoor exercise, comprise the most
rational method of constitutional treatment. Should the secretions of
the mouth give an acid reaction with litmus-paper, alkalies are
strongly indicated, topically and systemically. Avoidance of alcohol in
all forms is often absolutely essential.


Chronic Parenchymatous Glossitis.

The chronic parenchymatous form of glossitis is usually circumscribed.
When diffuse or general it has usually been a sequel of acute
parenchymatous glossitis. It is not a painful disorder, and as a rule
is not associated with constitutional manifestations. The circumscribed
tumefaction usually presents as an induration upon some portion of the
side of the tongue, being most frequently directly or indirectly due to
irritation sustained from a jagged tooth. Ordinary sensibility is much
diminished, and sometimes the sense of taste likewise. Sometimes the
indurated mass is ulcerated superficially. The enlargement of the organ
is not sufficient to keep it outside the mouth. Sometimes, indeed, the
tongue, {368} as a whole, has undergone atrophy, unilateral or
bilateral. Chronic abscess of the tongue sometimes supervenes, chiefly
in scrofulous subjects.

PATHOLOGY AND MORBID ANATOMY.--This consists merely in interstitial
connective-tissue hyperplasia, with atrophy of muscular fibres from
compression.

SYMPTOMS.--In addition to the objective symptoms of induration or
circumscribed tumefaction, the subjective symptoms may be summed up as
general hypersensitiveness to sapid and acrid substances; diminished
tactile sensibility at the part affected; slight stinging sensations
while the parts are at rest; occasional or continuous local pains; and
a sense of impediment in the movements of the tongue in articulation
and even in deglutition.

DIAGNOSIS.--Inspection reveals the swelling, and palpation its
induration. In addition, the adjacent source of irritation, a jagged
tooth or two, is seen. Abscess is recognized by special prominence at
one point of the swelling and by indistinct sense of fluctuation.

Cystic tumor is liable to be mistaken for abscess, but the
exploring-needle will solve the difficulty. Circumscribed induration
may be confounded with tumor or with epithelioma.

PROGNOSIS.--This is good, provided the source of irritation can be
removed or suppressed.

TREATMENT.--The first element in the treatment is the removal or repair
of any offending tooth, and next attention to any underlying malady,
constitutional or local. Weak solutions of iodine locally are said to
be of service. Abscesses require incision and evacuation. Their walls
should be distended with solutions of carbolic acid or be touched with
solutions of iodine, silver nitrate, or cupric sulphate, to promote
reparative inflammation.


Glossanthrax (Carbuncle of the Tongue, Malignant Pustule of the
Tongue).

This is a special variety of gangrenous ulcerative glossitis,
presenting as an integral phenomenon of a disease peculiar to
slaughterers, who become infected from diseased cattle, usually by
means of the knife, which they are sometimes in the habit of holding in
the mouth (Heyfelder and others). It has been described chiefly by
Heyfelder,[72] Duhamel, Chavarrien d'Audebert, Felix Plata, Breschet et
Finot, and Maisonneuve.[73]

[Footnote 72: _Med. Vereins Zeitung_, 1834.]

[Footnote 73: _Des Tumeurs de la Langue_, Paris, 1848, These de
Concours.]

The period of incubation occupies about one day. The tongue then
undergoes rapid tumefaction and becomes the seat of intense pain. The
points of inoculation become hard, covered with vesicles containing
bloody serum, which blacken, rupture, and leave dark, livid, gangrenous
patches of ulceration. Profound cachexia rapidly ensues under typhoid
manifestations, and death may result in less than twenty-four hours,
though usually not until sixty hours. The prognosis, therefore, is of
the gravest character.

The chief treatment consists in thorough cauterization of the
inoculated {369} points by means of the actual cautery, followed by
deep incisions into the body of the tongue if the glossitis be severe.


Ulceration of the Tongue.

Apart from the ulcerations of the tongue incidentally mentioned in the
foregoing pages, there are two forms of ulcer, both of sufficiently
frequent occurrence in ordinary practice to require special
description: these are the tuberculous ulcer and the syphilitic ulcer.

Tuberculous Ulcer of the Tongue.--Tuberculous ulceration of the tongue
occurs in a certain number of cases of advanced tuberculosis of the
lungs or of the lungs and larynx. It has even been asserted to precede
pulmonary tuberculosis. It is most frequently observed upon the upper
surface of one side of the organ, sometimes at the tip, sometimes
farther back, and usually on the same side upon which the disease is
most advanced in the lungs or the larynx. It is often associated with
previous or subsequent tuberculous ulcerations of the palate or of the
pharynx or contiguous structures. It gradually extends, and rarely if
ever heals. It is characterized by a superficial excavation, and by
being covered with a grayish detritus entirely different from the
purulent layers seen on other kinds of ulcers. When of long standing
its base is indurated, and this may give rise at first to suspicion of
squamous-celled carcinoma. Small yellowish elevations are sometimes
observed in the reddened mucous membrane around the ulcer--an
appearance deemed sometimes characteristic of the tuberculous nature of
the lesion (Trelat[74]).

[Footnote 74: _Bull. de l'Acad. de Med._, 1869, or _Arch. gen. de
Med._, 1870.]

PATHOLOGY AND MORBID ANATOMY.--Nodular tuberculous infiltration takes
place beneath the mucous membrane, which becomes elevated in small,
semiglobular, yellow protuberances of one or more millimeters in
diameter, around which the mucous membrane is red and swollen. The
epithelium becomes shed without undergoing renewal, and thus a little
point of superficial ulceration remains. When several such points are
sufficiently contiguous they coalesce into a single ulcer of irregular
contour, which gradually spreads without much other change.
Practically, it never heals.

SYMPTOMS.--In addition to the superficial ulceration described, and in
addition to the constitutional and local symptoms of advanced
tuberculosis of the lungs or lungs and larynx, as may be, there are no
special symptoms attending the tuberculous ulcer of the tongue. Saliva
is sometimes secreted in excess, but that is not characteristic. There
is little pain and little impediment to the movements of the tongue
until the disease has advanced.

DIAGNOSIS.--The presence in a tuberculous subject of a unilateral,
irregular ulcer of the tongue surmounted with grayish detritus and
surrounded by reddened edges, should suffice for the recognition of its
presumptive tuberculous character. It is most difficult perhaps to
differentiate from a small ulcerated squamous-celled carcinoma, and the
two indeed sometimes coexist, rendering the discrimination extremely
difficult until the advanced progress of the carcinoma places the
diagnosis beyond doubt.

{370} In the early stages, however, it is distinguished by lack of the
peculiar lancinating pains of carcinoma, which, however, are not
invariably attendant, and by lack of secondary involvements of the
cervical lymphatic glands. At all times it should be distinguishable
from the carcinomatous ulcer by lack of the fungus-like appearance of
the bed of the ulcer which is usual in carcinoma.

From syphilitic ulcer it is distinguishable by the history of the case,
its tendency to be unilateral, and its failure to respond to
antisyphilitic treatment. Syphilitic ulceration of the tongue may
represent the primary, the secondary, or the tertiary manifestation of
the specific disease. The former will not be discussed in this
connection.

Secondary ulcers occur on the upper surface of the tongue, most
frequently at the anterior portion, as fissures, usually longitudinal,
the floors of which are ulcerated. They occur likewise at the sides,
tip, and even lower surface of the organ. They are often associated
with secondary ulceration in the mucous membrane of some portion of the
mouth. They are quite painful, especially to the contact of pungent
articles of food. Some ulcers occur as simple superficial excoriations
at some portion of the edge or tip of the tongue, giving little
evidence of any specific character.

Tertiary ulcers are usually sequelae of gummata. They are much deeper
than secondary ulcers, sanious at bottom, often serpiginous in
configuration, and apt to extend in depth as well as in superficies,
sometimes penetrating through and through the organ. They are most
frequent in the very central portion of the tongue, or are
symmetrically disposed on either side of it.

PROGNOSIS.--The prognosis of tuberculous ulceration is bad, both as
regards tongue and patient.

TREATMENT.--The only topical treatment offering any prospect of local
cure is the bodily destruction of the ulcer and the surrounding tissue
with caustics, the best of which are the incandescent metals, or else
the excision, with the incandescent knife, of a portion of the tongue
comprising all the affected tissue. In the former case the tuberculous
process often reappears about the cicatrix; in the latter, at some more
distant point.

Tincture of iodine locally, detergent washes, and the like, often
secure a certain amount of comfort as palliatives. The same indications
prevail as in simple chronic glossitis, superficial and deep-seated.
Iodoform locally is of benefit, inasmuch as it relieves pain and
reduces collateral inflammation, but it is powerless to arrest the
onward march of the ulcerative process.


Hemorrhage from the Mouth.

DEFINITION.--A loss of blood from the mouth.

SYNONYM.--Stomatorrhagia.

ETIOLOGY.--Hemorrhage from the mouth is usually a symptom of some
disease or injury of the mouth, tongue, gums, palate, pharynx, or nose.
It may, however, occur as one of the phenomena of scorbutus or of
haemophilia. It is said to occur occasionally as a vicarious {371}
menstruation. It may be slight, so as barely to tinge the saliva, or it
may be profuse enough to terminate fatally. Between these extremes
there is an infinity of gradations. As a result of disease it may be
caused by simple hyperaemia of the mucous membrane, by rupture of
dilated blood-vessels, by ulceration, by gangrene. As a result of
injury it may arise from wounds of various kinds, accidental or
self-inflicted.

The gums are the most frequent source of slight hemorrhage from the
mouth. The pharynx, probably, is the next most frequent seat.
Hemorrhage from the tongue, cheeks, lips, and palate is usually
traumatic or the result of ulceration.

SYMPTOMATOLOGY, COURSE, DURATION, COMPLICATIONS, TERMINATIONS, AND
SEQUELAE.--The symptoms of hemorrhage from the mouth are the presence
of blood in the saliva or in the mouth itself, or in the expelled
products of expectoration, emesis, or catharsis, for sometimes the
blood is swallowed, and occasionally inhaled into the air-passages. The
course, duration, complications, and terminations of stomatorrhagia
depend upon its cause. Prolonged hemorrhage will entail anaemia;
profuse hemorrhage may terminate fatally.

DIAGNOSIS.--Careful examination of the mouth, tongue, pharynx, and
posterior nares, both by direct and by reflected light, may be
necessary to discover the source of the hemorrhage and discriminate it
from haemoptysis and haematemesis.

PROGNOSIS.--The prognosis will depend upon the nature of the cause, its
susceptibility of arrest, the quantity of blood lost, and the general
health of the patient. It is grave, as a rule, in the subjects of
haemophilia, as there is a constitutional malnutrition of the
blood-vessel system which cannot be counteracted.

TREATMENT.--Ergot or oil of turpentine internally, astringent
mouth-washes, and recumbency constitute the main features in treatment.


Morbid Dentition.

DEFINITION.--Departure from the physiological processes concerned in
the eruption of teeth, entailing certain local and systemic disorders.

SYNONYMS.--Dentitio difficilis, Pathological dentition, Odontitis
infantum.

The correct comprehension of the subject will be facilitated by
considering its etiology, pathology, and symptomatology in connection.
Indeed, morbid dentition has been assigned so prominent a part in the
etiology of various affections elsewhere discussed that a satisfactory
consideration of its own causation would require the repetition of much
that belongs more appropriately under other titles. While in some
infants the teeth erupt so quietly that the parents are astonished by
the accidental discovery of their presence above the gum, few children
escape a greater or less amount of local and constitutional disturbance
while passing through the process of dentition. So severe may these
disturbances become that, according to the mortality-tables of London,
as cited by West,[75] teething was assigned as the cause of death of
4.8 per cent. of all children dying under one year old, and of 7.3 per
cent. of those who died between the {372} ages of twelve months and
three years. It is furthermore well recognized that the period of
greatest mortality among children is that of the first dentition.
Associating these facts, we see, on the one hand, that while disorders
of dentition may act a causative part in the production of systemic
diseases or aggravate morbid processes due to ordinary causes, on the
other hand they may be but one expression of some profound
constitutional disturbance; or both aberration in the eruption of the
teeth and systemic disease may be dependent upon the influence of
dyscrasia. The period is one of active organic processes; the child is
becoming fitted for a new manner of existence; and change and
development are going on throughout nervous, vascular, respiratory, and
alimentary systems. Hence there exists peculiar susceptibility to
morbid influences; and any process, physiological or pathological, once
started, goes through its stages with excessive energy.

[Footnote 75: _Lectures on the Diseases of Infancy and Childhood_,
Philada., 1860, p. 425.]

Although the periods of normal eruption of the deciduous teeth vary
within extensive limits, and an invariable order in eruption is not
observed in all subjects, it may be stated as a rule that the lower
central incisors are cut in quick succession about the seventh month.
Some infants get these teeth during the fourth month (Vogel), and
others have to wait until the tenth or eleventh month, some even
longer. A few weeks after the appearance of these lower
incisors--within fourteen days in some subjects, not until nine or more
weeks in others--the central incisors of the upper jaw are cut, and its
lateral incisors shortly afterward, followed in their turn by the
lateral incisors of the lower jaw. In some instances--the majority,
according to Vogel--the eruption of the inferior lateral incisors is
delayed until the anterior molars are about to become exposed, usually
from the twelfth to the fifteenth month. Sometimes the upper molars are
cut before the lower, sometimes after them. From the sixteenth to the
twentieth, or even the twenty-fourth, month the canine teeth are cut,
and the four posterior molars follow between the twentieth and
thirtieth months, rarely delayed until the thirty-sixth
month,--completing the process of the first dentition.

From this it will be seen that the teeth erupt as a rule in pairs, and
that a longer or shorter interval of repose takes place between the
eruption of successive pairs.

Variations from the usual order beyond the limits noted above may be
considered abnormal. Numerous cases are on record both of precipitate
and of tardy dentition. Tanner cites from Haller nineteen examples in
which one or more of the central incisors have been found through the
gums at birth, and have had to be removed to prevent injury to the
mother's nipple; from Crump, a case of full dentition at birth,
reported to the Virginia Society of Dentists; and from Ashburner, a
case of a child beginning to cut its first tooth, an incisor in the
upper jaw, during its twenty-third month, the infant being very
delicate, with a large head, tumid abdomen, and peculiarly small-sized
extremities. The same author quotes from Serres cases of persons
passing through several years of life--in one instance seven--before
cutting their first teeth, and mentions on the authority of Tomes that
Boxalli and Baumes have each recorded an instance in which the patient
reached old age without a single tooth having ever appeared.

Rachitis is often the cause of tardy dentition, and in the subjects of
this {373} diathesis not alone are the teeth retarded in development,
but they decay early and even fall from their sockets.

The first indication of approaching dentition is the markedly increased
production of saliva. For some little time after birth the salivary
glands seem to remain wholly inactive, and until the fourth or fifth
month of extra-uterine life they furnish very little secretion. At this
period a decided change occurs. The mouth is constantly filled with
saliva, which dribbles from its corners. To this continual slobbering,
wetting the garments covering the chest, has been attributed the
bronchial catarrh which attends some infants; and diarrhoea has
likewise been referred to the swallowing of large quantities of saliva,
acting as a mild laxative by virtue of its saline constituents.

There may be no further manifestation until the seventh month, beyond
the broadening of the dental ridge. The exact position of each tooth is
usually indicated by greater prominence of the gum above it for some
time before it comes through, its entire outline being very distinct in
the upper central incisors. As the tooth approaches the surface the gum
becomes hot, shining, tense, and tumid, often painful. A slight amount
of catarrhal stomatitis is almost invariable. There is some elevation
of temperature; flushing of the cheek may occur; the child is restless,
peevish, and fretful; its sleep may be broken; it may cry out with
pain; its thumb, its fingers, any hard substance it can obtain, are
thrust into its mouth to allay the irritation of the gums. Otalgia is
not uncommon, and its occurrence may be inferred from the fact that the
child pokes its thumb or finger into the auditory canal or firmly
presses the tragus down over the external meatus. These may comprise
all the disordered manifestations, local or constitutional, or there
may be in addition loss of appetite, diarrhoea, vomiting, and the
various disturbances of reflex nervous origin to be alluded to later;
or, in the not common yet not rare instances already mentioned, there
may be absolutely no appreciable disturbance whatever.

Sometimes a disposition exists to the formation of small aphthous
ulcerations on the tongue or elsewhere in the mouth, particularly at
the duplicature of the lip and the outer surface of the alveoli.
Ulceration occurs most frequently at the tip of the tongue, probably
occasioned by friction from the new teeth. Usually there is a single
flat, round ulcer, its edges somewhat infiltrated, its bed covered with
a yellow lardaceous substance. It is extremely painful to the touch,
and thus every movement of the tongue occasions distress. It may heal
within a few days or continue for weeks. Ulcers in other situations are
less obstinate.

Occasionally--and more frequently in debilitated subjects or those
exposed to unhygienic surroundings--there is an unusual amount of heat
and swelling of the gum, which becomes excessively tender, usually over
the summit of a particular tooth--in which case there will be a little
tumor-like elevation--or around a tooth which has partially pierced
through it. Small sloughy ulcerations form in this situation. There is
great pain, and usually high fever and severe gastro-intestinal
disorder. This affection, often difficult of cure, is termed by some
writers odontitis infantum. So severe is the pain, and so great its
tendency to aggravate constitutional disturbances, that life may be
placed in jeopardy, and even fatal results ensue.

{374} Less severe than either of the forms just described, and yet far
more intense than the mild stomatitis which many authors regard as
physiological, is an aggravated form of catarrhal stomatitis sometimes
attendant upon morbid dentition, in which there is swelling of the
submaxillary glands and infiltration of the adjacent connective tissue.
In this case there is usually considerable pyrexia.

The constitutional disturbances of reflex nervous origin occasioned by
morbid dentition are of the most varied character, both in their degree
of gravity and in the manner and locality of their manifestation.
Doubtless the extensive ramifications of the great vagus nerve, and its
connections both of origin and distribution with the exquisitely
sensitive fifth nerve, as well as with the facial nerve and with the
sympathetic system, will explain why the irritation should now be
seated in the gastro-intestinal tract, giving rise to vomiting and
diarrhoea (gastritis, gastro-enteritis, enteritis, entero-colitis,
cholera infantum); now in the respiratory tract, provoking cough more
or less severe, or even a well-marked bronchitis; now manifest itself
in various cutaneous eruptions (urticaria, eczema, impetigo, lichen,
prurigo, herpes); and now accumulate in the cerebro-spinal axis,
manifesting its presence by slight spasms (dysuria, muscular
twitchings), or discharging with terrific force in some of those
convulsive seizures which are the dread of mothers and the cause of
much anxiety to physicians.

The mechanical causation of diarrhoea and bronchitis, insisted upon
particularly by Vogel, has already been alluded to. While this may be
one element, most certainly the nervous factor is too important to be
disregarded. Bronchitis, not attributable to ordinary exposure, occurs
coincidently with teething even in children who have been protected
against wetting of the chest; and the fact that more purely nervous
phenomena, and especially the dreaded brain symptoms, are usually
absent in children who have an excessive flow of saliva, and
particularly if there be also a moderate diarrhoea, would conduce to
the belief that nervous irritation, discharging itself in this manner,
does not accumulate in the centres.

Doubts have been expressed whether dentition can give rise to
convulsions in perfectly healthy children, although its role as an
exciting cause in predisposed subjects is admitted (Hillier). That
dentition alone, in the absence of any other predisposing or exciting
influence, will provoke any of the disorders with which it is
associated may be doubted in view of the fact already cited, that in
some infants there are no untoward occurrences. But there seems to be
no valid reason for separating the disturbances purely in the domain of
the nervous system from the other pathological processes originated or
aggravated by morbid dentition. Doubtless predisposition often
determines the direction and severity of the reflected phenomena; and
in the same manner reflected irritation may bring an organ within the
influence of the ordinary disease-producing cause.

The convulsive phenomena associated with dentition may take the form of
general eclampsia or spasms of particular groups of muscles. These
latter are very common--according to Vogel, universal--and vary in
intensity from that slight contraction of the facial muscles which
sends the mother into raptures of delight over the heavenly smile of
her {375} sleeping babe to the distressing seizure of laryngismus
stridulus. Sometimes the child may sleep with its eyes half open, the
eyeballs directed upward, and only the white sclerotic to be seen
through the gap between the lids, "producing an appearance which is
unnatural and alarming to the laity."

The attacks of general eclampsia are usually sudden. The child has been
to all appearances perfectly healthy, when, without warning, there
occurs a series of tetanic spasms like a succession of electric shocks.
The individual eclamptic shock cannot be distinguished from an
epileptic seizure. These convulsions sometimes continue for several
days, but frequently they cease after a few minutes. They may pass off
and leave nothing to testify to their occurrence; very frequently they
occasion permanent distressing lesions. Partial, so-called essential
paralyses, squint, or even idiocy, are cited among their sequelae;
infants subject to repeated convulsions while cutting successive teeth
have eventually perished from cerebro-spinal meningitis; death has not
infrequently been an immediate result. In these graver cases teething
is probably but one of the morbid influences at work.

Purulent otitis media follows dentition in some infants, usually, if
not invariably, of a scrofulous diathesis. At the clinic of the
Jefferson Medical College Hospital fully one-third of all the cases of
otorrhoea in children are said to be so occasioned.

Blennorrhoeal conjunctivitis is a rare complication of teething, and
when it occurs usually accompanies the eruption of the upper molars and
canines (eye teeth). It is attributed to direct extension of the
gingival inflammation by continuity through the antrum of Highmore and
the nasal passages. By some it is said to occur only in strumous
subjects. It is unilateral, and is not contagious, so that there is no
cause for alarm concerning the unaffected eye. The lids soon swell
enormously and the eyeball is exposed with difficulty. There is
considerable pain. The secretion is more mucous, translucent, and
stringy than in genuine blennorrhoea. The eyeball always remains intact
and the prognosis is always favorable (Vogel). Milder forms of
catarrhal conjunctivitis are not very uncommon.

Thus far, we have considered only the process of the first dentition.
Before the shedding of any of the deciduous teeth, the first permanent
molars inaugurate the second dentition, appearing in position at about
the sixth year. Next, displacing their temporary predecessors, come the
central incisors, between the sixth and eighth years, the inferior pair
generally preceding the superior ones. The lateral incisors are cut
between the seventh and ninth years; the anterior bicuspids between the
ninth and tenth years; the posterior bicuspids between the tenth and
eleventh years; the canines between the eleventh and thirteenth years;
the second molars between the twelfth and fourteenth years; the third
molars, or wisdom teeth, between the seventeenth and twenty-first years
as a rule, occasionally much earlier, sometimes later.

The eruption of the permanent teeth does not usually occasion any very
great amount of distress; nevertheless, it sometimes acts both as a
predisposing and as an exciting cause of various disorders, local and
systemic. The various forms of stomatitis, tonsillitis, sore throat,
gastro-intestinal derangements, febrile disturbances, bronchitis,
internal rhinitis, {376} diseases of the eye, of the ear, of the skin,
chorea, epilepsy, etc., have all been noted as accompanying, if not
occasioned by, the second dentition. Ashburner[76] records, among other
similar instances, that of a lad twelve years old who presented a
marked case of chorea, and after three months' continuance of the
twitchings fell into a violent epileptic fit, from difficulty in the
eruption of the second pair of permanent molars of the upper jaw. The
use of the gum lancet relieved the convulsion, and there was no return
of the chorea.

[Footnote 76: _On Dentition and some Coincident Disorders_, London,
1834, cited by Tanner.]

Quite frequently, the eruption of the inferior dentes sapientiae
occasions great and protracted suffering, especially when they appear
very close to or partially under the coronoid processes. Considerable
irritation is occasioned, in which the gums and adjacent tissues
participate. Inflammation may result and extend to the fauces;
mastication becomes impossible; severe odynphagia is excited.
Suppuration may ensue, and then the pus burrows in various directions,
finding exit at points more or less remote, internal or external. Among
the consequences of the eruption of a wisdom tooth into a crowded arch,
White[77] cites fistulae, necrosis, exostosis, ulceration and sloughing
of the soft tissues, cystic and other tumors, ankylosis of the jaw,
amaurosis, otalgia, otorrhoea, deafness, facial paralysis, hemicrania,
oesophagismus, tonsillitis, erysipelas, aphonia, hysteria, neuralgia,
chorea, epilepsy, tetanus, death.

[Footnote 77: "Pathological Dentition," extract from annual supplement
to the _Obstet. Journ. of Great Britain and Ireland_, April, 1878.]

DIAGNOSIS.--The age of the child and the appearances already described
will afford a basis for diagnosis so far as the local manifestations in
the mouth are concerned. The diagnosis of local disorders at a
distance, or of systemic disturbances of whatever character, can be
made out only by careful consideration of all the attending
circumstances; and it is always to be borne in mind that while the
process of dentition is to be recognized as one of the causative
factors, grave injustice might be done the little patient, and its life
perhaps endangered, by failure to recognize the presence of other and
perhaps more potent morbid influences.

In cases of chorea or epilepsy, of eye or ear troubles, or of any
morbid condition not otherwise accounted for, occurring during the
period of the second dentition, especially at the sixth, twelfth, and
seventeenth years, or until the wisdom teeth are fully erupted, it is
well to inspect the mouth and to think of dentition as the possible
cause.

PROGNOSIS.--The prognosis will depend upon the character and gravity of
the associated symptoms, the presence or absence of diathesis, and the
etiological importance attached to dentition. It is impossible to lay
down a general law.

TREATMENT.--The treatment of the deuteropathic or associated disorders
is to be conducted on the general principles applicable to those
diseases; for a consideration of which the reader is referred to the
appropriate articles of this work. We have here to consider general
prophylaxis and local measures. The proper management of the child
during the period of the first dentition is a matter of great
importance, and may avert serious complications. The child should be as
much as possible in the open air whenever the weather is favorable. The
head may be daily sponged with cold water, and caps and warm
head-coverings of all kinds should {377} be forbidden.[78] Frequent
rubbing of the gums with a crust or other hard substance, or with the
finger, is advisable; and something for the child to bite on,
preferably a silver piece, should be provided. Orris-root, calamus, and
other vegetable substances frequently given to children for this
purpose are objectionable; their fermentation is apt to lead to thrush.
The secretions must be kept active. The diet should be carefully
regulated, and cooling drinks be freely given in order that the child
may not overload its stomach by too frequent suckling in its efforts to
relieve the local heat by moisture. The mother should be warned not to
put it too frequently to the breast. Weaned children will often be
found unable to digest their ordinary food, and in that case still
greater care will be required. Slight diarrhoea does not call for
interference, and is often beneficial in relieving nervous tension and
thus averting a tendency to convulsions. Indeed, when the bowels are
not relaxed gentle aperients should be given, especially in plethoric
subjects or in those with cutaneous eruptions (Clarke). Cutaneous
eruptions do not call for treatment, and there seems to be ground for
the popular fear that they may be driven inward; at least, cases are on
record in which their disappearance under treatment, and even
spontaneously, has been followed by more or less severe convulsions.

[Footnote 78: Tanner after Clarke.]

In cases where bronchitis can be traced wholly or in part to soaking of
the clothing, due protection of the chest by an oil-cloth or waterproof
bib may be prophylactic against future attacks. In children who have
suffered from any special set of morbid manifestations during the
eruption of one pair of teeth, similar disturbances may be expected,
and should be guarded against, in the future.

Aphthous ulcerations are usually associated with disorders of
digestion, the relief of which must be the main object of treatment.
Locally, the treatment does not differ from that of aphthous stomatitis
in general. Obstinate ulceration of the tongue may require the use of
silver nitrate. In that form of ulceration called odontitis infantum,
in addition to proper attention to the diet and secretions and mild
antiphlogistic medication, local depletion by leeches, preferably at
the angle of the jaw, is often beneficial. Some writers advise the
application of leeches directly to the gum. Potassium chlorate
internally, two grains every four hours to a child twelve months old,
is curative in the majority of cases. It may be given dissolved in
sweetened water. Solutions of borax, and, in severe cases, of silver
nitrate, may be applied locally. The use of the lancet is
contraindicated, for the cut surfaces would be liable to ulceration.

[Illustration: FIG. 17. Incision for a cuspid (White).]

[Illustration: FIG. 18. Incision for a molar (White).]

The propriety of resort to the lancet for cure of systemic disturbances
by obviating the source of local irritation is one which deserves
consideration. It can only be decided upon the indications presented by
the individual case. The knife is not a panacea for all the disorders
of childhood occurring during dentition, and its indiscriminate use is
to be discountenanced. Nevertheless, there can be no doubt that
engorged and inflamed gums demand incision for their relief, on the
same general principles of surgery applicable to similar conditions
elsewhere. Where it is probable that systemic disease, even if not
solely caused, is aggravated by the irritation and pain of a tooth
unable to make its way to the surface unaided, it is clearly the duty
of the physician to give his little patient that modicum of relief, if
not of cure, which will be afforded by a proper incision of {378} the
gum. It will not do merely to score the gums, but cuts should be made
deep enough to reach the presenting surface and extend even beyond its
boundaries. The developing enamel cannot be injured unless undue force
be exerted. The best instrument to employ is a curved double-edged
bistoury, so wrapped as to prevent injury to tongue, cheek, or lips.
The child should be firmly held by another person, and in such a
position that the parts may be well illuminated. The jaws can be
separated by the operator's left hand, and the fingers so disposed as
to protect the tongue and lips. Sometimes the insertion of a small cork
between the jaws will be of advantage. The cuts should be made with
special reference to the form of the presenting tooth. James W.
White[79] recommends for the incisors and cuspids a division of the gum
in the line of the arch; for the molars a crucial incision, thus X, the
centre of the crown as near as can be determined indicating the point
of decussation. A cuspid partially erupted needs severance of the
fibrous ring on the anterior and posterior as well as on the lateral
surfaces (Fig. 17). All the cups of a molar may have erupted, and yet
strong fibrous bands maintain a decided resistance. In this case White
thinks that all the boundaries of the tooth should be traced by the
lancet and all such bands completely severed, or else a crucial
incision, as in the figure (Fig. 18), should be made so as to ensure
perfect release from pressure. The only contraindication to the use of
the lancet, except in ulcerative odontitis, as before mentioned, is the
existence of a hemorrhagic diathesis.

[Footnote 79: _Op. cit._]




{379}

DISEASES OF THE TONSILS.

BY J. SOLIS COHEN, M.D.


Tonsillitis.

DEFINITION.--An acute inflammation of the tonsil or tonsils; or
inflammation of the tonsil or tonsils, with inflammation of the
peritonsillar connective tissue and of the palatine folds.

VARIETIES.--When the inflammatory process is confined to the mucous
membrane the disease is erythematous, superficial, or catarrhal
tonsillitis; when it involves the lacunae it constitutes lacunal or
follicular tonsillitis; when it involves the gland as a whole it
constitutes parenchymatous, phlegmonous, or suppurative tonsillitis.
The two latter varieties may present in combination. When the
superficial inflammatory process is a vesicular one, eventually
sheathing the surface of the organ in whole or in part with a
membranous envelope, it constitutes herpetic or membranous tonsillitis.
This variety may complicate superficial tonsillitis. When the
inflammation of the tonsil, usually superficial, is due to the presence
of a cryptogamic growth, it is a mycotic or parasitic tonsillitis,
benign or malignant (diphtheria), as may be. When the inflammation of
the tonsil is due to rheumatism, it is rheumatic or constitutional
tonsillitis.

SYNONYMS.--Inflammation of the tonsils, Amygdalitis, Quinsy, Angina
tonsillaris, Angina phlegmonosa, Phlegmonous sore throat, Cynanche
tonsillaris. Lacunal tonsillitis is more generally known as folliculous
tonsillitis (tonsillitis follicularis). Common membranous or
pseudo-membranous sore throat (angina membranosa communis) is used as a
synonym for herpetic or membranous tonsillitis (tonsillitis herpetica
seu membranosa). Mycosis tonsillaris is a synonym for mycotic
tonsillitis (tonsillitis mycotica benigna or tonsillitis parasitica).
The tonsillitis of diphtheria is sometimes termed tonsillitis
diphtheritica, tonsillitis mycotica maligna; that of rheumatism,
tonsillitis rheumatica, angina rheumatica, rheumatic sore throat.

HISTORY.--Tonsillitis was described by Hippocrates. Of recent authors,
Sauvages, Cullen, Louis for researches on the effects of blood-letting;
Bell on the specific value of guaiacum; Velpeau as to the use of
powdered alum and nitrate of silver; Bourgeoise on the use of tartar
emetic; Maingault on paralytic sequelae; Hering on mycosis; and the
authors of the various encyclopaedias and dictionaries,--may be
mentioned as chief among the numerous observers whose contributions
have been of most value. The bibliographical references appended to the
{380} compilations last cited will guide the student in gaining access
to the more important special observations of anomalous cases.

ETIOLOGY.--Predisposing and Exciting Causes.--Tonsillitis may be
idiopathic, deuteropathic or symptomatic, or traumatic.

The predisposing cause of idiopathic tonsillitis is usually diathetic,
and is associated with congenital or inherited vulnerability of the
organ. Of diathetic causes, scrofula is undoubtedly the most
provocative, but even rheumatism and gout are likewise so considered,
though in a far more limited degree. Acute articular rheumatism is, in
fact, sometimes preceded by rather a sharp attack of tonsillitis
(rheumatic tonsillitis), which subsides spontaneously in a very few
days, sometimes within one day, sometimes suddenly and synchronously
with the onset of the ordinary manifestations of rheumatism, though the
latter are often slight and transient, as if the force of the attack
had been spent on the tonsils. Tonsillitis, non-specific in character,
is apt to be prevalent during epidemics of scarlatina, diphtheria,
rubeola, and variola. Membranous tonsillitis is common before and after
epidemics of diphtheria. Epidemics of tonsillitis have been recorded,
but in the face of their extreme rarity it becomes questionable whether
they were not extensive examples of the proclivity just alluded to.

Tonsillitis is more frequent in individuals with chronically diseased
tonsils than in individuals in whom these glands are healthy. Such
individuals, too, are more liable to recurrences; and such recurrences
often follow very slight provocations.

Idiopathic tonsillitis is rare in infancy. At the period of eruption of
the permanent teeth it is much more liable to occur than before that
period, and the liability increases progressively until the second
dentition has been completed. It is most frequent during the decennium
immediately following puberty--that is to say, in adolescents and young
adults--or from the fifteenth to the twenty-fifth year. The disposition
or predisposition to renewed attacks continues marked during the
decennium immediately succeeding; after which attacks are more and more
infrequent. Certain anatomical changes occurring in the tonsils, as the
rule about the fortieth year, may diminish their proclivity to
inflammation. Nevertheless, the disease occasionally occurs in advanced
age.[1]

[Footnote 1: Solomon Solis Cohen, "Abscess of the Tonsil in an
Octogenarian," _Med. News_, Philada., Feb. 16, 1884, p. 186.]

Deuteropathic tonsillitis is quite frequent in infancy, being excited
by the infection of scarlet fever, diphtheria, measles, and small-pox,
as discussed under these headings respectively. Under similar
circumstances it occurs in the adolescent and the adult likewise. It is
also produced in carcinoma and sarcoma of the tonsil.

Rheumatic tonsillitis, a deuteropathic variety, is most prevalent
during atmospheric changes.

Herpetic tonsillitis, often a deuteropathic variety, seems sometimes of
nervous origin exclusively. It is sometimes traceable to defective
drainage. It is sometimes prevalent during epidemics of diphtheria,
when its membranous character renders it extremely liable to be
mistaken for the tonsillitis of diphtheria.

Traumatic tonsillitis occurs occasionally. The causes are--inspiration
of irritant gases, the deglutition of chemically acrid substances, the
{381} accumulation of calcareous concretions in the crypts or in the
lacunae, direct and indirect gunshot and other wounds, the impaction of
fish-bones, fragments of toothpicks, cherry-stones, and other foreign
bodies, and the like.

Mycotic tonsillitis is due to the development of a cryptogam upon
tonsils probably already in a state of catarrhal inflammation in
individuals with health impaired by previous disease or unfavorable
hygienic influences.

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND
SEQUELAE.--The onset of tonsillitis, sometimes preceded by headache and
general malaise, is often accompanied by a chill, pyrexia following
within twenty-four hours. The temperature may reach 105 degrees F.,
being at its maximum, as a rule, about the third day. It is rarely
below 101 degrees F. The pulse is accelerated to 120 beats per minute.
Simultaneously with the constitutional symptoms local distress is
usually manifested, but either set of disturbances may precede the
other by several hours or by an entire day. Heat and soreness of the
throat are early complained of, gradually increasing in severity to
actual pain. The pain may become intense, especially during
deglutition. When the posterior palatine fold is put upon the stretch,
additional pain is referred to the ear, for this fold encloses the
staphylo-salpingeus muscle, which runs from the palate to the
pharyngeal orifice of the Eustachian tube. This pain in the ear,
sometimes the principal cause of complaint, is often premonitory of
suppuration. Noises in the ears on the one hand, and impairment of
hearing on the other, often attend extension of the inflammation in
this direction, the enlarged tonsil sometimes pressing the posterior
palatine fold against the pharyngeal orifice of the Eustachian tube.

On inspecting the throat early in the disease, one of the tonsils will
be seen to be swollen into an irregularly tumid, much-inflamed mass,
usually of a vivid red color. Occasionally both tonsils are involved
simultaneously, but this is far less frequent than involvement of the
second tonsil a few days later or after subsidence of the process in
its fellow. In many instances the inflammation affects one tonsil only.

The inflammatory process is seldom confined to the tonsil. All the
structures of the throat, even to the base of the tongue, are often
involved, and it is rarely indeed that the anterior palatine fold,
distended over the surface of the tumefied gland, escapes inflammation.
It is this stretching of the anterior palatine fold which occasions
much of the exquisite pain that forms so prominent a subjective symptom
in severe cases. The soft palate, hanging forward in the cavity of the
pharynx, is often inflamed or intensely congested, and the uvula
tumefied, elongated, and oedematous. It may be flaccid upon the
posterior part of the tongue or hang immediately over the epiglottis or
upon it, and induce painful and tiresome efforts at deglutition and
expectoration to relieve the consequent titillation. Sometimes it
adheres by viscid secretion to the side of the swollen tonsil.

The inflamed tonsil or the tonsil and its coverings project far into
the cavity of the pharynx, often as far as the middle line, touching
its fellow when both are involved, so that ulceration sometimes ensues
at the points of contact. The posterior surface of the anterior
palatine fold sometimes becomes unfolded, as it were, in the
tumefaction of the gland, and remains {382} stretched over it in a thin
continuous layer without any line of demarcation. The swollen palate
projects upon the enlarged tonsil like a shelf, from which depends the
uvula, the latter being often oedematous, usually anteriorly, but
sometimes posteriorly.

Inflammation of the connective tissue about the lower jaw, especially
when at or near the articulation, often renders it difficult or even
impracticable to open the mouth sufficiently to permit direct
inspection of the parts; but it is rarely that sufficient space cannot
be made to allow partial protrusion of the tongue on the one hand, and
the introduction of a fore finger for exploratory purposes on the
other, though both of these acts are sometimes impossible. The
tumefaction of the parts impairs the freedom and ease of deglutition,
which may become so painful as to prevent the swallowing of the saliva,
which then may dribble from the mouth.

The pain experienced in swallowing is often manifested by convulsive
action of the muscles of deglutition and of the muscles of the face.
The swollen tonsils prevent the soft palate from being applied to the
surface of the pharynx, as usual in deglutition; and as the upper or
retro-nasal portion of the pharynx thus fails to be shut off from the
lower oesophageal portion, liquids are often forced up into the nasal
passages posteriorly, and are regurgitated through the nostrils, thus
rendering it impracticable, for the time, to slake thirst or to swallow
liquid nourishment.

At first sensations of dryness and pastiness in the throat are
complained of, but in a few hours these symptoms become relieved by a
more copious secretion of mucus or mucus and saliva. This secretion
soon becomes viscid, and so adherent to the parts as to be detached
only with difficulty, thus causing harassing efforts for its
dislodgment by hawking and expectoration, or equally distressing
efforts to swallow it. Should the inflammatory process extend to the
salivary glands, as is not infrequently the case, secondary ptyalism
often results, with increased distress from this source, and the
patient lies or sits with his head inclined upon the diseased or most
diseased side to favor the uninterrupted flow of saliva from the mouth.

Extension of the inflammatory process to the submaxillary glands, or to
the parotid, or to the connective tissue surrounding them, is indicated
by tumefaction externally, which is often exquisitively sensitive to
pressure.

The timbre or quality of the voice is often impaired in a peculiar
manner by the tumefaction of the throat and the immobility of the soft
palate. The voice is thick, throaty, or guttural, having a
characteristic harsh, rasping aspiration in enunciation, while
articulation is much impeded by impairment in the movements of the jaw,
palate, tongue, and lips. At times it is also painful. Speech is
sometimes indistinguishable or impossible, and the voice may even
become suppressed, so that signs and writing remain the sole means of
communication.

Impairment of respiration, at least to any considerable degree, does
not occur, unless both tonsils are involved and swollen to an intense
degree--conditions under which dyspnoea may become pronounced, severe,
and even urgent, and suffocation become imminent. Painful respiration
is not uncommon in rheumatic tonsillitis.

The fever is sthenic in type. There are often severe aching pains in
{383} the limbs. Headache, restlessness, insomnia, nausea, and even
vomiting, may occur. The tongue is heavily coated, the breath is fetid,
appetite is impaired, and the bowels are constipated. The urine is
diminished in quantity, high-colored, and of high specific gravity. It
usually shows slight increase of urea and great diminution of
chlorides. Albuminuria occurs in rare instances.

The symptoms are proportionate to the severity of the attack. A first
attack is usually much severer than subsequent ones, and suppurative
cases more severe than those terminating by resolution. Resolution is
the usual termination, and the parts are restored to a normal condition
at the end of ten to fourteen days, sometimes earlier; in exceptional
cases not until three or four weeks. Sometimes permanent hypertrophy of
the tonsil remains.

Where the inflammatory process fails to subside, suddenly at the end of
five or six days, or a little later, or not until ten days to a
fortnight have passed, slight rigors supervene, announcing suppuration,
and the local distress is very great, with pulsation and lancinating
pains in the tonsils, until all at once the abscess bursts and its
contents are discharged with immediate relief. Sometimes the pus or
much of it is involuntarily swallowed; sometimes it is expectorated. In
exceptional instances the pus has escaped into the larynx and
suffocated the patient, usually during sleep.[2] In rare instances the
abscess, having burrowed beneath the pharyngeal muscles, may open at
the external angle of the jaw or behind the sterno-mastoid muscle. It
may discharge into the epiglotto-pharyngeal fold, and thence reach and
distend the epiglottis. It has been known to descend along the planes
of connective tissue into the mediastinum or into the lungs. Even
ulceration into the maxillary and carotid arteries has occurred,
usually with fatal result, occasionally with an opportunity to save
life by ligating the carotid (Erhmann).[3]

[Footnote 2: Stokes, _Med. Times and Gaz._, Aug. 29, 1874, p. 251;
Littlejohn, _Brit. Med. Journ._, Jan. 2, 1875, p. 16.]

[Footnote 3: _Gaz. med._, Paris, 1878, p. 42.]

The most frequent point of spontaneous rupture externally is at the
upper portion of the gland anteriorly, just beneath the anterior
palatine fold. Sometimes internal rupture occurs into the lacunae.

Termination by gangrene is exceptional, and is confined to individuals
with debilitated constitutions. It is much less frequent than
formerly--as a result, perhaps, of better methods of treatment.

Metastasis is one of the methods of termination as to joints or muscles
in rheumatic tonsillitis--to lungs, brain, or gastro-intestinal
tract--as formerly occurred with much more frequency under direct
depletory treatment.

In rare cases extension of the inflammation occurs to the epiglottis,
even to the larynx, and the laryngitis may be so severe as to threaten
life from the occurrence of oedema. Diffuse inflammation of the
retro-pharyngeal connective tissue or of the connective tissue of the
neck may constitute an unpleasant complication of the disease.

In a few instances paralysis of the palate occurs as a sequel of
tonsillitis, and in exceptional cases the paralysis may also affect the
arytenoid muscles of the larynx, and even the accommodator muscles of
the eyes.

PATHOLOGY AND MORBID ANATOMY.--Tonsillitis is almost always {384}
associated with inflammation of the tissues surrounding the tonsil and
those contiguous to it, even in the mildest and most frequent
manifestations of the affection. Thus, inflammation of the palate
(staphyllitis) and uvula, and even of the pharynx (pharyngitis), are
anatomically included with tonsillitis in angina or sore throat.

The mildest form of the malady is a catarrhal inflammation of the
mucous membrane covering the gland, and does not extend along the
lacunae which dip inward from the surface and divaricate toward the
interior of the organ. It is termed catarrhal tonsillitis, and, as has
been intimated, is almost always associated with catarrhal sore throat.
It is attributed to hyperaemia, with passive engorgement of the
vessels, following retrocession of blood from the cutaneous surface
after undue exposure to cold and moisture. A severer form of the malady
involves the lacunae in addition--several or all of them. This should
be termed lacunar tonsillitis, as suggested by Wagner. Primarily, at
least, it does not involve the follicles of the tonsils which open into
the lacunae, and is therefore incorrectly denominated follicular
tonsillitis, although it is most generally so described. The lacunae
are involutions of the mucous membrane, and in health furnish a
slightly turbid mucoid secretion which serves to lubricate the parts
and, as is generally believed, to facilitate deglutition. When the
lacunae are inflamed these products become pent up in them to a certain
extent, accumulate, and project in part at their orifices in turbid
creamy or curdy masses, plastered over the parts when thin in
consistence, or tightly imbedded when thick or desiccated. These masses
are usually white, but sometimes, owing to various admixtures, they are
more or less yellowish or gray or brown. They consist of epithelium
chiefly, with more or less pus and accumulation of cells similar to
those of which the follicles are composed--whether from follicles which
have become distended by proliferation of their constituents, and have
then burst, is not known. This epithelium has often undergone fatty
degeneration in part. Cholesterin is an occasional constituent, and
swarms of micrococci and bacteria abound when the masses are not
recent, especially if the inflammation is occurring in a tonsil long
the seat of chronic disease of the lacunae.

The tonsil itself is moderately swollen and its mucous membrane
hyperaemic. If the parenchyma of the tonsil be involved likewise, as
often occurs, the swelling will be much greater, so that the gland will
project a considerable distance beyond the margins of the palatine
folds. When a hypertrophied tonsil is the seat of the inflammation the
tumefaction will be much greater than when the inflamed tonsil has been
normal.

Acute inflammation of the palatine folds often coexists, especially of
the anterior fold. The soft palate may also be engaged in the morbid
process, which may involve the uvula likewise. Pharyngitis is an
occasional accompaniment, and stomatitis quite a rare one.

Lacunar tonsillitis sometimes subsides by spontaneous evacuation of the
pent-up contents of secretion and desquamation, the parts returning to
their normal condition. More frequently a desiccation of some of these
products ensues, with permanent chronic inflammation. Decomposition
then often takes place, fouling the breath by the escape of the gases.
Butyric acid has been recognized as one of the most prominent of these
fetid {385} gases. Calcareous change occurs in these contents of the
lacunae in some instances. Lacunar or follicular tonsillitis is often
associated with severe inflammation of the peritonsillar connective
tissue and the contiguous palatine fold, with serous or cellular
infiltration into these structures almost always terminating in
suppuration. This form of tonsillitis is very frequent, and is often
confounded with parenchymatous tonsillitis or with tonsillar abscess.
In these cases the abscess is in the peritonsillar tissue or in the
posterior leaflet of the anterior palatine fold. It bursts above the
tonsil at the angle between the two folds in the greater number of
cases. In some instances the suppurative inflammation affects the
anterior surface of the posterior palatine fold, sometimes contiguously
to the antero-tonsillar abscess, sometimes independently, constituting
a retro-tonsillar abscess. The follicles in the posterior palatine fold
are sometimes involved, the thickened anterior surface of this
structure becoming studded with small projections the size of ordinary
pinheads or larger, distended with whitish-yellow contents.

In another class of cases of tonsillitis the inflammatory process may
be chiefly parenchymatous, for rarely is it wholly so. That is to say,
it may involve the glandular structure of the organ wholly or in main
part. The disease is then an adenitis, an inflammation of
gland-tissue--tonsillitis per se. It is associated with superficial
inflammation of the surrounding mucous membrane, secondarily if not
primarily, and often with inflammation of the lacunae. In many
instances the parenchymatous inflammation is a direct extension of the
lacunar inflammation.

Parenchymatous tonsillitis may subside by resolution, or, as is quite
frequent, terminate by suppuration. A number of small abscesses may be
formed, which usually become confluent and rarely remain discrete.
Sometimes a single large abscess is formed. The confluent abscess may
discharge by several points. It is always associated with a severe
inflammation of the palatine folds and palate, especially the anterior
fold; sometimes of the adjoining half of the soft palate and the uvula;
sometimes of the entire velum and uvula. Sometimes these parts become
oedematous; sometimes suppuration ensues. Severe pharyngitis is not
uncommon. Glossitis, involving the posterior portion of the tongue
especially or exclusively, is an occasional accompaniment of
parenchymatous tonsillitis. (See GLOSSITIS.) Occasionally oedema takes
place in the epiglottis and upper margin of the larynx.

The character of the secretions varies. Sometimes these are semifluid;
sometimes soft, caseous, or pultaceous; sometimes fibrinous and
arranged in pseudo-membranes; sometimes hemorrhagic; sometimes moist
and viscid, sometimes very dry; often adherent, and always containing
cryptogams (leptothrix, Oidium albicans, bacteria, and micrococci).
Collections of caseous products accumulate not only in the crypts of
the tonsils and in their overlying mucous membrane, but likewise in the
follicles of the palatine folds below the tonsil, and thence toward the
base of the tongue.

The submaxillary glands often undergo engorgement, and become so tender
that external manipulation is painful, and sometimes they undergo
suppuration. The tumefaction due to the swollen glands and infiltrated
connective tissue around it is frequently incorrectly referred to the
tonsil itself, rather than to the accompanying inflamed palate, with
the {386} lymphatics of which these glands are in more direct
anatomical connection. The tonsil is at a considerable distance from
the inflamed glands, and cannot be felt from the exterior except under
unusual circumstances.

Herpetic tonsillitis is a rare form of inflammation of the tonsil, or
rather of its investing mucous membrane, characterized by the eruption
of herpetic vesicles on its surface. The vesicles soon undergo rupture,
and the resulting ulcers coalesce and become covered with a fibrinous
exudation. The disease is usually associated with similar vesicles upon
the palatine folds and upon the soft palate, and exceptionally with
vesicles on the pharynx. (See Herpetic Pharyngitis.) It is by some
fortuitous circumstance only that it is observed in the vesicular
stage. It is confined to one side of the throat in most instances, but
may be bilateral also.

Mycosis tonsillaris has been described by a few observers. B.
Fraenkel[4] has recorded three cases, E. Fraenkel[5] one, and Bayer[6]
two. In these cases the disease was not confined to the tonsils, but
implicated the calciform papillae of the tongue also, and one of
Bayer's cases some pharyngeal follicles in addition. E. Fraenkel's case
was in a male, and occupied but the right tonsil and base of tongue.
The white masses in this case were formed of spores and filaments
(Bacillus fasciculatus, Sadebeck), which are described as penetrating
some millimeters into the gland-tissue. These masses were tenacious,
and were reproduced rapidly after removal. In Bayer's cases, both
females, the same microphyte was recognized. In a female patient
observed at the Philadelphia Polyclinic[7] this affection followed
rheumatic tonsillitis, diphtheria being prevalent near her residence,
which was in a very unsalubrious locality. The deposit, confined to the
left tonsil, was so firmly adherent to the mucous membrane that the
implicated portion had to be torn away to get rid of the growth, which
was twice reproduced. The fungus was in its mycelial state, a few
spores and conidiferous filaments being recognized microscopically.

[Footnote 4: _Berlin. klin. Woch._, 1873, S. 94; _ibid._, 1880, No.
18.]

[Footnote 5: _Zeitschrift fur klin. Med._, iv., 1882.]

[Footnote 6: _Rev. mens. de Laryngologie, etc._, Nov., 1882, p. 329.]

[Footnote 7: S. Solis-Cohen, _The Polyclinic_, March, 1884, p. 133.]

Quite recently, and since the above was written, the results of an
elaborate study of this affection by Theodor Hering of Warsaw have been
published in a paper entitled "Pharynxmycosis leptothricia,"[8] read
before the Society of German Naturalists and Physicians. The author
collates fourteen cases, six of which were observed by himself. He
claims that the microphyte is simply the Leptothrix buccalis.

[Footnote 8: _Zeitschrift fur klinische Medicin_, Bd. vii. H. 4, 1884.]

The local subjective symptoms as collated by Hering vary from the
merest sense of discomfort in chronic cases to intense pain, difficulty
in speech and in deglutition, and various grades of cough in acute
ones. In some cases they are altogether wanting. Constitutional
disturbance may be entirely absent or may be presented in various
febrile or sub-febrile manifestations.

DIAGNOSIS.--The history of the attack, the appearances described, and
the symptoms narrated should ordinarily suffice for a correct
diagnosis. Still, mistakes do occur. An unsuspected tumor of the tonsil
observed for the first time during an ordinary sore throat might be
taken for an inflamed tonsil, but the progress of the case would soon
lead to its due {387} recognition. While tonsillitis is infrequent
after the fourth decennium, it occasionally occurs late in life, and
has been observed even in the ninth decennium; and reserve is proper as
to the cause of enlarged tonsils in the sore throats of those advanced
in life.

The deposit in follicular or lacunar tonsillitis or angina is pulpy and
not membraniform. It can be wiped from the surface with a fragment of
sponge, and does not tear from the surface in strips, as is the case
with the pseudo-membrane of diphtheria or of common membranous sore
throat. There is no abrasion of the mucous membrane beneath the
deposit. The patches are more prominent, usually more circumscribed,
and dip down into the lacunae, or rather project from the crypts upon
the surface of the tonsil. In its physical aspect the deposit more
closely resembles that observed in the sore throats accompanying
cachectic conditions, as in chronic tuberculosis, advanced syphilis,
some forms of scarlatina, typhus and typhoid fever, extreme old age
(agine pultacee, Fr.; cachectic angina); but the existence of previous
constitutional disease and actual debility should prevent the mistake
in diagnosis. In susceptible subjects the oncoming of an attack of
rheumatic tonsillitis may often be inferred, previous to the
manifestation of local symptoms, from the existence of otherwise
inexplicable odynphagia, the pain being especially intense upon
attempts to swallow saliva. Sometimes laryngoscopic inspection at this
early stage of the disease will reveal vivid redness of the mucous
membrane in the neighborhood of the crico-arytenoid articulations.[9]
The value of this early diagnosis lies in the opportunity it affords to
try abortive treatment.

[Footnote 9: S. Solis Cohen, _The Medical News_, Aug. 11, 1883, p.
146.]

PROGNOSIS.--The prognosis of catarrhal tonsillitis is almost invariably
favorable, except under very obviously unfavorable conditions, the
inflammatory process subsiding spontaneously within a few days. It is
favorable, as a rule, in phlegmonous tonsillitis subsiding within ten
or twelve days in most instances, even though all the stages be
completed to suppuration and discharge of the abscess. Sometimes two or
three weeks are consumed in the process. A certain amount of reserve is
requisite, nevertheless, in severe cases, in view of the possible
complications which may prevent recovery. If both tonsils are affected
to such an extent as to interfere seriously with respiration, death by
suffocation may ensue should the obstruction be not relieved by
excision of portions of the swollen glands or an artificial opening be
not made into the air-passage. Suppuration may perforate the internal
carotid or the external maxillary artery and produce sudden fatal
hemorrhage. The remembrance of such occurrences should screen a surgeon
from the imputation of carelessness should he be unfortunate enough to
incise an abscess under similar conditions. Some cases are on record of
fatal hemorrhage but a short period before a proposed operation could
have been performed.

Suffocation has ensued from discharge of the abscess into the
air-passage, usually during sleep; but it has occurred even during the
moment of speaking (Stokes).[10] Such results are accidental and
exceptional.

[Footnote 10: _Med. Times and Gaz._, Aug. 29, 1874, p. 251.]

Recurrences are frequent, especially in scrofulous subjects, and such
recurrences are apt to result in permanent hypertrophy and induration.

TREATMENT.--Mild cases of tonsillitis require no treatment except to
{388} keep the patient protected from exposure to abrupt changes of
temperature. The course of the affection both in mild cases and in
severe ones may often be materially shortened by prompt resort to the
use of guaiacum, both internally and topically. A gargle containing an
ounce each of ammoniated tincture of guaiacum and compound tincture of
cinchona to the pint, with the addition of three ounces of clarified
honey, and saturated with potassium chlorate (twenty grains to the
ounce), may be used, a drachm at a time, every two hours, hour, or half
hour, according to the urgency of the symptoms, and may likewise be
administered internally in drachm doses for an adult every two or more
hours. The beneficial effects will often be manifested within less than
twelve hours. Pellets of ice held in the mouth from time to time often
relieve pain and repress inflammation. Sodium bicarbonate locally, in
powder, affords great relief in some instances. In the presence of
marked pyrexia tincture of aconite may be given in drop doses every
hour until an impression has been made upon the heart, when its
continuance at intervals of four or more hours will be a matter for
consideration.

Guaiacum and aconite may be given with equal benefit in any form
preferred by the prescriber. At the same time saline laxatives may be
required from time to time. Regulation of the diet is often necessary.

When the tonsils are very much swollen, gargling of all kinds becomes
too painful, and therefore sprays of sedative and emollient mixtures
are to be substituted, or steam from water impregnated with volatile
substances, as benzoin, paregoric, hops, chamomile, and sage. When the
cervical glands are swollen, continuous hot and moist applications
externally afford great relief. If the suffering from the inflamed
tonsil be intense, scarification should be practised and the bleeding
be encouraged by warm water. When suppuration exists, the abscess
should be promptly evacuated by incision at the most prominent
accessible point.

Special symptoms require appropriate management on general principles.
The pain in swallowing can often be diminished by pulling on the lobe
of the ear at the moment of deglutition (Grewcock).[11] In debilitated
subjects, or during epidemics of diphtheria, quinia, iron, and
supporting measures are indicated.

[Footnote 11: _Lancet_, Nov., 1882, N.Y. reprint, p. 399.]

The rheumatic cases are best treated with sodium salicylate, ten to
fifteen grains every hour or two until relieved. Instituted in the
formative stage above alluded to, this treatment frequently seems to be
veritably abortive, especially when preceded by a full dose of an
alkaline purgative--say one ounce of Rochelle salts. Oil of gaultheria
may be used in small doses as an agreeable flavor to the mixture, or in
doses of ten to twenty minims, well diluted, as an adjuvant to the
salicylate, or even as a substitute for it. After subsidence of the
acute symptoms cinchonidine salicylate may be continued for a few days
in appropriate doses.

Herpetic tonsillitis requires the ordinary treatment for erythematous
tonsillitis, with additional topical treatment by sprays of alkaline
solutions, such as sodium borate or bicarbonate, five grains to the
ounce, or lime-water. Internally, small doses of mercuric chloride will
be of service, the dose varying, according to the age and size of the
patient, from one-forty-eighth to one-sixteenth of a grain every two
hours, until the stomach shows signs of irritation therefrom. In cases
of doubt as to {389} diagnosis from diphtheria the treatment for
diphtheria will be indicated as the safer measure. Here, again, the
mercuric chloride is sometimes equally valuable.

Mycosis of the tonsil does not seem amenable to medicinal treatment.
Thorough removal of the fungus with forceps or sharp spoons is
required, even though mucous membrane be detached with it. When this is
impracticable, ablation of the tonsil may be necessary. Raw or cut
surfaces left by any of these manipulations should be subjected to
thorough cauterization, electric cauterization being the most feasible
method.




{390}

DISEASES OF THE PHARYNX.

BY J. SOLIS COHEN, M.D.


Acute Pharyngitis.

DEFINITION.--An acute inflammation of the mucous membrane of the
pharynx, whether implicating the glandular structures or not, and
usually associated with inflammation of contiguous structures.[1] Acute
pharyngitis may be catarrhal or erythematous, phlegmonous or
suppurative, ulcerative, herpetic or membranous, gangrenous, and
erysipelatous.

[Footnote 1: In deference to the plan suggested by the editor of this
work, separate articles have been prepared under the heads of
Pharyngitis and Tonsillitis respectively. The two processes, however,
are so frequently associated that they should be studied together, the
more that both of them are likewise associated with extensions of the
inflammatory process to the palate, palatine folds, base of the tongue,
and other contiguous structures. The writer has always preferred to
describe these diseases under the head of sore throat, which does not
presuppose any limitation to individual anatomical structures.]

SYNONYMS.--Sore throat; Angina.

ETIOLOGY.--Acute pharyngitis may be idiopathic, deuteropathic,
traumatic, toxic, or parasitic. The predisposing cause may be
diathetic, as scrofula, rheumatism, gout, and syphilis; it may be a
depression of the vital powers from any cause, such as continued
exposure to foul air or impure water, improper diet or sedentary
occupations. There exists in some individuals a predisposition to
"catching cold," independent of any cachexia. Pharyngitis may occur at
any age, but is more frequent in the young. One attack increases
subsequent liability to the disease.

The exciting cause is usually exposure to cold and damp. Hence the
disease is more frequent at the seasons when these conditions prevail
or when sudden changes of temperature are taking place. Sudden chilling
of the body when overheated may occasion it in warm weather; for
instance, a plunge into the ocean while covered with perspiration. The
ulcerative variety, when not due to syphilis or tuberculosis, is
usually of septic origin, and is apt to occur in the debilitated
especially. The gangrenous form, which is rare, results from profound
blood-poisoning. The herpetic or membranous variety may be due to
disturbance of the trophic nervous system, and has been attributed to
mental emotion (Feron), to uterine disturbances (Bertholle), to the
contact of irritating substances and to miasmatic or fetid exhalations
(Peter). It prevails principally during epidemics of diphtheria or of
scarlet fever, and may be of cryptogamic origin. The cryptogam of
thrush is sometimes developed on the mucous membrane of the pharynx,
either primitively or as an extension of the disease from the oral
cavity. Certain conditions of the {391} atmosphere give rise at times
to so-called epidemic pharyngitis. Paludal or malarial pharyngitis may
arise from the same causes as malarial fevers. Pharyngitis occurs in
the various exanthemata as an essential part of the morbid process, and
is always more or less prevalent during epidemics of measles or scarlet
fever. It occurs not rarely in typhoid fever, and is an occasional
complication of pneumonia, rheumatism, herpes, pemphigus, and other
acute affections. It is one of the complications of facial erysipelas,
but erysipelatous pharyngitis may occur primarily. Pharyngitis may be
excited by the inhalation of deleterious solid, fluid, and gaseous
substances in the atmosphere which act mechanically or chemically on
the mucous membrane. Many drugs administered in poisonous or even in
medicinal doses may give rise to an attack of inflammation of the
pharynx; among them may be cited preparations of mercury, antimony,
iodine, arsenic, copper, lead, zinc, silver, stramonium, belladonna,
and most of the Solanaceae. Traumatic pharyngitis results from
deglutition of boiling water or of acrid or caustic substances; from
inhalation of hot air, of steam, or of flame, and is most usually
associated with traumatic oesophagitis or with laryngitis.

PATHOLOGY AND MORBID ANATOMY.--Acute pharyngitis, as most commonly
encountered, is a simple erythematous inflammation of the mucous
membrane; the palate and tonsils being likewise involved. In most
instances there is simply an active hyperaemia which may subside in a
day or two. When more intense than this the mucous membrane of the
palate, tonsils, and pharynx becomes congested and swollen, uniformly
or in circumscribed areas. In some instances the submucous tissue of
the pharynx is greatly relaxed, and the mucous membrane lies upon the
substructure in thick folds. In others there is more or less oedema.
The mucous follicles, especially those of the posterior palatine folds,
are frequently swollen. There is an abnormal though not excessive
secretion of viscid mucus, clear or turbid. The uvula is often swollen
or distended with serum, and its mucous membrane is relaxed. Sometimes
it appears as though pasted to one of the folds of the palate by viscid
secretion. The posterior palatine folds may be distended with serum,
and their arched appearance thus become obliterated. Resolution occurs
gradually in some instances, quickly in others.

Phlegmonous pharyngitis exhibits a still higher grade of inflammation.
It involves the submucous structures as well as the mucous membrane,
including at times the fibrous sheaths of the muscles. It may, in
addition, involve the palate, the tonsils, the base of the tongue, and
contiguous structures. Suppuration is common, usually circumscribed,
but not infrequently diffuse in patients of enfeebled constitution.

One variety of the disease is essentially a deep-seated pharyngitis;
and this form almost always progresses to suppuration (suppurative
pharyngitis). The process becomes then, not infrequently, a diffuse
suppurative inflammation of the subpharyngeal connective tissue,
extending sometimes downward along the oesophagus, into which the pus
may be discharged by spontaneous rupture, with a result of permanent
stricture from irregular cicatrization. Sometimes the suppurative
process extends anteriorly beneath the cervical fascia, and the pus may
gravitate so as to occlude the air-passages, partly or completely, by
direct pressure; or in other instances the entrance of {392} the larynx
may become blocked by the tumefaction of the pharynx. When phlegmonous
pharyngitis is of traumatic origin, there will be more or less
destruction of the mucous membrane according to the nature of the
injury, whether accidental or designed, whether due to burn, scald,
inhalation of hot air or steam, or to deglutition of alkaline, acid, or
other corrosive substances. In these cases the morbid process is rarely
confined to the pharynx, but the larynx, the oesophagus, and even the
stomach, are liable to be involved. If regurgitation of hot air or of
caustic fluids takes place through the nasal passages, the injury will
of course involve those regions.

Ulcerative pharyngitis is a low form of inflammation present in sore
throat, probably dependent upon septicaemia. The tonsils are somewhat
congested and swollen, and one or more white superficial ulcers form on
their surface, or on the palate, or on the pharynx. These ulcers are
generally round or oval, and vary greatly in size. When two or more
ulcers exist, they exhibit no tendency to confluence. Healing takes
place rapidly, usually without leaving any traces of the lesion.

Membranous pharyngitis, or herpes of the pharynx, is one of the
infrequent phenomena of a not uncommon sore throat, which exhibits at
first a collection of small vesicles the size of millet-seeds or
larger, isolated here and there or clustered in groups on the palate
and uvula, less frequently on the tonsils. Herpes of the mouth and lips
sometimes coexists. These vesicles are surrounded by inflammatory
areolae. Their contents are more or less turbid. In rare instances they
disappear without trace after a day or two. Usually they soon undergo
rupture, sometimes within a few hours, so that small ulcers are left,
which almost immediately become covered with a grayish-white exudation.
A number of patches will coalesce, forming limited sheets of false
membrane not unlike those of diphtheria. The disease is usually
confined to one side of the throat, the corresponding submaxillary or
cervical glands being affected moderately when at all involved. The
tonsil is swollen, and the mucous membrane of the palate and the
palatine folds is congested and often tumefied. There is an abnormal
secretion of viscid, ropy, turbid mucus. In a few days the ulcers heal
beneath the exudation, which becomes disintegrated and detached, the
inflammatory process subsiding by gradual resolution. Sometimes the
ulcers cicatrize without previous deposit of false membrane.
Occasionally there are at longer or shorter intervals successive crops
of vesicles, which may or may not undergo ulceration.

Gangrenous pharyngitis may supervene upon any form of pharyngitis, but
in the majority of instances its malignant character is inevitable from
the outset; so that some authors have even restricted the term
gangrenous to a form of sore throat characterized by primitive gangrene
of the pharyngeal mucous membrane originating independently of any
other malady. Whether an idiopathic disease, or whether it follows
scarlatina, measles, small-pox, dysentery, or enteric fever, it is
associated with that depraved condition of the system denominated
typhoid. At times it occurs in tuberculous phthisis. The initial
manifestations may be simply those of intense inflammation. The tongue
is covered with a dark creamy, pultaceous deposit consisting of
broken-down epithelium, pus-cells, bacteria, and molecular debris,
while similar masses are occasionally seen upon other mucous surfaces
of the mouth and throat. The tonsils, {393} palate, and pharynx are
livid and swollen, and sometimes oedematous. At an early period the
tonsils, the palatine folds, and the posterior wall of the pharynx
become covered with dark, ashy-colored ulcers with excavated edges.
Sometimes these spots are black from the first, and appear slightly
elevated. These soon slough out with more or less of the surrounding
tissues, and the ulcers left are covered with sanious, ichorous, fetid
secretion. In some instances a delicate pseudo-membrane has been found
in the bed of the ulcer after death (Mackenzie). The destructive
process rapidly extends--sometimes to the oesophagus in one direction
or to the nares in the other. The larynx is less frequently implicated;
should it be attacked, oedema is liable to occur. Occasionally the
process is limited to the tonsil, and there is no pharyngitis at all.
Erosion of the blood-vessels may give rise to fatal hemorrhage. In
those instances where the gangrene is circumscribed there are found,
post-mortem, depressed oval or circular patches from one-twentieth to
one-half an inch in diameter, varying in color from dark gray to
absolute black. The edges are of a brownish color and are
perpendicular. The bundles of muscular fibre are laid bare by
destruction of the mucous membrane and submucous connective tissue, but
as a rule escape implication of their substance. Similar patches have
been noted in the epiglottis and the upper part of the larynx as well
as in the mouth and pharynx--in some cases, indeed, in the trachea, the
lungs, the oesophagus, the stomach, and the intestines.

Erysipelatous pharyngitis is usually an extension of erysipelas from
the facial integument, which may take place by the lips and mucous
membrane of the mouth, by the nasal fossae, by the Eustachian tube from
the tympanum and external ear, or by the nasal fossae from the
conjunctiva and eyelids through the lachrymal duct. When the disease
begins in the pharynx the order of communication may be reversed. The
pathological processes are the same as in cutaneous erysipelas. The
mucous membrane of the pharynx will be diffusely red or purplish and
shiny. Sometimes little bullae are formed and become ruptured, leaving
a patch of softened whitish-yellow tissue, which is sometimes torn from
the surface beneath by the act of coughing or of deglutition. The
inability to swallow is not due to swelling of the tissues, but to
actual paresis of the muscles, probably from interstitial infiltration,
but perhaps from implication of their substance. The cervical and
submaxillary glands are rarely involved. Erysipelatous pharyngitis
usually terminates by resolution, desquamation of the greater part of
the epithelium of the mucous membrane often taking place; but it may be
followed by abscess or by gangrene. Extension may take place to the
larynx, and oedema may follow.

Exanthematous pharyngitis accompanies some cases of cutaneous
exanthemata. The pharyngitis of small-pox is occasioned by an eruption
upon the mucous membrane similar to that which appears on the skin.
Often in advance of the cutaneous eruption it occupies the inside of
the cheeks, the palate, uvula, and pharynx; sometimes the larynx as
well. Maturation occurs more rapidly than upon the skin, and there is
more or less purulent infiltration of the submucous connective tissues.
Ulceration of the larynx or trachea may ensue so severe in character as
to cause fatal termination by the local lesion.

{394} In measles an eruption similar to the cutaneous manifestation
occupies the air-tract from nostril to bronchi rather than the
food-passages. The Eustachian tubes may be involved, and the
inflammation is sometimes propagated along the lachrymal duct. The
throat may be affected a day or two before the external integument.
Small red points the size of a millet-seed or larger appear on the
palate, the tonsils, the posterior palatine folds, and the wall of the
pharynx. These disappear in a few days, though sometimes in bad cases
fibrinous exudation may accumulate. In other instances abscess or
ulceration takes place, chiefly in the larynx.

The pharyngitis of scarlatina develops a day or two prior to the
cutaneous eruption, the mucous membrane of the palate, tonsils, and
pharynx being deeply congested, uniformly or in patches, with slight
papulous elevations here and there. In the course of a day or two an
opalescent or milky deposit, consisting chiefly of detached epithelium
and viscid mucus, is observed on the swollen palate and tonsils. In the
anginose variety the hue of the inflamed structures is more dusky.
There is a pseudo-membranous deposit of a dirty-white, ash, or even
yellow color. It is not limited to the tonsils, but accumulates rather
on the palate, palatine folds, and posterior wall of the pharynx. The
mucous membrane beneath the patches is often ulcerated, and sometimes
gangrenous. There is much greater tumefaction of all the parts than in
simple scarlatina, the enlargement of the cervical and submaxillary
glands and the infiltration of contiguous connective tissue being so
great in some instances as to prevent the mouth from being opened. A
viscid and turbid secretion accumulates in the mouth. The nasal
secretions sometimes desiccate into firm crusts. Suppuration may occur.
Sometimes otitis media results from extension along the Eustachian
tube, and sometimes suppuration of the membrana tympani, suppurative
external otitis, or disease of the internal ear with extension to the
cerebrum. In malignant cases all the processes are aggravated.
Ulceration or gangrene soon ensues, the pseudo-membranous deposit being
dark, almost black, from extravasated blood. Oedema of the uvula and
soft palate is liable to occur, and if the larynx be involved there may
be oedema of the epiglottis and ary-epiglottic folds.

SYMPTOMATOLOGY.--Simple pharyngitis very often gives rise to but little
discomfort. There is usually more or less heat and dryness in the
parts, especially at first. There is some dysphagia, principally from
pain in swallowing, but in part from actual debility in the muscles of
deglutition. Hoarseness is not usual, and cough is infrequent if there
be no elongation of the uvula. Speech may be embarrassed by difficulty
of articulation. There is usually some febrile movement, with
acceleration of pulse and respiration. Some cases exhibit more intense
inflammatory action, with a corresponding aggravation of the
constitutional symptoms. The skin becomes markedly heated, the
body-temperature rises to 101 degrees F. or higher, the pulse reaching
100-120, in some instances 140, beats per minute, even in the adult.

In that variety known as rheumatic sore throat there will be in
addition pain and soreness in the neck, back, and limbs, often severe,
and increased by motion. There will be great accumulation of saliva in
the mouth because of the intense pain in swallowing it. Speech, and
even respiration, may become painful. These manifestations are
frequently {395} followed by the ordinary phenomena of acute articular
rheumatism, but they may subside in a few days, leaving only a general
feeling of muscular soreness or slight stiffness in one or more of the
joints. Sometimes a temporary torticollis follows.

In some cases of pharyngitis the cervical glands become swollen and
painful, but this is not common. In children the constitutional
disturbance is much greater than in adults. In malarial districts or in
subjects of malarial poisoning the manifestations may assume a periodic
character. Recovery takes place, as a rule, in from three to ten days.

In many instances the local phenomena are most prominently manifested
on one side of the throat. There will then exist great liability to
similar involvement of the other side after convalescence of a day or
two, and without care and avoidance of exposure the second attack may
be far more severe than the first.

The severe variety of pharyngitis denominated phlegmonous is often
ushered in with a decided chill, the phenomena of fever following
within twenty-four hours. The symptoms, both local and general, are of
much greater severity than in catarrhal pharyngitis, especially in
cases proceeding to suppuration.

Paralysis of the palate and other paralyses may follow either of the
forms of sore throat just described. Albuminuria sometimes results. In
extremely rare cases it is an accompaniment of the disease.

Superficial ulceration of the mucous membrane may occur in almost any
form of pharyngitis or of sore throat. Some authors have separated a
special form of ulcerative sore throat occurring in those enfeebled
from long exposure to unwholesome influences, such as nurses, hospital
attendants, etc., in whom the first symptom is pain in deglutition,
especially of saliva. The tongue is furred and the breath is offensive.
There is loss of appetite, with general lassitude, feebleness of
circulation, and more or less elevation of temperature. Intense
headache is often present. Under suitable treatment recovery is rapid.

The ulcerative sore throats of syphilis and of tuberculosis require
separate consideration.

Common membranous pharyngitis frequently gives rise to but slight
symptoms, differing very little from those of other forms of
pharyngitis; but there may be high fever of sthenic or of asthenic
type, very often preceded by general malaise, sometimes by a decided
chill. The pain in deglutition and the local heat and dryness are
sometimes much greater than in the more ordinary forms of pharyngitis.
The distress may extend into the ear, sometimes to the nasal passages,
in rare instances to the larynx. The disease lasts for a week or ten
days, usually terminating in recovery. In occasional instances, chiefly
in children, it terminates fatally by apnoea from extension of the
membrane into the larynx. Paralytic sequelae are not rare.

The advent of gangrenous pharyngitis is sometimes indicated by sthenic
phenomena, but usually from the first it is marked by extreme
prostration, comparable in some instances to the collapse of cholera.
There is a low type of fever. The pulse is feeble and infrequent. The
skin, especially of the extremities, is cold and blue. The eye is
glassy, the countenance haggard. The pain, as a rule, is not severe,
sensation being benumbed. The disease is often accompanied by an
irregular erythematous cutaneous {396} eruption. The secretions and
excretions escape by the mouth and nose, and they are extremely fetid.
There is indeed a peculiar odor, which once encountered can scarcely be
mistaken. If the lungs become affected there will be copious
haemoptysis. In some cases the tendency to hemorrhage is general, blood
oozing or gushing simultaneously from lungs, bowels, nose, and mouth,
and sometimes extravasating beneath the skin. Sphacelus ultimately
takes place at the points of ecchymosis. Diarrhoea, abundant and fetid,
due to invasion of the alimentary tract, often sets in before the
close, and may be regarded as a sure precursor of death. Death usually
takes place from syncope, intelligence often remaining unaffected to
the last. When these cases recover a horrible amount of deformity often
remains to mark the ravages of the disease. During cicatrization the
positions of contiguous parts become very much altered. The palate may
become adherent by its sides, and by more or less of its posterior
surface, to the pharynx, sometimes resulting in complete occlusion of
the nasal portion of the pharynx.

The constitutional symptoms of erysipelas of the pharynx are those that
attend the usual manifestations of external erysipelas, the febrile
phenomena, epigastric pain, nausea, and so on, being increased in
severity. There will be great pain and difficulty of deglutition. If
there be serious oedema, symptoms of suffocation will occur. Laryngitis
will be indicated by pain referred to the larynx. The duration of the
disease varies from forty-eight hours to a week, rarely longer. Death
may occur within two or three days from oedema of the larynx or from
other causes frequently indiscernible. Resolution usually takes place
in those cases which recover. Occasionally abscess occurs.

DIAGNOSIS.--The diagnosis rests upon the conditions already described
under the heads of Pathology and Symptomatology. Under ordinary
circumstances it presents no difficulty, but during the prevalence of
epidemics of scarlatina or diphtheria even the mildest sore throat
demands careful attention and frequent inspection until the exclusion
of the graver maladies may be positively determined. The greatest
difficulty will present in cases of common membranous sore throat, for
it is sometimes impossible to make the differentiation from diphtheria,
especially as the vesicular stage is rarely seen. Sometimes, it is
said, it is possible to detect one or more of the small ulcers left by
the rupture of the vesicles; sometimes small isolated spots of false
membrane will by their transparency indicate recent formation, and by
their circular shape the previous existence of a vesicle (Peter, cited
by Mackenzie). The coexistence of cutaneous herpes is corroborative of
the diagnosis, but by no means an infallible sign. It must not be
forgotten in this connection that membranous sore throat may predispose
to an attack of diphtheria. In gangrenous sore throat the grayish-black
patches may be mistaken for the pseudo-membranes of diphtheria, but
their color is dark from the outset, while in diphtheria they become
dark only as the disease progresses. They always represent actual death
of the tissues, which is not an essential lesion of diphtheria.
Swelling of the cervical glands is unusual. Finally, the characteristic
odor of gangrene is almost unmistakable.

PROGNOSIS.--The prognosis is favorable in catarrhal pharyngitis and in
the milder forms of the phlegmonous, non-specific, ulcerative, and
{397} common membranous varieties. It is unfavorable in intense
suppurative pharyngitis, though cases often get well. In gangrenous
pharyngitis the prognosis is extremely grave, but recovery is not
impossible. In traumatic pharyngitis the prognosis will of course
depend upon the nature and extent of the injury, being not unfavorable
if this be confined to the pharynx, though even in limited cases there
may be stenosis or other ill results from cicatrization. Erysipelatous
pharyngitis is of grave prognosis when the result of extension of the
disease from the face, but recovery is frequent when the pharyngeal
disease is primary.

TREATMENT.--The treatment of superficial pharyngitis is very simple.
Unless the case be so light that no special medicinal treatment seems
advisable, the patient should be confined to a bed or lounge to secure
rest, a light coverlid being thrown over the body to equalize the heat
of the surface. If a meal has recently been taken, a mild emetic is
often of service to empty the stomach and save the labors of digestion.
A gentle laxative or, if the patient be of costive habit, a saline
purge is indicated to facilitate the passage of matters already in the
intestinal canal. In cases of actual constipation a drastic cathartic
may be required. If there be considerable pain a small dose of morphine
may be advantageously combined with the aperient. If frequent pulse or
high temperature exist, especially in severe cases, tincture of
aconite, in doses of one or two drops every hour or two hours at first,
will be useful. As soon as any marked effect has been produced the
aconite may be discontinued or the intervals between administrations
lengthened. Locally, the free use of demulcent drinks, and of pellets
of ice when cold is agreeable, will relieve the pain in the throat and
sometimes repress excessive secretion. Cold compresses to the neck
anteriorly are often soothing, and sponging the entire surface of the
body with tepid water, acidulated or alcoholized, will allay the
intense heat of the skin. The diet should be light and nutritious. Very
often the emetic, rest, and regulation of diet will constitute the
entire treatment required.

When the local distress is very great, astringent lozenges (catechu,
krameria) may be allowed to dissolve in the mouth, or sprays of weak
solutions of alum or of carbolic acid may be propelled upon the mucous
membrane. Tannin, potassium chlorate, and cupric sulphate are often
used for this purpose. When the uvula is elongated or oedematous it is
often a constant source of irritation and discomfort. Scarification to
give vent to pent-up blood or puncture to allow the escape of effused
serum will afford prompt relief. Excision is never necessary.

In phlegmonous pharyngitis the treatment will necessarily be more
active. Here an early emetic is of great service. A saline laxative may
be administered every three or four hours for a day or two, each dose
containing a drop or two of the tincture of aconite, with the addition
of morphine if indicated by pain. Drop-doses of aconite at more
frequent intervals sometimes serve a better purpose. Inhalation of
steam, or of steam from water impregnated with hops, chamomile-flowers,
paregoric, compound tincture of benzoin, juice of conium, or the
aqueous extract of opium, belladonna, or conium, will afford great
relief, as will the frequent projection of sprays of warm water, simple
or slightly aromatized with cologne-water or with toilet vinegar. Warm
and moist applications externally are often very soothing. Gargling
entails too much pain to be of {398} service, but medicated sprays may
be used of aqueous solutions (twenty grains to the ounce) of tannin,
alum, zinc sulphate, or cupric sulphate, care being taken to guard
against the swallowing of any of these drugs. Powders of alum, tannin,
krameria, etc., diluted with liquorice, acacia, bismuth, lycopodium,
and the like, may be blown upon the parts, and are often efficient.
Sodium bicarbonate frequently affords relief. The topical application
of silver nitrate is rarely practicable and generally unnecessary.

When the inflammatory process is of a higher grade and not likely to
yield to purely medicinal treatment, leeching or venesection may be
employed, but should not be resorted to without urgent reason. The
recognition of abscess is an indication for its immediate discharge by
incision or aspiration. In suppurative cases quinia and iron should be
given in large doses. The general treatment is like that of simple sore
throat. When liquid food cannot be swallowed, nourishment by enema is
requisite. Efforts at deglutition should be spared as much as possible,
and with this view medicines which can be administered by inhalation,
by enema, or by hypodermatic injection are to be preferred.

In pharyngeal sore throat, whether catarrhal or phlegmonous, depending
on rheumatic or gouty diathesis, salicylic acid or the salicylates will
prove useful, either alone or in conjunction with other measures.

The treatment of ulcerative pharyngitis is practically the same as that
recommended for phlegmonous pharyngitis. Antiseptic gargles may be used
locally, but as a rule the pain is so great that inhalations of
soothing vapors, as before recommended, will answer a better purpose.
When the process is very acute fragments of ice will be most useful.
Ice to the head will afford relief to pain. A little good wine, with
quinia and iron, comprises the medicinal measure requisite.

Gangrenous pharyngitis calls for the most active and supporting
treatment. Eggs, milk, cream, nutritious soups (up to the limits of the
patient's capacity for swallowing, and by enema when necessary),
quinia, tincture of the chloride of iron, and alcohol in large doses,
are indicated. Local treatment is of high importance. Agents to destroy
diseased tissue promptly and prevent the extension of the gangrenous
process, such as bromine, strong nitric or hydrochloric acid, acid
solution of mercuric nitrate, or caustic potassa, are to be thoroughly
applied, in the hope of exposing a healthy surface beneath which will
heal by granulation. When this treatment is unsuccessful or too
hazardous, as in cases where the blood-vessels are probably involved,
we can only palliate the symptoms by applying weak solutions of acids
and astringents, to which opium may be added, relying on constitutional
measures for restraining the destructive process. Washes and sprays of
potassium chlorate, eucalyptol, thymol, hydrogen peroxide, etc., or the
agents employed in common sore throat, are often agreeable to the
patient, and may be useful in restraining fetor, but they have no
direct therapeutic influence on the progress of the disease. If the
ulceration is extending into the vicinity of the great vessels of the
neck, measures for compression should be at hand, in the use of which
the nurse should be instructed, and preparations be made to facilitate
ligation of the carotid artery in an emergency. Tracheotomy may be
necessitated by oedema of the larynx. The deformities resulting from
gangrenous sore throat in cases that recover usually require surgical
treatment.

{399} Traumatic pharyngitis must be treated on general principles. When
due to contact of caustic or corrosive substances, an attempt may be
made to neutralize the effects by a chemical antidote, but the
physician is usually summoned too late to accomplish much in this
manner. Morphine should be given in full doses, hypodermatically.
Insufflations of morphine in powder, soothing inhalations, fragments of
ice in the mouth, cold compresses, and, where possible, oleaginous
drinks, are indicated to relieve topical distress. Rectal alimentation
should be resorted to where the difficulties of deglutition are at all
great. If symptoms of suffocation occur, tracheotomy must be performed.
The results of traumatic pharyngitis require treatment according to
their special indications.

Erysipelatous pharyngitis is to be treated by the administration, by
enema if necessary, of large doses of quinia, tincture of the chloride
of iron, brandy, and diffusible stimulants. Alimentation is to be kept
up by mouth or rectum, as may be necessary, with as much food as can be
given containing the most nutrition in the smallest bulk possible.
Locally, a strong solution of silver nitrate (sixty grains to the
ounce) should be so applied as to cover a margin of unaffected
structures. Sedative inhalations are of service. Extension to the
larynx demands scarification or tracheotomy.

When the diagnosis of common membranous sore throat can be made out
with certainty, there is nothing calling for special treatment, but the
treatment pursued in ordinary sore throat may be generally followed
with advantage. When fetor exists, as during the detachment of patches
of exudation, antiseptic and detergent sprays may be employed.
Solutions of borax, boric acid, carbolic acid, potassium chlorate,
potassium permanganate, etc. are appropriate. In some individuals,
especially strumous and tuberculous subjects, there is a constitutional
proclivity to chronicity or to the recurrence of the peculiar
manifestations. More active measures will be required in these cases.
Locally, frequent application of the dilute acids (_i.e._ every day or
two) affords the most satisfactory results. Internally, iron and
cinchona preparations should be administered. Opium in small doses has
a special application--not as a narcotic, but as a gentle stimulant or
nervous tonic. Nux vomica or arsenic may be employed for a similar
purpose. The diet should be highly nutritious and easily assimilable.
Unnecessary exposure should be avoided, and supporting measures
generally, hygienic, as well as medicinal, should be persisted in.
Membranous pharyngitis sometimes exhibits a tendency to phagedaena. The
treatment for gangrenous sore throat is then indicated. It may invite
an attack of diphtheria or the diagnosis may be in doubt. In that case
the prudent course is to treat it as diphtheria, but to avoid the
recommendation for diphtheria of some indifferent remedy, during the
exhibition of which a case of membranous sore throat has recovered.
When extension to the larynx occurs threatening suffocation,
tracheotomy to avert death should be performed, as in croup or
diphtheria.

The sore throats of the exanthemata, of typhoid fever, etc., are to be
treated on the general principles applicable to catarrhal or
phlegmonous pharyngitis. Oedema or tumefaction, as in malignant
scarlatina, of a sufficient extent to obstruct respiration, is to be
relieved by scarification, and when this is inefficient resort must be
had to tracheotomy. The sore {400} throats caused by drugs are to be
treated first by removal of the cause, and afterward according to the
special indications.


Tuberculous Pharyngitis.

DEFINITION.--An acute ulcerative pharyngitis due to infiltration with
miliary and granular tubercle and the consequent destructive
metamorphosis.

SYNONYMS.--Acute tuberculous sore throat, Acute tuberculous
pharyngitis, Tuberculosis of the pharynx, Phthisis of the pharynx.

HISTORY.--Only of late years has tuberculosis of the pharynx been
distinctly recognized as a tuberculous disease. The tubercular sore
throat or pharyngitis described by Green of New York, and other authors
following him, is an affection of entirely different character, and not
tuberculosis at all. The chronic tuberculous sore throat of advanced
tuberculosis is likewise a different affection clinically, though of
the same histological character.

To the late Isambert[2] of Paris belongs the credit of definitively
recognizing the specificity of acute tuberculous sore throat or
pharyngitis, and to him likewise the credit of indicating its
differentiation from syphilitic sore throat, with which it had long
been confounded. To B. Fraenkel of Berlin[3] is likewise due the credit
of an accurate comprehension and elucidation of the clinical and
histological pathology of this disease.

[Footnote 2: _Annales des Maladies de l'Oreille, du Larynx, etc._, vol.
xi., 1875, p. 162; _Conferences cliniques sur les Maladies du Larynx et
des premieres Voices_, Paris, 1877, p. 219.]

[Footnote 3: _Berlin. klin. Woch._, Nov., 1876; _London Med. Record_,
Jan. 15, Feb. 15, 1877.]

ETIOLOGY.--Acute tuberculous pharyngitis is quite a rare disease. Its
predisposing causes, in all probability, are identical with those of
acute tuberculosis. Its exciting cause, in some cases at least, is some
unusual exposure to cold and wet. It is not certain that the throat is
affected before the lungs; but if this be the case, it is certain that
the lungs become affected soon afterward. The disease occurs in young
children, Isambert having recorded a case at four and a half years of
age, but it is much more frequent in adolescents and young adults. It
is impossible, as yet, to assign the reason why the pharynx rather than
other structures undergoes tubercularization in these exceptional cases
of pharyngitis. Syphilis sometimes coexists in the adult certainly, and
it may be questioned whether hereditary taint may not be an important
factor in determining tuberculosis in a region so frequently ravaged by
syphilis.

PATHOLOGY AND MORBID ANATOMY.--The local disease is essentially an
ulcerative pharyngitis or pharyngo-laryngitis, as may be, extremely
rapid in its progress, and terminating fatally within a few weeks, or a
few months at farthest. The ulcerative process usually begins on the
palatine folds or else on the lateral wall of the pharynx, thence
extending to the palatine folds, soft palate, uvula, and hard palate in
one direction, and toward the posterior wall of the pharynx in the
other. The uvula sometimes becomes thickened into a club-shaped,
gelatinous-looking mass, somewhat characteristic. Previous to
ulceration the mucous membrane is subjected to abundant infiltration
with miliary and granular tubercle just beneath the epithelial layer.
Macroscopically, these infiltrated portions of {401} tissue present as
irregular chagrinated groups of patches, generally confluent, which
when abundant or prominent are liable to be confounded with syphilitic
patches. Just beneath the surface the collections of tubercle project
as little semi-transparent grayish nodules, in size and form recalling
the appearance of vermicelli-seeds or fish-eggs. They steadily increase
in volume and in number, lose their translucency, and finally undergo
disintegration into lenticular ulcers with caseous bottoms and
undermined hyperaemic edges. The ulcers extend steadily in periphery
and in depth, and coalesce by necrosis of intervening mucous membrane.
Polypoid excrescences springing from the beds of the ulcers have been
described (Fraenkel). Collateral tumefaction takes place in some
instances, due, it is stated (Isambert), to infiltration of the tissues
by a gelatinous material, possibly a mucoid degeneration of the
connective tissue. The usual tendency of the disease, however, is to
incite atrophic metamorphosis of the adjacent tissues not undergoing
actual tubercularization. In many instances extension to the upper
portion of the larynx takes place; in some, extension to the vault of
the pharynx. Extension to the oesophagus, as has been remarked by
Mackenzie, and to the posterior nasal outlets, has not been noticed.
Enlargement of the cervical lymphatic glands is quite common.

Microscopic examination of the tissues of the pharynx has revealed
profuse infiltration with round cells--most frequently in the mucous
membrane and submucous connective tissue only, occasionally in the
muscular fibres likewise. The muscles sometimes undergo the fatty
degeneration, and the mucous glands both fatty and colloid
degeneration.

SYMPTOMATOLOGY.--The chief and characteristic subjective symptom is
extreme pain in swallowing (odynphagia)--pain much more intense than in
other morbid processes in the same locality, and inexplicable by the
extent of the visible disease merely. This pain often extends toward
the ears. Cough, adynamic fever, rapid emaciation, and so on are
present, as in acute tuberculosis generally.

DIAGNOSIS.--It cannot be stated that the diagnosis is easy. The two
distinguishing characteristics are the exquisite pain in swallowing and
the absence of pus from the surface of the ulcers. The aspect of the
ulcers differs, furthermore, from that of syphilitic ulcers by the lack
of opalescence and of inflammatory areolae. The gray nodules in the
affected mucous membrane are different from what is observed in any
other disease. These points, with the history of the attack, the family
history, and the probable evidence of tuberculosis in the lungs, will
usually serve to discriminate the disease from syphilis, for which it
is most likely to be mistaken. In cases of doubt ophthalmoscopic
examination of the choroid and iris may reveal tubercle. The bacillus
tuberculosis has been found in the detritus from the ulcers (Guttman,
Gurovitch). The fact must not be ignored that syphilitic and
tuberculous pharyngitis may exist together. Febrile symptoms, typhoidal
in type, in a case of supposed syphilitic sore throat will most likely
be indicative of tuberculosis.

PROGNOSIS.--The disease is rapidly fatal, apparently inevitably so. An
exceptional case has been recorded, however (Cadier[4]), living {402}
several years after the diagnosis had been made by Isambert and many
others.

[Footnote 4: _Annales des Maladies de l'Oreille, du Larynx, etc._,
July, 1883, p. 136.]

Death takes place by asthenia in from six weeks to six months;
occasionally within a fortnight from the apparent onset.

TREATMENT.--The little that can be accomplished in the way of treatment
is limited to improving the diet and hygienic surroundings, with the
administration of such constitutional remedial agents as are given in
acute tuberculosis, and palliative treatment of the local suffering.
For the latter purpose insufflations of iodoform and morphine are to be
recommended, two or three grains of the former with one-fourth to
one-half grain of the latter, once a day or oftener. Such insufflations
should be preceded by douches or sprays of sodium borate or
bicarbonate, to rid the parts of mucus and detritus. A drop or two of
carbolic acid, of eucalyptol, or of a solution of thymol may be
advantageously added for purposes of disinfection. Solution of hydrogen
peroxide (2 per cent. or weaker) is a very valuable agent for use in
spray or douche. It may be rendered more agreeable by the addition of a
few drops of some balsamic.

When swallowing is impracticable, nourishment by enema is indicated,
with forced feeding by means of a catheter passed through the larger of
the two nasal passages into the oesophagus.


Chronic Pharyngitis.

DEFINITION.--A chronic inflammation of the mucous membrane of the
pharynx, whether implicating the glandular structures or not, and
commonly associated with similar chronic inflammation of contiguous
structures.

SYNONYMS.--Chronic sore throat, Chronic angina.

Chronic pharyngitis presents in two varieties: 1, simple chronic
pharyngitis (chronic catarrhal pharyngitis, chronic catarrhal sore
throat), in which the disease does not affect, or affects but slightly,
the glandular structures of the mucous membrane; and 2, follicular
pharyngitis (granular pharyngitis, clergyman's sore throat), in which
groups of the follicular glands of the mucous membrane are enlarged,
and sometimes inflamed.

ETIOLOGY.--The predisposing causes of chronic catarrhal pharyngitis are
those enumerated under the head of the acute form of the affection, and
the exciting causes are repeated attacks of the acute malady.

The predisposing causes of chronic follicular pharyngitis are
overcrowding, and sedentary occupations; and the exciting causes are
chiefly improper use of the voice and exposure to local irritations,
mechanical and chemical, including too free use of condiments, tobacco,
and alcohol, gormandizing, and the alternations of hot food, cold
drinks, ices, and hot drinks at meals. It is not so often a direct
sequel of attacks of acute sore throat as a result of prolonged
catarrhal pharyngitis; and sometimes it appears to be chronic, so to
speak, from the outset.

Both forms of chronic pharyngitis are frequently associated with
chronic inflammations of the mucous membranes elsewhere, particularly
of the nasal passages and of the stomach, and, to a less extent, of the
genito-urinary apparatus; the entire train of phenomena, in some
instances, {403} being due to passive congestion dependent upon
impaired cardiac power. Similarly, it presents at times as one of the
accompaniments of exophthalmic goitre. It is often associated with
phthisis, and is sometimes found in phthisical subjects prior to the
detection of the pulmonary disease. It is sometimes coincident with
chronic cutaneous eruptions, and may depend on the same causes, whether
dietetic or nervous.

Uterine disturbances may give rise to chronic pharyngitis, probably by
reflex nervous influence, and so do other chronic and dispiriting
complaints. In like manner, depression of spirits and impairment of
bodily vigor from domestic, financial, and social chagrin provoke a
train of phenomena in which chronic pharyngitis may be a prominent
manifestation.

PATHOLOGY AND MORBID ANATOMY.--Simple chronic pharyngitis is a chronic
catarrhal inflammation of the mucous membrane and submucous connective
tissue of the pharynx, with irregular hyperplasia of all the
histological elements, chiefly affecting the epithelial layers and the
most superficial strata of the submucosa. The pharynx, the posterior
surface of the palate, and the pharyngo-palatine folds are the
structures most generally implicated, but the glosso-palatine folds,
the base of the tongue, and even the anterior surface of the palate,
are sometimes involved. At an advanced stage of the affection extension
may take place to the vault of the pharynx and the posterior nasal
outlets, and in occasional instances to the larynx.

The initial hyperaemia of diffuse congestion finally leads to permanent
dilatation of tracts of capillaries varying in area and mode of
distribution, sometimes recalling the territorial outlines upon a map.
The mucous membrane is bright red in color and irregularly thickened,
sometimes into prominent welts or folds. The palate is often relaxed.
Hypersecretion takes place over the entire diseased surface, and there
is considerable desquamation of turbid epithelium, which sometimes
accumulates in masses. Glands are dilated and hypertrophied here and
there, but not in every instance, or if so indiscernibly, at least, to
the naked eye.

In some cases enlarged follicles are very prominent in the
infra-tonsillar space, between the anterior and posterior palatine
folds, and along the lateral walls of the pharynx down toward the base
of the tongue. The circumvallate papillae may also be enlarged, and the
fungiform papillae are sometimes very prominent and deeply congested.

In the folliculous variety of the disease the hyperplasia affects
chiefly the mucous glands and follicles, isolated or in groups,
together with zones of connective tissue surrounding them and the
epithelial investment of the mucous membrane in their immediate
neighborhood. A number of small projections, from the size of pinheads
to that of peas, mostly somewhat hemispheroidal, sometimes ellipsoidal
or quite irregular in configuration, stud the pharynx irregularly. When
clustered they are more apt to occupy the lateral angles of the
pharynx. In this locality indeed the chains of glands and their
enveloping mucous membrane sometimes present in longitudinal ridges
which simulate additional or adventitious post-palatine folds. The
projections are usually opaque, deeper in color than the surrounding
congested mucous membrane, and velvety from loss of squamous
epithelium. Sometimes they are translucent, as if filled with colloid
material, probably retained and degenerated secretion. {404} Very often
their contents undergo caseous degeneration, and sometimes even
calcification--a variety designated tubercular by Green, Gibb, and
others, but far different histologically from true tuberculosis of the
pharyngeal glands, which does occur occasionally in phthisical
patients.

Delicate red lines of engorged capillaries usually surround the base of
these projections. There is great disposition to the accumulation of
viscid, discolored mucus on the surface of the mucous membrane. As the
disease progresses all the processes become more widely extended, until
finally nearly the entire pharyngeal and oral mucous membrane becomes
involved. The soft palate becomes relaxed and the uvula thickened and
elongated, sometimes to an extreme degree. Chronic folliculous
tonsillitis exists in many cases.

When either form of chronic pharyngitis continues for a long while
unchecked, there may result atrophy of the glandular structures and
epithelial elements generally, giving rise to pharyngitis sicca or
atrophic pharyngitis (so-called dry catarrh). There is then but scanty
secretion, and this dries rapidly upon the surface of the thin mucous
membrane, which becomes rough, inflexible, and glazed.

SYMPTOMATOLOGY.--Cough, expectoration, impairment of voice, dysphagia,
and uncomfortable sensations in the throat present in various degrees
according to the stage of the disease and the temperament of the
patient. Hemming and hawking to clear the throat often become habitual,
especially in cases associated with chronic internal rhinitis, being
provoked in many instances by secretory products which drop into the
pharynx or glide along its walls. It is sometimes important to
distinguish this habit from the cough of laryngeal or bronchial
irritation.

In cases associated with chronic gastritis the loss of appetite and
consequent emaciation accompanying the symptoms of pharyngitis
sometimes lead friends of the patient to a mistaken diagnosis of
consumption; and when, as is not infrequent, chronic bronchitis also
coexists, even the physician may be misled.

In many instances of chronic folliculous pharyngitis evidently of long
standing, and accidentally discovered at times to the surprise of the
patient, no history of the classical group of symptoms can be obtained.

DIAGNOSIS.--The diffuse congestion of the mucous membrane and the
absence of marked involvement of the follicles are, with the history of
the case, the main discriminative features in the diagnosis of chronic
catarrhal pharyngitis. The regular or irregular masses of tissue
projecting beyond the general surface of the mucous membrane are the
distinguishing characteristics of chronic folliculous pharyngitis. The
vascular network of dilated capillaries mapping the surface into
numerous irregular small areas of different sizes is not peculiar to
either variety.

PROGNOSIS.--The prognosis of chronic catarrhal pharyngitis is favorable
when no irremediable malady of body or mind exists. Much depends on the
practicability of improving the dietetic and hygienic environment of
the patient. The prognosis is likewise good in chronic folliculous
pharyngitis under favorable surroundings, so far as relief from
suffering is concerned; but the follicles, when long hypertrophied, so
rarely undergo absorption under any treatment that their destruction
becomes necessary--quite a different thing from their cure. The
enlarged follicles once destroyed, the collateral irritative
inflammation caused by {405} them usually subsides. Impairment of
voice, a result of the disease, may be remedied in young subjects, who
will learn to use the voice with the abdomen in distension; but much
improvement cannot be expected in old subjects and in those in whom the
disease has been produced by improper methods of declamation, which are
beyond correction.

TREATMENT.--In chronic catarrhal pharyngitis constitutional treatment
adapted to the diathetic condition is required in the first instance.
Alkaline laxatives are usually indicated by the irregularly coated
tongue and the tendency to costiveness. These may be advantageously
administered in half a pint of hot water one hour or so before meals,
with a view of washing the stomach free from accumulations of mucus,
epithelium, and retained products of digestion and decomposition, so
that its condition may be improved for the reception and digestion of
the ensuing meal. Topical medication of the throat is likewise
requisite. This should be of a soothing character. Mild astringents are
applicable, but strong astringents are often actually injurious. Silver
nitrate and cupric sulphate in stick or strong solution should not be
used; but sprays of dilute solutions (one or two grains to the ounce of
distilled water), twice or thrice a day, are often of service. Zinc
sulphate (five grains to the ounce) may be used in the same manner.
Zinc chloride (ten grains to the ounce), carefully applied to the
surface daily with a broad brush or soft cotton wad, is a useful
remedy. Tannin in ether sometimes answers admirably, a delicate film
being left for some time on the surface. Solutions of bismuth nitrate
or borate in glycerin applied locally often relieve uneasiness. A broad
flat brush is the best instrument for making these applications, placed
low in the pharynx so as to paint the entire posterior wall by a single
movement from below upward.

For home use, sprays, three or four times a day, of tar-water,
containing five or ten grains to the ounce, of sodium borate or
bicarbonate, or sodium, potassium, or ammonium chloride, or sodium,
potassium, or ammonium iodide, are soothing and efficacious, and much
superior to gargles. They are often preferred warm. Demulcent lozenges
(gelatin, acacia, althaea, glycyrrhiza) slowly dissolved in the mouth
often relieve topical discomfort.

Much more active treatment is required in chronic folliculous
pharyngitis. Judicious constitutional treatment is of great importance.
Topical medication is of equal importance. In recent cases of moderate
intensity the ordinary treatment for the catarrhal variety sometimes
suffices. In cases of long standing strong solutions of silver nitrate
(sixty to one hundred and twenty grains to the ounce), carefully
applied with the broad flat brush twice or thrice a week, are often of
great remedial effect. Iodine (one drachm to the ounce of glycerin),
alone or in combination with equal parts of carbolic acid, applied
daily, may be serviceable in cases unimproved by the silver nitrate.
Dilatation of the capillaries may sometimes be benefited by
applications of ergot (fluid extract) or ergotin (grs. x-xx to the
ounce). Enlarged follicles of long standing are rarely amenable to
astringent and alterant topical treatment. They require destruction.
The agent to be used is a matter of indifference as a rule, and,
according to the taste or resources of the practitioner, may be the
solid silver nitrate, caustic potash, London paste, zinc chloride,
{406} or the incandescent cautery, whether heated by fire, hot naphtha,
or electricity.

The sprays and lozenges already mentioned are useful in this variety of
pharyngitis also. They may be medicated with sedative ingredients
according to indications for the relief of pain and discomfort.

In cases resisting the plan of treatment suggested mercuric chloride
may be successfully used, both internally (gr. 1/16 two or three times
a day) and in spray, a drachm or less night and morning (one grain to
four ounces). External counter-irritation by repeated blistering over
the larynx and under the angles of the jaws is useful in some
instances. During treatment the voice should be used as sparingly as
practicable.

In chronic atrophic pharyngitis the treatment, constitutional and
local, should be such as favors secretion from mucous
membranes--internally, cubeb, pyrethrum, calamus, xanthoxylum,
jaborandi, ammonium chloride; topically, sprays, four or more times a
day, of hot water, glycerin and water, ammonium chloride. Patients
sleeping with the mouth open should wear an apparatus, extemporized or
made to order, to keep the lower jaw closed in sleep.


Syphilitic Pharyngitis.

DEFINITION.--A specific inflammation of the mucous membrane of the
pharynx or of the mucous membrane and submucous tissues, the result of
syphilis, and often associated with like disease in contiguous
structures.

SYNONYMS.--Pharyngitis syphilitica, Pharyngitis specifica, Syphilitic
sore throat, Syphilis of the pharynx.

ETIOLOGY.--Contamination by syphilitic virus is the sole cause, whether
by direct inoculation or by systemic poisoning, hereditary or acquired.
Direct inoculation proceeds from primary sores on the lips, tongue,
cheek, and hard palate, themselves the result of actual contact with
sores in other individuals. Initial sores have been seen upon the
tonsils, palatine folds, pharynx, and even the epiglottis. Direct
inoculation from secondary sores may be communicated by the
tooth-brush, blow-pipe, pipe-stem, trumpet, mouth-piece of
feeding-bottle, pap-boat, or similar article previously used by an
infected individual. Uncleansed surgical instruments convey the disease
in like manner.

PATHOLOGY AND MORBID ANATOMY.--Syphilitic pharyngitis--or, more
strictly speaking, syphilitic sore throat--occurs in all varieties,
primary, secondary, tertiary, and hereditary. Secondary manifestations
are the most frequent, and primary sores the most infrequent. The
primary sore is soft in some instances, and hard in others. Phagedaenic
ulceration may ensue. Secondary manifestations are usually bilateral,
and often symmetric in configuration and distribution. They appear from
a few weeks to a few months after infection, and are among the most
frequent early manifestations of secondary syphilis. The inflammatory
process begins in erythema, usually diffuse, often punctated, sometimes
in patches. It extends from above downward more frequently than in the
reverse direction, but may spread in any direction. The lesion
commences upon the soft palate and tonsils more frequently than {407}
on the pharynx, but may commence in any portion of the oro-guttural
cavity. Tumefaction ensues, with lividity of the surface. The
epithelial cells become distended; the resulting opalescence, somewhat
characteristic, eventually subsides into a central opacity, the true
mucous patch or condyloma latum. Mucous patches vary in size from mere
specks to large irregular surfaces, often the result of coalescences.
They sometimes become red and granular and covered with purulent
products. Microscopically (Cornil), they consist of thickened
epithelium upon a base of proliferated lymphoid cells, which often
infiltrate the deeper tissues extensively. They may disappear in the
course of a few weeks by resolution and absorption. Sometimes
suppuration occurs in small superficial abscesses which discharge upon
the surface. Several abscesses discharging simultaneously in
coalescence, an extensive ulcer may result, which, in repair, leaves a
cicatricial trace of its site. Flat and circular bluish-white patches,
due to thickening of epithelium, appear after the first year of
constitutional syphilis, and may exist in association with the true
mucous patch. They bleed readily on rough handling, but rarely undergo
ulceration.

Tertiary manifestations may present within a few months after infection
or not until many years. Gummatous infiltration of the connective
tissue, diffused or circumscribed (syphiloma), follows diffuse or
localized erythema, and then the gummata break down, discharge by
ulceration, and leave deep-seated irregular ulcers with undermined
edges and surrounded with inflammatory areolae. These manifestations
are much more frequent in the palate than in the pharynx, and the
ulcerative process often destroys the uvula and large portions of the
palate and palatine folds. When the pharynx and posterior surface of
the palate are both ulcerated, cicatricial adhesions are sometimes
inevitable, and thus serious stricture of the suprapalatine pharyngeal
canal may ensue. The lesion may be quite limited in extent or may
involve the entire pharynx. The ravages may become sufficiently
extensive to involve the vertebra and the skull or to perforate the
large blood-vessels. Cicatrization in the pharynx is vertical or
stellate as the rule, and the peculiar pallid lustre of the cicatrices
is quite characteristic of the syphilitic lesion. In many instances
secondary and tertiary manifestations commingle. Ulceration is then
more likely to extend superficially than in depth.

Hereditary manifestations pursue much the same course as tertiary
manifestations. They usually occur before puberty, but are occasionally
delayed until after maturity. Deferred tertiary and late hereditary
manifestations sometimes present the characteristic ulceration of the
commingled secondary and tertiary disease; and this form of ulceration
is often incorrectly attributed to scrofulosis and to lupus.

SYMPTOMATOLOGY, COURSE, DURATION, COMPLICATIONS, AND SEQUELAE.--The
subjective symptoms of syphilitic pharyngitis are those of erythematous
and ulcerative pharyngitis of like grade, except that there is very
little pain. The course is chronic unless specific treatment be
instituted, when prompt repair may be expected unless the general
health has been much undermined. The duration is indefinite. The
manifestations subside under treatment, and recur if it is not
sufficiently prolonged. Complications occur with similar manifestations
of syphilis in adjacent or contiguous or distant structures, as may be.
The most frequent sequel in neglected cases is cicatricial stricture.

{408} DIAGNOSIS.--Bilateral inflammation in symmetric distribution is
very characteristic of syphilis. Irregular ulcers with undermined
borders and surrounded by inflammatory areolae are similarly
characteristic. Acknowledged history of syphilis or the detection of
syphilitic manifestations elsewhere serves to confirm the diagnosis. In
cases of doubt a few days' treatment with specific remedies in large
doses will almost invariably serve to clear up the diagnosis.

PROGNOSIS.--The prognosis as to life is good unless the ulcerations
have become so extensive as to threaten perforation into blood-vessels
or the patient has become greatly debilitated. The prognosis as to
freedom from cicatricial adhesions and stricture is not good in the
presence of lesions which have destroyed large territories of tissue,
even under very careful management.

TREATMENT.--Specific medicines in positive doses constitute the most
effectual treatment. Mercury is indicated in secondary lesions.
Extensive ulcerative tertiary and hereditary lesions are peculiarly
susceptible to large doses (30 to 90 or more grains daily) of potassium
iodide, under the influence of which they often heal without any local
applications whatever. As soon as a positive impression has been
produced the dose may be diminished. The parts should be kept clean and
comfortable by periodic douching with sprays of alkaline solutions, or,
what is still more serviceable, with a ten-volume solution of hydrogen
peroxide diluted with one or more parts of distilled water. The best
local application to the edges of the pharyngeal syphilitic ulcers is
the solid cupric sulphate. Chromic acid (1:8) is a serviceable local
stimulant to indolent ulcers. Necrosed fragments of bone should be
removed. Should any impediment to respiration take place during
administration of the iodides, oedema of the larynx may be suspected,
and should be looked for. Professional supervision is requisite for
many months after the lesions have healed. Cicatricial sequelae of
stricture require surgical interference.




{409}

DISEASES OF THE OESOPHAGUS.

BY J. SOLIS COHEN, M.D.


Oesophagitis.

DEFINITION.--Inflammation of the oesophagus.

SYNONYMS.--Inflammatory dysphagia, Inflammation of the gullet.

Oesophagitis may be acute or chronic. Either form may be idiopathic,
deuteropathic, or traumatic.


Acute Oesophagitis.

DEFINITION.--Acute inflammation of the gullet.

SYNONYM.--Oesophagitis acuta.

HISTORY.--Until the publication in 1829 of a thesis by J. T. Mondiere
entitled _Recherches sur l'Inflammation de l'Oesophage, et sur quelques
points de l'anatomie pathologique de cet organ_, little study had been
devoted to acute inflammation of the oesophagus; and since that time
Mondiere's researches have been largely utilized by subsequent writers.
It has been taken for granted that Galen's mention of pain in the
oesophagus[1] has indicated his recognition of the disease. Fernel[2]
mentions phlegmon of the oesophagus; Honkoop[3] describes inflammation
of the oesophagus; J. P. Frank[4] describes an oesophageal angina; and
Joseph Frank[5] seems to have been the first author to use the term
oesophagitis. Since the publication of Mondiere's monograph the
principal systematic descriptions have been those of Hamburger[6] Von
Oppolzer[7] Zenker and Ziemssen[8] Luton,[9] and Bernheim.[10]

[Footnote 1: _De locis affectis_, lib. iv. cap. iii.; lib. v. cap. v.]

[Footnote 2: _De partium mortis et sympt._, lib. vi. p. 277.]

[Footnote 3: _Specimen inaugurale de morbo oesophagi inflammatorie_,
Lugd. Batav., 1774.]

[Footnote 4: _De curandis hominem morbis, Epitome praelectionibus
academicis dicata_, Mannheim, Stuttgardt, and Vienna, 1792-1820.]

[Footnote 5: _Praxeous medica praecepta universa_, Lipsiae, 1826-32.]

[Footnote 6: _Klinik der Oesophaguskrankheiten_, Erlangen, 1871.]

[Footnote 7: _Vorlesungen uber specielle Pathologie und Therapie_,
Erlangen, 1872; Englished in abstract by the writer in _Philada. Med.
Times_, 1872.]

[Footnote 8: _Handbuch der speciellen Pathologie und Therapie_, 1877;
English translation, New York, 1878, vol. viii.]

[Footnote 9: _Dictionnaire de Medecine et de Chirurgie pratiques_,
Paris, 1877, vol. xxiv.]

[Footnote 10: _Dict. Encyclopediques des Sciences medicales_, Paris,
1880, vol. xiv.]

ETIOLOGY.--Acute oesophagitis is quite a rare disease. It occurs
idiopathically, deuteropathically, and traumatically--traumatically far
the most {410} frequently, and idiopathically least frequently. It is
doubtful whether any special predisposing causes of oesophagitis can be
indicated. Nevertheless, infancy has been so cited by some authors
(Mondiere, Billard, Behier, and Steffan). Slight idiopathic
catarrhal--or rather erythematous--oesophagitis occasionally ensues in
the adult from sudden or prolonged exposure to cold and moisture, and
under such circumstances may sometimes be regarded as rheumatic in
origin, subsiding after a few hours' continuance, to be immediately
succeeded by manifestations of articular rheumatism, acute or subacute,
as in some analogous examples of rheumatic pharyngitis. Exceptionally,
severe oesophagitis may follow a simple cold (Noveene, cited by
Bernheim), or presents as an extension of sore throat, the result of
cold (Graves[11]). It is induced also by the habitual use of very hot
drinks and food, and occasionally by the opposite extremes, the use of
very cold articles of food and drink (Mondiere, Bourguet, Hamburger).
The abuse of tobacco and alcohol is alleged as quite a frequent cause
of mild oesophagitis, usually occurring, however, in association with
pharyngitis from the same causes.

[Footnote 11: _Lon. Med. and Surg. Journ._, 1836-37, No. 172, and
_Clinical Lectures_, Dublin, 1864, p. 592.]

Oesophagitis sometimes follows the deglutition of irritating medicines
or moderately caustic poisonous substances not sufficiently acid to
produce veritable traumatic oesophagitis. Mercury, codeina, and
particularly tartar emetic, are cited as capable of exciting
oesophagitis.

Large doses of tartar emetic, as formerly administered in pneumonia
(Laennec[12]), sometimes produced a peculiar form of pustulous
oesophagitis, not unlike the pustulous oesophagitis sometimes occurring
as part of the local manifestations of small-pox.

[Footnote 12: _Traite de l'Auscultation medicale, etc._, Paris, 1837,
vol. iii. p. 560, illustrated; Laboulbene, _Anatomie pathologique_, and
_Nouveau Dict. de Med. et de Chir._, vol. xxiv. p. 370, illustrated;
Von Oppolzer, _op. cit._, p. 109.]

Deuteropathic catarrhal oesophagitis occurs sometimes as an extension
of catarrhal pharyngitis on the one hand, and of catarrhal gastritis on
the other. It also occurs in scarlet fever, measles, and typhus fever.
It is likewise consecutive to the various diseases and surgical lesions
of the tube itself. Parasitic oesophagitis occurs as an extension of
parasitic stomatitis or thrush. Deuteropathic circumscribed phlegmonous
oesophagitis is sometimes produced by extension of inflammation from
softened caseous bronchial glands at the bifurcation of the trachea,
and by pressure from mediastinal tumors, aneurism of the aorta, etc.

Pseudo-membranous oesophagitis is almost always deuteropathic. It has
been encountered chiefly in association with pseudo-membranous
pharyngitis or diphtheria, and with croupous pneumonia, but likewise in
enteric and typhus fever, in cholera and in dysentery, in measles,
scarlatina, and small-pox, in nephritis, tuberculosis, carcinoma, and
pyaemia.

In a case of hysteria, to be mentioned later, the entire epithelial
coat of two-thirds of the oesophagus was discharged by emesis. In this
respect the local disease--in that instance at least--resembles
pseudo-membranous enteritis.

Traumatic oesophagitis is produced by the deglutition of corrosive
substances, which destroy portions of the mucous membrane in their
passage or excite a suppurative inflammatory process, or is produced by
the {411} passage of foreign bodies of sharp and irregular contour, or
by the passage of surgical appliances, whether used for actual
operations or for explorations merely.

In rare cases traumatic oesophagitis is the result of wounds with
firearms or other weapons.

Phlegmonous oesophagitis may be the result of disease or injury of the
interior of the oesophagus, or of its external coat by extension of
disease from tissues surrounding it. Foreign bodies, arrested in the
oesophagus or wounding it in their passage to the stomach; injuries
from surgical appliances, exploratory or operative, employed in
treatment for foreign bodies in the tube or in cases of stricture and
morbid growth; and chemical irritants swallowed by accident or
design,--are the chief causes in the former class of cases; but
pustulous and pseudo-membranous oesophagitis must likewise be regarded
as occasional causes. The causes operating upon the exterior of the
tube primarily are suppurative laryngitis and tracheitis, tumefaction
and softening of bronchial and tracheal lymphatic glands, and caries of
the spine. Isolated cases have been attributed to emboli in connection
with valvular diseases of the heart (Parenski, cited by Daton), and to
fits of anger (J. Frank and Rigal, cited by Daton). In certain cases
the cause is unassignable, and is then usually attributed to some
dyscrasia, syphilis in particular.

PATHOLOGY AND MORBID ANATOMY.--Acute oesophagitis presents both as a
diffused inflammation and a circumscribed process, annular or irregular
in contour. It does not appear from the post-mortem records consulted
that any special portion of the tube is particularly liable to
circumscribed inflammation, though the lower fourth appears most
frequently affected. The inflammatory process may be simply superficial
or erythematous, catarrhal or desquamative (Zenker and Ziemssen), or it
may be phlegmonous, and thus interest the submucous tissues as well as
the mucous membrane. This may terminate in abscess or in diffuse
suppuration with ulcerations. In occasional instances gangrene ensues.
Both in diphtheria and in croupous pneumonia, pseudo-membranous
oesophagitis is an occasional complication; and the same process is
said to have been observed in typhus fever, measles, scarlatina,
cholera, pyaemia, dysentery, tuberculosis, and carcinoma (Von Oppolzer
and others).

Pustulous oesophagitis occurs in small-pox, and occasionally follows
the use of tartar emetic in large doses.

The morbid anatomy of acute idiopathic oesophagitis, though usually
detailed in descriptions of the disease, must be known by theory much
more than by demonstration, few examples coming under the inspection of
the pathologist in time to distinguish the progressive stages of the
inflammatory process, and still fewer being revealed by oesophagoscopy
during life. The lesions most frequently observed post-mortem are
thickening, softening, and desquamation of the epithelium, with very
scanty accumulations of viscid mucus here and there upon the mucous
membrane. The mucous membrane is seen to have suffered numbers of
pinhead or slightly larger superficial circumscribed erosions, rounded
or longitudinal, and likewise a few actual ulcerations. The follicles
of the mucous membrane are often both swollen and hypertrophied,
reaching the size of peas, especially in the upper portion of the tube.

The desquamation of the epithelium usually takes place in small {412}
patches. One case, however, has been recorded (Birch-Hirschfeld[13]) in
which a young hysterical woman, after suffering three days with acute
oesophagitis without assignable cause, ejected by emesis a membranous
tube two-thirds of the entire length of the oesophagus, and shown under
examination to have been the completely detached epithelial coat of the
oesophagus, wholly normal in its upper layers and infiltrated with
agglomerated round cells in its lower layers. It was supposed that the
mass had been detached in consequence of acute subepithelial
suppuration.

[Footnote 13: _Lehrbuch der pathologische Anatomie_, Ziemssen, 1877, p.
818; English translation, vol. viii. p. 140.]

In addition to swollen and hypertrophied follicles there may be some
evidence of ulcerative destruction of these follicles. Mondiere and
others declare that this folliculous inflammation and ulceration may
exist without any other change whatever in the remaining constituents
of the mucous membrane; and therefore this form of oesophagitis was
termed folliculeuse by Mondiere (folliculous oesophagitis). This form
of the disease has been observed in typhus fever, in croup (Mondiere),
and in tuberculosis. Ulceration of the oesophagus occurs, likewise, in
carcinoma and in oesophagitis from corrosive fluids, wounds, and other
injuries.

In pseudo-membranous oesophagitis the exudation occurs usually in small
circumscribed gray-yellow or brownish flakes or stripes distributed
over different portions of the surface, more closely, however, at the
upper portion of the tube. Superficial erosions are sometimes observed
beneath these deposits, and occasionally ulcerations, at times
sufficient to give rise to severe hemorrhage (Zenker and Ziemssen).
Usually the mucous membrane is but slightly hyperaemic. In some
instances pseudo-membrane is so massed in plugs as to occlude the
cavity of the tube, as with obturators. In cases associated with
pseudo-membranous gastritis the oesophageal manifestations are greatest
in the vicinity of the cardiac extremity. Somewhat allied to
pseudo-membranous oesophagitis, and apt to be confounded therewith, is
the parasitic deposit of the Oidium albicans in cases of thrush; in
connection with which subject this point has already received
attention.

The pustules of small-pox may interest any portion of the mucous
membrane, but are most numerous at the upper portion of the tube. They
may be discrete or confluent. The pustules from tartar-emetic poisoning
are most numerous at the two extremities of the canal. It is contended
that the so-called pustules of variolous oesophagitis are really
superficial variolous ulcers, the antecedent specific lesions having
been lenticular papules merely, with abrasion of the softened
epithelial layer.[14] Variolous oesophagitis may excite an accompanying
catarrhal or pseudo-membranous oesophagitis. The local lesions, be they
pustular or ulcerous, heal without cicatrices.

[Footnote 14: _Virchow's Deutsche Klinik_, 1858, No. 31, p. 306; Zenker
and Ziemssen, _op. cit._, p. 146.]

Phlegmonous oesophagitis presents both as a diffuse and as a
circumscribed inflammation. Examined after death, there is abundant
purulent infiltration into the submucous connective tissue, which has
undergone destruction in portions of its extent. The infiltration
pushes the folds of mucous membrane outward to the interior of the
tube, and thus diminishes its calibre considerably when the
infiltration is annular. {413} The mucous membrane is congested,
ecchymosed, and covered with mucus, and has usually suffered
desquamation of portions of its epithelium. Ulcerations through the
mucous membrane will have taken place in some instances. Cicatrices
mark the location of ulcers which have healed.

In the diffuse variety the oesophagus is inflamed and swollen, as a
whole, in proportion to the extent of the disease. In the circumscribed
variety the morbid appearances are circumscribed. It has been known to
continue into the stomach (Belfrage and Hederius, cited by Zenker and
Ziemssen), and to extend therefrom (Ackermann, _idem_).

As described by Zenker and Ziemssen, chiefly from ten autopsies by
themselves and one by Belfrage and Hederius, phlegmonous oesophagitis
begins with a submucous purulent infiltration, transforming the areolar
tissue into an apparent layer of pus, although microscopic examination
shows the bundles of connective tissue to be intact at first. At a
later period they become really destroyed, leaving mere crevices filled
with pus. The mucous membrane, but little involved, may remain normal
or may present the evidence of catarrhal inflammation, desquamation of
epithelium, congestion, and slight deposits of mucus. The muscular
coat, intact to the unaided eye, under the microscope gives some
evidence of purulent infiltrations. The pus may finally escape through
the mucous membrane, in extensive infiltrations, at several points,
which give the parts a sieve-like appearance when the perforations are
closely grouped.

Gangrene sometimes occurs as a result of intense phlegmonous
oesophagitis, but this is far more rare than the gangrene supervening
after injuries by caustic substances. Sometimes it results from
capillary embolism (Rokitansky, Virchow, cited by Luton, _op. cit._).

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATION, COMPLICATIONS, AND
SEQUELAE.--The main subjective symptoms of oesophagitis are pain and
difficulty in swallowing, with febrile phenomena superadded in severe
cases. In simple oesophagitis of mild character these symptoms may be
so slight as to be attributed to other causes or be disregarded
altogether. In most instances there is a dull, steady pain beneath the
sternum, some sense of impediment to deglutition or absolute pain in
swallowing (odynphagia), and occasional regurgitation of viscid, glairy
mucus, food, or acid products from the stomach. In severe cases the
substernal pain is more acute and more diffused, and is frequently
associated with pain between the scapulae and to the left side. This
latter pain may be attributable to acid from the stomach. Sometimes the
pain is described as acute, especially during the passage of large
boluses, particularly if they are very hot, or even very cold. The seat
of pain, however, does not always indicate the seat of inflammation,
even though the pain be always referred to the same locality. When the
cervical portion of the tube is implicated, tenderness may sometimes be
detected by external pressure or by special movements of the head and
vertebrae.

The amount and character of the dysphagia vary greatly. Sometimes there
is a sense of impediment to the passage of food, solid or liquid, or
solid only, through and beyond the painful region. This sensation may
be accompanied or be followed at a brief interval by regurgitation of
food or mucus, or food enveloped with mucus, the latter in some
instances tinged with blood. The deglutition or the regurgitation may
be {414} accompanied by spasm of the muscular coat of the oesophagus.
The dysphagia is not always due to tumefaction of the mucous membrane,
but usually in part to coexisting inflammation of the muscular coat or
infiltration between the sheaths of muscular fibres, paralyzing their
efforts at contraction.

There are no subjective symptoms which permit discrimination between
desquamative catarrhal oesophagitis and folliculous oesophagitis. The
only symptom particularly indicating pseudo-membranous oesophagitis is
the expulsion of shreds of the membrane by hawking or by emesis; but a
strong inference is justifiable when the ordinary symptoms of
oesophagitis occur in cases of pseudo-membranous pharyngitis or
croupous pneumonia.

Phlegmonous oesophagitis is indicated by the presence of pus or of dead
mucous membrane in the matter regurgitated or vomited. In severe cases
there is considerable febrile reaction. In children, convulsions may
supervene from reflex irritation conveyed along the pneumogastric
nerve.

The course of acute catarrhal oesophagitis is, as a rule, short, the
pain and dysphagia usually subsiding in a few days, with complete
resolution and no unfavorable sequelae. When due to obstruction, the
course is indefinitely prolonged. Sometimes it subsides into a mild or
unsuspected chronic oesophagitis. In the symptomatic oesophagitis of
febrile diseases, the course is longer and unequal. In severer forms
and in phlegmonous oesophagitis, the disease may be protracted by
suppuration, abscess, gangrene, perforation of the oesophagus, and
other complications. It often terminates fatally--in three or four days
in some cases--sometimes under symptoms of collapse. Cases may recover
without important sequelae, but stricture very often results from
cicatricial complications. Chronic oesophagitis is a more frequent
sequel of the phlegmonous variety than of the catarrhal. It, in its
turn, may give rise to dilatation of the oesophagus, annular or
diverticular, from detention of food and consequent pressure.

DIAGNOSIS.--The diagnosis will rest upon the interpretation of the
coexistence of a certain number of the symptoms mentioned. Idiopathic
phlegmonous oesophagitis may readily be mistaken for dorsal myelitis by
the location of the pain--the more so that the spinal disease is
occasionally attended with spasm of the oesophagus, and the myelitis by
difficulty in deglutition; but the differentiation may be determined by
the inability to produce oesophageal pain by pressure made along the
dorsal vertebrae. In deuteropathic or traumatic phlegmonous
oesophagitis, the history of the attack will indicate the probable
nature of the malady, and prevent the mistake. Diffused oesophagitis is
suspected when the general pain or the painful dysphagia appears to
extend along the entire tract of the oesophagus, or at least a large
portion of it.

Circumscribed oesophagitis is usually indicated by odynphagia at a
certain point of the tube after completing the act of deglutition. The
location of the inflammation can sometimes be determined by
auscultation of the descent of the alimentary bolus or of a swallow of
water (Hamburger), which may yield evidence to the ear of arrest or
impediment to its passage. Auscultation of the oesophagus, however, is
less useful in acute oesophagitis than in stenosis, stricture, and
mechanical obstruction. When available in oesophagitis, the normal
sound of the passage of water down {415} the gullet becomes masked, and
accompanied by that of regurgitative ascent of small bubbles of air.
Sometimes there is a slight friction sound during the act of
deglutition itself. In circumscribed oesophagitis, especially when
annular, as is most frequently the case, sounds are heard attributable
to marked obstruction to the descent of the bolus. Abscess cannot be
positively diagnosticated until after its rupture and the appearance of
pus in the matters regurgitated or otherwise expelled from the
oesophagus.

Catheterism of the oesophagus is hardly justifiable as a method of
diagnosticating oesophagitis, though proper enough when it becomes
important to determine the locality of attendant obstruction.

It is important that inflammation of the oesophagus be differentiated
from spasm, stricture, stenosis, carcinoma, and other oesophageal
maladies; nearly all of which present the same main subjective
symptoms--pain and impediment to deglutition. The history of the case
is in itself a guide of great diagnostic value, often quite sufficient
for the purpose; but in its absence or retention other data must be
gathered.

Spasm of the oesophagus is most frequent in neurotic subjects. Its
manifestations are often sudden. It is evanescent or intermittent. It
is not a febrile affection. It is often overcome in a moment by
catheterization.

Stricture presents often an additional symptom of oesophagitis, the
regurgitation of mucus and food. The differentiation is made, in cases
of doubt, by the passage of the bougie or catheter.

Carcinoma of the oesophagus, while recent, may present much similitude
to oesophagitis, but as the case advances, the glandular involvements,
the cachexia, the expulsion of cancerous fragments, and the vomiting of
blood seem sufficient to prevent further confusion.

PROGNOSIS.--The prognosis is favorable in acute catarrhal oesophagitis,
the manifestations often subsiding within a few days; sometimes,
indeed, within a few hours, and that, too, without special medication.
It is therefore largely dependent on the cause of the oesophagitis and
the severity and extent of the malady. The only unfavorable
prognostications arise from the impediment to nourishment and the
complications which may ensue.

In presumptive pustulous oesophagitis from the use of preparations of
antimony, the manifestations usually subside within a few days upon
suspension of the remedy. Sometimes, however, these cases terminate
fatally.

Pseudo-membranous oesophagitis is usually fatal in its significance,
and the same may be said of the pustulous or ulcero-papular
oesophagitis of small-pox.

Phlegmonous oesophagitis is of grave augury, though many cases recover.
It may prove fatal within two or three days, though life is usually
prolonged for several days, even in fatal cases. When not fatal,
abscesses are apt to form, which, discharging internally or externally,
are followed by stricture or fistulae.

Both ulcerative oesophagitis and intense catarrhal oesophagitis may
terminate in chronic thickening of the walls of the oesophagus and in
cicatricial adhesions more or less extensive.

TREATMENT.--Mild oesophagitis requires no special treatment. The
patient should be kept within doors, and be fed on rice-water, {416}
barley-water, and other mucilaginous articles of diet, so as to avoid
all sources of local irritation. These drinks are usually better borne
hot than cold, but sometimes cold is quite agreeable. When cold can be
well borne the frequent deglutition of pellets of ice is useful as well
as agreeable, and ice-cream becomes a medicinal article of diet.

In severe cases the measures indicated become still more requisite, and
the use of the voice should be restrained in addition. All unnecessary
efforts at deglutition should be avoided, and anodyne medicaments
(opium, hyoscyamus, belladonna) should be added to the demulcent food
or beverages. When swallowing is impracticable or very painful,
nutriment should be given by the bowel, and medicines by the bowel or
by the skin. Thirst may be allayed by retaining fragments of ice in the
mouth from time to time, by rinsing the mouth with simple or acidulated
water, by sucking the juice of acid fruits, or by allowing compressed
effervescent lozenges to dissolve slowly in the mouth.

The external application of cold compresses, continuously or in
frequent renewals, is also indicated.

Febrile phenomena require ordinary antiphlogistic medication. When this
is impracticable, the indications may be met by using the cold bath or
the wet sheet, and by administering antipyretics hypodermatically.
Traumatic oesophagitis from a foreign body requires removal of the
object if still in the oesophagus; that from swallowing alkalies is met
by the use of acidulated beverages (vinegar and water, Orfila); that
from swallowing acids, by the use of alkaline drinks, of which the
handiest is usually soap and water. As soon as they can be procured
this may be changed for lime-water and calcined magnesia.
Theoretically, the carbonates of the alkalies are indicated likewise,
but it is contended (Hamburger, Oppolzer) that the extrication of the
carbonic acid gas renders mechanical rupture of the corroded oesophagus
imminent. Subsequently, fresh water should be freely drunk, or be
injected into the oesophagus when swallowing is impracticable. The
subsequent treatment is to be instituted upon general principles.


Chronic Oesophagitis.

DEFINITION.--A chronic inflammation of some of the tissues of the
oesophagus.

SYNONYM.--Oesophagitis chronica.

ETIOLOGY.--Chronic oesophagitis is sometimes a sequel of the acute
affection. More frequently it is the result of excessive use of strong
alcoholic beverages or of very hot drinks. It is said to be sometimes
the result of passive congestion in chronic pulmonary and cardiac
diseases. It follows the prolonged sojourn of foreign bodies in the
oesophagus. It exists in connection with carcinoma of the oesophagus,
with dilatation, and with stricture of the oesophagus, and with other
diseases obstructing the tube externally or internally. It is sometimes
produced by caries of the vertebrae, both scrofulous and syphilitic,
and by the pressure of aneurismal and other tumors.

PATHOLOGY AND MORBID ANATOMY.--Hypertrophy of the mucous membrane of
the oesophagus, of the submucous connective tissue, and {417} even of
the muscular coat, are the processes which take place in chronic
oesophagitis, especially when it has been of long continuance. This
hypertrophy, when at or near the cardiac extremity, may produce
stricture (Rokitansky and others), with subsequent dilatation of the
oesophagus from its frequent and prolonged distension by food which
should have passed on at once into the stomach.

On post-mortem examination the main evidences of disease are most
frequent in the lower third of the organ. Its folds of mucous membrane
are thick and prominent, dirty red, brownish-red, or gray, as may be,
abraded here and there, and covered with viscid muco-purulent
secretions. Abscesses and ulceration are not uncommon in cases due to
prolonged pressure or extension of disease from outside the tube. Such
ulceration has not uncommonly been the source of serious hemorrhage.

Diffuse inflammation of the peri- or retro-oesophageal connective
tissue has been noted as an occasional sequel to the inflammatory
process in the walls of the oesophagus.

SYMPTOMATOLOGY, ETC.--The symptoms of simple chronic oesophagitis are
similar in the main to those of mild acute oesophagitis, but are often
still more moderate, and therefore likely to be overlooked. In severe
cases the symptoms are chiefly those of the disease, usually stenotic,
which has excited the chronic inflammatory process. The course is
prolonged and the duration indefinite. Stricture is a frequent sequel.

DIAGNOSIS.--The diagnosis rests on the same principles and inferences
as in acute oesophagitis, the symptoms, however, being of longer
duration. The auscultatory signs of arrest or impediment in the descent
of the solid or liquid bolus are usually more definite than in acute
oesophagitis. The same differentiations are available in excluding
spasm, stricture, and malignant diseases. The use of the sound or
catheter is much more justifiable than in the acute variety.

PROGNOSIS.--The prognosis is usually unfavorable, on account of the
great liability to stricture and occlusion from organization of
inflammatory products.

TREATMENT.--Chronic oesophagitis may require both local and
constitutional treatment. The constitutional treatment will have to be
adapted to the cause of the disease. If due to obstructed circulation
in consequence of valvular disease of the heart, digitalis and remedies
of its class will be indicated. If due to obstructive pulmonic disease,
chloride of ammonium and alkaline remedies will be indicated.
Syphilitic inflammation requires the mixed treatment, with mercuric
chloride and potassium iodide or their equivalent. Iodides, indeed, are
often required in non-specific cases, and are useful particularly in
ordinary circumscribed oesophagitis. Under all conditions alcoholic
beverages should be interdicted, and so should the deglutition of all
irritating food and drink. Mild, bland, and mucilaginous substances
should be largely employed in food and drink. The copious use of
carbonic-acid waters is also recommended (Oppolzer). Sinapisms and
revulsives to the side of the cervical and dorsal vertebrae are also
recommended by some writers (Oppolzer).

The topical treatment consists in the systematic use every few days of
aqueous solutions of astringents (alum, tannin, ten to thirty grains to
the ounce) or alterants (compound solution of iodine, twenty minims to
the {418} ounce) passed gently over the diseased surfaces by means of a
piece of soft surgical sponge securely attached to a flexible staff.

Severe pain of rather sudden occurrence is usually attributable to
circumscribed ulceration, and is best treated by superficial
cauterization, as above, with a dilute solution of silver nitrate (ten
grains to the ounce). These remedies may be used in the form of
ointments of the same strength smeared upon a rather large flexible
bougie. To relieve pain and sense of constriction belladonna or
stramonium ointment, applied in the same manner, sometimes fulfils a
useful indication. Before making these applications attempts should be
made by auscultation to locate the seat of disease or obstruction.
After subsidence of the disease, occasional catheterization may be
practised at intervals of several weeks, in order to detect any
recommencing stenosis.


Ulcerations of the Oesophagus.

DEFINITION.--Circumscribed destruction of portions of the mucous
membrane of the oesophagus, the result of inflammatory processes.

ETIOLOGY.--Ulceration of the oesophagus occurs as a result of
inflammation of the organ, as discussed in connection with
Oesophagitis, and the cause varies with the character of the
oesophagitis, whether idiopathic, traumatic, or symptomatic of disease
elsewhere. Diseases, constitutional or local, provocative of ulceration
of the oesophagus, usually implicate some portion of either the
alimentary or the respiratory tract.

SYMPTOMATOLOGY.--The symptoms are in the main those described under
Acute Oesophagitis, particularly the expulsion of sanguinolent products
or of unmixed blood. Perforation into the trachea is indicated by
expectoration of food or drink; perforation into the great vessels, by
haematemesis, usually fatal; and perforation into the mediastinum, by
emphysema and purulent cellulitis. When large or extensive ulcerations
have cicatrized they occasion symptoms of organic stricture.

PATHOLOGY AND MORBID ANATOMY.--Referring to the corresponding section
under Oesophagitis, attention may be directed here to the liability of
deep-seated ulcers of the oesophagus to perforate the gullet and
establish fistulae with the trachea, bronchi, mediastinum, aorta, and
carotid artery, according to the locality of the lesion. These lesions
are usually necessarily fatal.

DIAGNOSIS.--The presence of blood in matters regurgitated or vomited
forms the chief diagnostic indication of ulceration of the oesophagus,
taken in connection with the usual symptoms of acute or chronic
oesophagitis.

PROGNOSIS.--The prognosis is altogether dependent on the nature of the
disease which has given rise to the ulceration.

TREATMENT.--The constitutional treatment will depend on the nature of
the disease which has occasioned ulceration. Ergot and turpentine are
administered in case of hemorrhage--the former best, perhaps,
hypodermatically. Attempts are sometimes made to cauterize the ulcer or
ulcers with nitrate-of-silver stick conveyed in a covered slotted
canula, to be exposed when the fenestrum reaches the ulcerated
locality, previously {419} determined by catheterization, or inferred
to be reached by the sensations of the patient. The practice is
uncertain in its manipulation and questionable in its results.


Stricture of the Oesophagus.

DEFINITION.--A constriction of the calibre of the oesophagus, whether
spasmodic or organic in character. This definition excludes stenosis
due to pressure from without.


Spasmodic Stricture of the Oesophagus.

DEFINITION.--A contraction of the muscles of the oesophagus, of
variable duration, causing partial or complete stenosis of the gullet
and interfering with the passage of food or of food and drink to the
stomach.

SYNONYMS.--Oesophagismus, Spasm of the oesophagus, Cramp of the
oesophagus, Convulsive dysphagia, Spasmodic dysphagia, Spasmodic
stenosis of the oesophagus, Spastic stricture of the oesophagus.

HISTORY.--On this subject there is little of importance in medical
annals previous to the observations of Frederick Hoffmann,[15] and
little of importance subsequently save the observations of
Mondiere,[16] though numerous personal observations are on record, as
well as a number of excellent compilations in various monographs,
text-books, encyclopaedias, and dictionaries.

[Footnote 15: _De spasmo gulae inferioris_, Halae, 1733; _De morbis
oesophagi spasmodicis_, Opera omnia, vol. iii., Geneva, 1761.]

[Footnote 16: "Recherches sur l'Oesophagisme ou Spasme de l'Oesophage,"
_Arch. gen. de Med._, April, 1833.]

ETIOLOGY.--Spasmodic stricture of the oesophagus is a neurosis often
hysterical. It is much more frequent in females than in males, and,
although observed in young subjects and less frequently in old ones, is
most common between the ages of twenty and fifty. It is sometimes
observed in several members of a neurotic family. It is often
associated with other evidences of neurosis, but sometimes constitutes
the sole manifestation. Sometimes the cause defies detection. Sometimes
it can be traced to a fear of strangulation, induced primarily by some
accidental impediment to deglutition or the entrance of a foreign body.
Strong mental emotion, such as the dread of hydrophobia after having
been bitten by a dog, sometimes produces the affection.

It occurs in connection with organic lesions of the oesophagus, organic
lesions of the stomach, organic lesions of the larynx and trachea, and
organic lesions of the lungs, heart, large blood-vessels, and
perioesophageal tissues, but likewise as a reflex disorder, with
lesions of distant organs, as the genito-urinary tract, the intestines,
the brain and spinal cord. Even pregnancy may produce reflex
oesophagismus. It sometimes occurs as a direct or reflex manifestation
of gout and of rheumatism. In a few instances it occurs as one of the
manifestations of tetanus and of hydrophobia.

SYMPTOMATOLOGY, COURSE, DURATION, ETC.--The spasm may affect {420} the
oesophagus only, or may be associated with spasm of the muscles of the
pharynx. It is usually manifested in a sudden inability to swallow or
to complete the acts of deglutition. This may be transitory or may
continue for a number of hours. The relaxation of the spasm is
sometimes followed by the discharge of flatus and the copious secretion
of pale urine. The spasm may recur at irregular intervals or be more or
less distinctly intermittent. Sometimes it precedes every effort at
deglutition. In some instances it occurs only upon attempts to swallow
certain kinds of food, and the articles of food vary with different
patients. Cold viands sometimes produce spasm when warm and hot food is
tolerated. Consciousness of a liability to spasm increases the
dysphagia for the time being, or brings it on suddenly when this
liability had been forgotten. The spasm is sometimes painless and
sometimes painful. In some instances it is associated with partial
regurgitation of a mass of air (the globus hystericus).

The dysphagia is rarely complete, instances in which no liquids can be
swallowed being infrequent. The aliment swallowed usually passes on
into the stomach, upon relaxation of the spasm, after a certain period
of detention varying from a number of seconds to many minutes. In cases
of prolonged or persistent spasm the aliment is usually rejected,
either at once or after a time, according as the contraction takes
place at the pharyngeal extremity of the oesophagus or lower down. When
rejected after some detention in the gullet, the aliments are usually
enveloped with mucus or followed by expulsion of mucus and of flatus.

In some subjects the pain in swallowing is severe. Sometimes it is
associated with spasm of the diaphragm (hiccough), spasm of the
air-passages, palpitation of the heart, and syncope.

The liability to spasm sometimes continues for years. Sometimes it
ceases permanently as suddenly and as unexpectedly as it began.

The seat of the spasm is referred by the patient to different regions,
which in their totality comprise the entire extent of the oesophagus.
In some patients the seat varies on different occasions. The actual
seat of any individual spasm is best determined by exploration with the
oesophageal bougie or by auscultating the oesophagus during the passage
of a bolus. It is most frequent perhaps at the upper extremity, and
then perhaps at the cardiac extremity. When habitually low down, there
is some liability to permanent distension of the oesophagus from
repeated retentions of food at the same place for hours together. In
some instances food is regurgitated from the oesophagus after its
retention for a day or even longer. When the spasm is high up, the
regurgitation may follow the act of deglutition almost immediately.

PATHOLOGY AND MORBID ANATOMY.--The affection being usually a pure
neurosis, there is no oesophageal lesion to be cited. In some of the
few autopsies recorded, constriction has been noted without lesion of
tissue.

DIAGNOSIS.--The diagnosis is based on the sudden onset of the spasm
without assignable cause, its intermittent or recurrent character, its
manifestation in advance of the effort at deglutition, the symptoms of
regurgitation, the coexistence of some of the affections mentioned in
connection with its etiology, and on the satisfactory result of
exploration with the oesophageal bougie; which differentiates the
affection from organic stricture or mechanical obstruction. In
catheterization of the oesophagus {421} in cases of pure spasm,
although the sound is usually arrested at the seat of constriction, it
passes onward after a few moments by sudden relaxation of the spasm.
Sometimes, indeed, the very first manipulation of this kind overcomes
the spasm permanently.

In the absence of other indications the differentiation from spasm of
organic origin rests, in great measure, on the conservation of
nutrition, cases being few in which the spasm is persistent enough to
interfere so materially with the ingestion of aliment as to produce
emaciation.

PROGNOSIS.--The prognosis is usually favorable in spasm of the
oesophagus, except in cases where the underlying malady is itself a
grave one. Patients do not die of neurotic spasm of the oesophagus. In
the majority of cases it is susceptible of cure within a few weeks,
sometimes much more promptly. Even when it continues for months or for
years there is little fear of permanent injury to the general health,
inasmuch as sufficient nutriment of some kind or other can be ingested
to sustain the patient.

The duration of the affection depends upon the surroundings of the
patient, his amenability to treatment, and the existence or absence of
disease in the oesophagus or elsewhere. In cases dependent upon
diseased conditions in the oesophagus or elsewhere the character of the
disease controls the prognosis, both immediate and ultimate. Thus,
aneurism of the aorta, tuberculosis, ulceration of the larynx and
trachea, carcinoma of the stomach, tetanus, and hydrophobia present the
highest unfavorable indications. Purely neurotic cases are extremely
prone to recurrence.

TREATMENT.--The treatment to be pursued will depend upon the nature of
the case. If due to organic lesion in the oesophagus or in some other
organ, the treatment will be directed to that affection, whatever it
may be. If due to emotional disturbance, therapeutic efforts will be
directed to their suppression or removal. If purely hysterical,
appropriate constitutional remedies for that condition will be
prescribed. These comprise asafoetida, valerian, camphor, musk, oxide
of zinc, bromides, belladonna, conium, and so on, best administered in
small doses at frequent intervals.

Local treatment is almost always necessary, both for its beneficial
mechanical effects and for its emotional influence. This consists in
the systematic passage of the bougie; and it is by far the best
practice to insist upon the patient's submission to it without an
anaesthetic. In cases of intense hyperaesthesia, which are rare, and in
the initial exploratory passage of the instrument in highly excitable
or uncontrollable subjects, anaesthesia may be resorted to if there be
no contraindication. The mere passage of the bougie will often effect
immediate relaxation of the spasm. When required, the manipulation may
be repeated a few times at intervals of several days. Should the
passage of the bougie determine the stricture to be purely spasmodic,
the patient should be made to partake of food in the physician's
presence at first, and afterward under the supervision of an efficient
attendant, until it becomes evident that there is no absolute
impediment to the passage of food. The presence of the physician during
early attempts at taking ordinary food imparts such confidence in the
patient that he soon overcomes his dread of strangling and learns to
eat again as he should do. Meantime, it may be necessary from time to
time to pass the bougie just before food is taken. {422} In such cases
it is well to smear the instrument with ointment of belladonna, so as
to deposit it more or less along the entire tract of the oesophagus.
Failing by these methods, success may follow the occasional passage, at
intervals of a few days, of a sponge probang saturated with a very weak
solution of iodine or of silver nitrate.

Counter-irritation along the course of the pneumogastric nerve or along
the spine is sometimes useful.

Electricity is sometimes employed to overcome the spasm; but
intra-oesophageal electrization of every kind is risky from the danger
of exciting fatal syncope from irritation of the pneumogastric nerve.
This objection is not applicable to percutaneous electrization, save in
a much more limited degree. Caution is requisite even with external
manipulations along the tract of the pneumogastric nerve; and such
manipulations, therefore, should not be undertaken without sufficient
familiarity with the effects of electric currents in that situation.

Taken all in all, the best results seem to follow the systematic use of
the bougie and enforced deglutition under the eye of an attendant in
whom the patient feels reliance can be placed in case the food should
"go the wrong way" or become impacted in the gullet.


Organic Stricture of the Oesophagus.

DEFINITION.--Diminution in the calibre of the oesophagus in consequence
of organic alterations in its walls, whether interstitial, cicatricial,
or malignant.

SYNONYM.--Stenosis of the oesophagus.

HISTORY.--As mentioned in connection with other affections of the
oesophagus, so with organic stricture: though much more has been
written on the subject, it is to the observations and publications of
Mondiere, so frequently cited, that we must credit medical literature
with a due appreciation of this topic. The last thirty years especially
have been prolific in the record of cases, and their study has been
further stimulated by the attention directed to the operation of
gastrostomy as a means of prolonging life in cases otherwise hopelessly
fatal.

ETIOLOGY.--Organic stricture of the oesophagus is occasionally
congenital. As a rule, life is rarely prolonged under such conditions,
but cases are on record in which it has been preserved to quite
advanced age. Thus, in a female who died from inanition at fifty-nine
years of age, after lifelong symptoms of stricture (Everard Homes[17]),
there was an annular stricture behind the first ring of the trachea;
and in a male subject who died with pneumonia at seventy-four years of
age, after lifelong symptoms of stricture,[18] the stricture was found
at the cardiac extremity of the oesophagus, which was enormously
dilated its entire length above the constriction.

[Footnote 17: _Biblioth. med._, t. viii. p. 260; Michel, _Dict.
Encyclopedique_, t. xiv. p. 466.]

[Footnote 18: Wilks, _Path. Trans. London_, xvii. p. 130; Holmes, _The
Surgical Treatment of the Diseases of Infancy and Childhood_, 2d ed.,
p. 137.]

In the majority of cases the stricture is due to cicatricial
obliteration of more or less of the calibre of the oesophagus, the
result of losses of substance following scalds produced by caustic
substances swallowed, mostly by accident and sometimes by design.
Wounds of all kinds, {423} whether from the interior, as in the case of
foreign bodies and instruments of extraction, or from the exterior, as
in the case of surgical operations, wounds from firearms, and the like,
are apt in their cicatrization to give rise to this form of stricture.

Though denied by some authorities, syphilitic disease of the oesophagus
is an undoubted cause of stricture. Setting aside disputed records of
older authorities, we may cite recent cases reported by Lancereaux,
West,[19] Wilks, Virchow, and Lublinski,[20] the latter-named going
deeply into the bibliography, pathology, and therapeutics of stricture
from syphilis. The author could add his personal testimony were it
requisite.

[Footnote 19: _The Lancet_, 1872.]

[Footnote 20: _Berlin. klin. Woch._, Aug. 20, 1883; _London Medical
Record_, Nov. 15, 1883, p. 489.]

Stricture of the oesophagus is likewise occasioned by the presence of
papillomatous, fibroid, and other morbid growths. Carcinoma is quite a
frequent cause.

The frequent deglutition of undiluted spirituous liquors is said to
give occasion at times to stricture of the oesophagus, but in these
instances this result is usually due to precedent chronic oesophagitis
thereby excited, and terminating in infiltration and hyperplasia of the
submucous connective tissue, and sometimes great thickening of the
epithelium as well.

Males are more frequently the subjects of stricture of the oesophagus,
and early adult life the most frequent period for its occurrence,
though it may present at any age.

SYMPTOMATOLOGY.--Except in traumatic cases, the earliest symptoms,
preceded in some instances by indications of mild oesophagitis, perhaps
unnoticed or unrecognized, are occasional impediments to deglutition of
large and firm boluses, or rather a mechanical obstacle to completion
of the act of glutition occurring at intervals of a few meals or a few
days. After a while the swallowing of a large solid bolus becomes
permanently impracticable. Then, sometimes, repeated efforts become
necessary to swallow small masses of solid food; and even to do this
may require external manipulation, or at least the additional pressure
of liquids swallowed immediately after the solid bolus. These efforts
are sometimes attended with spasm, regurgitation, and pain, and may be
accompanied in addition with tracheal dyspnoea, and with nervousness in
consequence. As the disease progresses it becomes impossible to swallow
solid food, and subsequently even fluid food in extreme cases. The
bolus is then often regurgitated immediately after its deglutition, and
may be covered with mucus, blood, pus, or fragments or detritus of
ulcerated malignant growth, according to the nature of the case. Pain
and sensations of rawness are often felt at the point of constriction,
whence the pain often radiates toward one or both scapulae. If the tube
is much dilated above the stricture, the food may be detained in the
sac for several hours, and then be regurgitated in a softened,
partially-decomposed condition. Should the mass be so situated as to
compress the trachea, suffocative symptoms may be produced.

In stricture due to organic disease there may be dysphonia from
pressure or injury to the recurrent laryngeal nerve producing paralysis
of the vocal band. The anatomical relations of the left recurrent nerve
renders it the much more liable of the two to become implicated.
Moderate dyspnoea may result from this paralysis by reason of the
reduced space of the glottis.

{424} PATHOLOGY AND MORBID ANATOMY.--Organic stricture of the
oesophagus is usually due to disease or structural change involving the
mucous membrane and submucous connective tissue; but the muscular
structure may become involved likewise. It may, however, be due to
abnormal laxity of the mucous membrane, permitting a fold to occupy a
position impeding the passage of the bolus.

In cases which are not carcinomatous the diminution in the actual
calibre of the tube is usually due to submucous proliferation of
connective tissue and to thickening of the mucous membrane. The
encroachment on the calibre of the tube may be quite slight, or may be
so great as to amount to almost complete occlusion.

The seat of stricture is at the upper portion of the oesophagus most
frequently, then at the cardiac extremity, at the point of crossing by
the left bronchus, and at the point of passage through the
diaphragm--all localities slightly constricted normally--but it may
occur at any portion.

In most instances the stricture is single. There may, however, be two,
three, or even four strictures. Multiple strictures are most common
after deglutition of caustic substances which have made their way clear
down into the stomach.

Syphilitic strictures are usually single, and so, as a rule, are
strictures of malignant origin. The latter are much larger in extent.

Cicatricial strictures from caustic substances may be in the form of
bands, rings, or longitudinal stripes or folds. Sometimes they are
quite extensive, and have been known to interest fully one-third of the
length of the oesophagus. The circumference, length, calibre, and
thickness of the stricture, however, vary within the most extreme
limits. Occasionally occlusion of the tube is complete.

The detention of food above the stricture usually dilates the
oesophagus, producing hypertrophy of the mucous membrane and submucous
connective tissue, followed in its turn by fatty degeneration. Atrophy
of the oesophagus may ensue below the stricture if at all tight, and
the mucous membrane becomes thrown into longitudinal folds.

DIAGNOSIS.--The diagnosis of organic stricture of the oesophagus rarely
presents difficulty. Dysphagia, spasm, and regurgitation are quite
characteristic of stricture. When the constriction is high up, the
vomiting or regurgitation of food may closely follow its deglutition;
when low down, this act may be delayed ten or fifteen minutes, in some
cases for hours. Alkaline reaction of the vomited matters is indicative
of their having failed to reach the stomach. The presence of
blood-cells, pus-cells, and cancer-cells indicates ulceration,
suppuration, and malignant disease, respectively.

Auscultation of the oesophagus during deglutition of water will
indicate the seat of stricture by revealing the ascent of consecutive
air-bubbles even when palpation with bougies fails. The passage of
oesophageal bougies or the stomach-tube into the oesophagus will often
reveal the point of stricture. Its length is estimated by the distance
of the resistance offered to the passage of the instrument; its
diameter, by the size of the largest instrument which can be passed
through it; and its consistence, by the character of the resistance.
Care is requisite in manipulating with these instruments, lest by undue
exertion of force they be passed through an ulcerated portion of the
wall of the tube or {425} a diverticulum. The character of the
resistance is sometimes the sole means of differentiating stricture
from stenosis due to compression of the oesophageal wall from its
outside.

It sometimes happens, in individuals with impaired sensitiveness of the
epiglottis or vestibule of the larynx, that the exploratory bougie is
introduced into the air-passage instead of the gullet. The usual
premonitory phenomena of suffocation will indicate the mistake. There
is some likelihood, too, of entering the larynx in individuals with
unusually prominent cervical vertebrae and in cases of stricture at the
extreme upper portion of the oesophagus. In introducing these
instruments into the oesophagus, therefore, it is well that they be
guided along the fore finger of the disengaged hand, and passed deeply
into the throat, either to the side of the larynx or behind it. By
keeping to the side and reaching the oesophagus by way of the
laryngo-pharyngeal sinus the risk of entering the larynx may be
avoided. Before introducing the tube the case should be carefully
examined for aneurism, which by pressure sometimes gives rise to the
ordinary subjective symptoms of stricture. Should aneurism be detected,
passage of the tube would be hazardous.

PROGNOSIS.--The prognosis is in most instances unfavorable. It is
comparatively favorable in cases of moderate stricture due to causes
apparently remediable. The extent and volume of the stricture progress
more or less slowly according to the nature of its cause, and in
non-malignant cases, such as are due to the action of caustic
substances, it may last for years before the patient, if not relieved,
succumbs, as he does, from gradual inanition. In the earlier stages,
before the hypertrophied muscles above the stricture undergo fatty
metamorphosis, the increased muscular power is sufficient to force
nourishment through the stricture; but when this becomes no longer
possible progressive marasmus must ensue. Meantime, abscess may become
developed in consequence of the pressure of retained food, and
tuberculous degeneration of the lung and local gangrene may take place
in consequence of the malnutrition.

TREATMENT.--The treatment of organic stricture of the oesophagus
resolves itself into maintenance of the general health, the
administration of the iodides to promote absorption of effusions into
the connective tissue or the muscles, mechanical and operative measures
for removal of the causes of the constriction or the strictured tissues
themselves, and operations for securing artificial openings below the
point of stricture for the introduction of nourishment (oesophagostomy
and gastrostomy). Nourishment by enema is of great value.

In carcinomatous stricture local measures are in the main
unjustifiable, as they usually entail injury which may prove very
serious. Arsenic internally is thought to retard the progress of
malignant disease when administered early and persistently. Morphine is
used hypodermically to assuage pain.

In cancerous and tuberculous disease great caution is requisite in
determining upon mechanical or surgical procedures. In cicatricial
stenosis from the effects of caustic substances, such measures may be
undertaken with much less consideration.

The local treatment consists in systematic mechanical dilatation with
bougies or mechanical dilators properly constructed. These are employed
{426} daily, every other day, or at more prolonged intervals, according
to the tolerance of the parts and the progressive improvement. They are
retained several moments at each introduction, and followed by the
passage and immediate withdrawal of an instrument of larger size. It is
often advisable that the final dilatation of each series be made with a
stomach-tube, so that liquid food may be poured through it from a
syphon or a small-lipped vessel, that there may be no necessity for
swallowing food for some hours thereafter. This method is continued
until it becomes evident that nothing further is to be gained by its
continuance. In cases that have been at all successful, the
introduction of the instrument should be repeated every week or two for
a long time, to prevent or retard recurrence of the constriction, which
is very liable to take place. M. Krishaber has reported[21] cases in
which a tube passed through the nose was retained from forty to three
hundred and five days; and from this success he deduces the
practicability of continuous dilatation in this manner. Billroth and
Rokitansky have encountered cases in which frequent dilatation had set
up inflammation of the surrounding connective tissue, which had caused
fatal pleurisy by continuity.

[Footnote 21: _Trans. Internat. Med. Congress_, London, 1881, vol. ii.]

Forcible dilatation by mechanical separation of the sides of a double
metallic sound has been employed with success in some instances. It is
a risky procedure.

Destruction of cicatricial tissue by caustics has been attempted, and,
though successes occasionally attend the practice, it is hardly
considered sufficiently promising.

Division of the stricture by internal oesophagotomy, with subsequent
dilatation, has been practised of late years, and offers some chances
of success. Oesophagostomy and gastrostomy have been performed in some
cases of impassable stricture, and the latter operation is gaining in
favor. For surgical details, however, we must refer to works on
surgery.


Carcinoma of the Oesophagus.

DEFINITION.--Carcinomatous degeneration of the oesophagus, whatever the
variety.

SYNONYM.--Cancer of the oesophagus.

ETIOLOGY.--Carcinoma is the most frequent disease of the oesophagus
that comes under professional observation. The most frequent variety is
the squamous-celled (53 out of 57, Butlin). Spheroidal-celled and
glandular-celled varieties are much less frequent. In some instances
the morbid product is a combination of the two. Colloid degeneration is
occasionally met with. Carcinoma is usually primitive. Its cause is
undetermined, but, as it is most frequent at the constricted portions
of the tube, pressure is supposed to be the exciting cause. It does not
always give rise to secondary infection. Sometimes it is an extension
from the tongue, epiglottis, or larynx, or from the stomach. It is most
frequent in males, and more so in the intemperate than in the
abstinent.

The immediate exciting cause is often attributed to local injury from
retention of foreign bodies or the deglutition of hot, acrid, or
indigestible substances.

{427} There appears to be some disposition to carcinoma of the
oesophagus in tuberculous subjects (Hamburger), while the children of
tuberculous parents may have carcinoma of the oesophagus, and their
offspring, again, tuberculosis.

SYMPTOMS.--The earliest local symptom is slight dysphagia, with
impediment to completion of the act of glutition--an evidence of
commencing stricture. Subsequently, inverted peristaltic action is
added, an evidence of dilatation above the stricture, with partial
retention of food. At a later stage vomiting will occur, with
admixtures of pus and sanguinolent fragments of cancerous tissue.

Progressive emaciation and impaired physical endurance usually precede
these local symptoms, but actual cachectic depression may come on quite
tardily. At first there is no pain; subsequently there comes on
considerable uneasiness at some portion of the tube. Finally, there may
be severe local burning or lancinating pains, particularly after meals.
If the disease be high up, there may be pain between the shoulders,
along the neck, and even in the head, with radiating pains toward
either shoulder and along the arm. If low down, there may be intense
cardialgia and even cardiac spasm. If the trachea or larynx be
compressed or displaced, dyspnoea will be produced. If the recurrent
laryngeal nerve be compressed, there will be dysphonia or aphonia.
Perforation of the larynx will be indicated by cough, expectoration,
hoarseness, or loss of voice; of the trachea, by paroxysmal cough,
dyspnoea, or suffocative spasm; of the lungs, by acute pneumonitis,
especially if food shall have escaped, and expectoration of blood, pus,
and matters swallowed, as may be; of the pleura, by pneumothorax; of
the mediastinum, by emphysema; of the pericardium, by pericarditis; of
the large vessels, by hemorrhage. Perforation of the aorta or pulmonary
artery is often followed by sudden death from hemorrhage, and of the
lungs by rapid death from pneumonitis.

PATHOLOGY AND MORBID ANATOMY.--Primitive carcinoma is usually
circumscribed. It is most frequent at the cardiac extremity, but often
occurs where the oesophagus is crossed by the left bronchus, and
sometimes occupies the entire length of the tube. The greater
proclivity of the lower third of the oesophagus has been attributed to
mechanical pressure where it passes through the diaphragm; that of the
middle third, to pressure of its anterior wall against the left
bronchus by the bolus. It begins, either nodulated or diffuse, in the
submucous connective tissue, implicates the mucous membrane, encroaches
upon the calibre of the tube, undergoes softening and ulceration, and
becomes covered with exuberant granulations. When the entire
circumference of the oesophagus is involved stricture results,
sometimes amounting eventually to complete obstruction. Ulceration
taking place, the calibre again becomes permeable. The oesophagus
becomes dilated above the constriction and collapsed below it.

As the disease progresses the adjoining tissues become involved.
Adhesions may take place with trachea, bronchi, bronchial glands,
lungs, diaphragm, or even the spinal column (Newman[22]). Perforation
may take place into the trachea, usually just above the bifurcation, or
into the lungs, pleura, mediastinum, pericardium, aorta, or pulmonary
artery. Abscesses are formed, the contents of which undergo
putrefaction. There {428} may be involvement of the pneumogastric
nerve, with reflex influence on the spinal nerves and the sympathetic
(Gurmay[23]).

[Footnote 22: _N.Y. Med. Journ._, Aug., 1879, p. 158.]

[Footnote 23: _Bull. med. de l'Aisne_, 1869; _Gaz. med. Paris_, April,
1872.]

DIAGNOSIS.--The diagnosis will rest on due appreciation of the symptoms
enumerated and the ultimate evidence of the cancerous cachexia.
Auscultation will often reveal the location of the disease. This may be
further confirmed by palpation with the bougie, but the manipulation
should be made without using any appreciable force. Laryngoscopic
inspection and digital exploration are sufficient when the entrance
into the oesophagus is involved.

Differential diagnosis is difficult at an early stage, and often to be
based solely on negative phenomena. At a later stage it is easy,
especially when cancerous fragments are expelled. In some instances a
tumor can be felt externally. Such a tumor, however, has been known to
have been the head of the pancreas (Reid[24]).

[Footnote 24: _N.Y. Med. Journ._, Oct., 1877, p. 404.]

Cancer of the oesophagus is liable to be confounded with chronic
oesophagitis, cicatricial stenosis, diverticulum, extraneous
compression, abscess, and non-malignant morbid growths.

PROGNOSIS.--The prognosis is unfavorable, the disease incurable. Death
may be expected in from one to two years, though sometimes delayed for
longer periods. Inanition or marasmus is the usual cause of death in
uncomplicated cases. Sometimes it takes place by haematemesis,
sometimes following involvement of the stomach, and sometimes wholly
unassociated with any direct disease of the walls of the stomach. Death
takes place not infrequently from perforation into adjoining organs,
and sometimes from secondary inflammation of other vital organs, as the
brain and the lungs.

TREATMENT.--There is little to be done in the way of treatment apart
from the constitutional measures indicated in carcinoma generally and
in chronic diseases of the oesophagus. The cautious use of the
stomach-tube to convey nourishment into the stomach is allowable during
the earlier stages of the disease only. It is dangerous after
ulceration has taken place, from the risk of perforating the walls of
the oesophagus, and thus hurrying on the fatal issue by injury to the
intrathoracic tissues.

When deglutition becomes impracticable or the passage of the oesophagus
absolutely impermeable to nutriment, food and alcoholic stimuli should
be administered by enema. Indeed, it is good practice to begin to give
nourishment occasionally by the bowel before it becomes absolutely
necessary, so as to accustom the part and the patient to the
manipulation. Narcotics to relieve pain are best administered
hypodermatically, so as to avoid unnecessary irritation of the rectum.

The passage of dilators, as in stricture of cicatricial origin, is very
hazardous. They produce irritation, which hastens the softening of the
tissues, and are open to the risk of penetrating the softened tissues
and passing through the walls of the oesophagus into the pleura, lung,
or mediastinum. Fatal accidents of this nature are on record.

Gastrostomy is sometimes performed to prolong life.


{429} Paralysis of the Oesophagus.

DEFINITION.--Loss of motive-force in the muscular tissue of the
oesophagus, whether intrinsic or reflex in origin.

SYNONYMS.--Gulae imbecillitas, Paralytic dysphagia, Atonic dysphagia.

ETIOLOGY.--Paralysis of the oesophagus may be caused by impairment of
function in one or more of the nervous tracts distributed to the
muscles concerned in dilating the upper orifice of the gullet or in
those concerned in the peristaltic movements which propel the bolus to
the stomach. These impairments of function may be nutritive in origin,
as in softening and atrophy of the nerve-trunk, or, as is more
frequent, they may be pressure-phenomena from extravasations of blood,
purulent accumulations, exostoses, tumors, and the like.

The paralysis may be due to disease or wounds of the nerves themselves
or of their motor roots, or of the cerebro-spinal axis, implicating
their origin, or to pressure and atrophy of a trunk-nerve in some
portion of its tract. It is likewise due to neurasthenia from
hemorrhage or from protracted disease (enteric fever, yellow fever,
cholera), or to systemic poisoning in diphtheria, syphilis, and
plumbism. It may be due to muscular atrophy or intermuscular
proliferations of connective tissue, to dilatation of the oesophagus,
and to disease in the tube. It may be due to mechanical restraint from
external adhesions of the oesophagus to intrathoracic tumors
(Finny[25]). It may result from sudden shock or fright. It may follow
the sudden reaction of cold upon the overheated body. It is one of the
manifestations of hysteria and of the hysteria of pregnancy.

[Footnote 25: _Dub. Journ. Med. Sci._, Oct., 1877.]

SYMPTOMS.--Partial paralysis may give rise to no symptoms at all. The
earliest manifestations are those of impediment to the prompt passage
of the bolus to the stomach, repeated acts of deglutition or additional
swallows of food or drink being necessary. Large masses are swallowed
and propelled onward more readily than small ones, and solids more
readily than fluids. There is often a characteristic gurgling attending
the passage of fluids along the tube. Swallowing is best performed in
the erect posture. These symptoms increase in severity as the paralysis
increases. There is little pain or none at all. In some cases there is
no regurgitation of food; in others, this is more or less frequent.
When the paralysis is complete, deglutition becomes impossible, and the
food attempted to be swallowed is expelled from the mouth and nose in a
paroxysm of cough. Sometimes the food enters the larynx and produces
paroxysms of suffocation or threatens asphyxia.

There is more or less flow of saliva from the mouth in consequence of
the inability to swallow it; and in some cases the losses of material
from the blood are so great as to reduce the patient very rapidly.

PATHOLOGY AND MORBID ANATOMY.--Paralysis of the oesophagus may be
partial or complete. It may be associated with paralysis of the
pharynx, palate, tongue, epiglottis, or larynx; with so-called bulbar
paralysis; with general paralysis; with cerebro-spinal disseminated
sclerosis.

DIAGNOSIS.--The diagnosis rests mainly on the symptoms of dysphagia,
especially when associated with paralyses elsewhere. It is
differentiated {430} from paralysis of the pharynx by the ability to
swallow the bolus and the apparent arrest of the bolus at some portion
of the tube. Auscultation of the oesophagus will determine the locality
of the arrest. It likewise affords presumptive evidence of an
alteration in the usual form of the bolus, which, being subjected to
compression at its upper portion only, assumes the form of an inverted
cone. The remaining auscultatory indications are similar to those of
dilatation.

There is no impediment to the passage of the stomach-tube or
oesophageal sound, or to its free manipulation when within the
oesophagus.

When the symptoms quickly reach a maximum, they indicate a paralysis
due to apoplexy, and so they do when the symptoms are sudden, hysteria
being eliminated. Paralysis due to gumma or other cerebral tumor is
much slower in its course.

PROGNOSIS.--In idiopathic paralysis, the local or special affection to
which it is due being curable, the prognosis is favorable, especially
if the paralysis be confined to the oesophagus. Recovery, however, is
often slow, even in curable cases. In hysterical paralysis the
prognosis is good. In deuteropathic paralysis the prognosis is much
less favorable, and will depend upon the nature of the causal
disease--apoplexy, insanity, cerebral tumor, syphilis, etc.

TREATMENT.--The treatment varies with the nature of the cause as far as
combating the origin of the disease is concerned. With regard to the
intrinsic paralysis of the oesophagus itself, strychnine and its
congeners are indicated, and may be administered hypodermatically if
the difficulty in swallowing be very great. If the paralysis be
partial, it is better to give nux vomica or Ignatia amara by the mouth,
in hopes of getting some beneficial astringent influence on the walls
of the oesophagus.

In all instances the feeding of the patient is an important element in
treatment. Masses of food arrested in the tube should be forced onward
with the sound. In some cases nourishment must be habitually introduced
through the stomach-tube and nutritive enemata be resorted to.

Electricity, though sometimes successful, is a risky agent to employ,
because, as announced by Duchenne, the use of an oesophageal electrode
is attended with some risk of unduly exciting the pneumogastric nerve
and thereby inducing syncope.


Dilatation of the Oesophagus.

DEFINITION.--An abnormal distension of a portion of the oesophagus or
of the entire tube, whether general, annular, or pouched.

SYNONYMS.--Oesophagocele, Hernia of the oesophagus, Diverticulum of the
oesophagus.

ETIOLOGY.--Dilatation of the oesophagus is occasionally met as a
congenital affection (Hanney,[26] Grisolle,[27] and others). The cause
under these circumstances is obscure. Usually, however, dilatation of
the oesophagus is of mechanical origin, due to distension by food or
water above a stricture or an impacted foreign body. Presumptive
paralysis of the muscular coat in chronic oesophagitis is alleged as a
source of similar distension.

[Footnote 26: _Edinb. Med. and Surg. Journ._, July, 1883.]

[Footnote 27: _Traite Element. de Path. int._, Paris, 1883, ii. p.
358.]

{431} General dilatation is presumed to be the mechanical result of
constriction of the cardiac extremity, leading to distension of the
oesophagus by the accumulation of large quantities of liquids.
Sometimes it is due to paralysis of the muscular coat, permitting its
distension by food.

Annular dilatation is sometimes due to distension just above the seat
of a stricture. Sometimes it is due to impaction of a foreign body;
sometimes there is no mechanical impediment; occasionally it is
observed as a congenital anomaly.

Pouched dilatation (diverticulum) is usually due to retention of food
immediately above an impacted foreign body or some obstruction of
another character. Some of the muscular fibres of the oesophageal wall
become separated and spread asunder, allowing the mucous membrane to be
gradually forced through them by repeated efforts of deglutition upon
retained masses of food or drink, until finally a pouch is formed,
hernia-like, outside of the tube. Another mode of production is said
(Rokitansky[28]) to consist in the subsidence of tumefied glands
outside the oesophagus, after adhesions had been contracted with the
oesophagus during the inflammatory process. The shrinking of these
enlarged glands to their normal volume sometimes draws the tube outward
into a funnel-shaped sac constricted at its margin by the muscular
coat, which has receded from the pouch or has been stripped loose. The
same form of dilatation is likewise an occasional result of rupture of
the muscular coat sustained in blows or falls. It occasionally exists,
too, as a congenital defect, and this has been attributed (Bardeleben
and Billroth[29]) to partial closing of one of the branchial fissures
externally, while the internal opening has remained patent.

[Footnote 28: _Archiv. gen. de Med._, 1840, p. 329.]

[Footnote 29: _Trans. Clin. Soc. London_, 1881, p. 130.]

SYMPTOMATOLOGY.--The symptoms, at first, are usually those of
obstruction to the passage of food, but before this obstruction occurs
dilatation may have existed without symptoms. In some cases of
diverticulum high up, there is a tumor, usually on the left side of the
neck. Rokitansky has reported one the size of the fist situated on the
right side of the neck, and Hankel[30] and others a tumor upon each
side. The tumor varies in bulk from time to time according as it may be
empty or may be distended with food, drink, or gas.

[Footnote 30: _Rust's Mag._, 1833; _Dict. Encycl._, _loc. cit._]

Food caught in the pouch can often be forced out into the pharynx by
external pressure over the tumor in the neck. The retention of food
above a constriction or in a sac is usually accompanied by some
distress after indulgence in too much food. This uneasiness becomes
relieved upon regurgitation or vomiting. Deglutition is impeded to a
less extent when the disease does not implicate the upper portion of
the gut.

Complete dilatation is sometimes indicated by long addiction to habits
of rumination. In some instances this rumination is an agreeable
sensuous process. In pouched dilatation it is very often disagreeable,
the regurgitated matters being acrid, owing to acid fermentation of the
contents of the sac.

While the dilatation remains moderate there may be little dysphagia or
none at all, the muscles continuing sufficiently vigorous to propel the
food; but after the muscles become paralyzed by distension the
dysphagia gradually increases and may culminate in complete aphagia.
One {432} of the special indications of diverticulum is that the
regurgitation does not take place until several hours after a meal. As
the sac enlarges there may be less and less complaint of dysphagia,
because it becomes able to contain larger quantities of food. At the
same time it may so compress the main tube as to occlude its calibre
and prevent access of food to the stomach.

The symptoms of annular dilatation are similar to those of stricture
with retention of food above it, the regurgitation usually following
deglutition more quickly.

In some cases of dilatation, circumscribed and general, food is
sometimes retained for an entire day or more before it is ejected. The
decomposition of the retained food usually produces a more or less
continuous foul odor from the mouth.

The course of the affection is progressively from bad to worse, and
entails ultimate emaciation. Some patients succumb early, and some live
to advanced age. Perforation of the oesophagus ensues in some
instances, and death results in consequence of the injuries sustained
by perioesophageal structures by the escape of the contents of the
oesophagus. Perforation is indicated by sudden collapse and by
emphysema from swallowed air.

PATHOLOGY AND MORBID ANATOMY.--Dilatation of the oesophagus is either
general or partial, according as it takes place in the whole or greater
portion of the oesophagus or in a circumscribed portion. Partial
dilatation may involve the entire circumference of the canal (annular
dilatation), or it may implicate but a portion of the wall, which
becomes pouched into a sac externally (diverticulum or saccular
dilatation).

General dilatation, though sometimes congenital, is, as mentioned under
Etiology, more frequently the mechanical result of distension of the
oesophagus by food or drink prevented from ready entrance into the
stomach by a constriction at the cardiac orifice. This form of
dilatation is sometimes discovered as a post-mortem curiosity. The
muscles have usually undergone great hypertrophy, and the mucous
membrane some thickening and congestion, with erosions and sometimes
ulcerations, indicative of chronic oesophagitis. In some instances all
the coats of the oesophagus have undergone hypertrophy. The dilatation
may vary from slight enlargement to the thickness of an ordinary man's
arm or larger (Rokitansky[31]); in rare cases, even a capacity nearly
equal to that of the stomach (Luschka[32] and others). (See Fig. 19.)

[Footnote 31: _Path. Anat._]

[Footnote 32: _Arch. fur Anat., etc._, March, 1868, p. 473.]

[Illustration: FIG. 19. Fusiform Dilatation of Oesophagus (Luschka). A,
Larynx; B, Thyroid gland; C, Trachea; D, Oesophagus; E, Stomach.]

The oesophagus is usually fusiform or spindle-shaped, being constricted
at those portions at which it is normally slightly constricted.
Sometimes the dilatation takes place between the lobes of the lungs
(Raymond[33]).

[Footnote 33: _Gaz. med. de Paris_, 1869, No. 7, p. 91.]

Annular dilatation is usually due to circumferential distension just
above a stricture. When not due to stricture its seat is usually just
above the diaphragm, where the oesophagus is normally liable to
constriction. The upper portion of the dilatation is larger than the
lower portion, and the muscular walls are usually hypertrophied.

Pouched dilatation (diverticulum) is usually formed chiefly of mucous
membrane and submucous tissue pushed through gaps in the fibres of the
{433} muscular coat, produced by distension. It sometimes involves the
entire coat in cases in which the oesophageal wall has become adherent
to enlarged lymphatic glands, which subsequently undergo subsidence in
volume and drag the adherent portion of the wall after them
(Rokitansky). The muscular walls are then usually hypertrophied, the
mucous membrane sometimes hypertrophied, sometimes atrophied. The
diverticulum is usually located in the upper portion of the oesophagus,
just below the inferior constrictor muscle of the pharynx. It may thus
be, in part, a pharyngocele also. It may be located behind the point of
bifurcation of the trachea or where the oesophagus is crossed by the
left bronchus. Its direction may be to the left side in the upper
portion of the oesophagus, to the right side, or upon both sides; but
when situated lower down it is usually directed backward, between the
posterior wall of the tube and the spinal column. Hence its distension
with food completely blocks up the calibre of the oesophagus. The
orifice by which the oesophageal wall remains in communication with the
pouch is round or elliptic in shape and variable in size, sometimes
being about an inch in its long diameter, sometimes much smaller. The
size of the diverticulum varies; a common size is that of a duck egg,
but the size of a fist has been attained. Sometimes the diverticulum
drags the oesophagus out of position and forms a sort of blind pouch in
the direct line of its axis, so that it becomes filled with food which
fails to reach the stomach. Sometimes there are several dilatations.

The dilatations become enlarged by retention of food, and are liable to
undergo inflammation, ulceration, and perforation.

DIAGNOSIS.--The diagnosis will depend upon the symptoms of dysphagia,
regurgitation, and so on, and upon the evidence furnished by
auscultatory indications, palpation with the oesophageal sound, and, in
some instances, the existence of a tumor in the neck, enlarging after
meals, and {434} from which food or mucus can be forced up into the
pharynx by pressure externally.

Stethoscopic auscultation of the oesophagus during the deglutition of
water indicates an alteration in the usual form of the gulp, which
seems to trickle rapidly in a larger or smaller stream according to the
degree of dilatation. If the dilatation be annular and located high up,
auscultation is said to give the impression of a general sprinkling of
fluid deflected from its course. The peculiar gurgle is often audible
without the aid of stethoscopy. Palpation with the oesophageal bougie
is competent to reveal the existence of a large sac by the facility
with which the terminal extremity of the sound can be moved in the
cavity. In the case of a diverticulum, however, the sound may glide
past the mouth of the pouch without entering it, although arrested at
the bottom of the sac in most instances.

In annular dilatation any constriction below it is usually perceptible
to the touch through the sound; but, on the other hand, the ready
passage of the bougie into the stomach, while excluding stricture, does
not positively disprove the existence of a circumscribed dilatation. If
high up, the dilatation may be detected externally by its enlargement
when filled with food after a meal, and the subsidence of tumefaction
when the sac is emptied by pressure from without, or by regurgitation.
If the dilatation occupy a position which exercises compression of the
trachea, dyspnoea will ensue when it is distended. The intermittence of
the tumefaction serves to differentiate the swelling from abscess or
morbid growth. From aneurism of the aorta, which it may simulate
(Davy[34]), it is to be discriminated by absence of the usual
stethoscopic and circulatory manifestations. The diagnosis of
congenital dilatation is based upon a history of difficulty in
deglutition dating from the earliest period of recollection.

[Footnote 34: _Irish Hosp. Gaz._, 1874, p. 129; _Med. Press and
Circular_, May, 1874.]

PROGNOSIS.--The prognosis is not favorable in any given case unless the
cause can be removed, and not even then unless food can be prevented
from accumulating in the distended portion of the tube. Nevertheless,
cases sometimes go on into advanced age. On the other hand, they may
terminate fatally within a year (Lindau[35]). The danger of perforation
adds additional gravity to the prognosis, for life may be suddenly lost
by this accident. Death usually takes place by inanition. A case of
death by suffocation has been recorded, attributed to the pressure of
the distended oesophagus upon the intrathoracic vessels (Hannay[36]).

[Footnote 35: _Casper's Wochenschrift_, 1840, No. 22; _Arch. gen. de
Med._, 1841, p. 498; _Dict. de Med et de Chir._, xxiv. p. 410.]

[Footnote 36: _Edinb. Med. and Surg. Journ._, July 1, 1833.]

TREATMENT.--If the dilatation be due to stricture or to an impacted
foreign body, the treatment should be directed to overcoming the one
and removing the other.

General dilatation from chronic oesophagitis requires treatment for
that disease.

Much depends upon preventing the accumulation of food in a sac or
diverticle; the best means of accomplishing which is the systematic
administration of all nutriment by means of the stomach-tube. When this
is not advisable, care must be exercised in the selection of such food
as is least likely to irritate the parts if detained in the pouch.

{435} As far as general treatment is concerned, stimulants are usually
indicated, as the patients become much reduced. If paralysis of the
muscular coat of the oesophagus is believed to exist, the
administration of preparations of phosphorus and of strychnine are
indicated on general principles of therapeutics. Stimulation of
muscular contractility by the oesophageal electrode has been
recommended, but the prospects of success hardly justify the risks of
serious injury in the domain of the pneumogastric nerve.

It has not yet been determined whether surgical procedures are
competent to relieve dilatation. In cases of pouched dilatation high up
it would not be difficult, as suggested by Michel,[37] to expose the
sac and excise it in such a manner that the sutures uniting the walls
of the oesophagus shall occupy the site of the mouth of the
diverticulum, and, thus obliterating it by cicatrization, restore the
normal path of the food from the pharynx to the oesophagus.
Gastrostomy, too, should hold out some hope of rescue, no matter what
portion of the oesophagus be dilated.

[Footnote 37: _Dict. Encyclop._, xiv. p. 465.]




{436}

FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH.

BY SAMUEL G. ARMOR, M.D., LL.D.


Functional Dyspepsia (Atonic Dyspepsia, Indigestion).

To difficulty in the physiological process of digestion the familiar
name of dyspepsia has been given, while to a merely disturbed condition
of the function the term indigestion is more frequently applied. This
distinction, difficult at all times to make, may appear more arbitrary
than real; and inasmuch as it involves no important practical point,
the author of the present article will use the terms interchangeably as
indicating functional disturbance of the stomach--_i.e._ disturbance of
the digestive process not associated with changes of an inflammatory
character, so far as we know.

Since it is one of the most common of all complaints from its
association with various other morbid conditions, the term is not
unfrequently vaguely employed. It is difficult, of course, to define a
disease whose etiology is so directly related to so many distinct
morbid conditions. Indeed, there are few diseases, general or local,
which are not at some time in their history associated with more or
less derangement of the digestive process. For purposes of limitation,
therefore, it will be understood that we now refer to chronic
functional forms of indigestion which depend largely, at least, on a
purely nervous element, and for this reason are not infrequently
described as sympathetic dyspepsia. Doubt has been expressed as to
whether such forms of disease ever exist, but that we encounter purely
functional forms of dyspepsia, corresponding to the dyspepsia apyretica
of Broussais, would appear to be a well-recognized clinical fact.

What the precise relation is between digestive disturbances and the
nervous system we may not fully understand, no more than we understand
how a healthy condition of nervous endowment is essential to all vital
processes. Even lesions of nutrition are now known to depend upon
primary disturbance of nervous influence. This is seen in certain skin
diseases, such as herpes zoster, which closely follows the destruction
of certain nerves. And it is well known that injury of nerve-trunks is
not unfrequently followed by impaired nutrition and failure in
reparative power in the parts to which such nerves are distributed.
Indeed, so marked is the influence of the nervous system over the
nutritive operations that the question has been considered as to
whether there are {437} trophic nerves distributed to tissue-elements
themselves whose special function is to keep these elements in a
healthy state of nutrition. The proof, at least, that the digestive
process is, in some unexplained way, under the immediate influence of
the nervous system, either cerebro-spinal or trophic, is both varied
and abundant. The digestive secretions are known to be the products of
living cells which are abundantly supplied with nerve-fibres, and we
can readily believe that the potential energy of this cell-force is
probably vital and trophic. At any rate, it is unknown in the domain of
ordinary chemistry. The digestive ferments, as clearly pointed out by
Roberts, are the direct products of living cells. Their mode of action,
he claims, bears no resemblance to that of ordinary chemical affinity.
It has a distinctly physiological character. Nor do they derive their
vital endowments from material substances. "They give nothing material
to, and take nothing from, the substances acted on. The albuminoid
matter which constitutes their mass is evidently no more than the
material substance of a special kind of energy--just as the steel of a
magnet is the material substratum of the magnetic energy, but is not
itself that energy" (Roberts). That this living cell-force is partly,
at least, derived from the nervous system is clear from the well-known
effects of mental emotion, such as acute grief, despair, etc., in
putting an immediate stop to the digestive process. Experiments on the
lower animals have also shown the direct influence of the nervous
system over gastric secretion. Wilson Philip showed by various
experiments on rabbits and other animals that if the eighth pair of
nerves be divided in the neck, any food which the creatures may
afterward eat remains in the stomach undigested, and after death, when
the nerve has been divided, the coats of the stomach are not found
digested, however long the animal may have been dead. Bernard also
excited a copious secretion by galvanization of the pneumogastric, and
by section of the same nerve stopped the process of digestion and
produced "pallor and flaccidity of the stomach." Recently doubt has
been thrown on these statements of Bernard and Frerichs. Goltz
concludes, from observations made on frogs, that nerve-ganglia,
connected by numerous intercommunicating bundles of nerve-fibres, exist
in the walls of the stomach, the irritation of which gives rise to
local contractions and peristaltic movements of the stomach, and that
these ganglia influence the gastric secretion. However this may be, it
still remains true that these gastric ganglia are in connection,
through the vagi, with the medulla oblongata, and are thus influenced
by the cerebro-spinal nerve-centres. And clinical observation confirms
what theoretical considerations would suggest. Thus, strong mental
impressions are known to produce sudden arrest of secretion, and that
which arrests secretion may, if continued, lead to perversion of the
same.

Impressions made upon the nerves of special sense are also known to
affect the salivary and gastric secretions. The flow of saliva is
stimulated by the sight, the smell, the taste, and even thought, of
food. Bidder and Schmidt made interesting experiments on dogs bearing
upon this point. They ascertained by placing meat before dogs that had
been kept fasting that gastric juice was copiously effused into the
stomach. Other secretions are known to be similarly affected. Carpenter
by a series of well-observed cases has shown the direct influence of
mental conditions on the {438} mammary secretion. The nervous
association of diabetes and chronic Bright's disease is interesting in
this connection, and the direct nervous connection betwixt the brain
and the liver has been shown by numerous experiments. It is maintained
by modern physiologists that "the liver--indeed each of the
viscera--has its representative area in the brain, just as much as the
arm or leg is represented in a distant localized area" (Hughlings
Jackson). And in harmony with this view Carpenter long since pointed
out the fact that if the volitional direction of the consciousness to a
part be automatically kept up for a length of time, both the functional
action and the nutrition of the part may suffer. It has been described
by him as expectant attention, and it has, as we shall see, important
practical bearings on the management of gastric affections. Sympathetic
disturbance of the stomach is also connected with direct disease of the
brain. This is seen in cases of concussion. The almost immediate
effects of a blow are nausea and vomiting, and the same thing is
observed in local inflammation of the meninges of the brain.

Many forms of functional dyspepsia due to nervous disturbance of a
reflex character will be pointed out when discussing the etiology of
the disease.

ETIOLOGY.--Among the agencies affecting the digestive process in atonic
forms of dyspepsia may be mentioned--

First, predisposing causes;

Second, exciting causes.

In general terms it may be said that all conditions of depressed
vitality predispose to the varied forms of atonic dyspepsia. These
conditions range through an endless combination of causes, both
predisposing and exciting. There is not a disturbed condition of life,
extrinsic or intrinsic, that may not contribute to this end. In some
cases it may be the effects of hot and enervating climates; in others
the alterations in the elementary constituents of the blood may be
apparent; while in still others the cause may be exhausting discharges,
hemorrhages, profuse suppuration, venereal excesses, sedentary
occupations, and long-continued mental and moral emotions.

Heredity may also predispose to functional dyspepsia. Certain faulty
states of the nervous system are specially liable to be transmitted
from parent to offspring--not always in the exact form in which they
appeared in the parent, but in forms determined by the individual life
of the offspring. For obvious reasons, growing out of our modern
American civilization, the inheritance of a faulty nervous organization
is apt to spend itself upon the digestive apparatus. The inordinate
mental activity, the active competitions of life, the struggle for
existence, the haste to get rich, the disappointments of failure,--all
contribute to this end. The general tendency of American life is also
in the direction of a highly-developed and morbidly sensitive nervous
system, and functional dyspepsia is a natural sequence of this. The
symptoms of dyspepsia thus caused usually manifest themselves at an
early period of life.

Age also predisposes to weak digestion. The stomach becomes weak as age
advances, in common with all the functions of the body, and consequent
upon this weakness there is diminished excitability of the gastric
nerves, with diminished muscular action of the walls of the stomach and
deficient secretion of the gastric juice. Chronic structural changes
are {439} also apt to occur in advanced life. The gastric glands become
atrophied and the arteries become atheromatous, so that with symptoms
of indigestion there are often associated loss of consciousness at
times, vertigo, irregular action of the heart, etc. These general facts
have an important bearing upon the hygienic management of dyspepsia in
the aged. They require, as a rule, less food than the young and
vigorous. In times when famine was more frequent than now it was found
that the older a human being was, the better deficiency of food was
borne. Hippocrates tells us, in his _Aphorisms_, that old men suffer
least from abstinence. Their food should be such, both in quantity and
quality, as the enfeebled stomach can digest. There is less demand for
the materials of growth, and consequently for animal food. Moderate
quantities of alcohol, judiciously used, are also specially adapted to
the indigestion of the aged. It has the double effect of stimulating
the digestive process and at the same time checking the activity of
destructive assimilation, which in old age exhausts the vital force.
And in order to more effectively arrest destructive metamorphosis great
caution should be taken against excessive muscular fatigue, as well as
against sudden extremes of temperature. Loss of appetite from deficient
formation of gastric juice is a common symptom in old age. This is not
often successfully treated by drugs, and yet medicines are not without
value. The sesquicarbonate of ammonium acts as a stimulant to the
mucous membrane and to the vaso-motor nerve, and in this way becomes a
valuable addition to the simple vegetable bitters. Dilute hydrochloric
acid with the vegetable bitters may also be tried. Condiments with the
food directly stimulate the action of the enfeebled stomach. The old
remedy of mustard-seed is not unfrequently useful, and pepper, cayenne,
horseradish, and curries act in a similar manner in torpid digestion.
And in cases of great exhaustion associated with anaemia benefit may be
derived from small doses of iron added to tincture of columbo or
gentian.

Nor should it be forgotten that in the opposite extreme of life the
digestive capacity is extremely limited. The infant's digestion is
readily disturbed by unsuitable alimentation. For obvious reasons it
does not easily digest starchy substances. The diastasic ferment does
not exist in the saliva of young sucking animals, at least to any
extent. No food is so suitable for early infantile life as the mother's
milk, provided the mother herself is healthy. It contains in an easily
digestible form all the constituents necessary to the rapidly-growing
young animal. Van Helmont's substitute of bread boiled in beer and
honey for milk, or Baron Liebig's food for infants, cannot take the
place of nature's type of food, which we find in milk. If a substitute
has to be selected, there is nothing so good as cow's milk diluted with
an equal quantity of soft water, or, what in many cases is better,
barley-water, to which may be added a teaspoonful of powdered sugar of
milk and a pinch of table-salt and phosphate of lime. Lime-water may be
added with advantage. Dilution of alimentary substances is an important
condition of absorption in the infant stomach.

Anaemia is a common predisposing cause of indigestion. Indeed, as a
widely-prevailing pathological condition few causes stand out so
prominent. It affects at once the great nutritive processes, and these
in turn disturb the functional activity of all the organs of the body.
Not only are the gastric and intestinal glands diminished in their
{440} functional activity by impoverished or altered blood, but the
movements of the stomach are retarded by weakened muscular action. It
is impossible to separate altered blood from perverted tissue-structure
and altered secretion. Indigestion produced by anaemia is difficult of
treatment, on account of the complexity of the pathological conditions
usually present, the anaemia itself being generally a secondary
condition. Careful inquiry should be made, therefore, into the probable
cause of the anaemia, and this should, if possible, be removed as an
important part of the treatment of the dyspepsia. Nothing will more
promptly restore the digestive capacity in such cases than good,
healthy, well-oxidized blood. Indeed, healthy blood is a condition
precedent to the normal functional activity of the stomach.

To these general predisposing causes may be added indigestion occurring
in febrile states of the system. The cause here is obvious. In all
general febrile conditions the secretions are markedly disturbed; the
tongue is dry and furred; the urine is scanty; the excretions lessened;
the bowels constipated; and the appetite gone. The nervous system also
participates in the general disturbance. In this condition the gastric
juice is changed both quantitatively and qualitatively, and digestion,
as a consequence, becomes weak and imperfect--a fact that should be
taken into account in regulating the diet of febrile patients. From
mere theoretical considerations there can be no doubt that fever
patients are often overfed. To counteract the relatively increased
tissue-metamorphosis known to exist, and the consequent excessive
waste, forced nutrition is frequently resorted to. Then the traditional
saying of the justly-celebrated Graves, that he fed fevers, has also
rendered popular the practice. Within certain bounds alimentation is
undoubtedly an important part of the treatment of all the essential
forms of fever. But if more food is crowded upon the stomach than can
be digested and assimilated, it merely imposes a burden instead of
supplying a want. The excess of food beyond the digestive capacity
decomposes, giving rise to fetid gases, and often to troublesome
intestinal complications. The true mode of restoring strength in such
cases is to administer only such quantities of food as the patient is
capable of digesting and assimilating. To this end resort has been had
to food in a partially predigested state, such as peptonized milk, milk
gruel, soups, jellies, and beef-tea; and clinical experience has thus
far shown encouraging results from such nutrition in the management of
general fevers. In these febrile conditions, and in all cases of
general debility, the weak digestion does not necessarily involve
positive disease of the stomach, for by regulating the diet according
to the digestive capacity healthy digestion may be obtained for an
indefinite time.

Exhaustion of the nerves of organic life strongly predisposes to the
atonic forms of dyspepsia. We have already seen how markedly the
digestive process is influenced by certain mental states, and it is a
well-recognized fact that the sympathetic system of nerves is
intimately associated with all the vegetative functions of the body.
Without a certain amount of nervous energy derived from this portion of
the nervous system, there is failure of the two most important
conditions of digestion--viz. muscular movements of the stomach and
healthy secretion of gastric juice. This form of indigestion is
peculiar to {441} the ill-fed and badly-nourished. It follows in the
wake of privation and want, and is often seen in the peculiarly
careworn and sallow classes who throng our public dispensaries. In this
dyspepsia of exhaustion the solvent power of the stomach is so
diminished that if food is forced upon the patient it is apt to be
followed by flatulence, headache, uneasy or painful sensations in the
stomach, and sometimes by nausea and diarrhoea. It is best treated by
improving in every possible way the general system of nutrition, and by
adapting the food, both in quantity and quality, to the enfeebled
condition of the digestive powers. Hygienic measures are also of great
importance in the management of this form of dyspepsia, and especially
such as restore the lost energy of the nervous system. If it occur in
badly-nourished persons who take little outdoor exercise, the food
should be adapted to the feeble digestive power. It should consist for
a time largely of milk and eggs, oatmeal, peptonized milk gruels, stale
bread; to which should be added digestible nitrogenous meat diet in
proportion to increased muscular exercise. Systematic outdoor exercise
should be insisted upon as a sine qua non. Much benefit may be derived
from the employment of electric currents, and hydrotherapy has also
given excellent results. If the indigestion occur in the badly-fed
outdoor day-laborer, his food should be more generous and mixed. It
should consist largely, however, of digestible nitrogenous food, and
meat, par excellence, should be increased in proportion to the exercise
taken. Medicinally, such cases should be treated on general principles.
Benefit may be derived from the mineral acids added to simple bitters,
or in cases of extreme nervous prostration small doses of nux vomica
are a valuable addition to dilute hydrochloric acid. The not unfrequent
resort to phosphorus in such cases is of more than doubtful utility.
Some interesting contributions have been recently made to this subject
of gastric neuroses by Buchard, See, and Mathieu. Buchard claims that
atonic dilatation of the stomach is a very frequent result of an
adynamic state of the general system. He compares it to certain forms
of cardiac dilatation--both expressions of myasthenia. It may result
from profound anaemia or from psychical causes. Mathieu regards mental
depression as only second in frequency. Much stress is laid upon
poisons generated by fermenting food in the stomach in such cases. It
may cause a true toxaemia, just as renal diseases give rise to uraemia.
Of course treatment in such cases must be addressed principally to the
general constitution.

But of all predisposing causes of dyspepsia, deficient gastric
secretion, with resulting fermentation of food, is perhaps the most
prevalent. It is true this deficient secretion may be, and often is, a
secondary condition; many causes contribute to its production; but
still, the practical fact remains that the immediate cause of the
indigestion is disproportion between the quantity of gastric juice
secreted and the amount of food taken into the stomach. In all such
cases we have what is popularly known as torpidity of digestion, and
the condition described is that of atony of the stomach. The two main
constituents of gastric juice--namely, acid and pepsin--may be
deficient in quantity or disturbed in their relative proportions. A
certain amount of acid is absolutely essential to the digestive
process, while a small amount of pepsin may be sufficient to digest a
large amount of albuminoid food. {442} Pure unmixed gastric juice was
first analyzed by Bidder and Schmidt. The mean analyses of ten
specimens free from saliva, procured from dogs, gave the following
results:

  _Gastric Juice of a Dog_.
  Water                        973.06
  Solids                        26.94
    Containing--Peptone and pepsin   17.19
    Free hydrochloric acid            3.05
    Alkaline chlorides                4.26
    Ammonium chloride                 0.47
    Chlorine                          5.06
               | Lime                 1.73
    Phosphates | Magnesia             0.23
               | Iron                 0.08

They proved by the most careful analyses that fresh gastric juice
contains only one mineral acid--namely, hydrochloric; since which time
Richet has been able to prove that "this acid does not exist in a free
state, but in loose combination with an organic substance known as
lucin," the chloride of lucin. And just here the curious and puzzling
question arises as to the secretion of a mineral acid from alkaline
blood. Ewald, the distinguished lecturer in the Royal University of
Berlin, tells us that "a brilliant experiment of Maly's has thrown
unexpected light upon this. There are fluids of alkaline reaction which
may contain two acid and alkaline mutually inoffensive salts, but still
have an alkaline reaction, because the acid reaction is to a certain
extent eclipsed; for instance, a solution of neutral phosphate of soda
(Na_{2}HPO_{4}) and acid phosphate of soda (NaH_{2}PO_{4}) is alkaline.
Such a solution placed in a dialyzer after a short time gives up its
acid salt to the surrounding distilled water, and one has in the
dialyzer an alkaline fluid outside an acid fluid." He thus proved that
the acid phosphate of sodium is present in the blood in spite of its
alkaline reaction.

Lack of the normal amount of the gastric secretion must be met by
restoring the physiological conditions upon which the secretion
depends. In the mean time, hydrochloric and lactic acids may be tried
for the purpose of strengthening the solvent powers of the gastric
secretion.

EXCITING CAUSES.--The immediate causes of dyspepsia are such as act
more directly on the stomach. They embrace all causes which produce
conditions of gastric catarrh, such as excess in eating and drinking,
imperfect mastication and insalivation, the use of indigestible or
unwholesome food and of alcohol, the imperfect arrangement of meals,
over-drugging, etc.

Of exciting causes, errors of diet are amongst the most constantly
operative, and of these errors excess of food is doubtless the most
common. The influence of this as an etiological factor in derangement
of digestion can scarcely be exaggerated. In very many instances more
food is taken into the stomach than is actually required to restore
tissue-waste, and the effects of such excess upon the organism are as
numerous as they are hurtful. Indeed, few elements of disease are more
constantly operative in a great variety of ailments. In the first
place, if food be introduced into the stomach beyond
tissue-requirements, symptoms of indigestion at once manifest
themselves. The natural balance betwixt {443} supply and demand is
disturbed; the general nutrition of the body is interfered with; local
disturbances of nutrition follow; and mal-products of digestion find
their way into the blood. Especially is this the case when the
excessive amount of food contains a disproportionate amount of
nitrogenous matter. All proteid principles require a considerable
amount of chemical alteration before they are fitted for the metabolic
changes of the organism; the processes of assimilative conversion are
more complex than those undergone by fats and amyloids; and it follows
that there is proportional danger of disturbance of these processes
from overwork. Moreover, if nitrogenous food is in excess of
tissue-requirement, it undergoes certain oxidation changes in the blood
without becoming previously woven into tissue, with resulting compounds
which become positive poisons in the economy. The kidneys and skin are
largely concerned in the elimination of these compounds, and the
frequency with which these organs become diseased is largely due, no
doubt, to the excessive use of unassimilated nitrogenous food. Then,
again, if food be introduced in excess of the digestive capacity, the
undigested portion acts directly upon the stomach as a foreign body,
and in undergoing decomposition and putrefying changes frets and
irritates the mucous membrane. It can scarcely be a matter of doubt
that large groups of diseases have for their principal causes excess of
alimentation beyond the actual requirements of the system. All such
patients suffer from symptoms of catarrhal indigestion, such as gastric
uneasiness, headache, vertigo, a general feeling of lassitude,
constipation, and high-colored urine with abundant urates, together
with varied skin eruptions. Such cases are greatly relieved by reducing
the amount of food taken, especially nitrogenous food, and by a
systematic and somewhat prolonged course of purgative mineral waters.
Europe is especially rich in these springs. The waters of Carlsbad,
Ems, Seltzer, Friedrichshall, and Marienbad, and many of the alkaline
purgative waters of our own country, not unfrequently prove valuable to
those who can afford to try them, and their value shows how often
deranged primary assimilation is at the foundation of many human
ailments. The absurd height to which so-called restorative medicine has
attained within the last twenty years or more has contributed largely
to the production of inflammatory forms of indigestion, with all the
evil consequences growing out of general deranged nutrition.

The use of indigestible and unwholesome food entails somewhat the same
consequences. This may consist in the use of food essentially unhealthy
or indigestible, or made so by imperfect preparation (cooking, etc.).
Certain substances taken as food cannot be dissolved by the gastric or
intestinal secretions: the seeds, the skins, and rinds of fruit, the
husks of corn and bran, and gristle and elastic tissue, as well as
hairs in animal food, are thrown off as they are swallowed, and if
taken in excess they mechanically irritate the gastro-intestinal mucous
membrane and excite symptoms of acute dyspepsia, and not unfrequently
give rise to pain of a griping character accompanied by diarrhoea.
Symptoms of acute dyspepsia also frequently follow the ingestion of
special kinds of food, such as mushrooms, shellfish, or indeed fish of
any kind; and food not adapted to the individual organism is apt to
excite dyspeptic symptoms. Appetite and digestion are also very much
influenced by the life and {444} habits of the individual. The diet,
for instance, of bodily labor should consist largely of digestible
nitrogenous food, and meat, par excellence, should be increased in
proportion as muscular exercise is increased. For all sorts of muscular
laborers a mixed diet is best in which animal food enters as a
prominent ingredient. Thus, it has been found, according to the
researches of Chambers, that in forced military marches meat extract
has greater sustaining properties than any other kind of food. But with
those who do not take much outdoor exercise the error is apt to be, as
already pointed out, in the direction of over-feeding. It cannot be
doubted at the present time that over-eating (gluttony) is one of our
popular vices. Hufeland says: "In general we find that men who live
sparingly attain to the greatest age." While preventive medicine in the
way of improved hygiene--better drainage, better ventilation, etc.--is
contributing largely to the longevity of the race, we unfortunately
encounter in more recent times an antagonizing influence in the elegant
art of cookery. Every conceivable ingenuity is resorted to to tempt men
to eat more than their stomachs can properly or easily digest or
tissue-changes require. The injurious consequences of such over-feeding
may finally correct itself by destroying the capacity of the stomach to
digest the food.

But, on the other hand, in many nervous forms of dyspepsia the weak
stomach is not unfrequently made weaker by severely restricted regimen,
and especially is this the case with mental workers. Theoretical and
fanciful considerations sometimes lead to physical starvation. This is
apt to be the case with dyspeptics. Men who toil with their brain
rather than their muscles, whether dyspeptic or not, require good,
easily-digested mixed diet. It is a popular error to suppose that drugs
can take the place of such food, especially drugs which are supposed to
have a reconstructive influence over the nervous system, such as iron
and phosphorus. The expression of Buchner, "No thinking without
phosphorus," captivating to theoretical minds, has gained much
notoriety, and has doubtless led to the excessive use of that drug in
nervous forms of indigestion. There never was a period when phosphorus
was so universally prescribed as the present. It enters into endless
combinations with so-called nerve-tonics. Of the injurious influence of
the drug in many cases of functional indigestion there can be no doubt;
and the statement itself, so often quoted, that "the amount of
phosphorus in the blood passing through the brain bears an exact
proportion to the intensity of thought," is calculated to mislead. T.
K. Chambers, author of the excellent _Manual of Diet_, makes the
statement that "a captive lion, tiger, leopard, or hare assimilates and
parts with a greater amount of phosphorus than a hard-thinking man;
while the beaver, noted for its power of contrivance, excretes so
little phosphorus that chemical analysis cannot find it in its
excreta." In the wonderful adaptations and regulative mechanisms of
nature we may trust largely to the natural law of supply and demand in
maintaining a proper equilibrium. It may be doubted, indeed, whether we
require at any time more phosphorus for brain- and nerve-tissue than
can be found in such food as contains digestible phosphatic salts. The
natural demand for food grows out of healthy tissue-change. An appetite
to be healthy should commence in processes outside of the stomach.

Food may also be introduced into the stomach in an undigestible form
{445} from defects of cookery. The process of cooking food produces
certain well-known chemical changes in alimentary substances which
render them more digestible than in the uncooked state. By the use of
fire in cooking his food new sources of strength have been opened up to
man which have doubtless contributed immeasurably to his physical
development, and has led to his classification as the cooking animal.
With regard to most articles the practice of cooking his food
beforehand is wellnigh universal; and especially is this the case with
all farinaceous articles of food. The gluten of wheat is almost
indigestible in the uncooked state. By the process of cooking the
starchy matter of the grain is not only liberated from its protecting
envelopes, but it is converted into a gelatinous condition which
readily yields to the diastasic ferments. Roberts, in his lectures on
the _Digestive Ferments_, points out the fact that when men under the
stress of circumstances have been compelled to subsist on uncooked
grains of the cereals, they soon fell into a state of inanition and
disease.

Animal diet is also more easily digested in the cooked than in the raw
state. The advantage consists chiefly in the effects of heat on the
connective tissue and in the separation of the muscular fibre. In this
respect cooking aids the digestive process. The gastric juice cannot
get at the albumen-containing fibrillae until the connective tissue is
broken up, removed, or dissolved. Hot water softens and removes this
connective tissue. Hence raw meat is less easily digestible.
Carnivorous animals, that get their food at long intervals, digest it
slowly. By cutting, bruising, and scraping meat we to a certain extent
imitate the process of cooking. In many cases, indeed, ill-nourished
children and dyspeptics digest raw beef thus comminuted better than
cooked, and it is a matter of observation that steamed and underdone
roast meats are more digestible than when submitted to greater heat.

Some interesting observations have been made by Roberts on the effects
of the digestive ferments on cooked and uncooked albuminoids. He
employed in his experiments a solution of egg albumen made by mixing
white of egg with nine times its volume of water. "This solution," says
Roberts, "when boiled in the water-bath does not coagulate nor sensibly
change its appearance, but its behavior with the digestive ferments is
completely altered. In the raw state this solution is attacked very
slowly by pepsin and acid, and pancreatic extract has no effect on it;
but after being cooked in the water-bath the albumen is rapidly and
entirely digested by artificial gastric juice, and a moiety of it is
rapidly digested by pancreatic extract."

It is a mistake, however, to suppose that cooking is equally necessary
for all kinds of albuminoids. The oyster, at least, is quite
exceptional, for it contains a digestive ferment--the hepatic
diastase--which is wholly destroyed by cooking. Milk may be
indifferently used either in the cooked or uncooked state, and fruits,
which owe their value chiefly to sugar, are not altered by cooking.

The object in introducing here these remarks on cooking food is to show
that it forms an important integral part of the work of digestion, and
has a direct bearing on the management of all forms of dyspepsia.

Haste in eating, with imperfect mastication, is a common cause of
indigestion in this country. Mastication is the first step in the
digestive {446} process. It is important, therefore, that we have good
teeth and that we take time to thoroughly masticate our food, for by so
doing we prepare it for being acted upon by the juices of the stomach.
Time is also necessary in order that the salivary secretion may be
incorporated with the alimentary substances. By the salivary diastase
starch is converted into sugar and albuminoids are prepared for the
action of the gastric juice. If these changes take place imperfectly,
the stomach can scarcely regain in gastric digestion what was lost in
imperfect mastication and insalivation. Haste in eating is one of the
American vices. It grows out of the temperament of our people. We are
jealous of lost time, and unfortunately this time is too often taken
from the stomach. We bolt our food with unseemly haste, and pay the
penalty in ruined stomachs. Many cases of indigestion are greatly
relieved, if not permanently cured, by simply doubling or quadrupling
the time occupied in eating.

Irregularity in the intervals between meals, such as taking one meal
only in twenty-four hours or taking food before the preceding supply
has been digested, is another fruitful source of indigestion. The
digestive process, in the natural order of change, is confused; changes
which should take place are delayed; and the results are such as arise
from excessive eating. Moreover, the stomach lacks the rest so
essential to digestion. The necessary interval, however, between meals
varies with the nature of the food taken. "Between the extremes of the
carnivorae," says Ewald, "which feed once in twenty-four hours, and the
herbivorae, which never have done with the business of feeding, man
holds a middle place, but not without permitting the recognition in the
course of his life of a sort of transition from the herbivora to the
carnivora. Infants should have the breast during the first three weeks
as often as they wake; after that every two hours to the third month;
then up to dentition every three hours; and later there should be five
meals in twenty-four hours." But to this general statement there are,
of course, many exceptions. Under certain pathological conditions food
should be taken in small quantities at short intervals. This is
especially the case in chronic gastric catarrh and in feeble digestion
of nervous subjects. Such patients are not unfrequently improved by
becoming again infants or herbivorae. By the use of an exclusive milk
diet or peptonized milk gruels, given in small quantities at
comparatively short intervals of time, the stomach may be so
accommodated that it will digest without discomfort a large amount of
nourishment within a given time. To S. Weir Mitchell of Philadelphia we
are indebted for some valuable observations bearing upon this point of
forced alimentation.

To the causes of indigestion already alluded to may be added the habit
of spirit-drinking, especially the habit of taking alcohol undiluted on
an empty stomach, which rarely fails after a time to engender dyspeptic
symptoms. It is a prominent factor in the production of chronic gastric
catarrh--a condition more frequently present in painful indigestion
than any that have been named. It is one of the most common diseases
met with in practice. Indeed, all causes already alluded to involve,
sooner or later, if they are constantly operative, irritative and
catarrhal conditions of the mucous membrane of the stomach, so that we
find it difficult at times--indeed impossible--to separate purely
functional from subacute inflammatory forms of dyspepsia. Practically,
we simply study the {447} subject in the relative degrees of prominence
of the one condition or the other.

But, in a still more comprehensive sense, indigestion is caused by
disturbance of organs directly associated with the stomach in the
digestive process. All organs closely associated with each other in
their physiological functions are apt to become associated in morbid
action. The clinical recognition of this is a matter of great
importance in the management of gastric affections. And first in the
order of importance in such association is the liver. So closely,
indeed, are the liver and stomach functionally associated in the
process of primary assimilation that they may be considered parts of
the same great digestive apparatus. Hence disturbance of the
liver--either in the formation of glycogen, the destruction of
albuminoid matter, or the secretion of bile--is immediately
communicated to the stomach. It may be difficult to say which of these
separate and distinct functions of the liver is most at fault; that can
only be a matter of physiological inference. In the one case, for
instance, the dyspeptic may be fairly well nourished, yet his
elimination may be bad. In the other there is no failure of the
destructive and excreting functions, but those concerned in the
assimilation of fat and peptones are disordered, so that the patient is
not well nourished, so far as the fatty element is concerned. This is
the more common form, and a form not unfrequently associated with
pulmonary consumption. The liver finally becomes fatty--a condition
usually found associated with the constitutional forms of phthisis.

The pancreas is also closely associated with the stomach, and its
secretion is of essential value in the digestive process. It is to be
regretted that our precise knowledge of its diseases is in such
striking contrast with its importance in the animal economy, and yet it
can scarcely be doubted that in dyspeptic symptoms associated with
failure of digestion of starchy, albuminous, and fatty elements of food
there is disorder of the secretion of the pancreas. Hence in the
treatment of the early stages of pulmonary consumption and other
disorders associated with deficient digestion and assimilation of fatty
substances the importance of directing our attention to the condition
of the liver and pancreas, as well as to the stomach.

That morbid states of the intestinal track occupy a prominent place in
the etiology of dyspepsia is also a well-recognized clinical fact.
Indeed, constipation of the bowels is an almost universal accompaniment
of deranged digestion, and when persistent for years it is apt to lead
to the most disastrous consequences. These are mainly in the direction
of lessened elimination from the intestinal glandulae. The general
symptomatology of deficient excretion from these glandulae is closely
analogous to the same condition of the liver: there is impairment of
the general health; the clear florid complexion disappears; the patient
becomes of a greenish or sallow hue; the blood is altered in quality;
fatigue is experienced after the slightest exertion; the nights are
restless; and there is great tendency to mental despondency. Moreover,
constipation often precedes the gastric symptoms. The diminished
muscular activity of the intestinal track extends to the stomach; its
movements are diminished; food is not properly mixed with the gastric
juice, and by being too long retained in the stomach in a comparatively
undigested state acetous fermentation in the saccharine and starchy
articles of diet is set {448} up, acid eructations and a sour taste in
the mouth being commonly complained of. Dyspepsia associated with this
condition of the intestinal track cannot be relieved until the
constipation is relieved, and by overcoming the constipation the
dyspeptic symptoms often disappear.

Mention has been made of the baneful influence of certain mental states
in the production of dyspeptic symptoms. But there are forms of
indigestion due to local nervous disturbance existing elsewhere than in
the nerve-centres. This was ascribed by the older writers to what they
termed consensus nervorum, or sympathy, by which "the operation of a
stimulus is not limited to the nerves immediately irritated, but is
extended to distant parts in known or unknown connection with the
irritated nerves." An intimate acquaintance with this law of sympathy
is of the utmost importance in the study of the functional forms of
dyspepsia, for no other organ of the body is subjected to such a wide
range of reflected nervous disturbance as the stomach. Morbid
sympathetic impressions are transmitted mainly through branches of the
vaso-motor nerve of the semilunar ganglia of the abdomen, and from the
pneumogastric to the stomach. Thus, a pregnant uterus not unfrequently
produces very troublesome vomiting; some females suffer from nausea and
indigestion during each menstrual period; and the more chronic forms of
pelvic irritation, such as a flexed uterus, and endometritis,
cervicitis, or tender ovary, may be the continuous exciting cause of
most troublesome forms of nervous dyspepsia. There is also close
sympathy of the stomach with the lungs and heart through the
distribution of the pneumogastric. So also may fixed points of
irritation in any part of the nervous system be reflexly transmitted to
the stomach, giving rise to most pronounced symptoms of indigestion.
And it is evident that in all such cases but little can be accomplished
in the way of relieving the dyspeptic symptoms until the cause upon
which they depend is removed. The treatment must have reference mainly
to the removal of such cause.

Lastly, all the causes mentioned finally concur in producing
irregularities of the mechanism of digestion; and this may be done by
disturbing either the muscular movements of the stomach or in
suspending or perverting the gastric solvents, or in these two
conditions combined.

SYMPTOMS.--1st. Referable to the Stomach.--The symptoms which attend
and indicate the presence of functional dyspepsia are such as accompany
in a greater or less degree almost all cases of chronic gastritis.
Clinically, so far as the direct gastric symptoms are concerned, it is
difficult to separate them. The more prominent of the local symptoms
are--a sense of fulness and distension after meals, discomfort during
the digestive process, derangement of appetite, acid eructations,
flatulence, regurgitations of food, and sometimes nausea and vomiting.
There is seldom severe pain; the sensation is rather that of
uneasiness. Exceptionally, however, there may be pain, which radiates
from the stomach to the shoulders, and may pass down the left arm so as
to simulate angina pectoris. But it may be readily distinguished from
that complaint by coming on after food, and not after exertion. In
other cases a sense of constriction may be accompanied by dyspnoea,
arising from impeded movements of the diaphragm from being pushed
upward by the distended stomach, or there may be heartburn, with an
ill-defined sense of burning felt in the epigastrium; {449} but thirst,
so frequently present in chronic gastritis, is, as a rule, absent in
functional dyspepsia. These symptoms are manifested in varying degrees
of prominence in individual cases, and some of them are rarely found
present. Thus, nausea and vomiting are not characteristic features of
the chronic forms of functional dyspepsia, and as a rule epigastric
tenderness is entirely absent. In markedly hysterical subjects or in
persons whose nervous system has been unduly excited by alcohol there
may be shrinking from the slightest touch upon pressure; but in these
cases the tenderness is not confined to the stomach, nor is it
increased by deep pressure. In some cases there is an unnatural craving
for food--a symptom rarely if ever observed in structural lesions of
the stomach--and now and then it happens that the appetite becomes
depraved, especially with hysterical patients. They crave indigestible
and unnatural substances, such as earth, chalk, and substances wholly
devoid of alimentary properties. Impairment of appetite, however, is
the more common feature of this form of indigestion.

Flatulence and eructations are generally complained of, the flatulence
being accompanied by a painful sense of fulness, affecting in equal
degree the stomach and small intestines. It is derived principally from
putrefactive or fermentative changes of the ingesta, which are
imperfectly elaborated in the stomach. The gases consist of carbonic
acid, sulphuretted hydrogen, hydrogen, nitrogen, and the hydrocarbons,
the butyric and acetic fermentations furnishing the hydrogen and
carbonic acid gas. In addition to these marsh gas is formed by a
special fermentation, the basis of which exists in the cellulose taken
with vegetable food. In excessive meteorism from paralysis of the
intestines the gas is principally nitrogen; the marsh-gas fermentation
results from the ingestion of certain easily-fermentable vegetables,
such as cabbage, cauliflower, etc.

In a certain proportion of cases regurgitation occurs from the stomach.
The liquor regurgitated may be intensely acid from the presence of some
of the fatty acids, probably butyric, lactic, or acetic. Exceptionally,
it may be insipid or brackish, constituting what is known as pyrosis,
or water-brash. The fluid is usually tasteless and without smell, and
in reaction it is neutral to test-paper. It contains sulphocyanuret of
potassium, and it has been supposed therefore to be only saliva. The
quantity thrown up may vary from a spoonful to a pint or more. It
affects females more than males, and especially those who subsist upon
coarse and indigestible food. It is best treated by astringents--such
as kino, krameria, logwood, or tannin--administered in the intervals
between digestion, so that they may act directly on the mucous
membrane. The oxide and nitrate of silver are thought by some to be
superior to the vegetable astringents.

Cardialgia is a painful condition of the stomach, usually referred to
its cardiac orifice, and is popularly known as heartburn. It is met
with in both functional and organic disease of the stomach. It is very
constantly present in chronic catarrhal gastritis, and evidently
depends upon the presence of an acid, for it is usually promptly
relieved by alkalies, such as chalk, magnesia, soda, or alkaline saline
waters. Food containing much fat, starch, or sugar should be avoided.

Nausea and vomiting are only occasional symptoms of functional
dyspepsia. When vomiting does occur it may take place at different
times {450} and with varying degrees of severity, differing in this
respect from the nausea and vomiting of subacute gastritis, which takes
place, if at all, soon after the ingestion of food. The time of
vomiting and the character of the matter ejected are liable to great
variation in functional dyspepsia. It may be the result of direct
irritation of morbidly sensitive gastric nerves, or it may be a reflex
phenomenon; it may follow soon after the ingestion of food, or it may
come on when the stomach is empty; the material vomited may be simply
food but little altered or an alkaline ropy mucus; it may consist in
the acid juices of the stomach or in a neutral watery fluid; or the
ingesta may have undergone fermentative and putrefactive changes from
either insufficient amount of the gastric solvent or from narrowing
(constriction) of the pyloric extremity, in which case the yeast fungus
(Torula cerevisiae) or the Sarcina ventriculi may be found in great
abundance in the vomited matter. Vomiting of this kind usually occurs
some time after eating. The gastric juice itself checks putrefaction;
so also does the admixture of bile. In the absence of these natural
antiseptics fermentation takes place. But it would be erroneous to
suppose that the fermentative dyspepsia is the primary disease; it is a
symptom which can be permanently corrected only by correcting the
condition upon which it depends.

Among the most noticeable of the phenomena referable to other organs
than the stomach are those connected with the liver and the alimentary
canal. The tongue in dyspeptic troubles varies much in character. In
reflex sympathetic indigestion it is not unfrequently clean; in hepatic
dyspepsia it is generally thickly coated with a white or yellow fur.
The symptoms are such as pertain more especially to chronic
gastro-duodenal catarrh, such as nausea, epigastric oppression, furred
tongue, heartburn, acid eructations, flatulent distension of the
stomach and bowels, unpleasant taste in the mouth, offensive breath,
loaded urine, frontal headache, irritability, and hypochondriasis.

Constipation, as we have seen, is an almost universal accompaniment of
functional dyspepsia, sustaining to it not unfrequently a causative
relation. It is undoubtedly one of the most common of the slighter
ailments of civilized life, and exerts a wide influence in deranging
the general health. "It is quite extraordinary how many different
derangements of health may result from imperfect action or a torpid
state of the secreting and expelling structures of the large bowel.
There may be violent and persistent nerve-pains, referred to the back,
or hip, or groin, and certain other symptoms which lead pessimist
practitioners, excelling in the discovery of neuroses, to diagnose
structural changes in some part of the spinal cord or the antecedent
state which is supposed to lead to them" (Beale). Pains in the loins
and thighs, violent lumbar pain, and certain remediable forms of
sciatica are sometimes due to imperfect excretion of the lower part of
the alimentary canal. And it is even possible that a condition of
hypochondria bordering on insanity may be brought about by
long-continued defective action of the bowels. In exceptional cases of
dyspepsia diarrhoea may be present. This is more frequently the case
when indigestion is associated with a congested state of the liver, in
which case the symptom should be regarded as curative. Excessive
irritability of the muscular walls of the stomach, superadded to weak
digestion, may also be followed by lienteric forms of diarrhoea.
Undigested {451} food hastily finds its way into the intestinal track,
and not unfrequently appears in the fecal evacuations.

Functional derangements of the stomach are often accompanied by pale
urate deposits in the urine. It may contain an excess of phosphates,
and in microscopical examination crystals of the oxalate of lime are
frequently found, constituting a special affection described by
Golding-Bird as oxaluria. He associated it with irritative dyspepsia,
hypochondriasis, and exhaustion of nerve-power. This form of dyspepsia
is best managed by the mineral, vegetable, and acid tonics, to which
may be added small doses of nux vomica, with the usual adjuvants of
good air and exercise, freedom from anxiety and care, cold sea-water
baths, and well-selected, generous animal diet.

Another form of dyspepsia is sometimes associated with a peculiar form
of dizziness--gastric vertigo. German writers speak of it as abdominal
dizziness, and Trousseau calls it vertigo stomicale. It is usually an
acute symptom, begins without any premonition, and is liable to be
confounded with disease of the brain. It sometimes occurs soon after a
meal, but more often when the stomach is empty (Trousseau). It perhaps,
in a majority of cases, depends upon dyspepsia, but it has to be
differentiated from organic brain disease, from cerebral anaemia,
cerebral hyperaemia, the slighter forms of epilepsy, Miniere's disease,
and general nervous exhaustion and depression. But in many cases it
will be found that treatment directed against the dyspepsia cures the
vertigo.

Dyspeptic patients are also liable to skin diseases, and especially is
this observed in the gastro-duodenal forms of indigestion. Disorders of
the skin, such as urticaria, erythema, lichen, eczema, and other allied
conditions, are well-recognized external indications at times of
disordered conditions of the gastro-intestinal mucous membrane. Thus,
it is a matter of common observation that the gastric symptoms increase
when the eruption on the surface disappears.

The general influence of the nervous system over the function of
digestion is perhaps the most remarkable feature of the disease, so
that disturbed innervation becomes conspicuous in its symptomatology.
The phenomenon varies in individual cases. Languor, drowsiness after
taking food, depression of spirits, irritability, hypochondriasis,
sleeplessness, palpitation, dry cough, dyspnoea, are all of common
occurrence; and the mental disturbance--the anxiety, gloom, and
sadness--is to many dyspeptics more distressing than absolute pain.

It is impossible, however, to present, in this connection, a complete
clinical history of functional dyspepsia, for the reason that it is
associated with so many separate and distinct affections, the dyspepsia
itself being symptomatic of these affections.

PATHOLOGY.--But little is known of the pathology of the purely
functional forms of dyspepsia beyond what is expressed by the terms
atony and asthenia. These express simply certain states of the system
with which atonic dyspepsia is so frequently found associated.
Pathological anatomy has shown, however, that some cases are dependent
upon, or associated with, certain appreciable alterations of the
stomach, such as atrophy of the mucous membrane or fatty degeneration
of its walls; and not unfrequently it is the seat of the so-called
amyloid or lardaceous degeneration, although this albuminoid
infiltration or cloudy {452} swelling is more frequently the
accompaniment of chronic inflammatory process. But Jones and Fenwick
have shown that these conditions may occur independently of
inflammation. However, upon this point we are compelled to speak with
caution. The boundary-line between functional and structural diseases
is not always clearly defined. Functional and structural troubles of
the stomach are certainly very intimately associated. Moreover,
symptoms of purely functional dyspepsia are so frequently associated
with the subacute forms of gastritis that the pathology of the disease
becomes, from necessity, doubtful and complex. It can only be studied
in connection with certain states or conditions of which functional
derangement of the stomach is a symptom readily recognized during life.
In the light of more advanced physiological and pathological researches
we may expect the limits of purely functional dyspepsia to be much
restricted.

DIAGNOSIS.--The diagnosis of atonic dyspepsia must have special
reference to its etiology. It is usually a chronic disease, and has to
be discriminated from subacute or chronic inflammation of the stomach.
This is the more difficult because many symptoms exist in common in
both varieties of indigestion. But in functional or atonic dyspepsia
the symptoms are not so continuous; there is less epigastric
uneasiness, less tenderness, less nausea or loathing of food, less
thirst, and less acidity and heartburn, less emaciation, less cerebral
and nervous disturbance, and the constitutional symptoms are also less
severe. The tongue, as a rule, is not so thickly coated, is not so red
or broad and flabby, the papillae are less marked, the breath less
offensive, and the urine, instead of showing a condition of lithaemia,
is not unfrequently pale and sometimes neutral, depositing oxalates and
phosphates, especially in feeble, broken-down conditions of the nervous
system.

With other painful affections of the stomach, such as ulcer and cancer,
it is not likely to be confounded, especially when in these affections
pain, vomiting, and haematemesis are present.

TREATMENT.--The first and leading indication is to remove, as far as
possible, all causes of the disease, and this requires patient research
and much diagnostic skill. Suggestive hints of treatment may be found
in connection with the discussion of the varied etiology of the
disease. We can, in conclusion, only allude to the matter in a very
general way. Special cases must furnish their own indications of
treatment.

In many cases a condition of nervous asthenia will be found prominently
present. A leading indication, therefore, irrespective of the special
determining cause, is to improve the general health of the patient; and
this is accomplished by all means which invigorate the system
generally. And first in the order of importance are diet and regimen.
It is evident that if a patient eat too much or too often, or if he eat
indigestible or unwholesome food, or lead an indolent and luxurious
life, nothing can be accomplished by way of drugs in the relief of the
disease. Excessive alimentation is, as we have seen, a most prolific
source of the disease. Tempted to excess by great variety and by the
ingenuity of culinary refinements, the stomach is burdened beyond its
capacity of digestion and beyond the actual requirements of the system;
and especially is this the case with those who live sedentary, indoor
lives. In all such cases it is absolutely essential that the digestive
organs have rest. {453} Better even in cases of doubt reduce the diet
for a time below the actual wants of the system until waste products
are thoroughly removed and appetite is revived. The benefit derived in
some instances from the protracted use of purgative mineral waters is
largely attributable to the restricted regimen enforced and to the
washing out of the system the waste products.

On the other hand, too great or too protracted abstemiousness may
equally impair the digestive process. In ordinary forms of atonic
dyspepsia we should seek rather, by appropriate treatment, to raise the
digestive capacity to the level of digesting good, healthy, nutritious
food, than to reduce the food to the low standard of feeble digestion.
But it is a mistake to suppose that this can be accomplished by simply
forcing food upon a stomach that lacks capacity of digestion.

As to the kind of diet, no precise rule is suited to all cases. Within
certain limits individual experience must be consulted. But these
experiences are not always reliable. Dyspeptic patients, more than any
others, are apt to have fancies. Certain general rules, therefore,
should be insisted upon. The food should be wholesome and digestible;
it should be well cooked, well masticated, and taken at regular and not
too long intervals. The intervals of time between meals depend upon
circumstances already referred to. In some cases small quantities of
easily-digested food should be taken at short intervals. In cases of
feeble digestion of nervous subjects milk diluted in Seltzer water, or
milk and lime-water, or peptonized milk, may be taken in liberal
quantities at comparatively short intervals of time. Sometimes
isinglass, arrowroot, or ground rice may be advantageously combined
with the milk, to which tender, undone meats may be added.

Peptonized Food.--Recently the attention of the profession has been
attracted to artificially digested food. The essential acts of
digestion are known to be chemical transmutations. Albuminoid
substances are changed into peptones and starchy matters are changed
into dextrin and sugar. To Roberts, in his excellent lectures delivered
in the Lumleian course before the Royal College of Physicians of London
in 1880, we are indebted for valuable information on the digestive
ferments and in the preparation and use of artificially-digested food;
and from these lectures we shall derive most of the information we
possess at present. It has been demonstrated that an extract of the
stomach or pancreas, in water, has to a certain extent the same powers
as the natural secretions of these organs. Hence, says Roberts, it is
possible for us to subject articles of food beforehand to complete or
partial digestion. Heat approximatively accomplishes the same thing. In
the practice of cookery we have, as it were, a foreshadowing of this
art of artificial digestion. Heat and digestive ferments alike aid
gastric digestion. In case of the lower animals the whole process has
to be accomplished by the labor of their own digestive organs.

Artificially digested food may be prepared in two ways--either by
following the gastric method with pepsin and hydrochloric acid, or by
following the intestinal method and using extract of pancreas. Both of
these plans have had special advocates. Roberts claims that the latter
yields by far the better results. "The pancreas not only acts upon
albuminous substances, but also upon starch. Pepsin, on the other hand,
is {454} quite inert in regard to starch. Moreover, the products of
artificial digestion with pepsin and acid are much less agreeable to
the taste and smell than those produced by pancreatic extract." The
pancreas of the pig, according to Roberts, yields the most active
preparation, but the pancreas of the ox or the sheep may be employed.
The pancreas of the calf is not active on starchy materials. A very
active extract of pancreas is now prepared, and is easily obtainable,
with directions for making peptonized milk, milk gruel, milk punch,
soups, jellies, blanc-manges, beef-tea, enemata, etc. It is important
to remember that peptonized foods do not keep well, especially in warm
weather. If a quantity sufficient for twenty-four hours be prepared at
any one time, the quantity which remains over twelve hours should be
reboiled before using. Food thus peptonized is indicated in feeble
conditions of digestion and when the derangement of digestion results
from causes pertaining to the condition of the stomach itself--_i.e._
catarrhal forms of dyspepsia.

As a rule, the food should be such as will require the least possible
exertion on the part of the stomach. Raw vegetables should be
forbidden; pastries, fried dishes, and all rich and greasy compounds
should be eschewed; and whatever food be taken should be eaten slowly
and well masticated. Many patients digest animal better than vegetable
food. Tender brown meats, plainly but well cooked, such as beef,
mutton, and game, are to be preferred. Lightly-cooked mutton is more
digestible than beef, pork, or lamb, and roast beef is more digestible
than boiled. Pork and veal and salted and preserved meats are
comparatively indigestible. Bread should never be eaten hot or
fresh--better be slightly stale--and bread made from the whole meal is
better than that made from the mere starchy part of the grain. Milk and
eggs and well-boiled rice are of special value.

But to all these general dietetic rules there may be exceptions growing
out of the peculiarities of individual cases. These should be carefully
studied. The aged, for obvious reasons, require less food than the
young; the middle-aged, inclined to obesity and troubled with feeble
digestion, should avoid potatoes, sweets, and fatty substances and
spirituous liquors; persons suffering from functional derangements of
the liver should be put, for a time, on the most restricted regimen;
while, on the contrary, the illy fed and badly-nourished require the
most nutritious food that can be digested with comfort to the patient.

The general regimen should be tonic and invigorating. The patient
should have the benefit of the best possible hygiene. Under this head
may be mentioned suitable clothing, fresh air, moderate exercise,
sunlight, baths, rest, regular hours, and the abandonment of all bad
habits. No single measure has such marked influence on the digestive
powers of the stomach as systematic, well-regulated muscular exercise
in the open air, and especially if the exercise be accompanied by a
cheerful mental state. For this reason outdoor sports are of benefit.
Hunting, fishing, boating, are known to excite the keenest appetite for
food, and the stomach will digest substances that would distress it
under other circumstances. Exhaustion, however, is to be carefully
avoided. Horseback exercise is a remedy of much value, especially in
the hepatic forms of indigestion.

The mental and moral treatment of the purely functional forms of {455}
indigestion are amongst the most powerful means we possess. As an
etiological factor certain morbid mental states rank first, as we have
seen, in the order of importance. Grief, despondency, and despair are
effectual barriers to digestion, and in a less degree mental worry
seriously interferes with the process. It is a matter of prime
importance, therefore, that the patient's mind be pleasantly occupied,
that he should be free from all care and mental worry, and that he
especially be kept from dwelling, if possible, upon his own bodily
ailments. This is often best accomplished by travel, when practicable,
in foreign countries, where everything will be novel and new and
calculated to lead him away from himself. Get him to travel, says
Watson, in search of his health, and the chances are in favor of his
finding it. We have the authority of Sir James Johnson also for saying
that no case of purely functional dyspepsia can resist a pedestrian
tour over the Alps.

We come now to discuss the medical treatment of dyspepsia, which,
though not unimportant, is subordinate to the general hygienic measures
already referred to. General hints of treatment have been made in
connection with special causes mentioned in the text. We seek, in a
general way, by therapeutic measures--

1st. To stimulate the secreting and muscular coats of the stomach;

2d. To supply materials in which it is supposed the gastric juice is
defective;

3d. To lessen abnormal irritability;

4th. To combat special symptoms or conditions which may hinder the
digestive process.

To meet these indications innumerable remedies have been recommended,
but they are of benefit only as they counteract the conditions upon
which the dyspepsia depends. For loss of appetite, if there are no
contraindications to their use, the vegetable bitters are often useful,
such as quassia, gentian, and columbo. Of these columbo is the simplest
of its class, but none more generally useful than mistura gentianae
with soda. The Hydrastis canadensis has also peculiar claims as a
bitter stomachic. It, perhaps more than any of the bitters, promotes
gastric secretion in feeble digestion, and has at the same time
peculiar salutary effects on the enfeebled condition of the chronically
inflamed gastric mucous membrane. It is supposed also to have a
stimulating effect on the pancreatic secretion. It may be given in the
form of a fluid extract combined with glycerin and small doses of nux
vomica.

Among the specific stimulating nerve-tonics, nux vomica, or its
alkaloid, strychnia, deserves special mention. In small tonic doses it
is specially indicated in conditions of general nervous prostration
associated with a tendency to hypochondriasis. In such cases we
frequently observe pale urine, containing an excess of the phosphates.
The mineral acids are valuable additions to the bitter tonics in all
broken-down conditions of the nervous system. In administering nux
vomica care should be taken as to limitation of time and dose. The
excessive or prolonged use of the drug is apt to produce serious
general nervous disturbance, the secondary condition being often the
opposite to that for which it was prescribed. Temporary saccharine
diabetes is not unfrequently one of the results.

In atony of the mucous membrane, with morbid sensibility and slow {456}
digestion, ipecacuanha is a remedy of much value. It was first brought
into prominent notice in connection with gastric affections by Budd,
since which time it has been more or less used by the profession. In
torpid, slow digestion, with depraved or lessened gastric secretion, it
is of undoubted value. It should be given on an empty stomach at least
half an hour before meals. The dose should be short of producing
nausea. We may commence with two to four drops of the tincture or wine
of ipecac, and gradually increase until we find the point of tolerance;
or it may be given in the form of pill in doses of a quarter or a half
grain before meals, combining it with rhubarb in three- or four-grain
doses. Ipecacuanha may be administered at the same time we are giving
the mineral acids, or mineral acids with pepsin.

Adjuvants to Digestion.--In atony of the stomach the gastric mucous
membrane responds feebly to the stimulus of food. There is failure in
both muscular movement and gastric secretion, with slowness of
digestion as a result. To meet this condition we seek to increase the
digestive power by the addition of certain principles natural to the
digestive process--viz. the mineral acids, pepsin, and pancreatin. Of
these acids, the hydrochloric should be preferred, because it is the
natural acid of the gastric juice. Lactic, nitro-hydrochloric, and
phosphoric acids have also been used with benefit. There can be no
doubt of the efficacy of either of these preparations. They are best
given when the stomach is empty, so that they may directly act on the
relaxed atonic mucous membrane. Half an hour before or two hours after
a meal is the best time for their administration, and to be of benefit
they should be administered for a length of time. From fifteen to
twenty minims of the dilute hydrochloric or nitro-hydrochloric acid may
be given in some bitter tincture or infusion for months. An elegant
preparation may be made by adding the acid to tincture of orange-peel
and syrup of lemon. Aromatic tincture, tincture of ginger, or glycerin
may be added in some cases. It is important that remedies administered
in gastric affections should be made pleasant as possible to the
patient.

Metallic preparations are of use in some cases. If for any reason they
are preferred, the perchloride of iron is one of the very best
preparations. Arsenic and zinc may also be tried in small doses.

Pepsin and its Uses.--Of the efficacy of pepsin as an artificial
substitute for the normal solvent of the food adverse opinions have
been expressed, but in spite of the most critical scepticism as to its
action its use since first introduced into medicine has steadily
increased. It has been shown to be the natural constituent of the
gastric juice and glands, and as a natural ferment, when combined with
hydrochloric acid, it constitutes the most important solvent of the
nitrogenous portions of our diet (Habershon). There is a vast number of
different preparations of pepsin in the market, and some of them are
doubtless of little value. We ought to be quite sure that the article
is what it purports to be. The pepsina porce is the best preparation,
one grain of which, says Beale, ought to thoroughly digest one hundred
grains of boiled white of egg in three or four hours at a temperature
of 100 degrees F. His test as to the value of pepsin is as follows:
"One hundred grains of hard-boiled white of egg, cut into thin slices,
may be placed in a wide-mouthed bottle or flask with one ounce of water
and twenty drops of dilute hydrochloric acid. One {457} grain of pepsin
powder is to be added, and the mixture placed before a fire at a
temperature of about 100 degrees F. The flask is to be shaken from time
to time. In about an hour the white of egg begins to look transparent
at the edges, and in about four hours it will be completely dissolved
if the pepsin is good." In cases of feeble digestion from deficiency of
gastric juice pepsin is a valuable adjuvant to the digestive power, and
may be given with advantage in connection with the mineral acids or
with ipecacuanha or capsicum before meals.

Special Remedies.--There are certain symptoms characteristic of the
different forms and complications of dyspepsia that require special
remedies. Bismuth is often useful. It is especially indicated where
there is a morbid painful condition of the gastric nerves. The
subnitrate or carbonate of bismuth may be given in ten- or twenty-grain
doses, suspended in water by means of mucilage of acacia, and flavored
with ginger or peppermint. It should always be given on an empty
stomach. Other elegant preparations supposed to be improvements upon
these have been recommended, and may be tried.

In cases of anaemia, if there are no contraindications, iron may be
tried. If digested and assimilated, it improves the blood, and this is
often the first step in the direction of restoring functional activity.
Of the preparations of iron, none is perhaps superior to the
perchloride. The saccharo-carbonate and the ammonio-citrate are also
valuable and unirritating salts of iron, and may be given with other
tonics. Ferruginous mineral waters slightly charged with carbonic acid
are well tolerated in small doses. The free dilution favors the action,
and is frequently more acceptable to the stomach than the more
concentrated forms. From one-half to one glassful may be taken at a
time; and the use of iron in this form may be preceded or accompanied
by the administration of small doses of quinia and of the bitter
tonics. But it is a mistake to commence the treatment by the
indiscriminate use of iron, quinine, and nerve-tonics. The
contraindications to the use of iron are irritable and inflammatory
states of the mucous membrane, or dyspepsia associated with deranged
conditions of secretion, as manifested by dirty tongue and loaded
urine.

When the nervous system is prominently at fault, nux vomica, arsenic,
and the nitrate and oxide of silver often prove to be valuable
remedies. Here also benefit may be derived from the lighter ferruginous
preparations; indeed, few combinations have greater influence over the
nervous system than the joint action of arsenic and iron. Much benefit
may also be derived, in special cases, from methodical
hydro-therapeutic treatment. If judiciously used it strengthens the
nervous system, stimulates the organic functions, and increases the
power of vital resistance. And in some cases of nervous dyspepsia
electricity gives good results. In all cases of nervous prostration as
much wholesome food should be taken as the stomach can easily digest.

In hepatic forms of indigestion there is no substitute for an
occasional mercurial cathartic, for, notwithstanding adverse criticism,
clinical experience has taught the great value of this drug upon the
upper portion of the intestinal track. The mode of operation may be
doubtful, but the result is unquestionable. In functional disturbance
of the liver or morbid conditions of the upper portion of the
intestinal track, as indicated {458} by the loaded tongue, sallow
complexion, want of appetite, and lithaemia, no remedy will give so
much relief as a few broken doses of calomel, followed by a saline
aperient; or eight or ten grains of blue mass, with a grain of
ipecacuanha, may be administered at bedtime, followed by a saline
draught in the morning. After the bowels are thoroughly unloaded by a
mercurial, great advantage may be derived from a systematic course of
the aperient mineral waters--the Friedrichshall, the Hunyadi, Carlsbad,
or some of the mineral waters of our own country. The hepatic form of
indigestion cannot be relieved until we relieve the congested hepatic
portal system, and this is best accomplished by the general line of
treatment here indicated. The simple vegetable bitters, with or without
alkalies, may be used at the same time or subsequent to this treatment;
but they are often worse than useless until we secure freedom of
abdominal circulation. The diet should be light and nourishing, and the
patient should spend most of his time out of doors. Horseback exercise
is peculiarly advantageous.

But in many cases of the more chronic forms of dyspepsia the colon is
as atonic as the stomach, and therefore the bowels require special
attention. In colonic dyspepsia all active purgation should be avoided,
and salines, such as sulphate of magnesia, the Hunyadi and other saline
mineral waters, should be specially prohibited. The most useful
aperients in such cases are rhubarb, aloes, senna, colocynth, or
podophyllin. Few laxatives answer a better purpose than the ordinary
compound rhubarb pill. It may be improved, in special cases, by
combining with it extract of nux vomica or belladonna. When there is no
affection of the rectum to forbid its use, the watery extract of aloes
answers very well, and, unlike many cathartic substances, the dose need
not be increased, nor does it disturb the digestive process. It may be
given in one-sixth of a grain up to a grain or more, and its purgative
action may be improved by being reduced to a state of very minute
division and combining with it small doses of belladonna. Belladonna
itself is a useful remedy. According to the observations of Harley, it
"tones and tightens the longitudinal fibre, while it relaxes the
circular;" and long before this theory of its action was suggested,
Trousseau called attention to its singular efficacy in producing easy
and natural evacuations from the bowels. It is important to observe its
mode of use. It should be given in sixth of a grain doses of the
extract in the morning a half hour or hour before breakfast. Its
efficacy may be increased by combining with it small doses of the
watery extract of aloes. In colicky conditions of the bowels two- or
three-drop doses of tincture of colocynth sometimes act wonderfully
well. In obstinate constipation the free use of diluents at the
termination of digestion is often attended with excellent results. But
the hygienic and dietetic treatment of constipation is even more
important than the medicinal, such as outdoor exercise, the cold bath,
rubbing, kneading the bowels, and the use of bread made of whole meal,
oatmeal, and an abundant supply of fresh vegetables and fruits.

Nausea and vomiting, occasional symptoms of functional dyspepsia, may
be relieved by various agents, such as effervescing draughts,
lime-water, oxalate of cerium, hydrocyanic acid, creasote, ice, and
alkalies.

When vomiting is dependent on fermentation or putrid action of the
contents of the stomach with development of sarcinae, it may be checked
{459} by carbolic acid or by creasote, or by the sulphite of soda or
sulphurous acid; and in irritable conditions of the stomach bismuth is
a valuable remedy. It may be given with alkalies or with
finely-triturated animal charcoal.

Gastric pain needs treatment appropriate to the circumstances under
which it arises. Sometimes it is relieved by regulating the ingesta or
the intervals at which it is taken; sometimes by warm carminative
stimulants or by chloric ether, ginger, or brandy. If the pain is more
constant, approaching a condition of gastralgia, hydrocyanic acid and
bismuth are more effective remedies. But it cannot be too strongly
stated, in conclusion, that in the management of the atonic forms of
dyspepsia hygienic treatment is of prime importance. The hopeful future
of medicine lies in the direction of promoting healthy nutrition, and
this is best accomplished by the careful adaptation of food and
exercise and modes of living to individual cases of disease.


Gastralgia (Gastrodynia, Cardialgia, Spasm of the Stomach).

Under the head of neuroses of the stomach have been variously described
the conditions indicated in the heading of this section; and a certain
amount of confusion has arisen in the use of these terms from the fact
that they represent subjective sensations common alike to organic and
functional forms of indigestion: pain, for instance, is felt in
gastritis, cancer of the stomach, and ulcer of the stomach. Indeed, it
rarely occurs independently of some disorder of digestion or structural
lesion of the stomach.

By gastralgia, considered as a distinct affection, however, we mean a
purely neuralgic condition of the sensory fibres of the stomach,
excluding inflammatory and structural changes on the one hand and
chronic forms of atonic dyspepsia on the other. The attacks are usually
periodical in character, with constricting pain in the pit of the
stomach, and the intervals are not necessarily associated with symptoms
of dyspepsia. It chiefly occurs in females of nervous temperament at
the catamenial periods.

Two forms of the disease have been described--one depending on
hyperaesthesia of the sensory fibres of the pneumogastric, the other on
hyperaesthesia of the solar plexus. This may be correct in theory, but
practically it can be of little importance to make the discrimination,
even if it were possible to do so.

Clinically, the disease is presented to us in two forms. In one the
pain is agonizing, comes on without premonition, is sometimes
intermittent or remittent in character, and conveys to the sufferer the
idea of spasm; hence it has often been described as colic of the
stomach. If not relieved by appropriate remedies, the pain may last for
hours or days. This is the acute form. In the other the pain is more of
a neuralgic character and is not so severe. There may be varying
exacerbations which may last for months or years. This is not an
unfrequent form, and may consist simply in the more acute form becoming
chronic.

ETIOLOGY.--With the limitation indicated, we have naturally to seek the
causes of the affection, says Ziemssen, in two directions: either in
the abnormal nature of the irritants to which the gastric nerves are
subjected, {460} or in an altered condition of the nerves themselves,
which therefore react abnormally with the normal degree of irritation.
This briefly covers the whole ground of the etiological relations of
the disease.

The predisposing causes are such as produce general depressed vitality,
embracing at the same time special conditions of extreme nervous
excitability. Some of these general conditions were pointed out while
speaking of atonic forms of dyspepsia. Indeed, the two conditions are
often associated, and practically it may be difficult to separate them,
although the connection between them is not necessarily an invariable
one. Like atonic dyspepsia, gastralgia is apt to affect anaemic
persons, and notably anaemic females at menstrual periods. Thus, the
association between gastralgia, chlorosis, and hysteria is a matter of
common observation. Of 350 cases noted by Briquet, only 30 had no signs
of gastralgia; and this observation is a fair average expression of the
experience of others.

Certain blood-poisons are also known to give rise to the disease.
Infection of the blood by malaria was observed by Niemeyer to produce
spasm of the stomach instead of the paroxysms of intermittent fever;
and in malarious regions of the United States the same observation has
been made. Gout and rheumatism are also known to sustain causative
relations to the disease. Certain idiosyncrasies also enter as a factor
into the somewhat complex etiology of the disease. Thus, some persons
suffer immediately from eating certain kinds of food and fruits, such
as shellfish, strawberries, honey, and even milk and coffee. The pain
and spasm are produced by direct contact with the sensory fibres of the
stomach; _i.e._ they react abnormally to normal stimulation. But
disease of the nerve-centres may enter into the causation. This is seen
by the effects of morbid growths impinging upon nerve-trunks; their
terminal branches often become extremely irritable and painful, and
this condition may be intensified by idiosyncrasy. Excessive acidity of
the stomach, seeds of fruit, certain articles of food, the presence of
worms in the stomach, and draughts of ice-water may simply act as
exciting causes to a centric predisposition.

Of the more direct causes operating upon nerve-centres, all the
depressing passions and emotions deserve special mention; so do all
causes which produce an exhausted state of innervation, such as
venereal excesses, onanism, the abuse of narcotics, etc.

But chief among the causes are those of a reflex kind. Painful
affections of the kidneys, irritable conditions of the bladder,
diseases of the liver, and, above all, morbid conditions of the female
genital organs, sustain a direct and close relation to painful and
spasmodic conditions of the stomach. It is a common accompaniment of
versions, flexions, prolapses, inflammations, erosions of the os, as
well as diseased conditions of the ovaries. When such local conditions
are associated with anaemia and hysteria, patients rarely fail to have
painful gastric complications.

SYMPTOMS.--The symptoms of gastralgia, like most of the neuroses, are
characterized by severe pain occurring in paroxysms, followed by
remissions, and sometimes by complete intermissions, again to recur
with varying degrees of severity. The pain in the acute variety is of a
violent, spasmodic character, and is referred to the epigastrium
immediately beneath the ensiform cartilage. Frequently it extends from
the epigastrium to the back and chest and into the right and left
hypochondrium. {461} No one has so briefly and so accurately described
the immediate attack of gastralgia as Romberg: "Suddenly, or after a
precedent feeling of pressure, there is severe griping pain in the pit
of the stomach, usually extending into the back, with a feeling of
faintness, shrunken countenance, cold hands and feet, and small,
intermittent pulse. The pain becomes so excessive that the patient
cries out. The epigastrium is either puffed out like a ball, or, as is
more frequently the case, retracted, with tension of the abdominal
walls. There is often pulsation in the epigastrium. External pressure
is well borne, and not unfrequently the patient presses the pit of the
stomach against some firm substance or compresses it with his hands.
Sympathetic pains often occur in the thorax under the sternum, in the
oesophageal branches of the pneumogastric, while they are rare on the
exterior of the body. The attack lasts from a few minutes to half an
hour; then the pain gradually subsides, leaving the patient much
exhausted, or else it ceases suddenly with eructation of gas or watery
fluid, with vomiting, with a gentle soft perspiration, or with the
passage of reddish urine."

Besides the violent paroxysmal pain referred to the stomach, symptoms
of derangement of other organs are often present. Prominent among these
are hysterical phenomena which are protean in their manifestations, and
if not recognized they are liable to mislead. Thus, with gastric pain
there may be violent palpitation of the heart, with shortness of
breath, cough, globus, hiccough, and convulsive affections, and in a
certain proportion of cases there is marked melancholia or
hypochondriasis.

The stomach is variously modified in its function. In many cases it is
entirely unaffected. The desire for food may be indeed increased, and
its ingestion may give a sense of relief. In others vomiting may be
severe, while in still others there may be merely a condition of
anorexia. The tongue is, as a rule, clean, the skin cool, the
temperature undisturbed, and there is absence of tenderness over the
epigastrium. Generally pressure relieves the pain.

DIAGNOSIS.--Functional and structural troubles of the stomach very
markedly simulate each other; therefore the diagnosis requires to be
made with great caution, and this is best done by a most rigid and
careful exclusion; and this becomes difficult because the symptoms are
mainly subjective.

It is a matter of great moment in differentiating the disease to take
into account all constitutional states which predispose to nervous
asthenia. Thus in conditions of chlorosis and hysteria the presumption
is strong that the pain is neurotic or spasmodic in character; and this
presumption is intensified if there be no accompanying constitutional
symptoms which indicate inflammatory action. We exclude inflammatory
conditions of the stomach by the frequent and complete intermissions,
by the absence of thirst, tenderness, and all febrile movement.
Moreover, the pain of inflammatory affections, unless produced by
corrosive poisons, is rarely so severe as in neuralgic affections; nor
are nausea and vomiting so uniformly present in neurotic affections.
Then the time at which the pain is experienced is a matter of
importance. In inflammatory affections it is felt immediately on taking
food. In neurotic affections it may occur when the stomach is empty,
and it is not unfrequently relieved by food. In ulcer and cancer of the
stomach pain is a common element, and, as in {462} gastralgia, it is
referred to the epigastrium. But in gastric ulcer the pain is rarely
absent; it is of a dull, gnawing character, is strictly localized in
the centre of the epigastrium, and is aggravated by pressure and by
food. Moreover, the vomited matter often contains blood. In cancer of
the stomach the pain is not as severe and spasmodic in character as in
gastralgia, the vomiting is a more prominent symptom, and the material
vomited has the characteristic cancerous look. Cancer is more apt to
occur too in advanced life, and it is characterized by a steady
progressive emaciation.

Gastralgia may also be confounded with rheumatism of the abdominal
muscles as well as neuralgia of the inferior intercostal nerves, and it
is liable to be confounded with colic resulting from biliary calculi.
Colicky pains in the transverse portions of the colon may also be
mistaken for pains in the stomach. "It is no exaggeration to say," says
Trousseau, "that in perhaps half the cases which are called gastralgia
the affection is nothing more than cholalgia." The more fixed the pain
is to one spot, and the nearer it is to the median line, the greater is
the probability of its being gastric.

PROGNOSIS.--Notwithstanding the severe and apparently alarming nature
of the symptoms, the prognosis of gastralgia is in the main favorable,
although the prospect of a permanent and speedy cure is small. The
duration of the disease depends on the nature and persistence of the
exciting causes, and these are so often associated with an exhausted
state of innervation that speedy recovery from the disease cannot be
promised. In the simpler varieties, caused by improper food, the
disease will disappear by removing the cause, and the hysterical forms
are liable to disappear with advancing life. So also cases arising from
malaria, anaemia, chlorosis, uterine disease, rheumatism, and gout may
be relieved by removing the cause. But there are cases produced by
unknown causes, and especially cases associated with a general and
unexplained cachexia, in which the prognosis is not good.

TREATMENT.--This is both radical and palliative. The radical treatment
must have reference to the diseases which have given rise to it. If,
for instance, the gastralgia can be traced to sympathetic disturbances
of the uterine organs, no remedy can be permanently effective until the
cause is removed. Since chlorosis and anaemia are so often found
associated with it, benefit may be expected from the ferruginous
preparations in some form. Iron occupies a prominent place as a
remedial agent. The precipitated carbonate is to be preferred on
account of its peculiar influence over the nervous system, and
especially over painful neuralgic conditions. It may be given in drachm
doses, or even larger, combined with ginger or aromatic powder. If the
stomach will not tolerate it, other preparations may be tried.

Quinia is a valuable addition to iron, and it is specially valuable in
cases of suspected malarious origin. Sometimes a few large doses will
break up the paroxysmal pains as no other agent will.

In the more chronic forms of the disease arsenic is one of the most
reliable remedies we possess. It has a well-deserved reputation in the
treatment of a great variety of nervous affections, and in none more
than in the disease now under consideration. It should be given for a
length of time--three or four minims of Fowler's solution, gradually
increased and {463} given immediately after food--and in cases of
anaemia it should be associated with iron.

In irritable, broken-down conditions of the nervous system nux vomica,
or its alkaloid strychnia, is a useful remedy. But it is a powerful
stimulant to the spinal nerve-centre, and care should be used in the
too protracted use of the remedy or in its administration in too large
doses. It may be combined with the phosphate or the valerianate of
zinc, or either may be given separately. The nitrate and oxide of
silver have also been used with asserted success. Nitrate of silver may
be given in pill form with opium.

If there is a strong hysterical element, the bromides and
antispasmodics may be tried in connection with remedies calculated to
strengthen the nervous system. The judicious employment in such cases
of hydro-therapeutic measures is of great value. Good results are also
obtained from electricity. The constant current should be preferred.

Among palliative remedies--_i.e._ remedies that act directly on the
painful gastric nerves--the subnitrate of bismuth has long been
regarded with great favor. Its action is mainly local; it may be given,
therefore, in drachm doses or more three or four times a day. If there
is nothing to contraindicate its use, aconite or dilute hydrocyanic
acid may be given with the bismuth.

For the immediate relief of pain, however, there is no substitute for
opium. The subcutaneous injection of morphia will generally give
immediate relief. But there are many reasons why we should try other
palliative remedies. In a disease so painful in character a remedy that
gives such prompt relief is liable to abuse. The formation of the opium
habit should be carefully guarded against. Spirits of chloroform may be
tried, therefore, as a substitute for opium, followed by large draughts
of hot water--hot as the patient can possibly sip it. Hot water of
itself often gives immediate relief.

An important part of the treatment consists in well-regulated hygiene.
Change of air, travel, pleasant mental surroundings, together with
carefully regulated diet, are in a majority of cases more efficacious
than drugs.


Acute Gastritis (Acute Gastric Catarrh).

Reasoning from the great functional activity of the stomach, from its
daily periodical change of blood-supply, from its extensive glandular
arrangement, and from its important relations to the functions of
vegetative and animal life, we might readily infer that it would be
frequently the seat of acute and destructive inflammation. But it is
remarkable, all things considered, how seldom that is the case. Indeed,
acute spontaneous inflammation of the stomach is almost unknown. When
it occurs it most frequently results from toxic causes. In less severe
forms, however, not attended with immediate danger to life, it is
undoubtedly a disease of frequent occurrence, and in this more
comprehensive sense the subject will be considered in the present
section.

The mucous membrane alone is usually the seat of the disease, and for
this reason it has become the custom of late years to describe it as
gastric {464} catarrh. This may be objectionable, for the reason that
it does not include gastric inflammation of every grade of intensity.
The term catarrh is generally applied to much more simple anatomical
structures than those pertaining to the stomach. We shall consider the
subject therefore under two forms--namely, (1) Catarrhal; (2)
Erythematous gastritis.

ETIOLOGY.--Certain conditions predispose to the disease. Acute
catarrhal gastritis is specially liable to occur in those who
habitually suffer from a disordered stomach. This may arise from
functional disturbance of the digestive process on the one hand, or
mechanical obstruction on the other. Mechanical causes are widespread
in their influence. Thus, weak heart-action from any cause tends to
disturb the normal adjustment between the two sides of the
circulation--arterial and venous. An abnormal amount of blood
accumulates on the venous side of the circulation, and chronic passive
hyperaemia of the abdominal viscera is the result. The effect of this
upon the stomach is to lower its functional activity and to invite
inflammatory action. The same condition results from structural
diseases of the heart, lungs, or liver. Persons suffering from valvular
diseases of the heart, emphysema of the lungs, or cirrhosis of the
liver are strongly predisposed to diseases of the stomach. Gastric
troubles are also apt to supervene during the progress of various
diseases.

Gouty and rheumatic persons are specially prone to suffer from gastric
catarrh; and eruptive disorders, such as scarlatina, diphtheria, etc.,
tend to erythematous forms of gastric inflammation. Catarrhal gastritis
is also a very common sequence of the whole class of malarious fevers,
including yellow fever, intermittents, and remittents. In its more
acute form gastric inflammation supervenes in the course of yellow
fever; and what is observed here in an extreme degree exists in a minor
degree in all the so-called malarious fevers. Intermittent and
remittent fevers are always attended with gastro-duodenitis and
gastro-hepatitis. The degree of this inflammatory complication
determines the continued character of the fever. Upon this point the
writer has very decided views based upon a wide field of observation in
malarious regions of country. We have lost ground in the treatment of
these diseases by directing our attention almost exclusively to the
febrile and malarious, to the exclusion of the inflammatory, elements.
Quinia is inoperative in the cure of these troublesome and often fatal
complications. Indeed, it is more than that: it is often positively
injurious. Arrest the local phlegmasia and secure freedom of abdominal
circulation, and we at once get the action of the specific remedy. It
may be going too far to affirm, as did Broussais, that gastritis
sustains a causative relation to all forms of fever, but that
gastro-duodenitis is an important secondary condition in all forms of
malarious fever, complicating and perpetuating the febrile state, there
can be no doubt; and it is equally clear that it constitutes one of the
most dangerous complications. Excessive alimentation, with the
injudicious use of tonics and stimulants, so often resorted to in the
treatment of these fevers in their early stages, only serves to
intensify the local inflammation. Abolish the congestive and
inflammatory element of a remittent, and it at once becomes an
intermittent.

Mention has been made of weak heart-action as a factor in catarrhal
{465} gastritis; also mechanical impediments to the return of blood
from the stomach to the heart. The stomach is thereby kept in a
constant state of congestion, the nutrition of the mucous membrane is
less active than in health, and its solvent juices are more sparingly
secreted. Thus in long-continued congestion produced by mitral disease
of the heart Samuel Fenwick found the formation of pepsin impaired. He
made artificial gastric juice from the mucous membrane of three males
dying of heart disease, and he found, on the average, only 2-9 grs. of
albumen were dissolved, whereas the amount digested by the mucous
membrane of persons who had died of other maladies was 4 grains. In the
cases of three females a still smaller amount of solvent power was
displayed. These facts have important bearings upon the question of
alimentation in fevers and the conditions in which there is chronic
congestion on the venous side of the circulation. Long-continued
passive hyperaemia of the stomach from any cause not only impairs its
functional activity, but strongly predisposes to inflammatory
complication.

Acute erythematous gastritis is most frequently met with in children.
It is a very common form of disease in early life, and the local nature
of the malady is frequently overlooked. Few questions in practical
medicine are more embarrassing to the physician. It has been known and
described as gastric and remittent fever, as continued typhoid, and
even as acute hydrocephalus. Writers and teachers describe and
dogmatize, while practical men hesitate at the bedside. There is little
doubt but in the background of these febrile manifestations in children
there is often an acute erythematous gastritis, which is more
successfully treated by a rigid milk diet, small doses of calomel and
bismuth, mucilaginous drinks, cooling saline laxatives, and sometimes
leeches applied to the epigastrium, than by the heroic doses of quinia
so frequently resorted to.

We must not, in this connection, lose sight of the fact, so clearly
pointed out by Broussais, that inflammation of the stomach is often
secondarily repeated in the brain. The whole field of clinical
observation abounds in illustrations of this. How often, for instance,
we can trace the sick headache, the delirium, and even convulsive
movements of the voluntary muscles, to primary gastro-intestinal
irritation! In the play of the sympathies morbid irritative action is
transmitted from the organic to the cerebro-spinal nerves; and of all
portions of the abdominal viscera the stomach and upper portion of the
intestinal track are the most frequent seat of these intense morbid
sympathies. Remedies which cool the stomach and lessen inflammatory
action diminish the excitement of the brain, and vice versa.

EXCITING CAUSES.--Among the direct exciting causes of gastric
inflammation--exclusive of acrid or corrosive poisons--the most
frequent in this country is the excessive use of alcohol. It acts most
injuriously when it is but slightly diluted and taken on an empty
stomach. And next to this pernicious habit, in the order of importance,
is the use of large quantities of food--more than the stomach has
capacity to digest, and more than is necessary for the wants of the
system. Excessive alimentation is a prolific source of gastric
inflammation. It generally manifests itself, however, in a chronic or
subacute form.

Acute erythematous gastritis, so frequently met with in children, is
{466} often present in scarlatina. It is evidently not catarrhal in
character, for in the earlier stages there is no increased secretion of
mucus and but little injection of the mucous membrane. The changes are
observed in the deeper structures of the stomach, and principally in
the gastric tubules. They are much distended by granular, fatty, and
albuminous matter; and in this respect it is analogous to erythematous
affections of the skin with which it is associated in scarlatina.

Finally, acute gastric catarrh may be excited by all causes that weaken
the digestive power either by weakening the gastric juice or by
retarding the movements of the stomach.

ANATOMICAL CHARACTERS.--No disease requires more knowledge and caution
in determining post-mortem changes than those of the stomach. In the
first place, it presents in inflammatory conditions markedly different
degrees of intensity, with corresponding differences in anatomical
changes. Its diseases also present many special forms, and changes take
place after death which simulate morbid processes during life.
Moreover, intense vascular injections are apt to disappear in the small
superficial vessels after death. This applies to all mucous membranes,
but specially to the mucous membrane of the stomach, which is the seat
of varying amounts of blood in their physiological limits during life.
For this reason the observations of Beaumont made upon a living subject
are invested with peculiar interest. It will be remembered that in the
case of Alexis St. Martin the appearances noted were such as belong to
the milder forms of inflammation. Beaumont noticed in this case, after
indiscretions in eating or abuse of ardent spirits, a livid
erythematous redness of the gastric mucous membrane, with, at the same
time, dryness of the mouth, thirst, accelerated pulse, and, at the
height of the injection, an entire absence of gastric secretion. At
other times there was considerable muco-purulent matter, with oozing of
grumous blood, "resembling the discharge from the bowels in cases of
chronic dysentery." The fluid taken out through the fistulous opening
consisted mostly, however, of mucus and muco-pus which showed an
alkaline reaction. He describes also a condition of ecchymosis and
oozing of blood from certain red spots of the gastric mucous membrane,
and when thus limited the constitutional symptoms experienced by the
patient were correspondingly slight. Ecchymoses may be present in large
number, with exudates of false membrane, which Beaumont describes as
aphthous. Brinton also describes a severe form of gastritis which he
terms ulcerative, in which he observed hemorrhagic erosions.

In the catarrhal form of gastritis the mucous membrane is covered with
a thick, tenacious, stringy mucus; it is softer than usual, and
generally thickened. It presents at the same time a dead-white
appearance, corresponding to Virchow's cloudy swelling--a condition
analogous to that which is observed in acute Bright's disease. Even
casts of the tubes are sometimes met with.

This inflammatory change in the substance of the mucous membrane is
especially observed in the acute erythematous form of gastritis
complicating scarlatina. In the early stage there is no increased
secretion of mucus, and at a more advanced stage the membrane may be
even paler than usual.

In cases of acute toxic gastritis intense redness is seen over the
entire {467} surface of the mucous membrane, followed by rapid
exudations and sloughing of portions of the membrane.

In all forms of the disease there is a tendency to extension of the
inflammation into the duodenum and small intestines. In the more
chronic forms we almost invariably encounter the condition of
gastro-duodenitis.

SYMPTOMS.--The symptoms of inflammation of the stomach present wide
differences in their intensity, depending upon the degree of severity
in different cases. In acute inflammation caused by the direct action
of poisonous irritants they are pronounced and highly diagnostic. The
patient immediately complains of burning pain, referred to the
epigastrium, followed by intense thirst and vomiting. The thirst is apt
to be very great and the act of vomiting painful. The vomited matters
contain mucus, saliva, sometimes bile, and not unfrequently, in fatal
cases, black, grumous, coffee-ground material. There is marked
tenderness on pressure, the pulse is frequent and small, coldness of
the surface is marked, and hiccough is apt to occur. The expression of
the patient is anxious, the abdominal muscles rigid, and, in fatal
cases, the prostration becomes rapidly extreme. The patient dies by
asthenia. These symptoms apply to acute cases of marked severity,
usually of toxic origin.

In the milder forms of catarrhal gastritis more frequently met with
there is seldom complaint of pain. The sensation is rather that of
fulness, uneasiness, with more or less tenderness on pressure. The
symptoms are such as belong to acute indigestion and the embarras
gastrique of French authors. The phenomena may be those of a slight
bilious attack. The tongue is foul, the breath offensive, the bowels
confined, and the urine high-colored and scanty. There is also
generally a sense of fatigue, and soon secondary cerebral symptoms
supervene, such as cerebral hyperaemia, headache, vertigo, noises in
the ears, palpitation, sighing, yawning, dyspnoea, faintness, and in
severe cases marked physical and mental depression. Nausea and vomiting
are common, and if the inflammation extends to the duodenum and liver,
symptoms of gastro-hepatic catarrh manifest themselves. If fever
supervenes, urticaria sometimes complicates these attacks.

In young children the inflammation is apt to involve a general catarrh
of the whole intestinal track. Thirst is excessive, followed by
vomiting and diarrhoea. The discharges are liquid, watery, offensive,
acid, and out of all proportion to the amount of fluid absorbed by the
stomach. The pulse becomes weak and fluttering, the skin pale, the
features pinched, the eyes sunken, and the extremities cold. The
tendency is toward rapid collapse and fatal issue. The symptoms
describe what is usually known as cholera infantum. It has its analogue
in the cholera morbus of adults.

In erythematous gastritis nausea and vomiting are as general as in the
catarrhal form, but, unlike the catarrhal, pain at the epigastrium is a
prominent symptom. It comes on directly after taking food. In
phthisical cases the sensation is rather that of rawness of the
oesophagus and stomach. Thirst is a troublesome symptom; the tongue is
red or dry and glazed; tenderness of the epigastrium is marked;
diarrhoea is generally present; and, as in the catarrhal form, the
stools are fetid and unhealthy. The disease shows a marked tendency to
become chronic.

{468} DIAGNOSIS.--In the more acute forms of the disease the symptoms
are all highly diagnostic. Vomiting, burning pain of the stomach,
tenderness on pressure, intense thirst, with frequent and small pulse,
point with almost unerring certainty to acute gastric inflammation. But
vomiting of itself, however persistent, is not evidence of gastritis,
for it may be present from many other causes. If the vomiting be
attended by headache, it may be confounded with gastric irritability
from brain disease. Thus, chronic meningitis with persistent vomiting
strongly simulates gastritis, and in the case of children it is liable
to be mistaken for it. In gastritis the nausea is from the first a
pronounced feature of the disease. Vomiting in affections of the brain
is often unattended by nausea. In gastritis the tongue is more
frequently coated or red and glazed. Diarrhoea is also more frequently
present, especially in early life. In affections of the brain the
tongue may be clean and the bowels are usually obstinately confined.
When there is much fever, gastritis may be confounded with remittent or
typhoid fever. In periods of childhood this mistake is specially liable
to occur, for there are many symptoms in common. In all such cases the
early history of the case ought to be carefully inquired into. In
gastritis we may be able to detect the cause in any particular case.
The gastric symptoms are apt to occur suddenly, and, as already stated,
are prominent from the first. In meningitis the skin is more frequently
dry; in gastric catarrh perspirations are common. The more prominent
and characteristic symptoms of typhoid should also be carefully
excluded, such as the gradual invasion, peculiar eruption, bronchial
catarrh, enlargement of the spleen, gurgling in the right iliac fossae,
with tympanitic abdomen. Peritonitis, with vomiting, may be mistaken
for gastritis, but the diffuse tenderness, the fixedness of position,
the rigidity of the abdominal muscles, and the tympanitic distension
serve to guide us in our diagnosis.

PROGNOSIS.--The prognosis must have reference to the cause. The more
violent forms of the disease resulting from corrosive poisons are
generally fatal. Death is apt to take place in a few hours from a
condition of collapse. The immediate cause of death is failure of
heart-action. It is also a dangerous disease in the extremes of life.
In its acute form in children it is apt to terminate fatally,
especially if it is not recognized early and judiciously treated. The
complications of the disease may also render the prognosis unfavorable.
Milder cases tend to recovery.

TREATMENT.--The most important indication of treatment, applicable to
all forms of gastric inflammation, is to secure complete or partial
rest for the inflamed organ. In dangerous cases no food should be taken
into the stomach. The patient should be nourished exclusively by
nutrient enemata. If food is permitted, it should be restricted to milk
and lime-water, administered in small quantities at short intervals. In
acute and dangerous cases, suddenly manifesting themselves, the
exciting cause should be carefully inquired into, and speedily removed,
if possible, by an emetic, or, if need be, by the stomach-pump, if the
poison be one which can be ejected; and following this antidotes are to
be administered according to the nature of the poison.

To allay the intense thirst small pieces of ice should be swallowed at
frequent intervals, or, what is often more grateful to the patient,
iced {469} effervescing drinks in small doses oft repeated. Injections
of water may also tend to relieve thirst. To allay vomiting the
physician is often tempted to try a great variety of remedies which are
usually worse than useless, for they aggravate rather than relieve the
distressing symptom. For the purpose of quieting the stomach opium is
the most reliable remedy we possess. It is best administered
hypodermically. Fomentations may be applied over the epigastrium.
Stimulants are, of course, contraindicated on account of their
irritating action on the inflamed membrane, but in case of rapid
tendency to death by failure of heart-action they should be
administered by the rectum or hypodermically.

In milder cases--which are much the more common--physiological rest of
the organ is also a cardinal principle of treatment. Rest of the body
is equally essential. In cases of any severity the patient should be
kept quiet in bed. For the condition of acute indigestion known as
embarras gastrique ipecacuanha in six- or eight-grain doses, given
three times within twenty-four hours, will often produce healthy
bilious stools, and in this manner accomplish the cure. One or two
grains of calomel may be added to each dose of ipecacuanha with
benefit. In all forms of catarrhal gastritis, especially if symptoms of
portal congestion are present, mild mercurial cathartics are attended
with benefit. Six or eight grains of calomel may be rubbed up with
sugar of milk and placed dry on the tongue, followed by a cooling
saline aperient. When diarrhoea is present in such cases, it should be
regarded as conservative, and encouraged by the administration of
half-grain or grain doses of calomel, combined with bismuth and
bicarbonate of soda. The diet should be restricted to milk and
lime-water or milk mixed with Vichy or Seltzer water. Demulcent drinks
should be freely given. In the slighter attacks effervescing drinks are
grateful to the patient; and if there be excessive formation of acid in
the stomach, antacids and sedatives should be administered.

Bismuth has a peculiar sedative and antiseptic effect in the milder
forms of inflammatory action of mucous membranes. It is especially
valuable in gastro-intestinal troubles of children. Its action is
mainly local surface action, and may therefore be given in liberal
doses if necessary. Children may take from five to ten grains, and
adults twenty grains or more. Hydrocyanic acid adds to its sedative
qualities, or when pain is present, with diarrhoea, opium in some form
may be added. The salicylate of bismuth is specially indicated when we
want to add to the antiseptic qualities of bismuth.

The general principles of treatment indicated here are applicable to
the so-called remittent fevers of children--namely, calomel in small
doses, combined with bismuth and bicarbonate of soda, followed by
occasional cool saline laxatives. Ipecacuanha is also a valuable agent
in correcting morbid gastro-intestinal secretions. When there is early
epigastric tenderness, with hot skin and elevation of temperature, two
or three leeches should be applied to the epigastrium, followed by warm
poultices of linseed meal. Dry cupping may also be used with benefit;
and if decided remissions occur, with suspicions of a complicating
malarious element, a few liberal doses of quinia may be tried. In many
such cases, however, it will be found unnecessary, and not unfrequently
hurtful. In acute gastro-intestinal inflammations of children--the
{470} temperature reaching 105 degrees or more--no febrifuge, in the
opinion of the writer, is equal to the cool or cold bath, repeated from
time to time until there is a decided reduction of temperature. But the
gastric inflammation, rather than the fever, should mainly claim our
attention.

Great care is necessary during convalescence from acute gastric
disease, particularly as regards the hygienic management. The apparent
debility of the patient too often tempts the physician to the early and
injudicious use of tonics, stimulants, and excessive alimentation,
which, if persisted in, can scarcely fail to perpetuate a chronic form
of inflammatory action.


Chronic Gastritis (Chronic Gastric Catarrh).

There is perhaps no malady more frequently met with than chronic
gastric catarrh, and none more frequently misunderstood. It comprises
many different forms of gastric derangement, which are grouped under
the general head of inflammatory dyspepsia, with many symptoms strongly
simulating ordinary functional dyspepsia. It includes, in the author's
opinion, a large number of cases of obstinate chronic dyspepsia, which
are badly managed because not recognized as of inflammatory origin.

ETIOLOGY.--In a more or less chronic form it is frequently met with as
a result of the acute affections. Hence the etiology is mainly that of
acute gastric catarrh. It may be caused--

1. By functional disorders of the stomach.

2. By mechanical causes which interfere with the portal circulation.

3. In connection with certain constitutional states, such as gout,
rheumatism, phthisis, renal disease, certain eruptive diseases, and as
a sequence of malarious fevers.

4. By the excessive use of alcohol and other gastric irritants.

5. By errors of diet, especially excessive alimentation.

6. By decomposition of ingested aliment owing to deficiency of gastric
juice.

7. By all causes that weaken the digestive power and lower the general
tone of the system.

Of all these causes, errors of diet are most apt to produce it, and to
perpetuate it when once established. And next to this, in the order of
importance, is the immoderate use of alcohol, especially by persons
whose general health and digestive power are below a healthy standard.
Such persons are apt to suffer from irritative and inflammatory forms
of dyspepsia, which, in various degrees of intensity, alternate with
the acuter forms of embarras gastrique.

The injudicious use of drugs may also be mentioned. There can be no
doubt that many transient and functional forms of indigestion merge
into the more chronic inflammatory forms of dyspepsia from the abuse of
stimulants, tonics, and purgatives. Anxious for relief, and urged on by
hope of recovery, the victims of functional dyspepsia are apt to have
recourse to every grade of quacks and to be subjected to every form of
harassing and mischievous treatment. Indeed, the use of potential and
irritating drugs, administered for all kinds of ailments, real or
imaginary, enters largely into the etiology of chronic gastric catarrh.

Mechanical causes deserve also special consideration. These are mainly
{471} such as offer impediment to the return of blood from the stomach
to the heart. In acute cases the congestion may be very intense.
Congestion of the same kind, but more gradual in its occurrence and
less in degree, may be present from all conditions affecting the
circulation of venous blood through the liver. General anaemia, by
producing weak heart-action, disturbs the normal adjustment between the
arterial and venous sides of the circulation. Blood accumulates in the
veins and capillaries, and morbid action propagates itself in a
direction contrary to the circulation. Hence in all conditions of
general anaemia there is tendency to dyspnoea, pulmonary oedema,
bronchorrhoea, special forms of liver disease, gastric catarrh, and
even temporary albuminuria. All mechanical obstructions to the free
transit of blood through the heart, lungs, or liver are followed by the
same results. A free secretion of mucus into the stomach is one of the
most commonly recognized. It is often vomited in large quantities. This
alkaline mucus, while it dilutes the digestive juices of the stomach,
furnishes favorable conditions for the development of low
micro-organisms, which contribute to the fermentative process. We may
not duly estimate the effects of these organisms on a mucous membrane
softened by long-continued passive hyperaemia.

Malarious fevers, from their congestive tendency, give rise to the more
acute forms of gastro-enteric inflammation. In the more chronic forms
of intermittent and remittent fevers more or less gastric inflammation
is invariably present. Indeed, in all forms of fever gastric
inflammation is a complicating element, and the recognition of the fact
has an important bearing on the treatment.

Certain constitutional diseases appear to involve special liability to
this affection, such as scrofula, phthisis, gout, rheumatism, syphilis,
and many chronic forms of skin disease; and in many cases the cause is
not apparent.

ANATOMICAL CHARACTERS.--The gross appearance of the stomach in chronic
gastritis is thus admirably described by Broussais, who faithfully
recorded what he "observed during many years in the bodies of those who
have long suffered from distaste for food, nausea, and vomiting." These
observations were made long before morbid anatomy had thrown much light
on the more minute structural changes of organs, and the general
picture will be recognized as faithful to-day: "Softening, friability,
and the reduction into a kind of gelatinous mass commonly occurs in the
region of the lower part of the larger curvature of the stomach; and
when closely examined it is perceived that it is not only the mucous
membrane that has undergone that species of decomposition, but that the
muscular has participated in it, and that the whole of the cellular
tissue which united the three membranes has entirely disappeared. The
parietes of the viscus are then reduced to a very thin lamina of serous
membrane, commonly so fragile as to tear on the slightest handling, or
even already perforated without any effort on the part of the
anatomist. The pyloric region, on the contrary, has manifestly acquired
more consistence and thickness; the mucous membrane there presents
large folds, the muscular appears more developed, and the cellular and
vascular are injected; sometimes even a true scirrhous state is
observed there. The portion of the mucous membrane which covers this
scirrhus is sometimes {472} ulcerated, but that in the surrounding
parts and at the border of the ulcer, far from being softened, is, on
the contrary, tumefied, indurated, and injected. Finally, though there
may or may not be ulceration of the pylorus, it is always manifestly
hypertrophied, whilst the lower part of the great curvature is the seat
of softening and atrophy."

These were the observations of the great anatomist apparent to the
naked eye. At the present time we can only confirm them by stating that
structural changes are particularly noticed in the pyloric region of
the stomach. The mucous membrane generally is vascular and covered with
a grayish, tough, transparent mucus. It is more opaque and thicker than
natural. The surface is usually changed in color: it may be red, brown,
ash-gray, slate-colored, or even black in spots. The darkened spots are
due to pigmented matter, and this is generally most marked in the
pyloric half of the stomach. It is most commonly met with in cases of
prolonged passive congestion of the stomach from portal obstruction,
and requires for its production the rupture of capillaries in the
superficial layers of the membrane and the transformation of the
haematin into pigment. The same condition often produces ecchymoses and
hemorrhagic erosions in spots. In other cases the mucous membrane is
strikingly uneven, being studded with numerous little prominences
separated from each other by shallow depressions or furrows. This
condition, which has been compared to granulations upon wounds, is
called mammillation. It is the etat mamelonne of Louis, and is
considered by him as a sure and constant sign of inflammatory action.
Like many other structural changes, it is usually found in the
neighborhood of the pylorus. More rarely polypoid growths project from
the membrane, and little cysts also frequently appear in the mucous
membrane.

Chronic inflammation tends to thickening of the mucous membrane. It
sometimes is not only greatly thickened, but acquires an extreme degree
of toughness. Exceptionally, however, the membrane, either entire or in
spots, may be abnormally thin. The thickening of the walls of the
stomach, when it involves the pylorus, gives rise to constriction of
the orifice and consequent dilatation of the stomach.

When the disease has been of long standing the interstitial tissue
between the tubules becomes thickened, the stomach is changed in its
normal structure, and the tubules themselves become confused,
compressed, and much less straight and parallel than in the normal
state. Or they may in some cases be enlarged, according to Flint, in
consequence of swelling and parenchymatous or fatty degeneration of
their epithelial cells. Microscopic examination often shows changes
such as occur in other glandular organs. The glands and tubules become
the seat of degenerative changes, such as are observed in Bright's
disease of the kidney, and they are frequently found associated in the
same case. The mouths of the gastric tubules become blocked up, while
deeper parts are dilated into cysts; and at times they are atrophied or
filled with granular fatty matter.

Many cases of persistent anaemia may be traced, according to Flint, to
this degenerative process of the gastric tubules.

The SYMPTOMS of chronic gastritis are mainly those of difficult
digestion of an aggravated kind, and are liable to be mistaken for
those of {473} ordinary functional dyspepsia. Some points of
distinction were referred to in the section treating of functional
dyspepsia; and while there are many symptoms in common, it is vastly
important that the two forms of the disease should be early recognized,
for they are radically distinct in their pathology and treatment.

We now speak of what is usually known as inflammatory, irritative, or
gastric dyspepsia--a persistent and aggravated form of indigestion
which has its origin in the stomach itself, in contradistinction to
dyspepsia which originates largely from causes outside of the stomach
and transmitted to it through nervous impression. The one is functional
and indirect; the other is inflammatory and direct.

The symptoms referable directly to the stomach are mainly those of
difficult and painful digestion, and are alike characteristic of all
forms of indigestion, such as loss of appetite, sense of weight and
fulness of the epigastrium, distress after taking food, acidity,
eructations of gas, etc. But chronic gastritis is more frequently
accompanied by a burning sensation in the epigastric region,
accompanied by tenderness on pressure, which is generally increased
after meals. Sometimes this tenderness amounts to actual pain, which is
increased after meals. But we are liable to be misled by pain: gastric
pain is not a characteristic symptom; subacute forms of the disease may
exist without any fixed pain; the sensation is rather that of burning,
uneasiness, and oppression of the epigastric region. The appetite, as a
rule, is greatly impaired--indeed, the sense of hunger is rarely
experienced--and nausea and vomiting frequently follow the ingestion of
food. This is especially the case when catarrh of the stomach is
associated with renal disease, portal congestion, or chronic
alcoholism. Large quantities of mucus are brought up, the vomiting
taking place usually in the morning, and on examination of the mucus it
will frequently be found to contain sarcinae and large numbers of
bacterial organisms. When stricture of the pylorus is present the
vomiting of putrid, half-digested food usually takes place about the
termination of the digestive process.

The tongue presents characteristics peculiar to chronic inflammation of
the stomach. In some cases it is small and red, with enlarged and red
papillae; in others, it is broad and flabby and somewhat pale; but in
either case, on close inspection, the papillae will be found red and
enlarged, this being more apparent on the tip and edges. In children of
scrofulous habits and in older persons of tubercular tendency the whole
organ is redder than natural, the papillae standing out as vivid red
spots.

In other cases the catarrh of the stomach extends to the mucous
membrane of the mouth. In all cases of oral catarrh the tongue, instead
of being red and pointed, is large and apparently oedematous. It is
uniformly covered with a white or dirty brownish coat, and frequently
shows the impression of the teeth upon its edges. The secretions of the
mouth are depraved, the breath heavy and offensive, and the gums spongy
and unhealthy in appearance. Acidity is also common.

Thirst is a common symptom. It is rarely absent either in the acute or
chronic form of the disease. It is most marked in the intervals between
meals and in the evenings.

It is rare in gastric catarrh of long standing that it does not extend
to the intestines, and occasionally from the duodenum to the ductus
{474} choledochus; in which case we have the combined symptoms of
gastro-intestinal catarrh associated with jaundice. The nutritive
system becomes implicated, and patients are especially prone to develop
any diathesis to which they may be liable.

There remains a group of symptoms of great interest in the study of
gastric inflammation--important because liable to mislead as to the
real nature of the difficulty--namely, morbid conditions of the nervous
system. Few diseases have such a wide range of morbid sympathies, and
few, it may be added, are so generally misunderstood and
misinterpreted. Two main facts, as formulated by Broussais, deserve to
be restudied by the profession:

First, that irritations of the visceral parenchyma which do not
implicate their serous membranes only give rise to ill-defined
sensations, and they not painful;

Second, that most of the acute pains arising from visceral irritation
are rather referred to external parts than to the viscera themselves.

Unless the seat of very acute inflammation, mucous membranes are
remarkably free from pain, and yet the gastric mucous membrane is the
seat of a most exquisite internal visceral sense and has a wide range
of morbid sympathetic disturbances. These sympathetic phenomena are
often treated for primary neuralgias. No fact in the clinical study of
disease deserves more careful consideration than this. Absence of pain,
then, is calculated to mislead. It is often only the sensation of
uneasiness, depression and melancholy, want of appetite, thirst,
nausea, loathing of food, and derangement of the bilious and gastric
secretions, that directs our attention to the stomach. Moreover, in
gastro-enteric inflammations pain is more frequently felt in parts
sympathetically affected than in the stomach itself. "It is only when
irritations of mucous membranes are in the vicinity of the openings of
cavities that the irritations are distinctly perceptible in the seat
they occupy" (Broussais). Morbid irritative action commencing in the
stomach repeats itself in the cerebro-spinal system of nerves, and the
secondary irritation may develop a more immediately dangerous
inflammation than the primary. This is frequently observed in children,
who are specially prone to irritation of the visceral apparatus. Many
cases of primary gastric irritation terminate in acute cerebral
inflammation. Indeed, the greater number of phlegmasiae of the brain
are only sympathetic irritations issuing from primary inflammation of
the stomach. Short of inflammation, the transmitted irritation may
merely give rise to reflex convulsions, and in adults to sick headache,
or, if long continued, to conditions of hypochondria. Headache is a
prominent symptom of gastric irritation. It is not usually acute, but
rather a sense of fulness and pressure, sometimes felt in the frontal,
at other times in the occipital, region. Many cases commonly called
cerebral hyperaemia and cerebral anaemia are nothing more than
malassimilation from chronic gastric catarrh. This fact deserves to be
specially emphasized at present, for we are apt to consider the
cerebral the primary lesion. Vertigo, as in functional dyspepsia, is
also an occasional symptom, and very commonly patients complain of
extreme degrees of sleeplessness and disturbed dreams and nightmare.

The heart's action is often disturbed in its rhythm, and sympathetic
dyspnoea leads to suspicion of disease of the lungs. And to all these
{475} nervous phenomena may be added unusual languor, lassitude,
irritability of temper, and a feeling of inability for either mental or
physical exertion.

But in the play of morbid sympathies it must be borne in mind that the
stomach may be secondarily affected. Irritations of all organs are
constantly transmitted to the stomach from their very commencement.
Hence the frequent loss of appetite, the thirst, the embarrassed
digestion, the deranged gastric secretion, and the altered color of the
tongue. This is markedly the case in all the malarious and essential
forms of fever. Gastric complication in these fevers is rarely, if
ever, absent, and if aggravated by the too early use of tonics and
stimulants and by harsh irritating cathartics, it becomes too often a
fatal complication.

Gastric symptoms are also associated with other constitutional
disorders, such as phthisis, renal disease, rheumatism, gout, and
almost all forms of chronic eruptive diseases.

Intestinal symptoms are rarely absent. Constipation is often obstinate,
and especially is this the case if the catarrhal condition is confined
to the duodenum. The lower down the inflammation the greater the
probability of diarrhoea, and when present the stools are offensive and
frothy; sometimes they are dry and scybalous and coated with a tough,
tenacious mucus which may form casts of portions of the intestinal
track. In other cases patients suffer from distressing intestinal
flatulence and a sense of general discomfort. Piles is a complication
frequently present without reference to complication of the liver.

The urine is more frequently disordered than in any other form of
disturbance of digestion. The most common changes consist in an
abundant deposit of the urates; exceptionally, however--especially in
cases of long standing in which there are marked nervous symptoms
associated with defective secretion of the liver and pancreas--it may
be of low specific gravity and pale in color from the presence of
phosphates. Slight febrile movement is not uncommon.

Finally, in all cases of chronic gastric catarrh the nutritive system
becomes deeply implicated--much more so than in functional disturbances
of the stomach. Emaciation is almost constantly present, the patient
often showing signs of premature decay.

DIAGNOSIS.--The disease with which chronic gastritis is most liable to
be confounded is atonic dyspepsia, the chief points of distinction from
which have been already alluded to. In general terms it may be said
that in chronic gastritis there is more epigastric tenderness, more
burning sensation and feeling of heat in the stomach, more thirst, more
nausea, more persistent loss of appetite, more steady and progressive
loss of flesh, more acidity, more eructations of gas, more general
appearance of premature decay, and greater tendency to hypochondriasis.
And yet all these symptoms, in varying degrees of prominence, may be
present in all forms of indigestion. To the points of distinction
already mentioned, then, a few circumstances may be added which will
afford considerable assistance in coming to a correct diagnosis:

1. The length of time the disease has uninterruptedly lasted. It is
essentially a chronic disease.

2. The local symptoms are never entirely absent, as is not infrequently
the case in functional dyspepsia.

{476} 3. The uneasy sensations, nausea, oppression, or pain, as the
case may be, follow the ingestion of food. They are not so prominently
present when the stomach is empty.

4. The result of treatment. In chronic gastritis it will be found that
all the local symptoms are exasperated by the usual treatment of
functional dyspepsia.

5. Stimulants and stimulating food are not well borne. Alcohol,
especially on an empty stomach, produces gastric distress. There is
also frequently slight febrile disturbance.

Chronic gastritis, with nausea, vomiting, haematemesis, general pallor,
and loss of flesh, may be mistaken for cancer of the stomach. But in
cancer vomiting is about as apt to take place when the stomach is empty
as during the ingestion of food; pain is usually greater, especially
when the orifices of the stomach are involved; the tenderness is more
marked; the emaciation and pallor more steadily progressive; the
vomiting of coffee-ground material takes place more frequently; and the
disease is more rapid in its progress. The age and sex of the patient
may also aid us in our diagnosis. Cancer is more frequently a disease
of middle and advanced life, and localizes itself oftener in the
stomach of males than females. Finally, the discovery of a tumor would
remove all doubts. Haematemesis in chronic catarrh of the stomach is
almost invariably associated with obstruction to venous circulation in
the liver, heart, or lungs.

In rare cases it may be difficult to distinguish chronic gastric
catarrh from ulcer of the stomach. In ulcer of the stomach pain is a
more prominent and constant symptom; it is more centrally located; the
vomiting after taking food is more immediate and persistent; the tongue
may be clean; flatulence is not a constant symptom; the appetite is
seldom much affected; the bowels are generally confined; and there is
nothing characteristic about the urine.

TREATMENT.--In this, as in the more acute forms of the disease, rest of
the stomach is important. From mistaken notions of disease we are prone
to over-feed our patients, and thus seriously impair the digestive and
assimilative processes. In chronic inflammation of the stomach a
restricted diet is of prime importance. The physician should most
carefully select the patient's food, and urgently insist on its
exclusive use. This of itself, if faithfully persevered in, will often
effect a cure.

The exclusive use of a milk diet--especially skim-milk--should be
thoroughly tested. In testing it we should allow two or three weeks to
elapse before any other food is taken. At the end of that time
soft-boiled eggs, stale bread, and well-cooked rice may be added, with
an occasional chop once a day. Some patients do not tolerate raw milk
well. In such cases we should thoroughly test the peptonized or
pancreatized milk or the peptonized milk-gruel, as suggested by
Roberts. This artificially-digested milk agrees wonderfully well with
many stomachs that cannot digest plain milk. Milk, in whatever form
administered, should be given at comparatively short intervals of time,
and never in quantity beyond the digestive capacity. Better err on the
side of under- than over-feeding. Nothing should be left to the fancy
or caprice of the patient. The food should be carefully selected by the
medical adviser, and given in definite quantities at definite times.
Even the moral {477} effect of such discipline is healthful for the
patient. After testing milk diet for a time, we may gradually add small
quantities of rare and thoroughly minced meat. Milk, eggs, and rare
meat are more easily digested, as a rule, than starchy substances.
Farinaceous food is apt to give rise to excessive acidity. But stale
bread may be added to the milk, and, if there is tendency to acidity,
better have it toasted thoroughly brown.

In addition to the dietetic treatment of the disease, diluents,
timeously administered, are of essential service. As a rule, patients
are too much restricted from their use, under the supposition that they
dilute the gastric juice and thereby impair the digestive power. This
restriction is proper at, and for some time after, the ingestion of
food. But at the end of the first hour after taking food several ounces
of gum-water, or some mucilaginous fluid sweetened and rendered
palatable by a few drops of dilute muriatic acid, should be
administered, and repeated every hour during the digestive process.
Diluents, thus administered, are not only grateful in allaying the
thirst of the patient, but are at the same time an essential part of
the treatment. The free use of demulcents at the termination of
digestion in the stomach is especially useful.

Beyond these general principles of treatment, applicable to all
varieties of gastric catarrh, we must have reference to the varied
etiology of the disease. This, we have seen, is most complicated. Hence
the difficulty in prescribing any rules of treatment applicable to all
cases. We should seek here, as in all cases, to generalize the disease
and individualize our patient.

Chief among remedial agents may be mentioned the alkaline carbonates.
When combined with purgative salines they are specially valuable in
gastro-duodenal catarrhs associated with disease of the liver. These
are a very numerous class of cases, especially in malarious regions of
country, and when present in a chronic form lay the foundation of
widespread disorders of nutrition. No treatment in such cases is
effective until we diminish engorgements of the liver and spleen, and
nothing accomplishes this so well as the use of alkaline saline
laxatives. These may be assisted in their action by small doses of
mercurials. It was a cardinal principle among the older practitioners,
in the absence of more minute means of diagnosis, to look well to the
secretions; and what was their strength is, I fear, our weakness.

Wonderful results often follow a course of the Carlsbad, Pullna, or
Marienbad waters, taken on an empty stomach, fasting, in the morning.
While taking the waters a rigid and restricted diet is enforced. This
is an important part of the treatment. And the fact that so many varied
ailments are cured by a course of these mineral waters with enforced
dietetic regulations only shows the prevalence of gastro-duodenal
catarrhs and their relation to a great variety of human ailments. To a
certain extent the potassio-tartrate of sodium and other saline
laxatives may take the place of these waters if perseveringly used and
taken in the same way. In feebler subjects minute doses of strychnia or
some of the simple vegetable bitters may be used in conjunction with
the laxative salines.

In chronic inflammatory conditions of the gastric mucous membrane,
which frequently follow acute attacks, the protracted use of hot water
is often followed by excellent results. There can be no doubt of the
value {478} of hot water in subacute inflammation of mucous membranes
in any locality; and it is specially valuable in gastro-intestinal
catarrh associated with lithaemia. Hot water, laxative salines,
combined with restricted diet and healthful regimen, accomplish much in
correcting morbid conditions of primary assimilation; and by
accomplishing this many secondary ailments promptly disappear. A pint
of water, hot as the patient can drink it, should be taken on an empty
stomach on first rising in the morning, and it may be repeated again an
hour before each meal and at bedtime. A few grains of the bicarbonate
of sodium and a little table-salt may be added. In some cases three or
four drops of tincture of nux vomica or some of the simple bitters may
be taken at the same time with benefit. Alkaline bitters are natural to
the upper portion of the digestive track. No food should be taken for a
half hour or an hour after the hot water. This treatment, to be
effective, must be persevered in for a length of time. A most rigid
system of dietetics suited to individual cases should be enforced at
the same time. This is an important part of the treatment.

In irritable and morbidly sensitive conditions of the mucous membrane
the sedative plan of treatment is not unfrequently followed by good
results; and of remedies belonging to this class bismuth is the most
effective. It is specially indicated in the more irritable forms of
gastric disturbance in which there is a sense of uneasiness and pain at
the epigastrium after taking food. If there is much acidity present, it
may be combined with magnesia or a few grains of finely-pulverized
animal charcoal.

Chronic cases of long-continued inflammatory action, with intestinal
complication, are often much benefited by the use of mercurials in
small doses. The one-fifth of a grain of calomel, combined with bismuth
or the bicarbonate of sodium, may be given for weeks without danger of
salivation. Excellent results sometimes follow this treatment. In small
doses calomel is undoubtedly sedative to the mucous membrane of the
upper portion of the digestive track. In cases of long standing that
have resisted other modes of treatment the more direct astringents have
been found of great value. Of these, nitrate of silver is to be
preferred, alike for its sedative, astringent, and alterative
properties. It may be given in pill form in from one-quarter to
one-grain doses, combined with opium, a half hour before each meal. The
writer of this article can speak from much experience of the value of
this drug. It proves in many cases a valuable addition to the hot-water
and dietetic course already alluded to.

If large quantities of mucus are vomited from time to time, especially
in the morning, we may resort with benefit to the use of other
astringents, such as bismuth, oxalate of cerium, kino, and opium; and
if we have reason to suspect stricture of the pylorus in connection
with a catarrhal condition of the mucous membrane, the stomach-pump
gives the patient great relief. It should be used about three hours
after a meal, injecting tepid water, and then reversing the syringe
until the water comes out perfectly clear. Niemeyer speaks highly of it
in such cases. He says: "Even the first application of the pump
generally gives the patients such relief that, so far from dreading a
repetition of this by no means pleasant operation, they clamorously beg
for it."

The gastric catarrh of phthisis is difficult to relieve. Artificial
digestives may be tried, with dilute muriatic acid, as already
indicated; and {479} for the relief of pain and irritation there is no
remedy so efficacious as hydrocyanic acid, which may be combined with
bismuth and opium in case there is diarrhoea. Hot water may be also
tried, with restricted animal food.

Habitual constipation must be overcome by suitable laxatives and by
enemata. Castor oil is mild and efficient in these cases, or in cases
of unusual torpor of the muscular coat of the bowels small doses of
aloes and strychnia may be tried. The free use of diluents toward the
close of digestion favors free action of the bowels. All harsh and
irritating cathartics are to be carefully avoided.

When there is much tenderness of the epigastrium, benefit may be
derived from counter-irritation, and nothing is so effectual as the
repeated application of small blisters.

General hygienic measures are in all cases to be insisted upon. In
morbid conditions of the liver and the upper portion of the digestive
track the free supply of oxygen to the lungs is a remedy of much power.
Hence patients should live as much as possible in the open air. They
should be warmly clad, and, if not too feeble, frequent cold baths
should be resorted to.

After local irritation has been subdued by appropriate treatment,
tonics may be tried to counteract the enfeebled state of the stomach.
They are such as are appropriate for functional diseases of the
stomach. But they should be used with caution and judgment in irritable
and inflammatory forms of dyspepsia. If we attempt to force an appetite
by their use, and to crowd upon the stomach more food than it has
capacity to digest, we may intensify the trouble and thereby add to the
patient's general debility. Food and tonics fail to impart strength
because the stomach is not in a condition to digest them.

One thing should be mentioned, in conclusion, as an important item in
the treatment--namely, patience. Chronic gastric catarrh, it should be
remembered, is essentially a chronic disease, and time becomes an
important element in its cure.




{480}

SIMPLE ULCER OF THE STOMACH.

BY W. H. WELCH, M.D.


DEFINITION.--Simple ulcer of the stomach is usually round or oval. When
of recent formation it has smooth, clean-cut, or rounded borders,
without evidence of acute inflammation in its floor or in its borders.
When of long duration it usually has thickened and indurated margins.
The formation of the ulcer is usually attributed, in part at least, to
a disturbance in nutrition and to a subsequent solution by the gastric
juice of a circumscribed part of the wall of the stomach. The ulcer may
be latent in its course, but it is generally characterized by one or
more of the following symptoms: pain, vomiting, dyspepsia, hemorrhage
from the stomach, and loss of flesh and strength. It ends frequently in
recovery, but it may end in death by perforation of the stomach, by
hemorrhage, or by gradual exhaustion.

SYNONYMS.--The following epithets have been employed to designate this
form of ulcer: simple, chronic, round, perforating, corrosive,
digestive, peptic; ulcus ventriculi simplex, s. chronicum, s. rotundum,
s. perforans, s. corrosivum, s. ex digestione, s. pepticum.

HISTORY.--It is only since the description of gastric ulcer by
Cruveilhier in the year 1830 that especial attention has been paid to
this disease.

In the writings of the ancients only vague and doubtful references to
ulcer of the stomach are found (Galen, Celsus). It is probable that
cases of this disease were described under such names as passio
cardiaca, gastrodynia, haematemesis, and melaena.

After the revival of medicine in the sixteenth century, as post-mortem
examination of human bodies was made with greater frequency, the
existence of ulcers and of cicatrices in the stomach could not escape
attention. But only isolated and curious observations of gastric ulcer
are recorded up to near the end of the eighteenth century. One of the
earliest recorded unmistakable cases of perforating ulcer was observed
by John Bauhin, and is described in the _Sepulchretum_ of Bonetus,
published in 1679. Other cases belonging to this period were described
by Donatus, Courtial, Littre, Schenck, and Margagni.[1]

[Footnote 1: References to these and to other cases may be found in
Lebert's _Krankheiten des Magens_, Tubingen, 1878, p. 180 _et seq._]

To Matthew Baillie unquestionably belongs the credit of having first
accurately described, in 1793, the anatomical peculiarities of simple
gastric ulcer.[2] At a later date he published three good engravings of
{481} this disease.[3] Baillie's concise and admirable description of
the morbid anatomy of gastric ulcer was unaccompanied by clinical data,
and seems to have had little or no influence in directing increased
attention to this disease.

[Footnote 2: _The Morbid Anatomy of Some of the Most Important Parts of
the Human Body_, London, 1793, p. 87.]

[Footnote 3: _A Series of Engravings, accompanied with Explanations,
etc._, London, 1799.]

A valuable account of the symptoms of gastric ulcer was given by John
Abercrombie in 1824.[4] Nearly all of the symptoms now recognized as
belonging to this affection may be found in his article. He knew the
latent causes of the disease, the great diversity of symptoms in
different cases, and the modes of death by hemorrhage, by perforation,
and by asthenia. He regarded ulcer simply as a localized chronic
inflammation of the stomach, and did not distinguish carefully between
simple and cancerous ulceration.

[Footnote 4: "Contributions to the Pathology of the Stomach, the
Pancreas, and the Spleen," _Edinburgh Med. and Surg. Journ._, vol. xxi.
p. 1, Jan. 1, 1824. See also, by the same author, _Pathological and
Practical Researches on Diseases of the Stomach, etc._--an excellent
work which passed through several editions.]

Cruveilhier,[5] in the first volume of his great work on _Pathological
Anatomy_, published between the years 1829 and 1835, for the first time
clearly distinguished ulcer of the stomach from cancer of the stomach
and from ordinary gastritis. He gave an authoritative and full
description of gastric ulcer from the anatomical, the clinical, and the
therapeutical points of view.

[Footnote 5: J. Cruveilhier, _Anatomie pathologique du Corps humain_,
tome i., Paris, 1829-35, livr. x. and livr. xx.; and tome ii., Paris,
1835-42, livr. xxx. and livr. xxxi.]

Next to Cruveilhier, Rokitansky has had the greatest influence upon the
modern conception of gastric ulcer. In 1839 this pathologist gave a
description of the disease based upon an analysis of 79 cases.[6] The
anatomical part of his description has served as the model for all
subsequent writers upon this subject.

[Footnote 6: Rokitansky, _Oesterreich. med. Jahrb._, 1839, Bd. xviii.
(abstract in _Schmidt's Jahrb._, Bd. 25, p. 40).]

Since the ushering in by Cruveilhier and by Rokitansky of the modern
era in the history of gastric ulcer, medical literature abounds in
articles upon this disease. But it cannot be said that the importance
of these works is at all commensurate with their number or that they
have added very materially to the classical descriptions given by
Cruveilhier and by Rokitansky. Perhaps most worthy of mention of the
works of this later era are the article by Jaksch relating to
symptomatology and diagnosis, that of Virchow pertaining to etiology,
the statistical analyses by Brinton, and the contributions to the
treatment of the disease by Ziemssen and by Leube.[7] In 1860, Ludwig
Muller published an extensive monograph upon gastric ulcer.[8]

[Footnote 7: Jaksch, _Prager Vierteljahrschr._, Bd. 3, 1844; Virchow,
_Arch. f. path. Anat._, Bd. v. p. 362, 1853, and A. Beer, "Aus dem
path. anatom., Curse des Prof. R. Virchow in Berlin, Das einfache
duodenische (corrosive) Magengeschwur," _Wiener med. Wochenschr._, Nos.
26, 27, 1857; Brinton, _On the Pathology, Symptoms, and Treatment of
Ulcer of the Stomach_, London, 1857; V. Ziemssen, _Volkmann's Samml.
klin. Vortrage_, No. 15, 1871; Leube, _Ziemssen's Handb. d. spec. Path.
u. Therap._, Bd. vii., Leipzig, 1878.]

[Footnote 8: _Das corrosive Geschwur im Magen und Darmkanal_, Erlangen,
1860. Good descriptions of gastric ulcer are to be found in the
well-known works on diseases of the stomach by the English writers,
Budd, Chambers, Brinton, Habershon, Fenwick, and Wilson Fox.]

ETIOLOGY.--We have no means of determining accurately the average
frequency of simple gastric ulcer. The method usually adopted is to
observe the number of cases in which open ulcers and cicatrices are
found {482} in the stomach in a large number of autopsies. But this
method is open to two objections. The first objection is, that scars in
the stomach, particularly if they are small, are liable to be
overlooked or not to be noted in the record of the autopsy unless
special attention is directed to their search. The second objection is,
that it is not proven that all of the cicatrices found in the stomach
are the scars of healed simple ulcers, and that, in fact, it is
probable that many are not. In consequence of these defects (and others
might be mentioned) this method is of very limited value, although it
is perhaps the best which we have at our disposal.

In 32,052 autopsies made in Prague, Berlin, Dresden, Erlangen, and
Kiel,[9] there were found 1522 cases of open ulcer or of cicatrix in
the stomach. If all the scars be reckoned as healed ulcers, according
to these statistics gastric ulcer, either cicatrized or open, is found
in about 5 per cent. of persons dying from all causes.

[Footnote 9: The Prague statistics embrace 11,888 autopsies, compiled
from the following sources: 1, Jaksch, _Prager Vierteljahrschr._, vol.
iii.; 2, Dittrich, _ibid._, vols. vii., viii., ix., x., xii., xiv.; 3,
Willigk, _ibid._, vol. li.; 4, Eppinger, _ibid._, vol. cxvi.

The Berlin statistics are to be found in dissertations by Plange
(abstract in _Virchow's Archiv_, vol. xviii.), by Steiner, and by
Wollmann (abstracts in _Virchow und Hirsch's Jahresbericht_, 1868), and
by Berthold (1883).

The Dresden statistics are in a dissertation by Stachelhausen
(Wurzburg, 1874), referred to by Birch-Hirschfeld, _Lehrb. d. path.
Anat._, Bd. ii. p. 837, Leipzig, 1877.

The Erlangen statistics are reported by Ziemssen in _Volkmann's Samml.
klin. Vortrage_, No. 15.

The Kiel report is in an inaugural dissertation by Greiss (Kiel, 1879),
referred to in the _Deutsche med. Wochenschr._, Feb. 4, 1882, p. 79.

So far as possible, duodenal ulcers have been excluded. Only those
reports have been admitted which include both open ulcers and
cicatrices.]

It is important to note the relative frequency of open ulcers as
compared with that of cicatrices. In 11,888 bodies examined in Prague,
there were found 164, or 1.4 per cent., with open ulcers, and 373, or
3.1 per cent., with cicatrices. Here scars were found about two and
one-fourth times as frequently as open ulcers. The observations of
Grunfeld in Copenhagen show that when especial attention is given to
searching for cicatrices in the stomach, they are found much more
frequently than the figures here given would indicate.[10] It would be
a moderate estimate to place the ratio of cicatrices to open ulcers at
3 to 1.

[Footnote 10: Grunfeld (abstract in _Schmidt's Jahrb._, Bd. 198, p.
141, 1883) in 1150 autopsies found 124 cicatrices in the stomach, or 11
per cent., but in only 450 of these cases was his attention especially
directed to their search, and in these he found 92 cases, or 20 per
cent., with scars. Grunfeld's statistics relate only to persons over
fifty years of age. Gastric ulcer, moreover, is extraordinarily common
in Copenhagen.

The inexact nature of the ordinary statistics relating to cicatrices is
also evident from the fact that in the four collections of cases which
comprise the Prague statistics the percentage of open ulcers varies
only between 0.81 and 2.44, while the percentage of cicatrices varies
between 0.89 and 5.42.]

The statistics concerning the average frequency of open ulcers are much
more exact and trustworthy than those relating to cicatrices. It may be
considered reasonably certain that, at least in Europe, open gastric
ulcers are found on the average in from 1 to 2 per cent. of persons
dying from all causes.[11]

[Footnote 11: If in this estimate were included infants dying during
the first days of life, the percentage would be much smaller.]

It is manifestly impossible to form an accurate estimate of the
frequency of gastric ulcer from the number of cases diagnosed as such
{483} during life, because the diagnosis is in many cases uncertain.
Nevertheless, estimates upon this basis have practical clinical value.
In 41,688 cases constituting the clinical material of Lebert[12] in
Zurich and in Breslau between the years 1853 and 1873, the diagnosis of
gastric ulcer was made in 252 cases, or about 2/3 per cent.

[Footnote 12: Lebert, _op. cit._, p. 196.]

Of 1699 cases of gastric ulcer collected from various hospital
statistics[13] and examined post-mortem, 692, or 40 per cent., were in
males, and 1007, or 60 per cent., were in females. The result of this
analysis makes the ratio 2 males to 3 females.

[Footnote 13: These statistics include the previously-cited Prague,
Berlin, Dresden, and Erlangen cases so far as the sex is given, and in
addition the returns of Rokitansky, _op. cit._; Starcke (Jena),
_Deutsche Klinik_, 1870, Nos. 26-29; Lebert, _op. cit._; Chambers,
_London Journ. of Med._, July, 1852; Habershon, _Dis. of the Abdomen_,
3d ed.; Moore, _Trans. of London Path. Soc._, 1880; and the Munich
Hospital, _Annalen d. stadt. Allg. Krankenh. zu Munchen_, vols. i. and
ii.

Only series of cases from the post-examinations of a number of years
have been admitted. It is an error to include isolated cases from
journals, as Brinton has done, because an undue number of these are
cases of perforation, which is a more common event in females than in
males. Thus, of 43 cases of gastric ulcer presented to the London
Pathological Society since its foundation up to 1882, 19, or 44 per
cent., were cases of perforation. In my cases are included a few
duodenal ulcers not easily separated from the gastric ulcers in the
compilation.]

In order to determine from post-mortem records the age at which gastric
ulcer most frequently occurs, all cases in which only cicatrices are
found should be excluded, because a cicatrix gives no evidence as to
the age at which the ulcer existed.

The following table gives the age in 607 cases of open ulcer collected
from hospital statistics[14] (post-mortem material):

    Age.    | No. of cases. | Totals.
  ----------+---------------+--------
   1-10.    |        1      |
  10-20.    |       32      |   33
  ----------+---------------+--------
  20-30.    |      119      |
  30-40.    |      107      |  226
  ----------+---------------+--------
  40-50.    |      114      |
  50-60.    |      108      |  222
  ----------+---------------+--------
  60-70.    |       84      |
  70-80.    |       35      |  119
  ----------+---------------+--------
  80-90.    |        6      |
  90-100.   |      ...      |
  Over 100. |        1      |    7
  ----------+---------------+--------

From this table it is apparent that three-fourths of the cases are
found between the ages of twenty and sixty, and that the cases are
distributed with tolerable uniformity between these four decades. The
largest number of cases is found between twenty and thirty. The
frequency of gastric ulcer after sixty years diminishes, although it
remains quite considerable, especially in view of the comparatively
small number of those living after that period.

[Footnote 14: The sources of these statistics are the same as those of
the statistics relating to sex in the preceding foot-note. The age in
the Erlangen cases of open ulcer is given by Hauser (_Das chronische
Magengeschwur_, p. 191, Leipzig, 1883). It is evident that only about
two-fifths of the cases could be utilized, partly because in some the
age was not stated, but mainly on account of the necessity of excluding
scars--a self-evident precaution which Brinton did not take.]

The probability that many cases of ulcer included in the above table
existed for several years before death makes it desirable that
estimates as to the occurrence of the disease at different ages should
be made also from cases carefully diagnosed during life, although the
diagnosis must necessarily be less certain than that in the post-mortem
records. The best {484} statistics of this character which we possess
are those of Lebert, from whose work the following table has been
compiled:

_Age in 252 Cases of Gastric Ulcer diagnosed during Life by
Lebert_.[15]

    Age.    | No. of cases. | Totals. | Per cent.
  ----------+---------------+---------+----------
   5-10.    |        1      |         |
  11-20.    |       24      |   25    |    9.92
  ----------+---------------+---------+----------
  21-30.    |       87      |         |
  31-40.    |       84      |  171    |   67.85
  ----------+---------------+---------+----------
  41-50.    |       34      |         |
  51-60.    |       17      |   51    |   20.24
  ----------+---------------+---------+----------
  61-70.    |        5      |    5    |    1.99
  ----------+---------------+---------+----------

Of these cases, nearly seven-tenths were between twenty and forty years
of age--a preponderance sufficiently great to be of diagnostic
value.[16]

[Footnote 15: _Op. cit._, p. 199. Of these cases, 19 were fatal, and
the diagnosis was confirmed after death. All of the cases were studied
by Lebert in hospitals in Zurich and Breslau.]

[Footnote 16: In my opinion, clinical experience is more valuable than
are post-mortem records in determining the age at which gastric ulcer
most frequently develops. In support of this opinion are the following
facts: In many cases no positive conclusions as to the age of the ulcer
can be drawn from the post-mortem appearances, and sufficient clinical
history is often wanting; a considerable proportion of the cases of
gastric ulcer do not terminate fatally with the first attack, but are
subject to relapses which may prove fatal in advanced life; in most
general hospitals the number of patients in advanced life is relatively
in excess of those in youth and middle age. By his faulty method of
investigating this question, Brinton came to the erroneous conclusion
that the liability to gastric ulcer is greatest in old age--a
conclusion which is opposed to clinical experience.]

The oldest case on record is the one mentioned by Eppinger,[17] of an
old beggar whose age is stated at one hundred and twenty years.

[Footnote 17: _Prager Vierteljahrschrift_, Bd. 116.]

The occurrence of simple ulcer of the stomach under ten years of age is
extremely rare. Rokitansky, with his enormous experience, said that he
had never seen a case under fourteen years.[18] There are recorded,
however, a number of cases of gastric ulcer in infancy and childhood,
but there is doubt as to how many of these are genuine examples of
simple ulcer. Rehn in 1874 analyzed a number, although by no means all,
of the reputed cases, and found only six, or at the most seven, which
would stand criticism.[19] The age in these seven cases varied between
seven days and thirteen years. In one case (Donne) a cicatrix was found
in the stomach of a child three years old. Since the publication of
Rehn's article at least four apparently genuine cases have been
reported--namely, one by Reimer in a child three and a half years old;
one by Goodhart in an infant thirty hours after birth; one by Eross in
a girl twelve years old suffering from acute miliary tuberculosis, in
whom the ulcer perforated into the omental sac; and one by Malinowski
in a girl ten years of age.[20]

[Footnote 18: Communication to Von Gunz in _Jahrbuch d.
Kinderheilkunde_, Bd. 5, p. 161, 1862.]

[Footnote 19: _Jahrb. d. Kinderheilk._, N. F., Bd. 7, p. 19, 1874.]

[Footnote 20: Reimer, _ibid._, Bd. x. p. 289, 1876; Goodhart, _Trans.
London Path. Soc._, vol. xxxii. p. 79, 1881; Eross, _Jahrb. f.
Kinderheilk._, Bd. xix. p. 331, 1883; Malinowski, _Index Medicus_, vol.
v. p. 575, New York, 1883.

Rehn does not mention Buzzard's case of perforating ulcer in a girl
nine years old (_Trans. London Path. Soc._, vol. xii. p. 84, 1861). See
also Chvostek's case of round ulcer in a boy (_Arch. f. Kinderheilk._,
1881-82) and Wertheimber's case of recovery from gastric ulcer in a
girl ten years old (_Jahrb. f. Kinderheilk._, Bd. xix. p. 79).]

The mean age at which gastric ulcer develops is somewhat higher in
{485} the male than in the female. This is apparent from the following
collection of 332 cases of open ulcer in which both age and sex are
given:[21]

    Age.    | Males. | Females.
  ----------+--------+---------
  10-20.    |    9   |    13
  20-30.    |   33   |    35
  30-40.    |   44   |    25
  40-50.    |   39   |    25
  50-60.    |   37   |    18
  60-70.    |   20   |    18
  70-80.    |    5   |     9
  80-90.    |    1   |   ...
  90-100.   |  ...   |   ...
  Over 100. |    1   |   ...
  ----------+--------+---------
  Total.    |  189   |   143
  ----------+--------+---------

In males the largest number of cases is found between thirty and forty
years, and in females between twenty and thirty. In males 54-1/2 per
cent. of the cases occur after forty years of age, and in females 48.9
per cent.

[Footnote 21: These cases are obtained from the same sources as those
of the first table (page 483).]

The relation between age and perforation of gastric ulcer will be
discussed in connection with this symptom.

The conclusions concerning the age of occurrence of gastric ulcer may
be recapitulated as follows: Simple ulcer of the stomach most
frequently develops in the female between twenty and thirty, and in the
male between thirty and forty. At the post-mortem table it is found
with almost equal frequency in the four decades between twenty and
sixty, but clinically it appears with greatly diminished frequency
after forty years of age. In infancy and early childhood simple ulcer
of the stomach is a curiosity.

We have no positive information as to the influence of climate upon the
production of gastric ulcer. The disease seems to be somewhat unequal
in its geographical distribution, but the data bearing upon this point
are altogether insufficient.

According to the returns of Dahlerup and of Grunfeld, gastric ulcer is
unusually common in Copenhagen.[22] According to Starcke's
report[23]--which, however, is not based upon a large number of
cases--the percentage is also unusually high in Jena. Sperk says that
gastric ulcer is very common in Eastern Siberia.[24] Palgrave gives a
high percentage of its occurrence in Arabia.[25] The disease is less
common in France than in England or in Germany,[26] and in general
appears to be more common in northern than in southern countries. The
statement of DaCosta[27] coincides with my own impression that gastric
ulcer is less common in this country than in England or in Germany. I
have found 6 cases of open ulcer of the stomach in about 800 autopsies
made by me in New York.

[Footnote 22: Dahlerup in Copenhagen (abstract in _Canstatt's
Jahresbericht_, 1842) found 26 cases in 200 autopsies (13 per cent.)
made in the course of a year and a half. Grunfeld (_loc. cit._) found
124 cicatrices in 1150 autopsies (11 per cent.).]

[Footnote 23: Starke (_loc. cit._) found 39 cases in 384 autopsies (10
per cent.); cf. also Muller, _Jenaische Zeitschr._, v. 1870.]

[Footnote 24: _Deutsche Klinik_, 1867.]

[Footnote 25: _Narrative of a Year's Journey through Central and
Eastern Arabia_, London, 1865.]

[Footnote 26: Laveran and Teissier, _Nouveaux Elements de Path. et de
Clin. med._, t. ii. p. 1060, Paris, 1879; and Godin, _Essai sur
l'Ulcere de l'Estomac_, These, Paris, 1877, p. 8.]

[Footnote 27: _Medical Diagnosis_, 5th ed., Philada., 1881. Keating
expresses the same opinion in the _Proc. of Path. Soc. of
Philadelphia_, vol. i. p. 142.

In 444,564 deaths in New York City from 1868 to 1882, inclusive, ulcer
of the stomach was assigned as the cause of death only in 410 cases.
Little value can be assigned to these statistics as regards a disease
so difficult of diagnosis.]

{486} Gastric ulcer is more common among the poor than among the rich.
Anxiety, mental depression, scanty food, damp dwellings, insufficient
exercise, and exposure to extreme cold are among the depressing
influences which have been assigned as predisposing causes of gastric
ulcer, but without sufficient proof.

The comparative frequency of gastric ulcer among needlewomen,
maidservants, and female cooks has attracted the attention of all who
have had large opportunity for clinical observation.

Pressure upon the pit of the stomach, either by wearing tight belts or
in the pursuit of certain occupations, such as those of shoemaking, of
tailoring, and of weaving, is thought by Habershon and others to
predispose to ulcer of the stomach.[28]

[Footnote 28: Bernutz found gastric ulcer in a turner in porcelain, and
learned that other workmen in the same factory had vomited blood. He
thinks that in this and in similar occupations heavy particles of dust
collecting in the mouth and throat may be swallowed with the saliva,
and by their irritation cause gastric ulcer (_Gaz. des Hopitaux_, June
18, 1881).]

Vomiting of blood has been known in several instances to affect a
number of members of the same family, but beyond this unsatisfactory
evidence there is nothing to show hereditary influence in the origin of
gastric ulcer.

In a few cases injury of the region of the stomach, as by a fall or a
blow, has been assigned as the cause of ulcer. The efficacy of this
cause has been accepted by Gerhardt,[29] Lebert, Ziemssen, and others.
In many of the cases in which this cause has been assigned the symptoms
of ulcer appeared so long after the injury that it is doubtful whether
there was any connection between the two.

[Footnote 29: "Zur Aetiologie u. Therapie d. runden Magengeschwurz,"
_Wiener med. Presse_, No. 1, 1868.]

That loss of substance in the mucous membrane of the stomach may be the
result of injury directly or indirectly applied to this organ cannot
admit of question. But it is characteristic of these traumatic ulcers
that they rapidly heal unless the injury is so severe as to prove
speedily fatal. Thus, Duplay[30] relates three cases in which pain,
vomiting, repeated vomiting of blood, and dyspepsia followed contusions
of the region of the stomach. But these traumatic cases, which for a
time gave the symptoms of gastric ulcer, recovered in from two weeks to
two months, whereas the persistence of the symptoms is a characteristic
of simple ulcer.[31]

[Footnote 30: "Contusions de l'Estomac," _Arch. gen. de Med._, Sept.,
1881.]

[Footnote 31: In a case reported by Potain, however, the symptoms of
ulcer appeared immediately after injury to the stomach, and continued
up to the time of death (_Gaz. hebdom._, Sept. 12, 1856).]

In the same way, ulcers of the stomach produced by corrosive poisons as
a rule soon cicatrize, unless death follows after a short time the
action of the poison. That corrosive ulcers may, however, be closely
allied to simple ulcers is shown by an interesting case reported by
Wilson Fox,[32] in which the immediate effects of swallowing
hydrochloric acid were recovered from in about four days, but death
resulted from vomiting of blood two weeks after. At the autopsy the
source of the hemorrhage was found in an ulcer of the pyloric region of
the stomach. An equally striking case is reported by Williams.[33] A
boy who suffered severely for three or four days after drinking some
strong mineral acid recovered, so that he {487} ate and drank as usual.
Two months afterward he died suddenly from perforation of a gastric
ulcer.

[Footnote 32: _Trans. of the Path. Soc._, vol. xix. p. 239, London,
1868.]

[Footnote 33: _The Lancet_, April 9, 1842.]

While, then, it would be a great error to identify traumatic and
corrosive ulcers of the stomach with simple ulcer, it is possible that
either may become chronic if associated with those conditions of the
stomach or of the constitution, for the most part unknown to us, which
prevent the ready healing of simple ulcer.

Gastric ulcer is often associated with other diseases, but it occurs
also uncomplicated in a large number of cases. Most of the diseases
with which it has been found associated are to be regarded simply as
coincident or complicating affections; but as some of them have been
thought to cause the ulcer, they demand consideration in this
connection.

The large share taken by pulmonary phthisis in deaths from all causes
renders this disease a frequent associate of gastric ulcer. It is
probable that the lowered vitality of phthisical patients increases
somewhat their liability to gastric ulcer. Moreover, it would not be
strange if gastric ulcer, as well as other exhausting diseases, such as
diabetes and cancer, diminished the power of resisting tuberculous
infection. Genuine tuberculous ulcers occur rarely in the stomach, but
they are not to be identified with simple ulcer.

There is no proof that amenorrhoea or other disorders of menstruation
exert any direct influence in the production of gastric ulcer, although
Crisp went so far as to designate certain cases of gastric ulcer as the
menstrual ulcer.[34] Nevertheless, amenorrhoea is a very common symptom
or associated condition in the gastric ulcer of females between sixteen
and thirty years of age.

[Footnote 34: _The Lancet_, Aug. 5, 1843.]

Chlorosis and anaemia, especially in young women, favor the development
of gastric ulcer, but that there is no necessary relation between the
two is shown by the occurrence of ulcer in those previously robust.
Moreover, it is probable that in some cases in which the anaemia has
been thought to precede the ulcer it has, in fact, been a result rather
than a cause of the ulcer.

Especial interest attaches to the relation between gastric ulcer and
diseases of the heart and of the blood-vessels, because to disturbances
in the circulation in the stomach the largest share in the
pathenogenesis of ulcer has been assigned by Virchow. As might be
expected, valvular lesions of the heart and atheroma of the arteries
are not infrequently found in elderly people who are the subjects of
gastric ulcer. A small proportion of cases of ulcer has been associated
also with other diseases in which the arteries are often abnormal, such
as with chronic diffuse nephritis, syphilis, amyloid degeneration, and
endarteritis obliterans. But, after making the most generous allowance
for the influence of these diseases in the causation of ulcer of the
stomach, there remains a large number of cases of ulcer in which no
disease of the heart or of the arteries has been found.[35] Gastric
ulcer develops most frequently between fifteen and forty years of age,
a period when arterial diseases are not common. Changes in the {488}
blood-vessels of the stomach will be described in connection with the
morbid anatomy of gastric ulcer.

[Footnote 35: From Berlin are reported the largest number of cases of
gastric ulcer associated with diseases of the circulatory apparatus;
thus, by Berthold 170 out of 294 cases, and by Steiner 71 out of 110
cases of ulcer. Endocarditis and arterial atheroma (present in
one-third of Berthold's cases of ulcer) form the largest proportion of
these diseases.]

Chronic passive congestion of the stomach in cases of cirrhosis of the
liver, direct injury to the mucous membrane of the stomach by parasites
in trichinosis, hemorrhage into the coats of the stomach in scorbutus
and in dementia paralytica, persistent vomiting in pregnancy, and
anaemia induced by prolonged lactation, have each been assigned as
causes in a few cases of gastric ulcer, but they are not associated
with gastric ulcer in enough cases to make their causative influence at
all certain.

Galliard assigns diabetes mellitus as the cause in one case of gastric
ulcer.[36]

[Footnote 36: _Clin. med. de la Pitie_, Paris, 1877, p. 77.]

Rokitansky attributed some cases of gastric ulcer to intermittent
fever.

Those who believe in the inflammatory origin of ulcer of the stomach
think that chronic gastritis is an important predisposing cause.

The abuse of alcohol is admitted as an indirect cause of gastric ulcer
by the majority of writers.

Lastly, burns of the skin, which are an important factor in the
etiology of duodenal ulcers, have been followed only in a very few
instances by ulcer of the stomach.

The direct causes of ulcer of the stomach, concerning which our
positive knowledge is very limited, will be considered under the
pathenogenesis of the disease.

SYMPTOMATOLOGY.--The following classes of cases of gastric ulcer may be
distinguished:

First: Gastric ulcer may give rise to no symptoms pointing to its
existence, and be found accidentally at the autopsy when death has
occurred from some other disease. This latent course is most frequent
with gastric ulcers complicating chronic wasting diseases, such as
tuberculosis, and with gastric ulcers in elderly people.

Second: Gastric ulcer may give rise to no marked symptoms before
profuse hemorrhage from the stomach or perforation of the stomach,
resulting speedily in death, occurs. Acute ulcers in anaemic females
from fifteen to thirty years of age are those most liable to perforate
without previous symptoms.

Third: Gastric ulcer may occasion only the symptoms of chronic
gastritis, or of functional dyspepsia, or of purely nervous gastralgia,
so that its diagnosis is impossible. In this class of cases after a
time characteristic symptoms may develop. Here, too, sudden death may
occur from hemorrhage or from perforation.

Fourth: In typical cases characteristic symptoms are present, so that
the diagnosis can be made more or less positively. These symptoms are
pain, and hemorrhage from the stomach, associated usually with vomiting
and disturbances of digestion.

The different symptoms of gastric ulcer will now be described.

Of all the symptoms, pain is the most constant and is often the first
to attract attention. It is absent throughout the disease only in
exceptional cases. In different cases, and often in the same case at
different times, the pain varies in its quality, its intensity, its
situation, its duration, and in other characteristics.

The kind of pain which is most characteristic of gastric ulcer is
severe {489} paroxysmal pain strictly localized in a circumscribed spot
in the epigastrium, coming on soon after eating, and disappearing as
soon as the stomach is relieved of its contents.

More common, although less characteristic, than the strictly localized
pain are paroxysms of severe pain, usually called cardialgic[37] or
gastralgic, diffused over the epigastrium and often spreading into the
surrounding regions. This is like the neuralgic pain of nervous
gastralgia, which is not infrequent in chlorotic and hysterical
females. The pain may be so intense as to induce syncope, or even
convulsions, in very sensitive patients.

[Footnote 37: There is much confusion as to the meaning of the term
cardialgia. With most English and American writers it signifies
heartburn, while continental writers understand by cardialgia the
severe paroxysms of epigastric pain which we more frequently call
gastralgia.]

The strictly localized pain is probably caused by direct irritation
confined to the nerves in the floor of the ulcer. In the diffuse
gastralgic attacks the irritation radiates or is reflected to the
neighboring nerves, and sometimes to those at a distance.

In most cases of gastric ulcer localized epigastric pain and diffuse
gastralgic paroxysms are combined.

The painful sense of oppression and fulness in the epigastrium which is
felt in many cases of gastric ulcer after eating is simply a dyspeptic
symptom, and is probably referable to an associated chronic catarrhal
gastritis. This dyspeptic pain is of little value in diagnosis.

Most subjects of gastric ulcer feel in the intervals between the
paroxysms a more or less constant dull pain, or it may be only a sense
of uneasiness, in the epigastrium. When sharp epigastric pain is felt
continuously, it is usually inferred that the ulcer has extended to the
peritoneum and has caused a circumscribed peritonitis, but this
inference is not altogether trustworthy.

The quality of the pain caused by gastric ulcer is described variously
as burning, gnawing, boring, less frequently as lancinating.

More important than the quality is the situation of the pain. The
situation of the localized pain is usually at or a little below the
ensiform cartilage. It may, however, be felt as low as the umbilicus or
it may deviate to the hypochondria. In addition to pain in the
epigastrium (point epigastrique), Cruveilhier called attention to the
frequent presence of pain in the dorsal region (point rachidien). The
dorsal pain, which may be more severe than the epigastric, is sometimes
interscapular, and sometimes corresponds to the lowest dorsal or to the
upper lumbar vertebrae. It is usually a little to the left of the
spine. The pain is often described as extending from the pit of the
stomach through to the back.

According to Brinton, the situation of the localized pain gives a clue
to the situation of the ulcer, pain near the left border of the
ensiform cartilage indicating ulcer near the cardiac orifice, pain in
the median line and to the right of this indicating ulcer of the
pyloric region, and pain in the left hypochondrium indicating ulcer of
the fundus. It does not often happen that the pain remains so sharply
localized as to make possible this diagnosis, even if the situation of
the pain were a safe guide.

Of the various circumstances which influence the severity of the pain
in gastric ulcer, the most important is the effect of food. Pain
usually {490} comes on within a few minutes to half an hour after
taking food, although it may appear immediately after ingestion or be
delayed for an hour or more. The pain continues until the stomach is
relieved of its contents by vomiting or by their passage into the
duodenum. It is unsafe to attempt to diagnose the position of the ulcer
merely from the length of time which elapses between the ingestion of
food and the onset of pain. It has sometimes been noticed that as
improvement progresses pain comes on later and later after eating. As
might naturally be expected, coarse, indigestible,
imperfectly-masticated food, sour and spirituous liquids, and hot
substances are more irritating than bland articles of diet. In some
exceptional cases the ingestion of even coarse food, instead of
aggravating, has had no effect upon the pain, or at least for the time
being has even relieved it.

External pressure usually increases the intensity of the pain of
gastric ulcer; in rare instances pressure relieves the pain.

Rest and the recumbent posture as a rule alleviate the pain of ulcer of
the stomach. The position of the patient may affect the severity of the
pain in a more striking way. It may naturally be supposed that that
posture is most agreeable which removes from the ulcer the weight of
the food during digestion. Hence it was claimed by Osborne[38] that the
site of the ulcer could often be inferred from the effect of posture on
the pain. Thus, relief in the prone position would indicate ulcer of
the posterior wall; relief in the supine position, ulcer of the
anterior wall; relief on the left or on the right side, ulcer of the
pyloric or of the cardiac region respectively. As ulcer of the
posterior wall is the most frequent, relief should be obtained oftener
by bending forward or by lying on the face than in the supine position.
Experience has shown that the influence of posture on the pain is not a
safe guide in diagnosing the location of the ulcer.

[Footnote 38: Jonathan Osborne, _Dublin Journal of Medical Science_,
vol. xxvii. p. 357, 1845.]

Mental emotions--particularly anxiety and anger--fatigue, even moderate
exercise, exposure to cold, and the menstrual molimen may each cause
exacerbations of pain in some cases of gastric ulcer.

Tenderness on pressure is a common symptom of gastric ulcer. A
localized point of tenderness may be discovered even when the
subjective pain is not localized. Pain sometimes follows pressure not
immediately, but after a brief interval. A fixed point of tenderness
can often be determined when the stomach is empty more accurately than
when it is full. The tender spot can sometimes be covered by the
finger's end. In searching for a point of tenderness it should be
remembered that many persons are very sensitive to pressure in the
epigastrium, and also that pressure is not without danger to those who
are the subjects of gastric ulcer. Not only may pressure induce
paroxysms of pain, but it may cause even rupture of the ulcerated walls
of the stomach.[39] Hence pressure should be cautiously employed and
should not be often repeated.

[Footnote 39: Dalton has reported a case in which perforation of a
gastric ulcer occurred while the patient was subjected in a water-cure
establishment to kneading of the abdomen to relieve his flatulence
(_Trans. N.Y. Path. Soc._, vol. i. p. 263.)]

In some cases of gastric ulcer pain is felt in regions at a distance
from the stomach. The most frequent of these so-called radiation
neuralgias are--neuralgia of the lower intercostal spaces, combined
sometimes with {491} hyperaesthesia or with analgesia of the affected
region, pain in the right shoulder (perhaps due to adhesions between
the stomach and the liver or the diaphragm), pain in the left shoulder,
and pain in the loins. In a case of ulcer reported by Traube
terminating in perforation the sole complaint, besides loss of appetite
and retching, had been difficulty in breathing and oppression in the
chest. These symptoms, which may be combined with gastralgic paroxysms,
are referred by Traube to transference of the irritation from the
gastric to the pulmonary filaments of the pneumogastric nerve.[40]

[Footnote 40: _Deutsche Klinik_, 1861, No. 10. These symptoms evidently
correspond to the vagus neurosis described by Rosenbach, in which, as
the result of reflex irritation of the pneumogastric nerve in the
stomach, occur difficulty in breathing, oppression in the chest,
palpitation, arhythmical action of the heart, and epigastric pulsation
(_Deutsche med. Wochenschr._, 1879, Nos. 42, 43).]

Sometimes the pain of gastric ulcer intermits for days or even weeks.
When the intermission is of considerable duration it is probable that
cicatrization has been in progress. It should, however, be remembered
that gastralgic attacks may continue even after cicatrization of the
ulcer is completed, probably in consequence of compression of
nerve-filaments by the cicatricial tissue. Once in a while the pain
exhibits a marked periodicity in its appearance. Thus in a case of
ulcer ending fatally from hemorrhage the pain came on but once a day,
and that with considerable regularity at the same hour. In this case
the pain was relieved by taking food.[41] The pain of gastric ulcer may
be temporarily relieved by hemorrhage from the stomach, and perhaps by
division of the irritated nerve by sloughing (Habershon).

[Footnote 41: Case reported by Peacock, _Rep. of Proceedings of London
Path. Soc._, vol. i. p. 253, 1847.]

The causes of the pain of gastric ulcer are not far to seek. Foremost
is the irritation of nerve-filaments exposed by the ulcerative process.
The irritation may be by mechanical, chemical, or thermic agencies.
With our present imperfect knowledge it is profitless to discuss
whether the pneumogastric or the sympathetic nerves are the chief
carriers of the abnormal sensations.[42] In the next place, we may have
radiation of the irritation from these nerves to neighboring and even
to remote nerves. Furthermore, the extension of the inflammation to the
peritoneum and the surrounding parts, and the formation of adhesions,
are additional factors in some cases in causing pain. Finally, the
great differences in susceptibility to pain manifested by different
individuals is to be borne in mind.

[Footnote 42: Leven, without sufficient reason, distinguishes two kinds
of gastralgic attacks--the one having its point of departure in the
pneumogastric, the other in the sympathetic nerve; in the former the
pain is associated with dyspnoea and palpitation of the heart; in the
latter the pain is deeper, and is accompanied by vaso-motor (?)
troubles on one side of the body.]

Next to pain, vomiting is the most frequent symptom of gastric ulcer.
There is, however, little which is characteristic of ulcer in this
symptom, unless the vomited material contains blood. In some cases of
gastric ulcer vomiting is the most marked and most distressing symptom
of the disease. It may, however, be absent during the whole course of
gastric ulcer.

Vomiting occurs most frequently after taking food, and is greatly
aggravated by an unregulated diet. Sometimes nearly everything which is
taken into the stomach is vomited. The vomiting of mucus or of a {492}
thin fluid unmixed with food is indicative only of chronic catarrhal
gastritis. Alimentary vomiting, which is more indicative of gastric
ulcer, usually occurs not immediately after taking food, but at the
acme of a gastralgic attack caused by the food. Soon after the stomach
is emptied by one or more acts of vomiting the pain is relieved. The
act of vomiting is usually easy, and at times is hardly more than
regurgitation of the food. Sometimes the patient experiences an
excessively sour taste from the vomit.

Vomiting exhausts the patient by withdrawing nutriment, and when
persistent may even cause death from inanition. But in some cases of
gastric ulcer, especially in women, the vomiting seems to be mainly a
nervous symptom, and even when long continued may be attended by little
or no loss of flesh. Evidently, more food is retained in these cases
than might be supposed.

There are two evident causes of vomiting in gastric ulcer--namely,
chronic catarrhal gastritis, which is a frequent complication, and
direct irritation of the nerves in the ulcer. Vomiting due to
dilatation of the stomach is oftener a sequel than an immediate symptom
of gastric ulcer.

For the diagnosis of gastric ulcer hemorrhage from the stomach is the
most important symptom.

The frequency of only the larger hemorrhages can be determined with any
degree of exactness. If the blood be effused in small quantity or
slowly, it may be discharged solely with the stools and escape
detection. Such slight hemorrhages doubtless occur in most cases of
gastric ulcer. It is probable that easily-recognized hemorrhages from
the stomach occur in about one-third of the cases of gastric ulcer.[43]
Hemorrhage is absent as a rule in the acute perforating ulcer of the
stomach.

[Footnote 43: In consequence of the uncertainty of the diagnosis in
cases of gastric ulcer which recover without hemorrhage, the estimates
of the frequency of this symptom have a very limited value, and will
vary with different observers according to their standard of diagnosis
of this disease. Lebert observed gastric hemorrhage in four-fifths of
his carefully-studied cases, and in three-fifths of his cases there was
profuse haematemesis. Brinton estimates that the larger hemorrhages
occur in about one-third of the cases. Muller found them in one-fourth
of the cases which he analyzed.]

In most cases hemorrhage from gastric ulcer is preceded by pain,
vomiting, and disturbances of digestion. Antecedent symptoms may,
however, be absent, or may be so obscure that no suspicion of ulcer
exists until the hemorrhage occurs.

The hemorrhage may be slight, moderate, or excessive in amount
(Cruveilhier). The larger hemorrhages are those which are most
distinctive of gastric ulcer.

The blood may be vomited, or voided with the stools, or retained in the
stomach and the intestines.

As has been remarked, when the hemorrhage is scanty all the blood may
escape by the bowel. Sometimes, although much less frequently, blood
effused in large quantity is entirely evacuated with the stools. After
haematemesis more or less blood is discharged by the bowel, sometimes
for several days after the vomiting of blood has ceased. Blood which
has traversed the whole length of the intestinal canal acquires a tarry
consistence and a black or brownish color in consequence of the
production of dark-brown haematin by the action of the digestive juices
{493} upon the haemoglobin, and in consequence of the formation of
black sulphide of iron by the union of hydrogen sulphide in the lower
part of the intestine with the iron of the haematin. The passage of
these black viscid stools is called melaena. Inasmuch as we cannot
presume gastric hemorrhage to be absent simply because no blood has
been vomited, it is evidently important to examine the stools for blood
when the diagnosis of gastric ulcer is obscure, and also in cases of
gastric ulcer where there are symptoms of internal hemorrhage not
accounted for by blood vomited. It should be remembered that certain
drugs, particularly iron and bismuth, may blacken the feces.

In very exceptional cases of gastric ulcer the effusion of a large
volume of blood causes sudden death before any of the blood has been
vomited. The autopsy shows the stomach and more or less of the small
intestine distended with coagulated blood.

Hemorrhage from gastric ulcer is usually made manifest by the vomiting
of blood. The quantity of the vomited blood varies from mere traces to
several pounds. The color and the consistence of the blood depend upon
the quantity effused and the length of time that the blood has remained
in the stomach. Blood which has been acted upon by the gastric juice is
coagulated, has a grumous consistence, and acquires by the formation of
haematin out of haemoglobin a dark-brown color, often compared to that
of coffee-grounds. Blood effused in small quantity is usually vomited
only with the food, and has usually the coffee-grounds appearance. The
patient's condition is not appreciably influenced by this slight loss
of blood. A little blood expelled after repeated acts of vomiting has
no diagnostic importance. Vomiting usually occurs soon after a large
gastric hemorrhage. It is the mechanical distension of the stomach
rather than any irritating quality of the blood which causes the
vomiting. Blood which is rejected immediately after a large gastric
hemorrhage is alkaline, fluid, and of an arterial (rarely of a venous)
hue. Often, however, even with large hemorrhages, the blood remains
sufficiently long in the stomach to be partly coagulated and to be
darkened in color. Ulcer more frequently than any other disease of the
stomach causes the vomiting of unaltered blood in large quantity. But
this kind of haematemesis is not peculiar to simple ulcer. It may occur
in other diseases, such as gastric cancer, and coffee-ground vomiting
may be associated with ulcer.

Copious haematemesis in cases of gastric ulcer appears usually without
premonition, or it may be preceded for a day or two by increased pain.
Its occurrence is somewhat more common during the digestion of food
than in the intervals, but there have been cases of ulcer where the
bleeding was favored by an empty stomach and was checked by the
distension of the organ with food. The free use of stimulants and
violent physical or mental exertion may excite hemorrhage. With the
onset of the hemorrhage the patient experiences a sense of warmth and
of oppression at the epigastrium, followed by faintness, nausea, and
the vomiting of a large quantity of blood. An attack of syncope often
causes, at least temporarily, cessation of the hemorrhage. But the
thrombus which closes the eroded vessel may easily be washed away, so
that the hemorrhage often recurs and continues at intervals for several
days, thereby greatly increasing the danger to the patient. Thus, the
tendency is for {494} the hemorrhage from gastric ulcer to appear in
phases or periods occupying several days.

A single hemorrhage is rarely so profuse as to cause immediate death.
More frequently the patient dies after successive hemorrhages. In the
majority of cases the hemorrhage is not immediately dangerous to life,
but is followed by symptoms of anaemia, more or less profound according
to the strength of the patient and the amount of blood lost.
Prostration and pallor follow the larger hemorrhages. Dizziness,
ringing in the ears, and dimness of vision appear when the patient
attempts to leave the recumbent posture. Thirst is often a marked
symptom. The pulse is feeble and more frequent than normal. There is
often a moderate elevation of temperature (anaemic fever) after profuse
hemorrhage. The urine is pale, abundant, and sometimes contains albumen
(Quincke). After a few days anaemic cardiac murmurs can often be heard.
Under favorable circumstances these symptoms of anaemia disappear in
the course of a few weeks.

The other symptoms of ulcer, particularly the pain, are sometimes
notably relieved, and may even disappear, after an abundant hemorrhage.
They usually, however, return sooner or later. After a variable
interval one attack of haematemesis is likely to be followed by others.
There is much diversity in different cases as regards the frequency of
these attacks and the character of the symptoms in the intervals. In a
few cases recovery follows a single attack of gastric hemorrhage; in
other cases the hemorrhage recurs frequently after intervals of only a
few days, weeks, or months; in still other cases hemorrhage recurs only
after long intervals, perhaps of years, although other symptoms of
ulcer continue. Sometimes the disappearance of symptoms indicates only
an apparent cure, and later the patient dies suddenly while in apparent
health by a profuse gastric hemorrhage. In the rare cases of this last
variety Cruveilhier has found sometimes that the ulcer has cicatrized
except just over the eroded blood-vessel.

The sources of the hemorrhage in gastric ulcer will be described in
connection with the morbid anatomy.

The symptoms of gastric indigestion are commonly, although not
constantly, present in gastric ulcer. They may constitute the sole
symptoms, in which case the diagnosis of the lesion is impossible. The
most important local symptoms of gastric dyspepsia are diminution, less
frequently perversion or increase, of the appetite; increased thirst;
during digestion, and sometimes independent of digestion, a feeling of
discomfort merely or of painful oppression, or even of sharp pain, in
the epigastrium; nausea; vomiting of undigested food, of mucus, and of
bile; regurgitation of thin fluids; often acid, sometimes neutral or
alkaline, flatulence, with belching of gas, and constipation. In many
cases of gastric ulcer the appetite is not disturbed, but the patient
refrains from eating on account of the pain caused by taking food.
Among the so-called sympathetic symptoms of dyspepsia are headache,
dizziness, depression of spirits, oppression in the chest, and
irregularity of the heart's action. Dyspepsia contributes its share to
the production of the anaemia and of the loss of flesh and strength
which are present in some degree in most cases of chronic gastric
ulcer.

{495} In many cases of acute perforating ulcer, as well as in some
cases of chronic ulcer, the symptoms are either absent or they are but
slightly marked. It has been demonstrated that in many cases of gastric
ulcer the resorptive power of the mucous membrane of the stomach is
unimpaired.[44]

[Footnote 44: This is shown by the experiments of Pentzoldt and Faber,
who determined the length of time which elapsed between swallowing
gelatin capsules containing iodide of potassium and the appearance of
the iodide in the saliva (_Berl. klin. Wochenschr._, No. 21, 1882).
Quetsch observed rapid absorption from the stomach in two cases of
gastric ulcer (_ibid._, 1884, No. 23). It is believed that also the
duration of the digestive process in the stomach is often within normal
limits in cases of gastric ulcer, although exact experiments upon this
point, as they require the use of the stomach-pump, have not been made
in this disease (Leube).]

The most common cause of dyspepsia in gastric ulcer is the chronic
catarrhal gastritis which usually accompanies this disease. It is
probable that the movements of the stomach may be seriously interfered
with by destruction of the muscular coat of the stomach when the ulcer
is of considerable size and is seated in the pyloric region. Adhesions
of the stomach to surrounding parts may likewise impair the normal
movements of the stomach. It is possible that ulcers, especially those
which are very painful, may cause reflex disturbance of the peristaltic
movements of the stomach and alterations in the quality or the quantity
of the gastric juice. The serious digestive disturbances which are
caused by distortions and dilatation of the stomach resulting from
cicatricial contraction of gastric ulcer are not considered in this
article.

Although Niemeyer emphasized the frequency in gastric ulcer of a
strikingly red tongue with smooth or furrowed surface, it does not
appear that any especial importance is to be attached to this or to any
other condition of the tongue as a symptom of the disease.

Increased flow of saliva is a rare symptom, which, when it occurs, is
usually associated with dyspepsia.

Constipation is the rule in gastric ulcer. The most important of the
various circumstances which combine to produce this condition is the
small amount of solid food taken and retained by the patient. The
restraint caused by gastric ulcer and gastric catarrh in the normal
movements of the stomach may diminish by reflex action the peristalsis
of the intestines (Traube and Radziejewski). The passage of large
quantities of blood along the intestinal canal is often associated with
colicky pains and diarrhoea.

Amenorrhoea is a symptom which was formerly thought to be
characteristic of gastric ulcer, although there was much discussion as
to whether it was the cause or the result of the ulcer. Amenorrhoea is
indeed common in the gastric ulcer of young women, but there is nothing
strange in this when one considers the frequency of amenorrhoea in
general, and its causation by various debilitating and depressing
influences such as are to be found in gastric ulcer. Notwithstanding a
few striking cases which have been recorded, it has not been
demonstrated that hemorrhages vicarious of menstruation take place from
gastric ulcer.

Gastric ulcer is not a febrile disease. Temporary elevation of
temperature may follow profuse gastrorrhagia and may attend various
complications, of which the most important are gastritis and
peritonitis. It has been recently claimed by Peter that the
surface-temperature of the {496} epigastrium is elevated in gastric
ulcer, but the observations upon this point are as yet too few for any
positive conclusions.[45]

[Footnote 45: According to Peter, the normal surface-temperature of the
epigastrium is from 95-1/2 degrees to 96 degrees F. (35.3 degrees to
35.5 degrees C.), while in gastric ulcer the temperature may equal or
even exceed by one or two degrees the axillary temperature. It is said
to register the highest during attacks of pain and of vomiting and
after hemorrhages (_Gaz. des Hopitaux_, June 23 and 30, 1883). See also
Beaurieux (_Essai sur la Pseudo-gastralgie, etc._, These, Paris,
1879).]

The general health of the patient remains sometimes surprisingly good,
even in cases of gastric ulcer with symptoms sufficiently marked to
establish the diagnosis. But in most cases of chronic gastric ulcer the
general nutrition sooner or later becomes impaired. This cannot well be
otherwise when dyspepsia, vomiting, paroxysms of severe pain, and
hemorrhage are present, separately or in combination, for any great
length of time. In proportion to the severity and the continuance of
these symptoms the patient becomes pale, weak, and emaciated. The face,
thin, anxious, of a grayish-white color, and marked with sharp lines of
suffering, presents the appearance which the older writers called
facies abdominalis, to which even so recent an author as Brinton
attaches exaggerated diagnostic importance. A little cachectic dropsy
may appear about the ankles. While it is true that the general
nutrition is less rapidly, less continuously, and, as a rule, less
deeply, impaired in gastric ulcer than in gastric cancer, nevertheless
sometimes a cachexia develops in the former which is not to be
distinguished from that of cancer. Litten[46] relates a case of gastric
ulcer which simulated for a time pernicious anaemia. In this case the
profound anaemia could not be explained by vomiting, hemorrhage, or
other symptoms of ulcer.

[Footnote 46: _Berliner klin. Wochenschrift_, Dec. 6, 1880.]

Beyond determining the existence of a fixed point of epigastric
tenderness, physical examination of the region of the stomach is
usually only of negative value in the diagnosis of gastric ulcer. In
some cases of ulcer of the stomach epigastric pulsation is very marked,
and sometimes most marked during gastralgic attacks. In these cases
there may be dilatation of the aorta from paralysis of vaso-motor
nerves analogous to the dilatation of the carotid and temporal arteries
in certain forms of migraine (Rosenbach). When the diagnosis lies
between gastric ulcer and gastric cancer, the presence of epigastric
tumor is justly considered to weigh against ulcer; but it is important
to know that tumor may be associated with ulcer. Thickening of the
tissues around old ulcers and the presence of adhesions may give rise
to a tumor. A thickened portion of omentum which had become adherent
over an old gastric ulcer produced a tumor which led to a mistake in
the diagnosis.[47] Rosenbach[48] calls attention to the occasional
production of false tumors by spasm of the muscular coat of the stomach
around a gastric ulcer. These tumors disappear spontaneously or yield
to the artificial distension of the stomach by Seidlitz powders--a
procedure which one would not venture to adopt if he suspected gastric
ulcer. Fenwick thinks that in some cases of gastric ulcer fixation of
the stomach by adhesions can be made out by physical exploration.

[Footnote 47: A. Beer, _Wiener med. Wochenschrift_, No. 26, 1857.]

[Footnote 48: _Deutsche med. Wochenschrift_, 1882, p. 22.]

The gravest symptom which can occur in gastric ulcer is the perforation
of the ulcer into the general peritoneal cavity.

{497} Only rough estimates can be made of the frequency of this
symptom. These estimates vary from 2 to 25 per cent. From the data
which I have collected I infer that perforation into the general
peritoneal cavity occurs in about 6-1/2 per cent. of all cases of
gastric ulcer.[49]

[Footnote 49: Miquel (_Schmidt's Jahrb._, Bd. 125, p. 65, 1864) reckons
the frequency of perforation at 2 per cent. Brinton's estimate of
13-1/2 per cent. is the one generally accepted. He found 69 cases of
perforation in 257 open ulcers collected from various sources. He
doubles the number of open ulcers, as he considers cicatrized ulcers
twice as frequent as the open. The statistics of some of the authors to
whom he refers should not be used in this computation, either because
they do not give accurately the number of cases of perforation, or
because they include under perforation all cases of ulcer which have
penetrated all of the coats of the stomach, whereas of course only
perforation into the general peritoneal cavity should be here included.
Valuable and laborious as are Brinton's researches, his statistics upon
this point, as upon many others, are inaccurate.

In 249 fatal cases of open ulcer taken from the statistics of Jaksch,
Dittrich, Willigk, Wrany (_Prager Vierteljahr._, vols. xcv. and xcix.),
Eppinger, Starcke, Chambers, Moore, and Lebert (_loc. cit._), I find 50
cases of perforation into the peritoneal cavity. This makes the
percentage of perforations 6-1/2 if the open ulcers be multiplied by 3,
the number of cicatrized ulcers being taken as three times that of open
ulcers (p. 482). This method of computation, which is adopted by
Brinton, is defective on account of the uncertainty as to the proper
proportion between cicatrized and open ulcers.

Lebert observed 9 cases of perforation with fatal peritonitis in his
252 cases studied clinically. He places the frequency of perforation
with peritonitis at 3 to 5 per cent., which corresponds to Engel's
estimate of 5-1/2 per cent. (_Prager Vierteljahrschrift_, 1853, ii.).]

As regards sex, perforation occurs two to three times oftener in the
female than in the male. This increased liability is referable mainly
to the preponderance of the acute perforating ulcer in young women.[50]

[Footnote 50: The liability to perforation in females seems to be not
only absolutely, but also relatively, to the number of ulcers greater
than in males, although, on the contrary, Brinton holds that the excess
of perforations in females is not greater than that of ulcers. Berthold
found perforation in 3.1 per cent. of the cases of gastric ulcer in
males, and in 9.7 per cent. of the cases in females (_op. cit._, p.
28).]

In the female the liability to perforation of gastric ulcer is greatest
between fourteen and thirty years of age. In the male there seems to be
no greater liability to perforation at one age than at another.[51]

[Footnote 51: Of 139 cases of perforated ulcer in females, Brinton
found that four-fifths occurred before the age of thirty-five. He
calculates the average age at which perforation occurs in the female as
twenty-seven, and in the male as forty-two. He thinks that the average
liability to perforation in both sexes decreases as life advances,
although he holds that the liability to ulcer itself constantly
increases with age.]

As will be explained in considering the morbid anatomy, ulcers of the
anterior wall of the stomach perforate more frequently than those in
other situations.

As regards the symptoms which may have preceded perforation three
groups of cases can be distinguished:

In the first there has been no complaint of gastric disturbance. In the
midst of apparent health perforation may occur and cause death within a
few hours. This is the ulcere foudroyante of French writers. It is met
with more commonly in chlorotic young women than in any other class.

In the second group of cases, which are more frequent, gastric symptoms
have been present for a longer or shorter time, but have been so
ambiguous that the diagnosis of gastric ulcer is not clear until
perforation occurs. Then, unfortunately, the diagnosis is of little
more than retrospective interest.

In the third group of cases perforation takes place in the course of
gastric ulcer, the existence of which has been made evident by
characteristic symptoms, such as localized pain and profuse hemorrhage.

{498} The immediate cause of perforation of gastric ulcer is often some
agency which produces mechanical tension of the stomach, such as
distension of the organ with food or with gas, vomiting, straining at
stool, coughing, sneezing, pressure on the epigastrium, violent
exertion, and jolting of the body.

With the escape of the solid, the fluid, and the gaseous contents of
the stomach into the peritoneal cavity at the moment of perforation, an
agonizing pain is felt, beginning in the epigastrium and extending
rapidly over the abdomen, which becomes very sensitive to pressure. The
pain sometimes radiates to the shoulders. Symptoms of collapse often
appear immediately or they may develop gradually. The pulse becomes
small, rapid, and feeble. The face is pale, anxious, and drawn (facies
hippocratica). The surface of the body, particularly of the
extremities, is cold and covered with clammy sweat. The internal
temperature may be subnormal, normal, or elevated; after the
development of peritonitis it is usually, but not always, elevated.
Consciousness is usually retained to the last, although the patient is
apathetic. Vomiting is sometimes absent--a circumstance which may be of
value in diagnosis, and which Traube attributes to the readiness with
which the contents of the stomach can be discharged through the
abnormal opening into the peritoneal cavity. There is usually
constipation. The respirations become more and more frequent and costal
in type. Thirst is often urgent. Suppression of urine is not an
uncommon symptom, although there may be frequent and painful attempts
at micturition. Albumen and casts may appear temporarily in the urine.
Retraction of one testicle, like that in renal colic, has been observed
(Blomfield). The patient usually lies on his back with the knees drawn
up. The abdomen is often at first hard and retracted from spasmodic
contraction of the abdominal muscles, but later it usually becomes
tympanitic, sometimes to an extreme degree. The presence of tympanitic
resonance replacing hepatic dulness in front is usually considered the
most important physical sign of gas free in the peritoneal cavity, but
this sign is equivocal. On the one hand, the presence of adhesions over
the anterior surface of the liver may prevent the gas from getting
between the liver and the diaphragm;[52] and on the other hand, in
cases of meteorism coils of intestine may make their way between the
liver and the diaphragm, or the liver may be pushed upward and
backward, so that its anterior surface becomes superior and the hepatic
dulness in front disappears. Physical examination may reveal in the
dependent parts of the peritoneal cavity an accumulation of fluid
partly escaped from the stomach and partly an inflammatory exudate.[53]
For humane reasons one should not submit the patient to the pain of
movement in order to elicit a succussion sound or to determine change
in the position of the fluid upon changing the position of the
patient.[54] There is sometimes relief from pain for some hours before
death.

[Footnote 52: Even without these adhesions liver dulness may persist
after perforation of the stomach, as in a case of Nothnagel's in which
for twenty-four hours after a large perforation from gastric ulcer the
abdomen was retracted and hepatic dulness was well marked (Garmise,
_Ulcus Ventriculi cum peritonitide perforativa_, Inaug. Diss., Jena,
1879).]

[Footnote 53: In a case of peritonitis resulting from perforation of a
latent ulcer of the duodenum, Concato found in the acid fluid withdrawn
by aspiration from the peritoneal cavity Sarcina ventriculi (_Giorn.
internaz. delle Scienze Med._, 1879, No. 9).]

[Footnote 54: Other symptoms which have been thought to be diagnostic
of pneumo-peritoneum in {499} distinction from meteorism, but the value
of which is doubtful, are these: In pneumo-peritoneum the respiratory
murmur can be heard by auscultation over the entire abdomen, while in
meteorism it does not extend beyond the region of the stomach
(Cantani); in the former amphoric sounds synchronous with respiration
can sometimes be heard over the abdomen (Larghi); borborygmi are heard,
if at all, distantly and feebly; the percussion note of gas free over
the liver is different from that of tympanitic intestine (Traube); the
percussion note is of the same character over the whole anterior wall
of the abdomen; the epigastric region is more elastic to the feel than
in tympanites; the distension of the abdomen is more uniform than in
tympanites; and coils of distended intestine, sometimes showing
peristaltic movement, cannot be seen or felt as in some cases of
meteorism (Howitz).]

There are exceptional cases of perforation in which some of the most
important of the enumerated symptoms, such as pain, tenderness of the
abdomen on pressure, tympanites, and the symptoms of collapse, are
absent.

Death sometimes occurs from shock within six or eight hours after
perforation. More frequently life is prolonged from eighteen to
thirty-six hours, it may be even for three or four days, and, very
rarely, even longer.[55] When life is prolonged more than twelve hours
an acute diffuse peritonitis is usually but not always developed.

[Footnote 55: In the _Descriptive Catalogue of the Warren Anatomical
Museum_, by Dr. J. B. S. Jackson, p. 448, Boston, 1870, is described a
case of gastric ulcer in which, so far as can be judged by the symptoms
and the post-mortem appearances, the patient lived nineteen days after
perforation.]

The contents of the stomach, instead of being diffused throughout the
peritoneal cavity, may be confined by a rapidly-developed circumscribed
peritonitis to a space near the stomach, or perforation may occur into
a space previously shut off from the general peritoneal sac by
adhesions. In this way circumscribed peritoneal abscesses form in the
neighborhood of the stomach. Diffuse peritonitis may be caused either
by an extension of the inflammation or by the rupture of these
abscesses into the general peritoneal cavity. The cases of
circumscribed peritonitis following perforation of gastric ulcer, with
escape of the contents of the stomach, although more protracted than
those in which the whole peritoneal surface is at once involved,
generally terminate fatally sooner or later. The symptoms are often
very obscure.

The most interesting of these peritoneal abscesses is the variety to
which Leyden has given the name of pyo-pneumothorax subphrenicus (false
pneumothorax of Cossy), the diagnostic features of which first were
recognized by G. W. Barlow and Wilks in 1845.[56] Here there is a
cavity, circumscribed by adhesions, just beneath the diaphragm,
containing pus and gas and communicating with either the stomach or the
intestine. By the encroachment of this cavity upon the thoracic space
the symptoms and signs of pyo-pneumothorax are simulated. Barlow and
Leyden have diagnosed during life this affection when resulting from
perforated gastric ulcer. The points in diagnosis from genuine
pyo-pneumothorax are the presence of respiratory murmur from the
clavicle to the third rib, the extension of the respiratory murmur
downward by deep inspiration, history of preceding gastric disturbance
with circumscribed peritonitis, absence of preceding pulmonary
symptoms, rapid variations in the limits of dulness with changes in the
position of the body, absence or only slight evidence of increased
intrapleural pressure (such as bulging of the {500} thorax as a whole,
and of the intercostal spaces), displacement of the heart, displacement
of the liver downward, and, if necessary, the determination by means of
a manometer that the pressure in the abscess cavity rises during
inspiration and falls during expiration, the reverse being true in
genuine pneumothorax.[57]

[Footnote 56: Barlow and Wilks, _London Med. Gazette_, May, 1845;
Leyden, _Zeitschr. f. klin. Med._, i. Heft 2; Cossy, _Arch. gen. de
Med._, Nov., 1879; Tillmanns, _Arch. f. klin. Chirurg._, Bd. 27, p.
103, 1881.]

[Footnote 57: Schreiber has shown that this last diagnostic point,
which was given by Leyden, is not without exceptions, for the pressure
in the peritoneal cavity may sink during inspiration and rise during
expiration (as in the pleural cavity), especially when the diaphragm
takes little or no part in respiration ("Ueber Pleural- und
Peritonealdruck," _Deutsches Arch. f. klin. Med._, July 31, 1883).]

Through the medium of subphrenic abscess, or directly through adhesions
between the stomach and the diaphragm, gastric ulcer may perforate into
one of the pleural cavities (generally the left) and cause empyema or
pneumo-pyothorax. Adhesions may form between the diaphragm and the
pulmonary pleura, so that the ulcer perforates directly into the lung;
in which case pulmonary gangrene or pulmonary abscess is usually
developed. The diagnosis of the perforation into the lung has been made
by recognizing a sour odor and sour reaction of the expectoration, and
by finding in the sputum particles of food derived from the stomach.
Sudden death from suffocation has followed perforation of the stomach
into the lung.[58]

[Footnote 58: Tillmanns (_loc. cit._) has collected 12 cases of
communication between the stomach and the thoracic cavity from
perforation of gastric ulcer; all proved fatal. In Sturges's case of
recovery from pneumothorax supposed to be produced by perforation of a
gastric ulcer the diagnosis of the cause of the pneumothorax was very
doubtful (_The Lancet_, Feb. 7, 1874).]

Perforation of gastric ulcer into the transverse colon has been
followed by the vomiting of formed feces and by the passage of
undigested food by the bowel (Abercrombie). Enemata may be vomited, so
that, as suggested by Murchison, the introduction of colored enemata
may aid in the diagnosis.

Gastro-cutaneous fistulae are among the rare results of perforation of
gastric ulcer. In these cases food, sometimes only in liquid form,
escapes through the fistula.

The opening of gastric ulcer into the pericardium is one of the rare
causes of pneumo-pericardium.

Other varieties of perforation which are of pathological rather than of
clinical interest will be mentioned under the morbid anatomy of gastric
ulcer.

COURSE.--Few diseases are more variable in their course and duration
than is simple gastric ulcer. It is customary to distinguish between
acute and chronic forms of gastric ulcer, but this is a distinction
which cannot be sharply drawn. Those cases are called acute in which,
with absence or short duration of antecedent gastric symptoms,
perforation or gastrorrhagia suddenly causes death. But in some of
these cases the thickened and indurated margins of the ulcer found at
the autopsy show that the disease has been of much longer duration than
the clinical history would indicate. Still, there is reason to believe
that within the course of a few days ulcers may form and perforate all
of the coats of the stomach.

In the great majority of cases of gastric ulcer the tendency is to
assume a chronic course, so that the often-used term chronic gastric
ulcer is generally applicable.

{501} The great diversity of the symptoms in different cases makes it
impossible to give a generally applicable description of the course of
gastric ulcer. It is, however, useful to designate the main clinical
forms of the disease. Thus we may distinguish--

1. Latent ulcers, with entire absence of symptoms, and revealed as open
ulcers or as cicatrices at the autopsy.

2. Acute perforating ulcers. With or without a period of brief gastric
disturbance perforation occurs and causes speedy death.

3. Acute hemorrhagic form of gastric ulcer. After a latent or a brief
course of the ulcer profuse gastrorrhagia occurs, which may terminate
fatally or may be followed by the symptoms of chronic ulcer.

4. Gastralgic-dyspeptic form. In this, which is the most common form of
gastric ulcer gastralgia, dyspepsia and vomiting are the symptoms.
Sometimes one of the symptoms predominates greatly over the others, so
that Lebert distinguishes separately a gastralgic, a dyspeptic, and a
vomitive variety. Gastralgia is the most frequent symptom.

5. Chronic hemorrhagic form. Gastrorrhagia is a marked symptom, and
occurs usually in combination with the symptoms just mentioned.

6. Cachectic form. This usually corresponds only to the final stage of
one of the preceding forms, but the cachexia may develop so rapidly and
become so marked that the course of the disease closely resembles that
of gastric cancer.

7. Recurrent form. In this the symptoms of gastric ulcer disappear, and
then follow intervals, often of considerable duration, in which there
is apparent cure, but the symptoms return, especially after some
indiscretion in the mode of living. This intermittent course may
continue for many years. In these cases it is probable either that
fresh ulcers form or that the cicatrix of an old ulcer becomes
ulcerated.

8. Stenotic form. By the formation of cicatricial tissue in and around
the ulcer the pyloric orifice becomes obstructed and the symptoms of
dilatation of the stomach develop.

DURATION.--The average duration of gastric ulcer may be said to be from
three to five years, but this estimate is not of great value, on
account of the absence of any regularity in the course and duration of
the disease. In cases of very protracted duration, such as forty years
in a case of Habershon's and thirty-five in one of Brinton's, it is
uncertain whether the symptoms are referable to the persistence of one
ulcer or to the formation of new ulcers, or to sequels resulting from
cicatrization.

In 110 cases (44 fatal) analyzed by Lebert[59] the course was latent
until the occurrence of perforation or of profuse hemorrhage in 15 per
cent., the duration was less than one year in 18 per cent., from one to
six years in 46-1/2 per cent., from six to twenty years in 18 per
cent., from twenty to thirty-five years in 2-1/2 per cent.

[Footnote 59: _Op. cit._, p. 235.]

TERMINATIONS.--In the majority of cases gastric ulcer terminates in
recovery. The recovery is often complete. Various gastric disturbances
may, however, follow the cicatrization of gastric ulcer, especially if
the ulcer was large and of long duration. These sequential disturbances
are due to the contraction of the cicatrix, to adhesions between the
stomach and surrounding parts, to deformity of the stomach, and
especially to dilatation of the stomach by cicatricial stenosis of the
pylorus. Hence, {502} gastralgia, dyspepsia, and vomiting may continue
after the ulcer has healed, so that anatomical cure of the ulcer is not
always recovery in the clinical sense. Relapses may occur after
recovery, as those who have once had gastric ulcer are more prone to
the disease than are others. Not infrequently the patient recovers so
far as to be able to attend to the active duties of life, but to avoid
renewed attacks he is always obliged to be very careful as regards his
mode of living.

How often gastric ulcer ends in death it is impossible to say. It is
certain that Brinton under-estimates the number of recoveries when he
computes that only one-half of the ulcers cicatrize. Lebert reckons the
mortality from gastric ulcer as 10 per cent., which appears to be too
low an estimate. Perhaps 15 per cent. would be a more correct estimate
of the mortality.

The causes of death are perforation, hemorrhage, exhaustion, and
complicating diseases.

About 6-1/2 per cent. of the cases of gastric ulcer terminate fatally
by perforation into the peritoneal cavity. Although this estimate can
be considered only approximative, there is little doubt but that the
much larger percentages given by most writers are excessive, and are
referable to the undue frequency with which cases of perforation of
gastric ulcer have been published. Such cases naturally make a strong
impression upon the observer, and are more likely to be published than
those which terminate in other ways.

Death from hemorrhage occurs probably in from 3 to 5 per cent. of the
cases of gastric ulcer.[60] In many more cases hemorrhage is an
indirect cause of death by inducing anaemia. Unlike perforation, fatal
hemorrhage from gastric ulcer is more common in males than in
females--more common after than before forty years of age. The average
age at which fatal hemorrhage occurs is given by Brinton as forty-three
and a half years both for males and females.

[Footnote 60: In 270 fatal cases of open ulcer from the statistics of
Jaksch, Dittrich, Eppinger, Starcke, Chambers, Habershon, Moore, and
Lebert, I find 27 deaths by hemorrhage. Reckoning three cicatrices to
one ulcer, this would give a percentage of 3-1/3.]

In a considerable proportion of the fatal cases exhaustion is the cause
of death. According to Lebert, death from exhaustion occurs in about 4
per cent. of the cases of gastric ulcer. The causes of exhaustion are
the pain, hemorrhage, dyspepsia, and vomiting which constitute the
leading symptoms of the disease.

Finally, death may be due to some of the complications or sequels of
gastric ulcer.

COMPLICATIONS.--Some of the complications of gastric ulcer are directly
referable to the ulcer, others are only remotely related to it, and
others are merely accidental.

Pylephlebitis is among the most important of the complications directly
referable to the ulcer. This pylephlebitis is usually of the infectious
variety, and leads to abscesses in the liver, sometimes to abscesses in
the spleen and other organs.

As has already been mentioned, chronic catarrhal gastritis stands in
close relationship to gastric ulcer. Chronic peritonitis is a rare
complication of gastric ulcer (Moore, Vierordt). Chronic interstitial
gastritis, with contraction of the stomach and thickening of its walls,
was {503} associated with ulcer in a case under my observation. In a
case of ulcer under the care of Owen Rees[61] this condition of the
stomach was associated with chronic deforming peritonitis (thickening,
induration, and contraction of the peritoneum) and ascites, so that the
symptoms during life and the gross appearances after death resembled
cancerous diseases of the peritoneum. Simple ulcer and cancer may occur
together in the same stomach, or cancer may develop in an ulcer or its
cicatrix. Glasser reports a case of phlegmonous gastritis with gastric
ulcer.[62] Extension of inflammation to the pleura without perforation
of the diaphragm sometimes occurs. Fatty degeneration of the heart may
be the result of profound anaemia induced by gastric ulcer.[63] Embolic
pneumonia and broncho-pneumonia are occasional complications. A
moderate degree of cachectic dropsy is not very infrequent in the late
stages of gastric ulcer.

[Footnote 61: _Med. Times and Gaz._, April 24, 1869.]

[Footnote 62: _Berlin. klin. Wochenschrift_, 1883, No. 51.]

[Footnote 63: Shattuck, _Boston Med. and Surg. Journ._, June, 1880,
vol. ciii.]

Other complications, such as pulmonary tuberculosis, valvular disease
of the heart, general atheroma of the arteries, cirrhosis of the liver,
syphilis, chronic Bright's disease, waxy degenerations, and malaria,
have been considered under the Etiology, and some of them will be
referred to again in connection with the Pathology, of gastric ulcer.
In most instances when ulcer is associated with these diseases the
ulcer is secondary.

SEQUELAE.--The most important sequelae of gastric ulcer are changes in
the form of the stomach in consequence of adhesions and in consequence
of the formation and contraction of cicatrices. These lesions are most
conveniently described under the Morbid Anatomy. The symptoms of the
most important of these sequels--namely, stenosis of the pylorus with
dilatation of the stomach--will be described in another article.

MORBID ANATOMY.--As regards number, simple ulcer of the stomach is
usually single, but occasionally two or more ulcers are present. It is
not uncommon to meet in the same stomach open ulcers and the scars of
healed ulcers. According to Brinton, multiple ulcers are found in about
one-fifth of the cases. In one case O'Rorke found six ulcers on the
anterior wall of the stomach.[64] Berthold mentions a case in which
thirty-four ulcers were found in the same stomach.[65]

[Footnote 64: _Trans. of the New York Path. Soc._, vol. i. p. 241.
Wollmann mentions the occurrence of over eight simple ulcers in the
same stomach (_Virchow und Hirsch's Jahresb._, 1868, Bd. ii. p. 126).]

[Footnote 65: _Op. cit._, p. 21. It is expressly stated that these were
not hemorrhagic erosions, but deep corrosive ulcers.]

The usual position of simple gastric ulcer is the posterior wall of the
pyloric portion of the stomach on or near the lesser curvature. Ulcers
of the anterior wall are rare, but they carry a special danger from
their liability to perforate without protective adhesions. The least
frequent seats of ulcer are the greater curvature and the fundus.

The table on page 504 gives the situation of 793 ulcers recorded in
hospital statistics:[66] {504}

  Lesser curvature   288 (36.3 per cent.)
  Posterior wall     235 (29.6    "     )
  Pylorus             95 (12      "     )
  Anterior wall       69 ( 8.7    "     )
  Cardia              50 ( 6.3    "     )
  Fundus              29 ( 3.7    "     )
  Greater curvature   27 ( 3.4    "     )

From this table it is apparent that ulcers occupy the lesser curvature,
the posterior wall, and the pyloric region three and a half times more
frequently than they do the remaining larger segment of the stomach.

[Footnote 66: These statistics are collected from the previously-cited
works of Rokitansky, Jaksch, Wrany, Eppinger, Chambers, Habershon,
Steiner, Wollmann, Berthold, Starcke, Lebert, and Moore. They represent
566 cases. So far as noted, most of the ulcers on the posterior wall
were nearer to the lesser curvature than to the greater; those on the
lesser curvature extended more frequently to the posterior than to the
anterior wall. Although not apparent from the table, most of the ulcers
of the lesser curvature and of the posterior wall were in the pyloric
region. So far as possible, cicatrices were excluded. Pylorus and
cardia in the table indicate on or near those parts.]

Occasionally two ulcers are seated directly opposite to each other, the
one on the anterior, the other on the posterior, wall of the stomach.
The most plausible explanation of this is that the ulcers are caused by
a simultaneous affection of corresponding branches which are given off
symmetrically from the same arterial trunk as it runs along one of the
curvatures of the stomach (Virchow).[67]

[Footnote 67: A. Beer, "Aus dem path. Anatom. Curse et. Prof. R.
Virchow, etc.," _Wiener med. Wochenschr._, Nos. 26, 27, 1857.]

The ordinary size of the ulcer varies from a half inch to two inches in
diameter. The ulcer may be very minute, as in two cases reported by
Murchison, in each of which a pore-like hole was found leading into a
perforated artery from which fatal hemorrhage had occurred.[68] On the
other hand, the ulcer may attain an enormous size, extending sometimes
from the cardiac to the pyloric orifice and measuring five or six
inches in diameter.[69]

[Footnote 68: Murchison, _Trans. of the Path. Soc._, vol. xxi. p. 162,
London, 1870.]

[Footnote 69: In one of Cruveilhier's cases the ulcer was 6-1/2 inches
long and 3-1/3 inches wide. Law describes an ulcer measuring 6 inches
by 3 inches (_Dublin Hosp. Gaz._, ii. p. 51).]

The ulcer is usually round or oval in shape. The outline of the ulcer
may become irregular by unequal extension in the periphery, or by the
coalescence of two or more ulcers, or by partial cicatrization. Simple
ulcers, especially when seated near the lesser curvature, have a
tendency to extend transversely to the long axis of the stomach, thus
following the course of the blood-vessels. By this mode of extension,
or more frequently by the coalescence of several ulcers, are formed
girdle ulcers, which more or less completely surround the circumference
of the stomach, oftener in the pyloric region than elsewhere.

As the ulcer extends in depth it often destroys each successive layer
of the stomach in less extent than the preceding one, so that the form
of the ulcer is conical or funnel-shaped, with a terrace-like
appearance in its sloping edges. The apex of the truncated cone, which
is directed toward the peritoneum, is often not directly opposite to
the centre of the base or superior surface which occupies the mucous
membrane, so that one side of the cone may be vertical and the other
sloping. In the half of the stomach nearer the lesser curvature the
cone slopes upward, and in the lower half of the stomach it slopes
downward. The usual explanation of its conical shape is that the ulcer
exactly corresponds to the territory supplied by an artery with its
branches. Virchow finds an explanation for the oblique direction of the
funnel in the arrangement of the arteries of the stomach. These, coming
from different sources, run along the curvatures of the stomach, and
there give off symmetrically branches which run obliquely toward the
mucous membrane, so that one of these {505} branches with its
distributive twigs (arterial tree) would supply a part shaped like an
oblique funnel. One of the chief supports of the theory which refers
the origin of simple gastric ulcer to an arrest of the circulation is
this correspondence in shape of the ulcer to the area of distribution
of the branches of the arteries supplying the stomach.

All ulcers do not present the conical form and terraced edges which
have been described. These appearances are far from constant in fresh
ulcers, and they are usually absent in those of long duration.

The most characteristic anatomical feature of simple ulcer of the
stomach is the appearance of the edges and of the floor of the ulcer.
The edges of recently-formed ulcers (acute ulcers) are clean-cut,
smooth, and not swollen. To use Rokitansky's well-known comparison, the
hole in the mucous coat looks as if it had been punched out by an
instrument. The floor of the ulcer may be smooth and firm or soft and
pulpy. The floor and edges of fresh ulcers are often infiltrated with
blood, but they may be of a pale-grayish color. Usually no granulations
and no pus are to be seen on the surface of the ulcer.[70] In ulcers of
longer duration the margins become thickened, indurated, and abrupt;
the floor acquires a dense fibrous structure.

[Footnote 70: In rare instances granulations may be present, as in a
case of W. Muller's, in which their presence rendered difficult the
diagnosis of simple ulcer from carcinoma (_Jenaische Zeitschrift_, v.,
1870). The microscope may also be required to distinguish the
irregularly thickened margins of old ulcers from scirrhous cancer.]

The floor of the ulcer may be the submucous, the muscular, or the
serous coat, or, if the whole thickness of the stomach be perforated,
it may be some adjacent organ to which the stomach has become adherent,
this organ being usually the pancreas or the left lobe of the liver or
neighboring lymphatic glands.

The microscopic examination of recently-formed ulcers shows that the
tissue immediately surrounding the ulcer is composed of granular
material, disintegrated red blood-corpuscles, pale and swollen
fragments of connective-tissue fibres, and cells unaffected by
nuclear-staining dyes. The red blood-corpuscles are sometimes broken
into fragments of various sizes in about the same way as by the action
of heat. The gastric tubules are separated from each other and
compressed by infiltrated blood, and contain cells which do not stain.
Around this margin of molecular disintegration, which has evidently
been produced by the action of the gastric juice, there is often,
although not constantly, a zone of infiltration with small round cells,
probably emigrated white blood-corpuscles. These cells are most
abundant near the muscularis mucosae and in the submucosa. Extravasated
red blood-corpuscles extend a variable distance around the ulcer,
farthest as a rule in the submucous coat. Many of the blood-vessels in
the immediate neighborhood of the ulcer appear normal; others,
particularly the arterioles and the capillaries, may be filled with
hyaline thrombi. Clumps of hyaline material may also be seen in the
meshes of the tissue around the ulcer. Fine fatty granules may be seen
in the tissue near the ulcer. The interstices of the loose submucous
tissue and the lymphatic vessels are often filled with fibrillated
fibrin and scattered blood-corpuscles for a considerable distance
around the ulcer.

In the margins of old gastric ulcers there is also a zone of molecular
necrosis. The induration and the thickening of the edges of these
ulcers {506} are caused by a new growth of fibrillated connective
tissue, which blends together all of the coats invaded by the ulcer.
This new tissue is usually rich in lymphoid cells, which are often most
abundant in the lymphatic channels. In the fibrous edges and base of
old ulcers are arteries which are the seat of an obliterating
endarteritis, and which may be completely obliterated by this process.
An interstitial neuritis may affect the nerve-trunks involved in the
fibrous growth. Blood-pigment may be present as an evidence of an old
hemorrhagic infiltration.[71]

[Footnote 71: The histological changes here described are based upon
the examination of typical specimens both of recent and of old gastric
ulcers which have come under my observation.]

Cicatrization is accomplished by the development of fibrous tissue in
the floor and borders of the ulcer. By the contraction of this
new-formed tissue the edges of the mucous membrane are united to the
floor of the ulcer, and may be drawn together so as to close completely
the defect in the mucous membrane. The result is a white stellate
cicatrix, which is usually somewhat depressed and surrounded by
puckered mucous membrane. It is probable that small, superficial ulcers
may be closed so that the scar cannot be detected. The mucous membrane
which has been drawn over the cicatrix is intimately blended with the
fibrous substratum, and is usually itself invaded by fibrous tissue
which compresses and distorts the gastric tubules. Hauser[72] has shown
that the tubular glands grow down into the cicatricial tissue, where
they may branch in all directions. These new-formed tubules are lined
by clear cylindrical or cutical epithelial cells, and may undergo
cystic dilatation. Very irregular cicatrices may result from the
healing of large and irregular ulcers. When the ulcer is large and deep
and the stomach is adherent to surrounding parts, the edges of the
mucous membrane making the border of the ulcer cannot be united by the
contraction of the fibrous tissue in the floor of the ulcer. The
cicatrix of such ulcers consists of fibrous tissue uncovered by mucous
membrane. The closure of the ulcer is incomplete. Such cicatrices are
liable to be the seat of renewed ulceration.

[Footnote 72: _Das chronische Magengeschwur, etc._, Leipzig, 1883. In
the rare instances of carcinoma developing in the borders or in the
cicatrix of gastric ulcer, Hauser believes that the cancerous growth
starts from these glandular growths, which in general have only the
significance of Friedlander's atypical proliferation of epithelial
cells.]

The formation and contraction of the cicatrix may cause various
deformities of the stomach. The character of these deformities depends
upon the situation, the size, and the depth of the ulcer which is
cicatrized. Among the most important of these distortions are stenosis
of the pyloric orifice, followed by dilatation of the stomach, more
rarely stenosis of the cardiac orifice, with contraction of the
stomach, approximation of the cardiac and of the pyloric orifices by
the healing of ulcers on the lesser curvature, and an hour-glass form
of the stomach, produced by the cicatrization of girdle ulcers or of a
series of ulcers extending around the stomach. These abnormalities in
form of the stomach, particularly the constriction of the orifices, may
be attended by more serious symptoms than the original ulcer.

As the ulcer extends in depth a circumscribed peritonitis, resulting in
the formation of adhesions between the stomach and surrounding parts,
is usually excited before the serous coat is perforated, so that the
gravest of all possible accidents in the course of gastric
ulcer--namely, perforation {507} into the peritoneal sac--is
permanently or temporarily averted. It has been estimated that
adhesions form in about two-fifths of all cases of gastric ulcer
(Jaksch). On account of the usual position of the ulcer on the lesser
curvature or on the posterior wall of the stomach, the adhesions are
most frequently with the pancreas (in about one-half of all cases of
adhesion); next in frequency with the left lobe of the liver; rarely
with other parts, such as the lymphatic glands, the diaphragm, the
spleen, the kidney, the suprarenal capsule, the omentum, the colon, and
other parts of the intestine, the gall-bladder, the sternum, and the
anterior abdominal wall. Adhesions cannot readily form between the
anterior surface of the stomach and the anterior abdominal wall, on
account of the constant movement of these parts, so that ulcers of the
anterior gastric wall are those most liable to perforate into the
peritoneal cavity.

It is difficult to include in any description all of the various and
complicated lesions which may result from perforation by gastric ulcer
of all of the coats of the stomach. The consequences of perforation may
be conveniently classified as follows:

1. Some solid organ, usually the pancreas, the liver, or the lymphatic
glands, may close the hole in the stomach.

2. An intra-peritoneal sac shut in by adhesions may communicate through
the ulcer with the cavity of the stomach.

3. A fistulous communication may form either between the stomach and
the exterior (external gastric fistula) or between the stomach and some
hollow viscus (internal gastric fistula).

4. The ulcer may perforate into the general peritoneal cavity.

These lesions may be variously combined with each other. It is to be
noted that in the first three varieties protective adhesions are
present, and that in the last these adhesions are either absent or
ruptured.

When the pancreas, the liver, or the spleen form the floor of the
ulcer, they may be protected from extension of the ulcerative process
by a new growth of fibrous tissue extending from the floor of the ulcer
a variable depth into these organs. Sometimes, however, the ulcerative
process, aided doubtless by the corroding action of the gastric juice,
eats out large excavations in these organs. These excavations
communicate with the cavity of the stomach, and are usually filled with
ichorous pus. The pancreas, unlike the spleen and the liver, possesses
comparative immunity against this invasion by the ulcerative process.

The situation, the form, and the extent of circumscribed peritoneal
abscesses resulting from perforation of gastric ulcer depend upon the
parts with which the stomach has contracted adhesions. Should an ulcer
on the posterior wall of the stomach perforate before the formation of
adhesions, the perforation would of course be directly into the lesser
peritoneal cavity. An interesting example of this rare occurrence has
been communicated by Chiari.[73] In this case, the foramen of Winslow
being closed by adhesions, the lesser peritoneal cavity which
communicated with a gastric ulcer was filled with ichorous pus, and in
this floated the pancreas, which had necrosed in mass and had separated
as a sequestrum. That form of intra-peritoneal abscess known as
subphrenic pneumo-pyothorax has been already described under
Symptomatology. Peritoneal abscesses communicating with the stomach may
open into various places, {508} as into the general peritoneal cavity,
into the pleural cavity, into the retro-peritoneal tissue, through the
abdominal or thoracic walls, etc.

[Footnote 73: _Wiener med. Wochenschr._, 1876, No. 13.]

Gastro-cutaneous fistulae are a rare result of the perforation of
gastric ulcer.[74] The external opening is most frequently in the
umbilical region, but it may be in the epigastric or in the left
hypochondriac region or between the ribs. Fistulous communications
resulting from the perforation of gastric ulcer have been formed
between the stomach and one or more of the following hollow viscera or
cavities: the colon, the duodenum and other parts of the small
intestine, the gall-bladder, the common bile-duct, the pancreatic duct,
the pleura, the lung, the left bronchus, the pericardium, and the left
ventricle. Gastro-colic fistulae, in contrast to gastro-cutaneous
fistulae, are more frequently produced by cancer than by ulcer of the
stomach.[75] In rare instances the peritoneum over ulcers of the lesser
curvature has contracted adhesions with the pyloric portion of the
stomach or with the first part of the duodenum. To accomplish this it
is necessary that a sharp bend in the lesser curvature should take
place. By extension of the ulcerative process abnormal communication is
established between the left and the right half of the stomach or
between the stomach and the duodenum. In either case the right half of
the stomach is often converted into a large blind diverticulum, the
digested food passing through the abnormal opening.[76] Gastro-duodenal
fistulae are more frequently with the third than with the first part of
the duodenum. In one of Starcke's cases the stomach communicated with
the colon and through the medium of a subphrenic abscess with the left
lung.[77]

[Footnote 74: Of the 25 cases of gastro-cutaneous fistula collected by
Murchison, 18 were the result of disease. In 12 of these cases the
probable cause was simple gastric ulcer (_Med.-Chir. Trans._, vol. xli.
p. 11, London, 1858). Middeldorpf says that among the internal causes
of the 47 cases of external gastric fistula which he tabulated, simple
ulcer of the stomach played an important role (_Wiener med.
Wochenschr._, 1860).]

[Footnote 75: Of 33 cases of gastro-colic fistula collected by
Murchison, 21 were from gastric cancer and 9 or 10 probably from simple
ulcer. On the other hand, gastro-cutaneous fistulae are twice as
frequently the result of simple ulcer as of cancer (_Edinb. Med.
Journ._, vol. iii. 1857).]

[Footnote 76: Thierfelder has made the best study of the complicated
relations existing in these cases (_Deutsches Arch. f. klin. Med._, Bd.
iv. p. 33, 1868).]

[Footnote 77: _Deutsche Klinik_, 1870, No. 39. Habershon also reports a
case in which a subphrenic abscess communicated with the lung, the
stomach, and the colon, but he believes that the ulceration was primary
in the colon (_Guy's Hosp. Rep._, Ser. 3, vol. i. p. 109).]

Four cases of perforation of gastric ulcer into the pericardium,[78]
with the production of pneumo-pericardium, have been reported, and two
cases of perforation into the left ventricle.[79] Muller found
lumbricoid worms in a pleural cavity which had been perforated by
gastric ulcer.[80] Diaphragmatic hernia may result from perforation of
the pleural cavity by gastric ulcer.[81] In one instance the greater
part of the small intestines {509} passed through a hole in the
transverse meso-colon which had been caused by a gastric ulcer.

[Footnote 78: Hallin, _Schmidt's Jahrb._, cxix. S. 37; Saxinger,
_Prager med. Wochenschr._, 1865; Guttmann, _Berl. klin. Wochenschr._,
1880, No. 23. Murchison mentions a specimen in the museum of King's
College, London, of a simple gastric ulcer opening into the pericardium
(_Edinb. Med. Journ._, vol. iii. p. 6). In a case reported by Graves a
liver abscess burst into the stomach and into the pericardium (_Clin.
Lect._, ii. p. 237, Dublin, 1848).]

[Footnote 79: Oser, _Wiener med. Blatter_, 1880, No. 52; Brenner,
_Wiener med. Wochenschr._, 1881, No. 47.]

[Footnote 80: Muller, _Memorabilien_, xvii., Oct., 1872.]

[Footnote 81: Needon, _Wiener med. Presse_, 1869, No. 42. In a case of
Gunsburg's the hole in the diaphragm was as large as the hand, and the
left pleural cavity contained the upper half of the stomach and the
spleen (_Arch. f. phys. Heilk._, xi. 3, 1852).]

The various fistulae which have been mentioned may be either direct or
through the medium of an abscess. While some of them are only
pathological curiosities, others, particularly the communications of
the stomach with the pleural cavity and with the lung, are sufficiently
frequent to be of practical clinical interest.

As has already been explained, ulcers of the anterior wall are the ones
most liable to perforate into the general peritoneal cavity,[82] but on
account of their comparative infrequency perforation occurs oftener in
other situations, particularly in the lesser curvature and near the
pylorus. Except on the anterior wall the perforation is often brought
about by the rupture of adhesions which for a time had prevented this
accident. In a considerable number of cases, particularly of ulcers on
the anterior wall, the ulcer looks as if recently formed (acute
perforating ulcer); in other cases its thickened and indurated margins
indicate long duration. Chiari[83] describes a case in which rupture
into the peritoneal cavity took place through the cicatrix of an old
ulcer, probably in consequence of the distension of the stomach with
gas. The hole in the peritoneum is usually circular, smaller than the
inner surface of the ulcer, and has sharp, well-defined edges. Less
frequently the edges are ragged. Post-mortem digestion may, however, so
change the borders of the opening as to make it difficult or impossible
to tell from their post-mortem appearances alone whether perforation
has occurred before or after death. The peritoneal cavity after death
from perforation is found to contain gas and substances from the
stomach. Usually within a few hours after perforation septic
peritonitis is excited, but in exceptional cases no inflammation of the
peritoneum has occurred even when life has been prolonged twenty-four
hours after perforation.

[Footnote 82: According to Brinton, "the proportion of perforations to
ulcers is such that of every 100 ulcers in each of the following
situations, the numbers which perforate are--on the posterior surface,
about 2; the pyloric sac, 10; the middle of the organ, 13; the lesser
curvature, 18; the anterior and posterior surface at once, 28; the
cardiac extremity, 40; and the anterior surface, 85."]

[Footnote 83: _Wiener med. Blatter_, 1881, No. 3.]

Emphysema of the subcutaneous, subperitoneal, and other loose areolar
tissue of the body is a rare but remarkable result of the perforation
of gastric ulcer. The emphysema is sometimes observed shortly before
death, but it attains its maximum development after death, when it may
spread rapidly over the greater part of the body. The gas consists in
part of hydrogen, as it burns with a blue flame. It is generated, at
least in great part, by fermentation of the contents of the stomach.
The gas may enter the subserous tissue at the edges of the ulcer and
thence spread, or, after perforation of the stomach, it may make its
way from the peritoneal cavity into the loose subserous connective
tissue through some place in the parietal peritoneum which has been
macerated, perhaps by the digestive action of the gastric juice.[84]

[Footnote 84: Roger (_Arch. gen. de Med._, 1862) and Demarquay (_Essai
de Pneumatologie medicale_, Paris, 1866) deserve the credit of first
calling general attention to the occurrence of subcutaneous emphysema
after rupture of the digestive tract. The following writers have each
reported a case of emphysema following the perforation of gastric
ulcers: Cruveilhier, _Anat. Path._, t. i. livr. xx.; Bell, _Edinb. Med.
Journ._, vol. vi. p. 783; Thierfelder, _Deutsches Arch. f. klin. Med._,
iv., 1868, p. 33; Newman, _The Lancet_, 1868, vol. ii. p. 728;
Poensgen, _Das subcutane Emphysem nach continuitatstrennungen des
Digestionstractus, etc._, Inaug. Diss., Strassburg, 1879, p. 40;
Korach, _Deutsche med. Wochenschr._, 1880 p. 275; {510} Jurgensen,
_Deutsches Arch. f. klin. Med._, Bd. 31, p. 441, 1882. Doubtful cases
are reported by Lefevre, W. Mayer, and Burggraeve. The fullest
consideration of the subject is to be found in the dissertation of
Poensgen.]

In two cases of sudden death from gastric ulcer Jurgensen found gas in
the veins and arteries of various parts of the body. He believes that
this gas, which certainly was not the result of putrefaction after
death, was derived from the stomach, and that it entered during life
the circulation through vessels exposed in the borders of the ulcer,
thus causing death. In one of the cases a profuse hemorrhage preceded
death, and in the other the ulcer had perforated into the peritoneal
cavity.[85]

[Footnote 85: Jurgensen does not consider whether this gas may not have
made its way into the blood-vessels after death in a manner similar to
its extension through the cellular tissue of the body in the cases of
emphysema just mentioned. In the case which he has reported in full
interstitial and subserous emphysema could be traced from the ulcer
("Luft im Blute," _Deutsches Arch. f. klin. Med._, Bd. 31, p. 441,
1882).]

The source of hemorrhage from gastric ulcer is from blood-vessels
either in the stomach itself or in the neighborhood of the stomach.
Hemorrhages slight or of moderate severity occur from the capillaries
and small arteries and veins in the mucous and submucous coats.
Sometimes profuse and even fatal hemorrhage comes from arteries or from
veins in the submucous coat, especially when these vessels are dilated.
Quickly-fatal hemorrhages take place from the large vessels between the
muscular and the serous coats, particularly from the main trunks on the
curvatures. After the formation of adhesions, followed by the
perforation of all of the coats of the stomach, profuse bleeding may
proceed from the erosion of large vessels near the stomach, such as the
splenic, the hepatic, the pancreatico-duodenal arteries, the portal and
the splenic veins, and the mesenteric vessels. Bleeding may also occur
from vessels in the parenchyma of organs invaded by the ulcer. The most
common source of fatal hemorrhage is from the splenic artery, which
from its position is peculiarly exposed to invasion by ulcers of the
posterior wall of the stomach. The hemorrhage is usually arterial in
origin. It may come from miliary aneurisms of the gastric arteries or
from varicose veins in the wall of the stomach. As Cruveilhier has
pointed out, an ulcer may cicatrize except over one spot corresponding
to an artery from which fatal hemorrhage may occur. Ulcers which give
rise to large hemorrhages are usually chronic in their course. Those
seated on the middle of the anterior wall, although peculiarly liable
to perforate, are comparatively exempt from hemorrhage on account of
the small size of the blood-vessels there.

Changes in the blood-vessels of the stomach have been seen in a
considerable number of cases of gastric ulcer. Instances have been
recorded of the association with gastric ulcer of most of the diseases
to which blood-vessels are subject. An example in all respects
convincing of embolism of the artery supplying the ulcerated region of
the stomach has not been published. Probably the best case belonging
here is one of perforating ulcer of the stomach with hemorrhagic
infiltration in its walls, presented by Janeway to the New York
Pathological Society in 1871.[86] In this case there was in the
gastro-epiploic artery an ante-mortem fibrinous plug which was
continued into the nutrient artery of the ulcerated piece of the
stomach. No source for an embolus could be found. In one case Merkel
found an embolus in a small artery leading to an ulcer {511} of the
duodenum.[87] The arch of the aorta was atheromatous and contained a
thrombus. Patches of hemorrhagic infiltration existed in the stomach.

[Footnote 86: _Trans. of the N.Y. Path. Soc._, vol. ii. p. 1.]

[Footnote 87: _Wiener med. Presse_, vii. p. 30, 1866.]

In many cases thrombosis of the arteries, and especially of the veins
involved in the diseased tissue around an ulcer, has been observed, and
in some the thrombus was prolonged in the vessels for a considerable
distance from the ulcer. It is probable that in most of these cases the
thrombus was secondary to the ulcer. Hyaline thrombosis of the
capillaries near the ulcer is also to be mentioned.

In a certain, but not large, number of cases atheroma with
calcification or with fatty degeneration of the arteries of the stomach
has been found associated with gastric ulcer.[88] Reference has already
been made to the occurrence of obliterating endarteritis in the
thickened edges and floor of gastric ulcer, where it is doubtless
secondary. In one case of gastric ulcer I found a widespread
obliterating endarteritis affecting small and medium-sized arteries in
many parts of the body, including the stomach.[89]

[Footnote 88: For cases in point see Norman Moore, _Trans. of the Path.
Soc. of London_, vol. xxxiv. p. 94.]

[Footnote 89: On the posterior wall of the stomach, midway between the
greater and the lesser curvature and five inches to the right of the
cardiac orifice, was a round ulcer half an inch in diameter, with
smooth, sharp edges. In the floor of the ulcer, which extended to the
muscular coat, was a small perforated aneurism of a branch of the
coronary artery. In addition there were small, granular kidneys,
hypertrophied heart without valvular lesion, and chronic interstitial
splenitis. Small and medium-sized arteries in the kidneys, spleen,
heart, lymphatic glands, and stomach were the seat of a typical
endarteritis obliterans, resulting in some instances in complete
closure of the lumen of the vessel. The patient, who was attended by
Sassdorf, was seized during the night with vomiting of blood, which
continued at intervals for twenty-four hours until his death. The
patient was a man about fifty years of age, without previous history of
gastric ulcer or of syphilis.]

In one case Powell[90] found a small aneurism of the coronary artery in
an ulcer of the lesser curvature of the stomach. Hauser[91] found an
aneurismal dilatation of an atheromatous and thrombosed arterial twig
in the floor of a recent ulcer. In my case of obliterating endarteritis
just referred to there was a small aneurism in the floor of the ulcer.
These miliary aneurisms in the floor of gastric ulcers seem to be
analogous to those in the walls of phthisical cavities. Miliary
aneurisms occur in the stomach independently of gastric ulcer, and may
give rise to fatal haematemesis, as in four cases reported by
Galliard.[92]

[Footnote 90: _Trans. of the Path. Soc. of London_, vol. xxix.]

[Footnote 91: _Das chronische Magengeschwur, etc._, p. 11, Leipzig,
1883.]

[Footnote 92: _L'Union med._, Feb. 26, 1884. Curtis reported a case of
fatal haematemesis from an aneurism, not larger than a small pea,
seated in the cicatrix of an old ulcer (_Med. Annals of Albany_, Aug.,
1880).]

Gastric ulcer is occasionally associated with waxy degeneration of the
arteries of the stomach.[93] In most of these cases there were multiple
shallow ulcers. Haematemesis is generally absent in gastric ulcer
resulting from waxy disease of the gastric blood-vessels. As is well
known, the amyloid material itself resists the action of the gastric
juice.

[Footnote 93: Hauser (_op. cit._) alludes to a case in which, with waxy
degeneration of the stomach, over one hundred small ulcers were found
in different stages of development, from hemorrhagic infiltrations to
complete ulcers. Cases belonging here are reported by Fehr, _Ueber die
Amyloide Degeneration_, Inaug. Diss., Bern, 1866; Merkel, _Wiener med.
Presse_, 1869; Edinger, _Deutsches Arch. f. klin. Med._, Bd. 29, p.
568; Marchiafava, _Atti del Accad. Med. di Roma_, iii. p. 114; and
Mattei, _Deutsche med. Zeitung_, July 5, 1883.]

Finally, varicosities of the veins of the stomach have been once in a
{512} while found with gastric ulcer. In a large number, probably in
the majority, of cases of gastric ulcer no changes have been found in
the blood-vessels of the stomach except such as were manifestly
secondary to the ulcer.

That gastric ulcer is frequently complicated with chronic catarrhal
gastritis has been repeatedly mentioned in the course of this article.

PATHOGENESIS.--Without doubt, the most obscure chapter in the history
of gastric ulcer is that relating to its origin and to its persistence.
Notwithstanding a vast amount of investigation and of discussion,
unanimity of opinion upon these subjects has not been reached. In view
of this uncertainty it is desirable in this article to do little more
than to summarize the leading theories as to the development of gastric
ulcer.

Most observers are agreed that the digestive action of the gastric
juice has some share in the development and the progress of the ulcer,
but as to the first cause of the ulcer there are various hypotheses.

The earliest theory refers the origin of simple ulcer of the stomach to
inflammation. Since its advocacy by Abercrombie and by Cruveilhier this
theory has always had its adherents, particularly among French writers.
It is true that in stomachs which are the seat of simple ulcer
evidences of inflammation can often be found both in the neighborhood
of the ulcer and elsewhere. In recent times the supporters of the
inflammatory origin of gastric ulcer lay especial stress upon the
presence of foci of infiltration with small round cells in the mucous
and the submucous coats.[94] But it is difficult to explain by the
inflammatory theory the usually solitary occurrence and the funnel-like
shape of gastric ulcer.

[Footnote 94: Laveran, _Arch. de Phys. norm. et path._, 1876, p. 443;
Galliard, _Essai sur la Pathogenie de l'Ulcere simple de l'Estomac_,
These de Paris, 1882; Colombo, _Annali univ. di Med._, 1877.]

The theory that gastric ulcer is of neurotic origin has also been
advocated. Some refer the origin to the secretion of an excessively
acid gastric juice under abnormal nervous influence (Gunsburg), others
to vaso-motor disturbances, and others to trophic disturbances. Wilks
and Moxon compare simple gastric ulcer to ulcers of the cornea
resulting from paralysis of the trigeminus. The neurotic theory of the
origin of gastric ulcer is altogether speculative and has never gained
wide acceptance.[95]

[Footnote 95: The first to attribute gastric ulcer to nervous influence
was Siebert (_Casper's Wochenschr. f. d. Heilk._, 1842, No. 29, and
_Deutsche Klinik_, 1852). Cf. also Gunsburg, _Arch. f. phys. Heilk._,
xi., 1852; Wilks and Moxon, _Lect. on Path. Anat._, 2d ed., Philada.,
1875, p. 386. Osborne in 1845 attributed gastric ulcer to the secretion
of an abnormally acid juice by a circular group of the gastric glands
(_Dublin Journ. of Med. Sci._, vol. xxvii. p. 357).]

The view which has met with the greatest favor is that which attributes
the origin of gastric ulcer to impairment or arrest of the circulation
in a circumscribed part of the wall of the stomach, and to a subsequent
solution by the gastric juice of the part thus affected. Rokitansky
first suggested this view by assigning hemorrhagic necrosis of the
mucous membrane as the first step in the formation of the ulcer; but it
is Virchow who has most fully developed this view and has given it its
main support. The first cause of gastric ulcer, according to Virchow,
is a hemorrhagic infiltration of the coats of the stomach induced by
local disturbances in the circulation. The part the nutrition of which
is thus impaired or destroyed is dissolved by the gastric juice.

{513} The affections of the gastric blood-vessels to which importance
has been attached are (_a_) embolism and thrombosis; (_b_) diseases of
the coats of the vessels, as atheroma, obliterating endarteritis, fatty
degeneration, amyloid degeneration, and aneurismal and varicose
dilatations; (_c_) compression of the veins by spasm of the muscular
coats of the stomach in vomiting and in gastralgia; (_d_) passive
congestion of the stomach by obstruction in the portal circulation.

In support of this view are urged the following facts: First, it has
been proven by the experiments of Pavy that parts of the gastric wall
from which the circulation has been shut off undergo digestion; second,
hemorrhagic infarctions have been observed in the stomach, both alone
(Von Recklinghausen, Hedenius) and associated with gastric ulcer (Key,
Rindfleisch); third, the hemorrhagic infiltration in the walls of
recently-formed ulcers indicates a hemorrhagic origin; fourth, the
funnel-like shape of the ulcer resembles the funnel-shaped area of
distribution of an artery; fifth, gastric ulcers have been
experimentally produced by injecting emboli into the gastric arteries
(Panum, Cohnheim).[96]

[Footnote 96: Pavy, _Philosoph. Trans._, 1763, p. 161; V.
Recklinghausen, _Virchow's Archiv_, Bd. 30, p. 368; Axel Key, _Virchow
und Hirsch's Jahresb._, 1870, Bd. ii. p. 155; Rindfleisch, _Lehrb. d.
path. Gewebelehre_, 5te Aufl., Leipzig, 1878; Panum, _Virchow's
Archiv_, Bd. 25, p. 491; Cohnheim, _Vorles. uber allgem. Path._, Bd.
ii. p. 53, Berlin, 1880.]

The main objections to this view are the infrequency with which the
assumed changes in the blood-vessels have been demonstrated, the common
occurrence of gastric ulcer at an age earlier than that at which
diseases of the blood-vessels are usually present, and the absence of
gastric ulcer in the vast majority of cases of heart disease, with
widespread embolism of different organs of the body. To meet some of
these objections, Klebs[97] presupposes in many cases a local spasmodic
contraction of the gastric arteries, causing temporary interruption of
the circulation; Rindfleisch and Axel Key, compression of the gastric
veins, with resulting hemorrhagic infiltration by spasm of the muscular
coat of the stomach in vomiting and in gastralgic attacks. But these
are pure hypotheses.

[Footnote 97: _Handb. d. path. Anat._, Bd. i. p. 185, Berlin, 1869.]

What is actually known concerning diseases of the gastric blood-vessels
in ulcer of the stomach has already been stated under the morbid
anatomy. From this it may be inferred that the origin of gastric ulcer
in diseased conditions of the blood-vessels has been established only
for a comparatively small group of cases.

Bottcher's[98] view that gastric ulcer is of mycotic origin, being
produced by micrococci, has thus far met with no confirmation.

[Footnote 98: _Dorpater med. Zeitschr._, Bd. v. p. 148, 1874.]

There are those who hold an eclectic view concerning the origin of
gastric ulcer. They believe that ulcer of the stomach may be produced
by a variety of causes, such as inflammation, circulatory disturbances,
irritating substances introduced into the stomach, traumatism, etc. The
peculiarities of the ulcer are due not to any specific cause, but to
the solvent action of the gastric juice, which keeps clean the floor
and the sides of the ulcer. These clean edges and floor, which are
incident to all ulcers of the stomach, justify no conclusion as to the
cause of the ulcer. Engel[99] over thirty years ago held that gastric
ulcer might {514} originate in various ways--that there was nothing
specific about it. Brinton was also of similar opinion.

[Footnote 99: _Prager Vierteljahrschr._, 1853, ii.]

Gastric ulcers have been produced experimentally in animals in a
variety of ways, but these experiments have not materially elucidated
the pathenogenesis of ulcer in man. Schiff by lesions of various parts
of the brain, and later Ebstein by lesions of many parts of the central
and peripheral nervous system by injections of strychnine--in fact,
apparently by any means which greatly increased the
blood-pressure--produced in the stomachs of animals ecchymoses and
ulcers. Muller by ligation of the portal vein, Pavy by ligation of
arteries supplying the stomach, likewise produced hemorrhages and
ulcers. The results of Pavy could not be confirmed by Roth and others.
Panum, and afterward Cohnheim, produced gastric ulcers by introducing
multiple emboli into the gastric arteries. Daettwyler under Quincke's
direction caused, in dogs with gastric fistulae, ulcers of the stomach
by various mechanical, chemical, and thermic irritants applied to the
inner surface of the stomach. Aufrecht observed hemorrhages and ulcers
in the stomachs of rabbits after subcutaneous injections of
cantharidin.[100]

[Footnote 100: Schiff, _De vi motorea baseos encephali_, 1845, p. 41;
Ebstein, _Arch f. exp. Path. u. Pharm._, 1874, p. 183; Muller, _Das
corrosive Geschwur im Magen, etc._, p. 273, Erlangen, 1860; Pavy,
_Guy's Hosp. Rep._, vol. xiii., 1867; Roth, _Virchow's Archiv_, Bd. 45,
p. 300, 1869; Panum, _loc. cit._; Cohnheim, _op. cit._; Daettwyler,
Quincke, _Deutsche med. Wochenschr._, 1882, p. 79; Aufrecht,
_Centralbl. f. d. med. Wiss._, 1882, No. 31.]

The most interesting of these experiments are those of Cohnheim and of
Daettwyler, who demonstrated that in one essential point all of these
experimental ulcers differ from simple gastric ulcer in man--namely, in
the readiness with which they heal. To this ready healing the gastric
juice, much as it has been accused of causing the spread of gastric
ulcers in man, seems to have offered no obstacle. We know that similar
losses of substance in the human stomach heal equally well.[101] Hence
it has been maintained throughout this article that it is unjustifiable
to regard all of the scars found in the human stomach as the result of
simple ulcer.

[Footnote 101: Portions of the mucous membrane of the stomach,
sometimes with some of the submucous coat, have been in several
instances removed with the stomach-pump, but thus far no bad effects
have followed.]

It appears from these experiments, as well as from observations on man,
that it is more difficult to explain why ulcers in the stomach do not
heal than it is to understand how they may be produced. From this point
of view the observation of Daettwyler is of interest, that in dogs
which had been rendered anaemic by repeated abstraction of blood not
only did slighter irritants suffice to produce ulcers of the stomach,
but the ulcers healed much more slowly. Practically, it is important to
learn what are the obstacles to the repair of gastric ulcers, but our
positive knowledge of these is slight. It is probable that such
obstacles are to be found in constitutional causes, such as anaemia and
chlorosis, in abnormal states of the blood-vessels around the ulcer, in
catarrhal affections of the stomach, in irritating articles of food, in
improper modes of living, and in increased acidity of the gastric
juice.

DIAGNOSIS.--In many cases the diagnosis of gastric ulcer can be made
with reasonable certainty; in other cases the diagnosis amounts only to
a suspicion more or less strong, and in still other cases the diagnosis
is impossible.

{515} The diagnostic symptoms are epigastric pain, vomiting, and
gastric hemorrhage. The characteristics of the pain which aid in the
diagnosis are its fixation in one spot in the epigastric region, its
onset soon after eating, its dependence upon the quantity and the
quality of the food, its relief upon the complete expulsion of the
contents of the stomach, its alleviation by changes in posture, and its
increase by pressure. That the pain of gastric ulcer has not always
these characteristics has been mentioned under the Symptomatology.
Vomiting without haematemesis is the least characteristic of these
symptoms. It aids in the diagnosis when it occurs after eating at the
acme of a gastralgic attack and is followed by the relief of pain.
Haematemesis is the most valuable symptom in diagnosis. The more
profuse the hemorrhage and the younger the individual in whom it
occurs, the greater is the probability of gastric ulcer. It should not
be forgotten that the blood is sometimes discharged solely by the
stools.

The simultaneous occurrence of all these symptoms renders the diagnosis
of gastric ulcer easy.[102] In all cases in which gastrorrhagia is
absent the diagnosis is uncertain; but gastric ulcer should be
suspected whenever the ingestion of food is followed persistently by
severe epigastric pain and other causes of the pain have not been
positively determined. When the course of the ulcer is latent and when
the symptoms are only those of dyspepsia, the diagnosis is of course
impossible. In cases previously obscure a diagnosis in extremis is
sometimes made possible by the occurrence of perforation of the
stomach.

[Footnote 102: That even under the most favorable circumstances
absolute certainty in the diagnosis of gastric ulcer is not reached is
illustrated by a case reported with great precision and fulness by
Banti: A female servant, twenty-one years old, had every symptom of
gastric ulcer, including repeated haematemesis and the characteristic
epigastric pain. She was nourished by enemata. She died from an
ulcerative proctitis four days after the last hemorrhage from the
stomach. Only a slight catarrhal inflammation of the stomach was found
at the autopsy, without trace of ulcer, cicatrix, or ecchymosis ("Di un
Caso d'Ematemesi," _La Sperimentale_, Feb., 1880, p. 168). It would
seem as if there must have been an ulcer which had healed so completely
as to leave no recognizable scar.]

In making a differential diagnosis of gastric ulcer, as well as of any
disease, reliance should be placed more upon the whole complexion of
the case than upon any fancied pathognomonic symptoms.

The diseases which are most difficult to distinguish from gastric ulcer
are nervous affections of the stomach. Like gastric ulcer, most of
these are more common in women than in men, and especially in chlorotic
women with disordered menstruation and with hysterical manifestations.
These nervous affections are manifold and their leading characteristics
are not yet well defined. The most important of these affections are
nervous dyspepsia, nervous vomiting, nervous gastralgia, and gastric
crises.

The leading symptoms of nervous dyspepsia, as described by Leube,[103]
are the ordinary symptoms of dyspepsia without evidence of anatomical
alteration of the stomach, and with the proof by washing out the
stomach that the process of digestion is not delayed. Nervous dyspepsia
is often associated with other nervous affections, and is caused
especially by influences which depress the nervous system. Epigastric
pain, and especially tenderness on pressure over the stomach, are not
common symptoms in nervous dyspepsia. Only those rare cases of gastric
ulcer in which hemorrhage from the stomach is absent and epigastric
pain is not prominent {516} are likely to be confounded with nervous
dyspepsia. In such cases, although the diagnosis of nervous dyspepsia
is by far the most probable, the patient may be confined to bed and put
upon the strict regimen for gastric ulcer. If in the course of ten days
or two weeks essential relief is not obtained, ulcer may be excluded,
and the proper treatment for nervous dyspepsia with tonics and
electricity may be adopted (Leube).

[Footnote 103: _Deutches Arch. f. klin. Med._, Dec. 18, 1878.]

In nervous vomiting, which occurs most frequently in hysterical women,
other nervous manifestations are present; there are usually less
epigastric pain and tenderness than in ulcer; the nutrition is better
preserved; the vomiting is less dependent upon the ingestion of food
and more dependent on mental states; and there are longer intervals of
relief than in ulcer. Still, it may be necessary to resort to the
therapeutical diagnosis as in the preceding instance.

In this connection attention may be called to the importance of
searching for reflex causes of vomiting, such as beginning phthisis,
ovarian or uterine disease, cerebral disease, and pregnancy; also to
certain cases of chronic Bright's disease in which gastric disturbances
are the main symptoms.

Of all the nervous affections of the stomach, nervous gastralgia is the
one which presents the greatest similarity to gastric ulcer. Its
diagnosis from gastric ulcer is often extremely difficult, and may be
impossible. The points of difference given in the following table may
aid in the diagnosis:

      NERVOUS GASTRALGIA.         |      ULCER OF THE STOMACH.
                                  |
  1. Pain is often independent of |  1. Pain is mostly dependent upon
  the ingestion of food, and may  |  taking food, and its intensity
  even be relieved by taking food.|  varies with the quality and the
                                  |  quantity of the food.
                                  |
  2. Pain is often relieved by    |  2. Pain is increased by pressure.
  firm pressure.                  |
                                  |
  3. Pain is rarely relieved by   |  3. Pain after a meal is usually
  vomiting.                       |  relieved by vomiting.
                                  |
  4. Fixed point of tenderness and|  4. These are often present.
  of subjective pain not generally|
  present.                        |
                                  |
  5. Relief is usually complete   |  5. Some pain often continues
  between the paroxysms.          |  between the paroxysms.
                                  |
  6. Nutrition frequently well    |  6. Nutrition usually affected.
  preserved.                      |
                                  |
  7. Usually associated with other|  7. Neuropathic states less
  nervous affections, such as     |  constantly present.
  hysteria, neuralgia in other    |
  places, ovarian tenderness, etc.|
                                  |
  8. Benefited less by regulation |  8. Benefited not by electricity,
  of diet than by electricity and |  but by regulation of diet.
  tonic treatment.                |
                                  |
  9. Not followed by dilatation of|  9. Dilatation of stomach may
  stomach.                        |  supervene.

According to Peter,[104] the surface temperature of the epigastrium is
elevated in gastric ulcer, but not in nervous gastralgia.

[Footnote 104: _Gaz. des Hop._, June, 1883.]

Probably not a single one of the points mentioned in the table is
without exception. Nervous gastralgia may be associated with gastric
ulcer, and if the ulcer is otherwise latent the diagnosis is manifestly
impossible. A diagnosis of purely functional gastralgia has been
repeatedly overthrown by the occurrence of profuse haematemesis. There
is no symptom {517} upon which it is more unsatisfactory to base a
diagnosis than upon pain. There is much difference among physicians as
regards the frequency with which they diagnose gastric ulcer in the
class of cases here described. It is probable that the error is
oftenest a too frequent diagnosis of gastric ulcer than the reverse.
Nevertheless, when there is doubt it is well to submit the patient for
a time to the proper treatment for gastric ulcer.

In several instances gastric crises have been mistaken for gastric
ulcer. These gastric or gastralgic crises, as they are called by
Charcot, by whom they have been best described,[105] are most
frequently associated with locomotor ataxia, but they may occur in
connection with other diseases of the spinal cord (subacute myelitis,
general spinal paralysis, and disseminated sclerosis), and an analogous
affection has been described by Leyden[106] as an independent disease
under the name of periodical vomiting with severe gastralgic attacks.
Gastric crises have been most carefully studied as a symptom in the
prodromic stage of locomotor ataxia. The distinguishing features of
these crises are the sudden onset and the atrocious severity of the
gastric pain; the simultaneous occurrence of almost incessant vomiting;
the habitual continuance of the paroxysms, almost without remission,
for two or three days; the normal performance of the gastric functions
in the intervals between the paroxysms, which may be months apart; the
frequent association with other prodromic symptoms of locomotor ataxia,
such as ocular disorders and fulgurating pains in the extremities; and
the development after a time of ataxia. Leyden has observed during the
attacks retraction of the abdomen without tension of the abdominal
walls, obstinate constipation, scanty, dark-colored urine, even anuria
for twenty-four hours, and increased frequency of the pulse (also noted
by Charcot). Vulpian[107] mentions a case in which there was vomiting
of dark-colored blood, and in which naturally the diagnosis of gastric
ulcer had been made. In the autopsies of Leyden and of Charcot no
lesions of the stomach have been found.

[Footnote 105: _Lec. sur les Maladies du Syst. nerveux_, t. ii. p. 32,
Paris, 1877.]

[Footnote 106: _Zeitschr. f. klin. Med._, iv. p. 605, 1882.]

[Footnote 107: _Maladies du Syst. nerveux_, p. 273, Paris, 1879.]

The differential diagnosis of gastric ulcer from gastric cancer will be
considered in the article on GASTRIC CANCER.

It has already been said that a part of the symptoms of gastric ulcer
are due to an associated chronic catarrhal gastritis. Usually other
symptoms are present which render possible the diagnosis of the ulcer.
There is usually some apparent external or internal cause of chronic
catarrhal gastritis, whereas the etiology of ulcer is obscure; in
chronic gastritis gastralgic paroxysms and the peculiar fixed
epigastric pain of gastric ulcer are usually absent; in chronic
gastritis profuse haematemesis is a rare occurrence; and in gastritis
the relief obtained by rest and proper regulation of the diet, although
manifest, is usually less immediate and striking than in most cases of
gastric ulcer.

The passage of gall-stones is usually sufficiently distinguished from
gastric ulcer by the sudden onset and the sudden termination of the
pain, by the situation of the pain to the right of the median line, by
the complete relief in the intervals between the attacks, by the
occurrence of jaundice, by the recognition sometimes of enlargement of
the liver and of the gall-bladder, and by the detection of gall-stones
in the feces.

{518} There is not much danger of confounding abdominal aneurism and
lead colic with gastric ulcer, and the points in their differential
diagnosis are sufficiently apparent to require no description here. The
diagnosis of duodenal ulcer from gastric ulcer will be discussed
elsewhere. The different causes of gastric hemorrhage, a knowledge of
which is essential to the diagnosis of gastric ulcer, will be
considered in the article on HEMORRHAGE FROM THE STOMACH.

PROGNOSIS.--Although a decided majority of simple ulcers of the stomach
cicatrize, nevertheless, in view of the frequently insidious course of
the disease, the sudden perforations, the grave hemorrhages, the
relapses, and the sequels of the disease, the prognosis must be
pronounced serious.

The earlier the ulcer comes under treatment the better the prognosis.
Old ulcers with thickened indurated margins containing altered
blood-vessels naturally heal with greater difficulty than
recently-formed ulcers.

Profuse hemorrhage adds to the gravity of the diagnosis. It usually
indicates that the ulcer has penetrated to the serous coat of the
stomach. A hemorrhage may exert a favorable influence, in so far as to
convince the patient of the necessity of submitting to the repose and
the strict dietetic regimen which the physician prescribes.

The severity of the pain is of little value as a prognostic sign.
Vomiting and dyspepsia, if uncontrolled by regulation of the diet, lead
to a cachectic state which often ends in death.

Little basis as there is to hope for recovery after perforation into
the general peritoneal cavity, there nevertheless have been a very few
cases in which there is reason to believe that recovery has actually
taken place after this occurrence.[108]

[Footnote 108: The most convincing case of recovery after perforation
of gastric ulcer is one reported by Hughes, Ray, and Hilton in _Guy's
Hosp. Rep._, 1846, p. 332. A servant-girl was suddenly seized with all
of the symptoms of perforation. Fortunately, she had eaten nothing for
four hours before the attack, and then only gruel. She was placed at
once under the influence of opium, was kept in the recumbent posture,
and was fed by the rectum. She was discharged apparently cured after
fifty-two days. Two months afterward she was again suddenly seized with
the same symptoms, and she died in fourteen hours. Shortly before the
second perforation she had eaten cherries, strawberries, and
gooseberries, which were found in the peritoneal cavity. The autopsy
showed, in addition to a recent peritonitis, evidences of an old
peritonitis. There were adhesions of the coils of the intestines with
each other and between the stomach and adjacent viscera. In the stomach
were found a cicatrix and two open ulcers, one of which had perforated.

Other cases in which recovery followed after all of the symptoms of
perforation of gastric ulcer were present, but in which no subsequent
autopsy proved the correctness of the diagnosis, have been reported by
Redwood (_Lancet_, May 7, 1870); Ross (_ibid._, Jan. 21, 1871); Tinley
(_ibid._, April 15, 1871); Mancini (_La Sperimentale_, 1876, pp. 551,
665); and G. Johnson (_Brit. Med. Journ._, March 26, 1870).

Frazer's two cases, reported in the _Dublin Hosp. Gaz._, April 15,
1861, are not convincing. The case reported by Aufrecht (_Berl. kl.
Wochenschr._, 1870, No. 21) and the one by Starcke (_Deutsche Klinik_,
1870, No. 39), which are sometimes quoted as examples of recovery, were
cases of circumscribed peritonitis following perforation.

In an interesting case from Nothnagel's clinic reported by Luderitz,
the patient lived sixteen days after perforation into the peritoneal
cavity, followed by all of the symptoms of diffuse perforative
peritonitis. Death resulted from pneumonia secondary to the
peritonitis. At the autopsy were found adhesions over the whole
peritoneal surface and streaks of thickened pus between the coils of
intestine. The perforation in the stomach was closed by the left lobe
of the liver (_Berl. kl. Wochenschr._, 1879, No. 33).]

In estimating the prognosis one should bear in mind the possibility of
relapses; of a continuance of gastric disorders, particularly of
gastralgia, after cicatrization; of the formation of cicatricial
stenosis of {519} the orifices of the stomach; and of the development
of dilatation of the stomach.

After the worst has been said concerning the unfavorable issues of
gastric ulcer, it yet remains true that the essential tendency of the
ulcer when placed under favorable conditions is toward recovery, and
that in many cases the treatment of the disease affords most excellent
results, and is therefore a thankful undertaking for the physician.

TREATMENT.--In the absence of any agent which exerts a direct curative
influence upon gastric ulcer the main indication for treatment is the
removal of all sources of irritation from the ulcer, so that the
process of repair may be impeded as little as possible.

Theoretically, this is best accomplished by giving to the stomach
complete rest and by nourishing the patient by rectal alimentation.
Practically, this method of administering food is attended with many
difficulties, and, moreover, the nutrition of the patient eventually
suffers by persistence in its employment. In most cases the patient can
be more satisfactorily nourished by the stomach, and by proper
selection of the diet, without causing injurious irritation of the
ulcer.

At the beginning of the course of treatment it is often well to
withhold for two or three days all food from the stomach and to resort
to exclusive rectal feeding. In some cases with uncontrollable vomiting
and after-hemorrhage from the stomach it is necessary to feed the
patient exclusively by the rectum.

The substances best adapted for nutritive enemata are
artificially-digested foods, such as Leube's pancreatic meat-emulsion,
his beef-solution, and peptonized milk-gruel as recommended by
Roberts.[109] Beef-tea and eggs, which are often used for this purpose,
are not to be recommended, as the former has very little nutritive
value, and egg albumen is absorbed in but slight amount from the
rectum. Expressed beef-juice may also be used for rectal alimentation.
The peptones, although physiologically best adapted for nutritive
enemata, often irritate the mucous membrane of the rectum, so that they
cannot be retained. It has been proven that it is impossible to
completely nourish a human being by the rectum.[110] Rectal
alimentation can sometimes be advantageously combined with feeding by
the mouth.

[Footnote 109: Leube's pancreatic meat-emulsion is prepared by adding
to 4-8 ounces of scraped and finely-chopped beef l-2-1/2 ounces of
fresh finely-chopped oxen's or pig's pancreas freed from fat. To the
mixture is added a little lukewarm water until the consistence after
stirring is that of thick gruel. The syringe used to inject this
mixture should have a wide opening in the nozzle; Leube has constructed
one for the purpose (Leube, _Deutsches Arch. f. klin. Med._, Bd. x. p.
11).

The milk-gruel is prepared by adding a thick, well-boiled gruel made
from wheaten flour, arrowroot, or some other farinaceous article to an
equal quantity of milk. Just before administration a dessertspoonful of
liquor pancreaticus (Benger) or 5 grains of extractum pancreatis
(Fairchild Bros.), with 20 grains of bicarbonate of soda, are added to
the enema. This may be combined with peptonized beef-tea made according
to Roberts's formula (Roberts, _On the Digestive Ferments_, p. 74,
London, 1881).

Preparatory to beginning the treatment the bowels should be emptied by
a clyster, and this should be occasionally repeated. About three to six
ounces of the tepid nutritive fluid should be slowly injected into the
rectum. The injections may be repeated at intervals of from three to
six hours. If necessary, a few drops of laudanum may be occasionally
added to the enema.]

[Footnote 110: Voit u. Bauer, _Zeitschrift f. Biologie_, Bd. v.]

There is universal agreement that the dietetic treatment of gastric
ulcer is of much greater importance than the medicinal treatment. There
is {520} hardly another disease in which the beneficial effects of
proper regulation of the diet are so apparent as in gastric ulcer.
Those articles of food are most suitable which call into action least
vigorously the secretion of gastric juice and the peristaltic movements
of the stomach, which do not cause abnormal fermentations, which do not
remain a long time in the stomach, and which do not mechanically
irritate the surface of the ulcer. These requirements are met only by a
fluid diet, and are met most satisfactorily by milk and by Leube's
beef-solution.

The efficacy of a milk diet in this disease has been attested by long
and manifold experience. By its adoption in many cases the pain and the
vomiting are relieved, and finally disappear, and the ulcer heals. In
general, fresh milk is well borne. If not, skimmed milk may be
employed. If the digestion of the milk causes acidity, then a small
quantity of bicarbonate of soda or some lime-water (one-fourth to
one-half in bulk) may be added to the milk. Large quantities should not
be taken at once. Four ounces of milk taken every two hours are
generally well borne. Sometimes not more than a tablespoonful can be
taken at a time without causing vomiting, and then of course the milk
should be given at shorter intervals. It is desirable that the patient
should receive at least a quart, and if possible two quarts, during the
twenty-four hours. The milk should be slightly warmed, but in some
cases cold milk may be better retained. In some instances buttermilk
agrees with the patient better than sweet milk. Although many suppose
that they have some idiosyncrasy as regards the digestion of milk, this
idiosyncrasy is more frequently imaginary than real. Still, there are
cases in which milk cannot be retained, even in small quantity.

For such cases peptonized milk often proves serviceable.[111] The
artificial digestion of milk as well as of other articles of food is a
method generally applicable to the treatment of gastric ulcer. The main
objection to peptonized milk is the aversion to it that many patients
acquire on account of its bitter taste. The peptonization should not be
carried beyond a slightly bitter taste. The disagreeable taste may be
improved by the addition of a little Vichy or soda-water. Peptonized
milk has proved to be most valuable in the treatment of gastric ulcer.

[Footnote 111: Milk may be peptonized by adding to a pint of fresh
milk, warmed to a temperature of 100 degrees F., 5 grs. of extract
pancreatis (Fairchild Bros. and Foster) and 20 grs. of bicarb. sodii
dissolved in 4 ounces of tepid water. The mixture is allowed to digest
for about an hour at a temperature of 100 degrees F., which may be
conveniently done by placing the milk in a bowl in a pan of water
maintained at this temperature. It is then boiled, strained, and placed
on ice, or when the milk is to be taken immediately it is better not to
boil it, in order that the partial digestion may continue for a while
under the influence of the pancreatic ferment in the stomach. The milk
without boiling may be kept on ice without further digestion; and this
procedure has the advantage that the pancreatic ferments, although
inactive at a temperature near that of ice, are not destroyed. The
degree of digestion aimed at is indicated by the production of a
slightly, but not unpleasantly, bitter taste. When the digestion is
carried to completion, milk has a very bitter and disagreeable flavor.
Peptonized milk-gruel, mentioned on page 519, may also be employed.]

Leube's beef-solution[112] is a nutritious, unirritating, and
easily-digested article of diet. It can often be taken when milk is not
easily or {521} completely digested, or when milk becomes tiresome and
disagreeable to the patient. It is relied upon mainly by Leube in his
very successful treatment of gastric ulcer. A pot of the beef-solution
(corresponding to a half pound of beef) is to be taken during the
twenty-four hours. A tablespoonful or more may be given at a time in
unsalted or but slightly salted bouillon, to which, if desired, a
little of Liebig's beef-extract may be added to improve the taste. The
bouillon should be absolutely free from fat. Unfortunately, not a few
patients acquire such a distaste for the beef-solution that they cannot
be persuaded to continue its use for any considerable length of time.

[Footnote 112: By means of a high temperature and of hydrochloric acid
the meat enclosed in an air-tight vessel is converted into a fine
emulsion and is partly digested. Its soft consistence, highly
nutritious quality, and easy digestibility render this preparation of
the greatest value. The beef-solution is prepared in New York
satisfactorily by Mettenheimer, druggist, Sixth Avenue and Forty-fifth
street, and by Dr. Rudisch, whose preparation is sold by several
druggists.]

Freshly-expressed beef-juice is also a fairly nutritious food, which
can sometimes be employed with advantage. The juice is rendered more
palatable if it is pressed from scraped or finely-chopped beef which
has been slightly broiled with a little fresh butter and salt. The meat
should, however, remain very rare, and the fat should be carefully
removed from the juice.

To the articles of diet which have been mentioned can sometimes be
added raw or soft-boiled egg in small quantity, and as an addition to
the milk crumbled biscuit or wheaten bread which may be toasted, or
possibly powdered rice or arrowroot or some of the infant farinaceous
foods, such as Nestle's. Milk thickened with powdered cracker does not
coagulate in large masses in the stomach, and is therefore sometimes
better borne than ordinary milk.

For the first two or three weeks at least the patient should be
confined strictly to the bill of fare here given. Nothing should be
left to the discretion of the patient or of his friends. The treatment
should be methodic. It is not enough to direct the patient simply to
take easily-digested food, but precise directions should be given as to
what kind of food is to be taken, how much is to be taken at a time,
how often it is to be taken, and how it is to be prepared.

In all cases of any severity the patient should be treated in bed in
the recumbent posture, and warm fomentations should be kept over the
region of the stomach. Mental and physical fatigue should be avoided.

Usually, at the end of two or three weeks of this diet the patient's
condition is sufficiently improved to allow greater variety in his
food. Meat-broths may be given. Boiled white meat of a young fowl can
now usually be taken, and agreeable dishes can be prepared with milk,
beaten eggs, and farinaceous substances, such as arrowroot, rice,
corn-starch, tapioca, and sago. Boiled sweetbread is also admissible.
Boiled calf's brain and calf's feet are allowed by Leube at this stage
of the treatment.

To these articles can soon be added a very rare beefsteak made from the
soft mass scraped by a blunt instrument from a tenderloin of beef, so
that all coarse and tough fibres are left behind. This may be
superficially broiled with a little fresh butter. Boiled white fish,
particularly cod, may also be tried.

It is especially important to avoid all coarse, mechanically-irritating
food, such as brown bread, wheaten grits, oatmeal, etc.; also fatty
substances, pastry, acids, highly-seasoned food, vegetables, fruit, and
all kinds of spirituous liquor. The juice of oranges and of lemons can
usually be taken. The food should not be taken very hot or very cold.

For at least two or three months the patient should be confined to the
{522} easily-digested articles of diet mentioned. These afford
sufficient variety, and no license should be given to exceed the
dietary prescribed by the physician. Transgression in this respect is
liable to be severely punished by return of the symptoms. When there is
reason to believe that the ulcer is cicatrized, the patient may
gradually resume his usual diet, but often for a long time, and perhaps
for life, he may be compelled to guard his diet very carefully, lest
there should be a return of the disease. Should there be symptoms of a
relapse, the patient should resume at once the easily-digested diet
described above.

Medicinal treatment of gastric ulcer, although less efficacious than
the dietetic treatment, is not to be discarded. Since its advocacy by
Ziemssen the administration of Carlsbad salts or of similarly composed
salts belongs to the systematic treatment of gastric ulcer. The objects
intended to be accomplished by the use of these salts are the daily
evacuation of the contents of the stomach into the intestine by gentle
stimulation of the gastric peristaltic movements, the neutralization of
the acid of the stomach, and the prevention of acid fermentations in
the stomach. Of these objects the most important is the prevention of
stagnation of the contents of the stomach. The chief ingredients of the
Carlsbad waters are sulphate of sodium, carbonate of sodium, and
chloride of sodium. The most important of these ingredients is sulphate
of sodium (Glauber's salts), which by exciting peristalsis propels the
gastric contents into the intestine, and thus relieves the stomach of
its burden, prevents fermentation, and removes from the surface of the
ulcer an important source of irritation. The carbonate of sodium
neutralizes the acids of the stomach, but the main value of this
ingredient and of the chloride of sodium is that in some way they
correct the action of the Glauber's salts, so that the latter may be
taken in smaller quantity and without the usual unpleasant effects of
pure Glauber's salts.[113] The artificial Carlsbad salts are to be
preferred to the natural or the artificial Carlsbad water. The natural
Carlsbad salts and much of those sold as artificial Carlsbad salts
consist almost wholly of sulphate of sodium. It is therefore best to
prescribe in proper proportion the leading ingredients of these salts.
A suitable combination is sulphate of sodium five ounces, bicarbonate
of sodium two ounces, and chloride of sodium one ounce
(Leichtenstern[114]). The relative proportion of the ingredients may of
course be varied somewhat to suit individual cases. The salts are to be
taken daily before breakfast dissolved in a considerable quantity of
warm water. One or two heaping teaspoonfuls of the salts are dissolved
in one-half to one pint of water warmed to a {523} temperature of 95
degrees F. One-fourth of this is to be drunk at a time at intervals of
ten minutes. Breakfast is taken half an hour after the last draught.
After breakfast there should follow one or two loose movements of the
bowels. If this is not the case, the next day the quantity of the salts
is to be increased, or if more movements are produced the quantity is
to be diminished until the desired result is obtained. In case the
salts do not operate, an enema may be used. Usually, to obtain the same
effect, the quantity of salts may be gradually diminished to a
teaspoonful.

[Footnote 113: Water from the Sprudel spring contains in 16 ounces 18.2
grains of sulphate of sodium, 14.6 grains of bicarbonate of sodium, and
7.9 grains of chloride of sodium, and 11.8 cubic inches of carbonic
acid. Its natural temperature is 158 degrees F. The other Carlsbad
springs have the same fixed composition and vary only in temperature
and amount of CO_{2}.]

[Footnote 114: The second edition of the German Pharmacopoeia contains
a formula for making artificial Carlsbad salts, so that the ingredients
are in about the same proportion as in the natural water. The formula
is as follows: Dried sulphate of sodium 44 parts, sulphate of potassium
2 parts, chloride of sodium 18 parts, bicarbonate of sodium 36 parts.
These should be mixed so as to make a white dry powder. The Carlsbad
water is imitated by dissolving 6 grammes of this salt in 1 liter of
water (_Pharmacopoeia Germanica_, editio altera, Berlin, 1882, p. 232).

According to a prescription very commonly used in Germany, the Carlsbad
salts are made by taking sulphate of sodium 50 parts, bicarbonate of
sodium 6 parts, chloride of sodium 3 parts. Dose, a teaspoonful
dissolved in one or two tumblers of warm water (Ewald u. Ludecke,
_Handb. d. Allg. u. spec. Arzneiverordnungslehre_, Berlin, 1883, p.
480).]

The Carlsbad salts are directed especially against the chronic gastric
catarrh which complicates the majority of cases of ulcer of the
stomach. It is well known that the most effective method of treating
this morbid condition is the washing out of the stomach by means of the
stomach-tube. The propriety of adopting this procedure in gastric ulcer
comes, therefore, under consideration. Although the use of the
stomach-tube in gastric ulcer is discarded by Leube and by See on
account of its possible danger, nevertheless this instrument has been
employed with great benefit in many instances of this disease by
Schliep, Debore, and others.[115] No instance of perforation of an
ulcer by means of the stomach-tube has been reported, and in general no
evil effects have resulted; but Duguet cites a case of fatal hemorrhage
following washing out of the stomach.[116] In view of the great benefit
to be secured by washing out the stomach, and of the comparatively
slight danger which attends the process, it seems justifiable to adopt
this procedure cautiously and occasionally in cases of gastric ulcer
with severe gastric catarrh. Of course only the soft rubber tube should
be used, and the siphon process should be adopted.[117] The stomach may
be washed out with pure warm water or with water containing a little
bicarbonate of sodium (one-half drachm to a quart of water). The
occasional cleansing of the stomach in this way can hardly fail to
promote the healing of the ulcer. Recent or threatened hemorrhage from
the stomach would contraindicate the use of the stomach-tube.

[Footnote 115: Schliep, _Deutsch. Arch. f. klin. Med._, Bd. 13; Debore,
_L'Union med._, Dec. 30, 1882; Bianchi, _Gaz. degli Ospitali_, March
26, 1884.]

[Footnote 116: _Gaz. des Hop._, Apr. 29, 1884. In a case of gastric
ulcer of Cornillon severe hemorrhage followed washing out the stomach
(_Le Prog. med._, Apr. 28, 1883).]

[Footnote 117: Soft rubber stomach-tubes are made by Tiemann & Co. in
New York, and are sold by most medical instrument-makers. A description
of the appropriate tube and of the method of its use is given by W. B.
Platt ("The Mechanical Treatment of Diseases of the Stomach," _Maryland
Medical Journal_, March 8, 1884).]

Beyond the measures indicated there is little more to do in the way of
treatment directed toward the repair of the ulcer. Not much, if
anything, is to be expected from the employment of drugs which have
been claimed to exert a specific curative action on the ulcer. Of these
drugs those which have been held in the greatest repute are bismuth and
nitrate of silver. Trousseau[118] devised a somewhat complicated plan
for administering bismuth and nitrate of silver in succession for
several months in the treatment of gastric ulcer. There are few who any
longer cherish any faith in these drugs as curative of gastric ulcer.
The same may be said of other drugs which have been thought to have
similar specific virtue in the treatment of gastric ulcer, such as
acetate of lead, arsenic, chloral hydrate, iodoform, etc.

[Footnote 118: _Clinique medicale_, t. iii. p. 95, Paris, 1865.]

{524} It remains to consider therapeutic measures which may be
necessary to combat individual symptoms of gastric ulcer.

The pain of gastric ulcer is generally relieved in a few days by strict
adherence to the dietetic regimen which has been laid down. When this
is not the case, it may be best to withhold all food from the stomach
and to nourish by the rectum. But this cannot be continued long without
weakening the patient, and sometimes the pain persists in spite of the
rest afforded the stomach. Undoubtedly, the most effective means of
quieting the pain of gastric ulcer is the administration of opium in
some form. Opium should not, however, be resorted to without full
consideration of the possible consequences. When the use of this drug
is once begun, the patient is liable to become dependent upon it, and
may be inclined, consciously or unconsciously, to exaggerate the pain
in order to obtain the narcotic. When prescribing opium in this disease
the physician should have in mind the danger of establishing the opium
habit. Moreover, opium retards digestion, and is anything but an aid to
the proper dietetic regimen, which is all-important. If it is decided
to give opium, it does not matter much in what form it is administered,
but the dose should be as small as will answer the purpose. Hypodermic
injections of morphine over the region of the stomach may be
recommended. Codeia often produces less disturbance than opium or
morphine. A useful powder for the relief of pain is one containing 8 or
10 grains of subnitrate of bismuth, 1/12 grain of sulphate of morphia,
and 1/5 grain of extract of belladonna. Much of the beneficial effect
attributed to bismuth is in reality due to its customary combination
with a small quantity of morphine. Before resorting to opium in cases
of severe pain it will be well to try some of the other means for
relieving the pain of gastric ulcer, although they are less effective.
Gerhardt thinks that astringents are better than narcotics to relieve
the pain of ulcer, and he recommends for the purpose three or four
drops of solution of chloride of iron diluted with a wineglassful of
water, to be taken several times daily. Although this recommendation is
from high authority and is often quoted, sufficient confirmatory
evidence of its value is lacking. Other medicines recommended are
hyoscyamus, belladonna, choral hydrate, chloric ether, hydrocyanic
acid, bismuth, nitrate of silver, and compound kino powder. Sometimes
warm fomentations, at other times a light ice-bag over the epigastrium,
afford marked relief of the pain. Counter-irritation over the region of
the stomach has also given relief. This may be effected with a mustard
plaster or by croton oil. I have known the establishment of a small
nitric-acid issue in the pit of the stomach to relieve the pain, but
such severe measures of counter-irritation are generally unnecessary.
The application of a few leeches over the epigastrium has been highly
recommended, but this should be done without much loss of blood. The
effect of position of the body upon the relief of pain should be
determined. When the pain is due to flatulence or to acid fermentation
in the stomach, the treatment should be directed to those states.

The most effective means of controlling the vomiting in gastric ulcer
are the regulation of the diet and, if necessary, the resort to rectal
alimentation. Absolute rest should be enjoined. Whenever small
quantities of milk, peptonized or in any other form, cannot be
retained, then exclusive rectal feeding may be tried for a while. There
have been cases of gastric {525} ulcer when both the stomach and the
rectum have been intolerant of food. In such desperate cases the
attempt may be made to introduce food into the stomach by means of the
stomach-tube, for it is a singular fact that food introduced in this
way is sometimes retained when everything taken by the mouth is
vomited.[119] The cautious washing out of the stomach by the
stomach-tube may prove beneficial. In these cases the attempt has also
been made to nourish by subcutaneous injections of food. In a case of
gastric ulcer where no food could be retained either by the stomach or
by the rectum Whittaker[120] injected subcutaneously milk,
beef-extract, and warmed cod-liver oil. The oil was best borne. The
injections were continued for four days without food by the mouth or
rectum. The patient recovered. At the best, hypodermic alimentation can
afford but slight nourishment, and is to be regarded only as a last
refuge. If there is danger of death by exhaustion, transfusion may be
resorted to.

[Footnote 119: Debore, _L'Union medicale_, Dec. 30, 1882, and _Gaz. des
Hop._, April 29, 1884. For this reason Debore makes extensive use of
the stomach-tube in general in feeding patients affected with gastric
ulcer. He objects to an exclusive milk diet on account of the quantity
of fluid necessary to nourish the patient, which he says amounts to
three to four quarts of milk daily. To avoid these inconveniences, he
gives three times daily drachm viss of meat-powder and drachm iiss of
bicarbonate of sodium (or equal parts of calcined magnesia and bicarb.
sod.), well stirred into milk. This is to be introduced by the
stomach-tube on account of its disagreeable taste. He believes that the
addition of the large quantity of alkali prevents digestion from
beginning until the food has reached the intestine. He also gives daily
a quart of milk containing grs. xv of saccharate of lime. Debore's
method of preparing the meat-powder is described in _L'Union medicale_,
July 29, 1882, p. 160. He also uses a milk-powder (_ibid._, Dec. 30,
1882; see also _Le Progres med._, July 12, 1884).]

[Footnote 120: J. T. Whittaker, "Hypodermic Alimentation," _The
Clinic_, Jan. 22, 1876.

Bernutz practised successfully in two cases the hypodermic injection of
fresh dog's blood (_Gaz. des Hop._, 1882, No. 64).

Krueg (_Wiener med. Wochenschr._, 1875, No. 34) injected 15 cc. of
olive oil twice a day subcutaneously without causing abscesses.

Menzel and Porco were the first to employ hypodermic alimentation
(_ibid._, 1869, No. 31).]

Of remedies to check vomiting, first in importance are ice swallowed in
small fragments and morphine administered hypodermically. Effervescent
drinks, such as Vichy, soda-water, and iced champagne, may bring
relief. Other remedies which have been recommended are bismuth,
hydrocyanic acid, oxalate of cerium, creasote, iodine, bromide of
potash, calomel in small doses, and ingluvin. But in general it is best
to forego the use of drugs and to rely upon proper regulation of the
diet, such as iced milk taken in teaspoonful doses, and upon repose for
the stomach.

Hemorrhage from the stomach is best treated by absolute rest, the
administration of bits of ice by the mouth, and the application of a
flat, not too heavy, ice-bag over the stomach. The patient should lie
as quietly as possible in the supine position, with light coverings and
in a cool atmosphere. He should be cautioned to make no exertion. His
apprehensions should be quieted so far as possible. All food should be
withheld from the stomach, and for four or five days after the
cessation of profuse hemorrhage aliment should be given only by the
rectum. There is no proof that styptics administered by the mouth have
any control over the hemorrhage, and as they are liable to excite
vomiting they may do harm. Ergotin, dissolved in water (1 part to 10),
may be injected hypodermically in grain doses several times repeated if
necessary. If internal styptics {526} are to be used, perhaps the best
are alum-whey and a combination of gallic acid 10 grains and dilute
sulphuric acid 10 drops diluted with water. Fox praises acetate of
lead, and others ergot, tannin, and Monsell's solution. If there is
vomiting or much restlessness, morphine should be given hypodermically.
If the bleeding is profuse, elastic ligatures may be applied for a
short time around the upper part of one or more extremities, so as to
shut out temporarily from the circulation the blood contained in the
extremity. If syncope threatens, ammonia or a little ether may be
inhaled, or ether may be given hypodermically. Brandy, if administered,
should be given either by the rectum or hypodermically. Caution should
be exercised not to excite too vigorously the force of the circulation,
as the diminished force of the heart is an important agent in checking
hemorrhage. When life is threatened in consequence of the loss of
blood, then recourse may be had to transfusion, but experience has
shown that this act is liable to cause renewed hemorrhage in
consequence of the elevation of the blood-pressure which follows it.
Transfusion is therefore indicated more for the acute anaemia after the
hemorrhage has ceased and is not likely to be renewed. It should not be
employed immediately after profuse haematemesis, unless it is probable
that otherwise the patient will die from the loss of blood, and then it
is well to transfuse only a small quantity.[121]

[Footnote 121: Michel transfused successfully in a case of extreme
anaemia following gastrorrhagia (_Berl. klin. Wochenschr._, 1870, No.
49). In a case of profuse and repeated haematemesis which followed
washing out the stomach Michaelis infused into the veins 350 cc. of
solution of common salt. Reaction gradually followed, and the patient
recovered. This case, which was one of probable ulcer, illustrates the
advantages of infusing a small quantity (_ibid._, June 23, 1884). The
dangers are illustrated by a case reported by V. Hacker, who infused
1500 cc. of salt solution in a patient in a state of extreme collapse
resulting from hemorrhage from gastric ulcer. The patient rallied, but
he died three hours after the infusion from renewed hemorrhage (_Wiener
med. Wochenschr._, 1883, No. 37). In Legroux's case of gastric ulcer
renewed hemorrhage and death followed the transfusion of only 80
grammes of blood (_Arch. gen. de Med._, Nov., 1880). In a case quoted
by Roussel, Leroy transfused 130 grammes of blood in a girl twenty
years old who lay at the point of death from repeated hemorrhages from
a gastric ulcer. In the following night occurred renewed hemorrhage and
death (_Gaz. des Hop._, Sept. 22, 1883). According to the experiments
of Schwartz and V. Ott, the transfusion, or rather infusion, of
physiological salt solution is as useful as that of blood, and it is
simpler and unattended with some of the dangers of blood-transfusion.
The formula is chloride of sodium 6 parts, distilled water 1000.]

Schilling recommends, when the bleeding is so profuse that the
patient's life is threatened, to tampon the stomach by means of a
rubber balloon attached to the end of a soft-rubber stomach-tube.[122]
The external surface of the balloon is slightly oiled. It is introduced
into the stomach in a collapsed state, and after its introduction it is
moderately distended with air. When the balloon is to be withdrawn the
air should be allowed slowly to escape. Schilling tried this procedure
in one case of hemorrhage from gastric ulcer, allowing the inflated bag
to remain in the stomach twelve minutes. The hemorrhage ceased and was
not renewed. Experience only can determine whether this device, to
which there are manifest objections, will prove a valuable addition to
our meagre means of controlling hemorrhage from the stomach.

[Footnote 122: F. Schilling, _Aerztl. Intelligenzbl._, Jan. 8, 1884.
Schreiber, in order to determine the position of the stomach, was the
first to introduce and inflate in this organ a rubber balloon
(_Deutsches Arch. f. klin. Med._, June 5, 1877). Uhler recommends in
case of profuse gastric hemorrhage to pass a rubber bag into the
stomach and fill it with liquid (_Maryland Med. Journ._, Aug. 30, 1884,
p. 347).]

{527} The boldest suggestion ever made for stopping gastric hemorrhage
is that of Rydygier, who advocates in case hemorrhage from an ulcer
threatens to be fatal to cut down upon the stomach, search for the
bleeding ulcer, and then resect it.[123] Notwithstanding the great
advances made in gastric surgery during the last few years, Rydygier's
suggestion seems extravagant and unwarrantable.

[Footnote 123: _Berl. klin. Wochenschr._, Jan. 16, 1882.]

The most effectual treatment of the dyspepsia which is present in many
cases of gastric ulcer is adherence to the dietetic rules which have
been laid down, aided by the administration of Carlsbad salts and
perhaps in extreme cases the occasional and cautious use of the
stomach-tube. If eructations of gas and heartburn are troublesome,
antacids may be employed, but they should be given in small doses and
not frequently, as the ultimate effect of alkalies is to increase the
acid secretion of the stomach and to impair digestion. The best alkali
to use is bicarbonate of sodium, of which a few grains may be taken dry
upon the tongue or dissolved in a little water.

If perforation into the peritoneal cavity occur, then opium or
hypodermic injections of morphine should be given in large doses, as in
peritonitis. Bran poultices sprinkled with laudanum or other warm
fomentations should be applied over the abdomen, although in Germany
ice-bags are preferred. Food should be administered only by the rectum.
The chances of recovery are extremely slight, but the patient's
sufferings are thus relieved. In view of the almost certainly fatal
prognosis of perforation of gastric ulcer into the general peritoneal
cavity, and in view of the success attending various operations
requiring laparotomy, it would seem justifiable in these cases, after
arousing, if possible, the patient from collapse by the administration
of stimulants per rectum or hypodermically, to open the peritoneal
cavity and cleanse it with some tepid antiseptic solution, and then to
treat the perforation in the stomach and the case generally according
to established surgical methods.[124] This would be the more indicated
if it is known that the contents of the stomach at the time of
perforation are not of a bland nature.

[Footnote 124: Mikulicz has successfully treated by laparotomy a case
of purulent peritonitis resulting from perforation of the intestine
with extravasation of the intestinal contents. He says that the
operation is not contraindicated by existing peritonitis if the patient
is not already in a state of collapse or sepsis. The perforation is
closed by sutures after freshening the edges of the opening (abstract
in the _Medical News_, Philada., Sept. 6, 1884). Both Kuh and Rydygier
recommend opening the abdomen after perforation of gastric ulcer. The
borders of the ulcer are to be resected and the opening closed by
sutures (_Volkmann's Samml. klin. Vortrage_, No. 220, p. 12).]

It is important to maintain and to improve the patient's nutrition,
which often becomes greatly impaired from the effects of the ulcer.
This indication is not altogether compatible with the all-important one
of reducing to a minimum the digestive work of the stomach.
Nevertheless, some of the easily-digested articles of food which have
been mentioned are highly nutritious. By means of these and by good
hygienic management the physician should endeavor, without violating
the dietetic laws which have been laid down, to increase, so far as
possible, the strength of his patient. Starvation treatment in itself
is never indicated in gastric ulcer. Inunction of the body with oil is
useful in cases of gastric ulcer, as recommended by Pepper.[125]

[Footnote 125: _North Carolina Medical Journal_, 1880, vol. v. p. 5.]

{528} In view of Daettwyler's experiments, mentioned on page 514, it is
manifestly important to counteract the anaemia of gastric ulcer. Iron,
however, administered by the mouth, disturbs the stomach and is
decidedly contraindicated during the active stage of gastric ulcer.
During convalescence, only the blandest preparations of iron should be
given, and these not too soon, lest they cause a relapse. When the
indication to remove the anaemia is urgent, and especially when the
chlorotic form of anaemia exists, it may be well to try the hypodermic
method of administering iron, although this method has not yet been
made thoroughly satisfactory. Especially for the anaemia of gastric
ulcer would an efficient and unirritating preparation of iron for
hypodermic administration prove a great boon. Probably at present the
best preparation for hypodermic use is the citrate of iron, given in
one- to two-grain doses in a 10 per cent. aqueous solution, which when
used must be clear and not over a month old. The syringe and needle
shortly before using should be washed with carbolic acid. The
injections are best borne when made into the long muscles of the back
or into the nates, as recommended by Lewin for injections of corrosive
sublimate. A slight burning pain is felt for ten minutes after the
injection. This is the method employed by Quincke with good result and
without inflammatory reaction.[126] It is well to remember that
Kobert[127] has found by experiment on animals that large doses of iron
injected subcutaneously cause nephritis. Other preparations of iron
which have been recommended for hypodermic use are ferrum dialysatum
(DaCosta), ferrum pyrophosphoricum cum natr. citrico (Neuss), ferrum
pyrophosphoricum cum ammon. citr. (Huguenin), ferrum peptonatum and
ferrum oleinicum (Rosenthal).[128] When it becomes safe to administer
iron by the stomach, then the blander preparations should be used, such
as the pyrophosphate, lactate, effervescing citrate, ferrum redactum.
Leube recommends the following prescription: Ferr. redact. gr. 80,
Pulv. althaeae gr. 60, Gelatin q. s.; make 90 pills: at first one, and
afterward as many as three, of these pills may be taken three times a
day. When carefully prepared the pills are about as soft as butter.

[Footnote 126: Quincke, _Deutsch. Arch. f. klin. Med._, Bd. xx. p. 27;
Glaenecke, _Arch. f. exper. Path. u. Pharm._, Bd. 17, p. 466.]

[Footnote 127: _Arch. f. exper. Path. u. Pharm._, Bd. 16.]

[Footnote 128: DaCosta, _N.Y. Med. Record_, vol. xiii. p. 290; Neuss,
_Zeitschrift f. klin. Med._, Bd. 3, p. 1; Huguenin, _Correspondenzbl.
f. Schweiz. Aerzte_, 1876, No. 11; Rosenthal, _Wiener med. Presse_,
1878, Nos. 45-49, and 1884, Jan. 20.]

Various sequels of gastric ulcer may require treatment. Cicatrization
of the ulcer is by no means always cure in the clinical sense. As the
result of adhesions and the formation and contraction of cicatricial
tissue very serious disturbances of the functions of the stomach may
follow the repair of gastric ulcer. The most important of these sequels
is stenosis of the orifices of the stomach, particularly of the pyloric
orifice. Very considerable stenosis of the pylorus may be produced
before the ulcer is completely cicatrized. In three instances a
stenosing ulcer of the pylorus has been successfully extirpated.[129]
The most important of these sequels {529} of gastric ulcer will be
treated of hereafter. Here it need only be said that during
convalescence from gastric ulcer attention to diet is all-important.
For a long time the diet should be restricted to easily-digested food.
The first symptoms of relapse are to be met by prompt return to bland
diet, or, if necessary, to rectal alimentation.

[Footnote 129: The successful operators were Rydygier (_Berl. klin.
Wochenschr._, Jan. 16, 1882), Czerny (_Arch. f. klin. Chir._, Bd. xxx.
p. 1), and Van Kleef (_Virchow u. Hirsch's Jahresbericht_, 1882, Bd.
ii. p. 383). Cavazzani cut out by an elliptical incision an old
indurated ulcer of the stomach adherent to the anterior abdominal
walls. The patient died three years afterward of phthisis (_Centralbl.
f. Chir._, 1879, p. 711). Lauenstein resected the pylorus
unsuccessfully for what appears to have been an ulcer of the pylorus
with fibroid induration around it (_ibid._, 1882, No. 9). These four
cases (three successful) are all which I have found recorded of
resection of gastric ulcer. In my opinion the resection of gastric
ulcers which resist all other methods of treatment, and especially
those which cause progressive stricture of the pylorus, is a
justifiable operation.]


Addendum.

Ulcers of the stomach which do not belong to the category of simple
ulcer are for the most part of pathological rather than of clinical
interest.

Although miliary tubercles in the walls of the stomach are more
frequent than is generally supposed, genuine tuberculous ulcers of the
stomach are not common. The most important criterion of these ulcers is
the presence of tuberculous lymphatic glands in the neighborhood, and
of miliary tubercles upon the peritoneum corresponding to the ulcer.
Sometimes miliary tubercles can be discovered in the floor and sides of
the ulcer. Tuberculous gastric ulcers, when they occur, are usually
associated with tuberculous ulceration of the intestine. In an
undoubted case of tuberculous ulcer of the stomach reported by Litten,
however, this was the only ulcer to be found in the digestive
tract.[130] Tuberculous gastric ulcers generally produce no symptoms,
but they have been known to cause perforation of the stomach and
haematemesis. Many cases which have been recorded as tuberculous ulcers
of the stomach were in reality simple ulcers. Cheesy tubercles as large
as a pea, both ulcerated and non-ulcerated, have been found in the
stomach, but they are very rare.

[Footnote 130: Litten, _Virchow's Archiv_, Bd. 67, p. 615.]

Typhoid ulcers may also occur in the stomach, but they are infrequent.
Both perforation of the stomach and gastrorrhagia have been caused by
typhoid ulcers, which, as a rule, however, produce no symptoms
distinctly referable to the ulcer.

Syphilitic ulcers and syphilitic cicatrices of the stomach have been
described, without sufficient proof as to their being syphilitic in
origin.

Necrotic ulcers, probably mycotic in origin, may be found in the
stomach in cases of splenic fever, erysipelas, pyaemia, etc.

Ulceration occurring in toxic, in diphtheritic, and in phlegmonous
gastritis need not be discussed here.

Follicular and catarrhal ulcers of the stomach have been described, but
without sufficient ground for separating them from hemorrhagic erosion
on the one hand and simple ulcer on the other.

Hemorrhagic erosions of the stomach, to which formerly so much
importance was attached, are now believed to be without clinical
significance. They are found very frequently, and often very
abundantly, after death from a great variety of causes.




{530}

CANCER OF THE STOMACH.

BY W. H. WELCH, M.D.


DEFINITION.--Cancer of the stomach is characterized anatomically by the
formation in this organ of a new growth, composed of a
connective-tissue stroma so arranged as to enclose alveoli or spaces
containing cells resembling epithelial cells. The growth extends by
invading the tissues surrounding it, and frequently gives rise to
secondary cancerous deposits in other organs of the body. The forms of
cancer which occur primarily in the stomach are scirrhous, medullary,
colloid, and cylindrical epithelial cancer. The disease develops
usually in advanced life. Rarely latent, occasionally without symptoms
pointing to the stomach as the seat of disease, gastric cancer is
usually attended by the following symptoms: loss of appetite,
indigestion, vomiting with or without admixture with blood, pain, a
tumor in or near the epigastric region, progressive loss of flesh and
strength, and the development of the so-called cancerous cachexia. The
disease is not curable. After its recognition it rarely lasts longer
than from twelve to fifteen months.

SYNONYMS.--Carcinoma ventriculi; Malignant disease of the stomach. Of
the many synonyms for the special forms of cancer, the most common
are--for scirrhous, hard, fibrous; for medullary, encephaloid, soft,
fungoid; for colloid, gelatinous, mucoid, alveolar; and for cylindrical
epithelial, cylindrical-celled or cylindrical or columnar epithelioma,
cylindrical-celled cancroid, destructive adenoma.

HISTORY.--Cancer of the stomach was known to the ancients only by
certain disturbances of the gastric functions which it produces. The
disease itself was not clearly appreciated until its recognition by
post-mortem examinations, which began to be made with some frequency
after the revival of medicine in the sixteenth century. During the
seventeenth and eighteenth centuries several instances of gastric
cancer are recorded, the best described being those observed and
collected by Morgagni (1761). During this period scirrhus was regarded
as the type of cancerous disease. It was a common custom to call only
the ulcerated scirrhous tumors cancerous.

With the awakened interest in pathological anatomy which marked the
beginning of the present century, the gross anatomical characters of
cancer and the main forms of the disease came to be more clearly
recognized. After the description of encephaloid cancer by Laennec[1]
in 1812, {531} and the first clear recognition of colloid cancer by
Otto[2] in 1816, these two forms of cancer took rank with scirrhus as
constituting the varieties of cancer of the stomach as well as of
cancer elsewhere. All that it was possible to accomplish in the
description of cancer of the stomach from a purely gross anatomical
point of view reached its culmination in the great pathological works
of Cruveilhier (1829-35) and of Carswell (1838), both of whom admirably
delineated several specimens of gastric cancer.

[Footnote 1: _Dict. des Sciences med._, t. i. and t. xii., Paris,
1812-15.]

[Footnote 2: Otto, _Seltens Beobachtungen, etc._, 1816.]

During this period of active anatomical research the symptomatology of
gastric cancer was not neglected. The article on cancer by Bayle and
Cayol in the _Dictionnaire des Sciences medicales_, published in 1812,
shows how well the clinical history of gastric cancer was understood at
that period.

Cylindrical-celled epithelioma of the stomach could not be recognized
as a separate form of tumor until the application of the microscope to
the study and classification of tumors--an era introduced by Muller in
1838.[3] Cylindrical-celled epithelioma of the stomach was first
recognized by Reinhardt in 1851, was subsequently described by Bidder
and by Virchow, and received a full and accurate description from
Forster in 1858.[4]

[Footnote 3: _Ueber den feineren Ban, etc., der krankh. Geschwulste_,
Berlin, 1838.]

[Footnote 4: Reinhardt, _Annalen d. Charite_, ii. 1, 1851; Bidder,
_Muller's Archiv_, 1852, p. 178; Virchow, _Gaz. med. de Paris_, April
7, 1855; Forster, _Virchow's Archiv_, Bd. 14, p. 91, 1858.]

Until the publication by Waldeyer[5] in 1867 of his memorable article
on the development of cancers, it was generally accepted that gastric
cancer originated in the submucous coat of the stomach, and that the
cells in the cancerous alveoli were derived from connective-tissue
cells. Waldeyer attempted to establish for the stomach his doctrine
that all cancers are of epithelial origin. In all varieties of gastric
cancer he believed that he could demonstrate the origin of the
cancer-cells from epithelial cells of the gastric tubules--a mode of
origin which had previously been advocated for cylindrical epithelioma
by Cornil[6] (1864). Waldeyer's view has met with marked favor since
its publication, but there are eminent pathologists who have not given
adherence to it in the exclusive form advocated by its author.

[Footnote 5: _Virchow's Archiv_, Bd. 41.]

[Footnote 6: _Journ. de l'Anat. et de la Phys._, 1864.]

It is somewhat remarkable that although in the early part of the
present century several monographs on gastric cancer appeared,[7] all
the more recent contributions to the subject are to be found in theses,
scattered journal articles, and text-books. Of the more recent careful
and extensive articles on cancer of the stomach, those of Lebert and of
Brinton are perhaps most worthy of mention.[8]

[Footnote 7: Chardel, Benech, Daniel, Germain, Prus, Sharpey, Barras,
etc.]

[Footnote 8: Lebert, _Die Krankheiten des Magens_, Tubingen, 1878;
Brinton, _Brit. and For. Med.-Chir. Rev._, 1857.]

ETIOLOGY.--The data for estimating the frequency of gastric cancer are
the clinical statistics of hospitals, series of recorded autopsies, and
mortuary registration reports.

Statistics with reference to this point based exclusively upon the
clinical material of hospitals have only relative value, as they do not
{532} represent in proper proportion both sexes, all ages, all classes
in life, and all diseases. Statistics based upon autopsies surpass all
others in certainty of diagnosis, but they possess in even greater
degree the defects urged against hospital statistics. Not all the fatal
cases in hospitals are examined post-mortem, and gastric cancer is
among the diseases most likely to receive such examination. Hence
estimates of frequency based exclusively upon autopsies are liable to
be excessive. Estimates from mortuary registration reports, and
therefore from the diagnoses given in death-certificates, rest
manifestly upon a very untrustworthy basis as regards diagnosis, but in
other respects they represent the ideal point of view, including, as
these reports do, all causes of death among all classes of persons. It
is evident that in all methods of estimating the frequency of gastric
cancer inhere important sources of error. In general, the larger the
number of cases upon which the estimates rest the less prominent are
the errors. Such estimates as we possess are to be regarded only as
approximate, and subject to revision.

From mortuary statistics Tanchou estimates the frequency of gastric
cancer as compared with that of all causes of death at 0.6 per cent.;
Virchow, at 1.9 per cent.; Wyss, at 2 per cent.; and D'Espine, at 2-1/2
per cent.[9]

[Footnote 9: Tanchou, _Rech. sur le Traitement med. des Tumeurs du
Sein_, Paris, 1844. These statistics, which are based upon an analysis
of 382,851 deaths in the department of the Seine, are necessarily
subject to sources of error, but they do not seem to me to deserve the
harsh criticisms of Lebert and others.

Virchow, _Verhandl. d. phys.-med. Gesellsch. Wurzburg_, 1860, vol. x.
p. 49--analysis of 3390 deaths in Wurzburg during the years 1852-55.

Wyss, quoted by Ebstein in _Volkmann's Samml. klin. Vortrage_, No.
87--analysis of 4800 deaths in Zurich from 1872-74.

D'Espine, _Echo medical_, 1858, vol. ii.--mortuary statistics of the
canton of Geneva, considered to be particularly accurate.]

In 8468 autopsies, chiefly from English hospitals, Brinton[10] found
gastric cancer recorded in 1 per cent. of the cases. Gussenbauer and
Von Winiwarter[11] found gastric cancer recorded in 1-1/2 per cent. of
the 61,287 autopsies in the Pathological Anatomical Institute of the
Vienna University. From an analysis of 11,175 autopsies in Prague, I
find gastric cancer in 3-1/2 per cent. of the cases.[12]

[Footnote 10: _Loc. cit._]

[Footnote 11: _Arch. f. klin. Chirurg._, Bd. xix. p. 372.]

[Footnote 12: Statistics of Dittrich, Engel, Willigk, Wrany, and
Eppinger, in _Prager Vierteljahrschr._, vols. vii., viii., ix., x.,
xii., xiv., xxvii., l., xciv., xcix., and cxiv. Grunfeld found in 1150
autopsies in the general hospital for aged persons in Copenhagen 102
cancers of the stomach, or 9 per cent. (_Schmidt's Jahrb._, Bd. 198, p.
141).]

I have collected and analyzed with reference to this point the
statistics of death from all causes in the city of New York for the
fifteen years from 1868 to 1882, inclusive.[13] I find that of the
444,564 deaths during this period, cancer of the stomach was assigned
as the cause in 1548 cases and cancer of the liver in 867 cases.
Probably at least one-third of the primary cancers of the liver are to
be reckoned as gastric cancers. This would make the ratio of gastric
cancer to all causes of death about 0.4 per cent. This ratio becomes
about 1 per cent. (0.93) if only the deaths from twenty years of age
upward be taken: gastric cancer hardly ever occurs under that age. It
is probably fair to conclude that in New York not over 1 in 200 of the
deaths occurring at all ages and from all causes {533} is due to cancer
of the stomach, and that about 1 in 100 of the deaths from twenty years
of age upward is due to this cause.

[Footnote 13: These statistics are obtained from the records of the
Board of Health of the city of New York. These records are kept with
great care and system.]

The organs most frequently affected with primary cancer are the uterus
and stomach. In order to determine the relative frequency of cancer in
these situations, I have compiled the following table of statistics
from various sources:[14]

    Primary Cancers.           Stomach.        Uterus.
  -------------------------  --------------  --------------
  11,131 in Vienna           10   per cent.  31   per cent.
   7,150 in New York         25.7  "   "     24.2  "   "
   9,118 in Paris (Tanchou)  25.2  "   "     32.8  "   "
   1,378 in Paris (Salle)    31.9  "   "     32    "   "
     587 in Berlin           35.8  "   "     25    "   "
     183 in Wurzburg         34.9  "   "     19    "   "
   1,046 in Prague           37.6  "   "     33.3  "   "
     889 in Geneva           45    "   "     15.6  "   "
  ------                     ----            ----
  31,482 total               21.4 per cent.  29.5 per cent.

From this table it appears that in some collections of cases the uterus
is the most frequent seat of primary cancer, while in other collections
the stomach takes the first rank. If the sum-total of all the cases be
taken, the conclusion would be that about one-fifth of all primary
cancers are seated in the stomach, and somewhat less than one-third in
the uterus. Even if allowance be made for the apparently too low
percentage of cases of gastric cancer in the large Vienna
statistics,[15] I should still be inclined to place the uterus first in
the list of organs most frequently affected with primary cancer, and to
estimate the frequency of gastric cancer compared with that of primary
cancer elsewhere as not over 25 per cent.

[Footnote 14: Vienna cases: Gurlt, _Arch. f. klin. Chir._, Bd. xxv. p.
421--statistical analysis of 16,637 tumors observed in the three large
hospitals of Vienna from 1855 to 1878. New York cases: see preceding
foot-note. Paris cases: Tanchou, _op. cit._, and Salle, _Etiologie de
la Carcinose_, These, Paris, 1877, p. 145 _et seq._--fatal cases in
Paris hospitals, 1861-63. Berlin cases: Lange, _Ueber den Magenkrebs_,
Inaug. Diss., Berlin, 1877--post-mortem material. Wurzburg cases:
Virchow, _loc. cit._, and _Virchow's Archiv_, Bd. 27, p. 430. Prague
cases: reference given above--post-mortem material. Geneva cases:
D'Espine, _loc. cit._]

[Footnote 15: That this percentage is too low is apparent from the fact
that the number of cases of gastric cancer is only twice that of
primary cancer of liver in Gurlt's statistics.]

The liability to gastric cancer seems to be the same in both sexes. Of
2214 cases of gastric cancer which I have collected from hospital
statistics, and which were nearly all confirmed by autopsy, 1233 were
in males and 981 in females.[16] This makes the ratio of males to
females about 5 to 4. This difference is so slight that no importance
can be attached to it, especially in view of the fact that in most
hospitals the males are in excess of the females.

[Footnote 16: My statistics regarding sex are obtained from _Prager
Vierteljahrschr._, vols. xvii., l., xciv., xcix., cxiv.; Lange, _op.
cit._; Katzenellenbogen, _Beitr. zur Statistik d. Magencarcinoms_,
Jena, 1878; Leudet, _Bull. de l'Acad._, t. 29, p. 564; Gussenbauer and
V. Winiwarter, _loc. cit._; Lebert, _op. cit._; Habershon, _Diseases of
Abdomen_, Philada., 1879; and _Ann. d. Stadt. Allg. Krankenh. zu
Munchen_, Bd. i. and ii.

If to these accurate statistics be added collections of cases from
heterogeneous sources, including mortuary statistics (Brinton, Louis,
D'Espine, Virchow, Gurlt, Welch), there results a total of 5426 cases,
with 2843 males and 2583 females, the two sexes being more evenly
represented than in the more exact statistics given in the text. In
this collection of cases Gussenbauer and V. Winiwarter's cases only up
to the year 1855 are included, as the subsequent ones are doubtless in
great part included in Gurlt's statistics. According to Brinton,
gastric cancer is twice as frequent in males as in females.]

{534} The following table gives the age in 2038 cases of gastric cancer
obtained from trustworthy sources and arranged according to
decades:[17]

   Age.       Number of cases.  Per cent.
  ------      ----------------  ---------
  10-20.              2           0.1
  20-30.             55           2.7
  30-40.            271          13.3
  40-50.            499          24.5
  50-60.            620          30.4
  60-70.            428          21
  70-80.            140           6.85
  80-90.             20           1
  90-100.             2           0.1
  Over 100.           1           0.05

From this analysis we may conclude that three-fourths of all gastric
cancers occur between forty and seventy years of age. The absolutely
largest number is found between fifty and sixty years, but, taking into
consideration the number of those living, the liability to gastric
cancer is as great between sixty and seventy years of age.
Nevertheless, the number of cases between thirty and forty years is
considerable, and the occurrence of gastric cancer even between twenty
and thirty is not so exceptional as is often represented, and is by no
means to be ignored. The liability to gastric cancer seems to lessen
after seventy years of age, but here the number of cases and the number
of those living are so small that it is hazardous to draw positive
conclusions.

[Footnote 17: The sources of the statistics for age are--Dittrich
(160), _Prager Vierteljahrschr._, vol. xvii.; D'Espine (117), _loc.
cit._; Virchow (63), _Virchow's Archiv_, Bd. 27, p. 429; Leudet (69),
_loc. cit._; Lange (147), _op. cit._; Katzenellenbogen (60), _op.
cit._; Gussenbauer and Von Winiwarter (493 cases up to 1855), _loc.
cit._; Lebert (314), _op. cit._; Habershon (76), _op. cit._; Gurlt
(455), _loc. cit._; _Trans. N.Y. Path. Soc._, vol. i. (41); and _Trans.
London Path. Soc._, vols. i.-xxxiv. (43). The results correspond
closely to those of the smaller statistics of Brinton and of Lebert.]

Cancer of the stomach in childhood is among the rarest of diseases.
Steiner and Neureutter[18] failed to find a single gastric cancer in
2000 autopsies on children. Cullingworth[19] has reported with
microscopical examination a case of cylindrical-celled epithelioma in a
male infant dying at the age of five weeks; it is probable that the
tumor was congenital. It is not certain whether Wilkinson's[20]
often-quoted case of congenital scirrhus of the pylorus in an infant
five weeks old was a cancer or an instance of simple hypertrophy.
Kaulich[21] cites a case of colloid cancer affecting the stomach,
together with nearly all the abdominal organs, in a child a year and a
half old, but whether the growth in the stomach was primary or
secondary is not mentioned. The case which Widerhofer[22] has reported
as one of cancer of the stomach secondary to cancer of the
retro-peritoneal glands in an infant sixteen days old seems from the
description to be sarcoma. Scheffer[23] has reported a case of large
ulcerated encephaloid cancer of the fundus, involving the spleen, in a
boy fourteen years old. Jackson[24] has reported an interesting case of
encephaloid cancer in a boy fifteen years old in whom no evidence of
disease existed up {535} to ten weeks before death. These cases, which
are all that I have been able to find in children, are to be regarded
as pathological curiosities.[25]

[Footnote 18: _Prager Vierteljahrschr._, vol. lxxxix. p. 77.]

[Footnote 19: _British Med. Journ._, Aug. 25, 1877, p. 253.]

[Footnote 20: _London and Edinburgh Month. Journ. of Med._, 1841, vol.
i. p. 23.]

[Footnote 21: _Prager med. Wochenschr._, 1864, No. 34.]

[Footnote 22: _Jahrb. f. Kinderheilk. Alt. Reihe_, Bd. ii. Heft 4, p.
194.]

[Footnote 23: _Jahrb. f. Kinderheilk._, xv. p. 425, 1880.]

[Footnote 24: J. B. S. Jackson, _Extracts from the Records of the
Boston Society for Medical Improvement_, vol. v., Appendix, p. 109,
Boston, 1867.]

[Footnote 25: Mathien (_Du Cancer precoce de l'Estomac_, Paris, 1884)
has recently analyzed, chiefly from a clinical point of view, 27 cases
of gastric cancer occurring under thirty-four years of age. Of these, 3
were under twenty and 14 were between twenty and thirty years. He also
emphasizes the error of considering cancer of the stomach as
exclusively a disease of advanced life.]

Such statistics as we possess would make it appear that gastric cancer,
as well as cancer in general, is somewhat less common in the United
States than in the greater part of Europe.[26] These statistics,
however, are too inaccurate, and the problems involved in their
interpretation are too complex, to justify us in drawing any positive
conclusions as to this point. It is certain that cancer is not a rare
disease in the United States.

[Footnote 26: Of 1000 deaths in New York in 1882, 19.3 were from
cancer. The statistics on this point from some of the large European
cities are--Geneva, 53 deaths from cancer per mille; Frankfort, 47.6;
Copenhagen, 33.2; Christiania, 29; London, 28.7; Paris, 27; Edinburgh,
25.4; Berlin, 22.4; St. Petersburg, 15; Amsterdam, 12. These statistics
are obtained from the _Forty-fourth Annual Report of the
Registrar-General (for 1881)_, London, 1883; from _Preussische
Statistik_, Heft lxiii., Berlin, 1882; and from _Traite de la
Climatologie medicale_, Paris, 1877-80, by Lombard, in whose excellent
work will be found much information on this subject.

To judge from statistics in this country and in England, the death-rate
from cancer is undergoing a rapid annual increase. Whereas in New York
in 1868 this death-rate was only 12.6 per mille, in 1882 it was 19.3.
In England and Wales in 1858 the deaths from cancer per 1,000,000
persons living were 329, and in 1881 they were 520. It seems probable,
as suggested in the above report of the Registrar-General, that this
apparently increasing large death-rate is due to increased accuracy in
diagnosis. It may be also that decrease in infant mortality and
prolongation of life by improved sanitary regulations may account in
part for this increase. From this point of view Dunn makes the
paradoxical statement that the cancer-rate of a country may be accepted
as an index of its healthfulness (_Brit. Med. Journ._, 1883, i.).]

It is said on good authority that in Egypt and Turkey gastric cancer
and other forms of cancer are infrequent.[27] A similar infrequency has
been claimed for South America, the Indies, and in general for tropical
and subtropical countries; but all of these statements as to the
geographical distribution of cancer are to be accepted with great
reserve, as they do not rest upon sufficient statistical information.

[Footnote 27: Hirsch, _Handb. d. Historisch-geographische Pathologie_,
Bd. ii. p. 379, Erlangen, 1862-64.]

I have analyzed the frequency of gastric cancer among negroes upon a
basis of 7518 deaths among this race in New York, and I find the
proportion of deaths from this cause about one-third less than among
white persons.[28] It has been stated that cancer is an extremely rare
disease among negroes in Africa.[29] The admixture with white blood
makes it difficult to determine to what degree pure negroes in this
country are subject to cancer.

[Footnote 28: According to the Ninth Census Report of the United
States, in the census year 1870 the deaths from cancer among white
persons were 13.7 per mille, and among colored persons only 5.7 per
mille; but it is well known that the registration returns upon which
the vital statistics in these reports are based are very incomplete and
unsatisfactory.]

[Footnote 29: Bordier, _La Geographie medicale_, Paris, 1884, p. 464.
Livingstone speaks of the infrequency of cancer among the negroes in
Africa.]

The question as to what role is played by heredity in the causation of
gastric cancer belongs to the etiological study of cancer in general.
Probably in about 14 per cent. of the cases of cancer it can be
determined that other members of the family are or have been affected
with the disease.[30] {536} The influence of inheritance, therefore, is
apparent only in a comparatively small minority of the cases. As
suggested long ago by Matthew Baillie, this hereditary influence is
better interpreted as in favor of a local predisposition (embryonic
abnormality?) in the organ or part affected than in favor of the
inheritance of a cancerous diathesis. It has been claimed by D'Espine,
Paget, and others that cancer develops at an earlier age when there is
a family history of the disease than when such history is absent.

[Footnote 30: This statement is based upon the collection of 1744 cases
of cancer analyzed with reference to this question. Of these, a family
history of cancer was determined in 243 cases. The cases are obtained
from statistics of Paget and Baker, Sibley, Moore, Cooke, Lebert,
Lafond, Hess, Leichtenstern, Von Winiwarter, and Oldekop. There is
extraordinary variation in the conclusions of different observers upon
this point. Velpeau asserted that he could trace hereditary taint in 1
in 3 cancerous subjects; Paget, in 1 in 4; Cripps, in 1 in 28. My
conclusions agree with those obtained at the London Cancer Hospital
(Cooke, _On Cancer_, p. 11, London, 1865).

The most remarkable instance of inherited cancer on record is reported
by Broca (_Traite des Tumeurs_, vol. i. p. 151, Paris, 1866): 15 out of
26 descendants over thirty years of age of a woman who died in 1788 of
cancer of the breast were likewise affected with cancer. As is well
known, Napoleon the First, his father, and his sister died of cancer of
the stomach.]

It may be considered established that cancer sometimes develops in a
simple ulcer of the stomach, either open or cicatrized. It is most
likely to develop in large and deep ulcers with thickened edges, where
complete closure by cicatrization is very difficult or impossible. It
is difficult to prove anatomically that a gastric cancer has developed
from an ulcer, and hence such statements as that of Eppinger, that in
11.4 per cent. of cancers of the stomach this mode of development
existed, are of no especial value.[31] No etiological importance can be
attached to the occasional association of cancer with open or
cicatrized simple ulcers in different parts of the same stomach. Of the
comparatively few cases in which strict anatomical proof has been
brought of the origin of cancer in simple gastric ulcer, probably the
most carefully investigated and conclusive is one studied and reported
by Hauser.[32] It is, however, by no means proven that Hauser's view is
correct, that cancer develops from the atypical epithelial growths
often to be found in the cicatricial tissue of gastric ulcer. In a few
instances both the clinical history and the anatomical appearances
speak decisively for the development of cancer in a simple gastric
ulcer;[33] and the establishment of this fact is of clinical
importance.

[Footnote 31: _Prager Vierteljahrschr._, vol. cxiv.]

[Footnote 32: _Das chronische Maqengeschwur_, Leipzig, 1883, p. 61. See
also Heitler, "Entwicklung von Krebs auf narbigen Grunde in Magen,"
_Wien. med. Wochenschr._, 1883, p. 961. It seems to me that at present
there is a tendency to exaggerate the frequency with which cancer
develops from gastric ulcer.]

[Footnote 33: A particularly satisfactory case of this kind is reported
by Lebert, _op. cit._, p. 503.]

Many other factors in the causation of gastric cancer have been
alleged, but without proof of their efficacy. This is true of chronic
gastritis, which was once thought to be an important cause of gastric
cancer, and is even recently admitted by Leube to be of influence.[34]
Certainly the majority of cases of cancer of the stomach are not
preceded by symptoms of chronic gastritis. Although in a few instances
gastric cancer has followed an injury in the region of the stomach,
there is no reason to suppose that this was more than a coincidence.

[Footnote 34: In _Ziemssen's Handb. d. spec. Path. u. Therap._, Bd.
vii. p. 134, Leipzig, 1878.]

Few, if any, at present believe that depressing emotions, such as
grief, anxiety, disappointment, which were once considered important
causes of cancer, exert any such influence. Cancer of the stomach
occurs as {537} frequently in those of strong as in those of weak
constitution--as often among the temperate as among the intemperate.
If, as has been claimed (D'Espine), gastric cancer is relatively more
frequent among the rich than among the poor, this is probably due only
to the fact that a larger number of those in favorable conditions of
life attain the age at which there is greatest liability to this
disease. No previous condition of constitution, no previous disease, no
occupation, no station in life, can be said to exert any causative
influence in the production of gastric cancer.

It will be observed that the obscurity which surrounds the ultimate
causation of gastric cancer is in no way cleared up by the points which
have been here considered and which are usually considered under the
head of etiology. It is impossible to avoid the assumption of an
individual--and in my opinion a local--predisposition to gastric
cancer, vague as this assumption appears. All other supposed causes are
at the most merely occasional or exciting causes. The attempts to
explain in what this predisposition consists are of a speculative
nature, and will be briefly considered in connection with the
pathenogenesis of gastric cancer.

SYMPTOMATOLOGY.--We may distinguish the following groups of cases of
gastric cancer:

First: Latent cases, in which the cancer of the stomach has produced no
symptoms up to the time of death. Many secondary cancers of the stomach
belong to this class. Here also belong cases in which a cancer is found
unexpectedly in the stomach when death has resulted from other causes.
I have found a medullary cancer, slightly ulcerated, as large as a
hen's egg, seated upon the posterior wall and lesser curvature of the
stomach of a laboring man suddenly killed while in apparent health and
without previous complaint of gastric disturbance. These cases, in
which life is cut short before any manifestation of the disease, are
without clinical significance, save to indicate how fallacious it is to
estimate the duration of the cancerous growth from the first appearance
of the symptoms.

Second: Cases in which gastric symptoms are absent or insignificant,
whereas symptoms of general marasmus or of progressive anaemia or of
cachectic dropsy are prominent. Cases of this class are frequently
mistaken for pernicious anaemia, and occasionally for Bright's disease,
heart disease, or phthisis. It is difficult to explain in these cases
the tolerance of the stomach for the cancerous growth, but this
tolerance is most frequently manifested when the tumor does not invade
the orifices of the organ.

Third: Cases in which the symptoms of the primary gastric cancer are
insignificant, but the symptoms of secondary cancer, particularly of
cancer of the liver or of the peritoneum, predominate. In some, but not
in all, of these cases the primary growth is small or has spared the
orifices of the stomach.

Fourth: Cases in which the symptoms point to some disease of the
stomach, or at least to some abdominal disease; but the absence of
characteristic symptoms renders the diagnosis of gastric cancer
impossible or only conjectural.

Fifth: Typical cases in which symptoms sufficiently characteristic of
{538} gastric cancer are present, so that the diagnosis can be made
with reasonable positiveness.

It is not to be understood that these groups represent sharply-drawn
types of the disease. It often happens that the same case may present
at one period the features of one group, and at another period those of
another group. Nor is it supposed that every exceptional and erratic
case of gastric cancer can be classified in any of the groups which
have been mentioned.[35]

[Footnote 35: In the thesis of Chesnel may be found many curious
clinical disguises which may be assumed by cancer of the stomach, such
as simulation of Bright's disease, heart disease, phthisis, chronic
bronchitis, cirrhosis of the liver, etc. (_Etude clinique sur le Cancer
latent de l'Estomac_, Paris, 1877). Layman (_Med. Annals Albany_, 1883,
p. 207) reports a case of gastric cancer in which extra-uterine
foetation was suspected.]

A typical case of gastric cancer runs a course about as follows: A
person, usually beyond middle age, begins to suffer from disordered
digestion. His appetite is impaired, and a sense of uneasiness,
increasing in course of time to actual pain, is felt in the stomach.
These symptoms of dyspepsia are in no way peculiar, and probably at
first occasion little anxiety. It is, however, soon observed that the
patient is losing flesh and strength more rapidly than can be explained
by simple indigestion. He becomes depressed in spirits. The bowels are
constipated. Vomiting, which was usually absent at first, makes its
appearance and becomes more and more frequent. After a while it may be
that, without any improvement, the vomiting becomes less frequent,
comes on longer after a meal, but is more copious. In the later periods
of the disease a substance resembling coffee-grounds and consisting of
altered blood is often mingled with the vomit. By this time the patient
has assumed a cachectic look. He is wasted, and his complexion has the
peculiar pale yellowish tint of malignant disease. Perhaps there is a
little oedematous pitting about the ankles. During the progress of the
disease in the majority of cases an irregular hard tumor can be felt in
the epigastrium. While one or another of the symptoms may abate in
severity, the general progress of the disease is relentlessly downward.
Within six months to two years of the onset of the symptoms the patient
dies of exhaustion.

Too much stress should not be laid upon any so-called typical course of
gastric cancer. This course is modified by many circumstances, such as
the situation of the cancer, its size, its rapidity of growth, the
presence or absence of ulceration, the existence or non-existence of
secondary tumors, the presence of complications, and the individuality
of the patient. It is necessary, therefore, to consider in detail each
of the important symptoms of gastric cancer. But in thus fixing
attention upon individual symptoms one must not lose sight of the
clinical picture as a whole. It is not any single symptom which is
decisive; it is rather the combination, the mode of onset, and the
course of the symptoms, which are of most importance in diagnosis.

Impairment of the appetite is the rule in gastric cancer. Anorexia is
sometimes a marked symptom before pain, vomiting, and other evidences
of gastric indigestion are noted. There is often a special distaste for
meat. The appetite may be capricious; it is very rarely even increased.
There are exceptional cases in which the appetite is preserved
throughout the greater part or even the whole course of the disease.
This seems to {539} be more frequent with cancer of the cardia than
with cancer of other parts of the stomach. Loss of appetite is a much
more common symptom in gastric cancer than in gastric ulcer. In cancer,
as well as in ulcer, the patient sometimes refrains from food less on
account of disrelish for it than on account of the distress which it
causes him.

Pain is one of the most frequent symptoms of cancer of the stomach. If
the pain begins early in the disease, and continues, as it often does,
with increasing severity, it renders gastric cancer one of the most
distressing affections. The pain is usually felt in the epigastrium,
but it may be more intense in the hypochondria. It is sometimes felt in
the interscapular region, the shoulders, or even in the loins.[36] With
cancer of the cardia it is often referred to the point of the xiphoid
cartilage or behind the sternum. In general, however, there is so
little correspondence between the site of the cancer and the exact
locality of the pain that no weight can be attached to the situation of
the pain in diagnosing the region of the stomach involved in the
growth. Nor does any import attach to the quality of the pain, whether
it is described as burning, gnawing, dull, lancinating, etc. Severe
gastralgic paroxysms occur, although less frequently than in gastric
ulcer.

[Footnote 36: The pain in cases of gastric cancer may be felt in parts
of the body remote from the stomach. Thus, in a case of cancer of the
cardia reported by Minot the pain was felt, not in the epigastrium, but
in the left shoulder, the back of the neck, and the pharynx. In several
instances the pain has been interpreted as of renal origin. In a case
of gastric cancer reported by Palmer each attack of vomiting was
invariably preceded by pain in the middle of the shaft of the left
humerus (_Extr. fr. the Records of the Boston Soc. for Med.
Improvement_, vol. iv. p. 217).]

The pain is usually aggravated by ingestion of food, although it may
not become severe until the process of digestion is far advanced. Pain,
however, occurs independently of taking food, and is occasionally a
marked symptom when there are no evidences of dyspepsia. There can be
no doubt that the cancer, as such, produces pain by involvement of the
nerves of the stomach, but there is no specific cancerous pain, such as
has been described by Brinton and other writers. There is usually
tenderness on pressure over the stomach, and this tenderness is often
over the tumor, if such can be felt.

In general, it may be said that the pain of gastric cancer, as
contrasted with that of simple gastric ulcer, is often less dependent
upon taking food, less intense, less circumscribed, less paroxysmal,
less often relieved by vomiting; but there is so little constancy about
any of these points that no reliance is to be placed upon any
peculiarity of the pain in the diagnosis of gastric cancer.

The observation of several cases of gastric cancer without pain as a
marked symptom leads me to emphasize the fact that absence or trifling
severity of pain throughout the greater part or the whole of the
disease, although exceptional, is not extremely rare. The frequency of
painless gastric cancers is given by Lebert as 25 per cent., and by
Brinton as 8 per cent., of the whole number. For many reasons,
numerical computations as to the frequency of this and of other
symptoms of gastric cancer are of very limited value.[37] Absence of
pain is more common in {540} gastric cancers of old persons and in
cancers not involving the orifices of the stomach than it is at an
earlier period of life or when the gastric orifices are obstructed.

[Footnote 37: Gastric cancer cannot be considered as a disease with
uniform characters. It is irrational to group together cancers of the
pylorus, of the cardia, of the fundus, of the curvatures, cancers hard
and soft, ulcerated and not ulcerated, infiltrating and circumscribed,
and to say that pain or vomiting is present in so-and-so many cases of
cancer of the stomach. There is not a sufficient number of recorded
cases in which the symptoms are fully described with reference to the
peculiarities of the growth to enable us to apply to gastric cancer the
numerical method of clinical study with valuable results. The great
discrepancy between Lebert's and Brinton's statistics as to the
frequency of painless cancers of the stomach illustrates the present
inadequacy of the numerical method, which is misleading in so far as it
gives a false appearance of exactness.]

The functions of the stomach are almost invariably disordered in
gastric cancer. Sometimes, especially in the early stages, this
disorder is only moderate, and is manifested by the milder symptoms of
indigestion, such as uneasy sensations of weight and fulness after a
meal, nausea, flatulent distension of the stomach relieved by
eructation of gases, and heartburn. With the progress of the disease
the uneasy sensations become actually painful; watery fluids, and
sometimes offensive acrid fluids and gases, are regurgitated; and
nausea culminates in vomiting. The breath is often very fetid. The
eructation of inflammable gases has been observed in a few cases.

The most troublesome symptoms of indigestion occur with those cancers
which by obstructing the pyloric orifice lead to dilatation of the
stomach. Cases of gastric cancer in which the distressing symptoms of
dilatation of the stomach dominate the clinical history are frequent.
These symptoms are in no way peculiar to cancer of the stomach, but
belong to dilatation produced by pyloric stenosis from whatever cause,
and will be described in the article on DILATATION OF THE STOMACH.

Various causes combine to impair the normal performance of the gastric
functions in cancer of the stomach. Chronic catarrhal gastritis is a
factor in not a few cases. The destruction by the cancer of a certain
amount of secreting surface can be adduced as a sufficient cause only
in exceptional cases of extensive cancerous infiltration. Of more
importance is interference with the peristaltic movements of the
stomach, particularly in the pyloric region, where the cancer is most
frequently situated. As already mentioned, dilatation of the stomach is
a most important cause of indigestion in many cases. Of great interest
in this connection is the discovery by Von den Velden[38] that as a
rule (to which there are exceptions) the gastric juice in cases of
dilatation of the stomach due to cancer contains no free hydrochloric
acid, and that this gastric juice has comparatively feeble digestive
power, as proven by experiments. As this alteration of the gastric
juice interferes particularly with the digestion of albuminous
substances, it is explicable why many patients with gastric cancer have
an especial abhorrence for meat.

[Footnote 38: _Deutsches Arch. f. kl. Med._, Bd. 23, p. 369.]

During the progress of the disease the dyspeptic symptoms may improve,
but this improvement is usually only temporary. In exceptional cases of
gastric cancer dyspeptic symptoms, as well as other gastric symptoms,
may be absent or not sufficiently marked to attract attention.

Hiccough, sometimes very troublesome, has been observed not very
infrequently during the later periods of the disease.

There is nothing noteworthy about the appearance of the tongue, which
is often clean and moist, but may be furred or abnormally red and dry.
In the cachectic stage, toward the end of the disease, aphthous patches
{541} often appear on the tongue and buccal mucous membrane. An
increased flow of saliva has been occasionally observed in gastric
cancer as well as in other diseases of the stomach. Thirst is present
when there is profuse vomiting.

Vomiting usually appears after other symptoms of indigestion have been
present for some time. It may, however, be one of the earliest symptoms
of the disease. At first of occasional occurrence, it increases in
frequency until in some cases it becomes the most prominent of all
symptoms. Vomiting may occur in paroxysms which last for several days
or weeks, and then this symptom may improve, perhaps to be renewed
again and again, with remissions of comparative comfort. There are rare
cases of gastric cancer in which the first symptom to attract attention
is uncontrollable vomiting, accompanied often with pain and rapid
emaciation. Such cases may run so acute a course that a fatal
termination is reached within one to two months.[39] In these cases,
which have been interpreted as acutely-developed gastric cancers, it is
probable that the cancer has remained latent for weeks or months before
it gave rise to marked symptoms.

[Footnote 39: For example, Andral relates a case in which death took
place thirty-seven days after the onset of the symptoms, these being
obstinate vomiting, severe gastralgic paroxysms, marasmus, and, about
ten days before death, profuse black vomit. There was found a fungoid
tumor the size of a hen's egg projecting into the cavity of the stomach
near the pylorus. In this situation the walls of the stomach were
greatly thickened by colloid growth (_Arch. gen. de Med._, June, 1823).
Here may also be mentioned the fact that in several instances pregnancy
has been complicated with gastric cancer. Here the uncontrollable
vomiting which often exists has been referred to the pregnancy, and has
led to the production of premature labor.]

The situation of the cancer exerts great influence upon the frequency
of vomiting and the time of its occurrence after meals. When the cancer
involves the pyloric orifice, vomiting is rarely absent, and generally
occurs an hour or more after a meal. As this is the most frequent
situation of the cancer, it has been accepted as a general rule that
vomiting occurs at a longer interval after eating in cases of gastric
cancer than in cases of simple ulcer. But even with pyloric cancer the
vomiting may come on almost immediately after taking food, so that it
is not safe to diagnose the position of the cancer by the length of
time between eating and the occurrence of vomiting. As the cancer in
its growth obstructs more and more the pyloric orifice, the vomiting
acquires the peculiarities of that accompanying dilatation of the
stomach. The vomiting comes on longer after a meal--sometimes not until
twelve or twenty hours or even more have elapsed. It may be that
several days elapse between the acts of vomiting, which then present a
certain periodicity. The patient then vomits enormous quantities
containing undigested food, mucus, sarcinae, and gaseous and other
products of fermentation. Sometimes, especially toward the end of the
disease, the vomiting ceases altogether. This cessation has been
attributed to reopening of the pyloric orifice by sloughing of the
growth. It is not necessary to assume such an occurrence, as a similar
cessation of vomiting sometimes occurs in dilatation of the stomach due
to persistent stenosis of the pylorus. Cessation of vomiting in these
cases is by no means always a favorable symptom.

Next to pyloric cancer, it is cancer involving the cardiac orifice
which is most frequently accompanied by vomiting. Here the vomiting
occurs often immediately after taking food, but there are exceptions to
this rule. {542} If in consequence of stenosis of the cardiac orifice
the food does not enter the stomach, it is shortly regurgitated
unchanged or mingled simply with mucus. It is this regurgitation rather
than actual vomiting which in most common and characteristic of cardiac
cancer. Even in cases in which the passage of an oesophageal sound
reveals no obstruction at the cardiac orifice it sometimes happens that
food, including even liquids, is regurgitated almost immediately, as in
a case reported by Ebstein in which cold water was returned at once
after swallowing.[40] In these cases Ebstein with great plausibility
refers the regurgitation to reflex spasm of the oesophagus induced by
irritation of a cancer at or near the cardia through contact of food or
liquids, especially when cold, with its surface.

[Footnote 40: "Ueber den Magenkrebs," _Volkmann's Samml. klin.
Vortrage_, No. 87, p. 21.]

When the cancer is seated in other parts of the stomach and it does not
obstruct the orifices, vomiting is more frequently absent or of only
rare occurrence. Vomiting is absent, according to Lebert, in one-fifth,
according to Brinton in about one-eighth, of the cases of gastric
cancer. Absence of vomiting is sufficiently frequent in gastric cancer
to guard one against excluding the diagnosis of this disease on this
ground alone.

Although in many cases the vomiting of gastric cancer can be explained
on mechanical grounds by stenosis of the orifices, this is an
explanation not applicable to all cases. Mention has already been made
of spasm of the oesophagus as a cause of regurgitation of food in some
cases of cardiac cancer. A similar spasm of the muscle in the pyloric
region may explain the vomiting in certain cases in which during life
there were symptoms of pyloric stenosis, but after death no or slight
stenosis can be found. There is reason also to believe that atony of
the muscular coats of the stomach may cause stagnation of the contents
of the stomach and dilatation of the organ. In exceptional cases of
gastric cancer in which the stomach is so intolerant as to reject food
almost immediately after its entrance a special irritability of the
nerves of the stomach must be assumed. It is customary to refer this
form of vomiting to irritation of the ulcerated surface of the cancer
by analogy with a similar irritability of the stomach observed in some
cases of simple gastric ulcer. But there is little analogy between the
ulcerated surface of a cancer in which tissues of little vitality and
irritability are exposed and the surface of a simple ulcer in which the
normal or slightly altered tissues of the stomach are laid bare.
Finally, in the existence of chronic catarrhal gastritis is to be found
another cause of vomiting in many cases of gastric cancer.

The presence of fragments of the cancer in the contents removed by
washing out the stomach with the stomach-tube has been observed by
Rosenbach[41] in three cases of gastric cancer, and utilized for
diagnostic purposes. A cancerous structure could be made out in these
fragments by the aid of the microscope. Hitherto, the presence of
particles of the tumor in the vomited matter has been considered as
hardly more than a curiosity, and I have not been able to find a
well-authenticated instance in which such particles in the vomit have
been recognized by microscopical examination. According to Rosenbach,
the fragments of the tumor in the washings from the stomach can be
recognized by the naked eye by the red, reddish-brown, or black specks
on their surface, due to recent or old hemorrhages which have aided in
the detachment of the fragments. {543} By this means such particles are
distinguished macroscopically from bits of food. By employing
soft-rubber tubes and the syphon process there is no danger, in washing
out of the stomach, of detaching pieces of the normal mucous membrane,
which, moreover, can be distinguished from the fragments of the tumor
by the aid of the microscope and usually by the naked eye. It remains
to be seen how frequently such fragments of the tumor are to be found
in the fluids obtained by washing out the stomach. It is not probable
that they will be found so often as Rosenbach anticipates. According to
the experience of most observers, they are very rarely present. They
would naturally be most readily detached from soft, fungoid, and
ulcerating cancerous growths. In this connection may also be mentioned
the occasional separation of bits of the tumor by the passage of the
stomach-tube in cases of cancer of the cardia. The eye of the tube as
well as the washings from the stomach should be carefully examined for
such particles.

[Footnote 41: _Deutsche med. Wochenschr._, 1882, p. 452.]

The habitual absence of free hydrochloric acid in the gastric fluids in
dilatation of the stomach due to carcinoma of this organ was noted by
Von der Velden.[42] He found in eight cases of dilatation due to cancer
of the pylorus that the fluids removed by the stomach-pump were free
from hydrochloric acid, whereas in ten cases of dilatation due to other
causes, such as cicatrized simple ulcer of the pylorus, free
hydrochloric acid was only temporarily absent from the gastric juice.
Von der Velden therefore attributes to the presence or the absence of
free hydrochloric acid in the gastric juice in these cases great
diagnostic importance. The observations which have followed Von der
Velden's publication are not yet sufficient to justify us in drawing
positive conclusions in this matter. Recently, Kredel[43] has reported
from Riegel's clinic seventeen cases of simple dilatation in which free
hydrochloric acid was only exceptionally and temporarily absent from
the gastric fluids, and nineteen cases of cancerous dilatation in
which, with very rare exceptions, free hydrochloric acid was
continuously absent. Cases, however, have been observed by Ewald,
Seeman, and others in which free hydrochloric acid has been found in
stomachs dilated from gastric cancer. It is to be noted that free
hydrochloric acid is absent from the stomach in other conditions than
in gastrectasia due to cancer; of which conditions the most important
are fever, amyloid degeneration of the stomach (Edinger), and some
cases of gastric catarrh. Free hydrochloric acid is also usually absent
during the first twenty minutes to an hour after a meal. We have not
sufficient information as to the presence or absence of free
hydrochloric acid in cases of gastric cancer without dilatation of the
stomach. To Von der Velden's symptom no pathognomonic value can be
attached, but it may prove, in connection with other symptoms, an aid
in diagnosis. The presumption is against gastric cancer if free
hydrochloric acid be found continuously in a dilated stomach. Less
importance can be attached to the absence of free hydrochloric acid
unless the observations extend over several weeks and fever and amyloid
degeneration are excluded.

[Footnote 42: _Deutsches Arch. f. klin. Med._, Bd. 23, p. 369, 1879.]

[Footnote 43: _Zeitschrift f. klin. Med._, Bd. 6, p. 592, 1884.]

The tests for free hydrochloric acid are most satisfactorily applied to
the fluids withdrawn by the stomach-pump. After a sufficient quantity
for examination has been withdrawn the syphon process may be {544}
substituted. Tests may also be applied to vomited material, although
here the admixture of secretions from the nose, mouth, and throat may
render the results less conclusive. Edinger's method of swallowing bits
of sponge enclosed in gelatin capsules and attached to a string, by
which they can be withdrawn, may also be employed. The sponge should be
free from sand, deprived of alkaline carbonates by hydrochloric acid,
and rendered perfectly neutral by washing in distilled water.

For clinical purposes the most convenient tests are those which depend
upon certain changes in color produced in reagents which enable us to
distinguish inorganic from organic acids. In the gastric juice the only
inorganic acid which comes into consideration is hydrochloric acid, and
the most important organic acid is lactic.

1. Saturated aqueous solutions of tropaeolin, marked in the trade OO
(Von Miller, V. d. Velden). The solution should be perfectly clear and
of a lemon-yellow color. This solution is colored red by the addition
of hydrochloric acid even in very dilute solution (0.01 per cent.). A
similar change in color is produced by lactic acid in somewhat less
dilute solution (0.06 per cent.), but the red color produced by lactic
acid disappears upon shaking with ether, while that produced by
hydrochloric acid remains, unless the acid was present in very minute
quantity. Tropaeolin is therefore a very delicate test for free acid in
general, but it does not distinguish so well as some other tests
hydrochloric from lactic acid.

2. Aqueous solution of methyl-violet (an aniline dye) in the strength
of 0.025 per cent. (Witz, Maly). The solution should be of a violet
color, and in a test-tube should allow the light to pass readily
through it. The addition of hydrochloric acid in dilute solution
changes the violet to a blue color, in stronger solution to a greenish
tint. With lactic acid in stronger solution methyl-violet gives a
similar but less distinct reaction. Methyl-violet, while a less
delicate test than tropaeolin, is better adapted for distinguishing
hydrochloric from lactic acid.

3. Ferric chloride and carbolic acid test (Uffelmann). Mix 3 drops of
liquor ferri chloridi (German Pharmacopoeia, specific gravity 1482), 3
drops of very concentrated solution of carbolic acid, and 20 ccm. of
distilled water. The addition of even very dilute solutions of lactic
acid (0.05 per cent.) changes the amethyst-blue color of this
test-fluid to a yellow color, with a shade of green. Dilute solutions
of hydrochloric acid produce a steel-gray, and stronger solutions a
complete decolorization of the fluid. When both hydrochloric and lactic
acids are present the effect of the lactic acid predominates unless
only a mere trace of it is present. This is therefore a good test for
lactic acid. It is necessary to prepare the test-fluid fresh each time
before using.

4. It is well to test the digestive power of the filtered fluid from
the stomach by suspending in the fluid a floccule of washed fibrin and
keeping the fluid at a temperature of about 100 degrees F. If free
hydrochloric acid be present in moderate quantity, in a short time the
fibrin will begin to be dissolved, but if the acidity be due to organic
acid the fibrin will be dissolved very slowly or not at all.

In applying these various tests the fluids from the stomach should be
filtered and the filtrate used. It is best not to rely upon a single
test, but to employ them in combination. The fluids may be mixed in a
test-tube. The reaction is sometimes most distinct when the fluids are
allowed {545} to mingle upon a white porcelain dish. It is sometimes of
advantage to concentrate the mingled fluids by evaporation. The fluid
obtained by the stomach-pump five or six hours after a meal is the most
suitable for diagnostic tests. The presence of peptones and of
dissolved albumen makes the tests less delicate for the gastric fluids
than for simple aqueous solutions of the acids.[44]

[Footnote 44: For further information on this subject consult Von der
Velden, _loc. cit._; Uffelmann, _Deutsches Arch. f. klin. Med._, Bd.
26, p. 431; Edinger, _ibid._, Bd. 29, p. 555; and Kredel, _loc. cit._]

It is important to distinguish between the slight and the copious
hemorrhages of gastric cancer.

The admixture of a small quantity of blood with the vomit, giving to
the latter the so-called coffee-grounds appearance, is a very common
occurrence in gastric cancer. Melaenamesis, as the vomiting of brown or
black substance resembling coffee-grounds is called, is estimated to
occur in about one-half of the cases of cancer of the stomach. It is
observed particularly in the cachectic stage, in which it is not rare
for some brown or black sediment to be almost constantly present in the
vomit. The brown or black color is due to the conversion by the acids
of the stomach of the normal blood-coloring matter into dark-brown
haematin.

The presence of blood in the vomited matter can generally be recognized
by the naked eye. By the aid of the microscope red blood-corpuscles,
more or less changed, especially decolorized red blood-corpuscles (the
so-called shadows), can usually be detected. Sometimes only amorphous
masses of altered blood-pigment can be seen. The spectroscope may also
be employed, in which alkaline solutions of haematin produce an
absorption-band between C and D, usually reaching or passing D. The
presence of blood-coloring matter can also be readily detected by the
production of haemin crystals.[45] The slight hemorrhages are in most
cases the result of ulceration of the cancer, by which process a little
oozing of blood from the capillaries is produced.

[Footnote 45: Haemin crystals may be produced by boiling in a test-tube
a little of the suspected fluid or sediment with an excess of glacial
acetic acid and a few particles of common salt. After cooling, a drop
from the lower layers will show under the microscope the dark-brown
rhombic crystals of haemin in case blood-coloring matter was present in
not too minute quantity.]

Copious hemorrhages from the stomach are not common in gastric cancer.
They occur probably in not over 12 per cent. of the cases (Lebert).
According to Lebert, they are more liable to occur in males than in
females. Blood vomited in large quantity is either bright red or more
or less darkened in color according to the length of its sojourn in the
stomach. Following profuse haematemesis, some dark, tarry blood is
usually passed by the stools, constituting the symptom called melaena.
Copious hemorrhages from the stomach hasten the fatal termination and
may be its immediate forerunner. Cases of gastric cancer have been
reported in which death has occurred from gastrorrhagia before there
has been time for any blood to be either vomited or voided by stool. As
might naturally be expected, patients with gastric cancer do not
usually rally as readily from the effects of gastric hemorrhage as do
most patients with simple ulcer. Profuse gastric hemorrhage, if it
occur, is most common in the late stage of gastric cancer, but I have
known a {546} case of cancer of the stomach in which copious
haematemesis was the first symptom, with the exception of slight
dyspepsia.[46]

[Footnote 46: In a case of cancer of the lesser curvature observed by
Laborie fatal haematemesis occurred before there had been any distinct
symptoms of gastric cancer (Bouchut, _Nouv. Elements de la Path. gen._,
ed. 3, p. 288).]

Profuse haematemesis is more common with soft cancers than with other
forms. The source of profuse hemorrhage is in some large vessel eroded
by the ulcerative process. The same vessels may be the source of the
bleeding as have been enumerated in connection with gastric ulcer.
Cancers situated near the pylorus or on the lesser curvature are the
most likely to cause severe hemorrhage.

While it is true that coffee-grounds vomiting is most common in cancer,
and profuse haematemesis is most common in ulcer of the stomach, it is
important to remember that either disease may be attended by that form
of hemorrhage which is most common in the other.

Dysphagia is one of the most important symptoms of cancer of the
cardia. Dysphagia is sometimes one of the first symptoms to attract
attention, but it may not appear until late in the disease. It is
usually accompanied with painful sensations near the xiphoid cartilage
or behind the sternum, or sometimes in the pharynx. The sensation of
stoppage of the food is usually felt lower down than in ordinary cases
of stenosis of the oesophagus. Stenosis of the cardia can be
appreciated by the passage of an oesophageal bougie, but it is
important to bear in mind that dysphagia may exist in cases of cancer
of the cardia in which the oesophageal bougie does not reveal evidence
of stenosis. Dysphagia may be a prominent symptom in cancer occupying
parts of the stomach remote from the cardia.[47] The dysphagia here
considered is not likely to be confounded with the difficulty in
swallowing which is due to weakness or to aphthous inflammation of the
throat and gullet, which often attends the last days of gastric cancer.

[Footnote 47: A case in point has been reported by J. B. S. Jackson.
The cancer occupied the pyloric region (_American Journ. of Med. Sci._,
April, 1852, p. 364).]

From a diagnostic point of view the presence of a tumor is the most
important symptom of gastric cancer. In the absence of tumor the
diagnosis of gastric cancer can rarely be made with positiveness. A
tumor of the stomach can be felt in about 80 per cent. of the cases of
cancer of the stomach (Brinton, Lebert). With all of its importance, it
is nevertheless possible to exaggerate the diagnostic value of this
symptom. It is by no means always easy to determine whether an existing
tumor belongs to the stomach or not, and even if there is proved to be
a tumor of the stomach, there may be difficulty in deciding whether or
not it is a cancer. Many instances might be cited in which errors in
these respects have been made by experienced diagnosticians. The value
of tumor as a diagnostic symptom is somewhat lessened by the fact that
it often does not appear until comparatively late in the disease, so
that the diagnosis remains in doubt for a long time. It is to be
remembered also that tumor is absent in no less than one-fifth of the
cases of gastric cancer.

In order to understand in what situations cancers of the stomach are
likely to produce palpable tumors, it is necessary to have in mind
certain points concerning the situation and the relations of this
organ.

The stomach is placed obliquely in the left hypochondrium and the
epigastric regions of the abdomen, approaching the vertical more nearly
{547} than the horizontal position. The mesial plane of the body passes
through the pyloric portion of the stomach, so that, according to
Luschka, five-sixths of the stomach lie to the left of this plane. The
most fixed part of the stomach is the cardiac orifice, which lies
behind the left seventh costal cartilage, near the sternum, and is
overlapped by the left extremity of the liver. The pyloric orifice lies
usually in the sagittal plane passing through the right margin of the
sternum, and on a level with the inner extremity of the right eighth
costal cartilage. The pylorus is less fixed than the cardia. When the
stomach is empty the pylorus is to be found in the median line of the
body; when the stomach is greatly distended the pylorus may be pushed
two and a half to three inches to the right of the median line. The
pylorus is overlapped by a part of the liver, usually the lobus
quadratus or the umbilical fissure. About two-thirds of the stomach lie
in the left hypochondrium covered in by the ribs, and to the left and
posteriorly by the spleen. The highest point of the stomach is the top
of the fundus, which usually reaches to the left fifth rib. The lowest
point of the stomach is in the convexity of the greater curvature to
the left of the median line. The lower border of the stomach varies in
position more than any other part of the organ. In the median line this
border is situated on the average about midway between the base of the
xiphoid cartilage and the umbilicus, but within the limits of health it
may extend nearly to the umbilicus. The lesser curvature in the greater
part of its course extends from the cardia downward to the left of the
vertebral column and nearly parallel with it. The lesser curvature then
crosses to the right side on a level with the inner extremity of the
eighth rib, and in the median line lies about two and a half fingers'
breadth above the lower margin of the stomach. The lesser curvature and
the adjacent part of the anterior surface of the stomach are covered by
the left lobe of the liver.

It follows from this description that only the lower part of the
anterior surface of the stomach is in contact with the anterior
abdominal walls. This part in contact with the anterior abdominal walls
corresponds to a part of the body and of the pyloric region of the
stomach, and belongs to the epigastric region. The remainder of the
stomach is covered either by the liver or by the ribs, so that in the
normal condition it cannot be explored by palpation.

It is now evident that tumors in certain parts of the stomach can be
readily detected by palpation, whereas tumors in other parts of the
organ can be detected only with difficulty or not at all. Cancer of the
cardia cannot be felt by palpation of the abdomen unless the tumor
extends down upon the body of the stomach. Cancers of the fundus, the
lesser curvature, and the posterior wall of the stomach often escape
detection by palpation, but if they are of large size or if the stomach
becomes displaced by their growth, they may be felt. Cancerous tumors
of the anterior wall or of the greater curvature are rare, but they can
be detected even when of small size, unless there are special obstacles
to the physical examination of the abdomen. Cancerous tumors of the
pylorus can be made out by palpation in the majority of cases
notwithstanding the overlapping of this part by the liver. The pyloric
tumor may be so large as to project from beneath the border of the
liver, or the hand may be pressed beneath this border so that the tumor
can be felt, or, what is most frequently the {548} case, the weight of
the tumor or the distension of the stomach drags the pylorus downward.
The pylorus may, however, be so fixed by adhesions underneath the
liver, or the liver may be so enlarged, that tumors of this part cannot
be reached by palpation.

The situation in which cancerous tumors of the pylorus can be felt
varies considerably. The usual situation is in the lower part of the
epigastric region, a little to the right of the median line, but it is
almost as common for these tumors to be felt in the umbilical region,
and it is not rare for them to appear to the left of the median
line.[48] Brinton states that the tumor is in the umbilical region more
frequently in the female sex than in the male, in consequence of the
compression exercised by corsets. Occasionally pyloric cancers produce
tumors in the right hypochondrium. Exceptionally, pyloric tumors have
been felt as low as the iliac crest or even in the hypogastric region.

[Footnote 48: According to Jackson and Tyson, pyloric cancers are felt
more frequently to the left than to the right of the median line.]

Cancers of the stomach do not usually attain a very large size.
Sometimes they form visible protuberances. An important criterion of
cancerous tumors of the stomach is their gradual increase in size by
progressive growth.

The consistence of cancerous tumors of the stomach is nearly always
hard, as appreciated by palpation through the abdominal walls. The
surface of the tumor is usually nodulated or irregular, but
exceptionally it is smooth. The tumor may be movable or not, but in the
majority of cases it is rendered immovable by adhesions. Mobility of
the tumor, however, does not exclude the presence of adhesions. The
tumor sometimes follows the respiratory movements of the diaphragm,
especially when it is adherent to this structure or to the liver, but
more frequently the tumor is not affected or but slightly affected by
the movements of the diaphragm. If the tumor is not fixed by adhesions,
it may change its position somewhat according to the varying degrees of
distension of the stomach or in consequence of pressure of intestine
distended with gas or feces. In consequence of these movements or of an
overlying distended colon the tumor may even disappear temporarily. It
is possible that the tumor may lessen or disappear in consequence of
sloughing of the growth.[49] It is not rare for a certain amount of
pulsation to be communicated to the growth by the subjacent aorta. This
pulsation is most common with pyloric tumors.

[Footnote 49: Symptoms which have been considered as diagnostic of
sloughing of stenosing cancers of the pylorus are diminution in the
size of the tumor, alleviation of the vomiting, hemorrhage, replacement
of obstinate constipation by diarrhoeal stools which often contain
blood, increased pain after eating, and rapid progress of cachexia.]

The percussion note over the tumor is usually tympanitic dulness.
Sometimes there is very little alteration over the tumor of the normal
tympanitic note belonging to the stomach; on the other hand,
exceptionally there is absolute flatness over the tumor.

It is often of assistance in determining that a tumor belongs to the
pylorus to find dilatation of the stomach. An abnormal fulness of the
epigastric and umbilical regions may then be observed, and through the
abdominal walls, if thin, may be seen the peristaltic movements of the
stomach. Other signs and symptoms aid in the diagnosis of dilatation of
the stomach, and will be described in connection with this disease.

{549} It is to be noted that what one takes to be the primary tumor of
the stomach is not so very rarely a secondary cancerous mass in the
stomach or in adjacent lymph-glands or in the peritoneum. Such nodules
may also increase the apparent size of the original tumor. As has been
pointed out by Rosenbach,[50] spasm of the muscular coat near a cancer
or an ulcer of the stomach may produce a false tumor or enlarge a real
tumor.

[Footnote 50: _Deutsche med. Wochenschr._, 1882, p. 22.]

The cancer, instead of appearing as a circumscribed tumor, may
infiltrate diffusely the gastric walls, and so escape detection. When
the greater part or the whole of the stomach is the seat of this
diffuse cancerous infiltration, a sense of abnormal resistance may be
appreciated by palpation in the epigastric region. In these cases the
stomach is often much shrunken in size. The outlines of the thickened
organ can sometimes be made out, but the physical signs do not suffice
for the diagnosis of cancer.

With cancer of the cardia there is usually more or less atrophy of the
stomach, which is manifested by sinking in of the epigastric region.

Sometimes the tumor eludes discovery on account of special obstacles to
the physical examination of the abdomen, such as a thick layer of fat
in the abdominal walls or a large quantity of ascitic fluid. Every aid
in the physical examination of the abdomen should be resorted to. The
patient should be examined while lying on his back with the utmost
possible relaxation of the abdominal walls. If necessary, he should
also be examined while standing or in the knee-elbow position.
Sometimes a deep inspiration will force down a previously concealed
tumor. The emptying of a dilated stomach by means of a stomach-tube
will sometimes bring to prominence a gastric tumor.

The inflation of the stomach by the development in it of carbonic acid
gas may render valuable assistance in the diagnosis of tumors of this
organ and of surrounding parts. This method has been recommended by W.
Ph. H. Wagner among others, and especially by Rosenbach.[51] From 20 to
30 grains of bicarbonate of soda and from 15 to 20 grains of tartaric
acid may be introduced into the stomach. The soda, dissolved in
lukewarm water, may be given first and followed by the acid in
solution, or, better, the mixed powders may be swallowed in the dry
state and followed by a tumblerful of water. Some persons require a
larger quantity of the powder in order to inflate the stomach.
Occasionally the introduction of the effervescing powder fails to
produce any appreciable distension of the stomach. This negative result
may be due to the escape of the gas into the intestine in consequence
of incontinence of the pylorus--a condition which Ebstein[52] has
observed and described especially in connection with pyloric cancer.
When this pyloric insufficiency exists the resulting tympanitic
distension of the intestine is a hindrance to palpation of tumors of
the stomach. Failure to secure distension of the stomach is not always
due to this cause. It may be necessary to make repeated trials of the
effervescing mixture. It is well to have a stomach-tube at hand to
evacuate the gas if this should cause much distress.

[Footnote 51: W. Ph. H. Wagner, _Ueber die Percussion des Magens nach
Auftreibung mit Kohlensaure_, Marburg, 1869; O. Rosenbach, _Deutsche
med. Wochenschr._, 1882, p. 22.]

[Footnote 52: W. Ebstein, _Volkmann's Samml. klin. Vortrage_, No. 155.]

In some respects simpler and more easily controlled is the method of
{550} distending the stomach by injecting air into it through a
stomach-tube, as recommended by Runeberg.[53] For this purpose the
balloon of a Richardson's spray apparatus may be attached to a
soft-rubber stomach-tube. In this way the desired quantity of air can
be introduced and at any time allowed to escape through the tube.

[Footnote 53: J. W. Runeberg, _Deutsches Arch. f. kl. Med._, Bd. 34, p.
460, 1884.]

When the stomach has been inflated the contours of tumors of the
pylorus often become surprisingly distinct in consequence of the
changes in the position and the shape of the stomach. When the tumor is
fixed by adhesions, it may be possible to follow the contours of the
stomach into those of the tumor. False tumors produced by spasm of the
muscular walls of the stomach may be made to disappear by this
distension of the organ. This procedure enables one to distinguish
between tumors behind and those in front of the stomach, as the former
become indistinct or disappear when the stomach is inflated. By
bringing out the contours of the stomach the relations of the tumor to
surrounding organs may be rendered for the first time clear. Assistance
in diagnosis may also be afforded by distension of the colon with water
or with gas or with air, per rectum, in order to determine the course
of the colon and its relations to abdominal tumors (Mader, Ziemssen,
Runeberg). A manifest contraindication to distension of the stomach or
of the colon with gas exists if there is a suspicion that the coats of
these parts are so thinned by ulceration that they might rupture from
the distending force of the gas. There have been no cases recorded
where such an accident has happened.

Only in exceptional cases are the bowels regular throughout the course
of gastric cancer. Constipation is the rule, and not infrequently there
is obstinate constipation. This is to be expected when the patient eats
little and vomits a great deal, or when there is stenosis of the
pylorus. In cancer, as in many other diseases of the stomach, the
peristaltic movements of the intestine are inclined to be sluggish.

Occasional diarrhoea is also common in gastric cancer, being present,
according to Tripier,[54] at some period or other in over one-half the
cases. Constipation often gives place to diarrhoea during the last
months or during the last days of life. In other periods of the disease
diarrhoea not infrequently alternates with constipation. In rare cases
diarrhoea is an early symptom, and it may be present exceptionally
throughout the greater part of the disease. The irritation of
undigested food sometimes explains the diarrhoea. When diarrhoea is
persistent there probably exists catarrhal inflammation of the large
intestine, or in some instances there may be diphtheritic and
ulcerative inflammation of the colon, causing dysenteric symptoms
during the last stages of cancer of the stomach.

[Footnote 54: "Etude clinique sur la Diarrhee dans le Cancer de
l'Estomac," _Lyon Med._, 1881, Nos. 40, 41, 42.]

Black stools containing altered blood occur for some days after profuse
gastric hemorrhage. It is important to examine the stools for blood, as
bleeding may occur from cancer of the stomach without any vomiting of
blood.

There is no change in the urine characteristic of gastric cancer.
Deposits of urates are not uncommon. If there be profuse vomiting or
frequent washing out of the stomach, the urine often becomes alkaline
from fixed {551} alkali.[55] The amount of urea is diminished in
consequence of the slight activity of the nutritive processes of the
body. Rommelaere attaches unmerited diagnostic importance to this
diminution of urea. A similar diminution of urea occurs in other like
states of depressed nutrition.

[Footnote 55: According to Quincke, when the acid in the stomach is not
hydrochloric acid, but organic acid resulting from fermentation, then
vomiting and washing out the stomach do not reduce the acidity of the
urine (_Zeitschrift f. klin. Med._, Bd. 7, Suppl. Heft, p. 25).]

Albuminuria does not belong to the history of gastric cancer, although
a small quantity of albumen may be present in the urine as in other
anaemic and cachectic conditions. A larger quantity of albumen may be
due to parenchymatous and fatty degeneration of the kidney or to
chronic diffuse nephritis, which are infrequent but recognized
complications of gastric cancer. There is often an excess of indican in
the urine, to which, however, no diagnostic significance can be
attached.

The urine in gastric cancer sometimes contains an excess of aceton, or
at least of some substance which yields aceton upon the application of
various tests. This so-called acetonuria is present without any
symptoms referable to it, so far as we know. Allied to this so-called
acetonuria is that condition of the urine in which it is colored
burgundy-red upon the addition of ferric chloride in solution
(Gerhardt's reaction). It is not positively known what substance
imparts this last reaction to the urine. V. Jaksch, who has studied the
subject industriously, believes that the red coloring substance is
diacetic acid, and he proposes to call the condition diaceturia. Fresh
urine, which shows in a marked degree Gerhardt's reaction, often has a
peculiar aromatic, fruity odor, as has also the expired air. Gerhardt's
reaction has been studied mostly in diabetic urine, but it occurs
sometimes in cases of gastric cancer and in a variety of diseases. This
so-called diaceturia may be associated with a peculiar form of coma,
but it is oftener observed without any symptoms referable to it[56]
(see page 555).

[Footnote 56: The various tests for aceton in the urine are not
altogether satisfactory. They are to be found in an article by Von
Jaksch in the _Zeitschrift f. klin. Med._, Bd. viii. p. 115. For
English readers a good abstract of an article by Penzoldt on these
tests and on acetonaemia in general is to be found in _The Medical
News_ of Philadelphia, Aug. 9, 1884, p. 162, but this does not consider
the corrections and additions to be found in V. Jaksch's article cited
above. Acetonuria has been observed especially in diabetes mellitus,
fevers, carcinoma, and dyspepsia.

The substance which produces Gerhardt's reaction is to be distinguished
from other substances which may be present in the urine and give a red
color with ferric chloride--first, by the fact that boiling the urine
in a test-tube for five or six minutes destroys the first-named
substance, or causes the red color to disappear in case this has been
produced by ferric chloride; and, secondly, by the fact that ether
extracts the substance from acidified urine, and that the red color
produced in the ether extract by ferric chloride (it may be necessary
to first neutralize the acid) fades away in the course of a few days
(V. Jaksch, _Zeitschrift f. Heilkunde_, Bd. iii. p. 17). Urines which
respond to Gerhardt's reaction in a marked degree yield aceton on
distillation, but aceton or an aceton-yielding substance may be present
in considerable quantity without response of the urine to Gerhardt's
test.]

Disorders of nutrition embrace an important group of symptoms, such as
loss of flesh and strength, impoverished blood, and cachectic color of
the skin. Emaciation and debility are sometimes the first symptoms of
gastric cancer to attract attention, and often the first symptoms to
arouse anxiety. More frequently these symptoms of disordered nutrition
first appear after dyspeptic ailments or pain have existed for several
weeks or months. It may aid in the diagnosis of gastric cancer to weigh
the patient {552} from time to time, as carcinoma is generally attended
by progressive loss of weight.

The patient frequently becomes morose and depressed in spirits. His
strength fails, sometimes disproportionately to the loss of flesh.
There is no disease in which emaciation becomes more extreme than in
cases of gastric cancer.

In many cases profound anaemia develops, and sometimes in such a degree
that this symptom cannot be regarded always as simply co-ordinate with
the other disorders of nutrition, but is to be regarded rather as an
evidence of some special disturbance of the blood-forming organs. The
blood may present the same changes as are observed in pernicious
anaemia, such as extreme reduction in the number of red
blood-corpuscles (to one million or even half that number in a cubic
millimeter) and manifold deformed shapes of the corpuscles
(poikilocytosis). In extreme cases the proportion of haemoglobin in the
blood may be reduced to 50 or 60 per cent. of the normal quantity.[57]
There is occasionally a moderate increase in the number of white
blood-corpuscles. In one case of gastric cancer I observed a
leucocytosis in which there was one white to twenty red
blood-corpuscles without enlargement of the spleen.[58]

[Footnote 57: The granular disintegrating corpuscles
(Zerfallskorperchen of Riess) may also be found in the blood in
considerable number. Leichtenstern has observed that toward the end of
life the relative proportion of haemoglobin in the blood may be
increased, sometimes rapidly, and may even exceed the normal limit.
This is due to concentration of the blood in consequence of the loss of
water. In such cases the tissues appear abnormally dry and the blood
thick and tarry at the autopsy (_Ziemssen's Handb. d. spec. Path. u.
Therap._, Bd. viii. 1te Halfte, p. 344).

It seems to me proper to distinguish two kinds of anaemia in gastric
cancer--a simple anaemia, which is present in the majority of cases,
and can be explained by the development of the cancer and the
disturbance of the gastric functions; and a pernicious anaemia, which
is present only in exceptional cases, and has the typical symptoms of
progressive pernicious anaemia.]

[Footnote 58: In a case of large medullary cancer of the stomach
reported by H. Mayer there was one white to fifty red blood-corpuscles.
The spleen was not enlarged (Bayer, _Aerztl. Intelligenzblatt_, 1870,
No. 21). A similar case is related by Lebert, in which, however, the
spleen was enlarged (_op. cit._, p. 481).]

To the pallor of anaemia is added often a faded yellowish tint of the
skin which is considered characteristic of the cancerous cachexia. At
the same time, the skin is frequently dry and harsh, and may present
brownish spots (chloasma cachecticorum). The pallid lips, the pale
greenish-yellow color of the face, the furrowed lines, and the pinched
and despondent expression make up a characteristic physiognomy, which,
however, is neither peculiar to gastric cancer nor present in all cases
of the disease. There is no cachectic appearance which is pathognomonic
of cancer; and in this connection it is well to note that there are
cases of gastric ulcer, and particularly of non-cancerous stenosis of
the pylorus, in which all of the symptoms described as peculiar to the
cancerous cachexia are met with. Nevertheless, the weight of these
symptoms in the diagnosis of gastric cancer should not be
underestimated. There is no disease in which profound cachectic
symptoms so frequently and so rapidly develop as in gastric cancer.

The profound nutritive disturbances of gastric cancer are referable
partly to the cancer as such, and partly to the impairment of the
functions of the stomach. It is impossible to separate the effects of
these two sets of causes, and distinguish, as some have done, a
cachexia of cancer {553} and a cachexia of inanition. It is the
combination of these causes which renders the cachexia of cancer of the
stomach so common, so rapid in its development, and so profound as
compared with that of cancer in other situations. The relation of
cancer in general to cachexia need not here be discussed, save to say
that there is the best ground for believing that the cachexia is
directly dependent upon the growth and metamorphoses of the primary
cancer and its metastases, and that there is not reason to assume any
dyscrasia antedating the cancerous formation.

While the failure of the general health and the gastric symptoms in
general develop side by side, it is especially significant of gastric
cancer when the symptoms of impaired nutrition are more pronounced than
can be explained by the local gastric disturbance. When, however, as
sometimes happens, gastric symptoms are absent or no more than can be
explained by anaemia and marasmus, then in the absence of tumor a
positive diagnosis is impossible. Such cases of gastric cancer during
life often pass for essential or pernicious anaemia. Otherwise,
unexplained symptoms of anaemia with emaciation and debility,
particularly in elderly people, should lead to a careful search for
gastric cancer.

Finally, it is necessary to add that there are exceptional cases of
gastric cancer in which there is no emaciation, and in which the
general health appears to be astonishingly well preserved. In most of
these cases death occurs either from some accident of the disease or
from some complication.

Slight or moderate oedema about the ankles is a common symptom during
the cachectic stage of gastric cancer. This oedema is due to hydraemia.
This cachectic dropsy in rare cases becomes excessive and leads to
anasarca, with serous effusion in the peritoneal, pleural, and
pericardial sacs. Such cases are liable to be mistaken for heart
disease, particularly as a haemic murmur often coexists, or for
Bright's disease. Ascites may be the result not only of hydraemia, but
also of cancerous peritonitis or of pressure on the portal vein by
cancer. Many cases of gastric cancer associated with ascites have been
falsely diagnosed as cirrhosis of the liver, and sometimes the
distinction is extremely difficult or impossible.

During the greater part of the disease the pulse is usually normal;
toward the end it is not infrequently rapid, small, and compressible.
In consequence of weakness and anaemia any exertion may suffice to
increase the frequency of the pulse, and may induce palpitation of the
heart and syncope.

As might be expected as the result of anaemia, haemic murmurs in the
heart and blood-vessels are not rare in gastric cancer.

Epigastric pulsation is often very prominent in cases of gastric
cancer, as it may be in various other conditions. This pulsation is
sometimes of a paroxysmal nature.

Venous thrombosis is not a rare complication in the last stages of
gastric cancer. It is most common in the femoral and saphenous veins,
and is rapidly followed by painful oedematous swelling of the affected
extremity. Thrombosis of the subclavian and axillary veins is much less
frequent. When it occurs there are the same symptoms of phlegmasia alba
dolens in the upper extremity as have been mentioned for the lower.
Lebert has recorded a case of thrombosis of the right external jugular
{554} vein.[59] The thrombosis is the result of marasmus, and therefore
may occur in other gastric diseases besides gastric cancer, so that
this symptom has not all the diagnostic importance for gastric cancer
claimed by Trousseau. Being an evidence of great weakness of the
circulation, marantic thrombosis in cancer of the stomach is of grave
prognostic import.

[Footnote 59: _Op. cit._, p. 394.]

The temperature is often normal throughout the course of gastric
cancer. Febrile attacks, however, are not uncommon in this disease.
Elevation of temperature may occur without any complication to explain
it. During the second half of the disease there may be either irregular
febrile attacks or a more continuous fever, which is, however, usually
of a light grade, the temperature not generally exceeding 102 degrees.
Slight chills may be experienced. Lebert describes a light and a hectic
carcinomatous fever.

There may be subnormal temperature with collapse during the last days
of life, and in general anaemia and inactivity of nutritive processes
tend to produce a low temperature.

Dyspnoea on slight exertion may be present in gastric cancer as a
result of anaemia or of fatty heart. In a few cases of gastric cancer
have been observed symptoms pointing to a reflex vagus neurosis, such
as paroxysms of dyspnoea, oppression in the chest, and palpitation of
the heart, but these symptoms are less common in gastric cancer than in
some other diseases of the stomach. Watson[60] relates a case of
gastric cancer in which increasing dyspnoea and palpitation were such
prominent symptoms that he was led to diagnose fatty heart with portal
congestion as the sole trouble. At the autopsy the heart and lungs were
found healthy, but there was extensive cancer of the greater curvature
of the stomach. He subsequently ascertained that there had been
symptoms pointing to gastric disease.

[Footnote 60: Sir T. Watson, _Lectures on the Principles and Practice
of Physic_, vol. ii. p. 471, Philada., 1872.]

The various complications of gastric cancer which affect the
respiratory organs will be considered later.

Depression of spirits, lack of energy, headache, neuralgia,
sleeplessness, and vertigo are functional nervous disturbances which
are often the result of disordered digestion from whatever cause, and
are therefore not uncommon in gastric cancer. The theory that these
symptoms are due to the absorption of noxious substances produced in
the stomach and intestine by abnormal digestive processes is
plausible,[61] and more intelligible than reference to some undefined
sympathy between the digestive organs and the nervous system.

[Footnote 61: This theory is elaborated by Senator ("Ueber
Selbstinfection durch abnorme Zersetzungsvorgange, etc.," _Zeitschrift
f. klin. Med._, Bd. 7, p. 235).]

The intelligence is generally not impaired in the course of gastric
cancer.

Considerable interest belongs to coma as a symptom of cancer of the
stomach, and more particularly to the occurrence of coma with the
peculiar characters which have been described by Kussmaul as
distinguishing diabetic coma.[62] The most distinctive feature in
Kussmaul's group of symptoms is the accompaniment of the coma by a
peculiar {555} dyspnoea in which, without evidence of disease of the
lungs or air-passages, the respirations are strong and deep and often
attended with a groaning sound in expiration. The breathing is either
normal in frequency or oftener moderately increased. The pulse is
usually small and frequent. The temperature is not much elevated, and
sometimes is much below the normal. Sometimes the coma is preceded by a
period of excitement, with restlessness, and perhaps with screaming.
Gerhardt's reaction in the urine may or may not be present. When it is
present in a marked degree there is often an aromatic, chloroform-like
odor to the breath and to the fresh urine. The patient may come out of
the coma, but in the vast majority of cases the coma terminates
fatally.

[Footnote 62: _Deutsches Arch. f. klin. Med._, Bd. 14, p. 1.]

It is now known that this dyspnoeic coma is not confined to diabetes
mellitus, but that it occurs also in gastric cancer and in various
other diseases.[63] Its occurrence in gastric cancer is rare. In this
disease it does not usually appear until anaemia is far advanced, but
it may occur in cases of cancer in which the patient's general health
and nutrition are still fairly good. I recently made the post-mortem
examination of an elderly man, fairly well nourished, who was found in
the streets comatose and brought in this condition to Bellevue
Hospital, where he died in about twelve hours. While in the hospital
his breathing was increased in frequency, forcible, and deep. His
temperature was normal. The urine contained a small quantity of
albumen, but no sugar. No previous history could be obtained. Uraemic
coma was suspected. At the autopsy was found a large, soft, ulcerated
cancer of the lesser curvature and posterior wall of the stomach near
the pylorus. The kidneys, brain, heart, and other organs were
essentially healthy.

[Footnote 63: Von Jaksch was the first to describe this form of coma in
cancer of the stomach (_Wien. med. Wochenschr._, 1883, pp. 473, 512).
He adopted the term coma carcinomatosum, and more recently coma
diaceticum. L. Riess has reported seventeen cases of this coma
occurring in a variety of diseases, such as pernicious anaemia, gastric
cancer, gastric ulcer, tuberculosis, which all had in common profound
anaemia. He proposes the term dyspnoeic coma (_Zeitschrift f. klin.
Med._, Bd. 7, Suppl. Heft, p. 34, 1884). Senator has described two
cases of gastric cancer with this coma. He uses the terms dyscrasic
coma and Kussmaul's group of symptoms (_ibid._, Bd. 7, p. 235). In the
cases described by Litten under the name coma dyspepticum, dyspnoea was
absent, but Gerhardt's reaction in the urine was present. In Litten's
cases structural disease of the stomach was not supposed to be present.
The patients recovered from the coma (_ibid._, Suppl. Heft, p. 81).]

We possess no satisfactory explanation of this form of coma. In
diabetes it is considered to be due to the presence in the blood of
some intoxicating agent. For a time this agent was thought to be
aceton; it is now believed by Von Jaksch to be diacetic acid. Much
stress has been laid upon the aromatic, fruity odor of the breath and
of the fresh urine, and upon the presence of some substance in the
urine which imparts to it a burgundy-red color upon the addition of
liquor ferri chloridi (Gerhardt's reaction. See changes in the urine,
page 551). Although the whole aceton question is at present in a very
confused state, there is no proof that aceton or its allies possesses
the toxic properties assumed by this theory;[64] and it is certain that
dyspnoeic coma may occur in diabetes and in other diseases without the
presence of Gerhardt's reaction in the urine. It is also true that this
reaction often occurs without any clinical symptoms referable to it.
Riess and Senator believe that in non-diabetic {556} cases anaemia is
the most important factor in the production of this coma.[65]

[Footnote 64: Frerichs, _Zeitschrift f. klin. Med._, Bd. 6, p. 3.]

[Footnote 65: Riess refers the coma to the anaemia as such, whereas
Senator thinks that, in consequence of the depraved nutrition of the
body resulting from the anaemia, some toxic substance is developed
which enters the circulation.]

Coma, probably belonging to this same variety, may occur in gastric
cancer without the peculiar dyspnoea which has been described. There is
reason to believe that this dyspnoea is not a necessary symptom of the
so-called diabetic coma.

Chronic Bright's disease terminating with uraemic coma is an occasional
but not frequent complication of gastric cancer.

Coma and other cerebral symptoms may be produced by secondary cancerous
tumors in the brain.

Stupor deepening into coma may develop during the often-prolonged
death-agony of gastric cancer.

The distribution, origin, and frequency of cancerous growths secondary
to gastric cancer are most conveniently considered under Pathological
Anatomy. Symptoms referable to certain localizations of these secondary
cancerous deposits, however, are so common, and so interwoven with the
clinical history of cancer of the stomach, that it is desirable to
consider some of these symptoms in the present connection.

Cancer of the liver is the most important of these secondary cancerous
growths. It is estimated to be present in nearly one-third of the cases
of gastric cancer, but by no means in all these cases does it produce
symptoms. As a rule, the earlier hepatic cancer forms in the course of
gastric cancer the more likely is it to be attended by symptoms. The
most important symptoms of secondary cancer of the liver are
enlargement of the liver, peritoneal exudation, and persistent icterus.
When nodular growths can be felt in the free border or surface of the
liver, the diagnosis is generally easily established. Sometimes the
liver remains of normal size or is even contracted, and then the
diagnosis is difficult or impossible. Ascites or exudative peritonitis
is present in about one-half of the cases of cancer of the liver.
Jaundice is less frequently present. It is only persistent jaundice
which aids in the diagnosis of hepatic cancer.

The various combinations of gastric cancer with secondary hepatic
cancer may be clinically grouped as follows:

1. Symptoms of gastric cancer with latent hepatic cancer.

2. Symptoms of gastric cancer followed by symptoms of hepatic cancer.

3. Symptoms both of gastric cancer and of hepatic cancer present when
the case comes under observation.

4. Symptoms of hepatic cancer with latent gastric cancer.

5. Symptoms of hepatic cancer followed by symptoms of gastric cancer.

6. Both hepatic and gastric cancer latent. Symptoms of anaemia and
marasmus, or of chronic exudative peritonitis, or of chronic pleurisy.

From this grouping it is evident that the existence of secondary
hepatic cancer may aid in the diagnosis of cancer of the stomach, or
may mislead, or may be without influence. The greatest assistance in
diagnosis is rendered when the physical signs and the symptoms of
hepatic {557} cancer develop some time after the appearance of gastric
symptoms which may previously have been equivocal. Much more difficult
to diagnosticate are the cases of hepatic cancer accompanied or
followed by gastric symptoms, inasmuch as cancer of the liver, whether
primary or secondary, may be attended with marked disturbance of the
gastric functions, including haematemesis. In these cases, unless a
tumor of the stomach can be discovered, a positive diagnosis of gastric
cancer is impossible. In view of the infrequency of primary cancer of
the liver, however, there will be in many of these cases a strong
probability in favor of primary cancer of the stomach. When it is
remembered that over one-third of the cancers of the liver are
secondary to cancer of the stomach, it is evident that in cases which
appear to be primary hepatic cancer very careful attention should be
given to the exploration of the stomach. But even then diagnostic
errors will often be unavoidable.

Cancer of the peritoneum secondary to cancer of the stomach may produce
no symptoms, and so pass unrecognized. The diagnosis of peritoneal
cancer is readily made when, after the recognition of gastric cancer,
secondary cancerous nodules in the peritoneum can be felt through the
abdominal walls or through the vagina. There are cases of gastric
cancer in which the symptoms are all referable to secondary cancer of
the peritoneum. Cancer of the peritoneum is usually attended with fluid
exudation in the peritoneal cavity. The chemical and the microscopical
examination of this fluid withdrawn by paracentesis may aid in the
diagnosis of cancerous peritonitis. Whereas in dropsical accumulations
in the peritoneal cavity the quantity of albumen in the fluid is
usually less than 2-1/2 per cent., in cancerous peritonitis there is
usually from 3 to 4 per cent. of albumen, the percentage rarely falling
as low as 2-1/2 per cent., but sometimes being as high as from 5 to 6
per cent. The percentage of albumen in ordinary peritonitis is usually
over 4.[66] Clumps of cancer-cells are sometimes to be found by
microscopical examination of the fluid. These cells are large,
epithelioid in shape, and often contain vacuoles and fatty granules. It
is only when these cells are arranged in clumps or as so-called budding
cells, and when they are present in abundance, that they are
diagnostic. They are to be sought especially in fibrinous coagula. They
are present only when the cancerous alveoli actually communicate with
the peritoneal cavity.[67] The development of cancerous nodules in the
margins of an opening made in the abdominal walls by a trocar is also
evidence of cancerous disease of the peritoneum. The same thickening
and retraction of the mesentery and omentum may occur in cancerous as
in tuberculous peritonitis. In both the exudation is often hemorrhagic.

[Footnote 66: The conditions under which the estimation of the quantity
of albumen in the peritoneal exudation may prove of diagnostic aid are
fully considered by Runeberg (_Deutsches Arch. f. klin. Med._, Bd. 34,
p. 1). Here also are given methods for making this analysis for
clinical purposes.]

[Footnote 67: The literature on this subject is as follows: Foulis,
_Brit. Med. Journ._, July 20, Nov. 2, 1878; Thornton, _ibid._, Sept. 7,
1878; Quincke, _Deutsches Arch. f. klin. Med._, Bd. 30, p. 580;
Ehrlich, _Charite Annalen_, vii. p. 226; Brieger, _ibid._, viii.]

Importance has been attached to enlargement of the supraclavicular
lymphatic glands in the diagnosis of cancer of the stomach, but there
are so many causes of enlargement of these glands that not much
significance can be attached to this symptom, which, moreover, is
absent in most {558} cases. Still, under certain circumstances this
glandular enlargement may aid in the diagnosis. The same remarks apply
to enlargement of the inguinal glands, which is a common occurrence in
case cancer involves the peritoneum. One must not mistake abnormal
prominence of the lymphatic glands in consequence of emaciation for
actual enlargement.

Gastric cancer much less frequently than gastric ulcer causes
perforation of the stomach. Of 507 cases of gastric cancer collected by
Brinton, perforation into the general peritoneal cavity occurred in 17
(3-1/3 per cent.).[68] In two cases of gastric cancer reported by Ellis
perforative peritonitis was preceded by symptoms supposed to be only
those of ordinary dyspepsia, hemorrhage and vomiting being absent.[69]
Various fistulous communications like those described under gastric
ulcer may be the result of perforation of gastric cancer, but with the
exception of gastro-colic fistula they are much more frequently
produced by ulcer than by cancer. In 160 cases of gastric cancer
collected by Dittrich, gastro-colic fistula existed in 6 (3-3/4 per
cent.).[70] In 507 cases collected by Brinton this fistula existed in
11 (2.17 per cent.). In Lange's 210 cases gastro-colic fistula existed
in 8 (3.8 per cent.). Of 33 cases of gastro-colic fistula collected by
Murchison, 21 were caused by cancerous ulceration.[71] The symptoms
characteristic of fistulous communication between the stomach and the
colon are the vomiting of fecal matter and the passage of undigested
food by the stools. These symptoms are not present in all cases, so
that a diagnosis is not always possible. Fecal vomiting is influenced
by the size of the opening between the stomach and the colon. With
great obstruction at the pylorus, fecal vomiting, as might be expected,
is absent or infrequent, while the passage of undigested food by the
bowels is common. Under these circumstances vomiting is sometimes
relieved after the establishment of the fistula. Aid may be afforded in
the diagnosis of gastro-colic fistula by the introduction into the
rectum or into the stomach of colored or other easily recognizable
substances, and determining their presence in the vomit or in the
stools in consequence of their escape by the unnatural outlet. V.
Ziemssen has determined in a case of gastro-colic fistula due to cancer
the escape into the stomach of carbonic acid gas artificially generated
in the rectum, with failure to obtain distension of the colon.[72] A
number of instances of gastro-cutaneous fistula due to gastric cancer
have been recorded, but this form of fistula is much less common than
gastro-colic fistula, and much less frequently the result of cancer
than of ulcer of the stomach. Subcutaneous emphysema may precede the
formation of the fistula. Other gastric fistulous communications
resulting from cancer, such as with the pleura, the lungs, the small
intestine, are too infrequent to merit consideration under the
symptomatology of the disease.

[Footnote 68: _Loc. cit._ Lange (_op. cit._) records in 210 cases of
gastric cancer 12 perforations into the peritoneal cavity (5.7 per
cent.).]

[Footnote 69: _Extr. fr. the Rec. of the Boston Soc. for Med.
Improvement_, vol. iii. p. 116, and vol. iv. p. 109.]

[Footnote 70: _Prager Vierteljahrsch._, vol. xvii.]

[Footnote 71: _Edinb. Med. Journ._, vol. iii. p. 4, 1857.]

[Footnote 72: _Deutsches Arch. f. kl. Med._, Bd. 33, p. 237. He
recommends for extreme distension of the colon in an adult the
introduction, by means of a tube passed up the rectum, of a solution of
about 5 drachms of sodii bicarb. and 4-1/2 drachms of tartaric
acid--injected not all at once, but in three or four doses at intervals
of a few minutes, the tube being cleaned in the intervals by the
injection of three ounces of water, so as to avoid generation of gas in
the tube. The generation of a smaller quantity of gas would suffice for
the purpose here in view.]

{559} As a rule, patients with gastric cancer die from gradual
exhaustion. In a condition of extreme emaciation and feebleness the
patient sinks into a state of collapse, accompanied often with stupor,
sometimes with mild delirium. The death-agony is prolonged frequently
from twelve to twenty-four hours, and sometimes even longer. On the
other hand, death may occur somewhat suddenly in the last stages of
gastric cancer, and without satisfactory explanation.

Death from copious gastric hemorrhage does not occur probably in more
than 1 per cent. of the cases of cancer of the stomach.

In the rare cases of death from perforation of the stomach the patient
is sometimes so exhausted at the time of perforation that the
occurrence of this accident remains unrecognized in the absence of any
complaint of characteristic symptoms.

The coma which sometimes leads to the fatal termination of gastric
cancer has already been sufficiently considered.

Finally, death may be the result of certain complications more or less
dependent upon the cancer. Of these the most important are suppurative
peritonitis and pulmonary complications, particularly oedema, terminal
pneumonia, and embolism of the pulmonary artery.

DURATION.--It is evidently impossible to determine the exact duration
of a cancer of the stomach. Doubtless in all cases there is a period of
growth of the tumor before it produces symptoms, and the duration of
this latent period can never be determined. When symptoms appear they
are often at first so mild as to be readily overlooked, and so
ambiguous that even if recognized they are not clearly referable to the
cancer. Gastric symptoms may have preceded, perhaps for years, the
development of the cancer, so as to lead to the assumption of a longer
duration of the cancer than is really the case. Estimates, therefore,
of the duration of gastric cancer can be only of limited value.

From 198 cases Brinton[73] estimates the average duration of gastric
cancer as about twelve and a half months, the maximum duration as about
thirty-six months, and the minimum as one month. From 36 cases
Katzenellenbogen[74] estimates the average duration as eighteen months,
the maximum as five years and five months, the minimum as one month.
From 112 cases Lebert[75] makes the average duration fifteen months and
the maximum four years. In 4 per cent. of the cases Lebert found the
duration less than three months, in 62 per cent. between six and
eighteen months, in 42 per cent. between six and twelve months, in 17
per cent. between three and six months, and in the same number of cases
between eighteen months and four years.

[Footnote 73: _Loc. cit._]

[Footnote 74: _Op. cit._]

[Footnote 75: _Op. cit._]

Estimates of several years' duration (such as nine years in the case of
Napoleon) are to be received with scepticism. In these cases symptoms
of gastralgia or of dyspepsia or of gastric ulcer have preceded the
development of the cancer. It has already been mentioned that cancer
may develop in a simple ulcer of the stomach.

Mathieu,[76] from an analysis of 27 cases of gastric cancer occurring
under thirty-four years, found the average duration in early life to be
only three months. In only 2 out of 19 cases did the duration exceed
one year. Although this analysis is based upon too small a number of
cases, there {560} seems to be no doubt that gastric cancer pursues a
more rapid course in early life than it does in old people.

[Footnote 76: _Du Cancer precoce de l'Estomac_, Paris, 1884, p. 40.]

COMPLICATIONS.--Some of the complications of gastric cancer have been
mentioned under Symptomatology. Jaundice may appear in the course of
gastric cancer from a variety of causes, such as catarrhal
gastro-duodenitis, impaction of gall-stones in the common bile-duct,
and pressure on the bile-duct by cancerous growths in the pancreas, in
the portal lymphatic glands, or in the liver itself. Pylethrombosis,
which is likely to be suppurative, is a rare complication. In a case of
cancer of the anterior wall and greater curvature of the stomach
reported by Wickham Legg[77] the symptoms seem to have been mostly
referable to a complicating suppurative pylethrombosis. Simple and
cancerous pylethromboses also occur. Other forms of peritonitis than
the cancerous may complicate gastric cancer, such as suppurative,
sero-fibrinous, and chronic proliferative peritonitis. Catarrhal
enteritis, and particularly diphtheritic colitis, are not infrequent
complications, especially in the later stages of the disease. Chronic
diffuse nephritis, both in the form of the large and of the small
kidney, is a rare complication of cancer of the stomach. Hydrothorax,
sero-fibrinous pleurisy, and emphysema may develop either with or
without cancerous invasion of the pleura. Pericarditis is much less
common; it is most likely to occur with cancer of the cardia.
Pyo-pneumothorax, abscess, and gangrene of the lung may result from
perforation of the pleura or of the lung by gastric cancer. Oedema of
the lungs, splenization, and pneumonia, involving usually the lower
lobes, are common in the last days of gastric cancer. Emboli derived
from venous thrombi are sometimes carried into the pulmonary artery or
its branches. Although much has been written as to the exclusion of
tuberculosis by cancer, no such law exists. Both old and fresh
tubercles have been repeatedly observed in cases of gastric cancer.
Reference has already been made to the frequent development of aphthae
in the mouth, pharynx, and oesophagus in the final stage of gastric
cancer. Fatty degeneration of the heart may develop in gastric cancer
as in other anaemic states. Phlegmasia alba dolens has already been
mentioned. It is not probable that insanity is to be regarded as more
than an accidental complication of gastric cancer; still, it has been
noticed in several cases--for instance, of Dittrich's 160 cases, 5
patients were insane, 2 with violent mania. Amyloid degeneration has
been present in some cases. Purpura haemorrhagica has been present in a
few instances in the later stages (cachectic purpura). Chronic
catarrhal gastritis and dilatation of the stomach are less
complications than a part of the disease. The relation of cancer to
simple ulcer of the stomach has already been considered. The various
secondary cancerous deposits are most conveniently considered under the
Morbid Anatomy. It is to be remarked that many of the complications of
gastric cancer--as, for instance, pneumonia and peritonitis--may have a
very obscure clinical history, as they often occur when the patient is
greatly prostrated.

[Footnote 77: _St. Bartholomew's Hosp. Rep._, vol. x. p. 236.]

MORBID ANATOMY.--The following table gives the situation of the tumor
in 1300 cases of cancer of the stomach:[78] {561}

  Pyloric region.           791  60.8%
  Lesser curvature.         148  11.4%
  Cardia.                   104   8.0%
  Posterior wall.            68   5.2%
  The whole or the greater
    part of the stomach.     61   4.7%
  Multiple tumors.           45   3.5%
  Greater curvature.         34   2.6%
  Anterior wall.             30   2.3%
  Fundus.                    19   1.5%

From this table it appears that three-fifths of all gastric cancers
occupy the pyloric region, but it is not to be understood that in all
of these cases the pylorus itself is involved. In four-fifths of the
cases the comparatively small segment of the stomach represented by the
cardia, the lesser curvature, and the pyloric region is the part
affected by gastric cancer. The lesser curvature and the anterior and
the posterior walls are involved more frequently than appears from the
table, inasmuch as many cancers assigned to the pyloric region extend
to these parts. The fundus is the least frequent seat of cancer. In the
cases classified as involving the greater part of the stomach the
fundus often escapes.

[Footnote 78: These cases are collected from the following sources:
Lebert, _op. cit._; Prague statistics of Dittrich, Engel, Wrany, and
Eppinger, _loc. cit._; Habershon, _op. cit._; Katzenellenbogen, _op.
cit._; and Gussenbauer and V. Winiwarter, _loc. cit._ Gussenbauer and
V. Winiwarter assign to the class of cancers involving the whole
stomach all cases which they found designated simply as carcinoma
ventriculi without further description. This produces in their
statistics an excessive number of cancers under this class. I have
preferred, therefore, to estimate in their collection of cases the
number of cancers involving the whole stomach, according to the
percentage for this class obtained from the other authors above cited.]

As was shown by Rokitansky, it is the exception for cancer of the
pylorus to extend into the duodenum, whereas cancer of the cardia
usually invades for a certain distance the oesophagus.

The varieties of carcinoma which develop primarily in the stomach are
scirrhous, medullary, colloid, and cylindrical epithelial
carcinoma.[79] The distinction between scirrhous and medullary cancer
is based upon the difference in consistence, the former being hard and
the latter soft. Cylindrical-celled epithelioma cannot be recognized as
such by the naked eye. It presents usually the gross appearances of
medullary cancer. Soft cancer (including both cylindrical-celled
epithelioma and medullary carcinoma) is the most frequent form of
gastric cancer. Next in frequency is scirrhous cancer, and then comes
colloid cancer, which, although not rare, is much less frequent than
the other varieties.

[Footnote 79: I have not been able to find an authentic instance of
primary melanotic cancer of the stomach, although this form is included
by most authors in the list of primary gastric cancers. It is known
that most cases formerly described as melanotic cancers are melanotic
sarcomata, which originate usually in the skin or the eye and are
accompanied frequently with abundant metastases. Secondary melanotic
tumors have been several times found in the stomach. They were present
in 7 out of 50 cases of melanotic cancer (or sarcoma) analyzed by
Eiselt, although out of 104 cases not a single primary melanotic cancer
occurred in the stomach (_Prager Viertaljahrschr._, vol. lxxvi. p. 54).
The list of secondary melanotic sarcomata of the stomach might be still
further increased. Of course gastric cancers colored by pigment from
old blood-extravasations should not be confounded with melanotic
tumors.]

As all degrees of combination and of transition exist between the
different forms of cancer, and as a large number of cancers of the
stomach are of a medium consistence and would be classified by some
observers as scirrhous and by others as medullary, statistics as to the
relative frequency of the different varieties have very little value.
Moreover, in most statistics upon this point there is no evidence that
simple fibrous growths have not been confounded with scirrhous cancer,
and as a rule {562} little or no account is taken of cylindrical-celled
epithelioma, which is a common form of gastric cancer--according to
Cornil and Ranvier, the most common.[80]

[Footnote 80: For any who may be interested in such statistics I have
collected 1221 cases of gastric cancer, of which 791 (64.8 per cent.)
were medullary, 399 (32.7 per cent.) scirrhous, and 31 (2.5 per cent.)
colloid. 22 cases described as epithelial have been included with the
medullary; 29 cases described as fibro-medullary, and 1 as
fasciculated, have been included with the scirrhous. The cases are from
the previously-cited statistics of Lebert, Dittrich, Wrany, Eppinger,
Gussenbauer, and V. Winiwarter, and from Fenger (_Virchow u. Hirsch's
Jahresbericht_, 1874, Bd. i. p. 312).]

Cancer of the stomach may grow in the form of a more or less complete
ring around the circumference of the stomach, or as a circumscribed
tumor projecting into the cavity of the stomach, or as a diffuse
infiltration of the walls of the stomach. The annular form of growth is
observed most frequently in the pyloric region. Cancerous tumors which
project into the interior of the stomach are sometimes broad and
flattened, sometimes fungoid in shape, but most frequently they appear
as round or oval, more rarely irregular, crater-like ulcers, with
thickened, prominent walls and ragged floor. The free surface of the
tumor presents sometimes a cauliflower-like or dendritic appearance,
which characterizes the so-called villous cancer. Diffuse cancerous
infiltration is seated oftenest in the right half of the stomach, but
it may occupy the cardiac region or even the entire stomach.

The relation of the cancerous growth to the coats of the stomach varies
in different cases. The tumor usually begins in the mucous membrane and
rapidly extends through the muscularis mucosae into the submucous coat.
In this lax connective-tissue coat the tumor spreads often more rapidly
than in the mucous membrane, so that it may appear as if the cancer
originated in the submucosa. The mucous membrane, however, is usually
invaded, sooner or later, over the whole extent of the tumor. The dense
muscular coat offers more resistance to the invasion of the tumor.
Cancerous masses, however, penetrate along the connective-tissue septa
between the muscular bundles, which often increase in number and size.
In the muscular coat thus thickened can be seen the opaque white
fibrous and cancerous septa enclosing the grayish, translucent bundles
of smooth muscular tissue. Often, however, the whole muscular coat
beneath the tumor is replaced by the cancerous growth, and can no
longer be recognized. The serous and subserous connective tissue, like
the submucous coat, offers a favorable soil for the growth of the
tumor, which here appears usually in the form of large and small
nodules projecting from the peritoneum. Adhesions now form between the
stomach and surrounding parts, and opportunity is offered for the
continuous growth of the cancer into these parts. In the manner
described the tumor grows in all directions, sometimes more in depth,
sometimes more laterally, sometimes more into the interior of the
stomach.

Ulceration occurs in all forms of gastric cancer.[81] The ulceration is
caused either by fatty degeneration and molecular disintegration of the
surface of the tumor or by the separation of sloughy masses. Doubtless
the solvent action of the gastric juice aids in the process. The softer
and {563} the more rapid the growth of the cancer, the more extensive
is likely to be the ulcer. Such ulcers are usually round or oval in
shape, but their contours may be irregular from the coalescence of two
or more ulcers or from serpiginous growth. The edges are usually high,
soft in consistence, and often beset with polypoid excrescences. The
floor is generally sloughy and soft, and often presents warty
outgrowths. The edges and floor may, however, be hard and smooth. In
the more slowly-growing scirrhous and colloid cancers the ulcers are
more likely to be superficial. Partial cicatrization of cancerous
ulcers may take place. The development of cicatricial tissue may
destroy the cancerous elements to such an extent that only by careful
microscopical examination can the distinction be made between cancer
and simple ulcer or fibroid induration. The examination of secondary
cancerous deposits in adjacent lymphatic glands or other parts becomes,
then, an important aid in the diagnosis.

[Footnote 81: Ulceration was present in 60 per cent. of Lebert's cases,
and in 66-1/2 per cent. of Gussenbauer and V. Winiwarter's pyloric
cancers.]

Suppuration has been known to occur in gastric cancers, but it is
extremely rare.

Each form of gastric cancer has certain peculiarities which require
separate consideration.

Medullary carcinoma grows more rapidly than the other varieties of
cancer. It forms usually soft masses, which project into the stomach
and are prone to break down in the centre and develop into the
crater-like ulcers already described. All of the coats of the stomach
are rapidly invaded by the growth. The consistence of the tumor is
soft, the color upon section whitish or reddish-gray, sometimes over a
considerable extent hemorrhagic. Milky juice can be freely scraped from
the cut surface of the tumor. The so-called villous cancer and the
haematodes fungus are varieties of medullary carcinoma. Medullary
carcinoma is more frequently accompanied by metastases than the other
forms. In consequence of its tendency to deep ulceration medullary
cancer is more liable to give rise to hemorrhage and to perforation
than is scirrhous or colloid cancer. The continuous new formation of
cancerous tissue in the floor of the ulcer and the formation of
adhesions, however, greatly lessen the danger of perforation into the
peritoneal cavity.

Histologically, medullary cancer is composed of a scanty stroma of
connective tissue enclosing an abundance of cancerous alveoli filled
with polyhedrical or cylindrical epithelial cells. The stroma is often
richly infiltrated with lymphoid cells, and contains blood-vessels
which often present irregular dilatations of their lumen.

Waldeyer describes with much detail, for this as for the other forms of
gastric cancer, the origin of the tumor from the gastric tubules.
According to his description, a group of gastric tubules, ten to twenty
in number, sends prolongations downward into the submucous coat. These
tubular prolongations are filled with proliferating epithelial cells,
which make their way into the lymphatic spaces of the surrounding
tissue and give origin to the cells in the cancerous alveoli. A
small-celled infiltration of the surrounding connective tissue
accompanies this growth of the tubules.

The tissue beneath and at the margins of medullary cancer may be
predominantly fibrous in texture and contain comparatively few
cancerous alveoli. This scirrhous base is often exposed after the
destruction of the greater part of the soft cancer by ulceration and
sloughing. It is {564} probable that many of the scirrhous cancers are
formed in this way secondarily to medullary cancer (Ziegler).

Cylindrical-celled epithelioma presents the same gross appearances and
the same tendency to ulceration and to the formation of metastases
which characterize medullary cancer. The consistence of cylindrical
epithelioma may, however, be firm like that of scirrhus. Not
infrequently the alveoli are distended with mucus secreted by the
lining epithelium, and then the tumor presents in whole or in part
appearances similar to colloid cancer.

Upon microscopical examination are seen spaces resembling more or less
closely sections of tubular glands. These spaces are lined with
columnar epithelium. Often in certain parts of the tumor the alveolar
spaces are filled with cells, so that the structure is a combination of
that of ordinary cancer and of epithelioma. The stroma is generally
scanty and rich in cells, but it may be abundant. Cysts may be present
in this form of tumor, and in one case I have found such cysts nearly
filled with papillary growths covered with cylindrical epithelium, so
that the appearance resembled closely that of the so-called proliferous
cysto-sarcoma of the breast.

The origin of cylindrical epithelioma from the gastric tubules is
generally accepted, and is more readily demonstrable than the similar
origin claimed for the other forms of gastric cancer.

Scirrhous cancer assumes often the form of a diffuse thickening and
induration of the gastric walls, particularly in the pyloric region,
where it causes stenosis of the pyloric orifice. Scirrhus may, however,
appear as a circumscribed tumor. Irregular hard nodules frequently
project from diffuse scirrhous growths into the interior of the
stomach. Scirrhous cancer and medullary cancer are often combined with
each other.

The dense consistence of scirrhous cancer is due to the predominance of
the fibrous stroma, the cancerous alveoli being relatively small in
size and few in number.

Colloid cancer generally appears as a more or less uniform thickening
of the gastric walls. All of the coats of the stomach are converted
into the colloid growth. Nearly the whole of the stomach may be invaded
by the new growth.[82] The tumor has a tendency to spread to the omenta
and to the rest of the peritoneum, where it may form enormous masses,
but it rarely gives rise to metastases in the interior of organs.
Colloid cancer may, however, form a circumscribed projecting tumor in
the stomach, and in rare instances it causes abundant secondary colloid
deposits in the liver, the lungs, and other parts.

[Footnote 82: In a case reported by Storer the whole stomach, except a
little of the left extremity over an extent of about an inch, was
converted into a colloid mass in which no trace of the normal coats of
the stomach could be made out. The colloid growth replacing the gastric
wall measured seven-eighths of an inch in thickness in the pyloric
region. Digestion was less disturbed in this case than in most cases of
gastric cancer (_Boston Med. and Surg. Journ._, Oct. 10, 1872). In
Amidon's case (reported in the _Trans. of the N.Y. Path. Soc._, vol.
iii. p. 38) there seems to have been an equally extensive colloid
metamorphosis of the stomach.]

Colloid cancer presents, even to the naked eye, an exquisite alveolar
structure, whence the name alveolar cancer as a designation of this
tumor. Bands of opaque white or gray connective tissue enclose alveolar
meshes which are filled with the gelatinous, pellucid colloid {565}
substance. This colloid material is thought to be produced by a colloid
transformation of the epithelial cells in the alveoli, but the same
transformation seems to occur also in the stroma. Few or no intact
epithelial cells may be found in the alveoli. Colloid metamorphosis may
take place in all forms of gastric cancer, but it is particularly
common in cylindrical epithelioma. Colloid cancer may originate in the
peritoneum unconnected with any glandular structures. It occurs often
at an earlier age than other forms of cancer. Deep ulceration rarely
attacks colloid cancer.

Flat-celled epithelioma is found at the cardiac orifice and as a
metastatic growth in other parts of the stomach. Originating in the
oesophagus, it may extend downward into the stomach. By noting whether
the structure is that of squamous or of cylindrical epithelioma it is
often possible to determine whether a tumor at the cardiac orifice
originates in the oesophagus or in the stomach.

Secondary cancer of the stomach, although rare, is not such a curiosity
as is often represented. Without aiming at completeness, I have been
able to collect 37 cases of secondary cancer of the stomach, of which
the larger number will stand critical examination.[83] Of these cases,
17 were secondary to cancer of the breast, 8 to cancer of the
oesophagus, 3 to cancer of the mouth or nose, and the remainder to
cancer of other parts of the body. The large number of cases secondary
to cancer of the breast is explained by the large statistics relating
to mammary cancer which were consulted. Gastric cancer is more
frequently secondary to cancer of the oesophagus than to cancer of any
other part. In this category of course are not included cases of
continuous growth of oesophageal cancer into the stomach, but only
metastatic cancers of the stomach. A part at least of the gastric
cancers secondary to cancer of the alimentary tract above the stomach I
refer, with Klebs, to implantation in the mucous membrane of the
stomach of cancerous particles detached from the primary growth in the
oesophagus, pharynx, or mouth. This view is supported by the absence in
some cases of any involvement of the lymphatic glands. The secondary
deposits in the stomach conform in structure to the primary growth.
They are usually situated in the submucous coat, where they form one or
often several distinctly circumscribed tumors. The secondary tumors may
or may not ulcerate. They rarely produce symptoms.

[Footnote 83: These cases are from Dittrich, 2 (the remainder of his
cases I rejected); Cohnheim, 1; Petri, 2; Klebs, 3; Lucke, 1; Weigert,
1; Coupland, 1; Cruse, 1; Hausmann, 1; Bartholow, 1; Oldekop, 5; Edes,
1; V. Torok and V. Wittelshofer, 8; Grawitz, 4; Haren Noman, 5.
So-called melanotic cancers, cancers involving only the serous coat of
the stomach, and those extending by continuous growth into the stomach,
are not included in this list.]

Primary cancers may be present at the same time in different organs of
the body; for instance, in the uterus and in the stomach.[84] The
possibility of multiple primary cancers is to be borne in mind in
considering some of the apparently secondary cancers of the stomach, as
well as in determining whether certain cancers are secondary to gastric
cancer or not. Here the microscopical examination is often
decisive.[85]

[Footnote 84: Case of A. Clark's (_Trans. N.Y. Path. Soc._, vol. i. p.
260), and a similar one reported by J. B. S. Jackson in _Extr. from
Records of the Boston Soc. for Med. Improvement_, vol. i. p. 335.]

[Footnote 85: The subject of multiple primary cancers is considered by
Kauffmann (_Virchow's Arch._, Bd. 75, p. 317), and by Beck (_Prager
med. Wochenschr._, 1883, Nos. 18 and 19). V. Winiwarter reports a
cancer of the stomach in a patient who died one year seven and a half
months after extirpation of a cancer of the nose. He regards the case
as one of multiple primary cancer.]

{566} Gastric cancer often causes important secondary changes in the
coats and the lumen of the stomach. In the neighborhood of the tumor
are often found hypertrophy of the muscular coat and fibrous thickening
of the submucous coat. Polypoid hypertrophy of the mucous membrane near
the cancer is not rare. Not only near the tumor, but over the whole
stomach, chronic catarrhal gastritis usually exists.

The most important alterations are those dependent upon obstruction of
the orifices of the stomach. This obstruction may be caused either by a
tumor encroaching upon the orifice or by an annular thickening of the
walls of the orifices. Even without apparent stenosis, destruction of
the muscular layer at or near the pylorus may be an obstacle to the
propulsion of the gastric contents into the duodenum. As a result of
obstruction of the pyloric orifice the stomach becomes dilated,
sometimes enormously, so as to occupy most of the abdominal cavity. The
walls of the dilated stomach, particularly the muscular coat, are
usually thickened, but exceptionally they are thinned. Sometimes with
pyloric stenosis the stomach is reduced in size. This occurs
particularly when a scirrhous growth extends diffusely from the pyloric
region over a considerable part of the stomach. Obstruction of the
cardiac orifice or in the oesophagus leads to atrophy of the stomach,
although here also there are exceptions. Above the obstruction the
oesophagus is often dilated. An existing obstruction may be reduced or
removed by ulceration or sloughing of the tumor.

Both dilatation and contraction of the stomach may attend gastric
cancer without any involvement of the orifices of the stomach in the
cancerous growth. The cavity of the stomach may be so shrunken by
scirrhous thickening and contraction of the gastric walls that it will
hardly contain a hen's egg. Irregular deformities in the shape of the
stomach, such as an hour-glass shape and diverticular recesses, may be
caused by gastric cancer.

Changes in the shape of the stomach and the weight of the tumor may
cause displacements of pyloric cancers, so that these tumors have been
found in nearly all regions of the abdomen, and even in the true
pelvis.[86] Such displaced cancers usually contract adhesions with
surrounding parts.

[Footnote 86: Lebert, _op. cit._, p. 420.]

It is not necessary to dwell upon the formation of adhesions which may
bind the stomach to nearly all of the abdominal organs, most frequently
to the liver, the pancreas, the intestine, and the anterior abdominal
wall. Adhesions of pyloric cancers are found in at least two-thirds of
the cases, and probably oftener.[87]

[Footnote 87: Gussenbauer and V. Winiwarter found adhesions recorded in
370 out of 542 pyloric cancers. In considering the propriety of
resection of gastric cancers it has become a matter of importance to
know in what proportion of cases adhesions are present. I agree with
Ledderhose and with Rydygier in believing that adhesions are present
oftener than appears from Gussenbauer and V. Winiwarter's statistics.
The fact that adhesions are not noted in post-mortem records of gastric
cancer cannot be considered proof of their absence. Little has been
done in the study of gastric cancer from a surgical point of view.
Metastases and adhesions were absent in only 5 out of 52 cases of
pyloric cancer in which either pylorectomy or exploratory laparotomy
was performed (Rydygier).]

Cancer of the stomach in the majority of cases is accompanied with
{567} metastases in other parts of the body. In 1120 cases of gastric
cancer secondary cancers were present in 710, or 63.4 per cent., and
absent in 410, or 36.6 per cent.[88] In about two-thirds of the cases,
therefore, secondary deposits were present.

[Footnote 88: These cases are from Habershon, _op. cit._; Lebert, _op.
cit._; _Trans. N.Y. Path. Soc._, vol. i.; and Gussenbauer and Von
Winiwarter, _loc. cit._]

In order to determine the relative frequency of the secondary deposits
in various organs of the body, I have constructed the following table,
based upon an analysis of 1574 cases of cancer of the stomach in which
the situation of the metastases were given:[89]

  Lymphatic glands.                    551  35.0%
  Liver.                               475  30.2%
  Peritoneum, omentum, and intestine.  357  22.7%
  Pancreas.                            122   7.8%
  Pleura and lung.                      98   6.2%
  Spleen.                               26   1.7%
  Brain and meninges.                    9   0.6%
  Other parts of the body.              92   5.8%

[Footnote 89: These cases include, in addition to those cited in the
preceding foot-note, those of Dittrich (_Prager Vierteljahrschr._, vol.
xvii.), Wrany (_ibid._, vols. xciv. and xcix.), Katzenellenbogen (_op.
cit._), and Lange (_op. cit._). Metastases in the intestine formed only
a small number of those under the heading peritoneum, omentum, and
intestine, but as they were all included together in Gussenbauer's
large statistics, the intestinal metastases could not well be placed
separately. In 673 cases the peritoneum and omentum were cancerous in
21.7 per cent.]

Secondary cancerous deposits are probably even more frequent in the
lymphatic glands than appears from the table. In 1153 cases of gastric
cancer in which the situation of the affected lymphatic glands is
specified, the abdominal glands, and chiefly those near the stomach,
were the seat of cancer in 32-1/2 per cent. In Lange's 210 cases the
cervical glands were affected in 4.3 per cent. In other statistics this
percentage is much smaller. In nearly one-third of the cases there are
secondary cancers in the liver. These may attain an enormous size in
comparison with the tumor of the stomach. Cancer of the peritoneum and
of the omentum is found in about one-fifth of the cases of gastric
cancer. The spleen is rarely involved, except by continuous growth of a
cancer of the fundus or in cases of widespread distribution of cancer
through the aortic circulation. Cancer of the liver increases the
liability to metastases in the lungs, but the latter may be present
without any cancerous deposits in the liver. Secondary cancers may be
present in the suprarenal capsules, the kidneys, the ovaries, the
heart, the thoracic duct, the bones, the skin, etc. In an interesting
case reported by Finlay[90] the subcutaneous tissue of the trunk was
thickly studded with small nodules, of which two were excised during
life and found to be cylindrical epitheliomata. This led to the
diagnosis of a primary tumor of the same nature in the stomach or in
the intestine. At the autopsy was found a cylindrical epithelioma of
the stomach which had not given rise to characteristic symptoms.
Secondary cancer of the intestine is rare if the deposits in the
peritoneal coat be {568} excepted. Several cancerous ulcers or multiple
cancerous nodules may be found along the intestinal tract, involving
the mucous and the submucous coats.[91] These metastases seem best
explained by the theory of implantation of cancerous elements which
have been carried from the primary growth in the stomach into the
intestine. In some of the cases the idea of multiple primary cancers
may also be entertained.

[Footnote 90: _Trans. Path. Soc. London_, vol. xxxiv. p. 102.
Unfortunately, in Roseler's case of multiple skin-cancers with an
ulcerated cancer of the stomach no microscopical examination of the
skin-nodules was made. The interpretation of this case is therefore
doubtful (_Virchow's Archiv_, Bd. 77, p. 372).]

[Footnote 91: Cases in point are recorded by Wrany (_loc. cit._), Blix
(_Virchow u. Hirsch's Jahresbericht_, 1876, ii. p. 207), Lange,
Katzenellenbogen, and Lebert.]

It is not rare for gastric cancer to cause secondary deposits in the
stomach itself. Sometimes it is difficult to decide which of two or
more cancers in the stomach is the primary growth, as in Ripley's case
of ulcerated cancer of the cardiac orifice with a similar growth around
the pyloric orifice.[92] It is probable that in very rare instances
multiple primary cancers may develop in the stomach.

[Footnote 92: J. H. Ripley, _Trans. N.Y. Path. Soc._, vol. iv. p. 121.
Maurizio has also reported a case of scirrhous cancer of the cardia
with scirrhous cancer of the pylorus (_Annal. univ. di Medicina_, Oct.,
1869). A similar case was observed by Barth (_Gaz. hebdom._, 1856, No.
24, p. 424).]

Cancerous metastases are produced by the transportation of cancerous
elements by the lymphatic current or by the blood-current. In a number
of instances the portal vein or some of the branches which help to form
it have been found plugged with a cancerous mass which may or may not
be organized.[93] The cancer in these cases has burst through the walls
of the vessel into the lumen, where it may grow both in the direction
and against the direction of the current. On serous surfaces, and
probably also, although rarely, on mucous surfaces, secondary cancers
may develop from cancerous particles detached from a parent tumor and
scattered over the surface as a kind of seminium.

[Footnote 93: Cases of this kind have been reported with especial
fulness by Spaeth (_Virchow's Archiv_, Bd. 35, p. 432), Acker
(_Deutsches Arch. f. kl. Med._, Bd. 11, p. 173), and Audibert (_De la
Generalisation du Cancer de l'Estomac_, Paris, Thesis, 1877).]

Mention has already been made of the invasion of parts adjacent to the
stomach by the continuous growth of gastric cancer. In this way
lymphatic glands, the liver, the pancreas, the omenta, the transverse
colon, the spleen, the diaphragm, the anterior abdominal wall, the
vertebrae, the spinal cord and membranes, and other parts may be
involved in the cancerous growth.

Under the head of Complications reference has already been made to
various lesions which may be associated with gastric cancer. As regards
the manifold complications caused by perforation of gastric cancer, in
addition to what has already been said the article on gastric ulcer may
be consulted. In general, the various fistulous communications caused
by gastric cancer are less direct than those produced by gastric ulcer.
The wasting of various organs of the body in cases of gastric cancer
may be found on post-mortem examination to be extreme. Habershon
mentions a case in which the heart of a woman forty years old weighed
only 3-1/2 ounces after death from cancer of the pylorus. As in other
profoundly anaemic states, the embryonic or lymphoid alteration of the
marrow of the bones is often present in gastric cancer.

PATHENOGENESIS.--The problems relating to the ultimate causation and
origin of gastric cancer belong to the pathenogenesis of cancer in
general. Our knowledge with reference to these points is purely
hypothetical. It will suffice in this connection simply to call
attention to {569} Virchow's doctrine, that cancer develops most
frequently as the result of abnormal or of physiological irritation,
hence in the stomach most frequently at the orifices; and to Cohnheim's
theory, that cancer as well as other non-infectious tumors originate in
abnormalities in development, more specifically in persistent embryonic
cells. According to the latter view, gastric cancer develops only in
those whose stomachs from the time of birth contain such embryonic
remnants. These unused embryonic cells may lie dormant throughout life
or they may be incited to cancerous growth by irritation, senile
changes, etc. According to Cohnheim's theory, the orifices of the
stomach are the most frequent seat of cancer on account of complexity
in the development of these parts.

For a full consideration of these theories the reader is referred to
the section of this work on General Pathology.

DIAGNOSIS.--The presence of a recognizable tumor in the region of the
stomach outweighs in diagnostic value all other symptoms of gastric
cancer. The detection of fragments of cancer in the vomit or in
washings from the stomach is of equal diagnostic significance, but of
rare applicability. The discovery of secondary cancers in the liver, in
the peritoneum, or in lymphatic glands may render valuable aid in
diagnosis. Of the local gastric symptoms, coffee-ground vomiting is the
most important. The relation between the local and the general symptoms
may shed much light upon the case. While anorexia, indigestion,
vomiting, and epigastric pain and tenderness point to the existence of
a gastric affection, the malignant character of the affection may be
surmised by the development of anaemia, emaciation, and cachexia more
rapid and more profound than can be explained solely by the local
gastric symptoms. The value to be attached in the diagnosis of gastric
cancer to the absence of free hydrochloric acid from the contents of
the stomach must still be left sub judice. The age of the patient, the
duration, and the course of the disease are circumstances which are
also to be considered in making the diagnosis of gastric cancer. These
symptoms of gastric cancer have already been fully considered with
reference to their presence and absence and to their diagnostic
features.

It remains to call attention to the differential diagnosis between
gastric cancer and certain diseases with which it is likely to be
confounded. The points of contrast which are to be adduced relate
mostly to the intensity and the frequency of certain symptoms. There is
not a symptom or any combination of symptoms of gastric cancer which
may not occur in other diseases. Hence the diagnosis is reached by a
balancing of probabilities, and not by any positive proof.
Notwithstanding these difficulties, gastric cancer is diagnosed
correctly in the great majority of cases, although often not until a
late stage of the disease. Errors in diagnosis, however, are
unavoidable, not only in cases in which the symptoms are ambiguous or
misleading, but also in cases in which all the symptoms of gastric
cancer, including gastric hemorrhage and tumor, are present, and still
no gastric cancer exists. Cases of the latter variety are of course
rare.

In the absence of tumor the diseases for which gastric cancer is most
liable to be mistaken are gastric ulcer and chronic gastric catarrh. In
the following table are given the main points of contrast between these
three diseases: {570}

    GASTRIC CANCER.    |    GASTRIC ULCER.     |    CHRONIC CATARRHAL
                       |                       |        GASTRITIS.
                       |                       |
  1. Tumor is present  |  1. Tumor rare.       |  1. No tumor.
  in three-fourths of  |                       |
  the cases.           |                       |
                       |                       |
  2. Rare under forty  |  2. May occur at any  |  2. May occur at any
  years of age.        |  age after childhood. |  age.
                       |  Over one-half of the |
                       |  cases under forty    |
                       |  years of age.        |
                       |                       |
  3. Average duration  |  3. Duration          |  3. Duration
  about one year,      |  indefinite; may be   |  indefinite.
  rarely over two      |  for several years.   |
  years.               |                       |
                       |                       |
  4. Gastric hemorrhage|  4. Gastric hemorrhage|  4. Gastric
  frequent, but rarely |  less frequent than in|  hemorrhage rare.
  profuse; most common |  cancer, but oftener  |
  in the cachectic     |  profuse; not uncommon|
  stage.               |  when the general     |
                       |  health is but little |
                       |  impaired.            |
                       |                       |
  5. Vomiting often has|  5. Vomiting rarely   |  5. Vomiting may or
  the peculiarities of |  referable to         |  may not be present.
  that of dilatation of|  dilatation of the    |
  the stomach.         |  stomach, and then    |
                       |  only in a late stage |
                       |  of the disease.      |
                       |                       |
  6. Free hydrochloric |  6. Free hydrochloric |  6. Free hydrochloric
  acid usually absent  |  acid usually present |  acid may be present
  from the gastric     |  in the gastric       |  or absent.
  contents in cancerous|  contents.            |
  dilatation of the    |                       |
  stomach.             |                       |
                       |                       |
  7. Cancerous         |  7. Absent.           |  7. Absent.
  fragments may be     |                       |
  found in the washings|                       |
  from the stomach or  |                       |
  in the vomit (rare). |                       |
                       |                       |
  8. Secondary cancers |  8. Absent.           |  8. Absent.
  may be recognized in |                       |
  the liver, the       |                       |
  peritoneum, the      |                       |
  lymphatic glands, and|                       |
  rarely in other parts|                       |
  of the body.         |                       |
                       |                       |
  9. Loss of flesh and |  9. Cachectic         |  9. When
  strength and         |  appearance usually   |  uncomplicated,
  development of       |  less marked and of   |  usually no
  cachexia usually more|  later occurrence than|  appearance of
  marked and more rapid|  in cancer; and more  |  cachexia.
  than in ulcer or in  |  manifestly dependent |
  gastritis, and less  |  upon the gastric     |
  explicable by the    |  disorders.           |
  gastric symptoms.    |                       |
                       |                       |
  10. Epigastric pain  |  10. Pain is often    |  10. The pain or
  is often more        |  more paroxysmal, more|  distress induced by
  continuous, less     |  influenced by taking |  taking food is
  dependent upon taking|  food, oftener        |  usually less severe
  food, less relieved  |  relieved by vomiting,|  than in cancer or in
  by vomiting, and less|  and more sharply     |  ulcer. Fixed point
  localized, than in   |  localized, than in   |  of tenderness
  ulcer.               |  cancer.              |  usually absent.
                       |                       |
  11. Causation not    |  11. Causation not    |  11. Often referable
  known.               |  known.               |  to some known cause,
                       |                       |  such as abuse of
                       |                       |  alcohol,
                       |                       |  gormandizing, and
                       |                       |  certain diseases, as
                       |                       |  phthisis, Bright's
                       |                       |  disease, cirrhosis
                       |                       |  of the liver, etc.
                       |                       |
  12. No improvement or|  12. Sometimes a      |  12. May be a history
  only temporary       |  history of one or    |  of previous similar
  improvement in the   |  more previous similar|  attacks. More
  course of the        |  attacks. The course  |  amenable to
  disease.             |  may be irregular and |  regulation of diet
                       |  intermittent. Usually|  than is cancer.
                       |  marked improvement by|
                       |  regulation of diet.  |

{571} The diagnosis between gastric cancer and gastric ulcer is more
difficult than that between cancer and gastritis, and sometimes the
diagnosis is impossible. The differential points mentioned in the table
are of very unequal value. An age under thirty, profuse hemorrhage, and
absence of tumor are the most important points in favor of ulcer;
tumor, advanced age, and coffee-ground vomiting continued for weeks are
the most important points in favor of cancer. As cancer may have been
preceded by ulcer or chronic gastritis for years, it is evidently
unsafe to trust too much to the duration of the illness. As has already
been said, it is best to place no reliance in the differential
diagnosis upon the character of the pain. Any peculiarities of the
vomiting, the appetite, or the digestion are of little importance in
the differential diagnosis. Cachexia is of more importance, but it is
to be remembered that ulcer, and even chronic gastritis in rare
instances, may be attended by a cachexia indistinguishable from that of
cancer. Cases might be cited in which very decided temporary
improvement in the symptoms has been brought about in the course of
gastric cancer, so that too much stress should not be laid upon this
point. Enough has been said under the Symptomatology with reference to
the diagnostic bearings of the absence of free hydrochloric acid from
the stomach, of the presence of cancerous fragments in fluids from the
stomach, and of secondary cancers in different parts of the body.

One must not lose sight of the fact that the whole complex of symptoms,
the order of their occurrence, and the general aspect of the case, make
an impression which cannot be conveyed in any diagnostic table, but
which leads the experienced physician to a correct diagnosis more
surely than reliance upon any single symptom.

In the early part of the disease there may be danger of confounding
gastric cancer with nervous dyspepsia or with gastralgia, but with the
progress of the disease the error usually becomes apparent. What has
already been said concerning the symptomatology and the diagnosis of
gastric cancer furnishes a sufficient basis for the differential
diagnosis between this disease and nervous affections of the stomach.

Chronic interstitial gastritis or fibroid induration of the stomach
cannot be distinguished with any certainty from cancer of the stomach.
Fibroid induration of the stomach is of longer duration than gastric
cancer, and it is less frequently attended by severe pain and
hemorrhage. Sometimes a hard, smooth tumor presenting the contours of
the stomach can be felt, but this cannot be distinguished from diffuse
cancerous infiltration of the stomach.

Non-malignant stenosis of the pylorus is of longer duration than cancer
of the pylorus. The symptoms of dilatation of the stomach are common to
both diseases. Cicatricial stenosis is the most common form of
non-malignant pyloric stenosis. This is usually preceded by symptoms of
gastric ulcer which may date back for many years. Non-malignant
stenosis more frequently occurs under forty years of age than does
cancer. The diagnosis between malignant and non-malignant stenosis of
the pylorus is in some cases impossible.

Although the surest ground for the diagnosis of gastric cancer is the
appearance of tumor, there are cases in which it is difficult to decide
whether the tumor really belongs to the stomach, and even should it be
{572} established that the tumor is of the stomach, there may still be
doubt whether or not it is cancerous.

The diagnosis between cancerous and non-cancerous tumors of the
stomach, such as sarcoma, fibroma, myoma, etc., hardly comes into
consideration. The latter group of tumors rarely produces symptoms
unless the tumor is so situated as to obstruct one of the orifices of
the stomach. Even in this case a positive diagnosis of the nature of
the tumor is impossible.

Of greater importance is the distinction between cancerous tumors of
the stomach and tumors produced by thickening of the tissues and by
adhesions around old ulcers of the stomach. Besides the non-progressive
character of the small and usually indistinct tumors occasionally
caused by ulcers or their cicatrices, the main points in diagnosis are
the age of the patient and the existence, often for years, of symptoms
of gastric ulcer antedating the discovery of the tumor. The long
duration of symptoms of chronic catarrhal gastritis and of dilatation
of the stomach is also the main ground for distinguishing from cancer a
tumor produced by hypertrophic stenosis of the pylorus.

Tumors of organs near the stomach are liable to be mistaken for cancer
of the stomach. The differential diagnosis between gastric cancer on
the one hand, and tumors of the left lobe of the liver and tumors of
the pancreas on the other hand, is often one of great difficulty.

Tumors of the liver are generally depressed by inspiration, whereas
tumors of the stomach are much less frequently affected by the
respiratory movements. The percussion note over tumors of the liver is
flat, while a tympanitic quality is usually associated with the dulness
over tumors of the stomach. Light percussion will often bring out a
zone of tympanitic resonance between the hepatic flatness and the
dulness of gastric tumors. Gastric tumors are usually more movable than
hepatic tumors. By palpation the lower border of the liver can perhaps
be felt and separated from the tumor in case this belongs to the
stomach. Most of the points of distinction based upon these physical
signs fail in cases in which a gastric cancer becomes firmly adherent
to the liver. The basis for a diagnosis must then be sought in the
presence or the absence of marked disturbance of the gastric functions,
particularly of haematemesis, vomiting, and dilatation of the stomach.
On the other hand, ascites and persistent jaundice would speak in favor
of hepatic cancer. There are cases in which the diagnosis between
hepatic cancer and gastric cancer cannot be made. This is especially
true of tumors of the left lobe of the liver, which grow down over the
stomach and compress it, and which are accompanied by marked
derangement of the gastric functions. The frequency with which cancer
of the stomach is associated with secondary cancer of the liver should
be borne in mind in considering the diagnosis.

There are certain symptoms which in many cases justify a probable
diagnosis of cancer of the pancreas, but this disease can rarely be
distinguished with any certainty from cancer of the stomach. The
situation of the tumor is the same in both diseases. With pancreatic
cancer the pain is less influenced by taking food, the vomiting is less
prominent as a symptom, and anorexia, haematemesis, and dilatation of
the stomach are less common than with gastric cancer. Of the positive
symptoms in {573} favor of cancer of the pancreas, the most important
are jaundice, fatty stools, and sugar in the urine. Of these symptoms
jaundice is the most common.

Should there be any suspicion that the tumor is caused by impaction of
feces, a positive opinion should be withheld until laxatives have been
given.

Mistakes may occur as to the diagnosis between gastric cancer and
tumors of the omenta, the mesentery, the transverse colon, the
lymphatic glands, and even the spleen or the kidney. Encapsulated
peritoneal exudations near the stomach have been mistaken for gastric
cancer. Where a mistake is likely to occur each individual case
presents its own peculiarities, which it is impossible to deal with in
a general way. Of the utmost importance is a careful physical
exploration of the characters and relations of the tumor, aided, if
necessary, by artificial distension of the stomach or of the colon by
gas (see page 549). No less important is the attentive observance of
the symptoms of each case. In doubtful cases fluids withdrawn from the
stomach by the stomach-tube should be carefully examined for cancerous
fragments, and the gastric fluids may be tested for free hydrochloric
acid by methods already described.

Pyloric cancers which receive a marked pulsation from the aorta
sometimes raise a suspicion of aneurism, but the differential diagnosis
is not usually one of great difficulty. Gastric cancer when it presses
upon the aorta may simulate aneurism, not only by the presence of
pulsation, but also by the existence of a bruit over the tumor. The
tumor produced by aneurism is generally smoother and rounder than that
caused by cancer. The pulsation of an aneurism is expansile, but the
impulse of a tumor resting upon an artery is lifting and generally
without lateral expansion. The impulse transmitted to a tumor resting
upon the abdominal aorta may be lessened by placing the patient upon
his hands and knees. Sometimes the tumor can be moved with the hands
off from the artery, so that the pulsation momentarily ceases. A severe
boring pain in the back, shooting down into the loins and the lower
extremities, and not dependent upon the condition of the stomach,
characterizes abdominal aneurism, but is not to be expected in gastric
cancer. With aneurism gastric disorders and constitutional disturbance
are much less prominent than with cancer of the stomach.[94]

[Footnote 94: In a case of pulsating pyloric cancer observed by Bierner
the symptoms were much more in favor of aneurism than of cancer. The
cancer had extended to the retro-peritoneal glands, which partially
surrounded and compressed the aorta. There were marked lateral
pulsation of the tumor, distinct systolic bruit, diminution of the
femoral pulse, and severe lancinating pain in the back and sacral
region. With the exception of vomiting, the gastric symptoms were
insignificant. The patient was only thirty-three years old (Ott, _Zur
Path. des Magencarcinoms_, Zurich, 1867, p. 71).]

Spasm of the upper part of the rectus abdominis muscle may simulate a
tumor in the epigastric region. The diagnosis is made by noting the
correspondence in shape and position between the tumor and a division
of the rectus muscle, the superficial character of the tumor, the
effect of different positions of the body upon the distinctness of the
tumor, the tympanitic resonance over the tumor, and, should there still
be any doubt, by anaesthetizing the patient, when the phantom tumor
will disappear. Spasm of the rectus muscle has been observed in cases
of cancer of the stomach.

{574} Attention is also called to the possibility of mistaking in
emaciated persons the head of the normal pancreas, or less frequently
the mesentery and lymphatic glands, for a tumor.[95] As emaciation
progresses the at first doubtful tumor may even appear to increase in
size and distinctness.

[Footnote 95: In the case of the late Comte de Chambord the diagnosis
of gastric cancer was made upon what appeared to be very good grounds.
No cancer, however, existed, and the ill-defined tumor which was felt
during life in the epigastric region proved to be the mesentery
containing considerable fat (Vulpian, "La derniere Maladie de M. le
Comte de Chambord." _Gaz. hebd. de Med. et de Chir._, Sept. 14, 1883).]

It is sufficient to call attention to the danger of mistaking, in cases
where the gastric symptoms are not prominent and no tumor exists,
gastric cancer for pernicious anaemia, senile marasmus, or the chronic
phthisis of old age. In some of these cases the diagnosis is
impossible, but the physician should bear in mind the possibility of
gastric cancer in the class of cases here considered, and should search
carefully for a tumor or other symptom which may aid in the diagnosis.

The possibility of mistaking gastric cancer accompanied with peritoneal
exudation for cirrhosis of the liver or for tubercular peritonitis is
also to be borne in mind.

The diagnosis of the position of the cancer in the stomach can usually
be made in cases of cancer of the cardia or of the pylorus. The
symptoms diagnostic of cancer of the cardia are dysphagia,
regurgitation of food, obstruction in the passage of the oesophageal
bougie, and sinking in of the epigastric region in consequence of
atrophy of the stomach. It has already been said that catheterization
of the oesophagus does not always afford the evidence of obstruction
which one would expect. Cancerous stenosis of the cardia is to be
distinguished from cicatricial stenosis in this situation. The
diagnosis is based upon the history of the case, which is generally
decisive, and upon finding fragments of cancer in the tube passed down
the oesophagus.

That the cancer is seated at the pylorus is made evident by the
situation of the tumor (see p. 561) and by the existence of dilatation
of the stomach. There are many more causes of stenosis of the pylorus
than of stenosis of the cardia, so that, notwithstanding the absence of
tumor, cancer of the cardia is often more readily diagnosticated than
cancer of the pylorus.

The greatest difficulty in diagnosis is presented by cancers which do
not obstruct the orifices of the stomach. Many of these cancers run an
almost latent course so far as the gastric symptoms are concerned, and
in case they produce no recognizable tumor and are unattended with
hemorrhage, the difficulties in their diagnosis are almost
insurmountable.

In general, a diagnosis of the particular form of cancer which is
present cannot be made, nor is such a diagnosis of any practical value.
In very exceptional cases such a diagnosis might be made by the
examination of secondary subcutaneous cancers[96] or of fragments found
in the fluids obtained from the stomach.

[Footnote 96: As for example, in Finlay's case, already referred to (p.
567). It is not safe to trust implicitly in this criterion, as the
subcutaneous tumors may be of a different nature from the tumor of the
stomach, as in an interesting case observed by Leube (_op. cit._, p.
125).]

Although the diagnosis of gastric cancer can generally be made before
the death of the patient, unfortunately a positive diagnosis in the
early stages of the disease is usually impossible. Should resection of
cancer {575} of the stomach become a legitimate operation in surgery,
it will be of the utmost importance to make the diagnosis in an early
stage of the disease. Only those cases are suitable for resection in
which there are no secondary deposits, the general health of the
patient is in fair condition, and extensive adhesions have not been
formed. It was to be hoped that the ingenious instrument devised by
Mikulicz for exploring the interior of the stomach by electrical
illumination would prove a valuable aid in diagnosis. The gastroscope
in its present construction, however, has proved of little value.[97]
It is, moreover, difficult to manipulate, and is not free from danger
to the patient. We may be permitted, however, to hope for improvement
in this direction.

[Footnote 97: Mikulicz has observed with the gastroscope in a case of
pyloric cancer immobility of the pylorus and absence of rugae in the
mucous membrane of the pyloric region (_Wiener med. Wochenschr._, 1883,
No. 24). It does not seem probable that there can be anything peculiar
to cancer in these appearances.]

In cases in which there is reasonable suspicion of the existence of
gastric cancer, and in which there is proper ground to contemplate
resection of the tumor, it is justifiable to make an exploratory
incision into the abdomen. It can then be decided whether or not cancer
exists, and whether the case is suitable for operation. When this
incision is made with all of the precautions known to modern surgery,
it is attended with little or no danger,[98] and it should not be made
except by surgeons who are practically familiar with these precautions.

[Footnote 98: Of 20 exploratory incisions for tumor of the stomach
performed by Billroth, not one had ended fatally (_Deutsche med.
Wochenschrift_, 1882, ii.).]

PROGNOSIS.--There is no proof that cancer of the stomach has ever ended
in recovery. It may be admitted that partial cicatrization of gastric
cancer may occur. We have, however, no sufficient reason to believe
that cancer of the stomach has ever been completely destroyed by any
process of nature or by any medicinal treatment.

A successful resection of a cancer of the pylorus by Billroth in
January, 1881, made a great sensation in the medical world. Since that
time the operation has been performed successfully ten times, and with
fatal issue twenty-seven times. A radical cure has not, however, been
effected, although life has been prolonged for a year and a half after
the operation.[99] The possibility of permanent cure of gastric cancer
by extirpation must be admitted. Enthusiasm over this possibility,
however, is seriously lessened by the fact that a radical cure is not
to be expected unless the operation is undertaken when the tumor is of
small size, has produced no distant metastases, is free from many
adhesions, and the patient is not greatly prostrated. In view of the
difficulty of diagnosis in the early stages it is not likely that these
favorable conditions can be fulfilled except in the rarest instances.
Metastases may already exist when the tumor is small and before it has
given rise to any symptoms.[100] Pylorectomy, moreover, will probably
be successful in the hands of only comparatively few surgeons. It is
therefore but a feeble glimmer of hope {576} which is now admitted to
the hitherto relentlessly fatal forecast of this disease.

[Footnote 99: Several of the patients are still living (1884), but, so
far as I can learn, no patient has survived the operation more than a
year and a half.]

[Footnote 100: Birch-Hirschfeld relates a case in which a non-ulcerated
cancerous tumor not larger than a silver half-dollar was found in the
pyloric region of the stomach of a woman who died from injury. The
tumor had given rise to no symptoms. Nevertheless, numerous metastases
existed in the lymphatic glands of the omentum and of the lesser
curvature (_Jahresb. d. gesellschaft f. Natur u. Heilk. im Dresden_
[1882-83], 1883, p. 37).]

TREATMENT.--Even up to the present time various drugs have been vaunted
as effecting a radical cure of cancer of the stomach. Some of these,
such as mercury, are positively harmful; others, such as conium,
belladonna, and condurango, are often palliative; but not one has been
proven to be curative. Since its recommendation by Friedreich in 1874,
condurango has enjoyed the greatest vogue. The few observations in
which, under the use of this agent, tumors, real or apparent, of the
stomach have lessened in size or disappeared, admit of other
interpretations than as cures of gastric cancer. There is, however,
considerable testimony as to the virtues of condurango as a stomachic.
In some cases it relieves the pain, vomiting, and indigestion of
gastric cancer, but in many cases it is employed without benefit. The
drug which passes by the name of condurango in the market is a very
variable preparation. According to Friedreich's directions, decoction
of condurango is prepared as follows: Macerate oz. ss of cort.
condurango for twelve hours with fluidounce xij of water; then boil
down to fluidounce vj and strain. The dose is a tablespoonful two or
three times daily. The decoction of condurango may be combined with
syr. aurantii cort.

While all specific treatment of gastric cancer is to be abandoned, much
can be done for the relief and comfort of the patient. The treatment is
symptomatic.

In general, the indications are similar to those in gastric ulcer. It
is not necessary, however, to restrict the diet to the same extent as
in gastric ulcer. The patient's tastes may be consulted to a
considerable extent. Still, it will be found, as a rule, that the
patient is most comfortable when his diet is confined to
easily-digestible substances, such as milk, beef-juice, Leube's
beef-solution, rare beefsteak, and other articles mentioned under the
treatment of gastric ulcer.

The pain of gastric cancer will usually require the administration of
opium in some form. There is manifestly not the same objection to the
employment of narcotics in a necessarily fatal disease like cancer as
in ulcer of the stomach. Opium may be given in pill form or as the
tincture or deodorized tincture, or often most advantageously as
hypodermic injections of morphia, to which atropia may be added.

Vomiting is sometimes controlled by regulation of the diet,
particularly by iced milk. For this symptom also opium or morphia is
often necessary. In addition, the customary remedies for relief of
vomiting, such as bits of ice, iced champagne, soda-water, hydrocyanic
acid, oxalate of cerium, creasote, may be tried. Cold or hot
applications to the abdomen and mild counter-irritants, such as mustard
plaster or turpentine stupes, sometimes afford relief. If the vomiting
be incoercible, it may be well to administer food for a short time
exclusively by the rectum, and in case of stenosing cancer of the
cardia this method of administering food may be the only one possible.

Acid eructations and heartburn are often relieved by the antacids, as
bicarbonate of sodium, lime-water, or calcined magnesia. Against
fermentative processes in the stomach have been recommended salicylate
of sodium, creasote, carbolic acid, and the alkaline hyposulphites.
Charcoal tablets are as useful as, and less likely to disagree than,
other antifermentatives. {577} In view of V. d. Velden's
investigations, already mentioned, the administration of dilute
hydrochloric acid in an hour after a meal is indicated.

Excellent results have been obtained by regularly washing out the
stomach in cases of gastric cancer, particularly in pyloric cancer with
dilatation of the stomach. By this procedure pain, indigestion, and
vomiting are often greatly relieved, and the patient experiences a
renewed sense of well-being. Unfortunately, the benefit is only
temporary. The syphon process is most conveniently employed.
Contraindications to the use of the stomach-tube are copious
gastrorrhagia and great weakness of the patient.

When constipation is not relieved by washing out the stomach, enemata
should be employed. Drastic purgatives should not be given.

For diarrhoea opium may be given, particularly in the form of small
enemata of starch and laudanum.

Scanty hemorrhage in the form of coffee-grounds vomiting requires no
treatment. Copious haematemesis is to be treated according to the
principles laid down under the treatment of hemorrhage from gastric
ulcer.

Discussion of the surgical treatment of gastric cancer of course does
not belong to this work. The opinion entertained by the physician as to
the propriety of surgical interference in gastric cancer is not,
however, a matter of indifference, for cases of gastric cancer come
first into the hands of the physician, and generally only by his
recommendation into those of the surgeon. So long as the physician
stands absolutely powerless before this disease, his general attitude
as to the propriety of surgical interference should not be one of
hostility. Experience only can determine the justification of surgical
operation in cases of gastric cancer. As yet, it is too soon to express
a positive opinion as to the value of resection of gastric cancer. Of
37 published resections of cancer of the pylorus, 27 died from the
effects of the operation, and of the fatal cases 18 within the first
twenty-four hours. These results are certainly not calculated to awaken
much enthusiasm for the operation. Still, it would be wrong to draw
definite conclusions from the existing statistics of resection of the
cancerous pylorus, partly because the number of operations is as yet
too small, partly because the operation has been done when it was
certainly unwarrantable according to the best judges (Billroth,
Czerny), and chiefly because the number of operators in proportion to
the number of operations is too great. For the 37 published operations
there have been 27 operators. Ovariotomy was not considered a
justifiable operation until the excellent results of individual
operators were obtained. It is probable that to an even greater extent
resection of the pylorus will become the specialty of certain
operators. Therefore, before concluding as to the value of resection of
cancer of the stomach it is necessary to await the results of
individual surgeons in a series of cases.[101]

[Footnote 101: Already, from this point of view, the operation appears
more hopeful. Czerny has performed 6 resections of the stomach with
only 2 fatal results; 4 of the operations were pylorectomies for
cancer. Billroth has performed the operation 8 times with 3 fatal
results (_Wiener med. Wochenschrift_, 1884, Nos. 17 and 29).]

So much, however, is now certain, that with our present means of
diagnosis the number of cases suitable for extirpation is very
small.[102] A {578} radical cure is to be expected only in the rarest
instances, so that the value of the operation will depend chiefly upon
the condition of the patient after its performance. As regards this
point, the results in the successful cases have been encouraging. In
several instances the terrible sufferings of the patient have given
place to months of comparative health and comfort.

[Footnote 102: Billroth at the eleventh session of the Congress of
German Surgeons said that he was amazed at the number of resections of
the pylorus which had been performed. Out of 50 to 60 cases of gastric
cancer, only 1 appeared to him suitable for operation.]

In cases of extreme cancerous stenosis of the pylorus which are not
suitable for resection Wolfler proposed forming a fistulous
communication between the stomach and the small intestine
(gastro-enterostomy). The results of the operation have not been
encouraging. Out of six cases in which this operation has been
performed, only two patients lived after the operation.

For the same condition Schede proposed making a duodenal fistula
(duodenostomy), but I am not aware that the operation has been
performed.

The results of gastrostomy for relief of cancerous stenosis of the
cardia or of the oesophagus have not been encouraging.[103]

[Footnote 103: Of 76 cases of gastrostomy for the relief of cancer of
the oesophagus or of the cardia, only 14 lived over thirty days
(Leisrink and Alsberg, _Arch. f. klin. Chir._, Bd. 28, p. 760, 1882).]


Non-Cancerous Tumors of the Stomach.

Little clinical interest attaches to non-cancerous tumors of the
stomach. They are comparatively rare and usually unattended by
symptoms. Even should a tumor be discovered, there are no means of
determining the nature of the tumor; and if symptoms are produced by
the tumor, the case will probably be diagnosticated as one of cancer.
It is necessary, therefore, in the present work to do little more than
enumerate the different forms of non-cancerous tumor of the stomach.

The most common of benign gastric tumors are polypi projecting into the
interior of the stomach. These are usually so-called mucous or
adenomatous polypi, being composed of hypertrophied or hyperplastic
elements of the mucous membrane with or without new growth of submucous
tissue. They may be present in large number (one hundred and fifty to
two hundred in a case of Leudet's). Their development is usually
attributed to a chronic catarrhal gastritis, so that a gastritis
polypora has been distinguished. These polyps are important only when
they obstruct one of the orifices of the stomach, in which case they
may cause even fatal stenosis. This occurrence is very rare.

Benign adenomata appear less frequently as growths in the submucous
coat of the stomach (Winiwarter).

Myomata and myosarcomata, projecting sometimes as polyps either into
the gastric or the peritoneal cavity, may attain a very large size, as
in a case reported by Brodowski in which a cystic myosarcoma of the
stomach weighed twelve pounds.[104]

[Footnote 104: _Virchow's Archiv_, Bd. 67.]

Sarcoma, either as a primary or a secondary tumor of the stomach, is
rare. Two cases of secondary lympho-sarcoma of the stomach (primary of
the retro-peritoneal glands) without gastric symptoms have come under
my observation. In a similar case reported by Coupland the symptoms
resembled those of gastric cancer.[105]

[Footnote 105: _Trans. London Path. Soc._, vol. xxviii. p. 126.]

{579} In connection with gastric ulcer mention has already been made of
the occurrence of miliary aneurisms in the stomach, which may be the
cause of fatal haematemesis.

Sometimes the mucous membrane is studded with little cysts, as in a
case reported by Harris.[106]

[Footnote 106: _Am. Journ. Med. Sci._, April, 1869.]

Fibromata and lipomata are very rare.

Foreign bodies in the stomach, particularly balls of hair, have been
sometimes mistaken for tumors, particularly cancer, of this organ.
Schonborn removed successfully a ball of hair from the stomach by
gastrotomy.[107] Before the operation the tumor was considered to be a
movable kidney.

[Footnote 107: _Arch. f. kl. Chirurg._, Bd. xxix. p. 609.]




{580}

HEMORRHAGE FROM THE STOMACH.

BY W. H. WELCH, M.D.


Hemorrhage from the stomach is a symptom, and not a disease. It is a
result of a great variety of morbid conditions in the description of
which it receives more or less consideration. Already the
symptomatology and treatment of hemorrhage from the stomach have been
considered in connection with its two most important causes--namely,
gastric ulcer and gastric cancer. It remains to give a summary of the
etiology and diagnosis of gastric hemorrhage.

Hemorrhage from the stomach is also called gastrorrhagia. The term
haematemesis is not synonymous with gastric hemorrhage, for blood may
be vomited which has simply been swallowed or has passed from the
intestine into the stomach.

ETIOLOGY.--The causes of gastric hemorrhage are as follows:

1. Ulcer of the Stomach.--Simple gastric ulcer is the most frequent
cause of abundant hemorrhage from the stomach. Tuberculous gastric
ulcers, typhoid gastric ulcers, and the ulcers of phlegmonous gastritis
are extremely rare causes of hemorrhage. Hemorrhagic erosion of the
stomach, which by many writers is assigned an important place in the
etiology of gastric hemorrhage, is not an independent affection, and in
my opinion is without any clinical significance.

2. Cancer of the Stomach.--(Non-cancerous tumors of the stomach hardly
deserve mention in this connection, so infrequently are they the cause
of gastric hemorrhage.)

3. Traumatism (mechanical, chemical, thermic).--_a_. Acting from
without the stomach: severe injury to the abdomen, as by a blow or a
fall; penetrating wounds of the stomach.

_b_. Acting from within the stomach: foreign bodies, particularly
sharp-pointed ones; corrosive poisons, as acids and alkalies; other
toxic inflammatory irritants; and very hot substances. Here should also
be mentioned injury from an inflexible stomach-tube and aspiration of
mucous membrane with the stomach-pump.

4. Diseases of the Gastric Blood-vessels.--_a_. Aneurism of the
arteries of the stomach. Miliary aneurisms have been found by Galliard
and others as a cause of profuse and even fatal hemorrhage from the
stomach. Especially in obscure cases should careful search be made for
miliary aneurisms.

_b_. Varices of the veins are a not unimportant cause of gastric
hemorrhage. They are most frequently associated with chronic passive
{581} congestion of the stomach, but they may be found without any
apparent disturbance of the circulation.

_c_. Degenerations of the vessels, particularly fatty and atheromatous
degeneration of the arteries. Probably gastric hemorrhage in
phosphorus-poisoning is to be attributed to fatty degeneration of the
arteries. Amyloid degeneration of the blood-vessels is a doubtful cause
of hemorrhage.

5. Active Congestion of the Stomach.--Here is usually placed gastric
hemorrhage as a result of severe inflammation of the stomach (as acute
catarrhal gastritis), although in these cases the inflammatory
alteration of the vascular walls is an equally important factor.

With more probability the so-called vicarious hemorrhages from the
stomach are to be assigned to active congestion. Sceptical as one is
inclined to be as regards vicarious hemorrhages of the menses, the
occurrence of such hemorrhages, although rare, must be admitted.
Doubtful, however, are alleged cases of gastric hemorrhage taking the
place of suppressed hemorrhoidal bleeding or of epistaxis.

6. Passive Congestion of the Stomach.--This embraces an important group
of causes of gastric hemorrhage. This hemorrhage is the result of
venous congestion caused by some obstruction to the portal circulation.
The obstruction may be--

_a_. In the portal vein itself or its branches within the liver, as in
pylethrombosis, cirrhosis of the liver, tumors, such as cancer or
echinococcus cysts, compressing the portal vein, occlusion of
capillaries in the liver by pigment-deposits in melanaemia, and
dilatation of the bile-ducts in the liver from obstruction to the flow
of bile. Next to ulcer and to cancer of the stomach, cirrhosis of the
liver is the most frequent and important cause of gastrorrhagia.

_b_. In the pulmonary blood-vessels, as in pulmonary emphysema, chronic
pleurisy, and fibroid induration of the lungs.

_c_. In the heart in consequence of uncompensated valvular and other
diseases of the heart.

For evident reasons, obstruction of the pulmonary or of the cardiac
circulation is much less likely to cause gastric hemorrhage than is
obstruction in the portal vein or the liver.

Possibly, gastric hemorrhage which is caused by violent acts of
vomiting may be caused by venous congestion of the mucous membrane of
the stomach. In support of this view, Rindfleisch advances the idea
that the veins in the muscular layers of the stomach, in consequence of
the thinness of their coats, are much more likely than the arteries to
suffer from the compression of the muscle during its contraction.

The occasional occurrence of gastric hemorrhage during pregnancy has
also been attributed to passive congestion of the stomach.

7. Acute Infectious Diseases--namely, yellow fever, acute yellow
atrophy of the liver, relapsing fever; less frequently cholera, typhoid
fever, typhus fever, diphtheria, erysipelas, and the exanthematous
fevers, small-pox, measles, and scarlet fever.

The cause of gastric hemorrhage in these diseases is not understood.
The usual explanation attributes the hemorrhage to dissolution of the
blood-corpuscles and secondary alteration of the walls of the
blood-vessels. Plugging of the vessels with micro-organisms has been
found {582} in only a few instances. The gastrorrhagia of acute yellow
atrophy of the liver has been attributed to dissolution of the blood,
not only by some infectious agent, but also by constituents of the
bile, and also to obstruction of the portal circulation by destruction
and occlusion of capillaries in the liver.

8. Other Constitutional Affections.--_a_. Hemorrhagic
diatheses--namely, scorbutus, purpura, and haematophilia. Strictly
speaking, a hemorrhagic diathesis exists in other affections of this
class.

_b_. Malaria. Here we may distinguish, first, periodical malarial
hemorrhages from the stomach which are cured by quinia; second,
pernicious gastric malarial fever, of very grave prognosis; and third,
hemorrhages in malarial cachexia due to extreme anaemia. Cases which
have been described as malaria with scorbutic complications belong
mostly to the last variety. Mention has already been made of gastric
hemorrhages attributed to malarial pigmentation of the liver.

_c_. Profound Anaemias. The most important affections in this category
are progressive pernicious anaemia, leucocythaemia, and
pseudo-leucocythaemia, including the so-called splenic anaemia.

_d_. Cholaemia. The hemorrhage is attributed to dissolution of the
blood-corpuscles by the action of the biliary salts.

Gastric hemorrhage is a rare event in Bright's disease, occurring more
especially with small kidneys. In one such case I found that the fatal
hemorrhage was due to the bursting of a miliary aneurism of a small
artery in the submucous coat. Probably in all similar cases the
hemorrhage is referable to disease of the vascular walls.

9. Neuropathic Conditions.--Although ecchymoses in the mucous membrane
of the stomach can be experimentally produced by injury of various
parts of the brain and spinal cord, there is no proof that gastric
hemorrhage which is of any clinical importance is referable to
structural diseases of the nervous system. The occasional occurrence of
gastric hemorrhage in progressive paralysis of the insane, in
tuberculous meningitis, in epilepsy, is to be attributed to other
causes.

In lack of a better explanation, however, the gastric hemorrhages which
have been occasionally observed in hysterical women may be classified
here. These constitute not the least important class of gastric
hemorrhages. The hemorrhages from the stomach in chlorosis belong
partly here and partly to anaemia.

10. Melaena Neonatorum.--Although in some cases ulcers have been found
in the stomach or duodenum, and in others a general hemorrhagic
diathesis exists, it must be said that the etiology of this grave
disease is still very obscure.

11. Bursting of Aneurisms or of Abscesses from without into the
Stomach.

12. Idiopathic Causes.--Under this unsatisfactory designation are
included cases which are aptly described by Flint[1] in the following
words: "Hemorrhage sometimes occurs from the stomach, as from the
bronchial tubes, the Schneiderian membrane, and in other situations,
without any apparent pathological connections, neither following nor
preceding any appreciable morbid conditions. It is then to be
considered {583} as idiopathic." A person in apparent health has
suddenly a hemorrhage, often profuse, from the stomach, which is
followed only by symptoms immediately referable to the hemorrhage. The
hemorrhage is naturally the source of great anxiety. Ulcer or cancer of
the stomach or some other grave disease is usually suspected. But the
patient develops no further symptoms, and often never has another
hemorrhage. Whatever hypotheses one may construct for these cases of
so-called idiopathic hemorrhage, the recognition of the clinical fact
of their occurrence is important.

[Footnote 1: Austin Flint, _A Treatise on the Principles and Practice
of Medicine_, 5th ed., p. 513, Philada., 1881.]

Inasmuch as hemorrhage from the stomach is usually made manifest by the
vomiting of blood, it is important to bear in mind that gastric
hemorrhage is not the only cause of haematemesis. Blood may gain access
to the stomach by being swallowed in cases of hemorrhages from the
nose, mouth, throat, bronchi, lungs, and oesophagus. Blood may also
enter the stomach from the duodenum in cases of simple ulcer of the
duodenum or of typhoid ulcers situated in the upper part of the
intestine.

The SYMPTOMS of hemorrhage from the stomach have already been described
in connection with ULCER OF THE STOMACH.

MORBID ANATOMY.--As is evident from the enumeration of the causes of
gastric hemorrhage, the lesions found after death are manifold. A
description of these lesions, however, does not belong here. It is
necessary, however, to say a few words concerning the demonstration of
the source of the hemorrhage.

The hemorrhage is arterial, venous, or capillary in origin. Ulcerations
from the stomach into the heart, which have been mentioned in
connection with gastric ulcer, are too infrequent to come into
consideration in this connection. If the bleeding is from a large
artery or vein or from a medium-sized aneurism or varix, the
demonstration of its source is not difficult. Often, however, in cases
of fatal gastric hemorrhage the search for the source of the hemorrhage
has proved fruitless. It is supposed that in many such cases the
hemorrhage is due to diapedesis, and not to rupture of a blood-vessel
(rhexis). Doubtless, small gastric hemorrhages, particularly those into
the tissues of the stomach, are often the result of diapedesis, but in
cases of profuse hemorrhages from the stomach where the source of the
hemorrhage is not demonstrable after death, the convenient assumption
of hemorrhage by diapedesis, in my opinion, plays too important a role.
In most cases of profuse gastrorrhagia the symptoms point to a sudden
outpouring of blood into the stomach; and our knowledge of diapedesis
does not warrant the belief that the red blood-corpuscles can escape
through the unsuffused walls of the vessels with that combined rapidity
and abundance which would be necessary to explain the sudden and
profuse hemorrhage. In these cases hemorrhage by rhexis is altogether
more probable even when ruptured vessels cannot be demonstrated. It
often requires a long-continued and careful search to find a small
vessel which is ruptured. In the case above mentioned of fatal
haematemesis from miliary aneurism over an hour of continuous searching
was required to find the pinhole perforation in the mucous membrane in
the bottom of which lay the small aneurism. Chiari[2] has reported a
fatal gastric hemorrhage due to rupture of a submucous vein. The
erosion of the mucous membrane was not larger than a hempseed. The
examination of the mucous membrane is often much impeded by the {584}
closely-adherent mucus and blood, which have to be carefully removed.
Injection of the vessels of the stomach with fluid may aid in finding a
ruptured vessel. It is not intended to assert that in all cases of
fatal gastric hemorrhage a painstaking search would reveal the source
of the hemorrhage, but it is believed that cases of fatal gastric
hemorrhage would less frequently be reported with negative anatomical
result as hemorrhages by diapedesis, or by exhalation, or as
parenchymatous or capillary hemorrhages, if such a search were made.

[Footnote 2: _Prag. med. Wochenschr._, 1882, No. 50.]

DIAGNOSIS.--Undoubtedly, small hemorrhages into the stomach often occur
which are not recognized, and in the absence of vomiting even larger
hemorrhages may escape detection unless a careful examination of the
stools be made. The patient may die from abundant gastric hemorrhage
before any blood has been vomited or has passed by the bowels.

When there is doubt whether the black color of the stools is due to
blood or to the administration of iron or of bismuth, it generally
suffices to add water to the stools. If blood be present, the water
will acquire a reddish color. Should doubt still remain, then the
microscope, the spectroscope, or the test for haemin crystals may be
called into requisition (see p. 545).

Whether black, tarry stools are produced by hemorrhage from the stomach
or by hemorrhage in the upper part of the intestine can be decided only
by the clinical history. If haematemesis be likewise present, the
presumption is strongly in favor of gastric hemorrhage. The diagnosis,
however, between hemorrhage from duodenal ulcer and that from gastric
ulcer is very difficult, and can rarely be positively made.

The mere inspection of the vomit is generally sufficient to determine
whether it contain blood or not. Color more or less resembling that of
altered blood may be produced in the vomit by iron, bismuth, red wine,
various fruits, such as cranberries, and by bile. When a careful
inspection by the physician leaves doubt as to the presence of
blood--which will rarely be the case--then here also recourse may be
had to the microscope, spectroscope, and test for haemin crystals.

Sometimes blood is swallowed and then vomited by hysterical females or
by malingering soldiers or prisoners for purpose of deceit. In such
cases there are generally no evidences of acute anaemia or of gastric
disease. The blood of some animals can be distinguished by the
microscope from human blood. When suspicion of deceit exists, there are
generally various ways of entrapping the patient.

When blood is vomited by nursing infants the possibility of its coming
from the breast of the mother is to be thought of.

Sometimes blood from the nose or throat is swallowed, particularly when
the bleeding occurs during the night. This blood may subsequently be
vomited. The inspection of the nose or throat will generally reveal the
source of the hemorrhage in such cases.

The diagnosis between hemorrhage from the oesophagus and that from the
stomach must be based upon the clinical history. The oesophagoscope,
however, has been successfully employed for diagnostic purposes.
Several cases have been reported of fatal hemorrhage from varices of
the oesophagus. Such hemorrhage cannot be distinguished from gastric
hemorrhage.

Much more frequently arises the question whether the hemorrhage is from
the stomach or from the lungs. Sometimes the decision of this point
{585} is very difficult, and it may even be impossible, especially when
the physician is obliged to trust only to the statements of the patient
or his friends. Difficulty in the diagnosis results mainly from the
fact that coughing and vomiting of blood are often associated with each
other. With haemoptysis blood may be swallowed and then vomited, and
with haematemesis more or less coughing occurs. The diagnosis is to be
based upon the points contained in the following table:

          HAEMOPTYSIS.             |          HAEMATEMESIS.
                                   |
  1. Usually preceded by symptoms  |  1. Usually preceded by symptoms
  of pulmonary or of cardiac       |  of gastric or of hepatic
  disease. Bronchial hemorrhage,   |  disease, less frequently by
  however, without evidence of     |  other diseases (see Etiology).
  preceding disease, is not rare.  |
                                   |
  2. The attack begins with a      |  2. The attack begins with a
  tickling sensation in the throat |  feeling of fulness in the
  or behind the sternum. The blood |  stomach, followed by nausea. The
  is raised by coughing. Vomiting, |  blood is expelled by vomiting,
  if it occurs at all, follows the |  to which cough, if it occurs, is
  act of coughing.                 |  secondary.
                                   |
  3. The blood is bright red, fluid|  3. The blood is dark, often
  or but slightly coagulated,      |  black and grumous, sometimes
  alkaline, frothy, and frequently |  acid, and usually mingled with
  mixed with muco-pus.             |  the food and other contents of
                                   |  the stomach.
                                   |
  If the blood has remained some   |  If the blood is vomited at once
  time in the bronchi or a cavity, |  after its effusion, it is bright
  it becomes dark and coagulated.  |  red and alkaline, or it may be
                                   |  alkaline if it is effused into
                                   |  an empty stomach.
                                   |
  4. The attack is usually         |  4. After the attack the physical
  accompanied and followed by      |  examination of the lungs is
  localized moist rales in the     |  usually negative, but there are
  chest, and there may be other    |  generally symptoms and signs of
  physical signs of pulmonary or   |  gastric or hepatic disease.
  of cardiac disease.              |
                                   |
  Bloody sputum continues for some |  Black stools follow profuse
  time, often for days, after the  |  haematemesis.
  profuse hemorrhage ceases.       |

As it is important that the patient should be as quiet as possible
during and for some time after the hemorrhage, any physical examination
which disturbs the patient, such as percussing the posterior part of
the chest or palpating the abdomen, should be avoided.

The diagnosis of the many causes of gastric hemorrhage belongs to the
description of the various diseases which have been enumerated under
the etiology.

PROGNOSIS.--It is exceptional for gastric hemorrhage to prove
immediately fatal. According to Fox, such an occurrence is more
frequent with cirrhosis of the liver than with ulcer or cancer of the
stomach. The ultimate result of the hemorrhage depends greatly upon the
previous condition of the patient. If this condition was good, he often
rallies from the most desperate prostration immediately following the
hemorrhage. A previously enfeebled patient is of course more likely to
yield to the further anaemia and exhaustion caused by profuse
hemorrhage. Although the symptoms of gastric ulcer and of cirrhosis of
the liver are sometimes improved after hemorrhage from the stomach,
nevertheless this hemorrhage can never be regarded as a welcome event.

For the treatment of gastric hemorrhage see ULCER OF THE STOMACH.




{586}

DILATATION OF THE STOMACH.

BY W. H. WELCH, M.D.


DEFINITION.--By dilatation of the stomach is understood a condition in
which the stomach is abnormally large and is unequal to the performance
of its normal functions. It will be observed that this definition of
dilatation of the stomach includes an anatomical disturbance and a
physiological disturbance. A stomach which, although unusually large,
performs its functions perfectly well is not, in the clinical sense, a
dilated stomach. The most characteristic functional disturbance in
dilatation of the stomach is delay in the propulsion of the gastric
contents into the intestine in consequence of inability of the muscular
coat of the stomach to perform the work imposed upon it. This muscular
insufficiency, whether primary or secondary, necessarily involves
disorder of the digestive and absorptive powers of the stomach.

SYNONYMS.--Dilatatio ventriculi; Gastrectasia. It has been proposed to
call the early stages of the disease insufficiency of the stomach
(Rosenbach). The condition described by Chomel as dyspepsia of liquids
is undoubtedly dilatation of the stomach.

HISTORY.--Dilatation as a disease of the stomach is not mentioned by
writers of antiquity. Fabricius ab Aquapendente in 1623 was among the
first to record an observation of dilatation of the stomach. During the
following century cases of dilatation of the stomach were recorded more
as curiosities than as of clinical interest. Most cases were attributed
to eating or drinking inordinate quantities. In 1743, Widman clearly
recognized stenosis of the pylorus as a cause of gastric dilatation. In
the works of Van Swieten, Morgagni, Lieutaud, and J. P. Frank, during
the latter half of the last century, different causes of dilatation of
the stomach are recognized. The last writer especially distinguishes
clearly between dilatation due to stenosis and that due to atony. The
data as to the symptoms of the disease were still very imperfect. In
1833, Duplay[1] published an important article in which the main points
in the causation and symptomatology of dilatation of the stomach are
clearly described. After this time the important works on the practice
of medicine or on diseases of the stomach contain, in the main, correct
descriptions of the disease under consideration. Since the publication
in 1869 of Kussmaul's memorable article[2] on the treatment of
dilatation of the stomach by the {587} stomach-pump, much greater
attention has been paid to this disease than ever before, so that the
literature upon this subject during the last fifteen years is very
considerable. In 1875, Penzoldt published an excellent monograph upon
dilatation of the stomach.[3]

[Footnote 1: _Arch. gen. de Med._, Ser. 2, t. iii. pp. 165, 523.]

[Footnote 2: _Deutsches Arch. f. kl. Med._, Bd. vi., 1869. Kussmaul
first employed the stomach-pump in dilatation of the stomach in 1867,
and in that year he reported a successful result (_Schmidt's Jahrb._,
Bd. 136, p. 386).]

[Footnote 3: _Die Magenerweiterung_, Erlangen, 1875. To this work I am
indebted for most of the historical data in the text.]

ETIOLOGY.--Dilatation of the stomach is the result of inability of this
organ to propel its contents into the intestine within the normal space
of time. In the performance of this mechanical work three factors are
involved--namely, the muscular force of the stomach, the quantity and
quality of the gastric contents, and the size of the opening between
the stomach and the intestine. All causes of dilatation of the stomach
may be referred to abnormalities of one or more of these factors.

The most important group of causes is represented by stenosis of the
pyloric orifice or of the adjacent part of the stomach or of the
intestine.[4] Most cases of hypertrophic dilatation of the
stomach--that is, dilatation with hypertrophy of the muscular walls of
the stomach--are produced by causes belonging to this group.

[Footnote 4: Dilatation of the stomach in consequence of intestinal
obstruction below the duodenum is so rare that no further attention is
given to the subject in the present article. The term pyloric stenosis
is often used in the course of the article to include any obstruction
to the passage of the contents of the stomach into the intestine,
whether the obstruction be in the duodenum, the pyloric orifice, or the
pyloric region.]

The most frequent cause of pyloric stenosis is carcinoma, either in the
form of a diffuse infiltration of the gastric walls in this region or
as a tumor projecting into the cavity of the pyloric portion of the
stomach. Next in frequency are cicatricial growths resulting from
simple ulcer involving the pyloric region. Much less frequent are
similar cicatricial stenoses of the pylorus resulting from ulcers
produced by swallowing corrosive poisons. Simple hypertrophy of the
coats of the stomach in the pyloric region, particularly of the fibrous
and muscular coats, is an occasional cause of dilatation. Obstruction
of the pylorus by mucous polypi or by hypertrophic folds of mucous
membrane is so rare as to have little practical interest. Likewise,
stenosis caused by sarcomata, fibromata, myomata, lipomata, and cysts
need be mentioned only for the sake of completeness.

Narrowing of the pyloric orifice may be caused also by pressure from
outside of the stomach, as by tumors, particularly cancer, of the liver
and of the pancreas, and by the contraction of fibrous adhesions and
thickenings resulting from perigastritis. Obstruction of the duodenum
by tumors growing in its walls, by cicatrices resulting from ulcers,
and by external pressure may also cause dilatation of the stomach.
According to Barker, compression of the duodenum by a wandering right
kidney may induce dilatation of the stomach. The mere association of
dilatation of the stomach and movable right kidney, however, cannot be
considered proof that the former is caused by the latter, for the
subjects of movable kidney (most frequently women with flabby abdominal
walls who have borne many children) are often also favorable subjects
for atonic dilatation of the stomach.

Sometimes with dilatation of the stomach the pyloric orifice is found
abnormally small, without any thickening or other appreciable change in
the walls of the pylorus. These cases in adults have been described by
{588} Landerer under the name of congenital stenosis of the pylorus,
but his conclusions are not free from doubt.[5] Congenital stenosis,
and even complete occlusion of the pylorus, has been observed in
infants.[6]

[Footnote 5: _Ueber angeborene Stenose des Pylorus_, Inaug. Diss.,
Tubingen, 1879. In the ten cases studied by Landerer the patients were
all adults, mostly in advanced life. In only one case is it mentioned
that indigestion existed from childhood; the clinical history in all is
incomplete. With the exception of one case there was no marked
hypertrophy of the muscular coat of the stomach, such as is usually
found with benign pyloric stenosis and would naturally be expected with
a stenosis existing since birth. The pyloric orifice varied from 1-1/2
cm. to 2 mm. in diameter. Some of the specimens had been in alcohol for
a considerable time. In my opinion, Landerer has not brought forward
sufficient proof that in these cases stenosis of the pylorus existed
since birth.]

[Footnote 6: Wunsche, _Jahrb. d. Kinderheilk._, viii. 3, p. 367.
Andral, Forster, and Bull have found congenital stenosis and atresia of
the pylorus.]

Spasm of the pyloric muscle, which, according to Kussmaul, may be
referable to erosions, ulcers, and inflammations of the adjacent mucous
membrane, can be admitted only as a hypothetical explanation of some
cases of dilatation of the stomach.

Somewhat problematical, although not improbable, is the production of
stenosis of the pylorus or of the duodenum by torsion and by
displacement of these parts. Dilatation of the stomach is sometimes
associated with scrotal hernia, particularly with that containing
omentum or transverse colon. This dilatation Kussmaul explains by the
production of a sharp bend between the movable first part and
comparatively fixed second part of the duodenum, in consequence of the
dragging downward of the stomach by the displaced omentum or transverse
colon. In a similar way Kussmaul believes that the weight of an
over-distended stomach may produce stenosis, and by this mechanism he
explains the occasional occurrence of symptoms of complete pyloric
obstruction when a large quantity of material has accumulated in an
already dilated stomach, and the prompt relief of these symptoms when
the burden of the stomach is removed either by vomiting or by the
stomach-tube.[7]

[Footnote 7: Another explanation given by Kussmaul, and likewise based
upon experiments on the cadaver, is that when the stomach is
over-distended it may rotate upon its own axis, so that the pylorus
acquires a sagittal direction and impinges against the first part of
the duodenum. This rotation of the stomach, however, can occur only
when the abdominal walls are flabby (Kussmaul, "Die Peristaltische
Unruhe des Magens," _Volkmann's Samml. klin. Vortr._, No. 181).]

The manner in which stenosis of the pylorus causes dilatation of the
stomach is sufficiently obvious to require no especial explanation. It
is, however, important to know that stenosis of the pylorus may be
compensated, so that even a very considerable degree of obstruction of
this orifice may exist without any dilatation of the stomach. The
obstruction may be completely counteracted by hypertrophy of the
muscular coat of the stomach, particularly of that in the right half of
the organ. Leube suggests that this increased muscular force, by
increasing the peristaltic movements, may also hasten the digestion and
absorption of the food, so far as these processes take place in the
stomach.[8] The timely removal of the contents of the stomach by
vomiting may also prevent over-distension of the organ. Another
compensatory circumstance may be the reduction of the quantity of solid
and liquid food taken by the patient. Conditions are often present,
however, which oppose the development of these {589} compensatory
circumstances. Such conditions are feebleness of the patient,
degeneration of the muscular coat of the stomach, chronic catarrhal
gastritis, insufficient secretion of gastric juice, and delayed
absorption, causing stagnation and fermentation of the food in the
stomach.

[Footnote 8: Leube, in _V. Ziemssen's Handb. d. spec. Path. u. Ther._,
Bd. vii. 2te Halfte, p. 211, Leipzig, 1878.]

Dilatation of the stomach may occur without any obstacle to the
evacuation of the gastric contents into the intestine. The cases of
so-called atonic dilatation of the stomach belong to this class. The
degree of dilatation in these cases is rarely so great as when the
dilatation is caused by stenosis. The cause of gastric dilatation in
the absence of stenosis is not always clear, so that a variety of
hypotheses, more or less probable, have been broached to explain these
obscure cases.

Dilatation with unobstructed outlet of the stomach must be referable
either to abnormalities in the quantity or quality of the contents of
the stomach or to weakness of the muscular walls of the stomach. In
most cases both of these causes are combined, and it is not easy to
separate their action.

Abnormal gastric contents may be the result of improper ingesta or of
disturbances in gastric digestion. Although in former times the
frequency of excessive eating and drinking as a cause of dilatation of
the stomach was doubtless exaggerated, nevertheless the efficacy of
this cause cannot be doubted. Dilatation of the stomach is said to be
common in people who live almost exclusively upon a vegetable diet and
therefore require large quantities of food. The habitual drinking of
large quantities of beer may cause dilatation of the stomach. The
occasional association of a dilated stomach with diabetes is referred
to the inordinate appetite and thirst which characterize this disease.
If the food reaches the stomach imperfectly masticated, the process of
digestion is delayed, and as a result the stomach may become dilated.
Indigestible food, particularly that which readily ferments in the
stomach, may be an indirect cause of the disease under consideration. A
similar role may be played by swallowing foreign substances either by
accident or by design. It is not proven that dilatation of the stomach
may be referable to exhaustion of its muscular power by the abuse of
agents which at first excite peristalsis, such as emetics, purgatives,
alcoholics, tobacco, spices, etc. Equally doubtful is the production of
dilatation by the misuse of narcotics, such as opium, which restrain
peristalsis.

Of great importance in the production and continuance of gastrectasia
are all circumstances which cause stagnation and fermentation of the
contents of the stomach. These abnormalities of the gastric contents
are referable both to muscular and to chemical insufficiency of the
stomach, but in this connection it is desired to call attention
especially to chemical insufficiency, although in the production of
gastric dilatation this becomes always associated with muscular
insufficiency. In this way chronic catarrhal gastritis is operative in
the causation of gastric dilatation. In consequence of insufficient
secretion of normal gastric juice and of delayed absorption, the food
remains abnormally long undigested in the stomach, and fermentative
changes, with the development of gas, occur. No less important,
however, is the impairment of the muscular power of the stomach in
chronic gastritis. Stagnation and fermentation of the contents of the
stomach occur also in functional or atonic dyspepsia, which is to be
reckoned as a cause of dilatation of the stomach. {590} Naunyn[9]
emphasizes especially the importance of abnormal fermentations in the
stomach (alcoholic, butyric acid, lactic acid, acetic acid
fermentations) both as a cause and as a result of dilatation of the
stomach. Ulcer and cancer of the stomach may cause dilatation by
interfering with the normal digestive processes.

[Footnote 9: _Deutsches Arch. f. kl. Med._, Bd. 31.]

We come now to the third and final group of causes of dilatation of the
stomach--namely, those included under weakness of the muscular walls of
the stomach. In the last analysis all causes of gastric dilatation come
under this heading, for even with pyloric stenosis and with excessive
contents a stomach will not dilate so long as its muscular power is
equal to the proper performance of the work which is demanded. In this
connection, however, reference is had especially to those cases in
which impairment or restraint of the muscular movements of the stomach
may be regarded more or less directly as the primary cause of
dilatation of the stomach.

Clearest of comprehension are those cases in which the muscular power
of the stomach is impaired by organic changes in the muscular coat.
Here may be mentioned partial destruction of the muscular coat,
particularly of that in the pyloric region, by ulcers and by cancers.
Thus, ulcers and cancers which in no way obstruct the outlet of the
stomach may cause dilatation of the organ. Inflammatory infiltration
(inflammatory oedema) of the muscular coat has been adduced as a cause
of its weakness in chronic catarrhal gastritis and in peritonitis.
Whether this is the proper explanation or not, there is no doubt that
the muscular coat of the stomach may become paretic in cases of chronic
catarrhal gastritis, as well as the subjacent muscle in inflammations
of other mucous membranes, as in laryngitis or in cystitis. Our
knowledge of the relation between degeneration of the muscular coat of
the stomach and gastrectasia is very imperfect. Fatty and colloid
degeneration of the muscle of dilated stomachs is probably to be
interpreted as a secondary change. It is probable that amyloid
degeneration may be a cause of atonic dilatation of the stomach.[10]
Oedematous infiltration of the coats of the stomach in cases of
cirrhosis of the liver, pulmonary emphysema, cardiac disease, and
Bright's disease has been assigned as a cause of gastric dilatation,
but without satisfactory evidence. Chronic interstitial gastritis
(cirrhosis of the stomach) is more frequently a cause of contraction
than of dilatation of the stomach.

[Footnote 10: Edinger, _ibid._, Bd. 29.]

The restraint of the muscular movements of the stomach by adhesions and
by dragging downward of the organ in hernia may cause dilatation.
Relaxation of the abdominal walls, as in women who have borne many
children, by removing the normal support of the stomach, has been
thought to cause dilatation.

Atony of the muscular walls of the stomach may be a part of general
muscular weakness and impaired nutrition. Here belong cases of adynamic
dilatation of the stomach secondary to typhoid fever, cholera,
tuberculosis, anaemia, chlorosis, cachexia, senile marasmus,
neurasthenia.

Whether primary paralysis of the stomach can occur or not is wholly
uncertain. We have no positive knowledge as to the occurrence of
paresis of the stomach in consequence of organic or functional changes
{591} in the peripheral or central nervous system. Nor does our meagre
information as to the relation between the nervous system and the
muscular movements of the stomach justify the construction of any
hypotheses as to this point.

For the sake of clearness the various causes of dilatation of the
stomach according to the foregoing classification may be recapitulated
as follows. Some of the more doubtful and of the rarer causes are
omitted:

  A. Stenosis of the Pylorus or of the Duodenum.
    1. Cancerous;
    2. Cicatricial;
    3. Hypertrophic (of pylorus);
    4. From external pressure;
    5. Congenital (of pylorus)?;
    6. From torsion of duodenum?
  B. Abnormalities in Contents of Stomach.
    1. Ingesta:
      _a_. Excessive;
      _b_. Imperfectly masticated;
      _c_. Indigestible.
    2. Stagnation and fermentation in consequence of chemical
         insufficiency of the stomach, as in chronic catarrhal
         gastritis and functional dyspepsia.
  C. Impairment of Muscular Force of Stomach.
    1. Organic changes in muscular coat:
      _a_. Partial destruction by ulcers and cancers;
      _b_. Inflammation, as in chronic catarrhal gastritis and
             peritonitis;
      _c_. Degenerations (fatty, colloid, amyloid);
      _d_. Oedema?;
      _e_. Cirrhosis of stomach.
    2. Mechanical Restraint:
      _a_. By adhesions;
      _b_. By weight of herniae.
    3. Impaired Nutrition and General Muscular Weakness, Adynamic
         dilatation from typhoid fever, tuberculosis, anaemia, etc.
    4. Paresis from neuropathic causes?

As a rule, not a single one, but several, of the above-mentioned causes
are operative in the production of dilatation of the stomach, and it is
often impossible to say which is the primary cause. The various gastric
functions are so dependent upon each other that if one is disturbed the
others also suffer. If, for instance, atony of the muscular coat of the
stomach exists, then in consequence of enfeebled peristalsis the
secretion of gastric juice is insufficient, the food is not thoroughly
mingled with the gastric juice, and the absorption of the products of
digestion in the stomach is interfered with; in consequence of which
the accumulating peptones still further hinder the digestive process.
The pylorus remains contracted for an abnormal length of time, as it
naturally is closed until the process of chymification in the stomach
is far advanced, and this process is now delayed. The stagnating
contents of the stomach readily ferment, and the irritating products of
fermentation induce a chronic {592} catarrhal gastritis, which further
impairs the functions of the mucous and muscular coats of the stomach.
Thus, in a vicious circle one cause of dilatation induces another. To
assign to each cause its appropriate share in the production of the
final result is a matter of difficulty, and often of impossibility.
From this point of view the dispute as to whether in atonic dilatation
the most important factor in causation is chemical insufficiency of the
stomach (impaired secretion of gastric juice, fermentations) or
mechanical insufficiency (weakened muscular action, stagnation),
appears of little practical importance.

Of the causes of non-stenotic dilatation of the stomach, the first
place is to be assigned to chronic catarrhal gastritis and to atonic
dyspepsia, as this term is understood by most English and American
writers.

As regards frequency, gastric dilatation is a common result of cancer
of the pylorus. It is less frequently caused by simple ulcer. Other
forms of pyloric stenosis than the cancerous and the cicatricial are
rare.

Opinions differ as to the frequency of non-stenotic or atonic
dilatation of the stomach according to the manner in which one
interprets the cases. Non-stenotic dilatations which are comparable in
degree to those produced by stenosis are rare. The lesser grades of
atonic dilatation, however, are not rare; but here arises the
difficulty of distinguishing these cases from mere chemical or
mechanical insufficiency of the stomach, which often represents the
early stage of the process. Hence it has been proposed to discard
altogether the term dilatation, and to substitute that of insufficiency
of the stomach. But this latter term is applicable to many affections
of the stomach other than dilatation. A typical case of atonic
dilatation of the stomach is a well-defined disease, and because it is
difficult to diagnosticate its early stages is not sufficient reason
for discarding altogether the designation.

Gastrectasia may develop at any age. It is most frequent in middle and
advanced life. The largest number of cases of atonic dilatation is met
with between thirty and forty years of age. The disease is rare in
childhood.[11] The disease occurs in all classes of life. Atonic
dilatation seems to be comparatively more frequent in private practice
and among the favorably situated than in hospitals and among the poor.
Kussmaul says that the largest contingent of patients is furnished by
persons who lead a sedentary life and eat and drink a great deal.

[Footnote 11: Kundrat and Widerhofer mention no case of stenotic
dilatation of the stomach in children. They say, however, that atonic
dilatation due to over-feeding, and particularly to rachitis, is not
infrequent in children. Widerhofer reports a case of very large
dilatation of the stomach in a girl twelve years old. The cause of the
dilatation was not apparent, and the clinical history was imperfect
(_Gerhardt's Handb. d. Kinderkrankh._, Bd. iv. Abth. 2). Lafage
(_These_, Paris, 1881) reports a case of gastric dilatation at ten
years, and another at sixteen years of age. R. Demme (abstract in
_Berl. kl. Wochenschr._, 1883, No. 1) reports a case of large
dilatation of the stomach in a boy six and a half years old.
Cicatricial stenosis was suspected. Pauli (_De Ventriculi Dilatatione_,
Frankfurt, 1839) reports an enormous dilatation of the stomach,
believed to be due to congenital stenosis.]

SYMPTOMATOLOGY.--Inasmuch as dilatation of the stomach is usually
secondary to some other disease, the symptoms of the primary disease
have often existed a long time before those of dilatation appear.

The subjective symptoms of gastric dilatation are for the most part
directly referable to disturbances of the functions of the stomach.
These {593} subjective symptoms alone do not suffice for a positive
diagnosis of the disease. Of the greatest diagnostic importance are an
examination of the vomit and a careful physical exploration of the
stomach.

The appetite with dilatation of the stomach may be normal, diminished,
increased, or perverted. In the majority of cases the appetite is
diminished, and there may be complete anorexia. Sometimes the appetite
is increased even to voracity, which is explicable by the small amount
of nutriment which is absorbed. Polyphagia may therefore be a result as
well as a cause of dilatation of the stomach.

Often there is excessive thirst in consequence of the small quantity of
fluid absorbed.

Dilatation of the stomach in itself does not usually cause sharp
epigastric pain, although it is often associated with painful diseases
of the stomach.

There is usually in the region of the stomach a sense of fulness and
weight, which is often distressing and may be accompanied with dull
pain.

Heartburn and eructations of gas and of bitter or of acid fluids are
frequently present. The gas is often odorless, but sometimes it is very
offensive. It may contain sulphuretted hydrogen. In a number of
cases--which, however, are exceptional--the gas has been found
inflammable, burning usually with a colorless flame (hydrogen), but
rarely, as in a case from Frerichs' clinic, with a bright
yellowish-white flame (hydrocarbons). Detonation upon setting fire to
the gas has been noted. The analysis of the inflammable gas has shown
oxygen and nitrogen in approximately the same proportion as in the
atmosphere, in addition to large quantities of carbonic acid and of
hydrogen, also marsh gas, and in Frerichs' case olefiant gas in small
amount.[12] The oxygen and nitrogen are doubtless simply swallowed, but
the carbonic acid and hydrogen are the result of abnormal fermentations
in the stomach. The origin of the hydrocarbons in the gas is not clear,
but they are probably also produced by fermentation within the stomach.

[Footnote 12: One of the analyses in Frerichs' case gave carbonic acid,
17.40; hydrogen, 21.52; marsh gas, 2.71; olefiant gas, traces; oxygen,
11.91; nitrogen, 46.44. In another analysis were found marsh gas,
10.75, and olefiant gas, 0.20. Sulphuretted hydrogen was also present
(Ewald, in _Reichert und Du Bois-Reymond's Archiv_, 1874, p. 222).]

One of the most frequent symptoms, although not a constant one, of
dilatation of the stomach is vomiting. This symptom often presents
characters which, if not pathognomonic of dilatation, at least raise a
strong presumption in favor of its presence. The act of vomiting is
sometimes accomplished with such ease that it is hardly more than
regurgitation; at other times the act is accompanied with violent and
exhausting retching. A feature particularly characteristic of
dilatation of the stomach is the abundance of the vomited material. In
no other disease is such an enormous quantity evacuated from the
stomach at one time. Blumenthal relates a case in which the vomited
material amounted to sixteen pounds. Such large quantities can
accumulate in the stomach of course only when a considerable time
intervenes between the acts of vomiting. The vomiting of gastric
dilatation does not generally occur until some hours after a meal. It
often presents a certain periodicity, occurring, for instance, at
intervals of two or three days, and followed usually by temporary
relief. It is often observed that as the stomach {594} becomes larger
and larger the vomiting becomes less and less frequent, but at the same
time more abundant. Especially toward a fatal termination of the
disease the walls of the stomach may become so paralyzed and
insensible, and the patient so feeble, that the vomiting ceases
altogether. Another valuable diagnostic sign furnished by the vomit is
the presence of undigested food which has been taken a considerable
time, it may be many days, previously.[13] If the morning vomit
habitually contains undigested food which has been eaten the previous
day, gastric dilatation either exists or is almost sure to develop.

[Footnote 13: Ritter relates the case of a man who vomited cherry-pits,
although he had not eaten cherries for over a year (_Canstatt's
Jahresbericht_, 1851, iii. p. 260)!]

The vomited matter is almost always in a condition of fermentation. If
the vomit be allowed to stand in a vessel, it will separate into three
layers--an upper, frothy; a middle, of turbid fluid, usually yellowish
or brownish in color; and a lower layer, composed of solid particles,
mostly alimentary debris. The vomit often emits an extremely offensive
odor. The reaction is nearly always acid. Different kinds of
fermentation--alcoholic, acetous, lactic acid, and butyric acid--are
present, usually in combination with each other. The microscope
reveals, besides undigested and partly-digested food, crystals of fatty
acids, sarcinae ventriculi, fungus-spores, and various forms of
bacteria, particularly rod-shaped ones. The connection between sarcinae
and fermentative processes is not understood. There is no evidence that
sarcinae are capable of causing fermentation. Of greater importance is
the recognition by the microscope of the spores of the yeast-fungus
(Torula cerevisiae). These spores are rarely absent, and their constant
presence is evidence that fermentation is in progress. Fermentation
often exists in undilated stomachs, but, as has already been mentioned,
it is an important factor in the production of dilatation, so that its
early recognition, if followed by proper treatment (washing out the
stomach especially), may ward off the development of dilatation. The
article on GASTRIC CANCER is to be consulted with reference to the
habitual absence of free hydrochloric acid from the stomach in cases of
cancerous dilatation. If cancer or ulcer of the stomach exists, blood
is frequently present in the vomit, but even in the absence of ulcer or
cancer or other demonstrable source of hemorrhage the vomit in cases of
dilatation of the stomach may exceptionally contain blood, even for a
considerable length of time. If the dilatation be due to pyloric
stenosis, bile is not often found in the vomited material.

It has already been mentioned that vomiting is not a constant symptom
of dilatation of the stomach. It remains to add that vomiting may be
present without any of the distinctive features which have been
described. Gastric dilatation, especially in its early stages, is often
accompanied by attacks of acute indigestion (embarras gastrique) after
some indiscretion in diet.

Constipation is an almost constant symptom of dilatation of the
stomach. This is naturally to be expected when so little substance
passes from the stomach into the intestine. The constipation is also to
be explained in part by the absence of the usual reflex stimulus which
the stomach during digestion normally exerts upon intestinal
peristalsis, for the constipation is usually much relieved when the
overweighted stomach is systematically washed out.

{595} Occasionally, attacks of diarrhoea occur in cases of dilatation
of the stomach. The diarrhoea may perhaps be explained by the sudden
discharge of a large quantity of fermenting material from the stomach
into the intestine.

With marked dilatation of the stomach, especially when there is profuse
vomiting, the urine is often considerably diminished in quantity.
Particularly in cases treated by systematic washing out of the stomach,
but also in other cases, especially with abundant vomiting, the acidity
of the urine is often much reduced. The reaction may be even
continuously alkaline (Quincke). Crystals of phosphate of magnesium
have been occasionally found in the alkaline urine of gastrectasia
(Ebstein). The urine is prone to deposit abundant sediments. It often
contains an excess of indican.

The patient may suffer from attacks of dyspnoea and of palpitation of
the heart in consequence of flatulent distension of the stomach.

The general condition of the patient will of course depend chiefly upon
the character of the primary disease and upon the severity of the
gastric symptoms. A moderate degree of dilatation may exist without
much disturbance of the general health of the patient. But as the
disease progresses and the food stagnates more and more in the stomach,
finally to be rejected by vomiting, the patient cannot fail to lose
flesh and strength. In extreme cases of gastrectasia, even without
organic obstruction, the patient may be reduced to a degree of
emaciation and of cachexia indistinguishable from that of cancer. As in
so many other gastric diseases, the patient is usually mentally
depressed and hypochondriacal. His sleep is disturbed. He suffers much
from headache and vertigo. He feels incapable of physical or mental
exertion. The skin is dry and harsh; the extremities are cold. Toward
the last, cachectic oedema about the ankles can often be recognized.

Kussmaul was the first to call attention to the occurrence of tetanic
spasms in cases of dilatation of the stomach.[14] This symptom has been
observed almost exclusively in an advanced stage of the disease when
the patient has become anaemic and weak. The spasms come on chiefly
after attacks of profuse vomiting or after evacuating large quantities
by the stomach-tube. The spasms may be preceded by a sense of pain or
distress in the region of the stomach, by dyspnoea, by numbness of the
extremities, or by great prostration. The tetanic spasms affect
especially the flexor muscles of the hand and forearm, the muscles of
the calves of the legs, and the abdominal muscles. The spasm may be
confined to one or more of these groups of muscles, or there may be
general tetanic contraction of the muscles of the body. Sometimes
typical epileptiform convulsions with loss of consciousness occur. With
general tetanic spasms the pupils are usually contracted, and often
irresponsive to light. Sometimes there is abnormal sensitiveness upon
pressure over the contracted muscles. The spasms may last for only a
few minutes, or they may continue for several hours, or even for days.
After their disappearance the patient is left extremely prostrated.
Although tetanic spasms increase the gravity of the prognosis, they are
not necessarily fatal.

[Footnote 14: _Deutsches Arch. f. kl. Med._, Bd. vi. p. 481.]

Kussmaul considers that these spasms are analogous to those occurring
in cholera, and are referable to abnormal dryness of the tissues in
consequence of the extraction of fluid. This view is supported by the
usual {596} occurrence of the spasms after profuse vomiting or after
washing out the stomach. Another explanation, which is perhaps more
applicable to the epileptiform attacks, refers the convulsions to
auto-infection by toxic substances produced in the stomach by abnormal
fermentative and putrefactive changes (Bouchard).[15]

[Footnote 15: Laprevotte, _Des Accidents tetaniformes dans la
Dilatation de l'Estomac_, These, Paris, 1884, p. 48.]

Coma, with or without the peculiar dyspnoea of diabetic coma, is a rare
occurrence in gastrectasia. (For a description of this form of coma see
page 205.)

The temperature in gastric dilatation is generally unaffected.
Penzoldt, however, saw two cases with moderate rise of temperature in
the evening, which could not be explained by any complication. On the
other hand, abnormally low temperature with slow pulse has been
observed (Wagner).

Essential to the diagnosis of gastric dilatation is the physical
examination of the stomach.

If the stomach be markedly dilated, inspection may reveal an abnormal
prominence of the abdominal walls in the epigastric region and
extending a variable distance below the level of the umbilicus. This
prominence is most marked on the left side. When the abdominal walls
are sufficiently thin and relaxed, sometimes the outline of the greater
curvature between the umbilicus and pubes, less frequently that of the
lesser curvature, can be made out. Sometimes the peristaltic waves of
the stomach can be perceived through the thin abdominal walls. By
pressure or by passing the hand across the abdomen gastric peristalsis
may sometimes be excited. The peristaltic movements of the stomach,
however, are rarely perceived except when the dilatation is due to
stenosis and the muscular coat of the stomach is hypertrophied. The
peristaltic waves generally pass from left to right, rarely in the
opposite direction as well. Careful attention to the situation,
direction, and extent of these waves is necessary to distinguish them
from similar peristaltic movements of the intestine.[16] The diminution
in size of the abdominal prominence caused by a dilated stomach after
profuse vomiting or after washing out the stomach may aid in the
diagnosis.

[Footnote 16: Kussmaul says that vigorous peristaltic movements of the
stomach may be perceptible through the abdominal walls even when there
is no dilatation of the stomach. Under these circumstances he
attributes the peristaltic commotion to an independent neurosis of the
stomach ("Die Peristaltische Unruhe des Magens," _Volkmann's Samml.
klin. Vortrage_, No. 181).]

An important aid in bringing out the contours of the stomach is the
artificial distension of the organ by the generation within it of
carbonic acid gas, as first suggested by Frerichs. For this purpose
20-30 grains of bicarbonate of sodium and 15-20 grains of tartaric
acid, each dissolved in a little lukewarm water, may be given one after
the other. If the stomach be much dilated and relaxed, it may be
necessary to give much larger quantities of the powders (up to 2-2-1/2
drachms of the soda and a corresponding quantity of the acid). It is
well to have a stomach-tube at hand in order to withdraw the gas in
case unpleasant symptoms develop. Sometimes the stomach fails to become
distended by this procedure. This is due in some cases to the escape of
the gas through the pyloric orifice into the intestine--a condition
designated by Ebstein as incontinence of the pylorus. It may be that
sometimes the gas produces such firm {597} contraction of the gastric
walls that the stomach does not expand by the pressure of the gas.
Instead of generating gas, a similar result may be produced by simply
injecting air into the stomach through a stomach-tube, as recommended
by Oser and by Runeberg. The air may, however, escape along the side of
the tube.

Palpation of the distended stomach yields an elastic resistance which
has been compared to that of an air-cushion. By palpating carefully
from above downward the greater curvature can sometimes be appreciated,
but in general it is difficult to distinguish it from the transverse
colon. Peristaltic movements may perhaps be appreciated by palpation
when they are not evident on inspection. If a dilated stomach contains
considerable fluid and the abdominal walls are yielding, fluctuation
may be perceived by palpation. The lowest level at which this
fluctuation can be felt may afford a clue as to the position of the
lower border of the stomach, but not much dependence can be placed upon
this sense of fluctuation unless many sources of error in its
interpretation are excluded.

By pressing gently and repeatedly against the abdominal walls a
splashing sound can usually be heard in cases of well-marked dilatation
of the stomach (bruit de clapotement). This sound can best be brought
out when the patient is in the recumbent position, with relaxed
abdominal walls, by palpating near the left border of the ribs. The
same sound can be produced by shaking the patient (bruit de glou-glou).
This sound may be heard at a considerable distance from the patient, to
whom it may be a source of much annoyance. In itself this splashing
sound is without diagnostic significance, as the condition for its
production--namely, the simultaneous presence of gas and liquid in the
stomach--exists often in healthy persons. By paying attention, however,
to the time at which this sound can be produced after eating or
drinking, and to its greater or less constancy, some diagnostic
importance can be attached to this sign. If the splashing sound can be
usually produced two hours or longer after the ingestion of liquid or
six hours after an ordinary meal, it generally indicates that
dilatation of the stomach exists.[17] It is necessary to exclude
somewhat similar sounds which may be produced in the intestines,
particularly in the transverse colon and caecum. The series of gurgling
sounds which may sometimes be produced in the intestine by palpation
are not likely to be confounded with the single splashing sound
produced in the stomach, but under certain circumstances a splashing
sound may be produced in the transverse colon which cannot be
distinguished from the gastric sound. If a dilated stomach contains a
very large quantity of fluid, the splashing sound cannot readily be
produced.

[Footnote 17: Baradat, _Etude sur le Bruit de Clapotement stomacal_,
These, Paris, 1884. Baradat says that this bruit is also diagnostic of
dilatation when it can be produced by palpating below a horizontal line
passing through the junction of the ninth and tenth ribs, but it is
evident that motion might be transmitted to the stomach even when its
greater curvature is above this line by palpating below the level of
the umbilicus.]

Leube has pointed out that the end of the stomach-tube (of course the
hard tube), after it has been inserted into the stomach, can often be
felt through the abdominal walls.[18] He says that if the tube can be
felt below a horizontal line passing through the anterior superior
spinous processes of the ileum, dilatation of the stomach may be
positively diagnosed, {598} and the existence of dilatation is probable
if the tube can be felt much below the umbilicus. No force should be
used in trying to make the end of the tube palpable. Of course if the
abdominal walls are thick or very tense the tube cannot be felt.
Leube's method is simple and convenient, and applicable to many cases.
As will be explained hereafter, a position of the lower border of the
stomach even quite as low as Leube's rule demands cannot be considered
by itself positive evidence of dilatation.[19]

[Footnote 18: _Deutsches Arch. f. kl. Med._, Bd. xv. p. 394.]

[Footnote 19: According to Oser, there is a possible source of error in
Leube's method--namely, that the sound may slide along the greater
curvature of the stomach, and even reach the pylorus, so that the end
may be felt higher than the lowest point of the stomach. Considerable
objection has been made to Leube's method on the ground of its danger,
but this objection is based on the assumption that greater energy is
employed in pressing forward the sound than Leube recommends (Oser,
article "Magenerweiterung" in _Eulenburg's Real Encyclopadie_, Bd.
viii., 1881).]

The length to which the stomach-tube can be inserted before meeting
resistance may evidently give some idea as to the size of the stomach.
The attempt, however, to establish any general law with reference to
this point has not proven successful.

In many cases valuable information as to the size of the stomach is
afforded by percussion. Over the greater part of the stomach the
percussion note is tympanitic, sometimes with a metallic quality. Over
the most dependent part of the stomach a dull sound is produced on
percussion in case a sufficient quantity of fluid or solid material is
contained in the viscus. In the upright position, therefore, in
percussing over the stomach from above downward, the tympanitic note
gives place to a dull sound, and this zone of dulness will change with
the position of the patient, so that in the recumbent posture the
dulness may entirely disappear. In order to prove that the region of
dulness belongs to the stomach, Piorry caused the patient to drink a
large quantity of water (a pint to a quart). In a healthy empty stomach
this quantity of water suffices to produce a zone of dulness which does
not descend below the level of the umbilicus. If, however, the dulness
be produced below the level of the umbilicus, it is inferred that
dilatation exists. Penzoldt's modification of Piorry's method gives
more certain results.[20] By withdrawing the fluid from the stomach by
the stomach-tube the dulness may be made to disappear, and by injecting
more fluid the dulness may be made to reappear at will. By noting the
lower limit of the dulness thus produced the position of the lower
border of the stomach may be determined. The farther this lies below
the umbilicus the greater, presumptively, is the degree of dilatation.
The artificial distension of the stomach with gas may also aid in
determining its limits by percussion. It must be said that in general
the separation of the lower limits of the stomach from the transverse
colon by means of percussion is a matter of great difficulty, and
sometimes is impossible.

[Footnote 20: Penzoldt, _op. cit._, p. 48.]

Upon auscultation over a dilated stomach sometimes a fine crackling or
sizzling sound, like that audible upon first uncorking a bottle of
soda-water, can be heard.[21] This is referable to the fermentation
which is in progress in the stomach. Eichhorst says that a similar but
finer crackling sound can be heard over a stomach in which carbonic
acid gas is {599} being artificially generated, and that this sound
abruptly ceases when the ear passes below the limits of the greater
curvature.[22]

[Footnote 21: Pauli was the first to record this phenomenon (_De
Ventriculi Dilatatione_, Frankfurt, 1839).]

[Footnote 22: _Handb. d. spec. Path. u. Ther._, Bd. i. p. 750, 1883.]

The displacement of neighboring organs by a dilated stomach does not
generally give rise to important physical signs. As the tendency of a
dilated stomach is to sink down in the abdomen, there is not usually
much displacement of the thoracic viscera. If, however, the fundus of
the stomach be distended with gas, the heart may be pushed upward, and,
being pressed against the chest-wall, its apex-beat may be more
forcible and diffused than normal. The tympanitic stomach may impart a
metallic quality to the cardiac sounds.

MORBID ANATOMY.--Considerable degrees of dilatation of the stomach are
easily recognized by post-mortem examination. In extreme cases the
stomach occupies all of the anterior region of the abdomen, covering
over the intestines and extending down to the pubes or even into the
true pelvis. Many cases are recorded in which the stomach was capable
of holding six to twelve pints. Godon[23] describes under the name
ventriculi hydrops a hardly credible case in which it is said that the
stomach contained ninety pounds of fluid! In the ordinary cases of
gastrectasia the lower border of the stomach is found somewhere between
the umbilicus and the pubes, frequently about a hand's breadth below
the level of the umbilicus.

[Footnote 23: _Diss. de Hydrops Ventriculi_, London, 1646. This
celebrated case is described with much detail. For three years the
abdomen was enormously distended, but the patient, a woman, never
vomited. The affection was supposed to be dropsy of the peritoneum.
Death occurred in a condition of extreme marasmus. The pylorus was the
seat of a hydatid cyst which extended into the duodenum. The stomach,
which was enormously distended, contained ninety pounds of fluid, in
which floated a great number of hydatid cysts, some of which were
ruptured. The anterior wall of the stomach was adherent to the parietal
peritoneum. The two orifices of the stomach were drawn close to each
other. The length of the stomach equalled a Paris ell.]

The fundus, being the most dilatable part of the stomach, is in most
cases disproportionately dilated in comparison with the pyloric region.
This excessive dilatation of the fundus is most noticeable in
gastrectasia due to stenosis. In most cases of dilatation the pylorus
sinks down somewhat in the abdomen, but in consequence of the
distension of the lower segment of the stomach the long axis of the
organ is more nearly transverse than normal. If the pylorus be fixed,
the lesser curvature may be drawn down in its middle so as to acquire a
hooked shape. The lesser curvature, which should be covered by the
liver, may be found considerably below its normal level. The dilated
fundus may extend from the left hypochondrium into the left iliac
region.[24]

[Footnote 24: Fogt reports a case in which an enormously dilated
stomach occupied a scrotal hernia of the left side. He refers to two
other similar cases (_Aerztl. Intelligenzbl._, 1884, No. 26).]

More or less dilatation of the oesophagus is associated with marked
dilatation of the stomach. If dilatation of the stomach be due to
obstruction in the upper part of the intestine, then the pyloric
orifice and the intestine on the proximal side of the obstruction will
be found dilated.

The walls of a dilated stomach may be hypertrophied, and such cases are
called hypertrophic dilatation; or the walls may be of normal thickness
or may be thinned, and these cases are called atrophic or atonic
dilatation. In general, the thickness of the gastric walls in
gastrectasia {600} depends upon that of the muscular coat. As a rule,
in cases of pyloric stenosis the muscular coat of the stomach is
hypertrophied. This hypertrophy affects chiefly the muscle of the
pyloric region. The gastric walls in stenotic dilatation may, however,
be of normal thickness or even atrophied. In non-stenotic dilatation
the muscular coat may be either hypertrophied or atrophied, but it
rarely attains the thickness observed in cases of gastrectasia due to
obstruction. Maier and others have repeatedly observed fatty and
colloid degeneration of the muscular fibres of dilated stomachs.[25]
More frequently, however, no degenerative change has been found in the
muscle.

[Footnote 25: _Deutsches Archiv f. klin. Med._, Bd. vi. p. 480;
Landerer, _op. cit._ Maier designates as colloid degeneration a
peculiar homogeneous, glistening appearance of the muscular fibres.
This change is not such as would usually be called colloid, but this
term is loosely used to designate a great variety of pathological
changes. The form of muscular hypertrophy in gastrectasia is chiefly
the numerical.]

The mucous membrane in dilatation of the stomach is usually in the
condition of chronic catarrhal gastritis. Although there are various
statements as to atrophy of the gastric tubules and degeneration of the
epithelial cells in the tubes in cases of gastric dilatation,
satisfactory histological investigations of the mucous membrane of the
stomach in this disease are wanting.[26]

[Footnote 26: For satisfactory studies of this nature it is desirable
that alcohol or some preservative fluid should be injected into the
stomach immediately after death.]

Atrophy of various abdominal viscera--particularly of the spleen, which
is usually small in this disease--has been attributed to the pressure
of a dilated stomach. This atrophy, however, is probably in many cases
only a part of the general emaciation and anaemia.

While well-marked cases of dilatation of the stomach cannot be mistaken
on post-mortem examination, it is important to add that the
pathological anatomist cannot always decide whether or not dilatation
of the stomach exists in the clinical sense. The following
considerations will make this evident: In the first place, the stomach
is a very variable organ as regards its size, so that it is impossible
to set definite limits, and say that a stomach exceeding these is
necessarily dilated, while a stomach not exceeding these limits is
normal. In the second place, it belongs to the clinical definition of
dilatation of the stomach that the organ is insufficient for the
performance of its normal functions. This insufficiency cannot be
determined at the post-mortem table. To determine, therefore, whether
stomachs which fall within certain not easily definable limits of size
are pathologically dilated or not, it is necessary to correct and
complete the results of the post-mortem examination by a knowledge of
the clinical history.[27]

[Footnote 27: To deny all value to post-mortem examination in the
determination of dilatation of the stomach, as has been done, is
absurd. In the majority of cases this examination affords satisfactory
evidence, but for some cases a reservation like that in the text must
be made. Rosenbach in an able article shows the error of regarding
dilatation of the stomach too exclusively from the anatomical point of
view ("Der Mechanismus und die Diagnose der Mageninsufficienz,"
_Volkmann's Samml. klin. Vortrage_, No. 153).]

DIAGNOSIS.--A considerable degree of dilatation of the stomach can
generally be diagnosticated without difficulty by means of the symptoms
and physical signs which have been described. The most important
diagnostic features relate to the character of the vomiting and to the
physical signs, together with the information afforded by the use of
the {601} stomach-tube. The diagnostic characters of the vomiting are
the large quantity rejected, its occurrence several hours after a meal,
its periodicity with long intervals, the temporary relief afforded, the
presence of undigested food taken a considerable time previously, and
the existence of fermentation. Washing out the stomach will also afford
evidence of stagnation of food. The time generally occupied in the
digestion of an ordinary meal is not over six to seven hours, so that
in health the contents of the stomach removed by the stomach-tube at
the end of this time should usually be free from undigested food. There
are of course individual idiosyncrasies with reference to the time
occupied in digestion, so that implicit reliance cannot be placed on
this diagnostic test. Delayed digestion is in itself no evidence of the
existence of dilatation, but the establishment of the presence of this
symptom may confirm other points in the diagnosis.

Simple inspection, palpation, and percussion of the abdomen are
sometimes, although rarely, sufficient for the diagnosis of dilatation
of the stomach. Various devices have already been described which aid
in the physical examination of the stomach, such as the administration
of effervescing powders, the introduction of the stomach-tube, and
Piorry's and Penzoldt's methods of determining the lower border of the
stomach.[28] It {602} is not necessary to repeat here the diagnostic
evidence afforded by physical examination. Excellent service as these
devices often perform, it must be confessed that they do not always
answer the purpose intended. The artificial distension of the stomach
with gas does not enable us always to distinguish intestine from
stomach. If the abdominal walls are thick or very rigid, this method,
like most of the others, is of little or no assistance. Then, as
already mentioned, the administration of the powders may fail to
produce any distension of the stomach, and may possibly mislead by
causing distension of intestine. Moreover, the artificial tympanites
may cause the patient much discomfort. The method of determining the
lower border of the stomach by Piorry's or Penzoldt's method is not
always conclusive. If the stomach be much dilated, it may take a very
large quantity of water to produce an appreciable zone of dulness. If
the transverse colon be distended with feces, it will not be easy to
separate the dulness of the stomach from that of the colon. Moreover,
loops of intestine containing feces or gas may lie over the anterior
surface of the stomach. The use of the stomach-tube simply for
diagnostic purposes is, for various reasons, not always practicable.
With due recognition of the important additions during the last few
years to our means of exploring the stomach, it must be admitted that
we are still far from any positive and universally applicable method of
determining the size and position of this organ during life. This
admission is the more necessary in view of the extravagant claims which
have been made for various more or less complicated contrivances for
physical exploration of the stomach.

[Footnote 28: Several other methods have been suggested for determining
the size and position of the stomach, but they have not found general
acceptance. Thus, Schreiber attaches a soft rubber balloon to the end
of a stomach-tube, and after its insertion in the stomach inflates it
(_Deutsches Arch. f. kl. Med._, Bd. 19). In Neubauer's method the long
end of a syphon-tube communicating with the stomach is bent upward, and
a glass tube is placed in the bent portion. The fluid will evidently
stand at the same level in the tube as in the stomach in case the
atmospheric pressure in both is the same. The atmospheric pressure in
the stomach is produced by using a double tube or by passing a second
tube into the stomach (_Prager med. Wochenschr._, 1879). Purjesz
attached a manometer to a stomach-tube, and thought that he could fix
the position of the cardia by noting the moment when in the passage
downward of the tube the negative pressure changed to positive, but
Schreiber has shown that the manometer may indicate negative pressure
even after the tube has entered the stomach (_Deutsches Arch. f. kl.
Med._, Bd. 33, p. 425). It has been asserted that by means of
auscultatory percussion of a stomach artificially distended with gas
the boundaries of the organ can be determined. Leichtenstern considers
the metallic quality of the tone heard over the stomach under these
circumstances more or less characteristic, while Skamper compares the
characteristic tone to that produced by tapping with the finger on the
dorsal surface of the hand of which the valar surface is placed against
the external ear (_Inaug. Diss._, Berlin, 1879, p. 30). It has been
claimed that the sound as of water dropping into a large cavity, which
can be heard when the patient is drinking, can no longer be heard when
the auscultating ear passes beyond the greater curvature (V.
Bamberger). Wunderlich suggests the possibility of feeling the arteries
of the greater curvature through the abdominal walls. Ferber calls
attention in cases of gastrectasia to a strip of dulness, with absent
vocal and respiratory sounds, corresponding to the posterior inferior
border of the left lung. This dulness, which is produced by material in
the most dependent part of the dilated stomach, disappears when the
patient assumes the knee-elbow position (_Deutsche Zeitschr. f. prakt.
Med._, 1876, No. 42). When it is impossible by other methods to
distinguish the lower portion of the stomach from the transverse colon,
it has been proposed to distend the colon with water, with gas, or with
air injected through a tube passed into the rectum. Penzoldt (_op.
cit._) found that the length of a tube (hard) or bougie reaching the
bottom of the stomach, estimating from the upper incisor teeth, should
be in a normal stomach at least 5 cm. less than that of the vertebral
column (occiput to coccyx), and at the most not much more than
one-third of the length of the body (1:2.8-1:3.3). In three cases of
gastrectasia he found the length of the tube inserted into the stomach
considerably more than one-third of the length of the body (1:2.4); in
one of the cases this length even exceeded that of the vertebral
column, and in the others it nearly equalled the length of the
vertebral column. Rosenbach's method of determining the elastic and
contractile power of the stomach is ingenious, but hardly of practical
utility. By injecting air into the stomach through a bulb apparatus
attached to the end of a stomach-tube, he is able to tell when the
point of the tube passes beneath the surface of fluid in the stomach by
hearing on auscultation a characteristic moist bubbling sound.
Elevation or depression of the level of the fluid can be determined by
withdrawing or by pushing forward the tube. That quantity of fluid
which, introduced into an empty stomach, causes no elevation, or
perhaps causes a depression, of the level of the food in the stomach,
indicates the utmost limit of the elastic and contractile forces of the
stomach (Rosenbach, _Volkmann's Samml. klin. Vortrage_, No. 153).]

The determination of the position of the lower border of the stomach
does not in itself enable us to infer positively the size of the organ.
It may be taken as a general rule that if the lower border of the
stomach be found persistently below the level of the umbilicus, the
stomach is dilated; but there are many exceptions to this rule.
Sometimes an otherwise normal stomach preserves in adult life the
vertical position which it had in the foetus, so that its lowest point
may be below the umbilicus. According to Kussmaul, a vertical position
of the stomach is a predisposing cause of dilatation. Occasionally a
stomach has a looped shape, so that without any dilatation of the organ
the lowest point may fall below the level of the umbilicus. It is,
moreover, a clinical fact established by the experience of many
observers that the lower border of the stomach may be found below the
level of the umbilicus without the existence of any symptoms of
dilatation.

The uncertainty of the anatomical diagnosis of dilatation of the
stomach in some cases makes it all the more necessary, as has been
repeatedly urged in the course of this article, to make a careful study
of the evidences of disordered gastric functions. The symptoms of most
importance in determining whether the condition called insufficiency of
the stomach is present or not are fermentation of the gastric contents
and the {603} persistent presence of undigested food in the stomach
beyond the limits of normal digestion. It is true that these symptoms
may be present without any dilatation of the stomach, but they are
likely to lead to dilatation if unchecked, and, what is of practical
importance, they require essentially the same treatment as dilatation.

A differential diagnosis between chronic catarrhal gastritis and atonic
dyspepsia on the one hand, and the early stages of dilatation of the
stomach on the other, cannot be made with any positiveness.

Of course, with our present means of diagnosis the confounding of
dilated stomachs with ascites, ovarian cysts, pregnancy, hydatid cysts
(of each of these errors there are recorded instances), is inexcusable.

PROGNOSIS AND COURSE.--The prognosis of dilatation of the stomach
depends first of all upon the nature of the primary disease causing the
dilatation. The prognosis of cancerous dilatation is as unfavorable as
possible. In dilatation due to non-cancerous stenosis the prognosis is
in general more favorable. Life may be prolonged sometimes for many
years, and the patient's condition greatly benefited by proper
treatment. A permanent cure of stenotic dilatation is not impossible,
but it is rarely to be expected. Even if temporarily relieved, the
symptoms of dilatation are likely sooner or later to return and to lead
to a fatal termination. The progress of the disease depends upon the
degree and the stationary or advancing character of the stenosis. In
the article on GASTRIC ULCER mention has been made of the cure of a few
cases of desperate gastric dilatation due to cicatricial pyloric
stenosis by means of resection of the diseased pylorus.

In general, the prognosis is more favorable in dilatation without
stenosis. If the degree of dilatation be only moderate, a permanent
cure may often be effected by proper treatment. If, however, the
dilatation be considerable, while the symptoms may be relieved or even
made to disappear for a time, relapses are prone to occur, and a
permanent cure is rarely obtained. Undoubtedly, Kussmaul's publication
in 1869, in giving to us a most valuable method of treatment, at the
same time raised extravagant expectations of the frequency with which
dilatation of the stomach can be cured. Too often the treatment with
the stomach-tube proves only palliative and not curative.

The course of dilatation of the stomach is chronic. The mode of death
is usually by inanition, very rarely from rupture of the stomach.

TREATMENT.--Reference to the causation of dilatation of the stomach
will show that there is considerable scope for the prophylactic
treatment of dilatation not referable to stenosis or incurable organic
disease. Thus, the correction of the habits of eating or drinking
inordinate quantities, or of imperfectly masticating the food in
consequence of haste or bad teeth or vicious custom, may avert the
development of gastric dilatation. Of especial importance is the timely
treatment of cases of dyspepsia or of chronic catarrhal gastritis which
are accompanied with fermentation or delayed digestion--conditions in
which the stomach-tube is of great service.

Of the means at our disposal for meeting the causal and the symptomatic
indications of dilatation of the stomach, the most important by far is
the use of the stomach-tube for the purpose of emptying and of washing
out the stomach. The introduction of this procedure by Kussmaul in 1867
marked a new era in the treatment of gastric disorders.

{604} By washing out the stomach we accomplish three important things:
first, we remove the weight which helps to distend the organ; secondly,
we remove mucus and stagnating and fermenting material which irritates
and often inflames the stomach and impedes digestion; and, thirdly, we
cleanse the inner surface of the stomach and obtain the beneficial
influence of the direct application of water, to which various
medicinal substances can be added. It is probable that in removing the
fermenting contents of the stomach we also remove a possible source of
self-infection of the system (see page 596).

By accomplishing these things we may possibly also enable the stomach
to regain its lost elasticity and muscular contractility. But unless
the normal elastic and contractile powers of the stomach are restored,
the treatment with the stomach-tube, indispensable as it is for the
relief of symptoms, is only palliative and not curative. Whether or not
this restoration of the stomach to its normal functional activity is to
be expected depends chiefly upon the cause and the degree of the
dilatation. Unfortunately, as has already been stated under Prognosis,
the permanent cure of dilatation of the stomach due to organic
stenosis, although possible, is not to be expected, and the number of
cases in which largely dilated stomachs can be restored to their normal
volume or made to perform permanently their normal functions is small.
There remains, however, a considerable number of curable cases--to be
sure, not always easily diagnosticated--in which the muscular coat of
the stomach has not been seriously damaged and in which the dilatation
is generally only moderate. Furthermore, excellent results are obtained
by the use of the stomach-tube in the cases which have been designated
insufficiency of the stomach, and which are closely allied to
dilatation--in fact, often represent its early stage. As has already
been mentioned, the most important criteria of this so-called
insufficiency are the fermentation of the contents of the stomach and
the presence therein of undigested food after the period required for
normal digestion (six to seven hours for an ordinary meal).

There are two principal methods of washing out the stomach--one by the
stomach-pump, the other by the siphon process. The stomach-pump is the
older method, and still has its advocates. The pump used by Kussmaul is
the Wyman pump, described by Bowditch in the _American Journal of
Medical Sciences_, vol. xxiii. p. 320, 1852. This (which is also called
the Weiss pump), as well as other forms of stomach-pump, consists in
principle simply of an aspirating syringe having at its anterior
extremity two openings communicating with the barrel of the syringe.
These openings can be alternately opened and closed by means of an
arrangement of valves. Through one opening, which is made to
communicate with an incompressible tube inserted into the stomach (the
other opening being now closed), the gastric contents are drawn into
the barrel of the syringe. This opening is now closed, and through the
other opening the contents of the syringe are discharged through a tube
externally. In a similar way fluid can be drawn into the syringe and
pumped into the stomach.

In the siphon process the outer end of the tube inserted into the
stomach is connected with a piece of elastic tubing about three and a
half feet long, in the free end of which is inserted the extremity of a
medium-sized glass funnel. A single elastic tube about six feet long
may also be used. {605} When the funnel is elevated, water which has
been poured into it will run into the stomach. If now, before the water
has all run out, the funnel be depressed below the level of the
stomach, the fluid contents of the stomach will flow out through the
tube according to the principle of the siphon. Figs. 20 and 21 will
make clear the mode of operation of this process. (The tube shown in
these figures is the Faucher tube, commonly used in France, and
consisting, with the funnel, of one piece. A longer tube than that
shown in the figure should be used.)

[Illustration: FIG. 20.[29]]

[Illustration: FIG. 21.[29]]

[Footnote 29: From Souligoux, _De la Dilatation de l'Estomac_, Paris,
1883.]

Another convenient but somewhat more complicated method of employing
the siphon process is according to Rosenthal's principle, and is
represented in Fig. 22. To the outer end of the stomach-tube is
attached a Y-shaped glass tube, one arm of which is connected with an
elastic tube running to an irrigator, while the other arm is connected
with the discharging tube. Through the irrigating tube water runs into
the stomach, the discharging tube being compressed. If the discharging
tube be opened while the fluid is flowing from the irrigator, and if
then, after the establishment of a column of water in the discharging
tube, the irrigating tube be compressed or the stopcock of the
irrigator be closed, a siphon communicating with the stomach is formed
and empties this organ of its fluid contents.

[Illustration: FIG. 22.[30]]

[Footnote 30: From Leube, in _Ziemssen's Handb. d. spec. Path. u.
Therap._, Bd. vii.]

In the siphon process the tube inserted into the stomach may be an
incompressible hard-rubber tube like that employed with the
stomach-pump, but by far the simplest, most convenient, and safest form
of stomach-tube is the soft, flexible, red rubber tube, resembling the
Jacques catheter, but of course larger and longer.[31] This soft tube
can inflict no {606} injury, and in most cases it is readily
introduced. Generally, the patient himself can best manipulate the
introduction of the tube. After the tube is introduced into the
pharynx, the patient, who should be in a sitting posture, makes
repeated acts of swallowing, by means of which, accompanied by
directing and gently pushing the tube with the fingers, the tube passes
along the oesophagus into the stomach. Often at first the nervousness
and inexperience of the patient occasion some trouble, but after a
little practice he generally succeeds in introducing the tube without
discomfort or difficulty. Before its introduction the tube should be
anointed with a little vaseline or some similar substance. In an adult
the tube is introduced for a length of at least 20 to 25 inches, and in
cases of dilatation of the stomach of course for a greater distance.
Whatever form of stomach-tube be used, it is important that the tube
should be at least 30 inches long, and should be provided with one, and
preferably with two, large eyes at its distal extremity.

[Footnote 31: Such a tube (marked 19 A) is made by Tieman & Co. of New
York, and is to be had of most surgical instrument-makers. (For a
fuller description of the tube and the mode of its employment see
article by W. B. Platt, "The Mechanical Treatment of Diseases of the
Stomach," _Maryland Medical Journal_, March 8, 1884.)

Oser's tube is 2 meters long, and is made of mineralized rubber. There
are two sizes. The smaller has a lumen of 8 mm. The thickness of the
wall is 2-1/2 mm. In the larger tube the lumen is 10 mm., and the
thickness of the wall 3 mm. He generally uses the smaller tube.

Faucher's tube is 1-1/2 meters long. The external diameter of the tube
is 10 to 12 mm. The walls are of such thickness that the tube can be
bent without effacing its lumen. At one extremity is a lateral eye with
two orifices. To the other extremity is adapted a funnel with a
capacity of about 500 grammes.]

Although the stomach-pump has the advantage of more completely
evacuating the stomach and of removing coarser solid particles than is
possible with the siphon, nevertheless its disadvantages--namely, the
possibility of inflicting injury to the mucous membrane of the
stomach,[32] the expense and greater complexity of the instrument, and
the circumstance that it should be used only by the physician--in
contrast with the advantages of the siphon--namely, its cheapness,
simplicity, safety, and possible employment by the patient or his
attendants--have led to the general adoption of the latter process.
Only the soft-rubber stomach-tube should be left to the employment of
the patient.

[Footnote 32: A number of cases have been recorded in which pieces of
the mucous membrane of the stomach have been detached by the
stomach-pump. Although as yet no serious effects have followed this
accident, the possibility of its occurrence can certainly not be
regarded with equanimity.]

Sometimes the flow through the siphon is interrupted by occlusion of
the eye of the stomach-tube by a solid mass or by some cause not always
clear. As already mentioned, it is desirable that there should be two
openings at the gastric extremity of the tube. When the flow is {607}
interrupted the position of the tube in the stomach may be changed, or
the patient may be directed to cough or to exert the pressure of the
abdominal muscles, or more water may be allowed to run into the stomach
in order to displace an occluding mass in the tube. It is, however,
well for such cases to have, if possible, a stomach-pump and an
incompressible tube in reserve. Moreover, as is apparent from the
foregoing statement of the advantages of the stomach-pump, there are
cases in which this instrument is much more useful than the siphon, so
that one cannot decide unconditionally in favor of one instrument over
the other.

The stomach-tube should be secured so that there can be no possibility
of its being swallowed entirely. A string may be attached to the distal
end of the tube. Leube[33] has reported an instance in which the whole
tube disappeared into the stomach, and Jackson[34] has also narrated a
case in which an insane patient swallowed the stomach-tube. In both
cases the tube was subsequently rejected by vomiting.

[Footnote 33: _Deutsches Arch. f. klin. Med._, Bd. 33, p. 6.]

[Footnote 34: _Extracts from the Records of the Boston Society for
Medical Improvement_, vol. vi. p. 261.]

For washing out the stomach after the greater part of the contents have
been withdrawn, about a pint of tepid fluid is allowed to slowly run
into the stomach, and is then siphoned out. This process is to be
repeated several times. In general, tepid water suffices for washing
out the stomach, but it is often better to use, at least a part of the
time, a 1 to 2 per cent. solution of bicarbonate of sodium, which
facilitates the removal of mucus. The artificial and the natural Vichy
and Carlsbad waters are also excellent for this purpose. Various
additions are also made to the water with the view of counteracting
fermentative changes in the stomach. For this purpose perhaps the best
agents are salicylate of sodium (1 per cent. solution) or resorcin (2
per cent. solution). Other substances which have also been recommended
are carbolic acid, permanganate of potassium, hyposulphite of sodium,
creasote, benzine. Simple water, however, accomplishes about all that
is possible, and many are satisfied to use it without any medication.

As regards the frequency with which the stomach is to be washed out,
one is to be guided by the symptoms and the effect obtained by the use
of the stomach-tube. As a general rule, it suffices to wash out the
stomach once a day, and often the process need be repeated only every
second or third day.

Opinions are divided as to the best time of day to select for washing
out the stomach. Kussmaul recommends the morning before breakfast, and
the majority have followed his advice; others prefer the evening. There
is much, however, in favor of washing out the stomach about half an
hour before the principal meal of the day. The best opportunity has
been offered for the digestion and absorption of the food taken at the
previous main meal, and the stomach is placed in the best possible
condition for the reception of more food.

The habitual washing out of the stomach is not without its drawbacks.
We often remove, as has been pointed out especially by Leube, not only
noxious substances from the stomach, but also the completed products of
digestion. To withdraw from the nourishment of the body this chyme
which the stomach has laboriously manufactured cannot be a matter of
indifference. Still, with the weakened absorptive powers of the
stomach, {608} and its inability to properly propel its contents into
the intestine, it is a question how much of this chyme would eventually
be utilized for nutrition. Another point is worthy of attention. The
relief which the patient experiences when his overloaded stomach is
freed of its burden, and the knowledge that this method of relief is
always at hand, may make him careless in the observance of the dietetic
rules which are of great importance in the treatment of this disease.
It is well, therefore, not to wash out the stomach oftener than is
necessary, nor to continue the habitual use of the stomach-tube longer
than is required.

There are contraindications to the use of the stomach-tube. In very
rare instances the attempt to introduce the tube causes the patient so
much distress, produces such violent spasm of the pharyngeal and
adjacent muscles, or induces so much retching and vomiting, or is
attended with such prostration or even syncope, that this method of
treatment has to be abandoned. Great weakness, recent gastric
hemorrhage, ulcer of the stomach in most cases (see page 523), often
cancer of the cardia or of the oesophagus, and aneurism of the aorta,
are contraindications to the use of the stomach-tube.

If we group together the results obtained by the use of the
stomach-tube in gastric dilatation, we shall find cases in which no
benefit results; cases which are benefited, but are obliged to continue
the use of the stomach-tube throughout life; cases in which recovery is
slow and gradual; cases with more or less speedy relief or apparent
cure, but followed by relapses; and cases of prompt relief and
permanent cure.

The regulation of the diet is never to be neglected in cases of
dilatation of the stomach. Here the guiding principles are that little
fluid should be taken, and that the food should be small in bulk,
nutritious, easily digestible, and not readily undergoing fermentation.
The patient should drink as little water as possible, and should
therefore avoid whatever occasions thirst. It is hardly practicable to
carry out the plan of giving water mostly by the rectum, as has been
proposed. In most cases milk is useful, but an exclusively milk diet is
not generally well borne on account of the quantity of fluid required.
Leube's beef-solution is often serviceable. Soft-boiled eggs and tender
meats are to be allowed, particularly the white meat of fowl and rare
beefsteak, especially that prepared from scraped and finely-chopped
beef, as recommended in the treatment of gastric ulcer (page 521).
Fatty, saccharine, and amylaceous articles of food--hence most
vegetables and fruits--are to be avoided on account of their tendency
to undergo fermentation in the stomach. Alcohol in any form is usually
detrimental. If gastric symptoms, particularly vomiting, be very
urgent, or if food introduced into the stomach affords little or no
nourishment, as in some cases of tight pyloric stricture, then rectal
alimentation is to be resorted to.

An important indication is to restore the tone and contractile power of
the muscular coat of the stomach. For this purpose electricity, in the
form both of the constant and of the faradic current, has been
beneficially employed. The best results are reported from the use of
the faradic current. Both poles may be applied over the region of the
stomach. The application of electricity to the inside of the stomach by
means of electrodes attached to stomach-tubes or bougies is a more
{609} difficult procedure, but has its advocates. Uniformly good
results are not obtained by the use of electricity in gastric
dilatation, but there can be no doubt that in some cases decided
benefit follows this method of treatment.

Nux vomica, particularly its alkaloid strychnia, has been much employed
with the view of stimulating the muscular power of the stomach.
Strychnia is given either internally or hypodermically. Hypodermic
injections of ergotin have also been used for the same purpose. It has
been hoped to increase the contraction of the stomach by cold
applications to the abdomen, as by ice-bags applied immediately after
washing out the stomach. The benefit derived from these various
attempts to increase the tonicity of the gastric muscle is not very
apparent.

A belt or bandage around the abdomen in order to support the stomach
sometimes makes the patient feel more comfortable; in other cases it
aggravates the symptoms.

In many cases digestion is promoted by giving dilute hydrochloric acid
with or without pepsin. About ten drops of dilute hydrochloric acid may
be given half an hour to an hour after each meal.

When the stomach is systematically washed out, the individual symptoms
of dilatation of the stomach will rarely require special treatment. The
sensation of fulness and weight in the stomach, the eructations, the
vomiting, and the constipation are generally relieved, at least
temporarily, by washing out the stomach. The appetite is improved, and
an increase in weight is usually soon noticeable.

If heartburn and eructations of gas continue troublesome, an antacid,
such as bicarbonate of sodium or prepared chalk, will be found useful.

Leube, in order to relieve constipation and to increase the peristalsis
of the stomach, administers Carlsbad water (see page 522). Not more
than five or six ounces of the water need be given, and this should be
taken slowly in divided doses. A laxative pill containing rhubarb may
be given occasionally.

If anaemia be the cause or a prominent accompaniment of dilatation of
the stomach, iron may be administered in a form as little disturbing
the digestion as possible, as the effervescing citrate or the lactate,
or arsenic in the form of Fowler's solution may be tried. In general,
however, all drugs which impair the appetite or digestion are to be
withheld. The digestion and the general condition of the patient are
often benefited by massage.

Resection of the pylorus in cases of cancerous and of cicatricial
stenosis of this orifice has been performed in several instances. The
subject, as regards its medical in distinction from its surgical
bearings, has already been discussed in connection with cancer of the
stomach (see page 577). Here it may be added that the propriety of
resection is less open for dispute in cases of non-cancerous pyloric
stenosis than it is in cancer of the pylorus.

Remarkable results have been reported by Loreta in cases of cicatricial
stenosis of the pylorus. After performing gastrotomy he inserts his
fingers through the constricted pyloric orifice and forcibly dilates
the stricture.[35] To judge from experience in divulsing strictures in
other parts of {610} the body, it does not seem probable that a
permanent cure can be often effected by this bold and dangerous
procedure.

[Footnote 35: Loreta has performed this operation successfully no less
than nine times (_The Lancet_, April 26, 1884).]


Acute Dilatation of the Stomach.

Under the name acute dilatation of the stomach[36] have been described
cases in which it has been supposed that a more or less suddenly
developed paralysis of the muscular coat of the stomach exists. But the
propriety of the term acute dilatation, and the very existence of an
acute paralysis of the stomach, are, to say the least, questionable.

[Footnote 36: The literature pertaining to the subject of acute
dilatation of the stomach is to be found in Poensgen, _Die Motorischen
Verrichtungen des Menschlichen Magens_, Strasburg, 1882, p. 95.]

As causes of this so-called acute dilatation of the stomach have been
assigned injuries, particularly those affecting the abdomen, surgical
operations involving the peritoneum, acute inflammations of the mucous
and of the peritoneal coats of the stomach, acute fevers, especially
during convalescence, and overloading the stomach with food or with
liquids.

The symptoms which have been chiefly emphasized are severe abdominal
pain, tympanitic distension of the stomach, and absence or cessation of
vomiting if this has previously existed. It will be noted that
inability to vomit under these circumstances implies not only paralysis
of the stomach, but also that of the abdominal muscles.

The prognosis depends on the character of the primary disease causing
the alleged paralysis.

If there be acute distension of the stomach with inability of the organ
to expel its contents either externally or into the intestine, the
stomach-tube may be employed to evacuate the gas and other material
present.

In a case described by Hilton Fagge[37] as acute dilatation of the
stomach the symptoms of dilatation appeared suddenly and ran an acute
course, but the autopsy showed that the dilatation was doubtless of
much longer development than the symptoms indicated. In a case reported
by Nauwerk[38] of extreme dilatation in consequence of hypertrophic
stenosis of the pylorus, after ten months of insignificant dyspeptic
symptoms there suddenly appeared, after excess in eating, symptoms of
dilatation of great severity, which continued until a fatal termination
at the end of three months. Thus it appears that chronic dilatation of
the stomach may cause little disturbance for a considerable time and
then run a rapid course.

[Footnote 37: "On Acute Dilatation of the Stomach," _Guy's Hosp. Rep._,
xviii. p. 4, 1873.]

[Footnote 38: _Deutsches Arch. f. kl. Med._, Bd. xxi. p. 573.]




{611}

MINOR ORGANIC AFFECTIONS OF THE STOMACH.

(CIRRHOSIS; HYPERTROPHIC STENOSIS OF PYLORUS; ATROPHY; ANOMALIES IN THE
FORM AND THE POSITION OF THE STOMACH; RUPTURE; GASTROMALACIA.)

BY W. H. WELCH, M.D.


CIRRHOSIS OF THE STOMACH.

DEFINITION.--Cirrhosis of the stomach is characterized by thickening of
the walls of the greater part or of the whole of the stomach in
consequence of a new growth of fibrous tissue, combined usually with
hypertrophy of the muscular layers of the stomach. The cavity of the
stomach is usually contracted, but sometimes it is of normal size or
even dilated.

SYNONYMS.--Fibroid induration of the stomach; Hypertrophy of the walls
of the stomach; Chronic interstitial gastritis; Sclerosis of the
stomach; Plastic linitis.

HISTORY.--The writings of the seventeenth and eighteenth centuries
contain many records of extremely contracted stomachs with uniformly
and greatly thickened walls (Butzen, Loseke, Storck, Portal, Lieutaud,
Pohl, etc.). In the works of Lieutaud and of Voigtel may be found
references to many such cases.[1] Doubtless, some of these cases were
examples of cirrhosis of the stomach, but in the absence of
microscopical examination it is not possible to separate these from
cancer.

[Footnote 1: Lieutaud, _Historia anat.-med._, t. i. p. 8, Venet., 1779;
Voigtel, _Handb. d. Path. Anat._, Bd. ii. p. 450, Halle, 1804. Here it
may be mentioned that Diemerbroeck's case, which is so often quoted to
prove that polyphagia instead of causing gastric dilatation may produce
hypertrophy of the muscular coat of the stomach, with contraction, was
probably an instance of cirrhosis of the stomach.]

Andral[2] was the first to describe fully and systematically
hypertrophy of the walls of the stomach. He attributed the lesion to
chronic inflammation. He erroneously supposed that scirrhus of the
stomach was only hypertrophy of the gastric walls. Cruveilhier[3]
distinguished between scirrhous induration and hypertrophy, which he
considered to be a final result of the irritation accompanying chronic
diseases of the stomach. Rokitansky's[4] description of fibroid
induration of the stomach, although brief, is accurate. He says that
the process usually involves the whole {612} stomach, and that it
originates in an inflammation of the submucous connective tissue. This
inflammation may occur either independently or in combination with
gastritis mucosa. Rokitansky emphasizes the error of confounding the
disease with scirrhous cancer. Bruch[5] made an elaborate study of
hypertrophy of the walls of the stomach, which he considered to be the
final stage of various chronic diseases of the stomach. Fibrous or
scirrhous cancer he considered to be nothing but this hypertrophy.

[Footnote 2: _Precis d'Anat. path._, Paris, 1829.]

[Footnote 3: _Anatomie pathologique_, Paris, 1830-42.]

[Footnote 4: _Lehrb. d. Path. Anat._, Wien, 1855-61.]

[Footnote 5: _Zeitschr. f. rat. Med._, Bd. vii., 1849.]

The best descriptions of cirrhosis of the stomach have been furnished
by English writers, by most of whom it is properly regarded as an
independent disease. Brinton[6] first employed the names cirrhosis of
the stomach and plastic linitis. Excellent descriptions of the disease
have been given by Hodgkin, Budd, Brinton, Habershon, H. Jones, Wilks,
Quain, and Smith.

[Footnote 6: _Diseases of the Stomach_.]

While in former times cirrhosis of the stomach was confounded with
cancer, in recent times it has not been separated by many from chronic
catarrhal gastritis. In German systematic works the disease receives,
as a rule, only passing mention in connection with chronic catarrhal
gastritis.

ETIOLOGY.--Cirrhosis of the stomach is rare, but it is not so
exceptional as to be without any clinical importance. I have met with
three cases at post-mortem examination.

The disease is more frequent in men than in women. A considerable
number of cases have occurred between thirty and forty years of age,
but the greatest frequency is after forty. At an earlier age than
twenty the disease is very rare.

The causation of cirrhosis of the stomach is obscure. Nearly all
writers upon the subject have emphasized the abuse of alcohol as an
important cause in this as in other diseases of the stomach.
Intemperance cannot, however, be the only cause; and here, as
elsewhere, it is not easy to say what importance is to be attached to
it as an etiological factor. In only one of the three cases which I
examined post-mortem could it be determined that the patient was an
immoderate drinker, and in one case intemperance could be positively
excluded. Other cases have been recorded in which the abuse of spirits
could be positively excluded. In one of my cases syphilis existed, as
was established by the presence of gummata in the liver. In some cases
the disease has been attributed to cicatrization of a gastric ulcer. In
a case reported by Snellen the disease followed an injury to the
epigastric region.[7]

[Footnote 7: _Canstatt's Jahresbericht_, 1856, iii. 302.]

Cirrhosis of the stomach, as well as cancer, ulcer, and most other
chronic structural diseases of this organ, is usually associated with
chronic catarrhal gastritis. There is, however, no proof of the
prevalent idea that chronic catarrhal gastritis is the cause of the
enormous new growth of fibrous tissue which characterizes typical cases
of this disease.

SYMPTOMATOLOGY AND DIAGNOSIS.--The symptoms of cirrhosis of the stomach
are not sufficiently characteristic to warrant a positive diagnosis.
Sometimes the disease pursues a latent course. Like cancer of the
stomach, it may put on various disguises. Thus, in a case of cirrhosis
of the stomach reported by Nothnagel[8] the symptoms were {613}
typically those of progressive pernicious anaemia. Association with
ascites or with chronic peritonitis may lead to a false diagnosis.
Thus, in one of the cases which I examined after death, and in which
there was chronic peritonitis with abundant fluid exudation, the
disease during life was diagnosticated as cirrhosis of the liver. Most
frequently, however, cirrhosis of the stomach is mistaken for gastric
cancer, from which, in fact, it can rarely be positively
diagnosticated.

[Footnote 8: _Deutsches Arch. f. kl. Med._, Bd. 24, p. 353.]

The symptoms are usually those of chronic dyspepsia, which sooner or
later assumes a severity which leads to the diagnosis of some grave
structural disease of the stomach, usually of cancer.

Indigestion, loss of appetite, oppression in the epigastrium, vomiting,
are the common but in no way characteristic symptoms of cirrhosis of
the stomach. There may be severe gastralgia, but in general the disease
is less painful than either ulcer or cancer of the stomach. The
inability to take more than a small quantity of food or of drink at a
time, with the sense of fulness which even this small quantity
occasions, has been considered somewhat characteristic of cirrhosis of
the stomach, but this symptom is too inconstant, and occurs in too many
other affections of the stomach, to be of much service in diagnosis.
The symptoms of dyspepsia are often of much longer duration than in
cancer, existing sometimes for many years (up to fifteen years), but on
the other hand there have been cases in which the clinical history of
gastric cirrhosis was as rapid in its progress as cancer. Moreover,
cancer may be preceded by dyspeptic symptoms of long duration, but long
duration is the exception with cancer and the rule with cirrhosis of
the stomach.

As the disease progresses the patient loses flesh and strength, and
usually dies in a condition of marasmus. Blood is rarely present in the
vomit, but in a few cases the vomiting of coffee-ground material has
been noted.

By physical examination sometimes a tumor in the region of the stomach
can be felt. Under favorable circumstances it can sometimes be
determined that this tumor is smooth, elastic, tympanitic on
percussion, and presents more or less distinctly the contours of the
stomach. By administering effervescing powder it may be possible to
obtain further evidence that the tumor corresponds in its form to the
stomach. The diagnosis of contraction of the cavity of the stomach is
not easy. Some information may be afforded by noting the length to
which the inflexible stomach-tube can be passed. The quantity of water
which can be poured into the stomach until it begins to run out of the
stomach-tube may also bring some confirmatory evidence as to the
existence of contraction of the stomach.

Even should the physical signs suffice to determine that the tumor is
the thickened and contracted stomach, still cancer cannot be excluded,
for this also may grow diffusely in the gastric walls and may cause
contraction of the cavity of the stomach. With our present means of
diagnosis, therefore, the most which can be said is, that a special
combination of favorable circumstances may render probable the
diagnosis of cirrhosis of the stomach, but a positive diagnosis is
impossible.

MORBID ANATOMY.--In most cases of cirrhosis of the stomach the stomach
is contracted. The cavity of the stomach has been found not larger than
would suffice to contain a hen's egg, but such extreme {614}
contraction is very rare. When the stomach in this disease is found
dilated, either the thickening involves only or chiefly the walls of
the pyloric portion, or the morbid process probably began there and was
followed by dilatation.

In typical cases the walls of the entire stomach are thickened, but
frequently the thickening is most marked in the pyloric region. The
walls may measure an inch and even more in thickness. The thickened
walls are dense and firm, so that often upon incision the stomach does
not collapse.

Upon transverse section the different coats of the stomach can be
distinguished. The mucous membrane is least affected, being sometimes
thickened, sometimes normal or atrophied. The muscularis mucosae is
hypertrophied, and is evident to the naked eye as a grayish band. The
submucous coat is of all the layers the most thickened, being sometimes
ten to fifteen times thicker than normal. It appears as a dense white
mass of fibrous tissue. The main muscular coat is also, as a rule,
greatly hypertrophied; the grayish, translucent muscular tissue is
pervaded with streaks of white fibrous tissue prolonged from the
submucous and subserous coats. This last coat resembles in appearance
the submucous coat, which, however, it does not equal in thickness,
although it is, proportionately to its normal thickness, much
hypertrophied. The free peritoneal surface usually appears opaque and
dense.

To the naked eye it is apparent that the new growth of fibrous tissue
is most extensive in the submucous coat, which it is probably correct
to regard as the starting-point of the disease. The hypertrophy of the
muscular layers is also in most cases an important element in the
increased thickness of the gastric walls.

Microscopical examination[9] shows sometimes a nearly normal mucous
membrane. The tubules, however, are usually more or less atrophied. In
the case reported by Nothnagel tubules could be found only in the
pyloric region of the stomach. The essential lesion is the new growth
of fibrillated connective tissue pervading all of the coats of the
stomach. In an interesting case reported by Marcy and Griffith,[10]
which was believed to be caused by an extensive cicatrized ulcer, a new
formation of smooth muscular tissue was found not only in the main
muscular tunic and the muscularis mucosae, but also throughout the
submucosa. This peculiarity was probably referable to the cicatrization
of the ulcer.

[Footnote 9: Microscopical examination is always necessary for a
positive diagnosis of cirrhosis of the stomach. In a case which I
examined post-mortem of double ovarian cancer, with multiple secondary
deposits in the peritoneum and with chronic peritonitis, the stomach
presented the typical gross appearances of cirrhosis, but here and
there were to be found nests of cancer-cells in the prevailing new
growth of fibrous tissue in the walls of the stomach.]

[Footnote 10: _Am. Journ. of the Med. Sci._, July, 1884, p. 182.]

Not infrequently adhesions exist between the stomach and surrounding
organs. Exceptionally, a diffuse growth of fibrous tissue may invade
the greater part of the peritoneum, particularly the visceral layer,
and cause a thickening similar to that existing in the stomach. In such
cases ascites is usually a marked symptom.

PROGNOSIS.--The prognosis of cirrhosis of the stomach is grave. The
disease runs a chronic course, and usually terminates in death by
asthenia. There is no reason to believe that the stomach can ever be
restored to its {615} normal condition. Still, cases have been reported
in which it has been supposed that cirrhosis of the stomach has
terminated in recovery.[11] The diagnosis, however, in such cases must
remain doubtful.

[Footnote 11: Lesser, _Cirrhosis Ventriculi_, Inaug. Diss., Berlin,
1876; Smith, "Cirrhosis of the Stomach," _Edinb. Med. Journ._, 1872, p.
521.]

TREATMENT.--The treatment is symptomatic, and is to be guided by the
general principles developed in previous articles concerning the
regulation of the diet and the administration of remedies.


HYPERTROPHIC STENOSIS OF THE PYLORUS.

The various causes of stenosis of the pylorus have already been
mentioned under DILATATION OF THE STOMACH, and the most important of
these causes have received full consideration in connection with ULCER
and with CANCER OF THE STOMACH.

Only one of the varieties of pyloric stenosis can claim consideration
as an independent disease. This variety is the so-called hypertrophic
stenosis of the pylorus (Lebert) or fibroid degeneration of the pylorus
(Habershon[12]). Under the name of hypertrophic stenosis have been
described cases in which the stenosis was due to hypertrophy of only
one of the coats of the stomach, usually either the submucous or the
muscular coat, sometimes only the mucous coat. In most cases, however,
all of the coats of the stomach are involved, and the lesion is similar
to that of cirrhosis of the stomach, but it is confined to the pylorus
or to the pyloric region. In such cases there is new growth of fibrous
tissue, most marked in the submucous coat, and hypertrophy of the
muscular coat. The appearance of the pylorus in some instances of
hypertrophic stenosis has been not inappropriately compared to that of
the cervix uteri.

[Footnote 12: Habershon, _On Diseases of the Abdomen_, London, 1862;
Lebert, _Die Krankh. d. Magens_, Tubingen, 1878; Nauwerk, _Deutsches
Arch. f. klin. Med._, Bd. 21, 1878.]

In the majority of cases the change here described is the result of
cicatrization of a gastric ulcer, and some believe that all cases of
so-called hypertrophic stenosis or fibroid degeneration of the pylorus
are referable to ulcer, although it may be very difficult to discover
the cicatrix of the ulcer. It is certainly not always possible to
detect either ulcer or cicatrix, so that it seems proper to regard the
hypertrophic stenosis in such cases as constituting an independent
affection.

The symptoms are those of dilatation of the stomach, sometimes preceded
by evidences of chronic catarrhal gastritis. The thickened pylorus can
sometimes be felt during life as a small, cylindrical, usually movable
tumor, either stationary in progress or of very slow growth.

In most cases the diagnosis of organic stenosis of the pylorus can be
made. Cancer may sometimes be excluded by the long duration of the
symptoms and the stationary character of the tumor if a tumor can be
felt. The exclusion of ulcer is more difficult and hardly possible, for
ulcer may have existed without producing characteristic symptoms.

The prognosis and treatment have been considered under DILATATION OF
THE STOMACH.


{616} ATROPHY OF THE STOMACH.

Atrophy of the stomach may be the result of stenosis of the cardia or
of the oesophagus. The stomach may participate with other organs in the
general atrophy attending inanition and marasmus. The walls of a
dilated stomach may be very thin.

Especial importance has been attached in recent years to degeneration
and atrophy of the gastric tubules. The glands of the stomach may
undergo degeneration and atrophy in various diseases of the stomach,
such as chronic catarrhal gastritis, phlegmonous gastritis, cirrhosis
of the stomach, and cancer of the stomach. Parenchymatous and fatty
degeneration of the glandular cells of the stomach occurs in acute
infectious diseases, as typhoid fever and yellow fever, also as a
result of poisoning with phosphorus, arsenic, and the mineral acids.

It is claimed by Fenwick that atrophy of the stomach may occur not only
as a secondary change, but also as a primary disease attended by grave
symptoms. Fenwick has described a number of cases in which the gastric
tubules were atrophied without thickening of the walls of the stomach
and without diminution in the size of the cavity of the stomach--cases,
therefore, which cannot be classified with cirrhosis of the
stomach.[13] He attributes in many cases the atrophy of the tubules to
an increase in the connective tissue of the mucous membrane, and draws
a comparison between atrophy of the stomach and the atrophic form of
chronic Bright's disease.

[Footnote 13: _The Lancet_, 1877, July 7 _et seq._]

In 1860, Flint[14] called attention to the relation between anaemia and
atrophy of the gastric glands. He expressed the opinion that some cases
of obscure and profound anaemia are dependent upon degeneration and
atrophy of the glands of the stomach. Since Flint's publication cases
have been reported by Fenwick, Quincke, Brabazon, and Nothnagel, in
which lesions supposed to be due to pernicious anaemia have been found
after death associated with atrophy of the gastric tubules.[15]
Nothnagel's case, which has already been mentioned, was one of
cirrhosis of the stomach.

[Footnote 14: A. Flint, _American Medical Times_, 1860. Further
contributions of Flint to this subject are to be found in the _New York
Medical Journal_, March, 1871, and in his _Treatise on the Principles
and Practice of Medicine_, p. 477, Philada., 1881.]

[Footnote 15: Fenwick, _loc. cit._; Quincke, _Volkmann's Samml. klin.
Vortrage_, No. 100 (case _b_); Brabazon, _British Med. Journ._, 1878,
July 27 (without microscopical examination!); Nothnagel, _Deutsches
Arch. f. kl. Med._, Bd. 24, p. 353.]

The symptoms which have been referred to primary atrophy of the stomach
are severe anaemia and disturbances of digestion, such as anorexia,
eructations, and vomiting. The digestive disturbances are often not
greater than are frequently observed in cases of severe anaemia.

In my opinion, the existence of atrophy of the stomach as a primary and
independent disease has not been established. In many cases which have
been described as primary atrophy the histological investigation of the
stomach has been very defective. Degeneration and atrophy of the
gastric tubules secondary to various diseases of the stomach and to
certain general diseases is an important lesion when it is extensive,
and must seriously impair the digestion, and consequently the
nutrition, of the patient.


{617} ANOMALIES IN THE FORM AND IN THE POSITION OF THE STOMACH.

These anomalies, so far as they have not received consideration in
previous articles, are of more anatomical than clinical interest, and
therefore here require only brief mention.

The stomach may have an hour-glass shape in consequence of a
constriction separating the cardiac from the pyloric half of the organ.
This constriction is sometimes congenital,[16] sometimes caused by
cicatrization of a gastric ulcer, and sometimes caused by spasmodic
contraction of the muscle, which may persist after death, but
disappears when the stomach is artificially distended. Hour-glass shape
of the stomach has been diagnosed during life by administering an
effervescing powder according to Frerichs' method.

[Footnote 16: A careful study of the congenital form of hour-glass
contraction of the stomach has been made by W. R. Williams ("Ten Cases
of Congenital Contraction of the Stomach," _Journ. of Anat. and
Physiology_, 1882-83, p. 460).]

Foreign substances of hard consistence which have been swallowed
sometimes cause diverticula of the stomach.

Sometimes the fundus of the stomach is but little developed, so that
the organ is long and narrow like a piece of intestine.

The stomach may be variously distorted by external pressure, as from
tumors and by adhesions.

The loop-shaped stomach and vertical position of the stomach have been
already considered in connection with DILATATION OF THE STOMACH (page
602).

In transposition of the viscera the stomach is also transposed. In such
a case difficulties may arise in the diagnosis of pyloric cancer, as in
a case described by Legroux.

The stomach may be found in hernial sacs. Mention has already been made
of the presence of dilated stomachs in scrotal hernia. More frequently
the stomach is found in umbilical hernias. In diaphragmatic hernia the
stomach is found more frequently in the thorax than is any other
abdominal viscus. In 266 diaphragmatic hernias collected by Lascher[17]
the stomach was found either wholly or partly in the thorax in 161
cases. The clinical consideration of diaphragmatic hernia, however,
does not belong here.

[Footnote 17: _Deutsches Arch. f. kl. Med._, Bd. 27.]

Furthermore, the stomach may be displaced by tumors, enlargement of
neighboring organs, tight-lacing, adhesions, and the weight of hernias.
These displacements, however, are generally inconsiderable and of
little importance.

In a case described by Mazotti[18] the stomach, of which the pyloric
portion was fixed by adhesions, was twisted around its long axis. Death
was caused by uncontrollable vomiting.

[Footnote 18: _Virchow und Hirsch's Jahresbericht_, 1874, ii. p. 249.]


{618} RUPTURE OF THE STOMACH.

Sufficient attention has already been given to perforation of the
stomach in consequence of diseases of its walls, such as ulcer, cancer,
abscesses, and toxic gastritis.

A healthy stomach may be ruptured by violent injury to the abdomen even
when no external wound is produced. An example of rupture of the
stomach from this cause is that sometimes produced when a person has
been run over by a heavy vehicle.

It has been claimed that a stomach with healthy walls may burst in
consequence of over-distension of the organ with solids or with gas.
The older literature is especially rich in reports of so-called
spontaneous rupture of the stomach. Most of these cases were examples
of perforation of gastric ulcer. In a case of apparently spontaneous
rupture of a stomach which had become abnormally distended with gas,
Chiari[19] found that the rupture was through the cicatrix of a simple
ulcer in the lesser curvature. It is hardly conceivable that rupture of
the healthy stomach from over-distension can occur so long as the
orifices of the organ are unobstructed.

[Footnote 19: _Wiener med. Blatter_, 1881, No. 3.]

Lautschner[20] reports a case of spontaneous rupture of the stomach in
a woman seventy years old with an enormous umbilical hernia which
contained the pyloric portion of the stomach. After drinking eight
glasses of water and two cups of tea and eating meat, she was seized
with vomiting, during which the stomach burst with a report which was
audible to the patient and to those around her. She passed into a state
of collapse and died in thirteen hours. A rent several centimeters long
was found in the posterior wall of the stomach. Lautschner thinks that
the pylorus was bent in the hernial sac so as to be obstructed. In the
walls of the stomach he found no evidence of pre-existing disease.

[Footnote 20: _Virchow und Hirsch's Jahresbericht_, 1881, ii.]

There is no satisfactory proof of the possibility of the occurrence of
rupture of a stomach with healthy walls except as a result of external
violence.

The symptoms and treatment of rupture of the stomach are those of
perforation of the stomach, and have already been described. The
prognosis is fatal.


GASTROMALACIA.

That the subject of gastromalacia should still occupy so much space in
medical works the purpose of which is mainly clinical proves that many
physicians still cling to the belief that this process may occur during
life. It is, nevertheless, certain that the condition which, according
to the ordinary and traditional use of the term, is designated
gastromalacia, is always a post-mortem process and is without the
slightest clinical significance. So long as the circulation of the
blood in the walls of the stomach is undisturbed, self-digestion of
this organ cannot occur. No one doubts {619} that parts of the gastric
walls in which the circulation has been arrested, and which are exposed
to the gastric juice, undergo self-digestion, as has already been set
forth in the article on GASTRIC ULCER. To describe cases of this nature
under the name of gastromalacia, however, is misleading, and can cause
only confusion, for the long-continued discussion as to whether
gastromalacia is a vital or a cadaveric process applied certainly to a
different conception of the term. In some of the cases which have been
published, even in recent years, in support of the vitalistic theory of
gastromalacia, and in which it has been proven that perforation of the
stomach occurred during life, the solution of continuity took place
through parts of the gastric walls in which the circulation had already
been obstructed, particularly by extensive hemorrhagic infiltration.
Some of these cases are probably also examples of perforation of
gastric ulcer or of rupture of cicatrices from over-distension of the
stomach, in which post-mortem digestion of the edges of the ulcer or of
the cicatrix obscured the real nature of the process. The subject of
gastromalacia should be relegated wholly to works on physiology and on
pathological anatomy.




{620}

INTESTINAL INDIGESTION.

BY W. W. JOHNSTON, M.D.


NATURE.--The term indigestion in its most common meaning refers to
gastric indigestion only. This limitation has arisen from the fact that
gastric digestion has been more thoroughly understood than intestinal
digestion, and because the symptoms, flatulence, acidity, eructations
of gas, pyrosis, and vomiting of unaltered food, are readily referred
to the stomach as their source. Intestinal digestion has not been well
known until within a recent date, and its phenomena in disease have
been mistaken for other pathological conditions.

From the important and complex function of the intestinal juices, and
the very great share they take in the solution of food, there must be
many phases of departure from the normal state. The processes of
intestinal digestion are more intricate than those of gastric
digestion, of a higher grade, and the chemical reactions are more
numerous, depending upon the participation of the bile, the pancreatic
juice, and the succus entericus; while intestinal absorption is a more
complex act than that of gastric absorption.

A brief review of the physiology of intestinal digestion will be of aid
in making clear its pathology.

The object of all digestion is to make such a solution of the ingesta
that they may pass through animal membrane and so enter the system.
Mechanical disintegration and simple solution do something toward this,
but for substances insoluble in water a more thorough change is brought
about by ferments which convert insoluble into soluble compounds.

The process of digestion begins in the mouth. Mastication breaks up the
masses of food; the saliva softens them, dissolves soluble substances,
as salt and sugar, and thus the pleasures of the palate are enhanced.
The ferment ptyalin acts upon starch (boiled starch being more rapidly
altered than unboiled), and changes it to dextrin and grape-sugar, both
of which are diffusible through animal membrane, entering lymph-spaces
and blood-vessels. The greater part of the saliva secreted is swallowed
with the food or in the intervals of eating. The amount formed in
twenty-four hours varies from 1500 gm. (Bidder and Schmidt) to 700 gm.
(Tuczek). It must therefore serve some ulterior purpose in the stomach.
Ewald[1] says that saliva converts starch into sugar in acid as well as
in alkaline and neutral solutions. But Langley[2] asserts that the
ferment of {621} saliva is destroyed by the hydrochloric acid of the
gastric juice. The longer food is subjected to mastication and
insalivation, the more thorough is the mouth digestion and the better
prepared is the mass for the action of the gastric and intestinal
juices. It is asserted that fatty matters are emulsified to a certain
extent by the alkaline ferments of the saliva.

[Footnote 1: _Lectures on Digestion_, New York, 1881, p. 37.]

[Footnote 2: "On the Destruction of Ferments in the Alimentary Canal,"
_Journal of Physiology_, London, Jan., 1882, p. 246.]

When the food enters the stomach the nitrogenous (albuminoid) elements
are attacked by the gastric juice, the bundles of muscular fibre are
broken up, the fibrillae are reduced to a granular mass, but not
completely dissolved (Frerichs), the fat-globules are freed from their
envelopes of connective tissue, milk is coagulated, and the casein is
dissolved.

"The tangible, practical object of this change is to form out of a
little-diffusible body (albumen) one easily diffusible (peptone), which
is capable of absorption through animal membrane in a higher degree
than ordinary albumen" (Ewald). Peptone is formed out of ordinary
albumen, as grape-sugar is formed out of starch, by taking up water; it
is therefore the hydrate of albumen.

The more tardy the digestion in the stomach the more highly charged
with acid is the gastric juice. According to Wright, the degree of
alkalinity of the saliva is in proportion to the acidity of the stomach
fluids, and Bence Jones has observed that during the excretion of acid
in the stomach the total alkalinity of all alkaline digestive fluids is
increased. The lesson is thus learned that a too careful preparation of
food, so as to shorten and lessen gastric labor, diminishes the
activity of the gastric juice as well as that of all other digestive
fluids.

Intestinal digestion begins when the softened mass passes through the
pylorus. This mass (chyme) is composed of (1) the products of gastric
digestion which have not been absorbed--peptone, dextrose, levulose,
peptonized gelatin, with mucus and gastric juice; (2) all matters which
have escaped digestion--the starch of vegetable substances, dissolved
gelatin and albumen which have not been peptonized, and some unaltered
muscle-structure; and (3) fat, fatty acids, and cellulose upon which
neither saliva nor gastric juice has had any influence (Ewald).

This complex semi-fluid mass with an acid reaction enters the duodenum
and comes in contact with fluids and ferments destined to work
remarkable changes in its composition. The first of these fluids is the
bile, which is alkaline and composed of the glycocholate and
taurocholate of sodium, cholesterin, soaps, etc., phosphates and
carbonates of lime and sodium, chlorides of potassium and sodium,
bile-pigment, etc. The outflow of bile is excited by the contact of the
chyme with the orifice of the bile-duct. When the alkaline bile is
mingled with the acid mass in the duodenum, it neutralizes its acidity,
precipitates the peptones, and therefore stops all further action of
the gastric juice. Fats containing free fatty acids are emulsified,
soaps being formed by a combination of the alkalies of the bile with
the fatty acids. Lastly, bile hinders fermentation in the intestine and
acts as a purgative by exciting peristalsis. Absorption is probably
also favored by bile, as it has been found that emulsified fats pass
more readily through an animal membrane which has been wet with
bile.[3]

[Footnote 3: Ewald thinks this result is doubtful: in animals killed
during digestion he has found an acid reaction in the contents of the
intestine beyond the opening of the bile-duct, with no precipitation of
the albumen (_op. cit._, p. 82).]

{622} As far as we now know, the function of the bile is to neutralize
the acidity of the duodenal contents, and thus pave the way for the
action of a digesting fluid of much greater potency and of much higher
function.[4]

[Footnote 4: In order still further to demonstrate the necessity of
bile-action as a preparation for pancreatic digestion, it may be
mentioned that in artificial experiments, with a heat equal to that of
the body, if antiseptics analogous to gastric juice and bile are not
used, there is a too rapid change from alkalinity to acidity, and
consequently all of the starch is not converted into sugar before it
develops lactic acid with putrefactive disorganization. A deficiency of
bile, therefore, is a cause of intestinal indigestion (Bartlett, _op.
cit._, pp. 12, 13).]

This fluid, the pancreatic juice, is composed of inorganic salts,
albuminoids, and certain specific ferments, and has an alkaline
reaction. It has a threefold operation upon the softened mass with
which it now comes in contact: 1. The starch of vegetable matter, which
has been only slightly acted on up to this time, is now rapidly
converted into grape-sugar by a peculiar diastatic ferment more active
than any other known ferment. 2. Albuminous matters (proteids) which
have escaped digestion in the stomach are changed into a soluble and
absorbable pancreas--peptone. Trypsin is the active ferment in this
case (Kuhne), and it is only in alkaline or neutral solutions that the
albuminoids are readily dissolved. The necessity of neutralization by
the alkaline bile is thus demonstrated. 3. A ferment distinct from the
others splits the fats into fatty acids and glycerin, and emulsifies
them so that they can be taken up by the lacteals lower down.

Experiments made by mixing albuminates with pancreatic gland-extract,
under favorable conditions, show after a certain time the presence of
leucin, tyrosin, hypoxanthin, and asparaginic acid. In a feebly
alkaline or neutral solution a faint putrefactive odor is soon noticed,
with the development of bacteria; ammonia, sulphuretted hydrogen,
hydrogen, and carbonic acid--evidences of the putrefaction of
albumen--are also detected.

It is difficult to tell when normal digestion in the intestines ends
and putrefaction begins. The conclusion is, that the normal action of
pancreatic juice (trypsin) gives origin to bodies met with in the
ordinary putrefaction of albumen.[5] This thin border-line between
normal intestinal digestion and the decomposition of the intestinal
contents has an important bearing on the facts of intestinal
indigestion.

[Footnote 5: Ewald, _op. cit._, p. 92.]

The intestinal juice performs a minor but independent part in
digestion. It converts albuminous matter into peptone, and hydrated
starch into sugar. Its function is therefore supplementary to that of
the gastric and pancreatic secretions.[6]

[Footnote 6: Ewald, _op. cit._, p. 103; also, "The Functions of the
Intestinal Juice," Charles L. Dana, _Med. News_, Philada., July 15,
1882, p. 59.]

When food enters the mouth the process of digestion begins, and all the
activities of the glands concerned in digestion are probably at once
set in motion. Mastication excites, by reflex action, pancreatic
secretion; the acid chyme touches the orifice of the common bile-duct
and stimulates the outflow of bile; the neutralized chyme next invites
pancreatic digestion. For the integrity of intestinal digestion it is
required that mastication and stomach digestion should be normally
performed.

The intestinal movements which are so necessary to digestion by making
successive changes in the position of the intestinal contents are {623}
controlled by nervous arrangements, but may occur independently of the
central nervous system. The ganglia of Auerbach and of Meissner in the
intestinal wall are sufficient for the development of peristaltic
waves. The irritation of the mucous membrane by food, hyperaemia, and
the pouring out of digestive juices, and intestinal movements, are
parts of one process. Paralysis by section of the splanchnic leads to
hyperaemia of the intestinal vessels and increased peristalsis;
stimulation of the splanchnic causes anaemia of the intestinal wall and
arrest of movement. Local cold by producing anaemia brings about the
same result.

The products of digestion as they pass toward the jejunum consist of
diffusible peptones, sugar, emulsified fats and oils, and substances
which have escaped digestion, as fragments of muscular fibre,
starch-corpuscles, connective tissue, hairs, or other foreign matters.
The bowel contains also carbonic acid, hydrogen, nitrogen, sulphuretted
hydrogen, and marsh gas. The mass, alkaline or neutral in the duodenum
and jejunum, becomes acid in the ileum from the putrefaction of albumen
and fermentation. The peptones and sugar pass by osmosis into the
blood-vessels of the portal system and thence to the liver. In the
liver the sugar is converted into glycogen (carbohydrate), and stored
in the liver-cells until needed for the maintenance of animal heat and
for the nutrition of the tissues. The peptones are used in part to
supply the nitrogenous waste of tissue, but much of the albuminoid
matter is broken up in the liver into glycogen and urea, the latter of
which is excreted by the kidneys as waste matter.

The minute granules of oil in emulsion are taken up by the epithelial
cells covering the villi; thence they enter the adenoid tissue of the
villi on their way to the lymphatic radicles, the lacteals. From here
the passage is open to the underlying lymphatic vessels and to the
larger abdominal lymph-vessels and the thoracic duct beyond.

Intestinal digestion is not completed and the body does not receive its
pabulum until the products of digestion have reached the liver and the
thoracic duct.

ETIOLOGY.--It is usually said that intestinal dyspepsia is more common
in women than in men, but the contrary is the rule. Some of its most
common causes--over-eating and the eating of indigestible food--are
especially vices of men.

It is more frequent between the ages of forty and fifty, but no age is
exempt. Infants at the breast, children of any age, adults, and old men
and women are alike subject to it. Men in middle life begin to suffer
from the imprudence and carelessness of youth and from the anxiety and
cares of business. The indulged children of rich parents and improperly
bottle-fed infants frequently suffer.

Heredity and idiosyncrasy have a certain influence in determining the
prevalence of intestinal dyspepsia. The distaste for and inability to
digest vegetables, fruits, and fats are often peculiarities of family
history. The occurrence of cases in the same family is often explained
by improper food, bad cooking, and irregular hours, to the evil
influences of which all the members are similarly subjected.

All conditions of the organism which result in a depraved or altered
blood-supply, as anaemia, primary and secondary rachitis, chronic
syphilis, and continued febrile diseases, are causes of intestinal
indigestion. {624} The connection of the indigestion of fats with the
strumous diathesis and with phthisis is undisputed. J. Hughes Bennett
traced the origin of phthisis to defective fat-digestion; strumous
indigestion and the indigestion of fat are synonymous terms.

Debilitating influences, such as bad air, want of cleanliness and
outdoor exercise, impair functional activity in the intestines as
elsewhere. Sexual excesses, but especially masturbation, have a special
influence for evil in this direction.

The influence of the mind upon the digestion of starch and fats is even
greater than upon gastric digestion, for no other reason perhaps than
that the former is a more complex function and less easily relieved
than the latter. Prolonged or excessive mental labor does not do so
much harm as mental worry, over-anxiety, and the strain and overwork of
business. Professional men--lawyers, physicians, and clergymen--who
become over-burdened with responsibilities, and who sympathize too much
with the distresses of others, are very prone to suffer. The careworn
face with lines about the mouth and forehead is one of the plainest
signs of duodenal defect. The proper secretion of the juices of the
intestine and normal peristalsis are impossible where brain and nerves
get no rest. The too rapid mental development of the children of the
present day is a fruitful source of weakened fat-and-starch digestion
and of impaired development. So long as children are sent to the public
school at four and six years of age, there will continue to grow up a
precocious race with active brains in feeble bodies.[7] This injurious
result is largely brought about by the direct interference of premature
brain-development with the complex intestinal processes of digestion
and absorption.

[Footnote 7: In eight of the States and Territories the minimum age for
entering the public school is fixed at four years; in seventeen States
at five years; in the others, except two, at six years. The two notable
exceptions are Alabama and New Mexico, where children do not enter
school until the age of seven.]

Wealth, with ease and inactivity, and sedentary occupations, contribute
to the same end by lessening the need of food, and thus debilitating
the organs of digestion by inaction. Sedentary pursuits, especially
those in which the body is bent forward and constricted or compressed
at the waist, interfere with active function in the intestine. This is
the case in tailors, shoemakers, etc. Tight-lacing in women and a too
tight trouser-band in men are injurious.

Hot climates, especially when combined with dampness, lead to disorder
in the intestine and liver. This effect is most marked among persons
coming from colder climates, as among the English in India, who keep up
the habits of eating to which they have been accustomed at home. The
lessened demand destroys the appetite, and stimulants and condiments
are resorted to to whip up the inactive functions. The intestine is
loaded with a mass of crude, unaltered matter which can with difficulty
be disposed of. Chronic indigestion results, varied with acute attacks
of diarrhoea or dysentery. The portal system is filled with an excess
of albuminoid material which the liver is unable to store away. The
excess is got rid of by conversion into uric acid. Lithaemia and
chronic congestion and enlargement of the overloaded liver result, with
their many attendant evils.

Over-eating occasions first gastric and then intestinal indigestion by
the {625} entrance of unaltered food into the duodenum. Eating without
hunger often involves the taking of food which the body does not need
and which the stomach cannot digest. Diners-out rarely go through a
season without one or more internal revolts. A too-varied diet, a
dinner of many dishes, is faulty in variety as well as in excess. On
the other hand, a too great sameness in diet and the prolonged use of
one or two articles of food which are not easy of digestion, and which
have a great deal of waste, fatigue and then disorder intestinal
digestion. This is a fault into which children are often allowed to
fall.

Indigestible food and an excess of starchy or fatty food conduce to
disorder of duodenal digestion. In conditions of debility and anaemia
and in the convalescence of fevers the deficiency of saliva involves an
inability to digest starch in the mouth and points to a corresponding
want in the duodenal secretions. The improper use of alcoholic liquors,
taking them on an empty stomach between meals and in excess, tends to
direct irritation of the mucous tract. Condiments in large quantity
have the same effect.

Irregularity in the hours of eating and a faulty distribution of the
amount of food disturb the perfect working of the mechanism of
digestion. Very light breakfasts and very late and large dinners are
injurious. The habit, now quite general in cities, of deferring the
breakfast proper until midday, leaves the system too long--fifteen to
sixteen hours--without proper food and weakens digestive activity.
Intestinal indigestion is very common among Americans who have lived
abroad and adopted European customs.

Another cause which is unfortunately very common is the imperfect
mastication and insalivation of food, due to too great haste in eating,
to defects in the teeth or gums, or to a deficiency of saliva. The
saliva no doubt sometimes possesses a feeble diastatic power, although
abundant in amount. Carnivorous animals bolt their food, but
vegetable-eaters must masticate. Slow mastication transforms starch
into sugar, and at the same time excites secretive activity in the
glands of the digestive tract, especially in the pancreas. The more
thoroughly this preliminary function is performed the better
preparation is there for the subsequent acts of digestion.[8]

[Footnote 8: "The familiar act of chewing is seldom a subject of
reflection, yet it throws into motion a more complicated system of
levers, accompanied by a drain of fluids from more curiously adapted
apparatus, than the arts can parallel" (Leared, _On Indigestion_,
London, 1863, p. 3).]

The chewing of tobacco, a wretched habit which is much less common now
than formerly, and to a less extent the habit of smoking, are causes of
deficient, altered, or depraved saliva, and secondarily of altered
pancreatic secretion. The thin smoker grows fat when he abandons the
weed.

The normal functions of the intestines are interfered with and
indigestion is set up by constipation. Every one has felt the activity
in digestion which accompanies the regular habit of defecation, and the
torpor and oppression which depend upon an unemptied colon. "There is a
concert of action in virtue of which the whole muscular apparatus of
the digestive tube sympathizes with that of the large intestine. This
concert of action, which induces pathological states, is the reason why
in the {626} physiological state a regular contraction of the whole
intestinal tube, including the stomach, is the consequence of the
regular contraction of the large intestine."[9]

[Footnote 9: Trousseau, "Les Dyspepsies," _L'Union medicale_, tome xi.,
1857, p. 313.]

An excess of acid in the stomach would enfeeble the solvent power of
the intestinal fluids by antagonizing neutralization by the alkaline
bile; the same effect follows any cause which prevents the outflow of
the bile, as the plugging of the common bile-duct by mucus and
epithelium in catarrh or by an impacted gall-stone. The emulsification
of fats is incomplete and decomposition in the intestine follows. The
antagonism of the saliva and the gastric juice, of the gastric juice
(or the chyme) and the bile, must preserve their delicate and nice
adjustment in order for digestion to be properly performed.

Diseases of the pancreas seriously embarrass digestion in the
intestine. Lesions of this organ, as catarrh of the duct, cancer, fatty
degeneration, etc., may result in impaired emulsification of fats,
fatty diarrhoea, and wasting.

Intestinal indigestion accompanies hyperaemia and catarrh of the
intestinal mucous membrane, diseases of the heart, lungs, and liver,
and all other causes which impede portal circulation.

SYMPTOMS.--Intestinal indigestion cannot be so clearly pictured as that
of gastric dyspepsia. This is owing to the frequent concurrence of the
two conditions, the gastric symptoms taking precedence of the others.
The more complex nature of the intestinal function is another reason,
intestinal indigestion having more modifications in its phenomena. In
the stomach there is only one active secretion; in the intestine there
are three, all participants in the act of solution. An alteration in
the quality or quantity of one of these--the bile, for example--would
lead to different symptomatic results than would follow another
defective secretion, as that of the pancreas, for instance. Clinical
study has not yet fully differentiated the forms of indigestion due to
these several deficiencies. But there are certain well-defined symptoms
associated with intestinal disorders which are distinguished by their
seat, time of their appearance, and their character from analogous
symptoms connected with the stomach.

Intestinal indigestion may be acute or chronic. The latter is the more
typical and more common form.

When a sudden attack of indigestion in the intestine results from the
entrance into the duodenum of food in such a state that it cannot be
digested, the result is the rapid development of pain, flatulence,
borborygmi, and frequently of fever, ending in diarrhoea, with the
escape perhaps of the offending matter: a condition then exists which
may be called acute or subacute intestinal catarrh or acute intestinal
indigestion. One name would be as correct as the other. Slight acute
forms are marked by a coated tongue, loss of appetite, headache, pains
in the limbs, distress in the epigastrium or right hypochondrium,
flatulence, and constipation. These might be accompanied by symptoms
indicating a disorder of the liver functions--light-colored stools,
slight jaundice, lithates in the urine. But intestinal indigestion
alone can cause these symptoms without the condition of so-called
biliousness being present. The local symptoms are due to the presence
in the intestine of an {627} imperfectly-altered mass and the
development of gas; some of the general symptoms are reflex; others, as
headache and lassitude and pain in the limbs, come from the absorption
into the blood of the gases, particularly sulphuretted hydrogen. The
participation of the stomach in acute attacks of this sort modifies the
symptoms as here described. Such attacks are apt to recur at intervals.

If the causes which bring about acute disorder in the intestine are
allowed to continue, the intervals between the acute or subacute
attacks diminish, and there is in time a fixed state of chronic
intestinal dyspepsia in which the partly-altered food coming from the
stomach is not properly prepared for absorption. Instead of digestion
there is decomposition; the transition is easy from the one to the
other of these states. The symptoms connected in this case with the
digestive organs are pain, occurring from two to six hours after
eating, in the right hypochondrium, the epigastrium, or the umbilical
region, due to distension of the intestine with gas. This pain is dull,
not always fixed, lasts from one to three hours, and is accompanied by
tenderness on pressure over its seat.

Tympanites, borborygmi, and a sensation of fulness in the abdomen
accompany the pain or may exist without it. Gaseous accumulations in
the intestine, the cause of these symptoms, have an independent source,
being produced by decomposition in the gut itself, and are not due to
the descent of gases from the stomach through the pylorus. What is a
physiological and temporary condition becomes in disease a distressing
symptom of long duration. In intestinal indigestion the gut is nearly
always inflated with gas, which in its movement produces rumbling
noises. In acute indigestion it is rapidly formed in large amount, and
by the stretching of the wall of the bowel and pressure on
nerve-filaments causes intense pain--colic. In the chronic form the
distension excites uneasy sensations, prevents sleep, and may be so
great as to cause dyspnoea by pushing the diaphragm upward. When the
small intestine is distended the greatest swelling may be about the
umbilicus, or the abdomen may be evenly rounded. When the colon is
chiefly or solely inflated, its outline across the upper part or at the
sides of the abdomen can be easily made out.

Constipation is a common feature. It is produced by a loss of
contractility of the intestinal wall. The more direct causes are
over-distension of the gut and disturbance in the circulation and
innervation of its walls. The stools are hard and dry, and are expelled
with difficulty. Sometimes they are coated with shreds or films of
mucus, the product of a chronic catarrh of the mucous membrane of the
colon, or mucus from the small intestine is intimately mixed with the
mass. Diarrhoea may alternate with constipation. The passage of
unaltered food, as fragments of meat, vegetables, or fruit, clearly
shows the extent to which indigestion exists. By the microscope
particles of food which have escaped complete disintegration may be
detected. The stools vary in color. Very dark-green or black discharges
show an excess of bile; light-yellow or gray slate-colored, a
deficiency. Stools of the latter character are highly offensive in
odor.

Hemorrhoids are often present, being due to the sluggish portal
circulation and to the pressure of hard fecal masses in the rectum. The
appetite is not impaired, as a rule, but it may be fitful or irregular.
A bad {628} taste in the mouth, and a swollen, relaxed, and coated
tongue may exist without any decided gastric disease.

The symptoms of disorder of the nervous system are more marked than in
gastric dyspepsia. This results not so much from the depressing
influences of pain as from the peculiar malnutrition of the
nerve-tissue. In order to have furnished to the blood the pabulum out
of which the nerve-elements are reconstructed the digestion of fat must
be normally performed. Lecithin, which is found conspicuously in the
brain and nerves, is a complex fat containing phosphorus and
nitrogen.[10] Anaemia and waste follow directly from interference with
the digestion and absorption of fats and starch in the intestine, but
the most delicate, the most easily-disorganized solid of the body, the
nerve-tissue, is the first to feel and to manifest its want of natural
supply. And so the dyspeptic whose intestine is at fault becomes
depressed in spirits, hypochondriacal, absorbed in the contemplation of
his sufferings, analyzing them and referring them to the most serious
organic changes. There are sleeplessness, disturbing dreams, the habit
of waking at a fixed hour, dizziness, uneasy sensations or pain in the
head, and disturbances of the special senses, as buzzing in the ears,
muscae volitantes, and attacks of blindness. Headache assumes often the
form of hemicrania; it may be in the forehead or about the eyes.
Attacks of vertigo and sensations as if the ground were rising beneath
the feet accompany intestinal flatulence. Confusion of thought, loss of
the power of application, and mental inertia are frequent sources of
anxiety. Paralysis has been noted as following indigestion.
Epileptiform convulsions and milder epileptic attacks can be traced to
undigested matter in the intestine.[11] Various modifications of
general sensibility also happen: there are pains in the back and limbs,
hyperaesthesia, and anaesthesia. An inaptitude for exertion, especially
for mental labor, forces the boy to give up school and college life.
Successful careers are abandoned by men who at the cost of neglecting
all the rules of health have succeeded for a brief period in passing
their fellows in the race. Sudden attacks of fainting have been noted,
with very grave collapse. These are the effect upon the nervous centres
of the absorption of sulphuretted hydrogen which has been evolved in
large quantities in the intestine.[12] The daily occurrence of
vertiginous and other morbid sensations, with melancholia, may be due
to the daily toxic absorption of gas from the intestine.

[Footnote 10: Fothergill, _Indigestion and Biliousness_, New York,
1881, p. 76.]

[Footnote 11: Chambers, _The Indigestions_, London, 1867, pp. 305-307.]

[Footnote 12: Tyrell, case of a man with eructations smelling of
sulphuretted hydrogen who had vertigo and sudden collapse; symptoms
relieved by purgative (_Pacific Med. and Surg. Journ._, May, 1882, p.
539).]

The action of the heart is disturbed as in stomach indigestion.
Irritability of the heart and palpitation are in part due to anaemia
and in part to mechanical pressure and reflex influences. The nervous,
anaemic, thin dyspeptic has among his chief troubles a throbbing heart,
which keeps him awake at night and fixes his attention upon this organ
as the seat of his disease. The general circulation is languid; cold
hands and feet and cold sweats testify to this, and the irregularity or
suppression of catamenia follows upon the irregular blood-supply.

The urine is usually high-colored, has an abnormally high density, is
acid, and on cooling deposits lithates, uric acid, and oxalate-of-lime
{629} crystals. The urine is most heavily loaded with sediment when
digestion has been recently completed. Therefore, the morning urine
after a heavy dinner of the night before contains the largest amount of
lithates. Albuminuria is occasionally a symptom of indigestion in the
bowel. The eating of cheese or pastry in excess may cause it.[13]
Seminal emissions at night frequently occur. The action and reaction
upon each other of this perversion of the sexual function, the
indigestion, and the mental disorder, reduce the poor sufferer to a
most pitiable condition of despondency and prostration.[14]

[Footnote 13: Warburton Begbie's _Works_, Sydenham Society's
Publications, 1882, p. 359.]

[Footnote 14: The writer has observed cases in which an exaggeration of
the sexual instinct in men of middle age was associated with intestinal
indigestion.]

Anaemia is one of the earliest indications of impaired nutrition. It
precedes loss of flesh and the wrinkled and dry condition of the skin
which may be a marked symptom in cases of long standing. Various
eruptions appear on the skin. In the strumous dyspepsia of children the
white, almost waxy, skin is covered with dry scales, which may be seen
over the whole body from head to foot. No symptom is more
characteristic of intestinal indigestion and of imperfect fat digestion
and absorption than this. Eczema and psoriasis, pityriasis, impetigo,
and porrigo decalvans are forms of skin eruption seen.

Closely allied to the symptoms caused by indigestion in the intestine
are those due to functional disorder of the liver. The liver completes
the work which the intestine has begun. It receives directly from the
intestine blood laden with the products of digestion, and further
transforms them into substances to be used in the economy. The symptoms
which result from disturbances in the performance of these functions
are, as has been said, closely connected with the symptoms of
intestinal indigestion. This association is shown by the tendency among
older writers to trace all such symptoms to the liver, the terms
bilious and biliousness including all the phenomena of derangement of
the function of digestion in the intestine, as well of the function of
the liver. Later writers excluded the part of the liver to a great
extent in giving rise to the so-called bilious symptoms. Recent
physiological study has shown how closely the intestine and the liver
are associated in health and in disease. When the liver is implicated
in indigestion the symptoms which follow are due either to a deficiency
of the secretion of bile, and the resultant disturbance of digestion in
the intestine, or to a derangement in the transformation in the liver
of the products of albuminoid digestion. When the disorganization of
the peptones is imperfectly performed in the liver, instead of urea
there is a production of lithates and lithic acid, constituting the
condition called lithaemia. The lithates pass into the urine and are
deposited. The occurrence of this urinary sediment after excesses and
imprudences in diet is well known. The continuance of lithaemia leads
to the development of symptoms more or less characteristic. These are a
loss of appetite and coated tongue, flatulence, oppression after
eating, and constipation. The nervous system is soon disturbed, and
often to a marked extent. Vertigo, headache, disturbances of the
special senses, sleeplessness at night, drowsiness during the day,
annoy the patient and induce extreme hypochondria. He is worried,
moreover, with numbness and tingling in one or both arms or in the
{630} legs, and hence spring fears of paralysis. The heart is disturbed
in action, and is irregular and feeble. Emaciation in previously
corpulent persons is not unfrequent.

COURSE, TERMINATION, AND SEQUELAE.--Acute dyspepsia in the bowel lasts
from a few hours to a day or two, and ends in leaving the patient as
well as before. A diarrhoea of indefinite duration may follow.

Chronic intestinal indigestion in infants and young children often
continues until the diet is changed to one suited to the powers of
digestion. In adults interference with so important a function cannot
but have the most serious results. While the progress is slow, lasting
many years, there is a steady march from bad to worse.

The character and conduct are so altered by the disease that a man may
be said to be just what his digestion makes him. Amiability under the
daily goad of intestinal dyspepsia is an impossibility. The
irreconcilables, the men out of joint with the world, are living
witnesses of the antagonism and disaffection within their intestines.
The deterioration in health paves the way for many diseases, and there
is hardly an organ in the body which may not ultimately become the seat
of organic change.

In the young, phthisis is frequently the ultimate result of the
malassimilation and malnutrition; in men beyond middle life
degenerative changes in the intestine, liver, and kidneys close the
series of morbid changes which began in the intestine. Thomas N.
Reynolds attributes bronchitis and phthisis in part to the local
influence of septic matter carried by the portal and lacteal vessels to
the lungs in cases of intestinal dyspepsia, with constipation and
septic fermentation of the ingesta.[15]

[Footnote 15: Paper read before section of Practical Medicine at
meeting of Am. Med. Assoc. in 1883.]

In many cases business and professions are abandoned, and men become,
under the influence of despair and complete absorption in their
symptoms, intellectual and moral wrecks, burdens to themselves and to
all around them. In this stage the primary cause, the dyspepsia, is
lost in the exaggerated prominence of the nervous symptoms.

DIAGNOSIS.--The acute variety is known by the seat of the abdominal
symptoms, the pain, distension, and movement of gas not being in the
stomach, but in the intestines. The pain is like colic; the abdomen is
sensitive to the touch; tympanites is general and may be very great. If
vomiting occurs, the symptoms continue after the stomach is empty.
Diarrhoea may quickly come on, and is followed by relief. The fever may
be quite high. There is no sleep, but restlessness, and in children
delirium. They may also have convulsions.

In the chronic form the history of the case and the study of the causes
are of great value in formulating an opinion. The persistent abuse of
the pleasures of the table sooner or later develops intestinal
indigestion. Inquiry into the mode of life, hours of eating, manner of
eating, kinds of food taken, etc. gives important information. The
teeth are defective, and mastication and insalivation are neglected.
There is distress in the pit of the stomach or in the right
hypochondrium, beginning about two hours after eating and lasting from
four to six hours; intestinal distension with gas, either in the small
intestine or colon, with borborygmi and constipation, is generally
present. The nervous symptoms are characteristic: they are depression
of spirits, irritability, sleeplessness, vertigo, and {631} headache.
The man is more completely altered mentally than in gastric dyspepsia.
The urine contains lithates in excess; anaemia and emaciation progress
rapidly. Seminal emissions and weight and heaviness about the loins are
present.

The following symptoms distinguish gastric dyspepsia, and do not occur
in intestinal indigestion unless the stomach is at the same time
involved: pain or weight in the epigastrium immediately after eating,
vomiting of unaltered food, of food in a state of acid fermentation,
eructations of ill-tasting or bad-smelling gas or of acid fluid,
water-brash, and heartburn. Loss of flesh may not take place to any
extent even in very bad forms.

The diagnosis of differences in the forms of indigestion due to defects
in the pancreatic, biliary, or intestinal secretions is not at present
a matter of precise knowledge. A pancreatic indigestion would be
followed, it might be supposed invariably, by fatty stools; but such is
not the case, since degeneration of the pancreas and closure of the
duct have occurred without fatty evacuations from the bowels.[16]
Moreover, ulceration of the duodenum is followed sometimes by fat in
the stools. Still, if the symptoms of intestinal indigestion include
rapid wasting and fatty diarrhoea, we may conclude that the pancreas is
at fault. The fat varies in appearance and amount. It may be seen as
oil-drops passed alone or with fecal matter, or as lumps of fat, pale
yellow and tallow-like. Glycosuria[17] bears some relation to
pancreatic diseases, and therefore may be an aid in diagnosis.

[Footnote 16: Ewald, _op. cit._, p. 95; D. S. Haldane, "Cancer of
Pancreas," _Edin. Monthly Journ. of Med. Sci._, xix. 1854, p. 77; J. S.
Bartrum, "Scirrhus of Pancreas and Stomach," _Assoc. Med. Journ._,
1855, p. 564; DaCosta, "Primary Cancer of Pancreas," _Proc. Path. Soc.
Philada._, 1857, vol. i., 1860, p. 8; S. W. Gross, "Primary Cancer of
Head of Pancreas," _ibid._, vol. iii., 1871, p. 94.]

[Footnote 17: Bright, "Cases and Observation connected with Diseases of
the Pancreas," _Med.-Chir. Trans._, vol. xviii. p. 1.]

A deficient excretion of bile is indicated by a whitish or yellowish
coating of the tongue, with loss of appetite and bad taste in the
mouth. The stools are scanty, dry, slate-colored or white, and
offensive in smell. The urine contains lithates. The complexion is pale
or muddy. The nervous system is much deranged. The patient is languid,
often irritable and hypochondriacal. He complains of headache, and is
dull and drowsy after eating. The heart's action is unsteady,
intermittent, or frequent. It is impossible to recognize indigestion
due solely to a deficiency of the intestinal juice or to feeble
peristalsis, granting that such forms exist.

PROGNOSIS.--A fatal result does not follow directly from intestinal
indigestion. Its complications and results are frequently the causes of
death. Treated early and with decision, a cure can be expected.
Everything depends upon the extent to which the patient submits to the
strict directions of his physician; his whole life must be made
subordinate to the plan of treatment.

When the general health has become profoundly altered there is less
chance to do good. Discouraging symptoms are anaemia, debility,
coexisting gastric dyspepsia, an inherited hypochondriacal tendency, or
the strumous diathesis in children.

When the disease has so far progressed that the patient is unable to
{632} rouse himself to the point of wishing to be well, only the most
severe measures directed to the control of an irresponsible person can
save him from ruin. In organic disease of the pancreas, intestine,
liver, or heart the result will depend upon the nature and curability
of the lesion.

TREATMENT.--Acute intestinal indigestion due to the presence of
undigested food and gas in the intestine is treated by relieving
present distress and procuring a free movement from the bowels. A large
enema or a quick cathartic followed by an opiate--hypodermic injection
of morphia, paregoric, or other preparation--may give early relief. A
strict diet, warm poultices over the abdomen, and an anodyne may be
needed for several days after.

The integrity of intestinal digestion depends upon the normal
performance of all the preceding stages of digestion. Perfect
insalivation, mastication, and gastric digestion are necessary to a
proper action of the intestinal juices. The first rule of treatment in
the chronic form is to examine into the condition of the mouth and
teeth--to insist upon a slow and thorough mastication of food,
especially of starchy food. Mastication is under the control of the
individual, and he refuses to exercise this salutary means of
prevention and cure at his own risk. The habit of chewing on both sides
should be cultivated. All habits which waste and weaken the saliva
should be given up, as smoking, chewing, and needless expectoration.
Where the teeth are imperfect they should be attended to; false teeth
should replace absent ones. All means should be used for improving
gastric digestion: complete solution of food here means easier work for
the intestine, and sometimes the cure of intestinal indigestion by
removal of its cause. The rules which more directly bear upon the
subject of intestinal dyspepsia are these: All the causes which have
acted to bring about the disease should be removed. A change from a hot
climate to a cooler and dry one will sometimes have an immediate good
effect. Especially is this the case if travel is combined with change
of scene. The substitution of exercise for inertia, of fresh for
confined air, and the abandoning of occupations and habits of dress
which hinder the freedom of movement of the abdominal muscles are of
the highest importance. The patient should be made to cultivate
pleasure instead of work if his mind has been overtaxed in his
profession or business. Relaxation of the strained energies is
indispensable to recovery. This rule is as applicable to
school-children as it is to the overworked adult, man or woman. The
benefits of travel, with change of scene and air, cannot be
overestimated. Pedestrian tours in the mountains for young men, a trip
to Europe for men and women in middle life, will secure the best
results. For men who work much with their brains nothing is more
conducive to aiding intestinal digestion than manual labor in the
garden or workshop as a recreation. Exercise on horseback is
pleasurable and improves a sluggish abdominal circulation. Rowing is
good for younger men if it is confined to the field of pleasure, and is
not made a task. For very feeble persons, especially for women, massage
serves the purpose of exercise. The Swedish movement cure expands the
thorax and abdomen, hastens the circulation, and quickens all the
functions of nutrition and secretion.

A course of treatment would be incomplete without suggestions as to
bathing. Life at the seashore would be of little service without the
daily plunge in the surf. Still salt-water bathing is better for
children and {633} delicate women. The reaction should be thorough to
secure the best results. It is much to be regretted that hydrotherapy
is not available and is not made use of more generally. A well-managed
establishment where appropriate regimen and good and sufficient food
could be combined with the renewal of the tissues by bathing would be
of great advantage in all forms of indigestion. Nearly all of the
benefit derived from the Hot Springs of Arkansas in chronic cachectic
diseases follows upon the immediate improvement of the digestion and
nutrition. The Warm and Hot Springs of Virginia have an equally good
effect upon torpid abdominal functions. The Russian bath, the very hot
bath, the cold plunge, the cold douche to the back or abdomen, and the
cold pack to the abdomen, are means which may be employed at home for
inducing a revolution ending in reform in the state of the digestive
organs.

Irregularity in the hours of eating is of so much injury that rules
must be given to enforce uniform habits. Instead of the light breakfast
and heavy dinner, a good breakfast, a midday dinner, and a light tea
are to be preferred. It is of much value to regulate the appetite
according to the needs of the body and to avoid excess in everything.
In this disease eating too little or starvation to a moderate degree
gives that rest to the intestine which is necessary to its restoration
to health.

The selection of the food should not be left to the patient; the
dietary should be chosen for him with a view to lessening intestinal
labor. In general terms, this should consist of a moderate amount of
albuminoid food of the most digestible kind, and of farinaceous food
and fats in an acceptable and digestible form. In other words, as the
intestine digests proteids, starch, and fats, no exclusive diet can be
devised which will secure a perfect result. In each case the
examination of the stools and experience with different articles of
diet must be made the means for determining upon a suitable regimen.

The exclusive milk diet is the best starting-point in feeding a patient
suffering from acute or chronic indigestion. In addition to the fact
that milk has all the elements of a perfect food, it contains sugar and
fat in the most favorable condition for absorption; the casein of milk
alone requires transformation into peptone. The pancreatic juice has
the greatest activity in its effect upon milk, as is easily
demonstrated by the artificial digestion of milk by pancreatic extract.
In milk, therefore, we find a most easily digestible and most highly
nutritious food for such cases. Instead of milk with cream, skimmed
milk will be found sometimes to serve better the purpose of an
exclusive diet, because it has less fat and because larger quantities
can be taken without distaste or a sense of repletion. Koumiss may be
added to the milk diet; it is digestible, palatable, and nutritious.

The peculiar and very active diastatic ferment of pancreatic juice
converts starch into sugar very readily. Farinaceous articles of diet
can be added to milk with advantage. Digestion takes place more slowly
and more thoroughly in consequence, and an additional article of
nutriment is obtained. Thus, milk can be diluted with a thick gruel of
barley or oatmeal, or some of the best of the various artificial foods
can be stirred in. To the milk diet may be added animal broths or soups
prepared with vegetables, animal jellies, or some of the ready-prepared
beef-essences. They may not in themselves be highly nutritious, but
they contain at least {634} the salts of meat, and act as stimulants to
the appetite and to the secreting glands.

Such a rigid diet cannot be kept up for a very long time without
change; the appetite craves variety. Therefore solid albuminoid food in
small quantity may be added to milk and farinaceous diet. Sweetbread
boiled in milk, without dressing of any kind, is well suited for a
beginning of animal diet. Oysters for some palates make an agreeable
variety without putting much strain upon the digestive powers. They
should be eaten uncooked, as cooking in any way renders them less
digestible, and for greater precaution the hard part, or the adductor
muscle which serves to keep the two shells together, should be removed.
Fish boiled or plainly cooked and eaten without sauce is very easily
digested. White-fleshed fish which has but little fat incorporated with
the muscle-fibre is to be preferred. The patient may have eggs uncooked
or slightly boiled, but one to two daily will be as much as he can well
digest. The meat of poultry and game, especially that from the wings
and breast, may be given even in a very feeble state of the digestive
organs. When a more solid or satisfying diet is craved the patient may
have beef or mutton cooked rare. Tripe and rabbit are suitable to some
cases.

Bread, one day old and made light and porous, need not be denied the
patient. Toast disagrees with some. To many, well-made biscuits or
crackers are agreeable.

Vegetables should be given in small quantities, as the intestine is
almost solely the seat of their digestion, and excess will tax too much
a function which should be allowed as much rest as possible. The green
vegetables contain less starch, and are therefore to be preferred.
Lettuce, cabbage, kale, spinach, and celery come under this class, but
even these are to be given to patients under treatment in moderation,
with the intention of pleasing the palate rather than for purposes of
nutrition. Macaroni and rice are easily digested.

Fruit contains very little nitrogenous matter and much water, and
therefore has but little nutritive value, but it may be given to
relieve the tedium of a restricted diet of milk or broths. Grapes,
oranges, figs, strawberries, blackberries, raspberries, and peaches are
the most digestible. But fruit should never be given as food.
Fruit-juices, especially if acid and fresh, are unobjectionable. Coffee
should not be allowed; its effect upon the nervous system is sufficient
objection to its use. Tea can be given diluted largely with milk;
cocoa, racahout, and broma are nutrient and make pleasant drinks. Sugar
need not be excluded if used sparingly, and butter and oil in
moderation may be permitted.

If the stomach is not disturbed thereby, wine may be taken with food to
excite appetite. But except in the case of those who have always taken
it, and cannot do without it, it is better to dispense with alcohol
altogether. A red wine well diluted with water is a pleasant addition
to the meal. Old wine is to be preferred to new, as being softer and
less alcoholic. Good pure American wine from California or Virginia
will answer the purpose when reliable French wine cannot be secured.

The value of mineral waters in the treatment of indigestion is great,
but without proper dietetic regimen they can accomplish but little. The
good results following a visit to Saratoga, Bedford, or other
watering-place are due to other causes than the waters. In combination,
however, {635} with the advantages of change of scene, air, good hours,
and a simple diet the mineral waters aid in bringing about a cure. They
are especially useful in men who drink too little water at home, in
gouty and plethoric subjects, and in states of acid stomach digestion
and chronic constipation. The alkaline and saline waters are the best,
the former containing a notable proportion of the carbonate or
bicarbonate of sodium, potassium, or lithium--the latter having neutral
salts in considerable quantity.

The articles of food to be avoided are pastry, cheese, much butter or
fat, meat richly dressed or over-cooked, pork, veal, lobsters, crabs,
vegetable matter in excess, very cold or very hot fluids or solids.

All of the methods so far described are designed to accelerate the
circulation in the abdominal organs and in the tissues generally, to
quicken the secretory and nutritive processes, and to give to the
intestinal secretions the foods which they can most readily digest. In
the event of such means failing to accomplish the desired end, is there
any direct stimulus which can be brought to bear on the intestinal
glands concerned in digestion? The pancreas being the most active and
most important of these, it would be desirable to have some agent which
could excite its gland-structure to greater activity. Sulphuric ether
has been found to have this effect; it may be given before meals. The
salivary secretion begins pancreatic digestion (the digestion of
starch), and therefore its outflow should be stimulated at the same
time; but thorough mastication does this usually without need of
further aid.

When all plans fail to secure a thorough digestion in the intestine,
and unaltered food and fat are passed, while the patient grows thinner
and feebler daily, artificially-digested food may be given. The
intestine is thus relieved of labor, and time is given for a
restoration of activity by rest and an improved tone of all the tissues
and organs. Rice, bread, baked flour, potatoes, or barley may be given
in combination with malt extract, which converts starch into
grape-sugar and dextrin.

As pancreatic juice acts both upon proteids and starch, an extract of
the pancreas has a more general application than an extract of the
stomach--pepsin. Roberts of Manchester has given full directions for
the method of digesting food by pancreatic extract. Beef, milk, and the
farinacea may be digested, the albuminoid substances being changed into
peptones, the starchy matters into dextrin and sugar, capable of being
absorbed readily with but little or no further alteration in the
digestive tract.[18] Pancreatic emulsion (Dobell) is another method of
giving fat emulsified.

[Footnote 18: Fresh pancreatic extract is made by cutting into small
pieces the pancreas of the pig (which is the best), the ox, or sheep.
The pancreas of the calf yields an extract which acts only on
albuminous substances, but not on starchy matters. The divided pieces
of the pancreas, well freed from fat, are put in a well-corked,
wide-mouthed bottle with four times their weight of dilute alcohol (one
part of rectified spirit to three parts of water). The mixture should
be agitated once daily: at the end of a week the mixture is filtered
through paper until it is clear. A well-made liquid extract of pancreas
is made and sold by Metcalfe of Boston, and a solid extract by
Fairchild Bros. & Foster of New York. No doubt improvements will be
made in the processes of manufacture of these extracts, and better
results will in time be obtained from their use.]

A less successful way of gaining the same object is by administering
the pancreatic extract internally. The difficulty lies in conveying the
extract (the ferment of which is destroyed by the acid gastric juice)
through the stomach in safety. This chemical danger is thought to be
obviated by giving the extract one to two hours after eating with a
{636} protecting guard of an alkali, the bicarbonate of sodium; but the
mechanical difficulty of securing direct transit through the stomach to
the intestine early enough and in quantity enough to digest the
duodenal contents is as great as the chemical obstacle. It is very
doubtful whether this method of use can be of any real service.

In those cases in which the form of indigestion is due to, or is
associated with, a deficient hepatic secretion--a condition indicated
by offensive and light-colored stools and other symptoms--it is
advisable to stimulate the liver to increased secretion. It is probable
that the same remedies which excite a flow of bile do at the same time
stimulate the pancreas. The best of these are euonymin, sanguinarin,
iridin, ipecacuanha, colocynth, jalap, podophyllin, sodium sulphate,
and potassium sulphate. Sodium benzoate, ammonium benzoate, and the
salicylate of sodium are also powerful hepatic stimulants. As one of
the purposes of the bile is to create the alkaline medium necessary for
pancreatic digestion, the administration of an alkaline[19] solution in
full doses, as in the form of mineral water, when gastric digestion is
finished, may make amends for the lack of bile. A combination of an
antiseptic and the alkali may to some extent supply the deficiency
still better, as the bile is the antiseptic of the intestinal canal.

[Footnote 19: The waters of Ems, Vichy (Grande Ville or Hopital
Springs), Vals, or Bilin may be used for this purpose.]

Atony of the intestinal wall leads to flatulence, colics, and
constipation, and would be a cause of indigestion if none other
existed. It is to be treated by the general rules already given, by
electrical stimulation of the abdominal muscles with the faradic
current, or by the effort to stimulate the intestinal wall more
effectively with the galvanic current. Strychnia in small doses should
be given for some time. In women of relaxed muscular fibre with
enlarged abdomens an elastic belt may be worn with advantage.

After the special aids to the parts concerned in digestion, tonics are
called for to combat the general want of tone and anaemia. The
saccharated iron, the carbonate, potassio-tartrate, lactate,
pyrophosphate, or the ferrum redactum may be given. The syrup of the
iodide of iron is the best form for children. The bitter tonics are
inadvisable except for loss of appetite in cases where the stomach is
not disordered. Quinia is available in a large number of cases in which
malarial influence plays a part. Strychnia is a good general tonic, and
may be prescribed combined with mineral acids, particularly with the
dilute hydrochloric acid.

The special symptoms which call for treatment are flatulence, abdominal
pains, and constipation. All the remedies already described are
directed toward their relief. But sometimes they appear in so
exaggerated a form as to need immediate attention. The many remedies
for colic and tympanitic distension which have the property of
relieving spasm and absorbing gas find application in these conditions.
Constipation is not to be treated by laxatives if it can be avoided.
But the bitter waters, Friedrichshall, Pullna, Hunyadi Janos, and
Rakoczy, by exciting bile outflow, are sometimes of undoubted curative
value.

The form of dyspepsia called strumous, as it occurs in children of
anaemic appearance with dry skin covered with minute scales, and with
bad breath and light ill-smelling stools, demands a very thorough and
{637} persevering treatment. The advantages of climate must be
sought--seashore in summer with bathing, dry and moderately warm air in
winter. Outdoor life in the sun, with active exercise, is to be had at
the expense of education within-doors. Study is not good for children
of this class except when health is made paramount to it. Cod-liver
oil, either pure, in phosphatic emulsion, or in the pancreatic
emulsion, is a necessity. Malt extract with the hypophosphites is
beneficial. The food must be carefully selected, and the child educated
to a varied diet, including fats. The skin should be anointed daily
with cocoanut oil, olive, cottonseed oil, or cod-liver oil.




{638}

CONSTIPATION.

BY W. W. JOHNSTON, M.D.


SYNONYMS.--Costiveness, Fecal retention, Fecal accumulation, Alvine
obstruction, Obstipation. _Ger._ Koprostase, Stuhlverstopfung,
Hartleibigkeit, Kothstanung. _Fr._ Constipation, Paresse du ventre,
Echauffement. _It._ Constipazione. Older synonyms: Constipatio vel
obstipatio alvi; Alvus tarda, dura, adstricta; Tarda alvi dejectio;
Obstipatio alvarina; Stypsis; Coprostasis (Good).

NATURE AND DEFINITION.--The act of defecation is almost wholly due to
the working of an involuntary mechanism which may be set in play by the
will, and is in part dominated by it, but which is frequently
independent and uncontrolled by volition. Deep inspiration, closure of
the glottis, downward pressure of the diaphragm, and contraction of the
abdominal muscles are accessory, but not essential, to the expulsion of
feces from the rectum. In certain persons, and occasionally in all
persons, especially in diseases where the fecal mass is in a semi-fluid
or fluid form, the strongest effort of the will cannot resist the
expulsive contractions of the rectal muscle. The sphincter is kept in a
state of tonic contraction by a nervous centre situated in the lumbar
portion of the spinal cord. The fecal mass, supported by the bladder
and the rectum, does not at first touch the sphincter; the rectum is
usually empty; but when the column has been well driven into the rectum
peristaltic action is excited in the rectal walls and the sphincter is
firmly pressed upon. The lumbar sphincter centre is now inhibited, and
the ring of muscle opens, the accessory and voluntary muscles contract,
and the expulsive act is completed. In the well-ordered and healthy
individual the rectal walls and the sphincter do not receive the
maximum of irritation from pressure of the advancing column but once in
twenty-four hours. The habit of having one movement in each day is, it
may be believed, in accordance with the natural and physiological
demand, although both the number and the hours of evacuating are fixed
to a great extent by education. The habit once established, the
mechanism of expulsion recurs at the same hour and entirely without the
direction of the will. If the desire be resisted, it will be most apt
not to return until the same hour on the next day.

Defecation depends for its normal character upon the healthy
functioning of the organism, but especially upon the normal processes
of digestion. The character of the rectal contents as to composition
and consistence, and the time of the arrival of the mass at the
sphincter, are {639} regulated by the taking of food at stated hours
and by its normal digestion and absorption. Unaltered or partly-changed
remains of the ingesta pass down the bowel, mingling with the secretion
from the intestinal glands and with mucus and epithelium. As this mass
passes into and through the colon, being propelled by regular
peristaltic waves, it acquires odor from the development of a substance
which is a final product of the putrefaction of albumen.[1] Gradually
the more fluid elements are absorbed, and in the descending colon a
less fluid or semi-solid consistence of the feces is reached. A healthy
digestion and assimilation, with active and regular contractile
movements of the muscular walls of the small and large intestines, are
essential to normal defecation.

[Footnote 1: Ewald, _Lectures on Digestion_, New York, 1881, p. 106.]

Constipation may be defined to be that condition in which there is a
prolonged retention of the feces or in which they are habitually
expelled with difficulty or in insufficient quantity.[2] While there
are individual peculiarities due to habit or nature, the custom with
most persons of having one movement in the twenty-four hours would
cause any longer retention of the rectal contents to be considered
constipation. The limits between health and disease are not well
defined, and a failure to evacuate the bowels for several days need not
be considered pathological nor require medical interference. In persons
otherwise in good health such an occurrence due to neglect, change of
habit or diet, as in travelling, would cause no interruption to health
or comfort. Nature brings relief sooner or later and re-establishes
order and regularity. In many cases constipation is a primary disease
and the cause of many secondary disturbances, but it is often the
effect or the symptom of various acute and chronic diseases. It may be
acute or chronic.

[Footnote 2: Cases of constipation due to mechanical obstruction from
changes in the wall of the intestine or to exterior pressure will not
be considered in this article.]

In long-continued constipation the intestinal contents are so retarded
in their progression along the canal that they undergo a too early and
too complete absorption of their fluid portion. In time there are an
accumulation and impaction of dry fecal masses in the rectum, sigmoid
flexure, descending transverse colon, or caecum. An obstacle is thus
created which may ultimately close the tube entirely and cause
intestinal obstruction.

ETIOLOGY.--1. Constipation occurs most frequently in advanced life. It
is the effect of loss of peristaltic force and of a diminution of
sensibility in the lower bowel, and is associated with general
functional inactivity and with muscular degeneration and obesity.
Infants are more subject to constipation than children of one year and
over. In many instances this is due to artificial feeding with cow's
milk, condensed milk, and the patent foods so largely used, or with any
diet unsuited to the digestive organs. Imperfect digestion of casein or
other food, the filling of the bowel with a dry mass difficult to
propel, and the consequent catarrhal state of the mucous membrane, are
causes of both constipation and diarrhoea. Feeble, delicate children
with imperfect muscular development, and children born rachitic,
scrofulous, or syphilitic, are generally constipated.

2. Women are prone to constipation much more than men. False modesty,
which imposes restraint upon young girls, and their ignorance {640} of
the necessity of regularity, their habits of indoor life, and avoidance
of exercise, are largely the causes of this. But the anatomical
structure and physiological life of the woman offer another
explanation. At every menstrual period the uterus enlarges and
exercises a greater compression upon the rectum. A tender and enlarged
ovary (and at the menstrual epoch the ovary is always tender and
enlarged) exercises an inhibiting action upon the muscles which bring
the feces in contact with it in their downward passage. In the married
woman recurring pregnancies lead to the habit of constipation from the
long-continued pressure upon the colon, sigmoid flexure, and rectum,
from the extreme stretching of the abdominal muscles, and from the
paralyzing effect of compression during labor. The relaxed condition of
the pelvic and abdominal organs after labor offers no resistance to the
distension of the rectum and sigmoid flexure. The cessation of the
catamenia is accompanied with constipation, nervousness, and a feeling
of ill-defined apprehension when the bowels are moved, or abdominal
pains deter many persons, chiefly women, from habits of regularity. All
uterine and ovarian derangements by mechanical or reflex means bring
about the same result. Chlorosis and anaemia in girls are almost
invariably associated with constipation.

3. Hereditary influence shows itself very markedly in the tendency to
constipation which is seen in many members of the same family. This is
probably more often apparent than real, and is the result of neglect of
the proper attention to the wants of children and of the perpetuation
of vicious habits of taking purgatives.

4. The habits of life and the occupation of the individual have much to
do with the causation of constipation. Those who lead active outdoor
lives are generally regular in their daily movements, but persons of
sedentary pursuits or who work in constrained attitudes--lawyers,
clerks, tailors, shoemakers, and seamstresses--are predisposed to
constipation. Intellectual work, not only from the muscular inactivity
which it entails, but from the diversion of energy to the
nerve-centres, develops the constipated habit as well as indigestion.
Men who are overworked in business, employes in banks, government
offices, shops, etc., bring on the habit from the hurry incident to
their occupations. Luxurious and enervating habits of life, over-eating
and sloth, with the over-indulgence in alcohol and tobacco, have the
same effect. All the influences which deteriorate health, such as bad
ventilation and over-heating of rooms, foul air, want of cleanliness of
the person, indigestible food, imperfect mastication, tight-lacing in
women, compression of the abdominal organs in men, can be said to share
in bringing it about. Servants, especially women, are constipated more
frequently than their masters. This is due to ignorance and neglect,
and sometimes to excessive tea-drinking and irregularity in eating.

5. Neglect to establish or continue a habit of daily regularity in
defecation leads to the accumulation in the rectum of masses of feces.
Resisting the desire to empty the bowel interrupts the necessary reflex
acts, and finally the muscular excitability and response to the
presence of feces are entirely wanting. The continued contact of fecal
matter with the mucous membrane wears out its susceptibility; the
over-distension of the rectum enfeebles the power of its muscular wall,
as is the case when all hollow muscular organs--stomach, heart,
bladder--are overstretched. Thus a {641} neglect to answer the demand
for a daily movement and the failure to completely empty the rectum
will gradually develop constipation in a person who has before been
perfectly well regulated. In childhood failure to teach and to insist
upon good habits is the cause of much of the trouble of after-life.

6. Acute and chronic diseases of the brain and spinal cord bring about
constipation. Meningitis, encephalitis, and myelitis, senile dementia
and softening, have it as a symptom at some time or other. In
encephalitis and myelitis there is an interruption of motor
nerve-currents. In meningitis and tetanus the muscular walls of the
bowel and the abdominal muscles are in a state of tonic contraction.

7. The use of aperients is an important agent in developing the
constipated habit by over-stimulating and wearing out muscular
activity. The idea that a daily movement is a necessity, and that an
occasional purgative is useful in relieving the system of morbid matter
which would otherwise induce disease, is the chief source of this
hurtful custom. The traditional meaning attached to the term
biliousness implied the resort to cathartics for its relief, and it is
much to be regretted that with our more advanced knowledge the effort
should be made to revive the use of this term, which was wellnigh
abandoned. More ignorance and erroneous treatment has hung upon the
theory of biliousness than upon any other doctrine of medicine within
the past thirty years: it is well for physicians to condemn it and to
resist its reintroduction into scientific phraseology.[3] If the term
bilious as applied to diseases were abandoned, much good would come of
it. The general use of purgative mineral waters has added to this evil.
Among the better classes these waters play the same part as the liver
regulators and vegetable pills do among laborers and servant-maids.
Both gratify the innate love for self-medication by a resort to
cathartics for the slightest ailment. At first the injurious effects
are not apparent, but in time the reflex function is not brought into
activity except by artificial aids. The intestinal and rectal muscles
must be whipped into action, their normal contractile power being lost.

[Footnote 3: For an excellent and dispassionate statement of the
reasons for abandoning the theory of the influences of bile as a cause
of disease, and the use of the term bilious, consult _The Bile,
Jaundice, and Bilious Diseases_, by J. Wickham Legg, chaps. viii. and
xxix. The Hippocratic and Galenical belief has been transmitted with
but little alteration through Stoll, Andrie, Abernethy, and Copland to
the writers of to-day on biliousness.]

8. Certain vegetable and mineral substances taken either intentionally
or by accident constipate the bowels. Chief among these stand opium and
its preparations. All opium-eaters are constipated. Lead which is
accidentally taken into the system by workers in metals, painters, etc.
invariably produces obstinate constipation. The use of tobacco in
excess has the effect of deranging digestion and causing constipation
in many persons, but this result is occasional only.

9. Chronic diseases of the lungs and heart, by enfeebling the muscular
movements which take part in defecation, as well as by the general
feebleness and the chronic intestinal catarrh and indigestion which
they create, are causes of constipation. Chronic diseases of the liver,
especially cirrhosis, are also causes. Constipation accompanies
obesity, for in very fat persons the abdominal walls have but little
power of contraction; the {642} muscle-layer is thin and flaccid. There
is also in such persons in advanced life an accumulation of fat in the
mesentery and around the colon. The muscle of the bowel is in a state
of fatty degeneration, and atony and dilatation of the gut follow.

10. Painful affections about the rectum and anus deter persons from
yielding to the desire for defecation. Fissure of the anus is the
principal one of these, but fistula, hemorrhoids, and local eczema have
a similar influence. A simple rigidity or spasmodic stricture of the
anal sphincter creates constipation.[4]

[Footnote 4: Kunemann, _De la Constipation compliques de Contraction du
Sphincter anal, et de son Traitement par la Dilatation de l'Anus_,
Paris, 1851.]

11. Constipation is a symptom in chronic cachexiae and wasting
diseases, in the convalescence of acute exhausting illness, as typhoid
fever and pneumonia, or in persons bedridden from any cause. Defective
nutrition and degeneration of the muscle-fibre of the intestine explain
these cases. In some of them, with improved nutrition, regeneration
takes place with a return of contractility.

12. Disorders of the digestive system have constipation as a
consequence and a symptom. The reflex sympathy between the movements of
the stomach and of the intestines brings this about in gastric
diseases.[5] It occurs in gastric cancer and ulcer, in acute and
chronic gastritis, in dilatation of the stomach, and in pyloric
stricture. The small amount of ingesta entering the duodenum in these
diseases diminishes the bulk of fecal matter. In acute intestinal
catarrh diarrhoea is the rule, but the bowels may be constipated in
intense inflammation and ulceration of the mucous membrane, as is often
the case in typhoid fever. In chronic intestinal catarrh constipation
is more common in the mild forms than diarrhoea. The thickening and
irritation of the mucous membrane lead to a diminution of reflex
excitability and loss of elasticity and contractility in the muscular
coat. Hence, except in cases where the inflammation is low down or
where ulcers have formed, constipation is a more frequent symptom than
diarrhoea. The alteration in the quantity and character of the
intestinal secretions in chronic catarrh is stated to be an important
element. This is to some extent true. Mucus, which is the chief product
of this condition, leads to indigestion and fermentation of the
intestinal contents and to increased irritation of the mucous membrane.
The evolved gas distends the bowel and weakens its contractile power.
The fecal mass when it reaches the rectum has an excess of mucus within
it or around it which makes its expulsion more difficult. But the
diminution or absence of bile does not constipate. In simple jaundice
diarrhoea is not uncommon, and an excess of bile does not of necessity
cause diarrhoea.[6]

[Footnote 5: Leube, in _Ziemssen's Cyclopaedia_, vol. vii. p. 211.]

[Footnote 6: Legg, _op. cit._, p. 271.]

The effects of the modifications of the pancreatic secretion are not
well known. Pancreatitis is attended by constipation. Fatty diarrhoea
is believed to follow occlusion of the pancreatic duct by pancreatic
calculi and chronic catarrh of the duct. Peristalsis is lost in
peritonitis from the muscular coat being infiltrated with serum and
paralyzed, but tuberculous peritonitis is frequently accompanied by
diarrhoea.

13. Loss of fluids by abundant perspiration, by diuresis, diabetes and
lactation, increases the dryness of the bowel contents and hinders free
{643} evacuations. This is observed as a result of the arrival in a
tropical climate and in very hot weather in any climate. The profuse
sweats accompanying phthisis, acute rheumatism, intermittent fever, and
unusual exercise cause constipation. Another explanation which applies
to this has been offered by Good and Eberle, who ascribe constipation
to the excessive action of the absorbents in the small intestine, by
which the fluid portion is too rapidly and too thoroughly removed.[7]
Exercise by promoting activity of the functions in general may induce
constipation in this way. In spermatorrhoea the stools are infrequent.
An insufficient amount of water taken with food is another cause.

[Footnote 7: Dick, _Braithwaite's Retrospect_, xvii. p. 152.]

14. Food which has but little waste to be got rid of--as milk or
beef--leaves a small residuum to be propelled along the intestine, and
therefore in one sense is constipating. Insufficient food acts in the
same way. An indigestible diet in excess, especially vegetable food, a
large part of which is insoluble, constipates by filling the bowel with
matter which cannot be got rid of, and chronic catarrh results. The
stones and seeds of fruits, as cherry- and plum-stones, raspberry- and
currant-seeds, husks of corn and oats, produce acute or chronic
constipation with serious symptoms. Intestinal worms (generally
lumbricoids) when in large numbers cause obstruction of the bowel;[8]
and various foreign substances taken by caprice or to take the place of
food have produced the same result: among these stick cinnamon,[9]
sawdust,[10] and clay (among the clay-eaters of the South) have been
mentioned. Magnesia, insoluble pills, and other medicines sometimes
form concretions in the bowel. Enteroliths and accidental concretions
form in the intestinal canal and are sources of obstruction. Any
foreign body is a nucleus around which concentric layers of phosphate
of lime are deposited, and thus a hard calculus is formed. Gall-stones
may pass into the canal and there accumulate in such numbers as to
interfere with the passage of the fecal matter.

[Footnote 8: Copland, _Medical Repository_, vol. xvii. p. 243.]

[Footnote 9: Ware, _Boston Med. and Surgical Journal_, 1858, vol.
lviii. p. 501.]

[Footnote 10: Bonney, _ibid._, 1859, vol. lix. p. 39.]

PATHOLOGICAL ANATOMY.--In cases where constipation has lasted many
years no alteration of the parts involved may be found. When lesions do
occur the pathological anatomy includes changes in the position,[11]
calibre, and in the walls and contents of the intestines. The most
common displacement is that of the transverse colon, which is depressed
in its centre; the acute angle of the descending part may reach as far
down as the hypogastrium. The caecum sometimes lies in the centre of
the abdomen. Dislocations of the intestines are congenital, due to
anomalies of intra-uterine development, in which case they become
causes of death in newly-born children from obstruction, or if
insufficient to cause death they establish habitual and incurable
constipation; or constipation may bring about displacement by the
greater weight of a portion of the bowel constantly loaded with fecal
matter.

[Footnote 11: Votsch, _Koprostase_, Erlangen, 1874.]

The sigmoid flexure is usually the seat of the greatest dilatation; its
expansion may be a cause or a consequence of constipation.[12] It may
reach a maximum of distension when it fills the entire abdominal
cavity, compressing all the abdominal organs and pushing the stomach,
liver, {644} and intestines into the thorax. In a case of this kind the
circumference of the dilated part was twenty-seven inches.[13] The
descending colon may be distended with the sigmoid flexure, or the
whole colon may be dilated from the upper part of the rectum to the
caecum;[14] the same thing happens rarely in the small intestine. In
one case, in which there was an accumulation of feces in the sigmoid
flexure, the large intestine presented itself as two immense cylinders
lying side by side, extending from the epigastrium to the pelvis.[15]
Each was about five and a half inches in diameter, and together they
filled the abdominal cavity. The circumference of the stretched colon
varies from ten to thirty inches. Pouches forming little rounded tumors
are seen on the outer surface of the colon; they are sometimes hernial
protrusions of the mucous membrane through the muscular coat (Wilks and
Moxon), or if large they are dilatations of the pouches of the
colon.[16]

[Footnote 12: Trastour, "De la Dilatation passive de l'Iliaque, et de
ses consequences," _Journal de Med. de l'Ouest_, 1878-79, tome xii. p.
165.]

[Footnote 13: Dupleix, _Le Progres medicale_, Paris, 1877, tome v. p.
953.]

[Footnote 14: Peacock, "Fatal Constipation, with Excessive Dilatation
of the Colon," _Tr. Path. Soc. London_, vol. xxiii. p. 104.]

[Footnote 15: Lewitt, _Chicago Med. Journ._, vol. xxiv., 1867, p. 359.]

[Footnote 16: Gay, "Sacculated Colon, Prolonged Constipation," _Tr.
Path. Soc. London_, vol. v. p. 174.]

The colon is sometimes much lengthened. But little weight can be
attached to this anomaly, as there is a difference in the length of the
colon in different nations and individuals, depending upon the
character of the food, being longer in those who eat largely of
vegetable food.[17]

[Footnote 17: _Ziemssen's Cyclopaedia_, vol. vii. p. 606.]

The mucous membrane is normal or hyperaemic, or is in various stages of
chronic catarrh. Proctitis may exist with follicular ulcers; ulcers
form in the caecum, sigmoid flexure, and in the bends of the colon;
perforations and peritonitis rarely occur. Chronic peritonitis has
resulted from the stretching of the bowel from retained and hardened
feces; adhesions may form which ultimately cause death by obstructing
the canal. The walls of the intestines are in long-standing cases much
thinned. There are many reasons to believe that fatty degeneration of
the smooth muscular fibre takes place, in consequence of which it loses
its contractile power and atrophies. This lesion is most common in
advanced life, and accompanies fatty accumulation and degeneration
elsewhere. Its results would be constipation, distension of the bowel
with gas, and sometimes symptoms of intestinal obstruction.[18] A
thinned and dilated bowel may easily be lacerated under unusual
stimulation, as from a purgative. In a case recently seen by the writer
such an accident, rupture of the colon and death from peritonitis,
occurred from the effects of an active purge taken to bring on
abortion. Hypertrophy of the wall, especially of the muscular coat,
coexists with dilatation, and is most common in the upper part of the
rectum and sigmoid flexure. It is caused by overwork in expelling fecal
accumulations. The walls never become as much thickened as in
constipation from organic stricture.

[Footnote 18: Cases are recorded of death with symptoms of intestinal
obstruction in which no lesion was found beyond a dilated colon; as,
for example, in _British Medical Journal_, April, 1879, p. 621.]

Collections of fecal matter may be found in any portion of the colon,
but more frequently in the rectum, sigmoid flexure, descending or {645}
transverse colon, or caecum. They lie within the intestinal tube,
partly or wholly occluding it, or within lateral pouches, forming
tumors which are sometimes quite large. In this last form there is no
obstacle to the free passage of feces along the canal. Fecal
accumulations occur as small round, oval, or irregularly-shaped lumps
(scybalae), and are often covered with layers of transparent semi-fluid
mucus, puriform mucus, or mucus in filaments. The small concretions
vary in density; they may be so hard as to resist the knife, and may be
mistaken for gall-stones; larger masses, semi-solid or solid, are most
commonly seen in the rectum and sigmoid flexure. Here the collection
may reach an immense size. In one case fifteen quarts of semi-solid,
greenish-colored fecal matter were removed at the autopsy.[19] In two
other cases the weight of the feces found in the bowel was thirteen and
a half[20] and twenty-six pounds[21] respectively. The whole colon from
the anus to the caecum may be filled with such a mass, as in a case
mentioned by Bristowe, where the colon "was completely full of
semi-solid olive-green colored feces. The small intestines were also
considerably distended, ... and were filled throughout with semi-fluid
olive-green contents."[22]

[Footnote 19: Peacock, _Tr. Path. Soc. London_, vol. xxiii. p. 104.]

[Footnote 20: Lamazurier, _Archives generales_, Paris, 1824, t. iv. p.
410.]

[Footnote 21: Chelius, _Heidelberg Med. Ann._, 1838, vol. iv. p. 55.]

[Footnote 22: Bristowe, "Diseases of Intestines and Peritoneum,"
_Wood's Library_, New York, 1879, p. 21.]

The color of these collections is black, reddish, deep green, or
yellow. In composition the scybalae, concretions, and larger masses
consist of fecal matter, with unaltered vegetable fibre; they may be
composed partly of skins of grapes, cherry-stones, biliary calculi,
hair, woody fibre, magnesia, or other foreign substances. Where fecal
concretions long remain in the intestine they acquire a hardness like
stone, and can with the microscope only be distinguished from mineral
matter.[23] Hemorrhoidal tumors, anal fissures, perirectal abscesses,
fistulae communicating externally or with the gut, are found in
connection with constipation. Abscess of the iliac fossa has been
observed in the same relationship.[24]

[Footnote 23: A remarkable case is recorded (_Dictionnaire de
Medecine_, Paris, 1834, t. viii. p. 435) in which an ulcerating cancer
of the fundus of the uterus had opened communication and formed
adhesions with the small intestine, from whence the feces passed into
the uterus and out through the vagina. The large intestine, totally
occluded, contained petrified fecal matter.]

[Footnote 24: Richet, "Abscess of Iliac Fossa," _Revue de Therapeutique
medico-chirurgicale_, 1876, p. 563.]

SYMPTOMS.--In persons who have a daily movement an occasional
interruption of two to four days may take place without local or
general signs of inconvenience. It is often asserted by patients that
one day's omission induces suffering, and recourse is immediately had
to laxatives. This may be justified sometimes, but in the majority of
cases no actual suffering follows a very rare and short
constipation.[25] If, however, symptoms do occur after a constipation
of one to three days, there is a sense of fulness and heat about the
rectum which is greater after stool; when the bowels are moved, it is
with effort (provided that no enema or purgative has been taken), and
the bulk of the expelled mass is much greater {646} than usual, being
moulded and hardened from its longer retention in the rectum. The
margins of the anus are tender, and the unsatisfied feeling after stool
is due to distension of the hemorrhoidal veins and oedema of the
tissues around them--a condition which ends in painful or bleeding
hemorrhoids. There are signs of impaired digestion, loss of appetite, a
coated tongue, oppression after eating and flatulence, and distension
of the abdomen. Headache is apt to be present, with flushing of the
face and general discomfort or irritability of temper. These phenomena
may all disappear within two or three days by a spontaneous stool or by
the use of a purgative.

[Footnote 25: Some interesting remarks in connection with the idea that
constipation is not necessarily hurtful, and is in some cases
beneficial, may be found in a pamphlet by C. I. Harris, _Is our
Physiology of the Large Intestine correct, and is Constipation in
certain cases as Injurious as is supposed?_ London, 1878.]

Acute symptoms of a violent nature are sometimes developed in persons
who have been constipated a long or short time, in consequence of
attempts at purgation or from the accumulation of indigestible food.
Violent paroxysmal pains in the abdomen and efforts at stool are soon
followed by symptoms of intestinal obstruction and serious collapse.
Quick relief follows a free movement from the bowels obtained by an
enema, or if not so relieved the case may terminate fatally.

A frequent recurrence of fecal retention from the causes mentioned will
in time develop the constipated habit. Distension of the rectum
increases its capacity and destroys its sensibility and expulsive
power. The colon above the point of stoppage is distended with gas and
weakened. The bowels are rarely moved spontaneously, and finally are
never emptied without artificial aid. The literature of medicine
contains many extraordinary records of prolonged fecal retention,
ranging from a few weeks to many months.[26]

[Footnote 26: _Am. Journ. Med. Sci._, Philada., 1846, p. 260 (three
months and twenty-two days); Renaudin, _Dict. des Sci. med._, t. vi. p.
257 (four months); Strong, _Am. Journ. Med. Sci._, Oct., 1874, p. 440
(eight months and sixteen days); Valentin, _Bull. des Sci. med._, t. x.
p. 74 (nine months); Staniland, _London Med. Gaz._, vol. xi. p. 245
(seven months); _Dublin Hosp. Reports_, vol. iv. p. 303 (eight months);
Inman, _Half-Yearly Abst. Med. Sci._, vol. xxxi. p. 275 (two years);
Devilliers, _Journ. de Med._, 1756, t. iv. p. 257 (two years); J.
Chalmers, _Med. Gaz._, London, 1843, vol. xxi. p. 20 (three years);
_Philada. Med. Museum_, 1805, vol. i. p. 304 (fourteen years).]

The evacuations in chronic constipation are harder and more dry than
they should be; they are passed in masses of various sizes, and in
color are brown, black, dark-green, or yellow. Sometimes a coating of
mucus is on the outside, and sometimes streaks of blood, or there is an
intimate admixture of mucus, giving a slimy, gelatinous appearance to
the mass. Semi-digested food, as partly-altered milk, meat, or
vegetable matter, is seen, and quite frequently there is an
intercurrent diarrhoea which alternates with costiveness.

The local symptoms about the pelvis and anal opening and in the lower
extremities come from the pressure of accumulations of feces. Thus,
compression of the iliac veins delays circulation in the lower
extremities; cold feet or oedema of the feet and ankles and varicose
veins follow. If the pressure is on the ilio-hypogastric and
ilio-inguinal nerves, there are neuralgic pains in the groin and over
the crest of the ilium. The sciatic and crural nerves may be the seats
of pain. Varicocele is the effect of weight upon the spermatic veins.
Erections and seminal emissions in men follow pressure on the pubic
veins and prostatic portion of the urethra. Retention of urine also may
come from the latter cause. If the kidneys and ureters are compressed
by fecal tumors in the descending or transverse {647} colon, nephritic
pain, albuminuria, or retraction of the testicle, with delay in the
escape of urine, may happen. Icterus and its consequences are owing to
pressure on the common bile-duct; the liver and other organs may be
displaced and the aortic circulation obstructed by fecal compression.
In women the retention of fecal matter in the rectum is the source of
special symptoms; it contributes largely to the occurrence of cervical
anti-flexion in the soft, pliable, growing uterus of girlhood (Thomas),
and unites with retroversion in women who have borne children to
produce great suffering.

An unnatural state of the digestive system, as a cause or result, is
the invariable accompaniment of chronic constipation. The appetite is
wanting; the tongue is coated, and may be pale, soft, and indented by
the teeth. Distress follows eating; the abdomen is distended with gas
and is hard; all the evidences of gastric or intestinal indigestion may
be found. Nutrition is imperfect, as is shown in loss of flesh and in
the signs of functional disorder to be next described.

The nervous system is soon deranged; sleep is unrefreshing, restless,
and disturbed by dreams. There are headache and mental and physical
indolence. The patient speaks of being giddy, faint, and nervous.
Disturbance of vision (muscae volitantes), of hearing (tinnitus
aurium), and alarming attacks of dyspnoea and cardialgia may occur.[27]
Heart-palpitations and profuse perspirations are the effect of
excitement or effort of any kind. Chilliness or violent chills can be
traced to this cause also. In women hysteria, disturbed menses,
anaemia, and chlorosis accompany constipation.

[Footnote 27: C. C. Melhose, _Hufeland's Journal_, 1841, xcii., Stuch
iv. p. 105.]

Nervous symptoms are very common in the young, and it is doubtful
whether they are consequences of constipation or whether they form a
part of a general state of malnutrition and anaemia. Hypochondria is
undoubtedly closely connected with the constipated habit, and the
failure to secure a daily movement becomes the subject of unceasing
thought and anxiety. Hallucinations and sudden loss of consciousness,
aphasia,[28] and delirium, have been found to depend upon fecal
accumulation.[29] The absorption of fluids and gases from
too-long-retained and decomposing feces may explain such cases. The
nerve-centres soon show the effect of the supply of altered or
contaminated blood.[30] It is probable that the marked nervous symptoms
are more due to this cause than to reflex influences.

[Footnote 28: Mattei, "Aphasia cured by relieving Constipation," _Bull.
de l'Acad. de Med._, Paris, t. xxx., 1864-65, p. 870.]

[Footnote 29: Pulitzer, _Wien. med. Presse_, 1866, x. p. 439. Case.--A
man aet. 42, with sleeplessness, hypochondriasis, hallucinations, and
one attack of sudden loss of consciousness; symptoms relieved by
removing a large quantity of fetid fecal matter from bowels. Also
Dujardin-Beaumetz, serious nervous symptoms due to constipation
(_Bulletin de Therap._, Paris, t. 89, 1875, p. 179).]

[Footnote 30: Bell, _Lancet_, London, 1880, i. 243-283.]

A coincidence exists between dislocation of the colon and various
states of mental disturbance. Ten cases of suicide were seen by Votsch
in which there were displacements of the colon. Laudenberger of
Stuttgart found that in ninety-four autopsies of insane persons there
were anomalies of position of the transverse colon in one-seventh of
the number (Votsch).

Fever is not infrequently due to constipation. During the course of
typhoid and other fevers an unusual elevation of temperature is often
{648} traced to a neglect to have the bowels emptied. But very high
temperature sometimes depends upon constipation alone, and is at once
reduced by removing the cause. This may occur in the course of chronic
diseases or in health, especially in children.[31] The temperature
rises from normal to 104 degrees F., and even higher, and immediately
drops to normal when the bowels are moved. When a sudden rise in
temperature comes with acute constipation, the influence must be a
reflected one from the mucous surface to the heat-centre.

[Footnote 31: F. Barnes, "On the Pyrexial Effects of Constipation,"
_Med. Press and Circular_, 1879, N. S. xxviii. p. 477. Also, C. H.
Jones, _Lancet_, London, 1879, ii. p. 229--a case in which there was a
temperature of 104.1 degrees, pulse 180, and delirium due to scybalae
in bowel; Cabot and Warren, "High Temperature from Constipation,"
_Boston Med. and Surg. Journ._, 1880, ciii. p. 1571.]

The urine is dark-colored and scanty, loaded often with urates, or it
may be limpid and of a very low specific gravity. The escape from the
bladder and through the ureters may be obstructed by compression, as
already mentioned. Suppression of urine has occurred, and been relieved
by removing large fecal collections.[32] In women catamenial
irregularity and dysuria are generally associated with constipation.
Disturbances in pelvic circulation and local pressure of a distended
rectum explain these conditions.

[Footnote 32: Barnwell, _Cincin. Med. News_, 1875, vol. viii. p.
353--female aet. 45. Had no movement for five days; suffered with
tympanites; severe pain in right iliac region, with persistent
vomiting; tumor in same region; complete suppression of urine. At the
end fifth day passed large quantity of apple-peelings and fecal matter.
Return of flow of urine; passed two gallons in ten hours.]

The skin is often parched, sallow, and is sometimes covered with
eruptions, as acne, psoriasis, eczema, erythema, or prurigo. Injuries,
wounds, and cracks of the skin heal slowly.

RESULTS AND COMPLICATIONS.--The lateral pouches of the colon, most
commonly at the sigmoid flexure, become distended, and deeper pouches
are formed, where fecal matter is retained.[33] This need not interfere
with the regular daily movements. Fecal tumors are thus formed, the
nature of which is often not recognized. The colon may be distended so
as to fill a large part of the abdomen. The pressure of hardened feces
brings about ulceration of the mucous membrane, perforation and
extravasation of the contents into the abdominal cavity, with fatal
peritonitis. Abscesses in the perirectal tissues, with fistulae,[34]
anal fissures, hemorrhoids, prolapse of the rectum, varices of the
prostate gland and bladder, owe their origin to fecal collections,
especially in advanced life.

[Footnote 33: Long, _Med. Times and Gazette_, 1856, vol. ii. p. 286.]

[Footnote 34: Bannerot, C., _Du Phlegmon pelvi-rectal inferieure et de
la Fistule de l'Anus consecutive causees par la Constipation_, Paris,
1880.]

Intussusception has been attributed to the weight of a mass of feces.
Typhlitis and perityphlitis may come from retention in the caecum.
Pressure upon the viscera brings about derangements in their functions,
many of which have already been described. From straining at stool a
hernia, haemoptysis, or cerebral hemorrhage may happen. Cases have been
reported of death from rupture of an aneurism of the aorta while at
stool, and J. F. Hartigan met with a case of spontaneous rupture of the
aorta, where the vessel was apparently but little diseased, occurring
in a man aged sixty during the act of defecation.[35]

[Footnote 35: Hartigan, _Tr. Med. Soc. District of Columbia_, vol. i.
No. 3, 1874, p. 55. See also same number for a valuable paper on
spontaneous rupture of aorta, by J. J. Woodward.]

{649} The effects upon the general system are those connected with
malnutrition. The health may be profoundly altered and death occur from
secondary diseases. Many general symptoms are due to the retention in
the blood of excrementitious matters or to their reabsorption.[36]

[Footnote 36: Sterk, "Ueber den schudlichen einfluss der chronischen
Stuhlverhatten auf den Gesamur organismus," _Wien. med. Presse_, xxii.,
1881, p. 330 _et seq._]

DIAGNOSIS.--The diagnosis of constipation is not difficult except in
hysterical women, who select this as one of their subjects of
deception. Primary must be distinguished from secondary constipation,
the last being a symptom of some general or local disease. The history
of the case and the predominating symptoms will be guides to a
decision, but constipation should be regarded as a symptom until it is
proved to be otherwise. The tendency is to look upon it and to treat it
as a distinct malady; important organic changes elsewhere may thus be
overlooked. Simple habitual constipation may be mistaken for
constipation due to lesions in the wall of the intestine or to closure
from the external pressure of tumors.

Slowly-developed symptoms of obstruction may come from polypoid growths
or benign tumors in the rectum, colon, caecum, duodenum, and ileum.
They are usually found in the rectum. The diagnosis can only be made
when the growth is in the rectum or when the tumor is expelled from the
bowel. Cancerous obstruction is accompanied by cachectic changes, by
the presence of an abdominal or rectal tumor, the passage of blood and
mucus, and violent rectal or abdominal pain. Primary cancer in the
small intestine appears in the form of lymphoma; it readily ulcerates,
and rather widens than narrows the channel of the bowel.[37]

[Footnote 37: Wilks and Moxon, _Path. Anat._, Philada., 1875, p. 417.]

Stricture of the bowel is most commonly found low down in the rectum or
sigmoid flexure, within reach of the finger or exploring bougie. If
high up, it can only be diagnosed by exclusion and by its slow
progression from bad to worse. Syphilis or dysentery has nearly always
preceded the development of stricture.

Tumors in the abdomen or pelvis compress the colon, and while they are
small they may be overlooked; sooner or later they grow so as to be
recognized.

The presence of gall-stones as obstructions may not be detected until
they are passed. The previous occurrence of attacks of hepatic colic,
followed by jaundice, gives rise to the suspicion that gall-stones are
in the intestine if they have been carefully looked for in the stool
but never found.[38] Enteroliths give no indication by which they could
be known to be in the bowel.

[Footnote 38: In a case seen by the author three separate attacks of
typhlitis occurred in a young woman suffering from chronic
constipation. After the last attack she passed from the bowel several
dark, irregularly-shaped concretions. The largest of these was a
gall-stone covered with fecal matter. Since this time--two years
ago--there has been no recurrence of inflammation and the constipation
is much better.]

All forms of constipation from organic modification of the walls grow
worse and have no remissions; some rapidly progress toward a fatal
termination. Simple constipation is subject to improvement and relapses
due to the character of the food, climate, exercise, etc. The etiology
is an important guide.

Stercoral tumors may be known by their position and character as {650}
ascertained by physical examinations and by their history. They are
found in the iliac, lumbar, or hypochondric regions, and sometimes in
other parts of the abdomen. The most common seat is in the sigmoid
flexure and descending colon. They are nodulated, movable, painless,
can be made to change shape or are indented by pressure, and have a
doughy feel. Exploration of the rectum, by detecting impaction, will
make the diagnosis clear when the obstruction is low down. The
distension of the abdomen above the point of obstruction is limited at
first to the region of the colon; but if the colon is much dilated with
gas or is displaced, the enlargement becomes more central and more
general. On percussion the sound is of a dull tympanitic quality, and
never absolutely dull even in cases of great fecal accumulation.[39]

[Footnote 39: Case referred to by Guttmann (_Physical Diagnosis_,
Sydenham ed., p. 360), in which the sound was dull tympanitic over two
large fecal tumors which weighed when removed at the post-mortem six
kilogrammes (sixteen pounds).]

Fecal tumors[40] are preceded by habitual constipation, and are most
common in elderly people; they are changed in position and size or made
to disappear by cathartics or rectal injections. Persistent treatment
will bring away scybalae which by their color and consistence show that
they have long been in the canal. But the free movement of the bowels
and the non-disappearance of the tumors are no proof that they are not
fecal.

[Footnote 40: _Tumeurs stercorales_, Paris, Thesis No. 240, 1878.]

Fecal accumulations have been mistaken for ovarian tumors,[41]
cancerous tumors of the mesentery, uterine fibroids, and retro-uterine
haematocele. Fecal tumors in the transverse colon have been taken for
enlargement of the liver and spleen. In one instance obstruction of the
bowel from fecal impaction was supposed to be a strangulated gut in a
patient suffering from hernia: an operation was performed, the patient
dying in sixteen hours afterward.[42] Ovarian tumors in their early
stages are sometimes thought to be fecal.[43]

[Footnote 41: Jas. Y. Simpson, _Med. Times and Gazette_, London, 1859,
vol. ii. p. 549.]

[Footnote 42: Thomas Bryant, _Med. Times and Gazette_, London, vol. i.,
1872, p. 303.]

[Footnote 43: J. B. Brown, _Lancet_, London, 1850, vol. ii. p. 48.]

Fecal impaction in the rectum, with ulceration and bloody and mucous
stools, may for a time be called cancerous ulceration. Sacculated
scybalae cannot be distinguished from submucous tumors even by the hand
pressing on them in the rectum.[44]

[Footnote 44: H. R. Storer, _Gynaecological Journ._, 1869, vol. i. p.
80.]

The history of each individual case, a full knowledge of etiological
factors, and a careful physical examination will in most instances lead
to a proper diagnosis.

PROGNOSIS.--The result of treatment depends upon the age. Although in
infancy constipation is very common, cure is the usual result where a
mixed diet begins to be taken in childhood. At from one to fourteen
years of age regular movements can usually be secured, unless there is
a radical defect in the organization of the child. In young girls at
puberty and after, if constipation once is established it is apt to
become inveterate, associated as it is with imperfect development and
with uterine displacements. In middle life in men the result depends
upon the cause and upon attention to the physician's counsel. If
intestinal catarrh or atony is the cause, a persistent subordination of
the life of the individual to the object in view will generally end in
cure. In women who have borne {651} children the hope of relief depends
upon the duration of the malady before treatment. It is a dispiriting
task to attack a constipation of many years' standing in women with
relaxed abdomens, uterine prolapsus or retroversion, and general
debility. In old age the causes are generally such as cannot be
removed. The bowels can be moved when the occasions demand, but there
is very little expectation of establishing a spontaneous habit of
regular fecal movements.

At every age and from whatever cause perseverance and hope on the part
of the patient and doctor are the chief elements of success. In
neglected cases the worst results may happen: dilatation of the colon,
ulceration, fecal impaction and obstruction, perforation; or in milder
cases chronic indigestion, hypochondria, etc.

TREATMENT.--The physician can render great service by giving to parents
advice which will prevent constipation in children. He should insist
upon the importance of habits of regularity in defecation. At the
period of puberty in young girls this is of even greater moment, and no
opportunity should be lost for pointing out the danger of neglect. As a
prophylactic measure in adults counsel should be given suited to the
occupation. To persons leading sedentary lives the necessity of
exercise ought to be made clear. In the trades little can be done, but
in the case of literary men and those who read or write for many hours
prevention is easier than cure. Daily exercise, walking or riding,
frequent bathing with active sponging and friction of the surface,
especially over the abdomen, will be of much service. Avoiding
constrained positions where pressure is brought to bear upon the
abdomen, as in bending forward to write, is quite an important item.
Among ignorant people advice of this kind is rarely attended to, but
even here the doctrine of regularity should never cease to be preached.
Active business-men, especially young men, need emphatic teaching. They
cannot plead ignorance for the habitual and persistent neglect of the
simplest rules of health of which they are in this country so often
guilty. The symptoms of indigestion which are precursors of
constipation should receive due attention, and a mode of life and
dietary suited to a complete digestion of the food will favor the
timely and proper expulsion of waste matter.

Acute constipation in a previously healthy person, lasting for one to
three days, does better without interference. No harm attends temporary
inaction of the bowel, and if a spontaneous stool takes place at the
end of this time it is a sign of a healthful and vigorous condition.
After this the normal regularity is restored. The habitual clearing out
of the bowel by a purgative pill or dose of mineral water whenever such
a state of matters occurs creates the necessity for the interference.
The man who never lets himself go over a day without an action is
miserable if he misses his purgative and its effects.

In the onset of acute diseases the custom of giving a preliminary
purgative is generally unnecessary, often injurious. It disturbs the
rest which such cases need; it produces exhaustion in some diseases, as
pneumonia, pleurisy, and rheumatism; it irritates the mucous membrane
when irritation involves danger, as in intestinal catarrh and typhoid
fever.

When it is desirable to empty the bowel in acute constipation a
warm-water enema for adults and children is the best means. When a
laxative is necessary in case of a failure of the enema, one mild in
its operation {652} should be chosen--a compound rhubarb pill, one to
five grains of calomel, a teaspoonful of Rochelle salts, or half a
bottle to a bottle of the solution of the citrate of magnesia or the
tartro-citrate of sodium. For children calomel, in doses of one-third
of a grain to one grain, is one of the most certain and least
objectionable. One grain of powdered rhubarb can be added to this for a
more active effect.

Under such circumstances as a blocking up of the bowel with a mass of
partially digested or undigested food, fruit-stones, skins, or other
foreign bodies, where the symptoms are violent pain, tympanites, and
vomiting, the best method is to give large enemata of warm water
through a long rectal tube passed as high up as possible, and to
administer calomel in doses of one to three grains, repeated every two
to three hours until the bowels are moved. Cold can be applied to the
abdomen to diminish tympanites and prevent inflammation. Should the
constipation not yield and the pain, vomiting, and tympanites augment,
the case will then be considered one of intestinal obstruction, and be
treated as such.

When called upon to treat chronic constipation, the physician should
remember that it is not the symptom, but its causes, to which he should
direct attention. Constipation is so often a symptom, a complication,
of other diseased states that its management is a matter of secondary
importance. Moreover, its causes are so peculiar to the individual and
depend upon so many variable habits of life that each case asks for
special study. The cure is only to be found by learning the particular
cause--the habit of neglect, hurried eating, the use of aperients,
uterine displacement, or any of the many causes enumerated.

The digestion and all that concerns it is of primary importance, and to
it attention should be at once directed. The stomach and intestinal
digestion should be examined separately, and the relative power to
digest different articles of food determined. A diet, then, should be
selected, not with a view to correcting the constipation, but as to its
suitability to the digestive capacity of the patient. No system of diet
can be fixed upon as suited to every case: the aim is to secure normal
digestion and absorption and normal peristalsis. Many trials may have
to be made before a proper dietary can be chosen. When there is
indigestion of fats and malnutrition, with pale offensive stools
containing much mucus, an exclusive nitrogenous and easily digestible
diet--such as is advised in the article on INTESTINAL
INDIGESTION--should be prescribed. In constipation connected with
membranous enteritis a similar system of diet is proper. The drugs
given should be those which aid intestinal digestion, and reference
must be made again to this subject, already treated of. Many cases of
constipation can only be cured by this treatment; the routine treatment
by purgatives and a diet of vegetables and fruits would aggravate and
not relieve. A course of exclusive milk or skim-milk diet, if
persevered in for some weeks, will cure cases of constipation of this
kind without the use of laxatives. Of course a purgative must sometimes
be given if enemata fail, but the least irritating one should be
selected.

The mineral waters best suited to constipation depending upon
intestinal catarrh are in this country those of the Rockbridge Alum
Springs and Capon Springs (Va.), the California Seltzer Springs, and
the milder {653} waters of Saratoga. The most suitable from Europe are
the waters of Apollinaris, Vichy, Buda, Vals, Ems, Salzbrunn, Selters,
Mt. Dore, and Kissengen. The warm baths of Virginia (Warm Springs, Hot
Springs) are useful in increasing the activity of the skin and in
giving relief to the catarrhal state. A month spent at the Warm
Springs, with a daily bath the natural heat of which is 98 degrees,
will work a complete transformation in the abdominal circulation. This
should be conjoined, of course, with a properly-regulated diet and
exercise. Another month spent at the Rockbridge Alum Springs will
complete the restoration of the bowel to a normal state. It is much to
be regretted that the really valuable mineral springs of Virginia lack
so many of the comforts which the invalid requires. In cases where it
is more convenient a stay at the Arkansas Hot Springs is to be
suggested, and for obstinate cases of intestinal catarrh with sluggish
circulation, obesity, and gouty tendencies these springs are to be
preferred. A season at some of the mineral baths of Europe, as
Aix-la-Chapelle, followed by the strict regimen of the grape cure (as
at Bingen, Durkheim, Vevay, Montreux, or Meran), is a rational mode of
treatment which offers an almost certain prospect of cure.

If the case is one of atony of the colon due to impaction of the rectum
and dilatation of the rectum and colon, without gastric or intestinal
indigestion, a quite different regimen is required. The constitution
and mode of life are the guides to the general plan to be followed.
Sedentary pursuits are to be given up as far as possible. Long
vacations and travel must be insisted on, with active exercise by
walking and riding; also cold bathing or sponging, with brisk friction
of the whole body. Sea-bathing is useful both as an exercise and for
the effect upon the sluggish peripheral circulation, but the slothful
life at the seashore, with over-indulgence in eating and drinking, is a
source of more harm than good. Warm baths, and cold douches to the
abdomen, compresses of cold water or of alcohol, the cold douche to the
spine while in the hot bath, are all beneficial. Massage for women,
children, and feeble persons takes the place of exercise. The kneading
of the muscles over the abdomen can be combined advantageously with an
effort to accelerate the passage of the contents of the colon by
manipulation in the direction of movement.

The interrupted electrical current, used for the purpose of developing
the feeble abdominal muscles, is a source of much advantage.[45] But to
be of service it should be persevered in for months, the patient
himself making the application under the direction of the physician. In
addition, the introduction of one insulated electrode into the rectum,
while the other is in contact with the abdominal muscles or along the
line of the large intestine, has been advised. The Swedish movement
cure may be a useful aid in some cases. The movements exercise the
muscles of expulsion. These are deep inspiration, flexion and extension
of thighs or trunk, twisting the trunk, pressure on the abdomen and
colon, stroking in the direction of fecal movement.

[Footnote 45: S. T. Stern, "Die faradische Behandlung der Obstipation
und der nervosen Enteropathie," _Centralblatt fur Newenheil_, 5 Jahrg.,
Mai, 1882, p. 201; also, I. Althaus, "Treatment of Obstinate
Constipation by Faradization of the Bowel," _Lancet_, London, 1867, ii.
606.]

In the relaxed condition of the abdomen in women who have borne {654}
children or in old persons the wearing of an abdominal support
sometimes gives help and comfort.

The best diet for cases of atony of the colon and rectum is one which
is easily digested and has a moderate amount of waste, as a full colon
will stimulate muscular action. Various articles are suggested with a
view to excite peristalsis by irritation of the mucous surface, but as
such substances are in themselves insoluble and innutritious, it is
unwise to resort to them. The following list includes the foods
suitable to such cases: Fresh vegetables, as spinach, raw or stewed
tomatoes, lettuce, kale, salsify, peas, asparagus, kohlrabi, and other
summer vegetables; in winter canned vegetables, if well prepared, take
their place. Among fruits, fresh fruit in general, especially grapes,
peaches, and oranges; dried fruit, as figs, raisins in small quantity,
stewed prunes, and baked or stewed apples, can be tried.

Too much vegetable matter is harmful, as the bowel is filled with an
excess of waste, much of which is undigested food; the quantity must be
regulated by the appearance of the stools and by the success of the
regimen. If the blockade continues obstinately, the vegetable diet
should be reduced. The microscope in many cases can alone decide the
amount of undigested vegetable matter. Meats are all advisable in
moderation. The least digestible, as ham and veal, are to be avoided.
Graham-flour bread, brown bread, or bran bread are better than bread
made of the best bolted flour. The first is more digestible, and bran
bread[46] is thought to increase peristalsis, but this is a doubtful
effect. Oatmeal well boiled, fine hominy, corn meal, or cracked wheat
with milk are pleasant and digestible. A cup of cafe au lait at
breakfast or before breakfast is the best morning drink;[47] it has a
laxative influence. Tea is thought to have the opposite effect. Milk at
breakfast answers well for those who take it with relish. An orange on
rising in the morning is a pleasant remedy.

[Footnote 46: "The Efficacy of Bran Bread in relieving Despondency ...
dependent on an Irregular and Constipated State of the Bowels," _Journ.
Ment. Sci._, London, 1858-59, v. 408-411.]

[Footnote 47: "Treatment by Cafe au Lait," _Gaz. des Medecins prat._,
1840, No. 4, p. 13.]

Certain drugs are called for to aid these measures in giving tone
directly or indirectly to the weakened bowel muscles. Strychnia stands
first, but it woefully disappoints one who trusts much in the
theoretical arguments for its use. In fact, it may be said of all drugs
given for constipation that they stand in a very subordinate rank to
the measures already discussed. They should be thought of last, not
first, and but little confidence should be put in the vaunted value of
new drugs. Strychnia can be combined in anaemia and debility with the
dried sulphate or carbonate of iron, and with quinia or arsenic,[48] or
in feeble digestion with dilute hydrochloric acid and pepsin.
Belladonna was advised by Trousseau as a stimulant to unstriped
muscular fibre, and it can well be given with strychnia; ipecacuanha
and atropia are approved of in conjunction.[49] A pill of ergot,
belladonna, and strychnia would answer the indication of a feeble
peristalsis. DaCosta has suggested giving one drop {655} of the fluid
extract of belladonna with compound tincture of gentian or cinchona
three times daily after meals. The sulphate or valerianate of zinc,
oxide of zinc, extract of valerian or gentian, capsicum, or black
pepper can be tried in pill form with belladonna and strychnia.

[Footnote 48: Bartholow thinks arsenic overcomes constipation when due
to deficient secretion and dryness of the feces (_Mat. Med._, New York,
1879, p. 129).]

[Footnote 49: Legros and Onimus, _Journal de l'Anat. et de la Phys._,
t. vi. pp. 37 et 163. Ringer says one grain of ipecacuanha taken while
fasting each morning will relieve constipation from torpor
(_Therapeutics_, New York, 1882, p. 438).]

These remedies are slow-acting, and in the mean while the bowels must
be moved artificially, methodically, and taught to act at stated hours.
For this purpose a small enema of cool or cold water at the same hour
every day after breakfast does well. It is irrational to distend the
bowel, already weakened by distension, with large enemata of warm
water. Recourse should not be had to this until all hopes of effecting
a cure are gone, or only as an occasional remedy in impacted
accumulations where the mass must be softened before it can be removed.
If the enema does not in time empty the colon sufficiently, laxatives
will have to be taken with some regularity until the habit is created.
A tumblerful of water with or without a teaspoonful of salt, or a
tumblerful of any alkaline water charged with carbonic acid, taken on
rising in the morning, may prove effective. A tablespoonful of sweet
oil at night acts well as a lubricator and softens the feces. If these
more simple means fail, it becomes unfortunately necessary to give a
purgative drug: any one of this class can be combined with strychnia,
belladonna, vegetable tonics, and iron. Those to be preferred are
aloes, colocynth,[50] and podophyllin. The compound podophyllin pill or
a pill of one-sixth of a grain of belladonna and podophyllin at night
or three times daily, the pill of aloes and myrrh, or the Lady Webster
pill, are well-approved forms of administration. A compound rhubarb
pill acts well if taken after dinner.

[Footnote 50: A few drops of the Prussian tincture of colocynth several
times daily is advised by Ringer (_Therapeutics_, New York, 1882, p.
642).]

If one desires to select a purgative which will probably increase the
outflow of bile, selection can be made from the following drugs:
podophyllin, aloes, rhubarb, colchicum, euonymin, colocynth, calomel,
jalap, sodium sulphate, potassium sulphate, cream of tartar; and among
the rarer alkaloids iridin, sanguinarin, physostigma, and juglandin.
These, according to Rutherford, Vignal, and Dodds, increase the
secretion of bile in fasting animals. Ox-gall and pig-gall are
laxatives only; they have no effect on the liver, but can be added to
other purgatives in pill forms.

Salines largely diluted may be given to strong adults: Epsom or
Rochelle salts quite early in the morning, a solution of sulphate of
magnesia with dilute sulphuric acid, to which dried sulphate of iron
may be added, are quite popular; and of the bitter waters, Hunyadi
Janos, Friedrichshall, or Pullna water serves the purpose. One grain of
sulphate of quinia added to a saline will increase its effect. The
milder laxative waters are to be preferred to the bitter waters. The
Saratoga waters, Congress, Geyser, Hathorn, answer the purpose taken
early in the morning, or among the European springs those of Kissengen,
Plombieres, Marienbad, Homburg, Seltzer, or Leamington in England, are
not too active in their effects. In atonic constipation, the form now
under consideration, the laxative chalybeate waters are indicated where
there is anaemia or debility. These are represented by the Columbian,
Pavilion, Eureka, and Excelsior Rock among the Saratoga waters, and by
the Bedford Springs water.

{656} It is well to administer a number of drugs in rotation in
habitual constipation, as the susceptibility to a particular drug is
lost after continued use. Increase of the dose is the usual method to
offset this result, but it is irrational to meet exhaustion by
over-stimulation. Rest of the part stimulated by using a remedy which
brings about the result in a different way is the wiser course. The
dose should be gradually reduced, tempting the bowel to act more and
more without aid. Among the laxatives which can be borne in mind in
alternating treatment the following list includes some which can be
used with advantage: the fluid extracts of rhamnus (buckthorn) and
cascara sagrada; alum, which is called for in certain forms of atony;
sulphur in the form of confection or sulphur with guaiacum[51] (half a
drachm of each in powder at night); the wine of colchicum (five drops
or more three times daily), advantageously used in gouty or rheumatic
persons; the infusion or tincture of euonymus; the tincture of benzoin;
senna in fluid extract and in the compound powder of liquorice.

[Footnote 51: Fuller, _Lancet_, London, April 23, 1864, p. 459.]

Infants and children should be cured of constipation without purgatives
if possible. Attention to the diet of the infant, and close inspection
of the stools to see the effect of the food given, will guide to a
proper system of feeding. Breast-milk is the best remedy; next, a food
which most nearly resembles mother's milk--cow's milk properly diluted
with barley-water, oatmeal-water, or rice-water--stands first.
Condensed milk, given in barley- or oatmeal-water, is a second and
excellent substitute in cities. Antacids prevent a too rapid
coagulation of the casein and the formation of curdy lumps. Lime-water
with milk or bicarbonate of potassium or of sodium may be administered
with the food or before it. The quantity of food must be lessened until
the child can digest all it takes.

The infant should be taught to empty the bowel at the same hour daily
by always placing it at this hour in a position favorable to and
suggestive of defecation. Dilating the sphincter at the same time with
the soap suppository or the small end of a Davidson's syringe, or just
touching the margins of the anus, will excite the necessary reflex
movement. If defecation is painful, examine the inner edge of the anus
for small cracks or for eczema ani.[52] Over-stretching the sphincter
with the finger in cases of rigid or spasmodic contractions will
sometimes produce permanent relief.

[Footnote 52: Betz, "Eczematous Proctitis," _Memorabilien_, iv., Dec.
28, 1859, S. 190.]

In children the question of diet is equally important. Most cases of
constipation in them originate in intestinal catarrh from improper diet
and over-feeding. Strict rules of diet should be rigidly enforced, and
each case receive special study in order to determine upon the best
dietary. The minutest details of the child's life, its habits and
surroundings, are to be controlled so as to secure the best possible
influences for health. Feeble development and muscular inertia must be
remedied by change of climate and tonics--iron, strychnia, and
cod-liver oil. When other methods fail to give early relief, a
purgative may be needed. Rhubarb, magnesia, calomel, Friedrichshall or
Hunyadi water, given in milk, the compound liquorice powder, the
compound anise {657} powder, are better than the more active
cathartics.[53] Habitual administration of laxatives to children ought
to be regarded as a confession that the case is incurable; it is a last
resort, for which necessity is the only argument.

[Footnote 53: The compound anise powder, a non-officinal preparation in
use in Washington, is a convenient form of administration: heavy
calcined magnesia, 360 grs.; rhubarb powdered, 180 grs.; oil of anise,
40 minims; stronger alcohol, one fluidrachm. The bicarbonate or fluid
magnesia is also a good preparation. Ringer knows nothing so effectual
in bringing back the proper consistence and yellow color to the motions
of children as podophyllin. Dissolve one grain of the resin in one
drachm of alcohol, and of this give one or two drops on a lump of sugar
twice or three times a day (_op. cit._, p. 458). Bouchut suggests the
same solution, with simple syrup as a menstruum.]

In old persons tonics should be combined with the laxatives, as
strychnia, iron, quinia, gentian with aloes, colocynth, rhubarb, or
podophyllin. The rectum should always be examined, as impacted fecal
masses will often be found there.




{658}

ENTERALGIA (INTESTINAL COLIC).

BY W. W. JOHNSTON, M.D.


SYNONYMS.--Enterodynia, Tormina, Colicodynia, Colalgia, Dolor colicus,
Passio colica, Spasmus intestinorum, Ileus spasmodicus, Spasmus
ventriculi, Neuralgia mesenterica; Spasm of the bowels, Cholick or
Cholick Colic, and Pain in the Belly; _Ger._, Das Banchgrimmem, Die
Kolik; _Fr._, La colique.

HISTORY.--Colic is described by Hippocrates.[1] He recommended the use
of emetics and gave other sound advice regarding the treatment of the
affection. Galen[2] administered sedatives, as opium and henbane, and
he advised them to be combined with carminatives. Aretaeus[3] speaks of
the pain of colic extending to the back, limbs, and testicles, and also
states that when affecting the sides of the body it may be confounded
with pleurisy, hepatitis, or splenitis. Alexander[4] points out the
differential diagnosis of the disease and directs a proper course of
treatment. Cupping, friction of the extremities, and dry fomentations
were recommended by Celsus;[5] and internally he advocated a mixture of
poppy, anise, pepper, etc. Aetius[6] describes the affection.
Serapion[7] and Avicenna[8] treated of colic more clearly than any
previous writers had done, and advised narcotics administered by the
mouth and rectum. Atony of the bowels is given as a cause of the
disease by Haly Abbas,[9] and Alsaharavius adds[10] to the etiology a
hot intemperament, indurated feces, and poisonous medicines. Rhazes[11]
directs the administration of emetics when the colic is due to
indigestion.

[Footnote 1: _De Affect._, xv.]

[Footnote 2: _De Med. Sec._, loc. ix.; iv., de loc. _Affect._, vi. 2.]

[Footnote 3: _Morb. Acut._, ii. 6; _Chron._, ii. 8.]

[Footnote 4: Lib. x. 1.]

[Footnote 5: _Medicina_, Libri octo, iv. 14.]

[Footnote 6: Lib. iii. 1, 29.]

[Footnote 7: iii. 32.]

[Footnote 8: iii. 16, 4.]

[Footnote 9: _Pract._, vii. 28.]

[Footnote 10: _Ibid._, xvii. 2, 12.]

[Footnote 11: Divis. 69.]

NATURE AND DEFINITION.--Enteralgia is the name given to intestinal pain
which is independent of indigestion and of inflammation or other
organic change in the wall of the bowel, and corresponds to gastralgia
and other visceral neuralgias. It involves the nerves which pass to the
intestine along the line of attachment of the mesentery, and which are
derived from the superior mesenteric plexus, with a prolongation from
the junction of the right pneumogastric nerve with the coeliac
plexus.[12]

[Footnote 12: The very extensive distribution of terminal
nerve-filaments in the intestine is an explanation of the frequency and
severity of attacks of intestinal pain. "We may form some estimate of
the extent to which the nervous system of the intestines is developed
from the fact that about one hundred ganglia belonging to the submucous
and over two thousand to the myenteric plexus are to be found in one
square inch of the intestine of the rabbit" (Frey, _Histology_, New
York, 1875, p. 493).]

{659} The pain of enteralgia is not spasmodic, and is not accompanied
by flatulence, borborygmi, or other signs of indigestion and gaseous
distension of the bowels.

Colic, on the other hand, applies to intestinal pain accompanied by
indigestion, distension of the bowel with gas, or the contact of
irritating ingesta. The pain is spasmodic, and is relieved by the
passage of gas and other contents from the bowel. The pain is due to
the local irritation of the richly-gangliated plexus of nerves seated
in the submucous layer and which extends from the pylorus to the anus.

At present enteralgia must be considered from its symptoms and from
post-mortem examinations as a pure neurosis of the sympathetic system.
Opportunities are rarely offered for studying the post-mortem
appearances of the disease, from the fact that when idiopathic it
seldom ends fatally. Out of forty-nine autopsies on patients who had
suffered from colic due to lead-poisoning, only one was found with any
change of the abdominal ganglia of the sympathetic. Segoud found the
ganglia and some of the fibres of the sympathetic hypertrophied and
indurated,[13] and "in recent times Kussmaul and Maier have published
an example of sclerosis of the coeliac and superior cervical
ganglia."[14]

[Footnote 13: Segoud, _Essai sur la Nevralgie du Grand Sympathique_,
Paris, 1837.]

[Footnote 14: M. Rosenthal, "Diseases of the Nervous System," _Wood's
Library_, New York, 1879, vol. ii. p. 265.]

The pathology of enteralgia due to a vitiated state of the system, a
morbid condition of the tissues of the intestines, the presence of
irritating ingesta, or to reflexion from other organs, differs in no
wise from a neuralgia of other parts arising from constitutional,
local, or reflex causes. Pain will likewise manifest itself here in
consequence of deleterious substances circulating in the blood, as in
Bright's disease, rheumatism, gout, or lead-poisoning. The terminal
nerve-fibres of the intestines are irritated in attacks of colic by
substances or food within the alimentary canal; gases are generated
from the decomposition of the ingesta. The consequent dilatation of the
gut produces loss of tone and abolition of the contractile power of the
muscular coat. Constipation and pain from pressure exercised on the
neighboring nerves will be the result.

Obstinate constipation, and even symptoms resembling ileus, may arise
from a portion of the intestine thus distended becoming bent upon
itself, the sharp angular flexure interrupting or completely
obstructing the passage of the feces.[15]

[Footnote 15: F. H. Hamilton, _Med. Gaz._, New York, 1880, vii. p. 3.]

ETIOLOGY.--Enteralgia may be either idiopathic or symptomatic. The
causes can best be considered by dividing them into general and reflex.

Under the head of general causes may be mentioned an inherited neurotic
temperament, particularly in individuals of a hypochondriacal tendency.
Females are far more apt to suffer from this affection than males, on
account of their more impressionable nature and greater liability to
nervous diseases in general. Hereditary tendencies, overtaxing the
mental powers during the developmental period of youth, and later in
life excessive mental labor and anxiety of business affairs, are
causes. It may occur in the cachexia developed during the course of
many chronic diseases, as diarrhoea, rheumatism, gout, phthisis,
cancer, Bright's disease, etc. Various morbid conditions of the blood
are followed by {660} enteralgia, as anaemia arising from prolonged
lactation, masturbation, or venereal excesses, and the presence of
various blood-poisons, as syphilis, malaria, lead, copper, and arsenic.
Other causes are living in cold, damp climates, with sudden changes of
temperature and chilling of the body. Persons addicted to the use of
tobacco or alcohol and to dissipations of various kinds may become
predisposed to enteralgia. Idiosyncrasy is a predisposing cause.

Enteralgia is often secondary to ovarian, uterine, or other distant
disease. Also, owing to intimate sympathetic relations, pain is often
felt in the bowels as a result of disease situated in some of the solid
abdominal viscera, as the liver, spleen, and pancreas. In the same way,
organic affections of the brain and spinal cord, especially acute
myelitis and spinal sclerosis and lesions of the vertebral bones,
excite intestinal pain. Emotion may also bring it about. The
application of cold to the feet or catching cold in general is followed
by pain which is due to reflex influence.

There may be a predisposition to colic from hereditary influence and
the neurotic temperament. A feeble digestion is a source of constant
risk. Much of the pain occurring in the course of dysentery, catarrh of
the bowel, invagination, fecal impaction, and other structural
affections is of the nature of colic. The most frequent by far of the
local causes is the direct irritation of the terminal nerve-fibrils by
substances within the alimentary canal and by over-distension of the
bowel with contained gas. Some of these irritants are partly-digested
and indigestible articles of food; food taken cold or in excessive
quantity; the decomposition of food and consequent distension of the
bowel by gas. Acid drinks and alcohol have the same effect.
Constipation with scybalae may produce colic in an otherwise healthy
person. A morbid state of the intestinal secretions, either as regards
quantity or quality, is said to have a like result, but this is a
doubtful cause. Foreign bodies within the canal, as fruit-stones,
various concretions, worms, and gall-stones if of large size, may
produce pain during their passage through the bowel. Cathartic
medicines may be enumerated as among the local causes, and also various
poisonous drugs. Lesions of any sort seated in the intestinal wall, as
ulcers and neoplasms, induce paroxysmal pains.

SYMPTOMS.--The pain of enteralgia occurs in attacks which come on
slowly and continue for a variable time--some hours or days. The pain
is situated about the umbilicus, and is relieved by deep pressure,
although at the same time there may be hyperaesthesia of the skin. The
intensity of suffering ranges from a dull heavy pain to one which is
acute and lancinating. Retraction of the abdomen is common, but there
may be tympanites. No signs of indigestion may appear, but eructations
of tasteless gas, or even borborygmi, may be complained of.

The duration of an attack of enteralgia is variable and depends to a
great extent upon the cause. Usually, when the symptoms are severe, the
duration is short. It may pass off in less than an hour, or a
succession of paroxysms continue to recur, and the attack will be kept
up for several days, weeks, or even a month. One seizure predisposes to
another, and each is liable to be more severe than its predecessor.

The malady may end gradually or as rapidly as it was ushered in.
Attacks are often mitigated, or even terminated, by the occurrence of
some other morbid condition--by a profuse sweat, the discharge of
lochia, {661} the menses, or some secretion which has been checked. The
development of rheumatism or gout may relieve it. Attacks often
terminate with vomiting, belching, and more especially with movements
of the bowels and discharge of flatus. A free emission of pale,
colorless urine is sometimes followed by relief. This occurs in
hysterical cases, and the disease is generally accompanied with some
uterine disorder and with tenderness along the spine.

The attack of intestinal colic may be developed suddenly and with full
intensity, or it may be preceded a short time, usually a few hours, and
rarely much longer, by prodromic symptoms. These are nausea, a
sensation of weight in the epigastrium, anorexia, eructations,
tympanites, rumbling, and slight griping pains. The patient is
irritable and restless, his bowels are usually confined, and urination
is often rendered painful by the distended bowels pressing upon the
bladder.

These symptoms, which are in truth but a part of the attack, being only
of a lower grade, increase in severity and the pain becomes more acute
and distinctly paroxysmal. It is of a sharp cutting, twisting, or most
frequently griping character, and is in the earlier part of the attack
usually referred to the umbilicus or to one of the iliac fossae, and
sometimes radiating thence in different directions. Generally it
becomes concentrated about the umbilicus. The exacerbations of pain
vary in degree of severity, in duration, and in frequency of
recurrence, while the intervals may afford complete relief or merely a
remission of the acute suffering. The sufferer either lies quietly upon
his abdomen or upon one side or the other, with his body bent forward
and thighs flexed, or he is restless and writhes in pain, groaning and
crying out from the intensity of suffering. He may seek relief by
trying a variety of positions and by pressure applied with the hands or
some solid object against the abdomen. Anxiety and pain are depicted in
his features. His face and extremities are cool and covered with a
clammy sweat. The pulse is small, hard, and generally slower than
normal. Breathing is sometimes oppressed, as a result of spasmodic
contraction of the abdominal and thoracic muscles. Often the muscles of
the hands, calves of the legs, and the feet are similarly affected. The
tongue is moist and as a rule clean. The bowels are constipated--at
times so much so as to amount to obstruction--or, again, diarrhoea and
tenesmus may be present.

Other abdominal symptoms are nausea or vomiting, eructation of gas, and
borborygmi. Micturition is at times urgent and painful, and the
testicles are frequently retracted.

The abdomen is occasionally tender, but pressure generally affords
relief. It is distended with gas, especially over the large bowel.
Palpation often reveals lumps or knots situated within the abdominal
walls and due to spasmodic contraction of its muscles, particularly of
the recti. In thin persons the constricted and dilated coils of the
intestines can also be distinguished as nodular masses which rapidly
alter in shape and position.

The severity of attacks of colic varies from a few slight griping pains
felt at intervals to a seizure of such intensity that the patient
suffers agony and presents symptoms of an alarming nature. Fortunately,
these grave cases are comparatively seldom observed. In them the local
and general symptoms are aggravated. Pain is more intense and {662}
constant, having less marked intervals of relief, and the patient may
pass into collapse, with a small, rapid, and wavering pulse, restricted
respiration, shivering and chilliness, and a cool, clammy skin. The
abdomen is greatly distended; hiccough comes on, also stercoraceous
vomiting, tenesmus, and in the worst cases involuntary stools and
suppression of urine. Nervous symptoms have been observed, as dizziness
or fainting, and finally delirium and convulsions may end the scene.

VARIETIES.--Attention has been called to a distinct form of enteralgia
due to the effects of alcohol.[16] It affects steady drinkers, and is,
as a rule, met with only during the hot months. The presence of
undigested food within the alimentary canal or exposure to cold may act
as exciting causes of the disease. The development is usually gradual.
Dull pains, felt at first over the abdomen, become later more
continuous and fixed about the epigastrium or umbilicus. Sometimes they
are complained of more over the bladder. Bilious vomiting and hiccough
are prominent symptoms; the patient is thirsty, and the liquids taken
only promote vomiting; and the bowels are constipated. There is
restlessness, and sleep is obtained with difficulty. Paralysis at times
supervenes, and affects the lower as well as upper extremities. In the
worst cases delirium and even convulsions occur. The disease nearly
always ends in recovery in from three to ten days. Severe intestinal
and gastric pain occurs in opium-eaters, but especially in women who
use morphia in excess. The suffering is always greater when the opiate
is reduced, but can only be cured by breaking up the bad habit.

[Footnote 16: Colica bacchanalium, J. H. Claiborne, _Med. Monthly_, New
York, 1855, p. 227.]

A variety of colic which occurs epidemically[17] in some of the
inter-tropical countries has been studied and described by different
observers. It is known by various names, such as colique seche; colique
vegetale; rachialgie vegetal; colic of Poitou, of Devonshire, of
Madrid, of Java, of Surinam; colique nerveuse; endemique des Pays
Chauds (Fonssagrives); endemic colic, dry colic, bilious colic, nervous
colic; girafy; dandy, etc. Segoud called it a neurosis of the great
sympathetic, and attributed the disease to the effect of cold.[18] The
symptoms resemble, in many respects, those of lead colic, and at one
time they were erroneously considered identical with it.[19] Thompson
and Chisholm,[20] after an {663} experience with the disease in the
West Indies, assert that such is not the case. Epidemics which occurred
in Madrid and several of the Spanish provinces, and many hundred cases
witnessed among the French soldiers by other observers, were
ascertained not to be due to lead-poisoning.

[Footnote 17: Colique vegetale, or endemic and epidemic colic, did not
escape the notice of the older writers. It is mentioned by Aretaeus;
Paulus AEgineta describes an epidemic of the disease which extended
through Italy and a large part of the Roman empire, and he states that
attacks were often followed by paralysis. Francois Citois gives an
account of an epidemic which raged at Poitou in 1616. Monson Smith
described the disease in 1717. In 1724 it appeared in Devonshire,
England, and presented the characteristic symptoms and sequelae. In
more recent times epidemics of the disease have occurred in nearly all
the countries of Europe. It prevailed in the northern part of France
and in Belgium from 1853 to 1859, inclusive. It has likewise visited
the Caribbee Isles, Cayenne, Guadaloupe, Madagascar, India, the West
Indies, some of the provinces of Spain, Java, the west coast of Africa,
the Antilles, Senegal, New Zealand, Brazil, and various other
localities. The disease occurs in all seasons, but is more prevalent in
summer and in the commencement of autumn.]

[Footnote 18: Segoud, _Essai sur la Nevralgie du Grand Sympathique_,
Paris, 1837.]

[Footnote 19: The disease frequently appeared on board of French
war-vessels, and was regarded by Lefevre (_Recherches sur les Causes de
la Colique seche_) as due to lead-poisoning. He asserts that lead is
more used in French ships than in those of other nations, and accounts
for its being epidemic in tropical countries because a warm climate
aids in developing the affection, and because there men drink more
freely of water. (See also Dutrouleau, _Arch. gen._, 1855, "Mal des
Europeens dans les Pays Chauds.")]

[Footnote 20: Quoted by Oppolzer, _Wien. med. Woch._, Bd. xvi., 1867,
p. 724.]

The affection is not accompanied with any constant lesion. Pascal[21]
made post-mortem examinations in six cases and found the mucous
membrane of the duodenum a little reddened: the gall-bladder contained
thick bile, and in a few cases there was congestion of the sympathetic
ganglia. The attack is usually marked by certain prodromic symptoms.
The patient complains of malaise, loss of appetite, a load in the
epigastrium, embarras gastrique, dull pains in the colon, borborygmi,
and cramps or tingling in the limbs. For the first few days the bowels
generally move several times daily. The stools are difficult, painful,
and of a black or dark-green color, offensive odor, and accompanied
with the discharge of flatus. As the disease progresses the bowels
become constipated and the discharge of gas ceases. After a few days
the pain is more severe and radiates to the lumbar region, the
testicles, or the thighs. It is seated principally in the epigastrium,
in the line of the transverse colon, or it may involve the whole
abdomen. Movement aggravates the pain, while pressure often relieves
it. The tongue is large, trembling, and coated white or yellow; the
breath is fetid, the saliva viscid, and mouth sticky. Anorexia is
complete; there are hiccough, nausea, vomiting of undigested food and
mucous or bilious matters, and constipation with hard black stools. The
patient is restless and sleepless. The abdomen may be distended or
retracted, and micturition is often painful and the urine high-colored.
The pulse is generally slower than in health, but becomes accelerated
when the attack is over. The skin is pale, the conjunctiva often
stained with bile, and in the later stages oedema of the lids and
emaciation come on. The effect upon the nervous system may manifest
itself by amaurosis, deafness, delirium, mania, coma, epileptiform
convulsions, or paralysis. The paralysis affects the extensors of the
hand, arm, and leg, or it may become general and end in death.

[Footnote 21: "Recherches anatomico-pathologique sur la Colique dite de
Madrid," _Rec. de Mem. de Med. mil._, Paris, 1826, xix. pp. 98-113.]

The duration of the disease is from eight to fifteen days, but in some
cases it becomes chronic. Relapses frequently occur. At times
intermittent or remittent symptoms develop, and occasionally the
affection is complicated with enteritis or peritonitis. The prognosis
depends very much upon the character of the epidemic, and the most
serious cases are those accompanied with either cerebral symptoms or
peritonitis.

The paralysis sometimes passes off in a few days, but oftener lasts
indefinitely. Emetics, purgatives, and anodynes are recommended in the
treatment of the disease, and frequently a change of climate is
necessary in order to recover fully from the affection.

DIAGNOSIS.--The diagnosis of enteralgia usually presents some
difficulty even when the symptoms are well marked. That the disease is
a true neuralgia is apparent from the periodical recurrence of the
pain, its sharp and darting character, from the sudden cessation
followed by complete relief, and from the absence of symptoms of
indigestion. Affections bearing a certain resemblance to enteralgia are
to be excluded.

In lumbo-abdominal neuralgia the pain is unilateral and extends around
{664} to the back. Tender spots can usually be detected by pressure on
the umbilical or hypogastric regions or on the spinous processes of the
vertebrae. In dermalgia the soreness is superficial, and light pressure
gives more pain than deep compression, while nervous and hysterical
symptoms are constantly associated with this form. Gastralgia is more
frequent than enteralgia, and the pain is located about the ensiform
cartilage. In myalgia of the abdominal parietes pressure causes pain,
as do also movements of the body, coughing, sneezing, etc. Rheumatic
pains would likely be felt in other muscles. In ileus the pain is more
continuous, the tenderness localized; there is constipation of a most
obstinate character, and vomiting of stercoraceous matter. The patient
has an anxious expression and a rapid, feeble pulse. In renal calculus
the pain is situated in the course of the ureter and shoots down to the
pubes and thighs. There is frequent desire to urinate, accompanied by a
scanty discharge of urine, and a copious flow of urine is followed by
cessation of pain. The maximum of pain in hepatic colic is situated in
the right hypochondrium, and is often reflected into the shoulder of
the same side. Icterus may also be expected. Colic arising from
lead-poisoning is usually associated with sufficiently characteristic
symptoms to render the diagnosis easy. When syphilitic the pain is apt
to be most severe at night.

In catarrh of the bowel the skin is hot and dry, the pulse accelerated,
and other indications of a symptomatic fever are presented. The pain is
more constant, more localized, and pressure causes it to be increased.
Tenderness on pressure is not invariably met with, but the rule holds
good that when deep pressure increases the pain inflammation rather
than enteralgia is indicated.

If colic is due to indigestible food, a sensation of weight will be
complained of at the epigastrium, griping pains occur at short
intervals, with flatulence, vomiting, and later diarrhoea. If the
attack be wind colic, the abdomen is enlarged by tympanitic distension;
borborygmi and belching occur. If it is the result of accumulation of
feces, there would be a previous history of constipation, and the lump
of feculent matter can be located by palpation and percussion.

PROGNOSIS.--The prognosis of idiopathic enteralgia is favorable, the
disease generally terminating after a variable period. Attacks are very
apt to recur, and each one will, in all probability, prove more severe
than the preceding. In symptomatic enteralgia the prognosis will depend
upon the nature of the fundamental disease.

Colic terminates favorably in nearly every case. Death has rarely
occurred from complications, as convulsions, and rupture of the bowel
has been observed from great distension.

TREATMENT.--If attacks of enteralgia are associated with hysterical
symptoms, it would be proper to employ antispasmodic sedatives. The
compound spirit of ether is very useful in these cases, especially if
they are accompanied with flatulence. Rubbing the spine with
stimulating or anodyne liniments frequently promises well. The
hypodermic dose of morphia gives relief more quickly than can be got in
any other way, but in pure enteralgia with frequently recurring
paroxysms care must be taken not to create the demand for the remedy by
giving it often. The radical cure of the disease is a more important
matter than the treatment of the acute attacks.

{665} If the cause of enteralgia be located in some of the solid
viscera or in the nervous system, remedies should be addressed to these
parts, and the reflex nervous impressions allayed by the bromides or
other nervous sedatives. The valerianate of zinc in doses of one grain
three or four times a day is extremely useful in neuralgia from reflex
irritation of the female pelvic organs. Constitutional remedies are
indicated in the cases due to a morbid condition of the blood--iodide
of potassium and mercury if a syphilitic poison or if of a rheumatic or
plumbic origin; colchicum if gouty; quinia if malarial; and iron when
an anaemic state is presented. H. C. Wood states that alum is used with
success; being of service when there is no lead in the primae viae, it
must act in some other way than as a chemical antidote. Arsenic is very
highly recommended in idiopathic enteralgia. Excellent results have
been reported from the use of nitrate of silver,[22] hydrocyanic acid,
belladonna,[23] and iodoform. Change of climate and travel may have to
be resorted to in obstinate cases.

[Footnote 22: Nauman, _Deutsche Klinik_, Bd. iii., 1851, p. 388.]

[Footnote 23: _Lancet_, vol. i., 1867, p. 81.]

The objects of treatment in colic are to relieve suffering and
terminate the attack as soon as possible. For this purpose the various
anodyne and antispasmodic remedies, as opium, hyoscyamus, chloral,
ether, chloroform, Indian hemp, and camphor, may be employed.
Carminatives are most useful, alone or combined with anodynes and
cathartics. Oleum cajuputi often affords immediate relief. Warm teas of
chamomile, ginger, valerian, or peppermint sometimes do good. When the
suffering is very acute nothing acts so promptly as a hypodermic
injection of morphia, either alone or combined with atropia.

The surface of the body should be kept warm, and hot applications to
the abdomen assist in relieving pain. The heat may be conveniently
applied by means of poultices, hot salt- or sand-bags, or rubber
bottles filled with hot water. Cold,[24] used externally, is more
grateful in some cases, and is preferable if there be much tympanites.
Sinapisms, turpentine stupes, and stimulating and rubefacient liniments
answer well in some cases, and should be tried. Anodyne applications to
the spine occasionally do good, and cold, applied by means of the
spinal ice-bag, is recommended by Ringer.

[Footnote 24: Roux, _Journal de Medecine_, Paris, 1765, p. 48.]

In order to treat the disease successfully and bring the attack to an
end, its cause should be ascertained if possible, and remedies directed
to its removal. If it be the result of indigestion, the contents of the
stomach should be removed by emetics. Drastic or powerful cathartics
will only tend to aggravate the disease, and on that account mild
laxatives are to be preferred in all cases. Castor oil, calomel, pil.
rhei comp., senna, etc. may very properly be prescribed.

In flatulent colic means should be directed to expel the gas.
Anodynes--preferably chloroform--and carminatives should be
administered by the mouth, and enemata containing turpentine or
asafoetida injected into the rectum. In severe cases a clyster with ten
or fifteen drops of liquor ammoniae is said to do good. If distension
of the bowel be so great as to threaten rupture, it may with propriety
and safety be relieved by puncturing the colon with an exploring-needle
or a fine trocar. In cases of flatulent colic where the gas arises from
the decomposition of food {666} remedies to check fermentation, such as
alkalies, creasote, carbolic acid, or the sulphites, would be
indicated. Good sometimes results from pressure and massage of the
abdomen. Rubbing with etherized oils and electricity have also been
used successfully. If the attack be from fecal impaction, it may be
possible to liquefy and remove the mass by using saline cathartics, as
sulphate of magnesium, aided by large oily or mucilaginous clysters,
which in obstinate cases should be injected through a flexible rubber
tube passed up the rectum as far as possible. Injections of an infusion
of tobacco are now seldom used for this purpose, on account of the
dangerous symptoms which often supervene. If pain or tenderness be
present at the seat of impaction, cathartics should be used very
cautiously or not at all, and opium given instead. The administration
of this drug, by relieving pain and allaying spasmodic action, is often
followed by free catharsis.

Persons subject to attacks of colic may diminish the intensity, or even
prevent the recurrence, of the disease by employing during the
intervals such remedies as would be indicated in their individual
cases. Phosphate of sodium has been highly recommended for preventing
the recurrence of attacks of colic. R. N. Taylor states[25] that his
experience with the use of the drug is quite extensive, and he found
the treatment uniformly successful. Thirty grains dissolved in a
glassful of water may be taken three times a day--preferably before
meals--and this quantity should be reduced if it causes any irritation
of the stomach. The bowels should be regulated and strict attention
given to diet. A milk diet is of course best in obstinate cases. Any
article of food known to disagree must be excluded, and tea, coffee,
and alcoholic drinks should also be prohibited.

[Footnote 25: _Med. Herald_, Louisville, 1880-81, ii. p. 348.]




{667}

ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS, COLITIS,
PROCTITIS).

BY W. W. JOHNSTON, M.D.


SYNONYMS.--Enteritis, Catarrhal enteritis, Mucous enteritis,
Endo-enteritis, Ileo-colitis, Entero-colitis, Diarrhoea. Older
synonyms: Chordapsus, Cauma enteritis, Enterophlogia, Enterophlogosis,
Colica acuta seu inflammatoria, Ileus inflammatorius, Enteralgia
inflammatoria, Febris intestinorum seu Iliaca inflammatoria, Colique
inflammatoire.

HISTORY.--It is interesting to start at the fountain-head of the two
streams of inquiry--the clinical and the anatomical--and to follow each
in its widely-diverging wanderings until they unite to give to the
phenomena of intestinal inflammation a just interpretation.

The symptom diarrhoea was fully described by the earliest writers in
medicine.[1] The symptomatic differences between diarrhoea, dysentery,
and lientery and the different forms of diarrhoea (bilious, watery,
etc.) were given in detail by the Greek and Roman physicians. The
Arabians had a much more elaborate classification of the fluxes.
Avicenna made seven varieties of simple diarrhoea. European writers
followed closely in these footsteps. Sennert made twelve and Sauvages
twenty-one varieties of diarrhoea, depending upon as many different
causes, as undigested food, worms, the bile, etc. Many recent writers
have adhered closely to the older authors in their method of treating
of diarrhoea, regarding it as a disease and dividing it into varieties
based on the causes or on the appearances of the stools. Among them may
be mentioned Cullen (1789), Good (1825), Tweedie (1841), G. B. Wood
(1852), Trousseau (1865), and Habershon (1879).

[Footnote 1: J. J. Woodward, _Med. and Surg. Hist. of the War_, Part 2,
Medical Volume, foot-note, p. 273 _et seq._]

It was only after many years of laborious investigation that the
appropriate lesion was affixed to a symptom so well understood and
described in its clinical aspects. The first conception of abdominal
and intestinal inflammation had no relation to diarrhoea. Under the
name [Greek: eileos], Hippocrates described abdominal symptoms of
intestinal obstruction and inflammation. For Sennert (1641)
inflammation of the intestines meant peritonitis. Bonet (1679), Hoffman
(1710), and Boerhaave (1758) included under this head peritonitis,
ileus, and all febrile and painful abdominal affections. Sauvages
(1763) and Morgagni (1779) gave in detail the symptoms of peritonitis
and called the disease intestinal inflammation--enteritis. In 1784,
Cullen made an advance in subdividing {668} enteritis into e.
phlegmonodoea and e. erythematica--the one involving the entire wall of
the intestine and the peritoneum, the other the mucous membrane lining
the intestine. John Hunter (1794) first fixed the place of peritonitis
as a distinct affection from inflammation of the mucous membrane of the
intestines.[2]

[Footnote 2: J. Hunter, _A Treatise on the Blood, Inflammation, and
Gun-shot Wounds_, London, 1794, p. 284.]

Up to this time constipation was the chief symptom of enteritis. The
meeting of the streams, the affixing the symptom diarrhoea to its
appropriate lesion, was brought about hypothetically at first by J.
Carmichael Smith in these words: "I think it is probable (for we can
have no positive evidence of the fact) that in diarrhoeas from catching
cold the villous or interior coat of the stomach is sometimes slightly
inflamed."[3]

[Footnote 3: Paper read Jan. 8, 1788, _Med. Communications_, London,
vol. ii., 1790, p. 168.]

On the Continent enteritis soon after this was limited in its meaning
by Pinel (1798) to inflammation of the mucous membrane of any part of
the intestines. He gave the name catarrhal diarrhoea to the same
condition. A still further restriction of its meaning was made by
Broussais (1821), who defined enteritis to be an inflammation of the
mucous membrane of the small intestine; he gave the name colitis to the
same disease in the colon. This distinction was adopted by Rostan
(1826), Andral (1836), C. H. Fuchs (1846), G. B. Wood (1852),
Wunderlich (1856), Grisolle (1865), Flint (1866), and Aitkin (1868).
According to the views of some authors, chiefly English, as Copland
(1844), Bristowe (1871), Roberts (1874), Habershon (1879), enteritis
includes inflammation of the serous as well as of the mucous coat of
the intestines.

Niemeyer (1864), Jaccoud (1869), Leube (1875), Bartholow (1880), and
most German and French authors prefer the name intestinal catarrh as
applied to inflammation of the mucous coat; inflammation of the serous
coat is peritonitis; the word enteritis is abandoned as involving a
pathological error.

NATURE AND CLASSIFICATION.--Catarrh of the intestines is an
inflammation of the mucous membrane of the intestinal tract. There are
various peculiarities of the catarrhal process due to the anatomical
structure of the parts involved, the presence of open glands, lymphatic
follicles, etc. This disease is to be distinguished from inflammation
of the serous coat of the intestine (peritonitis). The two are quite
distinct in their etiology, pathological anatomy, and symptomatology,
although they have been often confounded under the same name,
enteritis.[4] As so much confusion prevails as to the proper meaning of
enteritis, it is best to abandon the word altogether.

[Footnote 4: For cases called enteritis in which the lesions of
peritonitis were found, see Hamilton, _Edin. Med. Journ._, vol. ii.,
1857, p. 304; also Breed, _Chicago Med. Examiner_, Oct., 1869, p. 579.]

Diarrhoea is still regarded by some authors (J. J. Woodward) as
synonymous with intestinal catarrh; by others it is considered
separately as a disease distinct from catarrh. Habershon describes the
lesions of catarrhal diarrhoea and mucous enteritis almost in the same
words.[5] It is an unscientific method to take one symptom of a
pathological state, to {669} erect it into a disease, subdividing it
into varieties which are but differences in the intensity of its
manifestation, and to assign to it no fixed lesion. Diarrhoea is in
reality but a sequence and symptom of hyperaemia or inflammation of the
intestinal mucous membrane.

[Footnote 5: Such a method of treating the subject involves a
repetition, with an inversion, of the same description. Thus, catarrhal
diarrhoea has as its lesion mucous enteritis; mucous enteritis has for
its symptom (catarrhal) diarrhoea.]

ETIOLOGY.--Intestinal inflammation is more prevalent in the Northern,
Middle, and Western than in the Southern States. There is no relation
between the distribution of malarial and intestinal diseases: in some
regions where malarial disease is rife there is very little disease of
the intestines. Limited areas in Lower Mississippi, Eastern Kentucky,
Eastern North Carolina, etc. have a special predisposition to diseases
of this class.[6]

[Footnote 6: F. A. Walker, _Statistical Atlas_, 1874, table v. p. 3;
also plates xlii. and xlv.]

During the Civil War diarrhoea and dysentery were more frequent and
fatal in the central region than in the Atlantic and Pacific regions.

It is difficult to compare the relative liabilibity of the native and
foreign-born populations in the United States to intestinal disease.
Inasmuch as children, among whom the bulk of such cases occur, bear
such a small proportion to the adult foreign population, allowing for
differences due to this cause, statistics show that the foreign-born
race has a very distinct predisposition to these forms of disease.[7]
The Swedes, Norwegians, and Danes have a marked susceptibility to
intestinal diseases; the English and Welsh have the same tendency; but
the Irish have a comparative immunity. The colored race is more prone
to intestinal than to malarial diseases in the Middle States, but there
is the reverse susceptibility in the Northern and Southern States.

[Footnote 7: The number of children under ten to 1000 native population
is 306; number of children under ten in 1000 foreign population, 47 (F.
A. Walker, "Relations of Race and Nationality to Mortality in the
United States," _Statistical Atlas_, 1874, p. 213).]

Under ten years more males than females have enteritis, in the
proportion represented by the figures 362 and 299. After ten the
predisposition of the two sexes is about the same.

The summer is the season when diarrhoea is most prevalent and most
fatal. June, July, and August are the months in which the greatest
number of cases occur and in which there is the highest mortality. The
extraordinary death-rate in these months in cities is of course due to
the influence of summer heat on children, and the death-rate from
diarrhoea and entero-colitis is chiefly among infants under one year.
But among adults the same rule holds. The highest monthly mortality
from acute diarrhoea among the U.S. troops (white) between 1861 and
1866 was 147, in July, 1862; the next highest was 114, in August, 1862.
June and September were after these the most fatal months. According to
the census of 1870, the most fatal month is August.

Elevation of temperature in the summer months is the cause of the
prevalence of intestinal catarrh and of its great mortality among
infants and children. The number of deaths bears a direct ratio to the
degree of heat, the highest death-rate occurring in seasons of unusual
high temperature.[8] The effect of excessive or prolonged heat is to
arrest or weaken the digestive processes; undigested masses in the
stomach or the intestines act as foreign bodies and produce
inflammation.

[Footnote 8: Among the numerous publications bearing on this subject,
those contained in _The Sanitary Care and Treatment of Children and
their Diseases_ (Boston, 1881) are of especial value. S. C. Busey's
article contains much valuable matter on the relation of summer heat to
illness and mortality among children.]

{670} Sudden changes of temperature from cold to heat or from heat to
cold develop diarrhoea. If the air is at the same time saturated with
moisture, the effect of a change in temperature is greatly intensified.
In the first hot days of June there is on the Atlantic coast,
especially in cities, a rapid increase in the number of cases of
gastro-intestinal disturbance. A larger number of children are taken
ill in June than in August. The child in time becomes habituated to
heat, and if not attacked early runs less risk of illness in the later
months. A sudden or unusual exposure to low temperature, as in lying on
damp ground, leads to the same result. The check to perspiration after
violent exercise is especially provocative of diarrhoea. In these
instances the congestion and consequent inflammation of the mucous
membrane are brought about through the effect of heat or cold upon the
peripheral nervous system. Cold may act more directly by the driving of
suddenly-cooled blood from the surface of the body to the interior.
External burns belong to the same category, as they lead to extensive
inflammation, sometimes to ulceration, of the duodenal mucous membrane
through reflex influence. A case is reported of a boy aged twelve years
who after an external superficial burn of the left thigh was taken with
profuse diarrhoea which ended fatally in three hours (Ziemssen).

Contamination of the atmosphere with emanations the result of the
overcrowding of many human beings together, as in prisons, camps, or
asylums, especially where decomposition of organic matter is going on,
is of great influence in causing diarrhoea. Persons living in
badly-ventilated houses, or in houses improperly drained where the air
is vitiated by escaping gas from sewer-pipes, are especially prone to
be attacked. But sewer-gas, per se, does not cause diarrhoea any more
than it causes diphtheria or scarlatina.[9] It is a step backward to
hang upon this ready explanation all our doubts and our ignorance of
the origin of disease. The specific germ of the zymotic diseases may be
conveyed in the gases from sewers, but there are other and more direct
modes of communication which should receive equal attention.

[Footnote 9: Longstaff (_Brit. Med. Journ._, London, 1880, vol. i. p.
519) believes that summer diarrhoea has a specific poison which is
intimately connected with the process of putrefaction, and that the
infective material has its source in the public sewers.]

Children are much more liable to intestinal inflammation than adults.
This is due to the greater susceptibility of the mucous membrane in
them to congestion and catarrh from external influences and from direct
irritation. In infants fed upon an unsuitable diet--cow's milk or other
substitutes for mother's milk--this susceptibility is much increased.
The age most liable to attack is under one year, or from the first to
the second year, when, in consequence of dentition, weaning, and a
change from a diet chiefly or almost wholly liquid to one of solids,
there is a great liability to a disturbance of the normal equilibrium.
Intestinal catarrh forms almost one-third of the total number of the
affections of childhood. According to the census of 1870, 761 out of
every 1000 deaths from diarrhoea, dysentery, and enteritis occurred
under the tenth year. In old age a similar predisposition exists, and a
mild attack will in old persons induce more serious symptoms than in
middle life. Epidemics of diarrhoea among the aged in asylums and
hospitals are not uncommon.

{671} Temperament and idiosyncrasy are causes of differences in
predisposition. Many persons in consequence of taking cold invariably
have diarrhoea, while others as invariably have nasal catarrh or
bronchitis. Certain articles of food, as oysters and eggs, lead always
in some persons to intestinal disturbance. An exaggerated sensibility
of the mucous membrane to particular impressions is the cause of this
peculiarity.

Previous attacks of intestinal inflammation render the individual
liable to recurrences from very slight causes. The suppression of the
menses and of hemorrhoidal discharges and the healing of eruptions are
said to be followed by serious diarrhoea, but such an occurrence is
probably more often a coincidence than a result.

Sedentary life, by enfeebling muscular movement and by inducing
indigestion and constipation, brings on diarrhoea. Constipation impairs
the muscular tone of the bowel, and hardened fecal accumulations act as
irritants which sometimes provoke acute catarrhal processes--diarrhoea
and dysentery. Insufficient clothing in children and in adults makes
the skin more susceptible to changes of temperature and conduces to
intestinal congestion. Smoking in excess and the use of narcotics and
stimulants are mentioned as debilitating causes which pave the way for
disease in the intestine; the habitual use of the stronger liquors, by
keeping up chronic engorgement of the mucous membrane, is undoubtedly a
potent cause. Occupations which involve deprivation of fresh air and
sunlight, and all trades which enfeeble the individual, make him liable
to all digestive disorders. A feeble constitution, debility from
disease, from over-fatigue, or from loss of sleep, or any perturbing
influence, puts the body in a state favorable to indigestion and
diarrhoea.

The eruptive fevers are accompanied more or less by gastro-enteric
catarrh. In scarlet fever, measles, and variola there is a state of
equilibrium between the skin and the intestinal mucous membrane. When
the morbid manifestation does not normally appear upon the skin there
is a transference of irritation to the intestine. The administration of
purgatives in the early periods of scarlet fever and measles delays,
sometimes prevents, the outburst of the eruption on the skin. The
intestinal catarrh of the eruptive fevers has sometimes the
significance of an exanthem and sometimes of a secondary complication.
In measles it is more frequently the former; in scarlatina and variola
it comes later as a complication.

Uraemia, malarial infection, chronic suppuration, pyaemia and
septicaemia, cancerous and strumous disease of the mesenteric glands,
scurvy, tuberculosis, Bright's disease, and chronic wasting diseases in
general, are conditions in which diarrhoea appears as a result of the
defective nutrition of the vessels of the intestinal wall and their
liability to dilatation and hyperaemia, or from the presence in the
blood of septic matter.[10]

[Footnote 10: For experiments relating to the production of intestinal
catarrh by injections of irritating or putrid matter into the blood
consult _Traite clinique et experimentelle des Fievres dites
essentielles_, Gaspard et Bouillaud; also, _Path. anat._, Lebert, tome
ii., Texte, Paris, 1861, p. 205.]

The ingestion of a larger quantity of food than the stomach and
intestines are able to soften, and the taking of food essentially
indigestible or improperly prepared by cooking, are causes of the
passage of masses of food more or less unaltered along the intestinal
tract. Hyperaemia {672} follows the mechanical irritation of the mucous
surface. When articles of food are in a partial state of putrefaction,
so that the antiseptic properties of the gastric juice cannot be
quickly enough brought into play, there is a rapid fermentation in the
stomach, with the development of symptoms of gastric and subsequently
of intestinal catarrh. Unripe fruit, vegetables composed of hard
tissue, as early potatoes, cucumbers, pineapples, and cherries, by
their indigestible nature, are frequent causes. Oysters, crabs, fish,
and lobsters often occasion acute diarrhoea in consequence of being in
an unfit condition for food. Cheese has been known to produce violent
illness with symptoms of intense intestinal irritation; these effects
are due to some poisonous substance, hitherto undiscovered, developed
in the course of putrefaction. New coffee causes diarrhoea; six months
is usually the time before coffee grown in Ceylon reaches the European
and American markets; by this time it does not have this effect.[11]

[Footnote 11: J. Stevenson, "Medical Notes from Ceylon," _Edin. Med.
Journ._, Feb., 1862, p. 693.]

The irritant and caustic poisons, as mineral acids, caustic alkalies,
corrosive sublimate, arsenic, oxalic acid, tartar emetic, and carbolic
acid, kindle an intense inflammation of the mucous membrane of the
stomach, duodenum, and of the lower portion of the intestinal canal.
Softening of the coats of the intestines from corrosion, with
perforation, is not an infrequent result.

Drastic purgatives act as irritant poisons in producing acute
hyperaemia of the mucous coat with excessive transudation of serum; or,
in other words, an acute catarrh. A discharge of vitiated bile or an
excess of bile is given by recent[12] as well as by older writers as a
provoking cause of diarrhoea. The proper relationship is the reverse of
this: an intestinal catarrh the result of irritant action upon the
mucous surface entails a more active outflow of bile, just as some
cathartics by irritating the duodenum excite the gall-bladder to empty
itself.[13] Impacted fecal masses are direct irritants, exciting
inflammation (typhlitis, dysentery); putrefactive changes in
long-retained fecal collections have an additional power of irritation.
Foreign bodies accidentally or purposely swallowed, intestinal
parasites, the pus from an abscess which bursts into the intestine,
likewise are excitants of disease. Tubercle nodules, typhoid ulcers,
cancer, or other neoplasms in the wall are surrounded by areas of
inflammation.

[Footnote 12: Roberts, _Th. and Pract. Medicine_, Am. ed., Philada.,
1880, p. 160.]

[Footnote 13: "The propositions which are the foundation of the whole
theory that bile can cause diarrhoea, and that its absence leads to
costiveness, cannot be looked upon as proved" (J. Wickham Legg, _On the
Bile, Jaundice, and Bilious Diseases_, New York, 1880, p. 661).]

Alcohol taken in excess, as in a debauch, leads to acute
gastro-intestinal catarrh. The stomach symptoms are the earliest to
develop and are the most prominent. Habitual alcoholic indulgence is a
more common source of chronic than of acute intestinal catarrh.

The influence of unwholesome drinking-water as a cause of diarrhoea has
been carefully examined by Woodward.[14] Turbid or muddy water holding
inorganic matters in suspension, he concludes from the evidence, is not
a source of disease, and the injurious effects of such waters have been
grossly exaggerated. Water containing inorganic substances in solution
produce diarrhoea, and are purgative if the dissolved matters have
purgative properties. Limestone-water may produce {673} temporary
disturbance of the bowels, but is wholesome. Carbonate and sulphate of
lime and magnesium in solution are more cathartic, but not as much so
as selenitic waters which contain an excess of sulphate of lime. The
salts of sodium and potassium in the waters of Colorado, New Mexico,
and Utah are still more liable to produce diarrhoea.

[Footnote 14: _Med. and Surg. History of the War_, Part 2, Medical
Volume, p. 599 _et seq._]

Water contaminated with organic matters of vegetable origin, which are
found in states of decomposition in marshes and stagnant pools, does
not, in the opinion of Woodward and Parkes, have very great influence
in the production of diarrhoea or dysentery. Impurities from
decomposition of animal matters are unhealthful. This is especially
true of water impregnated with soakage from privies and sewers; and yet
epidemics of diarrhoea cannot as often be clearly traced to this source
as can outbreaks of typhoid fever. Parkes says water contaminated with
three to ten grains per gallon of putrescent animal matter may be
hurtful.

Contusions and injuries of the bowel by sudden pressure or shock to the
abdominal wall may lead to intestinal inflammation. The large intestine
is more exposed from its size and position to such injuries. Pressure
upon the bowel by a tumor, as an enlarged or retroverted uterus, may
cause diarrhoea, the source of which may be overlooked. Early-morning
diarrhoea from a displaced womb is of frequent occurrence.

Emotional influence, as sudden fright or grief, will produce sudden
diarrhoea. Lesions of nerve-centres--corona radiata, optic thalamus, or
corpus callosum--induce hyperaemia, softening, and ulceration of the
mucous membrane of the small intestine.[15]

[Footnote 15: Rosenthal, "Diseases of the Nervous System," _Wood's
Library_, New York, 1879, vol. ii. p. 266.]

Minute organisms (bacteria) are thought by some observers to be the
cause of diarrhoea, especially of a zymotic form, which prevails in the
summer months. In accordance with this theory, the dejecta from
infected persons are the vehicle of the contagious poison which by air-
and water-contamination infects others.[16]

[Footnote 16: Wm. Johnston, _Lancet_, London, 1878, vol. ii. p. 397;
also, _Brit. Med. Journ._, London, 1879, p. 81; also, G. E. Paget, "On
the Etiology of Zymotic Diarrhoea," _Brit. Med. Journ._, Nov. 19, 1881,
p. 819.]

PATHOLOGICAL ANATOMY.--A description of the morbid anatomy of acute
intestinal catarrh includes the changes which are observed (1) in the
exterior appearances of the intestines, (2) in their contents, and (3)
in the condition of their mucous lining.

1. The external appearances of the intestines depend upon the degree of
distension of the tube, the character of the contents, and the presence
or absence of inflammation of the serous coat. Great distension of the
colon, of the caecum, and of the small intestines is met with in acute
intestinal catarrh of some duration, and is due to relaxation of the
muscular coat. The colon usually presents the greatest distension. The
calibre of the tube may be lessened by strong contraction of the
muscular layer in acute intestinal inflammation of great intensity with
early and fatal termination. The color of the exterior varies with the
tension of the wall, the color of the contents, and the amount of
vascular injection. If the bowel is much distended with gas, the color
is pale; the mingling of bile with the feces causes a yellowish or
brownish color; if blood is in the tube a dull red hue is given to the
walls. If the intestine is congested or inflamed, the vessels are
outlined distinctly and can be seen in {674} different layers. The
areas of external redness generally correspond to internal hyperaemic
patches. The serous membrane shows arborescent congestion at the
mesenteric attachment or is inflamed from perforation; the signs of
peritonitis are most marked in the neighborhood of the
irregularly-shaped, round, oval, or pin-point openings in the gut. The
abdominal cavity may contain fecal matter, food, medicines, or worms
which have passed through the perforation.

2. The intestinal contents, instead of being homogeneous, of
pale-yellow color, and pea-soup-like appearance in the small intestine,
brown and more condensed in the lower part of the large intestine, may
present various changes. The fluid is usually increased in quantity,
and is thinner than normal in the colon: the color is greenish from the
bile, very pale from the closure of the bile-duct, red or black from
blood. The odor is absent from excess of serum, or very offensive from
decomposition due sometimes to the closure of the common bile-duct and
the want of bile. Shreds or masses of mucus may float in the liquid.
Undissolved pills or drugs, as bismuth, accumulated seeds, skins of
fruits or vegetables, parasites, or foreign bodies are seen. Epithelial
cells, the debris of digestion, micrococci, and bacteria are visible
under the microscope.

3. Inflammation involving the mucous membrane of the whole intestinal
canal is rarely or never met with. The nearest approach to generalized
catarrh of the bowel is found in eruptive fevers, especially measles.
Inflammation extending throughout the whole length of either the small
or large intestine alone, and affecting all parts equally, is also
rare. The ileum is the part of the small intestine most frequently the
seat of disease, but the ileum is rarely affected alone. Inflammation
is more frequently limited to the colon than to the small intestine.
The most common form of intestinal inflammation is ileo-colitis, where
the lower part of the ileum and a part of the colon, sometimes of
considerable extent, are inflamed. The duodenum is sometimes the seat
of a local inflammation, but this rarely happens except in the case of
external burns; duodenitis is most frequently an extension of catarrh
from the stomach, but the pathological anatomy of the duodenum presents
some peculiarities which will be described hereafter.

(_a_) Hyperaemia of the intestinal mucous membrane may exist without
inflammation. The engorgement of the veins by mechanical retardation in
disease of the liver, heart, or lungs does not constitute catarrh,
although it is sooner or later followed by catarrhal processes, usually
of a chronic nature. Gravitation of blood to the most dependent parts
in cases of long illness distends the vessels, and post-mortem
hypostasis leads to the passage of serum and coloring matter into the
meshes of the mucous and submucous tissue. In fatal cases of acute
diarrhoea sometimes no lesion has been observed. The hyperaemic
membrane pales after death, as does the skin in scarlatina and
erysipelas.[17] The presence or absence of hyperaemia is therefore no
positive proof of the previous existence or non-existence of
inflammation. To constitute inflammation there must be other changes
besides hyperaemia, as oedema, softening, and infiltration with
cell-elements.

[Footnote 17: It is difficult to recognize post-mortem hyperaemia in
the mucous membrane of the mouth or throat where intense inflammation
has been seen in life.]

{675} A degree of vascular turgescence visible to the naked eye is
nearly always present in the mucous and submucous tissues which have
been the seat of catarrh. It is usually found in the lower part of the
ileum, the caecum, sigmoid flexure, and other parts of the colon. The
redness is diffused over a surface of several feet in length or is
circumscribed in patches of varying size. When vessels of small size
are distended with blood, red branching lines are seen (arborescent or
ramiform injection) which have their starting-point in the insertion of
the mesentery. When the capillary system is engorged a fine interlacing
network can be discovered, which gives to the membrane a more uniform
red color. Parallel lines or bands of redness extend in a transverse
direction across the axis of the canal corresponding to the folds of
mucous membrane in the small and large intestine.

The shades of color depend upon the intensity and duration of the
congestion. In acute mild forms the color is light red; in more intense
grades the membrane is more vivid or purplish. Brown and slate-colored
tints show a passage into the chronic stage. A black hue occurs in
gangrenous inflammation. Minute dots (speckled redness) are due to
minute extravasations, and ecchymotic irregular patches are sometimes
seen.

Bile-staining of the mucous surface is met with; this cannot be removed
by washing. In metallic poisoning the redness is more vivid and the
mucous membrane is eroded.[18]

[Footnote 18: For colored plates illustrating hyperaemia and
inflammation of the intestines see Carswell, _Path. Anat._, London,
1838, plate ii. figs. 1 and 2. These are beautiful representations of
(1) ramiform vascular injection passing into (2) capilliform injection,
which becomes (3) uniformly red, or from its intensity (4) ecchymotic
or hemorrhagic. See also Annesley, _Morbid Anatomy_, London, 1828,
plates x. (Fig. 2), xiii., xxii., xxiv., and xxv. Many of these are
illustrations of peritonitis as a complication of enteritis. See also
Kupferlafelnzer, Lesser, _Ueber die entzundung und Verschwarung der
Schleimhaut des Verdauungskals_, Berlin, 1830, tab. iv. fr. 3; also J.
Hope, _Illustrations of Morbid Anatomy_, London, 1834, figs. 116, 118,
124, and 125. These plates are wonderful in their truthfulness and
execution.]

(_b_) Acute oedema and increase in the cell-elements in the inflamed
parts give rise to swelling and to softening, so that the mucous
membrane seems to be easily scraped off. This is not always the case,
as no loss of firmness of the reddened tissue is often found. In the
small intestine the villi, which in health are not seen, become
enlarged, giving a "plush-like" or velvety appearance to the mucous
membrane; they are sometimes club-shaped from epithelial accumulations
on their free extremities.

(_c_) When the small intestine is examined the solitary glands, which
in the normal state are barely visible, are so enlarged that they
appear as rounded prominences. They are described as looking like
grains of mustard-seed on a red ground, and are the size of pinheads.
When they are distinctly seen it may be concluded that they are
enlarged. In children the glands are enlarged when there has been
slight or no diarrhoea.

Peyer's patches are also tumefied, and are more distinct from being
elevated above the surface, but they have not in intestinal catarrh as
great a relative enlargement when compared with the solitary glands as
in typhoid fever. The interfollicular substance of the patch may
hypertrophy without any increase in the size of the follicles; a
reticulated {676} appearance is then given to the gland. The color of
the swollen follicles in recent inflammation is translucent from
oedema; later they are gray and opaque. These changes are more marked
at the lower end of the ileum, because the isolated follicles and
Peyer's patches are more numerous there.

(_d_) Catarrhal ulcers--erosions--are produced by the loss of
epithelium or from a process of vesicle-forming and rupture, as in
stomatitis. They may enlarge, undermine, and coalesce, thus reaching
quite a large size. They may deepen and perforate the wall of the
bowel, causing peritonitis, or they may heal, forming cicatrices which
in contracting may narrow the canal.

Small follicular ulcers are found on the mucous surface. They result
from the breaking down of the exposed wall of the closed follicle from
over-distension. The ulcer is either on the apex of the dome of an
isolated follicle or is within the area of a Peyer's patch. Sometimes
several ulcers may be seen on the surface of the swollen patch.[19] The
ulcerative process is sometimes very rapid. In the case of a child aged
eight years, with no previous intestinal disease, who died in the
Children's Hospital, Washington, in June, 1882, after a two days'
illness with watery discharges and rapid prostration, the solitary
glands throughout the ileum were many of them enlarged. As many as a
dozen small ulcers were seen at the apices of the enlarged follicles.

[Footnote 19: See photograph facing page 302 of _Med. and Surg. History
of the War_.]

In the large intestine the same lesions are found, but in a more
advanced stage, especially in the caecum and descending colon. Enlarged
solitary glands of the size of a pinhead or small bird-shot are
scattered along the canal.

Follicular ulcers[20] are found in the large intestine, occupying the
summit of the enlarged follicles and involving a large extent of mucous
surface. Pigment-deposits are seen which give rise to the appearances
described as occurring in chronic intestinal catarrh.

[Footnote 20: For description of the mode of formation and growth of
follicular ulcers see article on CHRONIC INTESTINAL CATARRH.]

(_e_) The mucous surface is covered, especially in the areas of
redness, with an adhesive, opaque mucus of neutral or alkaline reaction
and of yellow, red, or brown hue, depending upon the relative amount of
bile or blood. It is composed of mucus-corpuscles, epithelium-cells of
cylindrical and prismatic form, pus-cells, and sometimes
blood-corpuscles. Vibrios and bacteria also are seen.

The chief distinction between the lesions of acute intestinal catarrh
and typhoid fever are these: In typhoid fever the number of Peyer's
patches involved is larger; there will be a chain of enlarged glands
from the ileo-caecal valve throughout the ileum, those nearest the
ileum being the most altered. Near the valve there is usually some
ulceration, so that the gland acquires a ragged appearance. In catarrh
of the bowel there is a more irregular distribution of enlarged glands;
they project less above the surface, and if ulcerated have one or two
spots of erosion. In typhoid fever the Peyer's patch has the most
prominence. In catarrh of the bowel the solitary glands are the most
enlarged. In catarrh the large intestine may be the seat of the most
advanced lesion; in typhoid fever, except with rare exceptions, the
lesions in the ileum are most advanced.

{677} (_f_) The mesenteric glands are enlarged, but not so uniformly so
or to the same extent as in typhoid fever. The stomach is sometimes
found inflamed, the mucous membrane being reddened, thickened, or
softened. The liver, spleen, and kidneys are normal or present
accidental conditions of disease. In the respiratory organs pulmonary
congestion, pleurisy, and pneumonia are found. The heart contains clots
which are fibrinous or soft and red; they are found on both sides, but
when one cavity alone is filled the right is the common seat. The brain
is usually normal; fluid may be in the subarachnoid space, and thrombi
in the cerebral sinuses.

PATHOLOGICAL HISTOLOGY.--In the genesis of catarrh of the intestinal
mucous membrane the first effect of the exciting cause is an
over-distension of the capillaries and small vessels; this congestion
is most marked in the meshwork of vessels around the closed follicles.
A transudation of serum takes place into the mucous layer, and in more
marked congestion into the submucous layer also; these tissues become
more or less oedematous and swollen. Transudation of serum into the
intestinal tube follows. From over-stretching the walls of minute
vessels may rupture and small extravasations take place, staining the
tissue red. These subsequently become black pigment-spots. Post-mortem
extravasations are due to decomposition of the wall of the vessel.
Rupture of vessels on the surface leads to escape of blood into the
bowel, which is mixed with the transuded serum. The proper secretion,
intestinal juice, is diminished as a result of these changes, but an
excess of the mucus with which the mucous membrane is always coated
immediately follows. The origin of the mucus is not to be sought for in
the activity of the glands alone, but in the transformation of the
protoplasm of the epithelial cells.[21] The varying proportions of
serum, mucus, and blood cause the stools to be serous, mucous, slimy,
or bloody, hence the terms serous, mucous, and bloody diarrhoea.

[Footnote 21: Rindfleisch, _Path. Histology_, Sydenham ed., vol. i. p.
412.]

Hypernutrition, swift life of the mucous membrane, the result of
continued excess of blood, entails the increase of the cell-elements.
Lymphoid cells accumulate in the submucous layer, especially where
these cells are normally most numerous. There is a saturation of the
membrane with an excess of plasma. Cells also appear in increasing
numbers in the interfibrillary spaces of the mucous membrane, which
increase its bulk, and the follicles of Lieberkuhn appear as if pushed
apart. Lymph-corpuscles accumulate in the meshes of the closed
follicles, which are distended and project above the surface as
described. Multiplication of the cells within the follicle (follicular
suppuration) causes over-stretching and the wall bursts, forming the
first stage of the follicular ulcer. The appearance upon the epithelial
surface of an increased number of loosened cells, which are sometimes
epithelial in character and at other times resembling pus-cells
(epithelial and purulent catarrh), is believed to be due to a rapid
manufacture and exfoliation of epithelial elements, and to constitute
one of the essential features of catarrh. Desquamation of the
epithelium in catarrh of the bowel, even in that of Asiatic cholera,
has been called in question by Woodward, who thinks that the stripping
off of epithelium is cadaveric.

SYMPTOMS.--Owing to the difference in the intensity and extent of {678}
the catarrhal process there is every possible variation in the symptoms
of intestinal inflammation. No one symptomatic picture will properly
represent all cases, and with a view to greater convenience and
exactitude of illustration a division may be made into mild and severer
forms.

Under the head of mild forms can be included all cases of intestinal
catarrh which by their short duration and benignant character point to
a mild degree of inflammation. They correspond to the following
anatomical states: hyperaemia of the mucous membrane of parts of the
small or large intestine, or of parts of both simultaneously; slight or
moderate swelling of the membrane from serous saturation; transudation
of serum into the canal; increase of lymphoid cells in the mucous and
submucous tissues; and increased manufacture of epithelial cells, but
without any marked tumefaction or ulceration of the closed follicles.
The termination is by resolution, which is reached in a few days
usually, and the membrane is rapidly and entirely restored to the
normal state. Between the normal condition of the mucous membrane, with
its recurring periods of physiological hyperaemia, and the hyperaemia
with exaggerated secretion and peristalsis which leads to diarrhoea,
there is no well-defined border-line. Diarrhoea may be regarded as the
most certain sign of the catarrhal process. Whenever the frequency and
fluidity of the stools are such as to be regarded as pathological, some
stage or other of catarrhal inflammation may be assumed to exist.

In a large number of mild forms the onset is sudden. After a meal of
indigestible food or an unusual excess pain will be felt in the
abdomen, recurring in paroxysms, which start in the neighborhood of the
umbilicus and radiate throughout the abdomen. The pain is accompanied
by borborygmi, and is succeeded sooner or later by a desire to go to
stool. The first one or two movements, which follow each other in quick
succession, are more or less consistent or moulded, but in a short time
diarrhoea is established by frequent discharges of watery fluid,
containing perhaps some undigested fragments of food, which may have
been the exciting cause of the illness by mechanical irritation. Each
stool is preceded by colics, griping pains in the abdomen, which are
relieved by the evacuation. An attack beginning in this way and from
such causes may cease in a few hours, and be unattended by any general
symptoms if proper precautions are taken. A slight dryness and coating
of the tongue, with loss of appetite and occasional griping pains or a
tendency to looseness of the stools, may continue for a day or two.
Indiscretions in diet or other imprudences, as fatigue, may prolong the
mildest attack during one or more weeks, but the character of the
illness is here due not to the nature of the disease, but to the
addition of fresh causes which delay the natural progress toward
recovery.

Severer forms either begin suddenly, as in the milder forms just
described, or are preceded for a time by symptoms of gastric or
intestinal indigestion. The patient may have complained of distress
after eating, flatulence, colicky pains, distension of the abdomen and
tenderness on pressure, loss of appetite, with a general feeling of
ill-health--symptoms which point to the existence of a condition of the
mucous membrane of the gastro-intestinal canal favorable to the action
of an exciting cause.

A feeling of chilliness ushers in the attack. This is accompanied by
fever, which at first, and sometimes throughout, is of a marked
remittent type. {679} The griping pains, colics, which at first are
infrequent and dull, now recur at short intervals and become sharper.
They are sometimes attended with vomiting of food or of a greenish
fluid. The intensity of suffering may be so great as to cause pallor of
the countenance, a feeling of faintness, and coldness of the surface
with sweating. The paroxysm usually precedes a movement. The more
severe pains extend to the lower extremities and the scrotum.

Movement of gas in the intestines produces rumbling, gurgling, or
splashing sounds, called borborygmi. They are paroxysmal, lasting a few
moments, or are coincident with pain, and frequently are the immediate
precursors of an evacuation. The cause for their production is the
quick propulsion of the fluids by strong peristaltic action from one
part of the bowel to the other or the rapid movement of gas within the
bowel. Relief is obtained both from the pain and from the sense of
distension by expulsion of flatus.

Tympanites is closely connected with the symptoms just described. An
excess of gases within the bowel is not primarily a result of the
inflammation of the mucous membrane, but is an early phenomenon due to
the decomposition of indigestible food in its transit through the
intestine. Later, the gases are developed very readily by the
decomposition of even the most digestible articles of food, the mucus,
which is the product of the catarrh, acting as a ferment.

The distension of the intestinal canal produces an intumescence of the
abdomen which is commonly uniform, but may be greater in some portions
of the tract than in others. Thus the transverse and descending colon
are more projecting and more distinctly outlined than other portions of
the canal.

Sensibility of the abdomen to pressure exists along the line of the
colon or over a considerable area. But no defined limitation of the
affected part can usually be made by the location of pain to the touch.
If there is any local tenderness, it is over the descending colon. In
one form of enteritis--typhlitis--the localization of the inflammation
in the caecum produces subjective pain and pain on pressure in a
restricted region--a peculiarity which results no doubt from the early
intensity of the inflammation and the implication of the connective
tissue behind the bowel. But this is not true of inflammation of any
other part of the intestinal canal.

A sensation of soreness on movement, as in turning in bed, standing, or
walking, is not uncommon, even when the attack is of no great gravity.
The patient on standing bends forward to relieve tension, and he may
feel nervous when the bed is shaken.

Diarrhoea is the most important symptom, as it is directly related to
catarrh. The number of evacuations varies from one or two to twenty or
more in the day. In cases of medium intensity there are from six to ten
in twenty-four hours, the interval between the movements being two to
three hours during the day and somewhat longer at night. The matters
passed in quantity range from two ounces to a pint; the average is
about four fluidounces. This, however, is subject to great variations,
depending upon the intensity of the disease; the more choleriform the
attack the greater the amount of fluid passed. The weight of the
evacuations varies from five ounces to forty pounds in twenty-four
hours; this increase does not depend upon the greater quantity of water
only, but the solid constituents are in greater amount.

{680} The normal brown color, which is due to hydrobilirubin, changes
as the movements become thinner to yellowish-brown or pale yellow from
dilution of the fecal matter with water. An excess of serum or mucus
renders them colorless. A greenish-brown, greenish-yellow, or green hue
is due to the presence of bile. The rapid descent of the contents of
the bowel delays or prevents the reabsorption of bile,[22] or the fluid
is expelled before the usual transformations in color take place.[23]
The bile-pigment is also absent in duodenal catarrh from closure of the
opening of the ductus choledochus.

[Footnote 22: L. Brunton, "On the Action of Purgative Medicines," _The
Practitioner_, London, June, 1874, p. 403.]

[Footnote 23: The reaction of bile-pigment with nitric acid, which does
not take place in the contents of the colon or in normal feces, is seen
in the green stools of acute intestinal catarrh, especially in
children.]

The coloration of the stools further depends upon the character of the
food and drink and upon the drugs given. From an exclusive milk diet
the discharges are pale or contain undigested whitish lumps of casein.
The preparations of bismuth and iron give a black color and the
sulphate of copper a dark-green hue. A green or greenish-brown tint is
observed after the use of calomel, and while the experiments of the
Edinburgh committee demonstrated that no increase of bile follows its
administration in dogs, yet the opinion is still general that the green
stools contain an excess of bile.

Blood appears in three forms in the stools: as a coffee-ground or black
powder from hemorrhage in the stomach or upper bowel; as a reddish
fluid with small coagula in flakes, which come from intense congestion
or ulceration of the intestine; or an abundant hemorrhage may result
from deep ulceration in the duodenum or elsewhere.

The characteristic odor of the feces is altered in several ways. As the
movements become less solid they acquire a nauseous or sour smell, due
essentially to the volatile products formed in connection with the
decomposition of fatty matters.[24] When very thin and containing
little or no feculent matter the discharges lose odor, as in cholera,
or they become excessively offensive--cadaveric--in intense and fatal
inflammation and in ulceration of the bowels. After exposure to the air
the stools of diarrhoea undergo decomposition and develop offensive
smells more rapidly than in health. The absence of bile, whether there
is diarrhoea or not, gives rise to a peculiar and unpleasant odor,
showing that this secretion is to some extent an antiseptic. The escape
of fetid gas from the anus is rarely an accompaniment of a decomposed
state of the rectal contents. In children the stools are more variable
in quantity, color, and odor than in adults, and are more readily
affected by the ingesta.

[Footnote 24: Guttmann, _Physical Diagnosis_, Sydenham Soc. ed., p.
404. The odor of normal feces is due to a substance isolated by
Briequer, called scatol, which is a final product of the putrefaction
of albumen (Ewald, _Lectures on Digestion_, New York, 1881, p. 106).]

In the diarrhoea of old persons the discharges are thin, yellow,
offensive, and often frothy.

The disorder of the digestive apparatus is attended with other
symptoms. The tongue is normal in some cases; in others red at the
point and edges with a central whitish coat, or the surface is red,
polished, and dry. Marked change in the appearance of the tongue is due
to a complicating gastric catarrh. There is thirst, with loss of
appetite, and a tendency to {681} nausea and vomiting in children and
feeble persons. The breath has a peculiarly offensive odor (spoken of
as fecal) in some instances.

Fever is not always present. In cases of moderate severity it occurs in
the beginning of the illness, but declines rapidly under treatment by
rest and diet. The course of fever does not conform to any type even in
severe cases, although it so nearly resembles that of typhoid fever in
its first week as to lead to mistakes in diagnosis. The height of the
fever and its duration are measures of the extent of the lesions and
their gravity. Sudden outbursts of fever point to some complication. In
catarrh of the bowel due to cold the fever is higher than when
indigestion is the cause. In very feeble persons, in children, and in
any case from neglect and improper feeding the body-heat may be very
high.

The urine is diminished and high-colored. Very little disturbance of
the nervous system is seen except in young and old patients; some
headache and restlessness are all that may be observed. Moderate
delirium at night accompanies very acute attacks. In children
convulsions are not unusual in the onset and at the end of the attack.
In the aged exhaustion from the illness soon lapses into stupor or
coma.

Paraplegia and contraction of the muscles of the extremities are
referred by some observers to gastro-intestinal inflammation.[25]

[Footnote 25: Potain, _Le Praticien_, Paris, 1879-80, p. 88.]

In uncomplicated mild cases of intestinal catarrh there is a movement
toward recovery after a few days' illness. The stools become less
frequent, smaller, and more consistent. In a week to ten days the
tongue cleans, the thirst ceases, the appetite returns, the tympanites
and pain diminish. The fever declines, and ceases before the diarrhoea
is completely arrested. There are always more or less emaciation and
loss of strength from the fever and arrest of nutrition. The liability
to relapse is great, and the patient by indiscretions reproduces the
same symptoms, thus prolonging the attack for several weeks. Acute
intestinal catarrh may pass into the chronic form by a disappearance of
fever and amelioration of all the abdominal symptoms. The patient
begins to take solid food, gains strength and flesh, but complete
recovery does not come. The diarrhoea recurs at variable intervals as
the result of indulgences in a mixed diet, over-exercise, or exposure
to cold, and in time we have some degree of chronic catarrh permanently
established.

Very mild cases may be prolonged by the neglect of the patient to
consider his painless diarrhoea of sufficient moment to need attention.

In inflammation of the more intense kind the picture is somewhat
different. The prodromes are longer and the general symptoms more
severe. Restlessness, a sense of prostration, delirium, and high fever
mark the early stages and continue for a longer time. The patient loses
flesh and strength quickly. The features express anxiety and illness,
the skin is hot and dry, and the thirst great. Vomiting is repeated.
Borborygmi, the tension of the abdomen, pain, and sensibility to
pressure are all intensified. The stools are at first yellow and thin,
but change much from day to day. They may be green or very thin and
dark or grayish, and are sometimes very offensive in odor. Blood and
mucus may be seen in them, being slimy or grumous and bloody. When the
patient is very weak the discharges are involuntary; the tongue is
coated white, with bright red tip and edges, and is often dry.

{682} The severer forms last from three to six weeks. After a tedious
period of alternate improvement and relapse the illness becomes chronic
or the patient dies from asthenia, perforation and peritonitis, or some
other complication.

In the most intense varieties which find examples among Europeans and
Americans in intertropical countries, or result from acute mineral
poisoning and from rapidly-progressing cases of acute ulceration of the
intestinal wall, especially in children, there is a sharper and more
violent invasion. The strength is reduced in a very short time, and
there is rapid emaciation; the features assume an anxious expression;
the complexion is leaden or livid; the skin is cold and clammy; the
pulse is small, weak, and rapid; the breath comes quick and short, and
is frequently complicated with hiccough. In the early stages vomiting
occurs, due to a concurrent gastritis; in cases of poisoning vomiting
is incessant.

The pain in the abdomen is intense, and less paroxysmal than in other
forms. The abdomen is tympanitic and excessively tender to the touch,
and the knees are drawn up to relieve the tension of the abdominal
muscles. Thin, black, or reddish stools are passed every few moments.
As the attack progresses the urine is suppressed, the voice becomes
whispering, and collapse is developed. This is marked by cold
extremities, dyspnoea, feeble and finally imperceptible pulse. Death
may end the scene in a few hours or the patient may rally and recover
slowly.

Choleriform diarrhoea occurs chiefly in children during hot weather.

VARIETIES DUE TO SEAT.--The symptoms and progress of acute catarrh of
the intestines present numerous differences depending upon the seat of
the inflammation. The symptomatology already given is that of the most
common form (ileo-colitis), in which the lower part of the ileum and a
considerable portion of the colon are simultaneously involved. Many
cases no doubt occur in which the disease is limited and in which early
recovery is the rule. The pathological anatomy of cases of generalized
catarrh is better known, as they form the bulk of the fatal cases.

I. Acute Duodenitis.--The most common form of duodenitis is that in
which the inflammation spreads by continuity of tissue from the stomach
to the duodenum, as in acute gastric catarrh after a debauch. The
prominence of the gastric symptoms disguises the intestinal lesion,
unless the catarrh, as is frequently the case, extends into and
obstructs the common bile-duct and its branches, and suddenly develops
icterus with clayey stools and altered urine. Besides icterus, a
careful isolation of symptoms will show that some cannot be attributed
to the stomach: there is a dull pain seated in the right hypochondrium,
extending to the right shoulder or shoulder-blade, which is increased
by pressure upon the region of the duodenum. As the gastric symptoms
improve there is no change in the icterus, which continues for some
days or weeks longer. The connection between burns of the integument
and ulcer of the duodenum is well known. Symptoms of perforation, with
death, may be the first sign of this lesion, but vomiting of blood,
icterus, purging of blood, indigestion, and cardialgia occur from
duodenal ulcers.

The typical acute duodenitis described by authors as an independent
{683} affection is of rare occurrence. An epidemic of duodenitis[26]
has been reported where many persons were simultaneously attacked, all
the cases having had the same traits--headache, pain in the line of the
duodenum at the left edge of the right hypochondrium, pain in the first
and second lumbar vertebrae, constipation, jaundice, slow pulse, and
mental depression. Gangrenous inflammation of the duodenum[27] has been
once seen, and produced a chill, a severe sense of weight and pain in
the epigastrium, retching and eructations of gas, tenderness on
pressure, frequent pulse, and high temperature. There was obstinate
constipation, with dyspnoea, death ensuing in a few days. At the
autopsy gangrenous inflammation of the duodenum was found, which ended
abruptly twelve inches from the pylorus. There was a large gall-stone
in the gall-bladder.

[Footnote 26: McGaughey, _Philada. Med. Times_, Aug. 1, 1872, ii. p.
407; also, T. N. Reynolds, _Detroit Clinic_, June 7, 1882, p. 181.]

[Footnote 27: Eskridge, _Philada. Med. Times_, Feb. 15, 1879, ix. p.
239.]

A fatal case of duodenitis is recorded[28] in which the following
symptoms were observed: sudden and severe pain in the right
hypochondrium, increased by pressure; rigors, vomiting and purging of a
green flocculent fluid, and later of blood; jaundice, fever, delirium,
collapse, and death. The pylorus and two-thirds of the duodenal mucous
membrane were much inflamed and the orifice of the bile-duct closed.

[Footnote 28: _Die Krankheiten des Duodenums_, Mayer, quoted by Leube
in _Ziemssen's Cyclopaedia_, Am. ed., vol. vii. p. 373.]

II. Acute Ileitis, Acute Jejunitis.--When the ileum, with or without
the jejunum, is the seat of catarrh, diarrhoea may not be present,
provided the inflammation is slight and there is no increase of colon
peristalsis. The symptoms then are borborygmi, pain and fulness about
and below the umbilicus or between it and the right ileum, especially
after eating, and the general symptoms arising from indigestion and
malnutrition. Fever is slight or absent; there are malaise and loss of
strength. The feces give important indications. They contain unaltered
bile and fragments of muscular fibre and starch-granules in excess of
the quantity found in health. An increased quantity of mucus, diffused
evenly in a fluid evacuation, or globules of mucus stained with bile,
or bile-stained epithelium, denote inflammation confined to the small
intestine. A larger amount of indican in the urine than is normally
present is a sign of the same lesion.[29]

[Footnote 29: These conclusions are based upon the results of one
thousand examinations of feces made by H. Nothnagel, and reported in
_Zur Klinik der Darmkrankheiten; Zeitschrift fur klin. Medicin_, iv.,
1882, p. 223.]

Intense inflammation of the small intestine may exist without diarrhoea
or other symptoms betokening the real nature of the attack. Flint[30]
mentions having met with three such instances, and Goodhart[31] records
thirteen cases of enteritis with marked lesions in which no diagnosis
had been made before death. Rilliet and Barthez report twenty-four
autopsies in children with intestinal lesions in which no symptoms had
been observed.[32]

[Footnote 30: _Clinical Medicine_, Philada., 1879, p. 280.]

[Footnote 31: _Guy's Hospital Gazette_, Sept., 1878, p. 98 _et seq._]

[Footnote 32: _Maladies des Enfants_, Paris, 1861, tome i. p. 748.]

III. Acute Colitis.--Fifty years ago colitis was synonymous with
enteritis, and not with dysentery, as at a more recent date.[33] The
older {684} signification expressed the fact that inflammation in the
colon is essential to diarrhoea. Later the term was used synonymously
with dysentery.[34]

[Footnote 33: _Journal general de Medecine_, Paris, 1825, t. xci. p.
18.]

[Footnote 34: Tweedie, _System of the Practice of Medicine_, 1841.]

The colon is a conducting tube; the contents are composed of matters
unabsorbed in the small intestines. At first the mass entering the
colon is fluid, but by the gradual absorption of its watery part it
approaches solidity. The discharge from the rectum of a fluid shows
that the propulsion through the large intestine is so rapid that the
process of drying does not take place, or that from inflammation of the
colon there is an excess of fluid transudation from the intestinal
wall. The superficial position of the colon, its great size and length,
expose it to the action of external cold, to blows, etc.

In catarrh limited to the colon there are essentially the same symptoms
as in ileo-colitis, inasmuch as the inflammation of the colon gives to
that form its characteristic features--borborygmi, diarrhoea, and
tympanites. When the disease in the colon preponderates or exists
alone, the pain and tenderness are more superficial and confined to the
line of the large intestine. The distended colon projects and the
abdominal swelling is not so uniform. If the attack is subacute or
mild, the stools contain normal feces mixed with a great deal of mucus;
when the inflammation is in the sigmoid flexure, pure mucus is passed.
Blood mixed with mucus and tenesmus accompany inflammation low down.
Blood may, however, come from intense inflammation of the ascending and
transverse colon without disease of the lower bowel.[35]

[Footnote 35: In a case seen by the writer of colitis terminating
fatally from perforation of the transverse colon this point was
illustrated. A woman aged fifty was taken with diarrhoea in August,
1873. In November the symptoms became worse: tongue dry and red;
abdominal pain; tympanites; frequent stools, ten to seventeen in
twenty-four hours; quantity large, of a yellow or brownish-red color
with floating flakes. General symptoms grew worse; blood in stools from
time to time. November 24, sudden cessation of discharges from the
bowels, and the following day sudden collapse and death. Autopsy:
Descending colon and sigmoid flexure comparatively healthy. Transverse
colon adherent to stomach; deposits of lymph on colon and small
intestines; fluid and feces in the peritoneal cavity. The mucous
membrane of the ascending and transverse colon in a state of black
pulpy disintegration. In the transverse colon the walls were thinned by
ulceration and easily torn; gangrenous appearance of mucous coat;
perforation of the colon wall below greater curvature of the stomach.]

IV. Proctitis.--The rectum may be the seat of simple catarrh, which
differs in its symptoms from catarrh of other portions of the canal. By
many this form is called simple, non-infective dysentery. But as it is
a form of intestinal catarrh, it is right that it should be considered
in connection with colitis. The first indication of its onset is a
frequent desire to go to stool, with an unsatisfied feeling after each
effort. Normal fecal matter is first expelled in solid form, coated
with mucus which may be streaked with blood. Soon, however, the
discharges consist of jelly-like mucus, alone or mixed with blood. A
small quantity of this is passed with tenesmus at short intervals. The
patient complains of a burning feeling in the rectum and a constant and
irresistible desire to strain. The same spasmodic contraction may
involve the bladder.

This affection rarely assumes a serious form. It usually ends in
recovery spontaneously or under treatment by the cessation of the mucus
and blood and the discharge of normal fecal matter.

DIAGNOSIS.--A combination of the symptoms described as belonging to
inflammation of the small and large intestine gives the most common
{685} form of intestinal catarrh, ileo-colitis. This union is diagnosed
by the following symptoms: fever; general distension of the abdomen;
paroxysmal pains starting from the umbilicus, but having a general
distribution; noisy movements of gas; diarrhoea, the stools being
large, thin, stained more or less with bile, containing more or less
mucus intimately mixed with fluid matter and with particles of
partially-digested or unaltered food. It is possible in many cases to
recognize the part of the intestinal canal which is the seat of disease
from differences in symptoms which have already been described. But
great care in observation is needed, combined with a minute inspection
and microscopical examination of the stools, to arrive at accurate and
well-founded conclusions.

Acute follicular ulceration may be thought to have begun if after a
week or more of illness thin and sometimes putrescent stools are passed
containing small blood-coagula, with mucus and pus.[36] This opinion
would be confirmed by an increase in abdominal tenderness and the
persistence of the diarrhoea or tendency to relapse notwithstanding
careful treatment and diet. The transition of the disease into the
chronic form would give additional support to this view of the nature
of the lesion.[37]

[Footnote 36: "The intestinal mucous membrane, especially that of the
small intestine, scarcely ever produces pus without ulceration"
(Virchow's _Cellular Pathology_, Philada., 1863, p. 492).]

[Footnote 37: For a more detailed account of the symptoms and diagnosis
of follicular ulceration see article on CHRONIC INTESTINAL CATARRH.]

Some or all of the symptoms of acute intestinal catarrh are, however,
found in other diseases. It is well, therefore, to devote some
attention to differential diagnosis, giving a resume of the salient
points of distinction.

Typhoid fever in many of its features resembles intestinal catarrh, and
in many cases is confounded with it. Until within quite recent times
the symptoms of typhoid fever were grouped under the names
gastro-enteritis and follicular enteritis. In the first week of the
illness there is reasonable ground for delay in making a positive
diagnosis. Etiological data are here of great help. The occurrence of
the symptoms in children under two years and in adults beyond fifty
years points strongly to intestinal catarrh. Spring and early summer
are the seasons for diarrhoea; typhoid belongs to late summer and to
autumn. A sudden onset after errors in diet or exposure to cold, with
the early development of pain in the bowels, rumbling of gas,
diarrhoea, would be easily recognized as a local disorder. In typhoid
fever there is a less sudden onset, with prodromal debility, anaemia,
indigestion, and nocturnal fever. To these symptoms the diarrhoea,
which is attended with little or no pain, plays a very subordinate
part. In many cases of mild typhoid the development is sudden, with
rigors. A week's study of the temperature, if no rose-spots appear,
will be needed before the diagnosis can be made. There is not much
difficulty in making the distinction when the attack has reached its
second week. At this period in catarrh of the bowel the high fever,
with regular morning remissions and evening exacerbations, is not
constant, as in typhoid fever; there is tenderness on pressure over the
abdomen and gurgling, but no great meteorism; sibilant rales are not
heard in the chest; there are no rose-spots; rarely cerebral symptoms
except insomnia; and delirium is uncommon. The spleen is not enlarged.
The prostration is proportioned to the diarrhoea, and is by no means as
{686} great as at the same period in enteric fever. The colicky pains
preceding and accompanying the stools are a more marked feature of
intestinal catarrh; they are absent in enteric fever or have a feeble
intensity.

In children between the ages of two and seven years there are certain
peculiarities which augment the difficulties of diagnosis. Intestinal
catarrh in them is accompanied by an abundant, frequently painless
diarrhoea, by tympanites, cerebral disturbances, a dry and coated
tongue, with sordes on the lips and gums, and by a rapidly-developed
anaemia, emaciation, and exhaustion. Typhoid fever in children of this
age is generally benignant; vomiting is more common than in adults;
high grades of meteorism are infrequent; tenderness of the caecal
region is determined with greater difficulty; and severe nervous
phenomena and fatal intestinal complications rarely occur.[38] In other
words, in young children intestinal catarrh by its severity and enteric
fever by its benignity more nearly approach each other than in adults;
in many instances the diagnosis must be undecided until late in the
attack.

[Footnote 38: Consult "Diseases of Children," Henoch, _Wood's Library_,
New York, 1882, p. 300.]

Typhoid fever can of course be known if rose-spots, a splenic tumor, or
the characteristic delirium are manifested, or if the fever-curve
conforms to the type; but in children all these symptoms may be
negative; even the fever has great variability. If fever is continued
beyond ten days, and is accompanied by progressive anaemia and
emaciation and debility, the attack is enteric fever if all local
causes of fever can be excluded. There is no minimum limit to the
temperature in typhoid fever, and no matter how low the maxima of the
fastigium may be, typhoid fever cannot be excluded.[39]

[Footnote 39: Johnston, "On the Diagnosis of Mild Cases of Typhoid
Fever," _Am. Journ. Med. Sci._, Oct., 1875, p. 372; also, "On the Mild
Forms of Continued Fever in Washington," _Am. Journ. Med. Sci._, Oct.,
1882, p. 387.]

The large watery stools and the absence of tenesmus mark the difference
between diarrhoea and dysentery. Blood may be present in colitis, owing
to a high grade of inflammation and to ulceration. Simple catarrh of
the rectum, proctitis, is not readily distinguished from infective
dysentery. Small mucous and bloody stools may be catarrhal. In the
present state of our knowledge dysentery would be known by marked
tenesmus, by the grave general symptoms, the reddish fluid stools with
flocculi, and by its occurrence in epidemic form.

Enteralgia presents the following features which distinguish it from
intestinal catarrh: The tongue in enteralgia is clean or coated white,
but with no red tip and edges; the appetite is capricious, but not
lost; the bowels are constipated; the pain bears no relation to the
ingestion of food or drink, as in enteritis. Fever is accidental, and
there are other nervous phenomena. In lead colic there is no fever,
tympanites, nor diarrhoea. In rheumatism of the abdominal walls the
pain is superficial and sharp, not griping, and is increased by
movements of the trunk. The digestive system is in no way disordered.
From peritonitis intestinal catarrh is distinguished by a less degree
of illness and by its usually favorable result, by diarrhoea, a greater
freedom in movement, and by a less degree of suffering on palpating the
abdomen. Tympanites, constipation, great tenderness on pressure over
the abdomen, and a small, quick pulse, point to peritonitis.

{687} PROGNOSIS.--A simple intestinal catarrh of the form first
described involves no danger, and if treated by rest and diet soon
recovers. The more severe form, beginning as a primary disease, when
rationally treated ends in recovery in most instances.

Unfavorable predisposing causes are--a hot climate (India, the West
Indies, and intertropical climates in general); very hot weather of the
summer and autumn months; a very early or very advanced age; the
contaminated atmosphere of prisons, camps, etc.; all bad hygienic
influences; and previous or coexisting illness. When diarrhoea occurs
as a complication of the acute infectious diseases it has a special
gravity. In typhoid fever, scarlatina, measles, acute tuberculosis,
etc. it adds another element of illness and danger. During the progress
of chronic general diseases (malaria, scurvy, tuberculosis) it becomes
an obstinate and sometimes a fatal complication. Among the exciting
causes mineral poisons induce the most dangerous form of intestinal
catarrh. Unfavorable symptoms occurring during the course of acute
diarrhoea are the early development of high temperature, cerebral
disturbance, great sensibility to pressure over the abdomen, thin and
bloody or highly offensive stools, involuntary discharges, and very
rapid emaciation and loss of strength.

TREATMENT.--There have been many fluctuations of opinion as to the
relative value of modes of treatment in this disease. Various
therapeutic measures have been suggested which, after enjoying favor
for a time, have been abandoned, and revived after long periods of
disfavor. Venesection was alternately recommended and forbidden.
Emetics and evacuants, mercurials, diuretics, diaphoretics, have been
in turn warmly supported and vigorously opposed. Opium, belladonna, the
various astringents, and cinchona-bark have run through many changes of
favor. Individual drugs give curious evidence of inconstancy. Oxide of
zinc, suggested by James Adair in 1785 and by Hendy in 1784, after a
hundred years of weak approval is commended highly by Penrose (1863),
Brakenridge, and Mackey (1873),[40] and by more recent writers. Acetate
of lead, which dates back to Paracelsus, had varying fortunes of repute
and disrepute. In the end of the seventeenth century it had a name for
curing diarrhoea, but in the following century it was spoken of by
Boerhaave as a deceitful and destructive poison, and Cullen in 1789
said that hardly any one then thought of using lead internally.[41] In
1799 it had warm advocates in this country; among them, Thomas Ewall of
Washington, who wrote in 1808. Since then it has come into very general
use and favor, which it still holds.

[Footnote 40: J. J. Woodward, _op. cit._, p. 776.]

[Footnote 41: Ibid., _op. cit._, p. 780 _et seq._]

In view of the many changes of faith in systems of treatment and in
drugs, we have no right to assume that we have as yet reached the
perfection of treatment. In fact, experience brings the conviction that
our systems are quite imperfect and that drugs fail in our hands when
they are most needed.

The prophylactic treatment is of importance, especially in children,
delicate persons, and in those suffering from disease or predisposed by
idiosyncrasy to intestinal catarrh. Directions must be given by the
physician as to the food for children appropriate to their age and
digestive capacity. Summer heat and city life being so fatal to them,
they should {688} be sent to the cool climate of the seashore or
mountains during the first and second years of life. In warm weather
laxatives should not be given to children, except with precautions
against their acting too freely; the same rule applies to the aged. Too
great care in diet in older children predisposes to indigestion and
diarrhoea. Variety in food is of service, therefore. It is not well to
give children food prepared so as to do away with the necessity for
mastication and for active gastric movements. The stomach gains
strength by exercise. All reasonable care should be used not to take
food in excess of the individual's power of digestion. Unripe fruit,
stale vegetables or fruits, cheese, pork, shellfish which are not
absolutely fresh, are among the aliments which may produce diarrhoea,
and are to be avoided. Many people have to be told what food is
unsuited to them, and certain articles of food in individual cases
invariably excite diarrhoea. Alcohol is often to be blamed for
diarrhoeas which are attributed to indigestible food, and frequent
recurrences of intestinal catarrh can only be prevented by abandoning
stimulants altogether. The bad effects of sudden changes in temperature
are warded off by wearing flannel next to the body. This is an
important rule for adults as for children. Even in summer thin flannel
or gauze gives protection. Well-ventilated rooms, good house-drainage,
personal cleanliness, with all other hygienic aids, are means of
prevention. Persistent disinfection of sources of air- and
water-contamination should be practised, especially in hot weather. In
the country the open privies and wells need frequent clearing out.
Cases of fatal diarrhoea are met with in elevated regions where the
continued low temperature renders it improbable that heat could have
anything to do with their causation.[42] Water should not be used which
could in any way be tainted with soakage from privies, barnyards, or
other places where animal decomposition is going on.[43] Avoiding the
use of cathartics in the onset of acute illness, the nature of which is
not known, is a useful prophylactic measure. A fatal diarrhoea may
result from injudicious purging in such cases. Care in the use of
laxatives should be observed in the chronic wasting
diseases--tuberculosis, rachitis, cancer, etc.

[Footnote 42: The yearly occurrence of typhoid fever and diarrhoea at
seashore hotels shows that there is great danger in crowding persons
together and saturating the soil with the excreta. In the summer of
1882 in a boarding-house in the mountains of Maryland, where the
temperature was never above 75 degrees, there were three fatal cases of
diarrhoea in children, and several others of diarrhoea and dysentery
which recovered.]

[Footnote 43: The drinking-water supplying a country boarding-house
visited by the writer passed through iron pipes imbedded in the
manure-heap of a barnyard.]

The selection of a plan of treatment for intestinal catarrh will depend
upon the nature and cause of the symptoms. The diagnosis of the case is
incomplete and the treatment irrational until the indications furnished
by etiology have been obtained.

If cold has been the exciting cause, the patient should be confined to
bed. In the beginning a full dose of pilocarpin, hypodermically,[44] or
of the fluid extract of jaborandi by the mouth, may cause a powerful
diversion from the bowel to the skin. A hot-water or vapor bath has the
same object in view. Hot fomentations or mustard poultices can be next
applied to the abdomen. This should be succeeded by a febrifuge {689}
mixture containing the tincture of aconite-root, to which an opiate
(the deodorized tincture of opium or morphia) is to be added if there
is much pain or diarrhoea. A hypodermic injection of morphia given on
the first day of the attack immediately after a hot bath will give a
quiet night and diminish the intensity of the illness. The subsequent
treatment is that common to all the acute forms.

[Footnote 44: Atropia can be given with pilocarpin to diminish its
effect on the heart; atropia is the antidote for pilocarpin. (See
Schuk, _Centralb. f. d. med. Wissen._, Bd. 20, 1882, p. 357; also,
Frohnmuller, _Med.-Chir. Centralb._, July 14, 1882.)]

If summer heat has been the cause in adults or children, artificial
cooling of the temperature of the room by the evaporation of ice-water
or by one of the refrigerating machines yet to be perfected meet the
indication. If there is much body-heat (thermic fever), cold sponging,
the application of cold to the head, or the giving of pounded ice to
satisfy the intense thirst, are all advisable. Such cases are benefited
by a change of climate when the acute symptoms subside. The form of
diarrhoea due to malaria is to be treated by quinia and change of air
to a more healthful climate. Iron, with quinia or arsenic, is needed in
obstinate cases.

Intestinal catarrh which proceeds from the presence of undigested food
or hard fecal lumps in the bowel is benefited by early removal of the
irritating cause. It is not often that substances of this kind are
retained when the stools are large and frequent. The peristalsis is
here as active as it need be, and no good, but only harm, can come from
over-stimulating the contractile muscles. In those instances where
there is a distinct history of the taking of indigestible food,
especially fruit with seeds or skins, and where the efforts at stool
are frequent, ineffectual, and accompanied by colic and borborygmi, or
where scybalae are found floating in the fluid passed, a large enema of
warm water given slowly will excite the bowel to successful expulsive
efforts. If this does not give a certain amount of prompt relief, a
moderate dose of castor oil, calomel, Rochelle or Epsom salts ought to
be prescribed, and repeated after some hours until a free fluid or
semi-fluid stool results; one or two doses will usually suffice. If the
inflammation is localized in the caecum (typhlitis), as indicated by
local pain, tenderness on pressure in the right iliac or right lumbar
regions, constipation, flexing of the right thigh on the trunk, and
vomiting, a purgative should not be given, nor should prolonged efforts
be made to empty the bowel by injection through long rectal tubes. If
there is doubt as to whether typhlitis or undigested food and fecal
impaction is the cause of the local pain, it is better to err on the
safe side, and not to give a purgative unless the case is seen in the
onset before the more pronounced symptoms appear; then calomel or
castor oil may be tried once, but not repeated in case of failure.

As the diarrhoea of Bright's disease is salutary, no effort should be
made to arrest it. Its periodical recurrence prolongs life. In
tuberculosis the special character of the diarrhoea must be considered,
and every effort must be made to control it. In the eruptive fevers an
early diarrhoea, as in scarlet fever, does harm; it delays or prevents
the normal development of the eruption. In the later stages it is of
service sometimes, as in measles, when it leads to a rapid fall of
temperature. The course of action depends upon the nature of the
specific disease and upon the time of the appearance of diarrhoea.

There are certain principles, founded on the knowledge derived from
pathological study and from the experience of the past in the treatment
{690} of intestinal catarrh, which guide us to a treatment which is
more or less rational in all cases.

Rest is essential to the cure of the inflamed intestine, but absolute
inertia of the bowel is undesirable, even injurious. The retention of
fluids, transuded serum, bile, intestinal juices, and partly-altered
food is hurtful. Decomposition sets in and gas is developed, which by
distending the bowel causes great suffering and increases the
inflammation. The movements of the intestine are not entirely under
control; the patient must be fed; digestion and assimilation involve
the activity of inflamed parts. The stomach can be made to do most of
the work, but the sympathy of action is so close between the stomach
and intestines that one cannot function without the other being excited
into activity.

The first rule of treatment is to put the patient to bed and to keep
him in a horizontal position. Even in mild cases time will be saved by
resorting to absolute rest at once. If the attack is at all severe, the
bed-pan should be used; the effort to rise and the straining at stool
exaggerate peristaltic movement, increasing the frequency of the
evacuations. Additional rest can be given to the intestines by applying
a flannel binder around the trunk, compressing the abdomen; broad
strips of adhesive plaster could be used for the same purpose. In cases
where the diarrhoea, tympanites, and griping pain are not relieved by
other measures this suggestion may be of service.

In order to lessen intestinal hyperaemia and allay suffering,
counter-irritants and soothing external applications are employed.
Local blood-letting, although in vogue during more than two centuries,
has fallen into disuse. Recent authors still continue to advise the
application of leeches to the anus in order to deplete the portal
circulation,[45] but it is a decided objection to this remedy that the
fluid stools irritate the leech-bites and cause much discomfort.
Sinapisms or turpentine stupes may be of some service apart from the
relief which they give to pain. Blisters might be more generally used
than they are when the tenderness on pressure is confined to the colon.
In intense inflammation they should always be tried. Hot poultices of
flaxseed meal or hot fomentations of any sort applied over the entire
abdomen have a soothing and beneficial effect. A flannel compress
saturated with alcohol and covered with gutta-percha cloth makes a most
agreeable application.

[Footnote 45: Niemeyer, _Practice of Medicine, Intestinal Catarrh_.]

The directions for diet should be carefully and explicitly given. In
the onset of the attack entire deprivation of all food for twenty-four
or forty-eight hours is expedient. To relieve thirst, cracked ice,
carbonic-acid water, Apollinaris, Seltzer, or Deep Rock water can be
ordered; barley- or rice-water is slightly nourishing and relieves
thirst, but all liquids should be given in moderation. When it becomes
necessary to give food, the stomach must be made to do the work of
digestion, and, as far as possible, of absorption also. Such substances
are to be chosen as are converted in the stomach into peptones, and
which do not require contact with the intestinal juices for their
absorption.

The peptones transformed in the stomach from nitrogenous alimentary
principles are highly soluble and diffusible. Milk is better suited to
the conditions of intestinal catarrh than any other nitrogenous food.
It is palatable, relieves the thirst, and can be taken for a long time
without {691} aversion. By removing the cream, the fat, which would
require intestinal digestion, is partly got rid of. Skimmed milk does
not produce a feeling of distaste and what is called biliousness, as
does milk unskimmed. In cases where there is gastric catarrh the milk
can be made more digestible by adding an equal quantity of barley-water
or rice-water. The casein is then more slowly acted on by the gastric
juice and more thoroughly digested. Milk should be given in small
quantities at short intervals, as in this way the stomach performs the
entire work more thoroughly. If a large quantity is given, a portion of
it passes into the intestine unaltered. Buttermilk contains less fatty
matter than skimmed milk, and is a pleasant substitute for it. Koumiss,
if it could be properly prepared, would be an excellent food for
diarrhoea. Even the imperfect imitations are retained and digested when
other aliments fail. The whey of milk contains lactin, salts, a little
casein, and fatty matter. It may be made by adding to milk rennet,
sherry or other wine, cream of tartar, tamarind-juice, or alum.
Milk-whey is slightly nourishing, and is said to be sudorific; when
prepared with wine it is a mild stimulant well suited to the cases of
children.

Where it is desired to give as little work to the digestive organs as
is possible, milk and other foods can be given already partly digested,
as peptonized milk prepared according to the formulae of Roberts and
Fothergill.[46] Eggs are changed quickly in the stomach. Egg albumen is
more easily digested by artificial gastric juice than by pancreatic
extract (Roberts). A solution of egg albumen boiled in the water-bath
is swiftly and entirely transformed by pepsin and hydrochloric acid.
Raw eggs have been thought to be the most digestible, but Roberts found
that a solution of egg albumen when raw was very slowly acted on by
pepsin and acid, but after being cooked it was rapidly and entirely
digested. Eggs are best given, therefore, boiled slightly at a slow
heat; when an egg is plunged in boiling water the white sets hard,
leaving the yelk soft. The albumen of the white and the yelk should be
equally cooked throughout.

[Footnote 46: J. M. Fothergill, _Indigestion and Biliousness_, New
York, 1881, p. 63 _et seq._ See also quote to article on CHRONIC
INTESTINAL CATARRH.]

Beef-tea is said by the chemist to possess little nutritive value;
practical experience convinces the physician that it supports life.
Peptonized beef-tea may be substituted when thought best. Animal broths
thickened with rice, barley, or with peptonized gruel, as advised by
Fothergill, or with the addition of vermicelli, are valuable aids when
the palate is capricious. Raw beef is not as digestible as when the
tendinous and aponeurotic structures of the muscular fibre have been
softened, disintegrated, and converted into the soluble and
easily-digested form of gelatin by cooking.[47] Scraped raw beef, when
the pulp is removed from much of the connective tissue, is easily
digested by children as well as by adults.

[Footnote 47: Ibid., _op. cit._, p. 47.]

In most cases of acute intestinal catarrh the patient can be well
sustained by a diet consisting of one or other of the aliments
described. For the largest number milk alone--that is, skimmed milk or
milk diluted with barley-water, rice-water, or Seltzer water--is all
that is necessary to support strength during the attack. Although
starch after deglutition is {692} acted on in the intestine only, it
becomes desirable sometimes to give farinaceous food in some form or
other; milk may be undigested and animal broths may become distasteful;
the palate craves some change. In this case a blanc mange made after
the formula of Meigs and Pepper is as well suited to adults as to
children,[48] the proportion of cream and arrowroot being made larger
for adults. Sago[49] and tapioca[50] can be tried to tempt the palate.
The flour of the Egyptian lentil[51] is made into a gruel also. Most of
the patent foods for infants and invalids contain starch in some form
or other. Racahout is one of the pleasantest and best of these.
Nestle's food contains baked biscuits of wheat flour ground to a
powder. Liebig's food is made of wheat flour, malt flour, and a little
bicarbonate of potassium. Revalenta Arabica is an attractive name for
the flour of Arabian lentil with barley flour. Any of these may be
advantageously employed in cases of some duration and in the later
stages of convalescence.

[Footnote 48: Meigs and Pepper, _Diseases of Children_, Philada., 1870,
p. 304.]

[Footnote 49: Put half an ounce of sago into an enamelled saucepan with
three-quarters of a pint of cold water, and boil gently for an hour and
a quarter. Skim when it comes to the boil, and stir frequently. Sweeten
with a dessertspoonful of sifted loaf sugar. If wine be ordered, two
dessertspoonfuls; and if brandy, one dessertspoonful.]

[Footnote 50: Half an ounce of the best tapioca to a pint and a quarter
of new milk. Simmer gently for two hours and a quarter, stirring
frequently; sweeten with a dessertspoonful of sifted sugar.]

[Footnote 51: Take three tablespoonfuls of lentil flour, a
salt-spoonful of salt, and one pint of water. Mix the flour and salt
into a paste with the water and boil ten minutes, stirring (_Food for
the Invalid_, Fothergill and Wood, New York, 1880).]

The diet for convalescence should be controlled by the physician until
the patient has been well for at least two weeks. Liquid preparations
give place to fine hominy, corn meal or oatmeal porridge, with milk.
Then bread or crackers may be given, the intervals between the meals
increasing to three or four hours. Raw oysters, sweetbreads, tender
rare steak or mutton finely divided and well masticated, rice, and ripe
peaches, succeed the simpler diet. Much saccharine, starchy, or fatty
food is to be avoided for at least two weeks after entire recovery.

When the indications derived from the study of the cause have been
acted on, and the patient has been placed under a rigid discipline of
rest and diet, the treatment of symptoms comes next in order.

In mild cases, where the cause has been irritating ingesta, diet may
relieve the symptoms in a short time without medicine. If diarrhoea
with slight colicky pains and flatulence continue after a few hours, a
mixture holding in suspension subnitrate of bismuth, with five drops of
the deodorized tincture of opium in each dose, or a pill of lead and
opium, will suffice in a short time to give relief. In severer attacks
the fever heat may mount to a high point, giving great distress to the
patient. If a temperature of 103 degrees to 104 degrees F. is
reached--which is not unusual in children--a warm bath is a sedative
and antipyretic remedy, or a bath of 95 degrees can be gradually cooled
down to 75 degrees or 65 degrees F.--a procedure which will bring down
the body-heat two or three degrees. A substitution for the bath is
sponging with cool or cold water, to which vinegar or bay rum may be
added; or towels wrung out of cold water can be applied to the trunk
and extremities (Ringer) with a very happy effect.

Quinia can be used antipyretically in full doses, dissolved in dilute
hydrochloric acid. Pills, especially the sugar- or gelatin-coated
pills, {693} should not be given, as they irritate the mucous membrane
whether they are dissolved or not. In diarrhoea quinia pills often pass
unaltered.

Flatulence, eructations of gas, and borborygmi are controlled by strict
diet according to the rules given. Bismuth subnitrate or subcarbonate
unites with sulphuretted hydrogen and absorbs it. The alkalies, sodium
and potassium bicarbonate, sodium hyposulphite, the aromatic spirits of
ammonia, either relieve acidity or prevent fermentation and the
development of gas. A satisfactory formula for the early stages of
intestinal catarrh is one containing bismuth subcarbonate, sodium
bicarbonate, aromatic spirits of ammonia in water or cinnamon-water.
When the abdominal distension is great enough to be a cause of
distress, external cold--dry cold--is the best, applied with a rubber
bag filled with cracked ice or ice-water; it causes absorption of gas.
Abdominal compression with a bandage may be of some service also.
Mineral acids, especially the dilute hydrochloric acid, by affording
aid to the digestion prevent acid fermentation.

Diarrhoea is the central symptom and the best standard by which to
measure the intensity of the catarrh and its progress. But it is only a
symptom, and the mind ought to be directed to the lesion and not to it.
Having the cause in view, the object in all cases is to allay the
inflammation. This done, the diarrhoea decreases, then ceases. Shall
the effort be made to check the discharges, or shall they be allowed to
continue? The evacuant plan of treatment has been advocated, on the
ground that the purgative, by increasing intestinal secretion, relieves
the congestion of the intestinal blood-vessels and leaves the membrane
in a better state than before.[52] But inasmuch as a purgative only
acts by bringing about an intestinal hyperaemia and catarrh, there is
no good reason for, and many reasons against, treatment by evacuation.

[Footnote 52: Woodward, _op. cit._, pp. 727, 728.]

A preliminary purgative, as has already been stated, is necessary to
expel undigested food and scybalae, but for the purpose of increasing
intestinal or biliary secretion and diminishing engorgement of the
vessels this method is unsuccessful and unnecessary. When irritating
substances have been removed (and this is done usually without the
physician's aid by the spontaneous expulsive movements of the bowel)
the effort to check the discharge and to give rest is one and the same.
Opium is the one invaluable remedy which we cannot do without.[53] As
little of it should be given as is necessary to relieve the intensity
of the symptoms. The aim should not be to stop the pain and check
diarrhoea, but to take the edge off the sharp agony and to lengthen the
interval between the stools. Thus gradually the spasms of peristalsis
cease, and there is a diminution, and finally cessation, of the fluid
accumulation in the bowel. The diarrhoea is relieved entirely in a
period ranging from an hour after the giving of the first dose to one
week, according to the severity of the attack. Opium is given in pill
form, in the deodorized tincture, Dover's powder, or one of the salts
of morphia may be preferred. Any of these may be combined with antacid
and antifermentative mixtures, relieving the colic, gaseous distension,
and diarrhoea. If opium is combined with, {694} or followed by,
evacuants, its effects are thwarted, and it might as well not be given
at all.

[Footnote 53: The objections urged against opium, that it increases
thirst and nervousness, causes a retention of fermenting products,
produces opium intoxication, and that it is a routine practice to give
it, and does not cure the inflammation, may be valid, but we cannot do
without opium, nevertheless.]

It is the custom to combine astringents with opium, but in acute cases
of short duration it is a question whether astringents do not do more
harm than good. When good does come from the combination, it is the
opium which acts promptly and decidedly. The astringent lags behind,
and in cases of some duration and severity supplements the work of the
active partner. Bismuth is classed under this head, although it is not
an astringent. Its action is mechanical; much that is taken is passed
from the bowel as the black sulphide, which appears as a black granular
powder in the fluid stool. This is no proof that it may not have been
of service in its transit.[54] After death, when large doses have been
given, it has been found lining the whole intestinal canal.[55] The
subnitrate or subcarbonate can be given in powder on an empty stomach
in doses of five to twenty grains alone or in combination with opium,
or it can be dispensed with alkalies in water. The enormous doses (one
hundred and fifty to nine hundred grains daily), as given by Monneret,
are useless or hurtful. The value of bismuth is based on empirical
grounds only, but it is irrational to load the bowel with an insoluble
powder which if retained must cause irritation. As the discoloration of
the stools is an objection to bismuth when it is desired to study their
character for diagnosis, oxide of zinc may be substituted for it, as
the latter is an absorbent of acids and gases.[56] Gubler has insisted
upon combining it with bicarbonate of sodium to prevent the formation
of the irritating chloride of zinc in the stomach.[57] One of the
oldest and most popular remedies tor diarrhoea is lime in the form of
the carbonate or lime-water. The officinal mistura cretae is perhaps
more generally used for children than any other remedy. Lime-water is
added with advantage to milk when given to adults as well as children.
Carrara-water, made by dissolving the bicarbonate of lime with an
excess of carbonic acid, is less nauseous than liquor calcis, and may
be mixed with an equal part of milk.[58] Chalk and its preparations are
less beneficial than bismuth as astringents, but may be used merely for
their antacid effect.

[Footnote 54: Headland asserted that bismuth was insoluble, but it has
been detected in the liver, in milk, in urine, and in the serum of
dropsy by Orfila, Sewald, Bergeret, and Mayencon (_Materia Med._,
Phillips, vol. ii. p. 81).]

[Footnote 55: Levick, _Am. Journ. Med. Sci._, July, 1858, p. 101.]

[Footnote 56: Bonamy, "Du Traitement des Diarrhees rebelles par l'Oxyde
de Zinc," _Bull. gen. de Ther._, t. xcii., 1877, p. 251; also, J.
Jacquier, _De l'Emploi de l'Oxyde de Zinc dans la Diarrhee_, Paris,
Thesis, 1878, No. 118.]

[Footnote 57: Gubler, _Principles of Therapeutics_, Philada., 1881, p.
25.]

[Footnote 58: Phillips, _Materia Medica_, vol. ii. p. 105.]

The sugar of lead is a valuable astringent, because unirritating and
sedative to the mucous membrane. With opium in pill form, in doses of
one to three grains, it checks diarrhoea if the inflammation has not
lasted long and is not extensive. If there are cases where the bile is
passed in quantity, it is especially called for, as it is the only
astringent which diminishes the flow of bile.

The mineral acids--dilute hydrochloric, nitric, and sulphuric
acids--are given with some success. The first aids gastric digestion,
and in small doses with pepsin can be directed after food irrespective
of other treatment. The great repute which it has enjoyed in the
diarrhoea of typhoid is no doubt due to the improved digestion and
assimilation {695} which follow its use. The acid principle is what is
lacking in the gastric juice in fever and debility.[59] In all cases of
intestinal catarrh rapidity of gastric digestion should be sought for.
Nitric acid is of doubtful utility. Without an opiate in combination
there is little reason to hope for any result from its use; all the
suggested formulae contain opiates.[60] Dilute sulphuric acid is
thought to be more astringent than the others. If it has any efficacy,
it is due to the local astringent or alterative effect by contact with
the inflamed surface. Much testimony is to be found in its support in
cases tending to become chronic and where astringents combined with
opiates have failed after some days' trial. It should be administered
in doses of five to twenty drops in the form of mixture with mucilage
or some aromatic, as lavender and cardamom. An opiate should not be
combined with it if it is desired to test it fairly. It would be called
for when the stools are pale, abundant, watery, and alkaline.

[Footnote 59: Manassein, _Virchow's Archiv_, lv., 1872, p. 451.]

[Footnote 60: The favor in which nitric acid is held is due to the
advocacy of nitrous acid by Hope ("Observations on the Powerful Effects
of a Mixture containing Nitrous Acid and Opium in curing Dysentery,
Cholera, and Diarrhoea," _Edin. Med. and Surg. Journ._, vol. xxvi.,
1826, p. 35). Nitrous acid, the same as the fuming nitric acid of the
shops, is a reddish-yellow fluid highly charged with nitrogen trioxide.
Hope said that ordinary nitric acid did not produce the same effects,
and yet nitric acid is now given with the belief that it is of
service.]

Calomel is of ancient repute as a remedy in the early stages of
diarrhoea. According to recent views, it acts as a sedative to the
gastro-intestinal mucous membrane and checks fermentation. It should be
given in small doses (one-twelfth to one-eighth of a grain to children,
one-fourth to one-half of a grain to adults); it should not be
continued for more than two or three days. In combination with Dover's
powder it acts well, but it is doubtful which of the two remedies
should receive the greater praise for the resulting improvement. A very
small dose of the bichloride of mercury has been found beneficial by
Ringer for clayey, pasty stools or straining stools containing slime
and blood. His formula is--Hydrarg. bichloridi gr. j; Aquae fluidounce
x; a teaspoonful frequently during the day. The gray powder is not as
much thought of now as formerly; it is not so good for the early stages
of diarrhoea as calomel, but may be tried as an alterative when the
stools are green and offensive.

In the vegetable materia medica there are many and ancient remedies.
Tannin represents a large class, and there is nothing more than fancy
in preferring to it kino, catechu, haematoxylon, or blackberry-root.
Tannin is precipitated in the stomach as an inert tannate; gallic acid
is to be preferred for this reason, and also for its pleasant taste and
less irritating effect on the mucous membrane. It is well borne by
children, even in large doses, when given with water and syrup. It is
to be hoped that the unsightly and unsavory combinations of the
astringent tinctures with chalk mixture will be soon given up. They are
given chiefly to children, who are repelled by the sight, and still
more by the taste, of such compounds. The syrup of krameria is the
least objectionable, and catechu and krameria are made into troches
which are sometimes available.

Ipecacuanha is said by Bartholow to be extremely serviceable in the
diarrhoea of teething children with greenish stools containing mucus or
blood. He prescribes it with bismuth and pepsin.

{696} Recently some favor has been paid to coto-bark and its active
principle, cotoin. The latter is advised to be given in the following
formula:

  Rx. Cotoinae,        gr. j;
      Aquae distillat. fluidounce iv;
      Alcohol,         gtt. x;
      Syrupi,          fluidounce j.

A tablespoonful every hour. Five to eight drops of the fluid extract of
coto are given. It is said to have a speedy and certain effect in acute
diarrhoea.[61]

[Footnote 61: Coto-bark was imported into Europe from Bolivia in 1873,
and was called quinquina coto. Wittstein of Munich and Julius Jobst of
Stuttgart made the first analyses (_Neues Repertorium fur Pharmacie_,
xxiv. and xxv.). Von Gietl (_idem_, xxv.) first concluded from
experiments that it was of use in diarrhoea. Cotoin and paracotoin were
separated by Jobst. It has been found successful in the treatment of
diarrhoea in Germany and of cholera in Japan (Baelz, _Centralb. f. d.
med. Wissen._, 1878, xvi. p. 482). Cotoin sometimes disturbs the
digestion to a marked degree. Paracotoin may be used hypodermically.]

Salicin,[62] ergot, guarana, have all been spoken of by enthusiasts as
possessing valuable properties in diarrhoea.

[Footnote 62: Lawson, "Diarrhoea and its Treatment at the London
Hospitals," _Med. Times and Gaz._, vol. ii., 1868, p. 122; Bishop,
"Salicin in Diarrhoea and Dysentery," _Southern Med. Rec._, vol. iv.,
1874, p. 585; "Comparative Value of Opium and Salicin in Diarrhoea and
Dysentery," _Detroit Review of Med. and Pharm._, vol. x., 1875, p.
387.]

Alum is not often prescribed. Sulphate of copper is fitted for cases in
danger of passing into the chronic stage. Sulphate of zinc might be
more generally ordered than is the case. The sulphate of iron and the
fluid preparations of iron--tincture of the chloride, solution of the
pernitrite, and persulphate--are astringents, and could be tried if
other remedies fail. The effect of nitrate of silver is to constrict
vessels, to coagulate and disinfect excretions, and to form an adherent
protecting membrane (Phillips). It occupies the next place to lead, and
is suited to a subacute stage when acute symptoms have subsided. It is
warmly recommended by William Pepper and others.[63] The oxide of
silver has been preferred by some writers.[64] For the protracted
diarrhoea of children, in whom follicular ulcers form so rapidly, the
nitrate of silver is of special value. To adults it is administered in
a pill freshly made in doses of one-eighth to one grain. A solution in
distilled water with syrup answers well for children, the dose varying
from one-twentieth to one-fourth of a grain.

[Footnote 63: J. Maggregor, "On the Internal Use of Nitrate of Silver
in Inflammation of the Intestines," _Lancet_, 1841, vol. ii. p. 937.]

[Footnote 64: Lane, _Med.-Chir. Rev._, July, 1840, p. 289 _et seq._;
Eyre, _The Stomach and its Difficulties_, London, 1852.]

The theory of the germ origin of diarrhoea has naturally brought into
notice antiseptic remedies. Carbolic acid,[65] creasote,[66]
naphtha,[67] sulpho-carbolate of calcium,[68] salicylic acid,[69] and
chlorine-water have each been advocated. Practice does not support
their claim to be considered remedies for intestinal inflammation.

[Footnote 65: Habershon, _Lancet_, London, 1868, vol. i. p. 7; C. G.
Rothe, _Berliner klin. Wochenschrift_, 1871, p. 527.]

[Footnote 66: _Southern Med. and Surg. Journ._, vol. ii., 1846, p. 583;
_ibid._, vol. iii., 1847, p. 147; _London Med. Gaz._, vol. ix., 1849,
p. 254; _ibid._, vol. xii., 1851, p. 235.]

[Footnote 67: _Gaz. des Hopitaux_, 1849, p. 46.]

[Footnote 68: _Tr. Obstet. Soc. Lond._, vol. xii., 1870, p. 12.]

[Footnote 69: W. Wagner, _Kolbe's Journ. fur prakt. Chemie_, Bd. xi.,
1875, S. 60.]

{697} Treatment by the rectum may be employed when medicines are
rejected by the stomach or when it is desired to bring the drugs into
more direct contact with the inflamed colon. Opiates, astringents, and
alteratives are employed in this way. Laudanum in two to four ounces of
warm water or in warm milk or starch-water can be thrown into the
rectum, the fluid being allowed to remain. The injections are to be
given often enough to relieve pain and lessen the number of discharges.
With the laudanum, or without it, the mineral astringents can be used
by enema. Acetate of lead or sulphate of zinc is to be preferred. The
objection that but a small portion of the inflamed surface is reached
by the fluid is a valid one, and therefore those cases are most
benefited where the catarrh is in the lower colon and rectum.
Ringer[70] says that it is not at all necessary for the fluid to reach
that part of the intestine which is the seat of the catarrh; the
impression made on one part is communicated to the other by sympathy.
It was the practice with O'Beirne,[71] Hare,[72] and others to inject
fluid by a long flexible tube passed beyond the sigmoid flexure. This
method is advocated and employed in Europe by Mosler, Winterinz, and
Monti. Quite recently Dulles has drawn attention to irrigation of the
large intestine as a means of treating inflammation of the colon,
according to the plan of Alois Monti of Vienna.[73] Henoch has tried
with partial success in children the throwing into the rectum of a
large quantity of water holding in solution acetate of lead, alum, or
tannin. His method contemplates medication above the sigmoid flexure; a
part of the fluid escapes, while the rest remains five or ten minutes
in the bowel.[74] Monti says as much as two pints can be injected into
the bowel of a nursing child--for older children twice this quantity.

[Footnote 70: _Therapeutics_, New York, 1882, p. 99.]

[Footnote 71: _New Views of the Process of Defecation_, Washington,
1834, p. 85.]

[Footnote 72: E. Hare, "On the Treatment of Tropical Dysentery by means
of Enemata of Tepid Water," _Edin. Med. and Surg. Journ._, vol. lxxii.,
1849, p. 40.]

[Footnote 73: Dulles, "Irrigation of the Colon," _Philada. Med. News_,
Aug. 19, 1882, p. 199. The patient is placed on the side, back, or on
belly, with the hips elevated. A large flexible catheter if a child, a
stomach-tube if an adult, is inserted into the rectum. The tube is
connected with a reservoir of water elevated above the patient. The
rectum is first distended with water, and the tube is gradually made to
follow the course of the bowel until it finds its way into the
descending colon. Thus the water may be made to distend the whole of
the colon to the caecum. The fluid remains from a few minutes to half
an hour.]

[Footnote 74: Henoch, _Diseases of Children_, Am. ed., New York, 1882,
p. 206.]

Messemer[75] reported three cases (one child and two adults) treated in
this way with the most striking success. His object at first was to
cleanse the rectum, but warm water did not check the diarrhoea. Cold
water was tried, and (probably by reflex influences) diminished rapidly
the number of the discharges. And Ewald[76] has imitated Messemer's
method with results which are surprisingly good. He injected 200 and
300 cc. of cold water, which was expelled by pressure on the abdomen;
50 cc. were then thrown in and allowed to remain. He has used the
treatment in a large number of cases in children. The question as to
the ability to force water thrown into the rectum through the sigmoid
flexure and distend the colon has been settled by the experiment of
Mosler in a case where there was a caecal fistula. Water injected into
the {698} rectum traversed the colon and escaped through the fistula in
two minutes.[77]

[Footnote 75: J. B. Messemer, "Cold-Water Enemata as a Therapeutic
Agent in Chronic Diarrhoea," _American Journal of the Med. Sci._, vol.
lxxvi., 1878, p. 133.]

[Footnote 76: _Lectures on Digestion_, New York, 1881, p. 149.]

[Footnote 77: _Berlin. klin. Woch._, No. 45, 1873, p. 533. Woodward, in
discussing the claims of Battey of Georgia to priority in the discovery
of the permeability of the entire alimentary canal by enema (see paper
by Battey in _Virginia Med. Monthly_, vol. v., 1878, p. 551), quotes
from A. Guaynerius, who lived in the fifteenth century, from J. M. de
Gradibus (1502), Sennertus (1626), and from others among the older
writers to show that it was well known that suppositories and enemata
introduced into the rectum are sometimes thrown up by the mouth. He
mentions experiments by Alfred Hall (1845), G. Simon (1873), and F.
Koster (1874) which demonstrated that large quantities of water may be
forced from the rectum into the stomach. (See Woodward, _op. cit._,
foot-note, p. 836.)]

When ulcers are thought to be present, the remedies of particular value
are nitrate of silver, bismuth or turpentine, and the mineral acids,
given in conjunction with a rigid system of diet.

In hemorrhagic diarrhoea ice externally or ice-water injections, opium,
acetate of lead in large doses (ten to fifteen grains), gallic or
tannic acid, and ergot are the appropriate remedies.

Some modifications of treatment are required for the choleraic form (in
children, cholera infantum); the danger here is imminent from the drain
of water and collapse. For the vomiting of the early stages, pounded
ice eaten freely, potassium or sodium bromide in ice-water, and
counter-irritants over the abdomen, with cold sponging or cold baths
and ice to the head if there is much body-heat. Brandy, whiskey, or
coffee in full doses is called for early. Iced coffee can be given to
children. Spirit of camphor in five-drop doses every ten minutes aids
in averting collapse. Small doses of calomel every hour or two may
benefit nausea and vomiting. Arsenic is said to do well for vomiting
and profuse watery diarrhoea. For adults, morphia hypodermically is
perhaps the best remedy for the vomiting and purging; even for
children, minute doses given in this way are best for alarming illness.
Hypodermic injections of ether have also been suggested.

For the relief of duodenitis means are used to relieve the digestion of
the want of the biliary and pancreatic secretions. Nitrogenous food is
to be taken, but no fats or starch. Counter-irritation over the
epigastrium and right hypochondrium by a blister or iodine is of direct
service. If icterus accompany duodenitis and catarrh of the bile-ducts,
all treatment must be directed to the duodenum. For ileo-colitis and
colitis the rules already given apply.




{699}

CHRONIC INTESTINAL CATARRH.

BY W. W. JOHNSTON, M.D.


ETIOLOGY.--Chronic intestinal catarrh has many of the same causes as
the acute form; it is the expression of a large number of different
pathological states and complicates many general and local diseases.

It is very common in children under two years of age, and is associated
with change in diet in weaning and with the irritability of all the
tissues during dentition. It is also a frequent disease in old persons,
being due to imperfect mastication, the weakness of digestion, portal
congestion, the gouty diathesis, and other causes.[1] Men have the
disease more frequently than women. Hereditary influence and
idiosyncrasy predispose to chronic catarrh of the bowel as to catarrh
of the bronchi. Bad hygiene, want of cleanliness with an unhealthy
condition of the skin, constant breathing of foul air due to want of
proper ventilation, animal decomposition, or overcrowding predisposes
to chronic diarrhoea. The chronic diarrhoeas among soldiers in
camps,[2] among the inmates of prisons, workhouses, and asylums, are
examples of these influences. Overwork, especially mental overwork with
anxiety, and privation of sleep act in the same direction. In the
chronic constitutional diseases and in many chronic diseases of organs
diarrhoea sooner or later appears, and very generally is the immediate
cause of death. In phthisis pulmonum, whether tubercular or not, simple
catarrh of the bowel is nearly always present.

[Footnote 1: _La Diarrhee chez les Viellards_, Paris, Thesis, 1865, No.
112. See also works of Durand-Fardel and Charcot and Loomis.]

[Footnote 2: According to the statistics prepared in 1871 by T. B. Hood
of the U.S. Pension Office, chronic diarrhoea was the disease for which
a pension was granted in 20 per cent. of all cases of disability from
disease and in 75 per cent. of all the diseases of the digestive system
(_Report of Commissioner of Pensions_, 1871).]

During the course of chronic Bright's disease, more frequently in the
cirrhotic form, lesions are developed in the intestine which cause
obstinate diarrhoea. The discharge of urea into the intestine, and its
conversion into carbonate of ammonium, which acts as an irritant to the
mucous membrane, is the reason of the diarrhoea in this disease,
according to Luton and Treitz;[3] and in so far as the discharge
represents the escape of urea by the bowel, it may be regarded as
salutary. In gout, especially in old persons, periodical diarrhoea
gives relief. Chronic gouty subjects assert that they are not benefited
by colchicum until it has purged them. The {700} lithic-acid diathesis,
pyaemia, septicaemia, scurvy,[4] diabetes, leucocythaemia, Addison's
disease, and syphilis[5] have diarrhoea during some part of their
progress. The malarial cachexia is often attended with a diarrhoea
which quinia alone will relieve; this symptom may occur periodically or
be constant.

[Footnote 3: A. Luton, _Des Series morbides, Affections uremiques de
l'Intestin_, Paris, Thesis, 1859, No. 38, p. 45; also, Treitz, "Ueber
uramische Darmaffectionen," _Prager Vierteljahrschrift_, Bd. 64, 1859,
S. 143.]

[Footnote 4: See testimony as to the influence of scurvy in promoting
diarrhoea (Woodward, _Med. and Surg. History of the War_, Part 2,
Medical Volume, p. 638).]

[Footnote 5: A. Trousseau, "Comments on a Case of Syphilitic Diarrhoea
cured by Mercury," _Clinique med._, Paris, 1868, t. iii. p. 123.]

Disease of the liver, heart, or lungs, by retarding the circulation in
the portal system, causes venous stasis and catarrh in the
gastro-intestinal mucous membrane. The chief conditions which bring
this about are tumors compressing the mesenteric veins, cirrhosis of
the liver, tumors pressing on the ascending vena cava, valvular disease
of the right and left heart, fatty degeneration or dilatation of the
heart, cardiac debility from chronic exhausting diseases, fibroid
phthisis, chronic pneumonic phthisis, chronic pleurisy, and pulmonary
emphysema.

An unsuitable diet may not set up an acute catarrh, but may slowly
induce changes of a chronic nature in the mucous membrane. This is the
case in infants fed upon artificial food instead of breast-milk, or
when the digestion is overtaxed after weaning. In adults food difficult
of digestion and over-eating bring about the same result. Alcohol,
spices, and condiments, if taken in excess, and the habitual use of
purgatives, lead to chronic inflammation of the intestine.

Foreign bodies, such as fecal concretions, gall-stones, stones of
fruit, bones, coins, and pins, by remaining in contact with the mucous
membrane for a length of time, determine inflammation and
ulceration.[6]

[Footnote 6: Lothrop, "Case of a Child in whom seventeen plum-stones,
three cherry-stones, and seven small bones were impacted In the caecum
and ileum for a year. Inflammation, ulceration, and perforation of the
bowel resulted" (_Buffalo Med. and Surg. Journ._, March, 1882, p.
346).]

Neglect in the treatment of acute catarrh, the prolongation of an acute
attack, from its intensity and the incurability of the lesions,
establish chronic disease.

All chronic lesions of the bowel are complicated with chronic catarrh,
as chronic tubercular ulcer, neoplasms in the wall, pressure of a tumor
from without, etc.

PATHOLOGICAL ANATOMY.--The alterations in the intestines in chronic
catarrh involve the walls to a much greater extent than in the acute
form.

The intestinal tube is dilated, contracted, or irregularly dilated and
contracted. When the calibre is increased the walls are thinned.
Hypertrophy and hardening of the tunics, chiefly of the muscular and
submucous tissue, are accompanied by a narrowing of the canal, and this
change, most common in the rectum and sigmoid flexure, sometimes
involves a very considerable extent of the colon. Lebert records the
case of a woman who had diarrhoea for six weeks; constipation and
vomiting with abdominal tenderness ensued. There was hypertrophy of all
the coats of the stomach and of the ascending colon and rectum. The
rectum was so narrowed by the thickening of its wall that a female
catheter could not be passed through it.[7] In chronic catarrh the
mucous membrane {701} of the colon and of the lower part of the ileum
is the seat of the most characteristic lesions. The colon was alone the
seat of disease in 9 out of 99 cases analyzed by Woodward; in the
remaining 90 the two were involved together. In these the lesions in
the colon (especially in the rectum and sigmoid flexure) were always
more advanced and more serious than in the small intestine.

[Footnote 7: Lebert, _Path. Anat._, t. ii. pp. 247, 248; another case,
Laboulbene, _Anat. path._, Paris, 1879, p. 194.]

Gastric catarrh may by extension become duodenal catarrh, and from the
duodenum the disease may extend into the common bile-duct and its
branches. The duodenitis and catarrh of the ducts may persist, and
become chronic after the stomach lesion is gone.

The mucous lining of the intestine is changed in color, form,
thickness, consistence, and in the appearance of its glandular
structures. The shades of color in chronic inflammation are dark red,
livid, brown, drab, or slate-color, light blue, and greenish. The
coloration is not uniform. Dark-red and gray spots are seen on a pale
and uniform red ground; grayish streaks and patches are mingled with
red or whitish areas, giving rise to a mottled or marbled
appearance.[8] In some cases red predominates, in others the
slate-color.[9] Dark-brown, almost black, patches are also seen. These
different tints depend upon the intensity and character of the
inflammation and the stage which it has reached. Diffused bright-red
discolorations belong to acute inflammation, and are rarely seen in the
chronic form. Acute hyperaemic patches appearing in the midst of a
slate-colored membrane indicate intercurrent acute attacks. Dark-red
streaks or spots are caused by extravasations. Brown and slate-colored
areas represent the changes in old extravasations or pigment-deposits
where inflammation or ulceration has existed. Where the inflammation is
progressing toward the destruction of tissue the membrane is
dark-purplish or black in color, mottled with patches of dull reddish
hue and minute spots of bright red. Black dots are seen in the small
and large intestine isolated or in close proximity. They are due to
minute specks of black pigment deposited in the apices of the villi, in
the centres of solitary glands, in rings around them, or in the glands
of a Peyer's patch. The juxtaposition of pinhead black points gives
rise to the shaven-beard appearance[10] of the mucous membrane. Dark
streaks or wavy lines of pigment are also seen.[11]

[Footnote 8: For illustration of color of mucous membrane in chronic
inflammation see the following illustrations in color: _Med. and Surg.
Hist. of the War_, Part 2, Medical Volume--plates facing pp. 308, 518,
and 520; also, _Illustrations of Morbid Anatomy_, J. Hope, London,
1834, figs. 128, 129.]

[Footnote 9: For an excellent illustration of slate-color of chronic
inflammation, with supervening acute inflammation and hemorrhagic
patches, see Carswell, _Path. Anat._, Plate ii. fig. 4; also, Lebert,
_Path. Anat._, t. ii. Pl. cxiv. fig. 7.]

[Footnote 10: For an excellent illustration of this change see _Med.
and Surg. Hist. of the War_, volume cited, plates facing pp. 298, 304;
also, _Atlas d'Anatomie path._, Lancereaux, Paris, 1871, Pl. iii. figs.
3 and 4.]

[Footnote 11: See colored plates _Med. and Surg. History of the War_,
volume cited, facing p. 308.]

In the ileum the mucous folds are obliterated or swollen and thickened.
Obliteration of the folds occurs in connection with a dilated
intestine; when the intestine is contracted they are elevated,
tortuous, and close together. The villi are hypertrophied, looking
often like minute polypi. The mucous coat is usually thickened,
measuring from one-fifth to one-fourth of an inch. It is softened, and
more easily scraped off,[12] but quite {702} frequently there is
induration instead of softening. The solitary glands of the ileum are
hypertrophied and appear scattered over the mucous surface as small
rounded elevations. They are quite numerous or a few only may be seen.
A ring of vascular injection usually surrounds each enlarged follicle.
Peyer's patches may be unchanged or from swelling of the follicles are
more prominent than is normal, but relatively the enlargement of the
solitary glands is greater. In chronic catarrh the follicles acquire
greater size than in the acute form. The apices of the solitary glands
in the small intestine may be broken down, leaving small follicular
ulcers, with swollen rings around them formed of the undestroyed and
hypertrophied gland-structure. Here and there one or two of the
follicles in the Peyer's patch may have its centre indented by
ulceration. These changes are usually in the lower part of the ileum
near the caecum.

[Footnote 12: The mucous membrane is often tumefied and softened in
cases where there are thickening and contraction of the intestine with
great reduction of its calibre (Elliot Coues, _Med. and Surg. Rep._,
Philada., 1863, vol. x. p. 207).]

In the colon the enlarged solitary glands are in greater number, and
are dotted about more closely in the descending colon and sigmoid
flexure.[13] When there is ulceration the large intestine has many more
ulcers than the ileum, and they are more numerous in the lower part of
the colon. They appear as sharply-punched openings, and give to the
mucous surface a honeycombed look; their diameter varies from one-tenth
to one-fourth of an inch. Large ulcers formed by the confluence of
smaller ones measure from one-fourth to one inch in diameter; they may
be so deep as to have the muscular tunic for their base, and quite
often the bottom of the ulcers is black. A ragged or uneven appearance
is given to the surface by the ulcers being close together. Such
extensive destruction sometimes takes place that no normal mucous
membrane seems to be left. Perforating ulcers are occasionally seen in
the large intestine or ileum. Perforation occurred in two of Woodward's
ninety-nine cases. Healing ulcers[14] are found by the side of others
which are growing. Healed follicular ulcers are known by a puckered,
stellated appearance[15] of the mucous membrane, which is pigmented and
of a slate-gray or marbled-brown color[16] if the process has been long
completed. Larger dense cicatrices, pigmented also, mark the site of
more extensive ulcerations.

[Footnote 13: Illustration, _Kupfertafeln zu_ DR. LESSER _uber die
Entzundung und Verschwarung du Schleimhaut des Verdauungskanales_,
Berlin, 1830, Bei Enslin, Tab. ii. fig. 4.]

[Footnote 14: Illustration, J. Hope, _Illustrations of Morbid Anatomy_,
figs. 168, 169.]

[Footnote 15: Illustration, _Med. and Surg. Hist. of the War_, _tom.
cit._, p. 528.]

[Footnote 16: Illustration, Cruveilhier, _Anat. path._, xxx. livraison,
Pl. iii.; also, J. Hope, _Illustrations of Morbid Anatomy_, figs. 128,
129.]

Besides follicular ulcers the mucous membrane is disorganized by ulcers
which have their origin in a loss of epithelium and superficial
erosion. These deepen and may attain considerable size.

In addition to the lesions already described, the inflamed and
ulcerated surface is sometimes covered with a pseudo-membranous layer
of greenish-yellow color.

Chronic catarrh of the duodenum is the cause of dilatation of the
vessels and thickening of the coats. A varicose condition of the veins
may give rise to hemorrhage without ulceration.[17] The orifice of the
common bile-duct and the ducts for some distance are narrowed by
swelling of their lining membrane.[18] Ulcer of the upper part of the
duodenum {703} is found rarely in connection with external burns and
chronic Bright's disease. It is more common in men between thirty and
forty years of age. An embolized artery is the starting-point of the
lesion. The mucous layer, deprived of its nutrition in a limited area,
dies or is destroyed by the acid gastric juice; a round ulcer with
terraced edges is left, its base being the muscular or serous coat.
Adhesions may form between the peritoneum near the ulcer and the liver,
gall-bladder, or pancreas, or an opening may take place posteriorly in
the right seventh intercostal space or into the peritoneal cavity.
Cicatrization of the ulcer may lead to narrowing of the canal of the
bowel or of the pancreatic and common bile-ducts.[19]

[Footnote 17: G. Coulon, _Bull. de la Soc. Anat. de Paris_, 1879, p.
690.]

[Footnote 18: Duodenitis was made much of by Broussais and his
followers, and a great deal has been written about it. (See Boudin,
Paris, Thesis, 1837, No. 76, _Essai sur la Duodenite chronique_.)]

[Footnote 19: _Ziemssen's Cyclopaedia_, Amer. ed., vol. vii. p. 404.]

Suppuration in the wall of the duodenum is still rarer. One case only
is on record of pus being found in the intestinal wall.[20]

[Footnote 20: Picard, _Bull. de la Soc. Anat. Paris_, t. xv., 1840-41,
p. 393. See also microscopic view of suppuration in wall of duodenum,
Thierfelder, _Atlas d. path. Histologie_, 2 lief., Tab. x. fig. 6.]

Chronic proctitis or inflammation of the rectum may exist by itself.
The mucous membrane is swollen, hyperaemic, and the walls may be
indurated and thickened so as to reduce the calibre of the tube.
Superficial erosions or deep ulcers and perforation are due to the
retention of hard fecal matter in the distended pouches of the rectum.
Inflammation in the tissue around the rectum (periproctitis) is excited
by inflammation of the wall without perforation; abscesses form and
burst externally or into the bowel, thus establishing fistulae.

PATHOLOGICAL HISTOLOGY.--The essential primary feature of chronic
catarrh is the increase and persistence of cell-accumulation in the
reticular connective tissue of the mucous and submucous layer. After an
acute or subacute attack some time elapses before the large number of
cell-elements are disintegrated or absorbed. By remaining they offer a
constant invitation to causes of irritation, hence the necessity for
prolonged care in diet after acute attacks. Fresh causes--imprudence in
eating, etc.--induce additions to the number of cells, and the tissue
becomes overcharged with active elements of growth. Hypertrophy of
tissues results, the mucous and submucous tissues thicken, and the
glandular structures are stimulated to a condition of morbid activity.
The glands of Lieberkuhn elongate, the number of acini increases, and
the contained cells multiply. Accidental closure of the gland-openings
from outside pressure or over-accumulation of the contents leads to
cyst-formations. The lymph-cells in the reticular tissue of the closed
follicles undergo rapid increase; the follicle is over-distended,
projects above the surface, bursts, and a small ulcerating cavity is
left. This is now enlarged by the breaking down of the remaining tissue
of the follicle, then of the submucosa. The overhanging roof of mucous
membrane, deprived of its nutrition, sloughs off at the edges and the
exposed ulcerated surface is increased. By the confluence of two or
more burrowing ulcers more extensive destruction of the mucous and
submucous layers is brought about. The large deepened ulcers have the
mucous layer for their base. Cicatrization of the ulcers takes place by
the formation of cicatricial tissue at their base; the excavation is
filled up partially, by contraction the edges are brought together, and
the tissue solidifies. No villi or epithelium covers these cicatrices.

{704} There are rarer pathological changes. In catarrh of long duration
cysts are found, especially in the large intestine. They are about the
size of a small pea, projecting above the mucous surface. They have a
yellow or amber color, and contain a jelly-like yellow fluid which can
be pressed out. They originate in the distension of the dilating glands
of Lieberkuhn; according to Woodward, they find a favorable nidus for
their growth in the softening tissue of the solitary glands; hence the
cystic forms are seen occupying the interior of follicles undergoing
disintegration.[21] The presence of the glands of Lieberkuhn in the
interior of the closed follicles has been observed by other
pathologists, some of whom are unable to explain so remarkable a
lesion.[22] Around the edges or in the midst of healing ulcers in the
intestine granulation-like excrescences or polypoid growths are
observed as a rare lesion. These seem to be projections from
undestroyed islands of mucous membrane, being surrounded by the
ulcerated surface. The minute polypi originate in a process of growth
of the undestroyed mucous tissue. Cicatricial contractions around their
bases give them peculiar forms; they are club-shaped, simple, or
branched. This lesion has been described by Johann Wagner,[23] Carl
Rokitansky,[24] and J. J. Woodward[25] from original specimens.
According to Woodward, the growths (pseudo-polypi he calls them) are
composed of a central portion of connective tissue continuous with the
submucous connective tissue of the intestine and a peripheral portion
of diseased mucous membrane. The central connective tissue was filled
with large and numerous cells, and the glands of Lieberkuhn in the
mucous covering were elongated and branched and showed evidences of an
active hyperplasia.

[Footnote 21: J. J. Woodward, _op. cit._, pp. 570, 571.]

[Footnote 22: A. Laboulbene, _Anat. path._, Paris, 1879, p. 186.]

[Footnote 23: "Einige Formen von Darmgeschwuren; iii., die
Dysenterische Darmverschwarung," _Med. Jahrb. des k. k. ost. Staates_,
Bd. xi., 1832, S. 274.]

[Footnote 24: "Der dysenterische Prozess auf dem Dickdarme und der ihm
gleiche am Uterus, vom anatomischen Gesichtspuncte, beleuchtet,"
_ibid._, Bd. xxix., 1839, S. 88.]

[Footnote 25: "Pseudo-polypi of the Colon," _Am. Journ. Med. Sci._,
Jan., 1881, p. 142.]

Polypi of the colon have been seen and figured by other pathologists,
but they were not connected with ulceration and cicatrization of
ulcers. Luschka[26] saw the mucous membrane from the ileo-caecal valve
to the end of the rectum covered with polypi, club-shaped, the size of
a hempseed or bean, and made up of glandular tubes simple or branched.
Other cases have been described by Lebert, Heuriet, and others,[27] in
which polypi were distributed in the rectum, colon, caecum, or about
the ileo-caecal valve. This is the condition described by Virchow as
colitis polyposa.

[Footnote 26: _Virchow's Archiv_, vol. xx. p. 133.]

[Footnote 27: Heuriet, _Bull. de la Soc. Anat. Paris_, t. xlviii.,
1873, p. 250; _Tr. N.Y. Path. Soc._, vol. ii., 1877, p. 172. For
illustration of multiple polypi of colon and rectum, Lebert, _Path.
Anat._, tome ii., Pl. cxxii. figs. 1 and 2; granular elevations in
ileum, _idem_, Pl. cxxi. fig. 1. Also, mucous polypi of rectum,
Thierfelder, Tab. xiii. figs. 3, 3_a_, 3_c_; also, intestinal polypi of
rectum, Lancereaux, _Atlas Path. anat._, 1871, Paris, Pl. iv. fig. 4.
Polypi are rarely seen in the small intestine; see Bottcher, "Polyposes
Myom des Ileums," _Archiv der Heilkunde_, xi. Jahrgang, 1870, p. 125.]

Atrophy of the wall of the intestine, chiefly of the mucous layer,
supervenes upon catarrh. It is confined to certain areas, the rest
being normal or in a state of chronic catarrh. It is found in 80 per
cent. of the cases examined either in the large or small intestine. The
caecum is the most frequent seat; next in the order of frequency it is
seen in the ascending {705} colon, the lower part of the ileum, the
other parts of the colon, and is least common in the upper part of the
ileum. In children the lesion is more common in the small intestine
than in adults. The changes in the mucous membrane of the colon are a
diminution in its thickness and disappearance of the glands of
Lieberkuhn. The mucous layer is reduced to one-fifth of its normal
size, and no trace of the glands may be left; a layer of connective
tissue with imbedded round cells is all that remains. The surface of
the membrane is irregular and colored with yellowish pigment. In the
ileum the villi are shrunken, with few cells; in some cases they
disappear altogether. The muscular tunic may share in the atrophy.[28]

[Footnote 28: Nothnagel, "Zur Klinik der Darmkrankheiten," iii.
Abtheilung, Darmatrophie, _Zeitschr. f. klin. Med._, Berlin, 1882, iv.
p. 422; Virchow, "Ueber den Gang der amyloiden Degenerationen,"
_Virchow's Archiv_, Bd. viii. S. 364; E. Neumann, "Neue Beobachtungen
uber amyloide Degeneration," _Deutsche Klinik_, Bd. xii., 1860, S. 337,
353, and 373; Lambl, "Ueber amyloide und colloide Degeneration im
Allgemeinen und die des Darmsinsbesondere," _Beob. und Studien_ (_aus
dem Prager Kinder-Spitale_), Prag., 1860, S. 319; Frerichs, "Diseases
of the Liver," New York, 1879 (_Wood's Library_), vol. ii. p. 180; M.
G. Hayem, "Note sur la Degenerescence amyloide du Tube digestif,"
_Compte Rend. des Seances de la Soc. de Biologie_, Nov., 1865, 4me
Serie, t. ii. p. 191; also, _Gaz. med. de Paris_, t. xxi. p. 99.]

Lardaceous (amyloid or waxy) degeneration of the intestinal mucous
membrane is met with in chronic catarrh. The small arteries of the
villi and submucous layer, the muscular and other tissues, are
infiltrated with a new material allied to fibrin. The membrane to the
eye is paler than normal. When iodine is applied, a characteristic red
staining of the infiltrated parts is noticed. This lesion is a cause of
diarrhoea and of hemorrhage,[29] from the greater permeability and
greater fragility of the arteries. It is also associated with
follicular ulceration, and is probably a cause of disintegration of the
mucous membrane.[30]

[Footnote 29: T. Grainger Stewart, "On Hemorrhage from Waxy or Amyloid
Degeneration," _Br. and Foreign Med.-Chir. Rev._, vol. xli. p. 201.]

[Footnote 30: Frerichs, "Diseases of the Liver," New York, 1859
(_Wood's Library_), vol. ii. p. 180; also, E. Aufrecht, _Berl. klin.
Woch._, 1869, p. 315.]

The abdominal organs present other lesions in chronic intestinal
catarrh, few of which have any distinctive character. The peritoneum
shows signs of old or recent inflammation. The former is subacute or
chronic, and is recognized by the adhesions of opposed surfaces in a
limited area, frequently corresponding to the seat of intense
intestinal inflammation. Fatal perforations are delayed or prevented by
these adhesions. General peritonitis with soft lymph or sero-purulent
effusion is found with perforation. The mesenteric glands may be
enlarged. The liver is larger or sometimes smaller than normal, and its
tissue is softened and may be fatty. Abscess of the liver[31] is a very
rare result of chronic intestinal catarrh, with ulceration. The
gall-bladder is usually filled with bile. The spleen is small and firm
in texture; less commonly it is soft and friable. The pancreas is
healthy. The kidneys are large and pale; the cortical substance is
relatively increased and the tubules contain granular epithelium.

[Footnote 31: It occurred in 4 per cent. of Woodward's cases of chronic
follicular ulceration. See case reported by the writer in which the
ulcers healed before the death of the patient from hepatic abscess
(_Maryland Med. Journ._, March 15, 1883, p. 562).]

In the thorax the heart is flabby, pale, and small; clots are found in
the right and left side extending into the pulmonary artery and aorta.
Sudden death has been attributed to cardiac thrombosis. That coagula
{706} do form in the heart during life is shown by the sudden
occurrence of cerebral embolism with aphasia.[32]

[Footnote 32: The writer has seen one case of this kind occurring
during the effort at stool in a patient who was very feeble and very
anaemic from chronic intestinal inflammation with ulceration.]

Pneumonia is the most frequent pulmonary lesion; it may be single or
double. It was found in 18 of the 99 cases of Woodward, and in 21 out
of H. A. Allen's 41 cases. Inflammation of the pleura is not
infrequent. The brain and its membranes may be congested, and fluid is
found in the subarachnoid space, in some instances in cases which have
had a sudden termination. The cornea is ulcerated, and the eye
destroyed by opening of the anterior chamber in a small proportion of
cases. The sloughing process begins in the lower part of the cornea and
in the sclerotic.

SYMPTOMS.--When chronic intestinal catarrh succeeds the acute form, the
transition is marked by the disappearance of fever and an amelioration
of all the symptoms, with apparent recovery. The patient begins to go
about, but diarrhoea returns whenever there is any unusual fatigue or
excess in eating. In some cases there is no improvement in the
diarrhoea, but in the general symptoms only. When the malady is chronic
from the beginning, the onset is characterized by symptoms of
indigestion and occasional diarrhoea, which become more and more
pronounced according to the severity of the illness.

Mild forms of catarrh have constipation, or diarrhoea alternates with a
normal or constipated state of the bowels. The form in which
constipation is continuous is associated with mechanical stasis from
liver and heart lesions and with the gouty and uric-acid diathesis. The
mucous membrane is in a state of passive hyperaemia, an excess of mucus
being the product of the inflammatory process. Mucus coats the lining
tunic, lessens its irritability, interferes with digestion and
absorption, and acts as a ferment, exciting decomposition in the food.
The bowel is atonic and is distended with contained gas; there is great
feebleness of peristaltic contractions.

Intestinal indigestion and constipation are therefore the symptoms of
this form. The signs of indigestion occur one to three hours after
eating, according to the location of the maximum of catarrh and the
time taken by the food to reach this point. They are a sense of fulness
or distress in the abdomen from gaseous distension, slight colicky
pains, and a rumbling of gas, which may be prolonged during several
hours after a meal. The constipation is indicated by the spontaneous
passage of dry masses or scybalae coated with layers of mucus which are
clear or cloudy, or the mucus may be intimately mixed with solid
matter. Pure mucus is also expelled without fecal matter. There may be
no stool without a purgative, and then softened matter with scybalae
and mucus is passed. Altered mucus in the form of membraniform shreds
or cylinders occasionally pass in the so-called membranous enteritis.

The abdomen is full and not sensitive to pressure. The tongue is coated
and usually pale and flabby. In appearance the patient exhibits a
general want of tone; the skin is white or muddy, the muscles are soft,
and the expression indicates the depression of spirits, the lassitude,
and the inertia which he feels. Hemorrhoids are very likely to {707}
exist. Such a condition may last for months or years without much
change. Under proper treatment recovery may take place, but if entirely
neglected or improperly treated the disease inevitably becomes worse.

In a second mild form there is no permanent disease, only an
impressionability of the mucous membrane of the bowel to causes which
induce hyperaemia and excessive secretion ending in diarrhoea. Exposure
to cold, fatigue, or slight indiscretions in diet may bring it on; even
an emotional cause may do it. The attacks last one or several days, and
may at times assume some gravity. This predisposition to diarrhoea
lasting through a lifetime is analogous to the tendency to inflammation
of the nasal and other mucous membranes.

In severer and typical forms the symptoms point to permanent lesions.
The tongue is smooth, shining, or glazed, sometimes with a central
brown streak, but it may be also pale and covered with a white coat.
The appetite is diminished or lost, or it is capricious, craving
unsuitable food. If there is no gastric catarrh, the chief distress
does not come until some hours after eating, but the taking of food
sometimes excites pain and brings on an evacuation of the bowels
through reflex influence.

There may be slight tympanites or a retracted abdomen. The imperfect
digestion of food and the fermentation of the intestinal contents
develop gas which keeps the abdomen distended and causes slight pains
and borborygmi. Pain may, however, be entirely absent. A feeling of
abdominal soreness is not unusual; it is increased by coughing,
sneezing, or any sudden movement. Sensibility to pressure is usually
wanting; when it exists it is found along the line of the colon in most
cases.

The diarrhoea is the characteristic symptom. The number of the stools
varies from one to eight in twenty-four hours; four is about the
average number. They occur usually in the early morning hours, from two
to six o'clock, but food may at any time bring on peristaltic
contraction, so that a motion after every meal is not uncommon. In
quantity there is much variability; two to four ounces of fluid matter
is the rule perhaps, but a very much larger amount than this is often
passed with each evacuation. As a rule, the larger the quantity of
fluid the more extensive is the catarrh and the more advanced are the
lesions. The matters passed are composed chiefly of fecal matter
varying in consistence from a solid or semi-solid mass to a watery
fluid. In the soft stool, like thickened gruel, the consistence is due
to the presence of mucus; in the thinner evacuation water is the chief
element. Liquid stools are sometimes frothy. In color the dejecta are
brown, yellow, red, green, slate-color, or white. They may be colored
dark by medicines, as iron or bismuth, or by blood. The presence of
blood gives a pinkish, bright-red, dark-brown, or black color,
depending upon the amount of blood and the changes it has undergone in
the bowel from a longer or shorter retention. Blood, when it comes from
the rectum, is in bright-red streaks or small coagula. When its source
is higher up, it is much altered, being dark and granular.
Coffee-ground sediment in a fluid stool is blood from the upper part of
the intestine or stomach. The spreading of an ulcer may open a vessel
of some size, and a fatal hemorrhage follow. A yellow tint like that of
a child's movement may arise from a mixture of pus and fecal matter.
Pus, as a milky or creamy fluid which may be {708} streaked with blood,
is a frequent appearance in disease of the rectum and sigmoid flexure.
The odor of the stools is fecal, sour, or sickening from fermentation
or offensive from decomposition. In bad forms of chronic diarrhoea in
children the black watery stools have a most offensive odor.

Mucus is the most constant ingredient of the diarrhoeal stool, and is
in itself a sufficient evidence of catarrh, as it is not seen in normal
stools except as a temporary phenomenon. It is present in flakes in
watery evacuations, giving a jelly-like character to the fluid if it is
in excess, or it is mixed with semi-solid feces. Pure mucus may be
passed, if the catarrh is low down, in clear, glairy, or opaque masses.
The frog's-egg or boiled-sago particles supposed by Niemeyer and others
to point to follicular ulceration, and by Traube to be the swallowed
bronchial secretion, are said by Virchow to be partly-digested starch,
and also by Nothnagel to be of vegetable nature.[33] The stools may
contain small yellow or brownish masses which are mucoid in nature,
being yellow from bile-staining. Pavement epithelial cells are found in
the coating of mucus around a hard fecal lump. Cylindrical epithelium
is passed uncolored or stained with bile. These cells are separated,
and are deformed and shrunken, with a granular protoplasm and
indistinct nucleus. Goblet-cells are also seen. Round cells in the form
of mucus-corpuscles or giant-cells are mixed with shreds of mucus or
float in the thin stools. Crystals of triple phosphate, of neutral
phosphate, oxalate of lime, and other lime salts, and of cholesterin,
are also seen.

[Footnote 33: _Virchow's Archiv_, v. S. 329; Nothnagel, "Zur Klinik der
Darmkrankheiten," _Zeitschrift fur klin. Med._, iii., 1881, p. 241.]

Micrococci and bacteria have no pathological importance; they are seen
in different diseases and in health.

Unaltered food may be expelled (lientery) by rapid peristaltic
movements. But the microscope will detect what cannot be seen by the
eye--unaltered starch-granules, filaments of meat-fibre, or fat in
drops or in needle-shaped or feathery crystals.

The nervous system is disturbed after a certain time. There is languor,
with depression of spirits, mental weariness, and inaptitude for work
of any kind. The patient is querulous, morose; his sleep is restless,
but sometimes profound until disturbed by the demand to empty the
bowel. Melancholia is attributed to this as to other diseases of the
abdomen, but their influence in producing insanity is doubtful.[34]

[Footnote 34: Griesinger, _Mental Path. and Therap._, Am. ed., New
York, 1882, pp. 137, 138.]

No decided symptoms are exhibited in the respiratory and circulatory
systems. Even slight exertion will cause shortness of breath and
increased frequency or palpitation of the heart. This irritability of
the heart is a marked feature of the disease.[35]

[Footnote 35: DaCosta found that of 200 cases of irritable heart, 61
were in patients who had suffered from or still had diarrhoea (_Am.
Journ. Med. Sci._, vol. lxi., 1871, p. 37).]

The appearance of the urine is normal; it may be abundant, with
phosphatic deposit, or it is scanty and high-colored. In bad cases
albumen and casts have been found.[36]

[Footnote 36: Alonzo Clark, "Proc. of New York Path. Soc.," _Med. and
Surg. Reports_, vol. ix., 1862-63, p. 312.]

The symptom indicative of atrophy of the mucous membrane is believed by
Nothnagel to be the persistent passage of one soft, unformed stool
daily. Mucus and fat, which diminish the consistence of the stool, are
{709} excluded by microscopical examination. One stool daily shows that
there is no exaggerated peristalsis which hurries the food along so
rapidly that water cannot be absorbed.[37]

[Footnote 37: Nothnagel, "Zur Klinik der Darmkrankheiten," _Zeitschrift
fur klin. Med._, iv., 1882, p. 422.]

PROGRESS AND TERMINATION.--As the disease advances it is marked by
progressive emaciation and debility. The skin gradually acquires great
pallor, indicating profound anaemia. The loss of flesh is very rapid.
An exacerbation of the disease will in a few days cause the cheeks to
grow hollow, the eyes to appear sunken with dark rings around them. In
all cases of long duration the progress is intermittent; frequent
relapses occur from which the patient may rally and regain a moderate
degree of flesh. Recovery may take place in weeks or months--eighteen
months is the average duration[38]--but in most instances a tendency to
a recurrence of the diarrhoea from cold, fatigue, or indiscretions in
diet will continue throughout life. An incomplete recovery may take
place by the cessation of the diarrhoea and formation of a stricture
from the healing of an intestinal ulcer. In the worst cases there is no
rule as to the rapidity or regularity of the march of the disease.

[Footnote 38: C. H. Ralfe, Seamen's Hospital, London: see Aitken's
_Handbook of Treatment_, New York, 1882, p. 116.]

When the advance is toward a fatal issue the emaciation progresses
until it becomes extreme; nothing but skin and bone are left. The
cuticle is hard and dry, pale or brownish in color. The muscular
strength is so reduced that the patient is unable to move from bed. The
voice may sink to a whisper. The nervous depression and moroseness
assumes a more marked character. Among the soldiers during the Civil
War who had undergone great privations with insufficient or improper
diet the mental phenomena were those of dementia.[39] In them the
disease was modified also by the symptoms of scurvy and malarial
poisoning.

[Footnote 39: W. Kempler, "Entero-Colitis," _Am. Journ. of Med. Sci._,
vol. lii., 1866, p. 337.]

Fever is seen in the late stages; it is nocturnal at first, and later
assumes the features of hectic. The pulse grows more frequent and
thready; aphthous deposits appear on the inside of the mouth and
pharynx. Toward the end the discharges may become more frequent and
very abundant; they are more fluid, lighter colored or black, with
floating particles of blood and mucus. There may be a loss of odor or
they may have a cadaveric smell.

Death takes place in a few weeks or after years of alternate suffering
and relief. The immediate causes of death are exhaustion, marasmus from
starvation, collapse from perforation of an intestinal ulcer and
consecutive peritonitis, syncope from sudden exertion, pneumonia, or
acute pulmonary congestion, pleurisy, or subarachnoid effusion in the
brain, with coma and convulsions.

COMPLICATIONS.--General dropsy results from the hydraemia and languid
circulation of the late period of the disease. Other causes of this
symptom are coincident diseases of the liver, kidney, or the malarial
cachexia. Oedema of one extremity follows a thrombus in the crural
vein. Chronic bronchitis and pulmonary phthisis are sometimes met with.
Acute pneumonia[40] and acute pulmonary congestion are occasional {710}
causes of death. Peritonitis may occur with and without perforation.
The latter variety begins as a local inflammation of subacute or
chronic nature, and spreads slowly until it becomes general. Extensive
adhesions and abundant accumulations of serous, sero-purulent, or
purulent fluid in the abdominal cavity result.

[Footnote 40: Pneumonia (8 double and 12 single) occurred in 20 out of
41 fatal cases reported by Harrison Allen, _Tr. Path. Soc. Philada._,
1867, vol. ii. p. 161.]

The causal conditions which have been enumerated may be considered as
complications. They are tuberculosis, Bright's disease, cirrhosis of
the liver, abdominal tumors, scurvy, tubercular and other neoplasms in
the wall of the intestine; attacks of intercurrent, intermittent, or
remittent fever arise from the malarial influence to which the
intestinal catarrh is due. These fevers and rheumatism and
pseudo-rheumatism are complications in soldiers from the exposure to
malarial influences and to cold and dampness.[41]

[Footnote 41: Woodward, _op. cit._, p. 495.]

Ulceration of the cornea, escape of the aqueous humor, and collapse of
the eye were observed in quite a number of cases occurring among
soldiers.[42]

[Footnote 42: Elliot Coues, _Med. and Surg. Reporter_, Philada., 1863,
vol. x. p. 207, and H. Allen, _Tr. Path. Soc. Philada._, 1867, vol. ii.
p. 161.]

SEQUELAE.--The alteration of structure from long-standing inflammation
leaves the mucous membrane prone to recurrence of inflammation. Chronic
intestinal indigestion and permanent malnutrition come from the same
cause. The glandular and lymphatic structures of the intestine and the
mesenteric glands are so changed by disease that they imperfectly
perform their function. Tabes mesenterica is the ultimate phase of this
change. Constipation succeeds chronic diarrhoea, and is due to atony of
the muscular wall from long-continued distension, and probably from
degeneration of the muscular structure. A more serious cause of
constipation, and sometimes of intestinal obstruction, is found in
stenosis of the bowel from the healing of the ulcers of long-standing
chronic catarrh. Stricture is more common in the colon, sigmoid
flexure, and rectum. How frequently such a result follows the
cicatrization of intestinal ulcers is not definitely known. Woodward
concludes from a careful search of books and pathological museums that
stenosis from this cause is very rare.[43] Syphilis is the most common
cause of ulcer. Local or general peritonitis leads to the formation of
adhesions or fibrous bands uniting neighboring links of intestine. By
the contracting of these narrowing of the intestinal canal may result.
Paralysis, hemiplegia, paraplegia, etc. have been found to follow upon
diarrhoea of long standing.[44]

[Footnote 43: Woodward, _op. cit._, p. 504.]

[Footnote 44: Potain, "Paresie des Membres inferieurs ayant succede a
un Catarrhe gastro-intestinal," _Rev. de therap. Med.-Chir._, Paris,
1880, xlvii. p. 562; "Paralysis spinale secondaire a une Diarrhee
chronique," _Journ. des Conn. med. Prat._, Paris, 1880, 3, S. ii. p.
57.]

DIAGNOSIS.--The mild form of chronic catarrh of the intestines
associated with constipation has been confounded with hepatic
disorders, and the obscure symptoms attending it have been attributed
to excess or diminution of bile, and medicines to regulate the liver
have been given accordingly. In the absence of lesions in the liver, in
cases where symptoms such as have been described have preceded death,
the opinion is not justified that disease of this organ has existed. On
the contrary, alteration in the mucous membrane is almost always found,
which points to the true nature of the disease. The diagnosis is based
upon the accompanying {711} gastric catarrh and upon the symptoms of
intestinal indigestion and malnutrition. Greater sensibility to
pressure over the right hypochondrium and along the line of the colon,
pain one to two hours after eating, with distension of the abdomen, the
passage of well-formed and somewhat indurated feces mixed or coated
with mucus, are symptoms peculiar to these mild forms.

The tendency to diarrhoea from cold, indigestible food, etc. which
marks the second form of mild catarrh is easily recognized.

The characteristic symptom of the severe form is the persistent
diarrhoea. Paroxysmal pains, tympanites and rumbling of gas, tenderness
on pressure over the colon, the alternate periods of improvement and
relapse, with the constitutional signs of impaired nutrition and
progressive anaemia and debility, point out the nature and the seat of
the lesion with sufficient clearness. It is futile to attempt to
distinguish chronic intestinal diarrhoea from chronic dysentery. The
lesions of the two conditions are essentially the same; it depends upon
the fancy as to which name is given to the lesions described here under
the title chronic intestinal catarrh. A greater amount of blood and
mucus in the stool with tenesmus would more properly be called
dysenteric, but the same case may present at one time diarrhoeal, at
another dysenteric, symptoms.

Primary must be distinguished from secondary diarrhoea. Therefore the
liver, heart, and lungs must be examined to discover diseases which
might cause portal congestion. Any constitutional malady may be a cause
and an explanation: tuberculosis or pulmonary phthisis stands first in
its influence; next, chronic Bright's disease, septicaemia, scurvy,
syphilis, and gout are attended by intercurrent diarrhoea. If all
general disease can be excluded and the morbid process be located in
the intestine alone, its cause may be known by studying the habits,
occupation, and diet of the patient. Foreign bodies--hardened feces,
gall-stones, fruit-stones, etc.--are possible causes which the history
of the case may point to.

Having located the disease in the intestine and decided upon its
primary or secondary nature, it remains to determine more precisely
(_a_) the locality of the lesion, and (_b_) the stage of the
inflammatory process.

(_a_) In what part of the intestinal canal is the disease located? It
must be remembered that in typical and fatal cases the large intestine
is the home par excellence of the lesions of chronic catarrh, and that
the lower part of the ileum is often associated in the morbid
processes, but limited areas of the small or large intestine are
affected in mild forms which yield readily to treatment.

Icterus, clay-colored stools, and bile in the urine show that the
catarrh is in the duodenum and involves the opening of the common
bile-duct. The absence of diarrhoea, with flatulence and colics, limits
the area of inflammation to the duodenum. Symptoms of duodenal
indigestion accompany this form of catarrh; the failure of bile to
neutralize the acid chyme impairs the effect of the pancreatic
secretion. Fats are not digested and there is fatty diarrhoea. To this
may be added tenderness in the right hypochondrium, and pain and
oppression in the epigastrium and to the right one hour after eating.
There may be wasting and hypochondriasis.

{712} The lower part of the duodenum below the opening of the
bile-duct, the jejunum, and the ileum can be taken together as forming
the small intestine. Chronic catarrh of the small intestine is attended
with pain about the umbilicus, which comes on immediately or in one
hour after taking food. Tympanitic distension gives a full, rounded
prominence to the abdomen, which is more central than lateral, and
greater below the umbilicus than above it. It is accompanied by a sense
of oppression, which is greater after eating. Inability to digest food
consisting largely of starch or sugar, as well as tardiness in the
digestion of all foods, with resulting loss of flesh, are signs of
intestinal indigestion. There may be no diarrhoea; if there is,
important help to diagnosis can be gained by examining the stools. They
contain undigested or partly-altered meat-fibre and starch-granules,
discoverable only by the microscope. The discharges are soft and pulpy
from an intimate admixture of mucus. To the naked eye no mucus is
visible, but a thin layer under the microscope shows clear islets of
pure mucus, or mucus may only be detected by the adhesion of the
covering-glass to the slide. Bile-stained epithelium and globules of
stained mucus are seen in the liquid stools from catarrh of the small
intestine and of the ascending colon. There is the characteristic
reaction and play of color on testing for bile-pigment. These are
evidences that the stool with the bile has been hurried along the ileum
and colon, and expelled before the transformation in the coloring
matter has had time to take place.[45]

[Footnote 45: "II. Abtheilung, Diagnostische Bemerkungen zur
Localisation der Catarrhe," _Zeitschrift fur klinische Medicin_,
Berlin, 1882, iv. p. 223.]

In catarrh of the large intestine there is sensitiveness to pressure
along the line of the colon; the distension of the abdomen is not
uniform, depending upon the prominence of the transverse or descending
colon. The pains are more severe and precede the stools, which are more
frequent and larger than in catarrh of the ileum. The discharges are
pulpy or watery. Globules of mucus are visible to the naked eye, and
mucus is intimately mixed with fecal matter.

If the lower half of the colon is chiefly the seat of the disease, pure
mucus coats the more solid stool and is in its substance. With catarrh
limited to the descending colon scybalae are imbedded in mucus. From
the sigmoid flexure and rectum larger masses of mucus, without fecal
matter or with it, are expelled. Pure lumps of mucus, mixed or stained
with red blood and without fecal matter, indicate catarrh of the
rectum--proctitis.

(_b_) The stage of the process of inflammation is diagnosed by the
condition of the patient, the course of the disease, and the character
of the stools. As long as there is a pulpy fecal diarrhoea, with no
blood, pus, or fragments of tissue and no marked emaciation or fever,
and with a tendency to improvement under favorable conditions, there is
every reason to believe that there is no ulceration.

In follicular ulceration the course of the disease is essentially
chronic, and is marked by periods of improvement under careful
treatment, with exacerbations and relapses from slight causes of
irritation. There is progressive emaciation and debility, with fever of
hectic character, which is worse in the later stages. The abdomen may
be retracted. The movements are frequent and liquid, and are without
odor or fetid. They {713} contain mucus, glassy-gray or green,
pus-cells imbedded in masses of mucus, blood in small amount, but
sometimes abundant, and shreds of the tissue of the mucous membrane.
This last is an important aid to diagnosis.

The higher the ulcer the less marked is the diarrhoea. The lower its
situation the greater is the frequency of the stools and the more
liable are they to be accompanied by tenesmus and to contain blood and
pus. Toward the last, ulceration is accompanied by rapid emaciation,
fever, sweats, a feeble circulation, a dry tongue, great thirst, and
oedema of the feet and ankles. Death takes place by gradual exhaustion,
more rarely from perforation and peritonitis or from intestinal
hemorrhage.[46]

[Footnote 46: Nothnagel, "Die Symptomatologie der Darmgeschwure,"
_Klinische Vortrage Volkmann_, No. 200, Aug. 24, 1881.]

Duodenal ulcer is with difficulty recognized during life.[47] The
following are the symptoms which have preceded death from this lesion:
Profuse hemorrhage from the bowel, vomiting of food as well as blood,
icterus, dysphagia, hiccough, oppression in the epigastrium after
eating, attacks of cardialgia with tenderness on pressure in the right
hypochondrium, and sudden death with symptoms of collapse. If these
symptoms follow an extensive burn of the skin, they are easily referred
to a duodenal ulcer.

[Footnote 47: W. L. Loomis, "Perforating Ulcer of Duodenum and Sudden
Death." For two years the patient had suffered with dyspepsia and
epigastric pain after eating, was gouty, and had lost flesh. Autopsy:
atheroma of arteries, beginning cirrhosis of kidneys, walls of stomach
thickened, perforated ulcer one inch below pylorus (_Med. Record New
York_, 1879, vol. xv. p. 188; also _Boston City Hospital Report_, 1882,
p. 374).]

Tuberculous ulcers are distinguished from follicular ulcers by the
history of hereditary predisposition, the existence of pulmonary
tuberculosis, higher fever, and more rapid emaciation and debility.

A cancerous ulcer may be the cause of bloody stools; it is usually
within reach of the finger in the rectum; the mass exercises pressure
upon the prostate, and at times occludes the bowel, causing
obstruction. The cachexia and rapid decline are not seen in catarrhal
ulceration.

PROGNOSIS.--Chronic catarrh of the intestine is most fatal in children.
Among infants artificially fed, when the illness develops and continues
during hot weather, the mortality is very great. Recovery in the young
is rendered less probable if chronic diarrhoea is associated with
rickets, scrofula, or tuberculosis.

If the catarrh in adults is a complication of some previously existing
constitutional disease, as Bright's disease or scurvy, or is connected
with lesions of the liver, spleen, heart, or lungs, there is less hope
of cure. In old persons this disease has a special gravity.

The longer the disease has lasted before treatment is begun, and the
longer it continues without being influenced by treatment, the more
unfavorable will be the prognosis. Discouraging symptoms are an
uninterrupted loss of flesh and strength, lientery, hectic fever,
relapses notwithstanding care in diet, and the signs of
ulceration--blood, pus, and tissue-shreds in the stools, with an odor
of decomposition.

Favorable promises may be based upon a hearty willingness of the
patient to submit to the strictest regimen and to subordinate his life
to the plans of treatment, the absence of other diseases, early
improvement in his general condition and local symptoms under rest and
diet. A {714} complete cure cannot be assumed to exist unless the
patient has passed one or more years without a relapse.

TREATMENT.--As chronic intestinal catarrh is a complication of so many
conditions, the prevention of it becomes a matter of great importance
and of very general application. All rules for preserving
health--temperance in eating and drinking, bathing, exercise, good
ventilation, the avoidance of overwork, both mental and physical--are
so many means for escaping an intestinal catarrh which may present
itself as an indigestion with constipation or as a diarrhoea.

The special liability of infants and children, and to a less extent of
very old persons, and the greater dangers they run, call for the most
careful selection of appropriate diet at these periods of life.

Where there is hereditary predisposition, idiosyncrasy, chronic
diseases of organs, or constitutional diseases, an easily-digested
dietary should be supplemented by precautions against chilling of the
surface by the wearing of flannel underclothing and woollen socks.

The etiology of each case may at once suggest a line of treatment.
Among the causes which point to appropriate measures are--the continued
presence in the bowel of indigestible or undigested food, constant
exposure to cold or to changes of temperature, chronic cardiac disease
and portal congestion from any cause, chronic cachexiae, as syphilis,
malaria, tuberculosis, or Bright's disease, the crowding together of
individuals in prisons, asylums, etc.

1. The mildest form of intestinal catarrh characterized by intestinal
indigestion and constipation or by the passage of fecal matter more or
less solid, mixed or coated with mucus, is best treated by a diet such
as is advised for intestinal indigestion, bathing with friction,
outdoor life, exercise on horseback or by walking, pleasurable
occupations, and travel. Iron if there is anaemia, and strychnia if
there is a sluggish capillary circulation, with cold hands and feet,
are available and useful in many cases. Massage and the Swedish
movement treatment find useful application in feeble men and in women
who are not strong enough for outdoor exercise. To aid the digestion
the liquor pancreaticus as advised by Roberts, a teaspoonful one hour
and a half to two hours after each meal, with ten to twenty grains of
the bicarbonate of sodium, is, theoretically at least, to be warmly
recommended. The Rockbridge alum water, a small glass three times daily
between meals, has astringency enough for the hyperaemic membrane and
is of good service without increasing constipation.

Purgatives should be avoided as much as possible. An enema of cool
water, not more than a tumblerful, taken each morning after breakfast
if persevered in, may do all that is needed in this direction. If it
fails to empty the bowel completely, a larger enema of warm water--one
pint--holding in solution sulphate of zinc or alum in the strength of
one grain to three or four ounces, can be thrown high up with a rubber
tube once daily. This acts upon the mucous surface, constringes mildly
the congested vessels, and when expelled brings away the retained fecal
matter. These astringent rectal injections offer promise of cure in
many obstinate cases where the colon is chiefly the seat of disease.
Belladonna is advised for cases of this kind in combination with
strychnia for the constipation. Mild laxatives are often necessary.
Bedford mineral water, Hunyadi water, or other salines and the less
active vegetable {715} cathartics, can be given alternately.
Ipecacuanha has had quite a reputation in combination with purgatives
in intestinal catarrh. Aloin pills empty the bowel without much
attendant irritation.

2. The form of catarrh which shows itself in a tendency to diarrhoea
from indiscretions in diet or from exposure to cold must receive
prophylactic treatment. Especially in this form is it important to
improve the activity of the skin by bathing and friction, and to lead a
temperate life in all things, regulating the diet according to the
rules already stated. Tonics are called for in such cases. Fowler's
solution of arsenic (one drop before each meal, Ringer), the
potassio-tartrate or the tincture of the chloride of iron, dilute
sulphuric acid, nitro-muriatic or hydrochloric acid, are efficient in
improving digestive activity or in opposing the anaemia which is nearly
always present. Quinia is indicated in malarial anaemia with a
disposition to loose bowels. Quassia or other vegetable bitters can be
given if the appetite is languid; the bitters are, as a rule, of little
benefit, and may do harm if diarrhoea exists. Strychnia with quassia or
columbo stimulates the appetite and the gastric digestion. When
intercurrent attacks of diarrhoea come on with coated tongue,
flatulence, distress about the umbilicus after eating, bismuth given on
an empty stomach in full doses is serviceable. Small doses of morphia
or of opium in some form can be added to the bismuth if there is much
pain or when the stools are frequent.

In this and in other forms of intestinal catarrh mineral waters are
profitably employed. They are best taken at their sources; and here, as
in the case of sea-bathing, the benefit is largely due to the change of
air and scene and to the more simple mode of life. Any of the
watering-places where alkaline-saline waters or ferruginous waters are
found may be of benefit. A trip to Europe and a stay at Carlsbad will
break up many an obstinate case of chronic abdominal disorder; but
other beneficial waters in Europe are Tarosp, Rohitsch, Marienbad,
Kissengen, and Plombieres.

In this country the comfort and conveniences of the summer hotels and
climate are as much to be considered as the chemical composition of the
waters. For milder forms of catarrh with constipation a season at
Saratoga, with a life of temperance there, is a wise procedure. Bedford
Springs, Pa., offer the same advantages in part, but the waters are
best suited to catarrh with constipation. Many of the Virginia springs
benefit health-seekers who do not place too much reliance upon the
virtues of the waters, and who trust to the value of pure air,
exercise, diversion, and rest.

3. All plans of treatment for the more severe form of catarrh with
chronic diarrhoea (follicular enteritis) must be based upon a knowledge
of the lesions. Bearing in mind the alterations in the mucous and
submucous tissues, it is clear that no treatment can be successful
which is not carried out with the most careful attention to details,
and which is not continued for some time after all the symptoms of the
disease have ceased. The complete resolution of hypertrophied glandular
tissue, the scattering of cell-accumulations, and the healing of ulcers
can only be secured in this way. It is best to present the whole case
before the patient, so as to enlist in the task his intelligent
co-operation.

Directions for the guidance of cases of this kind must include every
{716} detail of the patient's life. The question of residence is of
importance to begin with. A cool and dry climate is better than a wet
and warm one, and where other means fail change of climate is sometimes
the only cure. A sea-voyage, a residence in a mountain-region, will
oftentimes promptly and effectually cure an obstinate diarrhoea.
House-drainage and ventilation should be examined into and improved.
The occupation may have developed the disease; in overwork may lie the
origin and the cause of its continuance. Rest from work is therefore in
some instances the one thing needed. In all cases the energies and the
brain should not be overtaxed. The bath to keep the skin active can be
combined with friction. The hot bath, as hot as can be borne, is the
best. It is a stimulant, not a depressant, as is the tepid bath, and it
is safer than the cold bath.

The cold sitz bath or the application of cold compresses diminishes
abdominal plethora, and is wisely advised in strong persons who are not
depressed or chilled by external cold. Sea-bathing is another
hydro-therapeutic measure which is of unquestioned advantage in all
forms of intestinal catarrh.

Permanent baths have been found very serviceable in many chronic
diseases, and there are many reasons for advising them in obstinate
diarrhoeas. There can be no better means for bringing to bear a strong
and continued influence upon the intestinal mucous membrane. The
patient should be kept in the warm bath for one, two, or three weeks,
according to his strength and the effect upon the disease. Systematic
hot bathing under the direction of a physician at Richfield, Sharon,
the Hot Springs of Virginia or Arkansas, is an invaluable aid.

Rest in the recumbent position for cases where the symptoms indicate
marked tissue-alteration is very often the most important part of the
treatment. Rest and diet are alone necessary to cure many cases, and
without these combined means relief is often impossible. The rest
should be absolute, the patient using a bed-pan and lying down all the
time. The contraindications for this method are a slight diarrhoea
which yields to other treatment, and loss of strength and appetite from
the deprivation of air and exercise.

If rest is not advisable, or does no good after a fair trial of two to
four weeks, outdoor life in fair weather by driving or walking slowly
can be suggested. A long drive will bring back a diarrhoea which has
taken many weeks to relieve.

The rules for diet must be clearly given and strictly enforced. An
exclusive milk diet should have a trial in every case. Skimmed milk can
be taken in larger quantities and with less repulsion, and is therefore
to be preferred. The exclusive milk diet can be varied with buttermilk,
koumiss, or wine-whey; and fruit-juices, as orange-juice, lime-juice,
or tamarind-water, please the patient without doing harm. In the case
of adults as well as children the milk is made more digestible by
diluting it with barley- or rice-water or by adding transformed
farinaceous food to milk in the form of Mellin's food and other foods
of this class.

Animal broths, as chicken-soup and beef-tea, are well digested if
properly made and given in small quantities. Raw meat scraped, beef or
mutton rare and thoroughly masticated, the breast of poultry, game,
broiled fish, raw oysters, raw or very slightly boiled eggs, or
sweetbread, are foods from which selection can be made to add variety
to the dietary. {717} Saccharine, starchy, and fatty foods are to be
given as little as possible. Vegetables may be added to the list as the
condition improves. Rice and fine hominy (grits) are to be thought of
first, as being easily digested and nourishing. Good wine in moderation
is not hurtful; the red wines diluted with water are the best, but good
port, tokay, and whiskey well diluted find application in particular
cases.

Whatever food be given, it should be taken in the quantities and at
hours prescribed by the physician, who by careful inspection of the
stools judges of the necessity of changes in his regulations and of the
success of his treatment.

The further treatment of chronic diarrhoea has for its object by the
aid of drugs to change the anatomical state of the mucous membrane.
Manifestly, the choice depends upon the state of this tissue. In the
earlier stages the increased vascularity and hypersecretion call for
mild astringents or for medicines which are believed empirically to
oppose these conditions. When drugs can be dispensed with, it is better
to do so; they should always be made subordinate to the careful regimen
already described.

Bismuth in large doses (ten to thirty grains) is a safe and efficacious
remedy in this stage. Nitrate of silver in pill form (one-sixth to
one-fourth of a grain) has the endorsement of Wm. Pepper and many other
practitioners. It should be continued for two or three weeks at least,
but it may be given in small doses during several months, with
intermissions, without danger of silver staining.[48]

[Footnote 48: A case is recorded of silver staining of the skin after
four weeks' administration (Woodward, _op. cit._, p. 780).]

A routine administration of any drug or class of drugs is
reprehensible, and from the numerous remedies which are advocated in
chronic diarrhoea selection can be made for trial in the course of
intractable cases. The list would include sulphate of copper
(one-fourth to one-half a grain), the liquid preparations of iron
(liquor ferri nitratis, tinct. ferri chloridi), dilute nitric and
sulphuric acids, gallic acid and other vegetable astringents, oxide or
sulphate of zinc, alum, precipitated phosphate of calcium, salicin,
corrosive sublimate (1/100 gr. every hour), the Indian bael-fruit, etc.
No remedy should be abandoned until it has been continuously given for
one or more weeks.

The Rockbridge (Va.) alum water is markedly astringent, is not
unpleasant, and may be used as a substitute for water with advantage.
In fact, there is no better way of introducing in quantity a mild
astringent into the intestine than by the drinking of this water.

Cold-water rectal irrigation has a sedative and astringent influence,
and when properly used is of great advantage to both children and
adults.[49] The patient should be placed in the proper position, and
the water made to enter the rectum as high up as possible. The number
of stools lessens almost immediately after this treatment, peristalsis
being inhibited thereby.

[Footnote 49: A long rectal rubber tube, such as advised by
Surgeon-General Wales, U.S.N., serves this purpose well.]

To the water used in irrigation astringents may be added in small
doses. Sulphate of zinc, sugar of lead, or alum may be given in this
way in the strength of one grain to four or six ounces of water. This
{718} method of treatment promises more and is more rational than the
internal administration of drugs.

Opium and its preparations should be avoided except to control frequent
or watery discharges or to relieve pain, but it is not often that this
is called for if wiser measures are first employed. Any of the remedies
spoken of may be given in the form of suppositories with greater
advantage often than by the mouth.

In that more severe class of cases called follicular ulceration, in
which the follicles are known to be ulcerated from a prolongation of
the illness, the obstinacy of the diarrhoea, the character of the
discharges, and the effect upon the general health, other measures are
to be adopted. The diet should be most strictly regulated and the
digestive power of the patient carefully studied. Cod-liver oil is
added with advantage to other foods if there is a lack of nutrition.
Aids to gastric digestion are called for.

The intestinal lesion is to be reached through the stomach or the
rectum. Nitrate of silver in small doses is more especially applicable,
and is to be preferred to all other drugs in this stage. It is to be
given in small doses and for several weeks.

Turpentine and copaiba have something in their favor in ulceration.
Ergot has been suggested, and where there is much hemorrhage from the
bowel may be prescribed.

Irrigations with solutions of nitrate of silver seem to be a direct and
certain remedy in cases where ulceration has existed for a long time.
Two and a half to three pints of distilled water, holding in solution
five grains of nitrate of silver, should be thrown up the rectum as
high as possible with a rubber tube; the effort should be made to
secure immediate exit to the fluid. This procedure is to be repeated
after the bowels are moved--once every day or every other day if the
rectum becomes irritable.[50]

[Footnote 50: See case reported by the writer to the Medical Society of
the District of Columbia, and published in the _Maryland Medical
Journal_, March 15, 1883, p. 562.]




{719}

CHOLERA MORBUS.

BY W. W. JOHNSTON, M.D.


SYNONYMS.--Cholera nostras, Sporadic cholera, European or English
cholera, Spasmodic cholera, Cholera biliosa, Passio cholerica,
Cholerhagia, Trousse-galant, Die Gallenruhr, Brechruhr.

DEFINITION.--An affection of the gastro-intestinal mucous membrane
characterized by violent abdominal pain, nausea, and sudden, violent,
and incessant vomiting, and by purging of a watery fluid containing
little albumen and bile; attended with spasms of the muscles of the
abdomen and extremities, a pinched and sunken countenance, pallor,
cyanosis, and coldness of the surface of the body; a feeble and rapid
pulse, oppressed respiration, and great restlessness; dryness of the
tongue, great thirst, and diminished or suppressed urinary secretion
and a state approaching collapse, which may rarely prove fatal, but is,
as a rule, followed by reaction.

HISTORY.--The term cholera has been in use since the time of
Hippocrates, but he confounded with it every disease which seemed to
him to come from acridity or corruption of humors, as colics and
meteorism with constipation.[1] He well described cholera morbus in
saying that "it is a disease which appears in summer, due to imprudence
in eating, at the same time as intermittent fever."[2] If Celsus be
correct in deriving the name from [Greek: chole] "bile," and [Greek:
reo] "I flow," it is more applicable to the disease now under
consideration than to the Asiatic disease, as it is the bile which is
absent in the colorless rice-water discharges of Asiatic cholera.
Trallian and Ruysch, however, ascribe it to [Greek: cholera] the
rain-gutter of a house.

[Footnote 1: _Append. au Traite du reg. les Maladies aigues_, 19, ii.
p. 495, ed. Littre.]

[Footnote 2: _Epidemies_, lib. v., ed. Littre, 71, p. 247.]

In the Old Testament mention is made of a disease resembling cholera
morbus.[3] Its true pathogeny was known to Galen, and it was accurately
described by Celsus,[4] and Aretaeus[5] mentions the nature of the
discharges and its frequency among young people and children.

[Footnote 3: _Hist. Med. des Maladies epidemiques_, Paris, 1825.]

[Footnote 4: Lib. iv. cap. 2.]

[Footnote 5: Lib. ii. cap. 5.]

The first mention of epidemics was in the sixteenth century. Various
epidemics in 1695, 1717, and 1718 in Germany were probably cholera
morbus. Forestus[6] reports seven observations from 1559 to 1565 of
attacks due to indigestible food or drastic medicines. F. Hoffman,[7]
{720} J. Frank,[8] and L. Riviere speak of the benignity of the disease
as contrasting it with its apparently dangerous symptoms.

[Footnote 6: _Opera Omnia_, Rothomagi, 1633, "De stomachi affectibus,"
lib. xxviii.]

[Footnote 7: _Medicina rationalis systemica_, t. iv. pt. 3, 1734.]

[Footnote 8: _Praxeos medicae universae praecepta_, Leipzig, 1826, p.
43.]

Sydenham's[9] description of the epidemics in England in 1669-72 is the
earliest account of the disease in modern literature, and it was he who
gave it the name cholera morbus.

[Footnote 9: Sydenham Soc. edition, vol. i. p. 163.]

NATURE.--There prevails at the present time a great diversity of
opinion in regard to its nature; the want of uniformity in the
appearances presented by post-mortem examinations may in some measure
account for this. The present state of our knowledge, derived both from
pathological anatomy and a study of the symptoms, will not warrant a
positive opinion in regard to it.

Niemeyer,[10] in common with most German and some French authors,
considers cholera morbus to be a variety of gastro-intestinal catarrh.
Leube[11] thinks it a variety of gastric catarrh with simultaneous
inflammation of the intestines and running a peculiar course. It is
certainly not identical with the specific Asiatic disease, although in
some cases the symptoms and morbid anatomy are exactly similar, and any
differentiation is impossible. By some it is believed that cholera
morbus is due to surviving germs implanted by previous epidemics of
Asiatic cholera.

[Footnote 10: _Pract. Med._, 1879, vol. i. p. 480.]

[Footnote 11: _Ziemssen's Cyclopaedia_, New York, 1876, vol. vii. p.
146.]

The slight changes found in some fatal cases would lead to the belief
that the effect of the exciting cause is something more than a
mechanical irritation of the gastro-intestinal mucous membrane.

The sudden onset, rapid development of symptoms, and dangerous collapse
justify the theory that there must be some previous change in the
individual or some peculiar result of food-decomposition. The nervous
system may be so enfeebled by prolonged heat that an irritant quickly
destroys its equilibrium and brings about vaso-motor paralysis of the
intestinal vessels and abundant serum transudation. Or the irritation
may be specific, depending upon the development of poison germs in food
which has been subjected to heat influences. There is a close
relationship between cholera morbus and cholera infantum in their
etiology, symptoms, and pathology.

ETIOLOGY.--Predisposing Causes.--The disease is more common in the
tropics, but is not confined to any climate. In temperate latitudes it
is more likely to occur in July and August, when the variation of
temperature between day and night is great, although the other months
of summer and autumn are not entirely exempt. It is said to be more
frequent and fatal in Southern Europe than in the northern and
temperate climates. In periods immediately preceding and following
epidemics of Asiatic cholera many persons are attacked, although there
is great liability to errors in diagnosis at these times.

It occurs more frequently in youth and adolescence than in advanced
life, and males seem to be more liable to attacks than females, but
difference in occupation may assist in this predisposition. Persons
endowed with an extreme sensibility of the nervous system and who are
subject to frequent attacks of intestinal catarrh are much more liable
to the disease. The exhaustion of the nervous system by heat, which is
the {721} probable explanation of the phenomena of cholera infantum,
has no doubt much to do with the development of cholera morbus. Mental
anxiety or overwork in summer increases this nerve-exhaustion and
renders the termini of nerves and the centres very susceptible to
peculiar irritation.

Exciting Causes.--It is probable that the cause of most attacks is a
septic material generated in the fermentation and decomposition of
food. This poison acts as an irritant upon the gastric and intestinal
nerves and gives rise to excessive peristaltic movements and vomiting.
Hence the quality of the food is an element of more importance in the
causation than the mere quantity ingested; and herein may reside the
chief difference between cholera morbus and Asiatic cholera, the latter
being due to a specific, imported, or acclimated poison which
invariably produces the same specific form in those exposed to its
action.[12] Unripe fruits, partially cooked or decaying meats and
vegetables, shellfish and fish some time from the water, may produce
the disease in those predisposed to it. The intemperate use of
ice-water and other cold drinks after a full meal or when the body is
exhausted by heat and fatigue, exposure to showers at the close of a
hot day, or passing from a heated room into damp cellars and
outbuildings, are frequent exciting causes.

[Footnote 12: "Bias the pugilist, naturally a great eater, had a sudden
choleraic attack after having eaten of succulent food" (Hippocrates,
lib. v. p. 247, ed. Littre).]

At times there exists a certain condition of inactivity of the
digestive organs when the gastric juice is not secreted in sufficient
quantity, and perfectly sound food may undergo fermentation and set up
an attack.

The offensive exhalation from a filthy alley which had been recently
cleaned was the exciting cause of a fatal epidemic in a London
school,[13] and Levier recounts an epidemic caused by the
drinking-water during the winter in Berne.[14]

[Footnote 13: _Lond. Med. and Surg. Gaz._, 1829, iv. p. 375.]

[Footnote 14: _Schweiz. Zeitschr. f. Heilk._, iii., 1864, p. 140.]

Nervous disturbance from other diseases may act as a cause. Leube
reports a case of intermittent fever which was followed by an annual
attack of cholera morbus preceded by febrile symptoms.[15]

[Footnote 15: Leube, _Ziemssen_, 1876, vol. vii. p. 148.]

Malaria, sewer-gas, and sudden and powerful mental emotions are
credited with the causation of some attacks.

PATHOLOGICAL ANATOMY.--In a few cases an examination of the body has
revealed no phenomena sufficient to account for the symptoms, even when
they have been the most severe during life. In these cases either the
inflammation has not passed the first stage of development and the
resulting hyperaemia has disappeared after death, or the irritation of
the gastro-intestinal nerves has been sufficiently intense to cause
death before the alimentary tract has undergone any consequent
structural change.

Usually, however, there are evidences of a general gastro-intestinal
catarrh: the mucous membrane is congested throughout and denuded of
epithelium. The solitary glands are enlarged and Peyer's patches
swollen and prominent. The blood is thickened and dark in color, and
the serous membranes dry, sticky, and covered with desquamated
epithelium. Indeed, the appearances may be identical with those
observed in true Asiatic {722} cholera. The kidneys are congested,
sometimes enlarged, and the tubules devoid of epithelium. In protracted
cases the general muscular system shows a beginning of granular
degeneration.

In no case, however, can a positive diagnosis between Asiatic cholera
and cholera morbus be made from post-mortem appearances.

SYMPTOMS.--The attack is usually sudden in its onset, but in some cases
is preceded by nausea, thirst, loss of appetite, and slight general
distress for some hours, or it may come on in the course of some
gastro-intestinal disturbance. Frequently it is developed during sleep,
particularly after midnight, the patient being aroused by a feeling of
pressure at the pit of the stomach, which is followed by nausea and
violent and incessant vomiting with intense pain, the contents of the
stomach being ejected with great force.

The matters first vomited consist mainly of the food last eaten, little
altered or mixed with gastric mucus and tinged with bile. In a certain
proportion of cases the amount of bile is increased, although it is
difficult to judge of the relative proportion by the color and taste of
the vomited liquid. The general belief that the liver is implicated and
the bile secreted in morbid quantity rests upon conjecture alone, and
has no solid basis. After a time only yellow, brown, or greenish mucus,
with more or less bile, is ejected, and in protracted cases hiccough is
most distressing.

Following the vomiting or at the same time with it purging comes on,
and it is usually preceded by borborygmi. In rare cases there is no
vomiting, but only intense pain in the bowels and copious alvine
discharges from the beginning to the end of the attack. The stools in
the beginning are normal in color, but soon become pulpy or semi-fluid.
As they increase in quantity they become watery, consisting of
blood-serum with mucus, cast-off epithelium and pus-cells, and are
nearly odorless, and sometimes resemble very closely the discharges of
Asiatic cholera, but almost invariably retain the yellow or green color
of the bile. Colorless rice-water discharges are observed in undoubted
cases of cholera morbus outside of any epidemic influence. The
discharges are acrid and irritating, and the neighboring parts become
red and excoriated.

At the same time there is intense burning or tearing pain in the
abdomen, generally centring at the umbilicus, great thirst and painful
contractions of the muscles of the abdomen and extremities,
particularly in the calves of the legs, and of the flexors of the
thighs, forearms, fingers, and toes. In the beginning there may be
tympanites, but this soon disappears, and the abdomen becomes retracted
and the muscles drawn up into knots. The cramps usually come on after
each act of vomiting and purging, but they may appear spontaneously.
Abdominal tenderness is either wanting or slight. As the transudation
continues the thirst becomes intense, the tongue cold, dry, and coated,
and the tissues shrivelled from loss of water. The skin is cold,
clammy, or covered with a viscid sweat, and the surface of the body is
cyanosed, violet, or in the extremities it may have a marbled
appearance. The nose is pointed, the eyes dark and sunken, and there is
a general appearance of collapse.

The mind may be clear throughout, but in protracted cases there is
great nervous prostration. The patient becomes dull and lethargic,
passing into stupor after great restlessness and jactitation. The voice
is faint {723} or whispering, the breath cold, and the respiration
sighing. The pulse in the beginning may be depressed, but soon becomes
rapid and often imperceptible, and there is great praecordial anxiety.

As the blood becomes thickened the urine is highly colored, small in
quantity, and it may be suppressed. An examination shows traces of
albumen, casts and desquamated epithelium, and a decrease in the amount
of urea and salts. In the last stages there may be a slight rise in
temperature, but it has no definite course and it is usually absent. In
collapse the temperature of the surface of the body sinks below normal,
but the temperature of the interior may rise as high as 101 degrees or
102 degrees F., as shown by the thermometer in the rectum or
vagina.[16]

[Footnote 16: _London Hosp. Reports_, 1856, vol. iii. p. 457.]

PROGRESS AND TERMINATION.--But, fortunately, the course of the disease
tends toward recovery in the large majority of cases. The discharges
gradually decrease in quantity, the intervals are longer, the
appearance becomes more natural, and a profuse perspiration is followed
by a refreshing sleep. The surface becomes warmer, the pulse slower and
more full, and the skin regains its normal color.

If the case has been a severe one or if it occurs in a person much
enfeebled by disease, it pursues a different course. The discharges
become almost uninterrupted, and at last are passed involuntarily. The
cramps are almost continuous or are convulsive, the pulse grows rapidly
weaker and is finally lost, coma succeeds stupor, and death follows in
collapse.

The duration of the disease varies from a few hours to two or three
days; death has occurred within twelve hours.

Recovery is generally complete after a few hours; and this rapid return
to the normal condition shows that there have been no textural change
of organs. Sometimes great emaciation, irritability of the stomach, and
slight diarrhoea persist for a few days, or symptoms of a general
gastro-enteritis may supervene.

DIAGNOSIS.--In making the diagnosis of cholera morbus it is necessary
to carefully differentiate it from epidemic cholera and the effects
produced by irritant poisons, such as the metallic salts, poisonous
fungi, etc.

Occurring during an epidemic of Asiatic cholera, it is not possible to
make a diagnosis, as the symptoms of cholera morbus and of mild cases
of the Asiatic disease are identical. From severe cases it is to be
distinguished by the absence of antecedent diarrhoea, by the presence
of bile in the vomited matters, and by the color and fecal odor of the
stools. The nausea and abdominal pain are more marked, while the
dyspnoea, cyanosis, and shrunken condition of the skin are less marked.
The mortality of cholera morbus is slight, whilst about one-half of
those attacked with epidemic cholera die.

In irritant poisoning the vomiting follows quickly after the ingestion
of a meal or poisonous matter; it continues for some time before
purging begins, and is out of all proportion to the diarrhoea. The
vomited matters contain blood and mucus and are never serous in
character. Corrosive poisons may cause redness, charring, or ulceration
of the mouth and throat and a burning sensation in the stomach. The
pain over the stomach is more constant and severe, particularly in the
intervals of {724} vomiting, and there may be abdominal tenderness and
bloody discharges. The expression is more anxious and the pulse rapid
and weak.

Elaterium and tartar emetic will bring on vomiting and purging which
resemble the symptoms of cholera morbus. Choleriform attacks due to
uraemia simulate cholera morbus. The distinction is to be made by the
previous history--pain and purging being relatively less prominent in
uraemia--by the presence of albumen and casts in the urine, and by the
early tendency to coma.

Acute peritonitis, attended by copious vomiting and purging, has been
mistaken for cholera morbus, and the true nature of the affection only
revealed by the autopsy.

PROGNOSIS.--As a rule, cholera morbus occurring in persons otherwise
healthy ends favorably in a few hours. Cases of secondary fever, with
gastro-intestinal catarrh, may prolong the attack from a few days to
two weeks. Should treatment have no effect in lessening the vomiting
and purging, and should the evidences of heart-failure become apparent,
a fatal result may be feared. Death has occurred within twelve hours,
and the mortality is 3 per cent. of uncomplicated cases.[17]

[Footnote 17: Bartholow, _Pract. Med._, New York, 1880, p. 58.]

Cases occurring in the course of other diseases possess a special
gravity.

TREATMENT.--During the summer months, and particularly in August and
September, when the hot days are succeeded by cool nights, iced drinks
should be used in moderate quantities; the diet should be light,
nutritious, and easy of digestion. Unripe fruits and articles of food
liable to fermentative changes should not be indulged in.

Exposure to the night air, particularly after a full meal, should be
especially avoided, and the clothing ought to be so arranged that
additions may be made as night approaches. Slight attacks of
indigestion should not be neglected, and any irregularity of the bowels
must receive immediate attention.

The period when the physician is called upon to prescribe for an attack
of cholera morbus is usually when the stomach has been emptied of food
and the patient is vomiting incessantly, purging, and writhing in pain.
If vomiting has not occurred and violent epigastric pain is the only
symptom, the stomach should be emptied by an emetic of hot water and
mustard repeated until the overcharged organ is completely emptied.
Partially-digested food in a state of acid fermentation will thus be
got rid of, and the sufferings may be immediately but not wholly
relieved.

If spontaneous vomiting has expelled the food, and the matters vomited
are green and watery, while pain and frequent stools with muscular
cramps, heart feebleness, and threatening collapse are the symptoms
presented, the remedy par excellence is a hypodermic injection of
sulphate of morphia (gr. 1/8 to 1/3) with sulphate of atropia (gr.
1/120 to 1/100). If one dose is not followed by decided mitigation of
suffering, the injection is to be repeated in a half hour or an hour,
not giving above one grain of morphia in divided doses. At the same
time, and while waiting for the full effect of the narcotic, efforts
can be directed to giving ease to the muscular spasms and pain by brisk
friction with stimulating lotions or by mustard poultices to the
abdomen and extremities. The morphia will be the best and quickest
stimulant which can be used; it will therefore be useless in most cases
to administer brandy, camphor, chloroform, {725} or other remedies of
that sort. Waiting and giving nothing by the mouth is the wiser course.
In twenty minutes to half an hour the most perfect bien etre succeeds
to the previous agony and exhaustion. In some cases the vomiting,
purging, and cramps cease more gradually, and six hours will pass
before the patient is at ease. The intense thirst is best treated by
the giving of cracked ice sparingly at first, more freely later.

Nothing substitutes morphia hypodermically with success, but in some
instances or when the stomach is not very irritable it may be necessary
to give medicine by the mouth. In this case chloroform (xv to xxx
drops), chlorodyne (x to xx drops), or spirits of camphor (v to x
drops) every quarter or half hour in ice-water may be directed.
Chloroform and camphor can be combined with the deodorized tincture of
opium in ten- to twenty-drop doses. Time is wasted in expecting relief
from remedies which are inevitably rejected as soon as taken; it is
only when the stomach is very tolerant that it is judicious to begin
with them.

The weakness of the heart's action must be combated by brandy or
whiskey, given by the mouth with pounded ice or administered
hypodermically. A considerable quantity of brandy or diluted alcohol
may be introduced by repeated injections beneath the skin. Iced
champagne may be tried with good effect. H. C. Wood quotes Hall[18] as
recommending hypodermic injections of chloral in the cold stage of
cholera. Five to eight grains in twenty minims of distilled water can
be thus given, and repeated at intervals of fifteen to twenty minutes
until some effect is perceived.

[Footnote 18: _Lancet_, May 2, 1874.]

If vomiting persists after the other symptoms--pain and muscular
spasms--are relieved, it is due to the intense gastric hyperaemia;
giving nothing which is not necessary is the wiser plan. Carbolic acid,
hydrocyanic acid, bismuth, bromide of sodium, or small doses of calomel
are remedies which meet the indication. Food should be withheld as long
as possible; then iced barley-water, followed by milk and lime-water in
very small quantities at short intervals, will test the power of the
stomach to retain and digest food.




{726}

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER.

BY J. LEWIS SMITH, M.D.


Entero-Colitis.

The summer affections of the intestines in children are chiefly of a
diarrhoeal character. Diarrhoeal attacks, as is well known, are much
more frequent and severe in the summer months than in other portions of
the year. Moreover, the diarrhoea of the summer season occurs chiefly
among children under the age of two and a half years, and is much more
common and fatal in the cities than in the country. In the large cities
this malady has heretofore been the annually-recurring scourge of
infancy, but of late years its prevalence has been in some degree
diminished and its severity controlled by the establishment of health
boards and the enforcement of sanitary regulations. Still, it remains
an important disease in all our cities, and one that largely increases
the aggregate mortality. The truth of this statement is shown by the
statistics of deaths taken at random from the mortuary records of any
large city. Thus, in New York City during 1882 the deaths from
diarrhoea reported to the Health Board, tabulated in months, were as
follows:

        Jan. Feb. Mar. Apr. May. June. July. Aug. Sept. Oct. Nov. Dec.
  Under
  five   34   32   50   50   72   231  1533  817   362  195   68   35
  years.
  Over
  five   14   15   14   20   15    19   131  149    84   55   31   24
  years.

Therefore, in 1882--and the statistics of other years correspond in
this particular--it is seen that nine times as many deaths of children
under the age of five years occurred from diarrhoea during the five
months from June 1st to October 31st as in the remaining seven months
of the year. It is also seen, in corroboration of the statement that
diarrhoea due to hot weather is chiefly a disease of infancy and early
childhood, that during these same five months, which embrace the summer
season, the number of deaths from diarrhoea under the age of five years
was seven and a half times greater than the number over that age. These
statistics agree with the general experience of physicians in city
practice. The summer diarrhoea would indeed be comparatively
unimportant were its death-rate as low in the first five years of life
as subsequently.

The following statistics show how great a destruction of life this
malady causes even under the surveillance of an energetic health board;
and before this board was established it was much greater, as I had
abundant opportunities to observe. The last annual report of the New
York Board of Health was made in 1875, since which time weekly
bulletins have been {727} issued. The deaths from diarrhoea at all ages
in the three last years in which annual reports were issued were as
follows:

              1873.  1874.  1875.
  January       94     43     46
  February      84     34     52
  March         97     40     58
  April        114     47     45
  May           95     61     89
  June         220    144    157
  July        1514   1205   1387
  August       967   1007   1012
  September    424    587    608
  October      213    255    185
  November      87    105     57
  December      53     56     50

Thus, in these three years the aggregate deaths from diarrhoea during
the months from June to October inclusive, in which months the summer
diarrhoea prevails, were 9885, while in the remaining seven months the
number was only 1407. How large a proportion of these deaths in the
warm season occurred in children we may infer from remarks made by the
Health Board in regard to another year. In their annual report for 1870
the board state: "The mortality from the diarrhoeal affections amounted
to 2789, or 33 per cent. of the total deaths; and of these deaths 95
per cent. occurred in children less than five years old, 92 per cent.
in children less than two years old, and 67 per cent. in those less
than a year old." Every year the reports of the Health Board furnish
similar statistics, but enough have been given to show how great a
sacrifice of life the summer complaint produces annually in this city.

What we observe in New York in reference to this disease is true also,
to a greater or less extent, in other cities of this country and
Europe, so far as we have reports. Not in every city is there the same
proportionate mortality from this cause as in New York, but the
frequency of the summer diarrhoea and the mortality which attends it
render it an important disease in, I believe, most cities of both
continents. In country towns, whether in villages or farm-houses, this
disease is comparatively unimportant, inasmuch as few cases occur in
them, and the few that do occur are of mild type, and consequently much
less fatal than in the cities.

The comparative immunity of the rural districts has an important
relation, as we will see, to the hygienic management of these cases.

ETIOLOGY.--In the causation of this disease two distinct factors are
recognized--the one atmospheric, the other dietetic.

The prevalence and severity of the summer diarrhoea correspond closely
with the degree of atmospheric heat, as may be inferred from the
foregoing statistics. In New York this disease begins in the month of
May--earlier in some years than in others--in a few scattered cases,
commonly of a mild type. Cases become more and more numerous and severe
as the weather grows warmer until July and August, when the diarrhoea
attains its maximum prevalence and severity. In these two months it is
by far the most frequent and fatal of all the diseases in cities. In
the middle of September new patients begin to be less common, and in
the latter part of this month and subsequently new cases do not occur,
unless under unusual circumstances which favor the development of this
malady. In New York a considerable number of deaths {728} of infants
occur from the diarrhoea in October. October is not a hot month in our
latitude--its average temperature is lower than that of May--and yet
the mortality from this disease is considerably larger in the former
than in the latter month. This fact, which seems to show that the
prevalence of the summer diarrhoea does not correspond with the degree
of atmospheric heat, is readily explained. The mortality in October,
and indeed in the latter part of September, is not that of new cases,
but is mainly of infants, as I have observed every year, who contract
the disease in July or August or earlier, and linger in a state of
emaciation and increasing weakness till they finally succumb, some even
in cool weather.

The fact is therefore undisputed, and is universally admitted, that the
summer season, stated in a general way, is the cause of this
annually-recurring diarrhoeal epidemic, but it is not so easy to
determine what are the exact causative conditions or agents which the
summer weather brings into activity. That atmospheric heat does not in
itself cause the diarrhoea is evident from the fact that in the rural
districts there is the same intensity of heat as in the cities, and yet
the summer complaint does not occur. The cause must be looked for in
that state of the atmosphere engendered by heat where unsanitary
conditions exist, as in large cities. Moreover, observations show that
the noxious effluvia with which the air becomes polluted under such
circumstances constitute or contain the morbific agent. Thus, in one of
the institutions of this city a few years since, on May 10, which
happened to be an unusually warm day for this month, an offensive odor
was noticed in the wards, which was traced to a large manure-heap that
was being upturned in an adjacent garden. On this day four young
children were severely attacked by diarrhoea, and one died. Many other
examples might be cited showing how the foul air of the city during the
hot months, when animal and vegetable decomposition is most active,
causes diarrhoea. Several years since, while serving as sanitary
inspector for the Citizens' Association in one of the city districts,
my attention was particularly called to one of the streets, in which a
house-to-house visitation disclosed the fact that nearly every infant
between two avenues had the diarrhoea, and usually in a severe form,
not a few dying. This street was compactly built with wooden
tenement-houses on each side, and contained a dense population, mainly
foreign, poor, ignorant, and filthy in their habits. It had no sewer,
and the refuse of the kitchens and bed-chambers was thrown into the
street, where it accumulated in heaps. Water trickled down over the
sidewalks from the houses into the gutters or was thrown out as slops,
so that it kept up a constant moisture of the refuse matter which
covered the street, and promoted the decay of the animal and vegetable
substances which it contained. The air in the domicils and street under
such conditions of impurity was necessarily foul in the extreme, and
stifling during the hot days and nights of July and August; and it was
evidently the important factor in producing the numerous and severe
diarrhoeal cases which were in these domicils.

In another locality, occupied by tripe-dealers and a low class of
butchers who carried on fat- and bone-boiling at night, the air was so
foul after dark that the peculiar impurity which tainted it could be
distinctly noticed in the mouth for a considerable time after a night
visit. In the street where {729} these nuisances existed and in
adjacent streets the summer diarrhoea was very prevalent and
destructive to human life. Murchison states that twenty out of
twenty-five boys were affected with purging and vomiting from inhaling
the effluvia from the contents of an old drain near their school-room.
Physicians are familiar with a similar fact showing this purgative
effect of impure air--that the atmosphere of a dissecting-room often
causes diarrhoea in those otherwise healthy.

The exact nature of the deleterious agent or agents in foul air which
cause the diarrhoea, whether they be gases or organisms, has not been
fully determined; but at a recent meeting of the Berliner Med.
Gesellschaft, A. Baginsky made a report on the bacilli of cholera
infantum, which he states he has found both in the dejections and in
the intestinal mucous membrane in the bodies of those who have perished
with this disease. In the stools, along with numerous other organisms,
Baginsky states that he found masses of zoogloea, and the same
organisms he detected on the surface of the small intestines, and could
trace their wanderings as far as the submucous tissue.[1] But it is
evidently very difficult to determine whether such organisms sustain a
causative relation to diarrhoea or spring into existence in consequence
of the foul secretions and decomposing fecal matters which are present.

[Footnote 1: _Allegem. Wien. Mediz. Zeitung_, Nov. 6, 1883.]

The impurities in the air of a large city are very numerous. Among
those of a gaseous nature are sulphurous acid, sulphuric acid,
sulphuretted hydrogen; various gases of the carbon group, as carbonic
acid, carburetted hydrogen, and carbonic oxide; gases of the nitrogen
group, as the acetate, sulphide, and carbonate of ammonium, nitrous and
nitric acids; and at times compounds of phosphorus and chlorine
(Parkes). A theory deserving consideration is that certain gaseous
impurities found in the air form purgative combinations. D. F. Lincoln,
in his interesting paper on the atmosphere in the _Cyclopaedia of
Medicine_, writes in regard to sulphuretted hydrogen: "When in the air,
freely exposed to the contact of oxygen, it becomes sulphuric acid.
Sulphide of ammonium in the same circumstances becomes a sulphate,
which, encountering common salt (chloride of sodium), produces sulphate
of sodium and chloride of ammonium. The sulphates form a characteristic
ingredient of the air in manufacturing districts." The sulphates, we
know, are for the most part purgatives, but whether they or other
chemical agents exist in the respired air in sufficient quantity to
disturb the action of the intestines, even where atmospheric impurities
are most abundant, is problematical and uncertain.

Again, the solid impurities in the air of a large city are very
numerous, as any one may observe by viewing a sunbeam in a darkened
room, which is made visible by the numerous particles floating in it.
These particles consist largely of organic matter, which sometimes has
been carried a long distance by the wind. The remarkable statement has
been made that in the air of Berlin organic forms have been found of
African production. Ehrenberg discovered fragments of insects of
various kinds--rhizopods, tardigrades, polygastrica, etc.--which,
existing in considerable quantity and inhaled in hot weather, when
decomposition and fermentation are most active, may be deleterious to
the system. Monads, bacteria, vibriones, amorphous dust containing
spores which {730} retain their vitality for months, are among the
substances found in the air of cities. The well-known hazy appearance
of the atmosphere resting over a large city like New York when viewed
from a distance is due to the gaseous and solid impurities with which
the air is so abundantly supplied--impurities which assume importance
in pathological studies, since minute organisms are now believed to
cause so many diseases the etiology of which has heretofore been
obscure. With our present knowledge we must be content with the general
statement that impure air is one of the two important factors which
cause summer diarrhoea, without being able to state positively which of
the elements in the air are most instrumental in causing this result.
But the theory is plausible that minute organisms rather than chemical
products are the chief cause. Henoch of Berlin, writing upon this
subject, calls attention to the disease known as intestinal mycosis,
its prominent symptom being a severe diarrhoea produced by eating
diseased meat containing a fungus. He believes that "a portion of the
fungus not destroyed by the gastric juice settles upon different parts
of the intestine, and there produces its effects;" and he adds, "At
present, however, we can regard the mykotic theory of cholera infantum
only as a very probable hypothesis. There is no doubt that high
atmospheric temperature increases the tendency to fermentation
dyspepsias which is present in imperfectly-nourished children at all
seasons, and causes them to appear not only epidemically, but also in
an extremely acute form which is not frequent under ordinary
circumstances. This would lead to the conclusion that, in addition to
the heat, infectious germs are present, which, being developed in great
masses by the former, enter the stomach with the food." The fungus
theory of the causative relation of atmospheric heat to the diarrhoea
of the summer season as thus explained by Henoch commands the readier
assent since it comports with the well-known facts relating to the
etiology of the summer complaint. This disease, as we have seen, is
most prevalent and fatal under precisely those conditions of dense
population, filthy domicils and streets, and atmospheric heat which are
favorable for the development of low organisms.

In those portions of our cities which are occupied by the poor, more
than anywhere else, those conditions prevail which render the
atmosphere deleterious. One accustomed to the pure air of the country
would scarcely believe how stifling and poisonous the atmosphere
becomes during the hot summer days and close summer nights in and
around the domicils in the poor quarters of the city. Among the causes
of this foul air may be mentioned too dense a population, the occupancy
of small rooms by large families, rigid economy and ceaseless endeavor
to make ends meet, so that in the absorbing interest sanitary
requirements are sadly neglected. Adults of such families, and children
of both sexes as soon as they are old enough, engage in laborious and
often filthy occupations. Many of them seldom bathe, and they often
wear for days the same undergarments, foul with perspiration and dirt.
The intemperate, vicious, and indolent, who always abound in the
quarters of the city poor, are notoriously filthy in their habits and
add to the insalubrity by their presence. Children old enough to be in
the streets and adults away at their occupations escape to a great
extent the evil effects of impure air, but the infantile population
always suffer severely.

Every physician who has witnessed the summer diarrhoea of infants is
{731} aware of the fact that the mode of feeding has much to do with
its occurrence. A large proportion of those who each summer fall
victims to it would doubtless escape if the feeding were exactly
proper. In New York City facts like the following are of common
occurrence in the practice of all physicians: Infants under the age of
eight months, if bottle-fed, nearly always contract diarrhoea, and
usually of an obstinate character, during the summer months. The
younger the infant, the less able is it to digest any other food than
breast-milk, and the more liable is it therefore to suffer from
diarrhoea if bottle-fed. In the institutions nearly every bottle-fed
infant under the age of four or even six months dies in the hot months
with symptoms of indigestion and intestinal catarrh, while the
wet-nursed of the same ages remain well. Sudden weaning, the sudden
substitution of cow's milk or any artificially-prepared food in place
of breast-milk in hot weather, almost always produces diarrhoea, often
of a severe and fatal nature. Feeding an infant in the hot months with
indigestible and improper food, as fruits with seeds or the ordinary
table-food prepared in such a way that it overtaxes the digestive
function of the infant, causes diarrhoea, and not infrequently that
severe form of it which will be described under the term cholera
infantum. Many obstinate cases of the summer complaint begin to improve
under change of diet, as by the substitution of one kind of milk for
another or the return of the infant to the breast after it has been
temporarily withdrawn from it. It is a common remark in the families of
the city poor that the second summer is the period of greatest danger
to infants. This increased liability of infants to contract diarrhoea
in the second summer is due to the fact that most infants in their
second year are table-fed, while in the first year they are wet-nursed.
Such facts, with which all physicians are familiar, show how important
the diet is as a factor in causing the summer complaint.

Occasionally, from continued ill-health, the milk of the mother or
wet-nurse does not agree with the nursling. Examined with the
microscope, it is found to contain colostrum. Under such circumstances
if a healthy wet-nurse be employed the diarrhoea ceases. It is very
important that any woman furnishing breast-milk to an infant should
lead a quiet and regular life, with regular meals and sleep. In the
_Louisville Med. Journal_, Aug. 19, 1882, R. B. Gilbert relates
striking cases in which venereal excesses on the part of wet-nurses
were immediately followed by fatal diarrhoea in the infants which they
suckled.

One not a resident would scarcely be able to appreciate the difficulty
which is experienced in a large city in obtaining proper diet for young
children, especially those of such an age that they require milk as the
basis of their food. Milk from cows stabled in the city or having a
limited pasturage near the city, and fed upon a mixture of hay with
garden and distillery products, the latter often largely predominating,
is unsuitable. It is deficient in nutritive properties, prone to
fermentation, and from microscopical and chemical examinations which
have been made it appears that it often contains deleterious
ingredients. If milk be obtained from distant farms where pasturage is
fresh and abundant--and in New York City this is the usual source of
the supply--considerable time elapses before it is served to customers,
so that, particularly in the hot months of July and August, it
frequently has begun to undergo {732} lactic-acid fermentation when the
infants receive it. That dispensed to families in the morning is the
milking of the previous morning and evening. The common result of the
use of this milk in midsummer by infants under the age of ten months is
more or less diarrhoea.

The ill-success of feeding with cow's milk has led to the preparation
of various kinds of food which the shops contain, but no dietetic
preparation has yet appeared which agrees so well with the digestive
function of the infant as breast-milk, and is at the same time
sufficiently nutritive.

In New York City improper diet, unaided by the conditions which hot
weather produces, is a common cause of diarrhoea in young infants, for
we meet with this diarrhoea in infants who are bottle-fed at all
seasons; but when the atmospheric conditions of hot weather and the use
of food unsuitable for the age of the infant are both present and
operative, this diarrhoea so increases in frequency and severity that
it is proper to designate it the summer epidemic of the cities. Several
years since, before the New York Foundling Asylum was established, the
foundlings of New York, more than a thousand annually, were taken to
the almshouse on Blackwell's Island and consigned to the care of the
pauper-women, who were mostly old, infirm, and filthy in their habits
and apparel. Their beds, in which the foundlings were also placed
alongside of them, were seldom clean, not properly aired and washed,
and under the beds were various garments and utensils which these
pauper-women had brought with them as their sole property from their
miserable abodes in the city. With such surroundings, the air which
these infants breathed day and night manifestly contained poisonous
emanations; while their diet was equally improper, for it was prepared
by these women from such milk and farinaceous food as were furnished
the almshouse. When assigned to duty in the almshouse, this service
being at that time a branch of Charity Hospital, I was informed that
all the foundlings died before the age of two months; one only was
pointed out as a curiosity which had been an exception to the rule. The
disease of which they perished was diarrhoea, and this malady in the
summer months was especially severe and rapidly fatal. The unpleasant
experiences in this institution furnished additional evidence, were any
wanting, that foul air and improper diet are the two important factors
in causing the summer diarrhoea of infants. Since that beneficial
charity, the New York Foundling Asylum, in East Sixty-eighth street,
came into existence, providing pure air and, for a considerable
proportion of the foundlings, breast-milk, many of these waifs have
been rescued from death.

I have already stated that this disease occurs, with an occasional
exception, under the age of two and a half years. The following table
embraces all the cases that came to one of the city dispensaries during
my service between the months of May and October, inclusive:

       Age.                Cases.
   5 months or under         58
   5 months to 12 months    212
  12 months to 18 months    174
  18 months to 24 months     93
  24 months to 36 months     36
                            ---
        Total               573

After the third year the liability to the summer complaint so rapidly
{733} diminishes that comparatively few are affected by it. It is seen
from the above statistics that by far the largest number of cases occur
during the period of first dentition; hence the prevalent opinion among
families that dentition causes the diarrhoea. It is the common belief
among the poor of New York that diarrhoea occurring during dentition is
conservative, and should not be checked. They believe that an infant
cutting its teeth suffers less, and may be saved from serious illness,
if it have frequent stools. Every summer I see infants reduced to a
state of imminent danger through the continuance of diarrhoea during
several weeks, nothing having been done to check it in consequence of
this absurd belief. The progressive loss of flesh and strength and
wasting of the features do not excite alarm, under the blinding
influence of this theory, till the diarrhoea has continued so long and
become so severe that it is with difficulty controlled, and the patient
is in a state of real danger when the physician is first summoned. The
following statistics, which comprise cases occurring during my service
in one of the city dispensaries, show the preponderance of cases during
the age when dental evolution is occurring:

                                              Cases.
  No teeth and no marked turgescence of gums    47
  Cutting incisors                             106
     "    anterior molars                       41
     "    canines                               40
     "    last molars                           20
  All the teeth cut                             28
                                               ---
        Total                                  282

It so happens that the period of dental evolution corresponds with that
of the most rapid development and the greatest functional activity of
the gastric and intestinal follicles, and the predisposition which
exists to diarrhoeal maladies at this age must be attributed to this
cause rather than to dentition.

SYMPTOMS.--The summer diarrhoea of infants commonly begins gradually
with languor, fretfulness, and slight febrile movement. The diarrhoea
at first usually attracts little attention from its mildness. The
stools, while they are thinner than natural, vary in appearance, being
yellow, brown, or green. Infants with milk diet are apt to pass green
and acid stools containing particles of undigested casein. The tongue
in the commencement of the attack is moist and covered with a slight
fur. At a more advanced stage it may be moist, but is often dry, and in
dangerous forms of the malady, accompanied by prostration, the buccal
surface is red and the gums more or less swollen and sometimes
ulcerated. Vomiting is common. It may commence simultaneously with the
diarrhoea, especially when food that is unusually indigestible and
irritating to the stomach has been given, but more frequently this
symptom does not appear until the diarrhoea has continued a few days. I
preserved memoranda of the date when vomiting began in the cases
treated in two consecutive summers, and found that ordinarily it was
toward the close of the first week. When it is an early and prominent
symptom it appears to be due to the presence in the stomach of
imperfectly digested or fermented and acid food, which, when ejected,
gives a decidedly acid reaction with appropriate tests. It contains
coagulated casein and undigested particles of whatever food has been
given. In many patients the progressive loss of flesh and {734}
strength is largely due to the indigestion and vomiting by which the
food, which is so much required for proper nourishment, is lost.

Emesis occurring at a late stage of the summer complaint is often due
to commencing spurious hydrocephalus, which is not an infrequent
complication, as we will see, of protracted cases. Perhaps when a late
symptom it may sometimes have an uraemic origin, for the urine is
usually quite scanty in advanced cases. It seems probable, however,
that deleterious effects from non-elimination of urea are to a
considerable extent prevented by the diarrhoea.

The fecal evacuations may remain nearly uniform in appearance during
the disease, but in many patients they vary in color and consistence at
different periods. In the same case they may be brown and offensive at
one time, green at another, and again they may contain masses of a
putty-like appearance, the partly-digested casein or altered epithelial
cells. The stools sometimes consist largely of mucus, with or without
occasional streaks of blood, indicating the predominance of
inflammation in the colon. This is the mucous diarrhoea of Barrier. The
stools are sometimes yellow when passed, but become green on exposure
to the air from chemical reaction due to admixture with the urine.

The character of the alvine discharges is interesting. In addition to
undigested casein I have found epithelial cells, single or in clusters
(sometimes regularly arranged as if detached in mass from the villi),
fibres of meat, crystalline formations, mucus, and occasionally blood,
as stated above. In one instance I observed an appearance resembling
three or four crypts of Lieberkuhn united, probably thrown off by
ulceration. If the stools are green, colored masses of various sizes,
but mostly small, are also seen under the microscope.

The pulse is accelerated according to the severity of the attack. The
heat of the surface is at first apt to be increased, though but
slightly in ordinary cases; but when the vital powers begin to fail
from the continuance of the diarrhoea the warmth of the surface
diminishes. In advanced cases approaching a fatal termination the face
and extremities are pallid and cool, and the pulse gradually becomes
more frequent and feeble. The skin is usually dry, and, as already
stated, the urinary secretion diminished. In severe cases attended by
frequent alvine discharges the infant does not pass urine oftener than
once or twice daily. The imperfect action of the skin and kidneys is
noteworthy.

Protracted cases of the summer complaint are apt to be complicated by
two cutaneous eruptions--erythema extending over the perineum and
frequently as far as the thighs and lower part of the abdomen, due to
the acid and irritating character of the stools; and boils upon the
forehead and scalp. The latter sometimes extend to the pericranium, and
in case of recovery leave permanent cicatrices. This furuncular
affection of the scalp has seemed to me useful in consequence of the
external irritation which it causes, since it occurs at a time when, on
account of the feeble heart's action and languid circulation, passive
congestion of the vessels of the brain and meninges is liable to be
present.

Patients who are weak and wasted in consequence of protracted
diarrhoea, remaining almost constantly in the recumbent position, often
have an occasional dry cough which continues till the close of life. It
is due to hypostatic congestion in the lungs, usually limited to the
posterior and {735} inferior portions of the lobes, extending but a
little way into the lungs. It is the result of prolonged recumbency
with feeble heart's action and feeble pulmonary circulation. Infants
reduced by chronic diseases, lying day after day in their cribs with
little movement of their bodies, are very liable to this passive
congestion of depending portions of their lungs, toward which the blood
gravitates, and into which but little air enters in consequence of
their distance and position and the feeble respirations. The hyperaemia
which results is of a passive character, a venous congestion, and the
affected lobules have a dusky-red color. This congestion, continuing,
soon results in pneumonitis of the catarrhal form, subacute and of a
low grade, for pulmonary lobules in which the blood remains stagnant
soon exhibit augmented cell-proliferation, perhaps from the irritating
effects of the elements of the blood now withdrawn from the
circulation.

I have made or procured a considerable number of microscopic
examinations in these cases of hypostatic pneumonia, and the
solidification of the pulmonary lobules has been found to be due to the
exaggerated development of the epithelial cells in the alveoli,
together with venous congestion. The affected lobules, whether in the
stage of hypostatic congestion or the more advanced stage of hypostatic
pneumonitis, when examined at the autopsy, were somewhat softer than in
health, of dark color, and many of the lobules could be inflated by
strong force of the breath; but in protracted cases the alveoli in
central parts of the inflamed area resisted insufflation. The lung in
hypostatic pneumonia, even when it is inflated, still feels firmer
between the fingers than normal lung.

Hypostatic pneumonia is so common in hospitals for infants that some
physicians whose observations have been chiefly in such institutions
have almost ignored other forms of pulmonary inflammation. Billard,
many years ago, wrote: "... The pneumonia of young children is
evidently the result of stagnation of blood in their lungs. Under these
circumstances the blood may be regarded as a kind of foreign body." Of
all the chronic and exhausting diseases of infancy, no one has,
according to my observations, been so frequently complicated by
hypostatic pneumonia as the disease which we are considering, although
it does not usually give rise to any more prominent symptom than an
occasional cough. Limited to a small and almost immovable part of the
lung, it does not ordinarily accelerate respiration or render it
painful, and the cough is also apparently painless.

When progressive loss of flesh and strength has continued several
weeks, and the patient is much exhausted, another complication is apt
to occur, known as spurious hydrocephalus or the hydrocephaloid
disease, the anatomical characters of which will be described in the
proper place. The commencement of spurious hydrocephalus is announced
by gradually increasing drowsiness, perhaps preceded by a period of
unusual fretfulness. Vomiting and rolling the head are occasional early
symptoms of this complication. As the drowsiness increases the pupils
become less sensitive to light than in their normal state, and are
usually contracted. When the drowsiness becomes profound and constant,
the pupils remain contracted as in sound sleep or in opium narcotism.
The functional activity of the organs is now also diminished, the
vomiting ceases, the stools become less frequent, the buccal surface
dry, and the urine more {736} scanty, while the pulse is more frequent
and feeble. Spurious hydrocephalus either continues till death, or by
stimulation the patient may emerge from it. When profound the usual
result is death.

Although the summer complaint in its commencement may be promptly
arrested by proper hygienic and medicinal treatment, if it continue a
few weeks the anatomical changes which occur are such that recovery, if
it take place, is necessarily slow and gradual. Improvement is shown by
better digestion, fewer stools and of better appearance, less frequent
vomiting, a more cheerful countenance, and the absence of symptoms
which indicate a complication. Many recover after days of anxious
watching and perhaps after many fluctuations.

Death may occur early from a sudden aggravation of symptoms and rapid
sinking, or the attack may be so violent from the first that the infant
quickly succumbs; but more frequently death takes place after a
prolonged sickness. Little by little the patient loses flesh and
strength, till a state of marked emaciation is reached. The eyes and
cheeks are sunken, the bony projections of the face, trunk, and limbs
become prominent, and the skin lies in wrinkles from the wasting. The
altered expression of the face makes the patient look older than the
actual age. The joints in contrast with the wasted extremities seem
enlarged and the fingers and toes elongated. The stools diminish in
frequency from diminished peristaltic and vermicular action, and
vomiting, if previously present, now ceases. A feeble, quick, and
scarcely appreciable pulse, slow respiration, and diminished inflation
of the lungs, sightless and contracted pupils, over which the eyelids
no longer close, announce the near approach of death. The drowsiness
increases and the limbs become cool, while perhaps the head is hot. The
infant no longer has the ability to nurse, or if bottle-fed the food
placed in the mouth flows back or is swallowed with apparent
indifference. So low is its vitality that it lies pallid and almost
motionless for hours or even days before death, and death occurs so
quietly that the moment of its occurrence is scarcely appreciable.

ANATOMICAL CHARACTERS.--Since the prominent and essential symptoms of
the disease which we are considering pertain to the digestive
apparatus, it is evident that the lesions which attend and characterize
it are to be found in this part of the system. Lesions elsewhere, so
far as they are appreciable to us, are secondary and not essential. I
have witnessed a large number of autopsies of infants who have perished
from the summer complaint, chiefly in institutions, and they have been
sufficiently marked and uniform to enable us to designate it an
entero-colitis. Several years since I preserved records of the
autopsical appearances in the intestinal catarrh of infants, most of
the cases being of summer diarrhoea. The number aggregated eighty-two.
Since then I have each summer witnessed autopsies in the institutions
in cases of this disease, and the lesions observed were the same as in
the eighty-two cases.

The question may properly be asked: Can inflammatory hyperaemia of the
intestinal mucous membrane be distinguished from simple congestion if
there be no ulceration and no appreciable thickening of the intestine?
It is possible that occasionally I have recorded as inflammatory what
was simply a congestive lesion, but I do not think I have incorporated
a {737} sufficient number of such cases to vitiate the statistics. In a
large proportion of the cases there was evident thickening of the
intestinal mucous membrane or other unequivocal evidence of
inflammation. The following is an analysis of the eighty-two cases:

The duodenum and jejunum presented the appearance of inflammatory
hyperaemia in 12 cases. The hyperaemia was usually in patches of
variable extent or of that form described by the term arborescent. In
51 cases the duodenal and jejunal mucous membrane was pale and without
any other appearance characteristic of catarrh or inflammation. In the
remaining 19 cases the appearance of the duodenum and jejunum was not
recorded, so that it was probably normal. On the other hand, in the
ileum inflammatory lesions were present as a rule. In 49 cases I found
the surface of the ileum distinctly hyperaemic, and in that portion of
it nearest the ileo-caecal valve, including the valve itself, the
inflammation had evidently been the most intense, since in this portion
the hyperaemia and thickening of the mucous membrane were most marked.
In 16 cases the surface of the ileum appeared nearly or quite normal;
in 14 hyperaemia in the small intestines in patches, streaks, or
arborescence was recorded, but the records do not state in which
division of the intestines they were observed.

Billard, with other observers, has noticed the frequency and intensity
of the inflammatory lesions in entero-colitis in the terminal portion
of the small intestines, and the thickening in many cases of the
ileo-caecal valve, and he asks whether the vomiting which is so common
and often obstinate in this disease may not be sometimes due to
obstruction to the passage of fecal matter at the valve in consequence
of the hyperaemia and swelling, but has not observed any retained fecal
matter above it, such as we find in any part of the colon, or any other
appearance which indicated sufficient obstruction to cause symptoms.
Still, it seems not improbable that the reason why the inflammatory
lesions are more pronounced at and immediately above the valve than in
other parts of the small intestine is that the fecal matter, so
commonly acid and irritating in this disease, is somewhat delayed in
its passage downward at this point.

Small superficial circular or oval ulcers were observed in the ileum in
4 cases, in 2 of which they were found also in the lower part of the
jejunum. In 1 case the records state that ulcers were in the jejunum,
but do not mention whether they were also in the ileum. In 1 case, in
which there was much thickening of the ileum next to the ileo-caecal
valve, many small granulations had sprouted up from the submucous
connective tissue, so that the mucous surface appeared as if studded
with small warts.

Softening of the mucous membrane was also apparent in certain cases.
The firmness of its attachment to the parts underneath varied
considerably in different specimens. I was able in cases in which there
was considerable softening to detach readily the mucous membrane with
the nail or handle of the scalpel within so short a period after death
that it was probable that the change of consistence was not cadaveric.
In some cases the vessels of the submucous tissue were injected and
this tissue infiltrated.

In all the cases except one lesions were present indicating
inflammation {738} of the mucous membrane of the colon. In 39
hyperaemia, thickening, and other signs of inflammation extended over
nearly or quite the entire colon; in 14 the colitis was confined to the
descending portion entirely or almost entirely; in 28 cases the records
state that inflammatory lesions were found in the colon, but their
exact location is not mentioned. In 18 of the autopsies the mucous
membrane of the colon was found ulcerated.

Therefore, according to these statistics--and autopsies which I have
witnessed that are not embraced in them disclosed similar
lesions--colitis is present, almost without exception, in cases of
summer diarrhoea, associated with more or less ileitis. The portion of
the colon which presents the most marked inflammatory lesions is that
in and immediately above the sigmoid flexure--that portion, therefore,
in which any fermenting fecal matter has reached its greatest degree of
fermentation, and consequently contains the most irritating elements,
and where, next to the caput coli, it is longest delayed in its passage
downward.

The solitary glands of both the large and small intestines and Peyer's
patches undergo hyperplasia. In cases of short duration, and in parts
of the intestine where the inflammatory action has been mild, the
solitary glands present a vascular appearance, like the surrounding
membrane, and are slightly enlarged. The enlargement is most apparent
if the intestine be viewed by transmitted light, when not only are the
glands seen to be swollen, but their central dark points are distinct.
If a higher grade of intestinal catarrh or a catarrh more protracted
have occurred, the volume of these follicles is so increased that they
rise above the common level and present a papillary appearance. Peyer's
patches are also distinct and punctate. The enlargement of Peyer's
patches, like that of the solitary glands, is due to hyperplasia, the
elementary cells being largely increased in number.

The small ulcers which, as we have seen from the above statistics, are
present in a certain proportion of cases in the mucous membrane of the
colon, and more rarely in that of the small intestine when the
inflammation has been protracted and of a severe type, appear to occur
in the solitary glands and in the mucous membrane surrounding them.
While some of these glands in a specimen are simply tumefied, others
are slightly ulcerated, and others still nearly or quite destroyed. The
ulcers are usually from one to three lines in diameter, circular or
oval, with edges slightly raised from infiltration. Rarely, I have seen
minute coagula of blood in one or more ulcers, and I have also observed
ulcers which have evidently been larger and have partially healed. The
ulcers are more frequently found in the descending colon than in other
portions of the intestines. When ulcers are present they commonly occur
in the descending colon, or if occurring elsewhere they are most
abundant in this situation.

According to my observations, these ulcers are found chiefly in infants
over the age of six months--during the time, therefore, when there is
greatest functional activity and most rapid development of the solitary
glands. Peyer's patches, though frequently prominent and distinct, have
not been ulcerated in any of the cases observed by me.

The appendix vermiformis participates in the catarrh when it occurs in
the caput coli, its mucous membrane being hyperaemic and thickened. In
{739} certain rare cases the inflammation is so intense that a thin
film of fibrin is exuded in places upon the surface of the colon. It is
apt to be overlooked or to be washed away in the examination. The
rectum usually presents no inflammatory lesions, or but slight lesions
in comparison with those in the colon. It usually remains of the normal
pale color, or but slightly vascular even when there is almost general
colitis. Hence the infrequency of tenesmus.

As might be expected from the nature of the disease, the secretion of
mucus from the intestinal surface is augmented. It is often seen
forming a layer upon the intestinal surface, and it appears in the
stools mixed with epithelial cells and sometimes with blood and pus.

The mesenteric glands in cases which have run the most protracted
course and end fatally are found more or less enlarged from
hyperplasia. They are frequently as large as a pea or larger, and of a
light color, the color being due not only to the hyperplasia, but in
part to the anaemia. Occasionally, when patients have been much reduced
from the long continuance of the diarrhoea, and are in a state of
marked cachexia at death, we find certain of these glands caseous.

The condition of the stomach is interesting, since indigestion and
vomiting are so commonly present. I have records of its appearance in
59 cases, in 42 of which it seemed normal, having the usual pale color
and exhibiting only such changes as occur in the cadaver. In the
remaining 17 cases the stomach was more or less hyperaemic, and in 3 of
them points of ulceration were observed in the mucous membrane.

All physicians familiar with this disease have remarked the frequency
of stomatitis. In protracted and grave cases it is a common
complication. The buccal surface in these cases is more vascular than
natural, and if the vital powers are much reduced superficial
ulcerations are not infrequent, oftener upon the gums than elsewhere.
The gums are apt to be spongy, more or less swollen, bleeding readily
when rubbed or pressed upon. Thrush is a common complication of the
summer complaint in infants under the age of three or four months, but
is infrequent in older infants. Occurring in those over the age of six
or eight months, it has an unfavorable prognostic significance,
indicating a form of summer diarrhoea which commonly eventuates in
death.

The belief has long been prevalent in the past that the liver is also
in fault. The green color of the stools was supposed to be due to
vitiated bile. But usually in the post-mortem examinations which I have
made I have found that the green coloration of the fecal matter did not
appear at the point where the bile enters the intestines, but at some
point below the ductus communis choledochus in the jejunum or ileum.
The green tinge, at first slight, becomes more and more distinct on
tracing it downward in the intestine. It appears to be due to admixture
of the intestinal secretions with the fecal matter.

I have notes of the appearance and state of the liver in 32 fatal
cases. Nothing could be seen in these examinations which indicated any
anatomical change in this organ that could be attributed to the
diarrhoeal malady. The size and weight of the liver varied considerably
in infants of the same age, but probably there was no greater
difference than usually obtains among glandular organs in a state of
health. The following was the weight of this organ in 20 cases: {740}

    Age.          Weight.  |    Age.           Weight.
  4 weeks   5     ounces.  | 10 months   6-3/4 ounces.
  2 months  3-1/2   "      | 13   "      6       "
  2   "     3-1/2   "      | 14   "      9       "
  4   "     5       "      | 15   "      6       "
  5   "     6-1/2   "      | 15   "      7-1/2   "
  5   "     9       "      | 15   "      9-1/2   "
  7   "     4-1/2   "      | 16   "      6       "
  7   "     6       "      | 19   "      4-1/2   "
  7   "     6-1/4   "      | 20   "      9-1/4   "
  9   "     8       "      | 23   "     15       "

In none of these cases did the size, weight, or appearance of this
organ seem to be different from that in health or in other diseases,
except in one in which fatty degeneration had occurred, but this was
probably due to tuberculosis, which was also present. In most of these
cases the liver was examined microscopically, and the only noteworthy
appearance observed was the variable amount of oil-globules in the
hepatic cells. In some specimens the oil-globules were in excess, in
others deficient, and in others still they were more abundant in one
part of the organ than in another. Little importance was attached to
these differences in the quantity of oily matter.

Hypostatic congestion of the posterior portions of the lungs, ending if
it continue in a form of subacute catarrhal pneumonia and giving rise
to an occasional painless cough, has been described in the preceding
pages. The character of the cough in connection with the wasting might
excite suspicions of the presence of tubercles in the lungs; but
tubercles are rare in this disease, and when present I should suspect a
strong hereditary predisposition. They occurred in only 1 of the 82
cases.

The state of the encephalon in those patients in whom spurious
hydrocephalus occurs is interesting. In protracted cases of the
diarrhoea the brain wastes like the body and limbs. In the young
infant, in whom the cranial bones are still ununited, the occipital and
sometimes the frontal bones become depressed and overlapped by the
parietal, the depression being of course proportionate to the
diminution in size of the encephalon. The cranium becomes quite uneven.
In older children, with the cranial bones consolidated, serous effusion
occurs according to the degree of waste, thus preserving the size of
the encephalon. The effusion is chiefly external to the brain, lying
over the convolutions from the base to the vertex. Its quantity varies
from one or two drachms to an ounce or more. Along with this serous
effusion, and antedating it, passive congestion of the cerebral veins
and sinuses is also present. This congestion is the obvious and
necessary result of the feebleness of the heart's action and the loss
of brain substance.

DIAGNOSIS.--The occurrence and continuance of diarrhoea in the warm
months, without any apparent cause except the agencies which hot
weather produces, indicate this disease. The exciting cause of the
attack may be the use of some indigestible and irritating substance,
dietetic or medicinal, as fruits with their seeds or a purgative
medicine; but if it continue after the immediate effects of the agent
have passed off, it is proper to attribute the diarrhoea to the summer
season.

In the adult abdominal tenderness is an important diagnostic symptom of
intestinal catarrh, but in the infant this symptom is lacking or is not
in general appreciable, so that it does not aid in diagnosis. When the
{741} diagnosis of the disease is established, the symptoms do not
usually indicate what part of the intestinal surface is chiefly
involved, but it may be assumed that it is the lower part of the ileum
and the colon. The presence of mucus or of mucus tinged with blood in
the stools shows the predominance of colitis.

PROGNOSIS.--Although this disease every summer largely increases the
death-rate of young children, most cases can be cured if the proper
hygienic and medicinal measures be early applied. It is obvious, from
what has been stated in the foregoing pages, that cholera infantum is
the form of this malady which involves greatest danger. Except in such
cases there is sufficient forewarning of a fatal result, for if death
occur it is after a lingering sickness, with fluctuations and gradual
loss of flesh and strength. Patients often recover from a state of
great prostration and emaciation, provided that no fatal complications
arise. The eyes may be sunken, the skin lie in folds from the wasting,
the strength may be so exhausted that any other than the recumbent
position is impossible, and yet the patient may recover by removal to
the country, by change of weather, or by the use of better diet and
remedies. Therefore an absolutely unfavorable prognosis should not be
made except in cases that are complicated or that border on collapse.
The most dangerous symptoms, except those which indicate commencing or
actual collapse, arise from the state of the brain. Rolling the head,
squinting, feeble action or permanent contraction of the pupils,
spasmodic or irregular movements of the limbs, indicate the near
approach of death, as do also coldness of face and extremities and
inability to swallow. It is obvious also that in making the prognosis
in ordinary cases we should consider the age of the patient, the state
of the weather, the time in the summer, whether in the beginning or
near its close, and the surroundings, especially in reference to the
impurity of the air, as well as the patient's condition.


Cholera Infantum, or Choleriform Diarrhoea.

This is the most severe form of the summer complaint. It receives the
name which designates it from the violence of its symptoms, which
closely resemble those of Asiatic cholera. It is, however, quite
distinct from that disease. It is characterized by frequent stools,
vomiting, great elevation of temperature, and rapid and great
emaciation and loss of strength. It commonly occurs under the age of
two years. It sometimes begins abruptly, the previous health having
been good; in other cases it is preceded by the ordinary form of summer
diarrhoea. The stools have been thinner than natural and somewhat more
frequent, but not such as to excite alarm, when suddenly they become
more frequent and watery, and the parents are surprised and frightened
by the rapid sinking and real danger of the infant.

The first evacuations, unless there have been previous diarrhoea, may
contain fecal matter, but subsequently they are so thin that they soak
into the diaper like urine, and in some cases they scarcely produce
more of a stain than does this secretion. Their odor is peculiar--not
fecal, but musty and offensive, and occasionally almost odorless.
Commencing simultaneously with the watery evacuations or soon after is
another {742} symptom, irritability of the stomach, which increases
greatly the prostration and danger. Whatever drinks are swallowed by
the infant are rejected immediately or after a few moments, or retching
may occur without vomiting. The appetite is lost and the thirst is
intense. Cold water is taken with avidity, and if the infant nurse it
eagerly seizes the breast in order to relieve the thirst. The tongue is
moist at first, and clean or covered with a light fur, pulse
accelerated, respiration either natural or somewhat increased in
frequency, and the surface warm, but the temperature is speedily
reduced in severe cases. The internal temperature or that of the blood
is always very high. In ordinary cases of cholera infantum the
thermometer introduced into the rectum rises to or above 105 degrees,
and I have seen it indicate 107 degrees. Although the infant may be
restless at first, it does not appear to have any abdominal pain or
tenderness. The restlessness is apparently due to thirst or to that
unpleasant sensation which the sick feel when the vital powers are
rapidly reduced. The urine is scanty in proportion to the gravity of
the attack, as it ordinarily is when the stools are frequent and
watery.

The emaciation and loss of strength are more rapid than in any other
disease which I can recall to mind, unless in Asiatic cholera. In a few
hours the parents scarcely recognize in the changed and melancholy
aspect of the infant any resemblance to the features which it exhibited
a day or two before. The eyes are sunken, the eyelids and lips are
permanently open from the feeble contractile power of the muscles which
close them, while the loss of the fluids from the tissues and the
emaciation are such that the bony angles become more prominent and the
skin in places lies in folds.

As the disease approaches a fatal termination, which often occurs in
two or three days, the infant remains quiet, not disturbed even by the
flies which alight upon its face. The limbs and face become cool, the
eyes bleared, pupils contracted, and the urine scanty or suppressed. In
some instances, when the patient is near death, the respiration becomes
accelerated, either from the effect of the disease upon the respiratory
centres or from pulmonary congestion resulting from the feeble
circulation. As the vital powers fail the pulse becomes progressively
more feeble, the surface has a clammy coldness, the contracted pupils
no longer respond to light, and the stupor deepens, from which it is
impossible to arouse the infant.

In the most favorable cases cholera infantum is checked before the
occurrence of these grave symptoms, and often in cases which are
ultimately fatal there is not such a speedy termination of the malady
as is indicated in the above description. The choleriform diarrhoea
abates and the case becomes one of ordinary summer complaint.

ANATOMICAL CHARACTERS.--Rilliet and Barthez, who of foreign writers
treat of cholera infantum at greatest length, describe it under the
name of gastro-intestinal choleriform catarrh. "The perusal," they
remark, "of anatomico-pathological descriptions, and especially the
study of the facts, show that the gastro-intestinal tube in subjects
who succumb to this disease may be in four different states: (_a_)
either the stomach is softened without any lesion of the digestive
tube; (_b_) or the stomach is softened at the same time that the mucous
membrane of the intestine, and especially its follicular apparatus, is
diseased; (_c_) or the stomach is healthy, {743} while the follicular
apparatus or the mucous membrane is diseased; (_d_) or, finally, the
gastro-intestinal tube is not the seat of any lesion appreciable to our
senses in the present state of our knowledge, or it presents lesions so
insignificant that they are not sufficient to explain the gravity of
the symptoms.

"So far, the disease resembles all the catarrhs, but what is special is
the abundance of serous secretion and the disturbance of the great
sympathetic nerve.

"The serous secretion, which appears to be produced by a perspiration
(analogous to that of the respiratory passages and of the skin) rather
than by a follicular secretion, shows, perhaps, that the elimination of
substances is effected by other organs than the follicles; perhaps,
also, we ought to see a proof that the materials to eliminate are not
the same as in simple catarrh. Upon all these points we are constrained
to remain in doubt. We content ourselves with pointing out the
fact."[2]

[Footnote 2: _Maladies des Enfants_.]

On the 1st of August, 1861, I made the autopsy of an infant sixteen
months old who died of cholera infantum with a sickness of less than
one day. The examination was made thirty hours after death. Nothing
unusual was observed in the brain, unless perhaps a little more than
the ordinary injection of vessels at the vertex. No marked anatomical
change was observed in the stomach and intestines, except enlargement
of the patches of Peyer as well as of the solitary and mesenteric
glands. Mucous membrane pale. In this and the following cases there was
apparently slight softening of the intestinal mucous membrane, but
whether it was pathological or cadaveric was uncertain, as the weather
was very warm. The liver seemed healthy. Examined by the microscope, it
was found to contain about the normal number of oil-globules.

The second case was that of an infant seven months old, wet-nursed, who
died July 26, 1862, after a sickness also of about one day. He was
previously emaciated, but without any marked ailment. The post-mortem
examination was made on the 28th. The brain was somewhat softer than
natural, but otherwise healthy. There was no abnormal vascularity of
the membranes of the brain, and no serous effusion within the cranium.
The mucous membrane of the intestines had nearly the normal color
throughout, but it seemed somewhat thickened and softened; the solitary
glands of the colon were prominent. The patches of Peyer were not
distinct.

In the New York Protestant Episcopal Orphan Asylum an infant twenty
months old, previously healthy, was seized with cholera infantum on the
25th of June, 1864. The alvine evacuations, as is usual with this
disease, were frequent and watery, and attended by obstinate vomiting.
Death occurred in slight spasms in thirty-six hours. The exciting cause
was probably the use of a few currants which were eaten in a cake the
day before, some of which fruit was contained in the first evacuations.
The brain was not examined. The only pathological changes which were
observed in the stomach and intestines were slightly vascular patches
in the small intestines and an unusual prominence of the solitary
glands in the colon. The glands resembled small beads imbedded in the
mucous membrane. The lungs in the above cases were healthy, excepting
hypostatic congestion.

{744} Since the date of these autopsies I have made others in cases
which terminated fatally after a brief duration, and have uniformly
found similar lesions--namely, the gastro-intestinal surface either
without vascularity or scantily vascular in streaks or patches,
sometimes presenting a whitish or soggy appearance and somewhat
softened, while the solitary glands were enlarged so as to be prominent
upon the surface. In cases which continue longer evident inflammatory
lesions soon appear which are identical with those which have already
been described in our remarks on the ordinary form of the summer
diarrhoea.

During my term of service in the New York Foundling Asylum in the
summer of 1884, an infant died after a brief illness with all the
symptoms of cholera infantum, and the intestines were sent to William
H. Welch, now of Johns Hopkins Hospital, for microscopic examination.
His report was as follows: "I found undoubted evidence of acute
inflammation. There was an increased number of small, round cells
(leucocytes) in the mucous and submucous coats. This accumulation of
new cells was most abundant in and around the solitary follicles, which
were greatly swollen. Clumps of lymphoid cells were found extending
even a little into the muscular coat. The epithelial lining of the
intestine was not demonstrable, but this is usually the case with
post-mortem specimens of human intestine, and justifies no inferences
as to pathological changes. The glands of Lieberkuhn were rich in the
so-called goblet-cells, and some of the glands were distended with
mucus and desquamated epithelium, so as to present sometimes the
appearance of little cysts. This was observed especially in the
neighborhood of the solitary follicles. The blood-vessels, especially
the veins of the submucous coat, were abnormally distended with blood.
I searched for micro-organisms, and found them in abundance upon the
free surface of the intestine in the mucous accumulations there, and
also in the mouths of the glands of Lieberkuhn. Both rod-shaped and
small round bacteria were found. I attach no especial importance to
finding bacteria upon the surface of the intestine. The general result
of the examination is to confirm the view that cholera infantum is
characterized by an acute intestinal inflammation."

NATURE.--Cholera infantum appears from its symptoms and lesions to be
the most severe form of intestinal catarrh to which infants are liable.
The alvine discharges, to which the rapid prostration is largely due,
probably consist in part of intestinal secretions and in part of serum
which has transuded from the capillaries of the intestines. That the
intestinal mucous membrane sometimes presents a pale appearance at the
autopsy of an infant who, previously well, has died of cholera infantum
after a sickness of twenty-four or forty-eight hours, is perhaps due to
the great amount of liquid secretion and transudation in which the
inflamed surface is bathed. Moreover, it is, I believe, a recognized
fact that the hyperaemia of an acutely-inflamed surface when of short
duration frequently disappears in the cadaver, as that of scarlet fever
and erysipelas. The early hyperplasia of the solitary and mesenteric
glands, and the hyperaemia and thickening of the surface of the ileum
and colon in those who have survived a few days, indicate the
inflammatory character of the malady.

The opinion has been expressed by certain observers that cholera {745}
infantum is identical with thermic fever or sunstroke. There is indeed
a resemblance to thermic fever as regards certain important symptoms.
In cholera infantum the temperature is from 105 degrees to 108 degrees;
in sunstroke it is also very high, often running above 108 degrees.
Great heat of head, contracted pupils, thin fecal evacuations,
embarrassed respiration, scanty urine, and cerebral symptoms are common
toward the close of cholera infantum, and they are the prominent
symptoms in sunstroke. Nevertheless, I cannot accept the theory which
regards these maladies as identical, and which removes cholera infantum
from the list of intestinal diseases. In cholera infantum the
gastro-intestinal symptoms always take the precedence, and are, except
in advanced cases, always more prominent than other symptoms. It does
not commence as by a stroke like coup de soleil, but it comes on more
gradually, though rapidly, and it often supervenes upon a diarrhoea or
some error of diet. In the commencement of cholera infantum the infant
is not apt to be drowsy, and it is often wide awake and restless from
the thirst. Contrast this with the alarming stupor of sunstroke.
Sunstroke only occurs during the hours of excessive heat, but cholera
infantum may occur at any hour or in any day during the hot weather,
provided that there be sufficient dietetic cause. Again, intestinal
inflammation is not common in sunstroke, while it is the common or, as
I believe, the essential lesion of cholera infantum. These facts show,
in my opinion, that the two maladies are essentially and entirely
distinct. Nevertheless, cases of apparent sunstroke sometimes occur in
the infant, and if the bowels are at the same time relaxed the disease
is apt to be regarded as cholera infantum, and if fatal is usually
reported as such to the health authorities. Cases of this kind I have
occasionally observed or they have been reported to me, although they
are not common.

With the exception of the organs of digestion no uniform lesions are
observed in any of the viscera in cholera infantum, except such as are
due to change in the quantity and fluidity of the blood and its
circulation. Writers describe an anaemic appearance of the thoracic and
abdominal viscera, and occasionally passive congestion of the cerebral
vessels. The cerebral symptoms often present toward the close of life
in unfavorable cases of cholera infantum are often due to spurious
hydrocephalus, which we have described above; but as the urinary
secretion is scanty or suppressed, cerebral symptoms may in certain
cases be due to uraemia.

DIAGNOSIS.--This form of the summer diarrhoea is diagnosticated by the
symptoms, and especially by the frequency and character of the stools.
The stools have already been described as frequent, often passed with
considerable force, deficient in fecal matter, and thin, so as to soak
into the diaper almost like urine. The vomiting, thirst, rapid sinking,
and emaciation serve to distinguish cholera infantum from other
diarrhoeal maladies.

When Asiatic cholera is prevalent the differential diagnosis between
the two is difficult if not impossible.

PROGNOSIS.--Cholera infantum is one of those diseases in regard to
which physicians often injure their reputation by not giving sufficient
notice of the danger, or even by expressing a favorable opinion when
the case soon after ends fatally. A favorable prognosis should seldom
be expressed without qualification. If the urgent symptoms be relieved,
{746} still the disease may continue as an ordinary intestinal
inflammation, which in hot weather is formidable and often fatal. If
the stools become more consistent and less frequent without the
occurrence of cerebral symptoms, while the limbs are warm and the pulse
good, we may confidently express the opinion that there is no present
danger.

The duration of true cholera infantum is short. It either ends fatally,
or it begins soon to abate and ceases, or it continues, and is not to
be distinguished in its subsequent course from an attack of summer
diarrhoea beginning in the ordinary manner.

TREATMENT.--Preventive Measures.--Obviously, efficient preventive
measures consist in the removal of infants so far as practicable from
the operation of the causes which produce the disease. Weaning just
before or in the hot weather should, if possible, be avoided, and
removal to the country should be recommended, especially for those who
are deprived of the breast-milk during the age when such nutriment is
required. If for any reason it is necessary to employ artificial
feeding for infants under the age of ten months, that food should
obviously be used which most closely resembles human milk in
digestibility and in nutritive properties. Care should be taken to
prevent fermentation in the food before its use, since much harm is
done by the employment of milk or other food in which fermentative
changes have occurred and which occur quickly in dietetic mixtures in
the hot months.

It is also very important that the infant receive its food in proper
quantity and at proper intervals, for if the mother or nurse in her
anxiety to have it thrive feed it too often or in too large quantity,
the surplus food which it cannot digest if not vomited undergoes
fermentation, and consequently becomes irritating to the
gastro-intestinal surface. The physician should be able to give advice
not only in reference to the frequency of feeding, but also in regard
to the quantity of food which the infant requires at each feeding.
Correct knowledge and advice in this matter aid in the prevention and
cure of the dyspeptic and diarrhoeal maladies of infancy.

Chadbourne of this city and myself made some observations in order to
ascertain how much food well-nourished infants receive daily. We
selected infants that had an abundance of breast-milk, and weighed them
before and after each nursing, so as to determine how much each infant
took during twenty-four hours. The avoirdupois ounce contains 437.5
grains, and we ascertained by careful weight and measurement, employing
the metric system for its greater accuracy, that one fluidounce of
human milk, with a specific gravity of 1.031, weighed 451.9 grains.
With these data it was easy to determine the quantity of milk in
fluidounces from its weight. Our first observations related to 12
infants under the age of five weeks, 8 of which nursed twelve times,
and the remaining 4 eight, nine, nine, and eleven times respectively,
in the twenty-four hours. The quantity of milk received by them in
twenty-four hours varied considerably in the different cases, but the
average was 12.41 fluidounces. Therefore if a baby in the first five
weeks nurse every two hours, it receives only a little more than one
fluidounce at each nursing.

The next observations were made upon 15 infants between the ages of
five weeks and ten months: 8 of the 15 were under the age of six {747}
months, and the remaining 7 were between the ages of six months and ten
months. The weighing showed that the younger took nearly the same
quantity per day, on the average, as the older infants in this group.
The average quantity received by each was twenty-four and six-tenths
fluidounces. Hence if the nursings were eight in the twenty-four hours,
three ounces were taken at each nursing; if the nursings were twelve,
the quantity each time was two ounces.

Biedert of Germany has also made similar observations in order to
determine the amount of nutriment required by infants. The results of
his weight-studies, as he designates them, were published in the
_Jahrbuch fur Kinderheilkunde_, xix. B., 3 H. His weighing showed that
infants during their first month, if fed on cow's milk, required from
160 to 200 grammes of milk daily, and in the third month 300 grammes.
These quantities in fluid measure are 5.44 to 6.83 ounces, the quantity
required each day in the first month, and 10.22 ounces, the quantity
required daily the second month. Therefore, both my weights and
Biedert's show that infants under the age of two months assimilate a
smaller quantity of milk than is usually supposed. For infants older
than two months he estimates the quantity of milk required by infants
by their weight. He believes that the greater the weight the greater is
the amount of food which the infant needs. The method pursued by
Chadbourne and myself is more simple, and it seems to indicate with
sufficient exactness the amount of food required.

Some infants, like adults, need more food than others, so that there
can be no exact schedule of the quantity which they require at each
feeding; but while in the first and second months they do not need more
than from one to one and a half fluidounces at each feeding, whether of
breast-milk, or of cow's milk prepared so as to resemble as closely as
possible human milk, infants as they grow older and their stomachs
enlarge can take food in larger quantity, and therefore require less
frequent feeding. Under the age of two months the stomach is so small
that it cannot receive much more than one or one and a half fluidounces
without undue distension. At the age of six months it can probably
receive and digest without discomfort three ounces, and in the last
half of the first year even four ounces. Infants nourished at the
breast should be allowed to nurse every two hours in the daytime,
whatever the age, after the second month, but less frequently at night,
for frequent nursing promotes the secretion of milk, and the milk is of
better quality than when it is long retained in the breast. If by the
fifth or sixth month mothers or wet-nurses find, as is frequently the
case, that they do not have sufficient milk, other food should be given
in addition, perhaps after each second nursing or every fourth hour.
The kind of food which it is best to employ to supplement the nursing
will be mentioned under the head of curative measures. By knowledge on
the part of the mother and nurse of the dietetic needs of the infant,
and by consequent judicious alimentation, and by measures also to
procure the utmost purity of the air, there can be no doubt that the
summer diarrhoea may to a great extent be prevented.

Curative Treatment.--The indications for treatment are--1st, to provide
the best possible food; 2d, to procure pure air; 3d, to aid the
digestive function of the infant; 4th, to employ such medicinal agents
as can be safely given to check the diarrhoea and cure the intestinal
catarrh.

{748} The infant with this disease is thirsty, and is therefore apt to
take more nutriment in the liquid form than it requires for its
sustenance. If nursing, it craves the breast, or if weaned, craves the
bottle, at short intervals to relieve the thirst. No more nutriment
should be allowed than is required for nutrition, for the reason stated
above, and the thirst may best be relieved by a little cold water,
gum-water, or barley-water, to which a few drops of brandy or whiskey
are added.

Since one of the two important factors in producing the summer
diarrhoea is the use of improper food, it is obviously very important
for the successful treatment of this disease that the food should be of
the right kind, properly prepared, and given in proper quantity. I need
not repeat that for infants under the age of one year no food is so
suitable as breast-milk, and one affected with the diarrhoea and
remaining in the city should, if possible, at least if under the age of
ten months, be provided with breast-milk. It can be more satisfactorily
treated and the chances of its recovery are much greater if it be
nourished with human milk than by any other kind of diet. If, however,
the mother's milk fail or become unsuitable from ill-health or
pregnancy, and on account of family circumstances a wet-nurse cannot be
procured, the important and difficult duty devolves upon the physician
of deciding how the infant should be fed. In order to solve this
problem it will be well to recall to mind the part performed in the
digestive function by the different secretions which digest food:

1st. The saliva is alkaline in health. It converts starch into glucose
or grape-sugar. It has no effect upon fat or the protein group. It is
the secretion of the parotid, submaxillary, and sublingual glands,
which in infants under the age of three months are very small, almost
rudimentary. The two parotid glands at the age of one month weigh only
thirty-four grains. The power to convert starch into sugar possessed by
saliva is due to a ferment which it contains called ptyalin.

2d. The gastric juice is a thin, nearly transparent, and colorless
fluid, acid from the presence of a little hydrochloric acid. It
produces no change in starch, grape-sugar, or the fats, except that it
dissolves the covering of the fat-cells. Its function is to convert the
proteids into peptone, which is effected by its active principle,
termed pepsin.

3d. The bile is alkaline and neutralizes the acid product of gastric
digestion. It has no effect on the proteids. It forms soaps with the
fatty acids and has a slight emulsifying action on fat. The soaps are
said to promote the emulsion of fat. Their emulsifying power is
believed to be increased by admixture with the pancreatic secretion.
Moreover, the absorption of oil is facilitated by the presence of bile
upon the surface through which it passes.

4th. The pancreatic juice appears to have the function of digesting
whatever alimentary substance has escaped digestion by the saliva,
gastric juice, and bile. It is a clear, viscid liquid of alkaline
reaction. It rapidly changes starch into glucose. It converts proteids
into peptones and emulsifies fats. While the gastric juice requires an
acid medium for the performance of its digestive function, the
pancreatic juice requires one that is alkaline. This important fact
should be borne in mind, that such a mistake as presenting pepsin with
chalk mixture, or the extractum pancreatis with dilute muriatic acid,
may be avoided.

{749} 5th. The intestinal secretions are mainly from the crypts of
Lieberkuhn, and their action in the digestive process is probably
comparatively unimportant, but in some animals they have been found to
digest starch. It will be observed that of all these secretions that
which digests the largest number of nutritive principles is the
pancreatic. It digests all those which are essential to the maintenance
of life except fat, and it aids the bile in emulsifying fat.

One of the most important conferences in paediatrics ever held convened
at Salzburg in 1881 for the purpose of considering the diet of infants.
Among those who participated in the discussion were men known
throughout the world as authorities in children's diseases, such as
Demme, Biedert, Gerhardt, Henoch, Steffen, Thomas, and Soltmann. None
of the physicians present dissented from the following proposition of
the chairman: That "all the advances made in physiology in respect to
the digestive organs of children only go to prove that the mother's
milk is the only true material which is quantitatively and
qualitatively suited to the development of the child, which preserves
the physiological functions of the organs of digestion, and under
favorable circumstances of growth unfolds the whole organism in its
completeness." All agreed that when the breast-milk fails animal milk
is the best substitute. Henoch, who was one of the conference,
expresses the same opinion in his well-known treatise on diseases of
children, as follows: "Cow's milk is the best substitute for mother's
milk during the entire period of infancy. I consider the administration
of other substances advisable only when good cow's milk cannot be
obtained or when it gives rise to constant vomiting and diarrhoea."

The many infants' foods contained in the shops were considered by the
conference, and, in the words of the chairman, "Now and evermore it is
unanimously agreed that these preparations can in no way be substituted
for mother's milk, and as exclusive food during the first year are to
be entirely and completely rejected." But, unfortunately, we soon learn
by experience that animal milk, although it is the best of the
substitutes for human milk, is, especially as dispensed in the cities,
faulty. It is digested with difficulty by young infants, and is apt to
cause in them diarrhoea and intestinal catarrh. Therefore in the hot
months its use is very apt to act as one of the dietetic causes of the
summer diarrhoea in infants exclusively fed upon it, unless it be
specially prepared so as to more closely resemble human milk. The
frequent unsatisfactory results of its use have led to the preparation
of the many proprietary substitutes for human milk which the shops
contain, and which have been so summarily discarded by the German
conference.

Woman's milk in health is always alkaline. It has a specific gravity of
1.0317; cow's milk has a specific gravity of 1.029. That of cows
stabled and fed upon other fodder than hay or grass is usually
decidedly acid. That from cows in the country with good pasturage is
said to be alkaline, but in two dairies in Central New York a hundred
miles apart, in midsummer, with an abundant pasturage, two competent
persons whom I requested to make the examinations found the milk
slightly acid immediately after the milking in all the cows.

The following results of a large number of analyses of woman's and
cow's milk, made by Konig and quoted by Leeds, and of several of the
{750} best known and most used preparations designed by their inventors
to be substitutes for human milk, show how far these substitutes
resemble the natural aliment in their chemical characters:

  -------------+-----------------------+-----------------------+
               |     Woman's Milk.     |      Cow's Milk.      |
               +-------+-------+-------+-------+-------+-------+
               |       | Mini- | Maxi- |       | Mini- | Maxi- |
               | Mean. | mum.  | mum.  | Mean. | mum.  | mum.  |
  ---------------------+-------+-------+-------+-------+-------+
  Water        | 87.09 | 83.69 | 90.90 | 87.41 | 80.32 | 91.50 |
  Total solids | 12.91 |  9.10 | 16.31 | 12.59 |  8.50 | 19.68 |
  Fat          |  3.90 |  1.71 |  7.60 |  3.66 |  1.15 |  7.09 |
  Milk-sugar   |  6.04 |  4.11 |  7.80 |  4.92 |  3.20 |  5.67 |
  Casein       |  0.63 |  0.18 |  1.90 |  3.01 |  1.17 |  7.40 |
  Albumen      |  1.31 |  0.39 |  2.35 |  0.75 |  0.21 |  5.04 |
  Albuminoids  |  1.94 |  0.57 |  4.25 |  3.76 |  1.38 | 12.44 |
  Ash          |  0.49 |  0.14 |  ...  |  0.70 |  0.50 |  0.87 |
  -------------+-------+-------+-------+-------+-------+-------+

The following analyses of the foods for infants found in the shops, and
which are in common use, were made by Leeds of Stevens's Institute:

                          _Farinaceous Foods_.
  ----------------+-------+-------+-------+-------+--------+-------+
                  |   1.  |   2.  |   3.  |   4.  |   5.   |   6.  |
                  |       | Hubb- |Imper- |       |        |Robin- |
                  |Blair's| ell's |  ial  |Ridge's|"A.B.C."| son's |
                  | Wheat | Wheat |Granum.| Food. | Cereal |Patent |
                  | Food. | Food. |       |       | Milk.  |Barley.|
  ----------------+-------+-------+-------+-------+--------+-------+
  Water           |  9.85 |  7.78 |  5.49 |  9.23 |  9.33  | 10.10 |
  Fat             |  1.56 |  0.41 |  1.01 |  0.63 |  1.01  |  0.97 |
  Grape-sugar     |  1.75 |  7.56 | Trace.|  2.40 |  4.60  |  3.08 |
  Cane-sugar      |  1.71 |  4.87 | Trace.|  2.20 | 15.40  |  0.90 |
  Starch          | 64.80 | 67.60 | 78.93 | 77.96 | 58.42  | 77.76 |
  Soluble         |       |       |       |       |        |       |
    carbohydrates | 13.69 | 14.29 |  3.56 |  5.19 | 20.00  |  4.11 |
  Albuminoids     |  7.16 | 10.13 | 10.51 |  9.24 | 11.08  |  5.13 |
  Gum, cellulose, |       |Undet- |       |       |        |       |
    etc.          |  2.94 |erm'd. |  0.50 |  ...  |  1.16  |  1.93 |
  Ash             |  1.06 |  1.00 |  1.16 |  0.60 |  ...   |  1.93 |
  ----------------+-------+-------+-------+-------+--------+-------+

                          _Liebig's Foods_.
  ----------------+------+------+-------+-------+------+------+------+
                  |      |      |       | Keas- |Savory|      |      |
                  | Mel- | Haw- | Hor-  |bey and| and  | Baby | Baby |
                  |lin's.|ley's.|lick's.| Matti-|Moor- | Sup  | Sup  |
                  |      |      |       | son's.| e's. |No. 1.|No. 2.|
  ----------------+------+------+-------+-------+------+------+------|
  Water           |  5.00|  6.60|  3.39 | 27.95 |  8.34|  5.54| 11.48|
  Fat             |  0.15|  0.61|  0.08 | None. |  0.40|  1.28|  0.62|
  Grape-sugar     | 44.69| 40.57| 34.99 | 36.75 | 20.41|  2.20|  2.44|
  Cane-sugar      |  3.51|  3.44| 12.45 |  7.58 |  9.08| 11.70|  2.48|
  Starch          | None.| 10.97| None. | None. | 36.36| 61.99| 51.95|
  Soluble         |      |      |       |       |      |      |      |
    carbohydrates | 85.44| 76.54| 87.20 | 71.50 | 44.83| 14.35| 22.79|
  Albuminoids     |  5.95|  5.38|  6.71 | None. |  9.63|  9.75|  7.92|
  Gum, cellulose, |      |      |       |       |      |      |      |
    etc.          |  ... |  ... |  ...  |  ...  |  0.44|  7.09|  5.24|
                  |      |      |       |       |      |Undet-|      |
  Ash             |  1.89|  1.50|  1.28 |  0.93 |  0.89|erm'd.|  1.59|
  ----------------+------+------+-------+-------+------+------+------+

  {751}                   _Milk Foods_.
  ----------------+-----------+-----------+-----------+-----------+
                  |           |   Anglo-  |           | American- |
                  | Nestle's. |   Swiss.  | Gerber's. |   Swiss.  |
  ----------------+-----------+-----------+-----------+-----------+
  Water           |    4.72   |    6.54   |    6.78   |    5.68   |
  Fat             |    1.91   |    2.72   |    2.21   |    6.81   |
  Grape-sugar and |           |           |           |           |
    milk-sugar    |    6.92   |   23.29   |    6.06   |    5.78   |
  Cane-sugar      |   32.93   |   21.40   |   30.50   |   36.43   |
  Starch          |   40.10   |   34.55   |   38.48   |   30.85   |
  Soluble         |           |           |           |           |
    carbohydrates |   44.88   |   46.43   |   44.76   |   45.35   |
  Albuminoids     |    8.23   |   10.26   |    9.56   |   10.54   |
  Ash             |    1.59   |    1.20   |    1.21   |    1.21   |
  ----------------+-----------+-----------+-----------+-----------+

It is seen by examination of the analyses of the above foods that all
except such as consist largely or wholly of cow's milk differ widely
from human milk in their composition, and although some of them--as the
Liebig preparations, in which starch is converted into glucose by the
action of the diastase of malt--may aid in the nutrition and be useful
as adjuncts to milk, physicians of experience and close observation
will, I think, agree with the German conference that when breast-milk
fails or is insufficient our main reliance for the successful nutrition
of the infant must be on animal milk. Nestle's Food, which consists of
wheat flour, the yelk of egg, condensed milk, and sugar, and which has
been so largely used in this country and in Europe, is probably
beneficial mainly from the large amount of Swiss condensed milk which
it contains.

Although the preference is to be given to animal milk over any other
kind of food as a substitute for human milk, yet even when obtained
fresh and from the best dairies and properly diluted it is very apt to
disagree with infants under the age of one year, producing indigestion
and diarrhoea. The close resemblance in chemical character of cow's,
ass's, and goat's milk to human milk would lead us to expect that
either would be a good substitute for the latter. The fact that the
milk of these animals is apt to cause indigestion and intestinal
catarrh, especially in the hot months, when the digestive function of
the infant is enfeebled from the heat, must be due to the quality
rather than quantity of its constituents. The difference in quality of
the casein of human and animal milk is well known, since that of human
milk coagulates in the stomach in flakes, and that of animal milk in
firm and large masses. The German conference saw at once the importance
of the problem which confronted them--_i.e._ how to modify cow's milk
so that it bears the closest possible resemblance to human milk. They
even discussed the difference of the milk of different breeds of cows,
and the proper feeding and care of cows, but the most important
suggestion made--and one which has already produced good results in
this country and in Europe, and promises to be instrumental in saving
the lives of many infants who by the old method of feeding would
inevitably perish--was made by Pfeiffer of Wiesbaden. I allude to the
peptonizing of milk. The pancreatic secretion digests milk that is
rendered alkaline at a temperature between 100 degrees and 150 degrees
F. Milk thus treated becomes in from twenty minutes to one hour
thinner, resembling human milk in appearance, and if the peptonizing be
continued beyond a certain point, and is more complete, its taste is
decidedly {752} bitter. The process should be watched and the
peptonizing suspended as soon as the bitterness becomes appreciable,
for, although more advanced peptonizing so changes the milk that it is
more easily digested by the infant than when the peptonizing is
partial, yet the bitterness which is imparted to it renders it very
disagreeable as a dietetic preparation. Milk thus prepared closely
resembles human milk in appearance, and its casein is so digested that
it is either not precipitated by acids or is precipitated, like that of
human milk, in flakes. By this process a digested or an easily-digested
casein is produced, instead of the casein of ordinary cow's milk, which
produces large and firm masses in the stomach--masses that the
digestive ferments penetrate with such difficulty that they cause
indigestion, and occur in the stools in coagula of greater or less
size. Pfeiffer pointed out that when peptonized milk is employed "the
feces showed absolutely no trace of the white cheesiness." Milk thus
prepared quickly spoils, and it is necessary to peptonize it in small
quantity and often during the twenty-four hours.

In New York City during the last year peptonized milk has been employed
largely as recommended by Pfeiffer, and with such results as to
encourage its further use. It is now used in the New York Infant Asylum
and New York Foundling Asylum. Five grains of extractum pancreatis
(Fairchild & Co.'s) and ten grains of sodium bicarbonate are added to
one gill of warm water. This is mixed with one pint of warm milk, and
the mixture, in some convenient vessel, is placed in water kept at a
temperature of 100 degrees F. for one hour, when it is placed upon ice
to prevent further digestion. It should be tasted frequently during the
peptonizing process, and if the least bitterness be observed the
process should be suspended before the expiration of the hour. With
some specimens of milk, especially at a temperature of 115 degrees to
120 degrees, a half hour or even less is sufficient. This artificial
digestion is arrested either by boiling the peptonized milk, which
destroys the ferment, or by reducing its temperature to near the
freezing-point, which renders it latent and inactive, but does not
destroy it. I need not add that placing the peptonized milk on ice is
preferable to boiling it, since we wish the ferment to continue to act
in the stomach of the infant. In the present state of our knowledge of
infant feeding, therefore, we can recommend no better substitute for
human milk than peptonized cow's milk.

Leeds recommended the following formula for peptonizing milk in his
very instructive remarks made before the New York County Medical
Association, July 16, 1884. In order that no mistake might be made, I
wrote to him for his formula, which he kindly sent me. The following is
an extract from his letter: "The formula which I ventured to suggest
for the preparation of humanized cow's milk was as follows: 1 gill of
cow's milk, fresh and unskimmed; 1 gill of water; 2 tablespoonfuls of
rich cream; 200 grains of milk-sugar; 1-1/2 grains of extractum
pancreatis; 4 grains of sodium bicarbonate. Put this in a
nursing-bottle; place the bottle in water made so warm that the whole
hand cannot be held in it without pain longer than one minute. Keep the
milk at this temperature for exactly twenty minutes. The milk should be
prepared just before using."

The object is of course to provide from cow's milk a food which will be
the nearest possible approximation to healthy human milk; and this
{753} appears to be achieved by the peptonizing process. Certainly,
what physicians have long been desiring--namely, some mode of preparing
cow's milk so that its casein will coagulate in flakes like that of
human milk--has been obtained by peptonizing.

It is a common error to expect too much of a new remedy which has a
real value, and we must not expect that all patients not in an utterly
hopeless state will begin to improve as soon as peptonized milk is
prepared for them, or that it is a full and exact substitute for human
milk, so that wet-nurses may be dispensed with. Healthy human milk is
the best of all food for infants under the age of twelve months, and
should always be preferred when it can be obtained, but we claim that
peptonized milk is a most useful addition to the dietetic preparations
for infants, probably surpassing in value the best of those in the
shops. We employ it in the belief that it affords important aid in
curing the dyspeptic and diarrhoeal maladies of infancy. Who first
formulated and recommended the process of peptonizing milk I am not
able to state, but I am informed that Roberts of Great Britain called
attention to it as a means of improving milk at a time antedating the
German conference.

Milk from healthy, properly-fed cows may be prepared without
peptonizing, so as to agree with many infants except in the warmest
weather, but is obviously less easily digested than peptonized milk. It
should be diluted as follows with water boiled so as to free it from
germs: In the first week after birth one-fourth milk with the addition
of a little sugar. The milk should be gradually increased, so that it
is one-third by the end of the fourth week, one-half by the end of the
third month, and two-thirds to three-fourths by the end of the sixth
month. After the sixth month it is still proper to add one-fourth
water, but pure milk may be given. Water increases the urination.

Before peptonizing--which, as we have seen, digests the casein to a
great extent, and changes that which is not digested so that it
coagulates in flakes in the stomach like breast-milk--was resorted to,
it was customary to use a thin barley- or oat-water in place of the
water used for diluting the milk. One heaped teaspoonful of barley
flour to two tablespoonfuls of water make a gruel of proper
consistence. A little farinaceous substance added to the milk by
mechanically separating the particles of casein tends to prevent their
coagulation in large and firm masses. This was the theory which
explained the beneficial action of the admixture. If for any reason
peptonized milk be not employed, milk prepared in the way I have
mentioned, by admixture with a farinaceous substance, is probably the
next best substitute for human milk.

It is very important to determine when and how farinaceous foods shall
be given in this disease. It is well known that infants under the age
of three months digest starch with difficulty and only in small
quantity, since the salivary and pancreatic glands which secrete the
ferments which digest starch are almost rudimentary at that age. The
artificial digestion of starch is, however, easily accomplished. Among
the last labors of the renowned chemist Baron Liebig was the
preparation of a food for infants in which the starch is digested and
transformed into grape-sugar, and thus infants at any age who are fed
with it are relieved of the burden of digesting it. The baron led the
way which has been so successfully followed since in the artificial
digestion of foods. A considerable part of the starch {754} in wheat
flour is converted into grape-sugar by the prolonged action of heat. I
frequently recommend that from three to five pounds of wheat flour be
packed dry in a firm muslin bag, so as to form a ball, and be placed in
water sufficient to cover it constantly and the bag kept over the fire
three or four days. During the nights the fire may go out for a few
hours. At the expiration of this time the external part, which is wet,
being peeled off, the remainder resembles a lump of yellowish chalk.
The flour grated from it gives a decided reaction of sugar by Fehling's
test. Starch is also quickly transformed into glucose by the action of
the diastase of malt, which indeed Liebig employed. If to a gruel of
barley flour, oatmeal, or other farinaceous substance, when hot, a
little of a good preparation of extract of malt, such as that prepared
by Trommer & Co. at Fremont, Ohio, which acts promptly, or by Reed &
Carnrick, be added, it becomes thinner. It is claimed that the starch
is thus quickly converted into glucose; which seems doubtful. It is,
however, so modified that it is apparently more readily digested and
assimilated. Farinaceous substances thus prepared may be employed with
peptonized or other milk. Infants frequently do better with this
admixture than when either the milk or gruel is used separately.

Of the foods contained in the shops which have been most prescribed,
and which have apparently been useful in certain cases, I may mention
those which have been prepared according to Liebig's formula, of which
there are several, the analyses of which I have given, and Nestle's
farina. In the use of those foods which contain no milk, as Ridge's
food, Imperial granum, etc., it is recommended that milk be added,
while for such as contain condensed milk, as Nestle's and the
Anglo-Swiss food, only water should be employed. The Anglo-Swiss food
contains about 60 per cent. condensed milk and about 20 per cent. each
of oatmeal and Russian wheat flour. It gives an acid reaction, unlike
Nestle's, which is alkaline. When Biedert's cream conserve was
announced great expectations were awakened from the fact that the
inventor is an authority in paediatrics, but, unfortunately, they have
not been realized in this country. Much of Biedert's conserve when it
reaches us is spoiled, and the directions for its use are too
complicated for ordinary family use, since a different mixture is
required for each month of the infant's age. I have employed this food,
but, with Henoch, "could not convince myself that it is more
efficacious than cow's milk." I am informed that the sale of it in this
country has ceased.

Condensed milk is largely used in the feeding of infants. The milk is
condensed in vacuo to one-third or one-fifth its volume, heated to 100
degrees C. (212 degrees F.) to kill any fungus which it contains, and
38 to 40 per cent. of cane-sugar is added to preserve it. In the first
month one part of milk should be added to sixteen of water, and the
proportion of water should be gradually reduced as the infant becomes
older. The large amount of sugar which condensed milk, preserved in
cans, contains renders it unsuitable in the dietetic role of the summer
diarrhoea of infants. The sugar is apt to produce acid fermentation and
diarrhoea in hot weather. Borden's condensed milk, freshly prepared, as
dispensed from the wagons, contains, I am informed by the agent, no
cane-sugar or other foreign substance, and on this account is to be
preferred to that in the cans. It is cow's milk of good quality, from
which 75 to 79 per cent. of the water {755} has been removed under
vacuum. The sole advantage which it possesses--and it is an important
one--is that it resists fermentation longer than the ordinary milk.

To select the best food for the infant from this considerable number of
dietetic preparations is one of the most important duties of the
physician. If called to an infant unfortunately deprived of wholesome
breast-milk, and suffering in consequence from indigestion and
diarrhoea, what diet shall we recommend? My recommendation would be as
follows: Use cow's milk of the best possible quality and peptonized in
the manner stated above, and peptonized in small quantity at a time,
such as a pint, or, better, half a pint. This may be the sole food till
the age of five or six months. Unfortunately, in the cities the milk
that is delivered in the morning is the milking of the preceding
evening, mixed with that of the preceding morning, brought often many
miles from the farms where it is produced. Milk twelve and twenty-four
hours old, notwithstanding the use of ice around the milk-cans, is apt
to undergo some fermentative change before it reaches the nursery. This
prevents the preparation of the best quality of peptonized milk, so
that in some instances during the heated term I have found that the
peptonized milk did not agree as well as the condensed milks, like
Borden's or Nestle's food. Not a few infants suffering from diarrhoeal
maladies seem to do better if some farinaceous food properly prepared
be added to the peptonized milk than when the milk is used alone. It is
better, I think, that the starch, or a considerable part of the starch,
be converted into glucose before the admixture. This can be done if a
few pounds of wheat flour be pressed dry in a bag, so as to form a
ball, and boiled three or four days, as I have elsewhere recommended.
The flour grated from the mass gives a decided sugar reaction to
Fehling's test. For infants under the age of six months one
tablespoonful of the flour thus prepared should be mixed with twelve
tablespoonfuls of water and boiled. When it has been removed from the
fire and become tepid, a small quantity of a good extract of malt, as
Trommer's or Reed & Carnrick's, may advantageously be added to the
gruel to increase the transformation of starch and render it more
digestible. To avoid the time and trouble of preparing the food in this
manner, one of the foods contained in the shops, in which the starch
has been transformed into glucose by the employment of Baron Liebig's
formula, may be used, as Mellin's or Horlick's, instead of the wheat
flour prepared by long boiling. The older the child, the thicker should
be the gruel.

Beef-, mutton-, or chicken-tea should not be employed, at least as it
is ordinarily made, since it is too laxative. Occasionally, for the
older infants, we may allow the expressed juice of beef, raw scraped
beef, or beef-tea prepared by adding half a pound of lean beef, finely
minced, to one pint of cold water, and after allowing it to stand for
half an hour warming it to a temperature not exceeding 110 degrees for
another half hour. By this process the albumen is preserved. Salt
should be added to it, and I am in the habit of adding to it also about
seven drops of dilute muriatic acid to facilitate its digestion. It is
chiefly for infants over the age of ten months that the meat-juices are
proper. A concentrated nutriment, prepared, it is stated, from beef,
mutton, and fruits, has lately been introduced in the shops under the
name Murdoch's Liquid Food. Young {756} infants with dyspeptic and
diarrhoeal symptoms can take it, and it appears to be readily
assimilated, as the quantity given at each feeding is small. It has its
advocates, and it appears to be of some service in cases of weak and
irritable stomach.

But since one of the two important factors in producing the summer
diarrhoea of infants is foul air, it is obvious that measures should be
employed to render the atmosphere in which the infant lives as free as
possible from noxious effluvia. Cleanliness of the person, of the
bedding, and of the house in which the patient resides, the prompt
removal of all refuse animal or vegetable matter, whether within or
around the premises, and allowing the infant to remain a considerable
part of the day in shaded localities where the air is pure, as in the
parks or suburbs of the city, are important measures. In New York great
benefit has resulted from the floating hospital which every second day
during the heated term carries a thousand sick children from the
stifling air of the tenement-houses down the bay and out to the fresh
air of the ocean.

But it is difficult to obtain an atmosphere that is entirely pure in a
large city with its many sources of insalubrity; and all physicians of
experience agree in the propriety of sending infants affected with the
summer diarrhoea to localities in the country which are free from
malaria and sparsely inhabited, in order that they may obtain the
benefits of a purer air. Many are the instances each summer in New York
City of infants removed to the country with intestinal inflammation,
with features haggard and shrunken, with limbs shrivelled and the skin
lying in folds, too weak to raise, or at least hold, their heads from
the pillow, vomiting nearly all the nutriment taken, stools frequent
and thin, resulting in great part from molecular disintegration of the
tissues--presenting, indeed, an appearance seldom observed in any other
disease except in the last stages of phthisis--and returning in late
autumn with the cheerfulness, vigor, and rotundity of health. The
localities usually preferred by the physicians of this city are the
elevated portions of New Jersey and Northern Pennsylvania, the
Highlands of the Hudson, the central and northern parts of New York
State, and Northern New England. Taken to a salubrious locality and
properly fed, the infant soon begins to improve if the disease be still
recent, unless it be exceptionally severe. If the disease have
continued several weeks at the time of the removal, little benefit may
be observed from the country residence until two or more weeks have
elapsed.

An infant weakened and wasted by the summer diarrhoea, removed to a
cool locality in the country, should be warmly dressed and kept indoor
when the heavy night dew is falling. Patients sometimes become worse
from injudicious exposure of this kind, the intestinal catarrh from
which they are suffering being aggravated by taking cold, and perhaps
rendered dysenteric.

Sometimes parents, not noticing the immediate improvement which they
have been led to expect, return to the city without giving the country
fair trial, and the life of the infant is then, as a rule, sacrificed.
Returned to the foul air of the city while the weather is still warm,
it sinks rapidly from an aggravation of the malady. Occasionally, the
change from one rural locality to another, like the change from one
wet-nurse to another, has a salutary effect. The infant, although it
{757} has recovered, should not be brought back while the weather is
still warm. One attack of the disease does not diminish, but increases,
the liability to a second seizure.

Medicinal Treatment.--The summer diarrhoea of infants requires, to some
extent, different treatment in its early and later stages. We have seen
that acids, especially the lactic and butyric, the results of faulty
digestion, are produced abundantly, causing acid stools. In a few days
the inflammatory irritation of the mucous follicles causes such an
exaggerated secretion of mucus which is alkaline that the acid is
nearly or quite neutralized. In the commencement of the attack these
acid and irritating products should be as quickly as possible
neutralized, while we endeavor to prevent their production by improving
the diet and assisting the digestion. In the second stage, when the
fecal matter is less acid and irritating from the large admixture of
mucus, medicines are required to improve digestion and check the
diarrhoea, while the indication for antacids is less urgent. Therefore
it is convenient to consider separately the treatment which is proper
in the commencement or first stage, and that which is required in the
subsequent course of the disease.

First stage, or during the first three or four days, perhaps the first
week.--Occasionally, it is proper to commence the treatment by the
employment of some gentle purgative, especially when the disease begins
abruptly after the use of indigestible and irritating food. A single
dose of castor oil or syrup of rhubarb, or the two mixed, will remove
the irritating substance, and afterward opiates or the remedies
designed to control the disease can be more successfully employed.
Ordinarily, such preliminary treatment is not required. Diarrhoea has
generally continued a few days when the physician is summoned, and no
irritating substance remains save the acid which is so abundantly
generated in the intestines in this disease, and which we have the
means of removing without purgation.

The same general plan of medicinal treatment is appropriate for the
summer diarrhoea of infants as for diarrhoea from other causes; but the
acid fermentation commonly present indicates the need of antacids,
which should be employed in most of the mixtures used in the first
stage as long as the stools have a decidedly acid reaction.

Those who accept the theory that this disease is produced by
micro-organisms which lodge on the gastro-intestinal surface and
produce diarrhoea by their irritating effect are naturally led to
employ antiseptic remedies. Guaita administered for this purpose sodium
benzoate. One drachm or a drachm and a half dissolved in three ounces
of water were administered in twenty-four hours with, it is stated,
good results.[3] I have no experience in the use of antiseptic
remedies.

[Footnote 3: _N.Y. Med. Rec._, May 31, 1884.]

If by the appearance of the stools or the substance ejected from the
stomach, or by the usual test of litmus-paper, the presence of an acid
in an irritating quantity be ascertained or suspected, lime-water or a
little sodium bicarbonate may be added to the food. The creta
praeparata of the Pharmacopoeia administered every two hours, or, which
is more convenient, the mistura cretae, is a useful antacid for such a
case. The chalk should be finely triturated. By the alkalies alone,
aided by the judicious use of stimulants, the disease is sometimes
arrested, but, unless {758} circumstances are favorable and the case be
mild, other remedies are required.

Opium has long been used, and it retains its place as one of the
important remedies in this disease. For the treatment of a young infant
paregoric is a convenient opiate preparation. For the age of one to two
months the dose is from three to five drops; for the age of six months,
twelve drops, repeated every three hours or at longer intervals
according to the state of the patient. After the age of six months the
stronger preparations of opium are more commonly used. The tinctura
opii deodorata or Squibb's liquor opii compositus may be given in doses
of one drop at the age of one year. Dover's powder in doses of
three-fourths of a grain, or the pulvis cretae comp. cum opio in
three-grain doses every third hour, may be given to an infant of one
year.

Opium is, however, in general best given in mixtures which will be
mentioned hereafter. It quiets the action of the intestines and
diminishes the number of the evacuations. It is contraindicated or
should be used with caution if cerebral symptoms are present. Sometimes
in the commencement of the disease, when it begins abruptly from some
error in diet, with high temperature, drowsiness, twitching of the
limbs--symptoms which threaten eclampsia--opiates should be given
cautiously before free evacuations occur from the bowels and the
offending substance is expelled. Under such circumstances a few doses
of the bromide of potassium are preferable. In the advanced stage of
the disease also, when symptoms of spurious hydrocephalus occur, opium
should be withheld or cautiously administered, since it might tend to
increase the fatal stupor in which severe cases are apt to terminate.

The vegetable astringents, although they have been largely employed in
the treatment of this as well as other forms of infantile diarrhoea,
are, I think, much less frequently prescribed than formerly. I have
entirely discarded them, since they are apt to be vomited and have not
proved efficient in my practice. As a substitute for them the
subnitrate of bismuth has come into use, and in much larger doses than
were formerly employed. While it aids in checking the diarrhoea, it is
an efficient antiemetic and antiseptic. It should be prescribed in ten
or twelve grains for an infant of twelve months; larger doses produce
no ill effect, for its action is almost entirely local and soothing to
the inflamed surface with which it comes in contact. It undergoes a
chemical change in the stomach and intestines, becoming black, being
converted into the bismuth sulphide, and it causes dark stools. Rarely
it gives rise in the infant to the well-known garlicky odor, like that
occasionally observed in adult patients, and which Squibb thinks may be
due to tellurium accidentally associated with the bismuth in its
natural state. For those cases in which the symptoms are chiefly due to
colitis, and the stools contain blood with a large proportion of mucus,
it has been customary to prescribe laudanum or some other form of opium
with castor oil. I prefer, however, the bismuth and opium for such
cases as are more decidedly dysenteric, as well as for cases of the
usual form of intestinal catarrh. In ordering bismuth in these large
doses it is important that a pure article be dispensed.

The following are convenient and useful formulae for a child of one
year: {759}

  Rx. Tinct. opii deodorat. minim xvj;
      Bismuth. subnitrat.   drachm ij;
      Syrupi,               fluidrachm ij;
      Misturae cretae,      fluidrachm xiv.  Misce.

Shake thoroughly and give one teaspoonful every two to four hours.

  Rx. Tinct. opii deodorat. minim xvj;
      Bismuth. subnitrat.   drachm ij;
      Syrupi,               fluidounce ss;
      Aq. cinnamomi,        fluidounce iss.  Misce.

Shake bottle; give one teaspoonful every two to four hours.

  Rx. Bismuth. subnitrat.        drachm ij;
      Pulv. cret. comp. c. opio, drachm ss.  Misce.

Divid in Chart No. X. Dose, one powder every three hours.

  Rx. Bismuth. subnitrat. drachm ij;
      Pulv. ipecac. comp. gr. ix.  Misce.

Divid in Chart No. XII. Dose, one powder every three hours.

Cholera infantum requires similar treatment to that which is proper for
the ordinary form of the summer diarrhoea, but there is no disease,
unless it is pseudo-membranous croup, in which early and appropriate
treatment is more urgently required, since the tendency is to rapid
sinking and death. As early as possible, therefore, proper instructions
should be given in regard to the feeding, and for an infant between the
ages of eight and twelve months either one of the above prescriptions
should be given or the following:

  Rx. Tinct. opii deodorat. minim xvj;
      Spts. ammon. aromat.  fluidrachm j;
      Bismuth. subnitrat.   drachm ij;
      Syrupi,               fluidounce ss;
      Misturae cretae,      fluidounce iss.  Misce.

Shake bottle. Give one teaspoonful every two or three hours.

An infant of six months can take one-half the dose, and one of three or
four months one-third or one-fourth the dose, of either of the above
mixtures.

If cerebral symptoms appear, as rolling the head, drowsiness, etc., I
usually write the prescription without the opiate; and with this
omission it may be given more frequently if the case require it, while
the opiate prescribed alone or with bromide of potassium is given
guardedly and at longer intervals. Although every day during the summer
months I have written the above prescriptions, it has been several
years since any case has occurred in my practice which led me to regret
the use of the opiate; but it must not be forgotten that there is
danger in the summer complaint, and especially in cholera infantum, of
the sudden supervention of stupor, amounting even to coma, and ending
fatally. A few instances have come to my knowledge in which, when death
occurred in this way, the friends believed that the melancholy result
was hastened by the medicine. But injury to the patient in this respect
can only occur, in my opinion, through carelessness in not giving
proper attention to his condition. It is chiefly in advanced cases,
when the vital powers are beginning to fail, when the innervation is
deficient, and the cerebral circulation sluggish, that the use of
opiates may involve danger. Explicit and positive directions should
{760} be given to omit the opiate or give it less frequently whenever
the evacuations are checked wholly or partially and signs of stupor
appear.

Second Stage.--The summer complaint in a large proportion of cases
begins in such a gradual way that the treatment which we are about to
recommend is proper in many instances at the first visit of the
physician, who is frequently not summoned till the attack has continued
one or two weeks. The alkaline treatment recommended above for the
diarrhoea in its commencement does not aid digestion sufficiently to
justify its continuance as the main remedy after the first few days. In
a large number of instances, however, one of the above alkaline
mixtures may be given with advantage midway between the nursings or
feedings, while those remedies, presently to be mentioned, which
facilitate digestion and assimilation are given at the time of the
reception of food.

Some physicians of large experience, as Henoch of Berlin, recommend
small doses of calomel, as the twelfth or twentieth of a grain, three
or four times daily for infants with faulty digestion and diarrhoea. To
me, this seems an uncertain remedy, without sufficient indications for
its use, and I have therefore no experience with it. The following are
formulae which I employ in my own practice, and which have been
employed with apparent good results in the institutions of New York:

  Rx. Acid. muriat. dilut.               minim xvj;
      Pepsinae saccharat.
        (Hawley's or other good pepsin), drachm j;
      Bismuth. subnitrat.                drachm ij;
      Syrupi,                            fluidrachm ij;
      Aquae,                             fluidrachm xiv.  M.

Shake bottle; give one teaspoonful before each feeding or nursing to an
infant of one year; half a teaspoonful to one of six months.

  Rx. Tinct. opii deodorat. minim xvj;
      Acid. muriat. dilut.  minim xvj;
      Pepsinae saccharat.   drachm j;
      Bismuth. subnitrat.   drachm ij;
      Syrupi,               fluidrachm ij;
      Aquae,                fluidrachm xiv.  Misce.

Shake bottle; give one teaspoonful every three hours to a child of one
year; half a teaspoonful to one of six months.

  Rx. Pepsinae saccharat. drachm j-ij;
      Bismuth. subnitrat. drachm ij.  Misce.

Divid in Chart No. XII. One powder every three hours to a child of one
year; half a powder to one of six months.

I have also obtained apparent benefit from lactopeptin, given as a
substitute for one of the above mixtures before each feeding or
nursing. In several instances which I recall to mind I have ordered as
much as could be placed on a ten-cent piece to be given every second or
third hour, while midway between the feedings in some instances of
considerable diarrhoea one of the mixtures of bismuth and chalk
recommended above was employed, and the result has been good.

Enemata.--It will be recollected, from our remarks on the anatomical
characters, that inflammatory lesions are commonly present in the
entire length of the colon, and that at the sigmoid flexure, where acid
and irritating fecal matter is probably longest delayed in its passage
downward, the colitis is usually most severe. Aware of this fact, I was
{761} led to prescribe at my first visit a large clyster of warm water,
given with the fountain or Davidson's rubber syringe, especially in
cases in which the stools showed mucus or mucus tinged with blood.
This, given with the lower part of the body raised a little above the
level of the shoulders, washes out the large intestine and has a
soothing effect upon its surface. The benzoate of sodium may be added
to the water for its antiseptic effect, as in the following formula:

  Rx. Sodii benzoat. drachm j;
      Aquae,         pint j.  Misce.

In occasional cases in which the stomach is very irritable, so that
medicines given by the mouth are in great part rejected, our reliance
must be largely on rectal medication, and especially on clysters
containing an opiate. Laudanum may be given in this manner with marked
benefit. It may be given mixed with a little starch-water, and the best
instrument for administering it is a small glass or gutta-percha
syringe, the nurse retaining the enema for a time by means of a
compress. Beck in his _Infant Therapeutics_ advises to give by the
clyster twice as much of the opiate as would be required by the mouth.
A somewhat larger proportion may, however, be safely employed. The
following formula for a clyster has given me more satisfaction than any
other medicated enema which I have employed:

  Rx. Argent. nitrat.     gr. iv;
      Bismuth. subnitrat. oz. ss;
      Mucilag. acaciae,
      Aquae,         _aa_ fluidounce ij.  Misce.

One-quarter to one half of this should be given at a time, with the
addition of as much laudanum as is thought proper; and it should be
retained by the compress. It is especially useful when from the large
amount of mucus or mucus tinged with blood it is probable that the
descending colon is chiefly involved.

Alcoholic stimulants are required almost from the commencement of the
disease, and they should be employed in all protracted cases. Whiskey
or brandy is the best of these stimulants, and it should be given in
small doses at intervals of two hours. I usually order three or four
drops for an infant of one month, and an additional drop or two drops
for each additional month. The stimulant is not only useful in
sustaining the vital powers, but it also aids in relieving the
irritability of the stomach and in preventing hypostasis in depending
portions of the lung and brain, which, as we have seen, is so frequent
in advanced cases.

The vomiting which is so common a symptom in many cases greatly
increases the prostration, and should be immediately relieved if
possible. The following formulae will be found useful for it:

  Rx. Bismuth. subnitrat.  drachm ij;
      Spts. ammon. aromat. fluidrachm ss-fluidrachm j;
      Syrupi,
      Aquae,          _aa_ fluidounce j.  Misce.

Shake bottle. Dose, one teaspoonful half-hourly or hourly if required,
made cold by a piece of ice.

  Rx. Acid. carbolic. gtt. ij;
      Liquor. calcis, fluidounce ij.  Misce.

Dose, one teaspoonful, with a teaspoonful of milk (breast-milk if the
baby nurse), to be repeated according to the nausea.

{762} Lime-water with an equal quantity of milk often relieves the
nausea when it is due to acids in the stomach, but it is rendered more
effectual in certain cases by the addition of carbolic acid, which
tends to check any fermentative process. Perhaps also some of the
recent antiseptic medicines introduced into our Pharmacopoeia, as the
benzoate of sodium, may be found useful for the vomiting. A minute dose
of tincture of ipecacuanha, as one-eighth of a drop in a teaspoonful of
ice-water, frequently repeated, has also been employed with alleged
benefit.

Of these various antiemetics, my preference is for the bismuth in large
doses, with the aromatic spirits of ammonia, properly diluted, that the
ammonia do not irritate the stomach. Nevertheless, in certain patients
the nausea is very obstinate, and all these remedies fail. In such
cases absolute quiet of the infant on its back, the administration of
but little nutriment at a time, mustard over the epigastrium, and the
use of an occasional small piece of ice or the use of carbonic acid
water with ice in it, may relieve this symptom.

In protracted cases, when the vital powers begin to fail, as indicated
by pallor, more or less emaciation, and loss of strength, the following
is the best tonic mixture with which I am acquainted. It aids in
restraining the diarrhoea, while it increases the appetite and
strength. It should not be prescribed until the inflammation has
assumed a subacute or chronic character:

  Rx. Tinct. calumbae,     fluidrachm iij;
      Liq. ferri nitratis, minim xxvij;
      Syrupi,              fluidounce iij.  Misce.

Dose, one teaspoonful every three or four hours to an infant of one
year.




{763}

PSEUDO-MEMBRANOUS ENTERITIS.

BY PHILIP S. WALES, M.D.


SYNONYMS.--Membranous enteritis; Infarctus (Kaempf); Diarrhoea
tubularis, Tubular looseness (Good); Follicular colonic dyspepsia,
Follicular duodenal dyspepsia (Todd); Pellicular enteritis (Simpson);
Pseudo-membranous enteritis (Cruveilhier); Pseudo-membraneuse enterite
(Laboulbene); Painful affection of the intestinal canal (Powell);
Mucous disease (Whitehead); Hypochondriasis pituitosa (Fracassini);
Fibrinous diarrhoea (Grantham); Mucous disease of the colon (Clark);
Chronic, catarrhal, or mucous diarrhoea; Colique glaireuse (of the
French); Chronic exudative enteritis (Hutchinson); Diarrhoea febrilis
(Van Swieten); Paraplexia rheumatica, Chlorosis pituitosis, Diarrhoea
pituitosa (Sauvages); Arthritis chlorotica (Musgrave); Colica pituitosa
(Sennertus); Scelotyrbe pituitosa (Perywinger); Mucositas intestinalis
colloides, Concretiones gelatiniformes intestinales (Laboulbene);
Tubular exudation-casts of the intestines (Hutchinson).

DEFINITION.--The disease is a non-febrile affection, consisting in a
peculiar, and usually persistent, morbid condition of the intestinal
mucous membrane, marked by the periodical formation of viscous,
shreddy, or tubular exudates composed chiefly of mucin, on the
discharge of which temporary amelioration of the accompanying acute
digestive and nervous symptoms occurs.

HISTORY.--Although no distinct and separate accounts of
pseudo-membranous enteritis occur in the medical writings of the
ancients, nor even in those dating up to the eighteenth century, yet
there may occasionally be detected in some of the descriptions of
certain pathological conditions grouped under such titles as colic,
passage of gall-stones, tenesmus, coeliac and pituitous affections,
diarrhoea, dysentery, etc., the peculiar features of the disease under
consideration. This confusion ruled up to a comparatively recent time.
J. Mason Good,[1] writing in the first quarter of the nineteenth
century, groups the disease as a species of diarrhoea--diarrhoea
tubularis--and remarks that he had "never hitherto seen this species
classified, and not often described, although it occurred frequently in
practice."

[Footnote 1: _Study of Medicine_, 1822.]

Aretaeus,[2] in the second century, in discussing the subject of
dysentery, speaks of alvine discharges sometimes occurring of a
substance of considerable length, in many respects not to be
distinguished from a sound piece of intestine, which he regarded as the
inner coating of the bowel. {764} This false interpretation of a fact
arose from the circumstance that the membranous exudate occasionally
assumes a tubular form, bearing the impress of the inner surface of the
bowel upon which it is formed, and was perpetuated up to a
comparatively recent period by successive authors. This error befell
Simpson,[3] Morgagni,[4] Lancisi, and Spindler;[5] the last of whom
describes the material discharged as worked up into a "materia alba,
longa, compacta."

[Footnote 2: Lib. ii. cap. ix.]

[Footnote 3: _Ed. Med. Essays_, vol. v. p. 153, 1752.]

[Footnote 4: 31st Epistle.]

[Footnote 5: _Actis Nat. Cur._, vol. v. p. 483.]

Bauer[6] under the title of "intestinal moles" describes in Haller's
_Disputations_ the discharges of this disease as "concreta fibrosa
quaedam pro parte pinguedine rara abducta, membranacea molarum ex utero
muliebri rejectarum formam accurate sistentia."

[Footnote 6: "De Moles Intestinorum," _Disputationes ad Morborum_,
Dresdae, 1747, p. 463.]

In the same volume Kaempf[7] discourses on this subject under the title
of "infarction of the intestinal vessels," and also in a separate
treatise[8] published somewhat later. In the latter he groups the
disease with others of a far different nature, their only point of
convergence being preternatural alvine discharges.

[Footnote 7: _De Infarctu Vasorum Ventriculi_, Basiliae, 1751.]

[Footnote 8: _Abhandlungen von einer neuer methode der hartnackigsten
Krankheiten die ihren Sitz im unterleibe haben, zu heilen_, Leipzig,
1784.]

Subsequent authors, as a rule, fell into the same error, and it was not
until 1818 that membranous enteritis was discriminated by Powell[9]
from that condition in which we recognize the presence of gall-stones.
Since then more correct views have prevailed, and the disease has now a
recognized place in nosology.

[Footnote 9: _Trans. of Col. of Phys. London_, vol. vi. p. 106.]

ETIOLOGY.--As in other diseases of obscure nature, so in this, there
has been much divergence of opinion as to its cause.

The influence of age is striking, as it is rarely seen in childhood or
in persons who have passed the forty-fifth year. Of my own cases, the
youngest was forty, and the oldest fifty-four. Rilliet and Barthez[10]
state that membranous formations in the intestinal canal of children
are very rare; that they always occupy the summits of the folds, rarely
the intervals, of the mucous membrane; and that they are detached in
layers of greater or less extent. They are not diphtheritic.
Heyfelder[11] has described similar exudations under the name of
enteritis exudatoria.

[Footnote 10: _Traite clinique pratique des Maladies des Enfants_, t.
i. p. 677, 1853.]

[Footnote 11: _Studien in Gabiete der Heilwissenschaft_, p. 173.]

Sex exerts as marked an influence as age, as the immense preponderance
of cases occurs in females. In an analysis of 100 cases, 4 only
occurred in males, 2 of which were children. All of my cases were
women; with the exception of two cases occurring in males, the same
experience is reported by Powell and by Copeland.

In regard to temperament, it is undoubted that the disease invades
nervous and hypochondriacal subjects oftener than others, but all
temperaments are liable in the presence of those enervative influences
that degrade physical health and impair nerve-power. All of my patients
belonged to the nervous type. Whitehead says that those of a phlegmatic
temperament, not easily excited into action, or persons deficient in
elasticity of fibre, compose all but a very small percentage of the
sufferers from this {765} complaint, and he had particularly noticed
that a large proportion of the women have light flaxen hair, fair
complexions, and white skins.

The determinative causes, whatever they may be, occasion perversion of
nutrition and innervation of the gastro-intestinal canal, principally,
I believe, by their action upon the ganglionic nerves presiding over
those functions originating the peculiar exudatory phenomena of this
disease. This condition of the nervous system once established, local
irritation of any sort may precipitate an attack, and hence the
multitudinous influences that have been assigned as exercising a
causative agency, as exposure to wet and cold, coarse, bad food, fecal
impaction, and the abuse of cathartic medicines, as alleged by
Grantham,[12] who asserts that the use of mercury, conjoined with a too
frequent use of aperient agents, is the cause of the disease in every
case.

[Footnote 12: _Facts and Observations in Med. and Surg._, 1849, p.
205.]

Farr considered the irritation of the intestinal canal owing to a
parasitic growth of a confervoid type (oscillatoria). This view is
supported by no other authority than that of himself and Bennett, as
nothing of this sort is recorded as occurring in the discharges of
patients of other observers; certainly in mine there was no parasitic
development. The presence of it in their cases may then be fairly
regarded as accidental, or at least unessential.

Habershon regarded ovarian diseases and painful menstruation in the
female, and prostatic diseases in the male, as exciting causes.

SYMPTOMS.--The most characteristic symptoms disclosing the presence of
pseudo-membranous enteritis are those arising from derangements of the
digestive organs. They are, in the beginning, vague and irregular in
occurrence, or so over-veiled by associated disorders of the
genito-urinary and nervous systems that their nature and import often
escape recognition until, weeks, and even months, of fruitless
medication addressed to these secondary phenomena having been expended,
the disease assumes such severity and presents such a complex of
peculiar symptoms that it no longer eludes identification.

The disease rarely starts as an acute affection; sometimes it is
subacute, but in the great majority of cases its course is chronic. Its
initiation is marked with symptoms of gastro-intestinal
disturbances--irregularity of the bowels, constipation and diarrhoea
alternately; and dyspeptic annoyance of one sort or another--capricious
appetite, nausea or vomiting, and pyrosis, usually increased by liquid
diet. In Dunhill's case there was almost daily vomiting of mucus and
pus streaked with blood, and occasionally pure blood. This prominence
of gastric derangement supplies an explanation why Todd conferred upon
the disease the title of follicular dyspepsia.

There is a sense of discomfort, soreness, or rawness of the abdomen,
especially along the line of the colon, and in two of my cases the
rectum was tender and raw, which augmented to decided pain in sitting
or riding, and the abdominal muscles were tense; a feeling of heat or
burning in the bowels often occurs, and almost always more or less
lassitude and mental depression. These symptoms aggravate, especially
upon indiscretions in diet, exposure to wet, or indeed under any sort
of enervative influences, at irregular intervals. Their persistence
finally induces grave disorders of nutrition, marked by the blood
becoming poor and thin, by sluggish {766} circulation and local
congestions in the pelvic and abdominal viscera, and loss of strength
and flesh. Yet certain patients seem to retain their flesh for a long
time, as I have seen, after suffering several years from the disease.
The depression of vital powers is still further manifested in a small,
slow, soft pulse and a temperature running below the normal standard.
The tongue is usually moist, pale, and flabby, and coated with a
pearl-white or yellowish-white coating; sometimes, however, it is raw,
red, tender, and fissured, or patchy from exfoliation of the mucous
coating. The gums and cheeks are usually pale and bloodless, and often
the seat of small roundish painful ulcers, which occasionally invade
the palate and throat. Grantham[13] says that ulceration of a
phagedaenic kind sometimes forms on the tonsils. The complexion usually
assumes a muddy or flavescent tint, which during the attack may deepen
to a jaundiced hue. At other times it presents a transparent or waxy
appearance.

[Footnote 13: _Op. cit._, p. 204.]

The skin is dry and furfy, sometimes cold and clammy, or, from
over-action of the sebaceous glands, greasy. There is a disposition,
especially on the chest, neck, and face, to papular eruptions or even
phlegmonous or carbuncular inflammation.

The urine is high-colored and loaded with abundant phosphates, which in
cooling precipitate as a heavy deposit. The bladder is often irritable,
and discharges more or less mucus. According to Grantham,[14] patients
occasionally pass urine with evident traces of albumen, and seldom
containing a normal quantity of phosphates. On an increase in fever or
mental excitement a larger quantity than natural of the lithate of
ammonium is found; frequently the mucous membrane of the bladder is
found thickened in these cases.

[Footnote 14: _Op. cit._, p. 204.]

The characteristic symptom, however, of this disease is the periodical
formation and discharge of mucous exudates varying in physical
appearances and frequency. The discharge may occur daily, with every
stool, or at irregular intervals--a week, month, or longer--but usually
in from twelve to fifteen days. The recurrence may be precipitated by
irregularity in diet, exposure to wet and cold, or by excesses of any
sort. The paroxysm is marked by tormina or severe pain, which may
resemble that of colic or that of the passage of a biliary calculus,
extending down the thighs or to the bladder, in the latter case
sometimes causing retention, requiring the use of the catheter. The
pain is usually referred to some part of the large intestine. In
certain cases the paroxysm is announced by chills radiating from some
point in the abdomen or even from other parts of the body.

After the paroxysm has endured two, three, or more days--usually a
week--membranous exudates, either with a spontaneous or with an
artificial movement of the bowels, are voided; after which there is a
gradual assuagement of the local and general symptoms, but the patient
experiences a sense of exhaustion or lassitude, and the tenderness of
the abdomen and the irregularity of the bowels usually persist.

During the attack there is anorexia, but in the intervals the appetite
remains fairly good, and the alvine discharges may assume quite a
natural condition.

In the course of the disease there is more or less disturbance in the
functions of the nervous system. During the paroxysm, when the {767}
sufferings are severe, the cast of symptoms running through the case is
of a decidedly hypochondriacal type. At times, with the expulsion of
the exudates and succeeding respite from suffering, there often occurs
a mental rebound which lifts the patient from the slough of despair to
the most hopeful anticipations of future health and happiness. In one
of my cases this transition was remarkable. This hysterical type is
common enough, and the irritability of the nervous system is still
further manifested in the occurrence of irregular contractions of
various groups of the voluntary muscles, as shown in hysterical
tetanus, general convulsions, or chorea in children, or by paralyses of
motion.

Copeland[15] reports a case of a lady in whom this disease was
complicated with the severest symptoms of hysteria, occasionally
amounting to catalepsy. The paroxysms of pain recurred at intervals
between four and six weeks, followed or attended by the discharge of
large quantities of false membrane in pieces, and sometimes in perfect
tubes. The menstrual flow was painful and irregular, accompanied with
shreds of false membrane--not, however, contemporaneous with those of
the intestine. The sensory nerves are often deranged, for in some cases
there is paraesthesia--anaesthesia or hyperaesthesia--in limited areas
of the skin. There is more or less headache, neuralgic pains in this or
that nerve, or in several at the same time.

[Footnote 15: _Dictionary of Medicine_, vol. ii. p. 669.]

The special senses do not escape; they manifest various forms of
functional derangement. In one of my cases there were constant buzzing
in the ears and perversion of the sense of smell, and in another the
vision was thought impaired and the services of an oculist sought.

The uterine functions are always involved in greater or less degree.
The menstruation is difficult and painful, and occasionally accompanied
with membranous discharges. In one of my cases there was a uterine
exudate, though the menopause had occurred several years before.
Leucorrhoea and cervical inflammation are common.

PATHOLOGY.--Despite the fact that the disease in question, without
being very frequent, is far from rare, little light has been shed upon
its pathology. Indeed, even its individuality as an independent and
distinct affection has been contested, although it is marked by a
complex of symptoms as peculiar and characteristic as those of any
other disease in the nosology.

There are those who maintain that the disease consists essentially in
an inflammatory condition of the intestinal mucous membrane, either of
the ordinary or of some specific type, croupous or diphtheritic.
Copeland says the formation of the membranes depends upon a latent and
prolonged state of inflammation extending along a very large portion,
sometimes the greater part, of the intestinal canal, as is evinced by
the quantity thrown off. Valleix[16] dismisses the subject summarily
with the delivery of the oracular judgment that the greater number of
cases of this disease are dysenteric, and the remainder diphtheritic.
Habershon is in full accord with this view, having, as he says, seen
these membranous exudates "follow severe disease of the intestines of a
dysenteric character, and sometimes associated with a state of chronic
congestion of the liver, and often perpetuated by the presence of
hemorrhoids, polypoid {768} growths, etc." Wilks and Clark,[17] after a
full examination of the enteric exudates submitted to them, concluded
that they are true casts of the large intestines produced by chronic
inflammatory action of the mucous membrane and subsequent exudation.
Conjectures have been ventured as to the exact anatomical structure in
which the process occurs. Thus, Todd[18] says that the proximate cause
of the disease is dependent upon a morbid condition of the intestinal
mucous follicles. Golding-Bird[19] holds similar language. He says: "It
is probable that the follicles are the principal seat of the disease,
for we know that they sometimes secrete a dense mucus differing little
in physical qualities from coagulated albumen or even fibrin."
Livedey[20] attributed the process to a morbid secretion into the
mucous crypts.

[Footnote 16: _Guide du Medecine practicien_, vol. iii. p. 10.]

[Footnote 17: _Trans. Path. Society_, vol. ix. p. 230.]

[Footnote 18: _Cyclopaedia of Practical Medicine_, vol. ii. p. 279.]

[Footnote 19: _Guy's Hospital Reports_.]

[Footnote 20: _L'Union medicale_, 1868.]

Among those believing in its croupous nature was Powell, who assumed
the character of the inflammation to be specific, and the exudate of
the same nature and formed in the same manner as that of ordinary
croup. This was the view entertained by Cruveilhier and Trousseau and
other French authors. Good was misled in a similar manner, as shown by
his statement that the exudation bears a striking resemblance to the
fibrous exudation thrown forth from the trachea in croup. He says,
however, that it is discharged in longer, firmer, and more compact
tubes. Serres,[21] in a dissertation upon pseudo-membranous colitis,
confounds the exudate with that of thrush, muguet, and infective
dysentery. Laboulbene,[22] a later writer, also remarks that there are
found in many treatises and in periodical literature a great number of
occurrences of false membranes in the dejecta. Most of these cases are
referable to dysentery, to muguet, hydatids, etc., but there remain a
certain number which are owing to different inflammatory and
non-diphtheritic affections of the digestive tube.

[Footnote 21: _These de Paris_, No. 39, 1836.]

[Footnote 22: _Recherches cliniques et anatomiques sur les Affections
pseudo-membraneuse_, Paris, 1861.]

Whitehead, in summing up his conclusions respecting the nature of the
disease, compares it with dermic inflammation. He says: "The mucous
membrane (intestinal), like the skin (and is not the one looked upon as
an inversion of the other?), is prone under certain conditions in
certain constitutions to develop products unnatural to its functions.
It is not natural for the skin to produce eczema, neither is it natural
for mucous surfaces to produce mucus in a concrete form; that the
proximate cause of the symptoms referable to this disease is the
hypersecretion and accumulation of mucus on the free surface of mucous
membranes; such accumulations sheathe and prevent the healthy
performance of the functions natural to the part, and thus induce
immediate and remote results, the effect of such suppressed functions;
that this hypersecretion indicates a want of balance between
nerve-force and germinal matter, and that the nerve-force is perverted
by irritation."

Simpson held similar views, and regarded the disease as a chronic
pellicular or eruptive inflammation of the mucous lining of the
bowels.[23] Other observers have been inclined to ignore the
inflammatory nature of the disease, at least as a primary condition,
and have sought the proximate cause in some as yet undefined
derangement of the nervous {769} system. Thus, Clark does not regard
the membranous exudates as the products of inflammation, properly so
called--that is, of capillary blood-stasis which has preceded their
formation--as the characteristic of such exudates is that they contain
fibrin. He says the abnormal cell-forms present arise in some other way
than by free cell-development out of an exuded blastema. Good[24]
asserts its dependence upon what he calls a "peculiar irritability of
the villous membranes of the large intestines, which in consequence
secrete an effusion of coagulating fibrin--fibrin mixed with
albumen--instead of secreting mucus, occasionally accompanied with some
degree of chronic inflammation."

[Footnote 23: _Obstet. Works_, Am. ed., p. 279.]

[Footnote 24: _Study of Medicine_, _op. cit._]

Also, DaCosta doubts whether the disease is originally inflammatory at
all. "Where inflammation," he says, "occurs, is it not secondary rather
than primary, the result rather than the cause?" "Is not the true
trouble in the nervous system, in the nerves presiding over secretion
and nutrition in the abdominal viscera?"

Bennett and Byford represent the opinions of a very small minority who
regard the disease as simply an expression of uterine derangement.

MORBID ANATOMY.--As none of the cases coming under my observation
terminated fatally, no opportunity was offered to me of making personal
investigation into the anatomical changes occurring in membranous
enteritis. Such opportunities have been so rarely met with that,
indeed, it may be said that the nature of these changes is wholly
unknown.

Simpson alludes to a case of phthisis in which the patient had passed
large quantities of "membranous crusts or tubes," and in which the
mucous membrane of the colon was covered with an immense number of
small spots of a clear white color, or vesicles, which, when punctured,
discharged a small quantity of clear fluid; and also refers to the case
of Wright, in which the mucous membrane of the colon and of the lower
portion of the small intestine was studded everywhere with a
thickly-set papular eruption.

My endoscopic examinations revealed, in the living subject, the
intestinal mucous membrane of a red, verging into a scarlet color,
thickened, and denuded of epithelium in patches of varying extent. This
condition does not always invade the ampulla of the rectum, but with
the long tube I am in the habit of using it was possible in all my
cases to reach a point where it existed. The extent of diseased surface
can only be conjectured by an inspection of the exudates and by
abdominal palpation.

In most cases the exudate is restricted to the large intestines--colon
and rectum--and often to a circumscribed portion of them; but in rare
cases its length and quantity would seem to indicate that extensive
portions of the surface are covered. One of the most remarkable cases
recorded is that of a woman forty years old who had been sick for five
years with gastro-intestinal derangement. Suddenly the case became
acute, and after much suffering she passed membranous exudates three
millimeters in thickness and many centimeters long, weighing in all
three kilograms.[25]

[Footnote 25: _Recueil de Memoires de Medecine, de Chirurgie, et de
Pharmacie militaires_, tome xxxvii. p. 297, 1855.]

Kaempf[26] gives another case, in which the length of the membranes
{770} discharged was sevenfold greater than the stature of the patient.
In Dunhill's[27] case the patient had suffered from this disease for a
long period, and during two years passed many yards of perfect
cylindrical shape, many of them several feet in length, and
sufficiently coherent to permit of their being handled, held up, etc.
In one of my cases a perfect cylinder three-quarters of a yard long was
voided.

[Footnote 26: _Op. cit._, p. 232.]

[Footnote 27: _Trans. of Path. Society of London_, vol. ix. p. 188.]

Laboulbene[28] describes the gastro-intestinal false membrane as thin,
soft, and granular, of a more or less yellow color, slightly adherent
to the mucous membrane, and when stripped off forming a yellow
pultaceous mass. He says it is first deposited in small, irregular,
sparsely-scattered patches, located on the summits of the intestinal
folds; afterward these patches increase, and cover the folds entirely
and almost the whole calibre of the intestinal canal. The mucous
membrane, he remarks, beneath the deposit is greatly inflamed.

[Footnote 28: _Op. cit._, p. 105.]

Powell believes that at times the deposit extends as high as the
duodenum, his opinion being solely based upon the clinical features of
the disease. In the first of his cases the membrane was found in
perfect tubes, some of them full half a yard in length, and certainly
sufficient in quantity, he says, to have lined the whole intestinal
canal.

In examining the membranes it is always best to float them from the
fecal or other foreign material by passing the discharges in a clean
vessel containing water. Their physical characters can then be readily
studied. They are best preserved in a 10 per cent. solution of alcohol.
The exudate consists usually of a single lamina, but at various points
in certain cases several superposed laminae may be observed, enclosing
between them particles of undigested food of various kinds. In most
cases the superficial layers are more opaque, drier, less elastic, and
friable than the deeper.

The configuration of the exudate varies greatly. The more common
variety is that occurring in loose, transparent, jelly-like masses,
like the white of an egg or glue, tinged often with various hues of
yellow. In three of my cases I noticed also the frequent occurrence of
a thin, serous, yellow discharge. In some cases the discharge resembles
pieces of macaroni, tallow, or wax; in others it assumes a shreddy or
ribbon-like form; and in a still rarer class it is tubular, being an
exact reprint of the surfaces from which detached. These tubular pieces
are, however, more or less torn and broken into smaller fragments of an
inch or two in length when discharged.

Its thickness also varies: sometimes it does not exceed that of the
thinnest film, and at others it is a quarter of an inch or more.

Its consistence ranges from that degree of loose aggregation that
permits elongation into stringy, breaking masses when fished up from
the water in which it floats, to a firmness and tenacity that will
enable it to be handled without fear of breakage.

The color differs in different cases. It is usually yellowish-white,
but this is often modified by tints dependent upon admixture with
extraneous matters from the intestinal canal--biliary coloring, blood
from the rupture of the vessels beneath the exudate, or with blood and
pus. It exhales a feculent odor.

The surfaces of the membranes are ordinarily smooth and uniform, but
sometimes reticulated. Certain observers have described the outer {771}
surface of the tubular exudate as uniformly smooth, and the inner as
broken and flaky at some points, at others ragged and flocculent, and
in many places thrown into shallow folds, lying in some situations
across, but chiefly along, the axis of the gut.

The microscopic characters of the exudate are pretty uniform. Wilks and
Clark[29] describe the surface of the tubes, examined with a linear
magnifying power of forty diameters, as exhibiting the appearance of a
gelatinous membraniform matrix traversed by a coarse network of opaque
yellow lines, studded at their points of intersection by similarly
colored rounded masses. From the larger network proceeds a smaller
secondary network, and in the recesses of this were found, at close and
regular intervals, well-defined round or oval openings, with elevated
margins, resembling in size and appearance the mouths of the follicles
of the great gut. With higher powers the exudate was found in many
cases to consist of a structureless basement membrane, which in certain
points showed a fibrous appearance, owing doubtless to the presence of
filaments of mucin. Numerous irregular granular cells, as well as
granules from the breaking up of these cells, thickly studded the
surface of the membrane. In the specimens of Wilks and Clark the
surface, besides being marked by the opaque yellow lines and dots,
presented various foreign matters, such as bile-pigment, earthy and
fatty granules, portions of husks of seed, gritty tissues of a pear, a
peculiar form of elastic tissue, stellate vegetable hairs, and a
mucedinous fungus. Clark, in describing the fibres found between the
layers of the exudates, says that they exhibited a very distinct and
regular transverse striation, approaching in character that found in
the ligamentum nuchae of the giraffe. Quekett and Brooke have met with
the same fibres in the feces. The transverse division depends probably
upon beginning decay. The division is sometimes so distinct and
complete as to lead, according to Beale,[30] to their confounding with
confervoid growths. Farre[31] actually describes the formation as of a
confervoid character.

[Footnote 29: _Op. cit._, p. 232.]

[Footnote 30: _The Microscope in Medicine_, p. 194.]

[Footnote 31: _Trans. Microscopical Society_.]

Here and there, in my specimens, were observed scattered epithelial
cells which were occasionally gathered in patches. Small colored masses
of irregular shape, doubtless of fecal origin, were also noticed. The
cells imbedded in the matrix, according to the above-quoted observers,
consisted of two kinds--one more or less spherical, the other more or
less cylindrical. In size the spherical cells varied from 1/2000 to
1/800 of an inch in diameter. The smaller cells had no distinct
cell-walls. Some of the larger cells were filled with fat-granules, and
represented granular cells; others had a single or double vesicular
nucleus; a few were acuminated at two opposite points and somewhat
compressed. All the other cells possessed demonstrable cell-walls. The
cylindrical cells resembled in their general characters those which
normally coat the mucous membrane of the larger gut, but they were much
more elongated, compressed, and firmly matted together. Many of the
more elongated cells were constricted in the middle, and exhibited a
nucleus on each side of the constriction. The more or less spherical
cells occupied the attached, and the cylindrical cells the free,
surface of the membranous tubes.

The perforations in the matrix were of uniform size and appearance,
{772} surrounded by elevated margins formed of closely-grouped
cylindrical cells, and led to two kinds of pits--one short and
flask-shaped, the other long and uniformly cylindrical. The
flask-shaped pits were about one-tenth of an inch in diameter and
distinctly hollow. The wall of each pit was made up of one or two
layers of subspheroidal cells, held together by an amorphous stroma. A
few of these follicles contained a deposit which was opaque in situ,
and which when broken up was found to consist of large flattened
nuclear cells, analogous to those met with in epithelial growths.

The cylindrical pits were also for the most part hollow, about
one-sixteenth of a line in length and one-thirty-first of a line in
breadth. These walls, devoid of membrane, were composed of small, more
or less spherical cells in various stages of development, imbedded in a
gelatinous matrix.

In examining the chemical characters of the specimens obtained in my
cases the membranes were thoroughly washed, when they were nearly as
colorless as the water in which they floated. They were drained on a
sieve, and presented a gelatinous appearance, much like the white of an
egg. Their specific gravity was about that of distilled water. When
treated with strong alcohol, the membranes shrank and assumed a
striated appearance. Chemical tests of tincture of guaiacum, peroxide
of hydrogen, and others failed to show the presence of fibrin or
albumen. Treated with ether, globules of fatty matter were obtained,
which were identified by their microscopical characters and by their
reaction with osmic acid. By boiling the liquid in which the membranes
had been soaked it became faintly hazy, indicating a trace only of
albumen. Faint evidence of the presence of this body was also presented
by picric acid and Mehu's test. Treated with a weak solution of caustic
potassa and heat, the membrane dissolved, leaving a little haziness.
The liquid was then filtered, and exactly neutralized with acetic acid,
and plumbic acetate added, when a copious precipitate was formed.
Mercuric chloride and potassic ferrocyanide failed to produce this
effect. From these and other tests used the conclusion was reached that
these membranes were composed essentially of mucin.

Both the microscopical and chemical characters of the exudates of the
disease under consideration show that they are widely different in
nature from those of other diseases. They are evidently a production of
the muciparous glands (follicles of Lieberkuhn) of the intestinal
canal, and consist essentially of mucin. Perroud[32] concluded from his
analysis that they contain a small quantity of albumen, but are
principally formed of the same substance as that which enters into the
composition of the epidermis. The exudates of other diseases of the
alimentary mucous membrane contain albumen and fibrin, as well as
molecular or homogeneous filaments. The ordinary croupous exudate,
according to Cornil and Ranvier, always contains filaments of fibrin,
sometimes mucin and pus-corpuscles mingled with the cellular
constituents, which vary in character with the locality of the
inflammation. The filaments form a reticulum in the meshes of which are
contained the other elements.

[Footnote 32: _Journal de Medecine de Lyon_, 1864.]

Diphtheritic exudates, as shown by Lehmann,[33] consist of fibrin, a
large {773} quantity of fatty matter, and 4 per cent. of earthy
phosphates, while its structure is made up of epithelial cells united
together, which, becoming infiltrated with an albuminous substance and
gradually losing their nuclei and walls, are finally converted into
homogeneous branching masses. The cells of these masses are liable to
undergo fibrinous degeneration. The inflammation determining the
exudate is not confined to the conglomerate glands, but involves all
the textural elements of the part affected, and the material of the
membrane originates from the capillary disturbance in them.

[Footnote 33: _Lehrbuch der Physiolog. Chemie_, Leipzig, 1855.]

Andrew Clark[34] states that he has observed in his studies of exuded
blastema, the product of diseased action in mucous membranes, three
varieties. The first is clear, jelly-like, and imperfectly membranous.
The second is yellowish, semi-opaque, flaky, and usually membranous.
The third is yellowish-white, dense, opaque, distinctly membranous,
tough, and rather firmly adherent to the subjacent surface. The first
contains only the merest trace of albumen, and no fibrin; the second
contains an abundance of albumen, and no fibrin; the third contains
both albumen and fibrin in abundance, the latter in a fibrillated form.
They all contain the same cell-forms. Yet it is to be noticed that in
the first variety there is no evidence of transudation or exudation; in
the second, no evidence of a true exudation; and that in the third, in
which the existence of a true inflammatory exudation is undeniable, the
only additional structural element present is fibre.

[Footnote 34: _Op. cit._, p. 133.]

DIAGNOSIS.--The diagnosis of membranous enteritis can never in its
advance, and rarely in its early stages, present much difficulty. Its
chronic course, irregular exacerbations, lack of febrile excitement,
the persistent derangement of the intestinal canal, the mental
depression, the gradual impairment of health, the various visceral
complications, and, lastly and chiefly, the peculiar character of the
alvine discharges,--stamp the disease with an individuality entirely
its own.

The mucous discharges of certain forms of chronic diarrhoea and the
membranous discharges of infective dysentery are all so different in
physical character, and are associated with such a different complex of
general symptoms, that they cannot be confounded with those of the
diseases in question. The peculiar irritative quickness of the pulse of
ordinary enteritis, according to Powell and Good, suffices to
differentiate this disease from membranous enteritis. The peculiarities
of the physical and chemical properties of these exudates, already
fully dwelt upon, not only distinguish them from those of the above
diseases, but also from such dejecta as may contain fragments of
undigested connective tissue, of hydatids, or of worms. The flakes of
mucus discharged from the bowels in protracted constipation, fissura
ani, and in the later stages of cirrhosis of the liver are composed of
mucus in which are found imbedded epithelial cells from the colon and
mucus-corpuscles. The microscope will also reveal the character of the
fatty discharges that may be associated with diseases of the pancreas,
liver, and duodenum. The mucous flakes of cholera stools are composed
of masses of intestinal epithelium mixed with amorphous and granular
matter, crystals of different substances, and, according to Davaine, of
parasitic forms, particularly the Circomonas hominis.

{774} Membranous casts from the upper part of the digestive track are,
in rare cases, passed by the bowels. One of the most curious instances
of this sort is reported by Villerme:[35] A woman swallowed a
tablespoonful of nitric acid, and seventy days afterward a long
membranous exudate, one or two lines thick and of a brown color, was
discharged, which corresponded in form with the oesophagus and stomach.
The patient died a few days later.

[Footnote 35: _Dictionnaire des Sciences medicales_, tome xxxii. p.
264.]

PROGNOSIS.--The prognosis of the disease as regards life is not
unfavorable, but as regards permanent restoration to health and
strength the case is entirely different. Theden[36] and Hoffman[37]
have, however, stated that the disease is not an unfrequent cause of
sudden death.

[Footnote 36: _Remarques et Experiences_, tome ii.]

[Footnote 37: _Med. Ration._, vol. v.]

Abercrombie[38] records a case of death from phthisis complicated with
this disease, and Wright another case in which the patient died in an
extreme state of marasmus. The acute and subacute forms are more
amenable to treatment, and the chances are correspondingly greater of
permanent recovery, though in all cases there is a strong tendency to
relapse. The chronic forms may almost be enrolled among the opprobria
medicorum when once they have made deep inroads upon nutrition and the
vital powers, and produced that condition named by Todd the pituitous
cachexia (cachexia pituitosa). These cases may, however, be alleviated
by judicious treatment, diet, and climatic changes, but repeated
relapses may be expected as the rule under slight exciting causes or
even without apparent cause. Patients under these circumstances drag
out a life of valetudinarianism, but it may be cut short at any time by
the supervention of some intercurrent disease, as phthisis, renal
degeneration, etc., or, according to Grantham, atrophy of the
intestines. Broca[39] records two cases of this disease, one of which
lasted ten and the other fifteen years. Three of my cases have endured
over six years.

[Footnote 38: _Inflamm. Affec. of Mucous Memb. of Intestines_, pp. 213,
279.]

[Footnote 39: _Bulletin de la Societe Anat. de Paris_, 1854.]

TREATMENT.--The treatment of membranous enteritis embraces medical and
hygienic measures. The medical means have for their object, first, the
removal of the membranous exudation when it has once formed; and,
second, to correct the conditions upon which its formation depends by
improving nutrition and invigorating the nervous system. The severe
sufferings of the paroxysms are greatly alleviated and the duration of
this stage cut short by freely emptying the bowels. The best means to
do this is by the injection of hot water with the long elastic bougie
three or four times a day, and to assist this with laxatives. Instead
of water, solutions of potassa, soda, and lime-water are preferred by
some practitioners. As a rule, the enemata cause considerable
discomfort, but in the end are followed by improvement in the condition
of the bowels. The best laxative is emulsion of castor oil, but
occasionally a mercurial, guarded by the extract of belladonna, will
furnish more marked relief. Powell and Copeland say that they have
employed with decided advantage a purgative consisting of the compound
infusion of gentian and infusion of senna, to which were added ten or
twenty minims of liquor potassae. This was repeated, so that four
stools in the twenty-four hours were obtained. Clark preferred to
regulate the bowels, when needed, with rhubarb, soda, and {775} ipecac,
conjoined or not, as required, with mercury and chalk. Good recommends
four grains of Plummer's pill every night, and the bowels kept open by
two drachms of sublimed sulphur daily. It should always be borne in
mind that all active or irritating purgatives are harmful. The bowels
by this treatment will not only be disembarrassed of the membranous
exudates, but also of any fecal collection the retention of which would
surely cause irritation, as occasionally happens even when there is an
apparent diarrhoea. This condition may be easily determined by
abdominal palpation. The relief from pain procured by free evacuation
of the intestine will be enhanced by the employment of hot fomentations
to the abdomen. Despite these means, its severity may, however, demand
the administration of narcotics. The best form will be a hypodermic
injection of a sixth or a quarter of a grain of morphia; enemata of
starch and laudanum are also beneficial. Burrows mentions a case in
which he succeeded in allaying nervous irritation by the nightly use of
thirty drops of laudanum. The patient noticed that the habitual
constipation was increased when the accustomed narcotic was omitted.
Bromide of potassium in large doses long continued will also be found
useful for the same purpose.

During the intervals of the paroxysms local medication of the bowels
and medical and hygienic measures should be had recourse to to prevent
the re-formation of the exudates by modifying the vital activities of
the intestinal mucous membrane and by restoring the general tone of the
constitutional powers. For local treatment the nitrate of silver,
sulphate of zinc, the sulphate of copper dissolved in glycerin, the
tincture of iodine, and carbolic acid cannot be over-prized. From five
to ten grains of the metallic salts, fifteen drops of tincture of
iodine, ten of the acid, administered through the long rubber tube, are
suitable doses to begin with. I am also in the habit of using stronger
solutions by mopping it on to the bowel through the endoscopic tube.
Kaempf made frequent and large injections of decoctions of various
plants--saponaria, taraxacum, etc.--which he imagined possessed
dissolvent and resolvent virtues. Cumming[40] speaks highly of the
efficacy of electricity.

[Footnote 40: _Lond. Med. Gazette_, 3d Series, vol. ix.]

For the purpose of improving the general health the preparations of
iron are advisable, of which the best are the tincture of the chloride,
pernitrate, pyrophosphate, lactate, and potassio-tartrate. Habershon
advises infusions of the bitter tonics with hydrocyanic and
nitro-muriatic acid. I have found a combination of these acids with
henbane and infusion of serpentaria useful. I also employ hot solutions
of the latter acid as a local bath over the abdominal region, applied
with a large sponge. Clark speaks favorably of the extract of nux
vomica and astringent remedies. Simpson praises the oleo-resins under
the form of pitch pills and tar, while Clark and others laud copaiba
and turpentine. Good advises the copaiba to be given by enema when it
cannot be borne by the stomach. Brodie used cubebs in small doses.

The alterative effects of small doses of arsenic, corrosive sublimate,
sulphate of copper, etc. may be tried in obstinate cases. Grantham in
the early stages of the complaint advises the use of ten grains of
iodide of potassium combined with one-quarter of a grain of morphia at
bed-time. He {776} also strongly urges the use of cod-liver oil, which,
he says, improves the strength and increases the flesh, lessens the
spasmodic pains, but does not check the discharges.

Counter-irritation of the abdominal region with tincture of iodine, fly
blisters, mustard, etc. has afforded little if any advantage. Dunhill
kept a blister open for six months without any good results.

The mineral waters of Pyrmont, Harrogate, and Carlsbad have been found
serviceable; the latter, Henoch[41] says, should be preferred before
all.

[Footnote 41: _Klinik der Unterleub. Krankheiten_, p. 668.]

The case will amend more speedily and surely by the adoption of those
sanitary measures, as regards clothing, diet, bathing, exercise, and
change of climate, which have such important influences upon health.
The healthy performance of the functions of the skin is of such
paramount necessity in maintaining that of the intestinal canal that
the patient should endeavor to avoid any exposure likely to lead to
checked perspiration, and should use flannel underwear and stimulate
the skin by friction with the hand or the flesh-brush. The diet should
be graded to the ability of the stomach to digest and the body to
assimilate. Our chief reliance will be upon milk, plain or peptonized,
eggs, and beef given in the various forms of acceptable preparations,
so as not to impair the tone of the stomach nor clog the appetite by
sameness. Such vegetables and fruits as agree with the patient may be
allowed. I have tried exclusive diets of milk, farinacea, and meat
without marked benefit. All stimulants, tea, and coffee should as a
rule be interdicted.

Systematic exercise in the open air and change of climate to a cool,
dry, bracing atmosphere will contribute to comfortable existence, if
not lead to recovery.




{777}

DYSENTERY.

BY JAMES T. WHITTAKER, M.D.


DEFINITION.--Dysentery is the clinical expression of a disease of the
large intestine, of specific and non-specific (catarrhal) origin and
form; characterized by hyperaemia, infiltration, and necrosis
(ulceration) of its mucous membrane; distinguished by discharges of
mucus, blood, pus, and tissue-debris; and attended with griping and
expulsive pains (tormina and tenesmus).

ETYMOLOGY.--The name is compounded of the two Greek words [Greek: dys
enteron], which, though untranslatable literally into English, have
long since received the exact Latin equivalent, difficultas
intestinorum. With appropriate alteration the same name is still
employed in every civilized language in the common as well as the
classical description of the disease. The French synonym, colite,
locates the anatomical seat of the disease, while the German Ruhr and
the English flux express one of its cardinal symptoms, the frequency
(flow) of the evacuations.

HISTORY.--Ancient.--In its clinical history dysentery is one of the
oldest known diseases, the name being found in common use before the
time of Hippocrates, as in the often-quoted passage from Herodotus (443
B.C.), who relates that it and the plague reduced the army of Xerxes on
the desert plains of Thessaly.

Fayrer informs us that in the ancient system of Hindoo medicine of the
Ayur Veda, and in the commentaries of Dhanwantari, Charaka, and
Sussutra, which carry us back nearly three thousand years, and in later
Sanskrit writers, dysentery is described by the name of atisar, under
two forms--amapake, or acute, and pakistar, or chronic; these again are
subdivided into six varieties, ascribed by those ancient sages to
changes in air, bile, phlegm, food, or to perturbations of the emotions
and passions.

Hippocrates (430 B.C.) makes frequent reference to the disease, the
nature of which he regards as a descent of the humors from the brain.
"Men of a phlegmatic temperament are liable to have dysenteries," he
says, "and women also, from the humidity of their bodies, the phlegm
descending downward from the brain."

"The disease is caused," he says more exactly in another place, "by the
overflow of phlegm and bile to the veins of the belly, producing
ulceration and erosion of the intestine." In his country, at least, it
seemed most to prevail in spring, but it was clearly connected with the
heat and moisture of this season in Greece--prime factors everywhere in
the genesis of the disease: "For when suffocating heat sets in all of a
{778} sudden while the earth is moistened by the vernal showers and by
the south wind, the heat is necessarily doubled from the earth, which
is thus soaked by the rain and heated by a burning sun, while at the
same time men's bellies are not in an orderly state, nor is the brain
properly dried." Of the prognosis he observes with great acumen,
"Dysenteries when they set in with fever ... or with inflammation of
the liver and hypochondrium or of the stomach, ... all these are bad.
But such dysenteries as are of a beneficial nature and are attended
with blood and scrapings of the bowels cease on the seventh or
thirtieth day, or within that period. In such cases even a pregnant
woman may recover and not suffer abortion;" whereas, "dysentery if it
commence with black bile is mortal." Galen comments upon this statement
that such a discharge is as incurable as cancer. The practitioner of
our day will interpret this assertion, which was repeated with singular
unanimity by all the writers of antiquity, with the belief that the
black bile was blood, and that such cases really were cancers. Indeed,
Paulus AEgineta distinctly says, "Dysentery arising from black bile is
necessarily fatal, as indicating an ulcerated cancer."

Thus, although dysentery is among the oldest of the known maladies, and
was recognized then as now by the same symptoms, the disease was by no
means closely defined or differentiated in ancient times. As Ackermann
long ago pointed out, many other affections were included under the
term dysentery, and some of the symptoms of true dysentery, notably the
tenesmus, were raised to the dignity of distinct diseases.

The gravity of the so-called lotura carnea, the fleshy stools, was
fully appreciated by Hippocrates, as is evidenced by the remark that
"if in a person ill of dysentery substances resembling flesh be
discharged from the bowels, it is a mortal symptom." Fleshy masses,
[Greek: xysmata], scrapings of the guts (originally epidermic
exfoliations from the bodies of gladiators, used in pills as a tonic),
were frequently alluded to by the older writers, more especially by
Aretaeus, in description of the discharges of dysentery. Hippocrates
was also aware of the fact that dysentery may be a secondary as well as
a primary malady. "One may expect," he says in speaking of the victims
of gangrene, "that such patients will be attacked with dysentery; for
dysentery usually supervenes in cases of mortification and of
hemorrhage from wounds." Finally, Hippocrates recognized the effects of
emesis in relief of the disease with the remark in one of his aphorisms
that a spontaneous vomiting cures dysentery.

Celsus (25 B.C.-45 A.D.), the great encyclopaedist, whose works
"constitute the greatest literary monument since the days of
Hippocrates," compiles all the information obtained up to his time; but
it is plain as regards dysentery, though he defines it in terms that
might stand in a modern text-book, that he has nothing new to add to
the knowledge of the Hippocratic school. He named the disease from one
of its most prominent symptoms, tormina (tenesmus he considered a
separate affection), speaks of the stools as being mixed with mucus and
fleshy masses, and in its treatment especially enjoins rest, "as all
motion proves injurious to the ulcer."

Aretaeus (50 A.D.), of all the authors of antiquity, wrote the most
perfect and at the same time the most picturesque account of the morbid
anatomy and symptomatology of this disease. The gross appearance of the
ulcers in the intestine and the common character of the discharges he
{779} describes with the accuracy of the modern pathologist and the
ardor of the true clinician. He speaks of the superficial, the
deep-seated, the irritable, and the callous ulcer. There is, he says,
"another larger species of ulcers, with thick edges, rough, unequal,
callous, as we would call a knot of wood; these are difficult to cure,
for they do not readily cicatrize, and the cicatrices are easily
dissolved." Their tendency to arrest and renewal and their general and
local effects he notices at length. "There may be a postponement of
their spreading for a long time," he says, "various changes taking
place in the ulcers, some subsiding and others swelling up like waves
in the sea. Such is the course of the ulcers; but if nature stand out
and the physician co-operate, the spreading may indeed be stopped, and
a fatal termination is not apprehended, but the intestines remain hard
and callous, and the recovery of such cases is protracted." Vivid
descriptions he gives of the stools: "Sometimes they are like chopped
tallow, sometimes merely mucus, prurient, small, round, pungent,
causing frequent dejections and a desire not without a pleasurable
sensation, but with very scanty evacuations." Again, they are "fetid
like a mortification;" composed of "food now undigested, as if only
masticated by voracious teeth, ... the dejection being discharged with
much flatulence and noise; it has the appearance of being larger than
its actual amount."

Galen (164 A.D.) attempted to correct the pathology of his
contemporaries, who considered all bloody discharges dysenteric. There
are four distinct varieties of bloody stools, he claims, only one of
which, that due to ulceration of the intestine, deserves to be called
dysentery. The bilious stool he derived from melancholy, and the fleshy
stool from disease of the liver. But, though Galen regarded the
presence of blood as a necessity, he was well aware of the fact that
the stools contained ingredients other than blood. It was Galen who
first used the word scybala ([Greek: schybala], feces) to express the
small, solid masses of excrementitious matter often voided with the
stools. In his treatment of the disease he made much use of the various
drying earths, the Samian, Lemnian, Armenian, the sources of which he
made long journeys to visit in order to become better acquainted with
their properties, and which are better substituted in our day by
bismuth, chalk, magnesia, and the carbonate of iron. It is the
distinguished merit of Galen to have called special attention to the
anatomical seat of the disease. Ulceration of the intestine he claimed
as the very essence of the disease, and all the physicians of his day,
he maintained, regarded as dysenteric only such cases as are attended
with ulceration.

Galen was the exponent of the flower of Grecian, we might say of
ancient, medicine. With very few exceptions, the later writers, if they
do not obscure the original text with their speculations, are content
to simply paraphrase the observations of their predecessors, and the
subsequent contributions to the ancient history of dysentery may be
briefly summed up in a few additional notes.

Coelius Aurelianus (400 A.D.) adopted the humoralistic doctrine of
Hippocrates and regarded dysentery as an intestinal rheumatism
(catarrh) with ulceration. He seems to have been the first author to
recognize the cardinal fact that dysentery, notwithstanding the number
of its stools, should be classed with the diseases which constipate the
bowels, or, as it {780} was centuries later aptly put by Stoll, "ut
hanc morbis adnumeres alvum potius occludentibus," and he blames
Erasistratus for using nothing but astringents, whereas many cases of
dysentery require laxatives. It is worthy of note that Coelius
Aurelianus ascribes the first use of opium in the treatment of
dysentery to Diocles of Carystus (300 B.C.), who administered the juice
of poppies combined with galls. By the time of Galen opium was so
freely used in the treatment of the fluxes as to call for protest
against its abuse.

Alexander of Tralles (575 A.D.) is often credited as having been the
first to locate the disease in the large intestine. The truth is, he
suggested various rules by which the seat of the disease, whether in
the small or large intestine, might be definitely determined. But none
of these rules--the seat of the pain, for instance, whether above or
below the umbilicus, and the interval of time between the pain and
discharges, whether long or short--possess the least diagnostic value
or add to the attempts in this direction of previous writers--Aretaeus,
Archigenes, and Galen. Like these, his predecessors, he recognized an
hepatic dysentery with discharges of bloody serum, which he attributed
with them to atony of the liver, but more boldly than they, and with
characteristic independence, he ventured to treat his patients with
fresh vegetables and fruits, damsons and grapes.

Paul of AEgina (660 A.D.) locates the disease in the rectum, and gives
a graphic account of its symptomatology. He made the mistake of many
later practitioners in regarding as a separate disease a symptom,
tenesmus, which he describes as an irresistible desire of evacuation,
"discharging nothing but some bloody humor, which is the cause of the
whole complaint, being an oedematous inflammation of the rectum which
creates the impression of feces lodged in the intestine and a desire of
evacuation." "Dysentery," he continues, "is an ulceration of the
intestines, sometimes arising from the translation of tenesmus, and
sometimes being of itself the primary affection; and is attended with
evacuations at first bilious and of various colors, then accordingly
bloody, and at last ichorous, like that which runs from dead bodies."

In curious contrast to these accurate observations is the absurd
suggestion of an obsolete therapy (Galen), that the dried dung of dogs
who had eaten bones, when drank in milk which has been curdled by
having heated pebbles put into it, is of great service; but as an
offset to this freak of fantasy is the renewed advocacy of warm milk,
fallen somewhat into disuse since the days of Hippocrates and Galen:
"And milk itself moderately boiled is an excellent thing"--a
recommendation of the milk diet which now plays such an important role
in the treatment of so many diseases of the alimentary canal.

Modern.--From this brief survey it is seen that the writers of
antiquity left nothing in the symptomatology of dysentery for
subsequent authors to describe. All further advance in our knowledge of
this, as of all diseases, was now rendered impossible by the extinction
of the light of science in the long night of the Middle Ages, whose
gloom deepens with succeeding centuries and whose shadows fall close up
to our own times.

The modern history of dysentery may be said to begin with Daniel
Sennertus, whose first _Tractatus de Dysenteria_ was published at {781}
Wittenberg in 1626. Sennert gave the deathblow to tenesmus as a
distinct disease, or as even a pathognomonic sign of dysentery, showing
that it is often present in purely local troubles, ulcers, fissures,
hemorrhoids, etc., or is due to disease of other organs--stone in the
bladder, tumors in the womb, etc. He recognized sporadic and epidemic
attacks of the disease, and described under the terms fiens and facta
forms which coarsely correspond to the catarrhal and diphtheritic
varieties of modern pathologists. Improper food, unripe fruits, at
least, cannot be the cause of dysentery, because, he shrewdly observes,
the epidemic of 1624 began in May, before the fruits were ripe, and
ceased in autumn, when they were ripe and in daily use. Moreover,
sucklings at the breast suffered with the disease. Nor could moisture
alone account for the disease, as this epidemic occurred after an
unusually hot and dry spring and early summer. Some other cause must be
invoked, and this other cause is perhaps the occult influence of the
constellations and planets--an explanation which he afterward admits to
be only an asylum of ignorance. In the treatment of the disease the
indication should be to heal the abraded or ulcerated intestine; but
since this cannot be done unless the cause is first removed, "the
abrading, eroding humor should be evacuated and absterged, at the same
time its acrimony mitigated and corrected; then the flux should be
checked by astringents, and the pain, if vehement, lenified and
removed." Purgatives should be repeated until all vicious humors are
discharged.

Sydenham colored his descriptions of the epidemic which he witnessed in
London in 1669-72 with the artistic touches of the master's hand. "The
disease sets in," he says, "with chills and shivers. After these come
the heat of the fever, then gripings of the belly, and lastly stools.
Occasionally there is no fever; in which case the gripes lead the way,
and the purging follows soon after. Great torment of the belly and
sinking of the intestines whenever motions are passed are constant; and
these motions are frequent as well as distressing, the bowels coming
down as they take place. They are always more slimy than stercoraceous,
feces being rarely present, and when present causing but little pain.
With these slimy motions appear streaks of blood, though not always.
Sometimes, indeed, there is no passage of any blood whatever from first
to last. Notwithstanding, provided that the motions be frequent, slimy,
and attended with griping, the disease is a true bloody flux or
dysentery." The efficacy of opium in its treatment causes him to break
out in praises of the great God who has vouchsafed us a remedy of so
much power. But Sydenham was too good a practitioner not to know that
all treatment must be prefaced with laxatives. For "after I had
diligently and maturely weighed in my mind," he says, "the various
symptoms which occur during this disease, I discovered that it was a
fever--a fever, indeed, of a kind of its own--turned inwardly upon the
bowels. By means of this fever the hot and acrid humors contained in
the mass of the blood, and irritating it accordingly, are deposited in
the aforesaid parts through the meseraic arteries." The indications
then were plain--viz. "after revulsion by venesection to draw off the
acrid humors by purging." It was the frequent and successful practice
of Sydenham also to drench the patient with liquids, per os et per
rectum--a mode of treatment which both he and the learned Butler, who
accompanied the {782} English ambassador to Morocco, where dysentery
was always epidemic, hit upon, "neither of us borrowing our practice of
the other." Butler declared that the method of deluging the dysentery
by liquids was the best. But many attacks are cured almost on the
expectant plan alone. This was the case with the excellent and learned
Daniel Coxe, Doctor of Physic, in whom "the gripes and bloody motions
ceased after the fourth clyster. He was kept to his bed, limited to
milk diet; and this was all that was necessary in order to restore him
to perfect health."

Zimmermann (1767) did not believe that improper food could be a cause
of dysentery, as in the epidemic of 1765 fresh grapes were plentifully
supplied to patients and proved an excellent remedy. He also noticed
the muscular pains (rheumatism) which had been mentioned by Sydenham
before him, and the paralyses first noticed by Fabricius in 1720, as
occurring in the course of, or as sequelae to, the disease. It was only
contagious, he thought, in bad cases, when the stools have a cadaveric
odor. But his main and most useful contributions were in the field of
therapy. He discarded venesection entirely, was among the first to
recognize the value of ipecacuanha, and objected strenuously to opium
until the cause of the evil was expelled. Hence he was vehemently
opposed to all astringents, to the use of which he ascribes the
rheumatisms and dropsies which sometimes occur. Wines and spices were
likewise put under ban; whey he permitted, but not milk, and water
freely, but always warm. Barley-water and cream of tartar were
sufficient food and medicine for ordinary cases, while camphor and
cinchona best sustain the strength in bad cases.

Pringle (1772) observed the frequent occurrence of dysentery
coincidently with malarial fever, and was a firm believer in the
contagion of the disease. He claimed that the foul straw upon which the
soldiers slept became infectious, but maintained that the chief source
of infection were the privies "after they had received the dysenteric
excrements of those who first sicken." It is spread in tents and in
hospitals, and may be carried by bedding and clothing, as in the
plague, small-pox, and measles. Neither food nor drink propagates the
disease, he thinks, for, so far as the fruits are concerned, he too had
seen it prevail before the fruits were ripe. The first cause of the
disease is "a stoppage of the pores, checking the perspiration and
turning inward of the humors upon the bowels." Antimony was his
specific in its treatment. He was also fond of Dover's powder in its
relief, and preferred fomentations to opium, which "only palliates and
augments the cause." The best drink for patients with dysentery was
lime-water (one-third) and milk.

This period of time is made memorable in the history of dysentery, as
of nearly all internal diseases, by the contributions from direct
observation upon the dead body by the father of pathological anatomy,
John Baptist Morgagni (1779). From the days of Hippocrates down, the
seat of the disease had been, as has been shown, pretty accurately
determined, and the same acumen which enabled the clinicians to
localize the affection had inspired them, as we have seen, to define
and describe its nature. But any descriptions from actual post-mortem
examinations were not put upon record until the beginning of the
sixteenth century, when were published the posthumous contributions of
Benivieni (1506-07). In his description of the lesions of the disease
he says that "the viscera displayed {783} internal erosion from which
sanies was continually discharged." Nearly three centuries elapsed
before Morgagni made his anatomical studies--an interval of time void
of any contributions from pathological anatomy; and so little attention
was paid to this branch of medical science that the descriptions of
Morgagni and of his more immediate successors failed to excite any
general interest or make any permanent impression. Morgagni himself,
while he fully recognized their significance, did not consider the
ulcerations of dysentery as absolutely essential to the disease, as
many cases, even fatal ones, did not exhibit them at all. They were not
liable to be mistaken for the lesions of typhoid fever, the ulceration
of Peyer's glands, because, though they may, they only rarely, coexist
in the same subject. As to the membranous fragments sometimes evacuated
with the discharges of dysentery, Morgagni showed that they are
occasionally true fragments or shreds of the intestinal coats, as has
been maintained by the older writers, Tulpius and Laucisius, but are
far more frequently nothing else than inspissated mucus--conceptions
which subsequent studies with the microscope have fully confirmed.

In view of the general disregard of direct observations, it is
therefore not surprising to learn that the nature of the intestinal
lesions gradually fell into oblivion or at least became underrated in
its import. But it is a matter of surprise that Stoll (1780) was able
to declare as the result of autopsies made by himself that, although
the colon is thickened and inflamed, ulcerations in dysenteries are
very rare. This distinguished author did not at all believe in the
contagion of the disease, as he had never seen it attack physicians or
nurses. It developed, he thought with the older writers, as the result
of exposure to cold during a perspiration. He emphatically insisted
upon the frequency of rheumatism as complicating the disease, and
describes in proof a number of cases of painful swollen joints during
and subsequent to the attack. It was his especial merit to have
succeeded in dispensing with the acrid bile as a cause of the disease,
maintaining that hepatic derangements were only accidental
complications, and thus disposed, but only for a time, of bilious
dysentery in so far as it was supposed to depend upon defective or
abnormal action of the liver.

But Annesley (1828) soon reinstated the liver in the pathology of
dysentery, with the exhibition of colored plates displaying abscess of
the liver in connection with the disease, as well as illustrating the
displacements and constrictions of the colon which sometimes occur in
its course.

The fourth decade of our century now brought in the anatomical
contributions of Cruveilhier and Rokitansky, to be followed later by
those of Virchow, upon which the modern morbid anatomy of the disease
is based; while the labors of the Indian physicians and of Copeland,
Parkes, and Vaidy put us in possession of the facts pertaining to its
general pathology. Fayrer has quite recently published the results of
his vast experience with dysentery in India, an important contribution
to the practical study of the disease, and Hirsch has treated
exhaustively of its medical geography. But the merit of publication of
the most complete chapter or work upon dysentery that has ever been
written anywhere belongs to, and is the especial pride of, our own
country. It constitutes the bulk of the second volume of the _Medical
and Surgical History of the War of the Rebellion_. It is a veritable
encyclopaedia of knowledge, not {784} only upon the subject of which it
treats, but upon all subjects immediately or even remotely collateral
to it, and is a lasting monument to the labor and the learning of its
author, Joseph J. Woodward, Surgeon of the United States Army.

GENERAL REMARKS.--Dysentery may be a primary or a secondary disease. As
a primary disease it occurs in sporadic, endemic (often closely,
sometimes curiously, circumscribed), or epidemic form, and is either
acute or chronic, according to the nature of its symptoms and lesions.
The ancient types of sthenic and asthenic or adynamic, typhoid,
bilious, and malarial dysenteries belong rather to history than to
modern medicine. The classification of cases in general use at
present--viz. the catarrhal and croupous or diphtheritic forms--has
reference rather exclusively to the nature of the lesion, and is hence
extremely defective. Nor are the divisions (as in cholera) into
sporadic and epidemic forms much more satisfactory, in that they
indicate simply the range or extent of the disease, and by no means
define a separate array of symptoms or lesions; precisely the same
symptoms or lesions being encountered in individual cases of either
form. None of these divisions clearly indicate differences in etiology,
upon which factor alone can any acceptable division of cases be based.
Perhaps less objection may be urged against the assumption of catarrhal
and specific forms, including under the provisional term catarrhal all
the cases which cannot as yet be accounted for by the action of a
special or specific cause.

It will become apparent in the study of the etiology of dysentery that
while any of the factors invoked may suffice to produce the catarrhal
(sporadic) form, none will explain the specific (epidemic) form of the
disease; both forms may be alike in their lesion and signs, but they
differ widely in their cause. In other words, dysentery is only a
clinical, and is in no way an etiological, expression of a disease. In
this respect dysentery finds its analogue in a much grosser lesion of
the bowels--namely, occlusion, acute or chronic, which, while it
presents pretty much the same train of symptoms, may depend upon a
great variety of causes, as impaction, strangulation, intussusception,
etc. While any of the causes cited may be sufficient to excite the
catarrhal form of the disease, the same causes may stand to the
specific form only in the relation of predisposing agents. Or, as
Maclean has better put it, "It appears that many of the so-called
causes of dysentery must be regarded more as acute agents of
propagation than of causation."

As a secondary disease dysentery occurs in the course of, or as a
sequel to (not infrequently as the terminal affection of), pyaemia and
septicaemia (puerperal fever), typhus and typhoid fevers, pneumonia,
Bright's disease, variola, scarlatina, abscess of the liver (though the
order of sequence is here oftener reversed), scorbutus, marasmus from
any cause, tuberculosis, and cancer. It must not be forgotten, however,
of these latter affections that each produces its own lesions in the
large intestine, which are not to be confounded with those of genuine
dysentery.

The view that dysentery shows a periodicity of recurrence at certain
distinct intervals or cycles--three, five, or ten years--is entirely
without foundation in fact; but there is strong ground for believing
that the disease is gradually abating both in frequency and virulence
with improvements in sanitation and hygiene. Thus, Heberden shows that
the {785} number of deaths set down in the seventeenth century under
the titles of bloody flux and gripings of the guts was never less than
1000 annually, and in some years exceeded 4000, whereas during the last
century the number gradually dwindled down to 20 (Watson)--a number
which is certainly a misprint for 200; and Aitken states that as a
cause of death it has been decreasing since 1852. Geissler also
remarks[1] that the variation in epidemics is nowhere so well
illustrated as in the case of dysentery. A noticeable reduction in the
number of cases in England began about 1850, and has continued almost
without interruption to the present time, so that now (1880) six to
eight times less cases occur than in the forties. The same diminution
has been noticed in Bavaria and Sweden. In Sweden the cases treated by
physicians in 1857 numbered no less than 37,000, with over 10,000
deaths; whereas now the number is reduced to 400-500 a year, and the
mortality has experienced a corresponding reduction from 20-30 to 6-8
per cent.

[Footnote 1: _Periodische Schwanderungen der wichtigsten Krankheiten_.]

At the same time, it is known of dysentery that it sometimes shows an
almost freakish recurrence after long intervals of time, appearing in a
place for many decades free from the disease, to establish itself there
for years as a regular endemic malady, not to disappear again for a
long series of years; in which respect, Hirsch remarks, it much
resembles malaria.

Allusion has been already made to the occasional curious
circumscription of the disease in definite localities. In fact,
dysentery, even when late to assume the proportions of a widespread
epidemic, begins, as a rule, and is confined for a time, in individual
enclosed regions--prisons, barracks, hospitals, etc.; and in the
process of dissemination it is rather characteristic of the disease to
leap over or to spare intervening territory and appear in new foci at
some distance from its original seat. A direct irradiation or linear
transmission of the disease is the exception, and not the rule. The
significance of this fact will become evident in the study of the
etiology of the disease.

Dysentery is pre-eminently a disease of army life, its victims among
soldiers numbering more than all other diseases together. Sir James
MacGrigor, Medical Superintendent of the British army, called it the
scourge of armies and the most fatal of all their diseases. Aitken says
that "it has followed the tracks of all the great armies which have
traversed Europe during the continental wars of the past two hundred
years." It decimated the French, Prussian, and Austrian armies in 1792.
In Cape Colony in 1804 every fourth man among the soldiers was attacked
with the disease, and of those attacked every fifth man died. In
Napoleon's campaign in Egypt dysentery numbered one-half more victims
than the plague; Kinglake says that 5000 men died of dysentery alone in
the war of the Crimea; and in our own country during our Civil War from
1861-65 chronic camp dysentery was the cause of more than one-fourth of
all the diseases reported, the mortality being at the rate of 12.36 per
1000.

Woodward relates that the dysenteries, acute and chronic, with
diarrhoeas, made their appearance in the new regiments at the beginning
of the war, and, though mild at first, quickly assumed a formidable
character. "Soon no army could move without leaving behind it a host of
the victims. They crowded the ambulance-trains, the railroad-cars, the
{786} steamboats. In the general hospitals they were often more
numerous than the sick from all other diseases, and rivalled the
wounded in multitude. They abounded in the convalescent camps, and
formed a large proportion of those discharged for disability." Most of
the prisoners died of this disease, and great numbers succumbed to it
on retirement to their homes after the cessation of the war. It is the
story of many a campaign, Eichhorst says, that dysentery kills more men
than the enemy's guns.

The fact that it sometimes shows itself in periodic form or with
periodic exacerbation, that it is sometimes successfully treated with
quinia, and that, as has been noticed from the days of Hippocrates
down, it prevails in greatest intensity in malarial regions, has given
rise to the view that dysentery is a malarial disease. This view, which
was strongly advocated by many of the older writers, Senac, Fournier,
Annesley, met with renewed support at the hands of many of the surgeons
in our Civil War. But wider observation has shown the fallacy of such a
view; for not only may the diseases prevail entirely independently of
each other in malarial regions, but there are regions where one does
and the other does not exist. Thus Huebner quotes from Rollo concerning
St. Lucie (West Indies), a town situated on a mountain in the midst of
a swampy country in which both dysentery and malaria abound, while the
town itself is almost free from dysentery; and Dutrolan cites Reunion
as a place where marsh fevers do not occur, while dysentery is very
common. Berenger-Feraud[2] scouts the idea of any such connection. "Let
us mention only St. Pierre de la Martinique," he says, "where there is
not a piece of marsh as big as a hand, but where dysentery has made
great ravage more than once. We might cite also Mauritius, Gibraltar,
Malta, New Caledonia--places exempt, or almost exempt, from malaria,
but often visited by dysentery."

[Footnote 2: _Traite theorique et clinique de la Dysenterie, etc._,
Paris, 1883.]

The view that dysentery is a form of typhus or typhoid fever
(Eisenmann) or scurvy needs no refutation in the light of existing
knowledge regarding the pathogenesis and pathology of these affections.
These diseases may often complicate, but can never cause, dysentery.

Dysentery is a disease which spares no age, sex, or social condition,
the seeming greater suffering of the poorer classes being due to the
filth, food, darkness, dampness--in short, to the bad sanitation--of
poverty.

Though the disease is often confined exclusively to soldiers in the
midst of a civil population, examples are not wanting of an exclusive
selection of civilians or of an indiscriminate attack in every
direction. Lastly, dysentery is a disease which may recur repeatedly in
the same individual, one attack rather predisposing to than preventing
another.

ETIOLOGY.--Dysentery is an omnipresent disease. "Wherever man is,"
Ayres observed of it nearly a quarter of a century ago, "there will
some of its forms appear." But the character of the form, and more
especially the extent and severity of the disease, vary in extreme
degree with the conditions surrounding the abode of man. No one of
these conditions affects the disease so markedly as the climate. It is
the testimony of Hirsch, based upon the study of seven hundred
epidemics of the disease, that no other disease is so dependent upon
the influence of the climate. The home of dysentery is the tropical
zone. It prevails in greatest frequency {787} and virulence in the
tropics, and in those regions of the tropics where the characteristics
of this zone are more pronounced, diminishes in intensity in the
temperate regions, and occurs only in sporadic form farther north. At
40 degrees latitude the line may be pretty sharply drawn; beyond it
dysentery as an epidemic is almost unknown.[3]

[Footnote 3: Shakespeare (_Troilus and Cressida_) cites "griping of the
guts" among the "rotten diseases of the south."]

India has been from time immemorial the hotbed of this disease.
Henderson says it is perhaps more fatal to natives than all other
diseases put together, and Hutchinson, Hunter, and Tytler observe that
it causes three-fourths of the deaths among the natives of Hindostan.
In Egypt the disease is indigenous, and is, according to Frank, post
pestem maxime timendus. Greisinger reports that one-half of all the
autopsies made by him in Egypt showed dysentery as a primary or
secondary affection. It is epidemic here at all times, Roser says, and
all fatal cases of acute or chronic disease finally perish with it.

Similar testimony might be adduced from a large part of Africa, much of
Asia, the Indian Archipelago, and the West Indies. It rages
"murderously" in Peru, causing a mortality in some epidemics of 60 to
80 per cent., and occurs in this country not only in the valleys, but
in cities and provinces at the lofty elevation of 8000 to 13,000 feet.

Heat, moisture, vegetable decomposition, and sudden atmospheric change
are the distinguishing characteristics of southern climes, and the
study of the etiology of a disease incident or indigenous to these
conditions calls for an investigation of these various factors.

It is well established of dysentery that it occurs for the most part in
the hottest season of the year. Of 546 epidemics tabulated by Hirsch,
404 prevailed in summer and fall, 113 in fall and winter, 16 in spring
and summer, and only 13 in winter. Fourteen-fifteenths of the whole
number of epidemics occurred in the months of June to September. And it
is corroborative of these conclusions that of 1500 deaths from
dysentery in the cities of Boston, New York, Philadelphia, and
Baltimore from 1816 to 1827, 1100 occurred in the months of July,
August, and September. In fact, the Census Reports (1860-70) of our
country show the maximum mortality in August and September, and the
minimum in January and February.

The prevalence of unusual heat may also call out an epidemic in places
where the disease usually shows itself only in endemic or sporadic
form. Thus, the severe epidemic of 1540 in England was preceded by a
heat so intense as to dry up the wells and small streams, in
consequence of which many cattle died of thirst; and the epidemics of
1583 in Germany, of 1758 in France, and of 1847 in our own country,
were characterized in the same way. Interesting in this connection is
the statement of Frick concerning the epidemic in Baltimore in 1849,
who found the cases to increase and decrease almost in proportion to
the elevation and depression of temperature. The epidemic of Weimar in
1868, where 12,000 people fell ill with the disease, illustrated the
rule when it ceased suddenly on the approach of cool weather at the end
of August.

But that heat alone is not sufficient to account for the genesis of the
disease is apparent from the occasional occurrence of it in the tropics
in the colder seasons of the year; in the colder climates, Russia,
Sweden, {788} and Canada; and in temperate regions during exceptionally
cool seasons, as in Plymouth in 1769, London in 1808, Massachusetts in
1817. Moreover, the temperate zone is often characterized by seasons of
unusual heat, during the prevalence of which dysentery may be almost
unknown. Thus, during the summer of 1881, in Cincinnati, the
thermometer scarcely fell below 95 degrees F. for weeks at a time, and
was often nearly 100 degrees during the entire night, but the records
at the Health Office show that while cases of heatstroke were
alarmingly frequent, dysentery was unusually rare during the entire
season.

That moisture cannot act more, at most, than as an occasional
predisposing cause of dysentery is sufficiently clear from the
statement of Hirsch, that of 119 epidemics, 62 commenced or were
preceded by wet and 57 by dry weather. In truth, dryness long continued
and excessive heat have already been invoked as remote causes of the
disease. But moisture, as contributing to, or being a necessary element
of, vegetable decomposition, the third characteristic of tropical
regions, is entitled to further consideration. Annesley observed that
among troops stationed in the vicinity of rivers, canals, and places
abounding with emanations from the decay of animal and vegetable
matters dysentery became extremely prevalent and assumed a more or less
malignant nature; and Baly, who studied the disease in its famous
outbreak in the Milbank Penitentiary, remarks that "it is greatest at
those seasons and in those states of the atmosphere which most favor
decomposition of organic matter in the soil."

In Africa it has been noticed that dysentery appears with the rainy
season, to disappear only at its close; and the same observation has
been made of Bengal, while in Lower Egypt the disease follows the
inundations of the Nile. Burkhardt says of 10,000 cases that one-half
occur in wet hot seasons, two-fifths in dry hot seasons, and but
one-tenth in cold seasons. Moreover, the removal of camping-grounds to
dry localities has often arrested the disease or checked its further
dissemination. Thus, Mursinna states that the removal of the army of
Prince Henry of Hesse from Nimes, where the disease raged fearfully, to
Leitmeritz was attended by its immediate cessation, notwithstanding the
fact that the soldiers ate large quantities of fruit. A statement of
Dillenius, quoted by Heubner, is in this connection exceedingly
instructive: "Dillenius had to march with a dysentery hospital of more
than 500 patients from July 26 to August 3, 1812, and it required four
whole days to accomplish an ordinary nine or ten hours' march. The
patients, extremely exhausted, were finally put into a sheep-shed.
Here, in the fresh air and lying on hay, they all improved very
quickly. By advice of the physician they ate for medicine the fresh
whortleberries which they themselves had picked." Werneck attributes
the exemption of the city of Halle since the end of the last century to
the draining and drying of the neighboring marshes.

On the other hand, numerous observations go to prove that dysentery is
likewise prevalent in dry sandy soils where the factors so necessary to
the production of malaria are entirely unknown. Thus, Hirsch quotes
from Harthill to the effect that dysentery never occurred among the
English troops in Afghanistan until they entered upon its thoroughly
dry and sandy plains; and from Lidell, who declared that the disease
prevailed most in Panama in March, the dry season at this place. Again,
a striking confirmation of exemption from dysentery in a marshy region
{789} is offered in the Antilles at Grande-Terre, "a wet, marshy plain
severely visited by malaria, but used by patients attacked with chronic
dysentery at Basse-Terre as the safest place of refuge and recovery."

The role of moisture and vegetable decomposition may be, then, summed
up in the words of Annesley, that "all situations which furnish
exhalations from the decay of animal or vegetable productions under the
operation of a moist and hot state of the atmosphere will always
occasion dysentery in the predisposed subject--_circumstances which,
with other causes_ [italics ours], combine to generate the disease."

Atmospheric vicissitudes, checking of perspiration, catching cold, are
synonyms in the present popular as in the ancient professional
conception of the genesis of dysentery. "Of the remote causes of
dysentery," Johnson says, "I need say little; they are the same in all
parts of the world--atmospheric vicissitudes." And in making this
statement the author expresses the almost universal testimony of the
Indian physicians. "Sudden change of temperature," observes
Kaputschinsky of the Trans-Caucasus, where dysentery is rife, "is in
this region no rarity. The sultry heat of noon often alternates with a
cutting cold wind, and vice versa. In the same place is now a warm, now
a cold, now a glowing hot breeze, and such changes most predispose to
dysentery." And McMullin says of the Barbadoes that "it is a curious
fact that this disease is most prevalent where from the immediate
contiguity of mountains sudden vicissitudes of temperature are
experienced." Didelot says also of South France, "It is not the fruits,
as people still believe to-day, which act as causes of dysentery, but
the sudden variations of the air." Ruthay remarks of the dysentery of
China that the most common cause is a chill caught by sleeping in a
draught uncovered or in the open air. Metzler attributes the exemption
of Stuttgart (since 1811) from any great epidemic to the fact that the
city lies in a valley open only to the east, which permits no contrast
of hot days and cold nights; and Seeger, in speaking of the epidemic
which occurred in Ludwigsberg in 1872 (a city of twelve thousand
population, where no epidemic of any kind had appeared since 1834, and
where 870 were suddenly attacked with dysentery) that it first broke
out in Kaffeeburg in two streets exposed to the wind, and thence spread
to different parts of the city. Exposure of the body, especially the
abdomen, during sleep or when perspiring, the sudden laying aside of
flannel body-clothes, are proceedings, Fayrer says, pregnant with
danger in dysenteric regions. A lamentable dysentery appeared,
according to Trotter, on board H.M.S. Berwick Oct., 1780, "in
consequence of the hurricane on the fifth of the month, by which the
clothes and bedding of the seamen, and indeed all parts of the ship,
were soaked in water, and many of the men slept for nights together on
the wet decks overcome with fatigue and debilitated from want of food."
Fayrer also quotes from Moseley the observation that "it often happens
that hundreds of men in a camp have been seized with the dysentery
almost at the same time after one shower of rain or from lying one
night in the wet and cold."

As illustrating the conjoined operation of all these various causes,
together with filth and foul effluvia, more especially exposure to
cold, the story of dysentery was never better told than by Sir James
MacGrigor, who, in speaking of the Peninsular campaign, remarks that
"the army during June as well as July was traversing Castile, where it
was {790} exposed to the direct influence of a burning sun darting its
rays through a sky without a single cloud, the troops marching and
fighting during the day, and bivouacking during the night on arid,
unsheltered plains. They felt at times every vicissitude of heat and
cold. In the rapid advance they could not be regularly supplied with
food or had not time to cook it, and not unfrequently indulged in bad
wine and unripe fruit." ... The thousands of sick (chiefly from
diarrhoea, dysentery, and remittent fever) were hurried off to Ciudad
Rodrigo, the nearest hospital-station to the frontier of Portugal, a
town "composed chiefly of ruins with very narrow streets," ... and from
having been "so much the object of contest, and alternately the site of
the hospitals of all the contending armies, nearly twenty thousand
bodies were calculated to have been put into the earth either in the
town or under its walls in the course of a few months." ... "It may
easily be conceived," the author adds, "in what state cases of
dysentery must have arrived after having sustained a journey in extent
from four to twenty days, conveyed chiefly in bullock-carts or on the
backs of mules, sometimes under incessant rain for several days
together."

It is really quite superfluous to cite further opinions or examples in
illustration of a fact which is so universally conceded as to be
exaggerated in its general significance. Taking cold is the common idea
of the cause of dysentery, and is always a satisfactory explanation in
a case of obscure origin in this or any disease, even though the
patient may be able to recall no possible exposure. The physician
himself contents himself only too easily with resort to this refuge,
and with further appeal to the locus minoris resistentiae, as the
explanation of the seat of the disease, which he hopes to cure with the
aid of the vis medicatrix naturae. But taking cold is only a popular
paraphrase for contracting a disease, and will bear no scientific
analysis of its meaning. Mere reduction of temperature will certainly
not produce a disease whose habitat is the hottest zone, nor will a
sudden chill of the surface be accepted as a sufficient cause so long
as men daily remain exempt after a sudden plunge into cold water. Some
other factor must be invoked to account for the outbreak of specific
(epidemic) dysentery.

The influence of the nervous system, the mechanical and chemical or
specific action of the ingesta and dejecta, remain to be especially
considered in the etiology of the disease.

The influence of the nervous system is more directly seen in the
production of diarrhoeas than dysenteries, but that sustained
disturbances of the emotions play an important part in the production
of dysentery is shown by the greater frequency of the disease among
prisoners of war. In the Franco-Prussian war the French prisoners
suffered more than the Germans, and the records of prison-life in our
own war, at Andersonville, Libby, and Salisbury, furnish ghastly
chapters in the history of this disease. Many other factors contribute
to the development of the disease under such circumstances--in fact,
all the cruelties of man's inhumanity to man--but the influence of the
nervous system is too plain to be mistaken. The communication between
the cervical ganglia and the sympathetic nerve-fibres which preside
over the cerebral circulation and regulate intestinal peristalsis has
been invoked (Glax) in explanation of the direct action of the brain
upon the intestinal canal. Curious in this {791} connection is the
claim of Savignac, who considered dysentery a disease of the nervous
system because in two cases he found spots of softening in the spinal
cord.

The noxious action of irritating articles of diet has been recognized
in the production of dysentery from the earliest times. Aretaeus
mentions acrid foods, and Aetius crudities, as directly causing the
disease; and unripe fruits have been especially stigmatized from the
days of Galen down. Decomposing, fermenting food and drink cause
diarrhoea much more frequently than dysentery, but if the irritation be
severe or prolonged, or be superimposed upon a catarrhal state, a
diarrhoea, it is claimed, may pass over into dysentery. Impurities in
drinking-water were charged with causing dysentery by Hippocrates
himself, with whom Avicenna fully coincided; and the view that
epidemics of the disease are caused in this way has been abundantly
advocated ever since. So far as running water is concerned, the
researches of Pettenkofer have shown that all impurities are speedily
destroyed, for even at the distance of a few rods from the reception of
sewage the water is perfectly safe. Nor does standing water lack the
means of purification, provided it be sufficiently exposed to the air.
The observations of Roth and Lex have shown that the water of the wells
of fifteen churchyards in Berlin contained nitrates in less quantity
than the average wells in the city; and Fleck made a similar statement
with regard to the wells of Dresden. But no one in our day would rely
upon a mere chemical analysis in the detection of the organic poisons
or particles of disease. It is the physiological test which remains the
most conclusive, and the evidence in favor of the production of
dysentery by the ingestion of drinking-water poisoned by the reception
of excrementitious matter, especially the dejecta of disease, is as
positive as in the case of typhoid fever. Thus, De Renzy found that the
number of cases of dysentery "immediately decreased at Sibsagor (India)
so soon as better drinking-water was obtained from wells deeply sunk
and lined with earthenware glazed pipes;" and Payne found that the
cases of dysentery (as well as diarrhoea and lumbrici) almost
disappeared from the asylum at Calcutta as soon as the habit of
drinking water from the latrines was stopped. In face of such facts,
which might be infinitely multiplied, one would hesitate to subscribe
to the statement of Fergusson that "true dysentery is the offspring of
heat and moisture, of moist cold in any shape after excessive heat; but
nothing that a man could put into him would ever give him a true
dysentery."

The relation of the action of the dejecta must be studied from the
double standpoint of the development and the dissemination of the
disease, as originating the catarrhal form by mechanical or chemical
irritation of the intestinal mucosa, and as spreading the specific form
by direct or indirect infection.

By the time the contents of the alimentary canal have reached the colon
they have become, through absorption of their fluids, more or less
inspissated, and hence as hard, globular masses fill the sacculi of the
large intestine. Mechanical irritations by crude, indigestible residue
of any kind of food, more especially of vegetable food, or chemical
irritations, as by fermenting food, accumulate in this region, fret the
mucous membrane into a state of inflammation, even ulceration, and
produce the anatomical picture and the clinical signs of dysentery. If
there be a superadded or {792} pre-existent catarrhal condition of the
mucosa or a defective peristalsis of the muscular coat, which is
sluggish enough at best, the development of a pathological state is
much facilitated. And there is no doubt that the dysentery of the
tropics is increased by the bulky, indigestible, feces-producing
character of the food.

The anatomical construction of the colon may also favor these processes
by its mere abnormal length or size or by duplicatures in its course.
The protracted constipation of the insane, in whom the transverse colon
is often found elongated or displaced--to assume the well-known M-form,
for instance--may partially account for the frequency of dysentery in
these cases (Virchow), though the neglect which comes of preoccupation
of the mind, with the general inhibition of peristalsis, is a more
frequent cause of the constipation.

Wernich (1879) sums up the action of the feces, independently of a
specific cause, in attributing the dysentery of the tropics, aside from
the great changes of temperature, to (1) bad aborts, the dejecta being
deposited in all parts of the towns or into an opening made in the
floor of the hut, with which is associated total lack of personal
cleanliness; (2) to the diet, which causes a large amount of feces; and
(3) to the relaxation of the intestine in general, permitting
accumulations of infecting matter.

Upon the question of the propagation of the disease by the dejecta rest
in great measure the all-important problems of a specific virus and of
the contagiousness of the disease.

It is the almost universal opinion of those who have had the
opportunity of widest observation that epidemic dysentery arises from,
or is due to, a specific cause, a miasm, a malaria (in its wide
etymologic sense, bad air), which emanates from the soil. The
simultaneous sudden attack of great numbers under the most diverse
surroundings admits of explanation in no other way. But the precise
nature of the morbific agent is still unknown. The similarity of
epidemic dysentery to malaria would indicate the existence of a low
form of vegetable life, a schizomycete, as the direct cause of the
disease. But the proof of the presence of a specific parasite or germ
is still lacking, and though its speedy disclosure by means of the
solid-culture soils may be confidently predicted, it cannot, in the
light of existing knowledge, be declared as yet.

Especial difficulty is encountered in the study of micro-organisms in
diseases of the alimentary canal because of the myriad variety in
enormous numbers found in healthy stools. Decomposition and
fermentation both begin in the large intestine, so that the feces swarm
with the bacteria and torulae productive of these processes. Woodward
declares that his own observations have satisfied him that "a large
part of the substance of the normal human feces is made up of these low
forms in numbers which must be estimated by hundreds of millions in the
feces of each day," bacteria, micrococci, and torulae being found
"floating in countless multitudes along with fragments of
partly-digested muscular fibres and other debris from the food;" but
while the torulae are increased, the other micro-organisms, bacteria,
etc., do not appear to be more numerous in the stools of dysentery than
in healthy feces.

The doctrine that dysentery depends upon parasites is very old in
medicine, and included animal as well as vegetable growths. Langius
(1659) declared that swarms of worms could be found in dysenteric
stools, and {793} Nyander (1760) went so far as to call dysentery a
scabies intestinorum interna; which extravagant conception would have
speedily met with merited oblivion had not his preceptor, the great
Linnaeus, incorporated the Acarus dysenteriae into his _Systema
Naturae_. Sydenham about this time (1670) expressed a much clearer
conviction of the cause of the disease when he spoke of "particles
mixed with the atmosphere which war against health and which determine
epidemic constitutions."

Baly (1849) first proclaimed the idea of a vegetable fungus, similar to
that described by Brittan and Swayne in cholera, as the parasite of the
disease; and Salisbury (1865) described algoid cells and species of
confervae as occurring abundantly in all well-marked cases. Klebs
(1867) found spore-heaps and rod-like bacteria in the stools of
dysentery as in cholera, but maintained that those of dysentery were
larger and thinner than those of cholera. Hallier (1869) maintained
that although there was no morphological difference in the
micro-organisms of the stools of dysentery, typhoid fever, and cholera,
he was able by culture-experiments to develop the micrococcus of
dysentery into a special fungus, which he called Leiosporium
dysentericum. Busch (1868) demonstrated nests and colonies of
micrococci, as well as mycelium, in the villi and among the glands of
the mucous and submucous tissues in the cases of dysentery from Mexico
which he examined, but Heubner (1870) was able to disclose them in
equal numbers in preserved preparations or fresh contents of healthy
intestines. Dyer[4] (1870) believes that the parasites constituting the
mildew or sweat which forms a viscous pellicle upon fruit is the agent
which directly produces and propagates the disease. Mere immaturity of
fruit gives rise only to diarrhoea. This parasite occurs in some years
more than others, which accounts for the irregularity of occurrence of
the disease. He avers that it is only necessary to clean fruit, more
especially plums, to prevent the disease. This suggestion merits place
only as a curiosity in the history of the mycology of dysentery.

[Footnote 4: _Journal f. Kinderkrankheiten_, No. 317.]

More important are the results of the experiments of Rajewski (1875),
who found the lymph-spaces filled with bacteria, and who was able to
produce a diphtheritic exudation upon the surface and in the substance
of the mucous membrane of the colon by the injection of fluids
impregnated with bacteria into the bowels or blood of rabbits; but this
result was only obtained when the mucous membrane had been previously
irritated or brought into a catarrhal state by the introduction of
dilute solutions of ammonia. It remains for subsequent investigation to
confirm these highly significant conclusions, which, when properly
interpreted, may explain the action of the predisposing and exciting
causes of the disease. Rajewski's bacteria, it is needless to state,
were simply the bacteria of common putrefaction. Lastly, Prior (1883)
describes a micrococcus as the special micro-organism of dysentery, and
Koch (1883), in prosecuting his studies of cholera in Egypt, remarks
incidentally upon a special bacillus which he encountered in the
intestinal canal in dysentery, though he is as yet by no means prepared
to ascribe to it pathogenetic properties.

The question of contagion hinges upon the specificness of the disease,
and cannot be definitely determined until this problem is finally
solved. The old writers believed in the contagion of dysentery.
Helidaeus {794} declared that he "had often seen it communicated by the
use of clyster-pipes previously used in the treatment of those
suffering with the disease, and not properly cleaned;" and Horstius and
Hildanus speak of the communicability of the disease from the latrines
contaminated by dysenteric excreta. Van Swieten maintained that
washerwomen contract it, and that physicians and nurses might be
affected. Degner saw the disease spread from street to street in
Nimeguen, while every one who came in contact with the disease became
affected. Pringle observed it spread from tent to tent in the same way;
and Tissot went so far as to declare, "Sil ya une maladie veritablement
contagieuse c'est celle ci." Ziemssen believed that the disease is only
contagious when the element of crowd-poisoning is superadded; and
Heubner states that trustworthy army surgeons in the Franco-Prussian
War frequently saw infection occur when many severe cases were heaped
together in a small space. Under these circumstances thorough
disinfection of the privies checked the spread of the disease. But it
was the universal testimony of these surgeons, as also of our own
surgeons of the Civil War, that the disease was never transported to
the civil population by any of the tens of thousands of cases on their
return to their homes.

By most modern writers dysentery is given a place, in respect to
contagion, between the exanthematous maladies, typhus and scarlatina,
which are without doubt contagious, and the purely miasmatic diseases,
malarial and yellow fevers, which are without doubt not contagious.
Dysentery is ranked with typhoid fever, which is contagious, not by
contact with the body, but with the discharges. It is not a question in
dysentery of epithelial drift or pulmonary exhalations, but of
ingestion or reception of the dejecta of the disease. By this
observation it is intended to convey the impression that dysentery,
like typhoid fever, is mostly spread in this way, but the reverse may
be true; it may be spread, like yellow fever and malaria, by poisons in
the air. But dysentery, as has been repeatedly remarked, is only a
clinical expression of a disease which may be caused in many ways; and
among these causes, least potent perhaps, but present nevertheless, is
contagion. For, not to mention the epidemics which were undoubtedly
spread in this way, as among the Allies at Valmy in 1792, among the
French in Poland in 1807, and in the hospital at Metz in 1870,
dysentery has been directly communicated by the use of clysters,
bed-pans, and privies in a most unmistakable way.

According to Eichhorst, the poison of dysentery is endowed with
extraordinary persistence of duration or tenacity of life in the
stools; for "observations are recorded where dysenteric stools have
been emptied into privies, and individuals employed to clean them out
after the lapse of ten years have been infected with the disease. These
observations go to prove, of this as of other similar affections
(typhoid fever), that the virus or microbe of the disease finds its
most favorable nidus in vaults, cesspools, sewers, etc. When the poison
is exposed to the air it is much more speedily destroyed, but is in the
mean time of course a possible conveyer of the disease." Fayrer quotes
from an anonymous writer, "whose views are as remarkable for their
force as for their originality," the rather extravagant assertion that
"if human excrement be not exposed to the air there can be no
dysentery."

{795} Knoewenagel has recently[5] opened up a new series of reflections
in his suggestion of a possible direct infection of the large intestine
per rectum, where the disease usually begins and is mostly best
expressed. He calls attention to the fact that people who suffer with
constipation indulge in longer sessions at stools and induce in
straining efforts a degree of relaxation of the rectal mucosa. The
mucous membrane at its orifice may become at the same time abraded by
hardened fecal masses, to leave open surfaces or crevices upon which
germs may lodge. Moreover, aspiration follows the efforts at expulsion,
and the air with its particles is drawn directly into the rectum, thus
affording all the conditions for immediate or direct infection.

[Footnote 5: _Schmidt's Jahrbucher_, Sept. 25, 1882.]

At any rate, it must be admitted that the evidence in favor of
contagion is in some cases too strong to be ignored. A single instance
may suffice for illustration: Flugel reports that the towns of
Nordhaben and Reichenbach, containing together twenty-two hundred
inhabitants, were visited by dysentery in 1873, when nearly four
hundred people were attacked. The visit of a relative carried the
disease from Reichenbach to the daughter of an innkeeper at Tauchnitz,
and from this house the disease spread over the whole place, so that in
a short time more than one hundred people fell ill. Four to six,
sometimes as many as eleven, members of one family were successively or
simultaneously affected. The use of the same bed was the surest means
of contagion.

The duration of the poison was proven in an exquisite case, which is,
however, not entirely free from objection: Two children of an officer
were severely affected in September and October, 1872. In January,
1873, the house was vacated and occupied by a successor in office,
whereupon in April, six months after dysentery had disappeared from the
place, the wife and child of the second officer were affected with the
disease.

To sum up the etiology of dysentery in a few words, it may be said that
few chapters in medicine are so thoroughly unsatisfactory, as the
prospect of reconciling the accumulated discordant facts is very
discouraging. Because of the singular uniformity in the symptoms and
lesions the temptation is strong to look for a common cause, and to
ascribe all cases to this cause, explaining differences by degree
rather than by kind. Such a view would find solid support in the
assumption of a specific germ, and would ally dysentery with typhoid
fever, a disease which has likewise, in all cases, uniform symptoms and
lesions, and which prevails in both sporadic and epidemic form. The
advocates of this view would fix the poison of the disease in the air
and alimentary canal (but not in the blood), and explain the existence
of individual cases, as well as the prevalence of epidemics, by
meteorological conditions as affecting the growth or dissemination of
specific germs. Nor would the adoption of this view exclude the
possibility of producing the catarrhal (sporadic) cases by many kinds
of noxious germs, including those of common putrefaction. Hot air and
wet air are notorious bearers and breeders of germs, and the law of
gravity keeps them near the surface of the earth--conditions which
coincide with the prevalence of the disease in the tropics and among
individuals (soldiers) who sleep upon the ground. If the contagion of
the disease be admitted, the existence of a {796} contagium animatum is
implied at once, for no chemical poison has the power of propagation.

But the germ of dysentery has not been found as yet, and until it has
been found, cultivated in suitable soil, and inoculated to produce the
disease, the evidence of its existence remains merely presumptive.

So that at the present time dysentery must be regarded as a malady
which stands in closer relation to, or finds a better analogue in,
cholera than typhoid fever; for cholera is a disease which has the same
geography, has likewise nearly uniform symptoms and lesions, so far as
it leaves any, and certainly has two distinct forms of origin--one
clearly specific, cholera Asiatica, and the other catarrhal, cholera
morbus.

PATHOLOGY.--Dysentery is a local malady, but, like every local malady
if sufficiently severe, it may show constitutional effects. It is
usually gradually ushered in from a lighter form of gastro-intestinal
catarrh. After a stage of incubation which lasts from a few hours to a
few days symptoms of dyspepsia and diarrhoea set in or increase,
attended with anorexia, heartburn, nausea, eructation or borborygmi,
pain in the abdomen, and copious fluid discharges. Hereupon ensue the
pains and the discharges characteristic of the disease. Violent griping
and colicky pains (tormina) traverse the abdomen, with sickening
sensations of depression. The desire of evacuation of the bowels
(tenesmus) becomes intense and more or less constant, and the discharge
itself is attended with little or no relief. At the same time the
region of the rectum, intensely inflamed, is the seat of intolerable
burning pain, which becomes excruciating with the introduction of a
speculum or the finger.

The discharges may be copious, dark-brown, thin, and highly offensive
(bilious dysentery), may contain occasional hard round fecal casts of
intestinal sacculi (scybalae), or may become more and more scant, until
with the most violent efforts only the minutest quantity is extruded of
mucus, generally streaked or tinged with blood (rose mucus) like the
rusty sputum of pneumonia. Later, all effort at emptying the alimentary
canal may be futile (dysenteria sicca), or the mucus may be pure or
commingled with pus to remain perfectly colorless (dysenteria alba), or
with blood in larger quantity (dysenteria rubra). In other cases, or at
other periods in the same case, the discharges consist of fleshy masses
composed of inspissated mucus or pus, blood, and tissue-debris (lotura
carnea). Sometimes, though rarely, the discharges consist of pure
blood, but oftener of a copious turbid fluid, which on standing
separates into a clear upper layer of serum and a sediment of
disintegrated lotura carnea. Or, lastly, the sediment is composed of
small round vitreous masses, evidently swollen by maceration to look
like sago-grains, which have been erroneously supposed to represent the
liberated contents of the intestinal follicles.

The general condition of the patient suffers correspondingly. There may
be fever or there may be none throughout the whole course of the
disease, but the pain and discharges quickly exhaust the strength of
the patient, and in severe or long-continued cases lead to emaciation
and profound prostration.

The skin is hot and dry; the tongue is heavily coated; the face wears
an anxious expression. The abdomen is tumid with gases, or in more
advanced cases sunken, discolored, and tender, especially in the course
{797} of the colon, whose thickened walls may often be felt beneath the
emaciated surface. The anus is spasmodically constricted, or in the
worst cases paralyzed, patulous, and livid or blue. Prolapse of the
rectum is common in children, and excoriation of the perineum by the
acrid discharges is not infrequent.

Finally, a typhoid state may set in or a pyaemia occur, when the
discharges may become involuntary or unconscious, and brain
symptoms--insomnia, stupor, delirium, and coma--supervene; or the
patient may linger long enough to perish by simple exhaustion or
marasmus.

Under favorable hygiene the great majority of cases of catarrhal
dysentery recover without special treatment in the course of from three
to ten days, but specific dysentery has no definite duration and but
little tendency to spontaneous cure. The worst cases are often quickly
controlled by appropriate interference, and the most surprising results
may be sometimes obtained in cases of even years' duration. On the
other hand, a certain percentage of cases is characterized by a
defiance to every kind of treatment, including the last resort, a
change of climate.

An acute case of catarrhal dysentery generally subsides without
lesions, and the natural duration of the attack may be much abbreviated
by proper treatment. Specific or epidemic dysentery lasts from two to
four weeks, or, becoming chronic, continues for years or for life, with
exacerbations and remissions.

Various complications are liable to occur in the course of the disease.
Three deserve especial mention--viz. affection of the joints
(rheumatism), paralysis, and abscess of the liver. Perforation and
peritonitis, always possibilities, and deformities of the colon,
thickenings, and constrictions, are not infrequently left.

MORBID ANATOMY.--The lesions of dysentery are the ordinary signs of
inflammation of a mucous membrane and its subjacent structures. They do
not differ in any essential way from those of any mucous surface in a
state of inflammation, the minor variations being due to differences in
the anatomy and physiology of the part affected. Thus, a description of
the pathological process in inflammation of the pharynx, bronchi, or
uterus would answer upon the post-mortem table for the same process in
the large intestine, and the finer microscopic lesions could be
differentiated in any case only by the histology of the part affected.

A slight lesion of any mucous membrane constitutes what is known as a
catarrhal process; a more grave affection, a diphtheritic process; a
more chronic inflammation, a hypertrophic or hyperplastic process.
Hence an easy distinction between sporadic and epidemic cases might be
based upon the character of the lesion found. But, as has been stated
already, it is impossible to draw a line between catarrhal and specific
cases, the same lesions being found in either form. The difference, so
far as the morbid anatomy is concerned, is wholly in degree or stage,
and not at all in kind, the specific (epidemic) form presenting the
graver lesion as a rule. So most cases of sporadic dysentery show only
catarrhal lesions, while most cases of epidemic dysentery show
diphtheritic lesions.

Catarrhal dysentery shows as its first obvious alteration a hyperaemia
of the mucous surface. It is limited exclusively to the large intestine
in the vast majority of cases, and only in rare exceptions affects the
small intestine, though cases have been mentioned as curiosities in
which the {798} process has reached the stomach in its upmost
prolongation. The hyperaemia is most marked, as a rule, in the lowest
parts of the large intestine, the rectum and descending colon, but
there is, as Virchow has pointed out, a peculiar predisposition to
affection at the seat of all the flexures, the iliac, hepatic, splenic,
sigmoid, where the additional element of fecal arrest or impaction is
superadded to the cause of the disease.

The catarrhal process occurs first in detached spots or streaks upon
the projecting folds or duplicatures of the mucous membrane; which
spots coalesce to form extensive surfaces. Examined by transmitted
light, these surfaces show a distinct arborescence of the vessels. Or
the disease may commence in the follicles in distinct areas of the
large intestine, and may remain confined to these structures to
constitute the variety known as follicular dysentery.

The hyperaemia of inflammation is attended with dilatation and paresis
of the vessel-walls and retardation of the circulation. The whole
process may be arrested at this stage, so that there escapes from the
vessels, at most, only serum to develop the oedema which, with the
defective nutrition from arrest of the circulation, gives rise to the
softening of the epithelial cells. These cells may be thus lifted from
their bed to constitute the process of desquamation, the fundamental
anatomical characteristic of acute dysentery, by which process the
submucous connective tissue is laid bare and the so-called catarrhal
ulcer results. Or the epithelium, but partially detached, may remain
upon the surface, "either raised in the shape of small vesicles which
contain clear serum, or it forms a grayish-white layer resembling the
mealy scurf of the epidermis--an appearance which probably induced
Linnaeus to term dysentery scabies intestinorum interna" (Rokitansky).

Kelsch maintains that the inflammatory process in dysentery commences
in the delicate connective tissue between the follicles, the network of
small spindle-shaped cells with multiple nuclei becoming speedily
penetrated by a number of very small, newly-formed vessels. Where the
epithelium is desquamated the surface is covered with granulations as
after a wound. The disposition of the follicles is soon deranged, for,
instead of standing in rows like gun-barrels, they are pushed asunder
and uplifted, so as to remain at different heights. Their interior
becomes blocked with mucus or their orifices occluded, so that
retention-cysts are formed to give rise to the appearance of the bead
necklace. Soon the walls of neighboring follicles coalesce, dissolve
away, and communication is established between them. The interior of
these communicating tubes or canals is filled with vitreous mucus; the
walls are stripped of their lining cells, but their "blind extremities
contain still adherent colossal epithelial cells." Moreover, the
follicles break into each other under the proliferative budding
process, so that the end of a distorted tube may be found in the
interior of another. Where follicles are destroyed the mucous membrane
above them or in their vicinity collapses--a condition observed and
described by Colin as effrondement. The mucosa in these regions may
appear perfectly uninjured, but by "blowing upon it with a tube it is
lifted up like an ampulla to show an opening in its centre," though
more frequently the mucous membrane collapses or sinks in at the region
of destruction. The inner surface of the mucosa is rendered
additionally uneven by the elevations or protuberances caused by the
{799} proliferations in the submucous connective tissue. The older
writers (Pringle, Hewson) regarded these projections as tumors of the
mucosa, and Rokitansky, who describes their true nature, speaks of them
as warty, tubercular (nodular) swellings or fungoid
excrescences--constituting a condition, he says, which Gely has termed
hypertrophie mamelonne. The alternate elevations and depressions thus
produced have been likened to the representations of bird's-eye views
of mountain-chains.

As a rule, occasional red blood-corpuscles are also permitted to escape
through the vessel walls in the process of diapedesis to give to the
surface mucus its characteristic tinge, and punctate submucous
hemorrhage is very frequently seen.

The pressure of the swollen, softened mucosa upon the sensitive nerves,
and the irritation of the acrid intestinal contents, are often invoked
to account for the constant desire of defecation (tenesmus) which
constitutes such an essential symptom of the disease; but both the
tenesmus and the colicky pains (tormina) precede the anatomical
changes, and are much more rationally explained by the direct action
upon the nerves of the cause of the disease, or by the derangement of
innervation effected through changes in the circulation.

An acute case of catarrhal dysentery may exhibit no further lesions,
and in the lightest cases even these may have entirely disappeared
post-mortem, so that no change at all may be observed at the autopsy.

In a more severe or protracted case the other alterations which
constitute the more complete cycle of the inflammatory process follow
the stage of hyperaemia. The arrest of circulation becomes more or less
complete, and the white corpuscles emigrate from the vessels to form
the pus-cells. Fibrin, or the elements which compose it, also escapes
to infiltrate the mucous membrane and remain upon its surface. The
pseudo-membranous or diphtheritic process is now developed, and may
vary in intensity from a mere frosting of the surface to dense
infiltration of the entire thickness. The false membrane, as well as
the mucous membrane, next suffers necrosis to form more or less
extensive sloughs. These sloughs are grayish-white when fresh,
dark-brown when stained by the intestinal contents, or greenish or
black when undergoing gangrene. They may cover patches of the mucosa or
the whole mucosa from the ileo-caecal valve to the rectum. They soon
become soft and pultaceous, hang in flaps or festoons in the interior
of the intestinal tube, or, detached, are voided in fragments or
shreds. One such fragment nine inches long is recorded in Woodward's
exhaustive description of the pathology of this disease. Examined under
the microscope, they are seen to consist of coagulated fibrin, red and
white blood-corpuscles, epithelial cells and debris, necrotic pieces of
mucosa, and myriads of micrococci and other micro-organisms.

The fall of the sloughs leaves the dysenteric ulcer. Its edges are
irregular and ragged, its base uneven like a crater, and its surface is
more or less covered with pultaceous debris. The submucous connective
tissue may form its base, or, this structure having been also
destroyed, the muscularis may be exposed, or in more extensive
necrobiosis the peritoneum itself may be laid bare. Occasionally this
last barrier is broken down, and perforation occurs. Or an acute
peritonitis may be developed, in dysentery as in typhoid fever, by
simple extension of the inflammatory {800} process without perforation.
Perforation is very rare in cases of follicular ulceration, and is by
no means frequent in the diphtheritic process, but it is the most
frequent cause of peritonitis in chronic dysentery. It may occur in any
part of the colon, but does occur most frequently in the caecum. The
resulting peritonitis is fatal as a rule, but the danger is obviated
sometimes, as in typhoid fever, by agglutination of the gut to a
contiguous structure or viscus. Perforation usually occurs late in the
disease, but it may occur very early. Thus Nagele reports from the
Franco-Prussian War a case in which perforation took place on the
fourth day, the diagnosis having been confirmed by an autopsy. In rare
cases a perityphlitis may ensue, with its natural consequences, or
periproctitis may be developed with perineal abscess, or, finally,
fistulae may form to burrow about and discharge themselves anywhere in
or upon the surface of the abdomen, the lumbar region, or the thigh.
Bamberger describes cases of perityphlitis attending dysentery, in some
of which resorption occurred, while in others pus was discharged upon
the surface of the abdomen; and the writer of this article once saw, in
consultation with T. A. Reamy, a case of fistula which extended from
the descending colon to the vagina. Through the opening made to
discharge the pus from a fluctuating abscess pointing in the vaginal
vault an india-rubber tube could be passed for six to eight inches. The
patient finally died from marasmus.

Chronic dysentery is distinguished by the alterations which occur in
inflammation developing more gradually and extending over a longer
period of time. Under the irritative changes resulting from an altered
circulation the connective tissue undergoes marked hyperplasia, so that
the wall of the intestine becomes at times enormously thickened, and
its calibre is often correspondingly diminished. Cornil observes that
acute or subacute dysentery is characterized by infiltration of the
submucous connective tissue, followed by destruction, while in chronic
dysentery the predominant lesion is essentially a proliferation and
thickening of the connective tissue of the large intestine. The
muscular tissue also undergoes hypertrophy, and the peritoneum becomes
thickened and opaque. Sometimes the peritoneum is covered with patches
of false membrane, or agglutination occurs with other portions of the
intestine to give rise to contortions or occlusions.

Ulceration shows itself in chronic dysentery in every grade and stage
of the process, from the first denudations to old cicatrizations. In
bad cases the whole course of the colon from the ileo-caecal valve to
the rectum may constitute one vast tract of suppuration. Blood-vessels
may be opened by the necrotic process, and copious, even fatal,
hemorrhage may ensue. When pure blood is discharged, the hemorrhage
usually occurs in this way per rhexem, but the quantities of blood
evacuated with other elements usually escape per diapedesem.

The cicatrization which results puckers the edges of the ulcers, and
may in cases of extensive or circular ulceration lead to more or less
stenosis of the intestinal tube. According to Rindfleisch, the scars of
dysenteric ulcers are very prone to contract, so that "the liability of
a subsequent stricture is directly proportionate to the extent of the
previous ulceration." The danger in these cases may be immediate from
entire, or more remote from partial, occlusion. Thus, Bamberger records
a case of {801} typhlitis due to impaction of feces above a stenosis
gradually developed from a dysenteric ulcer.

Although dysentery is a disease of the large intestine, its lesions are
not exclusively limited to this structure. It is always a purely local
disease at first, and, strictly speaking, continues so throughout its
course, yet it produces in severe or chronic cases widespread and
general effects. Rapid emaciation sets in, and anaemia is soon
pronounced in all the internal organs. The mesenteric glands show signs
of irritation or of absorption of specific products in hyperaemic
pigmentation and hyperplasia. The kidneys in acute cases exhibit venous
stasis, and in chronic cases may undergo parenchymatous change. The
joints are peculiarly liable to suffer in certain cases, and the
nervous system may exhibit lesions--points to be described in the
symptomatology of the disease. Should pyaemia occur, it superimposes
its own particular lesions in the serous membranes and internal organs.
All of these affections are to be regarded, however, rather as
complications than essential effects.

But the liver is found affected so frequently in dysentery as to
constitute more than a mere coincidence. Schneider has recently (1873)
reported of the results of his observations on 1400 cases of tropical
dysentery that in the 395 post-mortem examinations the liver was found
normal in but 10 cases. The abnormalities were as follows: hyperaemia
of various grades, 160; fatty degeneration, 62; abscess, 57; nutmeg
liver, 47; perihepatitis, 25; granular atrophy, 19; syphilitic atrophy,
8; cicatrices, 6; excavation with helminth, 1. Berenger-Feraud (1883)
reports of 411 fatal cases of dysentery observed at Senegal that the
liver appeared sound to the naked eye 98 times (23 per cent.) and
diseased "undeniably" 313 times (77 per cent.). Of the 313 cases of
hepatic affection there were found--hypertrophy, softening, or
hyperaemia, 123 times (39 per cent.); abscess, 143 times (46 per
cent.); simple discoloration, 29 times (9 per cent.); atrophy or
cirrhosis, 18 times (6 per cent.). Annesley found abscess of the liver
21 times in 29 cases of dysentery; Hospel, 13 times in 25 cases; and
Budd found ulceration of the large intestine 10 times in 17 cases of
hepatic abscess. Gluck had the opportunity of making 28 post-mortem
examinations in 151 cases of dysentery in Bucharest, finding abscess of
the liver 16 times. All these authors adopt the explanation first
offered by Budd of direct transfer of diseased products through the
mesenteric and portal veins.

But more extensive observation has developed the fact that the
frequency of abscess of the liver in connection with dysentery is a
peculiarity of tropical climates. In the temperate and colder regions
of the North this complication is not by any means so frequent.
Frerichs declares that of 16 observations collected by Louis and
Andral, "ulcers were present in only 3, and in 2 of these cases the
ulcers were tubercular; of his own 8 cases, there was intestinal
affection in none." Gluck believes that the liver is more prone to show
suppuration when already predisposed to it by a preceding amyloid or
cirrhotic change of malarial origin. Eichhorst calls attention to the
well-known fact that abscess of the liver is especially a disease of
the tropics independently of dysentery, and the frequency of its
occurrence here may be a mere coincidence. But it must be remembered
that opportunity for post-mortem examination, upon the {802} results of
which these statistics are based, does not occur in the great majority
of cases of dysentery, and abscess of the liver is very often
overlooked. Thus, Schneider cites cases where persons with abscess of
the liver of the size of the head were considered simulants up to
twenty-four hours before death. Since the diagnosis of hepatic abscess
has been made so easy by aspiration, cases begin to multiply; and it is
doubtless the experience of most practitioners, in the temperate zone
at least, that the decided majority of cases of hepatic abscess
acknowledge an existing or previous attack of dysentery. Certainly, few
authors would now venture to subscribe to the view of Annesley, that
the abscess of the liver was the primary malady and was the cause of
the dysentery.

SYMPTOMATOLOGY.--Dysentery, as stated, begins, as a rule, with the
general signs of a gastro-intestinal catarrh. So frequent is this mode
of inception, and so few are the exceptions, that it is impossible to
resist the conclusion that the disease is caused by the introduction of
a noxious element into the alimentary canal. The irritation thus
induced begins at the stomach, and is rapidly propagated throughout the
whole tract of the intestine. In the course of a few days the cause of
the disease becomes strictly localized to the large intestine, whose
greater capacity and more sluggish movement fit it for the easier
reception and longer retention of noxious matter.

But specific dysentery and the more intense forms of catarrhal
dysentery occasionally exhibit distinctive symptoms from the start, and
in rarer cases the disease is suddenly announced with such tempestuous
signs as to excite the suspicion of poisoning. Thus, a case (one of
five lighter cases) is reported from the Rudolfstiftung in Vienna
(1878) where the disease closely simulated Asiatic cholera, and where
it rapidly ran a fatal course, in spite of laudanum, soda-water, ice
pills, mustard plasters, injections of amyl nitrite, camphor, and
ether, and faradization of the phrenic nerve to stimulate the failing
respiration. Finger reports similar cases from the hospital at Prague.

Ordinarily, the peculiar pains of dysentery first proclaim the
character of the disease. The severe grinding, twisting pains, tormina,
are more or less localized in the course of the colon, and hence
surround or traverse the entire abdomen, the pains at the epigastrium
being due to spasmodic contractions of the transverse colon. The
patient in vain adopts various postures in relief or sits with his
hands firmly compressing the abdominal walls. The tormina are more or
less intermittent or remittent, and are usually experienced in greatest
severity toward evening. During their acme the face wears the aspect of
the intense suffering, which is expressed in outcries and groans. At
the same time there is upon pressure over the whole abdomen more or
less tenderness, which soon comes to be especially localized at the
caecum or sigmoid flexure.

The tenesmus (cupiditas egerendi) is a more distressing, and certainly
more distinctive, sign of dysentery. It is the feeling of heavy weight
or oppression, of the presence of a foreign body in the rectum, which
demands instant relief. At the same time intense heat is felt in the
rectum, which the patient likens sometimes to the passage of a red-hot
iron. The desire of evacuation becomes as frequent as urgent. In
well-marked cases the patient sits at stool half an hour or an hour at
a time, straining until faint {803} and exhausted, leaving the commode
with reluctance, only immediately or very soon to use it again.

Great depression is felt at the stomach at the same time, with nausea,
occasionally with vomiting; and strangury, with the discharge of only a
few drops of scalding urine or blood from the bladder, adds additional
suffering to the disease. Retraction of the testicle and prolapsus ani,
especially in children, are prone to occur in severe cases.

But neither the pain nor the prostration is so characteristic of
dysentery as the stools, which, though of very varied nature, are
nevertheless distinctive. After the discharge of the intestinal
contents the first evacuations consist of mucus in the form of glairy,
stringy matter, like the white of an egg, expressed as the result of
the violent efforts at straining. The mucus may be pure or tinged with
blood, but it is usually very scant in quantity, and stands in this
regard in marked contrast with the violence of the efforts to secure
its extrusion. It is the frequency of its discharge which constitutes
an especial distress. Twenty to forty, even two hundred, times in the
twenty-four hours the patient must go to stool. In the worst cases the
patient sits at stool or lies upon the bed-pan the most of the day.

The mucus is sooner or later mingled with pus or stained with blood.
The presence of pus by no means necessarily implies the existence of
ulceration, as the apparently pure mucus always shows occasional white
blood-corpuscles under the microscope, and even extensive suppurations
occur without apparent solutions of continuity.

The presence of blood is equally characteristic of dysenteric stools.
Usually it is intimately commingled with the mucus or pus or forms the
chief element of the copious so-called bilious discharge. The
evacuation of pure blood indicates erosion of vessels low in the colon,
often in the rectum itself, though enormous quantities of blood are
sometimes voided from unbroken surfaces. Thus Lecard reports the case
of a soldier who "while sitting restless at stool lost one and a half
quarts of blood." The patient died on the fifth day of the disease, and
at the autopsy there was found "apoplectiform congestion from the
ileo-caecal valve to the anus, but no ulcers anywhere, nor any broken
vessels."

Besides the mucus, pus, and blood, the dysenteric stools contain the
sloughs which have been torn off by violent peristalsis in cases of the
diphtheritic form. Usually they are separated in shreds and fragments,
but occasionally large sheets, even casts of a section of the colon,
are voided en masse. These were the cases considered by the older
authors to be detachments of the mucous membrane itself. As already
observed, these fragments consist for the most part of inspissated
mucus, pus, blood, and tissue-debris; but there is no doubt that in
some cases partially necrosed mucosa also enters into their
construction. One enormous tubular cast fourteen inches long, preserved
in our Army Medical Museum, was found to be "composed of
pseudo-membranous lymph in which no traces of the structure of the
mucous membrane could be detected" (Woodward).

There still remains to be mentioned the boiled-sago or frogs'-spawn
matter whose origin has given rise to such a curious mistake. Not
infrequently these vitreous-looking bodies compose the bulk of the
sediment in the stools of dysentery, and even some of our modern
authors, {804} unacquainted with the more searching investigations of
Virchow, have regarded them as expressed contents of intestinal
follicles. Virchow found that under the application of iodine they
always assumed a blue color, whereupon he ironically remarks that the
sago-like mucus is really mucus-like sago. They are simply granules of
starch ingested as food, to remain partially or wholly undigested.

The scybalae, the composite matter known as the lotura carnea, and the
micro-organisms found in the stools have already received mention
elsewhere.

Although the stools of dysentery are scant, as a rule, they are so
frequent as to discharge during the entire twenty-four hours a very
large quantity of albuminous matter. Oesterlen has made the curious
calculation to show that the mean daily loss of albuminates in
dysentery of moderate intensity is from 50 to 60 grammes during the
first fourteen days, and on an average about 20 grammes during the next
eight days. The total loss experienced in an attack of three weeks'
duration thus amounts to about 1000 grammes--in rough figures, two
pounds avoirdupois. The rapidity with which emaciation, hydrops, and
marasmus occur in severe cases is thus easily accounted for. Nagele
speaks of cases where patients were reduced to skeletons in eight to
fourteen days, so that the convalescence extended over six weeks to
eight months.

The alteration in the character of the secretion in dysentery is not
confined to the mucous membrane of the large intestine. On the
contrary, all the digestive juices are changed, in some cases entirely
checked. In the graver cases the saliva takes on an acid reaction and
loses its glycogenic properties; the gastric juice in the same cases
becomes alkaline and loses its peptonizing properties; while the
secretion of the bile is wholly arrested. Uffelmann, who had the rare
opportunity of studying the secretion of bile in a case of biliary
fistula, relates that during an attack of dysentery the bile ceased
entirely to flow, and only began to show itself again, at first
greenish, then greenish-brown, finally brown, during the process of
resolution on the ninth day of the disease. The anorexia, nausea, and
vomiting which so often mark the access or attend the course of
dysentery find thus easy explanation.

Should the disease continue, the general strength of the patient
becomes so profoundly reduced as to resemble the status typhosus. The
tongue, which has been hitherto thickly coated, now becomes black,
shows fissures, and bleeds, while the gums are covered with sordes. The
pulse becomes feeble, thready, or barely perceptible. The skin is dry
and harsh or scaly. The abdomen is tumid or collapsed, the anus
paralyzed, and the discharges continuously ooze out to excoriate the
perineum. While the brain is usually clear throughout the disease,
insomnia, stupor, or coma develop in the gravest cases from absorption
of disease-products (Senator), or death suddenly ensues from heart-clot
or from thrombus of the venous sinuses of the dura mater (Busey).

Pyaemia announces itself with a series of chills, followed by irregular
temperature, by the speedy occurrence of multiple abscesses in distant
organs, venous thromboses, affections of the serous membranes,
pleuritis, pericarditis, and embolic pneumonia. Gangrene of the
intestine, which may occur as early as the third day of the disease
(Nagele), is evidenced by the signs of general collapse.

{805} COMPLICATIONS AND SEQUELAE.--The lighter cases of dysentery, as
well as most of the grave cases, run their entire course without
complication, and often without sequelae. But a certain percentage of
cases is attended with complications on the part of the joints
(rheumatism), of the nervous system (paralysis), and on the part of the
liver and the kidneys.

Arthritis, when it occurs, shows itself, as a rule, in the second week
of the disease (Eichhorst), or after the disease has run its course,
during the period of convalescence (Huelte). That it is not a mere
coincidence is evidenced by the fact that it is present in a large
number of cases in certain epidemics, while it is not present
independently of dysentery. Thus, Braun of Stannenheim saw in the two
epidemics of 1833-34 more than forty cases of rheumatism, and Huelte
reports ten cases observed by himself in the epidemic at Montargis in
1854. Certain epidemics are distinguished by the rarity of this
complication, while most are marked by its absence altogether. In the
epidemic at Rahden (1872), 400 cases among 3800 inhabitants, Rapmund
saw inflammation of the joints set in only six times; and the entire
absence or extreme rarity of it in later epidemics have led most
physicians to deny any connection between the diseases, or to regard
the joint affection as incident to a complicating scorbutus or
neuralgia. All authors who admit it describe the knee-joint as being
the most frequent seat of the affection, but acknowledge that it is
mostly polyarticular; while there is much difference of opinion whether
it ever presents the general signs of true rheumatism--pyrexia,
diaphoresis, or its complications on the part of the heart. Huelte
maintains that it does not, and that it is allied to gonorrhoeal
rheumatism in this respect, while Eichhorst states that it may not only
show all these signs, but may be followed in exceptional cases by
suppuration and ankylosis. It usually lasts four to six weeks, but
neither its occurrence nor its severity stands in any relation to the
intensity of the attack of dysentery. It is probably to be regarded as
a manifestation of a light pyaemia or septicaemia, as it is a frequent
manifestation of this condition in or after scarlatina, puerperal
fever, and the septic fevers of surgery.

Paralysis has been observed to occur after dysentery ever since the
days of Galen, and, disregarding the observations of ancient and of the
older periods of modern times, we find occasional records of cases in
our own days. Leyden,[6] in reporting a case of paresis and rheumatic
pains following an attack of dysentery, says that although
post-dysenteric paralysis is now rarely mentioned, it was frequent in
the older reports, and claims it as an admitted fact that it occurs not
at all infrequently now. Joseph Frank quotes some observations of this
kind, and refers especially to the dissertation of Fabricius.[7] These
paralyses, Fabricius observes, have been seen after the premature
suppression of malignant epidemics of dysentery by opiates and
astringents. Observations were afterward recorded by Graves in which
paralysis occurred after colics and inflammation of the intestines; and
English veterinary surgeons mention the fact that paralytic weakness of
the posterior extremities of horses and cattle follow attacks of
intestinal inflammation. The paralysis, when it occurs, is usually
confined to the lower extremities, but may extend to {806} and involve
the upper extremities, by preference in the form of paralysis
transversa (opposite arm and leg). Brown-Sequard attributes it to
reflex contraction of the blood-vessels; Jaccoud, to exhaustion of the
nerve-centres; and Roser, to the contact of the inflamed transverse
colon with the solar plexus. Remak first suggested the idea of an
ascending neuritis--a view which would seem to be corroborated by the
paralysis observed after the experiments, by Lewisson, of crushing the
uterus, kidneys, bladder, or loop of intestine, and which finds
additional support, as Leyden remarks, in the length of time which
lapses before it appears. Landouzy[8] says that Finger found diffuse
myelitis in a patient affected with paralysis supervening upon cancer
of the intestine, and that Delioux and Savignac saw spots of softening
in the cervical and lumbar region of the cord in the case of a man
affected with post-dysenteric paralysis. Weir Mitchell suggests the
possibility of other factors--long marches, malaria, bad diet, and
injuries to the spine--in the genesis of the cases, mostly paraplegias,
observed by him; and Woodward calls attention to lead-poisoning (as by
treatment) in explanation of a certain number of cases.

[Footnote 6: "On Reflex Paralysis," _Volkmann's Sammlungen_.]

[Footnote 7: _Paralysis seu hemiplegia transversa resolutionem brachii
unius et pedis alterius exhibet_, Helmstedt, 1750.]

[Footnote 8: _Des Paralysies dans les Maladies aigues_.]

Abscess of the liver gives rise to few distinctive symptoms, and is
mostly recognized or suspected, in the absence of positive signs, by
the persistence or obstinacy of the dysentery. The ease and impunity
with which aspiration may be performed in its recognition justifies the
use of it in every doubtful case.

Regarding complications on the part of the kidneys, Zimmerman
recognizes four classes of cases: (1) mild cases, showing no albumen
and no casts; (2) severe, long-continued cases, with putrid stools,
status nervosus, and collapse, showing albumen; (3) cases commencing
with nervous symptoms, paralysis, scanty urine, showing kidneys filled
with exudation-cells and detritus; and (4) cases of speedy renal
complication and death. To these may be added the cases of protracted
chronic dysentery with long-continued suppuration, entailing the
possibility, of really rare actual occurrence, of amyloid degeneration
and chronic parenchymatous change (Bartels).

Dysentery may be further complicated by parotitis; by venous thrombosis
(phlegmasia dolens); by diphtheritic deposits on other mucous surfaces,
which Virchow declares to be exceedingly rare; and by hydrops, which is
oftener a concomitant of the period of convalescence.

Besides the deformities of the colon, which may ensue as a consequence
of ulceration or peritonitis, a long attack of dysentery is apt to
leave a hyperaesthetic or non-resistant state of the mucous surface, so
that every imprudence in exposure or in diet begets an intestinal
catarrh or a relapse of the disease.

DIAGNOSIS.--When dysentery presents itself with its whole train of
symptoms the recognition of the disease is very easy. The tormina and
tenesmus, the peculiar discharges, the rapid reduction of strength,
leave no doubt as to the nature of the affection. The prevalence of an
epidemic of the disease will often establish the character of a case
even when all the signs are not present or when anomalies occur.
Embarrassment in diagnosis only attends the recognition of catarrhal or
isolated cases, and in these cases there may be a doubt as between
dysentery and {807} diarrhoea--if such a symptom can be called a
disease--or typhoid fever, cholera, or some purely local affection of
the rectum, cancer, hemorrhoids, etc. In children difficulty of
diagnosis may arise as between dysentery and intussusception.

Dysentery is differentiated from that lighter form of intestinal
catarrh whose main symptom is diarrhoea by the presence of tenesmus in
dysentery, as well as by its mucous, muco-purulent, diphtheritic, and
bloody discharges. Dysentery lasts longer than diarrhoea as a rule, and
does not yield so readily to treatment.

Typhoid fever shows from the start brain symptoms, which are absent
from dysentery; has a typical temperature-curve, whereas there may be
no fever in dysentery, or, if any, of irregular remittent type; is
often prefaced by epistaxis and attended with bronchitis, both of which
are absent in dysentery; and exhibits ochre-colored pea-soup stools,
altogether different from those of dysentery.

Cholera morbus distinguishes itself from dysentery by its sudden onset,
its profuse vomiting and discharges, its violent cramps, and the speedy
collapse.

Cancer of the rectum can be usually felt, and hemorrhoids can be always
seen, so that no difficulty should be experienced in the recognition of
these cases.

Intussusception occurs mostly in children, and has, in common with
dysentery, vomiting, mucous or bloody stools, colic, tenesmus, nervous
unrest, and prostration, so that a differential diagnosis may be
impossible for a few days. The more strict localization of an
intussusception, which may sometimes be felt as a sausage-like mass,
most frequently in the right ileum and hypochondrium, the greater
frequency and persistency of the vomiting and pain, the presence
visibly or palpably of the invaginated gut at the anus or rectum, soon
enable the careful examiner to recognize the case.

PROGNOSIS.--The prognosis of dysentery varies between extremes. Some
cases are so mild as to merit the remark of Sydenham concerning certain
cases of scarlet fever: "Vix nomen morbi merebantur." They terminate of
themselves under favorable hygiene without especial treatment. On the
other hand, no known disease has a more frightful mortality than
dysentery in some of its epidemics, especially in army-life. It was
this class of cases which Trousseau had in mind when he called
dysentery the most murderous of all diseases. Sixty to eighty may be
the appalling percentage of death in these cases.

Under favorable surroundings the average mortality of dysentery amounts
to 5-10 per cent., but is much influenced by the age and the general
condition of the patient, as well as by the complications which occur
in its course. Thus, Sydenham said of it over two hundred years ago,
"It is not infrequently fatal to adults, and still more so to old men,
but is nevertheless exceedingly harmless to infants, who will bear it
for months together without suffering, provided only Nature be left to
herself." But dysentery is by no means always harmless to infants, for
in some epidemics this period of life has been visited with the
greatest severity. Thus, Pfeilstucker reports of Wurtemberg (1873-74)
that the greatest mortality, 39 per cent., occurred at the age of one
to seven years, and the least, 4 per cent., at the age of thirty-one to
fifty years; {808} and Oesterlen says of England that dysentery causes
20 per cent. of deaths from all causes in the first year of life.

Nor does the prevalence of a greater number of cases necessarily imply
a heavier mortality. For Bianchi reports of Rome that cases of
dysentery constituted but 2.28 per cent. of all the admissions into the
Ospedale di San Spirito in 1873, while in 1874 the percentage increased
to 3.68; yet the mortality of 1873 was 17.02 per cent., while that of
1874 was but 9.09 per cent.

Complications on the part of the nervous system, the status typhosus,
pyaemia, and great prostration, necessarily render the prognosis grave,
yet even these cases are not necessarily fatal. Thus, Jules Aron
reports from the epidemic at Joigny (1876) a case of recovery after
complete paralysis of the sphincter ani. The recognition and discharge
of an hepatic abscess relieves the patient from the dangers of this
complication. Peritonitis alarmingly aggravates the prognosis, and
perforation is almost of necessity fatal.

PROPHYLAXIS.--The improved sanitation of modern times has already
diminished the frequency and mitigated the severity of epidemics of
dysentery; and this fact, which is only an accidental observation as it
were, gives the clue to the means of its further prevention.

The selection of proper sites for camping-grounds, barracks, and
hospitals, the prevention of overcrowding in tenement-houses, ships,
and jails, the regulation of sewage, the care for the food and drink,
the observation of the strictest cleanliness by authoritative
control,--all these are general measures which suggest themselves in
the prophylaxis of this or any disease.

In the management of individual cases the first precaution is to
prevent the dissemination of the disease. Whether it be really
contagious or not, every case should be managed, as Bamberger suggests,
as though it were contagious; and this protection of others secures for
the individual patient the most favorable hygiene.

The bedding must be frequently changed; the windows kept open to secure
free ventilation, which, in the light of existing knowledge, is the
only true disinfectant; and all the furniture of the sick-room,
especially including the receptacles for the discharges, must be kept
perfectly clean. For this purpose the best purifier is very hot water.
The temperature of the sick-chamber, if it be subject to regulation,
should never be allowed to sink below or rise above 65-70 degrees F.

The drinking-water should be secured, during an epidemic, from the
purest possible source, and if good drinking-water cannot be had, what
there is should be thoroughly boiled.

The discharges should properly be mixed with sawdust or some
combustible substance and burned, or if this be impracticable should be
buried in the soil a few feet below the surface, and not emptied into
water-closets or privy-vaults used by others.

Such articles of food should be abjured as have a tendency to produce
intestinal catarrh. So unripe fruits, vegetables which readily undergo
fermentation--in short, all indigestible substances--should stand under
ban. But no prohibition should be put upon ripe fruits or simple
nutritious food of any kind.

Lastly, individuals should protect themselves from catching cold. The
{809} researches of Pasteur have disclosed the fact that certain germs
of disease will grow and multiply in the body of an animal whose
temperature is reduced, when they would not increase without it.

TREATMENT.--The first requisite in the treatment of an individual case
is perfect rest. Patients with even the lighter forms of catarrhal
dysentery should observe the recumbent posture, and cases of more
serious illness should be put to bed. Rest in bed, an exclusive diet of
milk--which should always have been boiled--and the time of a few days
is sufficient treatment for the mildest cases. Where there is objection
to milk, meat-soups, with or without farinaceous matters, rice, barley,
etc., may take its place.

A case which is somewhat more severe will require perhaps a light
saline laxative--a Seidlitz powder, a dose of Rochelle salts or Epsom
salts in broken doses--or a tablespoonful of castor oil or five to ten
grains of calomel, to effect a cure. For the relief of the pain of the
lighter cases nothing is equal to tincture of opium, of which five to
ten drops every three or four hours in a tablespoonful of camphor-water
acidulated with a few drops of nitric acid will generally suffice; or
Dover's powder in broken doses, one to three grains, with five to
fifteen grains of bismuth or soda, or both, is a good substitute for a
change.

The successful treatment of dysentery in any form depends upon a
recognition of the fact that the disease is local as to its seat, and
is probably specific as to its cause. The anodynes relieve the effects,
but the laxatives remove the cause. Consequently, the most rational
treatment of the severer cases is the irrigation of the large intestine
and the thorough flushing out of its contents. The use of clysters in
the treatment of dysentery dates from the most ancient times, with the
object, however, rather of medicating than washing out the bowel.
O'Beirne (1834) and Hare (1849) were the authors of the irrigation
treatment, which they executed by means of a long tube introduced into
and beyond the sigmoid flexure. Since Hegar has recently shown how the
whole tract of the large intestine can be thoroughly inundated and
flushed with a common funnel and rectal tube, the practice has
continually gained ground, until it is now admitted as the most
valuable method of treatment. H. C. Wood of Philadelphia, and later
Stephen Mackenzie of London, have reported a number of cases in which
irrigation of the bowel with large injections medicated with nitrate of
silver, drachm j-pint j, was attended with the most surprising
results--sometimes but a single injection effecting a cure; and the
writer of this article has reported one case almost in articulo mortis
where complete cure followed the irrigation of the bowel--on three
occasions with three pints of water containing three drachms of common
alum. This case was all the more instructive from the fact that a
relapse had occurred after very striking but only temporary relief had
been obtained with the nitrate of silver, the alum having been
substituted simply on the ground of expense.

Salicylic acid has also been extensively employed in this way with the
best effects, but carbolic acid has been discarded since the reports of
several cases of poisoning have been published. Should it become a
question of the necessity of a parasiticide, the bichloride of mercury
in extremely dilute solution, 1 to 1000, would be the agent par
excellence; but it is probable that the simple flushing of the bowel is
the chief {810} curative agent. The use of alum is not attended with
the dangers which have ensued from the absorption of carbolic acid, and
which might ensue from the bichloride of mercury. The water used in the
injections should always be cold. Ice-water injections alone give at
times the greatest relief. Wenzel uses injections of ice-water in all
recent and acute cases, whether slight or severe--in bad cases every
two hours. He seldom finds it necessary to use opium. The object is to
introduce as much water as possible without producing too much pain.
The large intestine of an adult holds, on an average, six imperial
pints, but in the author's experience not more than three or four pints
can be safely introduced. The patient should lie upon the back or the
left side with the hips elevated and the head low, while the injection
is slowly introduced from a funnel, fountain, or a bulb syringe whose
nozzle is thoroughly anointed with vaseline. In the absence of a
thoroughly competent assistant the operation should be performed by the
physician himself, for the proper use of an irrigating enema is a
practice which requires both judgment and skill. When pain is
experienced, the further influx of the fluid should cease for a few
minutes, when it may be resumed again and again until the largest
possible quantity is introduced. It is impossible to over-estimate the
value of this treatment in cleansing, disinfecting, and constringing
the foul and flabby surface of the whole seat of the disease. As was
said by Hare, "It changes a huge internal into an external abscess, and
enables us to cleanse the bowel of its putrid contents."

Of all the remedies which have been recommended in the relief of
dysentery besides the irrigation method, but one, ipecacuanha, deserves
the name of a specific. This remedy was first introduced into practice
in 1648 by the botanist Piso, who was led to adopt it from the popular
praise he had heard of it while travelling in Brazil. He considered it
the most exquisite gift of nature, and administered it in infusion
according to the Brazilian (subsequently known as the French) method.
Legros made three successive voyages to South America to import
supplies of the drug to France, but neither he nor the French merchant
Grenier, who had brought over more than one hundred and fifty pounds of
it, could secure its general use. Thereupon, Grenier acquainted Adrian
Helvetius, a Dutch physician practising in Paris at the time, with the
wonderful virtues of the Radix dysenterica, who, having experimented
with it first upon patients of the lower classes, was later successful
in curing the Dauphin of France. The further use of it, by permission
of the king, at the Hotel Dieu, enabled him to secure a monopoly of its
sale and secured for him a grant of a thousand pounds. Grenier hereupon
put in his claim for a division of the profits, and upon the refusal of
Helvetius instituted suit to obtain his rights. Justly indignant at the
loss of his suit, he revealed the secret, and ipecacuanha became common
property at once. Extravagant ideas were now entertained of its value,
but in the extreme reaction which followed every virtue of it was
disavowed, so that the drug came to be almost forgotten. From this
temporary oblivion the remedy was rescued by an English army surgeon,
E. Scott Docker, in 1858, who administered it, in combination with
laudanum, in his regiment, on the island of Mauritius, in all cases and
stages of the disease with such success that out of fifty cases he lost
but one. Although such indiscriminate use and such almost unvaried
success has not attended, and from the nature {811} of different cases
could not attend, its universal employment, there is no doubt of the
inestimable value of the service rendered in the restoration of the
remedy in the treatment of dysentery. Yet over twenty years elapsed
before its author received from his country, at the urgent solicitation
of the Director-General, in recognition of this service, a grant of
four hundred pounds.

Remarkable testimony as to its efficiency soon began to appear.
Ewart[9] recommends ipecacuanha in every form and type of acute
dysentery, as well as in the acute attacks supervening upon chronic
cases. Its advantages are simplicity, safety, comparative certainty,
promptitude of action, decrease of chronic cases and of complications,
especially abscess of the liver, and great reduction of mortality. "It
produces all the benefits that have been ascribed to bloodletting,
without robbing the system of one drop of blood; all the advantages of
mercurial and other purgatives, without their irritating action; all
the good results of antimony and other sudorifics, without their
uncertainty; all the benefits ascribed to opium, without irritating, if
not aggravating or masking, the disease." To the objections urged
against it he replies that the nausea is only temporary and
evanescent--that vomiting is exceptional and of but short duration;
moreover, it permits nourishment and assimilation and produces sleep.
If uncontrollable sickness and vomiting occur, they are probably due to
abscess of the liver, malaria, some other cachexia, Bright's disease,
strumous mesenteric glands, hypertrophy of the spleen, peritonitis, or
extensive sloughing.

[Footnote 9: _Indian Annals Med. Science_, April, 1863.]

Cunningham prefaces the treatment by a sinapism to the epigastrium and
half a drachm of the tincture of opium. Then from one to one and a half
drachms of ipecacuanha are administered in powder. It causes
considerable nausea, and vomiting occurs in one to two hours. During
the nausea copious perspiration breaks out, the pulse becomes fuller,
softer, and less frequent, the tenesmus and abdominal pains cease, and
the patient has no more stools for twelve to twenty-four hours. The
next evacuation is easy, fluid, but free from blood or mucus. Sometimes
the dose of ipecacuanha may require to be repeated.

Malun reports the results of treatment of 436 cases occurring in
twenty-one months. There were only 6 deaths, and in only 1 of these
could the remedy be fairly said to have failed. Under all other plans
of treatment the mortality has varied from 12 to 22.3 per cent.

Mr. Docker says that the mortality of dysentery in the British army
during the ten years that followed the adoption of the ipecacuanha
treatment fell from 11 to 5 per cent.

The remedy is best administered in large doses, 20 to 40 grains, and
should be repeated every four to twelve hours until permanent good
effects are secured. A dose of 15 to 30 drops of tincture of opium, or
morphia, one-fourth grain hypodermically, will best protect the patient
from too great exhaustion. The beneficial results are mostly obtained
in the acute cases, though surprising results sometimes follow in cases
of very long standing. Thus, Gayton records a case of severe chronic
dysentery of eighteen months' duration which was entirely cured by
ipecacuanha, and probably most physicians of large practice can recall
cases where the continual relapses of the dysenteric habit have been
completely broken up by {812} one course of active treatment. Should
the remedy fail to be of service in the course of forty-eight hours, it
should be discontinued.

Batiator, the bark of the root of the Ailanthus glandulosa; mudar, the
bark of the root of the Calotropis gigantea; and bael-fruit, more
especially in chronic cases,--have been proposed by Roberts, Duval,
Chuckerbutty, and others as substitutes for ipecacuanha, but are not
likely to soon supplant it.

Materia medica is rich in drugs whose virtues have been vaunted in
dysentery, and cases occur where the judicious physician will make his
selection according to the indications in a given case. Turpentine
internally, as well as externally in the form of a stupe (Copland), has
had advocates from ancient times; astringents, tannic acid or the
substances which contain it, kino, catechu, krameria; the acetate of
lead, nitrate of silver, etc.; antiseptics, carbolic acid, salicylic
acid, boracic acid; anodynes, opium and its preparations; and
quinia,--are among the agents most frequently employed.

Bonjean (1870) had occasion to laud the efficacy of ergotin in checking
hemorrhage and controlling the discharges in a report which
substantiates the claim of Rilliet and Lombard in the epidemic at
Geneva in 1853. Massolez had the same good results in the war of the
Crimea, as had also Andrea in the Spanish hospitals of Ceuta and
Tetuan.

Clysters of nitrate of silver, 4 grains to 5 ounces of water (Duchs),
or with a few drops of tincture of opium (Berger); of ipecacuanha
(Begbie and Duckworth); of laudanum and starch (Sydenham, Abercrombie);
of the various astringents,--may be tried in obstinate, more especially
chronic, cases.

Local inspection of the rectum by means of the speculum may possibly
reveal an ulcer, which is the chief or sole cause of the tenesmus and
bloody discharge. Maury reports such a case in which the ulcer was deep
enough to hide a small sponge. In such cases topical treatment may
effect a cure.

Dilatation may suffice to overcome a stricture in the rectum, the
result of cicatricial contraction, or colotomy may be necessary in
cases more refractory or situated higher in the bowel. Post[10]
reported a successful colotomy, with the formation of an artificial
anus in the left lumbar region, in such a case.

[Footnote 10: _New York Med. Record_, 1879, xvi. 24, p. 260.]

The food should be fluid, but nutritious, and milk best fulfils both
these requisites. Where milk cannot be tolerated it may be substituted
by soups, beef-tea, mutton-broths, chicken-soup, etc. But it should be
known of these substitutes that they contain little or no nutritious
matter on account of the insolubility of the albuminoids, and are
really only stimulants. Soft-boiled egg, thin custards, sweetbreads,
scraped or chopped raw beef--albumen thus in substance--constitute the
best food. But during the intensity of an attack the patient should
almost altogether abstain from food, both from lack of inclination for
it and from lack of ability to digest it. During convalescence the food
should be on the basis of animal diet, though ripe fruits and fresh
succulent vegetables should not be altogether withheld.

In all cases of pronounced prostration stimulants are to be freely
used, and of all stimulants alcohol is the best, as it has also
nutritive and {813} antiseptic properties. Alcohol is thus triply
indicated in the treatment of dysentery, but the choice of the form and
strength will be a matter of judgment in the individual case.

Where life is imperilled by hemorrhage or anaemia from any cause, a
forlorn hope is offered in transfusion, which in the hands of C.
Schmidt (1874) has proved successful in two cases.

Abscess of the liver is best treated by aspiration or hepatotomy;
rheumatism, by the salicylates; and paralysis, by the constant current
of electricity.

Obstinate cases of chronic or continually recurring dysentery are
thoroughly cured only by a sea-voyage, a sojourn at the seashore, a
mountain-excursion, or a permanent change of climate.




{814}

TYPHLITIS, PERITYPHLITIS, PARATYPHLITIS.

BY JAMES T. WHITTAKER, M.D.


HISTORY.--Typhlitis ([Greek: typhlos], blind), inflammation of or about
the head of the colon, more especially the vermiform process, is a
disease of modern recognition. Individual cases had been reported as
curiosities where foreign bodies or fecal accumulations had excited
inflammation in this part of the intestine, but it is undoubtedly to
Dupuytren[1] that the credit is due of having first individualized this
disease as a separate affection. About the same time (1827) Longer
Villermay published his communications in the _Archives gen._, t. v.
246, on the diseases of the vermiform process, to be followed in the
same year by Melier[2] and Hussar and Dance with observations on
inflammation of the connective tissue in the region of the caecum.
These affections, which had been hitherto described as inflammatory
tumors in the right iliac region, now received from Puchelt[3] the
distinct name perityphlitis.

[Footnote 1: _Lecons oral de Cliniq. chirurg._, t. iii. art. xii.]

[Footnote 2: _Arch, gen._, Sept., 1827.]

[Footnote 3: _Heidelberg klin. Annal._, i. 571 and viii. 524.]

Perhaps the most remarkable events in the history of these affections
since this time are the contributions of Stokes and Petrequin (1837) on
the value of opium in the treatment of perforation of the vermiform
appendix, of Albers,[4] who first distinguished the special form of
typhlitis stercoralis, and of Oppolzer (1858-64), who set apart,
perhaps as an unnecessary refinement in differential diagnosis, a
paratyphlitis, an inflammation of the post-caecal connective tissue.
Matterstock[5] (1880) deserves especial mention for having given such
prominence to anomalies of the vermiform appendix in the etiology of
the affection; and Kraussold[6] (1881) has connected his name with the
therapy of the disease by the boldness with which he expresses his
convictions regarding the necessity of early evacuation, by incision,
of inflammatory products, as first practised by Willard Parker in 1843.

[Footnote 4: _Beobacht. aus dem Gebiete der Pathologie_, ii. 1.]

[Footnote 5: _Handbuch d. Kinderkrank._, Bd. iv. p. 893.]

[Footnote 6: _Volkmann's Sammlung._, No. 191.]

GENERAL REMARKS.--Typhlitis, strictly speaking, is limited to
affections of the caecum and its appendix vermiformis; perityphlitis is
mostly due to extension of the inflammation to the peritoneal envelope
of these organs; while paratyphlitis signifies an involvement of the
extra-peritoneal and post-caecal connective tissues. Both perityphlitis
and paratyphlitis are therefore secondary processes, though they may,
in exceptional cases, arise from affections of organs other than the
caecum, as from {815} perinephritis, psoitis, vertebral caries, or as
an expression of metastatic processes in pyaemia, septicaemia
(puerperal fever), typhoid fever, etc.

ETIOLOGY.--Typhlitis and its allied affections or complications show
especial predilection for the male sex and the period of adolescence.
Nearly three-fourths (733) of the whole number (1030) of cases of
perityphlitis collected from the literature by Matterstock were males,
and this proportion holds good in infancy and early youth as well as in
adolescence. The greatest number of cases, 33 per cent., occurred at
the ages of 21-30; next, 30 per cent., at 11-20; while the ratio
gradually decreases toward both extremes of life. So the opinion is
expressed with singular unanimity by all authors that these diseases
pre-eminently affect the bloom of life.

The observation that typhlitis has so often been found to arise from
disease of the vermiform process has led to a closer study of its
anatomical relations, and developed the fact that this organ is subject
to great variation in size, shape, and situation.

Normally, the appendix vermiformis arises from the posterior interior
aspect of the caecum as a tube of the diameter of a goosequill and a
length of three to six inches, with a general direction upward and
inward behind the caecum. It is commonly provided with a small
mesentery, which retains it in its place. Its cavity communicates with
the cavity of the caecum by a small orifice which is at times guarded
by a valvular fold of mucous membrane, while its free closed end
terminates abruptly in a blunt point. It is commonly found filled with
mucus throughout its entire length. The existence of this superfluous
structure, which is found only in man and certain of the higher apes,
has given rise to much speculation among the anatomists and
physiologists, especially of the teleological school, as to its
possible use. It is now, however, the generally acknowledged opinion
that the appendix vermiformis is a relic or rudiment of a subsidiary
stomach in lower forms of life. The head of the large intestine, which
forms almost an additional stomach in the Gramnivora, and is three
times the length of the whole body in the marsupial koala, is very much
reduced in the Carnivora, whose food contains but little indigestible
matter, and is greatly reduced in the Omnivora, as in man. The
vermiform appendix is the shrivelled remnant of the great caecal
receptaculum of the lower animals. In the orang it is still a long
convoluted tube, but in man it is reduced, as stated, to the size of a
quill three or four inches in length, and is often entirely absent.

Kraussold, who complains that the vermiform process has hitherto
received only step-motherly treatment at the hands of anatomists and
clinicians, undertook a series of investigations which went to show how
often and what extreme anomalies do occur. In some cases the appendix
was disposed in an exactly opposite to the normal direction, its blind
end being turned upward along the ascending colon. In one case it was
found wound about the ileum; in another, spirally turned at its end and
lightly adherent to a hernial sac. Sometimes it was abnormally long or
short, open or closed with a valve, cylindrical, saccular, or bulbed,
fixed or free, curved or bent upon itself at a sharp angle, provided
with a short mesentery, and sometimes, as stated, it was entirely
absent.

But by far the most interesting point connected with this organ was the
frequency with which it was found the seat of ulceration or stricture
{816} from cicatrization somewhere in its course, the result of
dysentery, typhoid fever, syphilis, and more especially of
tuberculosis. Clinicians who have been struck with the frequency with
which typhlitis has occurred in tuberculous subjects find in this
discovery a satisfactory explanation of this very remarkable
coincidence.

Normally, the vermiform appendix is found filled, as stated, with a
tough vitreous mucus, but not infrequently masses of feces, foreign
bodies, intestinal worms, etc. find their way into it, where they may
remain innocuous or may excite a dangerous inflammation. This fact, in
connection with the general uselessness or superfluousness of this
structure, has led pathologists to characterize the vermiform process
with the significant appellation of a death-trap.

Two anatomical factors deserve especial emphasis in explanation of the
frequent origin of disease in the vermiform appendix. One is the
existence of the valvular fold of mucous membrane, already mentioned,
at or near the orifice of the tube in the caecum, the clinical
importance of which was first pointed out by Gerlach. This fold is most
marked between the ages of three and twelve, and when pronounced
narrows the orifice to one-half or one-third of the whole calibre of
the tube. As a rule, this fold, and the consequent diminution in the
size of the orifice, are but little marked in the first years of life
and in old age, which accounts for the relative infrequency of
typhlitis at these periods of life.

The second mechanical factor is the deformity caused by the abnormal
anatomical position of the organ, either as a congenital defect or as a
pathological change. Matterstock quotes from Zungel, who observed in 59
cases in the Hamburg hospital whole or partial obliteration 30 times,
catarrh and old fecal concretions 43 times, abnormal adhesions 12
times, and tubercular ulceration (without perforation) 11 times. Toft
claims as the result of 300 personal investigations that every third
person between the ages of twenty and seventy showed the traces of
present or past inflammation, and that actual ulceration existed in 5
per cent. of all bodies examined. Kraussold declares that this
percentage is rather too low than too high, and adds that among his
patients--who were, it should be stated, mostly phthisical--it was
remarkable how extraordinarily often the whole vermiform appendix was
the seat of an encroaching ulcer. In a number of cases cicatrices or
cicatricial alterations were found where typhoid fever or dysentery had
existed in the previous history.

Attention should at least be called to a last anatomical factor in
explanation of the frequency of ulceration and inflammation of this
structure, in that its walls are so sparsely endowed with muscular
tissue as to render it unable to empty itself of the virus or germs of
disease which enter it from the comparatively stagnant reservoir, the
caecum.

Constipation is usually invoked as a cardinal factor in the genesis of
typhlitis (typhlitis stercoralis). Speck calls attention to the
frequency of the disease in East Siberia, where the food, mostly
vegetable, contains a large amount of indigestible residue. But that
this condition cannot sufficiently account for the disease in most
cases is proved by the fact that constipation is more frequent in
advanced life and among females, in whom typhlitis with its associate
lesions is more infrequent. For the same reason a sedentary mode of
life loses force as an argument in its production. Perhaps the most
efficient cause of the condition is a local {817} paresis of the
muscular tissue of the caecum produced by the irritation of intestinal
catarrh, of disease virus, of a fecal concretion or a foreign body--an
irritation which may induce first a spasmodic action, and subsequently,
as a result, a partial paralysis or a paresis. The same condition may
be brought about more directly by the presence of a centre of
irritation--viz. by reflex inhibition of innervation. Accumulation and
impaction of feces must then necessarily ensue, and it is highly
probable that this accumulation occurs in this way as a result more
frequently than as a cause of the condition. For the symptoms of a
simple accumulation of feces (coprostasis) are never so severe, at
least at the start, as to mark the onset of a genuine typhlitis. Nor is
there anything in healthy feces to induce the signs of a severe
blood-poisoning which so commonly announces the advent or course of
typhlitis.

Room is here open for the surmise that most cases of typhlitis pur et
simple are due to the presence in the caecum of the germs or virus of
disease taken with the food or drink, and traversing innocuously the
whole length of the alimentary tract, to finally bring up in this most
stagnant part of the intestinal canal.

The role of pure mechanical causes cannot be ignored or underrated in
perityphlitis, understanding by this division processes which commence
in the vermiform appendix. For it is the rule to discover in the
vermiform appendix in these cases either fecal concretions or foreign
bodies. Haeckel and Buhl found concretions of meconium in a new-born
child, and fecal concretions, intestinal stones, are far more
frequently encountered than foreign bodies. In 146 accurately observed
adult cases recorded by Matterstock, fecal concretions were met with 63
times, foreign bodies 9 times, while in the other cases nothing could
be discovered; and in 49 cases among children, fecal concretions were
discovered 27 times, foreign bodies 3 times, and nothing abnormal in
the remaining cases. Not infrequently a small foreign body acts as a
centre of crystallization for feces which become superimposed in
successive layers. Hairs, as of the beard, sometimes officiate in this
way. Among other foreign bodies met with in fatal cases of perforation,
independently of feces, may be mentioned round-worms (Faber),
cherry-stones (Paterson), needles (Payne), fish-bones (Zungel),
gall-stones (Hallete), a mass of ascarides (Klebs), buttons (Gerhardt),
etc., etc. As already intimated, supposed foreign bodies are often
found on examination to be nothing else than intestinal concretions. As
to cherry-stones, which are so often accused of producing typhlitis,
Biermer and Bossard found it difficult or impossible to force them into
the vermiform process.

MORBID ANATOMY.--The lesions revealed upon the post-mortem table show
for the most part the ordinary picture of perforative peritonitis,
which is by far the most frequent cause of death. The peritoneum in the
vicinity of the perforation is found hyperaemic, swollen, necrosed,
covered with flakes of soft fibrin, or partially agglutinated to
contiguous structures. The wall of the bowel is very much thickened by
catarrhal swelling of its mucosa, proliferation of its submucous tissue
in more chronic cases, oedema of all its coats, or suppurative
processes. Not infrequently the mucous tissue is the seat of extensive
ulceration which may involve other structures of the gut or form an
abscess, even as large as a man's head, in its immediate vicinity. The
abscess may remain strictly localized or {818} may wander to discharge
itself into the ileum, caecum, duodenum, and diaphragm (Bamberger) with
resultant empyema (Duddenhausen), colon (Prudhomme), bladder (Bossard),
in which case the fecal concretion became the nucleus for a vesical
stone; acetabulum (Aubry), inferior vena cava (Demaux), or peritoneal
cavity, the most frequent eventuality. Duddenhausen saw in one case a
pylephlebitis result, Von Buhl a pylephlebitis and metastatic liver
abscess, which condition, Matterstock says, is noted 11 times in 146
autopsies; and older writers speak of discharges into the pleural sac,
into the lungs, pericardium, uterus, vagina, etc. A curious case was
observed by Eichhorst in Frerichs' clinic, where pus found escape
through the umbilicus. So cases of burrowing sinuses with abscesses at
distant seats, as in the groin or lumbar region, fistulae with
continuous discharge, and other curiosities, may be found among the
records by the curious.

In cases of more acute course the lesions are often found centred about
the vermiform appendix. The most various contortions, adhesions, or
erosions are observed in this structure. Occasionally a constriction
occludes the course of the tube, while the distal end is dilated into a
condition of hydrops. It may be found perforated in one or in several
places. The cicatrices or agglutinations of old attacks may be
encountered; it may be cut in two or three pieces (Matterstock), or
have been entirely absorbed. Kraussold records a case of this kind in a
colleague who died of typhlitis. Upon the post-mortem table no trace of
the vermiform appendix could be encountered except a dimple on the
mucous surface of the caecum, indicating the site of its former
orifice.

SYMPTOMATOLOGY.--Typhlitis announces itself in two ways--suddenly and
insidiously. In adults the disease begins as a rule with violent signs;
in children there is often a prodromatous stage which may last for days
or for months before a positive diagnosis can be established. There are
in these cases anorexia and vomiting, constipation and diarrhoea,
colicky pains, mostly concentrated about the ileo-caecal region. There
are at this time a disinclination to stand or walk, a stooped posture
or gait, occasionally a light icterus, a feeling of formication or
paresis in the right leg, and lastly an increased resistance or a
palpable tumor in the right ileum.

In the adult the disease is wont to begin with more tempestuous signs.
Not infrequently it is ushered in with a well-marked chill, upon which
immediately supervenes a sharp pain at the affected region. A general
collapse of strength soon follows, with fever, thirst, a husky voice, a
coated tongue, vomiting, singultus, and an expression of anxiety. The
impression of serious illness becomes apparent at once. The case early
bears the aspect of a grave infectious disease. A constant, dull,
boring, gnawing, or lancinating pain in the right iliac region first
excites the suspicion of the physician as to the real nature of the
disease. In children the pain is sometimes felt first in the
epigastrium; in three cases mentioned by Buchner, Herzfelder, and
Traube it was first experienced in the left ileum. There may be at this
time no tumor, but there is increased resistance to pressure and
exquisite tenderness to touch in the neighborhood of the caecum. The
whole abdomen is more or less tender, and often tumid. If there should
be also gurgling from displacement of gas, doubt is excited as to the
possible existence of typhoid fever.

{819} In the course of a few days the tumor takes shape. A typhlitis
stercoralis shows a distension of the whole ascending colon, a
sausage-shaped tumor, smooth or nodulated, along the entire right side
of the abdomen, with increased resistance also in the transverse colon.
More frequently in typhlitis--and, as a rule, in peri- and
paratyphlitis--the tumor or tumefaction is more localized about the
head of the colon. Frequently the swelling is so great as to be visible
as a protrusion or bulging of the affected region. Percussion shows
dulness, tanquam femoris, in cases of pure typhlitis, whereas in peri-,
and more especially in paratyphlitis, there is tympanites on light and
dulness only on deep percussion. Palpation or palpatory auscultation
occasionally, though very rarely, reveals a peritoneal friction sound
(Gerhardt).

The third cardinal symptom of the disease is the disturbance of
digestion, which, as stated, often precedes or attends the first
manifestation of the pain and the tumor. Anorexia, nausea, and
vomiting--which is in the last stage of the disease often substituted
by singultus--present themselves as occasional or constant signs of the
disease. Constipation remains as a rule throughout the whole course of
the disease with an obstinacy which sometimes excites apprehension of
an intestinal occlusion; or the constipation may alternate with
diarrhoea or dysenteric phenomena, more especially in the earlier
stages. The tongue is, as a rule, heavily coated, or in typhoid states
is dry, glazed, or fissured, and sordes covers the teeth and gums.

Fever is not a necessary factor in typhlitis, but when present
distinguishes itself by its irregular range. The pulse is usually
accelerated, full, and hard; the skin is dry and harsh; the urine is
scanty and high-colored, and contains "almost without exception
unusually large quantities of indican" (Eichhorst).

Perforation, when it occurs, is usually recognized at once by the signs
of more or less immediate collapse, which quickly results in death.

The abdomen becomes suddenly distended, meteoric over its entire
surface, the normal hepatic dulness giving place to a tympanitic
resonance.

Not infrequently perforation occurs as the result of an accident, as
after a push or blow upon the abdomen (Volz), heavy lifting
(Volperling), riding in a wagon (Marsh), after dancing (Cless), mere
turning of the body in bed (Langdon Downs), after emesis (Urban),
purgation (Stokes), enema (Melier), etc., etc. That the slightest
agitation may suffice at times to break down the last barrier of serous
tissue separating the intestinal and peritoneal cavity is shown in the
case recorded by With, where fatal perforative peritonitis occurred
after a fit of immoderate laughter.

Paratyphlitis distinguishes itself from the other forms of the disease
by its more insidious character. There is also in paratyphlitis, as a
rule, less disturbance in the alimentary canal. The caecum in
paratyphlitis is mostly empty or is filled with gas, whose presence is
recognized by tympanitic resonance on lighter percussion. On the other
hand, paratyphlitis is characterized by the greater frequency of
pressure signs in the right lower extremity. If the subjacent iliac and
psoas muscles be implicated, the thigh is flexed upon the leg in
decubitus. Various paraesthesiae, formication, numbness, pain, and
veritable paresis are experienced in the right leg. Dysuria, retraction
of the testicle, and priapism may also occur in this form of the
disease. Or pressure upon the iliac vein {820} induces thrombosis, with
oedema, milk leg. The long-continued process of suppuration in
paratyphlitis leads also at times to hectic fever or pyaemia, with slow
marasmus.

In all cases relapses are very frequent, as repeated occurrences of the
disease constitute the rule. Eichhorst records the case of a
court-officer who suffered five attacks of paratyphlitis in the short
space of one and a half years.

DIAGNOSIS.--The recognition of the disease is mostly simple. The pain,
the tumor, and the disturbances of digestion sufficiently, and for the
most part sufficiently early, distinguish the affection.

Simple impaction of feces is differentiated by the history of
constipation; by the feel of the hardened feces, which form an
elongated, nodulated, sausage-shaped tumor along the entire ascending
colon, and later in shifting along the transverse colon; by the
comparatively slight tenderness; and by the entire relief which follows
thorough irrigation of the bowel.

Cancer may be eliminated by regard of the age of the patient, the slow
development and course of the symptoms, and the gradual manifestation
of its cachexia.

Invagination is an affection for the most part of early childhood--is
marked by the sudden appearance of violent symptoms of disturbance of
digestion, vomiting, often stercoraceous, occlusion, diarrhoea, or
dysentery, with straining and discharges of blood.

DURATION.--Typhlitis and its complications have no definite duration. A
case may terminate fatally in the course of a few days or may extend
itself over months, or with its effects over years or for life. The
disease is, as a rule, much shorter in childhood than in adult life.
According to Matterstock, nearly one-half (44 per cent.) of children
succumb to the disease within the first three days. Wood records the
case of a girl aged ten who died in nine hours. The average duration of
cases of typhlitis without suppuration ranges from fourteen to
twenty-one days. The early evacuation of inflammatory products by
aspiration or incision may cut the disease short at any time, or
exacerbations and remissions may manifest themselves for months or
years--a condition especially liable to occur when burrowing sinuses or
fistulae develop, or when passive encapsulated abscesses are aroused
into activity by some accident or indiscretion on the part of the
patient.

PROGNOSIS.--A case of typhlitis stercoralis has no gravity, and should
terminate or be terminated within twenty-four to forty-eight hours
after its recognition. Neglected or unrecognized cases, however, are
not infrequently fatal from the circumscribed or more especially
diffuse peritonitis which may ensue.

Typhlitis independent of fecal impaction is always a grave affection,
requiring in every instance a very guarded prognosis.

Every form of typhlitis is more fatal in childhood than in adult life,
and any case of the disease may present grave complications or assume a
dangerous form at any time. The greater danger of childhood lies in the
greater liability to peritonitis. Most subsequent writers confirm this
statement, first made by Willard Parker, who also remarked that
suppurative processes, abscess formation, is more common in the adult.
The mortality of perityphlitis alone in childhood is 70 per cent., in
adult life 30 per {821} cent., so that the proportion of recoveries is
exactly the reverse of these figures at the different periods of life.

The general adoption of the opium treatment has, however, rendered the
prognosis of typhlitis far more favorable--has, in fact, reduced the
mortality in adult life from 80 per cent., the appalling figures of the
older statistics (Volz), to 30 per cent., the ratio of modern times.

The means of earlier detection and readier relief of accumulated pus
have also contributed much to reduce the mortality of typhlitis. In
1872, Bull of New York had to report of 67 cases of perityphlitic
abscess collected by him, mostly treated without operation, a mortality
of 47-1/2 per cent., while ten years later (1882) Noyes of Providence
was able to report of 100 cases treated by operation a mortality of
only 15 percent. (Pepper[7]).

[Footnote 7: "Contribution to the Clinical Study of Typhlitis, etc.,"
_Trans. Med. Soc. Penna._, 1883.]

The development of fistulae or wandering abscess, the occurrence of
pyaemia and peritonitis, necessarily aggravate the prognosis of a
simple case. Perforation is fatal of necessity, yet cases are not
wanting where recovery has occurred even after this gravest of all the
accidents of the disease. Thus, Patschkrowski reports, from Frerichs'
clinic, a case of recovery after perforation, and Pepper mentions the
results of an autopsy made upon an old man who died of vesical
hemorrhage, in whom he "found that there had, at some unknown previous
time, been perforation of the appendix."

PROPHYLAXIS.--The prevention of typhlitis has reference more especially
to cases of habitual recurrence of the disease in adults, or to the
earliest, prodromatous, stage in childhood. The slightest manifestation
of pain in the right iliac region should be looked upon with suspicion
in these cases, and absolute rest enjoined at once. Since in childhood
perforation has occurred in insidious cases after so slight an
irritation as a laxative or an enema, or even after a bath, every
provocation of this kind should be avoided. Injunction is to be put
upon all solid food in all cases in the inception as well as throughout
the course of the affection, that the element of coprostasis be not
superadded to the irritation of the disease. Adults subject to frequent
recurrences or relapses will thus avoid also the development or
aggravation of an intestinal catarrh, which in other cases of trivial
import may become dangerous to them. Many cases of typhlitis are
doubtless aborted at the start by the observance of absolute rest and
abstinence from food or rigid diet at the start.

TREATMENT.--Perhaps no disease requires such careful consideration of
its cause or form, inasmuch as the different varieties call for
entirely different treatment. A typhlitis stercoralis, for instance,
requires an exclusive evacuant treatment, whereas a peri- or
paratyphlitis demands a treatment that shall put the bowels at rest.

The safest and most effective method of emptying the caecum of impacted
feces is by irrigation of the bowels by means of the funnel syringe
devised by Hegar. The patient is put in the knee, elbow, or chest
posture, and warm water--which is the best solvent for hardened
feces--is allowed to slowly inundate the whole tract of the colon,
after the manner and with the precautions already pointed out in the
article on dysentery. Feeble or reduced patients should be supported in
this posture until as much water as possible is slowly introduced. As a
rule, a single thorough irrigation will suffice, or one or several
additional operations may be required {822} to secure the desired
effect. At the same time, broken doses, twenty grains, of sulphate of
magnesia may be administered every hour or two, not so much for the
purpose of exciting additional peristalsis as of turning water into the
intestinal canal from above.

The other varieties of the affection call for opium at the start, with
the double view of preventing the irregular, spasmodic, or tetanic
contraction of the muscular coat and of obviating the danger of
peritonitis. Opium is not contraindicated in these cases, even if the
element of fecal impaction be superadded, as all clinicians are
familiar with the fact that the bowels will move of themselves at times
even under its full narcotic effects.

The remedy is best given in fluid form, as in the tincture, that the
dose may be graduated in its repetition to secure its full effect
without danger. When a quick action is required, morphia hypodermically
may be preferred; yet it is to be remembered that opium with all its
active principles is of more value in the relief of peritonitis than
morphia alone. A careful watch should be kept upon all patients treated
with large or frequently-repeated doses of opium, that its toxic
effects be avoided. Not infrequently symptoms of poisoning have
supervened after a sudden relief of pain, necessitating the use of
means to keep the patient awake for a number of hours.

Hot embrocations, or poultices applied over large surfaces of the
abdomen, give great comfort to the patient, though the very opposite
treatment of an ice-bag, occasionally shifted or suspended, is more
agreeable in some cases in the inception of the disease.

So soon as a distinct doughy sensation or a more marked fluctuation
indicates the development of pus, steps should be undertaken at once to
secure its evacuation. In cases of doubt it is best to make a tentative
exploration with the needle of the aspirator, a large-sized needle
being preferred on account of the liability of occlusion with
tissue-shreds or other debris. It is quite surprising how rapidly a
case clears up at times after the evacuation of even only a drachm or
two of oedematous fluid. More frequently, however, the aspiration must
be repeated until a quantity of pus is secured and the abscess
completely discharged.

An abscess of more superficial situation, of larger size, or of
continuous formation is best relieved by free incision. As to the time
of the operation, the old rule, ubi pus ibi incisio, holds good here as
elsewhere. An early evacuation of the products of inflammation prevents
the supreme danger of perforative peritonitis or the formation of
burrowing sinuses, fistulae, amyloid degeneration, and marasmus.

Indurated tumors are sometimes made to soften under the long-continued
use of cataplasms, and chronic thickenings of the walls of the
intestine are relieved by general tonics, mild laxatives, mineral
waters, and gentle frictions with iodine or mercurial ointments.

Perforative peritonitis calls for opium in maximum doses as a means of
facilitating possible agglutinations or encapsulations, and a forlorn
hope is offered in an early laparotomy, which the bolder surgeons are
now undertaking in the equally desperate cases of perforation by gall-
or kidney-stones, etc.

Under no circumstances should a patient affected with typhlitis leave
the bed until the last trace of inflammation has subsided, as in no
disease is there greater liability to recurrence or relapse.




{823}

INTESTINAL ULCER.

BY JAMES T. WHITTAKER, M.D.


Intestinal ulcer, Ulcus intestinorum entero-helcosis ([Greek:
helchosis], ulcer), represents a solution of continuity in the wall of
the intestine, affecting first, as a rule, its mucous coat. Ulcer of
the intestine, like ulcer of the stomach, its occasional congener and
not infrequent associate, is the expression of an insult or injury
offered to the intestinal coat in its inner exposed surface, or of a
necrobiosis the result of a local occlusion in the general
blood-supply. Hence, ulcer of the intestine may be a purely local
disease, or be the local expression of a general, so-called
constitutional, disease. While in many cases the lines differentiating
these conditions may not be distinctly drawn, as many so-called
constitutional conditions (tuberculosis, typhoid fever, etc.) are
discovered to be--at first, at least--local processes, the toxic ulcer
(arsenic, mineral acids) may be taken as a type of the local process,
acting from within, and the syphilitic ulcer as the type of the general
process, acting from without. At the same time, it must be recognized
of syphilis that an ulcer may result from the dissolution or breaking
down of a gummatous mass anywhere in the course of the intestine, or
may be the effect of infection by extension into the rectum of
syphilitic processes about the genital organs, or, lastly, of direct
introduction of the disease in perverted intercourse (pederasty, coitus
heterotopicus).

Ulcer of the intestine is occasionally, though comparatively very
rarely, observed also as the result of pressure from within or without.
Such an ulcer is properly considered of traumatic or mechanical origin,
as it is induced as the direct effect of mechanical irritation or
arrest of blood-supply. Thus, dense masses of inspissated feces,
foreign bodies, indigestible residue of food, may fret the mucous
surface into a condition of hyperaemia, and, later, absolute
ulceration. Undue retention, as behind a cicatricial contraction, or an
occlusion from whatever cause at places where the intestinal tube
normally offers resistance (at the ileo-caecal valve, sigmoid flexure,
etc.), may lead to ulceration in the same way. Schonlein has called
attention to the paralytic condition of the intestinal muscularis in
age as a predisposing cause of mechanical intestinal ulcer; and Virchow
has noticed the same condition among the insane, whose intense
preoccupation leads to neglect of evacuation of the bowels. Certain
intestinal parasites, more especially ascarides, are admitted as
occasional causes of ulceration, and more superficial solutions of
continuity in the rectum have been noticed as the result of too
frequent or too careless use of enemata.

{824} Curling was the first to call attention to the fact that
extensive burns of the skin are sometimes followed by ulceration of the
intestines. The ulcerative process is almost exclusively confined to
the duodenum. Various attempts have been made to explain the intestinal
ulcer consequent upon burning of the skin, but a satisfactory
explanation is lacking as yet. Leube suggests an inhibition in the
force of the circulation by reason of accumulation of waste products in
the blood, while Billroth believes the ulcer to be the result of an
embolic process. Whatever the cause, the frequency of its occurrence
makes it more than a mere coincidence. According to Meyer, it is
observed most frequently in women, and shows its first symptoms in
seven to fourteen days after the initial burn.

Aside from toxic and traumatic causes, ulcer of the intestine occurs as
the result of dysentery, typhoid fever, and tuberculosis--diseases
mentioned in the order of frequency in the production of intestinal
ulcer. The ulcers of dysentery in the large intestine, and of typhoid
fever in the small intestine, assume such prominence in these
affections--having even been erroneously considered at one time as the
cause of these maladies--that their study belongs to the history of
these diseases. The ulcer of tuberculosis is rather an accident in the
course of this affection, and is now recognized as the occasional
result of direct infection by the ingestion of tuberculous flesh, or,
far more frequently, of the deglutition of tuberculous sputum. As a
rule, the tuberculous ulcer shows itself late in the course of
pulmonary phthisis, and is the cause of the obstinate and colliquative
diarrhoea which speedily exhausts the patient. Yet cases are
occasionally met in which numerous or extensive ulcers occur in the
intestinal canal early in the history of phthisis, before any serious
damage has been inflicted upon the lungs. The tuberculous ulcer
affects, and for the most part is confined to, the same structures
which form the seat of disease in typhoid fever--viz. the solitary and
agminated glands of the ileum. When the bacilli tuberculosis are
conveyed to the intestine by means of the lymph- and blood-supply
through the mesenteric vessels, the resulting ulcer takes the shape of
the vascular arrangement; that is, the long axis of the ulcer is at
right angles to the course of the tube. Thus, if sufficiently
extensive, the ulcer may be circular or form a girdle or ring entirely
around the tube. With the tubercular ulcer or ulcers are usually found
tubercular nodules or plaques in the serous coat, which are visible to
the naked eye as opacities or milky deposits beneath the peritoneal
coat. The glands of the mesentery may be at the same time so much
increased in size as to form visible or palpable tumors in the abdomen.

The frequency with which tuberculosis affects the vermiform appendix
has already been noticed in detail in the etiology of perityphlitis.

The ulcer of the intestine which is the result of a catarrhal process,
so called, belongs to the history of chronic diarrhoea and dysentery.

The true intestinal ulcer, per se, which has its analogue in the
stomach as the gastric ulcer, ulcus rotundum, is due to the same cause
as in the stomach--viz. to arrest of circulation and erosion by the
gastric juice. It is a well-established fact in physiology that gastric
digestion is continued--is, indeed, mainly effected--in the small
intestine; hence it is not surprising to learn that an arrest of
circulation in the small intestine {825} is attended by the same
result. The fact that this so-called peptic ulcer is found almost
exclusively in the duodenum speaks most emphatically for this origin of
the disease. Arrest of the circulation in the intestinal wall may be
due to embolus, which, according to the observations of Nothnagel and
Parenski, is not infrequently found in the branches of the duodenal
artery; to infarction, the condition so commonly encountered in pyaemia
and septicaemia; or to thrombotic occlusion, as seen in amyloid
degeneration--a disease process which selects by preference the vessels
of the alimentary canal, along with those of the kidney and spleen.

The duodenal resembles the gastric ulcer in form as well as origin. It
has the same appearance, in its recent stage at least, of having been
cut out with a punch, shows no inflammation, induration, or thickening
about its borders, and presents the same funnel-shape with terraced
walls, its apex below eccentrically situated, as a rule corresponding
to the situation of the artery. It is most frequently found in the
upper horizontal portion of the duodenum, but is occasionally, though
rarely, seen in the descending portion. In the further course of the
duodenum the gastric juice becomes gradually neutralized, so that
ulcers situated below the orifice of the gall-ducts are very great
exceptions. In Krauss' collection of 47 cases but 2 were found in the
lower sections of the duodenum. The intestinal like the gastric ulcer
is usually found single or alone, but occasionally two, three, or even
four ulcers are encountered. According to the tables of Morot, a single
ulcer is found in 81.8 per cent. of cases, two in 9.2 per cent., and
three and four in 4.5 per cent. each.

Duodenal like gastric ulcers are attended with the liability to
hemorrhage and perforation in equal if not greater degree. There is
also the same tendency to implication of contiguous structures. Stich
records a case of perforation of the aorta; Eichenhorst mentions the
formation of abnormal communication with the gall-bladder; and
Frerichs, a thrombosis of the vena porta in consequence of duodenal
ulcer. Lastly, the process of cicatrization may be followed by the same
disasters as occur in pyloric ulcers in consequence of contraction and
constriction. Thus, the orifices of the pancreatic or choledochus ducts
may be narrowed or completely closed, or the whole lumen of the
duodenum obliterated, with consecutive dilatation of the stomach and
oesophagus, as in the case narrated by Biermer. A very nice question in
differential diagnosis as between pyloric carcinoma and pyloric or
duodenal ulcer is sometimes raised in this way. In the vast majority of
cases it is safe, even in the absence of a palpable tumor and without
regard to the age of the patient, to decide this question in favor of
carcinoma. Cases of complete occlusion constitute the rule in
carcinoma, and the very great exception in ulcer.

It remains to be said that duodenal is much more rare than gastric
ulcer, in the ratio of 1 to 30, and that, unlike gastric ulcer, it
chiefly affects males. According to the statistics of Krauss, already
cited, the ratio of males to females is 9 to 1, and according to Trier
the ratio is 5 to 1. It occurs in greatest frequency between the ages
of thirty to forty, diminishing in frequency with advancing age.

SYMPTOMATOLOGY.--Ulcer of the intestines announces itself by symptoms
which are, as a rule, much more vague and indefinite than the same
process in the stomach. In a certain percentage of cases the symptoms
{826} may be entirely latent, and the cause of a sudden death be
revealed only on the post-mortem table. In less severe cases the entire
symptomatology of intestinal ulcer is grouped under the term dyspepsia,
no characteristic phenomena being manifest throughout the course of the
disease.

On the other hand, a very small ulcer may give rise to the most
dangerous symptoms--hemorrhage and perforative peritonitis, which may
be even fatal in the course of a few days or hours.

Among the symptoms that appear with prominence in the course of the
disease is pain. Although cases are abundantly on record marked by the
entire absence of pain, and although pain is by no means so universally
present as in gastric ulcer, it occurs in the great majority of cases
of ulcer of the intestine. The pain of intestinal ulcer distinguishes
itself from gastric ulcer by being more independent of the character of
the food or the time of taking it. For the most part, it occurs in
attacks of colic, which are characterized at times by their extreme
severity, long duration, and obstinacy to every means of relief. These
attacks occur in paroxysms with complete or only incomplete remissions,
and are ascribed, as in gastric ulcer, to the erosive action of the
gastric juice upon exposed nerve-fibres, the intervals of relief
corresponding to the periods of exhaustion of the nerve-centres. At the
same time, in exceptional cases, a long-continued localized tenderness
to pressure may indicate the seat of the disease.

Palpation may elicit, besides tenderness, points or regions of
induration or intumescence. Such a condition is more especially
encountered in cases of tuberculous disease, the so-called scrofula of
the intestine or the tabes mesenterica of childhood. More localized
enlargements are occasionally to be felt in the vicinity of the
duodenal or other intestinal ulcer in consequence of circumscribed
peritonitis, with its resultant agglutinations and adhesions. In this
connection caution must be exercised not to confound masses of impacted
feces with tumefactions. The history of constipation or the
administration of a light laxative will generally suffice to remove
this source of error.

Anorexia is a symptom of intestinal ulcer as a rule. The loss of
appetite may amount to a complete aversion to all food or only to the
more fatty articles of diet. A curious exception to this rule is not
infrequently seen in the unappeasable hunger of children the victims of
tuberculous ulceration. The contrast offered in the extreme emaciation
of these patients has been made the subject of frequent comment.

With this loss or perversion of appetite and defective digestion of the
food, the general condition soon begins to fail. Though cases are
occasionally met in which a bien-etre has been maintained for years, or
a condition of obesity has been retained, these cases form the
exception in the history of intestinal ulcer. More or less emaciation
gradually develops as a rule, and a reduction of the general strength
that is out of all proportion in its degree to the loss of flesh. At
the same time the mental condition of the patient suffers a degradation
to the level of the sufferer with chronic dyspepsia.

The disturbances of digestion which occur in intestinal ulcer present
many varieties in degree and kind. Some patients show none or but few
of the signs, while others run the gamut, so to speak, in the
semeiology of dyspepsia. Heartburn, eructations, pyrosis, borborygmi,
flatulence, gastralgias, pseudo-anginas, nausea, and vomiting, the
familiar {827} phenomena of gastric or intestinal catarrh, attend at
some time or other in the course of the disease most of the cases of
intestinal ulcer.

The condition of the discharges demands notice in detail, more
especially as abnormalities in the evacuations belong among the few of
the more constant symptoms of the disease.

Diarrhoea is the rule in intestinal ulcer. The discharges consist at
first of the undigested food and the digestive juices, which have been
hurried along the alimentary canal and prematurely evacuated on account
of the increase of peristalsis caused by the irritation in the upper
part of its tract. The arrest of the digestive process leads to early
decomposition of the ingested matters, and thus imparts to the
discharges an exceedingly offensive odor. While, in exceptional cases,
constipation may be present, or even obstipation of the bowels, the
discharges are usually so abundant as to constitute a diarrhoea, which
in some cases is so frequent or profuse as to become colliquative and
speedily exhaust the strength of the patient.

An ulceration situated in the colon or rectum would furnish the
discharges characteristic of dysentery, already described in detail,
while the same process in the ileum would show the evacuations
characteristic of typhoid fever or tuberculosis.

The most characteristic ingredient of the true duodenal ulcer is blood.
As stated in the article on HEMORRHAGE OF THE BOWELS, ulcer of the
intestine constitutes the most frequent source of this accident, which
is sometimes so grave as to destroy life in the course of a few days or
hours. The blood from an intestinal ulcer may be evacuated both by the
mouth and the anus, or may be retained in the alimentary canal and not
appear at all. Such cases constitute the condition known and described
under the heading of occult or concealed hemorrhage, which is
recognized by the rapid general collapse of the patient. When the blood
issues from a duodenal ulcer, it is intimately commingled with the
contents of the alimentary canal. The discharges in such cases are
usually black, tarry, and more or less fluid; whereas blood from the
colon or rectum still preserves its fresh red color and is discharged
separate from the feces or simply coats its exterior. Occasionally
cases are met where the blood coagulates in the interior of the
intestinal canal, to form a cast of its lumen or to accumulate in great
mass in the sigmoid flexure or rectum. In one case in the experience of
the author such an accumulation was the cause of a very severe
tenesmus, which was only relieved by the digital evacuation of large
masses of inspissated, coagulated blood.

The presence of pus would indicate lesion of the colon, as typically
shown in dysentery, as suppuration, at least with any visible products,
does not occur in ulcer of the duodenum.

DURATION.--Ulcer of the intestine has no definite duration. As in the
case of its prototype, gastric ulcer, it may speedily be covered with
cicatricial tissue and never appear again in the course of a long life.
But such a course is as unusual as in gastric ulcer. Frequent
recurrence constitutes the rule in intestinal ulcer, or a partial
recovery with frequent relapses, as in the course of ulcer of the
stomach. So ulcer of the intestine is not infrequently a lifetime
malady, with exacerbations and remissions dependent largely upon the
prudence or imprudence of the patient with regard to diet. It need
hardly be stated that ulcer of the intestine {828} may terminate
fatally even in the course of a few days from hemorrhage, circumscribed
and later diffuse peritonitis, or may drag out a slow length of years,
to finally destroy the patient with the general symptoms of inanition,
hydrops, and marasmus.

DIAGNOSIS.--From what has been already stated, it is seen that ulcer of
the intestine is often entirely overlooked or may be readily confounded
with other maladies of the digestive tract. Cases of traumatic or toxic
origin are generally readily recognized by the history of the patient,
and tuberculosis reveals itself by the youth of the individual, the
existence of the disease elsewhere, the gradual emaciation, the
premature senescence--in short, the general signs of the phthisical
habitus, the meteorism, and perhaps the presence of nodular
enlargements of the mesenteric glands.

The most characteristic symptom of the peptic ulcer is, as has been
stated, hemorrhage. But hemorrhage is present in only the minority of
cases, is, as a rule, occasional and transitory, and is at all times
difficult of differentiation as to its source. Blood from a gastric
ulcer may also be voided per rectum as well as per os, and the blood
from a duodenal ulcer after regurgitation may be wholly discharged by
vomiting. The absence of vomiting and the presence--more especially the
persistence--of tarry evacuations from the bowels would speak for ulcer
of the intestine. Dilatation of the duodenum, a condition of ectasia,
closure of the bile-duct with consecutive jaundice, or the presence of
fatty stools from occlusion of the pancreatic duct (a sign not now
regarded of the same value as in the days of Bright), would also
declare in favor of ulcer in the duodenum.

As between intestinal ulcer and catarrh or intestinal ulcer and
carcinoma, precisely the same rules would hold as in the case of the
stomach. A simple enteralgia would be recognized by its more frequent
occurrence among females or individuals of neurotic temperament; by its
connection with faults of diet, malaria, or exposure to cold; by the
absence of hemorrhage, diarrhoea, or peritonitis.

PROGNOSIS.--Too much caution cannot be exercised in the prognosis of
ulcer of the intestine; for even in the cases which run a perfectly
mild course the gravest, even fatal, accidents are liable to occur. The
danger of perforation in cases of typhoid fever from a single or from
one of the few ulcers that may be present imparts one of the chief
elements of gravity to this disease; and the same catastrophe may occur
at any time in dysentery or tuberculosis. The duodenal ulcer may
likewise have a sudden gravity imparted to a mild case by a copious
hemorrhage or a peritonitis, and, even though the patient escape all
possible complications, to recover with the surface of the ulcer healed
so that the loss of substance is filled in with firm cicatricial
tissue, the danger of contraction or stenosis still remains. The ulcers
of dysentery in the colon and of syphilis in the rectum are especially
liable to be followed by deformities of this kind, while the
tuberculous ulcer in the ileum not infrequently results in a more or
less complete stenosis. The ulcer of typhoid fever in its cicatrization
almost never reduces the size of the intestinal canal.

TREATMENT.--The most valuable therapeutic means of relieving the pain
and obviating the dangers of ulcer of the intestine consist in the
{829} regulation of the diet. The food should be light, easily
digestible, and during the acute stage of the disease as nearly fluid
in its consistency as may be. Milk would be the staple article of diet
in all cases were it not for the fact that in some cases constipation
attends its too exclusive use. The various soups, without solids,
broths, preparations of starch (sago, arrowroot, tapioca, etc.), may
sufficiently nourish the patient until the healing process shall have
commenced. Raw beef, chopped up and made into an emulsion, is perhaps
the most nutritious and least injurious of any kind of food. Bread,
potatoes and other vegetables should be ruled out altogether, because
of their liability to produce masses of feces whose inspissation may do
mechanical damage to ulcers in process of cicatrization.

Where there is failure in the general strength early resort should be
had to alcohol, which may be administered in the form of red wine (in
preference to white, because of the tannin it contains), wine-whey, or,
in more serious prostration, of sherry wine, milk punch, egg-nog made
with good whiskey or brandy.

In the worst cases, where all food irritates, feeding by the mouth may
be abandoned altogether for a time, and the strength of the patient
sustained by nutritive enemata of beef or pancreatic emulsion.

The diarrhoea should be controlled rather than entirely checked, for
fear of the greater evil of constipation. A little bismuth with
bicarbonate of sodium or oxide of zinc may suffice for the milder
cases, while in the more aggravated cases resort must be had sooner or
later to opium.

Constipation is best relieved by careful injections of warm water or by
the administration of the lighter laxatives--mineral waters, Seidlitz
powders, citrate of magnesia, castor oil, etc.

Vomiting is combated by ice, soda-water, champagne, cherry-laurel
water, and in graver cases morphia hypodermically.

Pain may be relieved by applications of hot water, cataplasms,
injections of hot water, and, when necessary, by morphia with or
without belladonna.

Hemorrhage is checked by ice internally and externally, turpentine,
ergot or preferably ergotin by hypodermic injection, and opium.

Peritonitis, more especially perforative peritonitis, calls
imperatively for the liberal use of opium.

Patients the victims of intestinal ulcer must maintain a guarded diet
for months, often for years, after all signs of the disease have
disappeared as the best prophylaxis against recurrence. Constant
vigilance is also required to avoid constipation, and the greatest
temperance exercised with regard to the use of alcohol. The author has
at the present time a patient under treatment who presents all the
symptoms of duodenal ulcer, including hemorrhage, with every indulgence
in strong drink, and in whom all symptoms disappear under entire
abstention. Sometimes a course of mineral waters, a sea-voyage, or
other change of life or scene constitutes the best means of avoiding
frequent relapse.

It need hardly be said that an ulcer in the rectum, which is readily
recognized by its attending tenesmus, calls for local treatment; and it
is equally plain that tuberculosis or syphilis requires appropriate
internal means of relief.




{830}

HEMORRHAGE OF THE BOWELS.

BY JAMES T. WHITTAKER, M.D.


GENERAL REMARKS.--Hemorrhage of the bowels occurs in both sexes, though
more frequently in the male, and at all ages, though more frequently at
the middle period of life. In the infant a form of it is sometimes
considered as a distinct affection under the head of melaena
neonatorum, and in age it sometimes shows itself as a distinct sign of
a disease characteristic of age--namely, cancer. According to the
tables of Bamberger, it is caused in the order of frequency by
dysentery, typhus fever, cancer (of the colon), mechanical injury,
poisons and foreign bodies, ulceration (tubercular, follicular), the
round ulcer of the duodenum, and aneurism; last and least frequent is
the so-called vicarious hemorrhage.

ETIOLOGY.--Hemorrhage from the intestinal canal arises from (1)
anomalies in the contents of the bowel; (2) disease of the wall of the
bowel; and (3) from general diseases.

(1) The inspissation of the natural contents of the bowel during
long-standing or habitual constipation may convert the feces into dense
masses which irritate and scratch the mucous membrane, and thus induce
hemorrhage directly by simple solution of continuity, or indirectly as
the result of extreme hyperaemia. Such hemorrhage is nearly always
slight, streaking or coating the surface of the scybalous mass or being
extruded from the anus as a small deposit of blood during the last act
of defecation; in which latter case it is found mostly associated with
hemorrhoids or fissure of the anus--conditions which require separate
description. Independent of these conditions, the hemorrhage nearly
always has its origin in the lowest regions of the large intestine,
where condensation of the feces is naturally greatest.

Foreign bodies in the intestinal canal descended from the stomach may
also be the cause of hemorrhage in the same way. Thus, stones of
fruits, bones of fish, fragments of oyster-shell, or other substances
in no way connected with aliments (false teeth, buttons, pins and
needles, etc.), may be swallowed accidentally or purposely (as by
children or the insane) to produce intestinal hemorrhage. Drastic
cathartics (podophyllin, gamboge, etc.) and poisons (arsenic, mineral
acids) occasionally act in the same way. Thus, Tardieu reports[1] the
case of a servant to whom was administered by a homoeopath veratrin
with coffee, with fatal effect in six days. At the autopsy, made by
Amussat and Reymond, the stomach and small {831} intestine were found
filled with a dark-brown or black bloody fluid, but there was no trace
of perforation, ulceration, or organic disease.

[Footnote 1: _Annales d'Hygiene_, July, 1854.]

Under this head mention should be made also of certain parasites whose
habitat is the intestinal canal, the walls of which they perforate. Two
varieties, the Anchylostoma duodenale and the Distoma hepaticum, are
frequent causes of hemorrhage, the former from the duodenum and
jejunum, the latter from the rectum, in hot climates, more especially
in India and Egypt.

(2) Anomalies in the intestinal walls produce hemorrhage as the result
of intense hyperaemia (per diapedesin) or of actual loss of substance
(per rhexin). Copious, even fatal, hemorrhage has thus ensued from
dysenteric and typhoid processes (and even without discoverable cause)
where no ulceration or loss of substance could be discovered on
autopsy; and this accident is so frequent as the result of ulceration
in the diseases mentioned as to constitute a characteristic sign or
complication. It must be said, however, that cases of alarming or fatal
hemorrhage without apparent cause during life or lesion after death
were more frequently reported in the literature of the times preceding
our more accurate knowledge of pathology and pathogeny. Few clinicians
or pathologists would now be content with reports made without full
knowledge of the history of the case or microscopic examination of the
intestinal walls. Thus, the report to the Societe Medicale d'Emulation,
April 2, 1834, by Dubois of a young man who quickly died of intestinal
hemorrhage five days after a severe headache, and on the same occasion
by Guillemot of several similar cases, would awaken the suspicion of
masked typhoid fever; and the case of an old man aged seventy-four who
died of intestinal hemorrhage after four days' diarrhoea, reported by
Husson,[2] would call for a close examination of the vessels in the
intestinal walls. In fact, Bricheteau, who reported a case from the
Hopital Neckar, was able on autopsy to discover a rupture in a small
artery of the intestines.

[Footnote 2: _Proceedings of the Anatomical Society at Paris_, 1835.]

Embolic processes leading to the formation of ulceration (by
predilection in the duodenum) are often attended with intestinal
hemorrhage, which would be more constantly present were it not for the
fact that, as in the stomach, the speedy establishment of collateral
circulation prevents the consequences of complete infarction.

Besides dysentery and typhoid fever, tuberculosis and syphilis are
occasional causes of ulceration and necrosis of the intestinal walls
which may be attended with hemorrhage. Cancer of the intestine most
frequently affects the rectum, but wherever situated may show
hemorrhage as one of its signs.

The local hyperplasia of the mucous tissue which constitutes a
polypus--and which in children, in whom it most frequently occurs, is
mostly situated in the rectum--is suspected to exist or is recognized
by the frequent discharge of blood from the bowels. A far more grave
affection of the intestinal walls, likewise most frequent in childhood,
is the peculiar dislocation known as intussusception or invagination.
This condition is so commonly attended with distressing evacuations of
blood and mucus as to simulate dysentery. The strangulation of the
intussuscepted mesentery with its vessels easily accounts for the
hemorrhage in such cases.

A more extensive compression is exercised at times by tumors in the
{832} abdominal cavity, as by pregnancy, ovarian growths, etc.,
occlusions in the course of the portal system (cirrhosis hepatis),
interference with the general circulation, as in diseases of the heart
or lungs, with intestinal hemorrhage as a consequence.

Diseases of the blood-vessels themselves, as amyloid degeneration,
aneurism, should not be omitted from the list of factors possibly
productive of this result.

(3) The general diseases attended with hemorrhage from the bowel are
characterized for the most part by more or less general disintegration
or dissolution of the blood, with the manifestation of hemorrhage in
various parts of the body--kidneys, uterus, subcutaneous tissue, etc.;
the enterorrhagia being an accidental localization, so to speak, of the
effusion. The most prolific causes of this disorganization are the
micro-organisms which "touch the life of the blood corruptibly;" and
hence the various acute infectious diseases may show in the severer
forms hemorrhage from the bowels. Under this head may be ranged
variola, which boasts even of a hemorrhagic form; typhus, yellow, and
malarial fevers; the forms of nephritis marked by uraemia, cholera,
icterus gravis, erysipelas, etc. Disintegration of the blood or partial
dissolution of its corpuscular elements occurs also in those obscure
affections which constitute the group, or are included in the
description, of the hemorrhagic diatheses, as haemophilia, leuchaemia,
pernicious anaemia, scurvy; of any of which enterorrhagia may be a
distinct or dangerous sign.

Melaena neonatorum is the distinct name given to a hemorrhage from the
bowels which occurs a few hours or days after birth, and which is often
so profuse as to cause death at once or in a short time. In most cases
no anatomical lesions can be discovered after death, save an intense
hyperaemia of the intestinal mucosa, so that the etiology of this
affection is involved in obscurity. The various causes assigned in its
production--ulceration of the stomach or duodenum (Bohn), embolism
(Landau), fatty degeneration (Steiner), premature ligature of the
umbilical cord (Kiwisch)--answer only for individual cases. Betz
reported a case in a family subject to haemophilia, and Trousseau once
saw twins thus affected; but that heredity cannot account for all cases
is shown by the fact that it occurs mostly in healthy children from
healthy parentage. Klebs is inclined to attribute the affection to the
action of micro-organisms, introduced perhaps as the result of
puerperal infection, but this cause can be assumed in only a small
minority of cases; at least, but a small percentage of cases coincide
with puerperal disease on the part of the mother.

The affection is fortunately rare. Eichhorst states that Hecker
observed it but once in 500 births, and Gemich but once in 1000 births.
According to Rilliet, the hemorrhage is oftener (8/14) intestinal,
rarer (4/14) gastric, and rarest (2/14) both. It is almost always
abundant and quickly repeated, the blood being mostly pure, in clots or
masses and fluid, though it is sometimes commingled with meconium. It
usually ceases within twenty-four hours, though it may continue for
three, five, or more days. Of 23 cases reported by this author, 12
recovered and 11 died.

MORBID ANATOMY.--Hemorrhage from the bowels, being only a symptom of
very many different conditions, is marked by lesions characteristic of
the condition in an individual case. These lesions are more
appropriately described in connection with the various diseases. Not
{833} infrequently in these cases the intestine is distinguished by the
absence of any lesion at all; but, from whatever cause, hemorrhage from
the bowels, like hemorrhage from any other source, shows a more or less
profound anaemia of all the internal organs, and in more chronic and
protracted cases leads to fatty degeneration, more especially of the
heart.

SYMPTOMATOLOGY.--Hemorrhage from the bowels is usually readily
recognized by the discharge of blood, either pure or mixed with the
natural contents of the alimentary canal. The actual seat of the
hemorrhage may, however, only rarely be recognized by the rectal
speculum. The colicky pains, borborygmi, or sensations of fluids in the
abdomen which are occasionally experienced may not be relied upon in
fixing the seat of the effusion. Should the hemorrhage occur in
quantity, or, more especially, should the seat of the effusion be low
in the intestinal canal, the blood which escapes is more or less pure.
When the hemorrhage is higher, or when the stay of the blood in the
bowel is longer, it becomes more or less incorporated with the contents
of the bowels or altered by the intestinal juices to present a
discharge of mushy or semi-fluid consistence, of dark-brown or black
color. So-called tarry stools are thus largely composed of blood.

But serious, even fatal, hemorrhage sometimes occurs without the escape
of any blood at all. Such are the so-called cases of concealed, occult,
or internal hemorrhage, in which the nature of the malady is only
suspected or recognized by the general symptoms attending the profuse
loss of blood. Should the hemorrhage be gradual, anaemia slowly
supervenes, with hydraemia and subcutaneous dropsy. Traube reports a
fatal case of oedema of the glottis from such a cause. Sudden
hemorrhage announces itself by pallor and prostration, dyspnoea,
vertigo, and syncope. Amaurosis, tinnitus aurium, formication, emesis,
and, if the disease be high up in the intestinal canal, haematemesis,
are the common attendants of serious hemorrhage. In the worst cases of
sudden effusion the patient may present the appearance of complete
collapse, and the intestinal canal be found on autopsy distended with
blood throughout a great part of its course, while no blood whatever
has escaped from the rectum. In such cases, or with more gradual loss
of blood, the patient experiences a sense of increasing weakness, the
skin becomes cold and bedewed with a clammy sweat, the pulse grows
feebler, the temperature falls, and death from exhaustion more or less
speedily ensues.

DIAGNOSIS.--The presence of blood in any quantity in the stools is
readily recognized by its coarser characteristics. Ridiculous errors
have been made by mistaking the coloration produced by bismuth, iron,
logwood, etc. administered internally, or by coloring matters
introduced into the discharges for purposes of deception. The
microscope, Zeichmann's test for blood-crystals, and in extremely
doubtful or medico-legal cases the spectroscope, furnish easy means of
detecting blood in whatever quantity or character.

It is the cause and seat, rather than the existence, of the hemorrhage
that mostly cause embarrassment in differential diagnosis. Hemorrhage
from the lungs, nose, or stomach is usually readily excluded by the
absence of any evidence of disease of these organs, and the presence of
the other symptoms of any general disease attended with enterorrhagia
makes a diagnosis in most cases easy enough. Alterations in the
contents of the {834} bowel, the presence of foreign bodies, are
recognized by the history of the case and by careful local examination,
while a diagnosis of anomalies in the walls of the bowel is usually
reached by exclusion. In no doubtful case should local inspection or
digital examination of the anus and rectum be omitted.

TREATMENT.--As in all cases of hemorrhage, the first requisite is
absolute rest. The patient should be at once put to bed and kept
perfectly quiet. Many a case of hemorrhage in typhoid fever is produced
by arising from bed to go to stool. The bed-pan is an absolute
necessity in the management of a case of typhoid fever after the second
week of the disease. Rest is the chief agent in prophylaxis as well as
therapy.

The most effective styptic in enterorrhagia is cold. An ice-bladder
should be laid upon or suspended immediately above the abdomen during
the whole duration of the flow. The injection of ice-water into the
bowel should be practised only in cases where the hemorrhage is
believed to come from the colon. Otherwise, the peristalsis it awakens
may only aggravate the danger. Should rest and cold fail to quickly
check the hemorrhage, resort should be had at once to ergot. This
remedy, in the form of ergotin, is most effective when introduced
beneath the skin. In cases of less imminent danger the practitioner may
be content to give the remedy by the mouth.

Small doses of the simple or camphorated tincture of opium frequently
repeated speedily arrest contractions of the bowel, and at the same
time feed the brain in threatening syncope. The astringents
proper--tannic acid or its preparations, acetate of lead, alum, the
perchloride of iron--are seldom necessary or advisable, but may be
called for in obstinate or protracted cases.

To turpentine has been ascribed, from time immemorial, specific virtues
in relief of hemorrhage of the bowels, and its administration is still
a routine system with many older practitioners. It is most effective in
large doses--one drachm, with milk or in emulsion, every hour or two
until the hemorrhage ceases.

In relief of collapse, alcohol, ether, and musk are imperatively
indicated, with the external application of heat; and in the treatment
of the anaemia and hydraemia the preparations of iron, including,
later, the mineral waters which contain it. In the worst cases of
sudden alarming hemorrhage the physician should not fail to practise
the transfusion of blood or solutions of salt or soda.

Milk is the best food and drink during the attack, and after it for
some days or weeks. Chopped or scraped raw beef may substitute it
later, while all farinaceous foods are to be strictly avoided for some
time.




{835}

INTESTINAL OBSTRUCTION.

BY HUNTER MCGUIRE, M.D.


When a mechanical impediment to the passage of the contents of the
bowel along the intestinal canal exists, the condition is known as
intestinal obstruction. The causes of this occurrence are numerous, the
symptoms urgent, the diagnosis difficult, the treatment uncertain, and
the termination, unless relieved by nature or art, speedily fatal.
There is no class of cases to which the practitioner is called more
important, or which demands on his part greater skill and judgment.

It is customary to divide the causes of obstruction of the bowels into
two great classes--acute and chronic.

In acute cases the attack is sudden, the symptoms violent, and, unless
the cause is speedily removed, life ends in a few hours or at most in a
few days. In chronic cases the causes act comparatively more slowly,
the symptoms are chronic and less urgent, and danger of death less
imminent. In this class the cause is not uncommonly spontaneously
relieved, and the individual restored to perfect health without the aid
of medicine or the surgeon's art. This result may happen in apparently
the most desperate cases.

This classification of acute and chronic obstruction is necessary for a
proper clinical study of the subject, but it should be remembered that
in practice there will be found some cases which partake of many of the
symptoms of both acute and chronic obstruction, making it difficult to
determine to which division the cases properly belong. It will also be
seen that some, at first, well-marked acute cases subside and become
chronic in character, and that (old) chronic cases of obstruction
sometimes suddenly change their nature and become acute. Again, some of
the causes mentioned as giving rise to acute obstruction of the bowel
in rare instances produce symptoms of chronic obstruction, and some of
the causes referred to as giving rise to symptoms of chronic
obstruction in rare instances provoke signs of acute obstruction. These
cases are exceptional. As a rule, the following list embraces
conditions which produce symptoms of acute obstruction:

1. Congenital malformations.

2. Impaction of foreign bodies, gall-stones, enteroliths, etc.

3. Twisting of the bowel--volvulus.

4. Internal strangulation by loops, bands, false membranes,
diverticula, mesenteric pouches, slipping of a portion of bowel into
natural or unnatural openings, diaphragmatic hernia, etc.

{836} 5. Invagination.

As a rule, the following causes produce symptoms of chronic intestinal
obstruction:

1. Constipation and fecal accumulation.

2. Stricture of the bowel, sometimes cancerous.

3. Compression of the bowel from abdominal tumors.

4. Contraction of the bowel from inflammatory changes, often
tuberculous.

A consideration of external hernia is, of course, not included in this
paper, but the possibility of the symptoms of intestinal obstruction
being due to this cause should never be overlooked.


Congenital Strictures and Malformations.

Cases of congenital strictures and malformations are confined almost
wholly to the rectum and anus, and come more properly under the
province of the surgeon. Some of the cases, however, belong to the
physician, the obstruction being so slight as not to require surgical
assistance. With all of them, however, the physician should be
familiar, that he may be able to distinguish between congenital
malformation giving rise to immediate obstruction and other forms of
intestinal occlusion. He should know, too, when to seek the aid of the
surgeon. For these reasons, as well as to make the history of the
causes of intestinal obstruction as complete as possible, it has been
thought proper to include in the list congenital occlusion and
malformation of the intestine. They will be treated, however, in the
briefest possible way, and the reader is referred to works on surgery
for a more detailed account of the pathology, symptoms, and treatment.

When congenital occlusion of the colon occurs, it is almost invariably
found in the sigmoid flexure, and is due, as most congenital atresia of
the intestine, to foetal peritonitis. Congenital occlusion may be found
in any portion of the small bowel, but a frequent site is the lower
part of the ileum and the ileo-caecal opening. The following case[1]
gives an example of a form of stricture of the duodenum in infants,
with the symptoms and pathological changes. The septum is supposed to
be an unnaturally developed valve, or two valvulae conniventes united:
"A child when born presented no unusual symptoms for the first
twenty-four hours. Vomiting then came on, and continued with short
intermissions until death, which took place some thirty-eight hours
after birth. The bowels were never relieved during life. The only
disease found was stricture of the duodenum close to the entrance of
the gall-duct, so that a probe passed down the latter entered the
duodenum immediately below the constriction. There was nothing to
indicate in what manner the constriction had occurred. On the gastric
side of the latter the duodenum was immensely distended--so much so
that at first sight it appeared like the pyloric end of the stomach
itself, and only by a more careful examination was the distinction
between the stomach and intestine detected by a ridge running around
their place of junction."

[Footnote 1: Quoted by Mr. Pollock in Holmes's _System of Surgery_,
from _Pathological Transactions_, vol. xii. p. 101.]

{837} Cases like this, a number of which are on record, are instructive
and of pathological interest; when, however, congenital occlusion
exists in the small intestines, no treatment can be suggested. If the
sigmoid flexure is the part involved and diagnosis can be made, opening
the intestine in the right groin and establishing an artificial anus
should be attempted.

In the development of the foetus the anal part of the bowel, beginning
below, develops upward, and the intestinal portion, commencing above,
grows downward; both portions, advancing, finally unite, making one
continuous tube. When, however, there is some interruption in the
foetal development of the intestine, and the two portions of bowel fail
to unite, we have malformation of the rectum and anus and intestinal
obstruction; or the two portions of bowel may have been united and
continuity of the intestinal track established, and subsequent
intra-uterine inflammation may obliterate the canal. Under these
circumstances a ligamentous cord represents the original tube. The cord
descends from the cul-de-sac in which the upper part of the bowel ends
to the skin about the anus, or is lost in the tissues about the neck of
the bladder. In congenital malformations the following conditions may
be found: 1st. The anal orifice may be so minute as not to allow the
feces to escape; or the aperture may be occluded by a membrane, through
which the meconium may be seen; or the anus may be entirely absent. 2d.
The rectum may be occluded by a membranous septum, the presence of
which is not suspected until symptoms of intestinal obstruction arise,
and then it is discovered by introducing the finger or a probe; or the
rectum may be entirely absent, the colon terminating in the iliac fossa
in a dilated pouch, or ending at the top of the sacrum or stopping at
any point between this and the normal anus, the place being determined
by the period of arrest of foetal development; or, the anus being
absent, the rectum may open into the vagina, bladder, urethra, and
other places. These cases belong exclusively to the surgeon.


Impaction of Foreign Bodies.

Intestinal obstruction may arise from the introduction, accidental or
otherwise, of foreign bodies into the stomach and bowels. Coins,
marbles, bullets, fruit-seeds, etc. are often swallowed by children,
sometimes intentionally, and if the object is round and small it rarely
gives rise to any serious trouble. The foreign body, however, if small,
may drop into the appendix vermiformis or some other diverticulum and
end in serious mischief, or if the individual has stricture of the
bowel the foreign body may be arrested by it.

Foreign bodies which are pointed or irregular in shape, swallowed by
accident or design, may give rise to dangerous and fatal symptoms, but
not unfrequently they escape per vias naturales. Thus, pins, needles,
pieces of bone, artificial plate and teeth, small pen-knives, and other
pointed or irregular-shaped bodies, have passed in this way.
Sharp-pointed bodies, as needles, sometimes make their way through the
walls of the stomach and present themselves at other and more distant
parts of the body. I have removed a needle from the calf of the leg
which {838} the patient had a month before accidentally swallowed.
Jugglers accidentally, in practising their calling, and insane people,
not unfrequently intentionally, introduce into the stomach all sorts of
foreign bodies, such as buckles, forks, spoons, knives, pieces of wood,
iron, bone, etc. Gross[2] records the case of a juggler who let a bar
of lead ten inches long and weighing a pound slip into his stomach.
Bell of Iowa removed it by gastrotomy, and the man recovered. Agnew[3]
reports a post-mortem of an insane woman in whose intestinal canal he
found three spools of cotton, two roller bandages, a number of skeins
of thread, and a pair of suspenders.

[Footnote 2: _System of Surgery_, by S. D. Gross, 6th ed., vol. ii. p.
616.]

[Footnote 3: _Agnew's Surgery_, vol. i. p. 393.]

The morbid appetite of some people, particularly girls and pregnant
women, sometimes induces them to swallow powdered chalk, magnesia, and
other substances, and when this practice is continued for a long time
the insoluble powder is deposited in the bowel and forms hard masses
which more or less completely obstruct the intestines.

Stony concretions or enteroliths are found generally in the caecum or
in the sacculi of the colon, very rarely in the small intestines. They
are round or oval, and when two or more are found together they have
facets. They consist usually of carbonate of lime or magnesia or
sesquioxide of iron. Other concretions are sometimes seen composed of
starch or the felted husks of oats, called oat-stones (avenoliths),
found particularly among the poorer classes of people in Scotland.
Other vegetable remains of husks, fibres, etc. may produce the same
thing. Young and middle-aged people more frequently suffer with these
concretions than the old. Foreign bodies made up by the gradual
accumulation of hair, string, and other substances are not unfrequently
found in the stomach and intestines. The mass produced in this way is
often very large. Sometimes the foreign body is arrested in the
oesophagus. In a post-mortem reported to the writer by Fairfax a large
copper coin, accidentally swallowed a few days before, was found lodged
in the gullet. Ulceration followed, a neighboring artery was opened,
and the patient died from hemorrhage.

Impaction of the bowel by gall-stones escaping from the gall-bladder
into the bowel is by no means an unfrequent cause of fatal obstruction.
Small gall-stones, after giving rise to intense pain and often grave
symptoms during their passage through the bile-ducts, may escape into
the duodenum and be discharged through the rectum, as any other small
foreign body. If, however, there is constriction or stricture of the
bowel at any point, the small gall-stone may lodge there, and if other
stones follow and lodge, the collection may soon be great enough to
produce obstruction. A very large single stone or a number of stones
forming a coherent mass may collect in the gall-bladder, slowly distend
the dilatable biliary passages, and escape into the bowel; or--and this
is more common--an opening made by ulceration between the distended
gall-bladder and the duodenum allows the concretion to escape into the
small intestine. These stones or aggregation of stones are sometimes
three, four, or five inches in circumference and from one to four
inches long. They occur, as a rule, in people over fifty years of age,
and more commonly in women. Brinton, in his excellent book on
_Intestinal Obstruction_, makes the average age in these cases
fifty-three and a half {839} years, and from the statistics he has
gathered it will be seen that their occurrence is four times as often
in females as in males. In 41 cases collected by Leichtenstern, 32 were
women and 9 men. The site of the impaction is always in the small
intestines. In 32 cases observed by Leichtenstern, 17 were found in the
lower part of the ileum, 10 occupied the duodenum and jejunum, and 5
the middle part of the ileum.

SYMPTOMS.--Foreign substances introduced into the stomach do not always
immediately give rise to serious symptoms. It is wonderful sometimes to
see how tolerant the stomach is of their presence. Many instances are
recorded of foreign bodies remaining in the stomach for months without
producing dangerous symptoms. The mass may be discharged by vomiting,
or it may escape through the pyloric opening into the intestine, and
ultimately be discharged through the rectum, or, lodging in the bowel,
give rise to symptoms of inflammation and obstruction. If, however, the
foreign mass remains in the stomach, and is not removed by the
surgeon's art or spontaneously discharged by ulceration, as in several
rare instances has been the case, it uniformly proves fatal.

Before the foreign body is discharged by ulceration through the walls
of the abdomen, adhesive inflammation unites that portion of the
alimentary canal, gastric or intestinal, in which the mass is lodged
with some part of the abdominal wall. By this union the cavity of the
peritoneum is protected, just as we see the peritoneal sac protected by
an effusion of lymph in hepatic abscess opening into the small
intestine. If the adhesion between the canal and abdominal wall is
imperfect, or by an undue amount of inflammation is disunited, the
foreign body or inflammatory products which surround it may escape into
the peritoneal sac and produce fatal peritonitis. Instead of passing
through the abdominal wall, the foreign substance may escape into the
bladder or vagina, or from the small intestine into the colon or
rectum. Dangerous peritonitis may follow the simple presence of the
foreign body in the alimentary canal from the obstruction it produces
when no attempt at discharge by ulceration has been made. If the size
and shape of the body permit its passage into the small intestine, it
makes its way very slowly along this tube, giving rise to occasional
attacks of colicky pains and symptoms of partial impermeability of the
bowel.

At any moment the foreign body may lodge, become impacted in the canal,
and all the grave symptoms of enteritis and general peritonitis present
themselves. Symptoms of inflammation may appear, and after a longer or
shorter time suddenly disappear, as if the foreign body had glided over
some point of obstruction and again begun its descent through the tube.
Its course is always irregular, passing quite rapidly over a portion of
the intestine, then going more slowly, then lodging for a time at some
point where it is obstructed by a fold or the contents of the bowel or
by spasmodic contraction of the muscular coat of the intestines. As the
calibre of the small intestine gradually diminishes as it approaches
the caecum, the passage of the foreign body becomes more and more
difficult as it is propelled onward toward the ileo-caecal valve. After
a time it may reach the caecum, where, of all places, it is most apt to
lodge; but it may continue its course to the rectum, where it gives
rise to tenesmus and a constant desire to go to stool. Finally,
spontaneously or aided by the finger of the physician or some
instrument, it is {840} evacuated per anum. Not unfrequently, the
foreign body can be felt through the abdominal walls, and its course
traced day after day as it makes its way along the canal.

It is a common practice with uninformed persons to give castor oil or
some purgative medicine when a pin, needle, coin, or other foreign
substance has accidentally passed from the mouth into the stomach. Such
practice is irrational and hurtful. Experience has shown that the
larger and more solid the alvine discharges, the more likely the
foreign body is to escape by the natural outlet; and the physician
should order such a regimen and diet as will probably secure this
condition of the contents of the bowel.

Long residence of a foreign mass at any point in the intestinal canal
is certain to produce some chronic enteritis and effusion of lymph and
subsequent stricture of the bowel, or the presence of the foreign body
may produce an ulcer; and when this is healed the resulting cicatrix
may end in serious obstruction from the natural tendency of the new
material to contract. Signs of constriction of the bowel may not be
noticed for some time after the escape of the foreign body.

Obstruction from the presence of intestinal stones and concretions is
almost invariably preceded by impaired health, emaciation, or cachectic
appearance, signs of partial impermeability of the bowels, and repeated
attacks of inflammation, especially in the region of the caecum. It
terminates sometimes by the concretion becoming encysted, by its
spontaneous evacuation, or by ulceration and perforation, or sometimes
by complete occlusion of the bowel, and death.

As occlusion of the bowel by the presence of gall-stones always occurs
in the small intestines, the symptoms are at once of the most urgent
and violent character. The signs are those of internal strangulation,
and the termination is often rapid in the extreme. Colicky, griping
pains are soon succeeded by violent agony; vomiting begins at once, and
is constant; at first bile is thrown up, and afterward feculent matter;
the pulse is small, wiry, and frequent; the belly is retracted; the
features are pinched, the extremities cold, and prostration soon comes
on, succeeded by collapse.

Evidences of disorder of the liver, symptoms of inflammation of the
peritoneum in that region, or attacks of hepatic colic sometimes
precede obstruction of the bowel by gall-stones; unfortunately,
however, for the purposes of diagnosis, these premonitory symptoms are
not invariably present.


Acute Internal Strangulation, Twisting, etc.

When a portion of bowel within the abdomen is constricted, its
circulation interfered with, and the passage of the contents of the
bowel interrupted, it gives rise to acute internal strangulation. This
condition is very similar to that of external strangulated hernia. The
difference is, that one is inside and the other outside of the cavity
of the abdomen.

Twisting of the gut upon its mesenteric axis, the passage of the bowel
through some natural or unnatural opening, the encircling of one
portion of bowel by another or by bands, false membranes, etc., may
cause {841} internal strangulation. It may happen at any age, and
involves generally the small intestine or the more movable parts of the
large bowel--viz. the sigmoid flexure and caecum.

Twisting, or torsion, is not an unfrequent cause of intestinal
obstruction, and may involve almost any portion of the intestinal tube.
Its most common site is the sigmoid flexure, and next in point of
frequency the caecum. It sometimes, but rarely, involves the small
intestines, and may occur as a simple twisting of one loop of
intestines upon another. Several conditions are necessary for its
production. First, the mesentery must be elongated. This change in the
mesenteric root may have been caused by the dragging of an old and
large hernia, or the mesentery may have been lengthened by relaxation
of the abdominal walls from childbearing or by the disappearance of
fat. However caused, before torsion of the gut takes place the
mesentery is elongated, so that the two ends are approximated and
something like a pedicle formed. Second, the portion of bowel attached
to the lengthened mesentery may become filled with an enormous quantity
of fecal matter and paralyzed by the great distension. In this paretic
condition it may be displaced by the living, moving parts around it,
and become bent and twisted, or the length of bowel belonging to the
elongated portion of the mesentery may be the seat of inflammation,
and, paralysis following, it becomes without resistance subject to the
pressure and movements of the active vital parts surrounding it. A
portion of bowel with its accumulated contents having a redundant
mesentery and paralyzed by enormous distension or by inflammation, or
by both, may readily be twisted more or less completely, and in some
cases several times upon itself.

The weight of the bowel and its contents, along with the rapid
distension of the intestine above, fixes the gut in this state of
torsion and effectually prevents it from untwisting. A semi-rotation of
the paretic and distended bowel about the mesenteric axis is sufficient
to interfere with the supply and return of blood and provoke enteritis.
Indeed, the rotation is rarely sufficiently great to produce complete
obstruction, and the symptoms are frequently rather those of
inflammation than of internal strangulation. For weeks before the final
attack the patient usually has symptoms of intestinal disorder, such as
flatulence, constipation, and spells of colic, due no doubt to the
changes provoked by the elongated mesentery and bent or curved
intestine. When torsion takes place the attack is sudden and the
symptoms violent and urgent. Vomiting, meteorism, insuperable
constipation, and frequently tenesmus, are soon followed by collapse
and speedy death. The patient may die in twenty-four hours; he rarely
lives beyond the fourth day. In some cases excessive tenesmus and
bloody stools are seen in the early stages of torsion of the bowel. The
condition may be mistaken for intussusception, but can usually be
distinguished by the premonitory symptoms of twisting and by the more
rapid course, the sudden meteorism, and quick collapse of the latter.

Still another way by which displacement of intestine may occasion
obstruction to the passage of its contents is when a portion of the
intestine has a long and narrow mesentery, and around this mesentery,
which is like a pedicle, another portion of the bowel is thrown,
encircling and compressing it. The accompanying figure, taken from
_Ziemssen's Cyclopaedia_, gives a good idea of this condition (Fig.
23). It represents a {842} loop of the small intestine placed around
the mesenteric pedicle of the sigmoid flexure. Leichtenstern calls this
"intertwining or knotting of two intestinal loops."

[Illustration: FIG. 23. Anterior view of the strangulated intestine and
stricture. _a_, gastric extremity; _b_, rectal extremity.]

[Illustration: FIG. 24. Posterior view of the strangulated intestine
and stricture. _a_, gastric extremity; _b_, rectal extremity.]

In consequence of inflammation of the peritoneum and effusion of lymph,
peritoneal surfaces are joined together, and before the lymph is fully
organized these surfaces are separated by the constant movements of the
organs and the change in the relationship of the parts, and strings and
bands of various shapes and sizes are formed in which a portion of the
intestine may become entangled and constricted. Sometimes the bowel
accidentally becomes engaged in a loop or noose of false membrane, or
becomes bound down under a band of fibrin; or, the peritoneal surfaces
of some of the organs having been joined together or to the wall of the
abdomen or pelvis, a loop of bowel may escape into a slit or opening
and become incarcerated; or a fold of bowel may fall into a fissure in
the omentum or mesentery or broad ligament of the uterus or suspensory
ligament of the liver, and become constricted; or the appendix
vermiformis may be twisted around the intestine in such a way as to
cause ligation of the tube, or, by becoming attached to some
neighboring part, it may form a loop through which the intestine may
pass and become obstructed. In the same way the bowel may be
constricted by a diverticulum. (This is well shown in Figs. 23, 24, and
25.) Bands entangling the bowel and causing strangulation may be
attached to the fimbriated process of the Fallopian tube or the ovary
or uterus. Indeed, it is impossible to describe in a limited space the
almost infinite ways in which these bands and strings may engage and
incarcerate the intestinal tube (Figs. 24, 25).

{843} [Illustration: FIG. 25. An appearance of the natural relations of
the diverticulum to the intestine. _a_, gastric extremity; _b_, rectal
extremity.]

Internal strangulated hernia may result from the bowel falling into a
pouch of the peritoneum and becoming ligated by the orifice of the
pouch, or passing into the foramen of Winslow, of which there are three
cases of strangulation recorded; or a retro-peritoneal hernia may be
formed; or, more common still, a hernia of the intestine through the
diaphragm.

In diaphragmatic hernia an opening is more frequently found in the
posterior part of this muscle. Two hundred and fifty-two cases of this
form of internal hernia have been collected by Leichtenstern, in which
the diagnosis was made in only five cases. He found the oesophageal
opening, a spot just behind the sternum, and a gap between the lumbar
and costal parts of the muscle, the weakest points in the diaphragm.

Diaphragmatic and other forms of internal hernia may exist and not
produce symptoms of strangulation either at the time of formation or
subsequently, just as we so commonly see in cases of external hernia.
When the bowel is constricted, however, and its circulation interfered
with, symptoms of internal strangulation come on, and are exactly like
the symptoms of external strangulated hernia. The attack is sudden, the
symptoms acute and urgent, and the course and termination very rapid.
Unless the constriction is relieved death may take place in twenty-four
hours; life is rarely protracted beyond three or four days.

The patient has first eructations, soon succeeded by nausea and
vomiting. The matter vomited consists of the contents of the stomach,
then of gastric fluid, bile, and the contents of the intestines. When
the last is ejected the vomiting is called fecal or stercoraceous. The
patient complains of a sense of constriction about the abdomen, griping
pains about the umbilicus, flatulence, tenesmus, and insuperable
constipation. One or two free stools from the large intestine below the
site of strangulation may be passed, but this should not deceive the
practitioner. As a rule, peritonitis soon follows strangulation. The
belly becomes tympanitic and tender, the pulse small and wiry, and the
face anxious. When gangrene supervenes the pain subsides, the pulse
becomes weak and intermittent, the surface cold and clammy, and the
patient soon dies in a state of collapse. Slight delirium may precede
death, or the mind remain unimpaired to the end. Very often, when
gangrene sets in and pain disappears, the patient has a grateful sense
of relief and is hopeful of recovery.


{844} Intussusception, Invagination.

One of the most frequent and important causes of intestinal obstruction
is intussusception or invagination of the bowel; by which term is meant
the protrusion or slipping of one portion of bowel into a portion
immediately adjoining.

This condition is sometimes found after death in persons old or young,
but particularly the latter, in whom during life there were no symptoms
of intestinal obstruction or intestinal trouble of any kind. The
displaced intestine in these subjects is easily reduced, is unattended
by any signs of inflammation, and is evidently the result of spasmodic
contraction of the transverse muscular fibres of the bowel at one part,
with distension and relaxation at another part, by which, just before
death, one piece of the bowel is pushed into an adjacent piece. Not
unfrequently two or more invaginations are seen in the same subject.
Flint[4] counted as many as fifteen in a child who died of typhoid
fever. This invagination of the death-struggle almost invariably
involves the small intestine, and may be the protrusion of a piece of
the bowel above into a piece immediately below, or the reverse, a
portion of bowel below being pushed into a portion above. It has been
suggested that this slight and temporary intussusception may occur
during life and give rise to temporary symptoms of intestinal
obstruction, which disappear when reduction of the displacement
spontaneously takes place.

[Footnote 4: _Practice of Medicine_.]

[Illustration: FIG. 26.]

[Illustration: FIG. 27.]

It will be seen by the diagrams that three successive portions of
intestine enter into the formation of an intussusception--an entering,
returning, and receiving portion. Two mucous surfaces and two serous
surfaces are thus brought into apposition. The mesentery attached to
the included lengths of bowel--viz. the entering and returning
lengths--is necessarily pulled down with the bowel in its descent, and
is also embraced by the receiving portion of the intestinal tube. The
traction excited by this portion of mesentery, thus wedged in between
the middle and inner layers of the bowel, materially alters what would
otherwise be the relationship of the parts. Fig. 26 shows simple
invagination of the ileum like the finger of a glove, in consequence of
the traction exerted. The entering or invaginated portion does not
always lie in the axis of the enveloping tube, but is more or less
curved, until very often its lower orifice is in contact with the wall
of the outer layer. The concavity of this curve looks {845} toward the
mesenteric edge of the invaginated portion of bowel, and the convexity
toward the opposite side of the receiving portion. The convex side of
the middle cylinder is often thrown into transverse folds or
convolutions. Intussusception, which gives rise to symptoms
characteristic of intestinal obstruction during life, is invariably
from above downward. It is doubtful whether there is on record a single
well-authenticated case of inflammatory invagination where the lower
segment of bowel protruded into the upper.

Reference to the diagrams will show that the lumen of the bowel is
diminished, and that more or less intestinal obstruction must follow
invagination. This obstruction is increased by the inflammation which
necessarily follows this condition. The large and numerous
blood-vessels of that portion of the mesentery involved in the
invagination are compressed and stretched; arterial supply, and
especially venous return, are interfered with; congestion quickly
follows, with copious inflammatory exudation; the layers of intestine
become swollen, and blood, sometimes in abundance, is poured out from
the mucous membrane. Peritonitis, limited sometimes to the invaginated
part, more often spreading to the peritoneum covering neighboring
structures, soon begins, and the contiguous serous surfaces are
agglutinated and the intussusception rendered irreducible. Lymph and
other inflammatory products are poured out freely; the coats of the
intestine become distended and thicker, and the inner and middle layers
of the invagination are separated by the deposit; the invaginated part
becomes more and more curved toward the mesenteric border of the outer
layer; and occlusion of the bowel, begun by the invagination, is made
more or less complete by the changes wrought by inflammation (Fig. 27).
That intestinal obstruction is not always complete in intussusception
is shown by the fact that fecal matter, often in considerable quantity,
is passed through the bent and narrowed tube, the intestine retaining,
at least for a time, its contractile power. The changes produced by
inflammation are chiefly seen in the inner and middle layers of
intestine, the receiving or outer layer of the invagination often
escaping any serious damage. These changes vary with the character and
duration of the inflammation. Sometimes they are limited to an
agglutination of the opposed serous membranes, an effusion of blood and
serum from the mucous surfaces, and an enormous distension and swelling
of all the invaginated parts; or the inflammation may end in
mortification of the middle or both the inner and middle cylinders, the
dead part coming away in shreds or in large fragments, or, if the
patient lives long enough, the entire invaginated tube being discharged
through the anus. If the inflammation involves the invaginated parts
unequally, strips and shreds of the bowel are detached by ulceration
and sloughing, and may escape in the discharge from the bowels in
pieces so small as to be unnoticed; but if the intussuscepted part dies
en masse, a circular line of demarcation is formed by ulceration, and
the dead segment is detached and drops into the cavity of the bowel
below, and escapes through the rectum. It is often so complete that the
inner and middle cylinders can be recognized, and the part of the
intestinal tube to which the expelled bowel belonged can be determined.
In favorable cases the blood-vessels of the healthy bowel above and
below the dead segment pour out a circular mass of coagulable lymph,
which, becoming organized, closes the breach and {846} completes the
intestinal tube. To accomplish this it is necessary that the ends of
the two portions of bowel should be accurately coaptated: if they are
not, some opening may be left through which the contents of the gut may
escape into the peritoneal cavity, producing fatal peritonitis; or the
new formation may be imperfectly organized, and burst during some
peristaltic movement of the bowel or from the pressure of gas
accumulating in the gut; or the supply of lymph may be so redundant as
to obstruct the calibre of the bowel, or end in cicatricial
contraction, stricture, and obstruction. Aitken[5] records four
instances where the curved end of the invaginated portion of bowel by
prolonged pressure caused ulceration and perforation of the coats of
the enclosing bowel, the invaginated portion passing through the side
of the enclosing segment and projecting into the cavity of the
peritoneum.

[Footnote 5: _Science and Practice of Medicine_.]

Gangrene and ulceration, however, do not always follow intussusception.
The mesenteric injuries may be sufficient to produce congestion and
exudation, and the patient survive the invagination for weeks, and
death eventually occur without sloughing or ulceration; or spontaneous
reduction of the invagination may take place and recovery of the
patient follow. The last termination must be rare, and impossible when
firm adhesion between the serous surfaces has taken place; but that it
does exceptionally occur is proved by cases where the diagnosis of
intussusception was undoubted, the invagination being felt in the
rectum or seen prolapsed through the anus. The most common termination,
if the patient survives, is mortification of the invaginated part and
separation in mass or by shreds or fragments.

Intussusception may occur in any portion of the intestinal canal, but
some points are more liable to it than others. 56 per cent. of the
cases collected by Brinton were ileo-caecal; in 32 per cent. the small
intestine alone was involved; 28 iliac and 4 jejunal; in 12 per cent.
the colon, including its sigmoid flexure, was the part implicated.

When the rectum is involved, it usually forms the outer layer of the
invagination, the middle and inner layers being formed by the bowel
which has passed from above into it; when prolapse of the rectum itself
occurs, the mucous membrane is generally alone involved, but along with
this the muscular coat may also descend and a true invagination of the
rectum be found.

The most common variety of intussusception is the ileo-caecal. It is in
this form that we find the greatest length of bowel involved. This
invagination begins generally at the ileo-caecal valve, the lips of
which at first turn toward, and descend into, the cavity of the caecum,
drawing with them the end of the ileum; in this case the valve forms
the lowest point of the invagination. If the invagination continues,
the end of the caecum is next inverted; and if the process still goes
on, more and more of the colon is invaginated, until in some rare cases
it traverses the whole of the large intestine, appearing just above or
even protruding through the anus. In this variety the vermiform
appendix lies between the middle and inner layers of the
intussusception, and its opening, usually stretched and enlarged by the
inverted caecum and inflammatory effusion, is found close to the
ileo-caecal orifice. In this intussusception the caecum and colon are
large and roomy, and the invaginated portion not so liable, {847} as it
is when the small intestine is alone implicated, to strangulation and
sloughing; nor is there seen in ileo-caecal intussusception, unless the
portion of bowel involved is very short, the marked curvature of the
invaginated portion so commonly found in the small intestine. In the
ileo-caecal form it is twisted or much convoluted rather than bent.

Another variety of ileo-caecal invagination--very rare, however--is
where the ileo-caecal orifice does not descend into the cavity of the
caecum, but the lower end of the ileum passes through the valve into
the large intestine. In this instance the invaginated portion is
tightly compressed by the valve, and strangulation is speedy and
complete. An invagination may occur in the lower part of the ileum, and
the inner and middle layers pass on to the ileo-caecal valve, and be
arrested at that point, and afterward, in consequence of violent
peristaltic action, the whole intussusception, inner, middle, and outer
layers, be invaginated into the colon. In this way the invagination
becomes doubled.

While intussusception may occur in either sex and at all periods of
life, it happens nearly twice as often in males as in females, and is
most frequently seen in childhood. Leichtenstern[6] found in his
statistics of 473 cases that one-half were seen in children under ten
years old, and one-fourth of all intussusceptions occurred in children
from four to twelve months old. Invagination of the small intestine is
found almost exclusively in adults. Brinton from his records gives the
mean age of its occurrence 34.6 years. According to the same author,
the average age of ileo-caecal invaginations is 18.57 years, and
one-half of all cases of this form of intussusception observed by him
were in children under seven years of age. Leichtenstern states that
the lower part of the ileum is the most frequent site of invagination
in the small intestine, and the descending colon and sigmoid flexure
the most common portion involved in intussusception occurring in the
large intestine.

[Footnote 6: _Op. cit._]

The mechanism of intussusception is probably not always the same. The
following is thought to be the most frequent process: A segment of
bowel becomes paralyzed by local peritonitis, some injury, diarrhoea,
or colic, and while in this state a segment of bowel above is subjected
to violent peristaltic action, and is forced into the unresisting
portion below. In this case the paretic segment forms the outer or
receiving layer of the intussusception. Leichtenstern believes that the
paretic portion is turned in and invaginated into the normal bowel
below, and that the clinical course of intussusception and post-mortem
appearance correspond with this explanation. If such is the case, the
paralyzed portion forms the inner layer, and the active bowel below the
receiving layer. Another theory, which applies with much force to the
most common of all invaginations--viz. the ileo-caecal--is, that as
violent anal tenesmus produces prolapse of the rectum, so prolonged and
powerful tenesmus at the ileo-caecal opening may cause prolapse of the
lips of this orifice, and, eventually, invagination of the ileum, or of
both this and the caecum, into the colon. When we remember that the
ileo-caecal valve is furnished with a sphincter muscle, the analogy is
complete. The idea so long entertained that intestinal worms may
occasion invagination of the bowel has generally been abandoned. A
polypoid tumor, by dragging down the portion of bowel to which it is
attached, may produce invagination; and {848} Brinton's statistics give
5 per cent. of cases of intussusception from this source. An
examination of a larger number of cases would probably show a much
smaller percentage due to this cause.

A majority of cases of intussusception, however, take place suddenly,
without previous diarrhoea, colic, traumatism, or ill-health of any
kind, and probably occur without any tenesmus or paresis of a portion
of bowel. It may be that the longitudinal fibres of a segment of gut
contract, dilating and shortening a portion of the bowel; while this
part is distended a portion immediately above may be lengthened and
narrowed by contraction of the circular fibres, and violent peristalsis
going on at this moment, aided, possibly, by contraction of the
muscular wall of the abdomen, forces the upper and narrow segment into
the lower and dilated one.

At first the invagination involves a small portion of the bowel, but,
active peristaltic action continuing, it rapidly increases in size.
This increase is made at the expense of the sheath or outer layer,
which turns in to form the middle layer. The length of the invagination
varies from two or three inches to three, four, or five feet.

The symptoms of intussusception generally come on suddenly, and
indicate both intestinal obstruction and inflammation. Pain resembling
violent colic, and referred to the site of the invagination, is a
prominent symptom. The pain is intense, paroxysmal in character, but
after a time it becomes continuous. At first pressure gives relief, but
in a few hours tenderness, denoting peritonitis, appears, limited to
the invagination or spreading gradually over the whole abdomen.
Vomiting soon follows, and, with rare exceptions, is persistent. After
two or three days occasionally blood and sometimes fecal matter are
ejected from the stomach. Diarrhoea, with bloody, mucoid stools, is
rarely ever absent, and is characteristic of invagination. The patient
has from fifteen to twenty passages a day. If the large intestine is
involved, the diarrhoea is accompanied with tenesmus. Above the
obstruction gas and ingesta accumulate, and produce abdominal
distension, sometimes well marked. Generally the tumor formed by the
invagination can be felt through the abdominal wall, and is a symptom
of great importance. Meteorism and peritonitis may render the existence
of the tumor obscure or altogether prevent its recognition, but in
intussusception of the colon and at the ileo-caecal valve the solid
cylindrical mass can usually be found, and frequently, when the small
bowel alone is implicated, a very careful and patient examination will
enable the observer to detect it. Sometimes it changes its site, size,
and shape; occasionally it can be felt in the rectum or is seen
protruding through the anus.

The urgency of the symptoms of invagination depends upon the portion of
bowel involved and the degree of constriction of the gut and its
attached mesentery. When the bowel is tightly constricted the symptoms
are acute, and the patient may die in a day or two; when the bowel is
not constricted the symptoms are chronic in character, and in the early
stages not urgent. The difference here is like that between
strangulated and incarcerated hernia.

In acute cases the attack is sudden, obstruction complete, and the
symptoms those of internal strangulation of the bowel, often followed
by collapse, which may destroy life in a few hours. These cases are
{849} chiefly jejunal and iliac invaginations, and the higher up in the
small intestine the seat of obstruction the more violent and urgent the
symptoms. Constriction, being great, is followed by engorgement and
inflammation of the invaginated bowel, and if the patient lives long
enough gangrene ensues, by which the obstructing mass is separated and
discharged en masse or in fragments through the anus. Not unfrequently
life is saved in this way. That gangrene has taken place and separation
of the invaginated segments is in progress are often known by the very
fetid character of the evacuations and by their admixture with blood
and shreds of necrosed bowel. When the sequestrum has been detached
entire, it is often passed with difficulty. Frequently it lodges at
some point in the bowel, producing temporary obstruction and giving
rise to tenesmus and pain as it passes along the large intestine. There
is no doubt that the continuity of the intestine above and below the
neck of the invagination has been established, and complete cures
effected in the way already mentioned. Usually, however, the patient
dies from collapse, peritonitis, or perforation of the bowel before the
obstructing mass can be removed by gangrene. Children almost invariably
die before this can take place, and adults live from the seventh to the
fourteenth day, according to the greater or less violence and acuteness
of the symptoms. When the slough has been discharged and the continuity
of intestine established, recovery is still uncertain, and death very
often happens for reasons referred to in speaking of the separation of
the sequestrum.

Separation of the invaginated portion and its expulsion, according to
Leichtenstern, in the majority of cases takes place from the eleventh
to the twenty-first day, but in chronic cases it is often delayed for
months. According to Brinton, separation of the sequestrum occurs
between the eighth and fifteenth in intussuscepted small intestine, and
between the fifteenth and twenty-second days in acute cases of
ileo-caecal and colic invaginations.

In chronic cases of intussusception, which usually embrace the
ileo-caecal and colic varieties, strangulation is not common and the
course of the disease is protracted. These cases often last for several
months, and the symptoms are not always well defined. At first the pain
is paroxysmal, with long intervals of ease. Vomiting succeeds, but is
not persistent; discharge of the contents of the bowel below the seat
of lesion takes place and afterward fecal matter from above this point,
because the permeability of the bowel is not usually lost in chronic
cases. Eventually the alvine discharges become bloody, mucoid, and
characteristic of intussusception; the severity of the symptoms may
gradually increase, the pain becoming greater, more constant, the
vomiting more incessant, the discharges from the bowels more frequent,
and in one, two, or three months the patient dies from asthenia.
Several authentic cases are related where the disease lasted one or two
years before terminating fatally. Very often some days before death the
pain and tenderness cease, and the operations become free from blood
and normal in character.


{850} Constipation.

Constipation is a prominent symptom in all of the conditions which give
rise to intestinal obstruction, and habitual constipation or loss of
the powers provided for the advance of the contents of the intestines
not unfrequently leads to permanent occlusion of the canal. It is
impossible to fix any definite rule as a standard of health for the
number and quantity of alvine evacuations. Some individuals have a
passage from the bowels once every day; others, in the enjoyment of as
good general health, suffer from the ordinary inconveniences of
constipation if they have less than two or three daily fecal
discharges; others, again, apparently equally as well, have a movement
from their bowels once in two or three days or once a week, or even
once in two weeks. Habershon[7] records the case of a "woman sixty
years old who from youth upward had had a passage from the bowels only
every six or eight days, and whose health had been perfect." A lady
under my own observation, for twenty years never had an alvine
discharge oftener than once in two weeks, and three times in her life
had passed two months without a movement of her bowels. This lady was
the mother of several children, and, although not in perfect health,
was able to attend to her ordinary household duties. Such cases are not
very uncommon, and occur, as far as I have been able to ascertain, more
frequently in women than in men.

[Footnote 7: _On Diseases of the Abdomen_, quoted by Leichtenstern in
_Ziemssen's Cyc. P. of Med._, vol. vii. p. 588.]

The number of fecal evacuations and the quantity discharged have been
shown by Bischoff and Voit to depend, to some extent, upon the
character of the food ingested, vegetable diet producing abundant, and
animal diet scanty, stools. Doubtless, the quality of the food partly
explains the quantity of the alvine evacuation, although, to some
extent, this must depend upon the time that the feces remain in the
colon, a long residence there taking away a greater part of the watery
constituents and making the fecal mass thicker and harder; but the
variations in the number of stools in persons living on the same diet
can only be explained by the variations in the activity of the
peristaltic action in different individuals, or in the same individual
at different periods and under different surroundings.

The causes of habitual constipation are of the most varied and
diversified character, and it is not always possible in an individual
case to point out the original or primary one. Not unfrequently several
causes are in operation at the same time to produce sluggishness of the
intestinal canal and constipation. Very often it begins with change of
scene and habits, by which the daily visit to the water-closet is
interfered with, or after confinement to bed with some temporary
indisposition. It is more likely to occur in men and women whose habits
are sedentary and who are constitutionally lazy and indolent. The feces
are allowed to remain in the rectum and colon, and every hour after the
ordinary time for going to stool diminishes the watery parts of the
fecal mass and makes it harder and more consistent. Many cases of
chronic constipation, begun in this way, have ended in dilatation and
thickening of the intestine, ulceration of the mucous membrane, and,
eventually, perforation of the coats and escape of the contents of the
gut into the peritoneal cavity. Rapid {851} excretion of water by the
kidneys, lungs, and skin produces constipation by withdrawing a large
proportion of the water from the fecal mass, rendering it unnaturally
dry and of diminished bulk. In diabetes, constipation arises from this
cause unless the patient makes up the loss by drinking an unusually
large quantity of water. Constipation in nursing-women is explained by
the loss of water in the secretion of milk. The profuse sweating which
attends malarial fever, phthisis, and other diseases readily accounts
for the constipation which often accompanies these disorders.

Certain articles of food not necessary to mention here produce
constipation. They fail to excite peristaltic action; or articles of
diet which at first act as a stimulus to the bowels, and even provoke
temporary diarrhoea, lose their power if kept up too long--just as
certain purgative medicines lose their force if continued for too long
a period. Gradually they cease to increase the peristaltic action, and
rather add than otherwise to the inactivity of the intestines. Eating
the same kind of food day after day is very apt, sooner or later, to
result in diminished sensibility of the intestinal canal, a reduction
of the peristaltic force, and deficiency in the secretion of the
digestive juices, which in itself is a common cause of constipation.
Frequent change of diet is generally needed to supply the stimulus
necessary for that intestinal motion which relieves the bowels.

Bile is looked upon as one of the most powerful agents in stimulating
peristaltic action, and when, from any cause, mechanical or otherwise,
it is not poured into the bowel, constipation ensues. Unnatural
flexures, congenital or acquired, of the large intestine are not
unfrequently the source of chronic constipation. These flexures, normal
or factitious, favor accumulation of feces, especially in subjects who
have diminished sensibility of the bowel and a paretic state of the
muscular coat. Certain injuries and diseases of the brain and spinal
cord reduce, and sometimes altogether prevent, intestinal activity.
Hysteria, if it exist for any length of time, is generally attended by
sluggishness of the bowels, and great mental depression (melancholia)
is sometimes preceded and sometimes followed by habitual constipation.
In treating such a case it is important to make the distinction.

Temporary paralysis of the muscular coat of the bowel, followed by
symptoms of intestinal constriction, with insuperable constipation,
sometimes attends violent contusion of the abdomen. In some cases
prolonged functional weakness of the muscular coat follows the injury.
Many chronic diseases leave the bowel in a sluggish condition by the
pathological changes produced in the intestine. The function of the
muscular coat is frequently injured by the infiltration which
accompanies peritonitis. The fibres are separated by the serous
effusion which attends this inflammation; they become overstretched,
and, losing their contractility, end in paralysis and obstinate
constipation. Occlusion of the canal from this cause may last for days,
and be accompanied with tympanitis, stercoraceous vomiting, and all the
signs of internal strangulation, ending in death. Post-mortem
examinations in such cases show no stricture or unnatural diminution in
the size of the canal, but that the fatal occlusion was due to
paralysis of the muscular coat of the bowel and arrest of its power.

The normal advance of the contents of the bowel is interfered with by
any cause which lessens the contractility of the muscular coat. Chronic
{852} diseases which debilitate the general muscular system affect at
the same time the contractile power of the muscular coat of the canal,
and the debility and degeneration of old age are felt here, and
sometimes occasion the constipation which often accompanies this period
of life. Leichtenstern[8] says that chronic intestinal catarrh is a
common factor of constipation--that when this catarrh is of long
standing it produces relaxation of the muscular coat and diminishes the
elasticity of the intestinal walls. He believes that this pathological
condition exists in a large proportion of the cases of habitual
constipation attended with mental depression, that the hypochondriasis
makes its appearance after the constipation has become chronic, and
that it is a secondary symptom. This affection is located chiefly in
the small intestine, and does not usually involve the colon.

[Footnote 8: _Op. cit._]

Probably the most common form of chronic constipation is that which
accompanies loss of sensibility and muscular inactivity of the colon
and rectum. The large bowel becomes sometimes so distended by the
accumulated fecal masses that it has been found after death to measure
ten or fifteen inches in circumference and to contain an astonishing
quantity of feces. Any part of the canal, except the last two inches of
the rectum, which is kept empty by the contraction of the sphincters,
may be occupied by the mass, but the accumulation is greatest in the
rectum, caecum, and sigmoid flexure. At the last-named location the
distension is so great that the mass can be readily felt through the
abdominal walls. The tumor may be as large as a foetal head, and may be
mistaken for a simple or malignant tumor of the omentum, stomach, or
other organ, or for pregnancy or ovarian growth. The dilatation may be
so enormous as to push the small intestines into the back part of the
abdominal cavity and to interfere with the function of any organ upon
which it encroaches. It may press upon the concave surface of the
liver, and, arresting the flow of bile, produce jaundice or
mechanically interfere with some portion of the track of the urinary
organs and cripple their functions. When situated in a portion of the
canal not tightly attached to the abdominal walls it is slightly
movable, more or less hard and consistent, according to its duration,
for it remains often for months unchanged, sometimes giving to the
fingers the impression of a rather soft, easily-indented swelling with
a uniform smooth surface--more often feeling like a hard, irregular,
elongated, and corrugated mass of fecal balls. Contraction here and
there of bundles of the circular muscular fibres of the gut produces
the irregular, corrugated impression imparted to the fingers. Their
shape and position may sometimes be changed by pressure through the
abdominal wall. If the accumulation occurs in the rectum, the
introduction of a tube or bougie is prevented by the impacted mass,
which can be gotten away only by the fingers or by some instrument. The
colon and rectum may be dilated to their utmost capacity with an
enormous amount of feces, enough to fill a common-sized pail, and both
the patient and medical attendant be deceived as to the sufferer's
condition by the fact that he has his daily number of stools. The
semi-fluid contents of the small intestines find their way through this
mass by some irregular and uncertain track, undermining and breaking
down sometimes a lump of the old fecal accumulation, which, if small in
size or broken up, may pass on and {853} escape by the anus, but if
large and hard may drop into the irregular and uncertain passage and
permanently close it; then sudden and complete intestinal occlusion
takes place, with all of its fearful consequences. If this, however,
should not occur, and the accumulation is not recognized and removed,
the enormous dilatation may go on until complete paralysis of the
muscular coat is produced, and entire stoppage of the current of feces,
with permanent occlusion of the bowel; or before this takes place
ulceration may set in, partly because of the great pressure of the
fecal mass upon the mucous membrane, and partly from the irritating
character of the contents of the bowel. Ulceration begins, most likely,
at some point where resistance is greatest, and perforation of the
bowel may ensue.

SYMPTOMS.--If the accumulation occupies only a portion of the colon, as
the caecum or sigmoid flexure, the distended part may become displaced
and twisted on its long axis. This condition scarcely ever happens in
the large intestines except at the parts mentioned. Torsion of the
caecum rarely takes place except in persons of from forty-five to sixty
years of age, while twisting of the sigmoid flexure may happen at any
period of life. When distended and very heavy from the weight of feces,
with probably some congenital defect about its mesenteric attachment,
the sigmoid flexure may become twisted and drop into the pelvis,
producing at once symptoms of internal strangulation.

Individuals accustomed to having one or more alvine evacuations a day
are made uncomfortable by two or three days of constipation. A feeling
of distension about the abdomen, with flatulence and heat, follows this
condition, and soon afterward headache, loss of appetite, and symptoms
of indigestion supervene. If this state of the bowels continues
unrelieved, pressure upon the hemorrhoidal veins takes place and
interference with venous return, producing congestion in the lower end
of the rectum. This is attended by straining, diarrhoea, evolution of
gaseous matter, colicky pains, and possibly sympathetic disturbance of
the genito-urinary organs. When at last the hardened and enlarged mass
is discharged, it produces some pain and burning about the anus, with
possibly rupture of the mucous membrane in that region. Fissure of the
anus may thus originate. In the case of a lad aged about nine years
under my care fissure of the anus began in this way, and after its
formation the pain of defecation was so intense that he resisted for
ten days every attempt of his bowels to move. After this time he passed
every day or two one or more hardened fecal balls, but always with such
atrocious pain that he looked forward to the next attempt with terror.
This case ended in fecal impaction, which nearly proved fatal.

Not unfrequently persons who habitually go two or three days without
having a passage from the bowels are not apparently inconvenienced, and
after a time any of the discomforts ordinarily felt from constipation
are not noticed, if indeed any exist.

Generally, however, chronic constipation leads to a host of troubles of
the most varied character. There is not an organ in the body that is
not more or less influenced by it. The generation of gas in the
intestines produces a sense of fulness of the abdomen and elevation of
the diaphragm which interferes with the action of the lungs and heart.
The sufferer is oppressed, sighs, and has difficult respiration and
attacks of {854} palpitation of the heart. The influence of the
abdominal pressure is conducted by the sympathetic nerves to the brain,
and the patient frequently has vertigo, headache, ringing in the ears,
faintness, etc., and in consequence of the pressure upon other nerves
or of hyperaemia of the spinal cord and its membranes he has dull
aching pains in his back, groins, genitals, or extremities. I have seen
in several instances pain in the legs, coming on after the patient has
retired and lasting until morning, violent enough to prevent sleep, at
once permanently relieved by an active cathartic after antiperiodics,
alteratives, and anodynes had failed to do any good.

A patient suffering from habitual constipation usually obtains
temporary relief by the bowels acting either spontaneously or after a
dose of medicine; but, the causes of constipation continuing, the
physical discomforts and suffering continue, varied in every
conceivable way. His digestion being disturbed, appetite poor, and
assimilation imperfect, he gradually loses flesh and his complexion
becomes sallow and unhealthy. In addition to this, he soon grows
irritable and fretful, trifling affairs trouble him, he has fits of
great mental depression, and soon settles down into hypochondriasis,
his life becoming a burden to himself and a nuisance to his friends.

If the constipation ends in fecal accumulation, the worst symptoms of
mechanical obstruction may present themselves at any time, and death of
the individual follow. The practitioner should always keep this fact in
mind in treating every case of intestinal obstruction, and search for
fecal impaction by examining the rectum and the whole length of the
large intestine through the anterior abdominal wall. Very often
symptoms of impaction come on gradually in one who has been ailing for
some weeks or months, but sometimes the onset is as sudden as in a case
of acute occlusion of the intestines. The patient is seized with pain
like that of colic and an urgent desire to empty his bowels, but all
attempts to do this are futile, and the straining is followed by great
exhaustion; borborygmus, nausea, vomiting, and possibly hiccough, soon
come on, with tympanitic distension of the belly. If the impaction is
not overcome, death by collapse or from peritonitis follows.
Post-mortem examination shows enormous fecal accumulation, peritonitis
as a consequence of the obstruction, perforating ulcer in some part of
the large bowel, more often the sigmoid flexure, or, in some cases,
absolute rupture of the caecum itself, and escape of its contents into
the peritoneal cavity.


Stricture of the Bowel.

In a report by George Pollock[9] of 127 cases of intestinal
obstruction, 77 belonged to the above class; and Brinton, in his
analysis of the whole group of cases collected by him, says stricture
constitutes about 73 per cent. In 124 cases of intestinal obstruction
reported by Mr. Bryant[10] from the post-mortem records of Guy's
Hospital, 47 were found to be stricture of the bowel. The above
statements show that stricture, or diminution of the calibre of the
bowel, is the most frequent cause of {855} intestinal obstruction, and
the subject is worthy of our earnest consideration.

[Footnote 9: _Medico-Chirurgical Review_, 1853.]

[Footnote 10: _Practice of Surgery_.]

While stricture of the bowel may be found in any portion of the
intestinal canal, it occurs most frequently in the sigmoid flexure and
rectum. Brinton found in 100 fatal cases of stricture 30 in the rectum
and 30 in the sigmoid flexure; only 8 cases in 100 were in the small
intestine. Brinton's statistics correspond very nearly with those of
other writers. The affection is more common in men than women, and the
average age at death is about forty-four years.

The most common cause of stricture is contraction following
cicatrization of ulcers of the mucous and submucous coats of the
intestine. The ulcer may involve the circumference of the bowel, and
the resulting cicatrix terminate in uniform constriction of its lumen,
or the ulceration may extend several inches along the side of the
intestine, ultimately causing contraction in the direction of its
longitudinal axis, marked stenosis, and kinking of the gut. When
ulceration, continuous or in patches, involves a large extent of bowel,
it may reduce the gut to a mass of indistinguishable cicatricial
tissue. Bristowe[11] says he has seen the whole caecum thus contracted
"into a channel barely capable of admitting a goose's quill."

[Footnote 11: Reynolds's _System of Medicine_.]

Stricture of the intestine often follows dysentery or tubercular and
syphilitic ulceration of the bowel. Follicular or hemorrhoidal
ulceration is sometimes the beginning of a stenosis which ends in
stricture of the rectum. Stercoral ulcers of the colon are not
unfrequently the starting-point of cicatricial contraction of the
calibre of the bowel. Sometimes, but rarely, ulcers of typhoid fever
end in constriction of the intestinal tube. The diameter of the gut is
also contracted by the effects of caustic substances, by ulceration
following the lodgment of foreign bodies, and by effusion of lymph or
thickening attendant upon long-standing hernia. Very often after death
it is impossible to determine what particular kind of inflammation and
ulceration caused the stricture. Generally, the cause which provokes
the ulceration sets up chronic peritonitis, which materially aids in
producing the obstruction. Spasm of the circular muscular fibres
usually accompanies these lesions, and materially contributes in many
cases to fatal intestinal obstruction. Some authors assert that spasm
without organic change can produce acute obstruction: such an
occurrence, except possibly in the rectum, must be very rare, if indeed
it ever happens.

The most common cause of stricture is cancer. This disease may
originate in the bowel itself, or, beginning in some neighboring organ
or tissue, gradually spreads and involves the gut. It may extend around
the bowel or be infiltrated along the sides of the canal for several
inches, and may be scirrhous, medullary, or epithelial in character.
Eighty per cent. of the cases of cancer of the bowel are situated in
the rectum. Usually, but not invariably, cancerous deposits are found
in persons who have passed middle age.

An impediment to the passage of fecal matter is invariably produced in
constriction of the intestine from the above causes, and it frequently
continues until fatal occlusion occurs. The contents of the bowel
accumulate above the block, producing distension of the gut and
thickening of the muscular coats above the stricture, with contraction
and atrophy {856} of the portion of intestine below. Dilatation of the
bowel above the seat of lesion is sometimes great enough to cause
rupture and peritoneal extravasation, or distension and stretching of
the coats of the canal may be sufficient to interfere with its
circulation, and ulceration ensue.

Occasionally cases of stricture or well-marked circumscribed
contraction of the bowel are seen which give rise to no marked symptoms
of constriction during life. Such was the case in the instance related
by Bristowe and referred to above. These instances are, however,
exceptional in the large intestine.

Symptoms of stricture vary according to the site, cause, and extent of
the lesion. They are gradually developed, and in this respect are
unlike the symptoms of internal strangulation or of intussusception,
which are generally acute and rapid in their course. When the
obstruction in stricture is complete, progress toward death is
comparatively slow. If the stricture is seated in the small intestine,
the symptoms are often so obscure that for a long time the presence of
the contraction may not be suspected; the contents of the small bowel
are usually fluid, and in this state readily pass through the
constricted part. The more solid the contents of the bowel, the greater
the difficulty in passing a contracted and narrow orifice, and the more
conclusive and characteristic the assemblage of symptoms of obstruction
from stricture.

The history of a case of intestinal obstruction from stricture is often
instructive. For weeks or months there have been colicky pains and
intestinal disorder; possibly, in the early stages, diarrhoea, but
later marked constipation, and probably previous attacks where
constipation was for a time insuperable and death from obstruction
imminent. Hemorrhage, except in cancer or when complicated with piles,
is rare. The attack may come on suddenly, or constipation become more
and more difficult to overcome; violent peristalsis presents itself,
accompanied by pain and abdominal distension, and followed by nausea
and vomiting, the latter often being stercoraceous. During the throes
of pain--for it is paroxysmal--the outline of the distended gut can be
felt and seen through the abdominal walls if they are thin and free
from fat. Unless the stricture is relieved the patient gradually dies
from asthenia. Inflammation is often absent throughout, but enteritis
or peritonitis may come on, or perforation and peritoneal extravasation
ensue and hasten the fatal termination.

When the obstruction is in the rectum it can be felt with the finger;
if in the sigmoid flexure, it may be felt with a gum bougie or probe,
but the use of the former is unreliable, and the latter, unless
carefully employed, dangerous. Obstruction at this point, however, is
attended with marked distension of the descending and transverse colon.
If seated in the small bowel, the large intestine is flaccid and
collapsed. Careful manual exploration often enables the practitioner to
determine the site of the contraction. Weight, pain, dulness, and
fulness are usually found about the stricture, but these signs may be
of little value when the abdominal wall is thick and unyielding, or
peritonitis or tumor is present, or the contracted portion of bowel is
compressed or drawn out of its proper site. Brinton suggests that the
site of stricture may be determined by the quantity of water which can
be injected through the anus into the bowel. Such an estimation must
often be erroneous, as stricture {857} is rarely ever complete and
fluid may be forced through the constricted part. Indeed, Battey of
Georgia has demonstrated upon dead and living subjects that fluid may
be made to pass through the entire canal from the anus to the stomach.

Obstruction due to cancer of the rectum can be determined by digital
examination. When seated in the small intestine or higher up in the
large bowel, the presence of a painful tumor, preceded for weeks by
evidences of impaired nutrition, emaciation, and followed by
lancinating pain, cancerous cachexia, etc., will indicate the character
of the trouble.


Compression and Contraction of the Bowel.

Obstruction of the bowel is sometimes occasioned by compression or
traction exerted on the intestine by abdominal tumors or cysts. Fibrous
tumors of the uterus, ovarian cysts, hydatid growths, or indeed any
form of abdominal tumor, may by pressure on some part of the intestinal
track produce fatal obstruction. Several inches of bowel may thus be
compressed and rendered impervious, or if traction is exerted by the
tumor, which is often adherent to the bowel, the tube may be sharply
bent or twisted and its action interfered with. A case is reported of
compression of the bowel from a great accumulation of fat about the
colon. Adhesions of intestinal coils from chronic peritoneal
inflammatory changes constitute a large and important class of cases of
intestinal obstruction. This condition is known as contraction of the
bowels: 23 of the 124 cases reported by Bryant were of this character.

The usual site of stricture is the large bowel: contraction is far more
frequently seen in the small intestine, and is caused by an effusion of
lymph following simple peritonitis or the inflammation attending the
formation of cancer or tubercle of the peritoneum. Coils of intestine
are matted together or to neighboring parts in this way by bands of
lymph or false membranes, and the action of the bowel interfered with
or obstructed. Constriction of a length of bowel may be found after
death, or a sharp, angular bend by which complete obstruction has been
produced.

Circumscribed peritonitis may produce adhesion of a portion of bowel by
bands of lymph to the uterus or its appendages, or to some part of the
large intestine, or to the abdominal wall, and the action of the bowel
become embarrassed by traction, constriction, or bending. In
consequence of the irritation following this condition, spasmodic
contraction may follow and add to the difficulty, or enteritis may
ensue; and this will especially be the case if the circulation of the
part is interfered with, and render complete what before was a partial
obstruction. Distension and fulness of the bowel above the obstruction,
with contraction and emptiness of the portion of the gut below, are
found after death in cases of contraction, just as we see in fatal
cases of stricture. The history of the case and presence of a tumor
will generally enable the practitioner to determine when obstruction is
due to the presence of some adventitious growth. When contraction is
complicated with the presence of tubercle or cancer, symptoms attending
these conditions will be present.

Obstruction of the intestines from contraction generally comes on {858}
insidiously. The patient may date the beginning of his trouble from an
old attack of circumscribed peritonitis which probably took place weeks
or months before. He has attacks of colicky pains, indigestion, and
constipation. The last is difficult to overcome, continuing for hours
before it is relieved by medicine or the efforts of nature. During the
attack of almost insurmountable constipation violent peristaltic
movement of the bowel above the impediment may be noticed. The patient
may gradually become more and more feeble from suffering and
interference with nutrition, and die from exhaustion, or fits of
obstinate constipation may continue to recur, until finally one of them
becomes insuperable and fatal.

The symptoms of contraction closely resemble those of stricture, but it
is important to distinguish one from the other, as the treatment,
especially if surgical interference is demanded, is very different. A
rigid analysis of all of the signs will usually, but not invariably,
enable the practitioner to make the distinction.

There is an important difference between the constipation of stricture
and that of contraction. In the former the difficulty is in defecation,
emptying the large bowel, the usual site of stricture; in the latter
the difficulty is in the passage of the contents of the gut along the
narrowed and contracted small intestine, the common site of
contraction. In stricture the calibre of the bowel is diminished by
some sharply-defined mechanical impediment seated in the cavity or in
the walls of the tube; in contraction the bowel is bent or kinked by
adhesions, or coils of intestine are matted and glued together and
peristalsis interfered with. In stricture defecation is difficult and
painful; in contraction the alvine discharges are painless. In the
former blood and mucus are not unfrequently seen in the feces; in the
latter the motions are healthy. In stricture constipation alternates
with diarrhoea; in contraction looseness of the bowels is rarely seen.
In stricture distension of the abdomen is lumbar and epigastric; in
contraction the distension is less and is central and hypogastric. In
both conditions violent distinct peristaltic action is seen during a
fit of constipation, and in both the bowel above the constriction is
distended and hypertrophied. In contraction the powerful, writhing
peristalsis involves the small intestine above the impediment, and in
stricture the large bowel above the obstruction. In both stricture and
contraction inflammation of the bowel and peritoneum may supervene. In
contraction, when inflammation sets in or when enteritis and
peritonitis are absent and the attack of constipation is
insurmountable, I have noticed that the symptoms are more urgent and
rapid in their course, and danger of death from collapse greater, than
when these conditions exist in stricture.

DIFFERENTIAL DIAGNOSIS.--In every case of intestinal obstruction a
careful examination should be made for external strangulated hernia.
All of the regions of the abdomen in which hernia may occur should be
thoroughly inspected, as the symptoms of the two conditions are
identical. A small or incomplete external strangulated hernia may
easily be overlooked. An individual with an old hernia may suddenly
have symptoms of intestinal obstruction, and it may be doubtful whether
the obstruction is due to internal constriction or to the external
hernia. Diagnosis is especially difficult when the chronic hernia is
irreducible in character. If the cause {859} of the impermeability is
internal and below the external hernia, that portion of intestine in
the hernial tumor becomes swollen, tense, and hard, and closely
resembles the local symptoms of strangulated hernia. If the external
hernia is reducible, reduction en masse may take place and a
retro-peritoneal hernia be formed. When the case is doubtful and
urgent, an operation for strangulated hernia should be performed.

Functional obstruction of the bowel is sometimes seen, closely
simulating obstruction from one of the structural changes mentioned.
Cases of functional obstruction are seen usually in hysterical or
nervous women, and are generally recognized by the history, course, and
termination of the malady. The fact that local enteritis, peritonitis,
or typhlitis, by paralyzing a portion of the bowel, may produce all the
signs of acute and complete obstruction, should not be lost sight of.

In cases of congenital stricture or malformation, or the presence of
foreign bodies in the intestine, or acute internal strangulation, or
twisting of a length of bowel, and generally in intussusception,
symptoms of acute obstruction are present. The individual may have been
in perfect health, and suddenly symptoms of the gravest character set
in. Intense pain, referred to some special part of the belly, is the
first sign of trouble. Nausea soon follows, and with it great
prostration; the depression of vital power approaches, and sometimes
reaches, syncope; the patient rolls and tosses in agony; his mental
distress is equally great, and if old enough he is conscious of his
danger and is anxious and despondent. Vomiting succeeds the nausea: at
first the contents of the stomach, and then those of the small
intestines, are thrown up; after a time the vomiting is stercoraceous.
The belly becomes swollen, tympanitic, and exquisitely tender; the
weight of the bed-clothes or the slightest touch of the finger upon his
abdomen is intolerable; he keeps his head and shoulders raised and his
lower limbs retracted to avoid pressure of the abdominal muscles.
Constipation is complete and insuperable. If the abdominal wall is
thin, the violent motion of the intestines can be seen and felt through
it. These painful peristaltic movements of the bowel are paroxysmal and
attended by loud rumbling or gurgling noises. The pain gradually
increases; the patient is very restless and complains of great thirst;
his pulse is small, hard, and frequent, his extremities cool and
features pinched. If not soon relieved, exhaustion comes on; he has
muttering delirium, cold clammy perspiration, hiccough, twitching of
the tendons, and death soon follows from collapse or from peritonitis
or gangrene, or from both. The average period of death is from six to
eight days. It may occur in thirty-six or forty-eight hours, or the
patient may last for two weeks.

In congenital occlusion and malformation the history of the case, the
age of the patient, and the fact that the deformity in such cases is
almost always confined to the anus and rectum, usually render the
diagnosis sufficiently easy.

Obstruction caused by foreign bodies impacted in the intestines can
generally be diagnosed. The history of the case may show that foreign
bodies have been swallowed or that the patient has been subjected to
some of the conditions which cause the formation of enteroliths. These
stony concretions are usually found in the caecum or colon, and
frequently give rise for days and weeks to symptoms of indigestion,
emaciation, {860} constipation, and other evidences of bad health
before complete occlusion of the intestine takes place. Not
unfrequently, before the sudden attack of impermeability of the bowel
the patient has had repeated attacks of typhlitis, and has been
conscious for a long time of the presence of a tumor in the region of
the caecum or colon. Possibly he has passed on some former occasion
pieces of the stony concretion.

Diagnosis of obstruction by gall-stones is often aided by the fact that
the patient has recently suffered characteristic pains of hepatic colic
and by the icterous condition of the skin. Possibly the individual has
suffered repeated attacks of hepatic trouble and has previously passed
a gall-stone. Obstruction from this cause is seen four times as often
in women as in men, and always after the middle period of life.

In obstruction occasioned by internal hernia or the presence of
membranous bands, loops, mesenteric pouches, the symptoms are often
such as to baffle all attempts at accurate and certain diagnosis. The
onset of the symptoms is sudden and the course of the disease rapid;
prostration of vital power is extreme, sometimes amounting to syncope;
vomiting incessant and persistent; pain constant and fixed. The most
characteristic symptom of internal strangulation is the very great and
prolonged depression of vital power; it occurs generally in early adult
life.

Erichsen states that in twisting of the bowel the abdomen is unevenly
distended, it being tympanitic on one side and flattened on the other.
This condition of the bowel is usually seen after middle age. In
intussusception the principal signs are, usually, the early age of the
patient--obstruction from other causes in children being rare--the
suddenness of the onset of symptoms, the frequent desire to go to
stool, the tenesmus, and the characteristic bloody mucus discharges. By
abdominal palpation frequently the sausage-like tumor can be
recognized, and very often the intussuscepted part can be felt in the
rectum or seen protruding through the anus. When invagination involves
the upper part of the small intestine, diagnosis of the cause of
occlusion is almost impracticable.

In obstruction of the bowel from fecal accumulation, inflamed and
thickened intestine, stricture, compression and traction, and
contraction of the gut from cancerous deposit, the symptoms are
gradually presented and chronic in character. They are unlike the signs
of acute obstruction, which occur in persons apparently in perfect
health and are sudden and violent from the beginning. In chronic
obstruction of the intestine the patient has probably been complaining
for some time, with symptoms of abdominal trouble. He has been unwell
for weeks, his appetite poor, digestion disordered, strength
diminished, and bowels constipated. The last symptom is the most
distressing of all. Purgatives do not give the relief ordinarily
obtained, but add to the griping, colicky pains, nausea, and general
depression. When his bowels do act, the stool is sometimes liquid,
sometimes very hard (scybalous), or the form of the matter passed is
tape-like or pipe-like. Sometimes, in his frequent attempts at stool,
the only discharge is blood and mucus or pus. Attacks of eructation and
vomiting often take place during the progress of the disease.
Stercoraceous vomiting is, however, rare, and only seen in the later
period of the attack. Abdominal distension is slow in making its
appearance, but after a time is well marked, and due more to tympanitis
than to {861} constipation; the tympanitic distension is accompanied by
loud rumbling and gurgling noises in the bowels. After a period which
varies much in different cases, inflammation, suddenly or gradually, is
set up, and all the symptoms of acute obstruction are presented,
grafted on signs of chronic occlusion. We have pain, nausea, vomiting,
great distension and tenderness of the abdomen, peristalsis plainly
seen and felt if the abdominal wall is thin, the small, frequent, wiry
pulse, clammy perspiration, prostration with hiccough, tendinous
twitchings, and death, very like that following a case of external
strangulated hernia.

Obstruction due to fecal accumulation generally happens in persons who
have passed middle age, and can often be diagnosed by digital rectal
examination and palpation of the abdomen, by the presence of fecal
tumors, and the history of long-existing constipation with its manifold
consequences; previous attacks of impermeability, and relief by
discharge of enormous masses of feces.

Obstruction caused by the presence of some abdominal tumor is generally
known by the history of the case, the fact of the existence of the
tumor being known to the patient or discovered by the physician by an
examination through the abdominal walls or through the vagina or
rectum. The progress of such cases is essentially chronic, but acute
symptoms may at any time come on. Diagnosis of obstruction due to
stricture is frequently made by examination of the rectum and sigmoid
flexure, the usual sites of constriction from this cause. Complete
occlusion from stricture is almost always preceded by well-marked
premonitory symptoms.

When the obstruction is situated in the lower part of the colon and
rectum, its precise seat can be determined by digital or manual
examination or the use of a bougie or tube. When the site of
obstruction is above the sigmoid flexure, it is difficult, and
occasionally impossible, to determine its exact locality. As a rule,
when the constriction is in the small intestine the symptoms are acute
and urgent; pain is intense, vomiting comes on soon, and prostration is
early and extreme. When the large intestine is involved, except in
volvulus, the symptoms are generally chronic. In twisting of the gut
the symptoms are rapid and uncommonly severe. The higher up the
obstruction, the earlier stercoraceous vomiting begins. Above the
constriction the bowel is distended and tympanitic; below the
constriction it is generally collapsed. In obstruction of the large
intestine the outline of the tympanitic and distended gut may be traced
with the eye and hand. In constriction of the small intestine the
secretion of urine, as has been shown by Hilton, G. Bird, and Barlow,
is less than where obstruction is seated in the large bowel. Besides
rectal and vaginal examinations, which should never be neglected in any
case of intestinal obstruction, abdominal palpation may also aid in
determining the site of constriction. It should not be forgotten,
however, when a tumor is found--as, for instance, in invagination--that
the bowel may be displaced; a distended caecum may be pushed into and
occupy the left side of the belly. Cases are not uncommon where the
symptoms are so combined and uncertain as to render accurate diagnosis
of the site of obstruction impracticable.

Very little light is thrown upon the diagnosis by pain, constipation,
or vomiting when these symptoms are considered separately. Pain is
common to many diseases of the abdomen; obstinate constipation, lasting
for {862} days and weeks, is often seen where there is no mechanical
obstruction; and vomiting attends many morbid conditions of the body.
But when these symptoms are combined and examined along with the
history of the case and mode of invasion, they are often characteristic
of constriction of the intestine. Pain in acute obstruction is fixed,
umbilical, and intermittent; in chronic cases it is more diffused and
increases with the distension. In acute cases constipation is complete
and insuperable; in chronic cases this symptom gradually increases; in
intussusception we have frequent discharges of a dysenteric character,
and hemorrhage, sometimes copious, when the small bowel is involved.
The bowel below the seat of complete constriction may be full of fecal
matter, and the discharge of this spontaneously or by the aid of
enemata may induce the attendant not to regard the case as one of
occlusion. Stercoraceous vomiting, as a rule, comes on early in acute
and late in chronic cases of complete occlusion of the gut; in
spasmodic ileus or impermeability not due to mechanical occlusion
feculent vomiting is only occasionally seen.

The duration of life in acute intestinal obstruction varies very much
in different cases: death may ensue in a few hours or not for ten or
twelve days; the average period is six days. The duration depends upon
the site of the constriction and the mechanical injury to the bowel;
the nearer to the pylorus the constriction, the more rapid the
progress. In volvulus involving the sigmoid flexure, when injury to the
bowel is great, the symptoms are acute in the extreme. After
peritonitis or enteritis begins, progress toward a fatal issue is very
rapid, the patient rarely living more than three or four days. In
occlusion from stricture, compression, fecal impaction, and chronic
intussusception the patient may live for weeks or even months.

The statistics of Leichtenstern show that from 5 to 10 fatal cases of
intestinal obstruction occur every year among every 100,000
inhabitants; and according to the mortuary records of England an
average of 1 death from this cause is seen in every 260 deaths. Brinton
reports 1 death from intestinal obstruction in every 280 deaths; his
statement is based upon 12,000 promiscuous autopsies. The first author
states that the statistical reports of the general hospital of Vienna
inform us that out of 60 cases of ileus, 6 or 10 per cent. recovered.
This report, however, is too meagre to be of much value. From Brinton's
statistics of 500 deaths from obstruction we find that out of 100
cases, 43 are intussusception, 17 stricture, 4.8 impaction of
gall-stones, 27.2 internal strangulation, and 8 torsion.

TREATMENT.--There are few conditions of the body which cause the
practitioner more anxiety and embarrassment than cases of intestinal
obstruction, and when the precise seat and nature of the occlusion are
not known the treatment is almost entirely empirical. The distinction,
however, between acute and chronic cases of obstruction of the bowels,
or of acute supervening upon chronic symptoms, can almost always be
made, and a patient investigation of the history of the case, the mode
of invasion, and a rigid analysis of all the symptoms presented will
generally enable the attendant to come to some positive conclusion as
to the cause and site of the occlusion. One fact in the treatment which
cannot be too strongly impressed upon the mind, especially of the young
practitioner, is not to use purgatives and irritating enemata, formerly
so much in vogue, {863} in the hope of forcing a passage through the
occluded bowel. The patient is urgently solicitous for medicine which
will open his bowels, but the use of purgatives to overcome internal
strangulation is as senseless and hurtful as when used to overcome the
constipation of external strangulated hernia. These agents only add to
the nausea, vomiting, pain, and peristalsis. The latter is violent
enough already to render coils of intestine visible, and with every
paroxysm is adding to the entanglement and impermeability. It is said
that cathartics in some instances have unlocked the bowel in intestinal
obstruction: these cases are exceptional, and many of them were
probably functional and not structural in character. The only exception
to the rule of avoiding purgatives is as stated by Jonathan Hutchinson:
"In certain cases when impaction of feces is suspected, and in cases of
stricture when fluidity of feces is desirable."

Formerly, some of the best practitioners resorted to the exhibition of
one or two pounds of quicksilver, in the hope of overcoming intestinal
obstruction by the weight of the metal. This plan has properly been
almost if not quite abandoned. Crude mercury is very slow to reach the
obstruction, is divided into small portions by the peristalsis, which
its presence increases, and if it should finally arrive at the point of
constriction in any considerable quantity, it is more liable to add to
than overcome the difficulty.

The great remedy in intestinal constriction is opium, in large or small
and repeated doses. Its use arrests the vomiting, stops the pain, and
quiets the violent movements of the bowel. Very often by it the
intestine is preserved and the life of the individual saved. No special
dose can be prescribed: it should be administered until slight narcosis
is obtained and pain and vomiting cease. Small doses of morphine, given
hypodermically and quickly repeated, is the best plan of exhibiting it.
It may be given by the stomach, but under such circumstances it is apt
to be rejected, or if retained absorption goes on slowly, or possibly
not at all. If for any reason its hypodermic use is impracticable, it
had better be given by the rectum. Opium lessens the danger of death
from collapse: it gives nature an opportunity to untwist the gut in
volvulus, or to unroll it in intussusception, or to cut off the
invaginated part by gangrene; and in internal hernia, morbid adhesions,
strangulation by bands of lymph, stricture, and other forms of
obstruction, it diminishes violent peristaltic action, postpones
inflammatory infiltration, fixation of the strangulated portion, and
keeps the parts in better condition for operative interference, which
in many cases offers the only hope of relief. To carry it farther than
slight narcosis and arrest of the most painful symptoms of obstruction
is an abuse of the remedy. By such abuse the symptoms will be masked
and both patient and practitioner deceived.

When obstruction is due to fecal impaction or spasm, the opium
treatment is still often indicated. Not unfrequently, after pain and
vomiting are relieved and slight narcosis kept up for some hours, the
bowels relax and spontaneous evacuation takes place. If not, discharge
of the contents of the bowel should be assisted by the administration
of castor oil, calomel, or repeated enemata of warm water. These agents
should not be used, however, as long as there is pain, tenderness of
the belly, or any evidence of peritonitis, but the opium treatment
continued until all signs of inflammation have disappeared. It has been
proposed to give {864} belladonna in place of opium; in small doses and
carefully watched it may be added to the opium, but should not be
substituted for it.

The local application of ice-water or pounded ice to the abdomen has
been recommended; and it is asserted that the danger of general
peritonitis is lessened, and that the strangulation itself has
disappeared, under the influence of cold. If, however, cold increases
pain and peristalsis, it should be abandoned. The local application of
moist heat or fomentations will more probably do good and give a
grateful sense of relief to the sufferer. General bleeding should never
be resorted to, and the use of leeches, except to ward off or subdue
some local inflammation, is of doubtful expediency. Blisters,
ointments, and cups are useless in such an emergency. Cracked ice,
strong coffee, and carbonated water in small quantities are valuable in
allaying thirst and nausea.

Cases are reported where obstruction of the bowels has been overcome by
the use of electricity; both the continuous and induced currents, but
chiefly the former, have been used; its value in such cases is
improbable.

Abdominal taxis or massage has been earnestly recommended and
frequently practised in cases of constriction. Successful results from
this procedure have been reported. It has been attempted while the
patient was in a warm bath or under chloroform or while taking large
enemata of warm water. Abdominal traction by the use of large cups to
the belly has also been advised. We can only hope for success from
these measures in the early stages of obstruction, before inflammatory
action or fixation of the strangulation has taken place, and any
attempt of this kind should be made with tact and gentleness. Inversion
of the body has also been suggested.

The injection of large quantities of warm water into the bowels to
overcome obstruction should never be omitted before resorting to
operative interference. The author has seen this plan in five or six
instances succeed after all other means had failed. Simple warm water
should be used, introduced by means of the common Davidson or a
fountain syringe. The injection should be made slowly, with occasional
intervals of rest, to allow the fluid time to pass through the
intestinal coils. During the operation the patient should be in the
knee-elbow or Sims's left lateral position, and under the influence of
an anaesthetic. One or two gallons of water may be used. In place of
water, the bowel may be inflated with air, introduced by a pair of
common bellows to the nozzle of which a piece of India-rubber tubing is
attached. The addition of castor oil, turpentine, carbonic acid gas,
and other irritants will more likely detract from than add to the
efficacy of these measures. In chronic intussusception, or in acute
cases when fixation of invagination is believed to have taken place,
and especially when inflammation is great, gangrene threatening or in
existence, injections of air or water should not, of course, be
attempted.

In invagination, when the intussuscepted part is low down in the rectum
or protruding from the anus, replacement by fingers or sound should be
tried; reduction begun in this way may be completed by injections of
air or water. The propriety of introducing the whole hand into the
rectum is very questionable. In occlusion of the gut by compression and
traction the cause should be found, and, if possible, removed. An
abdominal or pelvic tumor may be pushed out of the way of the
compressed bowel, a cyst punctured, a displaced womb replaced.

{865} Great care should be taken to support the strength of the patient
by concentrated and nutritious food, and in the later stages by
stimulants. When the bowels are distended by gas an injection into the
rectum of ten grains of sulphate of quinia will often give marked
relief.

It has been proposed to tap the distended gut with a fine trocar when
accumulation of gas is enormous, causing dyspnoea and great general
distress; temporary relief is often obtained by this plan, which is an
imitation of a common practice among veterinary surgeons. Something
more than temporary relief may, however, follow the tapping. In
twisting of the bowel, in internal strangulation by band or loop or
ring, and in some cases of invagination, the constriction is kept up by
the enormous gaseous distension. The obstruction is continued as much
by causes within as without the intestine. When tapped and the gas
drawn off, the bowel collapses, and may escape from its constriction
and return to its natural condition. Tapping is not always certain or
safe. The trocar or aspirating tube may pass between the convolutions
and no escape of gas take place, or it may be followed by fecal
extravasation into the peritoneal cavity. Notwithstanding the risk, the
plan is a valuable one, and in suitable cases should be resorted to.

SURGICAL TREATMENT.--In cases of acute obstruction of the bowel from
bands of lymph, diverticula, internal hernia, slipping of a portion of
gut into some opening, or twisting, when the treatment suggested has
been tried and fails, laparotomy should be performed; that is, the
abdomen should be laid open, the cause of the obstruction searched for,
and, if possible, removed. In acute cases a few hours, at most one day,
may be spent in trying the medical means recommended. After that time,
if the patient is not relieved, the sooner laparotomy is resorted to
the better the chance to save life. Acute internal strangulation of the
bowel from these causes has the same symptoms, course, and termination
that acute external strangulated hernia has. It demands the same
treatment--removal of the cause of the constriction. Delay in
performing the operation in the former is as certain to be followed by
peritonitis, gangrene, and death as it is in the latter; and the
surgeon who hesitates to open the abdomen and attempt to remove the
constriction in a case of acute obstruction after a fair trial and
failure of medical measures, is as culpable as the one who delays the
operation of herniotomy for unrelieved strangulated hernia.

In rare instances spontaneous self-reduction of external strangulated
hernia takes place; the cases are exceptional, and the fact is no
apology for postponing herniotomy. So in occasional instances acute
internal strangulation is spontaneously relieved; here too the cases
are exceptional, and the occurrence should be no excuse for delay in
laparotomy. To justify the operation it is not necessary that the
precise site and nature of the mechanical impediment should be
determined, although this can usually be done. It is only necessary to
know that the cause of the acute obstruction is not enteritis or
peritonitis, but a constriction mechanical in character, which no
medicine or manipulation or expectant treatment can relieve. When
diagnosis is clear and laparotomy is indicated to save or prolong life
in intestinal obstruction, the aid of the surgeon should at once be
invoked. Delay is fatal. Peritonitis beginning or in actual existence
makes abdominal section more dangerous and {866} lessens materially the
chances of recovery. To make the operation absolutely the last resort
when the bowel is injured beyond repair, when peritonitis is in full
progress, gangrene threatening, or the patient on the verge of
collapse, is a useless cruelty to the sufferer and his friends, and
only serves to bring surgery into disrepute. If the truth were known,
many of the cases of death following laparotomy should be ascribed not
to the fact that the knife was used, but to the fact that it was used
too late.

In intussusception not relieved by medical means the propriety of
abdominal section is questionable. The subjects of this condition are
usually children. Dislodging the invaginated bowel is not always
practicable, and the opium or expectant treatment may end in
spontaneous cure by the bowel righting itself or by sloughing of the
intussuscepted part. It is doubtless true that many of the so-called
cures from the latter process subsequently die from contraction of the
cicatrix at the site of the separation of the slough. In 43 cases
collected by Ashhurst of laparotomy for invagination, 13 recovered and
30 died. The record is bad, and to some extent the heavy mortality is
due to the fact that the operation was put off too long--delayed in
acute cases until sloughing had taken place, and in chronic cases until
adhesion of the invaginated parts had occurred. Indeed, some of the
cases reported were moribund when the operation was undertaken.
Recently many successful cases have been reported, and it is fair to
presume that the percentage of recoveries in the future will be greater
than they have been in the past.

In acute intestinal obstruction due to bands, internal hernia,
volvulus, or the presence of foreign bodies, as gall-stones, there is
no question that laparotomy should be performed after other measures
for relief have been employed and failed. Death in such cases is
inevitable and imminent, and operative interference should not be
postponed until peritonitis has set in. After the abdominal cavity has
been opened the distended gut can easily be found and the fingers of
the operator carried on down until the site of the constriction is
reached and the cause of the obstruction discovered. If the
constriction is due to the presence of bands or adhesions, they should
be cut or broken up and the gut relieved. If an internal hernia is
found or a portion of bowel has slipped into some fissure or pocket, it
should be withdrawn and the parts restored to their natural position.
If the cause of the obstruction is a volvulus, the bowel should be
untwisted. If a foreign body is felt impacted in the bowel and closing
it, unless it can be readily and without danger of lacerating the coats
of the gut pushed on by the fingers of the operator until it has passed
the ileo-caecal valve, the foreign body should be removed from the
bowel by an incision and the wound in the bowel afterward closed by
sutures. If the case is one of intussusception, the invaginated parts
should be pulled out: this is practicable where adhesions are absent or
slight, but if the adhesions are very firm, and it is impossible to
restore the parts to their natural position, the gut should be laid
open above the occlusion, the edges of the opening should be attached
to the margin of the external wound, and a fecal fistula established.
If the case of acute obstruction be due to stricture of the small
intestine, which is exceedingly rare, the gut may be laid open, and the
patient recover with fecal fistula, or entorectomy or resection of the
diseased part of the gut be resorted to. The operation of entorectomy
has been recommended by many {867} surgeons, and a large proportion of
the cases reported recovered. In one case by Koeberle six and a half
feet of the gut were successfully excised.

The following table by Ashhurst[12] shows the results of laparotomy. It
will be seen that in 230 cases 68 recovered:

                                   |        | Result  |        |
                                   |        | not     |        |
                                   |        | ascer-  | Recov- |
                                   | Cases. | tained. | ered.  | Died.
  ---------------------------------+--------+---------+--------+------
  Operations for--                 |        |         |        |
    Volvulus                       |   14   |    1    |    4   |   9
    Strangulation continuing after |        |         |        |
      herniotomy or taxis          |   18   |   ...   |    6   |  12
    Invagination                   |   43   |   ...   |   13   |  30
    Foreign bodies, impacted       |        |         |        |
      feces, gall-stones, etc.     |   18   |    1    |    7   |  10
    Strangulation by bands,        |        |         |        |
      adhesions, or diverticula    |   76   |    1    |   20   |  55
    Obstructions from tumors,      |        |         |        |
      strictures, ulcers, etc.     |   28   |    2    |    7   |  19
    Internal hernia and ileus      |   20   |    1    |    7   |  12
    Obstructions from other causes |    4   |   ...   |    1   |   3
    Causes of obstruction not      |        |         |        |
      ascertained                  |    9   |    1    |    3   |   5
  ---------------------------------+--------+---------+--------+------
               Aggregate           |  230   |    7    |   68   | 155
  ---------------------------------+--------+---------+--------+------

[Footnote 12: _Surgery_, p. 835.]

Enterotomy is an operation originally performed by Nelaton. It is done
by making an incision, preferably in the right groin, above the crest
of the ileum and parallel with Poupart's ligament. When the abdomen is
opened a coil of intestine is found and carefully stitched to the walls
of the incision. A very small opening is then made into the bowel, and
a fecal fistula established. Enterotomy is less dangerous than
laparotomy, as by it there is less interference with the peritoneum;
but no relief could be afforded by this procedure in cases of
intussusception or acute obstruction from bands, hernia, or volvulus.
It is applicable to cases of intestinal constriction when the
obstruction is about the lower part of the small or upper part of the
large intestine. It may be resorted to as a palliative measure when
exact diagnosis as to the character and site of the obstruction is not
clear, the case being otherwise hopeless, or in cases of obstruction
where severe symptoms persist and death is near, and yet for any reason
laparotomy or colotomy is inapplicable; or it may be performed in cases
of contractions after failure of patient and persistent medical
treatment. Many successful cases of enterotomy have lately been
reported, and the operation has been earnestly advocated by Trousseau,
Maunders, Wagstaffe, Bryant, and others. In chronic constriction due to
stricture or other mechanical obstructions, malignant or otherwise, not
remediable by any medical measures, colotomy should be performed. By
this operation the colon is opened and an artificial anus established.
The sigmoid flexure in the left lumbar region is the part selected for
the colotomy if the obstruction is situated in the gut below that
point. When the obstruction is higher up in the colon or its exact site
cannot be determined, the caecum in the right lumbar region is the part
chosen. In cases of obstruction from the mechanical pressure of tumors,
the possibility of relieving the compressed bowel by treating the
tumors should of course be considered before resorting to colotomy.




{868}

CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES.

BY I. E. ATKINSON, M.D.


The term cancer of the intestines is used here in a clinical sense to
designate new formations in the intestinal tract the tendency of which
is to destroy life, and has no reference to the histological characters
of the tumors, inasmuch as these are, during life, for the most part,
concealed from the eye of the pathologist. It so happens, however, that
in a histological as well as in a clinical sense the term is
appropriately applied to all but a very few of the malignant new
growths that develop in the parts under consideration, if we adopt, as
seems proper, the opinion of most modern pathologists, that cancer or
carcinoma should only include those tumors "consisting of cells of an
epithelial type, without any intercellular substance, grouped together
irregularly without the alveoli of a more or less dense fibroid
stroma."

Carcinoma of the intestines appears either as cylindrical-cell cancer,
as scirrhus, or as gelatinous or colloid cancer. Scirrhous cancer of
the intestines may resemble in appearance and texture the ordinary
medullary cancer, degrees of hardness or of softness depending upon the
predominance of the stroma or of the cellular elements in the
constitution of the tumor. Rarely, and in a purely clinical sense,
cancer of the bowels may exist as a lympho-sarcoma in the small
intestine, and then through progression from the glands of the
mesentery or elsewhere. Primary intestinal sarcoma has, however, been
observed. Similarly, melano-sarcoma has been detected in the intestine
as secondary to this form of sarcoma, originating in the skin or in the
eye.

Of the forms of carcinoma, cylinder-cell cancer is the most frequent.
Carcinoma gelatinosum or colloid cancer is of great relative frequency,
but it is altogether probable that here, as elsewhere, this represents
a degenerative form of ordinary carcinoma. At all events, it is certain
that it may be detected in many cases where the essential changes
reveal the ordinary glandular or cylinder-cell variety. These forms of
cancer may affect the bowel primarily or secondarily by extension from
adjacent organs and textures, or by metastasis. Primary cancer occurs
most frequently, metastatic cancer with great rarity. The relative
frequency of the different forms of cancer is not definitely known. In
the article on carcinoma in the _Dictionnaire Encyclopedique des
Sciences medicales_ (xii. pp. 576, 577) cancer of the bowels is said to
constitute about 8 per centum of all carcinomatous new growths.
Sibley[1] found that primary {869} carcinoma occurred in the alimentary
canal (exclusive of the mouth, tongue, and the annexed organs) in 6 per
centum of the cases collated by him. Tauchou's compilations of nine
thousand fatal cases of carcinoma show that intestinal cancer was
present in 4 per centum.[2] These computations include cancer of the
rectum. If statistics of cancer of the bowels exclusive of rectal
cancer were available, they would show, doubtless, a much smaller
proportion.

[Footnote 1: _Medico-Chir. Transact._, xlii., 1859.]

[Footnote 2: Leube, _Ziemssen's Cyclop._, vii. p. 432.]

Any portion of the intestinal tract is liable to be attacked by cancer,
though undoubtedly some parts of it with much greater frequency than
others. Kohler[3] reported that in thirty-four cases the cancer was
situated twenty-two times in the large intestine (the rectum excluded)
and twelve times in the small intestine (nine times in the duodenum).
It is not unlikely that in the cases of duodenal cancer the new growth
extended from the pylorus. At all events, primary cancer is seated with
far greater frequency in the large intestine, and, not including the
rectum, usually in either the sigmoid flexure or the caecum.
Grisolle[4] declares the large intestine to be four times more often
affected with cancer than the small intestine; that the sigmoid flexure
is attacked as often as all the rest of the colon taken together; and
that the caecum is still more often affected. Where the intestinal new
growth is secondary to carcinoma elsewhere, it is usually so by
extension from neighboring parts; thus, the ileum may become implicated
by contact with uterine cancer, etc., and cancer of the stomach, liver,
kidney, etc. may invade the colon.

[Footnote 3: _Ibid._, vii. p. 431.]

[Footnote 4: _Pathologie int._, 1865, ii.]

Cancer of the intestines usually begins after the middle period of
life, and apparently irrespective of sex. Nevertheless, young persons
are occasionally affected, and children sometimes develop malignant new
growths of the bowels (usually sarcomatous), either primarily, which is
rare, or secondarily, by extension from other parts. The influence of
heredity seems not to be well established. There can be no doubt that
chronic irritation may act as an exciting cause of cancer of the
bowels, as it may in cancer of other parts. It has been impossible to
recognize any specific influence from especial forms of irritation, and
it is not likely that such exist. Indeed, the etiological relations of
intestinal cancer remain exceedingly obscure.

SYMPTOMATOLOGY.--Up to a certain period of development cancer of the
bowels will give no sign of its presence; indeed, cases have been
observed where, death having occurred from other causes, the existence
of the malady became apparent only at the necropsy. In all cases the
symptoms are, at first, of an indefinite character and very inconstant.
Vague abdominal pains are experienced; these gradually tend to become
referable to a certain locality and to become associated with irregular
action of the bowels. Constipation, alternating with short intervals of
diarrhoea, supervenes, and a varying amount of meteorism is developed.
These symptoms may be attended by the signs of failing nutrition. The
body gradually shows the effects of chronic imperfect assimilation, and
becomes emaciated. The complexion slowly assumes the peculiar hue of
chloasma cachecticorum. Long before this occurs, however, the cancerous
new formation usually becomes perceptible as a more or less distinct
abdominal tumor, movable or fixed, as the part affected permits of free
movement {870} or is bound down to the neighboring parts either by
normal attachments or by adhesions resulting from inflammatory
processes or from the extension of the cancerous growth. When the tumor
is movable, it is generally situated in the small intestine or
transverse colon or sigmoid flexure, the other portions of the
intestinal canal being comparatively fixed. It should be mentioned,
however, that portions of the intestines normally freely movable may
become adherent to contiguous parts, as the transverse colon, with the
gall-bladder, liver, stomach, spleen, etc. etc.; the transverse colon
and small intestine, drawn down by the weight of the new growth, with
the pelvic organs, the bladder, uterus, uterine appendages, etc.; and
that, finally, different portions of the bowels may become involved in
one mass.

When the duodenum is the portion implicated the tumor may escape
observation or may be indistinguishable from cancer of the pylorus. It
occasionally happens that no tumor can be discovered until the malady
is far advanced whatever part of the bowel is affected. In nearly all
cases, however, before very long the tumor will be detected wherever
situated, but it will often remain difficult, owing to its situation,
to arrive at exact conclusions as to its precise character. Usually, it
offers considerable resistance to the touch, but its features may
readily be obscured by the fecal accumulation that forms above the
constricted portion of the gut and by the gaseous distension of the
bowel. This tumor will be slightly painful to pressure, and the patient
will refer to it a spontaneous pain, usually of a dull aching,
sometimes of a stabbing, character. Percussion yields a sound of
muffled resonance, due to the tubular nature of the tumor. Cancerous
neoplasms of the bowel, and of the duodenum especially, are apt to be
associated with a distinct pulsation caused by the subjacent abdominal
aorta. This may readily be distinguished from aneurismal pulsation by
the absence of an expansile character, by the disappearance of the
impulse that may sometimes be observed when the patient is made to
kneel upon all fours, and by the occasional mobility of the cancerous
tumor. By extension and by inflammatory infiltration the tumor
frequently becomes converted into a conglomerate mass where all
determination of locality becomes conjectural. The tumor is, with very
rare exceptions, single.

The symptoms that accompany the development of these growths depend
mostly upon their position in the alimentary tract. Pain alone seems
independent of this, but is at best a most uncertain concomitant. When
the duodenum is the part affected by extension from the pylorus, the
symptoms are indistinguishable from ordinary pyloric cancer. Even
primary cancer of this part may exactly simulate pyloric cancer. The
localized pain and tumor, the vomiting after meals, the frequent
presence of blood in the vomited matters, the progressive emaciation
from starvation, the absence of abdominal distension (a result of the
constriction of the gut at its upper extremity), the gastric
dilatation,--all combine to make the diagnosis difficult.

Cancer of the duodenum in its descending part may be suspected when
signs of hepatic and pancreatic obstructive difficulties point to
implication of the ducts, through which are produced jaundice upon the
one hand, and evidences of imperfect pancreatic digestion, in the
presence of undigested fat in the stools, upon the other. In the lower
portions of the {871} intestines the cancer becomes more and more
associated with meteorism and fecal accumulations. Constipation becomes
steadily more obstinate, but there are occasional fluid evacuations
containing blood, pus, and mucus, often stinking abominably. When the
tumor is toward the end of the large intestine--in the sigmoid flexure,
for example--fluid discharges occur with very great frequency at times;
but these are scanty in amount and but slightly fecal in character. In
these cases one does not usually observe the compressed, ribbon-like
stools that are seen in rectal cancer. These symptoms may precede the
appearance of the tumor, when the diagnosis will be less readily made.
The constipation will at first be more amenable to the use of
purgatives. (It is said to be due more to a loss of contractility of
the bowel than to the narrowing of its lumen.) Gradually these will
lose their efficacy, and finally complete obstruction of the lumen of
the gut is effected; in which event the symptoms of ileus will develop,
with cramps and vomiting, finally of a fecal character, and the fatal
issue quickly follow. Not unfrequently peritonitis is developed, and
may be of a chronic character or may destroy life within a day or two,
or the patient may die from exhaustion before the obstruction becomes
complete.

It may happen that the integument will become involved in the malignant
process, or may become continuous with the tumor by adhesive
inflammation. In such cases an opening may be formed by suppuration, or
the lancet may secure the passage of feces through an artificial anus,
and temporary respite be obtained. Sometimes a sudden disappearance of
the symptoms of obstruction--a result due to the softening and breaking
down of the cancerous mass, restoring temporarily the integrity of the
intestinal tube--may give an unjustifiable hope to the patient; or the
same effect may follow the establishment of a communication, by
ulceration, between the bowel above the tumor and some portion nearer
to the anal orifice. The progress of the new growth soon annuls the
benefits thus gained.

Not uncommonly, particles of the cancerous mass may become detached,
and, if diligently searched for, may be discovered in the feces.
Microscopic examination may then definitely determine the nature of the
disease. It has been claimed that colloid cancer may be diagnosticated
in this manner even before the appearance of other symptoms.[5] Death
may be hastened by the occurrence of metastatic deposits in other and
vital organs. Oedema of the lower extremities (of the left extremity in
cancer of the sigmoid flexure) will often be observed as a result of
the interference of the cancerous mass with the return of blood from
the extremities by pressure upon the large veins. The combination of
pain, tumor, constipation, tympanitis, progressive wasting, and the
cachexia that sooner or later supervenes, stamps eventually most cases
with unmistakable characters.

[Footnote 5: Charon and Ledegank, _Journ. de Med.-Chir. et de Pharm._,
v. lxviii., 1879, p. 493.]

The duration of intestinal cancer may extend from several months to
one, rarely two, years, the latter age sometimes being attained by
colloid cancer, the most chronic and least malignant form.

MORBID ANATOMY.--By far the most frequently encountered malignant new
growth of the bowel is carcinoma, in one or another of its forms. The
cylinder-cell epithelioma is probably the most common of {872} these,
and, as seen in the intestine, offers many naked-eye points of
resemblance with ordinary encephaloid carcinoma. It is soft, filled
with a milky juice, and may attain considerable size. The tumors appear
as discoid prominences of varying size and number. Later, these may
become fungoid and ulceration ensue. The growths early involve the
whole intestinal wall, and by their increase tend to obstruct the
passage of the intestinal contents. When ulcerated they present a
nodular, uneven surface, situated upon a thickened base consisting of
the infiltrated coats of the bowel. Villous prolongations (villous
cancer; the undestroyed connective-tissue stroma) may project into the
lumen of the bowel and give a peculiar tufted appearance to the part
implicated. One or more points may be invaded by cancerous growth, and
above each will be developed a dilatation of the gut (the result of
distension) containing uncertain quantities of fecal matter, upon the
removal of which the tumor will appear much smaller than it appeared
during life.

Scirrhus usually implicates the gut in its entire circumference, so
that a high degree of constriction may result from a small amount of
cancerous infiltration. It begins as small nodules or plates upon the
mucous membrane. As commonly observed, the lumen of the intestine is
narrowed by an annular band of gristly hardness. All the coats of the
bowel, with the peritoneum, become involved, and frequently the
contiguous parts are included in the cancerous infiltration, forming an
undefinable mass through which the contracted channel of the bowel may
be traced, though often impervious to any but the smallest articles (a
crow-quill, for example). The surface of the gut is generally
ulcerated, irregular, and nodular. The walls of the ulcer are irregular
and infiltrated. It will sometimes happen that the autopsy reveals
permeability of the bowel where total obstruction prevailed during the
latter days of life. This may be probably accounted for by the
disappearance of the hyperaemia that doubtless existed during life and
caused more or less turgidness of the growth. Sometimes the
connective-tissue element is less predominant, and gives place to a
more or less luxuriant cell-development; in a word, scirrhous carcinoma
is replaced by soft or encephaloid cancer. This difference is simply
one of degree, but is associated with greater rapidity and extent of
growth. Ulceration is extensive, and one may here also often discover
the villous, tufted appearance of villous cancer, caused by the
fringe-like shreds of stroma entangling cellular elements not yet
detached from the mass.

Colloid cancer, or carcinoma gelatinosum, may be associated with either
of the above-described forms as a degenerative form, or may,
apparently, develop as such from the beginning. It is a very frequent
variety of the malady. In 27 cases of intestinal cancer, colloid cancer
was present in 5, as reported by Lebert. It is most often observed in
the sigmoid flexure and caecum, as are the other forms of carcinoma. It
is composed of a considerable mass extending around the bowel.
Ulceration is less often found here than in the other forms, nor is
there the same tendency to secondary infiltrations. By the unaided eye
an alveolar structure may be detected, and when the mass is extensive a
soft, jelly-like consistency is presented, together with "a bright,
honey-yellow color." Small deposits of the colloid matter may be seen
upon the surface. These have been described as resembling wheals of
urticaria or herpetic or eczematous {873} vesicles (Bristowe). The
glairy fluid of colloid carcinoma oozes from the cut surface of the
tumor, bathes it, and is to be found in the intestine.

These different forms of cancer sooner or later invade neighboring
parts, as the peritoneum, mesenteric and retro-peritoneal glands, and
adjacent organs. On the other hand, the intestines may become invaded
by cancer of the peritoneum and other parts. It has even been observed,
reversing the usual order of things, as secondary to cancer of the
liver (Wilks and Moxon). Under these conditions the symptoms of
intestinal cancer will have been associated with those due to the
primary affection. Lympho-sarcoma will rarely be found as an extension
from the lymphatic glands and involving the small intestine. Melanotic
sarcoma may occur as metastatic from an original melano-sarcomatous
tumor of the skin or eyeball.

DIAGNOSIS.--In its earlier stages it is impossible to recognize cancer
of the intestines. After its symptoms have become established they may
resemble those of several disorders. Cancer of the duodenum cannot be
distinguished from that of the pylorus unless evidences of pancreatic
or biliary disturbances indicate obstruction to the passage of the bile
and pancreatic secretions. Previous to the appearance of a tumor one
must often remain in doubt. The alternations of constipation and
diarrhoea, the signs of partial obstruction, the localized pain usually
present, the gradual wasting, will arouse suspicions of cancer, though
chronic inflammatory affections of the bowels may induce symptoms not
altogether unlike these. The presence of a tumor will supply the
additional evidence necessary for a definite diagnosis. It will be
necessary to exclude fecal enlargements of the bowels. The cancerous
tumor will be somewhat painful, hard, nodulated. A tumor due to fecal
accumulation may closely simulate it, and is, indeed, usually
associated with it. By manipulation the fecal mass may be moulded, and
even displaced, and by appropriate purgative treatment may be caused to
entirely disappear. Foreign bodies, mesenteric tumors, and other
abdominal enlargements may offer physical resemblances to intestinal
cancer, but their symptomatology is usually so different that doubt may
be easily dispelled. Syphilitic gummy infiltration, with resulting
stricture, is more apt to occur in the rectum than in other parts of
the alimentary tract.

The presence of fragments of the new growths may sometimes be detected
in the stools, when microscopic examination will determine their
nature. With cylinder-cell epithelioma and glandular cancer this is not
common, but with colloid cancer much information may be gained by
examining the evacuations. According to Charon and Ledegank,[6] colloid
cancer of the intestine may be detected before symptoms develop, by the
presence of colloid matter in the feces. In the later stages, however,
the gelatinous change of all the histological elements may occasion
embarrassment, as at this stage the peculiarities of the cellular
structure will have been destroyed.

[Footnote 6: _Journ. de Med.-Chir. et de Pharm._, lxviii., 1879.]

PROGNOSIS.--Intestinal cancer always proves fatal. Death may result
from the debility resulting from the cancerous cachexia or from
intestinal occlusion or from peritonitis. The duration of the malady is
usually not long. It runs its course in from several months to one,
rarely to two, years.

{874} TREATMENT.--Treatment must be directed to the alleviation of the
distress caused by the disease. No curative treatment is known. When
the cancer is situated in the colon, especially in the sigmoid flexure,
the operation for artificial anus often affords great though temporary
relief. The diet should consist of such articles in the digestion of
which a large residue is not formed. Milk, eggs, soups, etc. should
compose the principal articles of food. Mild laxatives will be required
to secure the proper evacuation of the bowels, and to relieve pain and
discomfort opium is invaluable and should be freely used. When
obstruction is imminent nutrient enemata afford the most efficient
means of administering nourishment.


Lardaceous Degeneration of the Intestines.

SYNONYMS.--Albuminoid degeneration, Waxy degeneration, Amyloid
degeneration, etc.

Lardaceous degeneration of the intestines is an affection of quite
frequent occurrence in those persons who are the subjects of a like
change elsewhere; for although it has been asserted that it may be
present as a primary affection, it almost always succeeds the same form
of degeneration in other organs. Since, for the most part, it only
makes itself manifest at an advanced stage of the disease, its
importance is usually masked by the grave constitutional condition of
the patient, whose vital forces are wellnigh exhausted by the already
advanced degenerations present elsewhere. The extensive implication of
other organs and tissues in the same degenerative process also creates
great obscurity in the symptomatology of intestinal lardaceous disease,
and is doubtless the cause of the existing dearth of definite knowledge
upon the subject.

That the intestines are comparatively frequently involved in lardaceous
disease is shown by dead-house statistics. Thus, Charlewood Turner[7]
reported from the London Hospital that in 58 cases of lardaceous
disease the intestines were affected 10 times; and Goodhart[8] in 150
consecutive necropsies of lardaceous disease at Guy's Hospital reported
implication of the intestines 63 times.

[Footnote 7: _Transactions Path. Soc. London_, 1879, p. 517.]

[Footnote 8: _Ibid._, p. 533.]

Although the bowels do not become affected as early as several other
parts, they will almost certainly become involved should the patient's
life be prolonged; and in those cases where death is a direct result of
the degeneration the intestines share with the kidneys the chief
responsibility. It is not, however, until an advanced stage of
lardaceous degeneration that its presence in the alimentary canal is
revealed by symptoms; indeed, many cases do not, throughout life,
betray evidences of the pronounced alterations that are to be
discovered after death. Even in extreme cases there are no symptoms
that would, even with probability, be referred to lardaceous disease of
the bowels in the absence of the same degeneration in other organs and
parts. There are, then, no specific symptoms following lardaceous
degeneration of the bowels.

Where the normal functions of the intestines can no longer be properly
performed in consequences of the changes that have taken place in them,
there results a moderate diarrhoea. At first the number of movements
{875} may not be increased; the evacuated matters are fluid and of a
greenish or pale color. Usually, little or no pain is experienced,
though at times and in certain individuals this may be severe and
colicky. The diarrhoea is not always steadily progressive, but may from
time to time disappear. With the progress of the disease it may become
more free and persistent, and in the later stages hemorrhage from the
bowels may be superadded. This may vary in amount, and where, as is
often the case, the stomach participates in the degeneration,
haematemesis may also appear. These hemorrhages may be insignificant,
or may at once assume alarming proportions, and even bring to an
unexpected termination the life of the individual. Already, at the
outset of the intestinal symptoms, the general health will have shown
evidences of profound alteration, but upon the supervention of the
diarrhoea more rapid progress will be observed, consequent upon the
increased nutritive disturbance. The use of remedies in temporarily
controlling this diarrhoea may prolong for months the life they are
powerless to save.

So far as concerns the intestinal affection, there is no special
tendency toward febrile excitement. It must not be forgotten, however,
that acute inflammatory attacks of various tissues and organs
frequently arise in the course of lardaceous disease.

Though there seems to be reason to believe that mild degrees of
lardaceous degeneration may sometimes be cured, especially when
dependent on syphilis, there is but little hope of arresting its
progress at the late stage when the bowels become implicated. Indeed,
when pronounced degeneration of the bowels takes place the disease is
usually nearing the end of its course; for it is a well-settled fact
that in this degeneration extensive implications of organs may occur
without markedly reducing the patient's general condition, so long as
the kidneys and intestines remain unaffected. The cause of death is
usually to be traced to these organs. Dickinson[9] found that in 35
cases where death was apparently due to renal lardaceous disorder, the
immediate result was brought about by diarrhoea in 13 cases.
Presumably, in a large proportion of these lardaceous disease of the
bowel was present.

[Footnote 9: _Diseases of Kidney_, Part ii., 1877, p. 496.]

The degeneration usually affects the lower portion of the small and the
upper part of the large intestine. Occasionally it will be found to
have invaded the whole alimentary tract. As in lardaceous degeneration
generally, the process begins in the small arteries and capillaries and
veins, affecting primarily the arterial and venous muscular coats--not,
however, according to the latest authorities, the muscular fibres
themselves, but their perimysium and the cement substance, the
degeneration being one limited to the connective tissues.[10] In the
mildest cases only some of the small vessels of the mucous membrane are
involved, and no naked-eye changes can be detected. In more advanced
stages the mucous membrane is pale and shows evidence of catarrh.
Thickening occurs, and as the process advances a peculiar appearance is
revealed which has been compared to that of wet wash-leather (Wilks).
The iodine test now gives the mahogany-colored reaction of lardaceous
matter, with the tissues affected, or, if the methyl-aniline-violet
test of Cornil be employed, the lardaceous material will display a
red-violet color, while {876} normal structures will be tinged
blue-violet. It is said to be better to make the test near a Peyer's
patch, since the latter is seldom affected by the degeneration, and
brings out, by contrast, the surrounding lardaceous material.[11] This
distribution of the material cannot be considered as constant, however,
since Hayem found the patches of Peyer most frequently affected.

[Footnote 10: Cohnheim, _Allgem. Path._, 1882, p. 667.]

[Footnote 11: Wilks and Moxon, _Path. Anat._, p. 404; Kyber, _Virchow's
Archiv_, Bd. 81, H. 1 and 2.]

In more advanced stages the surface may become irregular from glandular
enlargement, and ulceration may occur. Microscopic examination shows
the lardaceous material in the vessels, and also in the stroma of the
mucous membrane and villi.[12] The epithelium is not involved. The
degeneration, at first confined to the mucous membrane, extends to the
submucous tissue, the proper muscular coat of the intestines being
often implicated--so far, at least, as concerns its connective tissue.
In the more severe cases Hayem found the agminated and solitary glands
extensively involved. Fine branches from affected vessels penetrate to
the interior of the glands. In such cases the mesenteric glands will be
found implicated. The degeneration of the vessels running through the
gland structure causes disappearance of this substance by fatty
degeneration, and occasions a reticulated arrangement of the lardaceous
material, and, secondarily, ulceration. In a similar manner ulcers may
arise in any part of the affected tract. Finally, the lardaceous
material may involve the whole thickness of the gut.

[Footnote 12: Eberth, _Virchow's Archiv_, 80, S. 138.]

The diagnosis of lardaceous disease of the bowels can only be made with
certainty in the presence of pronounced albuminoid disease of other
parts in association with the symptoms of intestinal disorder. It
possesses no characteristic symptoms.

Inasmuch as the disorder invades the bowels only at a late stage of its
existence, the prognosis acquires additional gravity. It is probable
that advanced albuminoid disease is never cured; so much the more
hopeless is it when affecting this tract. If unchecked, the diarrhoea
rapidly saps the powers of life; if temporarily alleviated, the
approach of death is more gradual.

Whatever attempts are to be made to cure the disease, they must be
through the general system, and are identical with those directed
toward the cure of lardaceous disease generally. Treatment directed to
the intestines must be palliative. The diarrhoea must be combated by
appropriate diet and the administration of such remedies as protect the
surface of the mucous membrane and control the intestinal movement.
Bismuth subnitrate in large doses is therefore indicated. Various
astringents may be employed, while the use of opium often secures most
gratifying relief. It should be given in generous doses. Preparations
of the crude drug seem to answer better than its salts. The necessity
of keeping the gut free from undigestible matters that may irritate the
already badly-damaged mucous membrane is apparent. Patients with this
form of lardaceous degeneration usually show the cachexia resulting
from profound modifications of nutrition, and their intestinal symptoms
can only be regarded as links in a long pathological chain. Hemorrhage
will call for remedies that under ordinary circumstances are employed
to control bleeding from the bowels.




{877}

DISEASES OF THE RECTUM AND ANUS.

BY THOMAS G. MORTON, M.D., AND HENRY M. WETHERILL, M.D., PH.G.


Diseases of the inferior and terminal portion of the large intestine
may be divided into primary and secondary--the former when the morbid
cause is local and independent of disease elsewhere, the latter when it
is consequent upon or incident to some other bodily affection. Among
the primary lesions may be classed congenital malformations, prolapse
of the rectum, hemorrhoids, and some varieties of new growths; also
diseases caused by local irritations, infection, or traumatism, such as
proctitis, ulceration, fissure, non-malignant stricture, chancroidal
invasion and primary syphilis, including obstruction of the bowel by
impacted feces and foreign bodies. Thread-worms and various cutaneous
eruptions about the anus may also be included among the causes of the
primary diseases of this portion of the alimentary canal.

The secondary affections are quite numerous, and may be caused by
direct extension of disease from the colon, as in the dysentery
following typhoid fever, and follicular enteritis, or entero-colitis of
children; by contiguity, from diseases in neighboring organs--_e.g._
ischio-rectal abscess causing fistula--or by changes in the nervous or
vascular supply, such as is seen in spasmodic contraction, paralysis,
epidemic dysentery, cholera, and the action of certain remedies.

The rectum, the third or terminal portion of the large intestine, has
no sharply-defined upper limits: it is usually understood to begin at
the sigmoid flexure, opposite the left sacro-iliac symphysis; it is
from six to eight inches in length and terminates in the anus. As the
sigmoid flexure is the narrowest portion of the colon, so the calibre
of the first part of the rectum is narrower than the portion below,
where it gradually becomes more commodious, and near the anus presents
a peculiar condition of the walls which gives it a capacity for
remarkable distension. The rectum, which is somewhat cone-shaped, in
its anatomical and pathological characters retains those of the large
intestine with slight variation. Upon the upper or first part of the
rectum the duplicature of the peritoneum is continued, forming the
meso-rectum, which invests the bowel, attaching it to the sacrum. Below
this the middle portion of the rectum (extending to the tip of the
coccyx) is attached to the sacrum by connective tissue only, but also
has a peritoneal investment on the upper portion of its anterior
surface.

{878} The third or terminal part of the rectum, which is only an inch
and a half in length, and is entirely without peritoneal covering,
terminates at the anus. The circular and transverse muscular fibres,
mucous crypts, and appendages throughout the rectum are identical with
those above, except that the general muscular tunic is thicker; but the
longitudinal fibres are less distinctly aggregated into bands than in
the colon, being disposed in a more uniform manner, except that, like
the circular fibres, they are especially aggregated between the
sacculi. The fact that the meso-rectum limits the mobility of the upper
and more narrow part of the rectum has led some to locate a third
sphincter at this point, but the existence of such an organ has not
been generally admitted. Van Buren characterizes it as an organ which
"anatomy and physiology had been equally unsuccessful in assigning
either certainty of location or certainty of function."[1]

[Footnote 1: Kelsey, _Diseases of the Rectum and Anus_, New York, 1882,
p. 20.]

The anus guards the outlet of the bowel by its double sphincter muscle,
which under normal circumstances affords voluntary control, within
certain limits, over defecation. The well-known peculiarity of the
vascular supply, a sort of erectile tissue being formed by the inferior
hemorrhoidal plexus and the passage of some of the efferent veins
through the sphincter muscle, by which they are subjected to pressure,
is very favorable to the development of certain forms of disease which
will be considered among the local disorders. As embryology has thrown
considerable light upon the pathology of morbid growths by
demonstrating relationships that were previously unsuspected, so a
consideration of the development of the lower portion of the intestinal
canal may lead to a better understanding of some of its diseases,
especially those which are symptomatic or secondary. In early foetal
life the third division of the primitive intestine, the pelvic portion,
terminates in a cloaca in common with the urachus; subsequently, about
the eighth week, a partition (the perineum) is formed which divides the
cavity into two portions, the uro-genital sinus and the anal cavity. In
the mean time, at an early period a depression occurs on the cutaneous
surface at the site of the anus, which deepens progressively until it
encounters the primitive intestine, with which it unites at the end of
the fourth week, and the continuity of the tube becomes established. It
therefore is seen that the rectum in its upper and middle portions is
derived from the internal and middle layers of the blastodermic
membrane, while its lower third, with the anus, like the buccal cavity,
is formed by the external and middle layers.

In its diseases, then, the greater part of the rectum would seem to
naturally participate in those of the large intestine, to which it
structurally belongs, while its inferior portion and the anus would
partake more in the disorders of the general cutaneous system. This
peculiarity of development also explains the difference noticed in the
vascular supply. The rectal veins are usually divided, like the rectal
arteries, into three sets--superior, middle, and inferior. They are
arranged so as to form two distinct venous systems, the rectal
returning its blood through the inferior mesenteric veins into the
portal system, the anal terminating in the internal iliac. The first
system is made up of the superior hemorrhoidal, the second of the
remaining veins.

The superior hemorrhoidal forms a venous plexus which surrounds the
{879} internal sphincter muscle; the inferior hemorrhoidal vein also
forms a plexus, but it is subcutaneous and principally below the
inferior border of the external sphincter.

There are, however, a number of communicating branches passing along
the walls of the rectum from one plexus to the other. The internal
hemorrhoidal veins also communicate freely with the branches of the
internal iliac around the trigone of the urinary bladder by means of
small vessels, which pass through the prostate gland and seminal
vesicles. By this method of anastomosis some relief is afforded when
there is an obstruction in the portal circulation, which is such a
common cause of turgescence of these veins, often resulting in
permanent dilatation or hemorrhoids.

At the lower part, or at the junction of the middle and lower third of
the rectum, the internal circular fibres of the muscular coat of the
intestine become quite numerous, forming what is called the internal
sphincter muscle; it is nearly an inch in breadth, and completely
surrounds the lowest part of the rectum. It is about an inch above the
margin of the anus; its muscular fibres are of the involuntary or
unstriped variety; in function it assists the external sphincter in
closing the anus and preventing the involuntary escape of the contents
of the bowel.

The external sphincter lies directly under the skin and upon the
internal sphincter and the levator ani muscle; its fibres encircle the
anus: arising from the coccyx, they are inserted into the tendinous
centre of the perineum, joining the transversus perinaei, the levator
ani, and accelerator urinae muscles. The sphincter ani is constantly in
a state of tonic contraction, but the force of its contraction may be
voluntarily increased. In the skin and superficial fascia are found
minute branches of the pudic and small sciatic nerves; in the
ischio-rectal space the internal pudic nerve; crossing about the centre
are the inferior hemorrhoidal nerves, which are distributed to the anus
and the lower portion of the rectum; the perineal nerve is especially
distributed to the anterior part of the anus.

Thus it is seen that the rectum and anus have vascular and nervous
supplies of considerable diversity and importance.


Congenital Malformations.

The simplest form of congenital malformation in this region consists in
an anus of insufficient size for the natural demands of the system, but
in no other manner abnormal. The most frequent variety of imperforate
anus is where complete occlusion is effected by the common integument
or by two cutaneo-mucous flaps, which owing to defective development
remain united without forming a raphe or perceptible line of union. The
rectum is not involved, and when the child strains the contained
meconium causes bulging of the part, which disappears under slight
pressure, but reappears when again free. In other cases the occluding
tissue is very firm, dense, with a disposition to pucker or form rugae.
The sphincter muscle is rarely perfect, and though an artificial anus
may be made, years may elapse before the child can control the
evacuation. In conjunction with an imperforate anus the colon may
terminate in a cul-de-sac, or it may communicate with the urethra, the
bladder, or the vagina.

{880} An imperforate rectum has been known to discharge at the
umbilicus, upon the face, under the scapula, upon the penis or the
anterior part of the scrotum. Sometimes, though very rarely, a common
cloaca has been found, as in fowls, common to the rectum and to the
genito-urinary organs; and still more rarely the rectum has opened in
abnormal sites upon the perineum and upon the buttocks.

The anus may be entirely absent. The rectum may be entirely absent or
it may be incomplete, terminating at various distances from the anus.
These malformations of the bowel may be associated with a perfect anus,
or with any of its imperforate forms, or with a fecal fistula. In
occlusion of the rectum the offending structure is in some cases a
hymen-like fold of mucous membrane, which, during straining, can be
recognized by the finger as a fluctuating protrusion; while in others
it consists of a mass of dense fibrous tissue which extends upward from
an inch to an inch and a half: in the former there is always found a
normal anus; in the latter there is either no trace of anus or one in a
more or less rudimentary state. In those cases where the rectum is
entirely absent the intestine terminates either in a cul-de-sac or a
fecal fistula; very rarely the rectum is replaced by a
fibro-ligamentous cord or band which springs from the colon, and,
descending toward the bladder, blends with the connective tissue of the
part. In the latter the pelvis is always in an imperfect state of
development, being much contracted in its lower diameters, and the anus
is absent; and Rokitansky and Curling lay stress upon the
non-development of the pelvis as a diagnostic guide in determining the
absence of the rectum. The passage of a sound into the bladder or
vagina is a procedure of some diagnostic value, as if its point
impinges directly against the sacrum it may be presumed that no rectum
exists. If the malformation is of such a character that the fecal
matter can find no exit, a train of symptoms ensues analogous to those
seen in the adult affected with intestinal obstruction: the infant
cries and is constantly restless, refuses food, vomits, the abdomen
distends, and death speedily ensues. A remarkable exception to this
rule was the case mentioned by Bodenhamer of a child with absence of
the rectum who was not operated on until three months after birth, and
who was apparently in perfect health. At the operation the intestine
was found three inches from the surface, and the child made a good
recovery.

Although the statistics of this class of malformations are somewhat
contradictory and confusing, it is safe to state that more male than
female children are so afflicted.

The prognosis in the large majority of these cases is grave, for unless
the operator can see or feel the fluctuating protrusion, or can
recognize it after a very slight exploratory incision, he is working
totally in the dark and in close proximity to the peritoneum.
Hemorrhage, peritonitis, pelvic cellulitis, and septicaemia diminish
the chances for recovery. Indeed, the majority of these cases are
scarcely amenable to surgical treatment.


{881} PRIMARY DISEASES OF THE RECTUM AND ANUS.


Prolapse and Procidentia of Rectum and Anus.

These conditions obtain most frequently at the two extremes of life,
infancy and senility, but have a very different causation in each.
Prolapse of the bowel may be partial or complete--partial when a
portion of the mucous membrane is extruded, and complete when the
entire rectum appears outside the anal orifice. A predisposing cause in
infants is found in the mobility of the bowel--in the fact that it and
the sacrum are much less curved than in the adult, and the abdominal
viscera are more voluminous: this, associated with the undeveloped
state of the muscular system, causes the weight and strain to act
directly and forcibly upon the sphincters, and the extrusion takes
place. It is often excited by allowing children to sit for a length of
time upon the chamber-vessel. It is frequently caused among children by
the presence of vesical calculi, by Oxyuris vermicularis, diarrhoea,
constipation, dysentery, polypi, and by the long-continued acts of
coughing and crying.

In adults and the aged it may be caused by loss of tone of the anus and
rectum in chronic diarrhoea and dysentery, or from the energetic action
of drastic cathartics, by urinary calculi, the long-continued use of
enemata, chronic cough, diarrhoea alternating with constipation,
stricture of the urethra, prostatic hypertrophy, tenesmus due to the
presence of polypi, and by the pressure of a pelvic tumor. It may
accompany procidentia uteri and hemorrhoids. An incomplete, reducible
prolapse consists of two or more overlapping plications of
normal-looking mucous membrane, sensitive but painless. In these cases
there is provoked a hyperplasia of much-elongated connective tissue in
the submucous space which undergoes serous infiltration and causes an
oedematous condition of the part. In a complete prolapse the entire
rectum--all of its component layers--is protruded through the anus. In
a recent case the folds of the gut are well marked, but in one where
the bowel has remained in this abnormal condition for some time the
submucous tissue becomes charged with inflammatory deposit which
effaces the plications and causes the bowel to become pale, hard, dry,
and tough; and finally pigmentation occurs and the part assumes
somewhat the character of true skin. These vary greatly in size, from
the slightest protrusion of mucous membrane to a tumor the size of a
melon. Usually they are reduced with ease, but their reappearance is
occasioned by the slightest tenesmus.

In old age the soft parts of the floor of the pelvis and the anal
sphincters lose to a great extent their tone and contractile vigor, and
the rectum, also participating in this change, is often unable to
withstand the increased thrust of the diaphragm and the compression of
the abdominal muscles during defecation; which act frequently demands
more exertion on account of a tendency to constipation in advanced
life.

In these long-standing cases of senile procidentia it is a matter of
experience, verified by post-mortem dissection, that the fibres of the
sphincters and of the levatores ani muscles are flattened, pale, and
stretched beyond the possibility of contraction, while the entire
perineum is in a state of atrophy.


{882} Polypi of the Rectum.

There are two varieties of these--the gelatinoid or soft, and the
fibroid or firm. The latter is of rare, the former of common,
occurrence, especially in children under the age of twelve years. The
fibroid polypus is only found in adults, and is composed of dense
connective-tissue elements and blood-vessels. The gelatinoid or soft
polypi are also partly composed of connective tissue and vessels, but
much finer than in the other: they contain hypertrophied follicles and
are covered with spherical epithelium. They resemble nasal polypi, but
are more dense. These growths are not malignant in character, but are
very troublesome, as they are almost always pedunculated, the stem
being from half an inch to four inches in length, which admits of the
descent of the tumor within the grasp of the sphincters during
defecation, and frequently admits of its escape from the anus. Their
presence is not free from danger, as they are very vascular, bleed
readily, and are sometimes detached by the breaking of the pedicle
during defecation. They frequently bleed spontaneously. The presence of
these abnormal growths teases the rectum and brings on tenesmus and
frequent desire to go to stool; the feces are flattened, and with them
escapes a quantity of glairy red mucus which has been compared to thin
currant-jelly. When caught in the grasp of the sphincters they often
bleed profusely, and especially is this the case with children so
affected. The presence of these bodies is accompanied with a sense of
weight and uneasiness in the bowel. They may be single or multiple;
they may be round, reniform, oval, fusiform, or irregular; they may be
smooth or villous. In size they vary from that of a marble or cherry to
that of a small hen's egg, and they are usually found about three
inches above the anus, but they vary in position from a point just
within the sphincter to one six inches up the rectum. Their presence is
usually diagnosticated without difficulty, or, if any is experienced, a
digital exploration will reveal them. A child with functional
disturbances of the bowels accompanied with frequent hemorrhages should
be examined for polypus. One of these growths sometimes unpleasantly
complicates a case of hemorrhoids.

A rectal polypus is an adenoma, consisting of dilated glands of
Lieberkuhn imbedded in connective tissue, also containing nerves and
blood-vessels, and is covered with the epithelium of the bowel.


Hemorrhoids, or Piles.

These are usually fibrous when situated below, or vascular when
situated above, the sphincter ani muscle. They are conveniently known
as external and internal piles, but in some instances it is impossible
to say whether these tumors are external or internal. In either variety
they are due to an abnormal state of the blood-vessels, and especially
of the plexus of superior, middle, and inferior hemorrhoidal veins
disposed around the lower extremity of the rectum immediately above the
internal sphincter muscle. The inferior mesenteric and internal iliac
veins receive a large portion of the blood from this plexus, so that a
very free intercommunication exists, around the lower portion of the
rectum, between the general {883} venous system and that of the liver.
It should be borne in mind that these veins are destitute of valves,
and are situated in a very dependent part, which is normally in a high
degree of functional activity.

External hemorrhoids are found at the very verge of the anus, and, when
not irritated or inflamed, appear like movable, dependent plications of
hypertrophied skin. They appear either singly or in groups, but it is
nothing unusual to find five or six of them together, and they are not
infrequently associated with the internal variety. These pendulous tabs
of integument are very prone to inflammation, and they then become
exquisitely tender, painful tumors, which vary in size from that of a
small pea to that of a pigeon's egg. That portion of the tumor
presenting toward the anus is covered with mucous membrane; the other
is covered with integument; the former is dark-colored, due to
engorgement of its vessels. These, being composed internally of
tortuous, dilated veins which have totally lost their normal
resiliency, bleed freely on section, but after a time they undergo the
following changes: the over-distended vein, of which each is mainly
composed, either becomes obliterated by the encroachment of
inflammatory deposit or its walls give way and the contained blood
escapes; its serum is absorbed, and the tumor now consists of a
blood-clot, the remains of a vessel, inflammatory lymph, a hyperplasia
of connective tissue, mucous membrane, and integument. It undergoes a
still further change by absorption, and remains a permanent pendulous
teat of cutaneous and connective tissue, bearing no trace of vascular
channels.

On account of the extremely sensitive nature of the mucous membrane and
skin of the anus, an inflamed condition of these tumors entails an
amount of suffering very disproportionate to their size: there is
torture in the act of defecation, constant tenesmus, spasm of the
sphincters, a sense of weight and heat in the perineum, and sometimes a
swollen, very painful, condition of the raphe, which stands out like a
cord.

Occasionally there is a total inability to urinate, combined with a
frequent desire to do so. When an attack such as this ends in
suppuration of the tumor a radical cure is effected, but a marginal
ulcer of the anus sometimes follows. An unclean and neglectful habit
provoking constipation, sexual incontinence, over-indulgence in
highly-seasoned food or in stimulating beverages, exposure to cold and
wet, and the straining attendant upon dysuria, will provoke an attack.
No age or sex is exempt from this affection (Gross). It is claimed that
before puberty females are more subject to it than males; after that
age the reverse obtains, except during pregnancy.

Internal hemorrhoids are round, oval, or sometimes cylindroid-shaped
tumors covered by mucous membrane; they are smooth, granular, or rough
to the touch, much less sensitive and painful than the inflamed
external variety, and are situated within the rectum it may be an inch
or two above the internal sphincter muscle. They occur in groups or
scattered over the surface of the bowel. In structure they are soft,
spongy, vascular tumors composed of dilated and tortuous blood-vessels,
the veins predominating over the arteries, their interstices scantily
supplied with connective tissue, and their covering is of mucous
membrane. In color they are dark red, but when compressed and
strangulated by the sphincters they assume a dusky purple hue. After
long exposure they take on a pseudo-cutaneous appearance.

{884} The columns of the rectum are the seat of the cylindroid pile,
which is brighter in color and much more arterial in its structure than
the ordinary variety, and bleeds very freely. Anything which causes
stasis and accumulation of blood in the hemorrhoidal plexus of veins
predisposes to this very common affection. Constipation is the usual
cause; and among others may be named diseases of the liver which cause
portal obstruction, pelvic tumors causing engorgement from pressure,
the gravid uterus, labor, prostatic hypertrophy, urinary calculi,
stricture of the urethra, stricture of the rectum, and rectal tumors.
Among other causes are horseback-riding, the erect posture, violent
cathartics, seat-worms, dysentery, diarrhoea, dyspepsia, and a
sedentary life, with a diet of rich, stimulating food.

These piles do not usually cause much suffering; they vary in size from
that of a pea to that of a pigeon's egg, and cause a sense of weight
and stuffing in the bowel; but when they are large and numerous they
cause severe pain, tenesmus, difficult defecation, spasm of the
sphincters, and prolapse of the anus. When the patient is at stool the
tumors are forced down and protrude in a bunch, surrounded and
constricted by a collar of prolapsed mucous membrane: under these
circumstances the tortuous and dilated vessels of which they are
composed give way and free arterio-venous hemorrhage takes place. In
some cases this happens at every stool, the patient losing from a few
ounces to a half pint of blood almost daily until alarmingly depleted.
Usually, the protruded piles are easily restored after a motion of the
bowels, and so remain until the next one occurs; but in other cases of
longer standing and of more gravity the sphincter loses all tone and
the piles remain constantly prolapsed. This affection is very chronic,
and the subject of it has to regulate his life with the greatest care,
as the least unusual effort or excess may provoke an exacerbation.
Excepting in the worst cases the general health is not materially
impaired. They occasionally become so strangulated as to slough off,
which effects a cure, but this is accompanied by grave constitutional
disturbance. The disease is rather rare before the age of puberty, but
is very common in both sexes in adult life, and is frequently
associated with fistula, polypus, fissure, or carcinoma of this region.
In females suffering with piles a free hemorrhage from them sometimes
takes the place of the menstrual flow. The presence of internal piles
causes a sense of weight and fulness and the sensation of a foreign
body or of feces remaining in the rectum, with troublesome and
obstinate itching about the anus. These symptoms, with the occurrence
of hemorrhage from the rupture, erosion, ulceration, or abrasion of the
dilated vessels, render the diagnosis easy. Should the piles not
protrude, they can readily be made to do so by directing the patient to
sit and strain over a vessel containing hot water. If the piles do not
appear, a digital examination should be made. Indeed, it would be
better to make one in every case of this kind.

About the margin of the anus the superficial veins are prone to great
dilatation, and when presenting form masses of a bluish color, often
very dark, covered partly by mucous membrane, partly by integument.
These are also commonly known as piles.


{885} Dilatation of the Rectal Pouches, or Physick's Encysted Rectum.

This is an uncommon disease, generally occurring in those advanced in
years, and consists of an hypertrophy, and sometimes of an
inflammation, of the natural rectal sacs. These pouches are quite small
in early life, and enlarge gradually as age advances, this condition
being favored by the lodgment in them of extraneous substances, such as
indurated fecal matter, inspissated mucus, the seeds of fruit, and
other undigested masses. Constipation, so usual with the old,
predisposes to this affection, as it keeps the bowel distended with
hardened feces. The pouches vary much in size, the largest of them
admitting the end of a finger. The disease is insidious and slow, but
is capable of producing intense suffering should inflammation,
suppuration, or ulceration attack them. Sometimes as many as a dozen
are involved.

The symptoms, which are rather misleading than suggestive of the
disorder, are a sensation of weight and uneasiness just within the anus
and uneasy sensations in the rectum, distressing itching, and, after a
time, pain following defecation and lasting often for hours. The pain,
which is aching and burning in character, is not confined to the parts
affected, but radiates down the thighs, toward the back, and into the
perineum. An increased secretion of mucus always exists in these cases,
but the discharge of purulent matter is uncommon, and its presence
indicates the existence of very active inflammation.

It is said that even in the worst cases no spasm of the sphincters
occurs. An exploration of the bowel with a blunt-pointed hook affords
the only reliable guide to correct diagnosis: this, as it is moved
about in the rectum, engages the rim of a sac, which may thus be drawn
down through the anus and examined.


Non-malignant Stricture of the Rectum.

In the absence of ulceration or syphilitic infection this is an
uncommon disease, and very many of the cases of so-called stricture of
the rectum are caused by spasm which always disappears during
anaesthesia.

The affection may be described as a narrowing of the lumen of the
rectum, more or less circumscribed, by the deposition of inflammatory
lymph or fibrous tissue in the mucous, submucous, or muscular tunic of
the bowel. It may be due to traumatic causes, such as the introduction
of foreign bodies, the frequent and careless use of enema-pipes, or the
presence of sharp or irritating substances swallowed, as pieces of
shell or bone. It is said to have been caused by indurated feces, but
no cases have been published in which this causation is clearly shown.
This condition has also been brought about by various operations upon
the mucous coat of the bowel, such as the application of nitric acid
and other escharotics and the removal of portions of mucous membrane
and of hemorrhoids.

Stricture may be secondary and a result of extension of an inflammation
outside the bowel, as pelvic cellulitis; and it is frequently caused by
syphilitic deposition and by chancroidal invasion--in the former by
{886} infiltration, ulceration, and cicatrization, in the latter by
unnatural sexual connection, or by infecting vaginal discharge running
into the bowel.

When the stricture involves only the mucous tunic, it imparts to the
finger the sensation of a ring-like elevation or a valve-like
projection, into which the finger enters or beyond which it passes
usually without much difficulty; but when it involves the submucous and
muscular layers, as after the cicatrization of a large rectal ulcer,
the finger encounters a dense fibrous mass which in some cases appears
to have no lumen, but in others will admit only the end of the finger.
In these grave cases of long standing there occurs considerable
dilatation of the rectum above the stricture due to fecal detention and
impaction at this point, and hypertrophy of the muscular coat of the
bowel produced by long-continued straining and expulsive efforts.

Allingham[2] speaks of chronic constipation as a cause, and says,
"Straining to evacuate the contents of the bowel forces down the upper
part of the rectum into the lower, causing an intussusception; it gets
within the grasp of the sphincter muscles, and this may be the
starting-point of the irritation." Stricture does not usually follow
proctitis, even when the latter is very chronic. The long-continued
pressure of the child's head in cases of delayed labor is said to have
caused stricture of the rectum.

[Footnote 2: _Diseases of the Rectum_, p. 195.]

This affection is a disease of adult life, and more cases of it occur
among women than among men. "If stricture of the rectum is found in a
young woman, it is probably due to chancre cicatrices; if it is met
with in old women and men, the inference should be that it is either
caused by cancer or by syphilitic infiltration and its consequences.
Only in those cases in which no cicatricial tissue has been
formed--that is, when the contraction is due to the infiltration
alone--will the results of the antisyphilitic treatment contribute
anything toward rendering the diagnosis more certain."

Stricture of the bowel may exist for months and years without being
recognized and without causing the patient much uneasiness; more
frequently, however, there is marked uneasiness, with an increased
desire to go to stool and a sense of weight or of a foreign body in the
bowel. Violent straining accompanies the act. It is given usually as
one of the most common and reliable symptoms of this condition that the
feces are flattened, ribbon-shaped, or triangular or wire-drawn: in
true stricture, according to Allingham, this is not the case, but the
characteristic stool consists of small, irregular, broken fecal
fragments. When the contents of the bowel happen to be watery, the
loose stool is spurted out with great force. In this disease diarrhoea
alternates with constipation; the intestines become distended with
quantities of gas and feces, which provoke frequent and severe attacks
of colic; the appetite and digestion fail; the complexion becomes
sallow; the patient emaciates; ulceration sets in, and the patient
slowly sinks from exhaustion. Usually, these cases do not give rise to
much pain, and what there is, is usually referred to the back, thighs,
penis, or perineum. A discharge of mucus resembling white of egg
immediately precedes each action of the bowels. Usually, these
strictures are within two and a half or three inches of the anus, but
sometimes they have been found high up in the sigmoid flexure, and
rarely at a greater distance. A syphilitic stricture by direct
inoculation {887} is found just within the sphincter muscle, and
consists of an infiltration of inflammatory lymph in a circumscribed
portion of the submucous tissue. It is tight, highly sensitive,
thickened, inflamed, and bathed in pus; there are also constitutional
symptoms, as fever, anorexia, and mental irritability. The subjects of
this variety are usually women. The tissues composing strictures of the
rectum of a very chronic character are found to be gray or bluish-white
in color, of very dense fibrous structure, and creaking under the knife
when cut, as a piece of cork would do.

Besides the before-mentioned stricture, due to the contraction of a
chancroidal ulcer, is another caused by submucous gummata of the
ano-rectal region, which is very rare; and yet another, the diffuse
gumma, or ano-syphiloma of Fournier, which is the most frequent of all
causes of stricture of the rectum. The diffuse gumma is one of the
later manifestations of syphilis, and consists in "an infiltration of
the ano-rectal walls by a neoplasm of as yet undetermined structure
originally, but susceptible of degenerating into a retractile fibrous
tissue, and thus giving rise to narrowing of the intestinal calibre to
a greater or less extent."


Proctitis, or Inflammation of the Rectum.

Inflammation and suppuration in the lower part of the rectum are even
more common than the corresponding affections of the caecum, and their
causes are quite as various. In many cases, no doubt, this affection is
traceable to ulceration (perforative or otherwise) of the mucous
membrane; in others it probably originates in the connective tissue
which surrounds the rectum (periproctitis). The rectum, still more
frequently than the caecum, becomes involved in inflammation and
suppuration originating in the various pelvic, and even in distant,
organs. Abscesses arising in the abdominal cavity or its parietes are
peculiarly apt to gravitate into the pelvis and to communicate with the
rectum.

Proctitis in its acute form has some symptoms in common with dysentery,
but it differs from it by the absence of abdominal pain, tenderness,
and severe constitutional symptoms. The pain in proctitis is usually
referred to the sacrum and perineum, and there is frequently dysuria
from sympathetic affection of the bladder. This disease may be acute or
chronic; the latter form occurs in those advanced in life. Frequent
attempts to evacuate the bowels, with great tenesmus, heat, weight, and
fulness in the bowel, and a mucous and bloody discharge in the absence
of impaction of the rectum, characterize the attack. Should it be
protracted and severe, the discharge will become purulent. A digital
exploration should always be made to ascertain if any foreign or
irritating substance is exciting the inflammation.

The presence in large numbers of Oxyuris vermicularis may excite
irritation and inflammation of the rectal mucous membrane, which is
sometimes very intense.[3]

[Footnote 3: Curschmann, _Ziem. Encyclop._, Am. ed., vol. viii. p.
848.]

Inflammation of the anus and buttocks, caused by the application of the
leaves of Rhus toxicodendron after defecation, has extended into the
{888} rectum and produced proctitis and peritonitis.[4] "In some cases
of dysentery the pathological lesions are limited to the rectum, which
would produce an apparently local inflammation very similar to
proctitis. The irritation of unnatural sexual intercourse and the
contact of gonorrhoeal poison have been known to excite intense
inflammation of the mucous membrane of the rectum, with a copious
discharge of pure pus, and accompanied by intense burning pain and
great heat of the parts involved."[5]

[Footnote 4: Case of Dunmire, _Philada. Med. Times_, vol. xii.]

[Footnote 5: Heubner, _Ziemssen's Cyclopaed._, vol. i. p. 552.]


Fissure of the Anus and Rectum.

The painful ulcer of Allingham is quite a common affection, attacking
women more frequently than men, and no age is exempt from it. Of 4000
consecutive cases of rectal and anal disease observed by Allingham, 446
presented fissure of the rectum. They are rarely multiple. Their usual
position is dorsal, although they may be found at any part of the
circumference of the anus, and just within the verge of the anus at the
junction of the skin and mucous membrane, extending upward toward the
rectum usually not more than half an inch, and appearing as a crack or
fissure, often very trifling in appearance, or a club-shaped
ulceration, the floor of which will be very red and inflamed if it is
recent, but if chronic the floor will be grayish, with hard,
well-defined margins. Sometimes there will be found at the external
extremity of the fissure a small club-shaped papilla or muco-cutaneous
polypoid growth; but this is not to be confounded with the ordinary
polypus, nor is it the cause of the fissure, but the result of
irritation caused by the latter. In other cases the external site of
the fissure is indicated by a very tender and swollen flap of
integument, which often becomes the seat of a small but very painful
fistula. The club-shaped papilla is said to indicate invariably the
existence of fissure.

Fissure of the rectum is often associated with anteversion and
retroflexion of the womb. In many of these cases the fissure will heal
spontaneously when the malposition is rectified. However treated, the
result will not be satisfactory while the uterine trouble remains
uncorrected.

Fissure is not infrequently caused by and accompanied with polypi: it
may be caused by any accident whereby the verge of the anus is torn or
superficially lacerated--by chronic diarrhoea, by violent expulsive,
straining efforts, as in labor, by the passage of very hard, dry
stools--and very frequently it is syphilitic in origin. The most
prominent symptom of this disease is pain, and this is very severe and
peculiar in character, coming on in most cases not during the act of
defecation, but twenty minutes to half an hour afterward, and is
preceded by a hot, burning, throbbing sensation at the anus: then comes
on spasmodic contraction of the sphincters, and the patient endures
agonizing pain, often for several hours, when relief is gradually
experienced, and no pain is felt until defecation again becomes
necessary. Now, it has been observed that in some cases where the local
lesion is very trifling the pain and spasm are intense and
long-continued; in other cases, where spasm and agonizing {889} pain
followed every act of defecation, no lesion of the anus or rectum could
be found. This led Dolbeau to consider the essence of fissure of the
anus neuralgic, and to define it as "a spasmodic neuralgia of the anus
with or without fissure." The mental depression is so much out of
proportion to the local disease that this may come within Curling's
observation, that "mental causes may produce local disease in the
rectum."


Rodent, or Lupoid, Ulcer of the Rectum.

This is, fortunately, a rare disease, and is peculiar and distinct from
any other form of ulceration in this region. It is not cancerous,
although bearing some resemblance to epithelioma. As it first appears
it is very like a syphilitic sore, and its situation and the character
of the pain might lead to the supposition that fissure existed. Rodent
ulcer is usually situated upon the mucous membrane, although it
occasionally invades the integument about the anus; its shape is
irregular, its edges sharp and well defined, and it does not undermine
the neighboring tissues. There is no induration about this sore, as
nature does not seem to attempt to limit it or to set up any reparative
action, and its surface is red and dry. The surrounding tissues seem
quite normal. It is very destructive, and seems to prefer mucous
membrane, although sometimes it destroys deeply. It does not cause
infiltration; it does not spread by the lymphatic system, forms no
secondary deposits, nor does it produce stricture. It may remain in a
quiescent state for some time, and a certain amount of cicatricial
tissue may form; but it never heals spontaneously, and an exacerbation
comes on which destroys in a very few hours the repair which may have
been the work of many days. This form of ulceration of the rectum is
usually considered incurable; the pain is intense, being compared to
that produced by hot iron, and of course being much aggravated by the
acts of defecation. Patients so affected die from exhaustion and pain,
although recovery may take place, I have known one case entirely cured
by complete excision. Spasm of the sphincters is a usual accompaniment,
and greatly augments the suffering of the patient. Of the four thousand
consecutive cases of rectal disease tabulated by Allingham, only two
were cases of rodent ulcer.


Obstruction of the Rectum.

This condition may be caused by foreign bodies introduced into the
anus, by indigestible substances swallowed, by impaction of feces, by
pressure of tumors external to the rectum, and by intestinal
concretions. Any condition which causes loss of muscular and nervous
tone in the large intestine favors its obstruction; thus, it is not
uncommon in the aged of both sexes, but especially is this the case in
women, and in them it often follows parturition. Hysterical, nervous,
and debilitated persons are particularly prone to it. The insane, if
not carefully watched and regulated, will become the subjects of it.
Impaction of feces is a very common cause of obstruction of the rectum,
and atony of this organ is usually the primary cause, the feces in
these cases being {890} either very hard and dry or clayey and
tenacious. These masses are of a more or less globular shape, and, as
they irritate the bowel and produce diarrhoea, the practitioner
sometimes falls into the error of prescribing doses of opium and the
astringents, misled by the appearance of feculent fluid which oozes
around the impacting mass. The impaction occurs just above the internal
sphincter. Habitual constipation soon stretches the rectum and robs it
of expulsive force, and an accumulation of months of fecal matter is
sometimes found. The appearance of persons so affected suggests
malignant disease: they are cachectic, sallow, dyspeptic, irritable,
and nervous. Vomiting, anorexia, thirst, cough, hectic, irregular and
profuse sweating, are also among its symptoms. Cases of melancholia and
of hypochondriasis have been cured simply by the discovery and removal
of rectal impactions. This condition has been mistaken for cancer,
phthisis, intermittent fever, and enlarged mesenteric glands.
Accompanying impaction, and as a result, is spasmodic contraction of
the sphincter ani, which causes the anus to protrude in a nipple shape
and to firmly resist the introduction of the finger. Usually, there is
no discharge from the anus in these cases. Tenesmus, a sense of weight
and of a body present in the bowel, are experienced. Young people are
not often subjects of impaction.

Concretions also cause obstruction of the rectum: these are more
frequently cylindroid in shape, and sometimes have a nucleus consisting
of some firm foreign body. Wetherill reports a case of a young adult,
who had been accustomed to the daily ingestion of a substance known as
hygienic bread (this substance is made from the husks of grain, and is
very coarse: it is used to excite peristaltic action), from whose
rectum he removed a very hard ball of this substance which was covered
with mucus, but which contained no nucleus. He reports another case in
which the offending substance was a globular mass of casein, stained
with bile and covered with mucus, and which had for a nucleus a small
mass of hardened fecal matter.

Gueneau de Mussy[6] reports a case in which there was an occlusion of
the rectum by a mass of magnesia, which was so firmly impacted that it
had to be removed by a mallet and chisel. A similar case occurred in
the practice of Dunlap of Norristown. Fendick[7] relates an instance of
impaction by a fish-bone near the anus, causing obstruction requiring
surgical interference; which illustrates the importance of examining
carefully all cases of acute piles and threatened abscess.

[Footnote 6: _Medical Times and Gazette_, 1879, vol. ii. p. 214.]

[Footnote 7: _Lancet_, 1880, vol. ii. p. 239.]

These concretions often consist of animal and vegetable fibres matted
together about a nucleus, the latter consisting of the seeds of fruit,
fragments of bone or gristle, hair, small coins, or pins. "Enteroliths
may lodge in the rectal ampullae" and cause obstruction. Indigestible
substances swallowed with the food may be arrested in the rectum, such
as grape-skins, fruit-pits, husks, and fibres, and where there already
exists stenosis of the bowel a dangerous form of obstruction may be
produced. Jones[8] reports a case of chronic impaction of the rectum by
plum-stones, which gave rise to trouble in defecation, and at the end
of eighteen months produced symptoms of piles; at the end of two years
impaction occurred, and the mass was removed by the surgeon. Hazelhurst
relates {891} a case of impaction in a negro where two hundred and
eighty plum-stones were removed from the rectum after having been there
for a week. The records of the Pennsylvania Hospital furnish the
following interesting case of obstruction:[9] "The patient (a male)
stated that twenty years before he swallowed a peach-stone. Two years
afterward he had symptoms of rectal irritation, tenesmus, constipation
alternating with diarrhoea, and liquid stools, etc. These symptoms had
continued ever since. His health had been markedly impaired. A digital
examination revealed a hard, stony mass two and a half inches above the
anus. Under ether Morton divided the external sphincter, and with a
pair of bone-forceps removed, with considerable difficulty, a
good-sized peach-stone which was lodged in the rectal tissues. The
stone was very sharp at the ends, and had evidently lodged crosswise
and become imbedded. The patient was discharged quite well and free
from all symptoms."

[Footnote 8: _Lancet_, 1856, vol. ii. p. 278.]

[Footnote 9: _Surgery in the Pennsylvania Hospital_, Phila., 1880, p.
335.]

Gall-stones may cause impaction or they may form the nuclei of
concretions. A case of impaction is related by Walker,[10] who removed
a gall-stone from the rectum which measured three and a half inches in
its longest and one and a quarter inches in its shortest diameter; also
one by Roberts,[11] in which he removed a gall-stone measuring five
inches in circumference from the rectum of a woman two weeks after
confinement. Mischievous, revengeful, insane, or intoxicated persons
sometimes force very curious foreign bodies into the rectum, among
which may be mentioned hot iron, bottles, cups, bougies, pieces of
wood, stones, a champagne flask, a goblet, slate-pencils, and the tail
of a pig with the bristles cut short. Some foreign bodies introduced
from below find their way through the sigmoid flexure and lodge in the
colon, or they may remain for a long time in the rectum. The caecum is
the favorite resting-place of foreign bodies. Turgis[12] removed by
linear rectotomy a cup which had been forced into the bowel. These
foreign substances, if not promptly removed, set up violent
inflammation. Obstruction of the rectum may be caused by vast numbers
of round- or thread-worms twining themselves together in a mass; and
when this happens in children or in adults of very nervous organization
a curious train of reflex symptoms may be developed, among which may be
mentioned choreic movements, convulsions, pruritus ani, insomnia,
irritability, melancholia, and hypochondriasis. Finally, the rectum may
be obstructed mechanically by pressure exerted from without. Such an
effect might be produced by morbid growths from the sacrum or ileum; by
deposits in Douglas' cul-de-sac; by ovarian disease; by pelvic
cellulitis causing stricture of the rectum; by vesical trouble; by
ascites with hepatic disease; and by various abnormalities of the
uterus, such as inflammation, morbid growths within or upon, simple
retroversion or retroflexion, or retroflexion of this organ in a gravid
state.

[Footnote 10: Flint, _Prac. Phys._, 460.]

[Footnote 11: _Bost. Med. Journ._, 1879, vol. ii. p. 116.]

[Footnote 12: _Societe de Chirug._, 1878.]

Impaction of feces under some circumstances may give rise to extensive
sphacelus of the rectum and the contiguous parts from pressure. This is
well illustrated in the following case of a woman aged sixty-five, who
was found to have an immense distension of the abdomen from ascites,
incident to a large omental scirrhus. The patient suffered greatly from
the pressure caused by the accumulation of water, and she was tapped.
Soon after this an impaction of feces was observed, which probably had
been forming {892} for some time prior to her coming under observation.
A week or ten days after the tapping the impaction was detected, but
not soon enough to prevent the formation of a large slough of the
posterior and inferior part of the rectum immediately above the anus.
The submucous tissues and the skin, owing to the greatly enfeebled
condition of the patient, soon gave way, leaving a large opening which
communicated with the bowel. The tissues adjacent were oedematous, red,
and painful. The finger carried into the bowel through the anus
discovered the slough to have involved a region of at least two and a
half inches in diameter.


Cutaneous Eruptions and Parasitic Conditions of the Anus.

These are quite numerous, and they almost invariably produce much
distress and excite painful pruritus, which is augmented rather than
relieved by scratching or friction of any sort. The application of the
leaves of Rhus toxicodendron after defecation is capable of exciting
considerable inflammation upon and around the anus, accompanied by
small pearly vesicles, which, when ruptured by scratching, seem to
spread the disease wherever the contained serum flows. Eczema, when
found in the anal region, is usually due to parasitic growth. Erythema
intertrigo is caused by the friction of moist opposing surfaces, as
between the nates of stout persons, who perspire freely, and infants.
The abraded derma exudes a sero-purulent fluid which excites
troublesome pruritus. When this condition exists about the anus it
causes painful defecation and spasm of the sphincters. Erythema
chronicum occurring in this locality is frequently a sequel to chronic
eczema and chronic lichen: the skin cracks, is moist, thickens, and the
epidermis exfoliates. The proximate cause in both of these conditions
is congestion of the vascular rete of the derma. In prurigo podicis
papules appear which itch intensely, and when scratched bleed, the
summit of each papule bearing a small black scab. If not cured, in time
a true psoriasis may develop. Herpes of the anus occurs similar to
herpes at the other mucous outlets of the body, and is usually
symptomatic of slight disorder of digestion. Wetherill has seen a case
of herpes zoster, (var. proserpens,) in which the vesicles extended
from the side of the scrotum along the perineum to the verge of the
anus. This condition was accompanied with neuralgia of the rectum,
painful defecation, and spasm of the sphincters. Furunculi sometimes
form at the verge of the anus, causing spasm, pain at stool, and
occasionally marginal fistulae. Various syphilodermata also appear in
this region. Gross was the first to describe a condition of trichiasis
of the anus--a very irritating complication to fissure--due to a
perverted recurvation of the hairs usually found in the anal region.
Villerme states that hairs have been found growing from the mucous
membrane of the rectum. The colonization of pediculus pubis about the
anus occasions a certain amount of irritation. Sarcoptes hominis is
sometimes found in this region, having been carried there by hands
infested with this parasite. The result is very distressing. The
peculiar tracks or burrows made by this little animal, and the use of
the microscope, make the diagnosis certain. The Acarus autumnalis, or
mower's mite, has been found in the skin of this part, and it is
capable of causing great distress. These do not furrow the {893}
integument longitudinally, but burrow vertically, and may be picked out
of the summits of the wheals, where they appear as small red points.


Ulceration of the Rectum and Anus.

This is a condition very different from fissure or the painful ulcer of
Allingham--much more grave, difficult to treat, and, in chronic cases,
much less hopeful of cure. It is not an uncommon affection, Allingham's
table of 4000 consecutive cases of diseases of the rectum and anus
furnishing 190 of the disease under consideration. An ulcer of the
rectum may be partly within, partly without, the internal sphincter,
but in most instances is found above that muscle, from an inch and a
half to two inches from the anus, situated dorsally.

The symptoms are unfortunately obscure and insidious, misleading not
only the patient, but also too frequently his medical adviser, and
gaining grave headway before a correct diagnosis is reached. Often the
very first symptom is a slight diarrhoea every morning as soon as the
patient rises, accompanied with a little discharge resembling
coffee-grounds; or, again, the discharge is like the white of an egg;
in some rare instances pus is formed. At this stage there is little or
no pain, but the patient suffers from tenesmus--which is not followed
by relief--and a sense of uneasiness in the part. Several stools of
this nature or streaked with blood may be passed during the earlier
part of the day, after which the patient feels partly relieved, and no
more evacuations occur until the following morning, when he again
experiences the same train of symptoms; and this repeats itself daily
for a long time. Finally, these discharges occur in the evening as well
as in the morning, then at various times during the day: his general
health begins to give way; the discharge becomes augmented in amount
and contains more blood and pus; and he suffers occasional pain from
flatulent distension. Local pain in the rectum is now felt, which is
not acute, but is very wearying, is augmented by much walking or by
long standing, and which has been described as similar to a dull
toothache. These ulcers may be multiple, and not infrequently lead to
stricture of the rectum, which condition is indicated by the
alternation of attacks of diarrhoea and constipation. As the ulcerative
process proceeds, nature makes efforts to limit the process, which
causes infiltration and thickening of the submucous and muscular
tissues, and produces narrowing of the lumen of the intestine, which in
time loses its tone and contractile power and becomes a passive tube,
utterly unfit to perform its normal duties. The sphincters give way and
the patient loses control over his evacuations. Finally, abscesses
form, which, burrowing toward the surface, form fistulae, and may
perforate the bladder, the vagina, or the peritoneal cavity. If one of
these ulcers be examined while yet in the acute stage, it will be found
to be oval in shape, with well-defined edges: the base will be either
grayish or very red and inflamed, the surrounding mucous membrane
appearing normal. The rectal glands will be found to be enlarged.
Should the ulcer be examined at a later stage, it will be found to be
much deeper and more extensive, with great thickening and nodulation of
the mucous membrane, and looking in places as though the latter {894}
had been torn off. At this stage the ulceration may be partial or may
involve the entire lower portion of the rectum. The suffering is now
intense, and a constant discharge of fetid pus and mucus takes place.
The appearance of the anus at this time suggests malignant disease: it
is covered with swollen, shiny, tender, club-shaped flaps of integument
constantly bathed in an ichorous discharge. The entire rectum and
sigmoid flexure have been involved in some cases, while in others
necrosis of the sacrum has occurred. Patients suffering from ulceration
and stricture are very liable to a low form of peritonitis, attended by
intense abdominal pain.

The causation of these ulcers of the rectum is frequently very obscure:
some are of syphilitic, others of strumous, origin. Some are of
traumatic origin, but more often the patient was in apparent health up
to the time of the appearance of the disease. The experience of
Allingham would indicate that neither chronic constipation nor
dysentery is a frequent forerunner of this malady. T. Claye Shaw,[13]
in an article entitled "On Some Intestinal Lesions of the Insane,"
says: "After death are found patches of ulceration sometimes so
extensive as to resemble a honeycomb network. The edges are usually
slightly raised, and perhaps hardened; but the ulcers are at other
times mere local punchings out of the mucous membrane, and there is
often a little loose gelatinous material." It is claimed that such
disorders are not infrequent among the insane.

[Footnote 13: _St. Bartholomew's Hospital Reports_, 1880.]

It is also claimed that the chronic mechanical irritation from foreign
bodies, impacted feces, and the like exert a causative influence in the
formation of ulcer of the rectum. Like typhlitis, this affection leads
to chronic inflammatory changes in the immediate neighborhood
(periproctitis), with the formation of fistulae and crater-shaped
ulcerations, and to the extensive destruction of the mucous membrane,
followed by wasting and contraction of the rectum. The healing of these
ulcers is much delayed by the fact that the ulcerated and undermined
mucous membrane is irritated by the fecal masses which are especially
apt to accumulate in the lower part of the bowel and around the anus.
We find also hemorrhoidal swelling and ulcerations, which may be
regarded as partly a cause, partly a result, of the ulcerative
proctitis.


Follicular Ulcerations.

In this condition the most extensive ravages are found in the rectum
and sigmoid flexure. The causes are identical with those of catarrh of
the large intestine, if we except the follicular disease produced by
dysenteric infection. In this form of the disease, at least in its
earlier stage, the form of these ulcers is always round and
funnel-shaped, with distinct thickening of the edges of the mucous
membrane around the ulcers. These appearances may be explained by the
mode in which the follicular ulcerations originate: "The solitary
follicles become swollen, a result of catarrhal irritation, and the
cellular elements accumulate in the reticulum, giving rise at first to
nodules which project above the level of the mucous membrane: then the
newly-formed tissue-elements become necrosed in consequence of the
mutual pressure of the cells upon {895} each other; finally, the apices
of the follicular nodules give way and the ulcers are formed. The
surrounding mucous membrane bends over downward toward the base of the
ulcer, so that the orifices of the crypts look down into the same."[14]
As the suppurative process extends, particularly in the submucosa, and
the tissue surrounding the follicles becomes destroyed, these small
ulcers coalesce to form larger ones, and the undermined edges of the
mucous membrane project over the base of the ulcers, bleed, and become
necrosed. Healing is possible by cicatrization, the borders of mucous
membrane becoming applied to the base of the ulcer and gradually drawn
together by the cicatricial tissue. Still, this result is extremely
rare if the ulcerative process has gained much headway. When, however,
a follicular ulcer of some size does heal, cicatricial stenosis may
result, followed by chronic constipation, just as in the case of simple
catarrhal ulceration. The situation of follicular ulcerations is almost
always in the large intestine, and they vary considerably in number:
sometimes only a few follicles are thus affected, while in other cases
the bowel is crowded with them.

[Footnote 14: Rokitansky, _Path. Anat._, iii. 1861, S. 226.]

The anus and rectum may become the seat of chancroidal invasion. An
ulcer of this character fairly within the rectum is very rarely met
with, especially in this country, and could scarcely be produced except
by unnatural intercourse. They are of not uncommon occurrence in the
anal region, and are met with in this situation more frequently among
females than among males. Occurring among the former, they no doubt
often arise from accidental contact during normal sexual intercourse.
When this condition is found in males, it rather indicates at least an
attempt at unnatural intercourse. Of 1271 males affected with
chancroids, only 3 were found with the disease in the anal region. Out
of 388 females similarly affected, 33 were found with chancroid of the
verge of the anus. The table of Debauge gives 23 cases among 206
females having chancroid in various other situations. The destruction
of tissue in these cases may be very serious should the nature of the
ulcer not be recognized, and stricture of the rectum or cicatricial
stenosis of the anus might result. Ulceration of the rectum may occur
during chronic proctitis; it may accompany advanced states of prolapse
and procidentia of the bowel; it may attack a stricture of the rectum
and cause peritonitis by erosion. Ulceration may accompany hemorrhoids,
or it may attack them and cause dangerous hemorrhage. Finally, a very
intractable form of ulceration may follow the clamp-and-cautery
operation upon piles. When this untoward result is seen, it is usually
due to the fact that the patient has been allowed to move about too
soon. Allingham claims to have seen these ulcerated stumps of piles
even ten days after operation.


Peri-anal and Peri-rectal Abscess.

The ischio-rectal fossa is peculiarly liable to attacks of inflammation
resulting in abscess, as it is filled with much loose connective tissue
which supports a considerable amount of fat, and is situated in a
region which is constantly exposed to injury both from within and
without. It is a very vascular part, being freely supplied by branches
of the inferior {896} hemorrhoidal arteries and veins; the latter,
being large and destitute of valves, empty into the portal circulation.
Abscess in this region is of very common occurrence, and may attack any
one at any period of life. It occurs more frequently among men than
among women, and usually during middle life.

Abscesses in this situation may be acute or chronic. The former variety
may be caused by injury to the anus or to the surrounding parts; by
exposure to cold and wet, and particularly by sitting upon damp seats
while the body is overheated; by impaction of feces, constipation, and
straining at stool. Irritating substances swallowed with the food, such
as small pieces of bone, oyster-shell, or the stones of fruit, may
excite abscess by their presence in the rectum. Among other causes are
general debility, an impoverished state of the blood, the scrofulous
and tuberculous diatheses. The disease sometimes occurs in quite young
infants. Wetherill reports the case of an infant attacked by an
enormous ischio-rectal abscess while nursing from the mother, who was
at the time suffering from a succession of boils. Many cases have been
traced to sitting upon the outside of damp omnibuses. Hepatic
disorders, causing engorgement and stasis of the blood in the
hemorrhoidal plexus, have frequently occasioned this condition. These
abscesses are not always situated in the ischio-rectal fossa;
frequently they are subcutaneous and just outside the anus: in other
cases the starting-point may be ulceration of the mucous membrane of
the rectum, with escape of fecal matter into the areolar tissue; they
also originate in the submucous connective tissue of the rectum. The
acute abscess is sudden and very severe in its onset; the pain is
continuous, throbbing, and augmented during defecation; dysuria is
almost always present, and in some cases there is total inability to
pass water. There is local tenderness, dusky redness, and fluctuating
prominence, and, if not interfered with, a rupture of the integument
will take place and the pus will escape externally. Sometimes their
formation is accompanied with a chill or with a succession of rigors:
there is always considerable constitutional disturbance, febrile
movement, loss of appetite, and malaise. This form of abscess is
usually circumscribed and does not burrow irregularly, and sudden
relief of pain and distress is coincident with their evacuation.

Chronic rectal abscess corresponds to the cold or chronic abscess in
other situations: it is apt to occur among those who are much
debilitated or among those of the scrofulous diathesis. These abscesses
have little disposition to open spontaneously upon the surface, but
they burrow extensively in all other directions--high up along the
outside of the rectum, laterally into the tissues of the buttock, or
downward and forward into the perineum. The process of formation may
occupy many months, and sad havoc may be occasioned before their
existence is suspected. They occasion no pain nor distress nor acute
febrile movement, but may be accompanied with a hectic condition,
erratic sweatings, and rapid loss of strength. Upon examination of the
anal region in these cases a painless flat, boggy, crepitating
enlargement is the only surface-indication of the probably extensive
damage sustained by the deeper structures.

This form of abscess may be of traumatic origin, but more frequently
the inflammatory process arises in the cellular tissue of the
ischio-rectal fossa; in some cases the morbid action is due to
ulceration of the rectum. {897} In either case peri-rectal or peri-anal
cellulitis will be induced. When these abscesses are of strumous origin
the pus is thin, curdy, and offensive.

Both the acute and the chronic abscesses of this region are often
difficult to heal, the external opening remaining permanently patulous,
communication with the bowel resulting from internal burrowing and
erosion, with the formation of extensive sinuses in all directions,
resulting in fistulae in ano.


Fistula in Ano.

This condition occurs more frequently than any other of the
abnormalities of this region, Mr. Allingham finding 1208 out of his
table of 4000 consecutive cases of diseases of the rectum and anus. He
found also that fistulae followed rectal abscess in 151 out of 196
cases, the abscesses which healed kindly and gave no further trouble
being only 45 in number. A fistula in ano is a linear ulceration with a
patulous orifice which discharges pus: it may or may not communicate
with the bowel, and it may have more than one external opening. The
great majority of fistulae in this region are caused by abscess, either
arising in the submucous areolar tissue of the bowel, or in the
subcutaneous connective tissue in the immediate neighborhood of the
anus, or in the ischio-rectal fossa, or in an ulcerated state of the
mucous membrane of the rectum: in other cases it is congenital, or it
may result from the presence of foreign bodies or worms in the bowel,
or from puncture of the rectum by pins, scales of shell, fragments of
bone, or other sharp substances swallowed with the food. Abscesses
leading to fistulae have followed kicks, blows, or wounds of the anal
region: in short, anything which induces an abscess here may result in
a fistula, and as in the former more cases occur in males than females,
and more during middle age than at any other period, the same is true
as to the latter. Fistula is quite common among the phthisical as a
result of malnutrition and septicaemia, aided by the constant
succussion of the perineum produced by efforts at coughing. Of the 4000
cases previously referred to, 1208 were cases of fistula; "of these,
172 presented more or less marked symptoms of lung trouble,
haemoptysis, cough, or impaired resonance in some portion of the
chest."

A fistula may be complete or incomplete. To be complete, it must have
two openings (it may have more)--one in the anus or rectum, and one
upon the surface. There are two forms of the incomplete or blind
fistula--one in which there exists an internal but no external opening,
and the other in which there is an external but no internal opening. In
complete fistula there may be more than one external opening, and this
is in the majority of cases not far from the anus, but it may open in
the perineum or upon any part of the gluteal region. When the openings
are multiple they usually converge to form a common tract or sinus. The
external opening presents nothing to the untutored eye to lead to the
suspicion of grave internal trouble: frequently the vent is so minute
and valvular or shielded by a thin pellicle as to be entirely
overlooked; in other cases a little teat formed of superabundant
granulations guards the entrance: there may or may not be
discoloration, elevation, or depression of the surrounding integument,
and erythema resulting from the {898} irritating nature of the
discharge. Inflamed and suppurating follicles in the integument about
the anus are not to be mistaken for the orifices of fistulous tracts.

The internal opening in anal fistula is situated between the sphincter
muscles, sometimes just within the anus, but oftener about half an inch
above; in rectal fistula the internal opening or openings may be at any
point above the internal sphincter. These sinuses may be very tortuous,
with pockets, blind passages, or diverticulae, and are known as
horseshoe fistulae when they commence at one side of the bowel and
ulcerate around it to a point opposite before making an opening.

Of the two varieties of incomplete fistulae, by far the least frequent
is that where no internal opening exists, but where there are one or
more external orifices: these do not invariably even run toward the
bowel, but may extend off through the tissues in any direction. In the
other variety, where there exists no external evidence of disease,
considerable damage may be done before its recognition. Fistula may
coexist with hemorrhoids, stricture, ulcer, or malignant growth: it may
be a very trivial affair, with the internal but a fraction of an inch
from the external opening, or it may be long, deep, and tortuous, with
sinuses running in all directions through the buttock.

Usually, fistulae become worse when not operated upon, but there are
cases which have healed without surgical interference--others in which
this condition has gone on for many years without getting any worse or
without the discharge increasing in amount. The fluid discharged from a
chronic fistula loses after a time much of its purulent character and
becomes serous and watery; but fresh abscess and inflammation is apt to
take place in these cases from feculent matter lodging in the sinus.
Those which burrow most readily are the internal fistulae with large
openings, into which the feces are pushed, with the sinus running
toward the anus, because of their funnel-shape.

The presence of fistula may be suspected if there are in the anal
region abscesses which have not completely healed, or which, having
apparently done so, break out from time to time and discharge pus; or
from the existence of a circumscribed hardness or swelling
unaccompanied by an opening which varies in size and is at times
painful; or if there exist any ulcerated moist openings. To make a
positive diagnosis the tract must be explored by a probe: enter the
oiled, blunt-pointed probe gently into the external opening and let it
find its way along without force, bending the probe if necessary, until
it has traversed the sinus as far as it will go; then pass the finger
into the rectum and feel about for an internal opening or for the point
of the probe. If the finger be introduced first, the relations of the
parts are interfered with and the internal opening, should one exist,
might not readily be found. Sometimes the bottom of the tract does not
correspond in situation to the internal opening, but extends beyond it.
In those cases where no external opening exists, the rectal speculum,
aided by judicious pressure, will discover an issue of pus from a sinus
upon the mucous membrane of the rectum.

In order to illustrate the amount of damage which a small foreign body
may cause when lodged in the rectum, Wetherill relates the following
case, which occurred in his practice at the Pennsylvania Hospital for
the Insane: The patient was a middle-aged man, intelligent, and an
{899} employe of the hospital. "Upon examination of the anal region I
found a small, tender, firm swelling, which did not fluctuate, about an
inch to the left of the anus: this had been forming for about a week,
and there was no history of painful defecation, of exposure to damp and
cold, nor of a blow or injury of the part. Without waiting for the
development of fluctuation, I made a free and deep incision into the
ischio-rectal space, and a large quantity of very fetid pus escaped:
upon introducing a large probe I found that it passed up into the fossa
to a depth of four and a quarter inches and turned but slightly toward
the bowel. Remembering the experience of Allingham, that when the pus
in these cases was very offensive there existed an opening in the
bowel, I questioned the patient again as to pain in the bowel or
painful defecation, which was answered in the negative. No
communication could be found with the finger in the bowel and a probe
in the wound, and poultices were applied, liquid diet ordered, and the
man kept in bed. The cavity was loosely filled with absorbent cotton
and the entire wound (apparently) healed slowly, but kindly, and in
about ten days after operation the patient left the house to all
appearance sound. About a week after the patient returned with the
report that he felt uneasy throbbing in the part, and that there was a
very slight discharge. Upon inspection I found in the surface-line of
the cicatrix a pinhole opening which yielded upon pressure a drop or
two of pus; upon entering a very fine probe it passed into a narrow
sinus to a depth of three and a quarter inches, but no communication
could be made with it with the finger in the bowel. Upon withdrawing
the probe it grated over something which felt like dead bone, about two
inches from the surface. I enlarged the opening, introduced a pair of
fine dressing-forceps, and withdrew a piece of the rib of a chicken
about half an inch in length and sharpened at one extremity to a fine
point. Upon making inquiry I found that he had not eaten any chicken
since the development of the abscess. He then suddenly remembered that
while he was at stool a few days prior to the formation of the abscess
he experienced a sudden pang of very acute pain in the rectum, which,
however, soon passed off. This was no doubt the moment when the piece
of chicken-bone pierced the rectum."


Hemorrhage from the Rectum.

Hemorrhage from the rectum may be accidental, primary, or
secondary--accidental when it follows the ulceration of internal piles
or the erosion of large arterial or venous trunks during the progress
of malignant disease, or when it occurs from the rupture of a rectum
during defecation--a very rare and curious occurrence reported by M. E.
Quenu;[15] primary when it occurs during, and secondary when it occurs
after, a surgical operation upon these parts.

[Footnote 15: _Revue de Chirurg.; Practitioner_, p. 29, Oct., 1882.]

Hemorrhage from the rectum without any structural lesions is quite
unusual, but occasionally copious losses of blood are seen in vicarious
menstruation, and several instances have been reported.

When ligatures separate after operations upon those of broken-down
constitution very copious and dangerous bleeding may occur without any
symptoms save a "sensation of something trickling in the bowel," {900}
a feeling of weight and fulness in the part, with increasing weakness
and syncope of the patient, until he expresses a desire to go to stool,
when suddenly a large quantity of blood escapes.


SECONDARY DISEASES OF THE RECTUM AND ANUS.

This class of affections depends upon constitutional infection, direct
extension of disease by contiguity, by contiguity from disease in
neighboring organs, or by abnormal conditions excited by disease of
remote origin; and are frequently due to changes in the nervous and
vascular supply.


Syphilis of the Rectum and Anus.

True primary syphilitic chancre of the rectum must be an extremely rare
lesion, and could have been acquired only by unnatural intercourse.
There are syphilographers who deny that the hard chancre has ever been
found within the sphincter muscles; but it certainly is not uncommonly
found in the anal region, and oftener among women than men. The table
of Jullien gives 12 instances of this lesion in males, and 1 instance
of chancre of the buttock, out of 77 cases, while among 82 cases
occurring in the opposite sex, 21 were of the anus and perineum and 4
of the buttocks. The French authorities give the frequency of this
condition in men as 1 case in every 119; in women, 1 case in every 12.

Anal chancres are easily overlooked, as they occupy the puckered folds
of the anus, which when not opened out to the fullest extent afford
perfect concealment: they may be either in the form of cracks or slight
fissures, elongated ulcerations, or firm papules. It has been claimed
that the initial lesion has provoked stricture of the rectum, but this
is not probable.

The secondary manifestations of this disease which show themselves in
the anal region are some of the syphilodermata, moist papules, mucous
patches, and moist papillomatous excrescences or condylomata. The
statistical tables of Davasse and Deville[16] in regard to the
occurrence of moist papules and mucous patches in women show that out
of 186 cases they appeared about the anus in 59 and on the perineum in
40. Bassereau's[17] statistics show that in men these lesions occurred
in the anal region 110 times out of 130 cases. These are, of course,
very contagious. Besides true syphilitic warts, which sometimes occur
in this region, it is quite usual to see the anus surrounded and the
entire gluteal cleft filled up with moist, offensive, papillomatous
excrescences, which remain obstinately so long as these surfaces are
permitted to rest in moist contact. Syphilitic stricture of the rectum
is one of the results of a later stage of infection, and occurs oftener
among women than men. It is stated by Jullien that of 60 cases only 7
were men, the remaining 53 women. They are invariably formed as
follows: A gummatous deposit in the {901} submucosa undergoes
ulceration, and the subsequent cicatricial contraction gives rise to
the stricture. Whether the stricture will be valvular or annular
depends upon the extent of rectal mucous membrane involved in the
ulcerative process. The diffuse gummatous infiltration of the
ano-rectal tissues and the subsequent deposition of contractile tissue
are the most usual causes of these specific strictures. The lower
portion of the rectum is commonly the situation of specific
ulcerations, usually of the secondary or tertiary stage, which lead to
the formation of stricture: this occurs more frequently among women
than men, and between the ages of seventeen and thirty years. Gosselin
and Mason regard strictures as the result of chancres, and not as the
result of constitutional infection; but it is known that ulcerations of
secondary syphilis may extend upward from affections about the anus,
and also that gummata do commonly give origin to this condition.
Gummata, and strictures following them, may be distinguished from other
affections on account of the greater distance from the anus at which
they occur, chancres or chancroid ulcers being usually within four or
five centimeters of the anal orifice. Strictures due to gummata are
more apt to occur late in life, but may therefore be easily confounded
with cancer. Condylomata at the anus are often associated with
syphilitic disease of the rectum.

[Footnote 16: _Internat. Encyclop. of Surgery_, vol. ii. p. 508.]

[Footnote 17: _Loc. cit._]


Scrofulous and Tuberculous Affections.

There are cases which yield abundant evidence of struma in the form of
enlarged glands, chronic abscess in the neck, swelling and abscess in
the vicinity of the articulations, and the like, in which ulceration of
the mucous membrane of the rectum has been found: this condition may
result in fistula in ano by erosion, permitting escape of flatus and
excrementitious products into the cellular tissue. A similar result may
follow by erosion of the bowel from a strumous abscess in the
connective tissue around the rectum; both these forms tend to the
production of that class of fistula which has no outlet at the surface,
but which has one or more openings upon the mucous membrane of the
rectum. Thus concealed (for often there is no marked surface indication
of either abscess or fistula), they may remain for a long time
unsuspected and acting as a serious drain upon the already impaired
constitution. The pus in these cases is watery, curdy, and offensive.
These chronic conditions are subject to intercurrent attacks of acute
inflammation, due to the lodgment in the abscess cavity or the
fistulous tract of fecal matter or indigestible solid substances. Any
or all of the abnormalities of this region may be complicated by the
existence of tubercular or scrofulous conditions of the system.
Tubercular ulceration of the rectum is now a well-recognized condition.
Rectal ulceration and tubercular disease of the lungs have not been
found to coexist in any marked preponderating number of tabulated
cases. The frequent association of fistula in ano and tubercular
disease of the lungs has long been recognized, Allingham having found
172 such cases among 1208 cases of fistula in ano.

The pathology of tubercular ulceration of the rectum is graphically
described in _Ziemssen's Encyclopaedia_ as follows: "These
[ulcerations] begin in the follicular apparatus with swelling of the
individual {902} follicles and their vicinity from tuberculous deposit.
The newly-formed cells become caseous, the superficial layer of the
tubercle breaks down, and thus ulcerations arise of a round funnel
shape. The enlargement of these ulcerations is probably produced by the
constant formation in the base and edges of the ulcers of new nodules,
which themselves caseate and ulcerate. This process of extension, to
which these tuberculous ulcerations of the intestines exhibit a marked
tendency, takes place chiefly in a transverse direction (girdle-shape),
following the direction of the blood-vessels. The infiltration and
necrosis may advance longitudinally, and, finally, the individual
ulcerations coalesce with each other: in this way may be explained in
part the dentate appearance of the edges of these ulcerations. The
ulceration extends also in depth, although usually the muscular coat
appears to be covered by a thick layer of connective tissue: the
destruction advances slowly in the muscularis, but in the lymphatic
vessels which pierce the muscularis less opposition is presented to the
progress of the tuberculosis; and thus it is not uncommon to find
tubercles ranged one after the other, like links in a chain, from the
base of the ulcer directly down to the serosa. Healing is extremely
rare. The most frequent situation is the lower end of the ileum, but
the process may extend upward to the stomach, or downward, involving
the rectum. There is almost invariably unmistakable signs of
tuberculosis in other organs. It is possibly never primary, but this is
a still-disputed point. It usually occurs with tuberculosis of the
lungs, and when so occurring it is always secondary. The clinical
symptoms of this state are by no means characteristic."

Dwelling upon the subject of intestinal tubercle, it has been suggested
by Klebs[18] that the intestinal disease is produced by swallowing
morbid products derived from phthisical lungs--an hypothesis supported
also by the fact that tubercle in the intestines tends so strongly to
spread downward. "The seat of the deposit is the submucous tissue or
the corium of the mucous membrane: it is certainly subjacent to the
basement membrane, and not contained in the follicles, as Creswell
taught."

[Footnote 18: Jones and Sieveking, London, pp. 593-595.]

Woodward, in his article upon diarrhoea,[19] says: "The lesions,
whether mild or severe, are most generally seated in the caecum and
colon, but more or less extensive tracts of the small intestine,
especially of the ileum, are often involved also." He continues:
"Tubercular disease of the lung was noted in nearly one-sixth of the
autopsies of fatal cases of forms of flux heretofore described.
Possibly the frequency in chronic cases may be explained by the fact
that protracted intestinal flux forms the development of lung phthisis
in the predisposed."

[Footnote 19: _Med. and Surg. History of the War of the Rebellion_, p.
266.]

The rectal fissure or painful ulcer may be connected with diathetic
causes, as struma or scrofula: it is doubtful if syphilis should be
included among its causes.


Cancer, Malignant Stricture, and Malignant Ulceration.

The forms of cancer met with in these regions are epitheliomatous,
scirrhous, encephaloid, and colloid. Considerable diversity of opinion
has {903} existed as to which variety occurs most frequently; but it is
now probably a matter of absolute knowledge that the epithelial form is
the one most commonly observed, and next to that in frequency the
scirrhous form. Encephaloid and colloid are of quite infrequent
occurrence. Again, as to the sex in which this affection appears the
most often, there is much disparity existing between surgical writers:
it is usually thought to be much more prevalent among women than among
men. This is not the experience of many of the authorities upon this
subject, yet the statistics of the Hotel Dieu, Paris, furnish
overwhelming evidence in favor of its preponderance in women. Carcinoma
of the rectum, occurring as a primary infiltration in the rectum,
probably occurs oftener in men, but there are among females so many
contiguous structures prone to cancerous degenerations, as the uterus,
the vagina, the ovaries, the Fallopian tubes, tumors and cancerous
masses occupying Douglas's cul-de-sac, that it would seem likely that
they would be more frequently the victims of secondary cancerous
deposit in the bowel or of erosion and extension of disease by
contiguity or continuity. Epithelioma in other situations attacks men
much more frequently than women. This form of disease usually occurs in
middle life and in old age, but to this general rule there have been
many exceptions; it has been seen in children. Allingham quotes its
occurrence in a lad of seventeen, and Gowland in one of thirteen. It
very rarely occurs as a secondary deposit of cancer in a remote region
or organ. In the table of 4000 cases of rectal and anal disease, before
referred to, cancer existed in 105. This disease is usually within easy
reach of the finger, except when the growth is in the sigmoid flexure,
being within an inch or two of the anus or from two and a half to three
inches above it. The epithelial form, when it commences at the anus, is
closely analogous to epithelioma of the lip: from the anal outlet it
spreads upward into the bowel, or it may be primarily seated there.
When occupying the junction of skin with mucous membrane it is
sometimes sluggish, and a long time may elapse before it takes on
aggressive action: induration, nodulation, obstinate fissure, or
fungous growth marks its inception; as the condition proceeds,
infiltration of surrounding structures takes place and large, hard,
irregular masses form, which ulcerate, split, and form cauliflower
excrescences. The rectum becomes blocked with fungoid growths: both
these and the cancer proper are very vascular, and frequent hemorrhages
occur, and an offensive muco-purulent discharge constantly oozes from
the bowel.

Scirrhus of the rectum commences as an infiltration of the submucosa,
which rapidly involves the other elements of the bowel, pushing hard
nodules upward into the lumen of the intestinal tube: these break down
and form ragged ulcers with indurated margins, and bleed profusely. Its
situation is usually not higher than three inches above the anus. It
has a tendency to invade all the neighboring organs and soft
structures, to bind them to itself in a firm, dense mass, and to form
communications with the vagina, bladder, uterus, perineum, and penis.
Abscesses and fistulae are common complications.

These neoplasms are insidious in their onset, and when seated at some
little distance from the anus do not excite much pain at first. In the
epithelial form the anus presents an abnormal appearance: it is
inflamed and is covered with irritated, hypertrophied tags of
integument bathed in {904} a sanious, offensive fluid. Difficult
defecation, of which the natural form is absent, with inordinate
tenesmus, a sense of weight and fulness in the bowel, and an irritable
condition of the bladder, are among the symptoms. The feces are passed
in little, irregular lumps or broken fragments, or this state is
accompanied by or alternates with small, liquid, offensive stools. As
the diseased action proceeds, very severe local and general pain is
endured: this is of a dull, lancinating character, and affects not only
the diseased bowel, but involves the entire contents of the pelvis,
shoots down the thighs, up the back, and into the penis: frequent and
exhausting hemorrhages take place; the patient exhales a peculiar
sickening odor; his complexion becomes cachectic; his strength fails;
and death ensues, after a variable period of intense suffering, from a
few months to two or three years after the first symptoms appeared. The
modes of termination of life in these cases are--exhaustion, secondary
deposition, septicaemia, peritonitis, and hemorrhage. Stricture of the
bowel and very extensive ulceration attend all of these advanced cases
of malignant rectal disease.

The encephaloid variety is prone to very sudden and rapid breaking
down, and may destroy life within a few months. If the finger be passed
into the bowel in a case of encephaloid degeneration, it will encounter
a large soft tumor occluding the gut: this is a very different
sensation from that imparted to the finger in a case of epithelioma or
scirrhus. In the former there will be felt a crepitating, as though due
to the giving way of a moist, friable substance; in the latter the
touch will perceive dense, irregular nodulations and ragged ulcerations
having very firm margins.

The rectum may also be involved and destroyed by any of these neoplasms
in neighboring organs. A middle-aged woman who was admitted to the
Pennsylvania Hospital in a very advanced stage of epithelioma of the
cervix uteri died from hemorrhage from the rectum and uterus in eight
minutes. At the autopsy it was found that the disease had almost
separated the cervix from the body of the uterus, had involved the
cul-de-sac of Douglas, and had eroded a large opening into the rectum.
Numerous ends of large vessels were observed which had undergone
erosion.

Carcinoma of distant organs does not seem to frequently involve the
rectum by secondary deposition. "In 160 cases of gastric cancer
examined at the Pathological Institution in Prague, Dittrich found
secondary cancer of the rectum only twice."[20]

[Footnote 20: Leube, _Ziemssen's Cyclopaed._, vol. vii. p. 235.]

In these cases of carcinomatous disease originating in the bowel the
neighboring lymphatic glands are indurated and enlarged, and secondary
deposition in neighboring and distant organs is the rule.

The lower portion of the intestinal tract may become involved in
disease by direct extension from the colon, as in dysentery following
enteritis or entero-colitis. Habersham says that diarrhoea arises
generally from an irritated condition of the large intestine, catarrhal
and mucous diarrhoea from slight inflammatory disease closely allied to
ordinary coryza affecting the mucous membrane of the large intestine.
"In the diarrhoea of soldiers the lesions of the large intestine have
been either those of congestion with varying degree of extravasation or
of ulceration more or less extensive. The colon in the former cases has
invariably presented {905} patches of intense congestion, and in
numerous instances extravasation, the amount and intensity varying in
different subjects, in a few the whole mucous surface of the intestine
having a livid red color; in others tracts of more or less intense
congestion at irregular intervals, as in the small intestines, would be
noticed. The ileo-caecal valve almost invariably presented intense
congestion. The rectum has uniformly presented intense congestion, with
more or less fibrinous exudation. Frequently the presence of fibrinous
exudation was a question of doubt."[21] The entero-colitis or ordinary
summer complaint of infants not infrequently causes a very troublesome
form of proctitis. Besides the ordinary causes of dysentery, Feyrer[22]
states that it is caused by irritation of the solar plexus of nerves,
also by the inhalation of sewer emanations and by the ingestion of
impure water.

[Footnote 21: _Med. and Surg. History of the War of the Rebellion_,
vol. ii. p. 102.]

[Footnote 22: _Times and Gazette_, 1881, p. 87.]

"In dysentery the anus becomes bluish-red, and is even marked with
cracks and rents; it is painful to the touch and tightly contracted. In
the later stages of severe cases it becomes large and gaping; then the
stools are generally discharged unconsciously, and the pain is slight,
paralysis of the sphincter ani having occurred. These symptoms indicate
generally that death is to be expected. In some of these cases the
pathological lesions are limited to the rectum. Dysentery may succeed
typhoid fever."[23]

[Footnote 23: Heubner, _Ziemssen_, vol. i. p. 552.]

"Pigmentation is common after dysentery, and also after typhoid fever
when dysentery has existed. Pigment-deposits are encountered in the
large intestine in those who have suffered from repeated attacks of
acute diarrhoea or from protracted flux. They may be seated as diffuse
patches on the general surface of the mucous membrane or may be more
especially localized in the closed glands. The diffuse form of these
deposits is more frequently encountered in the large than in the small
intestine, and is apt to be more intense in the former, producing
darker and more extensive discoloration; hence the ash- and
slate-colored, greenish, and blackish tracts which are so frequently
observed in the caecum, colon, and rectum."[24] Follicular ulceration
of the rectum sometimes follows chronic dysentery and typhoid fever.
Woodward has observed that a catarrhal condition of the rectum commonly
occurs in typhoid fever cases. Referring to typhoid fever lesions of
the large intestine, Rokitansky[25] says: "The ulcerative process is by
no means confined to the small intestine; we have seen the mucous
membrane of the large intestine riddled with ulcers. They were many of
them of large size, and had clean-cut, non-thickened margins. This
condition, indicating the absence of reparative action, is not nearly
so frequent as that of thickening and induration, which generally took
place to some extent in the edges of the ulcers. The bottoms of the
ulcers are commonly formed by the submucous tissue. Sometimes the
muscular fibres are completely exposed: this, however, is generally the
result of secondary advance subsequent to the reception of the morbid
action."

[Footnote 24: _Med. and Surg. History of War of Rebellion_, vol. ii. p.
308.]

[Footnote 25: Jones and Sieveking, p. 590.]

John Harley[26] calls attention to the intestinal lesions of scarlatina
as follows: "I know of no disease in which the morbid effects are more
{906} uniform. Scarlatina is essentially a disease of the lymphatic
system. It is attended with inflammatory action of this system of
glands, in which are included the agminated glands of the intestine. In
28 cases examined, 8 had the solitary glands of the large intestine
enlarged and inflamed; in 1 there was acute desquamation of the mucous
membrane of nearly the whole of the large intestine. In about half the
cases the large intestine was found healthy."

[Footnote 26: _Med.-Chir. Trans._, vol. iv. p. 102.]

The rectum and anus are frequently subject to attacks, by contiguity,
from diseases in neighboring organs. The most frequent of these is
doubtless that form of ischio-rectal abscess which invades the bowel,
causing fistula in ano. Various neoplasms having their seat in the
tissues or organs near the bowel may obstruct it by simple mechanical
pressure, or may cause inflammation, infiltration, and ulcerative
erosion. Mechanical encroachment by the pressure of a foreign body in
the vagina may cause grave interference with the normal functions of
the lower bowel. At the out-patient department of the Pennsylvania
Hospital in 1880, Arthur V. Meigs, assisted by Wetherill, removed a
large, hollow, glass ball-pessary from the upper end of the vagina of
an aged woman, who declared the pessary had been so placed by a
physician sixteen years before, and had remained ever since, despite
her repeated efforts to remove it with an ordinary table-fork. Upon its
extraction, which was accomplished with difficulty, a small portion of
its surface was found covered with scratches. Its presence had caused
constipation, impaction of feces, and atony of the rectum.

Interference with the rectal functions often follows tedious cases of
labor where the child's head remains long in the perineum.


The Effect of Abnormal Conditions of the Spinal Cord and its Membranes
upon the Rectum and Anus.

"In diseases of the spinal cord and its envelopes there is a great
tendency to constipation, owing to impairment of the secretion of the
intestinal juices. The intestinal movements are usually much affected,
either in the way of increase or diminution, in the former of which the
symptom is a frequent, watery, slimy diarrhoea; as a less common
condition it is even capable of being produced reflexly. Thus in a
patient with chronic myelitis I observed the regular evacuation of a
mucous fluid mass from the intestine as often as his bed-sores were
cleansed; and the like has been seen in dogs after division of the
lumbar cord. Much more commonly there is habitual, even excessively
obstinate, constipation, of which almost all chronic spinal patients
complain. The stool is slowly discharged, dry and hard, and the
evacuation occurs only at considerable intervals and after the
application of energetic remedies. Several causes doubtless contribute
to this: diminution of intestinal secretion and peristaltic
contraction, and probably also weakness of the abdominal muscles of
compression, which is often present. If there is an extreme degree of
weakness, meteorism and accumulation of feces are other consequences.
We do not know exactly from what portions of the cord these
disturbances proceed."[27]

[Footnote 27: Erb, _Ziemssen's Encyc._, xiii. p. 138.]

{907} "There are also in many diseases of the cord disturbances of
evacuation caused by paresis or paralysis of the sphincter ani. In mild
cases simple difficulty in retaining stool for any length of time
exists. There may be also great disturbance of sensibility, so that the
patient does not feel the call, and even if he possess some voluntary
control, he is surprised by the discharge, of which he feels
nothing."[28]

[Footnote 28: Erb, _loc. cit._, p. 139.]

The sphincter ani is affected in cases of myelitis, the usual symptoms
being those of paralysis; the same is true in softening of the cord or
myelo-malacia, and there is also diminished reflex excitability of the
anus.

Paralysis of the bladder and rectum is often delayed in cases of slow
compression of the cord; but if the compression exists to any
considerable extent, involuntary discharges of urine and feces will be
sure to occur. A pressure-myelitis of the lumbar portion of the cord
causes paralysis of the bowel, and in the later stage of some cases of
bulbar paralysis it also occurs.

Early in the course of spinal meningitis there exists a spasmodic
condition of the sphincters: these muscles are also paralyzed in spinal
and in meningeal hemorrhage, and from the pressure of tumors upon the
cord giving rise to paraplegia. "In acute ascending paralysis the
bladder and rectum are generally quite undisturbed in their functions.
In hemiplegia and in hemi-paraplegia specialis disturbances in the
evacuation of the bladder and bowels are almost always present, and in
the acute traumatic cases it is especially common to find severe
paralytic symptoms at the beginning of the attack (complete retention
or complete incontinence, involuntary stools, etc.), which, however,
generally soon recede and give place to lighter, more permanent
trouble, as weakness of the sphincters. Sometimes these disturbances
are very significant."[29]

[Footnote 29: Ibid., _loc. cit._, p. 740.]

The following is an extract from Gower's _Diagnosis and Diseases of the
Spinal Cord_:[30] "The spinal cord possesses centres, situated in the
lumbar enlargement, which preside over the action of the bladder and
rectum. They are probably complex reflex centres: that for the
sphincter ani is the more simple.... But if the volitional path in the
cord is damaged above the lumbar centres, the will can no longer
influence the reflex processes: as soon as the feces irritate the
rectum they are expelled by the reflex mechanism.... If the damage to
the cord involves also the sensory tract, the patient is unconscious of
this process; if the sensory tract is unaffected, the patient is aware
of the action of the bladder or bowel, but cannot control it. It is
often said that there is permanent relaxation of the sphincters, but
this is true only when the lumbar centres are inactive or destroyed. In
this condition evacuation occurs as soon as feces or urine enter; the
urine escapes continuously instead of being expelled at intervals....
We may, however, distinguish between the two states of the rectum by
the introduction of the finger: if the lumbar centre is inactive, there
is a momentary contraction due to local stimulation of the sphincter,
and then permanent relaxation. If, however, the reflex centre and motor
nerves from it are intact, the introduction of the finger is followed
first by relaxation, and then by gentle, firm, tonic contraction."

[Footnote 30: London, 1880, p. 37.]

{908} Morton has at this time in his wards at the Pennsylvania Hospital
two cases of rectal paresis following fracture of the vertebrae. The
first, a lad aged nineteen years, while crossing the Atlantic was
struck during a gale by a spar upon the back about the region of the
lower dorsal vertebrae. From the deformity and from other symptoms
there was undoubtedly a fracture destructive to the normal functions of
the cord. Upon the arrival of the steamer, some ten days after the
accident, the lad was brought to the hospital, where he has remained
for the past eighteen months. Total palsy of sensation and motion has
continued from the time of the accident to the present day, and extends
from the navel downward: the sphincter ani is constantly but feebly
contracted; the finger, when pressed into the anus, encounters slight
resistance, which continues during and after the simple passage of the
finger; very slight pressure, however, against the sphincter causes a
very marked relaxation, which continues so long as this is kept up.
With the removal of the finger the sphincter slowly and fairly
contracts. The second case is also one of vertebral fracture which has
been in the hospital about ten months. In this instance the sphincter
is always found contracted, but it readily yields under finger
pressure, and contracts quickly and regularly in the absence of this
pressure. Constipation and rectal impaction readily occur, and the
bowel requires to be regularly emptied. In another case, at the
Episcopal Hospital, under the care of W. B. Hopkins, there is fracture
of the spine, with total palsy below the seat of injury. The margins of
the anus were found in apposition, but in no firm contraction: mere
contact of the finger appeared to have little or no effect, but slight
pressure upon the sphincter caused a contraction, and very moderate
pressure upon the anus after the introduction of the finger produced
excessive dilatation. The action of the sphincter was in all respects
very tardy.

Two recent cases (August, 1883) of fracture of the dorsal vertebrae
have been admitted into the Pennsylvania Hospital. One, a lad aged ten
years, was struck by a bale of cotton which fell upon him; the other, a
man aged thirty years, fell from a second-story window. In both cases
total palsy occurred at once upon the receipt of injury, and in each
the same conditions of the anus have obtained as before described.

In the convulsive attacks incident to epilepsy the sphincters of the
bowel and urinary bladder are relaxed and the discharges are
involuntary; probably, also, one of the first symptoms indicative of
tumor of the base of the brain is recognized in involuntary rectal
evacuations. Rectal incontinence may be also due to tabes, while atony
and constipation are sometimes noticed as a result of excessive
intellectual exertion (DaCosta). The same may be said of chronic
lesions of the brain and spinal cord. Paresis of the rectum has been
noticed as a result of chronic congestions of the heart and in hepatic
disease. Allingham has observed failing nerve-power as a cause of
rectal atony: the latter, with constipation, is one of the commonest
troubles attendant upon melancholia and the chronic forms of insanity.
Seeley of Ovid, New York, related to Morton a case of paraplegia with
rectal paresis and dysenteric symptoms from malarial poisoning in a
married lady aged thirty years. An examination revealed an immense
rectal impaction. A free administration of quinia was followed by
complete recovery in a few weeks.


{909} Spasm or Spasmodic Contraction of the Rectum and Anus.

Apart from those cases in which spasm is induced by the irritating
stools of diarrhoea and dysentery, or by local ulcerations, fissures of
the anus, and intestinal worms, there are those in which painful spasm
occurs, due to the presence of a vesical calculus: it is also caused by
urethral stricture, impaction of feces, irritations and inflammations
involving the bladder or the adjacent organs. Spasm is also seen in
nervous females, without constipation; also in the varied irritations
of the female genito-urinary apparatus. In cases where spasm is due to
rectal impaction retraction of the anus is frequently seen.


Pruritus Ani.

This most painful, distressing, and obstinate affection belongs to the
class of neuroses, and is simply functional in character, without the
least structural change in the skin or mucous membrane of the anus or
rectum: the itching may be confined to the former or it may extend into
the latter. It may be brought about by a constipated state of the
bowels, but it is more often due to derangements of the digestive
apparatus.

Sufferers from pruritus ani are generally dyspeptics, although the
malady is observed in persons who are otherwise in most robust health.
Overwork, mental and physical exhaustion, have been charged with
producing pruritus, and in some instances spinal irritation seems to
have been unquestionably the exciting cause: now and again, pruritus
ani has been produced by the pregnant condition, and in some cases this
malady has persisted during the entire period of utero-gestation.
Intestinal worms, uterine maladies, rheumatism, and especially gout,
have unquestionably been exciting causes. Some years since a gentleman
having the most intense pruritus, which defied all treatment, was
suddenly relieved of all former distressing symptoms by the passage of
a small vesical calculus, the presence of which had never been
suspected, as no vesical symptoms had at any time existed. Some of the
most aggravated instances of anal pruritus are found in those far
advanced in diabetes mellitus. The nerves of the lumbar plexus in rare
instances have suffered from compression, more or less severe, from
fecal accumulations; in one case of spinal curvature detailed by
Portal[31] the rectum at its upper part was so narrowed by the
encroachment of the false ribs that excessive fecal accumulation
occurred which gave rise to remote pain in the great toe.

[Footnote 31: _Cours d'Anatomie medicale_, tome iv. p. 276.]


Neuralgia of the Rectum.

It seems to be unquestionable that there are instances of pure
neuralgia of the rectum, for in such cases the most carefully conducted
explorations have failed in demonstrating any evidences of disease. The
pain is doubtless reflex, due to depressing causes, to atmospheric
conditions, or to exposure to cold and wet. Neuralgia of the rectum has
also been noticed in malarial {910} poisoning, and especially in those
who have long been victims of intermittent fever. Neuralgia in this
region of the body is also due to general causes, as witnessed in cases
of rheumatism and of the gouty diathesis. Patients now and again
complain of "violent and painful pressure in the rectum, conjoined with
active pains in the perineum and anus and in the sexual parts: these
symptoms probably have a neuralgic character."[32] In many nervous
disorders, but especially in spinal irritations or inflammation, the
rectum is invaded by pains of a neuralgic nature more or less severe,
which are undoubtedly only functional in character. But 12 cases of
neuralgia were observed out of 4000 cases of rectal disease. Anstie[33]
says: "It needs some very powerful irritant to set up neuralgia in any
portion of the alimentary canal: ... this condition has been described
by Ashton.... In one case the patient complained of acute, paroxysmal,
cutting pain extending about an inch within the rectum.... The cause of
this attack was his getting chilled from sitting in his wet clothes."
Curling says that constantly directing the mind to this part of the
body will excite congestion and disease, possibly by producing abnormal
sensations, itching, and superficial inflammation.

[Footnote 32: Erb, _Ziemssen's Cyclop._, vol. xiii. p. 139.]

[Footnote 33: _Neuralgia and its Counterfeits_, p. 130.]

"In patients with piles hyperaemia of the spinal cord may become
habitual, returning regularly and frequently, and this may lead by
degrees to severer disturbance by the development of chronic
inflammation and proliferation."[34] Among some of the reflex troubles
arising from rectal disease are--sterility in women, simulation of
uterine disease, pruritus ani, pseudo-sciatica, pains in the legs and
feet, and impairment of co-ordination in the muscles of defecation.
There is a case reported[35] of a curious pain in the sole of a foot
caused by rectal disease; and another[36] in which irritation of the
eyes was caused by hemorrhoids.

[Footnote 34: _Ziemssen's Cyclop._, vol. xiii. p. 138.]

[Footnote 35: _Med. Times and Gazette_, 1868, vol. ii. p. 175.]

[Footnote 36: Cooper, _Lancet_, 1862, i. p. 625.]

There are some cases occasionally met with of so-called irritable
rectum. Now, a rectum may be irritable because irritated, but in some
of these instances there is no apparent cause. There occur frequent,
small stools expelled with force, but without pain: there must be
abnormal peristaltic action to cause this condition.


The Effects of Cholera and of Certain Poisons and Remedies upon the
Rectum.

After death from cholera there is found congestion and a swollen state
of the mucous membrane of the rectum: in some cases the epithelium of
the entire alimentary canal is almost absent. In slow poisoning by
arsenic the bowels show ulceration, but more particularly the rectum.
After phosphorus-poisoning the large intestine has been found inflamed
and contracted to the calibre of a quill. Among the effects of copper
have been seen ulceration and a peculiar green staining of the rectum;
of lead, no marked change of the mucous membrane except, in some
instances, hardening, but the muscularis was in an advanced state of
hardening and contraction. The action of croton oil is to render the
mucosa very soft and friable. Extensive destruction of the mucous
membrane of the rectum has resulted {911} from poisoning by bichromate
of potassium. The mineral acids and the caustic alkalies, when not
immediately fatal, cause corrosive ulceration of the rectum; the
soluble salts of zinc, tin, bismuth, and antimony produce a like
effect. Corrosive sublimate in its action upon the large intestine
produces a dysenteric condition; similar in their effects are
colocynth, jalap, elaterium, and cantharides. Strychnia causes a deep
violet congestion; alcohol, congestion and thickening; and tobacco,
redness of the mucous membrane with great engorgement of the vessels of
the rectum. One of the results of the long-continued abuse of morphia
is a catarrhal condition of the large intestine, accompanied with
exfoliation of the intestinal epithelium. Some persons are very
susceptible to the action of jaborandi, and in such its exhibition is
followed by hyperaesthesia and dull pain in the rectum and the urethra.

It is interesting to note that an abnormal condition in the rectum may
cause extensive disease in a remote organ; thus, a stricture of the
rectum may cause abscess in the liver. Wilkes[37] exhibited at the
Pathological Society a specimen in which an abscess, a diffuse,
purulent infiltration of the liver, and a gall-bladder filled with
purulent bile were distinctly traceable to the suppuration arising from
an ulcerating stricture of the rectum consisting of dense fibrous
tissue situated about four inches from the anus of a man aged
thirty-seven years. "Any form of suppurative intestinal disease seems
capable of producing hepatic abscesses of a metastatic or pyaemic
character."[38] It has not been found, however, that tubercular
ulceration of the intestines has ever given rise to hepatic abscess.

[Footnote 37: _Soc. Trans._, vol. ii.]

[Footnote 38: Darley, _On the Liver_, 1883, p. 536.]

Examinations and explorations of the abdominal viscera by the hand
introduced into the rectum, having for their object the detection of
tumors or morbid growths, are procedures which have fallen into merited
disrepute, and are mentioned here in condemnation. However, some years
since, Morton, in consultation with (J. Forsythe) Meigs, satisfactorily
demonstrated the absence of a suspected renal calculus by this method.

The distension of the rectum with water, either free or contained in a
rubber bag, in order to facilitate operations upon the pelvic viscera,
has been lately brought into notice by Garson at a meeting of the
British Medical Association. The most significant point brought out at
the meeting was that the water-distended rectum displaced the distended
urinary bladder upward and forward until it occupied a position quite
outside of the pelvic cavity, carrying along with it the peritoneum
both in front and behind. By this method of distension it was found
possible so to raise the peritoneum in front of the bladder as to leave
a clear working space of four centimeters between the upper border of
the symphysis pubis and the edge of the peritoneum: this may prove
useful in suprapubic lithotomy, as well as in operations upon the
uterus and its appendages during laparotomy.


RESUME OF THE THERAPEUTICAL AND SURGICAL TREATMENT.

FISSURE OF THE ANUS, in its true sense, is not to be confounded with
ulcerations either slight and superficial in extent, or with more grave
ulcerations involving not only the anus, but the mucous membrane of the
{912} rectum also. The true fissure is a mere linear crack or abrasion
or superficial ulceration. The pain accompanying this condition is out
of proportion to the length and depth of the fissure, varying from
slight uneasiness to as severe suffering as that caused by a deep and
extensive ulceration.

The treatment to be adopted in such cases is first to regulate the
bowels and to insist upon a scrupulous cleansing of the part after each
evacuation. Much sitting is to be avoided and a sedentary mode of life
is to be discouraged. Sometimes a few light topical applications of the
solid nitrate of silver will bring about a cure, or a lotion of the
same of the strength of from two to ten grains to the ounce of water
should be applied with a camel's-hair brush every other morning. The
ointment of the oxide of zinc, combined with any of the local
anaesthetics, will be found useful. As a dernier ressort in obstinate
cases an incision should be made through the fissure, together with a
thorough dilatation of the anal sphincter.

ULCER OF THE RECTUM, OR THE GRAVER FORM OF FISSURE OF THE ANUS.--In the
milder forms of this very common and painful affection the treatment
consists in thorough cleanliness of the part; the ulcerated surface may
be cauterized with nitrate of silver, and subsequently the application
of the red precipitate ointment or the lotio nigra. Should a vaginal
discharge exist, treatment should be instituted with a view to its
arrest, as the irritating fluid coming in contact with the ulcer would
prevent its healing. The treatment of that variety of ulceration where
the disease is situated partly without the anus and partly within the
rectum, besides the use of the means enumerated above, embraces the
daily introduction of a full-sized bougie made of wax or of yellow
soap. Henry Hartshorne says: "Experience leads me to have especial
confidence in collodion, to which one-fiftieth of glycerin has been
added to lessen its constricting effect." Glycerite of tannin and
tinct. benzoin. comp. have been useful. J. C. Peters[39] recommends the
use of iodoform suppositories. Tarnier[40] dusts the part with the same
drug in fine powder. Crequy[41] has had success with a dressing of
charpie saturated in a solution of hydrate of chloral. For the more
extensive and obstinate forms of ulceration the three methods of
treatment mainly relied on are--by cauterization, by dilatation, and by
incision. The caustics usually relied upon are the fuming nitric acid
and the acid nitrate of mercury, one application of either of these
often exciting healthy granulation. This application is to be followed
by the use of an ointment consisting of thirty grains of calomel and
three grains of morphia to one ounce of lard. If there is much spasm of
the sphincters, extract of belladonna may be added.[42] During this
treatment the bowels should be kept rather loose by the use of compound
licorice powder, and if much pain is experienced an opium suppository
should be used. Dilatation, first practised by Recamier, consists of
the introduction of the thumbs of the operator into the rectum, placing
them back to back, and then forcibly separating them from each other
until the sides of the bowel can be stretched out as far as the
tuberosities of the ischia. On account of the fact that both
cauterization and dilatation are not infrequently followed by relapse,
the method of operation which includes both incision and dilatation can
usually be relied {913} upon. The bowels should be thoroughly emptied
by a laxative, and an enema should be given three hours before the
operation.

[Footnote 39: _Philada. Med. Times_, Nov. 8, 1879.]

[Footnote 40: _Bull. gen. de Therap._, Sept. 30, 1875.]

[Footnote 41: Ashton, _On the Rectum_, p. 157.]

[Footnote 42: Agnew's _Surgery_, vol. i. p. 418.]

After full anaesthesia the ulcer may be readily exposed. The left index
finger of the operator is then carried into the rectum, and a
sharp-pointed curved bistoury is entered, three-quarters of an inch or
more from the side of the anus, to the depth of an inch or less, and
carried on toward the bowel until the point is felt by the finger
within, when it is made to puncture the mucous membrane, and then to
cut out to the surface. In some cases of deep fissure, before dividing
the sphincter the ulcer may be scraped freely or the entire ulcer may
be removed. The anus should now be well dilated with the fingers, after
which an opium suppository should be introduced and a fragment of lint
or linen well oiled be placed in the wound. The subsequent treatment
consists in keeping the patient in a recumbent position and confining
the bowels with opium. After three or four days a laxative may be
given. No dressing is necessary save attention to cleanliness.

The subcutaneous division of the sphincter has been proposed, but is
objected to on account of the liability of the extravasated blood
retained in the very loose cellular tissue of the part to form abscess.
In one case which Morton operated upon in this manner many years ago a
large abscess formed very rapidly, with serious constitutional
symptoms, which were relieved only after the freest opening and
division of the sphincter.

Should any polypi be found, their removal by ligation or by the knife
is an essential element of success in the operation; retention of urine
is not infrequent after operations upon fissure. When fissure or
ulceration makes its appearance in a syphilitic subject, it will
usually disappear under appropriate constitutional treatment.

TUBERCULOUS ULCER OF THE ANUS is best treated by the topical use of a
weak solution of chloral hydrate.

CHRONIC ULCER OF THE RECTUM.--In this condition the treatment should
include the use of anodyne and astringent lotions, suppositories or
enemata, and the internal administration of Ward's paste--_i.e._
confection of black pepper.

RODENT ULCER OF RECTUM.--In this rather rare, exceeding painful, and
generally incurable malady the patient sometimes dies merely from the
exhaustion of pain. Another mode of death is by diarrhoea; another by
hemorrhage. To quote Allingham:[43] "I have really nothing to offer as
regards treatment; all the various sedatives will be required in their
turn, and in the earlier stage I should recommend excision--not that I
have much hope that you will eradicate the malady, but you will remove
the pain, and for some time the sufferer will be comparatively
comfortable. I think also the application of fuming nitric acid should
be tried with the same object; one of my patients was fairly easy for
three months after I had destroyed the ulcer with the acid." Morton
accomplished the permanent healing of an undoubted rodent ulcer of the
rectum by the complete divulsion of all the involved tissues.

[Footnote 43: Page 30.]

CANCER OF THE RECTUM.--The medical treatment of this affection is
necessarily restricted to efforts to alleviate suffering and to obtain
sleep--anodynes in the form of suppositories of pil. saponis comp. or
of morphine mixed with ext. hyoscyamus in the proportion of a half
grain of the {914} salt to ten grains of the extract. Enemata of warm
water are useful. D'Arpene of Elba has suggested enemata of gastric
juice. The profuse discharge of sanious pus must be met by weak
injection of sulphate of copper and opium or a very dilute solution of
chloride of zinc. Now, as to the use of bougies in these cases, it may
be laid down as a general rule that their employment may be
mischievous, yet in certain cases justifiable--indeed, absolutely
necessary. When the disease is met with in its early stage, has not
ulcerated, is within reach of the finger, and is producing much
contraction of the calibre of the gut, a gum-elastic bougie, thoroughly
lubricated, may be introduced through the contraction. In case this
produces much suffering, the attempt must be abandoned; if not, once or
twice a week is often enough. Where no extensive ulceration exists the
patient can be much helped by this procedure. F. N. Otis[44] has
reported a case of malignant stricture in which he completely divided
the recto-vaginal septum, sphincter ani, and perineum with great
temporary relief to his patient. When large portions of a malignant
mass protrude from the anus, they may be removed by the application of
a paste of arsenite of copper or by the elastic ligature, the
destruction being safe and rapid. The injection of acetic acid into
these growths has been practised, but is useless and harmful.

[Footnote 44: _Arch. Clin. Surg._, 1877.]

As to operative procedure, when the morbid growth is an epithelioma
situated within a short distance of the anal opening an excision is not
only justifiable, but may be recommended. The results show that its
removal from this situation is as frequently successful as is its
removal from the lip. When a cancer completely fills the lumen of the
gut and plugs it so that the act of defecation becomes impossible,
excision of the rectum and the establishment of an artificial anus are
the two operative procedures open to the choice of the surgeon. A
decided reaction of opinion has lately taken place among members of the
profession relative to the latter of these; the few surgeons who did
practise excision of the rectum in cases of cancer were looked upon as
being rather unscientific and unsurgical. Billroth has excised the
rectum 16 times, with 4 fatal cases; Dieffenbach performed it 30 times;
Lisfranc had recourse to this operation as early as 1826; while the
operation has been performed very frequently in this country, and with
success.

Morton says: "In the spring of 1882, I was consulted in the case of a
lady aged fifty-six who had suffered for two years from what were
supposed to be internal hemorrhoids. An examination revealed the
existence of a large scirrhous mass encircling about two-thirds of the
gut, on the anterior part especially, and extending upward three
inches. The patient was worn down by long suffering, but was otherwise
in fair condition of health. With the assistance of Gross and Agnew, I
excised the mass, which included the entire lower part of the rectum.
The wound healed kindly, without an untoward symptom, and the patient
was very soon enabled to leave her home for the seaside, where she
passed the summer. The disease, however, resumed, but without any of
the severe pains which she had had prior to the operation. Death
occurred from gradual exhaustion seven months afterward."

He also relates the following case of excision of the rectum: The
patient, a female aged thirty-five years, first noticed some rectal
{915} irritation about four years ago. This was followed by distressing
pain during defecation and by hemorrhages; finally a tumor, which was
described by her medical attendant as being like an opened umbrella,
protruded, partly at first, then fully, through the anus. The growth
seemed to be spongy in character, and was very vascular. It was removed
by carrying a double-threaded needle through the mass, and thus
ligating it. Upon the seventh day after the operation a hemorrhage
occurred, which was controlled by plugging the rectum. Although the
growth was removed, the patient did not make a good recovery; symptoms
of rectal irritation continued. In September, 1884, the patient
presented herself in a wretched condition, with bearing-down pains and
frequent hemorrhages. Upon digital examination an elevated mass was
readily detected upon the sacral aspect of the bowel. By carrying the
fingers beyond this mass and making traction, it was brought down
within working distance, and was excised along with the entire lower
portion of the rectum. The freshly-cut edges of the gut were then drawn
down and stitched to the mucous membrane just above the anus. The
patient made a good recovery and has a serviceable anus.

R. J. Levis[45] has operated upon two cases of cancerous growth in the
rectum, removing the lower part of the bowel. The first case was that
of a man aged sixty, who made a very good recovery from the successful
operation, although three inches of the gut were removed. The second
case was that of a man aged fifty-two, who had a carcinomatous tumor
the size of a hen's egg at the right side of the rectum. The section of
gut excised was about one and a half inches in length. The patient died
of peritonitis upon the fourth day after operation. At the autopsy
there was no wound found in the peritoneum, the lowest point of which
was one inch above the end of the excised bowel.

[Footnote 45: _Surgery in the Pennsylvania Hospital_, pp. 81-83.]

The etherized patient, his bladder having been emptied, should be
placed in the lithotomy position. If a male, a sound should be passed
into the bladder. An incision is then carried from the centre of the
perineum along the raphe to the anterior margin of the anus, encircling
the latter by two semicircular cuts and continuing the division
directly back to the coccyx. In the female the incision should begin
just posterior to the vagina. If the anus is not included in the
diseased mass, the external sphincter may be spared by raising the skin
and the muscle together and turning them on each side. When the lower
end of the rectum is reached the dissection should be made entirely by
the fingers or by the handle of the knife, tying vessels as they
spring. Double ligatures should be introduced through the gut from its
mucous surface outward, and, when possible, then stitched to the skin
at the margins of the wound. The bowels should be controlled by opium
for the following eight or ten days.

The other operative procedure is lumbar colotomy. This was first
advocated by Amussat in 1839, when he appeared in a treatise upon the
subject entitled _On the Possibility of Establishing an Artificial Anus
in the Lumbar Region_. It is denied that he ever performed this
operation. It has happened to sound surgeons and skilful operators,
when the patient has been very muscular or very fat or when the colon
has been collapsed, that they have been at length compelled to abandon
the search for the gut {916} and to stitch up the external wound.
Allingham states that the cause of failure often is that the colon is
searched for too far from the spine, resulting, in the opening of the
peritoneum, in the starting up into the wound of a mass of small
intestine which baffles the operator very seriously. He, having made
more than fifty dissections, has come to this conclusion: "that the
descending colon is always normally situated half an inch posterior to
the centre of the crest of the ileum (the centre being the point midway
between the anterior, superior, and posterior-superior spinous
processes)." An incision four inches in length should be made midway
between the last rib and the crest of the ileum. The incision may be
made transverse, or, better, obliquely downward and forward, as
suggested by Bryant. Allingham says that care should be taken to
preserve the original length of the incision down through all
structures, lest when the operator approaches the gut he finds himself
working in the apex of a triangle the base of which is the line of the
wound. If the surgeon has reason to expect the gut to be collapsed, an
attempt should be made to distend it with some fluid. The intestine
should be drawn well out through the wound, and a longitudinal opening
an inch in length made in it. The edges of this are to be stitched to
the edges of the skin. Fecal matter is much less likely to flow into
the wound if the sutures are passed through the intestine previous to
opening it. A weak carbolated wash is all that is required as a
dressing. In one case of stricture of the rectum from a scirrhous mass,
in which Morton performed colotomy, an immense cyst of the kidney,
which was somewhat puzzling for a moment, protruded in the wound. After
emptying the cyst the gut was readily discovered and opened.

DILATATION AND INFLAMMATION OF THE RECTAL POUCHES.--This is a
comparatively rare condition of the rectum, called by Physick encysted
rectum, which is treated by bending the end of a probe into a hook,
passing it up into the bowel, and then withdrawing it with its
extremity resting against the surface, so as to engage and draw down
the pouches, the straining or bearing down of the patient assisting in
their extrusion; they may then be incised or cut off with a pair of
curved scissors.

LOSS OF CO-ORDINATION IN THE MUSCLES OF DEFECATION.--In those cases
where it can be ascertained that this curious trouble is not
symptomatic, sympathetic, nor reflex, the treatment must be directed to
the building up of the general health, such as electricity, baths,
asafoetida, and iron. Regular outdoor exercise should be enforced.

SPHINCTERISMUS.--This condition, though frequently attendant upon, may
exist in the absence of, any fissure, crack, or ulcer of the anus. It
is usually associated with constipation. In its treatment magnesia and
rhubarb are to be used, and the diet must be simple, unstimulating, and
taken at regular intervals. A hot hip-bath at night, with the use of a
belladonna suppository, often proves effective. In more obstinate cases
a bougie covered with ointment of belladonna should be used daily. In
still more intractable cases the muscle must be forcibly stretched with
the fingers. In the more obstinate cases which now and then occur it
becomes necessary to completely divide the fibres of the sphincter
muscle, followed by a thorough stretching of the parts.

{917} PRURITUS ANI.--This distressing and vexatious complaint proceeds
frequently from hemorrhoids. When caused by the presence of seat-worms,
they must be dislodged by purgatives and enemata of quassia or of one
composed of one part of carbolic acid to six parts of sweet oil, or of
turpentine and flaxseed tea. An enema of milk of asafoetida answers a
good purpose. If the pruritus is a result of the burrowing of the itch
insect, any wash, ointment, or dressing that evolves sulphuretted
hydrogen will rapidly bring relief. If caused by other parasites, an
application of ung. hydrarg. or red precipitate ointment, followed by a
warm bath, will be all that is necessary. In some it is a symptom of
dyspepsia, in others of a disordered state of the nerves of the anus
independent of local cause: in this case iron, quinia, and arsenic
should be given, and the patient should live an outdoor life as much as
possible. The remedies that have in turn been extolled and abandoned
during the treatment of this distressing condition it would require too
much space to even mention. The following are among the best: Sulphate
of zinc and alum, equal parts, are to be placed in an earthen vessel
and heated until a glassy mass is left, which is to be dissolved in a
little water and thrown into the bowel; palm soap pressed into the
anus, ointments of carbolic acid and morphia or of bromide of potassium
and cosmoline, citrine and other mercurial ointments, and suppositories
containing iodoform. Allingham uses a bone or a metallic plug of
peculiar construction, so as to keep the anus upon the stretch at night
without slipping into the bowel. The pressure which this exerts upon
the nerves and vessels prevents the itching. Hot (not warm) water
pressed against the anus with a sponge, or ten-drop doses internally of
tincture of gelsemium, or washes of dilute hydrocyanic acid or of
chloroform, or ointments of balsam of Peru or of veratria and aconitia,
or the corrosive chloride of mercury in solution applied locally, are a
few of the more reliable among this host.

STRICTURE OF THE RECTUM (NON-MALIGNANT).--The main modes of treatment
of non-malignant stricture of the rectum are two--by dilatation or by
linear incision (rectotomy). Dilatation may be practised by the finger
alone or by the finger covered with hollow rubber covers of various
sizes. These are open at the end, so that the guiding and recognizing
sense of touch may be left to the end of the finger. When the stricture
is out of reach of this method, either gum or metallic bougies must be
used, beginning with the smaller sizes and deliberately and carefully
adding sizes. When the lumen of a stricture is tortuous it is best to
use a long rather flexible rubber bougie having an olive-shaped
extremity. It is not necessary to leave these bougies standing for
hours in a stricture, according to the practice of some; this merely
excites inflammation. Should the stricture be irritable, every second
or third day would be sufficiently often to attempt dilatation. In
constrictions which are firm, but not sensitive, a good plan is to
insert a Molesworth elastic tube and gradually distend it by
hydrostatic pressure; Barnes's dilators have also been successfully
used. When the stricture is elastic and re-forms itself at once after
dilatation, incision should be practised. In those strictures which are
low down, the constriction may be nicked in several places by a hernia
knife, the blade of which is guided along a finger in the bowel; when
high up, a long double-bladed knife must be employed. In syphilitic
strictures, in addition to dilatation, proper alterative treatment is
{918} indispensable. As dilatation has often to be kept up for a long
time, the patient may be taught to practise this for himself.

PERI-ANAL AND PERI-RECTAL ABSCESS.--When acute, and when the surgeon is
called in time, the prompt application of leeches may abort the
abscess, but usually, by the time the surgeon sees it, it is necessary
to apply hot flaxseed poultices as fast as they become cool, keeping
the patient in bed upon light diet. The rule is to open deeply and
freely so soon as the least softening under the poultices indicates
that pus is within reach. After lancing, the poultices should be
continued for a few days: then the deep wound should be packed with a
strip of oiled lint and allowed to granulate from the bottom. As the
fetor of these abscesses is horrible, they should be injected with a
solution of permanganate of potash or liq. sodii chlorinata. When the
chronic variety of this abscess is discovered, it, with all its
sinuses, diverticula, and pockets, should be laid freely open upon a
director and packed with carbolized lint. It is often very necessary in
these chronic cases to use tonic and alterative treatment, such as
cod-liver oil and iodide of iron.

GONORRHOEA OF THE RECTUM.--Undoubted cases of gonorrhoea of the rectum
in the persons of prostitutes have been observed. Burning heat and
great pain are usually felt, with a free discharge of pure pus: the
mucous membrane is always intensely inflamed. The treatment is simple;
an injection of lead-water and laudanum or of sulphate of zinc answers
a good purpose. Primary syphilitic disease of the anus and rectum is
rarely seen, but of course the treatment indicated would be similar to
that laid down for primary syphilis in its usual localities.

IMPACTION OF FECES.--This condition usually occurs among the aged and
in women after parturition and in cases of paralysis. Those persons of
sedentary habits who do not pay sufficient attention to the necessity
of a daily alvine evacuation sometimes find themselves in this
condition. Impaction occurs not infrequently among the insane, and more
frequently among women than men. Allingham states that he has never
seen a case of impaction in a young person; but Wetherill now has under
his care a most obstinate case of this disorder in a young man whose
system has been completely broken down by intemperance in drink.

In paralysis of the rectum of traumatic origin impaction is almost
certain to take place unless great care is taken to prevent it.
Diarrhoea is a very misleading element in these cases, and is a symptom
which frequently deceives those who are not on their guard. The clayey
mass of feculent matter forms a hard ball in the distended bowel,
around which the small loose passages flow. Spasm of the sphincter ani
is the usual accompaniment of impaction, and the muscle should be
gently but thoroughly dilated before means can be used to free the
canal. The finger or the handle of a tablespoon is best to use in the
dislodgment of these masses, and should be oiled before introduction,
the accumulation broken up, and then washed out by an enema of soap,
turpentine, and warm water. Purgatives and hydragogue cathartics
usually fail to give relief, and add much to the patient's discomfort.
The bowel once freed, care must be taken to prevent a reaccumulation,
which very readily takes place, as the bowel in these cases is
distended and has lost tone. To this end frequent enemata of cold water
should be used, and the patient should {919} take a pill of dried
sulphate of iron, sulphate of quinia, extract of nux vomica, extract of
aloes, as recommended by Allingham. The diet should be restricted. An
excellent adjunct to this treatment is the local use of the faradic
galvanic current daily after breakfast. Let the patient lie upon a bed
and apply one pole or electrode to the anus, while the other one is
passed with pressure along the course of the large intestine. Not
infrequently it happens after this has been continued for a few minutes
that a very urgent desire is felt to go to stool. In the case mentioned
of the young man affected with impaction this treatment answered
admirably well, but before its use he had to take a small dose of
croton oil daily to cause an action of the bowels, all milder measures
having proved ineffectual. It is important in these cases to interdict
a sedentary mode of life.

IRRITABLE RECTUM.--A rectum is said to be irritable when it shows an
intolerance of the presence of feces or flatus, causing frequent desire
to go to stool. From such abnormal activity of the part there arise a
burning, uncomfortable impression of fulness and a soreness of the
anus. If after examination it is found that there is no local exciting
cause, a starch enema containing forty drops of laudanum should be
given and retained. This plan of treatment will usually afford relief.
Should the irritability prove to be obstinate, examine the rectum, and
if a spot of redness or increased vascularity be found, touch the spot
with strong nitric acid.

CONCRETIONS IN THE RECTUM.--These occur less frequently than do
impactions, and differ from them in being cylindrical and nucleated,
the nuclei being such bodies as balls or tangled masses of hair, or
coins, buttons, biliary calculi, or the like. Covering these are matted
animal or vegetable fibres or hardened fecal matter. They are not so
readily dislodged as are impactions, and it is necessary to dilate the
sphincter thoroughly and remove them with a scoop. Not infrequently
these bodies are bathed in pus and are very fetid.

PROCTITIS, OR INFLAMMATION OF THE RECTUM.--This may be either acute or
chronic, the latter being a disease of the aged. Allingham recommends
in this variety small doses of Barbadoes aloes to stimulate the bowel,
also such drugs as copaiba, turpentine, and black pepper. As an
injection in the acute form starch and laudanum, or bismuth suspended
in a mucilaginous vehicle, should be used. Probably the use of small,
smooth fragments of ice in the rectum would allay the tenesmus and help
to subdue the inflammation.

PROLAPSUS ANI AND PROCIDENTIA.--Prolapsus occurs much more frequently
in children than in adults, making its appearance at every movement of
the bowels. The child thus affected should not be allowed to sit upon
the chamber-vessel and strain, but should lie upon the side or stand,
while the nurse should be instructed to draw to one side one of the
buttocks so as to tighten the anal orifice. After the motion the
protruded part should be well washed in cold water, and afterward with
some astringent solution of oak-bark, matico, or a weak solution of
carbolic acid applied with a soft sponge. The bowel should then be
gently returned and the child be allowed to lie at rest for a while. If
there exists intestinal irritation, small doses of mercury with chalk,
with rhubarb at night, with wine of iron three times daily, would be
indicated. {920} The application of an anal pad and a T-bandage will
give sufficient support. If this treatment be carried out a cure
usually results in a few weeks. Some cases do not yield to this mode,
and then the surgeon has to make trial of ergotin given hypodermically,
each injection representing a grain of ergot, which is to be thrown
into the submucous tissue of the rectum every second day for two weeks.
Should relief not follow its use, cauterization is to be tried. The
cauterants usually applied are nitrate of silver, acid nitrate of
mercury, and nitric acid. Of these, nitric acid is the best. After
anaesthesia is complete every portion of the extrusion should be
touched with the acid, care being taken not to bring it into contact
with the skin; afterward the bowel is to be freely oiled and returned.
To prevent its extrusion the bowel should be filled with soft cotton
wool, a compress placed over the anus, and the buttocks strapped
tightly together with adhesive plaster. For a general quieting effect
the child should be given paregoric. About the fourth day the adhesive
plaster may be removed and a dose of castor oil administered, which
will bring away the cotton plug with the dejection.

Prolapsus and procidentia in the adult are much less manageable;
indeed, these conditions are usually very obstinate. There may exist
causes extraneous to the bowel, such as urethral stricture or enlarged
prostate or an impacted renal calculus or a calculus of the prostate.
The bowel should be searched for polypi or hemorrhoids, and the
prolapse may be cured by the removal of the irritating cause. Failing
to find any such cause, the surgeon has at his command either
cauterization or a removal of redundancy. The former may be by nitrate
of silver or acid nitrate of mercury or the actual cautery. It is well
not to apply these strong acids to the aged or those who are broken
down in health, as very destructive sloughing has followed their use in
these cases. When these are used, the same plan as that mentioned in
case of prolapse in children should be pursued. Strong carbolic acid
may be used in these cases with much less risk of sloughing than when
the acid is employed, and it may be applied oftener--indeed, daily if
desirable. Van Buren has recommended linear cauterization with the hot
iron to the mucous membrane, the bowel contracting as a result of
cicatrization. In adults generally, and especially in the aged, all the
forms of cauterization are less satisfactory as a means of relief than
either of the various modifications of Copeland's operation, which
consists in removing by ligation elliptical portions of the mucous and
submucous tissues of the prolapsed bowel. The most satisfactory of
these is either to excise two or three oval portions of the mucous
membrane with flat-curved scissors and bring the edges together with
interrupted suture, or to pinch up in several places the redundancy in
a Smith's clamp and cut off the folds in advance of the instrument,
applying to the stumps the hot iron. Allingham prefers ligatures of
horsehair in these operations, and mentions the carbolized catgut in
preference to silk. He cautions the operator not to carry his knife
into the submucous tissue, as free hemorrhage would inevitably occur.

In old cases of prolapsus or of procidentia that are not amenable to
operative treatment much can be done to render them comfortable: the
air-dilated gum pessary will sometimes afford relief, or a pad and
T-bandage will prevent the parts becoming ulcerated by friction.
Neither gallic {921} nor tannic acid answers the purpose so well as
acorn flour. The frequent use of cold water to the part is always
attended with comfort, and sometimes with relief. In these old cases of
great relaxation Nelaton has used strychnia by the mouth, and Weber (of
New York) hypodermically, with fair result. Vidal has cured three cases
by the repeated use of ergotin locally, hypodermically. In order to
bring about a radical cure in these very chronic cases, very decided
means sometimes are justifiable. The late Mr. Hey of Leeds was the
first to propose a plan by which, through cicatricial contraction and
inflammatory gluing together of the various tissues composing the
bowel, the anus and sphincter muscle might be strengthened and improved
in tone; to which end he proposed to cut away the pendulous flaps of
skin around the anus. In cases where these flaps are very redundant a
cure is sometimes effected by this procedure alone. Other cases will be
benefited by the operation proposed by Dupuytren, which consists in the
removal of radiating folds of the skin and mucous membrane at the edge
of the anus. To quote from Holmes's _System of Surgery_: "This
operation is effected by laying hold of the fold of skin on each side
of the anus with forceps, then with a sharp curved pair of scissors
removing both skin and mucous membrane. In very severe cases four or
six applications of the scissors may be necessary."

POLYPUS OF THE RECTUM.--The polypi of the rectum are the gelatinoid and
the fibroid, but as a very rare occurrence a villous or warty polypus
has been found. Polypoid growths are very different bodies, but they
are too frequently confounded with true polypi. The only treatment is
their removal, and the safest method is by ligation of the pedicle, and
either cutting off the growth in advance of the knot or returning it
into the bowel. The patient should remain quiet until the sloughing is
complete, and his bowels must be confined, otherwise profuse and very
troublesome hemorrhage might ensue. Their removal by the clamp and
cautery is equally safe. Their removal by torsion or by the scissors is
unsafe.

The peculiar villous polypus causes great and exhausting hemorrhage. A
case was successfully treated by the application of fuming nitric acid.

FISTULA IN ANO.--In the palliative treatment of this very common malady
no great amount of relief can be afforded. Those who are aged and
feeble or those who are much broken down will find comfort to attend
the free local use of warm water, and the sinuses should be injected
with dilute solutions of one of the mineral astringents, the strength
of these not exceeding two grains to the fluidounce of water.
Cosmoline, simple cerate, ointment of the oxide of zinc, and even fresh
lard, make the patient easier, as they prevent friction of the
buttocks. One of the forms of the radical treatment consists in the
division of all the structures between the fistulous tract and the
surface. This may be accomplished either by the use of the knife or by
seton. Stimulating injections or cauterization has been known
occasionally to permanently close fistulae in ano; but such plans of
treatment are unreliable, and usually unjustifiable. When the fistula
is not so high up in the bowel as to render the use of the knife
unsafe, this plan of treatment should be adopted. As an invariable
preliminary to all operations upon the rectum the bowels should be
thoroughly emptied and the patient should be placed under the influence
of {922} an anaesthetic. A flexible grooved director should then be
carried through the opening of the tract upon the surface and along the
tract to its opening in the bowel, should such exist. The forefinger
within the rectum will meet the point of the director as it emerges
from the internal opening, and the director should be pushed onward and
its extremity guided outward until it rests fairly upon the sound
integument outside, and all the included structures should be divided
along the groove of the director with a sharp-pointed curved bistoury.
Should the fore finger in the rectum not discover an internal opening,
one should be forced at the very bottom of the tract by rotating the
point of the director while making counter-pressure with the end of the
finger. Should several fistulae be found, they should be treated in
like manner. Sometimes it will be found that the incision is overlapped
by the dusky-red flaps composing its margins, in which case they should
be trimmed off with scissors. When the tract extends deeper than its
internal opening, the latter should be ignored and the sinus laid open
to its very bottom. When no external opening exists, one should be
made, and the guide for this incision will be a point of induration
felt by the finger at some point not far from the surface. The director
entering at this point will find the tract, and should be pushed
forward as described above. These opened sinuses should be packed with
lint soaked in carbolized oil and confined by a pad and a T-bandage. It
is the practice at the Pennsylvania Hospital to apply after division a
stick of caustic potassa, allowing it to remain in contact with the cut
surfaces for several seconds, after which the wounds are to be packed.
This procedure ensures their healing from the bottom. The bowels should
be confined for a few days, after which a dose of oil may be given.
Besides attention to cleanliness and a daily renewing of the packing no
further treatment will be demanded. The hemorrhage attending these
operations is usually trifling. Should a vessel spring, a ligature may
be thrown around it. When an abundant general oozing occurs, the rectum
must be packed and a compress and bandage firmly applied. Should the
surgeon prefer the seton operation, he should carry several threads of
stout silk or a piece of rubber cord on an eyed probe into the fistula
and out of its internal opening, and by tying their ends firmly down
upon the enclosed tissues slowly effect the same result as in the
cutting operation. When the seton used is silk, the ends should be
carried through holes in a round leaden plate or through those of an
ordinary button, and tied. These setons are to be drawn tighter every
three or four days until the division of the enclosed tissues is
complete. The subsequent treatment is the same as in the other
operation.

A difference of opinion exists among surgeons as to the propriety of
operating for fistula in ano in persons afflicted with tubercular
disease of the lungs. The practice of the present day is decidedly in
favor of operating, without reference to the condition of the lungs,
provided the patient is not too much reduced in strength.

An operation for fistula in ano has been proposed and practised by
Reeves, which is a compromise between cutting and ligation. He says:
"It consisted in passing a strong and well-waxed silk ligature along
the track of the fistula into the bowel. An ordinary surgical probe
with an eye in its end carried this thread into the rectum. My bivalve
expanding speculum was previously introduced, and by its use there was
no difficulty {923} in seeing and seizing the ligature and bringing it
out through the anus. The probe was then withdrawn, and the ends of the
silk were wound round two strong pieces of wood which were held between
the fingers of each hand. An assistant passed a finger on either side
of the track of the fistula to steady the tissues and to resist the
traction which was put on the silk thread. The two pieces of wood were
then drawn toward me with a rapid sawing motion, and the fistula was
quickly divided, with the loss of scarcely any blood. Some oiled lint
and a pad and bandage were applied in the usual way; and the wound
healed well. No anaesthetic was administered, and although the patient
did not relish the operation, still it was quite bearable, and what she
felt most was a burning sensation, due, doubtless, to the friction of
the silk."

HEMORRHOIDS.--The treatment of this form of rectal and anal disease is
either medical or surgical according to the gravity of the case and
according to the obstinacy with which it resists local and general
therapeutic agents. An ordinary acute attack of external piles, such as
is often produced by neglect of the bowels, causing constipation, may
be treated in the following manner: The patient should rest and avoid
stimulating food and beverages. He should employ cold bathing to the
part frequently: indeed, great comfort and relief often follow this
treatment alone. An ointment of tannic acid, glycerin, and simple
cerate, or one containing calomel and extract of opium, will be found
useful. Fresh lard, cosmoline, vaseline, cold cream, ointment of the
oxide of zinc (benzoated) or an ointment containing extract of opium,
extract of galls, and extract of belladonna or stramonium, are some
among many agents that have been extolled for their relief. H. C.
Wood[46] recommends enemata of solution of chlorate of potassium and
laudanum. Enemata of lime-water and linseed oil are recommended by
Agnew: "One of the very best formulas for allaying the irritation
incident to hemorrhoidal affections consists of the following
combination: Acetate of lead and tannin, of each fifteen grains;
carbonate of lead and extract of stramonium, of each thirty grains;
creasote, five drops. With a sufficient quantity of cocoa-butter mould
this into fifty suppositories."[47] The internal exhibition of the
balsam of copaiba, twenty drops in capsules taken four or five times
daily, or the use of fifteen drops of liquor potassa rubbed up with
half a drachm of the balsam into emulsion, taken three times a day, has
been much extolled, as has also the confection of black pepper.
Sometimes these various means will cure a chronic or long-standing case
of piles, either internal or external. Wetherill has found that the
topical application of rectified oil of amber has cured long-standing
cases of piles. This oil should not be applied in cases where much
inflammation exists, and where the piles are internal the best mode of
bringing it in contact with them is to incorporate from three to five
minims of the oil with sufficient cocoa-butter to make a suppository.
One of these, pushed into the bowel night and morning for a week, will
not infrequently cause the piles to shrink up and finally to disappear.
The bowels should be kept open with the compound powder of licorice. It
should be remembered that magnesia irritates hemorrhoids. Success has
followed the internal use of ergotin, of the fluid extract of hamamelis
virginica, of the corn blast (ustilago maidis), and of small doses of
aloes combined with hyoscyamus. {924} D. Young has had good results
follow the internal use of glycerin. Chronic cases of piles have been
cured by the application of ointments containing carbonate of lead,
creasote, carbolic acid, or iodoform. Ergotin used hypodermically in
the vicinity of the anus or injected into the piles has frequently
resulted in a complete cure, and the same may be said of the injection
of carbolic acid directly into the tumors. In the application of cold
water to inflamed piles it should be borne in mind that its forcible
impingement upon them in a fine stream acts far more efficiently than
the mere bathing them. Some cases do better under the use of warm water
or warm sedative and astringent lotions. A warm flaxseed poultice mixed
with laudanum is a very comfortable application. In obstinate cases of
prolapse Agnew[48] recommends the use of a rectal obturator or the use
of a hemorrhoidal truss.

[Footnote 46: _Philada. Med. Times_, Dec. 6, 1879.]

[Footnote 47: _Surgery in the Pennsylvania Hospital_, p. 210.]

[Footnote 48: Agnew's _Surgery_, vol. i. p. 445.]

Those who suffer from prolapse of piles should avoid the habitual use
of cushioned seats. They should assume a semi-erect posture during
defecation, or, when this is attended with difficulty or inconvenience,
they should contrive a portable water-closet seat by boring a hole an
inch and a half in diameter through a piece of planed board, bevelling
it so as to fit the person. These means will often prevent the
extrusion of the tumors. After defecation the patient should rest for a
little while in the recumbent attitude.

The careful touching of external piles with strong nitric acid is a
mode of treatment that has been quite successful in the hands of some
surgeons. The intolerable itching of these bodies can be allayed by
touching them with tincture of aconite-root or with a concentrated
tincture of prickly-ash bark. Freezing them with the ether spray allays
the pain and itching for the time being, but these symptoms return with
redoubled energy after the effect has subsided.

Should an attack of the external variety of piles not result in
absorption, but leave an excrescence, painless but inconvenient, and
liable at any time to become inflamed, excision would be in order.
Divide the integument by an incision radiating from the anus, separate
the skin from the tumor down to its base, and after seizing it with
toothed forceps cut it off with scissors curved on the flat. Little
flaps or tabs of skin remaining after piles may be snipped off with
scissors. It is not well to operate upon external piles unless they
obstinately resist all milder treatment. There are frequently venous
enlargements containing blood-clot, and when this condition exists
proceed as follows: Pinch up the little tumor between the thumb and
finger of the left hand; transfix its base with a curved bistoury, and
cut out; at the same time, by pressure with the thumb and finger,
extrude the clot. Fill the bottom of the little sac with cotton wool,
and the operation is complete. It is not necessary in these cases to
wait until the inflammation subsides before operating.

The operative treatment of the internal variety may be by
strangulation, by the cautery, by the ecraseur, and by the use of
caustics. The former of these is the safest and most convenient method,
and the one usually employed in the Pennsylvania Hospital, and should
be performed in the following manner: The lower bowel having been
thoroughly evacuated and the patient etherized, the operator should
gently but firmly stretch the sphincter. The patient should be placed
upon the side, with {925} the upper part of the body prone, the hips
elevated, and the thighs flexed upon the abdomen. Transfix the largest
tumor with a strong, long-handled tenaculum, cut through the skin at
the base with a knife or scissors around its external half, and hand
the hook to an assistant, instructing him to make gentle traction. Then
encircle the mass with a stout cord if the mass is not too large, or
pass a stout needle threaded with a double silk ligature, from without
inward, deeply through the base of the pile, drawing it through the
mucous membrane on the opposite side; cut loose the needle and tie
tightly, so as to completely strangulate the included tissues on either
side and leave the ends of the ligature long. Treat all the remaining
tumors in a similar manner seriatim, and then with scissors cut away
the strangulated bodies to within a safe distance of the ligatures, the
ends of which are now to be cut off close. Place an opium suppository
in the bowel, and the operation is complete.

When for any sufficiently good reason the patient will not bear the
ordinary anaesthetics, it will become necessary to modify the operation
as follows: The tumors having been well extruded by enema of warm water
or by the efforts of the patient, bend him forward over a chair and
direct an assistant to draw aside the buttocks. Then pass the double
ligatures as before indicated, but refrain from tying until all the
tumors are thus secured, as the operator will find it convenient to
draw upon the ligatures to keep the mass of piles within view and
working-distance. Then draw down each tumor, cut around its base, and
tie as before; cut off the ends of the ligatures and the greater
portion of each strangulated tumor, and return everything within the
bowel, and follow with an opium suppository. In many cases Morton has
used the nitrous oxide gas with the best results. The hook should then
be withdrawn, and each knot should be drawn more firmly down prior to
its reduplication. Following this procedure, if properly carried out,
the tumors will change color, becoming blue, thus indicating complete
strangulation.

The operation by the clamp and cautery is a good method when the
hemorrhoidal tumors are small. The operation is that of Mr. Cusack of
Dublin, and the clamp employed is that invented by Mr. H. Smith of
London. This instrument is so well known that a detailed description of
it would be unnecessary. In operating with it the tumor is to be drawn
well out and the clamp applied close up to its attachment with the
bowel. Strangulation is effected by means of the screw which runs
through the shafts of the handles. This accomplished, the strangulated
portion is cut off with scissors, which should leave a stump
three-eighths of an inch long. To this stump apply the actual cautery
at a dull red heat, touching its every portion, after which unscrew and
remove the clamp and look for hemorrhage. Should any occur, touch the
bleeding point with the hot iron. Confine the patient to bed for five
or six days and give sufficient opium to confine the bowels. After this
time has elapsed administer a dose of oil. Remember that but one pile
should be clamped at one time. "The taking two piles into the clamp at
once is sure to result in hemorrhage." Do not allow the cautery-iron to
touch the clamp. After the operation return the parts within the
sphincter and cut off any tabs of redundant integument with scissors.

The removal of internal piles by means of the ecraseur was the favorite
operation of Chassaignac, but it is a mode of procedure which is now
{926} regarded with disfavor by the best surgeons on account of the
liability to hemorrhage, and from the fact that troublesome and
injurious contractions of the anus have not infrequently followed its
use. The employment of iron or copper wire instead of the usual chain
has been recommended by those who prefer this mode of operation. The
plan adopted by Chassaignac was to pedunculate the piles by tying a
ligature around the base and drawing them down. The chain being then
applied, the strangulation and crushing off was slowly accomplished by
means of the lever of the instrument. It should take from twenty to
twenty-five minutes' crushing to accomplish this object.

For the treatment of internal piles by caustics Houston of Dublin used
strong nitric acid. A fenestrated speculum should be employed, and the
acid should be applied with a piece of wood or with a glass brush, care
being taken to limit its action to the tumors, the redundant liquid
being mopped up with a swab of lint or prepared absorbent cotton. The
entire surface should afterward be bathed in oil. The acid is relied
upon to produce a granulating surface, by the healing of which and by
the subsequent contraction a cure is sometimes achieved. At best, this
plan of treatment has proved tedious and unsatisfactory.

Chloride of zinc and caustic potassa are even more unsatisfactory
agents for this purpose than the acid, as they are very violent in
local destruction and their action is very difficult to limit. The use
of caustic potassa was last revived by Amussat, but failed to find
favor from his contemporaries, and soon fell into merited disuse. Van
Buren says: "From recent experience with the thermo-cautery of
Paquelin, I am disposed to regard it as more manageable than nitric
acid, and at least equally efficient." Allingham mentions favorably the
strong carbolic acid as a substitute for the nitric as an application
to vascular and granular surfaces. The reckless method employed by the
older surgeons of cutting off internal piles with the knife or with
scissors, without any precautions against bleeding, is merely mentioned
in condemnation. Usually no serious symptoms are to be expected after
operations for hemorrhoids, but to this general rule there are
exceptions. Morton knows of two consecutive cases of tetanus after this
operation performed in a hospital in this city, and both terminated
fatally. One of the most common occurrences after the ligation of piles
is retention of urine, generally lasting for a day or two and requiring
the use of the catheter.

HEMORRHAGE FROM THE RECTUM.--Bleeding from these parts is more usually
of a venous than an arterial character, but in some cases of
hemorrhoids the bleeding is either arterial or arterio-venous. The
latter occurs upon the detachment of a polypus, but not necessarily of
a polypoid growth. Arterial or mixed bleeding occurs in carcinoma and
in rodent ulcer, and also from the stumps of badly-occluded piles. In
cases of vicarious menstruation from the rectum the venous blood simply
oozes from the surface of the over-congested mucous membrane. This
condition should be readily diagnosed by the physical properties of the
blood and from the history of the patient. In almost all cases of
bleeding near the anus it will be possible to pick up the vessel or the
bleeding point on a tenaculum and ligate with silk, which is the most
satisfactory method to the surgeon. The rectum has been dragged down
with volsella forceps to apply a ligature to a point high up, but in
some of these cases the acupressure pin {927} with the twisted suture
will be found more convenient. Should hemorrhage occur after the
ligation of piles which cannot be checked by ligature, such as a
general oozing, pass all the ligatures through a hole made in the
centre of a small round sponge, then tie them across a piece of stick
(thus constructing a sort of tourniquet), and twist this around. Van
Buren cites a case in which a sudden laceration of the integument and
sphincter occurred during forcible dilatation in a case of hemorrhoids
in a very broken-down subject, with very copious hemorrhage. He passed
a sponge armed with a double ligature into the bowel, and, directing an
assistant to make traction upon the threads, the bleeding was checked.
Injecting ice-water and perchloride of iron into the rectum will often
check hemorrhage. Allingham prefers the persulphate of iron to any
other styptic for this purpose. Passing fragments of ice into the bowel
while holding a lump of ice upon the sacrum sometimes answers a good
purpose. In many cases of secondary hemorrhage from large venous
sinuses in a state of ulceration it will be impossible to ligate, and
the use of the ordinary styptics will be but the waste of valuable
time: the bowel must be tamponed as follows: Thread a strong silk
ligature through near the apex of a cone-shaped sponge, and bring it
back again, so that the apex of the sponge is held in a loop of thread.
Wet the sponge, squeeze it dry, and fill its meshes with ferric alum or
with persulphate of iron. Pass the left fore finger into the bowel, and
upon it push up the sponge, apex first, by means of a metal rod or any
other convenient body, fully five inches into the rectum. Now fill the
rectum below this with cotton-wool filled with the styptic. The bowel
having been completely filled, make traction upon the ligatures (thus
spreading out the bell-shaped sponge), while with the other hand push
up the packing. If this is carefully done no fear of bleeding need be
apprehended. In these cases the patient often suffers from collections
of flatus, which may be obviated at the time of packing by placing a
flexible catheter in the bowel and packing around it. These plugs
should remain for at least five or six days, and frequently eight or
ten days are none too long. The packing must then be picked carefully
away from the sponge. Agnew's rectal chemise answers the same purpose.
In describing its application he says: "Through the openings at the end
of the largest-sized gum catheter pass a strong silk thread; take three
square pieces of the material usually known as mosquito-netting,
placing them one on top of the other; at the centre of these squares or
pieces make an opening, and pass the catheter through it, securing the
two together by the threads. In applying the instrument the different
layers of the chemise must be moistened with water, and afterward well
filled with the persulphate of iron. It is then conducted some distance
into the rectum on a finger previously inserted; after which it is
expanded like a parachute by packing between the catheter and its hood
with long strips of lint thrust up on the end of a bougie until the
bowel is distended on every side. The catheter will serve to conduct
away the flatus, and when, after eight or ten days, its removal becomes
necessary, this is very easily effected by drawing out the ribbon-like
pieces of lint which were used as packing." Another method is to stuff
the bowel with fragments of sponge to which threads are tied, the ends
of which, protruding from the anus, facilitate their withdrawal. In
conjunction with these procedures the patient's pelvis should be
elevated. {928} After excision of portions of the mucous membrane the
risk of hemorrhage will be lessened by the surgeon introducing through
the edges of each incision a few fine sutures.

Enormous quantities of blood may escape into the bowel after operations
without any external symptom being apparent until the patient becomes
pallid and weak. In other cases the patient will complain of tenesmus
and desire to go to stool, or of a sensation of something trickling
into the bowel. Upon the recognition of these symptoms search should at
once be made for internal hemorrhage.


Rectal Alimentation.

Before taking leave of this very interesting class of diseases and of
their modes of treatment, it seems proper to introduce a few remarks
upon the subject of rectal alimentation, as it is now a well-recognized
and much-practised means of sustaining those whose stomachs are unequal
to the work which in health is so easily and unconsciously performed.
In the use of the lower bowel as an absorbent surface of alimentary
substances many failures have been reported, a fair proportion of
which, it is safe to infer, are due to the methods employed, to the
nutritive matters employed, and to the condition of the rectum at the
time. Firstly, as to the state of the rectum, it must be empty. Wait a
reasonable time, say an hour, after stool, so that the gut may be more
passive; have the patient in the recumbent posture; direct him to
resist tenesmus and to exert both the will and the muscular power to
retain the aliment. The syringe must be of hard rubber, must be
rectal-ended, and of the capacity of two fluidounces, and perfect in
action.

The preparation to be introduced, after being warmed to a temperature
of 98 degrees or 99 degrees F., should be very slowly injected with the
syringe, which should be also warmed and oiled. The enema must never
exceed in amount two fluidounces. If this be rejected, wait a
reasonable time and try again, using a less amount. If tenesmus proves
an insurmountable barrier to ordinary means, an opium suppository is to
be introduced three hours prior to another attempt. It has been
suggested, inasmuch as tenesmus is often relieved by the application of
cold to the rectum, to introduce the aliment in that state; but this
method is open to the objection that rectal digestion would be much
less likely to take place under this condition, as the bowel would then
have thrown upon it the additional work of warming up the substance
prior to absorbing it.

The usual errors made in applying this means of sustaining the patient
are, that the injections are too large, are too rapidly introduced, and
are not of the proper temperature. Allowing an interval of eight hours
between the enemata would afford three in the twenty-four hours, which
method has been found to offer the best results. This must be
persevered in at regular daily intervals for the patient to derive its
full benefit, and there is reason to suppose that the nervous system
gets expectant of these daily hours of support, as it does in the case
of our ordinary meal-times. An examination of the well-formed daily
stools of patients thus sustained will prove how close the analogy is
between this and digestion proper.

{929} Next, as to the substances to be employed. The best of these are
milk, eggs, concentrated beef-extracts or beef or chicken peptones, and
brandy or whiskey of good quality. These substances may be combined in
various proportions to suit the individual requirements of the case. A
very good mixture for this purpose is two tablespoonfuls of milk, one
tablespoonful of whiskey, and an egg, using both the yelk and the
albumen. To this add a little salt. This should be well beaten up and
properly warmed.

It is well to persevere in the use of these enemata even though at
first most of them appear to be rejected, as after a time, the rectum
becoming accustomed to their presence, absorption or so-called rectal
digestion may take place. This form of alimentation should be kept in
reserve in a case of chronic illness until all other methods of
sustaining the patient prove insufficient to support life. It is not
contraindicated even in some cases of chronic diarrhoea with persistent
vomiting and loss of peptic function, advantage being taken of the
intervals between the evacuations to introduce a small and very
concentrated nutrient enema. In ordinary cases not complicated by
diarrhoea the most convenient times will be found to be about seven
o'clock in the morning, three in the afternoon, and eleven at night.
Wetherill suggests the possibility of forming with solid extract of
beef, pepsin, and pure suet a nutrient suppository which might be
retained and absorbed in some cases in which it has been found
impossible to retain the enemata. A very small addition of white wax,
he thinks, would keep these solid during warm weather; if not, the suet
might be replaced by ol. theobroma (as in ordinary suppositories),
which is probably as likely to be absorbed as the suet.




{930}

INTESTINAL WORMS.

BY JOSEPH LEIDY, M.D.


All animals, except in general the simple cell-forms constituting the
sub-kingdom of protozoa, under ordinary circumstances are more or less
liable to be infested with others, called parasites, which commonly
live at the expense of their hosts, frequently with little or no
inconvenience, but often causing discomfort and suffering even unto
death. Parasites are distinguished as external and internal, the two
being mostly of a widely different character. The former chiefly
pertain to the division of arthropoda, or animals with jointed limbs,
as exemplified by lice, fleas, and flies of the class of insects, mites
of the class of arachnides, and epizoans and isopods of the class of
crustaceans.

Internal parasites, from their usual habitation named entozoa, are
commonly observed in the intestines of animals, and hence their
distinction as intestinal worms. The name has proved to be appropriate,
for investigations have shown that most entozoa, observed from time to
time in other parts of the bodies of animals, pass part of their life
in the intestinal canal of the same or of some other animal.

By far the greater number of entozoa are peculiar animals, constituting
the chief part of the scolecides, an extensive group of the sub-kingdom
of vermes or worms. Of this group they comprise the orders of CESTODES,
or tape-worms; the ACANTHOCEPHALI, or thorn-headed worms; the
TREMATODES, or fluke-worms; and the greater portion of the NEMATODES,
or thread-worms. Many entozoa also belong to the protozoa, but these,
so far as relates to man in a medical point of view, appear
unimportant, and will therefore not here enter into consideration.

In the course of their life entozoa undergo changes of form and
condition, and pass these in different organs of the same or of
different animals, and it may be for a brief period externally or in a
non-parasitic state. In many instances, as in the tape-worms and the
fluke-worms, the transformations accompanying the changes are of so
extraordinary a character that until their life-history was
investigated the successive metamorphoses were viewed as distinct
animals. Mostly, the entozoa pass one stage of existence within the
intestine of some animal, and another stage in different organs of
other animals. Many, perhaps most species, in each stage are peculiar
to one or a few nearly-related animals, but others of the same kind
infest a number of different animals. The animals infested by the same
parasite may be remotely as well as nearly related. Thus the Taenia
saginata, or beef tape-worm, in the mature state lives in the small
intestine of man {931} only, but in its juvenile or larval condition in
the flesh meat of the ox. The Taenia elliptica, the common tape-worm of
the intestine of the dog, in the larval condition lives in the louse of
this animal. The liver-fluke, Distomum hepaticum, occasionally found in
the liver of man, but of common occurrence in the sheep, to which it
proves so destructive in the affection known as rot, in the juvenile
condition lives in a little fresh-water snail of the genus Lymneus. The
guinea-worm, Filaria medinensis, which in the mature state is found
beneath the skin of man, in the larval condition inhabits the minute
crustacean cyclops of stagnant waters.

As would be reasonably supposed, entozoa commonly gain access to their
hosts through the food and drink, though in the case of aquatic animals
they also obtain entrance directly through the integument from the
surrounding medium. So long as they remain in the intestinal canal they
may occasion little trouble or inconvenience. When they are numerous in
this position or proportionately large, according to their peculiar
nature they may produce more or less suffering and even the most
serious consequences. Generally, however, it is when they occupy other
positions, to which they have migrated from the intestine, that they
induce aggravated symptoms proportioned to their numbers and the nature
of the organs they infest.

Many species of entozoa have been discovered in man, and most of them
are peculiar in kind. Many are common, and, while some are widely
extended, others are more or less restricted to certain localities.
They are variable in their frequency, largely proportioned to the
prevalence of habits which are favorable to their transmission, and
which, though under control, are more or less disregarded. Some species
are so rare in their occurrence that they seem to be accidental, and
therefore of comparatively little interest to the physician.

In general, the frequency of occurrence of intestinal worms is
proportioned to the extent of use of uncooked or insufficiently cooked
meats, the drinking of unfiltered standing waters, uncleanly habits,
and the intimacy of association with domestic animals. It therefore
follows that important prophylactics against infection by parasites are
properly-cooked food, the use of spring or freely-running water or
filtered standing water, cleanly habits, and the avoidance of intimacy
with domestic animals.


The Cestodes, or Tape-worms.

Tape-worms in the mature condition inhabit the intestines of vertebrate
animals, and are usually conspicuous for their long, tape-like
appearance and jointed character. In the juvenile or larval state they
infest the various organs, except the interior of the intestinal canal,
of both vertebrates and invertebrates, and in this condition are so
diminutive and inconspicuous that until a comparatively recent period
they for the most part remained unnoticed, and when known their
relationship with the mature forms was not recognized.

The mature tape-worm, as ordinarily observed, is a long, soft, flat,
white worm, which from its resemblance has received its familiar name.
{932} It has a small head, succeeded by a short, more slender neck
gradually widening into the body, which is divided transversely into
segments. These, which are usually called joints or links, and also
named proglottides, are so many individuals, and finally become
separated to hold an independent existence. The tape-worm clings to the
mucous membrane of the intestine by its head, which is provided for the
purpose with suckers, and in many cases also with circlets of hooks.
The segments of the body are incessantly produced by gradual growth and
successive division of the neck, and as they enlarge they become more
distinct and develop within a bisexual generative apparatus for each.
The worm has neither mouth nor intestine, but is nourished by
imbibition from the surrounding liquid in which it lies constantly
bathed. A pair of longitudinal vessels commences in the head and
extends throughout the body, one on each side, and in some genera is
joined by a transverse vessel at the fore and back part of every
segment. The mature segments have no body-cavity, but are occupied with
a complex bisexual generative apparatus, which is self-impregnating.
Finally the uterus, usually much ramified, becomes especially
conspicuous through distension with eggs, and the rest of the organs
for the most part become atrophied. The ripe segments successively
detach themselves from those in advance, often singly and not
infrequently several linked together. In this condition, often in
lively movement, they are discharged with the feces, and thus commonly
render themselves obvious to their host. Subsequently they may continue
to live a brief period externally in a non-parasitic condition.
Ordinarily, in moist excrement, or in water or similar materials, they
will remain alive for several days.

After the discharge of the tape-worm segments, together with the eggs
which had been previously laid by the latter and those still contained
within them, any or all may be swallowed by animals feeding in places
where the infected excrement has been deposited. When the proglottides
and eggs are taken into the stomach they are digested and the embryos
or proscolices are liberated.

The embryo or proscolex of the tape-worm is a microscopic spherical or
oval body, provided at one pole with three pairs of divergent spicules,
by which it is enabled to penetrate the walls of the stomach or
intestine of its host. From these positions the embryo migrates either
directly or through the blood-vessels to some other organ, most
frequently the liver or the muscles. Having reached its destination, it
becomes fixed in position, and for a time remains comparatively
quiescent, but undergoes further development. The embryo loses its
spicules and is transformed into the larval form or scolex. In most
species of tape-worms the scolex is simple or individual in character,
and consists of a head like that of the parent or mature worm, with a
neck ending in a capacious cyst, within which the head and neck are
inverted. In this form the scolex is contained in a sac of connective
tissue induced by the presence of the parasite. Such sacs, frequently
observed imbedded in the flesh, liver, lungs, and other organs of
animals, are familiarly known as measles. In this condition the
scolices of certain tape-worms have long been known, but as their
relationship was not recognized, they were viewed as distinct species
of parasites and described as cysticerci. In other species of
tape-worms the scolex is of compound character; that is to say, the
embryo {933} in its further development gives rise to the production of
one or more groups of individuals in conjunction. The compound scolex
thus forms a sac or a group of sacs, the basis of hydatid tumors. These
occur of various sizes, even up to that of a child's head, and may
occupy any organ of the body. They consist of a spherical sac or group
of sacs, simple in character or containing others, ranging in size from
that of a mustard-seed to that of a marble, or larger to that of a
walnut, enclosed in an envelope of connective tissue induced by the
presence of the parasite. The sacs are filled with liquid, and have,
attached within or free and floating, or less frequently attached
without, variable numbers of little white grains, which on examination
with the microscope exhibit the same constitution as the simple scolex
above described. As in the case of the cysticerci of measles, the
scolices of hydatids have long been known, but as their relationship
with the mature forms was unrecognized until lately, they were regarded
as distinct parasites and described as echinococci and coenuri.
Sometimes the compound scolex fails in development further than the
production of the sacs, which then constitute the so-called
acephalocysts.

Measles with their occupants, when retained in the muscles or other
organs, ordinarily undergo no further development, but ultimately,
after some months to a year or two, undergo degradation. The larva or
scolex dies and atrophies; the measle degenerates, and often becomes
the focus of calcareous deposit, shrinks to a little cicatrix, and may
finally disappear. Of a more serious nature is the tape-worm embryo
which produces the hydatid tumor. With the increase of this,
proportioned to the production of sacs and scolices, it may become so
large as greatly to interfere with the function of the organ it
occupies, and according to the nature of this organ will be the gravity
of the affection.

When, however, the flesh or other parts of animals affected with
measles or hydatids containing active scolices are used as food in a
raw or insufficiently cooked state, the meats are digested in the
stomach and the scolices liberated to pursue their further development.
Passing into the small intestine, the active scolex everts its head
from its caudal sac, which atrophies and disappears, and the parasite
attaches itself to the mucous membrane, and rapidly develops and grows
into the conspicuous and familiar form of the adult tape-worm. The
duration of life of the latter while maintaining its position in the
intestine is uncertain, but under favorable circumstances it commonly
continues for years, and thus, with the incessant production of ripe
segments charged with eggs, it becomes a constant focus of infection.

       *       *       *       *       *

Three species of tape-worm in the mature condition are common parasites
of man, living in the small intestine. They are the Taenia saginata,
Taenia solium, and Bothriocephalus latus.

       *       *       *       *       *

TAENIA SAGINATA.--SYNONYMS: Taenia mediocanellata; Beef tape-worm;
Unarmed tape-worm; Fat tape-worm.

Larval condition: Cysticercus saginata; Beef measle-worm.

This, which is now regarded as the most common tape-worm of man, is
named the beef tape-worm because it is derived from the beef used as
food. In the mature condition it lives only in the small intestine of
{934} man, and in the juvenile condition it lives in the ox. Its
frequency is proportioned to the prevalence of the custom of eating
beef in a raw or insufficiently cooked state, conjoined with the
careless habit of leaving human excrement in pastures where it is
accessible to cattle.

The mature beef tape-worm is commonly observed as a soft,
yellowish-white, thickish, band-like worm, ranging from six to twenty
feet or more in length. The head, about the size of a yellow
mustard-seed, is rounded quadrate and provided with four equidistant
hemispherical suckers. Succeeding the head is a short, slightly
narrower, flattened neck, which merges into the gradually widening and
segmented body. The segments, at first narrow fore and aft and several
times wider than the length, become successively larger,
proportionately longer, more distinct, and quadrate in outline; and
finally the length may exceed the breadth two or three times. A
full-grown tape-worm may possess twelve hundred segments and more, and
specimens are recorded as reaching a length of thirty feet. The larger
segments measure from a quarter of an inch to an inch long and from
three to four lines wide. The larger or riper segments exhibit on one
border, irregularly alternating on the two sides, at or near the
middle, a papilla in which is the external aperture of the genital
apparatus. In the fully-ripe segments the uterus, distended with eggs,
may be obscurely seen through the wall of the body, but is rendered
more visible by drying the segments, moderately compressed, between two
pieces of glass. It appears as a long, narrow, white or brownish median
line or tube, giving off laterally numerous short, transverse, more or
less branching tubes.

The worm in its usual position lies along the course of the intestine
in loose coils, and exhibits lively movements, alternately shortening
and elongating, expanding and contracting the head, and protruding and
retracting the suckers. The ripe segments spontaneously detach
themselves, and may be found scattered along the large intestine ready
to be discharged with the excrement, or, as is sometimes the case, they
may spontaneously creep from the anus. Rarely more than a single worm
infests a person at the time. The species is of rapid growth. According
to Perroncito, quoted by Cobbold, a mature worm was reared from a beef
measle, swallowed by a student, in fifty-four days.

It is estimated that the number of eggs in the mature segments of the
beef tape-worm amounts to about 35,000. As the full-grown worm may
consist of 1200 segments, and there is reason to believe these are
renewed several times annually, we learn that the whole number of eggs
produced by a single individual is enormous. The ripe segments,
attached to the parent or becoming spontaneously detached, lay their
eggs in the intestine to be discharged with the feces. When more or
less emptied they shrink and appear reduced in size, and in this
condition are expelled or spontaneously creep from the anus. If the
ripe segments are forcibly expelled and are alive, they will lay their
eggs in the feces externally. The ripe eggs are brown, oval, about 0.03
mm. long, and have a thick shell, with an outer vertically striated
envelope.

As previously intimated, the common source of the beef tape-worm in man
is the use of raw or insufficiently cooked beef affected with measles.
The ox becomes infested by swallowing the eggs, or, it may be, even the
entire segment, of a tape-worm deposited with feces in the {935}
pastures of cattle. The measles usually occur in the muscles, including
the heart, though they have also been noticed in the liver and lungs.
They appear, in beef, as oval, whitish bodies from the size of a
mustard-seed to that of a pea. They consist of a sac of connective
tissue containing the larval tape-worm or cysticercus. Measles under
ordinary circumstances are seldom noticed in beef, and when they occur
are commonly few in number.

According to the latest authorities--Leuckart, Cobbold, Stein, and
others--the beef tape-worm is the most common of the cestodes which
infest man. Until within about thirty years it was generally not
distinguished from the pork tape-worm, and this was accordingly
regarded as the most common human species. Since the writer distinctly
recognized the beef tape-worm within the last twenty years, all the
specimens of Taeniae, from people of Philadelphia and its vicinity,
that have been submitted to him for examination--perhaps in all about
fifty--have appeared to belong solely to Taenia saginata. The
prevalence of this species with us is no doubt due to the common custom
of eating underdone or too rare beef, while the pork tape-worm is
comparatively rare, as with us pork is only used in a well-cooked
condition.

       *       *       *       *       *

TAENIA SOLIUM.--SYNONYMS: The Pork tape-worm; Solitary tape-worm; Armed
tape-worm.

Larval condition: Cysticercus cellulosae; Pork measle-worm.

Until a recent period this species was generally regarded as the most
common tape-worm of man--a view which in great measure was due to the
circumstance that the beef tape-worm was not distinguished from it. It
was called the solitary tape-worm, still expressed by the specific
name, from the impression that it rarely occurred otherwise than single
at a time in a person. This has also proved to be incorrect, likewise
due to the two kinds of tape-worms having been confounded together; for
while the beef tape-worm most commonly occurs solitary, the pork
tape-worm not unfrequently occurs with several together.

The species is now appropriately named the pork tape-worm, as
indicating its common source--pork used as food. The frequency of the
parasite is proportioned to the prevalence of the custom of using pork
in a raw or imperfectly cooked state, conjoined with that of depositing
excrement where it may be accessible to hogs. In the mature condition
the pork tape-worm is peculiar to man and lives in the small intestine,
but in the larval condition, though especially infesting the hog, it
also occasionally infests man, and lives in any organs of the body, but
mostly the muscles, liver, and lungs.

The mature pork tape-worm, as commonly seen, is a soft white, thin,
band-like worm, from five to ten feet long and about four lines where
widest. The head is spheroid, about the size of that of an ordinary
pin, and smaller than that of the beef tape-worm. It is furnished with
four hemispherical cup-like suckers, and the summit forms a blunt
papilla armed with a double circle of twenty-five or twenty-six hooks.
The neck is narrow, thread-like, about an inch long, and merges into
the segmented body, which gradually widens to the extent mentioned. The
segments, at first much wider than long, as they successively enlarge
also become more distinct and proportionately longer, so that the more
{936} posterior ripe ones are as long as they are wide, and often
longer, though not to the same degree as in the beef tape-worm. The
genital papilla, with its external aperture, is marginal as in the
latter. The fully-developed uterus is quite distinctive in character
from that of the beef tape-worm. The median tube is coarser, and the
lateral branches are likewise coarser, much fewer--half the number or
fewer--less branched, and less crowded. The ripe and often
spontaneously detached segments are commonly longer than broad, more or
less elliptical in outline, with truncated ends, and usually measure
about half an inch in length by about a third in breadth. The ripe eggs
resemble those of the beef tape-worm, but are usually spheroid in
shape.

The common source of the pork tape-worm is pork affected with measles
eaten in the raw or insufficiently cooked state. The hog becomes
affected with measles when it has access to human excrement containing
eggs and ripe segments of the tape-worm, which it eats with avidity.
The eggs, with their already developed embryos, when swallowed, undergo
the same series of transformations and course as those indicated in the
account of the beef tape-worm. Pork affected with measles is much more
common than beef affected in the same way, and is frequently a subject
of ordinary observation. From the difference in habit of the hog and ox
this is what might have been suspected; and the fact that the beef
tape-worm is more common than the pork tape-worm is to be explained
from the circumstance that fresh beef is in more general use than pork,
and is usually employed less thoroughly cooked.

The pork measles are commonly seen as round or oval, hard, whitish
bodies, from the size of a hempseed to that of a pea, imbedded in the
connective tissue of the muscles or flesh. The measle consists of a sac
of connective tissue enclosing the scolex or larval tape-worm, which
resembles that of the beef tape-worm, but differs especially in the
possession of a double circlet of hooks to the head, as in the adult
worm. The scolex has long been known, and was regarded as a distinct
parasite, with the name of Cysticercus cellulosae. When fresh pork
measles are swallowed by man they are digested in the stomach, and the
cysticercus or scolex is released and passes into the small intestine.
Here, attaching itself to the mucous membrane by means of its suckers
and crown of hooks, it rapidly develops and grows into the adult
tape-worm. In this condition it lies in loose folds along the
intestine, to which it clings so tenaciously that commonly the neck
gives way when the greater part of the worm is forcibly detached by the
use of medicines. Fragments, consisting of the more mature segments,
frequently appear detached from the posterior part of the worm, and the
fully-ripe segments may be seen scattered singly in the course of the
large intestine. The isolated segments are thinner and more translucent
than those of the beef tape-worm, and in this condition are discharged
with the feces, but may also spontaneously creep from the anus, though
seldom as compared with the other species.

Experiments repeatedly made by swallowing pork measles prove that the
mature tape-worm may be developed in the course of three months. The
length of life attained by it under favorable circumstances is
uncertain, but it probably continues a dozen years or more.

The scolex of the pork tape-worm, or the cysticercus, so common in the
hog, is also less frequently a parasite of man, and in this condition
is a {937} more potent agent of danger than in its ordinary or mature
state. The infection is due to the introduction of eggs or mature
segments of the tape-worm into the stomach--a circumstance which may
readily occur through handling these objects and transferring them to
the mouth, or more rarely perhaps by their transference from the
intestine into the stomach through vomiting.

In the measle form the parasite may occur in any organ of the body, but
is mostly found in the muscles and subcutaneous tissue. Its
pathological significance depends on its number and position. Located
in the nerve-centres, it may occasion the most serious consequences.
Usually it occurs in small numbers and gives rise to no obvious
inconvenience, and is only accidentally detected in dissection after
death. It appears to maintain its vitality for some years, but finally
dies, and undergoes degradation. Only when it can be detected in such
position as the interior of the eye or beneath the conjunctiva can the
patient be relieved by surgical aid. Elsewhere, even if its presence is
suspected, it is ordinarily beyond the reach of medical treatment. The
writer a few years since, in dissecting the body of a colored man to
illustrate his lectures on the muscles, found two living measles, of
which one was in the diaphragm and the other in the transversalis
muscle of the abdomen, but none were detected elsewhere. The parasite
unquestionably gave no inconvenience to its host during life.

       *       *       *       *       *

Other species of Taenia which have been observed as parasitic in the
human intestine are mostly of rare occurrence.

       *       *       *       *       *

TAENIA CUCUMERINA, the common tape-worm of the dog, and TAENIA
ELLIPTICA, the common tape-worm of the cat, are very much alike in
appearance, and are regarded by many authorities as the same species.
They occur frequently in considerable numbers in these animals, living
in the small intestine. They have also been occasionally found in man,
especially children.

It is a comparatively delicate worm, chain-like in appearance, ranging
from four inches to a foot in length. The head is provided with four
suckers and a prominent rostellum armed with about sixty hooks. The
neck and anterior part of the body are thread-like. The mature segments
are elliptical in outline or like a melon-seed, whence the name. There
is a double set of sexual organs, and a genital orifice occupies the
middle of both lateral margins of the segments. The ripe segments
become readily detached and creep actively in the intestine, and are
either expelled with the feces or they spontaneously creep from the
anus. The eggs are comparatively few and measure 0.05 mm.

Late researches appear to show that the eggs adhering to the hair about
the anus or elsewhere are eaten by lice of the same animals, and within
these insects undergo further development. The dog and cat,
subsequently swallowing the lice, infect themselves with the mature
worms. Thus also persons, especially children, from too great
familiarity with these animals, directly or through their food, may
likewise become infected.

       *       *       *       *       *

TAENIA NANA, the Dwarf tape-worm, has been observed but once. It was
discovered by Bilharz, in Egypt, in a boy who died of meningitis. It
{938} is a little worm, about half an inch in length, and occurred in
large numbers in the duodenum.

       *       *       *       *       *

TAENIA TENELLA.--This is another small species, which has been but once
observed. It is described by Cobbold, who suspects it to be derived
from measles of the sheep.

       *       *       *       *       *

TAENIA FLAVOPUNCTATA is also a small species, from eight to ten inches
long, with ripe joints about one millimeter long and from one and a
half to two millimeters broad. It is described by Weinland, and has
also been but once observed. A half-dozen specimens were discharged
from a healthy child, of nineteen months, in Boston, Mass.

Since the above was written the author has had the opportunity of
examining some little tape-worms which he suspects to be of the same
kind as the former. They occurred in the practice of T. V. Crandall in
Philadelphia, and were expelled from a child of three years of age
after the use of santonin. About a dozen fragments appear to have
pertained to three worms, from twelve to fifteen inches in length. The
head in all was lost. The anterior part of the body is thread-like, the
posterior part about two and a quarter millimeters wide. The width of
the joints is more than twice the length. The ripe joints are pale
brown, and are remarkable for the comparative simplicity of the uterus,
which is distended with brown eggs. A peculiarity of the worm is the
repeated but irregular alternation of fertile with sterile joints.[1]

[Footnote 1: _Amer. Journ. of Medical Sciences_, 1884, p. 110.]

The species is probably more common than might be supposed, and from
its small size, and perhaps harmless character, has generally escaped
notice.

       *       *       *       *       *

TAENIA MADAGASCARIENSIS.--This species, described by Davaine, is
imperfectly known. Fragments of the worm have been twice observed in
the Comoro Islands.

       *       *       *       *       *

BOTHRIOCEPHALUS LATUS.--SYNONYMS: Dibothrium latum; Taenia lata; Broad
tape-worm.

This tape-worm, of another genus than the preceding, is a common
parasite of man in certain localities of Europe, but has not been found
as an indigenous product elsewhere. It occurs especially in Sweden and
Russia, East Prussia, Poland, and West Switzerland. In the latter
country it prevails to such an extent that it is reported that about
one-fourth of the inhabitants of Geneva are thus infested. Among the
tape-worms submitted to the writer from time to time for identification
a few years ago was a large specimen of Bothriocephalus latus, but it
proved to have been derived from a Swede who had arrived in this
country only a few months previously.

There are many species of Bothriocephalus, which in the adult condition
mainly live in fishes. The genus is distinguished from Taenia by many
points, chiefly in the form and construction of the head, the form of
the joints and uterus, and the position of the genital aperture, which
is situated centrally on one of the broad surfaces instead of the
lateral margin.

{939} The broad tape-worm is the largest of the tape-worms infesting
man, a full-grown specimen reaching to twenty-five feet in length with
a breadth of three-fourths of an inch, and consisting of upward of four
thousand segments. It is a soft, grayish, flat, band-like worm, with
head, neck, and segmented body holding the same proportions as in the
other tape-worms. The head is elongated, clavate, and is provided with
a long, narrow, elliptical sucker on each side. The narrower neck is
short and merges into the segmented body, which gradually widens to
half an inch or more. As the segments successively enlarge, they
increase proportionately to a greater extent in breadth, so that their
width for the most part measures from two to four times their length. A
few toward the end of the series become narrower and longer than those
in advance. In the ripe segments the uterus, distended with brownish
eggs, forms a central rosette-like group of pouches. The genital
aperture is central in the broad surface of the segments, and is always
on the same or ventral side.

The broad tape-worm inhabits the small intestine, and is usually found
single, but occasionally several together, and sometimes also in
association with one or both the other common tape-worms. The species
is also reported to be not infrequent in the dog.

Ripe portions of the broad tape-worm become detached in fragments of
variable length, to be discharged with the feces. The partially-emptied
appearance of the uteri in these fragments indicates the laying of the
eggs previous to the expulsion of the latter. The eggs are oval, of a
light-brown color, and measure about 0.07 mm. long. The shell at one
pole is furnished with an operculum or lid for the escape of the
embryo. This is developed subsequently to the discharge of the eggs
from the intestine. If the eggs are placed in water, in the course of
some months the embryos are developed and escape from the shell. The
embryo is a round or oval body furnished with three pairs of spicules,
as in that of the Taeniae, but differs in possessing a ciliated
envelope, by means of which it freely swims about in the water. After
some days the embryo discards its envelope and creeps about in an
amoeboid manner. Further than this, until recently, the fate of the
embryo was unknown. Braun of St. Petersburg, after determining the
presence of scolices of Bothriocephalus in the muscles, liver, and
organs of generation of the pike, trout, and eel-pout, by feeding these
to cats and dogs succeeded in rearing worms which differed in no
respect, except in being smaller, from the Bothriocephalus latus of
man. Such being the case, it becomes evident that man may ordinarily
become infested with the parasite by eating raw or insufficiently
cooked fishes of the kind mentioned.

       *       *       *       *       *

BOTHRIOCEPHALUS CORDATUS, described by Leuckart as a common species
infesting the dog in Greenland, has been reported as having once been
found in a woman. Bottger regards it as not distinct from
Bothriocephalus latus.

       *       *       *       *       *

BOTHRIOCEPHALUS CRISTATUS.--This species, but once observed, is
described by Davaine. It was passed by a child in Paris, and the worm
was upward of nine feet in length.

       *       *       *       *       *

SYMPTOMS OF TAPE-WORMS.--Whichever may be the species of {940}
tape-worm infesting the human intestine, the symptoms to which it gives
rise are mainly of the same character, modified of course in degree by
the size and number of the parasites and the susceptibilities of the
patient. Clinging by means of the head to the mucous membrane of the
intestine, and involved among the valvulae conniventes and villi, the
worm may extend in loose folds along the greater part of the course of
the intestine or lie coiled in an elongate mass. Besides being rendered
evident from time to time by the discharge of segments or fragments,
the beef tape-worm especially sometimes introduces itself to the notice
of its host through the segments creeping from the anus. Sometimes
segments of tape-worms are vomited, especially in women; and the
exhibition in this way, especially of the pork tape-worm, is to be
deplored, for should segments be retained in the stomach the patient
becomes further liable to be affected with measles or cysticerci.

Some persons continue infested with a tape-worm a long time without
suspecting its existence and with little or no inconvenience, and
perhaps first become aware of its presence by the accidental discovery
of segments discharged from the bowels. Usually, however, the parasite
creates more or less disturbance, and not unfrequently occasions great
discomfort. The symptoms are both local and of a general nature.
Itching at the extremities of the alimentary canal and various
dyspeptic symptoms are common; uncomfortable sensations in the abdomen,
uneasiness, fulness or emptiness, feeling of movement attributed to the
worm, and colicky pains; disordered appetite, sometimes deficient,
oftener craving; paleness, discoloration around the eyes, furred
tongue, fetid breath, and sometimes emaciation; fulness of the
forehead, dull headache, buzzing in the ears, twitching of the face,
and dizziness; often uncomfortable feelings in the abdomen increased by
fasting, which are temporarily relieved by taking a full meal. Certain
kinds of food also at times appear to produce greater uneasiness,
apparently due to more than usual disturbance of the parasite. Symptoms
of a more grave character are sensations of fainting, chorea, and
epileptic fits. Others of a chlorotic and hysterical character are not
unfrequent, especially in women, who also may suffer more or less from
uterine disorder.

All the ordinary symptoms are quickly relieved by the expulsion of the
tape-worm--permanently if it is entirely removed, but temporarily, as
is frequently the case, when only the greater bulk of the parasite is
discharged and the head continues to remain securely attached to the
intestine and ready to renew its many-segmented body. The tape-worms
are capable of a wonderful amount of extension from traction without
detachment; and from the delicacy of the neck and the anterior part of
the body, and the action of medicine on the peristaltic motion of the
intestine, the posterior part of the worm, including its great bulk, is
most apt to be torn away and discharged, while the head remains. So
long as this is the case, and the worm has not been poisoned or killed,
the anterior portion grows, and thus the parasite is renewed and
accompanied by a return of all the former symptoms. Under the
appropriate treatment the evacuations of the patient should be
carefully inspected, so as to satisfy both physician and patient that
the parasite has been completely expelled. To properly examine the
evacuations, they should be repeatedly drenched with clear water, and
the sediment, after the settling {941} of the washings, must be
inspected. It is only when the physician has seen the head of the
parasite that he can reasonably ensure his patient a permanent cure.

       *       *       *       *       *

TREATMENT.--To get rid of tape-worms many remedies have been employed,
though comparatively few retain a reputation for positive success. Some
act by powerfully operating on both bowels and worms, producing the
detachment and discharge of the latter without killing them, as is
often indicated in the lively movements they exhibit after their
expulsion. Others poison and kill the worms, and also cause their
detachment and expulsion from the bowel.

Before the administration of the appropriate medicine for tape-worms,
with the object of rendering it more effective it is advisable to bring
the alimentary canal into a condition which will render the parasites
most vulnerable. For this purpose fasting is to be recommended for
several days previously, and when food is used it should be in moderate
quantity, and of such a character as to leave little residue to
accumulate in the intestine. Wheat bread, the ordinary meats, milk and
coffee, are best, while the usual vegetables should be avoided.

One of the most effective remedies is the oil of turpentine in the dose
of one or two fluidounces, made into an emulsion with white of egg and
sugar; children require about half the quantity. The large dose is less
apt to produce the usual objectionable effects of that medicine than
small ones. The only inconvenience caused by it is the heat of the
stomach, some febrile excitement, and fulness of the head or headache
lasting for one or two days. The effects are more apt to occur when the
medicine does not act as a cathartic. The oil usually operates quickly,
killing the worm and producing its discharge. If it does not act in the
course of two or three hours, a full dose of castor oil may be given,
and, if necessary to aid the action of this, enemata may be employed.
To ensure the purgative action of the oil of turpentine it may be
advantageously associated with the castor oil, of each a fluidounce
made into an emulsion.

Another and effective remedy is the root of the male fern, Aspidium
filix-mas, used in decoction or electuary. Stein of Frankfort
recommends the ethereal extract as the best preparation, and prescribes
it in doses of from seven to ten grammes, enclosed in half the number
of gelatin capsules and administered at short intervals within half an
hour. It should be taken in the morning fasting, after taking a cup of
coffee, swallowing the capsules with the aid of a second cup. Half an
hour after the capsules are taken a mixture of castor oil, brandy, and
ginger syrup, of each fifteen grammes, should be administered. The
treatment has proved all that could be desired, and the worm, including
the head, is discharged altogether, rolled into a ball.

The bark of the pomegranate-root, Punica granatum, is also a powerful
and efficient remedy, but often proves very disagreeable from its
producing violent pains in the abdomen, with nausea and vomiting. It
also generally purges, occasioning the discharge of the worm.
Kuchenmeister prefers it to any other medicine, given in the form of
decoction prepared by macerating three ounces of the fresh bark in
twelve fluidounces of water for twelve hours, and concentrating the
infusion by gentle heat to one-half. He recommends it to be taken after
fasting a day and the {942} administration at night of two fluidounces
of castor oil. It is to be given in three or four doses within an hour.
Should the medicine not purge, it should be followed by another dose of
castor oil.

Recently, Feraud has recommended the tannate of pelletierin, the
alkaloid of which is derived from the pomegranate-root, as the most
powerful of remedies for tape-worm, the dose for an adult being
one-half to three-fourths of a grain. The patient should fast a day on
bread and milk, and the following morning, before rising, take an
infusion of one-third of an ounce of senna. This should be followed an
hour later by half the medicine diffused in a little water, and the
patient should remain quiet in bed to avoid nausea and vomiting. Half
an hour later the rest of the medicine is to be given, followed in
another half hour by a dose of castor oil. Should there be no stool
after an hour, purgative enemata may be used. In one case twelve beef
tape-worms were discharged together measuring, collectively, fifty
meters.

Kousso, the flower of Brayera anthelmintica, an Abyssinian herb, has
been of late much employed as a remedy for tape-worms, but with many
physicians of experience it has lost favor. Heller speaks of it highly,
and recommends it to be taken in the morning, an hour after the patient
has taken coffee. The dose is from half an ounce to an ounce, and is
conveniently taken in compressed balls or disks, coated with gelatin,
and swallowed at intervals in the course of an hour, aided by mouthfuls
of coffee. Any disposition to vomit should be repressed, which is
rendered easier by taking small mouthfuls of strong coffee or pieces of
ice.

Koussin, an alcoholic preparation of kousso, is also efficient, and has
the advantage over the latter that it does not occasion nausea. It has
been used in the medical clinic of Munich in the dose of 30 grains, and
it has been a very rare occurrence that the result was not all that
could be desired.

The seeds of the common pumpkin, Cucurbita pepo, are extolled by many
physicians as a remedy for tape-worms; and the writer has twice had the
opportunity of observing large specimens of the beef tape-worm which
were expelled after the administration of this medicine. The dose is an
ounce of the seeds bruised into a paste and made into an emulsion. It
should be taken in the morning, fasting, and followed in an hour or two
with a full dose of castor oil.

Santonin, a principle derived from santonica, Artemisia maritima, is
reported as a remedy for tape-worms, but its efficacy has also been
denied. The dose is from two to four grains for an adult, and from
one-quarter to one-half a grain for children over two years. It is best
administered in lozenges prepared with sugar and tragacanth.

The quinia sulphate has also been recommended as an effectual remedy
both in tape- and seat-worms.

As regards the prophylaxis of tape-worms, there are some important
points to which we direct attention.

The evacuations of patients containing tape-worms, their segments and
eggs, should not be carelessly thrown away, at least in places
accessible to animals which may become infected. They should be treated
with boiling water, the heat of which is sufficient to kill all animal
parasites. The handling of living tape-worms and segments should be
avoided, as eggs {943} which may adhere to the hands, if transferred to
the mouth and swallowed, will produce infection.

Meats visibly infested with measles are not fit and should not be used
as food. Raw meat should altogether be discarded as food, both for the
sick and well, and all meats should be thoroughly cooked. As a rule,
meat should not be used so long as it appears red or on cutting emits a
bloody liquid. A large piece of meat requires long boiling or roasting
for sufficient heat to penetrate to the interior to destroy any
parasites that may be present. Even salted meats and hams should be
cooked to ensure against parasitic infection. It is important also to
avoid food prepared by uncleanly persons who may be infested with
tape-worms.

As regards our domestic animals, which are the common source of the
infection of man with tape-worms, they should also be protected from
infection as far as possible. This is to be done by preventing them
from having access to human excrement. As Heller remarks, with this
object the barbarous custom of defecating in every place promiscuously
should be put down with a high hand.[2]

[Footnote 2: Several years since a physician of Texas sent to the
writer a piece of pork, making inquiry as to its condition, and stating
that all the pigs of his vicinity were diseased and their flesh
similarly affected. It contained a number of measles or larval
tape-worms. On giving the information and the probable cause of the
affection of the pigs, the doctor reported in return that there was not
a privy in his village. Until our people are more careful with the
raising of pigs, European governments will have reason for prohibiting
the importation of our pork.]

       *       *       *       *       *

TAENIA ECHINOCOCCUS.--SYNONYM: Hydatid tape-worm.

Larval condition: Echinococcus; E. hominis; E. veterinorum; E.
granulosis; E. scolicipariens; E. altricipariens; E. hydatidosus; E.
multilocularis; E. cyst; Hydatid; Hydatid cyst; Acephalocyst.

This tape-worm, in its mature state the most insignificant looking of
its kind, though not strictly an intestinal worm of man, in the
juvenile condition is one of his most dangerous parasites, as being the
source of hydatid tumors. The adult tape-worm lives in the small
intestine of the dog and wolf, in some localities often existing in
these animals in thousands together. From its diminutive size it may be
readily overlooked, concealed or obscured by the villi among which it
is suspended to the mucous membrane. It is about a fourth of an inch in
length, and consists of but four segments, of which the last alone
exhibits the ripe condition. The head resembles in construction that of
the pork tape-worm, being provided with four suckers and a prominent
crown, with from thirty to fifty hooks arranged in a double circle. The
terminal ripe segment exceeds in size all the preceding together, and
before it separates from the series another is ready to take its place.
The ripe eggs contain the usual six-spined embryo as in other
tape-worms.

The mature worm is remarkable for the comparative shortness of its
life, which, according to Siebold, is about seven weeks. Apparently to
compensate for the small number of its segments, the larval form is
endowed with the power of multiplying itself to a wonderful degree.

It is only in the larval condition that the hydatid tape-worm infests
man, and in this state also it infests the ape, the ox and sheep and
other ruminants, also the horse, hog, and indeed many other animals of
the same class.

{944} If the eggs of the tape-worm are swallowed, which may readily
happen by too free intimacy or association with infested dogs, the
liberated embryos obtain access to the intestine. Penetrating the
mucous membrane, the embryos thence may migrate to any part of the
body. From the comparative frequency of hydatid tumors in the liver we
may suspect they mostly enter the portal venous system and take the
course of the blood-current. It is, however, probable that they migrate
directly to their destination, for hydatid tumors are also frequently
seated in the neighboring organs and the abdominal walls. The embryo
tape-worm, once fixed in position, becomes the starting-point of a
hydatid tumor.

When dogs are fed on the liver, or other parts affected with hydatid
tumors, from the sheep or other animals, the scolices are liberated,
and, passing into the small intestine, are there developed into the
mature tape-worms.

Hydatid tumors occur in any of the organs of the body, but are more
frequent in the liver than in all others together. They are common in
the lungs, kidneys, spleen, omentum, and subperitoneal tissue of the
abdominal walls. They are less common in the heart, brain, spinal
canal, the pelvic viscera, and the bones. Mostly but a single tumor is
found in the same person, but occasionally several occur together in
the same or in different organs.

There are several varieties of the hydatid tumor. In man the more
common form consists of a cyst or a group of cysts enclosed in a
connective-tissue envelope induced by the presence of the parasite. The
simple cyst is produced through the transformation of the echinococcus
embryo, and the group of cysts is derived from the former by
proliferation; and hence the first has been called the parent cyst, and
the others the daughter cysts. These also in the same manner may
produce a third series, called granddaughter cysts. The parent cyst, at
first spherical, becomes modified in shape according to the space it
occupies and the resistance to which it is subjected, thus assuming an
oval, lobulated, or other form. It may increase in size to that of a
cocoanut or larger, and may remain simple, but usually is compounded by
proliferation in the production of daughter cysts. These may be few or
many up to hundreds, and range from a minute size up to that of a
walnut, and are spherical or modified in shape by mutual pressure or
other cause. The cysts are filled with a clear watery liquid of saline
taste, but without albumen.

The hydatid cysts are usually composed of an outer thick, translucent,
homogeneous, laminated, glistening, highly elastic membrane, the
ectocyst, and an inner thin, granular, and cellular layer, the
endocyst. From the endocyst originate minute buds, which become the
brood-capsules of the larval worms or scolices. These form little
groups of a few to a dozen individuals suspended within the
brood-capsules, but capable of eversion from them. The individual
scolices, which appear to the naked eye as mere white points, have the
form and construction of the head-segment of the mature Taenia
echinococcus. After death or by violence they become easily detached,
and then float free in the liquid containing them. In some cases the
echinococcus cysts develop no scolices, in which condition they
constitute acephalocysts. Occasionally the echinococcus embryo
undergoes imperfect development, constituting the multilocular hydatid
tumor, rarely found elsewhere than in the liver.

{945} Echinococcal tumors, especially those which have many daughter
cysts, when accessible are remarkable for exhibiting a tremulous
movement when grasped by the hand and quickly tapped with the finger.

Infection through the embryonic form of the Taenia echinococcus, as the
source of hydatid tumors, is productive of the most disastrous
consequences, and has ended in the destruction of many lives both of
men and domestic animals. The parasite is not directly productive of
suffering, but its effects and dangers are proportioned to the size of
the tumor it occasions and the character and importance to life of the
organ in which the latter is situated. With the increase of the hydatid
tumor, usually of very slow growth, it encroaches upon the surrounding
parts, and if these are not displaced they become disorganized and
atrophied.

The liability and frequency of infection with the hydatid disease
appear to be proportioned to the prevalence of intimate association
with the dog. In Iceland, in which it is said every peasant owns half a
dozen dogs, which share his dwelling with him, it is also reported that
one-sixth of all the deaths are due to the hydatid parasite.

Ordinarily, the hydatid disease is beyond the reach of medical
treatment. The mercurials and potassium iodide have been recommended,
but the results are very doubtful. Apparently as an indication how
little hydatid parasites may be influenced by medicine, the following
incident will show: The writer once received for dissection the body of
an English sailor which had been injected with zinc chloride for
preservation. In the abdominal wall in the right iliac region there was
a hydatid tumor the size of a fist. On examination of the tumor it was
found full of daughter cysts, and these contained living scolices,
though the man had been dead several days and the tissues were bleached
by the zinc solution.

Favorable results in the treatment of hydatid tumors are only to be
expected through surgical means when they are accessible.

As a prophylactic measure against infection the avoidance of too
intimate association with dogs is especially to be recommended.

In concluding the chapter on Taenia echinococcus, as a prophylactic
against this and other parasites Cobbold gives the advice that "all
entozoa which are not preserved for scientific investigation or
experiment should be destroyed by fire when practicable, and under no
circumstances whatever should they be thrown aside as harmless refuse."

       *       *       *       *       *

TAENIA ACANTHOTRIAS.

Larval condition: Cysticercus acanthotrias.

This species has been but once observed, and only in the larval
condition or that of the scolex, which was first described by Weinland.
About a dozen specimens were found by Jefferies Wyman of Boston in the
body of a woman of Virginia who died of phthisis. They were situated in
the connective tissue beneath the skin and in the muscles, except one,
which was attached to the dura mater. The scolex is distinguishable
from that of the other human tape-worms in possessing a triple circle
of hooks. The mature form of the worm remains unknown.


{946} The Trematodes, or Fluke-worms.

The trematodes or fluke-worms, though allied to the tape-worms, differ
in many important characters. In the mature condition, like the latter,
they are solid worms or are devoid of a body cavity or coelum, and are
with rare exceptions hermaphroditic. They are, however, never compound,
but simple or consist of single individuals, and are provided with a
mouth and alimentary canal, but this is closed or is without an anal
aperture. They have a water vascular system, communicating with the
exterior by a pore at the posterior extremity of the body. They are
commonly of flat, elliptical shape, with a sucker-like mouth at the
fore end, and with a second sucker situated ventrally near the middle.

The fluke-worms are remarkable for their successive transformations and
course of life, and, like the tape-worms, they pass the different
stages of their existence in different animals. A number of species
have been described as infesting man, but most of them are,
fortunately, of rare occurrence.

       *       *       *       *       *

DISTOMUM HEPATICUM.--SYNONYMS: Fasciola hepatica; Liver-fluke.

This species, the common liver-fluke, occasionally occurs in the human
body, but is especially frequent in the sheep and other ruminating
animals, as the ox, goat, and deer, and it likewise occurs in the
horse, hog, and some other animals. It usually inhabits the liver,
occupying the bile-ducts, but is also sometimes found in the portal and
other veins and in the intestine, and more rarely in abscesses beneath
the skin. It is the cause of the affection in sheep called rot, of
which many thousands die annually.

The liver-fluke is a flat, tongue-shaped, brownish worm about an inch
long and about half as wide. It is invested with minute scale-like
spines. The head end is somewhat prolonged, and terminates in a small
oral sucker, a short distance behind which is a small ventral sucker.
The intestine is forked and much branched. The genital aperture is
situated between the oral and ventral suckers. The commonly yellowish
eggs are numerous and large, oval, and measure about 0.135 mm. long.

The common liver-fluke frequently occurs in large numbers, even
hundreds, in the liver of the sheep, obstructing the bile-ducts and
occasioning more or less destruction of the organ. The eggs pass off
with the bile into the intestine, and are discharged with the
excrement. In water the eggs are hatched, and deliver a ciliated and
freely-swimming embryo. This in favorable positions, such as marshy
pastures, obtains access to small fresh-water snails and penetrates to
the interior of their body. Here the embryo sheds its ciliated
integument and is transformed into a sporocyst. This is an elliptical
pouch containing reproductive bodies, which become developed into
individuals of more elongated form than the sporocyst, provided with a
mouth and stomach, and named redias, or nurses. The nurse penetrates to
the liver of the snail, and there develops within itself new forms
called cercarias, which resemble the parent fluke-worm, but are
provided with a long, powerful tail and have no apparent generative
apparatus. The cercaria escapes through an aperture of the nurse, and
makes its way out of the snail into the water, where it swims about
actively by means of the tail, much in the manner of a tadpole. {947}
The cercaria after a time fixes itself to a submerged plant, becomes
encysted, shakes off its tail, and remains in a quiescent state. If in
this condition, in the feeding of sheep or other animals, the tailless
cercaria or incipient fluke-worm is transferred to the stomach, it
makes its way to the liver, and there grows and is developed into the
sexually mature worm.

Recently it has been ascertained both in England and Germany that the
juvenile state of the fluke-worm is passed especially in the little
fresh-water snail Lymneus truncatulus. As, however, the common
liver-fluke occurs in America, while the last-named species of Lymneus
does not, it is rendered probable that the juvenile condition of the
parasite also occurs in other species of snails. Incidentally, the
writer may here mention that he has found certain of our smallest
fresh-water snails, such as Planorbis parvus, frequenting meadows in
the vicinity of our rivers and creeks, swarming with nurses of several
different species of fluke-worms.

Notwithstanding the frequency of the common liver-fluke in the sheep
and other domestic animals, its occurrence has been rare in man, and in
all the cases reported it has been few in number, either single or from
two to half a dozen. In man it has been found to occupy the bile-ducts,
the portal vein, and abscesses beneath the skin.

       *       *       *       *       *

DISTOMUM LANCEOLATUM.--SYNONYM: Smaller Liver-fluke.

This species, much smaller than the preceding, is of lanceolate form,
acute behind, smooth, and about a third of an inch long. Its suckers
are moderately large, and the bifurcate intestine is unbranched. It
infests the liver of the sheep and ox and some other animals, and not
unfrequently is found in association with the former species. It
usually does not occur in such great numbers together as in the latter;
from which and other circumstances, as the smaller size and smooth
investment, it does not produce the same serious results. Its
continuous history remains unknown, though it is probable that its
course is similar to that of the common liver-fluke. Several cases are
reported of its occurrence as a parasite in man.

       *       *       *       *       *

DISTOMUM SINENSE.--Under this head Cobbold has recently described a
species somewhat larger than the D. lanceolatum. It occurs in the liver
of Chinese.

       *       *       *       *       *

DISTOMUM CONJUNCTUM.--Another species described by Cobbold under this
name, originally found in the liver of an American fox, has also been
detected in man. The worm is about one-fourth of an inch long.

       *       *       *       *       *

SYMPTOMS.--Cases of fluke-worms in the human liver have occurred so
rarely that we are not prepared to indicate with certainty what may be
the nature of the peculiar symptoms. If the parasites were numerous,
they would give rise to more or less obstruction of the bile-ducts,
with accumulation of bile, accompanied with jaundice and other symptoms
usually attendant on functional disturbance of the liver. As in sheep,
they would occasion dilatation of the bile-ducts, catarrhal
inflammation, incrustation with biliary matters, hyperplasia of the
surrounding {948} tissues, and more or less disorganization and atrophy
of the secretory structure.

TREATMENT.--As regards the treatment, we can say almost nothing. In the
destructive disease of rot in sheep there are no known means to expel
the parasites from the liver. If present in man, as they occur but few
in number, we may hope for their spontaneous expulsion in due time
without leaving any serious result. As a means of prophylaxis persons
should carefully avoid salads prepared from subaquatic vegetables, like
cress, which may harbor little fresh-water snails.

       *       *       *       *       *

DISTOMUM HETEROPHYES.--This is a small species, about half a line long,
with the fore part of the body covered with minute spines, and having a
large, nearly central, ventral disk. It has been but once observed, and
was reported by Bilharz, in Cairo, as having been found, in the
post-mortem examination of a boy, in the small intestine, in which it
existed in hundreds.

       *       *       *       *       *

DISTOMUM CRASSUM.--This is the largest of the fluke-worms infesting
man, and measures from one to three inches in length. It is elliptical,
comparatively thick, and smooth. The two suckers have nearly the same
relative size and position as in the D. hepaticum. It inhabits the
duodenum, and has been observed a number of times infesting inhabitants
of China and India.

       *       *       *       *       *

DISTOMUM RINGERI.--A species by this name, about half an inch long, has
recently been described by Cobbold as infesting the lungs of people in
Formosa and China.

       *       *       *       *       *

DISTOMUM OPHTHALMOBIUM.--A minute species, described under this name,
has been detected several times in the human eye.

       *       *       *       *       *

BILHARZIA HAEMATOBIA.--SYNONYM: Distomum haematobium.

As a human parasite this is the most important of the fluke-worms,
being the most common and dangerous. It is apparently restricted to
Africa and Arabia, and is especially frequent in Egypt, Abyssinia, the
Cape of Good Hope, and Natal. So far as known, it is peculiar to man
and monkeys, and inhabits the veins, especially those of the portal
system, and it lives on the blood.

The blood fluke-worm is remarkable among its kind in having the sexes
distinct. The female is slender, cylindrical, and tapering toward the
ends, looking more like an ordinary thread-worm than a fluke-worm, and
is about three-fourths of an inch long. The male is about half an inch
long, but wider than the female, which it partially embraces at
maturity by doubling upon it laterally.

This parasite, of the same essential nature as the more ordinary
fluke-worms, is most probably introduced in the juvenile condition into
the stomach by drinking unfiltered standing waters, and perhaps also by
eating vegetables which grow in wet places and upon which the young
fluke-worms may be encysted. From the stomach the worms gain access to
the portal venous system, within which they undergo development to
sexual maturity. The worms, proportioned to their number, {949}
occasion more or less sudden and dangerous haematuria. According to
Bilharz, who first discovered the parasite, it also induces
inflammation of the ureters, bladder, and rectum, accompanied with
ulceration and incrustations and concretions in the same, due to the
abundant deposit of eggs in the mucous membrane. The symptoms in the
haematuria are obvious; all treatment fails, but the prophylaxis is
evident.

       *       *       *       *       *

AMPHISTOMUM HOMINIS.--The genus Amphistomum is distinguished from
Distomum in having the ventral disk placed at the posterior extremity
of the body.

A species has been recently described by Cobbold under the above name,
and is reported as having been observed several times in natives of
India. It is a red worm, about the fourth of an inch long, and inhabits
the caecum and ascending colon, in which it was found in hundreds
together. The mucous membrane exhibited venous congestion and was
marked with numerous red spots resembling leech-bites, produced by the
parasites. One of the patients died of cholera.

We have too little information as to the symptoms induced by this
parasite, and of its treatment, to say anything. It is probable that
calomel, turpentine, and castor oil would be appropriate remedies.

Several other fluke-worms which have been reported as having been found
in the human body are generally viewed with doubt as to their
genuineness. Such are the Hexathyridium pinguicola, from a tumor of the
ovary; the H. venarum, said to have been found in the blood and in the
sputum of haemoptysis; and the Tetrastomum renale, said to have been
found in the urine.


The Acanthocephali, or Thorn-head Worms.

The thorn-head worms in the mature condition are comparatively robust
cylindrical worms, with a body-cavity or coelum, but devoid of mouth
and alimentary canal. They are provided with a protrusile and
retractile proboscis-like head armed with circular rows of recurved
hooks, by which they firmly cling to the wall of the intestine of their
host. The sexes are distinct. There are many species, which mostly in
the mature state live in fishes. In the juvenile or larval condition
they live in other animals, mostly crustaceans and insects. It is
doubtful whether any species naturally infests man.

       *       *       *       *       *

ECHINORHYNCHUS GIGAS.--The great thorn-head worm is a common parasite
of the hog, living in the small intestine. It is a large white worm,
the female of which reaches a foot in length, while the male is about
one-third the size. It is doubtful whether it occurs as a human
parasite, though a worm less than the fourth of an inch found in a man
in Prague has been attributed to this species.


The Nematodes, or Thread-worms.

The nematodes, or thread-worms, are slender, cylindrical, and
inarticulate, and usually more or less tapering toward one or both
extremities. {950} They have a distinct coelum or body-cavity, with
thick muscular walls limited by a transparent elastic, chitinous
integument, which is sometimes more or less distinctly and regularly
transversely wrinkled. The alimentary canal extends the length of the
coelum, with the mouth at the anterior extremity, and usually an anus
at or near the posterior extremity. In some forms in the mature
condition the intestine is atrophied and the anus absent. The sexes are
distinct, and commonly the male is very much smaller than the female.
The organs of generation occupy the coelum along the sides of the
intestine. The female aperture is commonly situated ventrally near or
in advance of the middle of the body, while the male aperture is at or
in the vicinity of the anus. Mostly, the worms are oviparous, but many
are viviparous. The development is direct, and usually the
transformations are inconspicuous, so that the embryos mostly differ
but little from the parent, except in the absence of the generative
apparatus.

       *       *       *       *       *

OXYURIS VERMICULARIS.--SYNONYMS: Ascaris vermicularis; Seat-worm;
Pin-worm; Maw-worm; Maggot-worm; Thread-worm; Ascarides.

The seat-worm is the most common intestinal parasite of man, prevails
everywhere, and is peculiar to him. It is a lively, wriggling creature
which inhabits the small and large intestines and feeds on their
contents. It frequently occurs in large numbers together, and in such
cases incessantly makes its appearance, associated with multitudes of
eggs, in the evacuations.

The female, which is ordinarily seen alone in the greatest abundance,
is a white cylindrical worm tapering toward both extremities. The head
end is thickened, and is provided with three prominent labial papillae
enclosing the mouth. The posterior end extends from the anal aperture
in a long and straight, narrow, conical, sharp-pointed tail. The double
uterine tube, distended with eggs, terminates in a vagina, the external
aperture of which is situated ventrally near the anterior third of the
body. The smaller male hardly tapers behind, but is incurved and ends
in a short, blunt, conical tail. The penis is a single chitinous
spicule, the end of which is usually seen projecting from the cloacal
aperture.

The young seat-worms, in various degrees of growth and development, and
the mature males are chiefly to be met in the lower portion of the
small intestine, while the pregnant and mature females chiefly occupy
the caecum.

The seat-worm is exceedingly prolific, it being estimated that a single
ripe female contains from 10,000 to 12,000 eggs, and these, it is
suspected, may be renewed several times before her functions become
exhausted. From time to time the ripe females proceed along the large
intestine to the rectum, in which position they lay most of their eggs.
These are discharged, together with many of the worms, in the feces.

The eggs are ovoid in shape and about 0.05 mm. long. After they are
laid under favorable conditions the embryos are rapidly developed. Left
in water, they soon die.

The investigations of the helminthologists of the day make it appear
that it is necessary that the eggs of the seat-worm should be swallowed
{951} and pass through the stomach, in which the embryos are freed,
before they can undergo development to sexual maturity. Moreover,
observations go to show that infection may, and probably ordinarily
does, occur from eggs scratched from the anus and conveyed to the mouth
directly or by being applied to food from uncleanly hands. It is
evident that itching of the anus, induced by the presence of the
parasites in the rectum, often accompanied by itching of the nose and
lips, may lead to alternate scratching of the parts and the
transference of eggs from one to the other. Thus, too, uncleanly nurses
who may be infested with seat-worms after scratching may handle food
and infest children under their charge. Children are commonly more
liable to the parasites than others, no doubt from the circumstance
that they are less capable of avoiding the conditions favorable to
infection. Seat-worms prevail in all conditions of society, but their
prevalence is largely proportioned to the more or less uncleanly
habits. Persons sleeping with others infested are liable to infection,
especially if they are uncleanly and in the habit of eating in bed.
Obvious hints to avoid the parasites are obtained by regarding the
statements thus given.

SYMPTOMS.--The presence of a few seat-worms is usually attended with no
obvious inconvenience, and they may remain unnoticed unless
accidentally observed in the evacuations. The symptoms occasioned by
them are in great measure proportioned to their quantity and the
susceptibility of the patient. The most prominent symptom is excessive
itching of the anus; often trifling or even absent during the day, it
becomes very annoying and distressing in the evening or during the
night. This periodic change appears to be due to the movement of the
worms to the rectum, apparently induced by the position and repose of
the patient and the increased warmth of the body in bed. Under these
circumstances the patient attempts to relieve the incessant itching by
scratching, and often by boring with the finger in the anus. In this
way eggs become adherent to the finger-nails, under which they have
been repeatedly detected, and may thus be inadvertently transferred to
the mouth. Occasionally, some of the worms wander from the anus, and in
women may thence penetrate into the vulva. The itching of the anus may
induce more or less sexual irritation, which in the young may further
lead to onanism and its attendant evils. Other symptoms of the presence
of the parasites are itching of the nose and lips, restlessness in
sleep, grinding of the teeth, startings, twitchings, and general
nervous disturbance. When the worms are very numerous they may produce
intestinal catarrh, with discharges of mucus, pain, and diarrhoea. In
children especially they may give rise to more serious nervous
symptoms, as epileptic fits and chorea.

TREATMENT.--Generally, persons are readily relieved of seat-worms.
Epsom salt alone or with senna as a purgative, repeated once or twice,
often answers to completely expel them. Castor oil, also alone or with
a few drops of the oil of turpentine or of wormseed, is also an
effectual remedy. The tincture of aloes, in the dose of from half a
fluidounce to two fluidounces, once or twice repeated, the writer has
found to fully answer the purpose. Besides the purgatives, medicated
suppositories, in obstinate cases injections of olive oil, and enemata
of a solution of castile soap introduced by means of an elastic tube,
so as to wash out the entire length of the large intestine, may be
employed.

       *       *       *       *       *

{952} ASCARIS LUMBRICOIDES.--SYNONYMS: Round-worm; Long round-worm;
Maw-worm; Lumbricus.

The round-worm is the largest of the nematodes which ordinarily infest
man, and is second only in frequency to the seat-worm. It is a
well-known parasite, and prevails everywhere in all conditions of
society. It is less lively in its movements than the seat-worm, and is
remarkable for possessing a peculiar disagreeable odor, which is
independent of the medium in which it lives. It inhabits the small
intestine and feeds on the contents. It also infests the hog and the
ox.

The round-worm is cylindrical, reddish or brownish, and tapering toward
both extremities. The head end terminates in three prominent labial
papillae surrounding the mouth, and the tail end is short and conical.
The female, as commonly seen, ranges from six inches to a foot in
length, and is about a fourth of an inch in thickness. The ovarian
tubes are long, thread-like, and tortuous, and, with the shorter,
nearly straight, and wider uterine tubes, contain many millions of
eggs. The genital aperture is situated ventrally near the anterior
third of the body. The male is about half the size of the female, but
is capable of considerable extension, and the tail end is incurved. The
penis consists of a pair of slender, clavate, chitinous spicules, the
ends of which protrude from the cloacal aperture at the root of the
tail.

The round-worm is exceedingly prolific, it being estimated that the
genital tubes of a large mature female contain the enormous number of
60,000,000 of eggs. The ripe eggs are laid in the intestine, and are
discharged with the evacuations in great numbers, and often in
considerable masses together. They are oval, about 0.05 mm. in length,
and are provided with a thick shell and an additional tuberculate
albuminoid envelope, usually colored by the intestinal contents.

The eggs of the round-worm after being expelled from the body are very
tenacious of life, and under ordinary favorable circumstances they may
remain in a condition capable of development for several years.
Experiments have shown that they have great power in resisting the
destructive influences of heat and cold, dryness, and the agencies of
decomposition. In water and moist earth they have been retained alive
for a year or two. When ripe eggs are placed in water the development
of the embryo is observed to proceed very slowly, and is only completed
after five or six months. The embryo while still contained within the
egg sheds its skin and becomes provided with a tooth-like spine to the
head end. The smallest examples of reputed round-worms found in the
human intestine measured only about a line in length.

The further history of the round-worm is unknown, nor has it yet been
positively ascertained in what manner man becomes infected with the
parasite. Repeated experiments, not only on the hog and other animals,
but on man himself, go to show that he is not directly infected by
swallowing the recently-laid ripe eggs. It is rendered probable that
the eggs are swallowed by some common but yet unknown minute aquatic
animal, within which the embryo may undergo further development, and in
this condition may be swallowed by man in drinking-water. In
confirmation of the view that man becomes infected in the latter way,
Davaine remarks that the "people of Paris, who drink only filtered
{953} water, are rarely infected with the round-worm, which is
otherwise the case in the rural districts of France."

The round-worm is most prevalent in warm climates, and especially among
the less-civilized peoples. The better classes among the more
enlightened nations suffer comparatively little from the parasite, and
it is the lower classes, especially the ill-fed and uncleanly, who are
most afflicted. It is exceedingly frequent in the Orient, in Africa,
the West Indies, and Brazil.

Most commonly, only a few round-worms--one, two, three, up to a
dozen--occur together in the same person, but they often occur in
considerable number, even to several hundreds. Not unfrequently they
are found in association with seat-worms. They are more frequent and
usually occur in greater abundance in children, perhaps in a measure
due to the circumstance that they are less able to discriminate the
conditions favorable to infection and avoided on other grounds by
adults.

The natural and ordinary habitation of the round-worm is the small
intestine, especially the jejunum, and it commonly only occurs in the
large intestine, mostly dead, on the way to be discharged with the
evacuations. Under disturbing circumstances, as the character of
certain irritating food, the parasite is disposed to become restless
and wander from its usual position. Not unfrequently it enters the
stomach, and thence may ascend to the mouth or nose, and perhaps the
first intimation of the presence of such an unwelcome guest is in its
expulsion from the mouth. From the pharynx the worm may enter the
larynx and trachea, or advance farther into the air-passages, giving
rise to the usual symptoms of foreign bodies in these parts.
Occasionally the parasite forces its way through the bile-ducts into
the liver and gall-bladder, creating disturbance in those organs
proportioned to the number and size of the worms and the extent of
their progress. In the liver it may occasion inflammation and the
formation of an abscess attended with all the usual symptoms of
hepatitis. It has been reported that it may penetrate the intestinal
wall and enter the peritoneal cavity, but it is generally regarded as
doubtful whether the worm can do so in a healthy state of the
intestine, but only where there may be ulceration or other similar
condition.

SYMPTOMS.--The symptoms indicating the presence of the round-worm in
the intestine vary with its numbers and with the age and susceptibility
of the patient. In general, the presence of one or two worms is
unattended with any marked disturbance, and is mostly unsuspected until
the parasite is accidentally seen in the discharges. The ordinary
symptoms are disordered appetite (usually increased), flatulence,
hiccough, foul breath, dyspepsia, abdominal pains, itching at the
extremities of the alimentary canal, furred tongue, darkening of the
eyelids, and emaciation. The nervous symptoms are restlessness in
sleep, unpleasant dreams, starting in fright, grating of the teeth, and
muscular twitchings. In more aggravated cases, especially in children,
epileptic fits may occur. If the parasites are numerous, they produce
diarrhoea with copious mucus discharges, and may induce enteritis with
all its attendant symptoms. When the worms wander into the stomach,
they induce colic, nausea, retching, and vomiting, all of which
disappear with the expulsion of the parasites.

TREATMENT.--The remedies employed for seat-worms often serve to {954}
expel the round-worm, and not unfrequently the two are discharged
together. Wormseed, or the seed of Chenopodium anthelminticum, has been
a favorite remedy for the round-worm, especially in children. The dose
in these cases is one or two scruples of the powdered seeds in
electuary with syrup or molasses, administered in the morning before
breakfast and at bedtime for three or four days. It should be followed
by calomel or other brisk cathartic. The volatile oil, in the dose of
from five to ten drops in emulsion, may be used in the same manner.

A much-extolled remedy to destroy and get rid of the round-worm is
santonin, given in doses of from one-third to one and a half grains
three or four times a day, the larger dose being used only for adults.
It should be followed by a purgative, for which a dose of castor oil
answers a good purpose.

       *       *       *       *       *

ASCARIS MYSTAX, the common round-worm of the cat and dog, has been
reported as occasionally infesting man. It resembles the former
species, but is much smaller, commonly from one to four inches in
length, and has the head end furnished with a pair of lateral narrow,
wing-like expansions of the integument. It inhabits the small
intestine, and when present in man would no doubt induce symptoms like
those of the ordinary round-worms which infest him.

       *       *       *       *       *

TRIOCEPHALUS DISPAR.--SYNONYMS: Long thread-worm; Whip-worm.

The long thread-worm is a not unfrequent intestinal parasite of man,
though rarely observed unless specially sought, as it ordinarily gives
rise to little or no disturbance. It is common in England, Southern
Europe, and the Orient. Davaine reports that half the cases of persons
investigated in Paris were infested with it; it also occurs in this
country. It inhabits the lower end of the ileum, the caecum, and
vermiform appendix, and feeds on the intestinal contents. It commonly
occurs in small numbers, two or three to a dozen, occasions no evident
inconvenience, and is rarely discharged with the evacuations.

The long thread-worm is yellowish-white and cylindrical, with the
anterior half or more of the body attenuated in a hair-like manner. The
female reaches about two inches in length, has the tail end conical,
and the anus subterminal. The male is about two-thirds the length of
the former, has the thicker portion of the body enrolled, and the tail
end blunt. The eggs are laid in the intestine and discharged with the
feces. The subsequent history of the parasite and its mode of infecting
man remain unknown.

Only in cases where long thread-worms are numerous do they give rise to
trouble. According to Leuckart, Pascal gives as constant symptoms of
the presence of large numbers of the parasite, headache, redness of the
face, prominence of the eyes, small, irregular, and intermittent pulse,
and pains in the lower part of the abdomen.

The usual remedies addressed to the seat-worm and round-worm will most
probably be equally applicable to the long thread-worm.

       *       *       *       *       *

LEPTODERA STERCORALIS.--SYNONYMS: Anguillula stercoralis; Rhabditis
stercoralis.

{955} This is a minute nematode worm recently observed infesting French
soldiers in Cochin China. It is about half a line in length, and
inhabits the small and large intestine, and also penetrates into the
biliary and pancreatic ducts. It occurs in myriads and occasions
diarrhoea and dysentery. Another species, Leptodera intestinalis,
nearly three times as large, has been noticed in smaller number
associated with the former. The eggs of these worms are laid in the
intestines, and both together are discharged in multitudes with the
feces. They are probably introduced into man by drinking stagnant
water, and undergo complete development after passing through the
stomach.

It is probable that the remedies employed in the treatment of the
familiar seat-worms and round-worms would be equally efficacious in the
expulsion of these parasites.

       *       *       *       *       *

ANCHYLOSTOMUM DUODENALE.--SYNONYMS: Strongylus duodenalis; Dochmius
duodenalis; Sclerostoma duodenale.

This intestinal parasite, first noticed in Milan by Dubini in 1838, is
of more dangerous character than any of the nematode worms previously
described. In Europe, besides Italy, it was frequently observed among
the workmen of the St. Gothard tunnel. It is exceedingly common in
Egypt, and Bilharz found it in nearly all his post-mortem examinations
of bodies. It probably prevails to a considerable extent in most
tropical countries, including the East and West Indies and Brazil.
There is also reason to suspect, from the nature of the affection it
induces, that it may exist in the Southern States.

The Anchylostomum is a red, cylindrical worm, with the anterior
extremity tapering and recurved. The head end, somewhat enlarged,
encloses a capacious oral capsule armed with strong hook-like teeth.
The caudal extremity of the female ends in a conical point, and the
genital aperture is situated behind the middle of the body. The caudal
extremity of the male ends in a trilobate pouch, within which projects
the bispiculate penis. The female is from five lines to three-fourths
of an inch long; the male is about half the size. The eggs are oval and
measure 0.05 mm. long.

The worm inhabits the small intestine, especially the duodenum and
jejunum, clinging tenaciously to the lining membrane by means of the
armed mouth. It penetrates the mucous membrane to the submucous coat,
from which it sucks the blood that forms its food. In the position of
its attachment it gives rise to little ecchymoses. It often occurs in
large numbers, even to hundreds and thousands. The eggs are laid in the
intestine and are discharged with the evacuations. Externally, in
water, the embryo undergoes development within the egg, and then
escapes to lead for some time an independent existence. Subsequently,
it is most probable that the worm obtains access to the human stomach
by drinking standing water, and completes its development in the
intestine.

The Anchylostomum proves to be a prolific source of wasting diseases in
tropical countries, and is pernicious to an extent proportioned to the
numbers infesting the intestine. By depriving the body of blood it
produces a greater or less degree of anaemia. The affection begins very
insidiously, and the general nutrition of the body may not be visibly
disturbed {956} until a late period. In moderate cases the disease is
indicated by general paleness of the skin and mucous membranes, fatigue
on slight exertion, and a tendency to palpitations and quickened pulse.
In more severe cases there is constantly increasing debility, with
increase of paleness, indisposition to exertion, excessive sleepiness,
and feeling of coldness. Dyspeptic symptoms sometimes appear, and loss
of appetite may alternate with ravenous hunger. Accompanying this there
is often a disposition to eat innutritious articles, as coal, clay,
wool, etc. Feeling of weight and oppression in the epigastrium and
abdominal pains are frequent. In the advance of the affection shortness
of breath appears, increased on exertion to violent dyspnoea.
Emaciation becomes obvious in the later stage of the disease. In the
worst cases the symptoms increase in severity, the patient becomes
dropsical, is attacked with profuse diarrhoea and vomiting, and finally
dies.

The severity of the affection is proportioned to the number of
parasites present and the quantity of blood they consume and cause to
be lost. Bad cases may end fatally in a few weeks, but generally the
disease lasts for months, and where the patient is provided with
abundance of good food it may continue for years.

The prognosis of the disease is rather unfavorable; if, however, the
nature of the affection is ascertained before it has greatly exhausted
the patient, and the parasites can be expelled, the result should be
favorable.

We have thus far obtained but little information as to the best
treatment for Anchylostomum. Calomel and turpentine have been
recommended, and, as these are most powerful vermicides, we have reason
to believe they would prove most effectual remedies.

In regard to the prophylaxis for Anchylostomum--and we may add in
general for all parasites which gain entrance to man through
drinking-water--all stagnant or standing waters should be filtered, so
as to remove any source of infection, whether by eggs or free embryos
of parasites or of larval forms existing within minute aquatic animals
which serve as intermediate hosts to parasites. Standing waters, such
as those of puddles, ditches, marshes, and ponds, more or less swarm
with minute animals, all of which may be entirely removed by
filtration. Even the water of cisterns and wells, if supplied from the
free surface of the country, may not be free from minute animals, and
especially eggs, and therefore requires filtration to be safe. Only
spring and freely-running water of rivers and creeks and of lakes is
commonly free from microscopic animals and their eggs, and therefore
devoid of all danger in these respects.

       *       *       *       *       *

STRONGYLUS LONGEVAGINATUS; S. bronchialis.--This nematode has been only
once satisfactorily observed. Many occurred in the lungs of a boy in
Germany, but the real cause of his death was not stated. The female
worm is about an inch long, the male about five-eighths of an inch.

Certain worms previously discovered in the bronchial glands of a case
of phthisis, and described under the name of Hamularia lymphatica, are
regarded by Cobbold as the same with the former; but the descriptions
of the two render this improbable. Treutler's drawing of Hamularia, as
copied by Leuckart, looks like an Ascaris upside down.

       *       *       *       *       *

{957} EUSTRONGYLUS GIGAS; Strongylus gigas; Palisade-worm;
Kidney-worm.--This worm, recorded in the catalogue of human parasites,
is doubtful as such. Pertaining to the same family as Anchylostomum, as
the common name indicates its usual habitation is the kidney. It is the
largest of the nematodes, and is a long, cylindrical red worm, slightly
tapering, and blunt at the ends. The mouth is enclosed by six rounded
labial papillae. The caudal extremity of the male ends in an inverted
cup-like pouch, from which the penal spiculum protrudes. The female
commonly ranges from one to three feet in length and from a fourth to
nearly half an inch in thickness. The male ranges from six inches to a
foot in length and from one to three lines in thickness.

The mature parasite is common in many fish-eating mammals, from which
it is inferred that fishes are the intermediate host for the juvenile
condition of the worm. It is frequent in the wolf, dog, mink, weasel,
raccoon, otter, and seal. It also occurs in the hog, and is reported to
have occurred in the horse, ox, and man. Usually it is solitary, and
occupies one of the kidneys coiled upon itself. Under its influence the
kidney is atrophied and reduced to the condition of a capsule of
connective tissue, often containing bony spicules. It feeds on blood
and on the purulent matter resulting from the inflammation it produces.
The worm is occasionally found in other positions, as the mesentery,
the abdominal cavity, the intestine, liver, urinary bladder, and lungs,
but perhaps in most of these cases has been derived from its usual
habitation. In this country the writer has repeatedly observed the
kidney-worm in the mink, the dog, and the wolf. In one instance in the
former animal he found a female and a male associated together in one
kidney, which was reduced to the condition of a fibrous capsule
containing in its wall a large radiated plate of bone.

The cases on record of the occurrence of this formidable parasite in
man are of very early date, and are mostly doubtful as to the authentic
nature of the worm, and are all unsatisfactory as to the attendant
phenomena.

       *       *       *       *       *

TRICHINA SPIRALIS.--The trichina, or flesh-worm, a minute nematode, is
a common parasite of man, and from its wide prevalence and results may
be regarded as the most dangerous of all. Perhaps from the earliest
ages it has been dealing death freely and indiscriminately to our kind
without its existence having been suspected until within the last
half-century. Frequently, the affection, now named trichinosis,
produced by its presence has been so prevalent in communities as to
appear epidemic. The parasite was first discovered, and is commonly
observed, as a little worm coiled up and imbedded in the flesh of man.
In the same manner it is frequently seen in the flesh of the hog. In
the adult or mature state it lives in the small intestine of both man
and the hog, but its duration of life in this position is comparatively
brief.

Trichinosis, or the disease induced by the introduction of trichinae
into the intestinal canal and the migration thence into the voluntary
muscles, varies in symptoms and gravity with the number, condition, and
position of the parasites and the susceptibility of the patient. The
presence of trichinae in the alimentary canal, though often accompanied
by violent symptoms, is comparatively free from danger, whereas in the
muscular {958} system they not only produce the greatest suffering, but
often the most disastrous results.

Man is ordinarily infected with the trichina by eating the raw or
insufficiently cooked meat of the hog, or pork in any of its varieties
of food. Infected meat often contains immense numbers of the parasite,
a single ounce at times being estimated to contain from 50,000 to
100,000 worms.

The trichina was first distinctly noticed in the muscles of the human
body by Paget in 1835, and was described by Owen with the name it now
bears. It was subsequently observed under the same circumstances by
other investigators. In 1846 the parasite was found by the writer in
the muscles of the hog, but neither he nor others for some time
afterward suspected the significance of the discovery. In 1860, Zenker
of Dresden treated a supposed case of typhus complicated with excessive
muscular pain and oedema. On post-mortem examination the muscles were
found swarming with trichinae, and to these the affection altogether
was attributed. Nearly at the same time the investigations of Leuckart
confirmed the relationship of the parasites as the cause of the
disease. In 1862, Friederich first diagnosticated the affection and
experimentally determined the presence of the worms in the living
patient.

The trichina is also found infesting other animals of the same class
besides man and the hog, especially the rat, mouse, rabbit, cat, and
fox. Experiments further prove that mammals are generally more or less
susceptible to infection with the parasite, though some appear to
resist its extension to the muscular system, as in the case of the dog.
The horse, ox, and sheep exhibit little disposition to artificial
infection of the muscles, and hence from this circumstance and the
nature of the food of these animals they are rarely found to be
infested with trichinae. In experiments on birds and lower classes of
animals, though trichinae were ascertained to advance in development in
the intestine, they failed to invade the muscular system.

Ordinarily, it appears that while man is infected with trichinae
through the hog, this animal becomes infected by eating infested rats,
mice, and cats, fragments of waste pork, and perhaps occasionally by
feeding on the excrements of infested animals.

The trichinae occupying the muscles are immature, and it is only after
they are swallowed and the parasites are freed by digestion of the
envelopes and pass into the intestine that they undergo development to
sexual maturity. In this state the female is viviparous and gives birth
to a multitude of active embryos, which immediately commence to migrate
to the muscular system. As it is estimated that each female may give
birth to upward of a thousand embryos, it is readily conceived to what
an extent the body may become infested from eating a few ounces of
trichinous pork.

The immature or larval trichinae are also distinguished as muscular,
and the sexually mature ones as intestinal, trichinae, in accordance
with their position in the two principal conditions.

Muscular trichinae vary in condition from the embryo, which works its
way among the muscular fibres or has obtained entrance into these, to
the coiled-up worm lying quiescent in a capsule imbedded among the
muscular fibres.

Infected flesh in the early state is scarcely distinguishable as such
with {959} the naked eye, but in old cases the trichina capsules become
imbued with calcareous matter, and are thus rendered visible as minute
white or grayish specks scattered through the red meat.

In the recent state of invasion the worms are found free among the
muscular fibres or within these. Later, they appear mostly solitary and
at rest, coiled within a fusiform mass of semi-liquid granular matter
resulting from the degradation of the muscular substance. Subsequently,
they become enclosed in an elliptical capsule, apparently derived from
the myolemma of the muscular fibre they had entered. The capsules,
situated among the bundles of sound muscular fibres, are arranged with
their long diameter parallel with the latter. The trichina capsules
commonly measure about one-fifth of a line long, and the coiled worm
within is scarcely a half-line long.

If muscular trichinae remain with their host, after a year or more they
exhibit signs of decay. Commonly, little fat-globules appear at the
poles of the capsules, and these become the seat of calcareous deposit.
Finally, the worms die and undergo degeneration.

When meat with living trichina capsules is swallowed, the freed worms
pass into the intestine, and here in the course of four or five days
reach maturity.

The adult intestinal trichina is a minute, filiform white worm, thicker
behind and tapering forward. The female is about an eighth of an inch
long, and has the genital aperture at the anterior fourth of the body.
The male is little more than half the length of the former, and has the
caudal end provided with a pair of conical processes, between which is
the genital aperture.

The ripe female trichinae give birth to living embryos, and continue
the function for about a month, after which they appear exhausted,
ordinarily die, and disappear from the intestinal canal. The new-born
embryos, about 1/200 of a line long, quickly leave the intestine to be
disseminated throughout the body. Penetrating the mucous membrane, they
probably enter the blood-vessels to be carried onward by the
blood-currents, and perhaps also, in part, directly migrate to their
destination in the muscles. The latter mode of progress is rendered the
more probable from the circumstance that the muscles contiguous to the
intestinal canal, as the diaphragm and those of the abdominal walls,
are commonly most abundantly infested with the parasites. In the
muscles of the limbs they are sometimes noticed to predominate toward
the extremities of the former, as if retarded in their course by the
tendinous connections.

It would appear that muscular trichinae, to be capable of producing
infection--that is to say, of further development--must have reached a
certain stage, corresponding with the encapsulated condition, before
they are swallowed. In this stage they may remain within their host
probably for a year or two.

Children seem to suffer less in proportion to the quantity of
trichinous meat they eat than adults, and they appear less susceptible
to muscular invasion of the parasites. The difference is probably in a
measure due to the greater susceptibility of the intestinal canal and
the consequent production of more copious diarrhoea in children, with
more complete expulsion of the worms.

SYMPTOMS.--In general, the effect produced by eating trichinous meat
{960} is proportioned to the number and condition of the trichinae
ingested and to the susceptibility of the patient. A few of the
parasites may pursue their entire career and die within their host
without ever exhibiting any obvious evidence of their presence.
Sometimes the symptoms of trichinosis are obscure or trifling,
sometimes sufficiently well marked, but moderate, and often they are
more or less striking and violent. The period of incubation of the
affection varies from a few hours to a week or more, and the duration
of the disease also varies--both in a measure proportioned to the
number and condition of the parasites.

In mild cases of trichinosis the patient may pass through the course of
the disease without being confined to bed, and in a few weeks may be
regarded as convalescent. The majority of cases pursue a slow course of
from six or seven weeks to three or four months. A fatal termination is
frequent, and is most common from the fourth to the sixth week, and
appears mainly to be due to the loss of respiratory power. Fatal cases
rarely happen after the seventh week.

From a few hours to a few days after eating trichinous meat the patient
may be seized with dyspeptic symptoms--nausea, cardialgia, flatulence,
eructations, and vomiting. These may be accompanied with complete loss
of appetite, excessive thirst, bad taste, and fetid breath. There is
also commonly a feeling of general uneasiness, with fulness of the
forehead or headache, and feeling of weakness and fatigue to exhaustion
or complete prostration. Neuralgic pains are felt in the abdomen and
limbs, and the muscles generally are more or less relaxed and flabby.

Violent disturbance of the alimentary canal occurs only when large
quantities of active trichinae are taken with the food. The subsequent
symptoms, due to invasion of the muscular system, may, but do not
necessarily, accord in degree with the former.

Diarrhoea usually comes on early, and the evacuations, at first more
consistent, become thin and clay-colored, like those of typhus or like
the rice-water stools of cholera. In the severest cases the patient may
die in this stage from extreme exhaustion and with all the appearance
of cholera. Sometimes the diarrhoea subsides and gives place to
obstinate constipation.

The muscular symptoms induced by the invasion of the trichinae may be
trifling or moderate, varying to a most violent character. They
commonly appear after a week, and later up to the sixth week. The
muscles become more or less swollen, hard and tender to the touch, or
highly painful under pressure. Motion is extremely painful, and the
patient usually lies in a helpless state with the limbs flexed--adults
on the back, children on the side. Difficulty, with pain, in chewing
and swallowing ensues, and even complete trismus, due to the presence
of the parasites in the muscles of mastication and deglutition.
Difficulty of breathing also arises from the presence of the trichinae
in the respiratory muscles, especially the diaphragm and those of the
larynx. Even movement of the eyes is painful, due to the parasites in
the orbital muscles. Bronchial catarrh comes on early, attended with
hoarseness and asthmatic cough.

Fever may be absent in mild cases of trichinosis, but is considerable
in the severer forms, though not in the first few days. The pulse
accords with the increase of temperature.

Profuse sweating is a common symptom of the affection, commencing {961}
early and continuing throughout. Generally there is considerable
decrease in the quantity of urine, which is highly colored.

Adults suffer with insomnia, while the reverse state prevails in
children, who commonly lie in a soporose condition. Formication and
dilatation of the pupils are frequent symptoms.

Oedema is a characteristic and pathognomonic symptom of trichinosis,
and is seldom so slight as to escape attention. It commonly appears in
the eyelids and face about the end of the first week, and may disappear
after several days, to recur after several weeks. It usually commences
in the limbs in the second week, and is more marked and persistent, and
increases, especially in severe cases.

Peritoneal and pleuritic irritation and inflammation, with bronchitis
and pneumonia, are not unfrequent complications in the more aggravated
form of trichinosis.

Most cases of the disease reaching the seventh week advance in
convalescence, while those of mild character by this time have
recovered, except from the weakness and emaciation, which remain as
evidences of serious illness.

Trichinosis in children is distinguished by greater mildness, less
danger, abundant oedema, less muscular pain, a dormant condition, and
more rapid convalescence.

The distinct recognition of trichinosis is difficult in isolated cases,
but becomes more evident where it occurs in numbers, as in an entire
family or in large portions of a community. The proof that the patient
has partaken of trichinous pork helps to establish the diagnosis.

In the beginning of severe cases of the affection symptoms of a more or
less violent gastro-intestinal catarrh are commonly present, often
associated with slight fever and almost invariably excessive
perspiration. Muscular lameness, both in mild and severe cases, is an
early symptom. The disease is distinguished from cholera by the profuse
perspiration and the peculiar muscular symptoms; from ordinary
rheumatism by the gastro-intestinal catarrh and general exhaustion.
With the appearance of oedema of the eyelids and face at the end of a
week the diagnosis becomes more certain. The further progress of the
affection is so characteristic that its distinction can scarcely remain
in doubt. The general prostration, the violent muscular symptoms, the
bronchial catarrh, the hoarseness and dyspnoea, the profuse sweating,
and the sleeplessness, render the case pretty clear.

In the prognosis of the disease no positive conclusion can be derived
from the severity or early appearance of the initial symptoms.
Commonly, the more speedily they occur and the more violent they are,
the less favorable will be the prognosis, while the later they appear,
the more propitious it is. Long-continued diarrhoea is especially
unfavorable, while a profuse diarrhoea at the beginning is to be viewed
as a fortunate event. The prognosis is more favorable in cases in which
sleep and the appetite are maintained, and in those in which the
disturbance of the respiratory organs is slight. A favorable
termination of the affection is the rule with children.

TREATMENT.--The treatment of trichinosis is not generally promising in
favorable results. No means have yet been discovered to destroy or
remove trichinae which have migrated from the intestinal canal. While
{962} the parasites continue within the latter we may have reasonable
hope of expelling them from the body by means of the usual remedies for
intestinal worms. Experience, however, with these remedies has not been
in accordance with expectations. In the mean time, until some more
potent vermicide is discovered applicable to the destruction and
removal of trichinae from the intestine, we are disposed to place most
reliance on such purgatives as oil of turpentine and castor oil and
calomel and jalap. Subsequently, a good nutritive diet with wine is
recommended to preserve the life of the patient until the affection has
reached that period when the parasites become capsulated and there is
no longer danger from them as irritants.

As a preventive of trichinosis, besides the avoidance of pork or its
varied preparations of ham, sausages, etc. when it is known or
suspected they may be infested, thorough cooking of meats is a certain
means. A boiling temperature surely kills all animal parasites, but
care is requisite that large pieces of meat should be cooked
sufficiently long that the desired heat may extend to the interior
throughout. The writer may add that it was in a slice of boiled ham,
from which he had partly made his dinner, that he first discovered
trichina in the hog.

       *       *       *       *       *

Of the nematode worms there are many species of comparatively long,
slender proportions, which constitute the family of Filaridae. As
parasites they rarely occupy the interior of the intestinal canal,
except by way of transit, and live in most other organs and tissues of
the body of both vertebrate and invertebrate animals.

       *       *       *       *       *

FILARIA MEDINENSIS.--SYNONYMS: Dracunculus; D. medinensis; Medina-worm;
Guinea-worm.

The Medina-worm has long been recognized as a parasite of man, and by
competent authorities has been regarded as the fiery serpent which
afflicted the children of Israel in the wilderness of Judea. It
prevails in the tropical regions of Africa and Asia, and thence has
been introduced into tropical America. It is ordinarily observed as a
long, white, cord-like worm, situated beneath the skin in any part of
the body, but mostly in the lower limbs, and especially in the vicinity
of the ankle. Though a frequent parasite, only the female is known. In
the mature condition it is nearly uniformly cylindrical, and ranges
from eighteen inches to three or four feet in length and less than a
line in thickness. The head end is rounded and furnished with a little
papillate plate, in the centre of which is situated a minute oral
aperture. The caudal end is conical and incurved. The intestinal canal
is atrophied and without an anal aperture. The coelum is mainly
occupied by a capacious uterus filled with free embryos. A generative
aperture appears also to be absent, and the young can only escape by
rupture of the parent.

Experiments made about a dozen years since in Turkestan by Fedschenko,
at the suggestion of Leuckart, have shown that when the embryos of the
Medina-worm are introduced into water containing the familiar little
crustacean cyclops, they penetrate into this, and within it undergo
transformation into the larval stage. The subsequent history of the
larval worms remains unknown, but from what we have learned of the
history of many parasitic worms it is reasonable to suppose that if
{963} the infested cyclops is swallowed in drinking-water, it may
explain the presence of the mature worm in the human body. The young
worms, liberated from their crustacean host by digestion in the
stomach, probably enter the intestine, and thence migrate to their
destination. In the young condition, advancing to maturity, the worms
have been found in all parts of the body except within the cranium and
eyeball. They appear to migrate in the course of the least-resisting
connective tissues, along the route of the principal blood-vessels,
until they reach the surface of the body.

Usually, a single worm is found in a person, though cases occur where
several, to a dozen or more, are present. Commonly, the parasite is
solitary, though two or three may be associated together. When deeply
seated the Medina-worm ordinarily produces but little discomfort,
though in some cases its movements are accompanied with more or less
severe pain. It also gives rise to inflammation and the formation of an
abscess, in the purulent matter of which the worm lies bathed. The
removal of the worm, when accessible, by the proper surgical aid is
followed by complete relief.

It is evident that filtration of the drinking-water would be a certain
prophylaxis for the Medina-worm.

       *       *       *       *       *

FILARIA SANGUINIS.--SYNONYMS: Filaria sanguinis hominis, Lewis; F.
sanguinolenta; F. Bancrofti, Cobbold.

Another species of Filaria, a more dangerous parasite of man and
indigenous to the tropics, is of frequent occurrence, though of
comparatively recent discovery. It has been observed in India, Africa,
Brazil, and the West Indies. It is commonly seen in the embryonic
condition, living in the blood of patients affected with elephantiasis
and certain other diseases, and is also found in the urine. In this
early condition it is a minute worm, scarcely more than the 1/100 of an
inch in length, and occurs together in immense numbers.

In the sexually mature condition the female filaria is a white
hair-like worm three or four inches in length, living in the lymphatic
vessels distally to the glands, especially in those of the lower limbs
and scrotum. The embryos after leaving the parent pass into the
lymphatic stream, and thence into the circulating blood. According to
recent observations of Manson, they enter the blood in the evening and
increase in number until midnight, after which they decrease and
disappear by morning, from which time during the day they remain absent
from the circulation. The investigations of the same authority have
shown that when the blood of infected persons is sucked by mosquitoes
these insects also imbibe the embryos, which subsequently undergo
transformation in the mosquitoes into the larval state. In this
condition the filariae may be transferred to water, by drinking which
man may become infected with the parasites. The larvae introduced into
the stomach appear thence to make their way to the lymphatics, within
which they undergo further development to maturity, and thus remain a
long time.

The presence of the worms in the lymphatics, with their numerous brood
in the circulating blood, gives rise to haematuria and chyluria. As
results of the obstruction of the lymphatic currents, the parasites
induce inflammation, suppuration, lymphatic abscesses, buboes,
lymphangiectasis, {964} oedema, ascites, chylous hydrocele,
elephantiasis,[3] and certain cutaneous affections.

[Footnote 3: Several years since, with the view of ascertaining the
presence of parasitic worms, the writer examined the blood of a case of
elephantiasis under the charge of T. G. Morton, but none were detected.
From what we have since been informed of the habits of Filaria
sanguinis, the absence of the parasites may have its explanation in the
circumstance that the blood examined was withdrawn in the daytime.]

TREATMENT.--While the treatment of the affection induced by the Filaria
sanguinis is varied and uncertain, the prophylactic measures are
obvious and certain. Under favorable conditions of bright light, high
temperature, and abundant food the stagnant waters of tropical
countries are especially prolific of the minute forms of animals which
harbor parasites. It hence becomes evident that all such waters,
whether obtained from puddles, ponds, tanks, or cisterns, should be
filtered before being used for drinking. Boiling is also effectual in
destroying all the animal life of waters, and thus rendering them
innocuous so far as parasites are concerned.

       *       *       *       *       *

Several other species of Filaria have been found in the human body, but
are little known and very rare in their occurrence.

       *       *       *       *       *

FILARIA LOA.--This species occurs in Western Africa, on the Gaboon
River, and is perhaps more frequent than now commonly supposed. It is
an active worm, little more than an inch in length, and is usually
found beneath the conjunctiva of the eye. It probably also occupies
other positions, and a missionary on the Gaboon informed the writer
that he had extracted one from the back of one of his own fingers. Its
presence produced an intense burning pain. The negroes are reported to
extract the worm by means of a thorn. The worm has also been observed
in Brazil and the West Indies.

       *       *       *       *       *

FILARIA RESTIFORMIS.--Under this name the writer recently described a
large Filaria reported to have been withdrawn from the urethra of a man
in West Virginia. It was obtained by C. L. Garnett, and sent, together
with an account of the case, to the Army Medical Museum of Washington,
where it is now preserved. It was a red cylindrical worm, twenty-six
inches in length, tapering at the head, and thick, incurved, and
obtusely rounded at the tail end.[4]

[Footnote 4: _Proceedings of the Academy of Natural Sciences_,
Philada., 1880, p. 130.]

       *       *       *       *       *

FILARIA OCULI HUMANI; FILARIA LENTIS.--A few cases are on record of the
occurrence of little worms in the aqueous humor and crystalline lens of
the human eye, to which the accompanying names have been applied.

       *       *       *       *       *

FILARIA TRACHEALIS.--Recently some minute worms found by Rainey in the
trachea and lungs have been described under this name.

       *       *       *       *       *

In conclusion, the writer acknowledges his indebtedness for much of the
information of this article to the articles on "Intestinal Parasites"
and "Diseases from Migratory Parasites" in _Ziemssen's Cyclopaedia of
the Practice of Medicine_, and to Glazier's _Report on Trichina and
Trichinosis_.




{965}

DISEASES OF THE LIVER.

BY ROBERTS BARTHOLOW, A.M., M.D., LL.D.


I. FUNCTIONAL DISORDERS.


Biliousness.

DEFINITION.--The term biliousness is used to signify a disturbance of
the gastro-intestinal digestion, with coincident excess in the
production of bile. According to the popular conception, both lay and
medical, the excess of bile is the cause of the symptoms; but when the
whole subject is carefully examined it will be found that biliousness
is made up of several factors, and that the hepatic disorder, if it
exist at all, is a mere incident.

PATHOGENY.--From the time of Galen biliousness has been regarded as a
morbid entity and the liver as the organ affected. Stoll, amongst
moderns, first revived the Galenical doctrines. Abernethy[1] was
amongst English physicians the most conspicuous advocate of the
condition called biliousness, and was the apostle of blue pill and
black draught. Copland in his great dictionary[2] more distinctly
formulated the views of the English school--especially that portion of
it influenced by the results of Indian practice--than had been
previously attempted, and hence his work best represents the opinions
and practice of the time amongst the English-speaking peoples. In this
country the great Rush first promulgated the notions of biliousness
which have since so dominated the medical opinion of this continent. A
large part of the United States has proved a fruitful soil for the
cultivation of theories of biliousness, since the condition known under
this name is a frequent accompaniment of malarial poisoning. To this
fact must be attributed the preponderating importance of biliary
derangements in the practice of the physicians of India also.

[Footnote 1: _Surgical Works_, London, 1811, vol. i. p. 36.]

[Footnote 2: _A Dictionary of Practical Medicine_, vol. ii. p. 723.]

It is a fact which will be hereafter more fully developed that malarial
infection may, and often does, derange the hepatic functions without
producing fever. The malarial poison irritates the liver, and thus more
bile is produced, but the quality deteriorates with the increase in
quantity. The functions of the liver are more disturbed during an
access of intermittent fever: the organ is swollen, the skin is muddy,
the eyes yellow, the tongue coated with a thick yellow fur, and the
urine is deeply tinged with bile-pigment.

Many of the metals employed as medicines and as poisons, as gold, {966}
silver, antimony, arsenic, phosphorus, etc., irritate the liver both in
their entrance and in their exit from the organism, and cause
biliousness; and the same fact is true of some vegetable alkaloids and
animal poisons. The liver excretes many of these substances, and in
their passage out from the blood the hepatic cells are irritated and an
increased production of bile is a result. Improper food, indulgence in
fats, sweets, condiments, and all kinds of fermented and alcoholic
liquors, intestinal indigestion arising from any cause, and
gastro-duodenal catarrh, are the most usual and obvious pathogenic
factors. In respect to food and indigestion as etiological factors
there are several points requiring more explicit statement. When
nitrogenous elements (albuminoids) are in excess in quantity or as
respects the power to digest and convert them, immature products, of
which uric acid is the chief, accumulate in the blood. When the fats,
sugars, and starches are in excess of the requirements of the organism
or are imperfectly disposed of in the small intestines, a local
irritation of the mucous membrane is produced, and various complicated,
immature products enter the blood. With these troubles and faults of
intestinal digestion a gastro-duodenal catarrh is usually associated.
Without the production of catarrhal jaundice, gastro-duodenal catarrh,
with the forms of indigestion accompanying it, keeps up a reflex
irritation of the liver. Just as the presence of normal chyme induces
the flow of bile, so the unhealthy products of intestinal indigestion
excite an irritation of the liver. The continued operation of this
cause maintains an abnormal activity of the liver, and more bile is
produced than is easily disposed of.

SYMPTOMS.--The condition of biliousness, as now understood, is made up
of derangement of the gastro-duodenal mucous membrane, with
bile-production in excess and bile-absorption probably delayed. The
symptoms are the product of these complicated conditions. The
complexion is muddy; the conjunctivae are yellow; the tongue is heavily
coated with a yellowish-white fur; a bitter taste persists in the
mouth; the breath is heavy in odor, even fetid; the appetite may be
keen or there may be complete anorexia; a sensation of nausea, of
heaviness, and fulness of the stomach is experienced, especially after
eating; the bowels are confined usually, but occasionally the movements
are relaxed, bilious in appearance, and cause heat and irritation about
the anus; headache is constantly present to some extent, and there is a
sense of fulness with more or less dizziness, and singing in the ears;
vision is rather blurred, and there is a hebetude of mind; the urine is
high-colored, high in specific gravity, and deposits lithates
abundantly on cooling. When these symptoms are conjoined with
hemicrania, nausea, and vomiting, the case is called bilious sick
headache, and when diarrhoea supervenes, the discharges apparently
containing much bile, it is bilious diarrhoea. The symptoms which above
all others give the character to the morbid complexus are the muddy
(bilious) complexion, the yellow-coated tongue, the yellow
conjunctivae, and the high-colored urine. The first departure from the
normal may be scarcely observed. Gradually, owing chiefly to errors of
diet, to climatic changes, or to malarial influences, or to these
several factors combined, the affected person drifts into the condition
of biliousness above described. Besides the general malaise, he
experiences no little despondency, inaptitude for exertion, and indeed
actual weakness. Finally, he is unable to apply himself to business,
relinquishes the effort, and seeks advice.

{967} COURSE, DURATION, AND TERMINATION.--Those who are accustomed to
experience attacks of biliousness suffer from them at certain intervals
which may be tolerably regular--at intervals of a few days, two, three,
or four weeks--when the cause is uniform; but they may happen very
irregularly when the conditions producing them are variable. The
duration of an attack is from two days to a week or more, according to
the severity of the symptoms and to the character of the measures
instituted for relief. The termination is in a return to the normal
state. If the conditions which produced it continue, when one attack is
ended the preparations for another begin at once, and at length
sufficient derangement of the organs concerned arises to constitute the
morbid complexus of biliousness.

TREATMENT.--Prophylaxis has great importance, since the causes of the
malady are to a considerable extent, at least, preventable. Errors of
diet in respect to the use of condiments, fats, meat, pastry, etc. must
be corrected. When there is pronounced gastro-duodenal catarrh and acid
fermentation in the duodenum, the saccharine, fatty, and starchy
elements of the food must rather be excluded and lean meats allowed.
Abundant exercise, bathing, and an open-air life in general should be
directed. Whenever a malarial infection is causative a change of
climate becomes imperative. Heredity cannot, of course, be excluded,
but the tendency to hepatic derangement can be rendered inoperative by
an abstemious life.

The remedial management includes the dietetic as well as the medicinal
treatment. When the distress has reached sufficient proportions to
justify such an extreme measure, the patient should be restricted to a
diet exclusively of skimmed milk, of which he is directed to take a
gill or more every three hours. This serves a double purpose, as
aliment and as a depurative agent, for this considerable quantity of
fluid promotes the urinary excretion and the elimination of waste
products. If the case is not severe enough to allow of such an
expedient, the diet should in any event be restricted to skimmed milk
hot, milk and hot water, hot lemonade, a little chicken or mutton
broth, a bit of dry toast, etc. As a rule, although not so palatable,
hot drinks are more beneficial than cold, but if the preference is
decidedly for cold, they may be allowed. After the more severe symptoms
have subsided a little lean meat broiled may be added, and as the cure
proceeds the succulent vegetables and acid fruits may be permitted.
Abstinence from potatoes, hominy, cracked wheat, and oatmeal should be
enjoined during the convalescence of those who suffer from habitual
attacks.

Medicines may not be necessary to those who have the resolution to
adhere to skimmed milk for several days or who can abstain from food
altogether for a day. Many experienced sufferers, especially through
the South and West and in England, procure rather prompt relief from a
blue pill of ten to fifteen grains or from one to five grains of
calomel at night, followed by a Seidlitz powder, Rochelle or Epsom
salts, or phosphate of soda on the following morning. Such patients
find that no other treatment is as serviceable. They get relief from
other measures, it is true, but neither as promptly nor as
satisfactorily. It is held by the advocates of this practice that the
mercurial acts on the liver--that the surplus bile is carried off; and
they point to the peculiar stools and to {968} the relief experienced
in evidence of the truth of this theory. Without entering on the
argument, which would occupy too much space, it must suffice here to
state that calomel and blue pill do not increase bile-production,[3]
but they do stimulate the intestinal glands and increase excretion from
them. The peculiar greenish stools produced by these mercurials do not
owe their characteristic appearance to the presence of bile, but rather
to the chemical transformations of the mercury itself and to the waste
products excreted by the intestinal glands. Since the researches of
Rutherford have been published, euonymin has been much prescribed in
cases of biliousness. From three to five grains are taken at the
bed-hour, and a mild laxative in the morning. In the same group of
cholagogues are ipecac, iridin, sanguinarin, and especially
podophyllin; but the serious objection to their use is that they
stimulate the liver when this organ is in an irritable state. As
calomel and blue pill have a sedative rather than a stimulant action on
the liver, they are more useful in biliousness than are the true
cholagogues. It should be borne in mind that one-half of a grain of
calomel will have a distinct purgative action on many persons, and that
one grain will rarely need to be exceeded.

[Footnote 3: That calomel, the type of a mercurial purgative, does not
increase the discharge of bile has been demonstrated on dogs by Rohrig
and Rutherford, and confirmed by observation of the effects of 20
grains on Westphalen's case of biliary fistula in man--a case in which,
for a time, all the bile escaped externally, and none apparently
entered the intestine (_Deutsch. Archiv f. klin. Med._, 1873, Band xi.
pp. 598 and 600).]

In general, notwithstanding the unquestionable utility of the
mercurial, it is better to relieve cases of biliousness by less
objectionable measures. A saline which acts at the same time on the
intestines and kidneys, as Rochelle salts, is usually effective in
bringing relief. A bottle of solution of magnesia citrate, of Saratoga
water (Congress, Hathorn, or High Rock), and of Blue Lick, the famous
sulphurous laxative of Kentucky, may remove the disorder in mild cases
if at the same time a suitable diet is enjoined. Phosphate of soda in
laxative doses, with or without Vichy water, is also a good remedy, if
somewhat slow. The warm purgatives, rhubarb, colocynth, aloes, etc.,
are useful when there is pronounced constipation.


Lithaemia.

DEFINITION.--By the term lithaemia is meant a condition of the system
in which uric (lithic) acid is produced in excess, and in which certain
derangements occur in consequence of the accumulation of this material
in the blood. Uricaemia was the term first suggested by Flint, Sr.,[4]
to express this state, and subsequently lithaemia was employed by
Murchison.[5] The latter has been more generally accepted. In one of
the most recent and valuable contributions to this subject by
DaCosta[6] lithaemia is the term used to designate the complex of
symptoms produced by uric acid in excess.

[Footnote 4: _The Principles and Practice of Medicine_, Philada.,
1882.]

[Footnote 5: _Clinical Lectures on Diseases of the Liver_, 2d ed., p.
565.]

[Footnote 6: _The Medical News_, vol. ii., 1883.]

PATHOGENY.--The ultimate product of albuminoid substances in the
organism prepared for final excretion is urea. That this substance is
{969} finally formed in the liver, to be excreted by the kidneys, seems
now well established.[7] In acute yellow atrophy of the liver, with the
disappearance of the proper structure of the organs urea ceases to be
produced, and instead leucin and tyrosin are excreted. In certain
states of the system characterized by deficient oxidation urea is not
sufficiently formed, and instead uric acid, a lower grade of oxidation
and a product of the disintegration of albuminoid substances, results.
An excess of urates is not always pathological. Their excretion seems
to be in a certain sense a safety-valve function. When albuminoid
matters are taken in excess of the power of the system to convert them,
or when the supply of oxygen to the blood is deficient from any cause,
urea is not formed, but uric acid and urates are abundantly excreted by
the urine.[8] Imperfect digestion of the albuminoids when they are not
taken in relatively too large an amount, and limitation below the
normal of the oxidation process when the supply of oxygen is not
insufficient, will have the same effect: in place of urea, uric acid
and urates will be formed and excreted. One of the early results of the
persistent presence of an excess of uric acid is the production of
lithaemia, the morbid complexus of which this excess is at once the
cause and the proof.

[Footnote 7: This proposition is not universally accepted. Valmont
(These de Paris, _Etude sur les Causes des Variations de l'Uree dans
quelques Maladies du Foie_, 1879) has carefully studied the excretion
of urea in several diseases in which the proper structure of the liver
is damaged--in atrophic cirrhosis and in cancer. As in these maladies
not all the secreting portion of the organ is destroyed, the argument
is so far weakened. His conclusions are as follows: "1. Patients with
cirrhosis or cancer of the liver who eat little excrete but little
urea. If they eat and do not absorb, or vomit or have diarrhoea, the
result is the same. When they partake largely of nitrogenous aliment
the proportion of urea rapidly increases. 2. In a cachectic or simply
anaemic patient the urea falls, apparently in proportion to the state
of the general nutrition and of the work done by the organic functions.
3. Absolute immobility of the patient seems to have an influence on the
amount of urea excreted. 4. In sclerosis or cancer the quantity of urea
falls rapidly on the occurrence of ascites or oedema, when a notable
quantity of urea is found in the fluid. 5. The digitalis often used in
the treatment also contributed to the loss of urea." If these
conclusions are verified, the formation of urea must depend on some
other function.]

[Footnote 8: Genevoix, _Essai sur les Variations de l'Uree et de
l'Acide urique dans les Maladies du Foie_, Paris, 1876.]

The persons who suffer from lithaemia are usually those who indulge in
the pleasures of the table and habitually consume much meat, pastry,
and highly-seasoned and rich food of all kinds. The idle, luxurious,
and indolent, literary men of sedentary habits, men who have led active
lives, but on retiring from business have continued to indulge in a
full diet, are apt to suffer from this malady. Women are less disposed
to it, but if subjected to the same conditions may also be similarly
affected. Especially do those suffer from lithaemia who indulge in malt
liquors or in alcoholic drinks of any kind. These substances act by
deranging digestion, and thus preventing the proper conversion of the
albuminoids, by inducing congestion of the liver, and also by
interfering with the process of oxidation.

SYMPTOMS.--The symptoms of lithaemia include derangements of the
digestive organs and of the liver, of the circulation, and of the
nervous system. As these subjects suffer from gastric and
gastro-duodenal catarrh, they present the usual symptomatology of these
affections, as a sense of weight and oppression at the epigastrium,
acidity, pyrosis, a capricious--sometimes voracious, sometimes
good--appetite, a coated {970} tongue, a bitter taste, etc. The bowels
are irregular, sometimes constipated, occasionally relaxed, with
scybalae. The stools may be liquid, almost black or light-yellow and
grayish. The motions are apt to be offensive, and a good deal of
offensive gas is discharged with them. Hemorrhoids are often present,
and there may be heat and irritation about the anus, and not
unfrequently intolerable itching. After meals there is much depression,
and often an insupportable drowsiness. Irregularity in the rhythm, even
intermissions, of the pulse are not infrequent.

The nervous symptoms, as DaCosta has lately insisted on, are the most
important and pronounced. The connection between oxaluria and mental
despondency has long been known, but the nature of the relation remains
undetermined. Headache, frontal and occipital, especially the former,
dizziness, tinnitus aurium, suffusion of the eyes, ecchymoses of the
conjunctiva, are usually present. Not unfrequently the subjects of this
affection experience sudden attacks of vertigo, accompanied by dimness
of vision and intense headache, and are supposed to have some organic
lesion of the brain. They are irritable, despondent, and often
intensely hypochondriacal, almost suicidal--are subject to neuralgic
attacks, and have aching in the limbs, a sense of weariness, and more
or less burning in the palms and soles.

The skin is rather dry and the complexion muddy. Urticaria is of
frequent occurrence, and sudden attacks of nausea, vomiting, and
intestinal pain coincide with the appearance of the eruption on the
skin.

The urine is usually rather increased in amount, its color heightened,
its acidity above normal, and floating in it, usually visible to the
naked eye, are reddish masses composed of uric acid. More or less pain
in the back, referable to the situation of the kidneys, and sometimes
extending along the course of the ureters, is common. The bladder is
rather irritable, and the passage of the urine produces heat and
scalding. The testicles are apt to feel sore and are somewhat
retracted. On standing, the urine may deposit uric acid and the urates
copiously, or the acid may be seen to form a cloud which slowly
subsides.

COURSE, DURATION, AND TERMINATION.--The course and duration of
lithaemia are much influenced by the habits of life of the person
affected. When unopposed by treatment and no change is made in the
conditions producing it, a gradual increase in the various disturbances
takes place. After a time structural changes occur in the liver; the
organs of circulation early undergo atheromatous degeneration; various
cerebral disorders due to degenerative changes arise; and acute
intercurrent affections may terminate life. Amongst the secondary
maladies due to lithaemia are gout, diabetes, renal calculi, and
nephritic colic. If the cases are subjected to appropriate treatment,
curative results may be certainly obtained. The prognosis, then, will
be influenced materially by the moral strength of the patient. If he is
one who can surrender his appetites and live abstemiously, a cure may
be promised. The case is far different with those who will continue the
use of malt, vinous, or alcoholic drinks, and will persist in indulging
in the pleasures of the table.

DIAGNOSIS.--The differentiation of lithaemia from other affections
offers no special difficulties. From gastro-duodenal catarrh it is
separated by the {971} excess of uric acid in the urine only, the other
symptoms being for the most part the same. The cerebral symptoms--the
vertigo, headache, etc.--are to be distinguished from the same due to
actual disease of the brain by the previous history, by the absence of
changes seen on ophthalmoscopic examination and of other signs of brain
disease, and by the subsequent behavior. Cases of cerebral mischief
producing such effects would rapidly develop into serious states,
whereas in lithaemia there are great fluctuations, but no apparent
progress in many months. In lithaemia also there are no changes in the
fundus oculi, whereas in brain diseases choked disk, hemorrhage into
the retina, white atrophy, etc. are often discovered. Further, in
lithaemia there are no disorders of sensibility, of motility, or of
intellection, whilst these are ordinary evidences of cerebral mischief.

TREATMENT.--Attention to diet is of the first importance. As uric acid
is an intermediate product in the metamorphosis of albumen, it might be
supposed that to diminish the quantity of this constituent of the food
would be sufficient. In some cases this suffices, but usually attention
must be given to the peculiarities of digestion characteristic of each
patient. More frequently trouble arises from indulgence in the starchy
and saccharine constituents of the diet; in some a very considerable
gastro-duodenal catarrh exists, and the mucus, acting as a ferment,
sets up an acetic fermentation in the starchy and saccharine
substances, with the necessary production of much carbonic acid gas. If
the fats disagree, the butyric fermentation also takes place, and very
irritating fat acids result. In these cases there is usually much gas
formed in the stomach and intestine, and an immediate ratio appears to
exist between the degree of mental despondency and the quantity of gas
in the intestinal canal. It follows, then, that in cases of lithaemia
the saccharine, starchy, and fatty constituents of an ordinary diet
should be omitted from the food of such subjects. Bread should be
partaken of very sparingly, and the foods containing starch, sugar, and
oil ought not to be partaken of at all. The succulent vegetables, as
lettuce, spinach, celery, cole-slaw, tomatoes, etc., ought to be
substituted. Lean fresh meats, poultry, game (plainly cooked), fresh
fish, oysters, eggs, etc. should constitute the basis of the diet. On
the other hand, there may be those who do better on a diet of
vegetables and fruit, excluding meat. In such we may suppose the fault
lies in the stomach digestion, where the albuminoids are converted into
peptones, the intestinal digestion being active and normal. All kinds
of wine and malt liquors should be prohibited. Coffee and tea must also
be relinquished. Without the carefully-regulated diet medicines can
accomplish but little; hence he who would obtain curative results must
give careful attention to every dietetic detail.

As deficient oxidation is an important factor in developing lithaemia,
active exercise must be enjoined. The amount of exercise must be
determined by the condition of the individual and the time, regulated
as far as may be by the period after meals. As when the food prepared
for assimilation is entering the circulation oxygen is needed to
perfect the final changes, it seems clear that exercise should be taken
three or four hours after the process of digestion has begun. Walking
exercise is better than any other for this purpose, but it should not
be carried to the point of exhaustion from fatigue. Sea-air and
sea-bathing are oxidizing agents of considerable value, and are
especially useful to the {972} subjects of lithaemia suffering at the
same time from malarial infection.

Medicines are administered with the view to accomplish two purposes: to
correct the disorders of digestion, to promote oxidation. One of the
most useful remedies is nitric acid, five to ten minims of the official
diluted acid being given before meals. It is more especially effective
when there is an excessive production of acid. The fermentation which
produces acid and the diffusion of acid-forming materials from the
blood are alike prevented by it. The injunction to administer it before
meals must be borne in mind when these purposes are to be subserved.
Nitric acid, as well as the other mineral acids, but in a greater
degree, promotes the flow of bile. This well-known clinical fact has
been confirmed by experiments. Under the use of nitric acid, as above
advised, uric acid and the urates disappear from the urine, being
excreted as urea, and hence this remedy accomplishes both of the
objects for which medicines are administered in this disorder. No other
mineral acid can fill its place in this connection.

Alkalies possess very decidedly the power to promote oxidation. The
soda salts are objectionable, for, combining with uric acid, they form
the insoluble urate of soda. The salts of potash and lithium, on the
other hand, form soluble combinations, and they also increase
elimination. Much depends on the time at which they are administered,
as Bence Jones,[9] and since Ralfe[10] especially, has shown. To
increase the alkalinity of the blood and urine, they must be taken
after meals, for then the acid materials of digestion are pouring into
the blood. For the same reason, if alkalies are administered to
neutralize the acidity of the intestinal canal, they must be given
after meals. The most useful alkaline remedies are liquor potassae,
bicarbonate of potash, Rochelle salts, citrate of lithium, etc. The
effervescing preparations of potash and of lithium are elegant and
palatable forms in which to administer these remedies. They may also be
taken dissolved in Vichy water, in our Saratoga Vichy, or in Carlsbad
or Bethesda. When the use of mineral waters is not contraindicated in
the state of the digestive organs, great good is accomplished by the
persistent use of Vichy, foreign or domestic, of Carlsbad, and the
alkaline waters of Wisconsin.

[Footnote 9: _Lectures on Pathology and Therapeutics_, by H. Bence
Jones, London, pp. 90, 280.]

[Footnote 10: _Physiological Chemistry_, by Charles Henry Ralfe,
London, 1883.]

The so-called cholagogues are unquestionably useful, but they become
less and less necessary according to the success achieved in the
dietetic course. Phosphate of soda is one of the most effective of this
group of medicines. As it acts as a compound, and not as a salt of soda
merely, it does not come within the prohibition against the use of soda
salts. It promotes the flow of bile and appears to remove the catarrhal
state of the mucous membrane. A teaspoonful three times a day is the
quantity usually required. Under some circumstances it may be
advantageously combined with arseniate of soda. Mercurials were
formerly almost universally used, but they have been largely supplanted
by podophyllin, euonymin, baptisin, etc., and by the phosphate of soda
above mentioned. Podophyllin is indicated when constipation is a
symptom. An efficient mode of giving it is in the form of granules, but
it must be continued without intermission for some time or during the
existence of {973} the lithaemia. The quantity given should be
sufficient to maintain the evacuations in a soluble state. Good results
are obtained from a combination of podophyllin with extracts of
physostigma, nux vomica, and belladonna. When distinct torpor of the
liver without constipation exists, euonymin, combined with physostigma,
may be advantageously used. For the vertigo and hypochondriasis no
remedy is more beneficial than arsenic (Fowler's solution) in small
doses kept up for some time, and it is also distinctly curative of the
catarrhal state of the mucous membrane. When malarial infection is the
cause of lithaemia, quinine becomes indispensable.

Topical agents in some cases render important aid to the other curative
measures. A daily sponge-bath, the water made more stimulating by the
addition of sea-salt, is very useful in the absence of sea-bathing.
Friction of the hepatic region with the official ointment of the red
iodide of mercury unquestionably stimulates the hepatic functions.
General faradization and faradic and galvanic excitation of the
chylopoietic system promotes activity of the digestive apparatus and of
the organic functions in general.


Hepatic Glycosuria (Temporary).

DEFINITION.--By the term hepatic glycosuria in this connection is meant
a temporary glycosuria due to excessive formation of glycogen. The
liver, unduly stimulated, produces more glycogen than can be disposed
of, and hence it is excreted by the kidneys as grape-sugar.

PATHOGENY.--In the normal condition it is supposed that the glycogen
produced by the liver is converted into grape-sugar, and soon oxidized
and thus consumed. One theory of diabetes maintained that in some way
the conversion of glycogen into grape-sugar was excessive and beyond
the oxidizing power of the blood, and hence this substance was
discharged in the urine. The recent discovery by Pavy[11] of glycogen
in considerable amount in the blood of all parts of the body renders it
certain that there are peculiar conditions necessary to the formation
of grape-sugar in sufficient quantity to constitute diabetes. It is
tolerably certain that an excess of acid in the intestinal canal,
diminishing thus the alkalinity of the blood, will have as a symptom
sugar in the urine. Persons disposed to the accumulation of fat, and
eating freely of sugar and starchy food, are apt to have intestinal
indigestion, and the acid produced by the fermentation of these
substances will, after its absorption, hinder the conversion of any
food-sugar. In such subjects also there may be an increased conversion
of the glycogen of the blood into sugar under the same conditions. Such
a glycosuria must necessarily be temporary and a purely functional
disorder.

[Footnote 11: _The Lancet_, vol. ii., 1883.]

SYMPTOMS.--The subjects of the malady under consideration are of full
habit, even obese. They habitually consume considerable quantities of
malt liquors and a diet composed largely of the starchy and saccharine
foods. If not in malt liquors, they at least indulge freely in bread,
potatoes, pastry, cakes--in all forms of farinaceous food, fats, and
sweets. They have a keen appetite, eat largely, and drink freely of
fluids. As {974} a rule, these subjects are but little disposed to
physical exercise and lead rather sedentary lives. Indulgence in such a
mode of life tends to increase the accumulation of fat, weakens the
muscles, and with them the heart-muscle, and slowly induces a
gastro-intestinal catarrh accompanied by stomachal and intestinal
indigestion. At first, heaviness, oppression, and drowsiness after
meals are experienced; then acidity, pyrosis, and eructations follow;
and ultimately the evidences of intestinal indigestion--flatulence,
pain, irregular and unhealthy evacuations, etc.--come on. Meanwhile,
the appetite is not usually impaired, and the disposition to drink
fluids increases; the amount of urine voided is greater, and to rise
during the night for the purpose of emptying the bladder comes to be a
fixed habit. The urine under these circumstances is copious,
high-colored, acid, and deposits on cooling abundantly of uric acid and
urates. The amount passed in twenty-four hours will reach sixty,
eighty, or more ounces, and the specific gravity will range from 1025
to 1035. On testing in the usual way, traces of sugar, more or less
distinct, will appear,[12] but not constantly, and hence repeated
examinations are necessary to determine the quantity. As a rule, the
evidence of the presence of sugar in small amount is satisfactory.

[Footnote 12: In testing for sugar, when the urine contains the urates
in such abundance there is danger of error. In using Trommer's,
Fehling's, or Moore's test, on heating, the urates will effect a
reduction of the copper or bismuth. It is necessary, therefore, to
separate them before applying the test. This is accomplished as
follows: The urine is evaporated to dryness on a water-bath; the sugar
in the evaporated residue is dissolved out by absolute alcohol, and
then an aqueous solution is prepared, to which the test is applied. An
experienced operator will not need to take such precautions, for,
familiar with the reactions, he can readily judge of the results.]

Various affections of the skin appear in the subjects of this malady,
and urticaria, prurigo, eczema, and boils are the forms most usual.

COURSE, DURATION, AND TERMINATION.--Slow in developing, this temporary
glycosuria is also slow in its course. It remains nearly stationary for
months, even years. Meanwhile the degenerative changes associated with
it slowly develop on all sides. The quantity of sugar does not greatly
increase, for its amount, being apparently dependent on the quantity of
acid entering the blood from the intestinal canal, must continue nearly
at the same standard. It is comparatively rare for true diabetes to
develop out of this state, although such a termination must be regarded
as a natural outcome. One reason, it may be, why such a conclusion is
not often reached is because of intercurrent maladies. It is an
important fact that acute serous--less often
parenchymatous--inflammations are very apt to occur during the
existence of even temporary glycosuria. Under appropriate management
this disorder is readily amenable to treatment. Hence the prognosis
will be favorable or not according to the skill exhibited in its
treatment.

DIAGNOSIS.--This malady offers no special difficulty in diagnosis. From
gastro-duodenal catarrh and from lithaemia it is distinguished by the
saccharine condition of the urine. From diabetes it is separated by the
rate of progress, by the protracted duration of the case without any
distinct advance, and by the temporary and fugitive character of the
glycosuria.

TREATMENT.--To carefully regulate the diet is the first consideration.
The traces of sugar and the excess of urates rapidly disappear when the
{975} starches, sugar, and fats are withdrawn from the diet. Indeed,
the rule as to alimentation must be as rigidly enforced as in true
diabetes, but after the gastro-intestinal catarrh has subsided the
ordinary mixed diet--that before the disturbance began--may be returned
to gradually. Active exercise must be enjoined under the same
conditions and for the same purpose as in the treatment of lithaemia.
In these obese subjects, unaccustomed to movement, exercise must be
cautiously undertaken; beginning with short excursions, it must be
gradually increased. Horseback riding is an excellent expedient, but
should not take the place of walking.

The merely medical measures have a twofold direction: to remove the
gastro-duodenal catarrh; to promote oxidation of the sugar in the blood
or prevent the conversion of glycogen into grape-sugar. Vichy water,
the potash salts, and alkalies generally serve to accomplish the
latter, and phosphate and arseniate of soda, tinctures of nux vomica,
and of physostigma, bismuth, and carbolic acid, relieve the former.
Small doses of Fowler's solution (two drops ter in die), and a minim
three times a day of a mixture in equal parts of tincture of iodine and
carbolic acid, are effective remedies in gastro-duodenal catarrh.


Jaundice (Icterus).

DEFINITION.--The term jaundice has its origin in the French word jaune,
yellow. Icterus, which has come to be a more technical word, is of
uncertain Greek origin, and is much employed by French writers as
ictere. The common German name is Gelbsucht, a highly expressive
designation. Jaundice signifies a yellow discoloration of the skin
caused by the presence of bile. It is a symptom rather than a disease.
As a symptom it will receive much consideration in the pages to follow,
but there is also a functional disorder--a jaundice due to a
disturbance in the biliary functions, without evidences of structural
change--which must be discussed here. This preliminary statement of our
present knowledge of jaundice will facilitate the comprehension of it
as a symptom, and will render unnecessary explanations that will be
merely a repetition of previous ones.

CAUSES.--The theories of the causation of jaundice may be reduced to
three: 1, that it is due to a disorganization of the blood in which the
coloring matter is set free, and hence is known as haematogenous; 2,
that the materials of the bile, which it is the office of the liver to
remove from the blood, are not so disposed of; 3, that the bile, after
being formed by the liver, is absorbed into the blood because of an
obstacle to its escape, and hence this is called hepatogenous jaundice.

The modern view of haematogenous jaundice had its origin in the
supposed discovery of the identity of haematoidin with bilirubin. If
the pigment of the blood has the same composition as the pigment of the
bile, haematogenous jaundice will be produced whenever haematoidin is
set free in the blood. Virchow[13] was the first investigator to show
the close resemblance between these two pigments. Since his observation
was made an identity of haematoidin and bilirubin has been maintained
by Zenker, Valentiner, Kuhne, and others, and as strenuously denied by
{976} Stadeler, Preyer, Young, and others. At the present time it
appears to be established that although the blood- and bile-pigments
are closely related, they are not identical.[14] Nevertheless, a
haematogenous jaundice is still admitted to exist by Leyden,[15]
Immermann,[16] Gubler,[17] Ponfick,[18] and some others. The existence
or non-existence of this form of jaundice is, however, of little
importance in this connection, since, if it ever occur, the malady of
which it is a symptom is not an affection of the liver, but of the
blood, as phosphorus-poisoning, pyaemia, etc.

[Footnote 13: _Archiv fur path. Anat., etc._, Band i. p. 370, 1847.]

[Footnote 14: Legg, J. Wickham, _On the Bile, Jaundice, and Bilious
Diseases_, p. 243.]

[Footnote 15: _Beitrage zur Pathologie des Icterus_, Berlin, 1866, p.
6.]

[Footnote 16: _Deutsch. Archiv fur klin. Med._, Band xii. p. 502.]

[Footnote 17: _Union medicale_, 1857, p. 503.]

[Footnote 18: _Ziemssen's Cyclopaedia_, vol. ix. p. 24.]

The second theory, that the bile is preformed in the blood and
separated by the liver, and that jaundice results because of the
failure of the liver to perform this office, is no longer entertained,
although largely held down to within a very recent period. As the bile
acids and bile-pigments are not to be found in the blood, chemistry
lends no support to the theory of jaundice by suppression of the
hepatic function. As they do not exist in the blood and are found in
the secretion of the liver, there can be no other view held than that
they are formed by this organ.[19]

[Footnote 19: The old doctrine of jaundice by suppression, which has
always been maintained by Harley (_On Jaundice_, London, 1863, p. 20
_et seq._), has been again restated and strongly advocated by him in
his treatise on _The Diseases of the Liver_, p. 83, which was issued in
1883. In the two following postulates he formulates his view:

"1. The biliary secretion can be actually retarded, and even totally
arrested, without alteration of hepatic tissue.

"2. When the liver strikes work and secretes no bile, the animal body
becomes jaundiced as a direct consequence thereof."

This view, he affirms, "can be made comparatively easy of absolute
proof."

The evidence on which he chiefly relies is exceedingly fallacious. It
rests on two facts: the existence of a case of jaundice in which the
ducts and gall-bladder contain no bile, but only ordinary mucus; the
appearances presented by a liver in a case of jaundice due to
obstruction of the common duct. The evidence afforded by the former is
entirely fallacious, because in an old case of jaundice with catarrh of
the bile-ducts such changes take place in the bile that it loses all of
its distinctive characteristics. This may be seen in an ancient example
of obstruction of the cystic duct, where the bile which the
gall-bladder contained is ultimately transformed into a whitish or
colorless mucus. The changes which occur in the so-called cysts of the
arachnoid are comparable, and exhibit the entire transformation of
blood-pigment, which is closely allied to bile-pigment.]

The third theory of jaundice--that which refers the disease to an
absorption of the bile into the blood after it has been formed by the
liver--is the one now most generally held, and, indeed, as one of the
causes is universally held. The bile is absorbed into the blood because
an obstacle to its passage by the bile-ducts exists at some point in
their course. This is the principal, but not the only, cause of
absorption. When the pressure in the vessels falls below that in the
ducts, bile will pass toward and into the vessels. Again, it sometimes
happens that a considerable part of the bile discharged into the
intestines is reabsorbed unchanged, and enters the portal vein and the
general circulation, thus causing jaundice.

The disturbances of the liver causing jaundice are various. It
sometimes occurs without cause, and the first intimation of it is the
peculiar tint of the skin. It is certainly true that powerful emotions
are causative; thus, a violent anger has brought on an attack. In such
a case we must suppose a depression of the vaso-motor system, and such
a lowering of the blood-pressure as to favor the passage of bile into
the {977} veins rather than into the bile-ducts. Thus, it has been
abundantly shown that a slight difference in pressure will divert the
bile in either direction. Heidenhain[20] has demonstrated that the bile
passes in the direction of least resistance, and in the case of the
considerable vaso-motor depression caused by extreme emotion the least
resistance is in the direction of the vessels. More frequently than
moral emotion is catarrh of the bile-ducts. It is not necessary for the
catarrhal swelling of the mucous membrane to close the ducts to have
the bile pass into the veins; such a degree of swelling as to make the
passage of the bile somewhat difficult suffices. A simple hyperaemia of
the mucous membrane may cause sufficient obstruction of the bile-ducts
to give rise to jaundice. Gastro-intestinal catarrh plays an important
part in the production of simple jaundice. Frerichs[21] ascertained
that of 41 cases, gastro-duodenal catarrh existed in 34. Ponfick[22]
considers catarrh of the ducts the principal factor. In fact, at the
present time there is but one dissenting voice on this point.[23]

[Footnote 20: Quoted by Legg, _supra_, p. 253.]

[Footnote 21: _Diseases of the Liver_, Syd. Soc. ed., by Murchison.]

[Footnote 22: _Ziemssen's Cyclopaedia_, vol. ix., _supra_.]

[Footnote 23: Harley, _Diseases of the Liver_, 1883, p. 440 _et seq._]

Gastro-duodenal catarrh extends by contiguity of tissue to the mucous
lining of the bile-ducts. The catarrhal state of the mucous membrane is
produced by errors of diet, acid indigestion, indulgence in condiments,
wines, and rich foods in general. Climatic changes, malarial infection,
exposure to cold and dampness, etc. are indirectly causative of
jaundice through the intermediation of gastro-duodenal catarrh.

Formerly, obstruction of the gall-ducts was supposed to be caused
sometimes by a spasmodic contraction of the organic muscular fibre
assumed to exist in the walls of the ducts. Although the presence of
these muscular elements has been denied, Heidenhain has lately,
apparently, demonstrated them. Audige has made observations
confirmatory of those of Heidenhain, and Dujardin-Beaumetz[24] has
verified the statements of Audige. It seems, therefore, in a high
degree probable that organic muscular elements exist in the walls of
the hepatic ducts, and that spasmodic icterus may therefore occur.

[Footnote 24: _Bull. gen. de Therapeutique_, vol. lxxxv. p. 385, 1873.]

SYMPTOMS.--Simple icterus may exist without any other obvious symptoms
than the yellow discoloration of the skin. In most cases, however, the
yellowness is preceded for a week or more by the symptoms of a
gastro-intestinal catarrh, or these symptoms accompany the jaundice.
There is much mental depression and a general malaise is experienced.
Headache, mental hebetude, a total loss of appetite, a furred tongue,
and a bitter taste, nausea and sometimes vomiting, constipation or
diarrhoea, precede or accompany the jaundice. When these symptoms
precede for some time the appearance of yellowness, it is probable that
the biliary derangement is secondary to the gastro-duodenal catarrh,
but when they occur with the jaundice it is probable that they are due
to the absence of bile from the intestine.

The yellowness first appears in the conjunctiva for a day or two before
the skin is tinted, and within forty-eight hours after the flow of bile
into the intestine has ceased. The face next becomes yellow, then the
body, {978} and afterward the limbs, but in some cases the limbs remain
free from discoloration. The lips do not exhibit any change of color,
but the roof of the mouth, the palate, and the mucous membrane under
the tongue are yellow. The saliva does not, as a rule, contain
bile-pigment or exhibit any changes of color unless mercurial
salivation is caused, when it becomes greenish in color and has a
bitter taste.[25] A yellow tint of the sweat, especially under the
arm-pits, is common. The milk very often contains bile-pigment or is
changed in color in some way.

[Footnote 25: Legg, _On the Bile, etc._, _supra_.]

The feces are colorless or have a grayish or clay-colored tint, and are
semi-solid, although sometimes hard and dry. In simple jaundice
diarrhoea is very often present. There may be considerable flatulence,
and more or less pain in consequence about the umbilicus, and the gas
when discharged is very offensive. The stools also, in some cases, have
an odor of decomposition, and if carefully examined particles of food,
undigested and decomposing, will be found. The feces may have a
parti-colored appearance--part whitish or grayish or clay-colored, and
part of a normal color. This condition is not difficult of explanation.
The obstruction to the flow of bile may be in a part, and indeed in a
small part comparatively, of the liver, and hence there may be
sufficient bile flow down to color the feces to a greater or less
extent. But a small amount of bile-pigment in the blood suffices to
tint the whole surface of the body.

The urine may exhibit changes in appearance before the conjunctiva
becomes yellow. It is colored in all possible degrees, from a merely
high normal hue to a deep brownish almost black tint. It may be deep
red and clear like dark brandy or brown like porter, and thick with
urates. Usually, the urine of jaundice deposits abundantly of urates,
but this fact is more especially true of those patients retaining
appetite or having a voracious appetite and indulging in a full diet
without restraint. The reaction of the urine is acid, and the specific
gravity does not often descend below 1010, and may be 1030. The amount
passed in twenty-four hours varies, but does not differ materially from
the normal. Toward the termination of some fatal cases the quantity of
urine has greatly diminished, and in a few instances was suppressed,
but in such examples other factors than hepatic disease were concerned.
More or less albumen is nearly constantly present in the urine of
jaundice, but the detection of a trace is very difficult when the
urine, as is so often the case, is cloudy. The urine should be
carefully filtered before applying the test, and a specimen for
comparison should be placed alongside of that being examined. If on
boiling no haze appears, it may be developed by dropping in some nitric
acid. The nitric-acid test, so often employed by allowing some drops of
urine to trickle down the test-tube and observing the reaction at the
point of contact, is, in the writer's experience, very fallacious. The
source of the albumen in jaundiced urine is obviously the
blood-globules. As Von Dusch first demonstrated, and Kuhne[26]
afterward clearly confirmed, the bile acids dissolve the red
corpuscles. As the quantity of albumen in the urine is small, it is
reasonable to conclude, as suggested by Legg, that the bile acids are
not present in the blood in any considerable amount.

[Footnote 26: _Archiv fur path. Anat._, Band xiv. p. 333.]

When any large quantity of bile is contained in the urine, its
detection is not difficult. A strip of muslin dipped in the urine will
be stained, and the underclothing of the patient will have the
yellowish spots {979} caused by bile. Gmelin's test is the most
convenient. This is applied as follows: Some nitric acid containing
nitrous--which is the case of the ordinary commercial article--is put
into a test-tube, and some of the suspected urine is allowed to trickle
down the side of the tube to come in contact, but not mix, with the
acid. At the point of contact, when the urine contains bile-pigment,
first a zone of green, then blue, violet, and finally red color,
develops. As this play of colors takes place on the instant, the
attention must be sharply fixed to see the changes. Rosenbach[27]
suggests this test be applied by filtering some urine containing bile
through filtering-paper and touching the paper with a drop of nitric
acid. The result is, a green circle forms at the point of contact. The
usual mode of applying Gmelin's test is to place on the bottom of a
common white plate or on a porcelain dish a thin film of the urine, and
carefully bring in contact with it a thin film of nitric acid. The
color reaction mentioned above takes place at the margin of contact.

[Footnote 27: _Centralblatt fur die medicin Wissenschaft_, 1876, p. 5.]

Besides the presence of bile and albumen, and some fatty epithelium
from the tubules, there is no material change in the composition of the
urine. At one time it was supposed that the amount of urea was greatly
lessened, but later and more accurate investigations have shown that
this excretion is in greater or less quantity according to the food
taken, and bears no relation to the jaundice. On the other hand,
Genevoix[28] maintains that the quantity of urea is increased in
spasmodic icterus, and in the same ratio the uric acid declines. As
regards the chlorides and other salts, there seems to be a tolerably
constant ratio in their variations with the changes of quantity of urea
and uric acid--are therefore nearly related to the amount of food
taken.

[Footnote 28: _Essai sur les Variations de l'Uree et de l'Acide urique
dans les Maladies du Foie_, Paris, 1876, p. 59 _et seq._]

As regards the condition of the liver, there is no apparent change. In
topography, in the area of hepatic dulness, and in the dimensions of
the right hypochondrium the local condition does not deviate from the
normal in simple jaundice. There may be more or less tenderness over
the epigastrium and along the inferior margin of the liver, but there
is rarely any actual pain.

The circulation of bile in the blood and the action of the bile acids
on the red corpuscles must have an influence on the functions of
various organs. In some cases of jaundice, but by no means in all, the
pulse is slow, in a few instances descending as low as 40 per minute,
and, according to Frerichs,[29] as low as 21 per minute. Usually, the
pulse-rate is not lower than 60. To observe the slowing of the heart
the patient must be recumbent, for the pulse rises to the normal or
above on assuming the erect posture and moving about. The occurrence of
fever also prevents the depression of the circulation. The slowing of
the heart is found to be due to the action of the bile acids on the
cardiac ganglia. The other elements of the bile were ascertained to
have no influence on the circulation. As the heart may be slowed by an
increase of inhibition through stimulation of the vagi or by a
paralyzing action on the cardiac muscle, it was necessary to eliminate
these effects to establish the influence of the bile acids on the
ganglia. By exclusion, and by ascertaining the effects {980} of the
bile acids on a properly prepared Stannius heart, Steiner and Legg have
succeeded in demonstrating this important point.[30]

[Footnote 29: _Diseases of the Liver_, Syd. Soc. ed., _supra_.]

[Footnote 30: _Archiv f. Anat. u. Physiol._, 1874, p. 474; Legg, _On
the Bile, etc._, _loc. cit._]

The temperature of jaundice is normal usually, sometimes below. When a
febrile affection occurs during the course of jaundice, the rise of
temperature belonging to it is prevented in considerable part,
sometimes entirely. The depression of temperature is referred by Legg
to the lessened activity of the hepatic functions; but it seems to the
writer more satisfactory to refer it to the action of the bile acids on
the red corpuscles, the conveyors of oxygen. Rohrig[31] has shown
experimentally that the injection of bile acids has this effect on the
temperature of animals.

[Footnote 31: _Archiv der Heilkunde_, 1863, p. 418.]

The nutrition of the body early suffers in jaundice; more or less loss
of flesh soon occurs, and debility and languor are experienced. There
are several factors concerned in this result. The diversion of the bile
from the intestine interferes in the digestion of certain materials;
when jaundice occurs, glycogen ceases to be formed--and this substance
has an important office in nutrition and force-evolution--and the
injury done to the red blood-globules interferes with oxidation
processes.

The functions of the nervous system are variously disturbed in
jaundice. Headache, frontal, occipital, or general, is present in most
cases to a greater or less extent. Hebetude of mind and despondency are
nearly if not quite invariable, although it is not unusual to see men
with jaundice engaged in their ordinary avocations. Drowsiness is a
common symptom. More or less wakefulness at night, or sleep with
disturbing dreams, not unfrequently coincide with drowsiness during the
waking moments. In severe cases of icterus dependent on structural
changes the cholaemia may produce stupor, delirium, convulsions, etc.,
but such formidable symptoms do not belong to the simple and merely
functional jaundice.

Vision is sometimes colored yellow, or, rather, white objects appear
yellow, but this must be a rare symptom, since Frerichs never met with
an example. Murchison[32] narrates a case, and the writer has seen one.
It is a fugitive symptom, rarely continuing longer than two or three
days. The term xanthopsy has been applied to it.

[Footnote 32: _Clinical Lectures on Diseases of the Liver_, New York,
1877, p. 321.]

A nervous symptom of common occurrence is pruritus of the skin. This
may be so severe as to prevent sleep, and in any case is a disagreeable
and persistent affection, always worse at night. It may appear before
the jaundice so long a period as ten days, as in a case mentioned by
Graves,[33] and two months in a case narrated by Flint.[34] It is most
severe at the beginning of the jaundice, and usually disappears before
the jaundice ceases, but it may continue to the end. It is not limited
to any particular part of the body. Pruritus is sometimes accompanied
by urticaria, and the irritation caused by the friction of the skin may
set up an eczema. Occasionally boils, and more rarely carbuncles,
appear during the course of jaundice. Another curious affection of the
skin which occurs during chronic jaundice is xanthelasma or
vitiligoidea. First mentioned by Rayer, this disease was afterward well
described by Addison and Gull[35] under the name vitiligoidea, and they
recognized two varieties, v. plana and v. tuberosa. The plane variety
is found on the {981} mucous membrane of the mouth, the eyelids, the
palms of the hands, and the flexures of the joints, and consists of a
yellowish-white soft eruption slightly raised above the surrounding
skin and varying in size from a pin's point to a dime in size. The
color is described as like that of a dead leaf or chamois-skin. The
tuberose variety consists of small tubercles from a millet-seed to a
pea in size. They have a yellowish color, are tense and shining, and
are placed on the ears, neck, knuckles, elbows, knees, and other parts.
Whilst the plane variety gives little if any uneasiness, the tuberose
is apt to become irritated and painful. From the pathological point of
view this eruption consists of proliferating connective-tissue
corpuscles, some of which have undergone fatty degeneration.[36] The
morbid process tends to occur symmetrically, as on the eyelids, to
which it may be confined, but it usually develops in patches, and may
indeed extend over the whole body, when it is called xanthelasma
multiplex.

[Footnote 33: _Clinical Lectures on the Practice of Medicine_, 2d ed.,
by Neligan, p. 637.]

[Footnote 34: _Philada. Med. Times_, 1878, p. 507.]

[Footnote 35: _Guy's Hospital Reports_, 1851, p. 265.]

[Footnote 36: Waldeyer, _Archiv fur path. Anatomie, etc._, vol. lii. p.
318.]

The disorganization of the blood caused by jaundice sets up a
hemorrhagic diathesis. This result, however, is not usual in simple
jaundice, but belongs rather to acute yellow atrophy, sclerosis, and
other chronic affections of the liver. It will therefore be more
appropriately considered in connection with those maladies.

COURSE, DURATION, AND TERMINATION.--When jaundice is a symptom merely,
it pursues a course determined by the peculiarities of the disease. The
duration of simple jaundice varies from one to four weeks, the average
being about three weeks. If it continues longer than two months,
suspicions may well be entertained that the case is of a more
formidable character than simple jaundice. The termination of this form
of the disease is always in health. A favorable prognosis can be given
only in the case of an accurate diagnosis. Those cases may terminate
more speedily which, being of malarial origin, are treated by efficient
doses of quinine. If delirium and coma come on, the apparently mild
case means, probably, acute yellow atrophy, which cannot at the onset
be distinguished from simple jaundice. If any nervous symptoms occur or
if hemorrhage appears, the case will prove to be serious. A rise of
temperature usually indicates mischief. When the stools begin to
exhibit the normal appearance from the presence of bile, a satisfactory
termination of the case may be soon expected. The yellowness of the
skin disappears slowly after the natural route of the bile has been
restored, and the urine is the last to lose the pigment, as it was the
first to exhibit its presence.

DIAGNOSIS.--The diagnosis of jaundice as a symptom is usually easy. It
should be remembered that jaundice cannot be detected at night by any
ordinary light, and when it is disappearing the tint varies, now being
distinct, again absent. Mental emotion when the color is fading
develops it. Browning by the sun's rays causes an appearance which
might be mistaken by a superficial observer for jaundice, but it is
only necessary to look at the parts protected and at the urine to
discover the true state of the case. The detection of bile in the urine
and the ocular evidence of its absence from the stools will be
conclusive. In some cases of jaundice the stools are golden yellow, and
in many instances they are offensive.

{982} It is important to mark out the limits of the gall-bladder, if it
is of sufficient size to do so, for any accumulation of bile in this
sac signifies an obstruction of the ductus communis choledochus. If the
jaundice has come on after the symptoms of gastro-duodenal catarrh, is
recent, continues but two or three weeks, and then subsides without any
nervous symptoms or hemorrhage, it is a case of simple jaundice,
probably due to catarrh or spasm of the bile-ducts. If the jaundice be
preceded by attacks of severe pain, nausea, and vomiting, and
disappears after a week or two, the case is one of hepatic calculi. If
the jaundice persists months after such an attack of acute pain, and
does not disappear after a year or more, it is probably due to an
impacted calculus. The other diagnostic relations of jaundice are more
properly considered in connection with the malady of which jaundice is
a symptom.

TREATMENT.--For jaundice the symptom the treatment is included in that
of the disease. Here the treatment of simple jaundice, the functional
disorder, is to be discussed. If there is much nausea, the tongue is
heavily coated, and, especially if the seizure has followed dietetic
excesses, an emetic of ipecac may be highly serviceable. Recent
experiments have proved the accuracy of the clinical observations which
recognized the cholagogue property of ipecac, and hence the emetic
effect of this remedy is aided by its power to promote the discharge of
bile. Emetics are of course contraindicated when jaundice is due to an
impacted calculus, to malignant disease, to echinococci or other kinds
of tumor. If there is much irritability of the gastro-intestinal mucous
membrane, as shown in vomiting and diarrhoea, small doses of calomel
(1/12 to 1/4 grain) three or four times a day are highly useful. If
calomel possessed the property ascribed to it of stimulating the liver,
it would be injurious; it is beneficial here because it has a sedative
effect at first, followed, when a sufficient amount has accumulated, by
an eliminant action. Such hepatic stimulants as euonymin, sanguinarin,
podophyllin, jalap, colocynth, rhubarb, etc. have long been used in
cases of jaundice with the view that the liver is torpid and needs
stimulating. It may be inquired, however, If the bile already formed
has no outlet by the proper route, what utility can there be in making
the organ produce more? The true reason for the administration of such
remedies in any case of obstructive jaundice is to cause such downward
pressure as to force out of the duct an obstructing plug of mucus. The
writer has known this result to be accomplished by a dose of compound
jalap powder when a great variety of remedies had been employed in
vain. One of the most efficient remedies--in the writer's considerable
experience the most efficient--is phosphate of sodium, of which a
drachm or more is administered three times a day. This remedy liquefies
mucous plugs and promotes the flow of bile without harshly and rudely
forcing the biliary secretion, and it also has a marked curative effect
in gastro-duodenal catarrh. It may be given advantageously with
arseniate of soda--the latter in dose of 1/20 grain--and dissolved in a
tumblerful of Vichy water or Saratoga Vichy water, or preferably in a
wineglassful of hot water. Free use of alkaline and laxative mineral
waters is desirable, for a double purpose--to act on the liver and on
intestinal digestion, and to promote the excretion of biliary matters
by the kidneys. In this country we have a number to select from--the
Saratoga, Bethesda, Michigan, and others. Certain sulphurous waters,
{983} as the Blue Lick of Kentucky, are highly useful in the more
chronic cases. Sulphur baths may be conjoined to the internal
administration of the waters.

Nitric and nitro-muriatic acids have long been celebrated for their
good effects in jaundice. It is the presence of the acid chyme in the
duodenum which excites the normal flow of bile, and Bernard found that
applying acid to the orifice of the common duct in the intestine has
the same effect. There is then a rational reason for the administration
of this remedy. A nitro-muriatic bath, both local and general, was
formerly more used than now. Its utility is questionable, and the
difficulties in the way of applying it great.

Recently, Gerhardt[37] has proposed to faradize the gall-bladder, and
by compression with the fingers to empty it, forcing the bile into the
intestine, and thus clearing out obstructions. This seems to be very
questionable if not dangerous practice, but repeated successes will
justify it.

[Footnote 37: _Sammlung klinische Vortrage_, Volkmann, p. 112.]

Regulation of the diet is of the first importance. Fats, starches, and
sweets cannot be well digested when no bile enters the small intestine,
where they undergo conversion. These substances fermenting, much acid
results, and hence if a catarrh exist it is increased. An exclusive
diet of skimmed milk, kept up for two weeks or as long as possible, is
the best mode of alimentation for this part of the treatment.
Afterward, the diet should be composed of milk, meat-broth, lemonade,
and subsequently of the succulent vegetables, acid fruits, and fresh
meat. Indulgence in malt liquors, wines, and spirits should be strictly
prohibited.

A new method of treating jaundice has been lately proposed by
Krull,[38] which has the merit that no injury is done by it if no good
is accomplished. It consists in injecting into the rectum from two to
four pints of water at 60 degrees F., which is retained as long as
possible. Each time the injection is repeated the temperature is raised
a little. Krull reports that he has uniformly succeeded, and has never
found it necessary to repeat the injection more than seven times. It
may be given twice or thrice a day.

[Footnote 38: _Berliner klinische Wochenschrift_, 1877, p. 159.]


II. STRUCTURAL DISEASES OF THE LIVER.


Hyperaemia of the Liver.

DEFINITION.--An abnormal quantity of blood in the liver, constantly
present, constitutes hyperaemia or congestion. During the period of
repose there is less, but during the period of activity more, blood
circulating in the liver, but the physiological hyperaemia is not, nor
does it contribute to, a diseased state unless abnormal conditions
continue it beyond the proper limits. The term hyperaemia, here used,
applies to a pathological state in which various structural alterations
grow out of the continual congestion of the blood-vessels of the organ.

CAUSES.--A physiological congestion of the liver ensues when the {984}
process of digestion is going on. The afferent vessels dilate, and not
only more blood, but various materials taken up from the foods and
products of digestion, many of them having directly stimulating
effects, also pass to the organ. Frequent and large indulgence in food,
especially if rich in quality and highly seasoned with spices, mustard,
etc., the consumption of malt liquors, wines, and alcoholic fluids in
general, the habitual use of strong coffee and tea, gradually induce a
state of hyperaemia. If to the consumption of a large quantity of
highly-stimulating food there is added the mischief of insufficient
waste, the danger of congestion of the liver is the greater. Persons
addicted to the pleasures of the table are apt to pursue sedentary
lives, and hence, besides the inappropriation of the material digested,
the process of oxidation is insufficient to burn off the surplus. A
sedentary life further tends to make the circulation in the hepatic
veins sluggish by lessening the number and depth of the respirations,
and with the obesity developed under these conditions the propelling
power of the heart is diminished by fatty degeneration or fatty
substitution of the cardiac muscle. Disease of the semilunar ganglion,
the solar plexus, and of the splanchnics under circumstances and of a
nature not now well understood may cause dilatation of the hepatic
vessels.

Suppression of a long-existing hemorrhage from piles and from the
uterine system has caused hyperaemia of the liver. Evidences of hepatic
congestion are comparatively common about the menstrual period in
consequence of the tardy appearance of the flow, of its insufficiency,
or of its sudden suppression. There is a form of jaundice known as
icterus menstrualis, and attacks of hepatic congestion are not uncommon
at the climacteric period.

The most important causes of hyperaemia of the liver are mechanical,
and consist in obstruction to the circulation in the ascending vena
cava from disease of the heart or lungs. Dilatation of the right
cavities, incompetence of the tricuspid, and stenosis of the mitral
orifice are the usual cardiac changes leading to congestion of the
liver. The same effect, to a much less extent, however, is produced by
any cause which weakens the propelling power of the heart, as
myocarditis, pericarditis, etc. Amongst the pulmonary lesions
obstructing the venous circulation are emphysema, interstitial and
croupous pneumonia, effusions into the pleura, intrathoracic aneurisms
or tumors, etc. It should not be forgotten that effusions into the left
pleura, as was demonstrated by Bartels[39] and confirmed by Roser,[40]
so push over the mediastinum toward the right and bend the vena cava in
the same direction, just as it emerges from the opening in the
diaphragm, that the circulation in this vessel is impeded, and
consequently congestion of the liver induced.

[Footnote 39: _Deutsches Archiv fur klin. Medicin_, Band iv. p. 265.]

[Footnote 40: _Archiv der Heilkunde_, Band vi. p. 40.]

The influence of climate, especially of long-continued high
temperature, has been warmly disputed. On the whole, it seems probable
that in warm climates congestion of the liver is much more common.
Malarial infection is an unquestionable cause. In the section on
Jaundice it was stated that this symptom may occur without the
phenomena of fever, and, indeed, without any other disturbance of the
system. In a large proportion of cases of intermittent fever, probably
in all, more or less congestion of the liver occurs.

{985} PATHOLOGICAL ANATOMY.--Congestion may take place in the portal
system, and be due to conditions of the gastro-intestinal mucous
membrane, or in the hepatic vein and radicles, due to obstructive
troubles in the heart or lungs. The appearances vary accordingly.
Restricting the observations to the hyperaemia, and not including
subsequent lesions, it suffices to say that the liver is somewhat
enlarged, rather darker in color than the normal, and uniformly so; the
radicles and branches of the portal vein in the liver, the trunk of the
vein itself, and the veins of the spleen, stomach, intestines,
mesentery, etc. are distended with black blood, and the tissue of the
liver rather wet, inclined to soften, and here and there marked by
minute hemorrhages from rupture of small vessels. The extravasations of
blood accompany the hepatic congestion of hot climates, and probably
are the preludes to suppurative inflammation. The portal system the
more readily suffers from a passive congestion because of the provision
for the alternate expansion and contraction of the tunics of the
vessel, scantily supplied with contractile elements. An acute
congestion of the liver produced by sudden dilatation of the
capillaries of the hepatic artery has not been described, but it would
appear to be possible.

The most important form of hepatic congestion is the mechanical,
arising from obstruction of the circulation in the heart or lungs. In
consequence of this obstruction the blood accumulates on the venous
side, and there is in consequence an ischaemia of the arterial side.
The hepatic vein becomes distended, and its terminal radicle in the
centre of each acinus--the central vein--enlarges with the increased
pressure. It follows that the minute capillaries emptying into the
central vein are also distended with blood, and finally the portal vein
and its radicles throughout are similarly affected. The same condition
of the hepatic circulation was long ago observed by Virchow[41] as a
result of weakness of the muscular tissue of the heart, and
consequently diminished propelling power of the organ. On section of
the liver much black blood flows out; each central vein is a distinct
dark object in the centre of each acinus, and contrasts strongly with
the surrounding paler substance, whence the common term for this
appearance is nutmeg liver. The long-continued distension of the
central vein leads to sclerosis of its walls,[42] and the neighboring
hepatic cells undergo atrophy in consequence of the greater pressure. A
relatively increased quantity of connective tissue seems to result, but
whether hyperplasia occurs is disputed. By Talamon[43] such increase of
the connective tissue is denied, but Thierfelder[44] admits that there
is an apparent and also in some cases a real increase. The atrophy of
the cells induces more or less shrinking and consolidation of the
liver; it is therefore smaller in size and firmer in texture, and
presents a brownish-red color. The atrophic change in the hepatic cells
is represented finally by some brownish or black pigment, but it is
rare, indeed, for all the cells of an acinus to disappear. To this
change has been applied the term cyanotic atrophy. In some instances
Liebermeister[45] {986} has found an increase of the connective tissue
of the liver; and this opinion is confirmed by Legg.[46] When this
multiplication of the connective tissue occurs, the condition of the
liver is entitled cyanotic induration. The sclerosis originating in
this way is distinguished from true cirrhosis by its less extent,
irregularity, situation, and the marked degree of hepatic congestion.

[Footnote 41: _Archiv fur path. Anat., etc._, Band v. p. 289.]

[Footnote 42: Talamon, _Recherches anatomo-pathologiques et cliniques
sur le Foie cardiaque_, Paris, 1881 (pamphlet).]

[Footnote 43: _Ibid._]

[Footnote 44: _Atlas_.]

[Footnote 45: _Beitrage zur path. Anat. u. Klinik der
Leberkrankheiten_, Tubingen, 1864, p. 209 _et seq._]

[Footnote 46: _Medico-Chirurgical Transactions_, vol. lviii. p. 345.]

SYMPTOMS.--Hyperaemia of the liver is usually one of the complex
conditions of a morbid state, and hence is associated in its
symptomatology with the connected maladies. On the one hand associated
with gastro-intestinal disorders, on the other with cardiac and
pulmonary diseases, the symptoms must be varied accordingly. It is
necessary, however, to indicate as clearly as may be those belonging to
the hepatic circulation.

Congestion of the portal circulation is a condition to which frequent
references are made, but which is rarely clearly defined. As seen in
the West and South, it signifies a gastro-intestinal catarrh more or
less acute, with an obvious condition of biliousness, as manifested in
a faint jaundiced tint of the skin and of the conjunctivae, uneasiness
in the right hypochondrium, with enlargement of the area of hepatic
dulness, the evacuations from the bowels being either grayish or
clay-colored, or more frequently bilious, acrid, and offensive.

The gastro-intestinal disorder which initiates the hepatic disturbance
should not be confounded with that which succeeds to congestion of the
hepatic veins. The latter invariably comes on after the obstruction at
the heart or lungs has continued for some time. There occurs in this
state very extensive hyperaemia of the gastro-intestinal mucous
membrane, and consequent disorders of stomachal and intestinal
digestion. The former is a reflex cause of disturbance, probably
through the intermediation of the solar plexus. The gastro-intestinal
irritation, by depressing the functions of the hepatic through the
solar plexus, induces a paresis of the muscular layer of the portal
system, and thus congestion ensues. Such a result is aided by high
temperature, but especially by the constitutional tendencies of some
subjects to hepatic disturbances. In such examples of hyperaemia the
symptoms consist of those belonging to gastro-intestinal catarrh,
succeeded by those referable to the liver, consisting in uneasiness,
heaviness, and fulness of the right hypochondrium, increase in the area
of hepatic dulness, soreness on pressure along the inferior margin of
the ribs and over the epigastric region, yellowness of the
conjunctivae, a fawn color of the skin generally, and high-colored
rather scanty urine, depositing abundantly uric acid and urates. A
liver considerably enlarged and projecting one or two fingers' breadths
below the ribs may be quickly relieved and return to the normal size on
the occurrence of hemorrhage from piles or after free watery
evacuations produced by a hydragogue cathartic.

The form of hepatic congestion most usually observed is that of the
hepatic vein, caused by obstructive troubles of the heart or lungs, and
known as the nutmeg liver. The increase of size of the liver under
these circumstances may be very considerable. To determine an increase
in the area of hepatic dulness the position of the organ must be
ascertained with reference to the position of the body, whether
recumbent or erect. In the former position the liver gravitates toward
the thorax; in the {987} latter, downward into the abdomen. If
palpation only were employed to detect an increase in the size of the
organ, an error might readily be committed in this respect. Some
congestion may doubtless exist without an actual increase of size
recognizable by our means of investigation; there may be merely some
distension manifested by a sense of increased resistance; the liver may
project a hand's breadth below the ribs; and between these extremes
there may be all possible degrees of enlargement. When the liver, in
consequence of hyperaemia, projects below the ribs, it offers to the
sense of touch the impression of a smooth, elastic, rather rounded
surface, and not the hardness and nodular character of sclerosis, and
not the sharpness of border and hardness of texture belonging to
amyloid disease. The enlargement of the liver due to hyperaemia is
further distinguished by the fact that it varies much in size at
different times, and may be much reduced by hemorrhage from the portal
system, and increased suddenly by an attack of dyspnoea.

When the liver is enlarged by hyperaemia the patient usually has a
distinct appreciation of the fact, feels a sense of weight, tenderness,
and oppression in the right hypochondrium, and experiences a painful
dragging from the right toward the left when turned on the left side.
In some cases pain is felt in the shoulder, or, if not pain, a feeling
of weight. A slight icteroid hue of the conjunctiva, face, upper
extremities, and trunk is often present, but the stools are not wanting
in bile and the urine contains but little pigment--facts indicating
that the obstruction is limited to a small number of ducts. If the
jaundice is decided, the stools clay-colored, and the urine loaded with
pigment, a catarrhal swelling of the common or hepatic duct exists.

As nutmeg liver is an incident in the course of the venous stasis from
cardiac or pulmonary obstructive disease, it is not unusual to find
ascites and general dropsy occur. When ascites precedes the other
manifestations of dropsy, and is relatively more important, the hepatic
congestion has led to atrophy of the cells and contraction of the
organ, or to cyanotic induration, as it has been designated in
contradistinction to cirrhotic induration.

The subjects of hepatic congestion, especially of that form of the
malady due to gastro-intestinal irritation, are apt to experience no
little mental depression, even hypochondriasis, as, indeed, is usual in
most cases of hepatic disease.

COURSE, DURATION, AND TERMINATION.--The behavior of any case of
hyperaemia of the liver is determined, first, by the character of the
cause, and, secondly, by the extension of the mischief and the atrophic
changes which ensue. The congestion arising from gastro-intestinal
irritation is comparatively short-lived, since the causal conditions
may usually be promptly removed. It is far different in the cases due
to pulmonary or cardiac disease. If caused by a left pleuritic
exudation, the congestion will disappear as soon as the bend in the
ascending vena cava is removed by paracentesis. If, however, produced
by a permanent pulmonary obstruction, the course of the hepatic disease
is toward cyanotic induration. The same is true of obstructive cardiac
lesions. If compensation--as, for example, of a mitral
regurgitation--is not effected, the continual congestion must lead to
the ultimate lesions of the liver; but if compensation can be brought
about, the liver will be saved the irremediable {988} changes. The
prognosis, therapeutical and pathological, must necessarily be
dependent on the lesions of which the hyperaemia of the liver is merely
a symptom.

DIAGNOSIS.--The decision in any case of hyperaemia of the liver must
rest on the determination of the gastro-intestinal, pulmonary, or
cardiac diseases causative. When, for example, to the gastro-intestinal
disturbance or cardiac disease there are added heaviness, uneasiness,
increased area of dulness of the right hypochondrium, a hyperaemia of
the liver may be concluded to exist. The extent to which the organ is
damaged may be judged from its size, the duration of the congestion,
and the character of the determining cause. If the area of hepatic
dulness declines steadily after having been increased, the causative
conditions continuing, the shrinking is due to atrophy. This view is
confirmed if ascites has appeared and increased out of proportion to
the general dropsy.

TREATMENT.--Those cases of hyperaemia dependent on excesses in eating
and drinking require the substitution of a diet composed of lean meat,
skimmed milk, acid fruits, and such succulent vegetables as lettuce,
tomatoes, celery, etc. When there is a high degree of gastro-intestinal
catarrh, an absolute milk diet may be enforced with great advantage.
The diet, exercise, bathing, etc. enjoined in the section devoted to
lithaemia are equally applicable here. Amongst the special plans of
diet sometimes advocated in the condition of abdominal plethora or
portal congestion are the grape cure, the whey cure, etc. Great good is
accomplished by a simple diet and a course of the Saratoga saline
laxative waters--the Congress, Hathorn, Geyser, etc. The alkaline
waters of Wisconsin and Michigan, the White Sulphur of Virginia, and
others having similar properties in this country may be employed for
the same purpose. The saline laxatives, Pullna, Friedrichshall, and
other purgative salines, may be used in robust, plethoric subjects with
much portal congestion, hemorrhoids, etc. Phosphate of soda, given in
sufficient quantity to maintain a soluble state of the bowels, is also
a useful remedy. The resinous cathartics, podophyllin, jalap, rhubarb,
aloes, euonymin, iridin, baptisin, etc., are all useful when the
indication is to unload the portal circulation. The mercurials,
formerly so much used, are now discredited to an unwarranted degree. In
an irritable state of the gastro-intestinal mucous membrane calomel in
small doses is remarkably useful.

The treatment of congestion of the hepatic vein is included in that of
the lesion causing it. In some rather exceptional cases the liver
enlarges considerably in consequence of incompetence of the mitral,
without there being any other conspicuous evidence of the lesion.
Remarkable relief is afforded to the hepatic symptoms by the
administration of digitalis. The important point in all cases due to
cardiac disease is to bring about compensation, and thus obviate the
consequences of the lesion. Remediable pulmonary affections should be
cured as promptly as possible, and the evil results of incurable
affections lessened by efforts to remove the hepatic hyperaemia.
Careful alimentation, saline laxatives, and diuretics are the most
efficient measures. It would be encroaching on the subjects of
pulmonary and of cardiac diseases to enter more minutely into the
therapeutical questions connected with a symptom of these affections.


{989} Perihepatitis.

DEFINITION.--By the term perihepatitis is meant an acute inflammation
of the serous envelope of the liver. It may be acute or chronic, very
rarely the latter, and it is usually a secondary affection, although
primary cases are not uncommon.

PATHOGENY.--Inflammation of the hepatic portion of the peritoneum may
arise by an extension of the morbid process from neighboring parts, as
in perforation of the stomach or duodenum, pleuritis of that part of
the membrane reflected from the diaphragm, etc. More frequently it
arises by contiguity from some disease of the liver itself, as chronic
interstitial hepatitis, abscess, echinococci cysts, cancer, etc. The
author has frequently (comparatively) seen perihepatitis follow the
passage of gall-stones. It is usual to find considerable organized
exudation at the hilus of the liver in the case of those who have had
several attacks of hepatic colic, and attachments to various
neighboring parts also. In those instances of secondary hepatitis there
may be more or less extensive connective-tissue formation and
compression of the hepatic substance (Budd).[47]

[Footnote 47: _Diseases of the Liver_; also, Bamberger, _Krankheiten
des Chlylopoietic Systems_, p. 495, 2d ed.]

Direct perihepatitis arises from traumatic causes--from contusions of
the right hypochondrium by spent balls, blows and falls, etc.
Tight-lacing and wearing a strap to support the trousers are supposed
to excite a slow, chronic hepatitis, but the latter is more certain to
bring about such a result than the former.

SYMPTOMS.--Acute perihepatitis, if of sufficient extent, causes more or
less fever; pain is felt in the right hypochondrium, and is increased
by pressure and by deep inspirations, and in some rare instances a
friction murmur is audible synchronous with the respiratory movements.
These symptoms succeed to attacks of hepatic colic, perforation of the
stomach or intestine, and contusions of the abdominal wall. The chronic
form is not febrile; there is a feeling of soreness instead of acute
pain; pressure, the movements of the body, respiration, etc. increase
the distress, and on turning on the left side a painful dragging is
experienced. A slight degree of icterus may be present in both acute
and chronic cases.

COURSE, DURATION, AND TERMINATION.--The course of the acute cases is
toward recovery. In two or three days the inflammation reaches the
maximum, adhesions form, and then the morbid process declines. The
whole course of an acute perihepatitis caused by external injury or by
the passage of gall-stones is terminated in a week or ten days. The
mischief done may not be limited to the adhesions formed. The large
quantity of newly-organized connective tissue may, in its subsequent
contraction, compress the common, cystic, or hepatic duct, or the
portal, or both ducts and vein. The course of the chronic cases is
determined by the causative lesion. The contraction of the new-formed
connective tissue may compress the organ and lead to sclerotic changes
which cannot be distinguished from cirrhosis. In some instances
contusions set up suppurative inflammation, and an abscess forms
between the parietal and glandular layer of the peritoneum. Such a case
will then present the phenomena of hepatic abscess.

DIAGNOSIS.--The determination of the character of the case will be
{990} largely influenced by the history. If the attack has followed a
blow on the side or a paroxysm of hepatic colic or the symptoms of
perforation, there will be no difficulty in determining its seat and
character. In the absence of the history the differentiation must be
made between perihepatitis and pleuritis. The distinction consists in
the fact that in the former the pain and soreness are below the line of
respiratory sounds, although synchronous with them. In chronic
perihepatitis the symptoms come on in the course of the hepatic
disorder, or are consequent on a local injury, as the pressure of stays
or a band.

TREATMENT.--If the symptoms are acute and the subject robust, the local
abstraction of blood by leeches affords relief and diminishes the
violence of the disease. A bandage should be tightly applied around the
body at the level of the hypochondrium to restrain the movements of the
affected organ. A turpentine stupe may be confined in this way, or a
compress of water may be utilized to serve the same purpose. If the
pain is acute and the peritonitis due to perforation or to the passage
of calculi, the hypodermatic injection of morphia is the most important
resource.


Interstitial Hepatitis; Sclerosis of the Liver; Cirrhosis.

DEFINITION.--The terms interstitial hepatitis and sclerosis of the
liver express the nature of the malady: they signify an inflammation of
the intervening connective tissue, resulting in a sclerosis--an
induration of the organ. The term cirrhosis, now so largely in use, was
originally proposed by Laennec[48] because of the yellowish tint of the
granulations, from the Greek word, [Greek: chirros], yellow. As
Laennec's theory of cirrhosis was erroneous, having regarded these
granulations as new formations, the word is a very faulty one, and
hence it would be preferable to use the term sclerosis, since a similar
change in other organs is thus designated, as sclerosis of the kidney,
sclerosis of the lungs, etc. It is also called in England gin-drinker's
liver, hobnail liver. Carswell[49] first described the anatomical
changes with accuracy, and illustrated them with correct drawings. The
following year Hallmann[50] confirmed the truth of Carswell's
descriptions, and contributed a good account of the morbid anatomy; and
subsequently French, German, and English authorities added new facts,
which will be set forth in the further discussion of the subject.

[Footnote 48: _Traite de l'Auscultatlon mediate_, tome ii. p. 501.]

[Footnote 49: _Illustrations of the Elementary Form of Diseases_,
fasciculus 10, plate 2.]

[Footnote 50: _De Cirrhosi hep._, Diss. Inaug., Berolini, 1839, quoted
by Thierfelder.]

CAUSES.--Sclerosis of the liver is, conspicuously, a disease of adult
life and onward. Except the congenital example mentioned below, the
earliest age at which the disease has occurred, so far as I am able to
ascertain, is four years--a case reported by Wettergreen[51] of
hypertrophic sclerosis, in which neither a syphilitic nor paludal cause
could be ascertained. Cayley[52] reports a case in a child of six;
Murchison,[53] Frerichs,[54] Griffith,[55] one each at ten. After this
period the increase relatively to age is rapid. The majority of cases
occur between thirty {991} and fifty years. Yet Virchow[56] has given
the details of a congenital example. According to Forster, of 31 cases
of cirrhosis, 16 were between forty and sixty years. The preponderance
of cases in the male sex is very decided. Of Bamberger's 51 cases, 39
were men, 12 were women; of Frerichs' 36 cases, 20 occurred in men and
16 in women--a larger proportion of women than any other author
records; of 12 cases observed by myself, only 1 was a woman.
Nationality does not affect the production of cirrhosis, except as
regards the personal habits of the people. This disease is
comparatively uncommon in wine- and beer-drinking countries, and
frequent amongst a spirit-drinking people.[57] The great etiological
factor is the abuse, the habitual use, of spirits, and hence the number
of cases observed in North Germany, England, Scotland, and the United
States. Murchison affirms that he has never seen a case produced in any
other way. Even in children of tender years the abuse of spirits can
usually be traced. Nevertheless, there are instances of the disease the
origin of which cannot be referred to alcoholic excess. The congenital
cases, as that narrated by Virchow, and the instances occurring in
children and adults not given to spirits in any form, indicate that
there are other pathogenetic influences which may bring about a
sclerosis of the liver. Virchow[58] was one of the first to illuminate
the subject of visceral syphilis and to demonstrate the occurrence of
sclerosis of the liver from syphilitic infection. Very often the
syphilitic cachexia coincides with alcoholic excess. There can be no
doubt that chronic malarial poisoning causes, or powerfully predisposes
to, cirrhosis. I have submitted elsewhere pathological evidence on this
point,[59] and the Italian physicians, who have the opportunity to
obtain accurate data, maintain that malarial toxaemia does bring about
this state. It is probable that the overgrowth of connective tissue is
induced by the repeated congestions of the malarial attacks, and by the
obstruction due to catarrh of the bile-ducts which so often occurs in
the febrile paroxysms.

[Footnote 51: _Hygeia_, 1880, quoted by _London Medical Record_, March
15, 1881.]

[Footnote 52: _Transactions of the Path. Society of London_, vol.
xxvii., 1876, pp. 186, 194.]

[Footnote 53: _Clinical Lectures_, _loc. cit._]

[Footnote 54: _Clinical Treatise, etc._, Syd. Soc. ed., by Murchison.]

[Footnote 55: _Clinical Lectures_, _loc. cit._]

[Footnote 56: _Archiv f. path. Anat._, Band xxii. p. 426.]

[Footnote 57: Baer, _Der Alcoholismus_, Berlin, 1878, p. 62 _et seq._]

[Footnote 58: _Virchow's Archiv_, vol. xv. p. 281; also, Lancereaux, _A
Treatise on Syphilis_, Syd. Soc. ed.]

[Footnote 59: _Memoirs of the Sanitary Commission_, medical volume.]

J. Wickham Legg[60] and Charcot[61] nearly simultaneously discovered
that obstruction of the bile-ducts, if continued a sufficient length of
time, sets up a hyperplasia of the connective tissue of the liver. The
evidence is pathological and experimental. Thus, Legg has seen a liver
markedly cirrhotic in a case where a small cancer of the duodenum
completely obstructed the flow of bile into the intestine.[62] By tying
the common duct in dogs it was found that a hyperplasia of the
connective tissue very soon occurred, and this was followed, of course,
by contraction of the new tissue and atrophy of the hepatic cells.
Closure of the hepatic vein has the same effect, and also, as
Solowieff[63] has asserted, closure of the portal vein; on the other
hand, by Frerichs and others the closure of the portal is attributed to
the sclerosis.

[Footnote 60: _On the Bile, Jaundice, etc._, _loc. cit._, p. 351 _et
seq._]

[Footnote 61: _Lecons sur les Maladies du Foie, etc._, p. 231 _et
seq._]

[Footnote 62: _On the Bile, Jaundice, etc._, _loc. cit._, p. 355.]

[Footnote 63: _Arch. f. path. Anat., etc._, Band lxii. p. 195.]

Certain poisons, as antimony, arsenic, notably phosphorus, have the
power to set up an irritative hyperplasia of the connective tissue of
the {992} liver. These metals accumulate in the liver in preparation
for excretion. Wegner,[64] in the study of the action of phosphorus on
dogs, rabbits, and other animals, has induced a marked degree of
sclerosis, but such results have not been observed in cases of
poisoning by phosphorus in man, except in an instance reported by
Kussner.

[Footnote 64: _Virchow's Archiv_, Band lv. p. 18.]

Finally, a condition of the liver corresponding in all respects to
cirrhosis has been induced by perihepatitis, by the organization of the
exudation and its subsequent contraction, and by the extension of the
morbid process from the capsule to the interlobular connective tissue
(Poulin[65]).

[Footnote 65: _Etude sur les Atrophies viscerales consecutives aux
Inflammations chroniques du Sereuses, etc._, These de Paris, 1880.]

PATHOLOGICAL ANATOMY.--Several forms of cirrhosis are recognized by the
modern French school of pathologists. According to Sabourin,[66] there
is an annular, a monolobular, and a multilobular form. These differ
merely in regard to the arrangement of the new connective tissue. At
the outset of the disease the liver is increased in size and
hyperaemic. Its consistence is also greater than normal. The outer
surface is at this period smooth, but on section the islets of the
parenchymatous tissue, yellowish in color, are distinctly visible
between the grayish or pale-rose tint of the intervening or
proliferating tissue. This reddish-gray material consists of fine
connective-tissue elements containing spindle-shaped cells.[67] The
development of this material is such as to even exceed in quantity the
proper glandular structure. The bands of newly-formed connective tissue
extend between individual lobules (monolobular cirrhosis) or between
groups of lobules (multilobular cirrhosis). A portion of the
spindle-shaped cells form new vessels communicating with the branches
of the hepatic artery.[68] Coincidently with the formation of the new
connective tissue ensues its contraction. The enlarged organ diminishes
in size from a slight degree to one-half its original volume;
especially in the left lobe is the diminution of size most marked. On
the surface it exhibits a knobbed or nodular aspect (hobnail liver),
and these knobs present through the capsule a yellow appearance. The
granulations, so called, consist of small prominences corresponding to
lobules or groups of lobules, and hence vary in size from that of a
pinhead to that of a pea.[69] Between these are the sharply-defined
masses of connective tissue. On section the organ is found to be of
firm almost cartilaginous hardness, and between the interlacing bundles
of connective tissue are the small islands of parenchymatous tissue
projecting above the cut surface and having a yellowish or
brownish-yellow color. As the terminal branches of the portal are
compressed in the process of shrinking undergone by the new connective
tissue, they are destroyed. The result of this obliteration of the
portal radicles is the impaired nutrition of the lobules and atrophy of
the cells. Formerly it was held that the atrophy of the hepatic cells
was due to the compression exercised by the contracting connective
tissue, and Beale[70] even maintained that the change began in {993}
the cells, the connective tissue contracting as the cells receded
before them. This view has been reaffirmed by Ackermann in a paper read
last year before the Congress of German Naturalists and Physicians, but
without any acknowledgment, so far as I can ascertain, of Beale's
long-before expressed opinions. In the discussion which followed the
reading of Ackermann's paper the position of its author was supported
by Aufrecht, Kussner, and others, but controverted by Rindfleisch. It
has been demonstrated by Cohnheim and Litten[71] that the lobule is
nourished not only by the portal radicles, but by the branches of the
hepatic artery, which enter, by the interlobular vein, the capillaries
of the lobule, and hence the nutrition of the cells suffers in
consequence of the lessened blood-supply; but it is probable also that
more or less compression is exercised. When the cells are destroyed,
their remains may be discerned in the mass of connective tissue as fine
fat-granules or masses of pigment yellowish or brownish in color. The
peculiar appearance to which the name cirrhosis is applied is due to
the lobules or groups of lobules which project on section above the
divided surface, and are colored yellowish by the bile-pigment, which
here exists in an exaggerated quantity. The cells themselves are not
normal: they are enlarged by compensatory hypertrophy, and they contain
much bile-pigment and a considerable quantity of fat. The compression
of the capillaries, especially their obliteration, leads to stasis of
the blood and its consequences in the whole chylopoietic system.

[Footnote 66: Ch. Sabourin, "Du Role que joue le Systeme veineux
sus-hepatique dans la topog. de la cirrhose du foie," _Revue de
Medecine_, June, 1882.]

[Footnote 67: Forster, _Lehrbuch der pathologischen Anatomie_, Jena,
1873, p. 264.]

[Footnote 68: Cornil, "Note sur l'Etat anatomique des Canaux biliaires
et des Vaisseaux sanguins dans la cirrhose du foie," _Gaz. med. de
Paris_, 1883.]

[Footnote 69: Charcot, _Lecons sur les Maladies du Foie, etc._, p.
226.]

[Footnote 70: _Archives of Medicine_, vol. ii. p. 82.]

[Footnote 71: _Archiv fur path. Anat._ (Virchow), Band lxvii. p. 153
_et seq._]

SYMPTOMS.--The development of sclerosis is usually very insidious.
After some years' indulgence in spirit-drinking or affected for a
length of time with the other causes of the malady, a gradual decline
of vigor occurs. The complexion takes on a fawn color, stigmata slowly
form on the face, there is more or less yellowness of the conjunctiva,
and attacks of headache, giddiness, and even severe vertigo, are
experienced. An increasing indisposition to mental effort, some
hebetude of mind, and a gradually deepening despondency are felt. The
appetite gradually fails, becomes capricious, and only highly-seasoned,
rather odd, or unusual articles of food can be taken. Such subjects
acquire a taste for condiments, for such uncooked vegetables as onions,
celery, raw cabbage, etc., for fruits, and get a distaste for
plainly-cooked meats and vegetables, for sweets, etc. The digestion is
as capricious as the appetite: at first there are times of appetite,
again of indifference, then of disgust; some heaviness is felt after
meals; gaseous eructations, acidity, pyrosis, nausea, occur day after
day as the case advances; and ultimately morning vomiting is regularly
experienced. Nausea is felt on rising; then with much straining and
distress a little glairy mucus and a teaspoonful of bile are brought
up; after which, it may be, a little food can be taken. It is only
after the case is fully declared that these troubles of stomach
digestion become constant; previously they occur now and then in a
paroxysmal way, whilst between there is only labored digestion.

As the compression of the portal radicles maintains, by reason of the
obstruction, a constant hyperaemia of the intestinal mucous membrane, a
catarrhal state, with fermentation of the fatty, starchy, and
saccharine constituents of the food, and hence complicated products of
an irritating kind, must result therefrom. Hemorrhoids, varying in size
according to {994} the degree of obstruction, form, sometimes bleeding
more or less profusely, again being merely troublesome or painful.
Fissures of the anus and fistula in ano not unfrequently complicate the
case. The bowels are necessarily rather relaxed than confined, but at
the onset of the malady they may be confined, afterward assuming more
or less of the characteristics of diarrhoea. The stools may be
offensive with the products of decomposition, rather clay-colored or
golden, or brownish and almost black from the presence of blood. In
some cases the stools are parti-colored--clay-colored in part, brownish
in part--and in exceptional examples continue normal or nearly so until
near the end. As the transudations from the portal vessels increase,
the mucous membrane of the intestinal canal becomes oedematous, and,
the normal secretions being arrested, the discharges finally consist of
a watery fluid, whitish or grayish, dark-brown or blackish, and very
offensive. The decomposition of foods instead of their proper digestion
and solution, and especially the fermentation of the starchy and
saccharine constituents of the aliment taken, produce a great quantity
of gas; hence meteorism comes to be an ordinary symptom. The
accumulation of gas is greatly promoted by the paretic state of the
muscular layer and by the relaxation of the abdominal walls consequent
on the oedema of the muscular tissue. A high degree of distress is
sometimes caused by the great accumulation of flatus; the abdomen is
greatly distended and the diaphragm is pushed up against the heart and
lungs, compelling the patient at length to sit up to breathe with ease.
Of course the accumulation of fluid may be greater, and the gas only
add to the discomfort.

A very common symptom is hemorrhage. Sometimes it happens, indeed, that
this is the only evidence of the portal obstruction at first observed.
Haematemesis is more common than intestinal hemorrhage. Now the blood
may be large in quantity, appear little changed from its usual
coagulated state, and be brought up promptly with slight effort of
vomiting; now it is passed by stool, is in coffee-colored, granular
masses or in a tar-like, semifluid state; and again it appears in
coffee-grounds mixed with the contents of the stomach. These variations
are due to the character, seat, and extent of the hemorrhage and to the
condition of the mucous membrane. Merely-distended capillaries,
yielding, may furnish a little blood, which, acted on by the gastric
juice, forms coffee-grounds, or, if not acted on in consequence of the
failure of the gastric glands to functionate, appears as bloody streaks
mixed with mucus. Enlarged veins, giving way, may furnish a large
quantity of partly-coagulated venous blood, charred or not as the state
of the juices will determine. In some cases hemorrhages into the
submucous tissue or thromboses of the submucous veins lead to solution
of the membrane thus deprived of its nutritional supply, and ulcers
form. Two admirable examples of this kind have been seen by the writer
in which large haematemesis occurred from ulcers near the pylorus. They
were round, smooth ulcers, containing coagula, and the eroded vessels
(veins) were readily seen opening into the cavity of each.

The obstruction to the portal circulation results also in an
enlargement of the spleen. There may be a simple enlargement due to the
hyperaemia merely; there may be an enlargement due to the hyperaemia
and to a resulting hyperplasia of the connective tissue; there may be
also, in {995} addition to the second form of enlargement, amyloid
degeneration, syphilitic hyperplasia, etc. The increased dimensions of
the spleen are by no means always made out, and authorities differ
greatly as to the proportion of cases in which the enlargement can be
detected. The organ may indeed be considerably enlarged whilst pushed
upward into the left hypochondrium by the effusion, and yet the attempt
to measure and define its dimensions may be fruitless. From a slight
increase due to the hyperaemia up to the enormous dimensions acquired
by the added amyloid material there are all possible variations in
size.

Partly in consequence of the increased blood-pressure in the vessels of
the peritoneum, and partly in consequence of the watery condition of
the blood itself, effusion takes place into the sac of the peritoneum.
Such an accumulation is known as ascites, or dropsy of the abdomen. The
time at which the effusion begins, the amount of it, and the degree of
contraction of the liver necessary to produce it, vary in each case.
Ascites may be the first symptom to announce the onset of cirrhosis; it
is more frequently amongst the later symptoms, and is the evidence of
much interference in the portal circulation. However, it is not due
wholly to hepatic disease. The blood in cirrhosis is much reduced and
watery, hence slight causes suffice to induce an outward diffusion.
Given a certain obstacle to the passage of the blood through the liver,
transudation will be the more prompt to appear the greater the anaemia.
In some cases an enormous quantity of fluid collects: from ten to
thirty pounds may be regarded as usual, and forty to sixty pounds as
exceptional, although the highest amount just given is not rare. The
fluid of ascites nearly represents the serum of the blood. It has a
straw color and is clear, but it may have a reddish tint from the
presence of blood, a greenish-yellow or brown from bile-pigment. The
solids of the serum are in the proportion of from 1 to 3 per cent., and
consist of albumen chiefly and salts, of which sodium chloride is the
principal. Hoppe's[72] analysis gives this result: 1.55 to 1.75 solids,
of which 0.62 to 0.77 is albumen. According to Frerichs, the amounts of
solids ranges from 2.04 to 2.48, and of these albumen constitutes 1.01
to 1.34.

[Footnote 72: _Virchow's Archiv fur path. Anat., etc._, Band ix.]

Oedema of the inferior extremities comes on after, usually--rarely
with--the ascites. If the mechanism of this oedematous swelling be as
supposed, the effusion into the areolar tissue necessarily succeeds to
the abdominal effusion. The pressure of the fluid in the cavity on the
ascending vena cava and iliac veins seems to be the principal factor;
but to this must also be added the intestinal gas, which in some
instances exerts a powerful force. The ankles have in rather rare cases
appeared swollen before the abdomen, but the detection of fluid in the
peritoneal cavity when in small quantity is not always easy. Obese
women, with much accumulation of fat in the omentum and flatus in the
intestines, have swollen feet and legs if erect for some time, the
effusion being due to pressure on the vena cava. The legs may become
enormously distended. The scrotum and penis in the male, the vulva in
the female, the buttocks and the abdominal wall, also become
oedematous, sometimes immensely. Walking grows increasingly difficult.
Warmth and moisture and the friction of the sensitive surfaces excite
vesicular and pustular eruptions where the {996} scrotum and labiae
come in contact with the thighs. Urination may be impeded by the oedema
of the prepuce.

An attempt at compensation for these evils growing out of the
obstruction in the portal system is made by the natural powers.
Anastomoses of veins through minute branches are made use of to convey
the blood of the obstructed portal circulation into the general venous
system, and to this end become greatly enlarged. The interlobular veins
being obliterated by the contracting connective tissue, the pressure in
the branches and trunk of the portal vein is much increased. Hence an
outlet is sought for in the veins which communicate between the portal
and the ascending vena cava. One of the most important of these is a
vein in the round ligament, at one time supposed to be the closed
umbilical vein, but proved by Sappey to be an accessory portal vein.
Bamberger,[73] however, has found the umbilical vein pervious, and
since, Hoffmann[74] has demonstrated the same fact. It is probable,
indeed, that Sappey's observation is correct for some cases. In either
event, the veins of the abdominal wall about the umbilicus
communicating with the epigastric become enormously distended, and in
some advanced cases of cirrhosis form a circle known as the caput
Medusae. Further communication between the portal and the veins of the
diaphragm takes place by means of the veins in the coronary and
suspensory ligaments. In some instances a new route is established
between the veins of the diaphragm and the portal by means of new
vessels formed in the organized connective tissue resulting from
perihepatitis. Still another channel of communication exists between
the inferior oesophageal veins, the azygos, and the coronary, and
finally between the inferior hemorrhoidal and the hypogastric. The more
completely can communication be established between these anastomosing
veins the less severe the results of portal obstruction.

[Footnote 73: _Krankheiten des Chylopoiet. Syst._, _loc. cit._]

[Footnote 74: Quoted by Thierfelder, _op. cit._]

Besides these indirect evidences of portal obstruction and a
contracting organ, there are direct means of ascertaining the condition
of the liver. By the methods of physical diagnosis we may acquire much
information. On auscultation, as our Jackson[75] was the first to show,
a grating or creaking like leather, or friction sound, is audible over
the right hypochondrium synchronously with the respiratory movements or
when produced by moving with the fingers the abdominal wall on the
liver. This sound is caused by the bands of false membrane which extend
between the two surfaces, and hence indicates a secondary
perihepatitis.

[Footnote 75: _The American Journal of the Medical Sciences_, July,
1850.]

To ascertain the dimensions of the liver--to mark out the area of
hepatic dulness--with accuracy is a most necessary procedure. The
period of the disease is an important element in the problem. When the
new material is deposited and the congestion of the portal system first
occurs, an increase in the dimensions of the organ is observed. This
enlargement, of brief duration, must not be confounded with the
hypertrophic sclerosis, another form of the malady. So considerable is
the increase in the size of the liver that there is an evident
enlargement of the right hypochondrium, and the whole abdomen seems
fuller. The organ may be felt, on palpation, projecting one, two, or
even three fingers' breadths below the margin of the ribs, and the left
lobe extends well across the epigastrium, increasing the sense of
resistance and the area {997} of dulness in this direction. The
enlarged liver, as felt below the ribs, appears firmer than is natural,
is yet smooth, and the margin is sharply defined. The duration of this
period of enlargement is indefinite, but it is rather brief, and is
followed by the contracting and atrophic stage. It is not often,
indeed, that the patient presents himself during the period of
enlargement. Sometimes a perihepatitis or an unwonted tenderness in the
right side compels attention during this stage, but more frequently it
escapes notice. If perihepatitis occur, there will be fever, pain, and
tenderness, a slight icterode hue of the skin, and possibly
Jackson's[76] friction sound. These symptoms, taken in conjunction with
the history of the case and the obvious enlargement of the organ, will
indicate the existence of the first stage of sclerosis.

[Footnote 76: _The American Journal of the Medical Sciences_, July,
1850, _supra_.]

The contraction of the liver, or, as it may be expressed, the atrophy
of the hepatic cells and the consequent shrinking of the interlobular
connective tissue, goes on slowly. Several months may be occupied in an
amount of atrophy distinct enough to be recognized by the narrowing of
the area of hepatic dulness. Especially difficult is the recognition of
the contraction when ascites has fully distended the abdomen. It may be
necessary under such circumstances to postpone a decision until tapping
has removed the fluid. If the organ can be felt by depressing the walls
of the abdomen, more or less unevenness of surface may be detected, and
the inferior margin may give the impression of hardness and sharpness
of outline. At the same time, the increased dulness of the epigastric
region observed during the hypertrophic stage will have gradually
ceased because of the shrinking of the left lobe. The liver may be
undergoing the atrophic degeneration to a marked extent and yet remain
large--larger even than normal. Such a state of things may be due to
conjoint amyloid or fatty degeneration of the organ, and, indeed, more
or less fatty change occurs in all cases of cirrhosis. The shrinking of
the liver persists until the area of dulness is not greater in area
than two or three ribs.

The disturbances of function in sclerosis of the liver are not limited
to the chylopoietic system. As the secreting structure of the liver is
continually lessened in extent by the atrophy, symptoms result from the
necessary interference in the hepatic functions. These symptoms are
concerned with the liver, with the nutrition of the tissues of the
body, and with the kidneys. As regards the biliary function of the
liver, the quantity of bile acids and pigment is reduced below the
normal in proportion to the damage done to the organ. As a rule, there
is little jaundice in sclerosis, and very little bile-pigment present
in the urine. Hence there must be little produced. Instead of a
jaundiced hue of the skin, it has a fawn color--an earthy, sallow tint
eminently characteristic of a chronic affection in which the power to
produce bile is much impaired. Occasionally it happens, particularly in
the early stages of cirrhosis, that a well-marked jaundice appears in
the face and body, but this probably is due to a catarrh of the
bile-ducts. In most cases the integument presents the earthy and sallow
hue above mentioned. Graves[77] appears to have been the first to
interpret aright the greater significance of this appearance of the
skin than the purely jaundiced tint. The glycogenic {998} function of
the liver must be impaired in the same ratio as the biliary. The
nutrition of the body suffers; the skin becomes dry and harsh; the fat
disappears; the temperature of the body, unless the conditions for
producing fever are present, is barely up to normal, if not somewhat
below; a marked degree of anaemia supervenes; and the action of the
heart becomes feeble and rapid after a period of slowness. The blood is
altered in quality, and hence hemorrhages--epistaxis especially--occur,
petechiae and ecchymoses appear in the skin, and stigmata are numerous
about the face and nose.

[Footnote 77: _Clinical Medicine_, _op. cit._]

The urine in cirrhosis is high-colored because of the abundance of
pigment, and in the early stages of the disease is increased in amount,
although of lower specific gravity. When much effusion takes place into
the peritoneal sac, the compression of the renal veins by the fluid
lessens the activity of the kidneys and diminishes the urinary flow.
Much discussion has taken place over the quantity of urea present in
the urine in cases of cirrhosis, but it has been established that the
relative quantity of urea lessens in proportion to the damage suffered
by the liver.[78] The urates are in excess.

[Footnote 78: Charcot, _Lecons sur les Maladies du Foie_, _loc. cit._,
p. 252; also, _Essai sur les Variations de l'Uree dans les Maladies du
Foie_, par F. Genevoix, Paris, 1876; _Des Rapports de l'Uree avec le
Foie_, par A. Martin, Paris, 1877; _Sur l'Uree et ces Variations dans
la Cirrhose_, These de Paris, Audiguier; _Contribution a l'Etude du
Role du Foie dans la Product. de l'Uree_, Reufflet.]

COURSE, DURATION, AND TERMINATION.--There are enormous variations in
the course of the disease as respects the rate of its progress. In
general, it may be said that the whole duration is from three months to
six years. The onset is often insidious, and little distress is
occasioned until effusion begins in the abdomen. In other cases there
is considerable pain in the right hypochondrium, severe disorders of
digestion and intestinal derangements, rapid emaciation, ascites, and
some intercurrent malady which terminates them, often quite
unexpectedly. The usual course is as follows: After the protracted use
of alcoholic stimulants the symptoms of gastro-intestinal catarrh
appear; there occur acidity, pyrosis, morning vomiting, and distress
after meals; the bowels are irregular, the stools rather dark and
offensive; the bodily vigor declines and the mental condition is
depressed and hypochondriacal; emaciation progresses; the skin becomes
dry, harsh, and fawn-colored; stigmata appear on the face; some
uneasiness is felt in the abdomen, through the right hypochondrium, and
about the umbilicus; presently the abdomen enlarges and the feet and
legs swell; after a time the abdominal enlargement is extreme and the
walls become thin, the genitals and thighs are greatly distended, and
the prepuce is so swollen that urination grows more and more difficult,
the penis almost disappearing in the surrounding oedema;
notwithstanding the immense size of the abdomen and lower extremities,
the chest, face, and upper extremities are wasted away; to lie down is
impossible, and only snatches of disturbed sleep are procured in the
upright sitting posture; breathing grows more and more difficult, and a
sense of suffocation is imminent; and, thus worn out by suffering and
want of sleep, the patient at last sinks into a soporose state and dies
comatose, if not cut off before by some acute serous
inflammation--pleuritis, peritonitis, peri- or endocarditis, pneumonia,
etc.

{999} The course of any case of cirrhosis is much influenced by the
amount of damage to the hepatic cells and by the extent of the
compensatory changes in the circulation. Ulcers of the stomach or
intestine, opening vessels, or hemorrhages from the mucous membranes
may have a pronounced effect on the progress of any case. A fatal
result was determined in a case under the writer's charge by hemorrhage
from ulcers near the pylorus, which were caused by thromboses of the
stomach veins at that point. Occasionally, the occurrence of thrombosis
of the portal vein adds an embarrassing and dangerous complication. The
liver, besides the change due to cirrhosis, may be affected by amyloid
or fatty degeneration, or by both combined. It should not be forgotten
that more or less fatty change takes place in the hepatic cells
undergoing atrophy, whence the appearance called cirrhosis. Sclerosis
may be a general condition in which several organs participate, the
kidneys notably. These organs are changed by a hyperplasia of the
connective tissue, and especially by fatty degeneration of the
epithelium. In the brain the sclerosis consists in chronic
pachymeningitis, adhesions of the dura, etc., and with these
connective-tissue changes are often associated extravasations of blood.
These lesions are probably due to chronic alcoholism rather than to the
cirrhosis--are simultaneous lesions, instead of consecutive.

The duration of cirrhosis must necessarily depend largely on the
occurrence of the complications above mentioned and on the appearance
of intercurrent diseases. The most usual intercurrent maladies are
peritonitis, pleuritis, and other serous inflammations. An attack of
cerebral (meningeal) hemorrhage may occur. Failure of the heart may be
due to fatty degeneration of its muscular tissue. Stupor, coma, and
insensibility may come on toward the close in consequence of the
retention of excrementitious matters. By Flint, Jr., these cerebral
symptoms were referred to the retained cholesterin, and hence he
designated this state cholesteraemia. Numerous experimentalists
(Pages,[79] Chomjakow,[80] Von Krusenstern,[81] Koloman Muller[82])
have studied this question, and only Muller has been able to confirm
Flint's theory. The condition is more suitably designated cholaemia,
which signifies blood-poisoning from the excrementitious biliary
matters retained in the system.

[Footnote 79: Quoted by Legg, p. 233.]

[Footnote 80: Quoted by Krusenstern.]

[Footnote 81: _Virchow's Archiv_, Band lxv. p. 412.]

[Footnote 82: _Archiv fur experimentelle Pathologie und Pharmakologie_,
Band i. p. 213.]

Any fully-developed case of cirrhosis can only terminate in one way,
for we possess no means of restoring the hepatic cells when once
destroyed. At the outset of the disease, before any serious changes
have taken place, it is probable it may be arrested. Proceeding to its
natural termination without complications or intercurrent affections,
death finally occurs from exhaustion. The emaciation becomes extreme,
the stomach gets to be excessively irritable, and an exhausting
diarrhoea consumes the last remains of strength. Then an oedema of the
lungs or failure of the heart or a deep coma ends the scene.

DIAGNOSIS.--Cirrhosis in its first stage is to be distinguished from
diseases which cause enlargement of the liver, and in its second or
contracting stage from diseases that induce contraction of the organ.
The history of alcoholic excess is an important means of
differentiating this {1000} from other affections. The enlargement
belonging to alcoholism is distinguished from that due to amyloid
disease by the permanent character of the latter and by its history of
chronic suppuration, in addition to, it may be, alcoholic excess; from
cancer, by the character of the enlargement, by its permanence, by the
secondary deposits in the mesentery and elsewhere, by the severe and
persistent pain; from hydatids or echinococci cysts by the painless
enlargement of the latter, by the absence, usually, of any interference
with the hepatic functions, by the purring thrill, and by the presence
of the characteristic hooklets in the fluid withdrawn. From the
maladies characterized by the contraction of the organ it is
distinguished by the rapidity with which the case is developed in acute
yellow atrophy, and by the profound constitutional disturbance
characteristic of this form of contraction. When the liver is lessened
in size in consequence of the compression exercised by the contracting
exudation of a local peritonitis, there is a history of pain and
soreness of the right hypochondrium, followed by the symptoms of
contraction--a very different history from that of cirrhosis, in which
the local attacks of pain and distress succeed to or accompany the
symptoms of contraction. Occlusion of the gall-ducts by a calculus may
set up a slow atrophy having some points of resemblance to cirrhosis;
but in this malady attacks of hepatic colic precede the signs of
obstruction, the jaundice, and gray evacuations, and the evidences of
contraction succeed to these very characteristic symptoms; whereas in
cirrhosis paroxysms of pain followed by jaundice are not known.
Occlusion of the portal vein may also be followed by atrophy, but this
is usually due to some other affection of the abdominal organs, and the
change in the condition of the liver occurs very promptly, there being
neither the history nor the course of symptoms belonging to cirrhosis.

TREATMENT.--As the abuse of alcoholic liquors--even their habitual use
in moderation--is the chief pathogenetic factor, they should be
entirely given up. Condiments, coffee and tea, highly-seasoned animal
foods, are of less importance as causes, but are sufficiently injurious
to require them to be discontinued. The food of such subjects should
not contain fat, because the bile is necessary to its right
assimilation, and should have but a small proportion relatively of
starch and sugar, since these articles readily ferment in the presence
of an excess of mucus and in the absence of the bile. The succulent
vegetables, as lettuce, celery, spinach, etc., should be substituted
for the starchy and saccharine. A diet largely composed of skimmed milk
renders an important service both as a nutrient and a diuretic and
depurant. Lean meats, acid fruits, and the weak alkaline mineral waters
should be the basis of a proper system of alimentation.

As malarial intoxication is a cause now distinctly recognized, patients
should be removed from such influences. If this be impracticable, the
effects of the poison should, as far as possible, be removed,
especially the glandular complications. To this end, such remedies
should be employed as will affect the overgrowth of the connective
tissue, as the compound solution of iodine, the bichloride of mercury,
and the chloride of gold (or gold and sodium). Quinine will be
necessary, according to circumstances.

Do we possess any means to check the overgrowth of connective tissue
{1001} in cases of sclerosis? The writer believes that those remedies
have this power to a less or greater extent which are separated by the
liver from the blood. These are chiefly the salts of gold, silver,
copper, arsenic, and mercury (chloride), and phosphorus. The most
useful of these are the chloride of gold and sodium and the chloride of
mercury, and some phosphates. The writer has had, he thinks, curative
results in the commencement of the disease from the chloride of gold
and sodium and the phosphate of sodium. German practitioners believe
that the chloride of ammonium is a powerful alterant and deobstruent,
and prescribe it in this affection to stop the overgrowth of connective
tissue. That it does have this effect can hardly be disputed, but the
daily quantity necessary is large, the taste very disagreeable, and the
stomachal effect that of an irritant. Hence it is by no means so
effective as the chlorides above mentioned. The chloride of gold and
sodium (1/10 grain) can be given at the same time with chloride of
mercury (1/20 grain) if it is desirable to combine their effects. The
writer has seen what appeared to be cases of cirrhosis in the first
stage yield to the persistent administration of phosphate of
sodium--drachm j ter in die--and the chloride of gold and sodium.

When contraction of the liver has ensued, and hemorrhages, effusion
into the cavity of the peritoneum, and a high degree of
gastro-intestinal catarrh have occurred, the relief of the secondary
symptoms takes the first place in importance. There are but three modes
by which an effusion into the abdomen can be removed: by the skin, by
the kidneys, by the intestinal canal. Each of these may be employed in
turn. By the skin warm baths, vapor baths, digitalis stupes, and
especially the subcutaneous injection of pilocarpin, may be employed.
These alone may be sufficient in some cases--rather rarely, however.
They may all be used simultaneously or in turn to effect the purpose. A
digitalis stupe may be made to have the effect of a vapor bath: a large
one is placed on the abdomen and the body is covered with blankets,
which results in the production of abundant sweating. The vapor bath is
applied in the ordinary way, so that no explanation is needed. If there
be no contraindication in the state of the heart, pilocarpin salts can
be injected in sufficient quantity to induce active diaphoresis. These
measures proving inadequate, an attempt should be made to dispose of
the fluid by acting on the kidneys and promoting diuresis. Amongst the
diuretics in ascites, Wilks places the resin of copaiba first. The dose
ranges from two to five grains, and it may be given in combination with
gold or mercury chloride. When this remedy increases the flow of urine,
it does good, but if the quantity of urine remains unchanged, it does
no good, and should be discontinued.

As the effusion of fluid is due to the portal obstruction, it follows
that depletion of the terminal radicles of this system will act most
directly on the origin of the troubles. Hydragogue cathartics have,
therefore, an important place in the treatment of ascites of hepatic
origin. One of the most generally efficient of these remedies is the
compound jalap powder, for whilst it produces free watery evacuations,
it also stimulates the kidneys somewhat. It is generally better to give
a full dose--one or two teaspoonfuls--in the early morning, so that the
disturbance caused by it will subside before the time for taking food.
Several free watery evacuations should be produced by it. Sometimes the
resin or extract of podophyllin is added to the compound jalap powder
to increase its activity. {1002} Purgative combinations of colocynth,
gamboge, and resin of podophyllin are also occasionally employed, but
the most efficient hydragogue is elaterium. The last-mentioned may act
very efficiently without causing any considerable depression, but the
results obtained by it are usually fleeting. After even a very free
discharge of fluid the effusion quickly increases, and further
purgation is required. Tapping is a palliative expedient which must
sometimes be considered. With the present improved aspirator and the
antiseptic method the fluid may be withdrawn with ease and safety. It
is not necessary in any case to remove all the fluid--merely that
quantity which will relieve the pressure on the diaphragm and on the
renal vessels. The author has seen general peritonitis result from
tapping. As such a complication will increase all the difficulties of a
case, it is very desirable to prevent it by careful application of the
antiseptic method and sealing of the punctured orifice to prevent the
entrance of germs.

In the protracted cases of cirrhosis there ensues, finally, a highly
catarrhal state of the mucous membrane, the bowels become very
irritable, and frequent offensive and watery discharges occur. If under
these circumstances the abdominal effusion increases, the remedies must
consist of diuretics and diaphoretics rather than purgatives. Indeed,
an exhaustive colliquative diarrhoea may require bismuth, copper, and
other astringents, combined with opium, to prevent the patient passing
into the condition of collapse. Hemorrhage by vomiting or by stool will
demand ice, subsulphate of iron, ipecac, ergotin in the form of
subcutaneous injection especially, and other remedies which have been
found useful in gastric or intestinal hemorrhage.

Topical remedies are not without utility if used early. When the
changes in the liver are secondary to peritonitis of the hepatic
portion, the application of leeches and cups renders an important
service. At any time during the course of cirrhosis wet or dry cups may
be used with advantage whenever local pain, tenderness, and a catching
respiration indicate the extension of mischief to the peritoneum. The
tincture of iodine or flying blisters, or both in turn, may be applied
over the right hypochondrium after cups and leeches, or at any time
when local distress indicates the need of counter-irritants. Probably
the most efficient topical application during the hypertrophic stage of
cirrhosis is the official ung. hydrarg. iodidi rubri. A piece the size
of a large pea should be thoroughly rubbed in over the hepatic region
daily until some irritation of the skin is produced. When this
irritation has subsided the applications should be renewed.


Suppurative Hepatitis; Abscess of the Liver.

DEFINITION.--Suppurative hepatitis is an acute inflammation of the
hepatic parenchyma, terminating in suppuration. The inflammation may be
primary or due to local conditions entirely, or it may arise from
morbid processes occurring in parts or organs in anatomical relation to
the liver.

CAUSES.--Climate exercises an unquestionable influence in the
production of hepatic abscess. Those warm countries visited by
dysentery, {1003} says Lombard,[83] are almost exclusively affected by
this disease. Hirsch,[84] whilst recognizing the influence of climate,
shows that the natives are not affected to the same extent as are
Europeans. Both writers maintain that hepatic abscess does not occur
frequently in the corresponding parallels of latitude in the United
States; which is true of the Atlantic border, but is not correct for
the interior continent, the valley of the Mississippi, and its
tributaries. In this vast region the conditions for the production of
hepatitis exist abundantly. The mean annual temperature, the
malaria-breeding soil, the social and personal habits of the people
(males), combine to favor the production of hepatic abscess. As the
native population and females in tropical countries are not affected,
there must be other influences to the action of which the high
temperature contributes. The rich and highly-seasoned food in which
Europeans indulge and the large consumption of alcoholic drinks are
doubtless responsible in a large measure for the occurrence of this
malady in such excessive proportions amongst them.

[Footnote 83: _Traite de Climatologie medicale_, tome iv. p. 386.]

[Footnote 84: _Handbuch der historisch-geographischen Pathologie_, Band
ii. p. 300.]

Sex has a remarkable influence in securing immunity against hepatic
abscess. According to the statistics of Rouis,[85] of 258 cases of
hepatic abscess, only 8 were in women. He rightly enough attributes
this exemption rather to the difference in habits of the two sexes than
to any merely sexual peculiarity. In 12 cases observed by the writer,
only 1 was in a woman. In Waring's[86] collection of 300 fatal cases of
tropical dysentery, only 9 occurred in women. These facts are most
conclusive regarding the relatively greater frequency of the affection
in men. As might be expected, the age at which this disease occurs is
the period of adult life, when exposure to the conditions developing it
is most likely to happen. In general, then, hepatic abscess may be
referred to the period mentioned by Rouis--from twelve to seventy-five
years of age. In my own cases the youngest was eleven years and the
oldest fifty-four years of age. It is not the broken-down subject of
mature age or the weakling of youth who is attacked by hepatic abscess,
but the more vigorous and able-bodied, who have, because of their
strength and activity, been exposed to the manifold conditions
producing it.

[Footnote 85: _Recherches sur les Suppurations endemiques du Foie
d'apres des Observations recueilles dans le Nord de l'Afrique_, par J.
L. Rouis, Paris, 1860, p. 189.]

[Footnote 86: _An Inquiry into the Statistics and Pathology of Some
Points connected with Abscess of the Liver_, by Ed. John Waring,
Resident Surgeon of Travancore, 1854, p. iii.]

Rouis finds that a combination of the lymphatic and nervous
temperaments seems most favorable to the production of this malady. It
is certain that those who have the bodily conditions influential in the
formation of gall-stones are not unfrequently attacked by abscess. The
passage of the calculi may induce a local peritonitis of considerable
severity; their arrest in the duct, with the result of ulcerating
through, producing peritonitis and adhesions, are conditions
eventuating in the formation of an abscess always large and sometimes
of enormous size. Under such circumstances the element of temperament
has a secondary place in the aggregate of causes.

Not very often hepatic abscess results from external blows, contusions,
and from penetrating wounds. The liver is so placed as to glide aside
when a blow is inflicted on the right hypochondrium, and thus escapes
{1004} direct compression. An injury which elsewhere would have but
little effect may excite suppurative inflammation in the tropical--or,
as it may be entitled, the hepatic--abscess zone. Climatic conditions,
or the changed habits of Europeans in tropical and subtropical regions,
exert a distinct influence in traumatic cases.

The most important causes of hepatic abscess exist in the state of the
portal vein, hepatic artery, and the hepatic veins. In the valley of
the Mississippi and its tributaries, where abscess of the liver is a
comparatively common disease, it has been found that in a large
proportion of the cases the initial stage is an affection of the
rectum--a form of dysentery properly entitled proctitis. So far as this
vast region is concerned, the intestinal disease which precedes abscess
of the liver, and stands in a causative relation to it, is an affection
of the mucous membrane from which the inferior hemorrhoidal veins
arise. This disease, although having a dysenteric form, is not ordinary
dysentery. The onset of the disease and its symptomatic expression are
those of a mild affection of the mucous membrane of the rectum--so
insignificant in some cases as to be recalled with difficulty. In
tropical countries abscess of the liver may be associated with
dysenteric ulcerations. This relation has been frequently observed, but
is far from constant. In Waring's[87] cases, which occurred in India,
31 per cent. of the fatal cases of hepatic abscess arose during the
course of acute or chronic dysentery. De Castro of Alexandria[88] finds
that dysentery is the most frequent cause of abscess in that region,
especially in the Greek hospital. Murchison[89] considers tropical
abscess of the liver as secondary to dysentery in a considerable
proportion of the cases, but by no means in all. In non-tropical
countries abscess of the liver is found to succeed to ulcerations of
the stomach, the intestines, the bile-ducts, etc. In the case of
ulceration of any part of the mucous membrane from which the portal
vein receives branches a morbific material may be conveyed to the
liver. This morbific material may be some unknown septic principle the
presence of which in the liver will excite suppurative inflammation; it
may consist of an embolus having septic power or a merely mechanical
irritant; it may be micrococci or some other living organisms, which,
arrested in the portal radicles, set up inflammatory foci, etc. There
are many examples of hepatic abscess connected with dysenteric
ulcerations of the intestine in which no embolus can be found.
Admitting the presence of the embolus originally, its disappearance is
readily understood by reference to the changes induced by suppuration.
Excepting these cases there must be many in which no embolus can be
found, because none existed; an unknown septic substance has excited
the suppurative inflammation. Emboli may be lodged in the liver from
thrombi formed in the peripheral distribution of the portal vein, or
from distant parts of the systemic circulation, as in bone diseases.
There has been no satisfactory explanation of the manner in which such
emboli pass the pulmonary capillaries to be lodged in the liver. At one
time there was supposed to be a special relation between injuries of
the bones of the head and hepatic abscess, but it is now known {1005}
that these cases are not more numerous than those due to osteo-myelitis
in any situation. Abscesses in the lungs are greatly more frequent than
in the liver in cases of this kind. According to Waldeyer,[90] whilst
in two-thirds of the cases of death from surgical diseases and injuries
there were abscesses in the lungs, in only 6 per cent. were there
abscesses of the liver. It is evident that the emboli entering the
systemic circulation are usually arrested in the pulmonary capillaries.
Klebs maintains that such emboli consist of parasitic organisms.

[Footnote 87: _On Abscess of the Liver_, _supra_.]

[Footnote 88: _Des Abces du Foie des Pays chauds, et de leur Traitement
chirurgical_, par le Dr. S. V. Castro (d'Alexandrie d'Egypte).]

[Footnote 89: _Clinical Lectures_, _loc. cit._, p. 178.]

[Footnote 90: _Virchow's Archiv fur path. Anat., etc._, Band xl. pp.
380, 408.]

Dilatation and ulceration of the bile-ducts were the principal causes
of hepatic abscess, as ascertained by Von Baerensprung, in the Berlin
Pathological Institute. Duodenal catarrh involving the orifice of the
common duct, catarrh of the biliary passages leading to obstruction,
and plugging with a gall-stone have resulted in abscess, the initial
lesion being probably rupture of one or more of the finer tubes or
inflammation leading to suppuration.[91]

[Footnote 91: Grainger Stewart, _The Edinburgh Medical Journal_,
January, 1873.]

Finally, a considerable proportion of cases of hepatic abscess arise
under unknown conditions. In such cases, however, it is usually found
that there has been more or less indulgence in alcoholic drinks, or the
liver has been taxed by excesses in the use of rich foods and
condiments, or exposure to extreme degrees of temperature has occurred.
In the interior valley of this continent, where hepatic abscess is
comparatively common, the causes are to be found in malarial
influences, in alcoholic indulgence, in dysenteric attacks the product
of climatic variations and improper alimentation, and in the formation
and arrest in transitu of hepatic calculi also the result of
long-continued gastro-duodenal and biliary catarrh.

PATHOLOGICAL ANATOMY.--Great differences of opinion have been expressed
as to the initial lesions in hepatic abscess. It is probable, however,
that these differences are due to the character of the abscess. Some
have their origin in the hepatic cells, others in the connective
tissue, and others still in the vessels. There may be a number of
points at which the suppurative process begins, or it may be limited to
one. Virchow[92] describes the initial lesion as beginning in the
cells, which first become coarsely granular, then opaque, and finally
soften, and pus appears. Klebs, who maintains the constant agency of
septic micrococci, affirms that the changes in the cells are due to
compression exerted by the mass of these organisms distending the
neighboring vessels, and then suppuration begins on the portal side of
the lobules. Liebermeister originally held that the initial lesion is
in the connective tissue; and this view is also supported by Koster,
who brings to bear experimental data. In the walls of the vessels of
the connective tissue and about them, between the hepatic cells, great
numbers of lymphoid cells accumulate. The intercellular spaces are also
distended with plasma and round cells, and in the vicinity of the
central vein the swollen hepatic cells are pressed together; soon
pus-corpuscles appear, and the proper anatomical elements are broken up
into a diffluent mass composed of fat-granules, pus-corpuscles, and
disintegrating hepatic cells.

[Footnote 92: _Archiv fur path. Anat., etc._, Band iv. p. 314.]

When suppurative hepatitis arises from an embolus, or emboli, the
{1006} first step is the change in the appearance of the acini, which
are enlarged and grow softer by disintegration of their cells; then at
the centre a yellowish spot appears, and is made up of the detritus,
granules of fat, and pus. Surrounding such softening portions of the
hepatic tissue is a zone of congestion. When the morbid processes are
excited by emboli, there will be as many centres of pus-formation as
there are particles distributed by the vessels--from two or three to
fifty or more. They may be uniformly distributed through the organ or
be collected in one part. Emboli conveyed by the portal vein will be
arranged with a certain regularity and through the substance of the
liver, whilst those coming from some part of the systemic circulation
tend to form at the periphery under the capsule. Small abscesses in
close proximity unite ultimately by the softening and disintegration of
the intervening tissue.

In the so-called tropical abscess, which is the variety so frequently
met with in the interior of this country, the mode of development is
different from the embolic, above described. Owing to the deposit of
some morbific matter whose nature is now unknown, the vessels dilate
and hyperaemia of the part to become the seat of suppuration ensues.
The cells become cloudy, granular, and opaque from the deposit of an
albuminous matter in them. Within the area of congestion a yellowish
spot soon appears, surrounded by a translucent, pale-gray ring, and
here suppuration begins; the neighboring cells disintegrate and a
purulent collection is formed, which enlarges by the destruction in
succession of the adjacent portions of hepatic tissue. Whilst this
process is going on there is a border of deep congestion about the
abscess, fading off gradually into the normal tint of the hepatic
parenchyma; the walls of the abscess are rough and irregular from
projections of tissue just beginning to disintegrate, and the pus
burrows in various directions more or less deeply into the softening
parts. The size to which such purulent collections attain is largely
determined by the condition of the liver as a whole. If the organ
attacked is healthy otherwise and the general health is not
deteriorated, the area of the abscess may be limited by a well-defined
membrane and continue inactive for a long time. This limiting membrane
is of inflammatory origin, developed from the connective tissue, and
varies in thickness from a mere line to several. It was formerly called
a pyogenic membrane, because the pus discharged was supposed to be
formed by it. When such a limiting inflammation cannot take place, the
abscess continually enlarges by the softening and destruction of the
adjacent hepatic tissue, and may finally attain to enormous
proportions. The embolic abscesses vary in size from that of a pea to
that of an orange. The so-called tropical abscesses are usually
single--in three-fourths of the cases, according to Rouis;[93] in 62.1
per cent., according to Waring.[94] Of the fatal cases collected by the
latter author, 285 in number, a single abscess existed in 177, and
multiple abscesses in 108. In 11 per cent. there were two abscesses; in
3.6 per cent., three; and in 5.6 per cent. there were four abscesses.
As regards the part of the liver in which abscess occurs, the
statistics show a great preponderance in favor of the right lobe. In
Waring's collection of 300 cases the right lobe was the {1007} seat of
the abscess in 163, or 67.3 per cent.; the left lobe was affected in
16, or 6.6 per cent.; and both lobes in 35, or 14.4 per cent. The
preponderance of cases affecting the right lobe is the more striking
when it is understood that, other parts being invaded, the right is
included with them in the morbid process. In my own cases the right
lobe was the seat of the abscess in 70 per cent.

[Footnote 93: _Recherches sur les Suppurations endemiques du Foie_,
_loc. cit._, p. 146.]

[Footnote 94: _An Inquiry into the Statistics and Pathology, etc.
connected with Abscess of the Liver_, _loc. cit._, p. 125.]

The contents of the abscesses are affected in character by the form of
the disease, whether embolic or tropical, by its rate of development,
by the condition of the hepatic parenchyma, by the formation of a
limiting membrane, etc. In the more chronic cases, surrounded by a
dense membrane, the pus is usually laudable or dry and cheesy; in the
acute embolic cases the pus is dark brown, ichorous or grumous, and
contains a good deal of detritus of the hepatic parenchyma; and in the
tropical cases it is of a sanguinolent, dark color, or more frequently
of a grayish purulent fluid; and in the acute forms contains much
broken-down tissue, whilst in the chronic cases, in direct ratio to
their duration, the pus approaches the laudable character. The source
of an abscess discharging from the neighborhood of the liver may be
ascertained by a microscopical examination and the discovery of the
hepatic elements (the cells) in the fluid. Bile may also be present in
the pus.

The abscesses not confined by a limiting membrane constantly enlarge by
the softening and disintegration of the adjacent liver substance, and
those enclosed or encysted after a period of quiescence of variable
duration begin active efforts to establish communication outwardly. The
point to which a purulent collection in the liver tends becomes an
important element in diagnosis and in treatment. As the abscess
approaches the surface of the liver the capsule inflames, and if
adhesions are not formed more or less sloughing occurs, and the
contents are discharged into the abdominal cavity. Adhesions may form
to the parietes, an external swelling appear, and after a time
discharge take place in the right hypochondrium at some point. Pus may
escape at the umbilicus, in the right inguinal region, posteriorly at
the sacro-iliac junction, and in other situations. Adhesions may form
to the stomach, duodenum, the ascending vena cava, to the diaphragm
opening the thoracic cavity, the pericardium, or the mediastinum; and
the accumulated pus may thus find a vent. According to Waring,[95] the
termination of hepatic abscess is as follows: Of 300 cases, 169, or
56.3 per cent., remained intact--that is, had not advanced beyond the
liver; 48 were evacuated by operation, or 16 per cent.; 14, or 4.6 per
cent., entered the thoracic cavity; 28, or 9.3 per cent., opened into
the right lung; 15, or 5 per cent., entered the abdominal cavity; 7, or
2.3 per cent., opened into the colon; 1 entered the stomach; 3 entered
the hepatic vein near the vena cava; 1 communicated with the hepatic
ducts, 2 with the right kidney, etc. The termination of 162 fatal
cases, according to Rouis,[96] was as follows: 125 proved fatal in
consequence of the extent of the abscess or of the severity of the
accompanying dysentery; 3 terminated by gangrene of the walls of the
abscess; 3 by peritonitis; 12 by opening of the abscess; 2 by rupture
of adhesions; 11 by opening of the abscess into the pleura; 2 by
intercurrent and 3 by secondary pneumonia. Notwithstanding the
differences {1008} in the mode of expressing the conditions, the
general results are the same.

[Footnote 95: _An Inquiry into the Statistics and Pathology, etc. of
Abscess in the Liver_, _loc. cit._]

[Footnote 96: _Recherches sur les Suppurations endemiques, etc._, p.
149.]

An abscess of the liver having discharged in a favorable way, healing
may take place. There may be such an extent of injury--the whole
secreting structure of the liver being destroyed--that repair is beyond
the power of the organism. The best results are attained when discharge
occurs by the most direct route externally; the next, by way of the
right lung; the third, by the stomach or intestine. Repair cannot be
hoped for when a large part of the normal hepatic structure is
destroyed. When the pus escapes the walls of the abscess approximate,
and union takes place by connective tissue, leaving a radiated or a
merely linear cicatrix to mark the site of the purulent collection. So
perfectly does repair take place in suitable subjects that no trace of
the lesion may remain.

Those portions of the liver outside the borders of the abscess, and
beyond the vascular derangements produced by it, may be entirely
healthy. In the cases terminating in recovery the portion of the liver
unaffected by abscess continues to functionate normally. More or less
of the liver may be destroyed; hence it follows that recovery may be
partial. According to the damage done to the proper secreting structure
of the organ will the recovery be partial, limited, or complete.

SYMPTOMS.--The existence of an abscess of the liver is determined by
systemic or general and by local symptoms, and they may be acute or
chronic.

Systemic.--In acute cases the beginning of mischief may be announced by
a rigor, but more frequently this indicates the onset of suppuration,
and is one of the phenomena of the chronic form. As the disease occurs
in this country, a chill takes place suddenly in a case which presents
the usual symptoms of proctitis (dysentery) during the course of this
affection or soon after its apparent cure; then a febrile movement
occurs, and subsequently an irregular intermittent, the rise of
temperature being preceded by rigors or mere transient chilliness. With
these febrile symptoms there may be associated uneasiness in the right
hypochondrium, acute pain, or a feeling of weight and pressure, with
jaundice, etc. The fever is septicaemic, intermittent, or remittent if
it have any special type. In the septicaemic form the rigors are
severe, occur irregularly, sometimes daily, sometimes twice a day, and
at intervals of two or three days or longer; the fever rises to a high
point--104 degrees, 105 degrees, or higher--and the sweats are profuse.
In the intermittent form the fever usually has the quotidian type; some
slight chilliness is experienced in the early morning as a rule, and
the exacerbation occurs in the afternoon and evening, the sweating
being slight toward the morning. More frequently, in the writer's
observation, the type of fever has been remittent, with periodical, but
not regularly so, exacerbations. In such cases the morning temperature
has been at 99 degrees or 100 degrees, and the evening 102 degrees or
103 degrees. Such a range of temperature may be present during three or
four weeks or even longer, the abscess gradually making its way
outwardly. Conclusions may be drawn from the behavior of the febrile
movement as to the character of the local affection, with the
limitations imposed by the necessary uncertainty of the data. If the
chills are decided rigors, the fever {1009} high, and the sweats
profuse, either pyaemic abscesses or large tropical abscesses
implicating neighboring organs exist. The simple intermittent,
especially the remittent, form of fever suggests abscesses of medium
size making their way outwardly, with only partial injury to the parts
traversed. In a certain portion of the cases the type of fever changes
when a large accumulation of pus takes place; after several weeks of a
mild remittent the fever becomes irregularly intermittent with rigors,
strong exacerbations, and profuse sweats. In protracted cases the fever
assumes the typhoid aspect; there is profound adynamia, dry tongue,
sordes, diarrhoea, and the usual symptoms of this state. When the
secreting structure of the liver is destroyed to a large extent, the
condition of acholia is superadded to the typhoid state.

The pulse is irritable and quick from the beginning of the symptoms. In
a few instances a slow pulse, such as occurs in jaundice, has been
observed, but generally the number of cardiac contractions is in a
direct ratio with the body temperature. When typhoid symptoms supervene
in advanced cases the pulse becomes weak and dicrotic.

Not every case presents the symptom sweating. The chronic cases with
mild remittent fever have little more than slight moisture of the
surface, whilst the acute and pyaemic cases are characterized by
profuse sweats. If to an irregular febrile movement, preceded by chills
and followed by sweats, there is added the tendency to sweat on all
occasions--on slight exertion, on sleeping, under any
excitement--suppuration may be suspected.

General malaise, a sense of fatigue and exhaustion, and progressive
decline in flesh and strength occur. It is remarkable, however, how
some obese subjects preserve their roundness and apparent fulness of
habit. Usually, however, emaciation advances pari passu with the
progress of the suppuration. The more acute the symptoms, the more
rapid the wasting. When an encysted abscess develops in the course of a
chronic dysentery, there may be no appreciable change in the condition
of the patient properly attributable to the additional lesion. The loss
of appetite, the frequent vomiting, and often the dysenteric troubles,
contribute materially to the exhaustion and the wasting of the tissues.
The stomachal derangements may be present with the initial symptoms,
but they are usually more pronounced when the abscess attains to
considerable size.

A peculiar tint of the skin, especially of the face, is observed in
those cases without jaundice. There is an earthy or sallow hue, which
to the practised eye signifies suppuration. Jaundice is present in a
less proportion of cases. In 13 of Waring's cases the skin is said to
be sallow. In Rouis's collection icterus was present in 17 per cent.,
or 26 times in 155 patients. According to Waring, jaundice is rarely
present. In the 12 cases in my own hands actual jaundice was not
present in one, but 9 had an earthy hue or presented some yellowness of
the conjunctiva. In fact, jaundice does not have the importance as a
symptom which might, a priori, have been expected.

The mental condition of these subjects is that of depression. They
sleep poorly, are disturbed by vivid dreams of a horrifying character,
and the nocturnal sweats increase the tendency to wakefulness.
Hypochondria, or at least marked symptoms of mental depression, as
{1010} Hammond[97] has shown, are present in many cases. So frequent,
indeed, seems to be the association of a depressed mental state with
hepatic abscess that in every case of the former the liver should be
carefully explored. Hammond goes so far as to say that in every case of
hypochondriasis puncture of the liver with the aspirator needle should
be practised when any symptom, however indefinite, indicates the
existence of an abscess. Besides the condition of hypochondriasis in
many cases, there may be stupor, hebetude of mind, confusion due to
acholia, cholaemia (Flint's cholesteraemia), when a large part of the
liver structure is destroyed.

[Footnote 97: _Neurological Contributions_, vol. i. No. 3, p. 68: "On
Obscure Abscesses of the Liver, their association with Hypochondria and
other Forms of Mental Derangement, and their Treatment."]

Sweating has already been referred to as a phenomenon connected with
the febrile movement. It is necessary to state further that this may
vary in amount from a mere moisture of the surface connected with
sleep, or it may be a profuse diaphoresis with which the febrile
paroxysm terminates. As a systemic symptom, sweating is strongly
suggestive of suppuration, and may therefore be extremely significant,
in this connection, of suppuration in the liver. According to Waring,
of 75 cases specifically interrogated on this point, 72 presented this
symptom. Rouis refers (p. 123) to it as very constantly present, coming
on chiefly at night--sometimes generally over the body, sometimes
limited to the head, and always accompanied by an accelerated pulse.

The urine in cases of hepatic abscess varies; it is never normal. There
may be merely an excess of urates--a symptom common enough in all
febrile affections and in suppuration. It is usually high-colored,
deficient in urea, and contains leucin and tyrosin, and not often
bile-pigment, except when jaundice is present, which, as we have seen,
is rather uncommon.

It should be borne in mind that whilst the above-described mental and
cerebral and other symptoms are often present, they are by no means
invariably so. There are cases, usually of encysted abscess, in which
no functional disturbance of any kind exists. But the systemic symptoms
are by no means so important as the local. To these we must now direct
attention.

Local.--The position, size, and shape of the liver are not without
significance, but it is strictly correct to say that an abscess of the
liver may exist without any change in the size of the organ or in its
relations to the surrounding organs. In 2 of 12 cases in the hands of
the writer there was no evidence of enlargement of the right
hypochondrium, but a difference in circumference of half an inch was
ascertained in favor of the left side. In 4 cases there was no
appreciable change in the size of the hepatic region; in one-half there
was an increase in the area of hepatic dulness. In one of the cases in
which the left side was the larger the abscess was of enormous extent,
and discharged by the stomach and intestine. The enlargement of the
liver may be very great. In one instance observed by the author the
abscess reached to the upper border of the third rib. Rarely does the
dulness extend more than two fingers' breadth below the inferior margin
of the ribs, although cases are reported in which the enlarged organ
reached to the crest of the ileum. As a rule, the diaphragm is pushed
up and the lung displaced, rather than the dulness is extended
downward. When the first tumefaction {1011} due to the initial
congestion takes place, the organ may be much larger than subsequently,
the pus becoming encysted and the normal state outside of the area of
suppuration being restored. The purulent collection in a large
proportion of the cases taking place in the right lobe, the extension
of dulness is in the same lines as the normal. When, however, the right
lobe is the seat of abscess, or a purulent collection forms around an
impacted calculus, the swelling may appear in the outer border of the
epigastrium next the ribs, and the increased area of dulness will be
across the epigastrium and occupying the superior portion of this
region. The general experience on these points corresponds to my own.
Thus, according to Waring, there was an evident enlargement of the
liver in 90 cases, and no enlargement in 11. In most cases the increase
in size gives the impression of a fulness or hardness of the liver or
of a diffused swelling or tumor of the epigastrium. In some instances
the right hypochondrium is bulged out, the intercostal spaces widened,
and the side appears to be or is actually elevated, and occasionally
enlarged veins form, as in cases of the obstructed portal circulation
of cirrhosis. In a case recently presented at Jefferson College
Hospital clinic by the author, a globular swelling formed in the walls
of the abdomen just below the inferior margin of the ribs near the site
of the gall-bladder, and was held by an eminent surgeon to be a tumor
of this locality; but it had the history of an hepatic abscess, and
ultimately proved to be one. Rouis furnishes statistical evidence of
the time when the increase in size of the liver occurs with respect to
the other symptoms. He has noted an enlargement of the organ 73 times
in 122 cases. Of 51 cases, the liver was enlarged in 12 before
suppuration, in 22 at the onset of suppuration, and in 17 after
suppuration was established. In 49 examples the liver was enlarged in 2
before any other symptom was manifest, in 8 at the onset of symptoms,
and in 39 after the symptoms were well declared.

Fluctuation is not referred to by the writers in general, and there are
no statistical data on this symptom, so far as our observation extends.
No symptom could be more uncertain in all doubtful cases. When a large
accumulation has taken place and the parietes of the sac are thin,
fluctuation may be detected, but it cannot then be regarded as
decisive. When an abscess in the interior of the right lobe is
encysted, no fluctuation can be effected. The best mode of eliciting
fluctuation, according to Hammond, is to place the extremities of the
fingers of the left hand in the depression between the ribs over the
most prominent part of the right hypochondrium, and gently tap with the
fingers of the right hand the right border of the epigastrium. In 3 out
of 12 cases this method has apparently elicited fluctuation in my own
experience. The elasticity of the hepatic structure is such that the
method of palpation, however practised, must return a sensation nearly
allied to that of fluctuation in a purulent accumulation. It is
certain, therefore, that errors of observation are liable to occur, and
hence conclusions based on an apparent fluctuation should be accepted
with caution; under any circumstances it should be very distinct, and
even then should not be acted on unless supported by other suggestive
evidence.

The uneasiness or pain felt in the right hypochondrium varies greatly
according to the position of the abscess, the degree and kind of
pressure exerted on neighboring organs, and the period of its
development. When {1012} the peritoneal layer of the liver is involved,
there will usually be acute pain, and this happens at two periods--when
the abscess first forms from an impacted calculus or from any cause
which includes the peritoneum, and subsequently when the pus, making
its way from the liver, excites inflammation in the peritoneal
investment of the liver, of the diaphragm, or affects ultimately the
pleural membrane. In the so-called pyaemic abscesses there is very
little pain, and in the case of the large single abscess in the
interior of the right lobe there is rather a sensation of weight or of
heaviness, of dragging than of acute pain. When the capsule of the
liver is put on the stretch or the peritoneal investment is inflamed,
then acute pain may be felt. More or less pain or local distress is, on
the whole, a usual symptom. According to Rouis,[98] local pain is
present in 141 out of 177 cases, or in 85 per cent. The statistics of
Waring[99] closely correspond, for of 173 patients affected with this
malady, in 153 there was more or less pain referable to the affected
organ. The position of the pain has some influence in determining the
seat of the malady, and often indicates the position of the abscess. As
respects the character of the pain, there is little uniformity; in
general it is a tensive, heavy, throbbing sensation, but under the
circumstances above mentioned this may have an acute or lancinating
character, as when the capsule or the peritoneal investment of the
organ becomes involved.

[Footnote 98: _Recherches, etc._, _loc. cit._]

[Footnote 99: _An Inquiry, etc. into Abscess of the Liver_, _loc.
cit._]

Besides the pain directly referable to the liver there are painful
sensations felt in the neighboring parts, of very considerable
significance. These are often described as sympathetic pains, and are
referred to the shoulder--to the right shoulder when the right lobe is
the seat of mischief, and to the left shoulder when the abscess forms
in the left lobe of the liver. Although this statement has many
limitations, it is not without diagnostic importance. Rouis ascertained
the existence of the shoulder pain in 17 per cent. of the cases, or in
28 in a total of 163. Waring reports that this symptom was observed in
52 in a total of 76 cases. The right shoulder seems to be affected in
about the same ratio as the right lobe of the liver in 25 times out of
26 cases, according to Rouis. The shoulder pain appears at the same
time, in a majority of cases, as the hepatic pain, but it is very
capricious. It is most frequently at the top of the shoulder, but it
may be at the end of the clavicle, in the scapula, or extend down the
arm. Its duration is very irregular, appearing occasionally during the
existence of the disease, coming on at the outset, and lasting weeks or
months, or only felt on pressure over the liver, on coughing, or on
taking a full inspiration. The character of the pain is equally
uncertain. It is usually heavy, tensive, stinging, or may be merely a
sensation of soreness or of uneasiness or of weariness. The behavior of
the shoulder pain is partly explicable by reference to the path by
which the reflex is conveyed. As Luschka[100] has shown, the filaments
of the phrenic nerve supplied to the suspensory ligament and capsule of
the liver, put on the stretch or irritated, convey the impression to
the cord, and it is reflected over the sensory fibres of the fourth
cervical distributed to the shoulder. Rouis reports an instance in
which the deltoid was wasted.

[Footnote 100: Quoted by Thierfelder, _op. cit._]

The decubitus of patients affected with hepatic abscess is often {1013}
extremely characteristic. To obviate the pressure on the swollen and
inflamed organ the position assumed is right lateral-dorsal, the body
inclined to the right, the right thigh flexed on the pelvis, and the
spinal column so curved as to relax the abdominal muscles of the right
side. When the pain and tenderness are not great there may be frequent
changes of position, but in repose the lateral-dorsal decubitus is
assumed. When the suppuration is well advanced and the accumulation
large, the patient keeps in that position nearly constantly. If
pressure interferes with the normal play of the lungs, and dyspnoea is
produced on assuming the recumbent posture, the attitude taken
expresses this state also: then the decubitus is lateral and partly
dorsal, but the body is raised to a half-upright. There are many
exceptions to these rules. Some lie easiest on the back, some on the
left side; but it is quite certain that much the largest number, when
uninfluenced by special circumstances, naturally place themselves as
above described.

Jaundice is amongst the rarer symptoms. Rouis finds it to be present in
17 per cent. of the cases, Thierfelder in 16 per cent., and Waring in
somewhat less than 6 per cent. Referring to my own observation,
jaundice has rarely been present, but some yellowness of the
conjunctivae and a faint yellow tint of the skin generally have been
evident. The peculiar aspect of the countenance connected with
suppuration has rarely been wanting. When jaundice does occur, it is
referable to two conditions--to a catarrhal swelling of the bile-ducts,
which may be coincident with the onset of the suppurative inflammation;
to the pressure of the abscess on the hepatic or common duct, which
must happen at a late period.

As an abscess of the liver forms and enlarges, pressure is exerted on
neighboring organs, producing very decided disturbances. Nausea and
vomiting, anorexia, a coated or glazed tongue, diarrhoea or dysentery,
are amongst the disorders of this kind involving the digestive
apparatus. Each of these symptoms will require examination.

There is nothing characteristic in the condition of the tongue which
does not belong to suppuration in any situation. Nevertheless, there
are some appearances that have a certain value in conjunction with
other diagnostic signs. At the onset of the suppurative inflammation
the tongue is more or less heavily coated, but as the case proceeds it
becomes dry and glazed in parts, whilst covered with a well-defined
membrane-like crust at the base and margins. This appearance is very
characteristic of the cases of suppuration, the abscess enlarging. In a
very important case observed by me lately there was a well-marked
diphtheritic-like exudation of the tongue and fauces toward the
termination of the case, the membrane forming as the pus accumulated.
This appearance was coincident with a typhoid state.

Nausea and vomiting appear with the beginning of symptoms, are
associated with the general signs of systemic disturbance, and are
especially prominent when an accumulation of pus takes place, being due
under these circumstances to pressure on the hepatic and solar plexuses
or to direct encroachment on the stomach--probably to both causes. The
frequency and persistence of the vomiting are points of much diagnostic
importance, according to Maclean[101] and Fayrer,[102] which I {1014}
am able to fully confirm from my own experience. The matters ejected by
vomiting consist of the contents of the stomach--glairy mucus, the
accumulation in the gall-bladder, altered blood (coffee-grounds)--and
the contents of the abscess if it discharge by the stomach. The
vomiting is most apt to occur during the febrile exacerbation or at the
time of sweating. The statistics are conclusive as to the frequency of
vomiting as a symptom. Of 84 cases in which special reference was made
to this point, in 74 nausea or vomiting existed. In my own experience
this symptom has never been wanting.

[Footnote 101: "The Diagnostic Value of Uncontrollable Vomiting," by W.
C. Maclean, _Brit. Med. Journ._, August 1, 1873.]

[Footnote 102: _Ibid._, September 26, 1873.]

The relation between abscess of the liver and dysentery has been much
discussed. Under the head of Causes the influence of dysentery as a
pathogenetic factor has already been examined. We have now to study its
symptomatic relations. A considerable proportion of the cases occurring
in this country have been preceded by proctitis--simple, sporadic
dysentery affecting the rectum. In India a close relationship has been
traced between ulcerations of the intestinal canal and abscess.
According to Waring, 75 per cent. of the cases have occurred in those
who were actually suffering from dysentery or recent or old
ulcerations. As observed by Rouis in Algiers, out of 143 cases there
were 128 with dysentery, or 90 per cent. Budd[103] long ago maintained
that a peculiar poison generated at an open ulceration in the intestine
was the true cause. Moxon,[104] Dickinson, and others have lately
reaffirmed this explanation. A case by the latter[105] casts a strong
light on this question: A patient had extensive dysenteric ulceration
of the intestine and an abscess of the liver, without any symptoms
indicating their existence. Such a case teaches the instructive lesson
that dysenteric ulcerations may escape detection, and hence the
connection between abscess and the intestinal lesion remains unknown.
In a small proportion of cases--about 5 per cent.--dysentery is a
result, apparently, of hepatic abscess. Whether the relation is
admitted to exist or not, it is a curious fact that in so many cases
ulcerative disease of the intestinal canal accompanies the hepatic
affection. Hemorrhoids, prolapse of the rectum, gastro-intestinal
catarrh, etc. are produced by the pressure of an enlarging abscess on
the portal vein.

[Footnote 103: _Diseases of the Liver_, 3d ed., p. 82.]

[Footnote 104: _Pathological Transactions_, 1862 and subsequently.
Numerous cases are recorded in the various volumes up to 1880.]

[Footnote 105: _Ibid._, vol. xiii. p. 120.]

The urine contains bile-pigment when jaundice is present, is usually
loaded with urates, and the amount of urea may be deficient when much
of the hepatic tissue is destroyed.

From the beginning of symptoms some cough is experienced: it is short
and dry, but after a time in many cases the cough is catching and
painful, and finally may be accompanied by profuse purulent
expectoration. The breathing is short and catching when by the upward
extension of the mischief the diaphragm is encroached on, and may
become very painful when the pleura is inflamed. Ulceration of an
abscess into the lungs is announced by the signs of a local
pleuro-pneumonia--by the catching inspiration, the friction sound, the
crepitant rale, the bronchophony and bronchial breathing, and bloody
sputa usually, etc. Some time before the abscess really reaches the
diaphragm, preparation is made in the lung for the discharge through a
bronchus. The author has seen {1015} many examples of this, and a very
striking illustration of the same fact is afforded in a case by
Dickinson,[106] in which an abscess holding about four ounces was
contained in the upper part of the right lobe; its walls were irregular
and not lined by a limiting membrane. It is further stated that the
"right pleura was coated with flocculent lymph, and the cavity
contained serous fluid," etc. Here, in advance of the abscess,
preparation was made for its discharge through the lung. The tendency
of an abscess of the abdomen to external discharge is manifested in two
directions: those of the upper part tend to discharge through the
lungs, those of the lower part through the natural openings below.
Abscesses of the liver come within the former rule, but it is not of
invariable application, since some discharge by the stomach or
intestine, some externally; yet a large proportion make their way
through the lungs. Another symptom referable to the pulmonary organs in
cases of hepatic abscess is singultus, or hiccough. This is a symptom
of the period of discharge rather, and is often extremely protracted
and exhausting. Pericarditis occurs in those cases in which discharge
takes place in this direction, and it may develop, as does pleuritis,
in advance of any change in the diaphragm. This preparation of the
thoracic organs for external discharge seems almost like a conscious
purpose, as if an intelligent supervision of these processes were
exercised.

[Footnote 106: _Transactions of the Pathological Society_, vol. xxxii.
p. 127.]

COURSE, DURATION, AND TERMINATION.--As the facts already given have
sufficiently shown, the course of abscess of the liver is extremely
uncertain. From the beginning to the end there may not be a single
indication of its presence. On the other hand, a well-marked case is
perfectly characteristic. Abscesses of the liver are acute and
chronic--the former of short duration, accompanying pyaemia, portal
phlebitis, and similar conditions; the latter, arising in the course of
chronic dysentery or from unknown causes, especially if encysted,
remaining latent for weeks or months. The course of an abscess is much
influenced by the direction taken by the pus in the attempt at
discharge. This portion of the subject requires careful statement and
thorough treatment, and we therefore present it somewhat in detail.
Beginning with his individual observations, the abscess in the author's
12 cases discharged--3 externally, 5 by the lungs, and 4 by the stomach
or intestines. In Waring's[107] collection of 300 fatal cases, 169
remained intact at death, 48 were operated on; consequently, only 83
are left for the purpose of this comparison. Of 83 cases of hepatic
abscess discharging spontaneously in some direction, 42 escaped into
the thoracic cavity or by the right lung (in 28); into the abdominal
cavity (15) or stomach (1) or intestine (7), 23; externally 2, besides
in special directions to be hereafter referred to. Rouis[108] has
tabulated the results in 30 cases of abscess fatal without an operative
influence. Of these, 2 discharged externally, 17 by the thorax (15 by
the lung), 5 by the stomach, 4 by the intestine, and 2 by the biliary
canals.

[Footnote 107: _An Inquiry, etc. into Abscess of the Liver_, _loc.
cit._, p. 131.]

[Footnote 108: _Recherches sur les Suppurations endemiques du Foie,
etc._, _loc. cit._, p. 148.]

The appearances presented when the discharge takes place through the
external parts are by no means uniform. When the epigastric or
umbilical region is the point of discharge, a globular tumor forms,
which may {1016} be mistaken for a fibroid or fatty growth; softening
in the centre of the mass occurs, and ultimately the pus is discharged.
If the pus makes its way outwardly through the right hypochondrium, the
tumor formed is furrowed by the attachment to the ribs, and several
openings usually occur. The pus may burrow under the skin for some
distance and point in the axilla, or, making its way along the
suspensory ligament, emerge at the navel, or, descending, appear in the
lumbar region or under Poupart's ligament.

As the statistics prove, the most usual route for discharge to take
place is by the thoracic cavity, especially the right lung. Some time
in advance of an opening in the diaphragm a localized pleuro-pneumonia
occurs, adhesions form between the pulmonary and costal pleura, and a
channel is tunnelled out for the passage of the pus to a bronchus. The
discharge of pus suddenly occurs after some days of cough and bloody
expectoration. Even in favorable cases the amount is so large that the
patient has extreme difficulty in disposing of it, and in unfavorable
cases, the quantity being large, the patient's life is ended by apnoea.
In still other cases an extensive purulent accumulation may form in the
pleural cavity, the lung is compressed, and all the phenomena of an
empyema superadded to those of a hepatic abscess. In a case reported by
Westphalen[109] all the bile secreted by the patient came out by an
opening in the fifth intercostal space. The empyema thus induced may
indeed be the principal lesion, as in the case of the late Gen.
Breckenridge, on whom thoracentesis was performed by Sayre of New York,
and in a case reported by Lower.[110] So far from this being uncommon,
as asserted by Thierfelder, when an abscess of the liver approaches the
diaphragm inflammatory symptoms begin on the pleural side, and thus
pyothorax may occur in advance of the perforation of this septum.

[Footnote 109: _Deutsches Archiv fur klin. Med._, 1873, Band xi. p.
588.]

[Footnote 110: _Berliner klinische Wochenschrift_, 1864, p. 461.]

The opening of an hepatic abscess into the pericardium is rare, since
in Waring's collection of 300 fatal cases there was not one. When it
does occur, pain is experienced about the heart; the action of the
organ becomes irregular; praecordial anxiety and oppression are felt;
suffocative attacks occur; and very soon the symptoms of pericarditis
arise. Perforation of the ascending vena cava or of the hepatic vein
happens in about 2 per cent. of the cases. When a quantity of pus is
thus turned into the circulation, disastrous results follow, not so
much from the infective nature of the pus as from the sudden increased
pressure within the vascular system and the labor imposed on the heart,
already failing.

The escape of the pus into the peritoneal cavity occurs in about 11 per
cent. of the cases of spontaneous evacuation, according to Waring. Of
the 162 fatal cases collected by Rouis, 14 opened into the
peritoneum--about the same proportion as Waring gives. When discharge
takes place into the peritoneum, the patient passes into a condition of
collapse, or peritonitis is excited and rapidly proves fatal. In rare
instances the inflammatory reaction is restricted to a small area,
ulceration takes place through the abdominal parietes, and thus
discharge is effected.

An opening may be made into the intestine or into the pelvis of the
kidney. In the former case pus is discharged by stool or by vomit, and
often in enormous quantity; in the latter by the urine, frequent and
{1017} painful micturition, with much pus, being the evidence of the
accident. In either case communication may be kept up with the abscess,
and the patient be worn out with the exhausting discharge maintained by
the intercommunication between the abscess and the canal through which
discharge takes place.

Cases of hepatic abscess prove fatal without perforation. In Waring's
collection of 300 cases, 169 remained intact, in the words of the
author--that is, did not extend beyond the boundaries of the liver. Of
203 cases collected by Rouis, 96 did not extend beyond the liver.
According to Thierfelder, about one-half of the cases of hepatic
abscess perforate the liver. These statistics therefore closely
correspond, and the general conclusion is very nearly expressed in the
formulated statement of Thierfelder.

The duration of hepatic abscess cannot readily be expressed in figures.
The acute cases terminate early by reason of the various complicating
conditions. The chronic cases are much influenced in their duration by
the presence of a limiting membrane, for if this be formed the duration
will be protracted over weeks or months; and those cases not thus
confined are necessarily of shorter duration. A period of latency may
result when the extension of the morbid process is thus hindered.
Forming a conclusion from the general conduct of the cases, it may be
said that the duration of hepatic abscess is from two weeks to six
months. Of 220 cases collected by Waring, the average duration was 39
days. Rouis fixes the average duration in 179 cases at 60 days. Of
Waring's cases, the largest number (59) terminated in from 10 to 20
days; whilst Rouis places the maximum number (104) at from 11 to 60
days, the shortest duration of any case being 10 days, and the longest
480 days.

The termination may be accelerated by the manner of discharge, as when
the abscess opens into the ascending vena cava, into the sac of the
pericardium, or into the peritoneal cavity. In my own cases, carefully
selected for these observations, death occurred in one during discharge
by the right lung, one within twelve hours after discharge by the
intestine, and one within ten days after discharge by the stomach and
intestine, the mortality of the whole being 75 per cent. In Waring's
collection of 300 fatal cases, 169 died whilst the abscess was still
intact--that is, in the liver.

The mortality from abscess of the liver is very large. In Rouis's
collection of 203 cases, 162 died, 39 recovered entirely, and 2
improved; 80 per cent., therefore, proved fatal. According to De
Castro,[111] whose observations were made at Alexandria, Egypt, 93 in
208 cases died, this being 72.5 per cent. According to Ramirez,[112] of
11 cases of which an account is given in his memoir, 10 died and 1
recovered--a mortality of 90 per cent. De Castro (p. 40) also gives the
results arrived at by the Medico-chirurgical Society of Alexandria, who
collected 72 cases of abscess, of which 58 died, making the percentage
of deaths 80.5. Various circumstances besides the abscess affect the
result. An early successful operation, the mode of discharge, the
amount of hepatic tissue destroyed by the {1018} suppuration, the
extent of pre-existing lesions--especially ulcerations of the
intestinal canal--are important factors in the result. In respect to
some of these we have valuable statistical data. The discharge through
the lungs is the most favorable route, next by the parietes of the
abdomen, and lastly by the intestinal canal. One-half of those cases in
which discharge is effected by the right lung get well. This is my own
experience, and it accords with the observations of Rouis, of De
Castro, and others. Rouis gives the result in 30 cases of hepatic
abscess discharging by the right lung; of these 15 recovered. Of 25
cases observed by De Castro, discharging by the lungs, 19 recovered.
Next to the discharge by the bronchi, the most favorable mode of exit
is externally, through the parietes of the abdomen; much less favorable
is by the stomach or intestine; but still more fatal is the discharge
into the cavity of the peritoneum. When the abscesses are multiple and
due to pyaemia, the termination is always in death. The numerous
lesions besides the hepatic accelerate the fatal issue. In the case of
large single abscesses the result is in a great measure due to
exhaustion from protracted suppuration. When in addition to the
formation of a great quantity of pus there is frequent vomiting and
rejection of aliment, the failure of strength is proportionally rapid.
In favorable cases, after an abscess is evacuated through the right
lung, recovery takes place promptly. When the discharge occurs through
the abdominal wall, the process is much slower, and often fistulous
passages with several orifices, very slow to heal, are formed. Complete
recovery may ultimately take place. The recovery will be incomplete in
those cases with large loss of hepatic substance, especially when this
coincides, as it usually does, with catarrh, ulceration, and other
lesions of the intestinal tube. Again, the recovery will be incomplete
in those cases where there are imperfect healing of the abscess site
and a fistulous communication with the exterior.

[Footnote 111: _Des Abces du Foie des Pays chauds, et de leur
Traitement chirurgical_, _loc. cit._, p. 40, Paris, 1870.]

[Footnote 112: _Du Traitement des Abces du Foie, Observations
receuilles a Mexico et en Espagne_, par Lino Ramirez, M.D., Paris,
1867, _loc. cit._]

It is possible for the arrest and healing of a suppurative inflammation
of the liver to take place without discharge. Under such circumstances
the watery part of the pus is absorbed, the solid constituents undergo
a fatty metamorphosis, are emulsionized, and thus absorbed, and
gradually closure of the damaged area is effected by a
connective-tissue formation. We must, however, accept with caution
those examples of this process which are supposed to have occurred
because radiating cicatrices are discovered on the surface of the
liver. In a case of hepatic abscess discharging through the lung, known
to the writer, after death, which occurred fifteen years subsequently,
there was no trace of the mischief, so perfectly had repair been
effected. Radiating cicatrices are so often of syphilitic origin that
they cannot be accepted as proof of the former existence of an abscess.

DIAGNOSIS.--He who finds the diagnosis of abscess of the liver easy
under all circumstances can have had but little experience with the
numerous difficulties in the way of a correct opinion. There are cases
so plain that the most casual inspection suffices to form a conclusion;
there are cases so difficult that the most elaborate study fails to
unravel the mystery. The maladies with which hepatic abscess may be
confounded are echinococcus of the liver, dropsy of the gall-bladder,
cancer, abscess of the abdominal wall, empyema, or hydrothorax, etc. As
regards echinococcus, the difference consists in the slow and painless
enlargement characteristic of echinococcus, and the absence of any
symptoms other than those {1019} due to the mere pressure of the
enlarging mass. In abscess there may be no apparent enlargement, or the
increase in the area of dulness may be very great, or after a period of
increase of size there may be contraction due to the formation of pus,
and hence limitation of the inflammation; finally, the accumulation of
fluid may be sufficient to cause dulness up to the inferior margin of
the second rib. There are no corresponding changes of size in the
echinococcus cyst. Furthermore, abscess of the liver large enough to be
recognized by the increased dimensions of the organ will be accompanied
by more or less pain in the right hypochondrium and by a septicaemic
fever. On the other hand, an echinococcus tumor is not accompanied by
fever, pain, or tenderness, and it has that peculiar elastic trembling
known as the purring tremor. The most certain means of differential
diagnosis is the use of an aspiration-needle and the withdrawal of a
portion of the fluid. The presence of pus with hepatic cells will be
conclusive of abscess, whilst a serous fluid with echinococci hooklets
will prove the existence of the echinococcus cyst.

In cases of dropsy of the gall-bladder there are no febrile symptoms,
no chills, and the tenderness when present is limited to the pyriform
body, the seat of the accumulation of fluid, and no general enlargement
of the liver can be made out. At the point of swelling fluctuation may
be detected, or if the gall-bladder is filled with calculi the
sensation imparted to the touch is that of a hard, nodular body of an
area and position corresponding to that of the gall-bladder. Tapping
the gall-bladder, an easy and safe procedure, will resolve all doubts.
When an impaction of a gall-stone is the cause of abscess, the clinical
history is eminently characteristic: there are attacks of hepatic
colic, after one of which the chills, fever, and sweats belonging to
hepatic abscess occur.

The differentiation of cancer of the liver from abscess rests on the
following considerations: In cancer there is slow enlargement, with
pain; a more or less nodular state of the organ without fluctuation;
usually ascites; no rigors; no fever and sweats. In abscess the liver
may or may not be enlarged; there are rigors, fever, and sweating, and
the surface of the organ, so far as it can be reached, is smooth and
elastic, and it may be fluctuating. Cancer happens in persons after
middle life, develops very slowly, and is accompanied by a peculiar
cachexia; abscess occurs at any period, very often succeeds to or is
accompanied by dysentery and by the usual phenomena of suppuration.

It is extremely difficult to separate an abscess in the abdominal wall,
in the right hypochondrium, or a tumor in this region, from an abscess
of the liver. The history of the case, the existence of a dysentery or
of an apparent intermittent or remittent fever before the appearance of
a purulent collection, will indicate the liver as the probable source
of the trouble. Attention has already been called to a case in which an
abscess of the liver was supposed by an eminent surgeon to be a tumor
of the abdominal wall. The history in this case of an obstinate
remittent fever, followed by the appearance of a tumor of the
hypochondrium and by a preliminary discharge at the umbilicus, clearly
indicated the nature of the trouble. In the absence of any history of
the case it is extremely difficult to fix the origin of a suppurating
tumor originating, apparently, in the depth of the right hypochondrium.

Mistakes are frequently made in the case of an abscess developing in
{1020} the convexity of the right lobe of the liver and pushing the
diaphragm up to the third, even to the second, rib, and thus producing
conditions identical with empyema of the right thorax. Such instances
of hepatic abscess are peculiarly difficult of recognition, because,
the physical signs being the same as those of empyema, the
differentiation must rest on the clinical history. In cases of empyema
proper the effusion in the chest is preceded by pain and accompanied by
an increasing difficulty of breathing; in hepatic abscess there are, as
a rule, symptoms of disturbance in the hepatic functions, fluctuation
in the hepatic region, dysentery, etc., long anterior to any
disturbance in the thoracic organs. Again, empyema may be a latent
affection, without any symptom except some obscure pain and a
progressive increase in the difficulty of breathing; on the other hand,
abscess of the liver is preceded by symptoms of liver disease and of
associated maladies. A dry, purposeless cough is present in many cases
of abscess; a painful cough with bloody expectoration occurs when
preparation is making for discharge through the lungs.

Errors of diagnosis are liable to occur in the consideration of
symptoms unquestionably hepatic in origin. Thus, the intermittent fever
accompanying some cases of hepatic colic, like the shivering fits and
fever which occur in cases of nephro-lithiasis, may be confounded with
the septicaemic fever of hepatic abscess. An attentive examination of
the attendant circumstances, especially a careful survey of the right
hypochondrium, can alone determine the nature of the symptoms. In all
doubtful cases the experimentum crucis of puncture with the
exploring-needle becomes a measure of necessity. When all diagnostic
indications are at fault, the needle of the aspirator may decide the
issue. An abundant experience has shown that a needle of suitable size
may be introduced into the right lobe without any ill result--often,
indeed, with distinctly good effects when there is no suppuration or
when pus cannot be detected. In the present state of our knowledge it
cannot be determined why puncture of the organ should be beneficial in
cases having the symptomatic type of hepatic abscess when none exists;
but of this fact there is no doubt.

TREATMENT.--As the formation of pus is coincident with or causative of
the first symptoms, it is obvious that treatment directed to prevent an
abscess can rarely succeed. Yet it is probable that now and then an
abscess just forming has been arrested and healing effected. At the
onset of symptoms some large doses of quinine, with a little morphine
(scruple j of the former and 1/8 gr. of the latter), every four or six
hours, may have a decided curative effect. During the course of the
septicaemic fever, with its chills and febrile exacerbations, quinine
in full doses and alcohol according to the conditions present are
necessary remedies. As the symptoms develop saline laxatives are useful
until the formation of pus becomes evident, when all perturbating
treatment of the intestinal canal should cease. If dysentery be present
when the hepatic symptoms arise, it should be cured as promptly as
possible; and of all remedies for this purpose, ipecac given in the
usual antidysenteric quantity offers the best prospect of relief. For
the dysentery which succeeds to abscess, and is probably, in part at
least, dependent on portal obstruction, the mineral astringents, as
copper sulphate, are the most effective remedies. As far as
practicable, after an abscess has formed the intestinal canal should be
kept quiet, for any considerable disturbance will {1021} endanger the
escape of pus into the peritoneal cavity. Persistent vomiting is very
significant of pressure by an enlarging abscess in the stomach, and
usually signifies an abscess associated with impacted calculus. It is
important in such cases to maintain, as far as can be done, a quiescent
condition of the stomach, for the purpose of preventing rupture into
the peritoneal cavity and to favor the nutrition which is seriously
endangered by the repeated vomiting. Effervescent soda powders are very
useful; carbolic acid in solution, or creasote-water with or without
bismuth, is beneficial; champagne, very dry and highly effervescent,
has been, in the writer's hands, remarkably efficient. As food becomes
a most important need in such cases, milk and lime-water, wine-whey,
egg-nog, and similar aliments must be given in small doses and
frequently. Nutrient enemata, prepared from eggs, milk, and beef-juice,
with the materials for digestion--acid and pepsin--may be made to
supplement the stomach, but such efforts have a very limited utility,
owing to the state of the hepatic functions and to the obstruction of
the portal circuit. In all cases it is necessary to maintain the
strength by suitable aliment and the judicious use of stimulants. The
long-continued and profuse suppuration makes an enormous demand on the
vital resources of the patient, and this must be compensated by
suitable food-supplies.

As the formation of pus has taken place in most cases when symptoms
have begun, the question of highest importance is, Shall the pus be
evacuated? The statistical evidence relating to this question becomes
then an extremely valuable guide. As in almost all cases of puncture of
the liver for the evacuation of an abscess some part of the liver
substance must be passed through, it is necessary to note how far this
can be done without inflicting permanent injury on the organ. Hammond
has punctured the liver in eight cases without the presence of an
abscess, and of these not one has presented any unfavorable symptom.
The author has punctured the liver, penetrating well into the interior,
in two cases in which no abscess was discovered, but the symptoms of
hepatitis existed, with the effect to improve the symptoms. In
Condon's[113] collection of 11 cases there were 8 of abscess evacuated
by the trocar, and 3 of acute hepatitis in which abscess had not
formed, but in which the puncture procured the most decided
amelioration of the symptoms. We have heretofore referred to Hammond's
experience in the puncture of the liver in cases of hypochondriasis,
this condition appearing to depend in some instances on the presence of
abscess. In a number of instances abscesses did exist, but in many
others there was no apparent lesion of the liver, but in these cases
the puncture of the organ was without any ill result. Testimony to the
same effect is given by Ramirez,[114] who asserts that he had not known
a single instance in which any ill result followed puncture of the
liver. It may therefore be regarded as certain that exploratory
puncture of the organ for the purpose of diagnosis as well as for
treatment can at any time be performed with suitable precautions in
respect to the size, condition, and character of the instrument.

[Footnote 113: "On the Use of the Aspirator in Hepatic Abscess," Dr. E.
H. Condon, _The Lancet_ (London), August, 1877.]

[Footnote 114: _Du Traitement des Abces du Foie, Observations
recueilles a Mexico et en Espagne_, par Lino Ramirez, M.D., Paris,
1867, p. 65.]

The authorities of most experience are agreed that, provided with the
{1022} aspirator, the abscess may be punctured as soon as a purulent
collection can be ascertained to exist. The obvious reason for tapping
the abscess is its tendency to extend in various directions, destroying
the hepatic substance. In those examples confined by a limiting
membrane, after a time of inactivity ulceration begins, and the pus
seeks an outlet in some direction. The early evacuation by a suitable
aspirator becomes then a measure of the highest necessity. The good
effects of puncture with even such a crude instrument as the trocar is
well exhibited in the statistics collected by Waring.[115] In a
collection of 81 cases opened by the knife or trocar there were 66
deaths, making the percentage of recoveries 18.5. In these cases the
operative procedure was a final measure, and the mischief had been done
almost if not quite in its entirety. The statistics of Waring are
concerned with a period anterior to 1850. Although they demonstrate the
value of the trocar and evacuation of the abscess, as compared with the
results of the natural course of the disease, the far greater success
of the treatment by the aspirator is shown by the statistics of recent
times. Thus in McConnell's[116] 14 cases, also of India, in which the
aspirator was used to empty the sac, 8 recovered and 6 died. The
statistics of Waring may also be profitably compared with those of
Condon,[117] in which, of 8 cases of abscess evacuated by the
aspirator, 4 recovered, or 50 per cent. They may also be compared with
Sach's[118] cases, 21 in number, of which 8 recovered, or 38 per cent.,
and with the cases of De Castro[119] of Alexandria, who reports 22
large abscesses operated on, the proportion of cures being 31.8 per
100, and 10 small abscesses, the proportion of cures being 70 per 100.
In a case seen in consultation with Collins, in this city, last year,
the aspirator was used by us about three months after the symptoms of
abscess declared themselves. About a quart of bloody pus was drawn off
at once, the opening sealed, and no subsequent accumulation occurred,
the patient entirely recovering, for after a year he was seen
(December, 1884) in complete health. From these data we draw the
important conclusion that early operation is desirable. This fact may
be formulated in the expression: In all cases of hepatic abscess use
the aspirator whenever the presence of pus is made out. When the
abscess is large, and especially when communication is established with
the parietes of the abdomen, a free opening, followed by the insertion
of a drainage-tube, is the proper method to pursue. If the pus
reaccumulates, it is good practice to inject the cavity with tincture
or compound solution of iodine after the pus is drawn off, provided the
dimensions of the abscess are not too great.

[Footnote 115: _An Inquiry into the Statistics of Abscess of the
Liver_, _loc. cit._]

[Footnote 116: "Remarks on Pneumatic Aspiration, with Cases of Abscess
of the Liver treated by this Method," _Indian Annals of Medical
Science_, July, 1872, quoted.]

[Footnote 117: _Lancet_, _supra_.]

[Footnote 118: _Ueber die Hepatitis der heissen Lander, etc._, von Dr.
Sachs in Cairo.]

[Footnote 119: _Des Abces du Foie des Pays chauds, et de leur
Traitement chirurgical_, par le Docteur S. V. de Castro (d'Alexandrie
d'Egypte), Paris, 1870, p. 59.]

As regards the mode of proceeding, the following are useful rules:
Ascertain, if possible, the existence of fluctuation; locate the point
where the walls of the abscess are thinnest; insert an
exploring-needle, and if the depot of pus is reached substitute a
trocar having a sufficient calibre to evacuate the contents of the
abscess; observe antiseptic precautions in respect to each detail of
the operative procedure, and after the removal of the canula or needle,
if a drainage-tube is not necessary, close the {1023} wound
antiseptically. If drainage is necessary, keep the cavity empty and use
proper solutions to prevent septic decomposition. When an abscess of
the liver is pointing, the best place to puncture is where the abscess
is most prominent and it walls thinnest, but if the accumulation of pus
is encysted and there is no attempt at effecting an exit, the
exploring-needle should be passed into the interior of the right lobe,
the most usual site of suppuration. If pus be reached, a larger trocar
may be inserted to evacuate the cavity thoroughly. Repeated insertion
of the needle-trocar is preferable when the abscess is small, but when
the accumulation is large and sufficiently firm attachments to the
abdominal parietes exist, a drainage-tube will be necessary.

In what direction soever discharge of an abscess may take place, the
general indications are to support the powers of life by food and
stimulants. The utmost quietude should be maintained. It is useful, by
the application of a firm flannel bandage, to keep the liver in its
proper position and maintain it there. When pointing of an abscess
occurs, a large flaxseed poultice is a soothing and a mechanically
supporting application.


Acute Yellow Atrophy.

DEFINITION.--By the term acute yellow atrophy is meant an acute
affection of the liver, characterized by rapid wasting or degeneration
of the organ, accompanied by the systemic symptoms belonging to an
acute acholia or cholaemia. It is an acute, diffused inflammation, with
atrophy of the proper gland-elements. It has been called icterus
gravis, malignant icterus, hemorrhagic icterus, malignant jaundice,
etc.

HISTORY.--Cases having a more or less exact resemblance to acute yellow
atrophy have been occasionally reported from the earliest period.
Amongst English physicians, Bright[120] was one of the first to give an
accurate account of the clinical history of some well-defined cases.
Rokitansky[121] was really the first to define the disease from the
pathological standpoint, and it was he who designated it acute yellow
atrophy, this term being intended to signify the nature of the
objective changes. The first treatise ever published on the disease as
a distinct morbid entity was the monograph of Horaezek,[122] which
appeared in 1843. Amongst the French, Ozonam in 1847 was the first to
recognize and describe the disease as a distinct affection, although
Andral[123] had several years before mentioned an affection of the
liver which corresponded in some of its features to this affection. In
1862, Wagner[124] asserted that many of the cases of acute yellow
atrophy were only examples of acute phosphorus-poisoning, and that no
real distinction exists between the two affections. This statement has
been warmly disputed by various German observers, but there is no doubt
a close resemblance between the two affections.

[Footnote 120: _Guy's Hospital Reports_, 1836, vol. i. p. 621.]

[Footnote 121: _Handbook of Pathological Anatomy_, Am. ed.]

[Footnote 122: Quoted by Legg, _On the Bile, Jaundice, and Bilious
Diseases_, _loc. cit._]

[Footnote 123: _Clinique medicale_, 1839, tome ii. p. 363.]

[Footnote 124: _Archiv der Heilkunde_, 1862, p. 364.]

CAUSES.--There can be no doubt that acute yellow atrophy is a very rare
disease, since so few examples are found post-mortem. In the course of
a very large experience in autopsical examinations I have met with but
{1024} one characteristic example.[125] According to Legg, it is "one
of the rarest diseases known to man."

[Footnote 125: _General Field Hospital_, December, 1863.]

Several theories have been proposed to explain the occurrence of this
affection, but without success. It has been ascribed to an excess in
the production of bile, to stasis in the bile, and to a sudden
saturation of the hepatic cells with biliary matters contained in the
portal vein. That these supposed causes are really influential in
producing the malady can hardly be entertained. That there is a
peculiar poison which has a causative relation to the disease is
rendered probable by the fact that a condition closely allied to this
disease is produced by phosphorus, antimony, arsenic, and other
poisons. Is it not a ptomaine generated under unknown conditions in the
intestine? Especially does the morbid anatomy of phosphorus-poisoning
nearly agree in all its details with icterus gravis--so nearly that by
many German authorities they are held to be identical.

Age has a certain influence in the causation of this disease. It is
rarely seen in early life, Lebert in a collection of 63 cases having
found only 2 before ten years of age, yet there has been a well-marked
case at three, and Hilton Fagge reports one at two and a half years of
age. Nevertheless, much the largest number occur between fifteen and
twenty-five years of age, and the maximum age may be fixed at sixty.

The influence of sex in the pathogeny is most remarkable. It is true in
Lebert's collection of 72 cases there were 44 men and 28 women, but it
is now known that he did not properly discriminate in his selection of
supposed examples of the disease. The statistics of all other observers
are opposed to those of Lebert. Thus, in Frerichs' collection of 31
cases, carefully sifted to eliminate error, there were 22 women and 9
men. Legg has also collected 100 cases of acute yellow atrophy, and of
these 69 were women or girls. The most active period of life--from
twenty to thirty years of age--is the usual period for the appearance
of this disease. More than one-half of Lebert's cases occurred between
fifteen and twenty-five; and of Frerichs', two-thirds happened between
twenty and thirty years of age. In Legg's collection of 100 cases, 76
were between fifteen and thirty-five years of age. What is the
condition of women at this period in life which renders them so
susceptible to this malady? There can be no doubt that pregnancy is the
great factor. Of 69 cases especially interrogated on this point,
examined into by Legg, in 25 pregnancy was ascertained to exist. In
Frerichs' collection one-half were women in the condition of pregnancy.
The period of pregnancy at which the disease appears varies from the
fourth to the ninth month, the greatest number occurring at the sixth
month. So long ago as 1848, Virchow drew attention to the remarkable
changes in the liver due to pregnancy. Sinety[126] has studied the
effect of lactation on the liver, and has ascertained the existence of
fatty degeneration. There is a form of jaundice which accompanies
menstruation, as shown by Senator,[127] Hirschberg, and others. These
facts indicate a certain relationship between the sexual system of the
female and the liver, but they do not indicate the nature of the
connection, if any exist, between this condition and acute yellow
atrophy.

[Footnote 126: _De l'Etat du Foie chez les Femelles en Lactation_,
Paris, 1873 (pamphlet).]

[Footnote 127: _Berliner klinische Wochenschrift_, 1872, p. 615, "Ueber
Menstruelle Gelbsucht."]

The influence of depressing emotions has been supposed to be effective
{1025} in producing this disease, but it is more than doubtful if such
a relationship exists. Lebert, however, refers 13 of his cases to this
cause, but Legg, who bases his statements on the study of 100
carefully-recorded cases, is sceptical regarding the effect of such
influences. Syphilis has in some instances appeared to be the
principal, if not the only, pathogenetic factor, and Legg[128] compares
the action of the virus of syphilis to the effect of phosphorus,
mercury, etc.

[Footnote 128: _On the Bile, Jaundice, and Bilious Diseases_, _loc.
cit._]

PATHOLOGICAL ANATOMY.--The anatomical changes occurring in this disease
indicate the existence of a systemic condition: the lesions are not
limited to the liver, but involve various other organs. The changes in
the liver should be first described, since the name of the disease is
derived from the alterations in this organ. As the name indicates, the
lesions are atrophic, but not all examples show this. In some cases
there is little change in the size of the organ; in others the wasting
is extreme; certainly in all typical examples the liver is reduced in
size. The variations in size observed are probably due to the stage at
which the inspection is made: if early, the organ may not be reduced in
size, may be even somewhat enlarged by the deposition of new material;
if later, the atrophic changes will be more or less pronounced. When
the atrophy has taken place, the size of the liver is reduced to
one-half, even to one-third, of its original dimensions; it is then
soft, almost like pulp, and cannot maintain its shape, but flattens out
on the table. The capsule is much wrinkled and the color of the organ
is yellowish, variegated by islets of reddish or brownish-red color,
these spots being somewhat depressed below the general surface and
having a firm texture. On section the boundaries of the lobules are
either lost or have become very indistinct, the line of section being
bloodless. The knife with which the sections are made becomes greasy.
In some instances ecchymoses are discovered under the capsule, and
rarely hemorrhagic extravasations in the substance of the liver. The
bile-ducts are found intact, as a rule. The greatest change in the size
of the liver is observed in the left lobe. The duration of the disease,
as has been indicated above, has a marked influence over the size and
condition of the liver. The atrophic shrinking of the liver occurs more
decidedly after the ninth day. In general, the tissue of the liver is
soft and pulpy in consistence. On microscopic examination the most
important alterations are seen to have occurred in the hepatic cells;
ultimately, these cells disappear, being replaced by fatty and
connective-tissue detritus; but before this stage is reached important
alterations have taken place in the form and structure of these bodies:
the cells become granular and fatty, and lose their sharpness and
regularity of contour, especially at the periphery of the lobule, but
ultimately all the cells within the lobule undergo atrophic
degeneration. In this atrophic degeneration of the hepatic cells, in
their fatty degeneration, and ultimately entire disappearance, consist
the real proofs of the disease. The red islets of tissue already
alluded to consist of the fatty detritus mixed with crystals of
haematoidin.

More or less increase of the connective tissue is noted in many of the
cases--increase of connective tissue with numerous young cells formed
around the vessels and the bile-ducts (Waldeyer[129]). The changes in
the {1026} liver would surely be incomplete without some references to
the minute organisms which play so important a part in modern
pathology. Waldeyer was the first to demonstrate the presence of
bacteria in the pigment-remains of the hepatic cells. Other observers
have been unable to detect them, so that at present the parasitic
origin of this affection remains sub judice.

[Footnote 129: _Arch. fur path. Anat._, 1868, p. 536, Band xliii.]

Important changes also take place in the spleen, but the opinions on
this point are somewhat contradictory. Frerichs found the spleen
enlarged in most of his cases; Liebermeister, on the other hand, and
Legg,[130] find that the spleen is enlarged in about one-third of the
cases. When the atrophic changes occur in the liver, more or less
swelling of the splenic veins must occur in consequence of portal
obstruction. The peritoneum, especially the omental part, is the seat
of multiple ecchymoses, and the endothelium is fatty. The mesenteric
glands are usually swollen. More or less blackish or brownish fluid,
consisting of altered blood, is usually found in the stomach, and the
same, assuming a tar-like consistence, in the large intestine.
Ecchymoses of rather small size are distributed over the stomach and
intestines. The epithelium of the stomach-glands is found granular and
disintegrating, and a catarrhal state of the gastro-intestinal mucous
membrane exists throughout. The secretions are never normal, and the
stools are wanting in bile or present a tarry appearance, due to the
presence of blood.

[Footnote 130: _On the Bile, Jaundice, and Bilious Diseases_, _supra_.]

Important changes take place in the kidneys. They consist essentially
in a granular and fatty degeneration of the tubular epithelium, whence
the altered appearance of the cortex. Multitudes of bacteria crowd the
pyramids. Ecchymoses also are found in the mucous membrane of the
pelvis of the kidney, in the bladder, and indeed all along the
genito-urinary tract.

The muscular tissue of the heart is in a state of acute fatty
degeneration, beginning with a granular change which may at the outset
be of very limited extent and involve but few fibres. The endo- and
pericardium are studded with ecchymoses or marked by hemorrhagic
extravasations, and the pleura presents similar appearances, but not to
the same extent.

The brain does not always show evidences of change, but in many
instances there are ecchymoses of the meninges; the walls of the
vessels are affected by fatty degeneration.

The tissues of the body are more or less deeply stained with bile. The
pathological change on which the jaundice depends has been variously
stated, but the most probable explanation is that which refers it to
mechanical obstruction of the bile-ducts, either by catarrhal swelling
or fatty degeneration of the epithelium. Notwithstanding the prominence
of the hepatic symptoms, acute atrophy of the liver is probably only
one element in a constitutional morbid complexus.

SYMPTOMS.--Acute yellow atrophy begins in two modes--the grave symptoms
preceded by mild prodromes, or the most serious symptoms appear at the
onset. The former mode is the more common. The usual prodromes are
referable to the gastro-intestinal canal, and consist of loss of
appetite, nausea, vomiting, a bitter taste in the mouth, headache, and
general malaise. Indeed, the opening attack may be much like an {1027}
ordinary bilious seizure or acute gastro-duodenal catarrh or a sick
headache. In some cases the initial symptoms--nausea and
diarrhoea--appear to be induced by an indigestible article of food.
Jaundice never fails to be present at some period, but is usually one
of the prodromic symptoms. It has no special characteristics by which
the gravity of the approaching seizure may be measured. It is usually
rather deep, and all parts are deeply stained, but the coloration may
be limited to the body and upper extremities. No change in pulse or
temperature, except the usual depression of both functions, is to be
observed; the urine is deeply stained with pigment, and the feces are
grayish, colorless, or parti-colored.

The period of time elapsing before the serious symptoms come on is not
constant; from one week to several months have been the variations
observed. In a minority of the cases no prodromes have occurred, but
the grave symptoms have declared themselves at once. From the
appearance of the jaundice up to the onset of severe symptoms the time
has varied from two weeks to several months, but has rarely exceeded
three months. During this time there may be nothing to indicate the
gravity of the approaching symptoms; in fact, the case then, as at the
onset, seems to be one of simple gastro-duodenal catarrh associated
with catarrhal jaundice. The onset of serious symptoms is most usually
announced by dilatation of the pupil. If, therefore, in a case of
apparently simple catarrhal jaundice, especially in a pregnant female,
there should occur without apparent reason a marked and persistent
dilatation of the pupil, the possibility of the case being one of acute
atrophy should be apprehended. This symptom is not, alone, of
sufficient value to decide the character of the case, but then an
obstinate insomnia comes on, violent headache is experienced, there is
more or less confusion of mind, and jactitations or an extreme
restlessness occurs. When such pronounced nervous symptoms appear the
character of the attack is explained.

Various divisions have been proposed to mark the type of the symptoms:
thus, the icteric period embraces the prodromal symptoms with jaundice;
the toxaemic period is that stage characterized by profound nervous
disturbances. Ozonam has divided the symptoms into those of the
prodromal period and those of the serious stage, the latter being
subdivided into the symptoms of excitation and those of collapse. There
may be no prodromal period, however; without any preliminary symptoms
the patient is suddenly seized with delirium and passes into a
condition of coma and insensibility, or the first evidence of serious
illness may be convulsions. It is probable, however, that in even the
most sudden cases mild prodromal symptoms had occurred, but were
overlooked. There is much variability in the symptoms of the toxaemic
period. There are three symptoms: excitement with delirium, sometimes
delirium ferox; coma, less or more profound; and convulsions. Legg has
numerically expressed the relative frequency of these symptoms thus: Of
100 cases of unquestionable acute atrophy, 76 had become comatose, 59
were delirious, and 32 had suffered convulsions.[131] According to the
same authority, delirium and coma were associated together in about
one-half of the cases, but in pregnant women coma often occurs alone
(Legg). Usually, when convulsions happen there has been either coma or
delirium. With these cerebral symptoms there are often present various
{1028} disturbances of motility and sensibility, such as local
convulsions, jactitations, hiccough, extreme restlessness, paralysis of
the sphincters, and incontinence of urine and feces or retention,
grinding of the teeth, exalted sensibility of the skin, or it may be
complete anaesthesia, severe itching of the surface, etc.

[Footnote 131: _On the Bile, Jaundice, and Bilious Diseases_, _loc.
cit._]

During the toxaemic period, and directly dependent on the retention of
excrementitious matters in the blood, hemorrhages occur from the mucous
surfaces, from wounds, and into the various serous membranes. A changed
state of the blood being present in all cases of this disease, the
proportion in which extravasations take place is high--in about 71.3
per cent. according to Liebermeister, and 80 per cent. according to
Legg. The latter author regards these estimates as rather low. When
hemorrhage occurs in the stomach in small amount, it presents itself as
coffee-grounds or as black vomit, and in the intestine in the form of
black, tarry stools or melaena. Hemorrhage may also occur from the
surface of an ulcer, from a fresh wound, a leech-bite, etc.; but the
most usual form of extravasation of blood after the gastro-intestinal
is epistaxis or bleeding from the nose. Women who abort, as they are
very apt to do when this disease comes on, may suffer from frightful
hemorrhage, and deaths have been thus caused. Various opinions have
been expressed as to the cause of the hemorrhagic condition--by some
attributed to the changes in the composition of the blood; by others to
the alterations of the vessel walls; both factors are doubtless
concerned.

During the prodromic period the temperature of the body, as in the case
of ordinary uncomplicated jaundice, is rather depressed below normal,
sometimes as much as two degrees; but when the toxaemic stage comes on
the body-heat rises to a variable extent, but usually over 100 degrees
F. In some cases no febrile movement can be detected; in others a very
considerable elevation of temperature occurs, but very rarely attains
to 105 degrees or 106 degrees F. The pulse becomes very rapid, in some
instances rising to 140; but without any apparent cause it may fall
suddenly to 70 or 80, and these fluctuations may take place several
times a day. The rise of temperature and a very rapid pulse may come on
in the final coma only; and immediately after death, as Legg points
out, the body-heat may attain the maximum elevation.

As the toxaemic period develops the tongue becomes dry, glazed,
fissured, sordes form on the teeth and lips, the breath becomes fetid,
and the breathing may assume the Cheyne-Stokes type. The nausea and
vomiting of the prodromal period persist, and the ominous
coffee-grounds appear in the rejected matters, or grumous masses--clots
acted on by the gastric juice--are brought up. Black, pitch-like, or
tarry stools, the result of hemorrhage, are passed toward the
end--involuntarily when liquid. When no blood is present the stools are
grayish and without bile. Constipation may be the condition instead of
diarrhoea in about one-third of the cases.

Various eruptions have been observed on the skin, such as petechiae,
roseola, eczema, etc., but their very variety, as their occasional
appearance, indicates their accidental relationship to the disease.

The urine is much altered in character, but it is usually acid in
reaction, although it has been observed neutral or alkaline. The
specific gravity is at or nearly normal, and it has a deep-brownish or
bilious hue {1029} due to the presence of bile-pigment. The most
important change in the composition of the urine is the diminished
quantity of urea or its entire disappearance; the phosphates, and
especially the chlorides, are also usually diminished in amount; and
albumen and leucin and tyrosin appear to a lesser or greater extent,
together with hyaline, fatty, and granular casts.

Although the observations are somewhat contradictory, it seems pretty
definitely established that the blood is more or less altered in
composition, morphological and chemical. The red corpuscles are
diminished in amount, and often deformed; the white corpuscles are
increased; and excrementitious products--urea, leucin, tyrosin, and
cholesterin--are found in greater or less quantity.

COURSE, DURATION, AND TERMINATION.--Although, as a rule, the course of
acute atrophy is rapid, it is not invariably so. In some instances the
prodromic symptoms have continued through several months, but,
according to Thierfelder, one-half of the cases terminate in from three
to five weeks, and in only 10 per cent. is the duration continued into
eight weeks. The course of the disease is extremely rapid in pregnant
females, rarely extending beyond the second week. An extended course of
the disease is due to delay in the prodromic stage, the toxaemic period
being always absolutely and relatively shorter. In the condition of
pregnancy the danger is increased by the hemorrhages, and the early
termination is due chiefly to this factor. When the duration of the
disease is protracted and its evolution normal, the accumulation of
hepatic excrementitious matters sets up cerebral disturbance, which
becomes a pronounced feature of the case.

The termination cannot probably be otherwise than fatal. As in the
course of the disease the hepatic cells undergo solution and
disintegration, their restoration can hardly be regarded as possible,
certainly not probable. Any curative result must, then, be wrought in
the prodromic period, when the diagnosis must be viewed with some
mistrust.

DIAGNOSIS.--George Harley[132] maintains the singular doctrine that
acute yellow atrophy is only the "sporadic form of the contagious
jaundice of the tropics," or yellow fever. He bases his opinion on the
identity of their symptoms, pathological anatomy, mortality, and
contagious character; for he affirms that acute yellow atrophy may
exhibit contagious power in temperate climates.

[Footnote 132: _Diseases of the Liver_, Amer. ed., 1882, p. 255.]

As acute yellow atrophy comes on as an ordinary catarrhal jaundice, it
is impossible to distinguish it from the latter affection during the
prodromal period. When cerebral symptoms, black vomit, and tarry stools
appear, the area of hepatic dulness very decidedly diminishes, and
leucin and tyrosin replace urea in the urine, acute atrophy may be
suspected.

Acute phosphorus-poisoning, as regards its symptomatology and morbid
anatomy, does not differ from acute yellow atrophy, and many cases of
the latter have been mistaken, it is supposed, for the former. To
distinguish between them the history of the case must be carefully
ascertained.

When, after the prodromal symptoms, which may not be accurately
diagnosticated, there occurs a rapid decline in the area of hepatic
dulness, hemorrhages take place from the mucous surfaces, stupor and
delirium {1030} supervene, and urea disappears from the urine, being
replaced by leucin and tyrosin, there can be no difficulty in coming to
a conclusion: the case must be one of acute yellow atrophy.

TREATMENT.--It was formerly supposed that a case of acute yellow
atrophy must necessarily prove fatal, but this opinion must now be
modified, since examples of cure of supposed cases have been reported
from Oppolzer's clinic,[133] by Lebert,[134] by Harley,[135] and
others. As at the onset the symptoms cannot be distinguished from a
bilious attack or from catarrhal jaundice, the treatment must be
appropriate to these states. When the serious symptoms begin, a large
dose (scruple j) of quinine should be at once administered, and half
the quantity at regular intervals to keep up the cinchonism. Phosphate
of soda, with some arseniate and such mild hepatic stimulants as
euonymin, iridin, etc., should be given to maintain a gentle aperient
action. Experience has proved that active or drastic cathartics do harm
rather than good; on the other hand, mild laxatives, especially those
having cholagogue action, seem to do good.

[Footnote 133: Thierfelder, _op. cit._]

[Footnote 134: _Ibid._]

[Footnote 135: _Diseases of the Liver_, Amer. ed., _supra_.]

Important symptoms arising during the toxaemic period require remedies
to combat them. Nausea and vomiting, and also diarrhoea, are best
relieved by carbolic acid and bismuth in combination. Hemorrhage
requires, when intestinal, the chloride and perchloride of iron; when
from other mucous surfaces, ergotin, gallic acid, and other
haemostatics. The depression of the vital forces should be treated by
small and frequently-repeated doses of alcohol, by quinine, by iron,
and, under some conditions, by digitalis. After the disintegration of
the hepatic cells has been produced no remedies can be of any service.
Until this occurs, however, it seems to the author well worth while to
attempt to stay the destruction by the administration of those remedies
which, by their accumulation in that organ, indicate a special affinity
for its tissue. These drugs are phosphorus, antimony, gold, silver, and
mercuric chloride. By the timely administration of one or more of these
would it not be possible to stay the progress of the atrophic
degeneration?


The Liver in Phosphorus-Poisoning.

DEFINITION.--Poisoning by phosphorus may seem to be a toxicological
question rather than a merely hepatic disease, but as the morbid
complexus thus induced is so similar to acute yellow atrophy that the
conditions are regarded as identical by many of our German colleagues,
it is necessary to enter into some details regarding it.

PATHOGENY.--Phosphorus-poisoning occurs at any period from youth to old
age, but is most common from twenty to thirty years of age. Women seem
more inclined to effect self-destruction in this way than are men,
probably because phosphorus matches are so readily obtained. Children
may munch match-heads in a spirit of mischief. That form of chronic
poisoning seen in workmen in match-factories, and consisting in
necrosis of bone, etc., does not come within the scope of the present
inquiry.

A body poisoned by phosphorus does not exhibit a tendency to
putrefactive decomposition within the usual period. The tissues are
more or less {1031} deeply stained by bile-pigment, and this coloration
extends to pathological fluids as well. The serous and mucous membranes
contain points of blood-extravasation, but they are especially numerous
in the serous membranes. Hemorrhages of this kind are due to two
causes--to the disorganization of the blood, and to fatty degeneration
of the arterioles. The heart is also more or less advanced in fatty
degeneration, the muscles granular, the striations obscure or
obliterated, and the whole soft and easily torn. The spleen is usually
enlarged--often, indeed, to twice its natural size. The liver presents
highly-characteristic alterations. When death occurs early the organ is
generally enlarged, infiltrated with fat, the connective tissue
undergoing hyperplasia; but in more advanced cases atrophy has taken
place, the cells have disappeared and are replaced by fat-granules,
crystals of leucin and tyrosin, connective tissue, etc.--in fact, the
changes characteristic of acute yellow atrophy. The jaundice has been
variously interpreted. As the bile-ducts in advanced cases are found to
contain no bile, but only a colorless mucus, the advocates of a
haematogenic jaundice hold that the jaundice is due to a failure of the
liver to excrete the biliary principles in the blood; whilst the
opponents of this view maintain the existence of an obstruction in the
ultimate ducts. Harley[136] has recently brought forward some strong
facts and arguments--which we believe can be successfully
controverted--maintaining the former view. The jaundice of
phosphorus-poisoning, if Harley's opinion prove to be correct, must be
regarded as a haematogenic jaundice.

[Footnote 136: _Diseases of the Liver_, _loc. cit._]

The mucous membrane of the stomach, as might be supposed, is more or
less ulcerated or in an advanced state of catarrh, and the gastric
glands are affected by fatty degeneration.

The kidneys are affected in a similar manner to the liver; the
epithelium is fatty and sometimes detached, and the same process is
found to occur in the vessels and epithelium of the cortex.

SYMPTOMS.--Not only in the morbid anatomy, but in the symptoms, do we
find that a very remarkable resemblance exists between acute yellow
atrophy and phosphorus-poisoning. As phosphorus is usually swallowed in
bulk, some hours may elapse before the local symptoms begin, for the
contents of the stomach and the tough mucus lining the mucous membrane
may, and usually do, prevent immediate contact of the poison with the
mucous membrane. When the stomach is entirely empty the symptoms may
begin in an hour or two. The symptoms produced may be arranged in two
groups--those due to the local irritation excited by the poison; those
due to its systemic impression. In the first group belong burning in
the gullet, pain, nausea, and vomiting. According to Lewin,[137] who
has collected a number of cases for analysis, vomiting occurs in 26 out
of 32 instances of poisoning. Some hours--often, indeed, three or four
days--then elapse before the systemic symptoms begin. Vomiting, which
was for the time being suspended, occurs again, and instead of the mere
contents of the stomach, containing more or less phosphorus, blood,
somewhat changed by the gastric juice--chocolate-colored or as
coffee-grounds--appears in the vomited matters. The evacuations from
the bowels may at first, as the contents of the stomach, appear
phosphorescent, and afterward exhibit the appearances due to the
presence in them {1032} of altered blood. At this time, if the liver be
examined it will be found somewhat enlarged and tender to pressure, and
on or about the third day jaundice appears; but it should not be
overlooked that jaundice, as Bamberger[138] has shown, may be postponed
to the second or third week after the phosphorus has been taken.

[Footnote 137: _Virchow's Archiv fur path. Anat., etc._, Band xxi. p.
514 _et seq._]

[Footnote 138: Legg, _On the Bile, Jaundice, and Bilious Diseases_,
_loc. cit._]

In favorable cases the area of hepatic dulness decreases and the
jaundice declines. In the fatal cases certain nervous phenomena become
prominent. There occur drowsiness, developing into coma, with
intercurrent attacks of delirium which may be of a maniacal character;
convulsions, spasmodic attacks, dilated pupils, and involuntary
evacuations. The disorganization of the blood and the fatty change in
the vessels are exhibited in the hemorrhages from the gastro-intestinal
mucous membrane. The nervous phenomena are due chiefly to the retention
in the blood of various excrementitious matters which it is the
function of the liver to separate from the blood. Flint's theory of
cholesteraemia has been so abundantly disproved that no one upholds it
at the present time, but the cerebral symptoms are properly referred to
the retention of all hepatic excrement.

The temperature in phosphorus-poisoning rises from 99 degrees to 102
degrees F., but it may reach in severe cases to 103 degrees to 105
degrees F., and at death or immediately afterward to 105 degrees, even
to 107 degrees F. The same fact is true of acute yellow atrophy. With
the jaundice the pulse declines, but in the further progress of the
case, especially toward the close, the pulse becomes rapid and small.

The changes occurring in the urine are highly significant. The amount
of urea decreases as the symptoms increase in severity, and leucin and
tyrosin take its place. If the case tends to recovery the urea again
increases in amount, but if the tendency is in the opposite direction
the quantity of urea steadily diminishes. Bile acids and bile-pigment
are found in quantity, and albumen is present in small amount.

COURSE, DURATION, AND TERMINATION.--Phosphorus-poisoning is necessarily
an acute affection, but the duration of cases is much influenced by the
form in which the poison is taken. If in a liquid and diffusible form,
as oleum phosphoratum, the local and systemic symptoms will develop in
a few hours, but if in solid masses, as particles of match-heads, many
hours (six to ten) may elapse before the local irritation begins. The
proportion of cures in phosphorus-poisoning varies from one-fourth to
one-half of the cases. Much depends, however, on the promptness and
efficiency of the treatment. The prognosis is the more favorable the
earlier proper measures of relief have been instituted. If the case has
proceeded to jaundice, hemorrhages, black vomit, etc. without the
administration of suitable antidotes, little can be expected from any
kind of treatment.

DIAGNOSIS.--The history of any case involved in doubt is indispensable
to a correct conclusion. The phosphorescent appearance of the matters
vomited or passed by stool may make the differentiation comparatively
easy; but if the case has passed beyond this stage,
phosphorus-poisoning can be separated from acute yellow atrophy only by
the history of the case. If the fact of the administration of
phosphorus is successfully concealed, no differentiation can be made,
since {1033} even the best authorities hold to the identity of the
toxic symptoms produced by this poison and of the morbid anatomy, with
the symptoms and lesions of acute yellow atrophy.

TREATMENT.--The poison should be evacuated as quickly as possible by
emetics and proper diluents. The best emetics are sulphate of copper,
apomorphia, and ipecacuanha, the antimonial and mercurial emetics being
unsuited, since their effects are similar to those of phosphorus.
Oleaginous protectives do not prevent, but really favor, the absorption
of phosphorus. Decoctions of flaxseed, slippery elm, acacia, etc. are
suitable demulcents and protectives. The fatty matter in food, eggs,
etc. will have an injurious effect by promoting the solution and
absorption of the phosphorus, and should hence be excluded from the
diet. The most effective antidote is oleum terebinthinae, and the most
suitable preparation is the French acid oil. Freshly-distilled
turpentine appears to be almost if not entirely useless. It is probable
that the American oil which is old and has been exposed to the air for
many months will answer the purpose, but it cannot be too strongly
insisted on that the turpentine which has proved to be efficient in
phosphorus-poisoning is the French acid oil. Turpentine when exposed to
the air absorbs oxygen as ozone, and to this principle are probably due
the curative effects of old turpentine. Phosphorus when acted on by
this agent is converted into a spermaceti-like substance entirely
devoid of toxic power. As rapidly as possible the poison should be
acted on by the antidote, and then the stomach should be evacuated,
using, caeteris paribus, the sulphate of copper, since this forms an
insoluble phosphide with any portion of free phosphorus, whilst at the
same time it empties the stomach of its contents. Although the
immediate results of the poison may be thus removed, the damage to the
red corpuscles and to the whole mass of the blood requires special
management. The success of transfusion, as practised by Jurgensen,[139]
proves that the substitution of fresh blood may save life when the
existing blood-supply is inadequate to the performance of its proper
functions. It follows that if the toxic effects of phosphorus have
continued for several days, blood-transfusion will be necessary in
those cases characterized by an inability to recuperate notwithstanding
the successful removal of the poison.

[Footnote 139: _Berliner klinische Wochenschrift_, No. 21, 1871.]

For the inflammatory symptoms produced by the local action of
phosphorus, opium in some form is indispensable. This remedy is equally
valuable as a means of maintaining the vital resources and to prevent
the evil results of shock and inflammation.


Carcinoma of the Liver.

DEFINITION.--Under the term carcinoma of the liver are included primary
and secondary cancer of the liver. The malady with which we are now
concerned is the primary affection, occurring in the organ proper or in
some pathological new formation connected with it.

ETIOLOGY.--Heredity is the most important factor. A careful
investigation of the reported examples demonstrates that from 15 to 20
per cent. owe their origin to hereditary influence clearly, and
probably {1034} considerably more are indirectly derived in this way
when the immediate connection may not be demonstrable. Next to
heredity, age must be regarded as the most important pathogenetic
influence, much the largest number occurring at from forty to sixty
years of age. It is a malady of advanced life, therefore, rather than
of youth or middle age. Excluding the female organs from consideration,
it is quite certain that sex has little special influence, and that
males and females are affected about equally.

Primary cancer of the liver is comparatively infrequent, occurring in
not more than one-fourth of the cases. Frerichs collected 91 cases, and
of these 46 were secondary to cancer in organs having vascular
communication with the liver.

PATHOLOGICAL ANATOMY.--Under the term cancer of the liver are included
several distinct forms of morbid growth, but united in the
characteristic of malignancy. From the merely clinical standpoint this
characteristic is the most decisive bond of union between them, and
serves as the point of departure in the study of this affection.
Primary cancer of the liver is divisible into two forms: 1, as a
single, defined tumor; 2, as an infiltration through the whole mass of
the organ.[140] Secondary cancer occurs in nodular masses, and with
extreme rarity as an infiltration. The form of cancer is really the
same; the differences in structure are only apparent, the variations
being due to the relative proportion of cells, fibres, and vessels. If
the fibrous stroma is abundant and the cells small in quantity, the
form of structure approaches scirrhus; on the other hand, if the cells
largely preponderate, the type is encephaloid; if vessels predominate,
it is called telangiectatic. The usual form in cancer of the liver is
the soft, cellular variety, encephaloid or medullary. When the
cancerous new formation is nodular, the masses vary in size from a pea
to a child's head,[141] and are numerous inversely as their size. When
the cancer occurs as a solitary tumor, it may attain to enormous
dimensions. It has a spherical shape usually, protrudes from the
surface of the organ somewhat irregularly, and the overlying peritoneum
is thickened, cloudy, and adherent from a local inflammation. The
central portion, whether there be one, several, or many nodules, is
depressed, giving an umbilicated appearance to the tumor; and this
central depression is found to be soft, almost diffluent, and full of
juice. The fibrous stroma which extends through this central soft
material has a reticulated arrangement and a shining, fibrous
appearance. The cancerous masses are not confined to these nodules, but
extend into the surrounding hepatic structure, push their way into the
portal (especially the hepatic) veins, block the ducts, and invade the
lymphatic glands in the fissure of the liver.

[Footnote 140: Virchow, _Krankhaften Geschwulste_, _loc. cit._; Perls,
_Virchow's Archiv fur path. Anat., etc._, Band lvi. p. 448 _et seq._;
Frerichs, _A Clinical Treatise, etc._, Syd. Soc. ed., _loc. cit._, vol.
ii. p. 281 _et seq._]

[Footnote 141: Forster, _Lehrbuch der Pathologischen Anatomie_, by
Seibert, Jena, 1873.]

When the cancerous new formation takes the form of an infiltration of
the organ instead of distinct nodules, the liver is usually uniformly
enlarged and its outlines preserved.[142] The peritoneum is opaque,
thickened, and adherent. The organ is traversed by fibrous bands, and
the {1035} intervening portion is a soft, juicy pulp, stained by the
imbibition of bile. In extreme cases hardly any portion of the proper
hepatic tissue remains, but is replaced by a cancerous new formation
having the same shape.

[Footnote 142: Perls, _Virchow's Archiv_, Band lvi. p. 448 _et seq._]

As regards the minute structure of cancer of the liver, it may be
regarded as a degeneration (cancerous) of the proper gland-cells and of
the epithelium of the bile-ducts. As cancer develops in the liver it is
to be noted that the cellular elements preponderate over the fibrous or
the stroma, and hence the new formation presents the characteristics of
softness, rapid growth, and a multitudinous cellular hyperplasia. As
regards the form of the new cells, it cannot now be doubted that they
are descendants of the secretory gland-cells and of the epithelial
lining of the ducts. According to some observers, it is to the
proliferation of the proper gland-cells that the new formations owe
their origin; according to others, to the hyperplasia of the cells
lining the ducts. As the growth of the new formation can take place
only through an adequate blood-supply, it becomes very important to
ascertain its source. There can be little doubt that primary cancer of
the liver receives its nutrient supply through the hepatic artery, in
connection with which new capillaries form in the pathological tissue.

Secondary cancer of the liver is the usual form of the specific
manifestation. From the merely clinical standpoint the primary
affection is the more important. From the pathological point of view
the secondary implication of the liver may be a true metastasis or a
mere communication by contiguity of tissue. The most usual metastasis
occurs from epithelial cancer of the face (Schuppel), but the ordinary
communication of the new formation is from primary cancer of the
stomach, intestine, pancreas, mesentery, etc. The cancer elements, as
the author has several times verified, crowd the lymphatics and veins,
and through these channels reach the liver and other parts. As the
cancer elements in the case of secondary implication of the liver are
distributed chiefly by the portal vein, it follows that there must be
numerous secondary foci and multiple nodes. Cancerous infiltration
under these circumstances is the rarest possible form for the new
growth to take. The size and number of nodes forming in these cases of
secondary implication of the organ vary greatly--from two or three to
twenty, or a hundred, or even more. As regards the form, structure, and
ultimate behavior of the secondary formation, they do not differ from
the primary. As respects the relative proportion of stroma and cellular
elements--fibres and cells--they vary greatly, some presenting the firm
texture of a predominating fibrous stroma, others the softness and
ready diffluence of the excessive cellular production. The latter is
undoubtedly the usual condition, and when the nodular masses are
incised an abundant creamy juice exudes. With the development of these
nodules an increase in the size of the liver takes place and the organ
has an uneven and indurated feel. As the cancerous masses develop the
proper hepatic structure undergoes atrophy, and finally little is left
of the organ but the cancerous new formation. The blood-vessels,
lymphatics, and peritoneal investment are invaded, the first mentioned
most decidedly; and especially are organized exudations the favorite
seats of cancer new formations, those, for example, about the
gall-bladder and cystic duct resulting from repeated attacks of passage
of calculi.

{1036} Secondary changes take place in the cancerous nodes. As the
cells develop pressure is brought to bear on the vessels supplying them
and on each other, with the result of fatty degeneration of the central
portion, which effects the change in the form of the nodules and in
their consistence, already mentioned. The blood-supply to the cancerous
nodes in the liver is derived from the hepatic artery, as Frerichs has
determined by carefully-made injections; they also are new formations
of exceedingly delicate structure, and form a network about the
periphery of each mass or node. By reference to these anatomical
considerations it is easy to understand the failure of nutrition of the
central portions of the nodes.

Pigment cancers of the liver are rare as secondary formations, and
excessively infrequent as primary formations. They are, properly
speaking, melano-sarcomas (Schuppel). They are more often metastatic
than merely secondary--that is, transferred from different parts, as in
the case of melanotic sarcoma of the choroid--than due to neighboring
disease transferred by contiguity of tissue. This variety of cancer, so
called, takes the form of multiple nodes or of diffused infiltration,
the former more frequently; but both modes of development may go on at
the same time. The nodes vary in size from a pea to a child's head,
have a grayish, brownish, or blackish tint, and exude on section a
fluid not creamy like true cancer-juice, but rather watery and
containing black particles floating in it. In the case of diffuse
infiltration the pigment masses are thoroughly distributed through the
original hepatic tissue. In both forms the size and weight of the organ
are enormously increased. In the case of the melanotic infiltration the
whole organ is uniformly enlarged, reaching in a few months the
enormous size of twelve to twenty pounds.

Sarcomas also occur very rarely as primary growths in the liver, but
secondary sarcomas are more frequent. There are fibro-sarcoma,
lympho-sarcoma, and osteo-sarcoma as secondary deposits, the first
being very firm in consistence, the second soft and medullary, and the
last of hard, bony consistence.

SYMPTOMS.--We are especially concerned here with primary cancer of the
liver. The secondary disease is so obscured by the main and primary
lesion that a diagnosis may be impossible. Furthermore, the progress of
the original disease is that which demands immediate consideration. As,
therefore, the secondary implication of the liver is of relatively
trifling importance, and only an incident in the course of the main
disease, the matter for consideration now is primary cancer of the
liver.

It is the fact that in some, even a considerable proportion, of the
cases the onset and progress of cancer of the liver are very obscure.
For some time the symptoms may be of the vaguest description. The usual
history is this: A person of forty to sixty years begins to fail in
flesh and strength, becomes sallow, has disorders of digestion, pain
and uneasiness in the right hypochondrium, and the bowels are now
confined, now relaxed. The abdomen, notwithstanding the general loss of
flesh, increases in size, and the superficial veins are enlarged; very
considerable pain is experienced in the right hypochondrium, and often
extreme tenderness to pressure is a pronounced symptom. The pains are
not limited to the hepatic region, out extend widely from this point in
all directions. On palpation the {1037} liver is found to be enlarged,
its texture indurated, and its outline irregular and nodular, and
pain--often, indeed, quite severe--is developed by pressure.

The condition of the liver on palpation is best ascertained by suddenly
depressing the abdominal wall with the tips of the fingers arranged in
a line. Displacing thus the movable bodies in the cavity, the liver is
quickly reached, and nodules, if they exist, are readily felt. If the
new formation has developed from exudations about the gall-bladder and
cystic duct, it may be felt by suddenly depressing the walls of the
abdomen over this organ in the usual position of the fissure.

In the case of general cancerous infiltration of the organ, with the
remarkable enlargement which occurs in such cases, there will be
present an obvious distension of the right hypochondrium; the
intercostal spaces will be forced outward and the arches of the ribs
rendered more prominent; the area of hepatic dulness, both vertical and
transverse, will be increased; and the limits of dulness will move with
a full inspiration downward, and with a full expiration upward. This
mobility of cancer-nodules of the liver with the inspiratory and
expiratory changes serves to distinguish them from tumors of the
abdominal walls. Seen early, the changes in the size of a nodule or of
the liver itself may be noted from week to week,[143] especially in
cases of rapidly-growing cancer.

[Footnote 143: Murchison, _Clinical Lectures_, p. 187.]

As the cancerous new formations extend into the portal system within
the liver, obstruction to the portal circulation results from the
blocking of the blood-current. Also, interference in the portal
circulation arises by compression of the vessels from without, either
through the accumulation of cancer-products in the liver or by the
enlargement of the lymphatics in the fissure of the organ. In what way
soever it may be produced, the practical fact remains that ascites is a
frequent symptom, occurring in somewhat more than one-half of the
cases. The character of the fluid varies. It may be a clear serum
containing a small proportion of albumen; it may be colored by bile or
be of a deeper greenish or reddish hue; it may contain flocculi of
lymph and numerous leucocytes floating in it; and the ordinary serum
may be rendered cloudy and be filled with shreds of exudation in
consequence of peritonitis, or bloody because of hemorrhage from a
softening nodule. When the fluid is considerable in amount the
difficulty of ascertaining the condition of the liver is greatly
enhanced, and symptoms due to the interference of the fluid with the
action of various organs are introduced into the complexus of morbid
signs. Especially is the upward pressure of the ascitic fluid, and the
consequent interference in the movements of the lungs and heart, a
source of considerable distress. First, a local and afterward a general
peritonitis ensues as a consequence of the extension outwardly of the
new formations to the peritoneal layer, and its implication by
contiguity of tissue or the rupture of a spreading fungous growth and
hemorrhagic extravasation into the cavity. The peritoneal complication
is not only a serious addition to the sufferings experienced by the
patient, but it adds to the difficulties of a diagnosis. In the case of
a celebrated savant who died of cancer of the liver (seen by the
writer) there was such a pronounced peritonitis that the diagnosis made
by the attending physician was chronic peritonitis. When this
complication occurs, there takes place {1038} a decided increase in the
local tenderness, and this increased sensibility to pressure quickly
extends over the abdomen, causing a general exquisite tenderness.
Besides this tenderness characteristic of most cases of peritonitis,
distension of the abdomen and the decubitus peculiar to this state are
obvious symptoms. It is therefore clear that the occurrence of
peritonitis not only contributes to the severity and painfulness of the
case, but seriously complicates the diagnosis.

It has been already stated that pain in the right hypochondrium is a
nearly constant symptom in cancer of the liver. With the initial
symptoms, uneasiness, heaviness, a sense of pressure in the hepatic
region are experienced, and as the case progresses more or less acute
pain develops as a rule. But there are exceptions. In cases of cancer
involving the deeper portion of the liver there may be little pain, and
in some rare cases of cancer involving the external part of the
liver--the capsule and peritoneum--but little pain is experienced. In
much the largest proportion of cases the pain is severe, and the
production of any considerable pain means the implication of the
hepatic plexus of nerves or the hepatic peritoneum. It follows, then,
that the pain in the former case is not limited to the locality of the
disease, but is more or less widely distributed through the anatomical
relations of the hepatic plexus, being felt in the epigastrium, the
walls of the chest, the shoulders, etc.

In secondary cancer of the liver, following cancer of the stomach,
vomiting is a constant symptom, but also in those cases of primary
disease in which the left lobe is especially enlarged, relatively, are
nausea and vomiting pronounced symptoms. At the onset of the malady the
appetite fails and a gastro-intestinal catarrh is set up. More or less
catarrh of the bile-ducts also ensues. The interference with nutrition
thus occasioned is enhanced in those cases in which the obstruction of
the ducts is sufficient to prevent the escape of bile into the
intestine. Jaundice is not a constant symptom, occurring in little more
than one-third of the cases. When it occurs, the peculiar stools are
present and the intestinal digestion is deranged, as in cases of
ordinary obstruction to the ducts. In two cases of cancer of the liver
occurring in the writer's practice, and examined by post-mortem, there
were calculi present in the gall-bladder; in one case the principal
calculus was egg-shaped and the size of a pullet's egg.

The nutrition rapidly fails from the beginning of cancer of the liver.
The downward pace is accelerated when the gastro-intestinal digestion
fails and vomiting occurs after taking food. The skin becomes dry and
wrinkled, and if not jaundiced has a peculiar tint, varying in depth of
color from an earthy or fawn-like hue to a deep bronze. Failure of
strength is a pronounced symptom from the beginning, and is out of
proportion to the loss of flesh. As the wasting advances the decline of
strength is accounted for, but the feeling of weakness and the distaste
for exertion which occur so early are very significant signs of
internal cancer, although they do not indicate the position of the
neoplasm. Emaciation finally becomes extreme.

The urine declines in amount as the case progresses. It is usually very
high-colored, contains bile-pigment when jaundice is present, and other
forms of pigment produced by conditions not at present known. Sometimes
albumen is present, and leucin and tyrosin rarely.

{1039} COURSE, DURATION, AND TERMINATION.--As has been already set
forth, cancer of the liver may present so few really distinctive
symptoms as to escape recognition. Under favorable circumstances the
diagnosis may be comparatively easy. In forming an opinion it is useful
to review the whole course of the malady and draw conclusions not only
from the characteristic signs, but from the development of the symptoms
as a whole.

A case of cancer of the liver occurs usually after the middle period of
life. The person so affected begins to decline in flesh and strength,
has uneasiness in the right hypochondrium, disorders of digestion, and
begins to have a pallid or earthy hue of the countenance. Presently,
much pain is felt in the hepatic region, the organ distinctly enlarges,
and some effusion of fluid and much flatus increase the dimensions of
the abdomen. Much tenderness, often exquisite sensibility, is produced
by pressure over the liver, and often over the whole abdomen. By
careful palpation nodules can be made out and their growth noted in
those cases free from peritoneal inflammation. The abdominal swelling
and tenderness incommodes the lungs, and a semi-erect decubitus is
assumed to relieve the pressure on them; the breathing becomes short,
catching, hurried, and painful, and sometimes a most distressing
hiccough is superadded to the other sufferings. Great wasting and
weakness ensue. Jaundice appears, or the earthy hue of the skin deepens
into a bronze discoloration. The case may be terminated by some
intercurrent disease--by an attack of pleuritis, pneumonia, by
peritonitis from rupture or perforation, by intra-peritoneal
hemorrhage, by an exhausting diarrhoea. The natural termination is by
gradual failure of the powers, by marasmus, the immediate cause of
death being due to cerebral anaemia, to failure of the heart from fatty
degeneration of the cardiac muscle, from thrombosis of the portal vein,
from the development of a hemorrhagic state, and hemorrhages from the
various mucous surfaces, etc. The duration is much influenced also by
the character of the cancer, whether scirrhous or medullary. The latter
are not only more rapidly growing, more destructive of the hepatic
tissue, and more rapidly distributed to neighboring organs, but more
quickly perforate the capsule and excite a fatal result by hemorrhage
or by peritonitis. The average duration of cancer of the liver is
variously stated. Having reference to my own personal observation,
controlled by the experience of other observers, the duration is from
three to nine months, one year being exceptional. There are cases in
which the symptoms are very acute, the progress rapid, the whole course
from the initial symptoms to the termination being completed in from
two to three months. It need hardly be observed that no case of cancer
of the liver has been cured. The invariable termination is in death. If
any case has seemed to be cured, it may be asserted with confidence
that cancer of the liver did not exist.

DIAGNOSIS.--The differential diagnosis is concerned, first, with the
existence of cancer; second, with its form. As cancer causes
enlargement of the liver in two textural conditions--namely, uniformly
smooth, and nodular--it must be differentiated from other diseases
producing similar results. Amyloid disease and echinococcus cysts
present us types of the former; cirrhosis and syphilis, of the latter.
The history of the amyloid disease and of the echinococcus cyst is very
different, and both {1040} develop much more slowly. Amyloid disease of
the liver arises simultaneously with the same form of degeneration in
other organs, and is connected with suppurative disease of some kind,
with syphilis, with chronic malarial poisoning, etc., and may occur at
any age. Echinococcus cysts enlarge painlessly and do not impair the
vital forces; the liver is elastic, and under favorable circumstances
presents by palpation the purring-tremor symptom. Cirrhosis may have to
be differentiated at two periods--during the time of enlargement,
which, however, is rather brief; and during the stage of contraction
and nodulation. The history in cancer and in cirrhosis is different:
the age, the habits of life, the rate of hepatic change, are opposed in
the two diseases; the diminution in size with nodulation is
characteristic of cirrhosis; enlargement with nodulation belongs to
cancer. The rapid progress of cancer, the wasting, the debility, the
cachexia, serve to distinguish it from all other affections of the
liver except acute yellow atrophy and phosphorus-poisoning; both,
however, are so different in history and development as not to require
differentiation. It may be quite impossible in latent cases to
distinguish primary cancer of the liver from secondary, but in those
examples of the disease occurring in the stomach, intestines, and
pancreas there is usually an antecedent history of the primary malady
which distinctly separates it in point of time and the character of the
symptoms from the secondary implication of the liver. Cancer of the
gall-bladder, and especially of the organized exudation about it, may
not be readily separated from cancer of the pancreas or of the
duodenum. In doubtful cases the history of attacks of hepatic colic
becomes an important element in making the differentiation.

TREATMENT.--As we are not in possession of a cure for cancer, the
treatment of cancer of the liver must be palliative. Anodynes to
relieve pain, paracentesis of the abdomen to remove accumulation of
fluid which causes distress, carbolic acid to check nausea and
vomiting, and the usual haemostatics for hemorrhage, are the measures
most necessary. In fact, the treatment must be throughout
symptomatic--for the relief of symptoms as they arise.


Amyloid Liver.

DEFINITION.--By amyloid liver is meant a deposit in the cells of the
organ, in its vessels and interstitial tissue, of a peculiar albuminoid
matter called amyloid because of a superficial resemblance to
starch-granules. Various designations have been applied to this
condition of the organ; thus it has been entitled waxy liver and
lardaceous liver, because of the apparent resemblance to wax and lard
respectively.

CAUSES.--There exists in the blood a peculiar material, albuminoid in
form, applied in the normal state to the structure of
tissue--dystropodextrin, as it is called by Seegen--which, when
precipitated under certain conditions not now known, assumes the
peculiar appearance with which we are now familiar under the term
amyloid. The character of the amyloid matter was first distinctly set
forth in 1858 by Virchow, who also discovered the characteristic
reaction by which it can always be detected. The reaction to iodine
gave to the material the designation amyloid, or starch-like, by which
it is chiefly known. The {1041} circumstances inducing the deposit of
this material are by no means clearly understood. It has long been
known that suppuration, especially in connection with bone, has had a
distinct influence. Syphilis, especially the tertiary lesions
accompanied by pus-formation, has an evident causative relation.
Chronic malarial infection has a more distant and doubtful, but still
recognized, power to develop this morbid state. Of the various causes
above mentioned, the most frequent is the suppuration of pulmonary
cavities. In regard to the influence of this, however, it must be
remembered that no form of suppurative disease is so common. The
relative frequency of the association between suppurating cavities and
amyloid disease is not greater than long-standing necrosis with an
extensive sequestrum is with the same state; but the actual number of
the former is greater. Amyloid disease of the liver is most frequent
between the ages of ten and thirty, but it may occur at any age, the
period in life being determined by the operation of the causes. Thus,
Frerichs' statistics are: under ten there were 3 cases, from ten to
twenty there were 19, and from twenty to fifty there were 37 cases. Men
are, relatively to sex, more frequently attacked, and in the proportion
of three-fourths, but this difference means, of course, the character
of men's occupations and their greater liability thereby to the
accidents and diseases incident to such employments.

Besides the pathogenetic factors above mentioned, it may be well to
refer in this connection to the effect of long-standing neoplasms. It
has been found that amyloid disease is produced in some subjects by the
cachexia resulting from the slow development and persistence of such a
new formation. The special character of the neoplasm is of less
importance in respect to this condition than the constitutional
condition--the cachexia--induced by its slow growth and interference
with nutrition. Although long-standing disease, especially of a
suppurative kind, is known to be necessary to cause amyloid disease,
Cohnheim[144] has lately published some facts which seem to prove that
the degeneration may occur more speedily than has been heretofore
supposed. He has shown, contrary to the previously-accepted view, that
amyloid degeneration may follow in three months after the reception of
a gunshot wound. He records three cases in which the amyloid deposits
ensued in six, five, and three months, respectively.

[Footnote 144: _Virchow's Archiv_, vol. liv. p. 271 _et seq._, "Zur
Kentniss der Amyloidentartung."]

According to the author's observation, a peculiar somatic type is
either necessary to, or at least is greatly promotive of, the amyloid
degeneration. If, for example, the same suppurative process occurs in a
person of a blond and lymphatic type and in another of brunette and
nervo-muscular type, the former will be much more likely to suffer from
amyloid change than the latter. "The gelatinous progeny of albuminous
parents" is the mode of expression used to designate this particular
type.

PATHOLOGICAL ANATOMY.--To use the term amyloid liver is rather
misleading, since this indicates the restriction of the morbid process
to the liver, whereas it is perfectly well known to be rather widely
distributed through various organs and tissues of the body. The term
amyloid is itself confusing, since the albuminoid material so
designated is not really starch-like. The corpora amylacea, so called,
differ materially from starch-granules, and still more from the amyloid
matter. According to {1042} Wagner,[145] these substances "have nothing
in common." In the study of the amyloid deposit it has not been
possible to separate it from the tissue in which it is imbedded; hence
the published analyses of this peculiar material are probably far from
correct. However, it has been rendered probable that the amyloid
deposit has close affinities with fibrin. One of the theories--that of
Dickinson of London--assumes that this material is fibrin deprived of
the potash associated intimately with it. According to Seegen,
dystropodextrin, a material existing in normal blood, agrees with
amyloid matter in its most essential characteristics. Although
Dickinson's theory is not tenable, it has served a useful purpose in
showing the close affinity of fibrin with this pathological product.
What view soever may be entertained of its nature, it is certain that
the material to which we apply the term amyloid is of albuminous
origin. Under circumstances with which we are now unacquainted this
material is deposited from the vessels, and, instead of undergoing
organization and contributing to the structure of tissues, remains
unorganized and unappropriated. It is known that this deposition of the
amyloid material is related to the process of suppuration and to
certain cachexiae, but the intermediate steps remain unknown and
inexplicable.

[Footnote 145: _A Manual of General Pathology_, by Prof. Dr. E. Wagner,
p. 325 _et seq._]

The amyloid matter is first exuded into the coats of the finest
ramifications of the hepatic artery, and therefore the first appearance
of the disease is in the middle zone of the lobules. In this respect
pathologists are agreed: that the amyloid deposits first appear in the
walls of the vessels. Wagner maintained, in opposition to Virchow, that
the exudation is limited to the vessels and does not extend to the
hepatic cells, which perish by pressure and consequent atrophy. This
point has not yet been decided. It seems most probable, however, that
the ramifications of the hepatic artery and all the capillaries of the
lobule are affected, and that the deposits in them lead to atrophic
degeneration of the cells.

In consequence of this extensive implication of the vascular system of
the liver important changes occur in the size, density, and appearance
of the liver. The organ is greatly enlarged in all its diameters. When
felt through the walls of the abdomen its outline is distinct, it is
firm, even hard, to the sense of touch, and it projects from a finger's
breadth to a hand's breadth below the margin of the ribs. The increase
of size of the amyloid liver is very great, attaining in weight, on the
average, twice that of the normal organ; but this size may be largely
exceeded in exceptional instances. In respect to shape and outline the
amyloid liver does not differ from the normal organ; for although its
dimensions are increased, its relations to the parts adjacent are not
altered. The weight of the amyloid liver may reach ten, twelve, even
sixteen pounds avoirdupois. The color of the amyloid liver is very
different from that of the normal organ: instead of having the
reddish-brown tint, it becomes grayish, yellowish, or reddish-gray. In
consistence the amyloid liver is firm and rather elastic and doughy,
and on section the margins of the incision are well defined, even
sharp. A very characteristic feature of the cut surface is its
paleness, anaemia, or bloodlessness, and scarcely any blood is exuded,
even from the large vessels. The appearance of the incised surface of
the liver has been described by comparison with various substances:
according to one, it is waxy; according to another, it is lardaceous. A
thin {1043} section of a part of the liver far advanced in the amyloid
change is distinctly translucent, almost transparent; but a marked
difference is observable between the amyloid matter and the lobules
proper, even in the cases of extreme deposit. The lobules are separated
by an opaque yellow border, and the centre of each is marked by a spot
of a similar yellow color.

The amyloid material is remarkable for its power to resist the action
of chemical agents and putrefactive decomposition. The test originally
proposed by Virchow--iodine--continues to be the most characteristic.
Orth[146] suggests a method of applying it which is very excellent in
respect to the clearness with which the reaction is shown: A large,
thin section of the affected liver is placed in a saucer of water
containing some iodine, and after the reaction has taken place is laid
on a white plate. Iodine tincture, diluted or the compound solution, is
brushed over the affected region, when the amyloid matter assumes a
deep mahogany tint and the normal tissues a merely yellowish hue. The
distinctness of the reaction may be increased by brushing over the
iodized surface some dilute sulphuric acid, when the amyloid matter
takes a deep violet, almost black, color.

[Footnote 146: _Diagnosis in Pathological Anatomy_, Riverside Press,
1878, p. 321.]

Only a part of the organ--namely, the smaller vessels--may be involved
in the degeneration, and this may be restricted to patches or parts of
the organ. With the amyloid change there may be associated syphilitic
gummata, or the liver may be more or less advanced in fatty
degeneration or in cirrhosis. Those parts of the organ not invaded by
the disease are not often entirely normal; they are more or less
darkened in color by venous congestion, distinctly softer, etc. The
amyloid change is not limited to the liver, but extends to the kidneys,
lymphatic glands, the intestinal mucous membrane, etc.

SYMPTOMS.--As the amyloid change in the liver is usually coincident
with a simultaneous alteration of other organs, and as the deposits
characteristic of the affection are dependent on long-previous disease
of an exhausting kind, it is not surprising that the subjects of this
affection present the evidences of a cachexia. To the effects of a
chronic malady we have added the complications growing out of the
amyloid change in the liver, associated, as it usually is, with amyloid
degeneration of other important organs.

The symptomatic expression of amyloid liver is therefore mixed up with
various derangements that occur simultaneously, but especially with the
causes inducing the existing cachexia, with chronic suppuration of
pulmonary cavities, or in connection with diseased bone, with the
syphilitic cachexia, or with chronic malarial toxaemia. With what cause
soever the cachexia may be associated, the symptomatology of amyloid
liver is secondary to, or ingrafted on, the conditions produced by the
cachexia. The liver is enlarged in all well-marked cases from a
finger's breadth to a hand's breadth or more below the inferior margin
of the ribs; it is also firm to the touch, well defined, elastic, and
its margin rounded, but yet well defined. There is usually no
tenderness nor pain, and, without any uneasy sensations to indicate the
change taking place, the organ is found to have slowly enlarged,
sometimes to an extraordinary extent. Careful palpation may also
demonstrate an enlargement of the spleen. When the abdominal muscles
are relaxed and there is no swelling of the abdomen by flatus or
peritoneal effusion, the very considerable enlargement of {1044} the
liver can be readily ascertained. If the effusion is not so great as to
distend the abdomen unduly, the increased consistence and dimensions of
the liver can still be made out with comparative ease. The hepatic
functions are not always sufficiently disturbed to produce
characteristic symptoms. In a small proportion--scarcely one-tenth--of
the cases does jaundice appear, and when present it is due, usually, to
enlargement of the lymphatics in the hilus of the organ, and thus
directly compressing the hepatic duct. In the writer's experience,
although jaundice has not occurred, there was present a peculiar dark
earthy or bronzed tint of the skin, significant of chronic hepatic
troubles. Obstruction of the portal circulation is rather unusual, and
the explanation is to be found in the fact that the amyloid
degeneration occurs first in the radicles of the hepatic artery. In
about one-fourth of the cases ascites is present, but in a somewhat
larger proportion hemorrhoids, blackish, tarry stools, and other
evidences of portal congestion. When the intestinal arterioles are
attacked, an intractable colliquative diarrhoea comes on; the stools
are offensive, sometimes light from the absence of bile, sometimes dark
from decomposition or the presence of blood. When the stomach
arterioles are also involved, which is usual under these circumstances,
the blandest and simplest articles of diet will pass unchanged or
simply decomposed. Blood may be vomited sometimes in large quantity
from thrombic ulcers, but the matter ejected from the stomach when the
case is well advanced is a thin, watery fluid, faintly acid or neutral,
and greenish or brownish in color.

An enlarged spleen is often present, produced by the same
conditions--by amyloid degeneration. The same change taking place in
the kidney, the urine becomes pale, abundant, of low specific gravity,
and albuminous. General dropsy supervenes in a majority of the cases
finally, due largely to the hydraemia; and of this condition ascites is
a part. In some cases enlargement of the abdomen is the first step in
the dropsical effusion, and may throughout be the most prominent, as
the author has seen. In other cases oedema of the feet and legs is the
first evidence of dropsy; in still others the dropsy is general from
the beginning.

Amyloid liver may coexist with a fairly good state of the bodily
nutrition, but if digestion and assimilation be interfered with by any
of the causes above mentioned, the strength rapidly declines and
emaciation reaches an extreme degree.

COURSE, DURATION, AND TERMINATION.--As amyloid liver is never a
substantive affection, but secondary to some constitutional malady or
to long-continued suppuration, its course must be considered in
relation to the agency producing it. It is very silent in its origin
and progress, and causes no pronounced symptoms until it attains
considerable size and its functions are interfered with by the extent
of the deposits. The history of the affection to which it is secondary
therefore precedes the onset of the amyloid change and accompanies it
throughout. The enlarged organ, with the results of its enlargement in
altered functions of the abdominal organs, is a symptom superadded to
existing disturbances. The period elapsing in the course of a chronic
suppurative disease before the amyloid change occurs differs greatly in
different cases, and may be stated as from three months (Cohnheim's
case) to many years. Many of the cases terminate by an intercurrent
disease; others by uraemic {1045} convulsions; a very few by hemorrhage
from the stomach or intestines; and those pursuing their course
uninterruptedly, by exhaustion.

The prognosis is very unfavorable. By some a cure at the beginning of
the morbid deposits is regarded as possible, and examples of cures have
been reported. The writer has seen supposed cases of amyloid liver
terminate in recovery. There must always remain an impression that in
such instances an error of diagnosis was committed. Those of syphilitic
origin are probably more curable, but syphiloma of the liver may be
confounded with amyloid disease, and hence the cure may be referred to
the latter.

DIAGNOSIS.--Amyloid degeneration of the liver may be confounded with
the various non-febrile enlargements of the organ. An important element
in making the differentiation is the history of suppuration in
connection with bone, with lung cavities, with constitutional syphilis,
with chronic malarial toxaemia, etc. From fatty liver, amyloid
degeneration is distinguished by the history as just sketched; by the
fatty tendencies of the body in the former, emaciation in the latter;
by the concomitant changes in the spleen, kidneys, and elsewhere; and
by the subsequent history, fatty liver terminating by a weak heart
usually, whilst the amyloid disease ends in the modes described in the
preceding paragraph. From hydatid disease, amyloid liver is
differentiated by the history, by the difference in the physical
characteristics of the enlargement, by the presence of the purring
tremor in the one, its absence in the other, and especially by the
subsequent course. In all doubtful cases the use of an aspirator-needle
and the withdrawal of some fluid containing the characteristic hooklets
of the echinococcus will serve to determine the nature of the growth.
From cancer, amyloid liver is separated by the previous history, by the
nodular character of the enlargement, by the pain, and by the cachexia
and associated derangements. Whilst amyloid liver is secondary to
suppurative diseases, cancer is usually secondary to cancer of the
stomach or other organ within the limits of the portal circulation.

TREATMENT.--As amyloid disease owes its origin to syphilis, to chronic
malarial toxaemia, to suppuration, these, so far as they are remediable
conditions, should be cured as speedily as may be, to prevent the
development of the amyloid disease or to arrest it if begun.
Unfortunately, the condition of the liver is not recognized until the
morbid change is effected, and therefore practically irremediable.

The treatment necessarily involves that of the morbid state to which
the amyloid deposits are owing. The syphilitic disease requires iodine
and mercury; the malarial, quinine, iodine and the iodides, eucalyptus,
iron, etc., according to the state of each case; and surgical diseases,
especially necrosis of bone, should be effectively treated by suitable
surgical expedients. The cause being removed if possible, what means,
if any, can be resorted to to cause the absorption of the amyloid
matter? The only specific plan of treatment hitherto proposed is that
of Dickinson,[147] based on his theory of the constitution of amyloid
matter; according to which the amyloid deposits consist of fibrin
altered by the separation of the potash and soda salts, which have been
eliminated in the pus. If this theory be admitted, the obvious
indication is to supply the alkaline materials. The cases reported by
Dickinson in which this theory was {1046} practically demonstrated were
not sufficiently improved to lend any empirical support to this method.

[Footnote 147: _The Pathology and Treatment of Albuminuria_, p. 214 _et
seq._]

The medicinal remedies which do any good are the iodides--notably the
iodides of ammonium, of iron, of manganese, etc., the compound solution
of iodine, and the double iodide of iron and manganese. As the
officinal ointment of the red iodide of mercury, rubbed in over the
splenic region, does so much good in chronic enlargement of the spleen,
it is probable that it will prove effective in this form of enlargement
of the liver. The writer has observed results from it in such cases
that justify him in strongly urging its employment. The method of its
application consists in rubbing perseveringly a piece of the ointment,
a large pea in size, over the whole hepatic area, and repeating it
daily until some irritation and desquamation of the skin is produced,
when it should be suspended until the parts will bear renewed
applications. Besides the topical application of the red iodide, this
remedy may be given internally with advantage without reference to
syphilitic infection. It seems to the writer probable that bichloride
of mercury may be as useful, as it is certainly more manageable. The
chloride of gold and sodium, arsenic in small doses, and the metallic
tonics, so called, may be useful carefully administered, especially the
first mentioned, which the writer believes has some real power over the
disease.

Dietetic rules are of great importance. As the hepatic functions are
much disturbed, if not entirely suspended, it is necessary to give
those foods which are converted into peptones in the stomach. As a
rule, fats, starches, and sweets are mischievous, and milk, meats,
oysters, and the nitrogenous foods best adapted to nourish the patient.
If the diarrhoea should prove exhausting, the mineral acids, with
opium, are the best remedies. Nausea and vomiting are best relieved by
carbolic acid mixture, and hemorrhages by the solution of the chloride
or subsulphate of iron.


Fatty Liver; Fatty Degeneration of the Liver (Hepar Adiposum).

DEFINITION.--By the term fatty liver is meant a change in the organ
characterized by the excessive quantity of fat- or oil-globules
contained in the cells of the parenchyma.

CAUSES.--The liver acts, under normal conditions, as a reservoir for
the surplus fat, which it gives out as the demand is made. It is not
only the fat brought to the liver by the blood which accumulates in the
organ, but it apparently possesses the power to transform certain
substances--albumen, for example--into fat. An important causative
element, therefore, is the quantity of fat present in the food
habitually consumed. This has been proved by the investigations of
Radziejewsky[148] and others, who have shown that the fat in the food
is stored up in the normal places of deposit, one of which, of course,
is the liver. Another causative element is the formation of fat from
the albumen of the hepatic cells in consequence of diminished
oxidation. In respect to both causes the consumption of oxygen is an
important factor. The insufficient supply of oxygen {1047} which is a
necessary result of a sedentary life leads thus, directly, to the
accumulation of fat in the liver-cells. A constitutional predisposition
is also an important factor. There are those who under certain
conditions of daily life store up large supplies of fat, and others who
under the same conditions continue lean. Women more than men are
subject to such inherited predispositions.

[Footnote 148: _Virchow's Archiv fur path. Anat., etc._, Band lvi. p.
211.]

Again, fatty liver occurs in the course of certain cachexiae, notably
phthisis. In this case the obstructive pulmonary lesions interfere with
the process of oxidation, and also maintain a constant hyperaemia of
the portal system. This condition of the liver also occurs in the
cancerous cachexia, in anaemia and chlorosis of long standing, in
chronic suppurative diseases, etc. The dyscrasia of chronic alcoholism
is a very common cause of fatty liver. At the same time that
hyperplasia of the connective tissue is taking place the fat is
accumulating in the hepatic cells. So great is the accumulation of fat
in the blood that the serum presents a milky appearance. This excess in
the quantity of fat is rather due to diminished oxidation, to lessened
combustion, than to increased production. Another causative element of
the fat-production in cases of alcoholism is the interference of
alcohol with the process of digestion and assimilation.

Poisoning by phosphorus, antimony, arsenic, and other metals sets up an
acute fatty degeneration of the liver. Pregnancy, lactation, and
suppuration also have the same effect, but to a slighter and less
permanent extent.

PATHOLOGICAL ANATOMY.--Fatty liver agrees with amyloid liver in that
the fatty deposits increase the size and weight of the organ. The
surface is smooth, the peritoneal investment unaltered, and the margins
rounded. Sometimes the organ is merely increased in thickness,
sometimes in diameter. It has a greasy feel and cuts like a mass of
fatty tissue. Examined at a low temperature--below freezing--it seems
like a mass of suet, the proper structure being almost extinguished in
the fatty metamorphosis. The outline of the lobules remains distinct
even in cases far advanced in the fatty degeneration, but in the
extreme cases it is obliterated, the cut surface presenting a uniformly
yellowish or grayish-yellow tint. The fatty liver is also wanting in
blood; it is dry, and on section only the largest vessels contain any
blood. When cardiac disease of a kind to produce congestion of the
venous system exists--for example, mitral or tricuspid lesions--the
same relative decrease in the quantity of blood in the liver is
observable after death, although during the life of the subject the
opposite condition may have been present. The cause of this
bloodlessness of the fatty liver is to be sought in the pressure
exerted by the growing fat-cells.

Not all cases of fatty liver are advanced to the degree indicated in
the above description. From the normal size up to the maximum attained
by the most advanced fatty liver there are numerous gradations in the
quantity of fat and in the dimensions of the organ. Fatty degeneration
may accompany cirrhosis, in which the liver is contracted. The deposits
of fat may take place in particular areas. In cases of fatty liver per
se the deposit occurs within the liver-cells, as may be demonstrated on
microscopic examination, the initial change consisting in the formation
of granules in the protoplasm which ultimately coalesce, thus producing
{1048} fat-globules or cells. The fatty change in the hepatic cells
proceeds in a certain methodical manner from the cells at the periphery
of each lobule to the centre. The quantity of fat deposited in the
liver in cases of fatty change is very great. In the normal condition
of the organ fat exists, according to Perls,[149] in the proportion of
3 per cent. of the weight of the liver. When the condition of fatty
liver exists the quantity of fat rises to 40, even 45, per
cent.--almost one-half. It is important to note, as was pointed out by
Frerichs, that in an inverse ratio with the increase of fat was the
quantity of water.

[Footnote 149: _Virchow's Archiv_, _supra_.]

That more or less fatty change in the liver is not incompatible with a
normal functional activity is quite certain, but the boundary between
health and disease is by no means well defined in respect to the
quantity of fatty change in the liver-cells. The liver, within certain
limits, is a mere reservoir of the surplus fat of the body, and hence a
variable, but not excessive, amount of accumulation of fat is not
incompatible with a normal functional performance of the organ. The
limits of a merely functional state and of a diseased state are not,
therefore, very clearly defined. In certain inferior animals, as
Frerichs has shown, a fatty condition of the liver is normal.

SYMPTOMS.--The signs and symptoms of fatty liver are by no means well
defined. This state of the organ, as a rule, accompanies the general
tendency to fatty metamorphosis and deposit in the body. It is a
symptom in the course of phthisis, of chronic alcoholism, and of
various forms of metallic poisoning, but under these circumstances
there is no material change in the course of the symptoms produced by
this complication. As an independent affection it rarely, if ever,
exists alone. So far as its symptoms can be defined, they are referable
to the organs of digestion and assimilation and to the liver itself.

The appetite is generally good, but distress after eating, acidity and
heartburn, eructations of acid liquid and of certain articles of diet,
are experienced. The stools are usually rather soft or liquid, wanting
in color, whitish or pasty, and occasionally dark, almost black, owing
to the presence of blood. Hemorrhoids are usually present. The
discharges are often offensive from the decomposition of certain
constituents of the food, acid and burning because of the presence of
acetic, butyric, and other fat acids, or merely offensive because of
the formation of hydrogen compounds with sulphur and phosphorus.
Notwithstanding the derangement of the stomachal and intestinal
digestion, the deposition of fat continues in an abnormal ratio. With
the increase in body-weight a decline in muscular power takes place.
The respiration is hurried on the slightest exertion, and dyspnoea is
produced by any prolonged muscular effort. The circulation is feeble
and the pulse slow in the state of repose, but on active exertion the
pulse becomes rapid and at the same time feeble. The sleep is disturbed
by horrifying dreams, and only on assuming a nearly sitting posture can
the patient sleep with any degree of quietude.

In these cases of fatty liver a very considerable mental inquietude,
despondency, even hypochondria and melancholia, result. The relation of
insufficient hepatic excretion to the mental state is yet sub judice,
but there can be no doubt that some connection exists. From the
earliest {1049} period hepatic derangements--as the term hypochondria
denotes--have been associated with certain disorders of the mind. This
relation certainly holds good in respect to the mental perturbation
occurring in cases of fatty liver. With a rotund countenance and a
well-nourished body there is associated very considerable mental
despondency.

Without distinct jaundice the skin has an earthen or tallow-like hue,
the conjunctiva is muddy or distinctly yellow, and now and then
well-defined jaundice appears.

The urine is rather scanty, high-colored because of the presence of
bile-pigments, and deposits urates abundantly. When jaundice
accompanies fatty liver the urine will be very dark, muddy, thick, and
will react to the usual tests for bile, urates, etc.

The area of hepatic dulness is, as a rule, enlarged in cases of fatty
liver. The deposition of fat in the cells adds to the gross size of the
organ, and hence the inferior margin extends below the border of the
ribs to a degree determined by the amount of increase in its substance.
If the liver can be felt, it is smooth, not hard and resisting, and is
free from nodules. Usually, however, owing to deposits of fat in the
omentum and in the abdominal walls, the outlines and condition of the
liver cannot be ascertained, and must remain merely conjectural.
Rather, therefore, by implication than by direct examination can the
condition of the liver be ascertained.

COURSE, DURATION, AND TERMINATION.--The course of fatty liver, as an
element in a general change not of a toxic character, is essentially of
a chronic character. The fatty liver of acute phosphorus, antimonial,
and other forms of poisoning is acute and fatal, but it is not these
forms with which we are here concerned. Acting the part of a reservoir
of the surplus fat stored up in the body, which may be disposed of
under normal and physiological conditions, the fatty liver becomes by
careful management a normal organ again. The course, duration, and
termination will therefore largely depend on the nature of the
management pursued. A fatty liver cannot, then, be regarded as fatal,
or even as dangerous to life per se. The course and termination will
therefore be those of the associated condition.

DIAGNOSIS.--The determination of the existence of fatty liver will not
be difficult in all those cases in which this condition may properly be
suspected; for example, in phthisis, in chronic alcoholismus, in
obesity, and in cases of habitual indulgence in eating and drinking. If
in these cases the organ is distinctly enlarged, is smooth, and is
flabby in outline; if at the same time the digestion is deranged, the
stools are light in color, there are hemorrhoids, flatulence, acid
indigestion, and torpid bowels,--a fatty liver may be reasonably
suspected. The subjects of fatty liver are usually obese, and present
the characteristics typical of that condition, or they are the victims
of alcoholismus or present the evidence of habitual indulgence in the
pleasures of the table. The differentiation of fatty liver from amyloid
degeneration, from cystic disease, and from other maladies causing
enlargement of the organ is made by reference to these points in the
etiological history--by a careful study of the condition of the organ
itself and of the organs associated with it in function. As the amyloid
liver is more likely to be confounded with the fatty liver, it should
be noted that the former is an outgrowth of the process of suppuration,
that the organ {1050} is hard in texture, and that amyloid change
occurs at the same time in other organs--conditions opposed to those
characteristic of the fatty liver. Cancer of the liver is accompanied
by a peculiar cachexia; the body wastes, and the enlarged liver is hard
and nodular instead of being smooth and flabby.

TREATMENT.--When fatty liver is a symptom merely, its treatment is
merged into that of the primary condition. Thus, in phthisis and in the
various forms of metallic and phosphorus-poisoning the condition of the
liver is quite secondary. There are cases of obesity, however, in which
the fatty change in the liver is a part of the general morbid process,
and must be treated accordingly. There are still other cases in which,
without a decided tendency to obesity, the food habitually consumed is
of a fatty or fat-forming nature. The first requisite in the treatment
of fatty liver is to amend the diet. From the time of Hippocrates down
to Mr. Banting it has been recognized that the starchy and saccharine
constituents of the food, as well as the fatty, contribute to the
formation of fat. In arranging a dietary in cases of fatty liver this
fact should be regarded. Besides excluding the fats, saccharine and
starchy substances should be cut off. The diet should be composed of
fresh animal foods, game, fish, oysters, and such succulent vegetables
as lettuce, celery, spinach, raw cabbage (cole-slaw), etc. Amongst the
articles excluded should be bread, but the greatest difficulty is
experienced in its withdrawal, many patients declaring themselves
unable to live without it. In such instances a small biscuit
(water-cracker) may be allowed, but, as far as may be accomplished,
bread should be cut off from the diet.

If there are acidity, heartburn, pyrosis, and regurgitation of acid
liquid, much good may be expected from the administration of diluted
nitric acid before meals, especially if there be considerable uric acid
in the urine. The simultaneous administration of tincture of nux vomica
will prove useful if the appetite is poor and the digestion feeble.
When the complexion is muddy, the conjunctivae yellow, and the tongue
coated, excellent results are had from the persistent use of phosphate
of sodium. Under these circumstances also arsenic is very beneficial.
Even better results may be had from a combination of the two agents, a
teaspoonful of the pulverized phosphate being given with one-fortieth
of a grain of the arseniate of sodium. Alkalies, as lithium citrate,
solution of potassa, etc., are unquestionably useful as remedies for
obesity and fatty liver, but they must be administered with a proper
caution. Also, the permanganate of potassium has seemed to the author
to be especially valuable as a remedy for these states.

Remedies to increase the activity of the portal circulation and
diminish congestion of the hepatic vessels are useful at the outset,
but the anaemia which succeeds renders their use improper at a later
period. Amongst the hepatic stimulants of great use in those cases
characterized by whitish, pasty stools, yellow conjunctivae, etc., are
resin of podophyllin, euonymin, baptisin, and others having the same
powers. Saline laxatives are also useful, but to a less extent. It must
be remembered, however, that these subjects are wanting in bodily
vigor, often suffer from weak heart, and always have flabby muscles, so
that they bear all depleting measures badly. The hepatic stimulant of
greatest utility in these cases is sulphate of manganese. The writer
has had excellent results from a {1051} combination of quinine and
manganese. For the general state, which denotes insufficient oxidation
according to the chemical pathologists, permanganate of potassium is a
remedy of value, as above mentioned. The best form in which to
administer this is the compressed tablet, and the dose usually is two
grains. As chalybeate tonics are indicated, the oxidizing power of the
succinate of the ferric peroxide, the remedy so warmly advocated by
Buckler, may be utilized with advantage. The combination of quinine,
iron, and manganese in pill form, or the syrup of the iodides of iron
and manganese, or the phosphate of iron, quinine, and strychnine, are
tonics adapted to the relief of the depression accompanying this
malady.


III. AFFECTIONS OF THE BILIARY PASSAGES.


Catarrh of the Bile-Ducts.

HISTORY AND DEFINITION.--Although catarrh of the bile-ducts had been
incidentally referred to by some previous writers, notably by Stokes of
Dublin, Virchow[150] was the first to treat of this condition
systematically. Amongst recent writers, Harley[151] appears to be the
only one disposed to question the importance of catarrh of the
bile-ducts as a factor in the production of jaundice. Even in
phosphorus-poisoning the appearance of jaundice, at one time supposed
to be haematogenic in source, has been referred to a catarrh of the
bile-ducts.[152] It seems probable that opinions have too decidedly
veered toward the importance of this condition as a factor in the
production of jaundice.

[Footnote 150: _Archiv fur path. Anat._, Band xxxii. p. 117 _et seq._]

[Footnote 151: _Diseases of the Liver_, _supra_.]

[Footnote 152: Wyss, _Archiv der Heilkunde_, 1867, p. 469 (Legg).]

CAUSES.--Catarrh of the bile-ducts has been referred to all those
causes which can excite a catarrhal process in any situation. These are
systemic and local. Amongst the systemic may be placed peculiarities of
constitution or idiosyncrasy. A tendency to hepatic disorders is a
feature in certain types of constitution, and, as such types are
transmitted, the hepatic disorders seem to be inherited. In such
persons, possessing the so-called bilious nature, catarrh of the
biliary passages is not uncommon, and a special susceptibility to it
apparently exists. The atmospherical and other causes which in some
subjects will set up a catarrh of the bronchi will in the bilious type
induce a catarrh of the duodenum and bile-ducts. The malady is not
inherited; only the character of bodily structure which favors it under
the necessary conditions.

Climatic changes and certain seasons, especially the autumn, are
influential causes. Exposure to cold and dampness, the body warm and
perspiring, will set up a catarrhal process in the bile-ducts and
intestine, especially in those having the special susceptibility which
belongs to certain bodily types. Malarial miasm is an especially active
cause in malarial regions. The writer has seen many examples in various
parts of the United States within the malaria-breeding zone. Other
miasmatic agencies are not without importance. The exhalations from the
{1052} freshly-upturned soil of some cities, the gases from cesspools
and sewers, and illuminating gas exert a causative influence. The bad
air thus made up has been happily called civic malaria.

The most influential causes of catarrh of the biliary passages are
local in origin and in action: they are the agencies which induce
catarrh of the duodenum. Disturbances of the portal circulation should
be first named. Whenever obstructive lesions of the cardiac orifices
exist, whenever the pulmonary circulation is impeded by disease of the
lungs, the portal vein is kept abnormally full, and as a necessary
result of the stasis a catarrh of the mucous membrane follows.
Congestion of the portal system may be a result of vaso-motor paresis.
The abdominal sympathetic may be the seat of various reflex
disturbances: those of a depressing kind induce stasis in the portal
system. Certain medicinal agents have this effect, and prolonged and
severe cutaneous irritation, it is probable, may act on the portal
circulation in the same way. The action of cold on the peripheral
nerves may be similarly explained.

Catarrh by contiguity of tissue is the most frequent factor. Catarrh of
the duodenal mucous membrane is the initial condition, and from thence
the process extends to the bile-ducts. Although the duodenum may be
alone affected, the usual state of things is a gastro-intestinal
catarrh, the stomach and the whole length of the small intestine being
simultaneously diseased. When the catarrhal process is thus diffused
the duodenal mucous membrane is most deranged, probably because the
acid and fermenting chyme is first received here, and what acridity
soever it may possess attacks this part in its greatest strength. It
must be remembered that the secretion of the duodenal glands and of the
pancreas and liver must also have an abnormal character; hence those
foods which in the healthy condition of things are digested in this
part of the canal undergo ordinary putrefactive decomposition and
furnish very irritating products. This observation is especially true
of the fats: the fat acids are in the highest degree irritating. The
digestive fluid of the duodenum has a more or less pathological
character, because the catarrhal process not only interferes with the
habitually easy flow of the gland secretions, but, extending to the
gland elements themselves, gradually alter their structure.

Gastro-intestinal catarrh results from the misuse of foods and the
abuse of certain condiments and of spirits. Excess in the quantity of
starchy, saccharine, and fatty foods which undergo conversion and
absorption in the intestine, habitually consumed, decomposition of such
portions as escape proper digestion ensues, and the products of this
decomposition exercise an irritant influence on the mucous membrane.
The daily consumption of sauces and condiments and of highly-seasoned
foods has a constant irritating action; but more influential than any
other causative agency is the abuse of malt liquors and spirit. Whilst
the latter acts more on the stomach and the liver proper, the former
affect more the duodenal mucous membrane and the bile-ducts.

To these causative agencies must be added a pathological state of the
bile itself. Under conditions not now known the bile seems to acquire
acrid properties and set up a catarrh in passing along the ducts.

PATHOLOGICAL ANATOMY.--The area affected by the catarrhal process
varies greatly. The termination of the common duct for a short space
may be the only part affected, but with this there is always more or
less, {1053} sometimes most extensive and severe, duodenal catarrh,
followed by jaundice. The extent to which the common duct is affected
may be exactly indicated by the staining with bile, which extends down
to the point of obstruction. The catarrhal process may invade the whole
extent of the common duct, the cystic duct, gall-bladder, and the
ramifications of the tube throughout the organ. The resulting
appearances will vary accordingly.

The first change observable is a more or less considerable hyperaemia
of the mucous membrane; but this is rarely seen, because the
examination cannot be made at the time when this condition is present.
The epithelial layer is swollen, sodden, the cells cloudy, undergoing
rapid multiplication and desquamating. The cast-off cylindrical
epithelium, mucous cells, and serum make up a turbid mixture, which,
with bile, fills the smaller ducts, and may in places, especially at
the orifice of the common duct, form an obstruction sufficient to
prevent the passage of the bile; which may, however, be readily pressed
out with a little force. Especially near the end of the common duct the
mucus is apt to accumulate, and a plug of it, often tenacious and
somewhat consistent, obstructs the orifice. It is probable that whilst
catarrh is the chief cause of jaundice, it may also, by a merely
intermittent activity, cause the condition of biliousness--now so far
relieved as to permit the bile to descend into the intestine, now so
much obstruction as to prevent the escape of any considerable part of
that formed. When the common duct is the seat of the catarrhal process,
and the outflow of bile thus prevented, it accumulates in the
gall-bladder, which may be so far distended as to present a
recognizable tumor of pyriform shape through the abdominal parietes.

When the catarrhal process invades the finer ducts the appearances are
somewhat different. There are no bile-stains along the course of the
common and cystic ducts, and the gall-bladder is empty, or at most
contains only some mucus, with altered bile. The tubes at or near their
ultimate ramifications contain a turbid mucus composed of cylindrical
epithelium and lymphoid cells, and tenacious enough to close them
firmly. More or less hyperaemia of the liver-structures proper, and
consequent increased dimensions of the organ, a more or less active
catarrhal condition of the duodenal mucous membrane, accompany the
changes in the finer ducts.

SYMPTOMS.--There are marked differences in the behavior of the more
acute cases of catarrh of the bile-ducts and the chronic examples of
the same disorder. The former is held to be the most frequent cause of
jaundice, whilst the latter is an important element in the so-called
bilious state, in lithaemia, and as a secondary condition in some
cardiac and pulmonary diseases. Also, the morbid complexus of catarrh
of the bile-ducts includes the symptoms of duodenal and gastro-duodenal
catarrh.

The acute form of this disease sets in with the symptoms of
gastro-duodenal catarrh. Usually, after indulgence in too highly
stimulating food or in some article having a specially irritating
character, an attack of acute indigestion supervenes. The tongue is
more or less heavily coated, the breath heavy, the taste bitter, pasty,
or sourish, the appetite poor or actual repugnance to food, especially
to the offending articles, is experienced, and nausea, not unfrequently
vomiting, ensues. The epigastrium and the hypochondriac regions have a
heavy, overloaded, distressed, {1054} and sore feeling; there is some
tenderness to pressure; sometimes the gall-bladder, abnormally full,
may be detected by careful palpation; and the area of hepatic dulness
will usually be increased. The abdomen is more or less distended by
gases, and eructations of offensive gases (hydrogen and sulphur
compounds, volatile fat acids, etc.) occur. Constipation exists when
the catarrhal process is limited to the duodenum, and the stools
consist of hard lumps having a light yellow, clay-colored, or whitish
appearance. When the whole extent of the small intestine is affected,
the stools will be soft, liquid, or watery, and will vary in color from
yellow to gray or white. In some cases the fecal matters will have an
offensive odor--the odor of decomposition--and considerable discharges
of very foul-smelling gas will attend the evacuations. This symptom
will occur when the intestinal digestion is suspended and the contents
of the bowel in consequence undergo putrefactive decomposition.

During the initial period of the disorder the urine will simply be
high-colored and loaded with urates and uric acid, but when jaundice
supervenes the pigment will convert the urine into a dark,
coffee-colored, and somewhat thick liquid.

With the onset of the malady symptoms referable to the nervous system
appear. Headache, dizziness, and hebetude of mind are present, and now
and then an attack of catarrh of the bile-ducts will have the objective
signs of an ordinary migraine or sick headache. Usually, however, as
the intestinal and hepatic troubles develop, headache and some mental
hebetude come on, but when jaundice supervenes the headache becomes
more severe, and very considerable mental depression, irritability of
temper, and moroseness are experienced. Chilly sensations, with flashes
of heat, are felt at the outset, but with the appearance of jaundice
the sensation of coldness predominates. In some cases, the intestinal
catarrh being extensive, there will be, after some preliminary
chilliness, a febrile movement, but this is never of a pronounced
character, and in the slighter cases of the disease or when the
catarrhal process is limited to the bile-ducts, there is no elevation
of temperature. With the first symptoms the pulse is somewhat
quickened, but as the bile acids accumulate in the blood they effect a
decided slowing of the heart's action, the pulse falling as low, it may
be, as 50 per minute. This lessened activity of the circulation is
accompanied by corresponding reduction of temperature, the body-heat
falling a degree or more.

The most distinctive symptom of catarrh of the bile-ducts is jaundice.
In the acute or quickly-developing form above described of catarrhal
icterus the symptoms of gastro-intestinal disturbance precede the first
indication of jaundice from five to eight days. Yellowness of the
conjunctiva and of those parts of the body exposed to the air is the
first manifestation; afterward the jaundice hue becomes general. The
tint varies in depth from a faint gamboge-yellow, only discernible in a
favorable light, to a deep greenish- or brownish-yellow.

In the more chronic cases of catarrh of the bile-ducts the symptoms are
simply those of a gastro-duodenal catarrh, to which some hepatic
disturbances are superadded. Some abdominal uneasiness felt in the
epigastrium and in the right hypochondrium, especially in two to three
hours after meals; flatulence, sometimes accompanied by colic; {1055}
constipation, persistent or alternating with diarrhoea--in the one case
in hard lumps with more or less mucus adherent, in the other soft or
liquid, and in both cases having a rather golden-yellow color, grayish
or black and tar-like appearance,--such are the symptoms referable to
the intestinal canal. The disturbances in the hepatic functions
produced by the catarrhal swelling of the mucous membrane of the ducts
are further exhibited in a somewhat sallow, earthy, or muddy
complexion, yellowish tint of the conjunctiva, high-colored, acid urine
loaded with urates and phosphates. Such subjects, although having, it
may be, a keen appetite, rather lose than gain in weight: they
experience lassitude, headache, much depression of spirits, and the
mental symptoms are most pronounced during the time intestinal
digestion is going on. In fact, the morbid complexus is rather that of
intestinal catarrh; nevertheless, the slight degree of obstruction to
the outflow of bile occurring in these cases has an influence both in
the intestinal digestion and in the nutritive functions. Any degree of
obstruction, as has already been pointed out, leads to serious
structural change of the liver, and this in turn produces well-defined
symptoms.

Disturbances of the hepatic functions, even jaundice, accompany the
paroxysms of malarial fever. Without the occurrence of fever, catarrhal
jaundice may come on during the course of chronic malarial poisoning.
Catarrh of the bile-ducts is the pathogenetic factor in these cases.
More especially in malarial regions, but also in temperate and warm
climates, paroxysmal attacks, with or without jaundice, are
comparatively frequent. These acute seizures occur in those having the
chronic form of the malady, and are excited by sudden climatic changes,
by excesses in eating, especially by the use of improper articles of
diet. Considerable nausea, flatulence, and constipation or diarrhoea,
weight, tension, and soreness in the right hypochondrium and sometimes
in the shoulder, chilliness, general malaise, headache, and an
increasing icterode tint of the skin, constitute the complexus of
symptoms belonging to these cases.

COURSE, DURATION, AND TERMINATION.--Acute catarrh of the bile-ducts
with jaundice has a well-defined course--in its mildest form, with
little gastric or gastro-intestinal disturbance--lasting ten days or
two weeks; in the ordinary form, with the accompanying gastro-duodenal
catarrh, running its course in a month to six weeks. In the chronic
form, with acute exacerbations due to indiscretions in diet or to
climatic influences, the course of the disease is chequered by
vicissitudes, the result of the causes just mentioned, and its duration
must therefore be indefinite and, as a rule, protracted. Catarrh of the
bile-ducts, or catarrhal jaundice, usually terminates in health after a
period of functional derangement of the intestines and liver. Without
exhibiting any features of a special character, some cases do not pass
through this benign course: the intestinal catarrh sets up an
ulcerative process at one or more points in the duodenum; but more
especially the obstruction to the free course of the bile caused by the
catarrhal swelling of the mucous lining of the ducts induces structural
changes in the liver--an hypertrophy of the connective-tissue elements,
a sclerosis.

DIAGNOSIS.--There are but two signs which indicate the nature of the
disorder, and only one that is really distinctive. Intestinal
indigestion with slight coincident biliary derangement is one, and
jaundice is the {1056} other. When, after the signs and symptoms of
gastro-duodenal catarrh have declared themselves, jaundice appears,
there can be no question as to the nature of the case. The diagnosis is
more difficult in the chronic cases with exacerbations due to the
exciting causes above mentioned, for the persistence of the jaundice
will suggest the occurrence of some permanent organic lesion. The
differentiation of the various kinds of jaundice has already been made.

TREATMENT.--Regulation of the diet is of the first importance. Those
foods requiring the intestinal juices for their solution and
absorption, and which cannot be properly digested when a duodenal
catarrh exists or when bile is absent, should of course be excluded
from the diet. These articles are the fats, starches, and sweets. The
mucus playing the part of a ferment, these substances are converted
into various secondary products of an irritating character. Flatulence
is caused by the evolution of carbonic acid gas and the hydrogen
compounds of sulphur and phosphorus; and acetic, butyric, and other
acids not only change the reaction of the intestinal juices, but are
directly irritating to the mucous membrane. In the acute cases a diet
of skimmed milk, taken hot and at three hours' interval, and after the
acute symptoms have subsided, in conjunction with some other aliment,
is the most appropriate mode of alimentation. Meats, fish, eggs, and
oysters are the chief articles of diet, besides the milk, during the
whole course of the more chronic cases; and to these may be added the
succulent vegetables, as lettuce, spinach, celery, raw cabbage, and
tomatoes. If, in consequence of irritability of the mucous membrane or
of idiosyncrasy, any article occasions distress, it should be omitted
from the diet.

The medicinal management includes the administration of remedies for
gastro-intestinal catarrh. The treatment of catarrhal jaundice has been
discussed. When constipation exists, saline laxatives, especially
phosphate of sodium and Rochelle salt, are useful. If there be
diarrhoea, the most appropriate remedies are bismuth, with or without
carbolic acid, Hope's mixture, oxides of zinc and silver, and other
mineral tonic astringents.

The propriety of the administration of special hepatic
stimulants--cholagogues--has been much disputed. When the disorder
consists merely in an obstruction to the outflow of bile, the utility
of stimulating the production of this secretion seems more than
doubtful. Much harm has been done by the indiscriminate use of mercury.
Its power to increase the production of bile having been assumed, and
the quantity of bile present in the feces being manifestly less in
cases of catarrhal jaundice, it followed that mercury should be
employed in this disorder. Modern experience has quite demonstrated its
inutility in the mode and for the purpose to which it was formerly
devoted. Nevertheless, good effects are had from calomel in small doses
as a sedative to the mucous membrane. When there are nausea, headache,
vertigo, and constipation present, excellent results may be had from
the 1/20 gr. to 1/10 gr. of calomel, exhibited at short intervals until
the bowels are moved. If calomel possessed the property formerly
ascribed to it, of stimulating the hepatic functions, it would be
contraindicated in catarrh of the bile-ducts. This contraindication
exists in respect to all hepatic stimulants.

If there be decided irritability of the stomach and constipation,
{1057} Seidlitz powders may be given at regular intervals. Phosphate of
sodium in drachm doses is highly useful for the double purpose of a
laxative effect and to prevent the tendency to inspissation of the
bile, which is one of the most important results of catarrh of the
bile-ducts and gall-bladder. In the more chronic cases the persistent
use of sodium phosphate is to be highly commended.

In this disease, especially as it occurs in gouty subjects, sulphate of
manganese is often decidedly serviceable. If anaemia and debility
coexist, this remedy can be combined with sulphate of iron and sulphate
of quinine--a combination which the writer has found peculiarly
effective under such circumstances. When oxidation is deficient and the
urates are present in the urine in excessive quantity, good effects are
had from the permanganate of potassium, a tablet containing two grains
being given four times a day. In the more chronic cases the salts of
silver, copper, and zinc are really very useful, especially the oxides
of silver and zinc; and of these the former is more efficient. Better
than any of those mentioned is arsenic, as arseniate of sodium or as
Fowler's solution, but the best results are had from small or medium
doses persistently used. If there be much intestinal catarrh and
consequent diarrhoea, bismuth and aromatic powder, oxide of silver,
Fowler's solution with a little opium, Hope's mixture, etc. are
appropriate remedies.

It is in catarrh of the bile-ducts that nitric and nitro-muriatic acids
have proved useful, rather than in cirrhosis and other diseases of the
liver-tissues. They prevent fermentation, promote oxidation, and
increase the activity of the assimilative functions. When there occurs
active fermentation of certain foods, and consequently considerable
flatulence, excellent results are obtained from the members of the
antiseptic group--from creasote or carbolic acid, salicylic acid,
biborate of sodium, the benzoates, etc. To these may be added quinine,
the dose of which will be determined by the purpose for which it is
prescribed. So often is catarrhal jaundice of malarial origin that
quinine becomes a remedy of high importance in the cases occurring in
the malarial-forming zone.

Certain special plans of treatment have been proposed for the cure of
catarrhal jaundice. One of the most effective of these is enemata of
cold water. By means of an irrigating apparatus the large intestine is
well distended with water once a day for several days. The first enema
has a temperature of 60 degrees F., and subsequent injections are a
little warmer. The increased peristalsis of the bowels and the reflex
contractions of the gall-bladder dislodge the mucus lining and
obstructing the gall-ducts. When the bile flows into the intestine,
digestion is resumed and the catarrhal inflammation subsides. But with
the irrigation method may be employed other remedies, as above
indicated.

Faradization of the gall-bladder has been used successfully for the
expulsion of the stored-up bile and the removal of the mucus
obstructing the ducts. It is applied by means of one moistened sponge
electrode placed directly over the gall-bladder, and the other on the
opposite side of the body and posteriorly. A slowly-interrupted faradic
current is then passed. This expedient is not suitable when the case is
acute in character.


{1058} Biliary Concretions; Gall-Stones; Hepatic Calculi; Hepatic
Colic.

DEFINITION.--There are two classes of concretions which may occasion
symptoms: inspissated bile and regularly-formed gall-stones.
Slowly-developing symptoms of jaundice from obstruction may arise from
the deposit of particles of inspissated bile in the hepatic ducts, or
sudden attacks of hepatic colic be due to the passage of concretions.
When biliary calculi reach the intestines, certain kinds of disturbance
may be caused by their presence there. Under the term biliary
concretions must be considered, therefore, the mechanism of their
production, their composition, the symptoms caused by their passage
through the ducts (hepatic colic), and the intestinal disturbance due
to their retention in the bowel.

Formation: Inspissated Bile.--Those concretions consisting of
inspissated bile are irregularly-shaped masses of a brownish,
greenish-brown, or reddish-brown color, friable and crumbling into a
gritty dust with slight pressure of the fingers. When recent and before
drying, they are softer, almost pultaceous, and may take the form of
the canal through which pressed. But as seen after drying they present
the appearance of a dark vegetable extract, dried and partly
pulverized. When examined as found in the gall-bladder or lodged in the
larger hepatic ducts or distributed in irregular fragments (gall-sand)
in the various hepatic passages, they present the shape, color, and
general characteristics of a partly-dried vegetable extract roughly
broken up, but still soft enough to take any shape from pressure. The
writer has seen them thus in situ accompanying regularly-formed
gall-stones in a case of gunshot wound of the liver. These masses of
inspissated bile differ from gall-stones in composition; they consist
of bile, but with a preponderance of the coloring matter. According to
Harley,[153] who has given a more correct account of these bodies than
any other systematic writer, their composition is as follows:

  Water    5.4
  Solids  94.6

The contents of the solids are--

  Bile-pigment                84.2
  Cholesterin                  0.6
  Salts (iron, potash, soda)  15.2

[Footnote 153: _The Diseases of the Liver, with and without Jaundice,
etc._, by George Harley, M.D., F.R.S., Philada., 1883, p. 349.]

Some years ago, before I was aware of the nature of such concretions. I
detected a number in examining the stools of a patient who had in quick
succession many attacks of hepatic colic, but as the usual form of
concretion was looked for and not found, the relation of these bodies
to the symptoms in the case was not understood. I now recognize the
value of Harley's observations on these bodies.

The biliary concretion which is properly a gall-stone has a definite
form and a more or less well-defined crystalline structure. The forms
taken are various. The most usual form is octagonal or hexagonal or
polyangular, with smooth facets, corresponding to points of contact of
other calculi. Instead of smooth facets and sharp angles, the
concretion may be studded with irregularly-shaped masses. When there
are numerous {1059} calculi present, they have smooth surfaces and
rather sharp angles, made, not by attrition, as has been supposed, but
by deposition of the new material under pressure. When they have this
form there are many present, but the number of facets does not indicate
the number of calculi, and the absence of facets is not proof of the
absence of other calculi. The smooth opposing surfaces are not always
plane, but may be convex or concave to fit the shape of the adjacent
bodies.

Calculi may be globular, ovoid, cylindrical, and truncated cones. The
largest in my collection is egg-shaped, and nearly filled the
gall-bladder which contained it, a little mucus free from bile-elements
only being present. If a concretion forms in a duct or a single one is
present in the gall-bladder, the shape is determined by the pressure of
the walls of the duct or of the gall-bladder, respectively. As found in
the stools, and still somewhat soft, the shape will represent the form
of the common duct through which it has been pressed. Such a soft,
recently-formed gall-stone will have the crystalline structure and
chemical constitution of these bodies, and will therefore differ from,
apparently, similar masses of inspissated bile. Although a round,
ovoid, or cylindrical calculus indicates the absence of others because
there are no evidences of mutual pressure and adaptation, a positive
conclusion cannot be reached in that way, for the gall-bladder may
contain numerous calculi of long-standing, and a recent concretion
formed in a duct be discharged with the usual symptoms.

The number of calculi which may be present at any time or be produced
in the course of years ranges from one to several thousand. The number
is in inverse ratio to the size. One case[154] is reported in which
7802 calculi were found in the gall-bladder, but they must have been
very minute in size. Of the specimens now in my collection, there are
230 obtained from one gall-bladder, which they entirely filled; they
are nearly uniform in size, have an average weight of two grains, and
contain four, five, and six smooth facets. Another collection of
calculi removed from a closed gall-bladder contains 45, of large size,
distending the organ and forming a tumor which projected beyond the
margin of the liver. Hepatic calculi are rarely solitary; hence if one
attack of hepatic colic occur, others may be expected.

[Footnote 154: Frerichs, _op. cit._, vol. ii. p. 499.]

In color gall-stones vary from a clear white to a dark-brown, almost
black, tint. The most usual tint of the mature calculi in the
gall-bladder is that of the ripe chestnut. Long stay in the intestines
increases the depth of the color, until it becomes almost black; on the
other hand, detention in the gall-bladder has a slightly bleaching
action; but the real cause of difference of color is the presence or
absence of pigment. If composed of pure cholesterin, the color will be
whitish, opaque, or glistening and almost translucent.

In size gall-stones vary from the smallest pea up to a hen's egg. When
several hundreds are contained in the gall-bladder, they will usually
be of the dimension of a medium-sized pea. Two large solitary
concretions in my possession are respectively 2 inches and 1-1/2 inches
in long diameter, and 1 inch and 3/4 of an inch transversely. Very much
larger calculi have, however, been recorded; thus, one mentioned by
Frerichs is 5 inches in length and 4 inches in circumference. The most
frequently {1060} encountered calculus, at least in this country, is
polyangular in shape and of the size of a large pea. Globular or ovoid
seems to be the prevailing form, and the dimensions that of a small
pea, in Germany, according to Frerichs and Von Schuppel, but this
statement must refer to the initial shape of these bodies.

Not all hepatic calculi have defined mathematical forms, but may
consist of branching cylinders composed of irregular nodular masses,
not unlike the concretions of inspissated bile. As a rule, in each case
where the calculi are multiple there is uniformity of color, shape, and
composition. This feature is well exhibited in my collection. The
calculi obtained from each subject are in one case white, polyangular,
rather unctuous, and nearly equal in size; in another, chestnut-brown
in color, polyangular in shape, and varying slightly in size, but
uniformly characteristic in shape; and in a third, singular in number,
ovoid in shape, dark-brown in color.

In composition gall-stones vary somewhat. When fresh they contain
considerable water, and at all times are hygroscopic. Dried in the air,
they are composed of--

  Water    4
  Solids  96
         ---
         100

The solids consist of--

  Cholesterin                  98
  Pigment                       1
  Inorganic or mineral matter   1
                              ---
                              100

Such are the constituents, according to Harley, of the usual
concretion, the cholesterin calculus. But as other varieties are
encountered occasionally, it may be well to give the composition of
these. The following table by Ritter, to be found in _Robin's Journal_
for 1872 (p. 60), is a correct representation of the contents of
different specimens:

---------------+------+------+------+------+------+------+------+-----
  Composition  |      |      |      |      |      |      |      |
  of Different |      |      |      |      |      |      |      |
  Kinds.       | 1st. |  2d. |  3d. | 4th. | 5th. | 6th. | 7th. | 8th.
---------------+------+------+------+------+------+------+------+-----
  Cholesterin  | 98.1 | 97.4 | 70.6 | 64.2 | 81.4 | 84.3 |trace.|  0
  Organic      |      |      |      |      |      |      |      |
    matter     |  1.5 |  2.1 | 22.9 | 27.4 | 15.4 | 12.4 | 75.2 | 18.1
  Inorganic    |      |      |      |      |      |      |      |
    matter     |  0.4 |  0.5 |  6.5 |  8.4 |  3.2 |  3.3 | 24.8 | 91.9
  Number of    |      |      |      |      |      |      |      |
    specimens  |  28  |  16  |  580 |  94  |  220 |  16  |   3  |   1
---------------+------+------+------+------+------+------+------+-----

The above may be regarded as the average composition, expressed in
round numbers. The variations from these figures will be comprehended
in two parts.

A calculus consists of three several parts: the nucleus, the body, the
rind. A calculus of small or medium size may be a nucleus for the
formation of a large one. Usually the nucleus consists of a bit of
mucus, casts of the biliary ducts (Thudicum), inspissated bile, a
blood-clot, a liver-fluke or other parasite, as a desiccated
round-worm, or some foreign body, as a seed, or, as in one reported
example, a globule of mercury.[155] {1061} The central mass of mucus
may contain a large proportion of pigment or crystals of cholesterin or
lime-salts, giving it special characteristics.[156] There may be
several nuclei. Fauconneau-Dufresne reports an instance in which a
pyramidal concretion contained four, and Guilbert a globular stone with
five, distinct nuclei. Such examples of calculi having multiple nuclei
are produced by the adhesion whilst in a soft state of two or more, and
the subsequent addition of material to the conjoint mass, welding it
into a single stone. A few calculi are homogeneous throughout, composed
of nearly pure cholesterin, mixed intimately with a little coloring
matter and lime salts. The cholesterin calculus will have a somewhat
translucent appearance, will be a dead white or a yellowish-white, or
present a greenish- or brownish-yellow tint through the white. Even the
white calculus, apparently composed of nearly pure cholesterin, will be
found on section to contain traces of a nucleus. By long detention in a
gall-bladder whose duct is permanently occluded, and is therefore free
of fluid, the mucus nucleus may so shrivel as to leave a cavity which
is merely stained. One of my specimens--a solitary calculus of large
size--exhibits this peculiarity.

[Footnote 155: Thudicum, J. L., _On Gall-stones_, London, 1863; also
Frerichs, _op. cit._, vol. ii. p. 503.]

[Footnote 156: Cyr, Jules, _Traite de l'Affection calculeuse du Foie_,
Paris, 1884, p. 11 _et seq._]

The body consists of cholesterin, nacreous or darkened by pigment,
deposited in radiating lines or in concentric layers, or in both
together. Pigment may be intimately incorporated with the cholesterin
or deposited between the layers of this substance, pure or nearly pure,
forming an alternating arrangement.

The crust or rind usually is smooth, unctuous to the touch, firm, but
when broken with the finger-nail readily crumbles. When composed of
lime salts, or when the cholesterin is mixed with varying proportions
of these salts and of pigment, the surface is still smooth, but
thicker, firmer, and darker in color. The rind may not be smooth, but
studded with wart-like projections, or it may consist of several layers
of earthy matter separated by pigment. These layers may be very
friable, and readily crumble and fall off. In some instances the crust,
several lines in thickness, is the body of the calculus, and the cavity
contains only a light honeycomb of mucus and pigment.

The specific gravity of gall-stones composed of crystallized
cholesterin is nearly that of water. Air-dried calculi will float on
water, but the recent ones, full of moisture, sink. The relation of the
weight of the calculus to that of the bile is more important. As the
specific gravity of bile ranges from 1020 to 1026, it is obvious that
on this fluid air-dried calculi will float, but, holding in the recent
state much water, ordinary gall-stones will sink. Those containing much
mineral matter will have a correspondingly high specific gravity--much
higher than bile.

ORIGIN AND FORMATION OF HEPATIC CALCULI.--Certain conditions are
necessary to the formation of these bodies on the part of the bile and
on the part of the gall-bladder and ducts. Constituted for the most
part of cholesterin, which exists in such small quantity in normal
bile, there must be some change in the composition of this fluid to
increase the quantity or to diminish the solubility of that
constituent. It will conduce to a better understanding of the subject
to premise the composition of the bile: {1062}

  Bile contains, in 1000 parts,
    Water            860
    Solids           140

  The solids of bile are,
    Glycocholate and Taurocholate of soda  90.8
    Fat                                     9.2
    Cholesterin                             2.6
    Mucus                                   1.4
    Pigment and extractive                 28.
    Salts                                   8.
                                          -----
                                          140.

Normal bile is neutral or slightly alkaline in reaction. If the
reaction become acid from any cause, the constituent cholesterin is
precipitated; and this occurs the more readily the larger the
proportion of this substance held in solution. Cholesterin is an
excrementitious material found in the blood and excreted by the liver.
It represents in part, probably, the waste of nervous matter, but more
certainly of the fatty tissues in general. Conditions of the system in
which the metamorphosis of the fatty elements occurs more freely--as
obesity, advancing life, etc.--are accompanied by an increased
production and excretion of cholesterin.

So long as the neutral state or the alkalinity of the bile is
maintained, the cholesterin will be kept in solution, although its
relative proportion may be in excess of the normal. A lack of the soda
constituent of the system is one factor, but the most important is a
catarrhal state of the mucous membrane of the bile-ducts and
gall-bladder. The mucus formed plays a double role: it furnishes a
nucleus about which cholesterin crystallizes; it acts as a ferment and
inaugurates a process of acid fermentation which results in the
precipitation of cholesterin. When all the conditions favorable to the
separation and crystallization of cholesterin are present, any foreign
body may serve the purpose of a nucleus. The articles which have thus
served have been enumerated.

A by no means infrequent combination is that of bilirubin with calcium;
and this may constitute the nucleus or form a part of the body or the
crust of a calculus. The mechanism of its formation is not unlike that
of the cholesterin concretion. Bilirubin is soluble in alkalies, and is
precipitated from its solution by acids. It follows that when acid
fermentation takes places under the influence of mucus, bilirubin may
be precipitated in combination with calcium. The salts of sodium and
potassium are much more abundant in bile than those of lime, but the
latter much more often enter into the formation of calculi because of
their slighter solubility. Other combinations of bile-pigments, mucus,
and the salts of the bile take place, but they are relatively less
frequent. The principal lime salt is the carbonate, and this combines
in varying proportions with the bile acids, the fat acids, and
bile-pigment.

Certain physical conditions are not less important than the chemical in
the production of hepatic calculi. Accumulation of bile in the
gall-bladder, stasis, and concentration are essential conditions. If
bile remains long in the gall-bladder, it becomes darker in color and
more viscid, its specific gravity rises, and the relative proportion of
solids increases, doubtless because of the absorption of a part of the
water. The reaction--which, as has been stated, is in the fresh state
neutral or {1063} alkaline--becomes acid in consequence of a
fermentative change (Von Gorup-Besanez) set up by the mucus. If a
catarrhal state of the mucous membrane exist, the mucus, epithelium,
and lymphoid cells cast off play the part of a ferment. The lime which
is so important a constituent of biliary concretions is not present
even in concentrated bile in sufficient amount to account for its
agency in the formation of these bodies, is furnished by the diseased
mucous membrane (Frerichs). Indeed, numerous crystals of carbonate of
lime have been seen in situ in contact with the mucous membrane in
cases of chronic catarrh. It follows, then, that catarrh of the biliary
passages has an important causative relation to that pathological
condition of the bile which precedes the formation of calculi. In this
connection we must not lose sight of the researches made by Ord[157] on
the action exerted by colloids on the formation of concretions. The
mucus is the colloid; cholesterin, lime, and soda salts are the
crystalloids. These latter diffusing through the colloid medium, the
resulting combinations assume spheroidal forms. The union of bilirubin
and lime salts illustrates the same principle.

[Footnote 157: _On the Influence of Colloids upon Crystalline Forms and
Cohesion, with Observations on the Structure and Mode of Formation of
Urinary and other Calculi_, by W. Miller Ord, M.D., F.R.C.P. Lond.,
etc., London, 1879.]

CAUSES.--We have here to consider the external conditions and the
general somatic influences which lead to the formation of biliary
concretions. Age has an important causative action. Besides other
agencies due to advancing life, the increase of cholesterin is an
influential factor. The less active state of the functions in general,
diminished oxidation, loss of water, and concentration of the bile are
influential factors in determining the formation of hepatic calculi in
advancing life, as the opposite conditions oppose their production in
early life. Although not unknown in infancy, at this period in life and
until twenty years of age they occur but rarely.
Fauconneau-Dufresne,[158] of 91 cases, had 4 in infants; Wolff[159] had
1 in a collection of 45 cases; and Cyr,[160] 2 cases under ten in a
group of 558 cases. The following table illustrates the influence of
age on the productivity of gall-stones:

  AUTHORS.

  HEIN.
    Whole No.           395
    From infancy to 30   18
    From 30-70          377

  FAUCONNEAU-DUFRESNE.
    Whole No.            91
    Before 20            10
    From 20-40           13
    From 40-90           68

  WOLFF.
    Whole No.            45
    Before 20             3
    From 30-60           42

  DURAND-FARDEL.
    Whole No.           230
    Before 20             2
    From 20-30           28
    From 30-60          162
    From 60-90           38

  CYR.
    Whole No.           558
    Before 20            20
    From 21-30          208
    From 31-40          185
    From 41-50           91
    From 51-60           48
    Above 60              6

[Footnote 158: _Traite de l'Affection calculeuse du Foie_, Paris,
1851.]

[Footnote 159: _Virchow's Archiv f. path. Anat., etc._, Band xx., 1861,
p. 1.]

[Footnote 160: _Traite de l'Affection calculeuse du Foie_, Paris, 1884,
p. 53.]

Although there is a general correspondence in the results of the
observations on the age most liable, there are differences. Thus, Cyr,
whose figures represent the experiences at Vichy, makes the age of
maximum liability from twenty to forty years--distinctly earlier than
any other observer; and hence it is necessary to bear in mind the
extreme latitude of his diagnosis. Of my own collection, 30 in number,
all doubtful cases {1064} excluded, there were 20 between thirty and
fifty years, and 10 between fifty and seventy. Of these, 22 occurred in
subjects between forty and sixty. The period of maximum liability is
about fifty years of age. Cyr refers the difference of his statistics
from those of other observers to the character of the patients. The
preponderance in the number of cases of hepatic calculi at or about the
fiftieth year is referable to the lessened activity of the nutritive
functions at this period, and to the increase in the relative
proportion of cholesterin in the blood in advanced life (Luton[161]).
Charcot[162] maintains that after sixty biliary calculi are more
frequent, but owing to the physiological conditions then existing the
migration of these bodies is effected without notable inconvenience.

[Footnote 161: Jaccoud's _Dictionnaire encycloped._, art. "Voies
Biliaires;" _idem._, _Bull. gen. de Therap._, March 15, 1866.]

[Footnote 162: _Lecons sur les Maladies du Foie, etc._, p. 145.]

According to most authorities, females are more liable to the formation
of gall-stones than are men. Thudicum, after an analysis of the
statistics given by the most experienced and celebrated authorities,
places the proportion at 3 to 2. Von Schuppel gives the same figures.
Cyr, whilst recognizing this estimate as true of the great mass of
observations on this point, finds that in his own cases the
preponderance of females over males was even greater, being 4 to
1--inversely to the liability of the sexes to gout; but this excess is
to be explained by the character of the subjects falling under his
observation. Women are subjected to influences which favor the
formation of these concretions, such as pregnancy, sedentary habits,
diet of a restricted character, the use of corsets, and the somatic
changes at the climacteric period.

The social state, by reason of the conditions associated with a good
position in life, has an influence in the production of calculi.
Luxurious habits and indulgence in the pleasures of the table are
important factors, and hence this malady is encountered amongst the
better class of patients in private practice rather than amongst
laboring people in the hospitals.

As the somatic conditions which exert a predisposing action, and the
social circumstances also favoring the formation of hepatic calculi,
are transmitted, heredity is by some classed among the etiological
factors, but it can only be regarded as indirect.

Malarial influences unquestionably exert a very powerful influence as
this malady occurs in this country. Paroxysms of intermittent either
induce or accompany the seizures of hepatic colic, and chronic malarial
poisoning exerts a direct causative influence through the hepatic
disturbances and the gastro-duodenal catarrh which are associated with
it. Attacks of hepatic colic are extremely frequent in the malarial
regions of the West and South. It may be, however, that this malady is
frequent rather in consequence of the diet of pork than of climatic
causes, for it is probable that indulgence in such food plays an
important part in the formation of biliary concretions (Harley). Due
allowance made for diet, climate is yet, no doubt, an influential
factor. In warm, especially in malarial, regions the functions of the
liver are taxed to compensate for the increased action of the skin and
lungs; but this organ is, besides, affected by the poison of malaria,
and to the congestion caused by it is superadded a catarrhal state of
the bile-ducts and of the duodenum. A {1065} pathological condition of
the bile itself is first induced; then the fermentative changes set up
by the mucus cause the separation and crystallization of pigment and
cholesterin.

Certain seasons favor the formation of biliary concretions, because
then the special influences which operate at all times are more active
and persistent. These seasons are fall, winter, and early spring, and
gall-stones are more numerous then in consequence of the activity of
the malarial poison, the character of the diet then employed, and the
lessened oxidation due to the more sedentary life. Climate is a factor
of some consequence, but not in the direction that might have been
supposed. Gall-stones are more common in temperate than in tropical
climates--a statement confirmed by the observation of the physicians of
India. They are, according to Harley, quite common in Russia, where
also they attain to extraordinary dimensions; but these circumstances
are not due to the climatic peculiarities of that country, so much as
to the diet habitually consumed, consisting so largely of fatty
substances.

Of all the conditions which favor the production of gall-stones, none
are so influential as the bodily state and the associated dietetic
peculiarities. Those troubled with these concretions, as they have
occurred under my observation, have been either obese or have had a
manifest tendency in that direction. They have had a strong inclination
for the fat-forming foods, also for starchy, saccharine, and fatty
articles, such as bread and butter, potatoes, beans and peas, pork,
bacon, and fat poultry, etc. Harley thinks indulgence in bacon (p. 367)
is a prime factor. Thudicum rejects this notion on chemical grounds,
for obesity and the free consumption of fat cannot be concerned in the
production of these bodies, because cholesterin is an alcohol.[163] The
agency of a fatty diet has been so strongly indicated in clinical
observations, and the relation of cholesterin to the fats so obvious,
that it can hardly be doubted the free consumption of fat in food
contributes directly to the formation of calculi. An indirect relation
may also be traced. A catarrhal state of the duodenal mucous membrane
existing, and the bile excluded by swelling and obstruction of the
bile-ducts, fats are decomposed, and the fat acids, absorbed into the
portal blood, contribute to those chemical changes in the bile which
result in the precipitation of cholesterin. Beneke[164] traces a
connection between atheromatous degeneration of the vessels and the
formation of biliary concretions. A general increase in the amount of
fat in the body is usually coincident with the atheromatous change, and
at the same time the relative proportion of cholesterin in the bile
becomes greater.

[Footnote 163: _A Treatise on Gall-stones_, p. 214.]

[Footnote 164: _Deut. Archiv fur klin. Med._, Band xviii.]

Indulgence in the starchy and saccharine foods plays a part in the
formation of gall-stones not less, if not more, important than the
consumption of fats. A diet of such materials is highly fattening, and
if the necessary local conditions exist they readily undergo
fermentation, and thus cause or keep up a catarrh of the mucous
membrane.

Too long intervals between meals, Frerichs[165] thinks, is more
influential than errors of diet in causing concretions. The bile
accumulates in the gall-bladder, and the condition of repose favors the
occurrence of those changes which induce the separation and
crystallization of cholesterin. {1066} Obstacles to outflow of every
kind have the same effect. The largest calculus in my possession was
obtained from a case of cancer of the gall-bladder which compressed,
and finally closed, the cystic duct. Sedentary habits have the same
mechanical effect, but, as already pointed out, insufficient air and
exercise act by lessening oxidation. Corpulent persons indulging in
rich food and avoiding all physical exertion, those of such habits
confined to bed by illness or injury, the literary, the well-to-do,
self-indulgent, lazy, are usual subjects of this malady. Any condition
of things which causes a considerable retardation in the outflow of
bile will have a pathogenetic importance, especially if the causes of
chemical change, the lessened quantity of taurocholic and glycocholic
acid, and an increased quantity of cholesterin, coexist. Moral causes,
as fear, anxiety, chagrin, anger, etc., have seemed to exercise a
causative influence in some instances (Cyr).

[Footnote 165: _A Clinical Treatise on Disease of the Liver_, Syd. Soc.
ed., vol. ii. p. 511.]

To the causes of retardation of the bile-flow mentioned above must be
added catarrh of the bile-ducts. This acts in a twofold way--as an
obstruction; a plug of mucus forming the nucleus. It has already been
shown that fermentative changes may be set up by the mucus, which plays
the part of a ferment, an acid state of the bile resulting.

Situation of Gall-stones, and their Destiny.--The gall-bladder is, of
course, the chief site for these bodies, but biliary concretions and
masses of inspissated bile may be found at any point in the course of
the ducts. Single stones may be impacted at any point in the cystic,
hepatic, or common duct, or masses composed of numerous small calculi
may take the form of a duct and branches, making a branching calculus
of the shape and size of the mould in which it is cast. Such casts may
be hollow, thus permitting an outlet to the bile, or they may
completely close the tube, and a cyst form, the walls of which grow
thicker with connective-tissue deposits. Stones of very large size may
be thus enclosed, Frerichs having seen one the size of a hen's egg
formed about a plum-seed, which was the nucleus. In some rare instances
the major part of the larger tubes have been filled with inspissated
bile, through which the fluid bile could only be slowly filtered.

Calculi are not often found in the hepatic duct, since they can only
lodge there in descending from the smaller tubes, and hence are too
small to become wedged in. The usual site, as has been sufficiently
explained, is the gall-bladder. At the entrance to the cystic duct and
at the terminus of the common duct in the duodenum are the points where
migrating calculi are most apt to be arrested.

Spontaneous disintegration of gall-stones sometimes occurs. Cholesterin
being dissolved off of the corners and edges, the cohesion of the mass
is impaired and it falls apart in several fragments. By very slight
mechanical injury air-dried calculi will be broken up. In the
gall-bladder two factors are in operation to effect the disintegration
of the contained calculi: the movements of the body, by which the
corners and the borders are crumbled; the solvent action of the
alkaline bile on the cholesterin. When, however, these concretions are
made up of lime and pigment, their integrity can be impaired only by
the process of cleavage; no solvent action can take place.

Various changes occur in the ducts or in the gall-bladder in
consequence of the presence of these concretions. Whilst a catarrhal
state of the mucous {1067} membrane of the ducts is an element of much
importance in the process by which concretions are formed, on the other
hand the presence of these bodies excites catarrh, ulceration,
perforation, and, it may be, abscess of the liver. When concretions
form or are deposited in the ducts, they cause inflammatory reaction,
the walls yield, and the neighboring hepatic structures may also be
affected by contiguity. The dilatation of the tube is usually
cylindrical, much more rarely sacciform. The neighboring connective
tissue may undergo hyperplasia and a more or less extensive sclerosis
occur. More frequently the calculus ulcerates through, and an abscess
is produced which will take the usual course of that malady. Very
rarely a calculus is found enclosed in a separate sac and surrounded by
healthy hepatic tissue (Roller).[166]

[Footnote 166: _Berliner klin. Wochensch._, No. 42, 1879; _ibid._, Nos.
16, 17, and 19 for 1877, Fargstein.]

As the gall-bladder is the usual place for the formation and storage of
gall-stones, the changes in connection with this organ are the most
important. The calculi may be so numerous or so large as to distend the
gall-bladder and cause it to project from under the inferior border of
the liver, so as to be felt by palpation of the abdominal wall. The
stones may be few in number and float in healthy bile, or they may fill
the bladder to the exclusion of fluid, the cystic duct being closed
permanently; or there may be, with one or more concretions, a fluid
composed of mucus, muco-pus, serum, and bilious matter. The mucous
membrane may be in a normal state, but this is rare; usually it is
affected by the catarrhal process, and atrophic degeneration has taken
place to a less or greater extent; the rugae are obliterated, the
muscular layer hypertrophied. When attacks of hepatic colic have
occurred, more or less inflammation of the peritoneal layer of the
gall-bladder and cystic duct is lighted up, and organized exudations
form, changing the shape and position of the organs concerned. It is
usual in old cases of hepatic colic to find the gall-bladder bound down
by strong adhesions, the cavity much contracted or even obliterated,
the cystic duct closed, and the neighboring portion of the liver the
seat of sclerosis. Such inflammatory exudations about the gall-bladder
may become the seat of malignant disease--of scirrhus. Several examples
of this have been reported, and one has occurred in my own practice.

The contact of a gall-stone, especially of a polyangular stone, may
cause ulceration of the mucous membrane. This is the more apt to occur
if the muscular layer of the gall-bladder is hypertrophied, especially
if certain fasciculi are thickened and overacting, leaving intervening
parts weak and yielding to the pressure of the stone forced in by the
spasmodically contracting muscles. Finally yielding, the stone and
other contents of the gall-bladder escape into the cavity of the
abdomen. Adhesions to neighboring parts may prevent rupture. Such
adhesions are contracted with the colon, the duodenum, the stomach, and
other organs. In some rare instances the closed gall-bladder has
undergone a gradual process of calcification, the mucous membrane
losing its proper structure, the muscular layer degenerating, and a
slow deposit of lime salts taking place, the ultimate result being that
the biliary concretions are enclosed in a permanent shell.

As above indicated, biliary concretions may remain where deposited for
an indefinite period. Very often they migrate from the point of
formation, the gall-bladder, into the duodenum, producing
characteristic {1068} symptoms called hepatic colic. As the size of the
ducts increases from above downward, obviously but little vis a tergo
is needed to propel the concretions onward. The chief agency in the
migration of these bodies is the discharge of bile. Common observation
shows that the symptoms of hepatic colic usually declare themselves in
two or three hours after a meal--at that time when the presence of the
chyme in the duodenum solicits the flow of bile. The gall-bladder
contracts on its contents with an energy in direct ratio to the amount
of bile present, and with the gush of fluid the concretion is whirled
into the duct. Once there, the cystic duct being unprovided with
muscular fibres, the onward progress of the stone must depend on the
flow of bile; and, as the canal is devious, this may not always carry
the concretion into the common duct. Just behind the neck of the
gall-bladder the duct makes an angle somewhat abrupt, and here also its
folds project into the canal, so that at this point the stone is apt to
lodge; but much depends on the size and shape of the calculus. If it
pass through the cystic duct, the inflammation resulting may close the
canal, several instances of which have fallen under my observation. The
next point where stoppage of the migrating calculus may, and frequently
does, occur is the orifice of the common duct in the duodenum. This
orifice has a funnel shape, the smaller extremity toward the intestine,
the object of this being to prevent the entrance into the duct of
foreign bodies from the intestine. A diverticulum is thereby made
(Vater's) in which a concretion may lodge, partly or wholly preventing
the escape of bile into the bowel. The various forces concerned in the
propulsion of the concretion onward from the common duct into the
intestine are the discharges of bile, the contraction of the few
muscular fibres in the walls of the duct, the respiratory movements,
especially forced expiration, coughing, sneezing, vomiting,
defecation--in fact, all of those acts in which the abdominal muscles,
the diaphragm, and the sphincters are simultaneously brought into
strong contraction. The symptoms produced by the migration and stoppage
of a concretion will vary according to the size and shape of the stone,
and the consequent diminution in the amount of bile discharged or its
complete arrest. In other words, the stone may be firmly wedged in,
completely closing the canal against the passage of bile, or it may lie
loosely in the diverticulum Vateri, acting as a sort of ball valve, now
permitting a gush of bile, and now stopping the passage-way more or
less tightly.

The migration of calculi may take place by ulcerating through into
neighboring hollow organs. Usually the first step consists in stoppage
of the bile. To the accumulating bile mucus is added, and the
gall-bladder or the duct--usually the common or cystic duct--dilates,
often to a considerable extent, and, adhesions forming, discharge
ultimately takes place through some neighboring hollow organ. The
routes pursued by such fistulous communications are various. The organs
most frequently penetrated are the stomach, duodenum, and colon, less
often the urinary passages, and very rarely the portal vein. Numerous
examples of external discharge of calculi have been reported. The most
usual, as it is the most direct, is the fistulous connection of the
gall-bladder or common duct with the duodenum. Solitary stones of
immense size have been thus discharged. Murchison[167] gives references
to many interesting {1069} examples, and the various volumes of
_Transactions of the Pathological Society_ are rich in illustrative
cases. The symptoms produced by the migration of calculi by the natural
route and by ulceration into other organs will be hereafter considered.

[Footnote 167: _Clinical Lectures on the Diseases of the Liver_, 2d
ed., p. 487 _et seq._]

SYMPTOMS DUE TO THE PRESENCE OF GALL-STONES AT THEIR ORIGINAL
SITE.--Very large calculi or numerous small ones may be present in the
biliary passages without causing any recognizable symptoms. The
migration of these bodies by the natural channel and by ulceration into
the duodenum may also be accomplished without any local or systemic
disturbance.[168] That the retention of calculi may not induce any
characteristic reaction by which they may be recognized is probably due
to the fact that the gall-bladder, in which they chiefly form,
possesses but slight sensibility, and as it is in a constantly changing
state of distension or emptiness according to the amount of bile
present, it is obvious that a foreign body made up of the biliary
constituents, and having nearly the same specific gravity as the bile,
is not likely to cause any uneasiness or recognizable functional
disturbances. Furthermore, the slowness with which biliary concretions
form enables the organ to accommodate itself to the new conditions. The
lack of sensibility which is a feature of the gall-bladder, and which I
have had the opportunity to ascertain by actual puncture in an
individual not anaesthetized, is in some instances supported by a
general state of lowered acuteness of perception. There are great
differences in respect to readiness of appreciation and promptness of
response to all kinds of excitation in different individuals. To what
cause soever we may ascribe the lack of sensibility, the fact remains
that in not a few cases of gall-stones in the gall-bladder there are no
symptoms to indicate their presence. On the other hand, there are some
disturbances that have a certain significance.

[Footnote 168: Amongst the numerous examples of this kind to be found
recorded may be mentioned the case reported by M. L. Garnier, Agrege a
la Faculte de Medecine de Nancy (_Archives de Physiologie normale et
pathologique_, No. 6, 1884, p. 176): An hepatic calculus, weighing 24.5
grammes, was discharged without any symptoms or even consciousness on
the part of the patient, a man of sixty years. He had had colic and
jaundice, but these subsided entirely, and there was no further
disturbance. As has happened in so many instances, this stone must have
ulcerated through into the bowel without causing any recognizable
symptoms.]

The subjective signs are uneasiness--a deep-seated sensation of
soreness--felt in the right hypochondrium, increased by taking a full
inspiration and by decubitus on the left side. Pain or soreness,
sometimes an acute pain, is experienced under the scapula near the
angle, at or about the acromion process, and sometimes at the nape of
the neck. In one case under my observation within the past year a
patient who had had several attacks of hepatic colic, the usual
polyangular stones having been recovered, had from time to time severe
pain over the right side of the neck, shoulder, and scapula,
accompanied by a severe herpes zoster in the district affected by the
pain. This is of course an extreme example, but it is very suggestive
of the relation which may exist between hepatic disturbances and
shingles. Attacks of gastric pain coming on some time after food, and
not soon after, as is the case in true gastralgia, are usual in the
early stage of the disease--are constant, according to Cyr,[169] who
quotes approvingly an observation of Leared on this point. Migraine
{1070} or sick headache and vertigo occur in many cases, but it may
well be doubted whether these symptoms are not due to the accompanying
gastro-duodenal catarrh, which is a nearly constant symptom. Acidity,
flatulence, epigastric oppression, a bitter taste, a muddy rather
bilious complexion, and constipation are symptoms belonging to catarrh
of the gastro-duodenal mucous membrane. Most of these symptoms are
rather indefinite. Some additional information may be supplied by
palpation. When the gall-bladder is distended with gall-stones, or is
in the enlarged state which occurs when the common duct is obstructed,
it may project beneath the inferior border of the liver far enough to
be felt. In thin persons a grating sound, produced by the friction of
the calculi, may be heard, the stethoscope being applied as palpation
is made over the hypochondrium. It is rare that these symptoms can be
elicited, since the calculous affection of the liver occurs for the
most part in persons of full habit, in whom the abdominal walls are too
thick to allow of the necessary manipulation. There may be also some
tenderness on pressure along the inferior margin of the ribs,
especially in the region of the gall-bladder.

[Footnote 169: _Traite de l'Affection calculeuse du Foie_, p. 71.]

SYMPTOMS DUE TO THE MIGRATION OF GALL-STONES BY THE NATURAL
CHANNELS.--A calculus passing into the cystic duct from the
gall-bladder causes the disturbance known as hepatic colic or bilious
colic, because of the jaundice which accompanies the major part of
these seizures. But jaundice is not a necessary element in these cases;
it is not until the concretion reaches the common duct that the passage
of bile into the intestine is interfered with. The gall-bladder has a
function rather conservative than essential, for its duct may be
permanently closed without apparently affecting the health.

The time when an attack of hepatic colic is most likely to occur would
seem to be determined by the flow of bile; for this, as has been
stated, is the chief factor in moving calculi along the ducts. As, no
doubt, the presence of the chyme in the duodenum is the stimulus for
the production of bile and also for the contractions of the
gall-bladder, it follows that a few hours after meals is the time when
the attacks of hepatic colic would a priori be expected. This is in
accord with experience, but there are exceptions. In one of the most
formidable cases with which the writer has had to deal--the diagnosis
confirmed by the recovery of the calculi--the most severe attacks
occurred in the early morning. According to Harley,[170] colic from the
passage of inspissated bile occurs when the stomach and duodenum are
most nearly empty--from ten at night until ten in the morning--and this
he relies on as a means of diagnosis, but the exceptions are too
numerous to assign much importance to this circumstance.

[Footnote 170: _On Diseases of the Liver_, p. 354.]

The onset of pain is usually sudden, but it may develop slowly from a
vague uneasiness in the region of the gall-bladder; or after some pain
and soreness at this point, accompanied by nausea, even vomiting, the
paroxysm will begin with very acute pain. The situation of the pain is
by no means constant, and usually varies in position in the same case.
The point of maximum intensity is near the ensiform cartilage, outward
and downward two or three inches, about the point of junction of the
cystic and common duct. From or about this region the pain radiates
through the epigastrium, the right hypochondrium, upward into the
chest, {1071} backward under the scapula, and downward and inward
toward the umbilicus. In some instances under my observation the most
acute suffering was located in the right iliac region, in others in the
lumbar region, and in still others in the epigastrium. The position of
the pain may be such as to draw attention from the liver, and thus
greatly confuse the diagnosis. In a well-defined attack the pain is
intense, shooting, and boring, irregularly paroxysmal; the patient
writhes in agony, screams and groans, rolls from side to side, or walks
partly bent, holding the part with a gentle pressure or rubbing with an
agonized tension of feeling. Meanwhile the countenance is expressive of
the intensest suffering, is pallid and drawn, and the body is covered
with a cold sweat. Nausea presently supervenes, and with the efforts to
vomit a keen thrust of pain and a sense of cramp dart through the
epigastrium and side. Very considerable depression of the vital powers
occurs; the pulse becomes small, feeble, and slow, or very rapid and
feeble. The patient may pass into a condition of collapse, and, indeed,
the pain of hepatic colic may cause death by sudden arrest of the
heart's action. The cases which prove fatal in this way are doubtless
examples of fatty heart, the degeneration of the cardiac muscle being a
result of the action of the same factors as those which cause
gall-stones to form, if the relation of general steatosis to these
bodies which I have set forth prove to be true. The pain is not
continuously so violent as above expressed: it remits from time to
time, and seems about to cease altogether when a sudden access of
anguish is experienced and the former suffering is renewed, and, it may
be, more savagely than before. The pain of an attack of hepatic colic
has no fixed duration. It will depend on the size of the calculus, on
the point where impacted, and on the impressionability of the subject.
The severity of the seizures varies within very wide limits. The attack
may consist in a transient colic-like pain, in a mere sense of
soreness, in epigastric uneasiness with nausea, or it may be an agony
sufficient to cause profound depression of the powers of life--to
destroy life, indeed. The usual attack of hepatic colic is one in which
severe suffering is experienced until relief is obtained by the
exhibition of anodynes. Under these circumstances the subsidence of the
pain may be rather gradual or it may be sudden: in the former case, as
the effects of the anodyne are produced, we may suppose that the spasm
subsides and the stone moves onward, at last dropping into the
intestine: an enchanting sense of relief is at once experienced. Very
serious nervous disturbances may accompany the pain. Paroxysms of
hysteria may be excited in the hysterical; convulsions occur in those
having the predisposition to them from any cause, and in the epileptic.

The onset of a severe seizure is announced by chilliness, sometimes by
a severe chill. Now and then the paroxysms commence with the chill, and
the pain follows. It occasionally happens that the attacks in respect
to the order in which the symptoms occur, and in their regularity as to
time, behave like an ordinary ague. In fact, there appear to be two
modes or manifestations of the attacks of hepatic colic in malarious
localities: those in which the phenomena are merely an outcome of the
passage of the calculi; those in which an attack of intermittent fever
is excited by the pain and disturbance of hepatic colic. To the first
Charcot[171] {1072} has applied the phrase fievre intermittente
hepatique. It is supposed to correspond pathogenetically to urethral
fever produced by the passage of a catheter. On the other hand, the
second form of intermittent can occur only under the conditions
producing ague. A calculus passing in a subject affected with chronic
malarial poisoning, the latent malarial influence is aroused into full
activity, and the resulting seizure is compounded of the two factors.
The truly malarial form of calculus fever differs from the traumatic in
its regular periodicity and the methodical sequence of the attacks,
which occur in the order of an intermittent quotidian or tertian.
During the attacks of hepatic colic, when protracted and severe, a
sense of chilliness or distinct chills occur, sometimes with the
regularity of an intermittent; but these differ from the seizures which
the chill inaugurates at distinct times, the intervening period being
free from disturbance.

[Footnote 171: _Lecons sur la Maladies du Foie_, p. 178.]

The fever which accompanies some severe paroxysms of hepatic colic has
a distinctly intermittent character, hence the name applied to it by
Charcot. There are two forms of this calculus fever as it occurs in
malarious localities: one intermittent, coming on during a protracted
case, and immediately connected with and dependent on the passage of
the stone; the other a regular intermittent quotidian or tertian, which
determines and accompanies the paroxysm of colic. A case occurring
under my observation very recently, in which these phenomena were
exhibited and the calculi recovered, proves the existence of such a
form of the malady. In this case with the onset of the pain a severe
chill occurred; then the fever rose, followed by the sweat, during
which the pain ceased, but much soreness and tenderness about the
region of the gall-bladder, and jaundice, followed in the usual way. At
the so-called septenary periods also attacks come on in accordance with
the usual laws of recurrence of malarial fevers.

Not all cases are accompanied by fever. In many instances, probably a
majority, the pulse is not accelerated, rather slowed, and the
temperature does not rise above normal. The inflammation which follows
an attack of hepatic colic will be accompanied by some elevation of the
body-heat, and fever will occur when ulceration of the duct and
perforation cause a local peritonitis; but these conditions are quite
apart from those which obtain in the migration of calculi by the
natural channel.

Nausea and vomiting are invariable symptoms of hepatic colic. First the
contents of the stomach are brought up, then some glairy mucus only,
with repeated and exhausting straining efforts; and with the sudden
cessation of the pain there may appear in the vomit a quantity of
bilious matter, the contents of the gall-bladder liberated by the
passage of the stone into the intestine. If bile is present in the
vomit from the beginning, it may be concluded that the obstruction is
not complete.

Constipation is the rule. The abdomen may be distended with gas--is
usually, indeed, when constipation exists. Free purgation gives great
relief. The stools are composed of scybalae chiefly at first, afterward
of a brownish offensive liquid, and when jaundice supervenes they
become whitish in color, pasty, and semi-solid. Now and then it happens
that a copious movement of the bowels takes place as the attack is
impending, but during the paroxysm no action occurs.

Jaundice is an important, but not an invariable, symptom. It comes on
within the first twenty-four hours succeeding the paroxysm, and appears
{1073} first in the conjunctiva, thence spreading over the body
generally. The intensity of the jaundice depends on the amount of the
obstruction: if complete, the body is intensely yellow; and if partial,
the tint may be very light. The very slight degree of obstruction which
suffices to determine the flow of bile backward has been already
stated. There may be no jaundice, although all the other symptoms of
the passage of gall-stones may be present. Such is the state of the
case when a calculus enters and is arrested in the cystic duct. Under
these circumstances the natural history differs from that which obtains
when the obstruction is in the common duct and ends abruptly by the
discharge of the calculus into the intestine. After the persistence of
the symptoms of hepatic colic for a variable period without jaundice,
this sign of obstruction may appear, indicating the removal of the
stone from the cystic into the common duct. The symptoms accompanying
the jaundice--the hebetude of mind, the slow pulse, the itching of the
skin, the dark-colored urine--have been sufficiently detailed in the
section on that topic in another part of this article.

The duration of the jaundice is different in different cases, and is
influenced by the degree and persistence of the obstruction. When the
obstruction is partial and the stone is soon removed, the jaundice will
be slight and will disappear in a day or two; on the other hand, when
the stone completely blocks the passage and is slowly dislodged, the
jaundice will be intense and will persist for ten days to two weeks.

After the paroxysm has passed, if severe, the liver will be swollen,
more or less tenderness will be developed by pressure, and in some
instances, a local peritonitis coming on, there will occur the usual
symptoms of that condition.

Although all the symptoms produced by the passage of biliary calculi
may be present, some uncertainty will always be felt unless the body
causing the disturbance is recovered from the feces. A
properly-conducted search is therefore necessary. As this is so often
done inefficiently and the calculus not found, an error of diagnosis
may seem to have occurred. Every stool should be examined in the mode
hereinafter described for a number of days after the attack until the
calculus is found. It should be remembered that only air-dried calculi
float on water. The stool, as soon as passed, should be slowly stirred
up in water sufficient to make a thin mixture, and all solid particles
removed for further examination, the thinner portion poured off, and
more water added from time to time until only solids remain at last. It
should not be forgotten that masses of inspissated bile, biliary sand,
may produce symptoms not unlike those due to gall-stones proper, and
hence all particles having the appearance of this material should be
examined chemically. Place some of the supposed bile on a white plate
and pour over it some drops of strong sulphuric acid, when the
biliverdin will take on a brilliant scarlet color.

The discharge of particles of inspissated bile causes symptoms not
unlike those due to the migration of biliary calculi, but there are
points of difference. A strongly-marked case diagnosticated biliary
calculi, and in which masses of inspissated bile were discharged in
great quantity, will furnish the symptomatology to be now described.
The onset of the paroxysms of pain is less abrupt than is the case with
gall-stones, and the attacks may occur at any time; the pain also
subsides more gradually, and hardly {1074} ceases at any time, but
revives every now and then, so that several days, even weeks, may be
occupied with one seizure. Jaundice is less apt to follow, and indeed
well-defined jaundice rarely occurs in this affection. There is much
swelling of the liver, also considerable tenderness, and relief is most
certainly afforded by free purgation, anodynes seeming rather to keep
up the disturbance, probably by checking the hepatic secretions.

Attacks of hepatic colic may be expected to recur when a calculus with
multiple facets migrates, but the time when its associates may be
expected to move cannot be predicated on any data now available. Single
attacks may happen at intervals of weeks, months, or years. The
migration of one large stone may so dilate the ducts as to facilitate
the passage of those that remain behind, thus ensuring a recurrence of
the seizures at an early period.

IMPACTION OF CALCULI AND MIGRATION BY ARTIFICIAL ROUTES.--The point at
which impaction takes place is an element of great importance. The size
of the calculus is far from being decisive as to the certainty of
impaction or as to the untoward results. A not unfrequent accident is
the blocking of the cystic duct at its opening, thus preventing the
influx or outgo of bile from the gall-bladder. If the stone does not
ulcerate through, in this position it does no damage, for the
gall-bladder, as has been stated, may be closed without any apparent
detriment. Just at the bend of the cystic duct, near its origin, is the
point where arrest of a calculus is most likely to take place. The next
most likely point is the duodenal end of the common duct. When
impaction occurs a local inflammation comes on, an exudation is poured
out, ulceration begins, and presently the peritoneum is reached.
Adhesions usually form with the neighboring organs, but now and then
perforation takes place, and bile, pus, and the calculus are
precipitated into the peritoneal cavity. A fatal peritonitis follows,
as a rule; but rarely the inflammation is localized, and an abscess
forms which pursues the usual course of such accumulations; or
adhesions may take place about the site of the perforation and prevent
a general inflammation of the peritoneum. In this way a very large sac
may be produced, with the ultimate result of rupture into the general
cavity, although a fistulous communication may be established with some
neighboring organ, permitting safe discharge in this direction.

A gall-stone impacted in one of the hepatic ducts or in the main duct,
ulcerating through, may form an abscess not distinguishable from other
solitary hepatic abscesses except by the presence of the concretion
causing the mischief and the absence of the usual conditions giving
rise to these accumulations of pus. It is probable that fatal abscesses
of the liver not infrequently are caused in this way in extra-tropical
countries. Adhesions forming to neighboring hollow organs or to the
external integument, such abscesses discharge, carrying out the
calculus with them. In this way may be explained the discharge by the
intestine of calculi much too large to have passed by the natural route
and unattended by the usual symptoms of hepatic colic. These
gastro-intestinal biliary fistulae extend from the gall-bladder and the
larger ducts to the stomach, to the duodenum, and to the transverse
colon; but of these the communication with the stomach is the least
common. The adhesion of the gall-bladder or common duct to the duodenum
or colon may be direct, exudations uniting {1075} the two parts without
the intervention of an abscess cavity, or such a sac or cavity may be
interposed. In some cases the discharge of biliary calculi is effected
through these routes with so little disturbance as to escape notice, or
the symptoms may be only vague indications of a local inflammation in
the neighborhood of the liver.

Biliary fistulae communicating externally, caused by the migration of
calculi, are comparatively common. They have the clinical history, and
are usually treated as cases, of hepatic abscess. Sometimes hundreds of
calculi are thus discharged. In such instances it may be assumed that
communication has been established with the gall-bladder. Hepatic
abscess thus due to the migration of calculi may discharge into the
pelvis of the kidney, into the ascending vena cava, or through the
lung, but these places of outlet are comparatively uncommon.

COURSES AND COMPLICATIONS.--Although symptoms cease for the time being
when the calculus passes into the duodenum, and although in most
instances no after unpleasant effects are experienced, there are cases
in which the presence of the concretion in the intestine proves to be
fruitful of mischief. Calculi of very large size--from a pigeon's to a
hen's egg--are also found in the intestine, without the occurrence of
symptoms indicative of their migration. It has been shown that this
silent migration of calculi from the liver-passages to the intestinal
is not uncommon. Hepatic concretions are distinguishable from the
intestinal by their crystalline form and by their composition. The
former are usually polyangular, and are composed of cholesterin
crystallized about a nucleus of bile-pigment, inspissated bile, or
mucus. After entrance into the intestine, lime salts and mucus are
deposited in successive layers, so that the form of the calculus is
modified and its size increased. The solitary ovoid concretion is most
frequently found in the intestine, without previous symptoms of hepatic
source, and, although increased in size in the intestine, it retains
its original shape. A specimen of this kind now in my possession
illustrates these points. It is composed of cholesterin crystallized in
radiating lines and concentric rings about a central nucleus of
inspissated bile. Around the hepatic concretion there have formed
layers of lime and mucus since it has reached the intestine, and after
drying this rind became brittle and was readily detached. The
polyangular calculus is apt to form the nucleus of a scybala-like mass
of feces; hence in the search for these bodies every such mass should
be broken up. An example of this has recently come under my own
observation. Concretions of all sizes, having reached the intestines,
as a rule pass down without creating any commotion, and are silently
discharged. But various disturbances occur in some instances.
Obstruction of the bowels is one of the results. A great may cases have
been collected by Murchison,[172] as many more by Leichtenstern,[173]
of impaction of the intestine produced by an accumulation of feces
about a biliary concretion. A calculus may be retained in a fold or
diverticulum of the small intestine, and may indeed cause a loop to be
formed which in turn readily twists, becoming an immovable obstruction.
This mode of obstructing the bowels is less common than the simple
impaction. It is affirmed by some authorities, especially by Von
Schuppel, that obstruction of the bowels--impaction--is more often
caused by stones that have ulcerated through into the {1076} intestines
than by those that have descended by the common duct; and this
conclusion must be reached if jaundice has not been present. It is not
only the size of the calculus which determines impaction, as has been
stated: several may be agglutinated in one mass, and reflex spasm of
the muscular layer may be induced by their presence in the bowel.
Nevertheless, some enormous concretions have been found in the canal,
and others have been discharged without special trouble. Hilton Fagge
exhibited to the Pathological Society[174] of London two gall-stones
passed with the stools, measuring 2-1/2 by 1-1/5 inches in long and
short diameter, and Fauconneau-Dufresne[175] refers to concretions of
the size of a hen's egg. Mention has been made of one in the writer's
possession of the size of a pullet's egg, which, until its discharge,
caused a train of characteristic symptoms. These immense bodies may
have ulcerated through from the gall-bladder or may have grown by
successive deposits of carbonate and phosphate of lime after reaching
the intestine.

[Footnote 172: _Lectures on Diseases of the Liver_, p. 573.]

[Footnote 173: _Ziemssen's Cyclopaedia_, vol. vii.]

[Footnote 174: _Transactions of the London Pathological Society_, vol.
xix. p. 254.]

[Footnote 175: _Op. cit._]

The symptoms caused by the presence of concretions in the intestines
are, when pronounced, sufficiently characteristic. At a variable period
after an attack or attacks of hepatic colic the disturbance begins. The
condition of impaction above referred to does not differ from ordinary
fecal accumulation. It is true that occasionally the intestinal
irritation due to the presence of these bodies in some instances
preceded the symptoms of impaction, but usually there is no evidence to
indicate that the stoppage of the bowel is due to anything else than
feces. The irritability manifested by the intestinal mucous membrane
when gall-stones are present varies remarkably. There may be only some
ill-defined pain which, as a rule, indicates the position of the
calculus, or it may be pain with a feeling of soreness, or it may take
the form of violent colic, with nausea, vomiting, and depression. In my
own cases pain was experienced at or near the ileo-caecal valve, where
one was lodged, and along the descending colon, where the others were;
the pain and soreness ceased when these bodies were discharged.

In a few instances gall-stones are brought up by vomiting. The most
remarkable example of this is a case to be found in the _Transactions
of the Pathological Society_ (vol. xii. p. 129): A woman ninety-four
years of age vomited a stone the size of a nutmeg. In the reported
examples violent pain, nausea, and much vomiting preceded the discharge
of the calculus.

Like other foreign bodies, a gall-stone may ulcerate through the
intestine, producing fatal peritonitis.

Many conditions due to the presence of biliary concretions, and which
arise during their migrations, may be viewed as complications. Many of
those produced directly have been described as a part of the proper
course of the malady; others are local and reflex, and these may with
propriety be considered as complications. First in importance are those
due to obstruction and the local inflammation.

The passage of a calculus along the duct excites an inflammation of the
mucous membrane, which by contiguity of tissue invades the peritoneal
layer if the stone is retained for a sufficient time, and especially if
it is immovably lodged. The stoppage in the flow of bile leads to
dilatation of the ducts, and a change takes place in the character of
that fluid, {1077} owing to the admixture of mucus with the bile and to
the pouring out of a pathological secretion: it loses the bilious
appearance and becomes a merely sero-purulent fluid. Serious changes
ensue in the structure of the liver, as was first suggested by O. Wyss
and Leyden, and afterward more especially by Wickham Legg[176] and
Charcot.[177] A ligature to the common duct in animals is followed in
so short a time as two weeks by hyperplasia of the connective tissue
and atrophy of the gland-elements. It has been ascertained that similar
changes ensue in man from the impaction of a calculus in the common
duct. Under these circumstances the size of the liver, as indicated by
the area of hepatic dulness, at first enlarges, and subsequently more
or less contraction, coincident with the atrophy, ensues. When the
cystic duct is obstructed the contents of the gall-bladder increase,
and become ultimately sero-purulent (dropsy). In some instances, the
walls of the abdomen being thin, a globular elastic tumor may be felt
projecting from beneath the liver.

[Footnote 176: _St. Bartholomew's Hospital Reports for 1873_. See also
_Treatise on Diseases of the Liver_, by the same author, _loc. cit._]

[Footnote 177: _Lecons_.]

Angiocholitis, or inflammation of the duct, is caused by the passage,
especially by the impaction, of a calculus. The inflammation may extend
by contiguity of tissue and involve the surrounding parts. Several
cases have been examined by the writer in which the gall-bladder and
the cystic and common duct were imbedded in a mass of organized
exudation. An extension of inflammation may take place, and be confined
to the hepatic peritoneum. Heavy organized exudations will form,
adhesions be contracted to the diaphragm, to the parietal peritoneum,
and to the neighboring organs, and the capsule, thickened and
contracting, will ultimately induce changes in the structure of the
adjacent part of the liver. When the inflammation extends to the
peritoneum there are the usual systemic symptoms, and locally acute
pain, increased by the respiratory movements and by pressure, and
assuming a constrictive character; nausea and frequent vomiting, and
often a very troublesome hiccough, caused, doubtless, by implication of
some branches of the phrenic nerve; constipation, etc.

The relation of biliary colic to cancer of the biliary passages was
first noted by Frerichs, who ascertained the occurrence of gall-stones
in 9 out of 11 cases of cancer of these parts. Hilton Fagge[178]
reports a case of the kind, and the writer can add another from his own
observations.

[Footnote 178: _Guy's Hosp. Rep._, 1875.]

The most important of the reflex symptoms are those pertaining to the
circulatory system. The action of the heart becomes irregular in rhythm
and diminishes in force. The circulation of the bile acids in the blood
causes slowing of the heart's action, as has been set forth in the
section on jaundice; but that is a direct consequence, and is not a
reflex impression. Potain was the first to show that the structure of
the heart is affected. A mitral murmur is a recognized symptom in the
icterus of gall-stones, but Potain[179] has shown that the real seat of
this murmur is the tricuspid, and that the affection of the heart is a
dilatation of the right cavities. The physiological reason for this
condition of the heart is the rise of tension in the pulmonary artery,
which is secondary to irritation of the splanchnic nerves; and to this
factor is also due the reduplication of the first sound and the
accentuation of the second sound--characteristic signs of the cardiac
change in these cases.

[Footnote 179: Cyr, _Traite de l'Affec. calc. de Foie_, _loc. cit._]

{1078} There are certain reflex nervous troubles in cases of hepatic
colic, some of them of great importance. One of the lesser troubles is
herpes zoster. A very violent attack in the course of the distribution
of the first, second, and third cervical nerves has happened in a case
under the writer's observation. There have been reported from time to
time cases of sudden death during the paroxysms of hepatic colic, in
which a calculus lodged in Vater's diverticulum, at the intestinal
extremity of the common duct, was the cause of the accident. An
explanation of this result is to be found in the intimate nervous
communications between the liver and the heart through the solar plexus
and the large number of ganglia contained in Vater's diverticulum. The
most severe pain is felt as the calculus is passing through the orifice
of the common duct into the intestine, and here also the spasm of the
muscular fibre is most tense. The so-called crushing-blow experiment of
Goltz illustrates how intense suffering, such as the passage of a
gall-stone, can paralyze the heart through the solar plexus. The
depression of the heart's action does not always occur on the instant,
but it may be gradual--several hours, even a day or two, being occupied
in the suspension of activity. Leigh of Liverpool[180] has reported an
example of death in six hours in a female of thirty, previously in good
health; Cornillon,[181] another in a female of fifty-three, who died in
twelve hours from the beginning of the paroxysm; Williamson,[182] a
female of fifty-one years, who expired on the fourth day;
Habershon,[183] two, who died during the paroxysms at a period not
stated; and Brouardel, one which was the subject of a medico-legal
investigation. In the first case the calculus was yet in the
gall-bladder, the appearances indicating that persistent spasms had
occurred to force the calculus into the cystic duct; in the others in
which the position of the stone is mentioned, it was engaged in the
orifice of the common duct or had reached the intestine.

[Footnote 180: _Medical Times and Gazette_, 1867, vol. i. p. 248.]

[Footnote 181: Cyr, _op. cit._, p. 185.]

[Footnote 182: _The Lancet_ (London), vol. ii. p. 780.]

[Footnote 183: _Lectures on the Pneumogastric_, 3d Lecture.]

In several instances sudden death has resulted from uncontrollable
vomiting induced by the paroxysms of hepatic colic. Trousseau[184]
mentions a case in which strangulated hernia and death ensued in
consequence of the violent vomiting brought on by the passage of a
calculus.

[Footnote 184: _Clinique medicale_.]

DIAGNOSIS.--Unless the distension of the gall-bladder is sufficient to
cause a recognizable tumor, gall-stones in that organ do not produce
symptoms by which they can be diagnosticated. If sudden attacks of
violent pain in the right hypochondrium, accompanied by nausea and
vomiting and followed by jaundice, have occurred from time to time,
then the presence of biliary concretions may be suspected if the
symptoms belonging to them are present in the intervals between the
seizures. The migrations of calculi produce symptoms so characteristic
that error is hardly possible. The only disorders with which an attack
of hepatic colic may be confounded are gastralgia and hepatalgia. As
regards the first, the distinction is made by the seat of pain, by the
absence of after jaundice, and by the lack of a concretion passed by
stool. As the diagnosis may depend on the finding a concretion, the
writer must again affirm the importance of a properly-conducted search
of all the stools passed for several days after the paroxysm.

{1079} Hepatalgia is diagnosticated with great difficulty, for the pain
has the same seat, the same character, but as a rule it does not
terminate so abruptly, is not accompanied by such severe vomiting and
depression, jaundice is absent, and no stone can be found in the
evacuations. Both gastralgia and hepatalgia occur in the subjects of
neurotic disturbances--in the pale, delicate, and hysterical--whereas,
as a rule, hepatic colic happens to the obese, to the persons of active
digestion addicted to the pleasures of the table.

The passage of calculi may be confounded with flatulent colic, with the
pain caused by lead and other mineral poisons, with impaction, internal
strangulation, local peritonitis, and similar causes of sudden and
violent pain. The differentiation is made by attention to the seat and
character of the pain, by the previous history, and especially by the
absence of jaundice and of a concretion. From renal colic the hepatic
is separated by the position of the pain, by the direction taken by it,
and by the retraction of the testicle, the irritability of the bladder,
and the appearance of blood in the urine--all characteristic symptoms
of the renal affection.

TREATMENT.--The treatment of biliary concretions includes the remedial
management for the calculi in position, for the paroxysms of hepatic
colic caused by the migration of these bodies, and for the results and
complications.

Treatment of the Calculus State: Of Inspissated Bile.--As the particles
of inspissated bile are deposited along the larger hepatic ducts, and
form in consequence of a deficiency in the amount of glycocholate and
taurocholate of soda, two methods of treatment are to be carried out:
free purgation by an active cholagogue to wash out the offending
substance, and the exhibition of a soda salt to promote the alkalinity
of the bile and the consequent solution of the bile-pigment. Harley's
method, which he strongly urges, consists in the administration of "one
or two drachms of sulphate of soda in a bitter infusion every morning
before breakfast, or from twenty to thirty grains of bicarbonate of
soda, along with a drachm of taraxacum-juice in a bitter infusion,
every night at bedtime at regulated intervals for a month or so,
according to the constitution of the patient and the severity of the
symptoms."

As persons who suffer from inspissation of the bile are naturally
bilious, it is of the first importance in the prophylactic treatment to
regulate the diet. Indulgence in malt liquors, in fatty and saccharine
articles of food, must be forbidden. Acid fermentation in the course of
duodenal digestion should be prevented by withholding the starches and
sugars. Peptonized foods, given with an alkali, are highly useful.
Milk, fresh meat, and the succulent vegetables are the proper
constituents of a diet for these subjects. Bread is one of the most
offending articles, and should be restricted in amount as much as
possible.

Next to a suitable diet, systematic exercise is a measure of the
highest utility in these cases. A daily morning sponge bath of a weak
alkaline water not only maintains the skin in a healthy state, but also
promotes the oxidation processes of the body. The alkaline mineral
waters of Wisconsin, Michigan, Virginia, and other States, especially
of the Bethesda Spring of Wisconsin, may be drunk with great advantage
to accomplish the same purpose.

{1080} We possess direct means for preventing inspissation of the
bile--remedies which act in the physiological way by increasing the
proportion of glycocholate and taurocholate of soda. Harley prefers the
sulphate and bicarbonate for this purpose, but my experience is in
favor of the cholate and phosphate of sodium, especially the latter;
for, whilst it plays the part of a soda salt, it exerts a decided
cholagogue action, thus effecting the results achieved by the combined
use of sulphate of soda and taraxacum. A cure may be confidently looked
for in this malady by the persistent use of sodium phosphate--drachm j
ter in die. It seems to act more efficiently when given dissolved in
hot water.

The paroxysms of hepatic colic due to the passage of inspissated bile
are to be treated in the same way as when this condition of things is
caused by the migration of formed calculi. The action of cholagogue
purgatives is more decidedly beneficial in the attacks due to the
passage of inspissated bile.

Biliary Calculi in Situ.--Notwithstanding their crystalline form and
firmness of texture, it is possible to effect the gradual solution of
biliary calculi. Outside of the body it is easy to dissolve a calculus
in chloroform, in Durande's remedy, etc., if time enough be given, but
the problem is a far more difficult one when the calculus is in
position in the gall-bladder or in a hepatic duct. As Trousseau[185]
has wisely observed, it is not safe to apply to conditions within the
body conclusions reached by experiments in the laboratory.
Nevertheless, facts are known which justify the belief that an
impression may be made on concretions in the gall-bladder. The motion
of respiration and the voluntary actions of the abdominal muscles cause
more or less attrition and breaking off of the angles and margins of
the crystals, thus permitting the solvent action of the bile. If,
however, the bile continues in the state in which it was at the time of
the crystallization of the cholesterin, it will make no impression on
this substance. We have now the means of restoring its power to
dissolve crystallized cholesterin. As a necessary preliminary, fracture
of the crystals must be effected. This may be accomplished, when the
natural forces have failed to effect it, by manipulation of the
gall-bladder through the walls of the abdomen, but especially by
faradization. Excellent results have been achieved by this
last-mentioned expedient, but no satisfactory explanation has been made
of its methodus medendi, unless we accept the mechanical effect of the
muscular movements. In applying the faradic current an electrode is
introduced into the rectum, and the other, a sponge well moistened, is
placed over the gall-bladder. An interrupted galvanic current is
indicated, the electrodes in the position just mentioned, when a
migrating calculus is stopped on its way. Such an application has
rendered important service in a few cases.

[Footnote 185: _Clinique medicale de l'Hotel Dieu de Paris_.]

Except that calculi have been found in a state of decay, their angles
and edges broken, divided by cleavage, there is no evidence that they
have undergone solution when in situ, except the clinical evidence
which consists in a disappearance of the symptoms. The remedy of
Durande, which consists in a mixture of ether and turpentine--three
parts of the former and two of the latter--has been celebrated since
the close of the last century, and is yet much employed in France,
notably at Vichy. It {1081} is preferred by Cyr,[186] who advises its
administration in capsules taken immediately before meals. Chloroform
readily dissolves calculi out of the body, and hence it has been
proposed, and indeed much used, for the purpose of effecting their
solution in the gall-bladder; but, as Trousseau urges, there is no
warrant for the belief. Corlieu,[187] who first proposed its use, and
afterward Bouchut,[188] maintained that chloroform does exert this
solvent action, and reported cases in confirmation; but there are so
many sources of fallacy that such evidence must be viewed with
suspicion. It has usually been administered in small doses (five
minims) three times a day for a long period. That it is beneficial by
stimulating the flow of pancreatic secretion and by allaying spasms is
probably true, but that any quantity which can be administered in
safety will act as a solvent of cholesterin concretions cannot be
believed.

[Footnote 186: _Traite de l'Affection calculeuse du Foie_, p. 287.]

[Footnote 187: _Gazette des Hopitaux_, 1856, June 19.]

[Footnote 188: _Bulletin gen. de Therap._, vol. lxi. p. 49.]

If solution of hepatic calculi is possible under any circumstances, the
most rational mode of effecting it would seem to be to restore that
condition of the bile which in the normal state maintains cholesterin
in the state of solution. Cholesterin is precipitated and crystallizes
about a nucleus when the glycocholate and taurocholate of soda are
deficient in amount. The agents most effective in restoring the solvent
power of the bile are the salts of soda, of which the sulphate is
preferred by Harley. In 1873 the cholate of soda was brought forward by
Schiff, who prescribed it in doses of 50 centigrammes (8 grains nearly)
three times a day, to be gradually increased until digestive or
circulatory troubles arose. This remedy, which is eminently rational
from the point of view above indicated, has apparently been of decided
service in many published cases and in the writer's experience. It will
be found, however, that five grains three times a day is as large a
quantity as can be easily borne.

Another soda salt which in my own hands has proved in a high degree
effective is the phosphate. As has been explained when referring to its
use in cases of disorders due to inspissated bile, it has a distinct
cholagogue action, but the chief sources of its utility in this
affection are its chemical and resolvent powers. The usual quantity is
one drachm three times a day, dissolved in sufficient warm water.

Bile itself, in the form of inspissated ox-gall, was formerly much
used, a scruple to a drachm being given three times a day, and not
without good results. It was also prescribed with chloride of ammonium.
For the gastro-duodenal catarrh and the accompanying catarrh of the
bile-ducts this combination is sometimes useful.

I have recently proposed a new expedient for effecting the solution of
hepatic calculi. This method consists in puncture of the gall-bladder
with a fine exploring-trocar, and the injection through the canula,
after withdrawing the stylet, of a suitable solvent. Durande's remedy,
chloroform, and other solvents can be introduced in this way without
injury to the parts. I have punctured the gall-bladder, removed its
contents, and explored its interior without damaging the organ in any
way and without leaving after traces. The measure proposed offers no
special difficulties in its execution.

The Paroxysms of Hepatic Colic.--The pain of hepatic colic being {1082}
the most acute suffering known to man--in its severest form at
least--the most powerful anodynes are required. The measures employed
for relief of pain happen to be the most efficient for promoting the
expulsion of the calculus and for limiting, if not preventing, the
subsequent inflammation. As soon as the character of the seizure is
manifest a hypodermatic injection of morphine and atropine--1/8 to 1/2
grain of the former and 1/200 to 1/80 grain of the latter--should be
given; ether administered by inhalation if necessary; and by the
stomach chloroform, chlorodyne, or chloral. As the stomach is usually
exceedingly irritable, the subcutaneous injection of remedies is a
precious resource: this failing or contraindicated, relief may be given
by the rectal injection of laudanum or chlorodyne. As relief is often
afforded by the act of vomiting, the attempts to empty the stomach
should be encouraged, and to this end large draughts of warm water
should be given. Hot fomentations and mustard plaster should be applied
over the right hypochondrium, and an entire warm bath may be used if
available.

Great relief is usually afforded by the action of purgatives. The
irritability of the stomach forbids the employment of drastic
purgatives, yet podophyllin resin is warmly commended by Dobell. It
must be given in small doses, and preferably dissolved in spirit.
Calomel in one-grain doses, every four hours until it purges, allays
nausea and lessens the after-uneasiness in the right hypochondrium, but
mercurial treatment given with a view to a supposed cholagogue effect
only does evil by prolonged administration, especially if ptyalism is
induced. If evidences of portal congestion are present, such remedies
as euonymin, iridin, baptisin, and others of the cholagogue group give
good results. The most effective of the remedies of this kind is
ipecacuanha, given in purgative doses: the emesis induced by it favors
the extrusion of the stone, and the powerful cholagogue effect relieves
the portal congestion. Twenty grains at once, and repeated if need be
in three hours, is a suitable quantity.

The various complications which may occur, and the results which follow
the migration of the calculus, require treatment adapted to the
conditions existing, and will be mentioned in the sections devoted to
these topics.


Occlusion of the Biliary Passages; Stenosis of the Ductus Communis
Choledochus.

DEFINITION.--By occlusion of the biliary passages is meant an
obstruction, internal or external, of the hepatic, cystic, or common
duct. The causes of the obstruction are various, but the results are
quite uniform; hence the term includes a complexus of symptoms of a
very distinctive type. Occlusion may be congenital or acquired: it is
the latter with which we have especially to deal.

Stenosis signifies a narrowing which in its extremest form produces a
nearly complete obstruction; when the canal is entirely closed the term
occlusion is applied. Stenosis also may be congenital or acquired.

PATHOGENY.--The conditions producing narrowing of a hepatic duct or its
complete obstruction are numerous, and some of them complex in their
relations. As regards the ducts themselves, the interference may {1083}
be entirely within the canal, or it may affect the walls, or it may be
wholly extraneous; as, for example, when a cancer of the pancreas
encroaches on the common duct. It will be convenient to consider the
causes of stenosis and obstruction from these points of view: 1,
internal; 2, of the duct walls; 3, extraneous.

The most usual situations for the occurrence of those changes that lead
to occlusion by inflammatory adhesions are the beginning of the cystic
duct, obstruction of which is of little moment, and the end of the
common duct, which finally proves fatal.

The passage of a large polyangular calculus may cause such irritation,
abrasion of the epithelium, and subsequent inflammatory exudation as to
effect a direct union of the opposing sides of the canal. This takes
place at the beginning of the cystic duct especially, since, owing to
the spasm of the gall-bladder and the absence of muscular fibres in the
walls of the duct, the stone crushes into, without passing through, the
canal. The inflammatory exudation thus excited may close the duct. Not
unfrequently the gall-bladder, full of calculi, is thus shut off from
the liver permanently. In one instance the writer has seen a calculus
wedged into the orifice of the cystic duct, whilst just beyond the
lumen was permanently obstructed by an organized exudation. Permanent
closure of the cystic duct is of far less consequence than of the
common duct, and may, indeed, be a conservative condition, as in the
case above mentioned, where numerous polyangular calculi may have
migrated, except the closure of the passage.

The most usual point of obstruction in the course of the common duct is
the intestinal end, but various processes are employed to effect it.
The first in importance is catarrhal inflammation. This seems the more
credible when it is remembered that to a simple catarrh of the mucous
membrane is due the temporary stoppage of the duct, producing jaundice
in much the largest proportion of cases. When the epithelium is
detached and granulations spring up from the basement membrane,
adhesions of the surfaces will readily take place, and the union may be
so complete as that all traces of the duct will disappear. It is
probable that in many, if not in most, of these cases the initial
condition of the canal is that of simple catarrh, the more positive
changes in the mucous membrane arising from peculiarities in the
tissues of the individual affected, or from local injury caused by the
passage of a concretion or irritation of pathological secretions of the
duodenum.

Stenosis, and finally occlusion, of the common duct may arise from the
cicatrization of an ulcer. Such ulcers may occur in several modes. They
may result from catarrhal inflammation of a chronic type, much new
connective-tissue material forming, and in the process of
cicatrization, with the contraction belonging to it, the lumen of the
canal is so far filled up that the passage of bile is effectually
prevented. They may be produced in that state of the tissues which
accompanies certain cachectic and profoundly adynamic conditions, as in
severe typhoid fever. Such ulcers may also be due to the mechanical
injury effected by the migration of a gall-stone. In cicatrizing, a
tight stricture, impermeable to the passage of bile, may result, or the
lumen of the canal be entirely obliterated. In the latter case the duct
itself may disappear and leave no trace. An ulcer situated at the
duodenal end of the common duct and extending into the {1084} duodenum
may also in the process of healing so contract as to render the orifice
impermeable to bile. The same effect may follow the cicatrization of an
ulcer of the duodenum in the immediate vicinity of the orifice of the
common duct.

Without the intervention of an ulcer as a means of explaining closure
of the common duct, this accident may be caused by a catarrhal
inflammation which effects denudation of the basement membrane, and
thence union may be produced by the mere contact of the
freshly-granulating surfaces. Congenital occlusion of the bile-ducts or
obstruction occurring in a few days after birth, it is probable, is
effected in this way, but no direct evidence of the process has thus
far been offered. During intra-uterine life, as at any period in
after-life, it seems necessary to the production of such changes that a
peculiar constitutional state must exist; otherwise, such a result
might happen to every case of catarrhal inflammation of the bile-ducts.
The extent of the changes is further evidence in the same direction;
for not only are the walls of the duct in permanent apposition and
adhesion, but the duct degenerates into a mere fibrous cord, and in
some instances is nearly, even entirely, obliterated.[189]

[Footnote 189: _Ziemssen's Cyclopaedia_, p. 589.]

The cystic or common duct--the latter to be chiefly considered--may be
occluded by the retention in its lumen of some foreign body. The
impaction of a biliary calculus has already been repeatedly referred
to, but there are some additional points demanding consideration. The
larger concretions may be stopped in the neck of the gall-bladder;
those small enough to enter the canal may be arrested at its bend
behind the neck, and the very entrance of the cystic duct may be
blocked, as in a case examined by the writer.

The hepatic duct is very rarely permanently occluded. As the calibre of
this canal continuously enlarges downward, there is no point at which a
stone is likely to be arrested; nevertheless, it occasionally happens
that such an obstruction does occur. An example has occurred under the
observation of the writer, but the cause was a gunshot wound of the
liver.

The most usual, and for very obvious reasons the most important, of the
sites where occlusion occurs is the common duct and at the termination
of the duct in the small intestine, the intestinal orifice. Just behind
and to the right of its orifice the duct is dilated into a fossa--the
diverticulum Vateri; and here concretions of a size to pass along the
common duct are stopped. It is not essential that the stone fit the
canal: it may do so and prevent any bile passing into the duodenum; it
may be a polyangular body, and, though wedged in, leave spaces through
which more or less can slowly trickle. The symptoms will be modified
accordingly. Again, the diverticulum may contain numerous concretions,
which distend the canal greatly, but through the interstices of which
some bile can flow.

Other foreign bodies very rarely close the intestinal end of the ductus
communis; thus, for example, a cherry-seed, a plum-seed, a mass of
raisin-seeds, may slip into the orifice after the passage of a
gall-stone has stretched it sufficiently. A much more common cause of
occlusion is an intestinal parasite, which crawls in and is fastened.
The common round-worm is the most frequent offender, and much less
often liver-flukes find a lodgment there.

{1085} The ductus communis choledochus may be closed by agencies acting
from without. They are various, but the most common are the
carcinomata. Primary cancer of the gall-bladder and gall-ducts,
although not of frequent occurrence, is by no means rare. It develops
in connection with the connective-tissue new formations produced by the
inflammation following the migration of large calculi. A very
instructive example has been examined by the writer. The patient, a
woman aged forty-eight, had had numerous paroxysms of hepatic colic,
and after death, which followed a protracted stage of jaundice by
obstruction, a large ovoid calculus, filling the gall-bladder, was
found, and an extensive organized exudation of inflammatory origin was
the seat of carcinomatous disease involving the cystic and common ducts
and closing the lumen of both. Cancer of the pylorus, of the duodenum,
of the pancreas, of the right kidney, and of the liver itself, not
unfrequently by exterior pressure permanently occlude the common duct.
To this category of obstructing causes must be added enlarged lymphatic
glands of the transverse fissure, large fecal accumulations, tumors of
the ovaries and uterus, aneurisms of the abdominal aorta, and
especially aneurism of the hepatic artery, several examples of which
have been reported, and one has occurred in a case seen by the writer.

The effects of obstruction are much less important when the cystic duct
is closed. The contents of the gall-bladder accumulate, constituting
the condition known as dropsy of the gall-bladder. A catarrhal state of
the mucous membrane is set up; the muco-pus formed mixes with the bile,
and the mixture undergoes fermentative changes which further alter its
character and impart to it irritating qualities, in consequence of
which the mucous membrane becomes more decidedly inflamed, and a still
more purulent fluid forms, so that ultimately the contents of the
gall-bladder are entirely purulent, and that organ may attain to
enormous size. Instead of a catarrhal inflammation leading to
suppuration, the mucous membrane may pour out serum abundantly, the
biliary contents and mucus disappear by absorption, and finally the
gall-bladder will be moderately distended by a serous-like fluid. No
further disturbance ensues, and the gall-bladder, thus shut off from
participation in the hepatic functions, ceases to give trouble.

The results are far different when the obstruction occurs in the
hepatic or common duct, for then the bile can no longer perform its
double function of secretion and excretion--of contributing materials
necessary to digestion and assimilation, and excreting substances whose
removal is necessary to health. The liver continuing to functionate
after closure of the duct is effected, obviously the secretion of bile
continues to accumulate, and the irritation of the mucous membrane
causes a catarrhal state; mucus is poured out, and serum escapes from
the distended vessels. If the hepatic duct only is obstructed, the
dilatation will not involve the cystic duct and gall-bladder, but as
the common duct at its termination is occluded, usually the whole
system of tubes will be affected by the ensuing changes. The
alterations already described as occurring in the gall-bladder take
place in all the hepatic ducts. The bile-elements are absorbed, and the
fluid distending the whole system of hepatic tubes becomes finally a
semi-transparent serum or a very thin sero-mucus, having in bulk a pale
sea-green color. Although an intense jaundice {1086} coexists with the
obstruction, no portion of the bile escapes into the ducts. At the
beginning of the obstruction more or less bile is in the tubes, and
then the fluid will have a distinct biliary character; but as it
accumulates, first the bile-constituents disappear, then the
mucus--which at the outset was formed freely--is absorbed, and at last
only a colorless serum remains. This fluid, which has been examined
chemically by Frerichs, is found to be slightly alkaline, to have only
2 per cent. of solids, and to present no trace of any biliary
constituent. As the fluid accumulates the gall-bladder and ducts
dilate, sometimes to an enormous extent, the fluid they contain
amounting to several pints. The walls of the ducts grow thinner, and
may finally give way with the pressure or from external violence, the
fluid exciting an intense and quickly-fatal peritonitis. Important
changes occur in the structure of the liver also. With the first
retention of bile the liver conspicuously enlarges, and may indeed
attain to twice its normal size, but it subsequently contracts, and may
lessen in as great a degree as it had enlarged. Changes begin in the
glandular structure as pressure is brought to bear on the cells by the
enlarging ducts. The liver-cells become anaemic and the protoplasm
cloudy, but granular and fatty degeneration does not take place. Even
more important as an agency affecting the condition of the hepatic
cells is the hyperplasia of the connective tissue, which ensues very
promptly when an obstruction to the flow of bile arises from any cause,
as has been shown by Legg[190] and Charcot.[191] The liver on section
has a rather dark olive-green color, and is firmer in texture, owing to
the increased development of the connective tissue; the cells are
bile-stained and contain granules of coloring matter and crystals of
bilirubin, and although they are at first not altered in outline,
subsequently more or less atrophy is produced by the contraction of the
newly-formed connective tissue and the pressure made by the dilated
hepatic ducts.

[Footnote 190: _On the Bile, Jaundice, and Bilious Diseases_, p. 352
_et seq._]

[Footnote 191: _Lecons sur les Maladies du Foie, etc._, p. 205 _et
seq._]

SYMPTOMS.--The symptoms produced by occlusion of the cystic duct are
not sufficiently characteristic to be diagnosticated with any
certainty. When an attack of hepatic colic has slowly subsided without
jaundice, and an elastic tumor, globular or pyriform in shape, has
appeared from under the inferior margin of the liver in the position of
the gall-bladder, dropsy of that organ may then be suspected. As
paracentesis of the gall-bladder may be performed with ease, safety,
and little pain, the diagnosis may be rendered more certain by the use
of the exploring-trocar.

Obstruction of the hepatic or common duct is accompanied by symptoms of
a very pronounced and distinctly diagnostic character. Without
referring now to the antecedent symptoms or to those belonging to the
obstructing cause, the complexus of disturbances following the
obstruction is the subject to which our attention must be directed. The
great fact dominating all other considerations is the stoppage of the
bile, whether this has occurred suddenly or slowly. Jaundice begins in
a few hours after the canal is blocked. At first there is yellowness of
the conjunctiva, then diffused jaundice, deepening into the intensest
color in two or three weeks, or, when the obstruction is sudden and
complete, in a few hours. At first the color is the vivid jaundice
tint, a citron or salmon or yellow-saffron hue, but this gradually
loses its bright appearance, grows darker, and passes successively into
a brownish, bronze-like, and ultimately a {1087} dark olive-green,
which becomes the permanent color. Under some moral emotional
influences there may be a sudden change to a brighter tint, lasting a
few minutes, but otherwise the general dark olive-green hue persists
throughout. In a few instances, after some weeks of jaundice, the
abnormal coloration entirely disappears, signifying that the liver is
too much damaged in its proper glandular structure to be in a condition
to produce bile. Such a cessation of the jaundice is therefore of evil
omen.

Pruritus, sometimes of a very intense character, accompanies the
jaundice, in most cases appears with it, and in the supposed curable
cases it has persisted after the cessation of the discoloration. The
irritation may become intolerable, destroying all comfort, rendering
sleep impossible, and so aggravating as to induce a highly nervous,
hysterical state. The scratching sets up an inflammation of the skin,
and presently a troublesome eczema is superadded. In some of the cases
a peculiar eruption occurs on the skin and mucous membranes, entitled
by Wilson[192] xanthelasma. It has been carefully studied by Wickham
Legg,[193] who has ascertained the character of the changes occurring
in the affected tissues, and also by Mr. Hutchinson.[194] As a rule,
this eruption appears after several months of jaundice, and manifests
itself first on the eyelids, then on the palms of the hands, where it
makes the most characteristic exhibit, and after a time on the lips and
tongue. It occurs in irregular plaques of a yellowish tint slightly
elevated above the general surface, and rarely assumes a tubercular
form. As was shown by Hilton Fagge, xanthelasma occurs more especially
in the milder cases of catarrhal icterus that had been protracted in
duration, but it is also occasionally seen in the jaundice of
obstruction.

[Footnote 192: _Diseases of the Skin_, 6th ed., Lond., p. 773.]

[Footnote 193: _On the Bile, Jaundice, and Bilious Diseases_, p. 317
_et seq._]

[Footnote 194: _Medico-Chirurgical Transactions_, vol. liv. p. 171.]

According to the stage of the disease during which the examination is
made the liver will be enlarged or contracted; more or less tenderness
may be developed by pressure in the area occupied by the ducts, and a
tumor in a position to effect compression may possibly be detected. The
area of hepatic dulness will be increased in the beginning of all the
cases in which the obstruction is complete, but will remain normal so
long as the flow of bile persists despite the obstruction. When
enlarged, the liver can be felt projecting below the inferior margin of
the ribs, and with it, in most cases, the elastic globular body, the
gall-bladder. The state of the hepatic secretion, and in consequence
the duration of the obstruction, may be ascertained by puncture of the
gall-bladder and withdrawal of some of its contents for examination.
The presence of unaltered bile will indicate recent obstruction; of
serum, will prove long-standing interruption of bile-production. The
presence of concretions in the gall-bladder will indicate the character
of the obstructing cause, and an increased amount of bile of a normal
or nearly normal kind will be conclusive evidence that the obstruction
is in the course of the common duct. In a fatal case of permanent
occlusion examined by myself the cystic duct was closed by inflammatory
adhesions and the common duct was stopped up by a calculus.

The enlarged area of hepatic dulness will, in a protracted case, not
continue. The proper secreting structure, the hepatic cells, undergo
atrophy, {1088} and the increased connective tissue--to the development
of which enlargement of the organ is mainly due--contracts. The
ultimate result is that the liver becomes sclerosed, and is distinctly
smaller, the area of hepatic dulness diminishing to a greater relative
extent than the area of dulness due to hypertrophic enlargement. The
contraction of the liver goes on at the rate that several months are
required to make the result evident on percussion and palpation. Not
unfrequently, the contraction is too slight to affect the percussion
note of the right hypochondrium, and then, to realize the condition of
the organ, the history and rational signs must be closely studied.

Whilst the liver thus varies in size, the gall-bladder remains enlarged
and projects from the under surface of the organ, elastic, globular,
and distinctive. The shrinking of the liver from around it makes the
impression of growing size; it may be increasing, indeed, but more
frequently the enlargement is merely apparent.

Whether the liver be enlarging or diminishing in size, its functions
are impaired, or indeed entirely suspended. As the digestive canal
receives the bile immediately on its production, it will be best to
begin with the gastro-intestinal disorders which accompany occlusion of
the bile-ducts. The appetite is either wanting entirely and food is
loathed, or an excessive or canine appetite is experienced. The latter
belongs rather to an early stage of the disorder, and comes on after
the first disturbance of the stomach belonging to the immediate effects
of the occlusion. The former is the result of long-standing
interference with the primary assimilation. The tongue is coated with a
thick yellowish fur, which, drying, is detached in flakes, leaving the
mucous membrane beneath red, raw, fissured, and easily bleeding. The
taste is bitter, and the mouth has a pasty, greasy, and unclean
feeling. There is much thirst, and as a rule the patient experiences a
keen desire for acid drinks and for fresh fruits. The stomach is rather
intolerant of food, and nausea comes on as soon as it enters the
stomach. The mucus and stomach-juice accumulating over night, in the
morning there is much retching and nausea until the acid and rather
foul contents of the organ come up. When food is retained it causes
much distress, gases of decomposition accumulate, distending the
stomach and giving prominence to the epigastrium, and eructations of
offensive gas, with some acid liquid, occur from time to time.
Similarly, in the intestines the foods undergo decomposition instead of
normal digestion; gases of putrefaction are evolved, the abdomen
generally is swollen, and flatulent colic results. Very irritating fat
acids are liberated by the decomposition of the fatty constituents of
the food, which, with the acid products of the fermentation occurring
in the starch and sugar of the diet, cause a sensation of heat and
distress through the abdomen. Usually, the bowels are torpid, but in
some cases the stools are relaxed, having the consistence and
presenting somewhat the appearance of oatmeal porridge. They may be
firm, moulded, even hard. The gas discharged and the stools are
offensive, with a carrion-like odor. Sometimes decomposing articles of
food can be detected in the stools by very casual inspection--always,
indeed, when the examination is intimate. An excess of fat is also a
characteristic of the condition induced by occlusion of the ducts,
especially when the pancreatic duct is closed, as does happen in cancer
of the head of the pancreas.

{1089} A significant change in the color of the stools takes place.
They lose their normal brownish-red tint and become yellowish or
clay-colored or white, pasty, or grayish. Sometimes the stools are very
dark, tar-like in color and consistence, or more thin like prune-juice,
or in black scybalae. The most usual appearance of the stools in
occlusion is grayish, mush-like, and coarsely granular. The very dark
hue assumed at times or in some cases signifies the presence of blood.
A dark tint of the evacuations may be caused by articles of food, as a
greenish hue may be due to the use of spinach; a clay-colored tint to
the almost exclusive use of milk; a grayish tint to the action of
bismuth; a bilious appearance to the action of rhubarb; and many
others. When the occlusion is partial, although it be permanent,
sufficient bile may descend into the duodenum to color the stools to
the normal tint, and yet all the other signs of obstruction be present.

The bile-pigment, not having an outlet by the natural route, by the
intestine, passes into the blood; all the tissues of the body and the
various secretions and excretions, notably the urine, are stained by
it, constituting the appearance known as jaundice or icterus. This
malady has been described (see ante), but it is necessary now to give a
more specialized account of those conditions due more especially to the
prolonged obstruction of the biliary flow. These are a morbid state of
the blood; changes in the kidneys and in the composition of the urine;
a peculiar form of fever known as hepatic intermittent fever; and a
group of nervous symptoms to which has been applied the term cholaemia.

It has already been shown that but little pressure is required to
divert the flow of bile from the ducts backward into the blood. Changes
consequently ensue in the constitution of the blood and in the action
of the heart and of the vessels. The bile acids lower the heart's
movements and lessen the arterial tension; hence the pulse is slower,
softer, and feebler than the normal. Should fever arise, this
depressing action of the bile acids is maintained; and hence, although
the temperature becomes elevated, the pulse-rate does not increase
correspondingly. There are exceptions to this, however, in so far that
the heart and arteries are in some instances little affected, but it is
probable under these circumstances that there are conditions present
which induce decomposition of the bile acids.

The most important result of the action of the bile on the constitution
of the blood is the hemorrhagic diathesis. Soon after the occlusion
occurs in very young subjects--at a later period in adults--the
occlusion having existed for many months, in some cases only near the
end, the disposition to hemorrhagic extravasations and to hemorrhages
manifests itself. From the surface of the mucous membranes, under the
serous, in the substance of muscles, the hemorrhages occur. Epistaxis,
or nasal hemorrhage, is usually the first to appear, and may be the
most difficult to arrest. The gums transude blood, and wherever
pressure is brought to bear on the integument ecchymoses follow. The
conjunctiva may be disfigured and the eyelids swollen and blackened by
extravasations, and the skin of the cheeks and nose marked by stigmata.
Haematemesis sometimes occurs, but the extravasations into the
intestinal canal more frequently--indeed, very constantly--take place
in a gradual manner, and impart to the stools a dark, almost black,
tar-like appearance. In the same way the urine may contain fluid blood
and coagula, or it may have a merely smoky {1090} appearance from
intimate admixture with the blood at the moment of secretion.

Both the bile-pigment and bile acids exert an injurious action on the
kidneys. In cases of prolonged obstruction not only are the tissues of
the organ stained by pigment in common with the tissues of the body,
but the epithelium of the tubules, of the straight and convoluted
tubes, are, according to Moebius,[195] infiltrated with pigment. In
consequence of the size and number of the masses of pigment, the tubes
may become obstructed and the secretion of urine much diminished. Other
changes occur, due chiefly to the action of the bile acids, according
to the same authority. These alterations consist in parenchymatous
degeneration. The urine contains traces of albumen in most cases, and,
according to Nothnagel,[196] always casts of the hyaline and granular
varieties stained with pigment. As the alterations in the structure of
the kidneys progress, fatty epithelium is cast off, and thus the
tubules come finally to be much obstructed and the function of the
organ seriously impaired. To cholaemia then are superadded the peculiar
disturbances belonging to retention of the urinary constituents.

[Footnote 195: _Archiv der Heilkunde_, vol. xviii. p. 83.]

[Footnote 196: _Deutsches Archiv fur klin. Med._, vol. xii. p. 326;
also, Harley, _op. cit._, p. 503.]

One of the most interesting complications which arises during the
existence of obstruction of the bile-ducts is the form of fever
entitled by Charcot[197] intermittent hepatic fever. Although its
character was first indicated by Monneret,[198] we owe the present
conception of its nature and its more accurate clinical history to
Charcot. It does not occur in all cases. As has already been pointed
out, the passage of a gall-stone may develop a latent malarial
infection or a febrile movement comparable to that caused by the
passage of a catheter, and known as urethral fever. Charcot supposes
that true intermittent hepatic fever is septicaemic in character, and
can therefore arise only in those cases accompanied by an angiocholitis
of the suppurative variety--such, for example, as that which follows
the passage of calculi. Illustrative cases of this fever, one of them
confirmed by an autopsy, have been recently reported by E. Wagner,[199]
who is rather inclined to accept Charcot's view of the pathogeny. A
remarkable case has been published by Regnard,[200] in which the
angiocholitis was induced by the extension of echinococcus cysts into
the common duct. Whilst there are some objections to Charcot's theory,
on the whole it is probably true that this intermittent hepatic fever
is produced by the absorption from the inflamed surface of the ducts of
a noxious material there produced. It may be likened to the fever which
can be caused by the injection of putrid pus into the veins of animals.

[Footnote 197: _Lecons sur les Maladies du Foie, etc._, p. 178 _et
seq._]

[Footnote 198: Cyr, _Traite de l'Affection calculeuse du Foie_, p.
193.]

[Footnote 199: _Deutsches Archiv fur klin. Medicin_, vol. xxxiv. p.
529.]

[Footnote 200: _Gazette med. de Paris_, No. 49, 1873, quoted by Wagner,
_supra_.]

Intermittent hepatic fever, as its name implies, is a paroxysmal fever,
having a striking resemblance to malarial fever, but differs from it in
less regularity of recurrence, in the fact that urea is below the
normal amount instead of increased, and in the effect of quinine, which
in the case of malarial fever is curative, but not curative in hepatic
fever. The paroxysms are sometimes quotidian, rarely double quotidian,
tertian, quartan, and even longer, and in the same case all of these
varieties may occur; on {1091} the other hand, there may be entire
regularity of the seizures. The severity of the chill, the maximum
temperature, and the amount of sweating vary within considerable
limits; there may be merely a slight sense of chilliness or a severe
rigor; the temperature may rise to 101 degrees or to 104 degrees F.,
and there may be a gentle moisture or a profuse sweat. There does not
seem to be any relation between the extent and severity of the local
mischief and the systemic condition.

The period of onset of intermittent hepatic fever, and its duration and
mode of termination, are by no means readily determined. Cyr fixes on
the paroxysms of colic as the beginning, but he obviously confounds the
chill and fever caused by the passage of a calculus with the true
intermittent hepatic fever. In a carefully-observed case, the facts
confirmed by an autopsy, E. Wagner[201] gives the clinical history of a
typical example of this malady: Gall-stones were found in the duodenum,
in the common and cystic ducts, but the most important one was a
polyangular stone obstructing the hepatic duct. There was an ulcer with
thickened margin at the entrance to the gall-bladder, and the mucous
membrane of the common duct near the intestinal orifice had a smooth,
cicatricial aspect of recent origin, indicating inflammatory
ulceration. The conditions favorable to the production of a morbid
material of a kind to induce septicaemic fever were therefore present.
The onset of fever occurred ten days after the last seizure, time being
thus afforded for the local changes necessary. The duration of the
fever in this case was five months, but the existence of pulmonary
phthisis with cavities will explain this apparently protracted hepatic
intermittent fever. The duration of the disease in its usual form is
uncertain, and ranges between a week and two months, or even three
months, according to Charcot.[202]

[Footnote 201: _Deutsches Archiv fur klinische Medicin_, Band xxxiv. p.
531, 1884.]

[Footnote 202: _Lecons sur les Maladies du Foie_, p. 180.]

Suspension of work by the liver necessarily involves retention in the
blood of various excrementitious matters. The attempt of Flint[203] to
establish the doctrine of cholesteraemia has not been supported by the
evidence of contemporary or subsequent physiologists. This theory
denies to the other constituents of the bile any morbific action, and
concentrates those disturbances known as cholaemia on the effects of
cholesterin. As uraemia signifies not merely the presence of urea in
the blood, but of all of the toxic substances excreted by the kidneys,
so the word cholaemia comprehends all the constituents of bile having
power to derange the organism by their presence in the blood.

[Footnote 203: _The American Journal of the Medical Sciences_, 1862, p.
349 _et seq._]

By cholaemia is meant those disturbances, chiefly nervous, which are
due to the presence of biliary excrementitious matters in the blood,
and not less to the effect on nutrition of the absence of bile from the
process of digestion in the intestine. As the atrophic changes proceed
in the liver, the quantity of urea and uric acid in the urine
diminishes, and presently leucin and tyrosin appear. Amongst the means
of differential diagnosis of hepatic intermittent fever from malarial
fever Charcot mentions the quantity of urea present--in the former
greatly lessened, in the latter much increased. There is, however, a
source of fallacy here not mentioned by Charcot: that is, the
variations in the amount of urea due to destruction of the hepatic
secreting structure. It follows that as changes {1092} occur in the
kidneys, to the condition of cholaemia is superadded the derangements
belonging to uraemia.

When the occlusion has existed for some time--a variable period, partly
due to peculiarities of individual structure--there come on certain
characteristic symptoms of nervous origin: headache, hebetude of mind,
dull hearing, obscure or hazy vision, xanthopsia; somnolence and
greatly increasing stupor, leading into coma; rambling and incoherence
of mind, passing into delirium; muscular twitching, subsultus; muscular
weakness, deepening into paralysis; and finally, it may be, general
convulsions. As these derangements of the nervous system develop, a
light febrile movement supervenes, so that the whole complexus has the
typhoid type, or, as it can be more definitely expressed, the patient
thus affected lapses into the typhoid state.

COURSE, DURATION, AND TERMINATION.--Occlusion of the gall-ducts is an
essentially chronic malady in the greatest number of cases. As a rule,
the causes of obstruction operate slowly, but to this rule there are
exceptions. Permanent occlusion may take place suddenly, as when a
gall-stone is impacted immovably in the common duct, or when a
round-worm makes its way into the duct and is firmly fixed there,
incapable of further movement.

When occlusion is once effected the gradual changes occurring in the
liver lead to slow decline of the nutrition; the bile-elements
circulating in the blood poison it and set up alterations in the
structure of the kidney, and ultimately, the brain becoming affected,
the end is reached by convulsions and coma. Although permanent
occlusion, if unrelieved, terminates in death, a small proportion of
cases get well, either in consequence of giving way of the obstructing
cause or from the opening of a new route to the intestine. Thus, a
calculus lodged in the fossa of Vater may suffer such injury to its
outer shell as to yield to the action of solvents, or, suppuration
occurring around it, the stone may be loosened and forced onward, or
ulceration may open a channel into the bowel. An incurable malady
causing the occlusion, the termination in death is only a question of
time. The duration of any case must be indefinite. There are several
factors, however, whose value can be approximately estimated. When the
obstructing cause is merely local--as, for example, a gall-stone or the
cicatrix of a simple ulcer--the duration of the case is determined by
the mere effect of the suspension of the hepatic functions. As the
eliminating action of the liver and the part played by the bile in the
intestinal digestion are necessary to life, it follows that the
complete cessation of these functions must lead to death. The rate at
which decline takes place under these circumstances varies somewhat in
different subjects. Probably two years may be regarded as the maximum,
and three months the minimum, period at which death ensues when no
other pathogenetic factor intervenes.

DIAGNOSIS.--To determine the fact of occlusion is by no means
difficult: the persistent jaundice, the absence of bile in the stools,
and the appearance of the bile-elements in the urine are sufficient. It
is far different when the cause of the occlusion is to be ascertained.

The ease and safety with which the exploring-trocar can be used in
cases of supposed obstruction of the cystic duct enable the physician
to decide with confidence points which before could only be matters of
mere {1093} conjecture. The writer of these lines was the first to
puncture the gall-bladder and to explore, by means of a flexible probe
passed through the canula, the course of the duct.[204] It is possible
in this way to ascertain the existence of gall-stones in the
gall-bladder, to find an obstruction at the entrance of the cystic
duct, to demonstrate the presence of echinococci cysts, and to remove
for microscopical examination pathological fluids of various kinds.
More recently, Whittaker and Ransohoff[205] of Cincinnati have
attempted the detection of a gall-stone impacted at any point by the
introduction of an exploring-needle; and this practice has been
imitated by Harley[206] of London, but without any reference to the
pioneer and prior investigation of his American colleagues. The case of
Whittaker and Ransohoff survived the exploratory puncture, but Harley's
case proved fatal from traumatic peritonitis. Notwithstanding this
untoward result, Harley persists in the advocacy of this method. It
must appear to any one familiar with the intricate arrangement of the
parts composing the anatomy of this region a most hazardous proceeding,
and hardly to be justified in view of the superior safety and certainty
of my method. To explore the interior of the gall-bladder an
aspirator-trocar is introduced; any fluid intended for microscopical
examination is then withdrawn, and through the canula a flexible
whalebone bougie is passed.

[Footnote 204: _The Cincinnati Lancet and Clinic_ for 1878-79; also, W.
W. Keen, M.D., "On Cholecystotomy," _The Medical News_, Sept., 1884.]

[Footnote 205: _Lancet and Clinic_, 1884.]

[Footnote 206: _Lancet_ (London), July, 1884.]

When icterus comes on in a few days after birth and persists until
death ensues by convulsions and coma, there can be no doubt regarding
congenital absence or impermeability of the common duct. Permanent
retention-jaundice, accompanied by the characteristic symptoms of that
condition immediately succeeding an attack of hepatic colic, is
probably due to impaction by a calculus. When, at or after middle life,
in a patient with a history of former attacks due to gall-stones, there
begins a fixed pain in the right hypochondrium, and subsequently
retention-jaundice, the existence of a malignant growth in connection
with the cicatricial tissue and ancient organized exudation should be
suspected; and this suspicion will be confirmed if subsequently a tumor
can be felt. If with a localized pain slowly-developing jaundice,
intestinal indigestion, fats and oils appearing unchanged in the
stools, and a condition of prostration more than is properly referable
to the derangement of the hepatic functions, come on in a man or woman
after thirty-five, cancer of the head of the pancreas should be
suspected; and this suspicion will be confirmed if a tumor can be
detected in that situation. It should not be forgotten, however, that
in emaciated subjects the head of the pancreas may be so prominent as
to be mistaken for a scirrhous growth.

A pulsating tumor of the right hypochondrium, accompanied by jaundice,
may be an aneurism of the hepatic artery. Pulsation may be communicated
to a bunch of enlarged portal lymphatic glands, which will compress the
common duct, but in this case, as the increase in the size of the
glands is due to caseous, amyloid, or cancerous deposits, there will be
found a source whence these morbid products are derived, and will
explain the nature of a tumor thus constituted.

The differentiation of hypertrophic cirrhosis from occlusion of a
slowly-forming character is by no means easy. In both jaundice {1094}
gradually appears; in both the liver is enlarged, but in hypertrophic
cirrhosis much more than in occlusion; and in the latter the
gall-bladder is full--may indeed be distended--whilst in the former it
is empty or contains but little bile. The history of the case may
indicate the nature of the symptoms. Previous attacks of hepatic colic,
and the symptoms of occlusion supervening on the last, are highly
significant of calculous occlusion.

TREATMENT.--To ascertain the nature of the occlusion is a necessary
preliminary to any exact treatment. In many cases this must remain a
mere conjecture, when, of course, the treatment is only symptomatic.
When it is probable or certain that the duct is obstructed by a
calculus, two methods may be resorted to for its removal: one method is
to break up the calculus by mechanical means; the other is to effect
its solution by chemical agents.

Fracture of an impacted calculus is not a merely fanciful expedient. If
the site of the obstruction is ascertained, an attempt may be made to
penetrate the calculus by an aspirator-needle passed through the
abdominal walls, according to the method of Whittaker and Ransohoff.
The dangers attendant on this mere puncture are great, and a fatal
result has occurred in one of the very few cases in which it has been
done. Less severe and dangerous methods for attempting the
disintegration of a calculus should be first tried, as follows: Make
firm friction with the fingers along the inferior margin of the ribs
and toward the epigastrium and umbilicus, whilst the opposite side
posteriorly is supported by the hand spread out and applied firmly. A
strong faradic current sent through the region of the gall-bladder and
ducts has in several instances seemed to do good--indeed, to remove
obstructions. A calculus impacted may be dislodged either by the
fracture of its surfaces or by the strong muscular contractions of the
abdominal walls and of the muscular layer of the duct. Most calculi are
easily broken, and when the smallest breach is made in the external
crust disintegration follows; and some calculi are so friable as to
yield to slight pressure. Furthermore, the slightest solution in the
continuity of the rind disposes the whole mass to dissolve in suitable
menstrua. Mechanical rupture is so important a step in the process of
disintegration of an impacted calculus that so serious an operation as
section of the abdomen as a preliminary to it should be considered. The
cavity exposed, the obstructed duct is found, and its retained calculus
is mashed without section of the duct. I find one instance[207] in
which this was done as a subordinate part of a cholecystotomy, and the
breaking up of the stone proved to be easy of accomplishment. It is
also the method of Tait, who proposes to mash the calculus by means of
suitable forceps fitted with padded blades.

[Footnote 207: Harley's case, _op. cit._]

I have suggested a means of effecting solution of an impacted calculus
which seems, on further reflection, well worthy of consideration. The
proposal is to inject, through a canula introduced into the
gall-bladder, one of the solvents of the cholesterin calculus before
mentioned. I have already used the canula as a duct for the passage of
an exploring-sound, and have by means of it explored the interior of
the gall-bladder. It is quite as feasible to inject through the canula
a solvent, successive charges of which can be thrown in and withdrawn
by the aspirator.

{1095} That the usual solvents introduced by the stomach can effect the
solution of impacted calculi has been declared impossible by
Trousseau;[208] and with this conclusion I unhesitatingly agree. I have
already discussed this part of the subject, and need now only refer the
reader to that section.

[Footnote 208: _Clinique medicale_, _loc. cit._]

The various causes of obstruction besides calculi do not offer an
inviting field for the exercise of therapeutical skill. Each case must
be treated according to the nature of the obstructing cause; hence to
make an accurate diagnosis is an essential preliminary to suitable
treatment.


IV. DISEASES OF THE PORTAL VEIN.


Thrombosis and Embolism of the Portal Vein; Stenosis; Pylephlebitis.

DEFINITION.--By the terms at the head of this section are meant the
various pathological processes which induce coagulation of the blood in
some part of the portal system. As the portal vein is made up of many
branches coming from the various organs of the abdominal cavity except
the kidneys, and as it empties, so to speak, into the liver, it is
obvious that various and complex derangements will ensue on the
formation of thrombi.

CAUSES.--Thrombosis of the portal vein occurs under three general
conditions: the blood is in a readily coagulable state; the action of
the heart is weak and the blood-current sluggish; the circulation
through the vein is impeded by external pressure. The coagulability of
the blood is increased in diseases characterized by an excess of its
fibrin-producing constituents, of which cirrhosis of the liver may be
mentioned as one having this peculiarity. In chronic maladies of a
depressing kind there may be simply a weak action of the heart, or the
muscular tissue of the organ may be affected by a fatty and atrophic
degeneration. The external pressure by which the blood-current through
the vein is impeded may be caused by the newly-formed connective tissue
of Glisson's capsule, by enlarged lymphatics in the hilus of the liver,
or by tumors of various kinds. The first named of these causes of
compression--atrophic cirrhosis--is most frequently acting. Very
rarely, organized exudations of the peritoneum may be so situated as to
compress the portal vein. This result can only happen when the hepatic
portion of the peritoneum is involved.

Pylephlebitis exists in two forms: the adhesive and suppurative. The
former results in changes not unlike those of simple thrombosis. The
blood coagulates in the affected part of the vessel, the clot is
organized, and the vessel ultimately forms a solid rounded cord which
is permanently occluded. The suppurative variety is so different in its
origin and in its results that it requires separate treatment, and I
therefore postpone the consideration of it to the next section.

{1096} SYMPTOMS OF THROMBOSIS AND ADHESIVE PYLEPHLEBITIS.--It is a
remarkable fact that the biliary function of the liver is not
necessarily affected in cases of occlusion of the portal vein. It is
true, in advanced cases of cirrhosis, when the interlobular veins are
obliterated by the pressure of the contracting newly-formed connective
tissue, the functions of the liver are arrested in so far as the damage
thus caused extends. Notwithstanding the blocking of the portal,
sufficient blood reaches the hepatic cells by the anastomosis between
the hepatic artery and the interlobular veins--an anatomical connection
demonstrated by Cohnheim and Litten.[209] So long as this anastomosis
continues bile will be formed, although the portal vein is occluded.

[Footnote 209: _Virchow's Archiv_, Band lxvii. p. 153, "Ueber
Circulationsstorungen in der Leber."]

The most significant symptoms of thrombosis of the portal vein are the
sudden formation of ascites, which quickly assumes a very high grade,
and equally sudden passive congestion of the gastro-intestinal mucous
membrane, enlargement of the spleen, and distension of the superficial
veins of the abdominal parietes. When these symptoms succeed to
cirrhosis of the liver, or appear after the formation of a tumor in the
hepatic region, or come on in the course of phthisis or chronic
inflammation of the hepatic peritoneum, the existence of thrombus of
the portal vein may be reasonably suspected.

Coincidently with the occlusion of the portal vein the
gastro-intestinal mucous membrane becomes the seat of a catarrhal
process, and to the fluid thus produced is added a much more abundant
transudation from the distended capillaries. Nausea, vomiting, and
diarrhoea result, the rejected matters being serous, watery, and in
many cases tinged with blood. Now and then quite a severe hemorrhage
takes place, and the blood is brought up by vomiting (haematemesis) or
is discharged by stool. Hemorrhoids form, and, in large masses
protruding, much pain is experienced, and free bleeding may result from
rupture of a distended vein.

The veins of the abdominal parietes, which in the normal state are
invisible or at least not prominent, and which form anastomoses with
the portal, when the obstruction occurs dilate, sometimes to a
remarkable extent. The most important anastomosis is that between the
femoral and saphena and internal mammary and epigastric veins. When the
hepatic branches of the portal are closed, but the trunk remains
pervious, the parumbilical vein enlarges greatly, and, communicating
with the superficial veins of the anterior part of the abdominal walls,
forms a radiating network of tortuous veins to which is given the
striking title of caput Medusae.

The most significant symptom of portal thrombosis is a quickly-forming
ascites. It is true, ascites is a common symptom in advanced cirrhosis,
but the rapid accumulation of fluid and the prompt filling of the
cavity after tapping distinguish that which arises from portal
thrombosis from all others. Besides its excessive extent, the ascites
presents the usual symptoms.

Due to the same cause as the enlargement of the superficial veins, the
hemorrhages, the ascites, etc., there occurs considerable hypertrophy
of the spleen in many of the cases. It sometimes happens that the new
compensatory circulation and the hemorrhages from some part in the
{1097} usual route of the portal so dispose of the blood that the
spleen does not enlarge sufficiently to be readily made out.

COURSE AND TERMINATION.--It is obvious that a condition such as that
induced by thrombosis of the portal must be comparatively quickly
fatal; but the cases vary in duration as the compensatory circulation
is more or less complete. Whilst the majority of cases terminate within
two weeks, instances of several months' duration are not unknown, but a
fatal termination, sooner or later, is inevitable in all cases.

Coming on in the course of some chronic affection of the liver or some
obstructing cause exterior to the organ, there soon follow ascites,
nausea and vomiting, haematemesis, bloody stools of a liquid character,
enlargement of the spleen, distension of the abdominal veins, and the
distressing symptoms produced by an excessive accumulation of fluid in
the peritoneal cavity.

DIAGNOSIS.--As there is no symptom of thrombosis of the portal which
may not be caused by advanced cirrhosis, the diagnosis rests on the
rapid production of the attendant phenomena and their conjoint
appearance.

TREATMENT.--A symptomatic treatment is alone possible. The highly
irritable and congested intestinal mucous membrane precludes the
employment of hydragogue cathartics. Salines which cause outward
diffusion from the vessels are the only cathartics which can be used
with propriety. Action of the kidneys and of the skin must be
maintained. To this end the resin of copaiba in pilular form and
pilocarpine subcutaneously may be used. If the strength of the patient
will permit, leeches around the anus can be applied, and much relief
may be expected from free bleeding. It is probable that opening a
swollen hemorrhoid would give the same kind of relief as that caused by
a free hemorrhage. In any case the benefit derived from treatment must
be merely palliative and temporary.


Suppurative Pylephlebitis.

PATHOGENY.--Primary pylephlebitis rarely if ever occurs. On the other
hand, the secondary form is by no means uncommon; it succeeds to
ulcerative or purulent inflammation at some point in the circuit of
origin of the portal radicles. The most frequently-occurring cause is
ulceration and suppuration of some part of the intestinal tube, and
hence the most common result is multiple abscess of the liver.
Pylephlebitis has often resulted from typhlitis; from ulcers of the
large intestine, as in dysentery; from such traumatic injuries as tying
hemorrhoids; from proctitis; from ulcers of the stomach and similar
morbid processes elsewhere within the range of origin of the portal
system. The pathogeny is clear. The inflammatory or ulcerative action
extends to and involves the walls of the veins, or some morbid material
diffuses through the vein walls. In either case coagulation of the
blood in the vessel ensues, and the clot undergoes a series of changes
resulting in the formation of emboli, which, carried into the main
current, are subsequently lodged in the hepatic capillaries.

There are three steps in the morbid process: the changes in the vein
wall; the production and transformation of the thrombus; and the
formation of secondary suppurating foci in the liver.

{1098} The appearance of the tunics of the inflamed vessels varies with
the stage at which they are examined. At first the walls of the vessels
are reddish from congestion, succulent, and swollen, infiltrated by
leucocytes and inflammatory exudation and the cellular elements
undergoing proliferation. The intima especially is much altered in its
appearance and structure, becoming thick, opaque, grayish or yellowish
in color, and having adherent to it a thrombus passing through its
characteristic changes. Ulceration of the intima then occurs, and the
purulent elements, with shreds of tissue, mingle with the degenerating
blood-clot, and ultimately there remains a purulent depot lined with
sloughing, even gangrenous, contents. Emboli detached from such
decomposing thrombus are arrested in the vessels of the liver, and
there set up a suppurating phlebitis, ending in an abscess formation,
or a quantity of pus from the original point of ulcerative phlebitis
passes into the portal vein, and is generally distributed through the
hepatic branches, here and there foci of suppuration being established
by the deposit of decomposing emboli. There may be numerous small
abscesses irregularly distributed through the liver, or there may be
one or two larger collections of pus. Very often the vessel whose
occlusion by a suppurating embolus has caused the mischief is
destroyed, and hence no communication with the abscess-cavity can then
be traced. These abscesses are not limited by a line of inflammatory
demarcation or by a limiting membrane, but the hepatic tissue adjacent
is congested and infiltrated with pus.

Ulceration, abscesses, or purulent inflammation occurring at any point
within the area of origin of the radicles of the portal vein may induce
pylephlebitis and consequent hepatic abscess. There are two points at
which, suppuration established, secondary pylephlebitis is most apt to
occur: the caecum; the rectum. As respects the former, the symptoms of
typhlitis precede the hepatic disturbance; and as respects the latter,
usually dysentery, or rather proctitis, is the initial disease. In both
sources of the hepatic trouble the inferior hemorrhoidal veins are
chiefly concerned--a fact explicable by reference to the sluggishness
of the circulation and the distended condition of these veins, whence
it is that thrombus is very readily induced. Numerous instances of
pylephlebitis following suppurative lesions of the caecum have been
reported. One of the most recent, and at the same time typical,
examples of such conditions is that published by Bradbury[210] of
Cambridge, England. The initial lesion was "an ulcer the size of a
split pea" situated near "the junction of the vermiform appendix and
caecum." "The hemorrhoidal veins and the inferior mesenteric above were
filled with breaking-down clot and pus," and "the liver contained many
abscesses of various sizes, the largest about the size of a lemon,
which had burst through the diaphragm." As is so often the case, the
ulcer of the caecum produced no recognizable disturbance, and important
symptoms were manifest only when the emboli lodged in the liver set up
suppuration, when there occurred the usual signs of hepatic abscess. In
the West and South hepatic abscess due to pylephlebitis, induced by
proctitis, with ulceration of the rectum, is a common incident. Various
examples of this kind have fallen under my own observation. The
relatively greater frequency of this form of pylephlebitis is due to
the fact above {1099} stated, that the inferior hemorrhoidal veins are
voluminous, have a sluggish current, and are liable to over-distension
by pressure of feces and by external abdominal bands and clothing.
Cases of a corresponding character arise from suppuration and
ulceration elsewhere within the portal circuit. Thus, Bristowe[211]
reports a case in which pylephlebitis resulted from an ulcer of the
stomach, the neighboring veins becoming implicated and the usual
results following.

[Footnote 210: _The Medical Times and Gazette_, Sept. 27, 1884, p. 450,
"Proceedings of the Cambridge Medical Society."]

[Footnote 211: _Transactions of the Pathological Society of London_,
vol. ix. p. 278.]

When inflammation has begun in a radicle of the portal vein, it may
proceed to the liver by contiguity of tissue, the whole intervening
portion of the vessel being affected. Probably more frequently the
intra-hepatic portion of the portal is inflamed by emboli, and the
adjacent hepatic tissue then undergoes suppuration, as has been already
set forth.

SYMPTOMS.--There being two points of disease--the primary lesion of the
peripheral vessel and the secondary results in the hepatic portion of
the portal--the symptomatology must have a corresponding expression.
The stomach, the caecum, or the rectum, or some other organ or tissue,
being occupied by a morbid process, there will be a characteristic
complex of symptoms. Taking up the most usual primary disturbance, a
typhlitis or an ulcer of the caecum, there will be pain, tenderness,
and possibly fever, occupying in point of time the period proper to
such a malady and an amount of disturbance of function determined by
the extent of the lesion. The symptoms caused by a single small ulcer
of the caecum, as in the example narrated by Bradbury, may present no
characteristic features and may have little apparent importance, and
yet the lesion is productive of very grave consequences.

When from any of the causes mentioned above a thrombus forms in a vein
of the portal system in consequence of the extension of the
inflammation about it, the case, what importance soever it previously
had, now takes on new characters. The onset of the inflammation of the
vein walls and the puriform degeneration of the thrombus is announced
by a chill--a severe rigor, or chilly sensations at least. At the time
of the chill, and sometimes before it, pain is felt, significant of the
lesion in the vein. When proctitis or typhlitis precedes the
pylephlebitis, pain appropriate to the malady is a significant symptom;
but the pain which comes on with the beginning of the inflammation in
the liver is a new sign. The most frequent sites of the pain are the
right hypochondrium and the epigastrium, but it may also be felt in the
left hypochondrium or in either iliac fossa. Unless there be diffuse
peritonitis the pain is accompanied by a strictly-localized tenderness
to pressure. The situation of the pain may afford an indication of the
vein attacked, and when there are two points at which pain is
experienced, one may originate at the first situation of the morbid
action; the other will be due to pylephlebitis.

The fever succeeding the chill is decided, and in some cases may attain
to extraordinary height--a manifestation indicative of the pyaemic
character of the affection. The fever intermits or remits, with a more
or less profuse perspiration. The febrile phenomena are similar in
their objective expression to malarial fever, but there is an important
difference in respect to the periods of recurrence of the chills. The
paroxysms are very irregular as to time: there may a daily seizure at
different hours, or there may be several chills on the same day. In
other words, the {1100} paroxysms have the pyaemic characteristics
rather than the malarial. After a time the intermittent phenomenon
ceases, and there occurs a remission merely, the exacerbation being
preceded by chilliness and succeeded by sweating. The sweats are
characteristically profuse and exhausting. During the sweating the
temperature begins to decline, and reaches its lowest point just before
the chilly sensations during the early morning announce the onset of
the daily exacerbation of the afternoon and evening. The thermal line
exhibits many irregularities until the febrile movement assumes the
remittent type, when there occur the morning remission and nocturnal
exacerbation. The maxima may be from 103 degrees F. to 105 degrees,
even to 106 degrees.

When the pain and chill come on, disturbances of the digestive organs
ensue. When a large vein of the portal system is occluded, the
remaining veins must be over-distended, and congestion of a part or of
all of the digestive tract will be a result. An acute gastric catarrh
is set up. The appetite is lost, the stomach becomes irritable, and
vomiting is a usual incident. Sometimes the disgust for food is
extreme, and the nausea and vomiting are almost incessant. The vomited
matters consist of a watery mucus mixed with thin bile after a time,
and now and then of a bloody mucus. Thrombosis of a stomach vein may
occur, to be followed by an acute ulcer, and from this considerable
hemorrhage may proceed, when the vomit will consist of blood. Such an
accident, happening to the mucous membrane of the intestine, will be
indicated by bloody stools if the ulceration is low down, or by
brownish, blackish, or chocolate-colored stools if higher up in the
small bowel.

The tongue has usually a characteristic coating in these cases. Large
patches of a rather heavy and darkish fur form, and, cast off from time
to time, leave a glazed and somewhat raw surface. Sometimes there is a
profuse salivary flow, but more frequently the mouth is dry. The lips
are fissured or contain patches of herpes, and the buccal cavity may be
more or less completely lined by patches of aphthae.

Diarrhoea is a usual symptom, the stools being dark when mixed with
blood, or grayish and pasty or clay-colored when there is jaundice.

Three-fourths of the cases of pylephlebitis are free from jaundice.
This symptom may occur at the onset when the common duct is obstructed
by a calculus, but in other cases it appears when the formation of pus
in the liver exerts sufficient compression of the hepatic ducts to
prevent the passage of the bile.

When jaundice occurs, it is accompanied by the usual symptoms. The
urine, previously unchanged, is now colored by bile-pigment, and the
alterations in the renal structure and function belonging to jaundice
also take place.

It sometimes happens that the obstruction of the portal vein is
sufficient to cause enlargement of the superficial veins of the
abdomen, but the duration of the disease is usually too brief to permit
much deviation from the normal, except rarely. In the cases
characterized by the occurrence of diffuse peritonitis the abdomen will
present a swollen and tense appearance, and there will be acute
tenderness to pressure. The area of hepatic and splenic dulness is not
increased from the outset, but is evident, as respects the spleen, soon
after the obstruction at the liver, and as respects the liver when the
formation of abscesses occurs.

{1101} COURSE, DURATION, AND TERMINATION.--The course of pylephlebitis
is compounded of the disturbance at the original point of disease, and
of the secondary inflammation at the several points in the liver where
emboli set up purulent inflammation. There are, therefore, two distinct
symptom-groups, and a short intervening period in which the first is
being merged into the second. The duration is variable, but the extreme
limits are not remote from each other, the condition of pylephlebitis
terminating in from two weeks to three months, the shorter being the
more usual. The termination is death, doubtless invariably; for, as in
true pyaemia arising from other causes, the septic changes in the blood
are such as to preclude the possibility of a return to the normal
condition.

DIAGNOSIS.--The main point in the diagnosis consists in the occurrence
of an evident local inflammation, followed by the signs of suppuration
in the hepatic region coming on subsequent to ulceration and
suppuration at some point in the peripheral expansion of the portal
system. Thus, when a proctitis with ulceration of the rectum has been
in existence for some time, there occur pain and tenderness in the
hepatic region, accompanied by an irregularly intermittent fever and by
profuse sweating, it can be assumed with considerable certainty that
emboli have been deposited in some one or more of the terminal branches
of the portal. The evidences of hepatic trouble--swelling of the organ,
jaundice, etc.--and of portal obstruction, which then supervene,
indicate with some precision the nature of the case.

TREATMENT.--Although pylephlebitis wears a most unfavorable aspect, the
possibility of a favorable result should always be entertained by the
therapeutist.

As absorption of medicaments must be slow--indeed, uncertain--by the
gastro-intestinal mucous membrane when there is portal occlusion, it is
well to attempt treatment by the skin and subcutaneous connective
tissue. Gastro-intestinal disturbance--nausea, vomiting, and
diarrhoea--should be treated by a combination of bismuth, creasote, and
glycerin--remedies acting locally chiefly. Ammonia--the carbonate and
solution of the acetate--is indicated, and should be given for the
purpose of dissolving thrombi and emboli. Corrosive sublimate, carbolic
acid, and quinine can be administered by the subcutaneous areolar
tissue. Quinine may also be introduced by friction with lard, and in
considerable quantity.


V. PARASITES OF THE LIVER.


Echinococcus of the Liver; Hydatids of the Liver.

DEFINITION.--The echinococcus is the intermediate or larval stage in
the development of the Taenia echinococcus--the completed
parasite--whose chief habitat is the intestine of the dog. As the
natural and clinical history of parasites is elsewhere treated of, the
subject is here confined to the development of echinococci cysts in the
liver, its ducts, and vessels.

CAUSES.--The presence of echinococcus vesicles in the liver is due to
{1102} the migration of the embryo from the intestinal canal. As
Davaine[212] has ascertained by analysis of all the recorded examples
previous to the publication of his treatise, echinococci are found in
as large a proportion in the liver as in all the other organs combined.
This statement is repeated with approval by Cobbold[213] and by
Heller.[214] The embryo, set free in the intestine from the food or
drink containing the ova, starts on its migration. There are several
reasons why the liver is selected for its habitat: it is the largest
accessible organ; the common duct and the portal vein offer the most
convenient roadway for reaching and penetrating its substance. The
exact route or routes of which the parasite avails itself in migrating
have not been definitely settled, although Friedreich has shown that
the portal vein is the medium of transmission of the Echinococcus
multilocularis. The comparative frequency with which the liver is
entered indicates that the portal vein is the favorite route of
migration.

[Footnote 212: _Traite des Entozoaires et des Maladies vermineuses,
etc._, par C. Davaine, Paris, 1877, p. 383.]

[Footnote 213: _Entozoa_, by T. Spencer Cobbold, M.D., F.R.S., London,
1874, p. 275.]

[Footnote 214: In vol. iii of _Ziemssen's Cyclopaedia_, p. 561.]

PATHOLOGY AND SYMPTOMS.--The number of echinococci reaching the liver
varies from one to ten or twelve or more. They increase in size from
the time of their deposit in the organ, and ultimately attain to large
proportions. The rapidity of growth depends somewhat on the character
of the tissue in which imbedded, and the amount of disturbance of
function is determined by the position of the parasite in the organ.
Echinococci may be deposited in any part of the liver--in the substance
of the organ, in the ducts, or in the vessels--but the most usual site
is near the capsule, and, developing outwardly in the direction of
least resistance, impart to the outline of the organ an irregular
contour. As the echinococci develop, the adjacent parts of the liver
pressed upon undergo atrophy, but the connective tissue of the organ
contributes to the formation of the dense capsule which envelops them.
But as the increase in size is not rapid, although continuous, if the
cysts are situated at the periphery and adjacent to the capsule, they
may be present for many months without causing any distinct symptoms.
In a case occurring under my own observation last year the only symptom
which attracted attention was an enlargement of the hepatic region, and
on examination a characteristic elastic, irregular, and painless tumor
could be readily detected by sight and touch occupying the right
hypochondrium and extending into the epigastric and umbilical regions.
When the echinococci cysts impinge on the portal vein or on the hepatic
duct, there will be caused the usual results of such pressure--ascites
or jaundice, or both conditions may occur simultaneously, with
obstruction of both vein and duct. When the cysts develop downwardly,
the stomach and intestines will be displaced, and nausea and vomiting,
diarrhoea or constipation, and, it may be, considerable pain of a
colic-like character, will be caused. An upward development of the
cysts gives rise to more pronounced disturbances. The diaphragm is
pushed upward, the heart displaced, and the lungs, especially the
right, compressed. Occasionally the diaphragm is softened and
perforated by the pressure of the enlarging cysts, and the lungs are
ultimately tunnelled, the parasites being discharged by the bronchi.

{1103} The growth of an echinococcus tumor may spontaneously cease, and
then retrograde changes take place, leading to its final disappearance.
This arrest of development may occur without any obvious cause, but now
and then such a change from the ordinary course of tumors may be
effected by an external injury, as a blow on the abdomen, but more
frequently the death of the parasite is caused by ulceration into a
bile-duct, and the entrance of bile, which is a poison to these
hydatids. It sometimes happens that, opening into a duct of large size,
the daughter and granddaughter vesicles are slowly discharged through
it into the intestine, and thus a cure is effected. Inflammatory action
occurring in the cysts, adhesions may form and rupture into a
neighboring cavity take place. Direct communication may be established
with the intestine, or the cavity of the pleura or peritoneum be
entered, with results entirely disastrous.

A necessarily fatal termination must also ensue when the hydatids
penetrate the ascending vena cava, but this accident is, fortunately,
very rare.

The passage outward through the abdominal wall is an exceedingly
uncommon but fortunate issue of echinococcus of the liver, for in this
mode the hydatids may be discharged without much difficulty.

The echinococcus vesicle is enveloped in a dense, resisting, and
elastic capsule, constructed out of the connective tissue of the part
in which it is deposited. The innermost layer of the vesicle is the
germinative (endocyst), and from its granular surface are developed the
brood-capsules and their scolices--_i.e._ the head with its suckers and
crown of hooklets.[215] Each vesicle may contain not only daughter, but
also granddaughter, progeny, numbering from a dozen up to many
thousands, and they will vary in size from the head of a pin to a
pullet's egg. It follows that the mother vesicles must also greatly
vary in size: they range from a large pin's head to a child's head. The
vesicles or sacs contain a clear, faintly yellowish, or opalescent
fluid, neutral or slightly alkaline in reaction, and holding in
solution a large per cent. of sodium chloride, but free from albumen.
The specific gravity of the fluid ranges from 1007 to 1015, according
to the quantity of sodium chloride present. Succinic acid and also
haematoidin are usual constituents, besides the ingredients already
mentioned.

[Footnote 215: _Entozoa_, Cobbold, p. 273 _et seq._, chapter viii.]

Although the form of hydatid or echinococcus cyst above described is
the usual one, there is occasionally produced an anomalous development
of the parasite, which from its resemblance to colloid cancer was
supposed to have this character until Virchow[216] unravelled the
mystery by demonstrating its true structure. This form of the parasite
is designated Echinococcus multilocularis. Its resemblance to colloid
cancer is the more striking because of the tendency of the interior of
the mass to undergo degeneration, to disintegrate, and to break up into
pus-sacs with greenish, cheesy, and bilious contents. An Echinococcus
multilocularis tumor is of almost stony hardness; it has a very dense
fibrous structure, intersected by cavities with thick gelatinous
contents. These minor cavities[217] are sacs of echinococci, but they
depart widely from the typical form, well-defined scolices being seldom
encountered.

[Footnote 216: _Archiv fur Anat._, Virchow, vol. xi. p. 80.]

[Footnote 217: Carriere, quoted by Davaine, _op. cit._, p. 961.]

{1104} Echinococci of the liver develop very slowly, and it is
characteristic of them to attain to very large proportions in most
cases without causing any very pronounced symptoms. There are certain
signs common to hydatids in any situation; there are others which are
due to particular circumstances.

A hydatid tumor of the liver is smooth but somewhat irregular in
outline, and elastic, when it develops downward, extending below the
margin of the ribs. If, however, it grows upward, the area of hepatic
dulness extends in that direction beyond the usual limits; the
diaphragm is pushed up, the lungs forced upward to the left and
compressed, and the heart also displaced upward toward the left. The
extension of the tumor downward, in the direction of least resistance,
is more usual. If the walls of the abdomen are sufficiently thin, the
tumor large enough, and if made up of many daughter vesicles, there may
be evoked by palpation the very characteristic sign known as hydatid
purring. To produce this effect an oscillation must be caused by a
sudden impulse communicated to the tumor on one side, the hand resting
against the other side. This sensation is likened to the impression on
the eye of the vibration of a bowl of jelly. Even when there is a
well-defined tumor this symptom is comparatively infrequent, but if
present it is pathognomonic, since no other kind of tumor possesses the
property of oscillation and elastic collision of its several
constituents.

When the tumor is so situated as to occlude the hepatic or common duct,
jaundice will be a symptom, and when the stomach is pressed upon there
will be epigastric oppression and nausea. If the vena cava is impinged
on or the portal vein, the usual results--ascites and oedema of the
lower extremities and of the scrotum--will be manifest. There is, of
course, nothing distinctive in these results.

The Echinococcus multilocularis, situated in the substance of the
liver, causes the usual disturbances of a new formation in such a
position. Much of the hepatic tissue is destroyed by its growth, and
many of the minor ducts closed. Jaundice is an early symptom--the
first, indeed, in many cases--and is also one of the most persistent.
It is present, according to Griesinger, in 10 out of 13 cases. The
usual gastro-intestinal disorders belonging to jaundice occur under
these circumstances; also the nervous disturbances of cholaemia.[218]

[Footnote 218: Davaine, _op. cit._, p. 962.]

Enlargement of the spleen is a very frequent symptom, being present,
according to Davaine, in 11 out of 13 cases, and, according to Heller,
in 25 out of 29 cases, in which this fact was made the subject of
direct inquiry.

Pressure on the vena cava causes oedema of the inferior extremities in
a small number of cases; and on the vena porta, ascites. There may
occur thrombosis of the portal, in which event the ascites will form
very quickly, and return as quickly after tapping.

The usually placid course pursued by echinococcus of the liver may be
much modified by inflammation and suppuration. Some external injury may
develop the inflammation. Having occurred, the clinical history
corresponds to other cases of hepatic abscess, and the reader is
therefore referred to the section on that topic for fuller information.

DIAGNOSIS.--At the outset of echinococcus of the liver the {1105}
differentiation of the tumor from other tumors, and of the disturbances
produced by it as contrasted with the effects of other morbid growths,
becomes exceedingly difficult, if not impossible. The size,
painlessness, elasticity, the purring tremor of the echinococcus tumor,
afford a sure basis for constructing a diagnosis, and as ultimately
developed they become the means of accurate differentiation from other
morbid growths of that locality. All doubt as to the nature of a given
hydatid tumor of the liver may be set at rest by the use of the
aspirator. The discovery of the characteristic hooklets of the scolex
in the fluid withdrawn from the tumor will be conclusive as to the
presence of echinococci. The hooklets may be absent, as in the case of
acephalocysts, but the fluid is characteristic in other respects: it
contains a large quantity of chloride of sodium and is free from
albumen.

Very great difficulty is experienced in diagnosticating an echinococcus
tumor developing from the upper surface of the liver, pushing the
diaphragm and lungs upward and displacing the heart to the left. Whilst
the physical signs may be, and are, usually alike when the condition
calling for diagnosis has existed for some time, there are means of
differentiating in the history of the cases and in the initial
symptoms.

The origin and growth of the echinococcus tumor are obscure and free
from constitutional disturbance; the onset of a pleuritic exudation is
marked by pain, fever, and hurried respiration and by physical signs of
a characteristic kind. It is true there are cases of so-called latent
pleurisy in which a hydrothorax forms without any well-marked
indications, but it will usually be found that some local pain, hurried
breathing, or other symptoms existed from the beginning. Those cases of
hydrothorax accompanying renal and cardiac diseases are readily enough
associated with their original cause.

Echinococcus of the liver may be confounded with abscess of the liver,
but a differentiation can be readily made by attention to a few
considerations, except in the rare condition of the Echinococcus
multilocularis which has proceeded to suppuration. In this latter
condition there are no means of differentiation, since an
abscess-formation has already occurred, nor is there any need to
attempt a distinction without the occasion of a difference.
Echinococcus differs from abscess in history, in the character of the
swelling, and in progress. Abscess of the liver is preceded by
paroxysms of hepatic colic, by inflammatory ulceration of some part of
the intestinal tract, or by local injury--traumatism. The onset of a
hydatid tumor is silent and painless. The swelling of the liver when an
abscess forms is not considerable at any time, and appears to be a
uniform enlargement of the organ, except when the pus tends to make its
way through the walls of the abdomen externally. An enlarging
echinococcus tumor is an obvious projection from the surface of the
liver at some point, and it does not have the characteristic
tenderness, the fluctuation of an abscess matured and ready to
discharge, and the constitutional disturbance; but it does have a
peculiar elasticity, and now and then may present that eminently
characteristic sign, the purring tremor. The use of the
exploring-trocar will usually suffice to clear up all doubts by the
withdrawal of the characteristic fluid of the hydatid cyst or of pus.

DURATION AND TERMINATION.--The progress of an echinococcus {1106} tumor
is exceedingly slow, and the development of symptoms produced by its
extension is early or late according to its position and to the nature
of the parts impinged on. A spontaneous cure may take place under the
rather rare circumstances of an opening into the hepatic duct or one of
its principal divisions, and the gradual discharge of the cysts by this
outlet into the intestine. Next to this mode of termination, the most
fortunate direction taken by the enlarging cysts is through the walls
of the abdomen externally. When the growth is upward through the lungs,
the symptoms belonging to empyema or hydrothorax, with pulmonary
abscess, ensue, and the termination is fatal after a protracted course.
Rupture into the peritoneal cavity is a fatal event. Ulceration into
the intestine, and the discharge of the cysts through the route thus
made, may effect a cure, but more frequently the fistulous
communication becomes a means of forming a fecal abscess.

The result in any case of hydatids of the liver is much influenced by
the mode of treatment adopted and the period at which it is undertaken.
As these parasites can be readily reached and destroyed by safe means,
obviously the more early the diagnosis is made and the treatment
carried out, the less the injury done to the hepatic structures and
neighboring parts.

TREATMENT.--Prophylactic.--As the intestine of the dog is the natural
habitat of the Taenia echinococcus, and as the hydatid is the first
stage in the development of the ovum and the second in the life-history
of the parasite, the means of prophylaxis consist in preventing
contamination of human food and water with the dog's excrement, which
contains the ova of the parasite. In Iceland, where hydatid disease is
very prevalent, dogs and human beings living in the same huts and
obtaining their water-supply by melting the snow just about them,
contamination of food and drink must readily occur. In this country
such conditions cannot exist; nevertheless, cases of hydatids are not
infrequent. The chief, if not the only, source of contamination is
through the consumption of such uncooked vegetables as lettuce, celery,
cabbage, etc., in the folds of which the ova may be retained, and from
which an ordinary washing does not suffice to detach them. It follows
that such articles of food should be minutely inspected and cleansed
before being placed on the table.

Boiling and filtration are the means of removing impurities of this
kind from potable waters.

Therapeutical.--The remedial management of cases of Taenia echinococcus
is necessarily restricted to that stage in their development when by
increasing size the functions of organs begin to be affected. Internal
medicines given with the view to arrest the growth of the parasite are
useless. Formerly, such attempts were made and successes were claimed,
but it is now known that no medicine can act on organisms enclosed as
these are in a dense capsule. It is needless to occupy space with
therapeutical details of this kind, but mention may be made of the
agents that were supposed to be effective. Laennec held that baths of a
solution of common salt had a distinct curative effect. The internal
use of iodide of potassium and the local application of iodine paint
were believed to cure a case in St. George's Hospital, London, in the
practice of Mr. Caesar Hawkins. Kameela was, in Iceland, supposed to
have a curative effect, but notwithstanding this the physicians of that
island resort to very heroical surgical methods in the treatment of
this affection.

{1107} The one means of relief consists in the removal of the vesicles,
either by suitable incisions or by compassing the death of the
parasite, after which the power of nature may be adequate to the cure.
In Iceland large incisions are made into the tumor at its most
prominent part, and, although accidents are not uncommon, the results
in many cases are eminently satisfactory. The accidents are shock,
hemorrhage, and especially peritonitis. Under favorable circumstances
now no procedure is more satisfactory in its results than free incision
and drainage. The tumor should be prominent, adherent all round to the
peritoneum, and the walls of the abdomen thin to ensure complete
success without accident. At the present time, so great have been the
advances in abdominal surgery, this operative procedure may be
preferable in some few cases presenting the favoring conditions above
mentioned.

Very simple expedients, however, suffice in most cases. The most simple
is puncture. This is now much practised in Iceland, and, as the
statistics show, with considerable success. Thus, Hjaltelin[219]
reports 100 cases cured in this way, and in his own hands this
expedient proved successful in 41 out of 50 cases operated on. In
Australia, where hydatid disease is also quite common, simple puncture
has effected a large proportion of cures,[220] and is the method of
treatment usually pursued. In England puncture has the approval of some
of the best authorities.[221]

[Footnote 219: Davaine, _op. cit._, p. 605.]

[Footnote 220: _The Medical Times and Gazette_, August, 1873, p. 164.]

[Footnote 221: _Transactions of the Clinical Society_ for 1872:
discussion participated in by Gull, Bryant, Greenhow, etc.]

The mode of performing this operation consists in the introduction of
an exploring-trocar into the most prominent part of the tumor. It may
be withdrawn at once or be permitted to remain for a few minutes to
several hours. The dangers are suppuration in the sac and peritonitis;
but the former, although sometimes accompanied by severe constitutional
symptoms, is not likely to endanger life, and even formidable
disturbances due to the latter are usually recovered from. The facts
show that puncture very rarely indeed causes dangerous, especially
fatal, symptoms. An eruption of urticaria has been observed to follow
puncture with the trocar, and also aspiration, in a considerable
proportion of the cases, but it has no special significance.

Since the introduction of the aspirateur, puncture and withdrawal of
the fluid by means of this instrument has been practised more
frequently, and this appears to be a more effective procedure, than
simple puncture with an exploring-trocar, although in most cases the
escape of the contained fluids suffices to destroy the parasite. The
aspirateur is less likely to permit the escape of fluid into the
peritoneal cavity or the entrance of air into a vein punctured by
accident. If puncture with the trocar or aspiration be practised, shall
all the fluid be withdrawn at once? The answer to this question may be
decided by the character of the sac. Does it contain daughter and
granddaughter vesicles? If so, one puncture may not permit the escape
of much fluid; but in any event it is the practice of the most
judicious and experienced authorities[222] to withdraw as much as
possible of the contents of the cysts at the first operation. Formerly,
a method practised by some French surgeons consisted in successive
tappings, a small quantity of fluid being drawn off each time.[223]
{1108} There is no good reason for this method of treatment now, and it
seems to have been discontinued.

[Footnote 222: _Transactions of the Clinical Society_, _loc. cit._]

[Footnote 223: Davaine, _supra_.]

Yet another method of treatment, but less effective than puncture or
aspiration, consists in injecting into the sac, after the removal of
its contained fluid, certain agents toxic to hydatids. A solution of
the extract of fern, alcohol, solution or tincture of iodine, and bile,
are the chief remedies thus employed. It has long been known that bile
is destructive of these parasites, and cases have occurred of
spontaneous cure in which the opening of the growing cysts into a
bile-duct has secured the entrance of bile and consequent arrest of
growth and atrophy of the hydatids. Several successful cases have been
reported in which the injection of aspidium (male fern) was the
effective agent, but the threatening symptoms produced by it, and the
comparative freedom of other methods of treatment from such
disturbances, do not recommend the injections of fern. In the case
reported by Pavy[224] the extract of fern was mixed with a solution of
potassa.

[Footnote 224: _Lancet_ (London), July, 1865.]

Injections of iodine in solution or in the form of tincture have been
more frequently practised than of any other material. Davaine,[225] who
finds it less successful than simple puncture and aspiration,
recommends, as affording the best results, a dilute aqueous solution of
iodine. Alcohol, a solution of permanganate of potassium, and various
antiseptic agents have been used to some extent, but none of them
possess any advantages over more simple measures.

[Footnote 225: _Op. cit._, p. 650.]

The latest proposal for the treatment of hydatid cysts, and probably
the most effective consistent with entire safety, is electrolysis.
Originally suggested by Althaus[226] to those who first employed the
measure on any considerable scale, it had been mentioned thirty years
before by Budd, and appears to have been first practised in Iceland on
a single case. The first elaborate attempt to establish electrolysis on
a sound basis as a regular procedure was made by C. Hilton Fagge and
Mr. Arthur E. Durham.[227] They operated on eight cases, and all were
successful. The method consists in the introduction of two needles
connected with the negative pole, and the application of the
positive--a moistened sponge--on the exterior in the neighborhood of
the hepatic region. The strength of current employed by Fagge and
Durham was that furnished by a battery of ten cells, and which by
previous trial was found to decompose a saline solution. The two
electrolytic needles, connected with wires attached to the negative
pole, were introduced into the most prominent part of the tumor about
two inches apart. The current was allowed to pass about ten minutes
usually, sometimes a little longer, the sponge on the exterior--the
positive pole--being shifted occasionally. The immediate effects are
not considerable. The tumor may be rendered somewhat more tense and
appear to be enlarged, but more frequently it becomes softer and is
lessened in size, the increase of size being due to the disengagement
of hydrogen gas, and the diminution caused by the escape of more or
less fluid. The immediate effects of the operation varied. In one case
no symptom followed, and in this the result was regarded as doubtful,
although a cure was considered probable. In the others more or less
{1109} constitutional disturbance followed, the symptoms being pain and
fever, the temperature ranging between 100 degrees and 103 degrees F.
The duration of the fever was from two to nineteen days, the latter in
one case only. As has been observed in some of the cases treated by
puncture or by aspiration, a rash appeared on the skin--in some
instances scarlatinous, in others of urticaria. It is a curious
circumstance that an eruption of urticaria is reported to have appeared
in one subject in whom a rupture of the sac into the peritoneal cavity
is supposed to have occurred.

[Footnote 226: _On the Electrolytic Treatment of Tumors, etc._, London,
1867.]

[Footnote 227: _Medico-Chirurgical Transactions_, 1871, p. 1 _et seq._]

Although so little change in the tumor occurs immediately after the
operation, yet it undergoes slow absorption, and ultimately disappears.
The time occupied in the disappearance of the tumor varies from a few
weeks to many months, the difference being due probably to the
situation of the growth, those occupying the substance of the liver
requiring a longer time to fill up.

Fagge and Durham report a case in which simple acupuncture was followed
by a result apparently as good as obtained by electrolysis, and other
similar experiences have been published. If the simple introduction of
a needle suffices to arrest the growth of a hydatid cyst and induce its
atrophy, of course the more complex procedures will be abandoned.

The tendency of the treatment of hydatid cysts has constantly been
toward simplicity, and the success occurs in a direct ratio thereto. In
forming an estimate of the relative value of the methods of treatment,
the average of mortality of each plan becomes the most important
factor. Simple tapping and paracentesis, the most frequently adopted
mode of treatment, is not without immediate and remote danger. Of 46
cases carefully tabulated by Murchison,[228] there were 3 deaths
properly attributable to the operation; but the after
results--suppuration of the cyst and its consequences, peritonitis,
etc.--cannot be measured so accurately. About two-thirds of the cases
thus treated result in cure, and in a majority of these a single
operation suffices. The injection of the various substances which have
been employed for that purpose does not seem to increase the proportion
of cures, and their use distinctly enhances the dangers of the
treatment. At present, the decision as to the method of treatment to be
employed in any case should be made between simple tapping,
electrolysis, and acupuncture. Of these, the last mentioned, it can
hardly be doubted, is the method which is most desirable, for although
it has not been employed so largely as the others, thus far the results
have been better: the percentage of recoveries without accident has
been higher relatively than by other methods of treatment. As
acupuncture presents no special difficulties or dangers, and is but
little painful, it may be tried first, reserving more formidable
measures for the failures by this simple expedient.

[Footnote 228: _Clinical Lectures on Diseases of the Liver_, _loc.
cit._]


Distoma hepaticum and Distoma lanceolatum (Liver-Flukes).

The Distoma hepaticum, entitled by Linnaeus Fasciola hepatica, occurs
very frequently in herbivorous animals and occasionally in the biliary
{1110} passages of man.[229] It is, however, less important than the
Distoma lanceolatum, which, although much smaller than the former,
occurs in much larger numbers.

[Footnote 229: Davaine, _Traite des Entozoaires_, Paris, 1877, p. 240
_et seq._; also, Cobbold, _Entozoa_, p. 148.]

Distoma hepaticum is a leech-like parasite from 25 to 30 mm. in length,
of a brownish color, smooth to the naked eye, but thickly covered with
minute spikes or spines to be seen with a low power, and provided with
a cephalic (entrance to oral cavity) and an abdominal sucking disk,
which are also organs of locomotion. The Distoma lanceolatum owes its
name to its lancet shape; it is smaller than D. hepaticum, measuring
about 8 mm. in length and half this or less in width; it is unprovided
with spines, but contains two suckers at the side. Both parasites are
hermaphrodite; the ova, according to Cobbold (p. 166), have "an average
longitudinal diameter of 1/180, whilst their greatest transversal
measurement is about 1/270." These ova are capable of some movement,
provided as they are with a ciliated envelope.

The disease known as the rot in sheep, and a peculiar cachexia entitled
by Davaine la cachexie aqueuse, are caused by the presence of distoma.
The ova gain access to man through the use of unwashed cress, lettuce,
and similar vegetables eaten in the raw state, and in drinking-water.
Fortunately, this accident is rare. The number of reported examples
collected from all sources by the indefatigable Davaine is twelve.[230]

[Footnote 230: _Ibid._, p. 253 _et seq._]

The larger distoma passes into the common and hepatic duct and
gall-bladder, whilst the smaller (lanceolatum) enters the finer
ramifications, and, there multiplying, several consequences may ensue.
The irritation caused by their presence and development will excite a
more or less severe cholangitis, or, accumulating in sufficient
numbers, an actual obstruction will be induced, and jaundice and
structural alterations of the liver will in turn be brought on.

The DIAGNOSIS of such a malady is, in the very nature of the case,
uncertain at best, and in most cases impossible. Nevertheless, it may
be made in rare instances. The existence of the rot may cast suspicion
on the mutton and kitchen vegetables so situated as to suggest the
possibility of contamination with the ova of distoma. Definite and
conclusive information will be afforded by the presence of the ova,
still more of the more or less fully-developed parasite, in the feces
of a patient effected by the symptoms of catarrhal jaundice or
occlusion of the biliary passages. By tapping the gall-bladder
parasites may be withdrawn.

The SYMPTOMS are those common to cases of catarrh of the bile-ducts
(cholangitis), catarrhal jaundice, or occlusion of the passages, as may
be. As these have been detailed under their respective heads, it is not
necessary to repeat the observations already made.

As regards the TREATMENT, in addition to the methods of management
recommended in such cases it may be stated that the use of certain
parasiticides offers a reasonable prospect of good results. Creasote,
bichloride of mercury, thymol, eucalyptol, oil of wintergreen
(gaultheria), and similar agents are rational remedies and should be
fairly tried.


{1111} Parasites in the Portal Vein.

The entozoon which by its presence in the blood causes the disease
chyluria also inhabits the portal vein. In some parts of the
world--Brazil more especially--this disease is exceedingly common. It
has occurred also in two or three instances in England, and the writer
has had a case within the past year (1884) in Philadelphia. The
parasites in this case were found in immense numbers in the urine.

The blood of the portal vein sometimes is actually filled, and the
liver substance itself is penetrated, by them, but nothing is known of
the alterations they induce in these organs. When cases of haematuria
or chylous urine due to the Filaria sanguinis hominis occur, the
changes are not confined to the urinary organs, but often, doubtless,
involve the liver. There are no signs in the present state of our
knowledge by which the existence of these parasites in the portal vein
and liver can be determined.




{1112}

DISEASES OF THE PANCREAS.

BY LOUIS STARR, M.D.


Until the middle of the seventeenth century the prevalent views upon
the functions and diseases of the pancreas were vague in the extreme.
By some the organ was regarded simply as a cushion provided for the
protection of the neighboring blood-vessels and nerves; by others it
was looked upon as the seat of lesion in many very diverse diseases, as
ague, hypochondriasis, melancholia, and so on.

In 1642, Wirsung's discovery of an excretory duct demonstrated the fact
that the pancreas was a special organ, and initiated the successful
investigation of the physiology and pathology of the gland. For many
years after this, however, little progress was made, and it is only
comparatively recent investigations that have furnished definite and
reliable information upon the subject. Even now our knowledge of the
clinical and pathological features of diseases of the pancreas is far
behind that of many of the other viscera of the body, the chief reasons
for this being the uncertainty in regard to the physiology of the gland
and the rarity with which its lesions are primary and uncomplicated.

ANATOMY AND PHYSIOLOGY.--The pancreas is a long, somewhat flattened,
narrow, acinous gland, pinkish-white in color, and of looser texture
than the salivary glands, which it otherwise closely resembles in
structure. It is hammer-shaped, measures from six to eight inches in
length, one and a half inches in breadth, and about three-fourths of an
inch in thickness, and varies in weight from three to five ounces. The
gland is situated in the upper part of the abdominal cavity; the
expanded portion, or head, lies in the concavity of the duodenum;
thence it extends transversely across the epigastric and both
hypochondriac regions on a level with the first lumbar vertebra and in
contact with the posterior abdominal wall. As it passes toward the left
it gradually decreases in size, and the narrowest part, or tail, rests
against the spleen. Behind the organ are the crura of the diaphragm,
the aorta, the inferior cava, the superior mesenteric vessels, and the
solar plexus; in front of it, the stomach and the left lobe of the
liver. Its anterior surface alone is invested with peritoneum, being
covered by the posterior layer of the lesser omentum. The ascending
portion of the head is intimately connected with the duodenum by dense
connective tissue, and at times the descending portion, by extending
backward and outward, forms an almost complete ring around the gut; the
body is loosely attached by connective tissue to the posterior
abdominal wall, and the {1113} left extremity and tail are joined to
the left kidney and suprarenal capsule and to the spleen by loose
areolar tissue. The gland is supplied with arterial blood by branches
springing from the pancreatico-duodenal and splenic vessels; its veins
join the splenic and superior mesenteric veins; its lymphatics
communicate with the lumbar glands; and its nerves are branches from
the solar plexus. The principal excretory duct, the canal of Wirsung,
has at its widest part the calibre of a goose-quill. It begins by the
union of five small branches at the tail, and extends transversely
through the substance of the gland from left to right, nearer the lower
than the upper border, and the anterior than the posterior surface; it
is joined throughout its course by numerous small branches from the
acini, which enter it at acute angles. In the head the duct curves
slightly downward, and as a rule opens with the ductus choledochus into
the ampulla of Vater in the second portion of the duodenum; sometimes,
however, it has a separate opening into the intestine. A second,
smaller, duct runs from the ascending portion of the head, and usually
joins the main duct, but may also open independently.

The acini of the gland are from .045 mm. to .090 mm. in diameter, and
are composed of a very thin membrane lined with pavement cells. The
thin walls of the excretory ducts are formed of connective tissue and
elastic fibres, and are lined by a single layer of small cylindrical
epithelial cells. The terminal extremities of the ducts form a complete
network around the glandular cells, resembling the intralobular biliary
canaliculi. The acini are imbedded in a mass of adipose tissue which
contains the vessels and nerves.

The topographical relation of the head of the pancreas to the ductus
choledochus is of clinical importance. As a rule (fifteen times in
twenty-two, Wyss), the bile-duct descends near the head, toward the
duodenum; frequently it runs through this part of the organ, being
either partially or entirely surrounded by the gland substance. Now,
when the bile-duct merely passes over the pancreas, any enlargement,
unless excessive, would simply push it aside, but when it passes
through the head, a comparatively slight amount of disease is
sufficient to close it entirely and cause jaundice.

It is only since the observations of Bernard in 1848 that the
prominence of the pancreatic juice as a digestive fluid has been
recognized. It fulfils several important purposes: in the first place,
it emulsifies the fatty articles of food; secondly, it converts starch
and cane-sugar into glucose; and, finally, it supplements the action of
the gastric juice upon nitrogenous materials and completes their
digestion. Each of these changes is probably brought about through the
agency of a special ferment (Danilewsky). The pancreatic juice is not
secreted continuously. According to the observations of Bernstein,
there are two separate secretory flows following each ingestion of
food--one occurring shortly after the food enters the stomach; the
other a few hours later, corresponding in time to the passage of the
food from the stomach into the intestine, the latter being followed by
a period of rest until the next meal. Both the condition of nausea and
the act of vomiting arrest the secretion. When the vagus is divided and
the central extremity of the cut nerve is irritated, the secretion is
also arrested, and remains checked {1114} for a long time. The arrest
in each instance is attributed to reflex action of the spinal cord and
sympathetic nerve. At the same time, irritation of the mucous membrane
of the stomach caused by the presence of food increases the flow of
pancreatic juice, and so too does simple section of the nerves which
accompany the arteries. It would seem, therefore, that the gland is
under the influence of two sets of nerves from the vagus--one
inhibiting, the other exciting, its secretion.

GENERAL ETIOLOGY.--Pancreatic disease occurs more frequently in men
than in women. No period of life is exempt from it, but it is most
commonly met with in the aged. The predisposing causes are
constitutional syphilis, pregnancy, and hereditary tendency. Among the
apparent exciting causes may be mentioned the habitual over-use of
alcoholic drinks, gluttony, the excessive use of tobacco, suppression
of the menstrual flux, the abuse of purgatives, excessive and prolonged
mercurial medication, and mechanical injuries, either prolonged
pressure or blows upon the epigastrium. As a secondary affection,
disease of the pancreas is associated with chronic diseases of the
heart, lungs, liver, alimentary canal, and abdominal glands, and the
organ may be the seat of metastatic abscesses and tumors.

GENERAL SYMPTOMATOLOGY.--The objective symptoms are--rapid and extreme
emaciation of the entire body; sialorrhoea; obstinate diarrhoea with
viscid stools; fatty stools; lipuria; and the presence of masses of
undigested striped muscular fibres in the stools.

The well-established fat-absorbing and peptonizing properties of the
pancreatic juice furnish a ready explanation of the wasting of the body
which occurs when this secretion is arrested, diminished in quantity,
or altered in quality by disease. Emaciation is not a constant symptom
of pancreatic disease. A number of cases are mentioned by Abercrombie,
Claessen, and Schiff in which, notwithstanding disease of the gland and
complete closure of the duct, revealed by post-mortem examination, the
patients during life were not only well nourished, but even moderately
corpulent. In such instances it is probable that the digestive
functions of the absent pancreatic juice are more or less adequately
performed by the bile and succus entericus. When present, emaciation is
an early symptom; it is at the same time progressive, and is usually
very intense in degree, being most marked in those cases where there is
associated hepatic disease or obstruction to the passage of bile into
the intestine, where the disease of the pancreas interferes
mechanically with the processes of nutrition by pressing upon the
pyloric extremity of the stomach or upon the duodenum, and when the
organ is the seat of carcinomatous growths. In the last-named
condition, in addition to the perversion or arrest of the secretion,
the loss of flesh is attributable to the general causes of malnutrition
attendant upon carcinoma wherever situated.

Sialorrhoea, or an excessive secretion from the salivary glands, is
noticeable as a symptom of disease of the pancreas only when there is
an associated lesion of the stomach, either of a catarrhal or cancerous
nature. Under these circumstances a quantity--six or eight
fluidounces--of a colorless, slightly opalescent, and adhesive and
alkaline fluid may be expelled from the mouth at once as an early
morning pyrosis; or by frequent and repeated acts of expectoration,
following a sudden filling of the mouth with fluid, a large bulk of
thin saliva may be expelled {1115} during the day. This hypersecretion
must not be looked upon as any indication of an especial sympathy
existing between the salivary glands and the pancreas, neither can it
be regarded as a pancreatic flux with a regurgitation of the fluid from
the duodenum into the stomach and thence through the oesophagus into
the mouth, since during the nausea that must always attend the passage
of the intestinal contents into the stomach the pancreatic secretion is
arrested, and since the liquid contains salivary, and not pancreatic,
elements.

The diarrhoea pancreatica is the least constant of all the objective
symptoms; in fact, constipation is present in many pancreatic
affections, notably carcinoma. The fecal evacuations in this condition
are frequent, thin, viscid, and contain an abundance of leucin. Under
the microscope the leucin appears either in the form of concentrically
sheathed globules, or as small crystalline rods and scales collected
together in the form of wheels or aggregated in clusters. This form of
diarrhoea may be attributed to a hypersecretion from the pancreas.

That the presence of fat in the stools is an important diagnostic
symptom of pancreatic disease is proved both by clinical and
experimental observations. The characters of these stools vary
considerably. The fat may appear mixed with the feces in small lumps,
ranging in size from a pea to a hazelnut, yellowish-white in color,
soluble in aether, and easily melted and burned. Again, after the
evacuation has become cool fat may be seen covering the fecal masses,
collected into a thick cake around the edges of the containing vessel,
or, when the feces are liquid, floating as free oil on the surface.
Finally, the fat may be in a crystalline form, the crystals being
needle-shaped and aggregated into sheaves and tufts. The quantity of
fat also varies. It may be present only in small quantities, or may
even be entirely absent from the evacuations in those cases in which
the secretion from the pancreas is simply diminished, and the amount is
greatest in those instances where there is a simultaneous arrest of the
pancreatic and hepatic secretions. It must be remembered, too, that
even in health the stools may contain fat; this occurs when an excess
of oleaginous food is consumed and after the administration of castor
oil or cod-liver oil. These conditions must be eliminated, therefore,
in estimating the value of fatty stools as a diagnostic symptom; if,
then, at the same time, coincident disease of the liver can be
excluded, the symptom becomes almost pathognomonic. The appearance of
fat in the stools may be due not only to an arrest of the pancreatic
secretion, but also to pressure upon the large lymphatic trunks,
interfering with the circulation of the chyle and checking the
absorption of fat from the intestine.

Usually, the amount of fat expelled is in direct proportion to the
quantity consumed, but occasionally the former greatly exceeds the
latter. In such cases there must be some other source for the evacuated
fat than the food; and it is probable that fat from the adipose tissue
passes into the blood, and thence through the mesenteric vessels into
the intestine. This theory would likewise account in part for the rapid
and extreme wasting, and for another less frequently observed
symptom--namely, lipuria. A case is recorded by Clark of medullary
cancer of the pancreas with nutmeg liver, and another by Bowditch of
cancer of the pancreas and liver in which lipuria was noted. The fat
was observed, after the urine had cooled, floating about on the surface
in masses or globules; differing, {1116} therefore, from chyluria, for
in this condition the fat is present in the form of an emulsion, and
gives the urine either a uniform milk-like appearance, or, after it has
been allowed to stand, rests upon the surface in a creamy layer.

When the pancreatic secretion is arrested, most of the animal food
which has escaped gastric digestion will pass unchanged through the
intestine and give rise to another characteristic condition of the
evacuations--namely, the presence in the feces of undigested striped
muscular fibres. The amount of these fibres, and indeed their
appearance at all in any given case, will depend directly upon the
nature of the food consumed.

SUBJECTIVE SYMPTOMS.--The subjective symptoms of disease of the
pancreas are abnormal sensations in the epigastrium, and pain.

The abnormal sensations in the epigastrium are weight and pressure,
attended at times by praecordial oppression and discomfort. The feeling
of weight is usually deep-seated, may be intermittent or constant, and
is generally increased or developed by pressure. It is often influenced
by position, the assumption of the erect posture or turning from side
to side giving rise to a stretching or dragging sensation, as if a
heavy body were falling downward or moving about in the upper abdomen.

The pain may be due either to an inflammation of the peritoneum
covering the gland or to pressure upon the solar plexus, and
consequently varies in character. When it depends upon localized
peritonitis, it is constant, circumscribed, and deeply seated in the
epigastrium at a point midway between the tip of the ensiform cartilage
and the umbilicus; it is rather acute, and is greatly augmented by
pressure. The second variety occurs in paroxysms, and is neuralgic in
character, the sharp, excessively severe lancinating pains extending
from the epigastrium through to the back, upward into the thorax, and
downward into the abdomen. These paroxysms--in reality attacks of
coeliac neuralgia--are attended by great anxiety, restlessness, and
oppression and a tendency to syncope. That calculi in the duct of
Wirsung, tightly grasped at the position of arrest, may give rise to
paroxysms of pain analogous to biliary colic, cannot be doubted, though
there are no positive facts in support of this view.

PRESSURE SYMPTOMS.--When the pancreas becomes enlarged it encroaches
upon the neighboring blood-vessels and viscera, interferes with their
functions, and thus produces prominent symptoms.

The ductus choledochus from its close relation to the head of the gland
is especially liable to become obstructed, with the consequent
production of chronic jaundice and the general effects of the absence
of bile from the intestinal canal. Pressure upon the portal vein gives
rise to enlargement of the spleen; on the inferior cava, to oedema of
the feet and legs; and on the aorta, occasionally, to aneurismal
dilatation of the vessel above the point of obstruction and to
subsequent alteration in the size of the heart. By encroaching on the
stomach an enlarged pancreas may cause either displacement of the
viscus or stenosis at its pyloric extremity, attended with occasional
vomiting of large quantities of grumous, fermenting liquid, pain,
constipation, general failure of health, and the distinctive physical
signs of dilatation of the stomach. The duodenum may also be pressed
upon and more or less occluded, and pain and vomiting occur several
hours after food is taken. Occasionally hydronephrosis is {1117}
produced, the accumulation being usually in the right kidney and due to
obstruction of the corresponding ureter.

A sufficient number of cases have been collected to show that there is
an intimate connection between disease of the pancreas and diabetes
mellitus. One or other condition may take the precedence, melituria
occurring during the progress of pancreatic disease, demonstrating the
onset of diabetes, and the appearance of fatty stools in diabetes a
secondary involvement of the pancreas. Various theories have been
advanced to account for this association, but the true explanation
seems to be based upon the experiments of Munk and Klebs. By
experimenting upon dogs these observers found that extirpation of the
solar plexus produced either permanent or temporary diabetes, whereas
section of the hepatic and splanchnic nerves, removal of the pancreas,
or ligature of the duct of Wirsung was without effect. From the
intimate anatomical relation of the pancreas to the solar plexus it is
easy to understand how disease of the gland may give rise to
alterations in the nerve-structure, either by direct pressure or by the
extension of inflammation along the nerve-fibres connecting the gland
with the ganglia; and these alterations in time produce diabetes. In
the instances in which diabetes is the primary affection the condition
of the pancreas, as proved by post-mortem section, is usually one of
simple or fatty atrophy; and it may be assumed that a lesion of the
solar plexus is the cause of both diseases, the changes in the pancreas
being produced in a similar way to the atrophy of the submaxillary
gland after section of the vaso-motor nerves in Bernard's experiments.

The same nerve-lesion may give rise to bronzing of the skin, and two
cases are recorded in which disease of the pancreas (cheesy
infiltration, cancer) was attended by this symptom.

PHYSICAL SIGNS.--To make a successful exploration of the pancreas the
stomach and colon should be as far as possible empty, and the patient
placed in a position, with the head and shoulders slightly elevated and
the thighs drawn up toward the belly, to relax the abdominal muscles;
or if necessary this relaxation must be brought about by the
administration of aether. The knee-elbow position is often preferable
to the dorsal position in practising palpation.

The condition of the gland giving rise to physical signs is one of
enlargement, affecting chiefly and primarily its head, and due
generally to the presence of some morbid growth.

Inspection reveals either a diffuse bulging of the upper third of the
abdomen to the right of the median line, or a well-defined tumor
situated beneath the right costal border, about the line of junction of
the right hypochondriac and epigastric regions. Often the pancreatic
tumor does not come in direct contact with the abdominal wall, but
presses against and thrusts forward the left lobe of the liver,
producing simply a prominence in the epigastrium. In the first
condition palpation elicits an ill-defined sense of resistance; in the
second, the fingers readily outline a tumor, which is slightly movable,
rounded in shape, firm or fluctuating, with a smooth or nodulated
surface, usually tender to the touch, and often giving a false impulse
transmitted from the aorta lying beneath; and in the third, the smooth
surface and the sharp edge of the left lobe of the liver are easily
distinguishable.

{1118} Percussion over a pancreatic tumor is commonly dully-tympanitic,
absolute flatness occurring only when it is very large and comes
directly in contact with the abdominal wall, pushing aside the stomach
and intestines.

On auscultation a blowing murmur may, in some instances, be heard over
the tumor. These murmurs are due to pressure upon the aorta, and must
be distinguished from the sound produced in aneurism of this vessel.

The various complications of pancreatic disease, such as dilatation of
the stomach, ascites, and secondary lesions of the liver, greatly
modify the physical signs, and sometimes entirely prevent an
exploration of the gland.


INFLAMMATORY AFFECTIONS OF THE PANCREAS.


Acute Idiopathic Pancreatitis.

This is a rare disease. It occurs most frequently in males during and
after adult life, and the strumous diathesis appears to predispose to
it. Intemperance, the suppression of normal or morbid discharges, and
traumatism act as exciting causes.

ANATOMICAL APPEARANCES.--The pathological changes may be divided into
two stages. In the first the gland is deep red in color, intensely
injected with blood, greatly increased in consistence, enlarged to the
extent of two or three times its normal size, and when an incision is
made the divided lobules feel firm and crisp. The interlobular tissue
is sometimes dotted with bloody points, and the same hemorrhagic
changes may occur in the connective tissue surrounding the gland. In
this stage resolution may occur or the inflammation may pass into
suppuration. At the beginning of the second, or suppurative, stage
numerous minute collections of pus are seen scattered throughout the
gland in the interacinous tissue; these gradually collect into a single
large abscess, and at times the whole gland is converted into a mere
pus-sac, the capsule being much thickened. In other instances the
formation of pus is entirely peripancreatic. The pus is usually
inodorous and creamy, but is sometimes grayish-white or greenish in
color; it then has a faint disagreeable odor, and occasionally is very
fetid. When mixed with pancreatic juice it becomes clear and yellowish
in color, and contains numerous minute curd-like masses.

In the first stage secondary peritonitis may arise from a simple
extension of the inflammatory process, and bands of lymph are formed,
gluing the pancreas to the neighboring organs. In the second, fatal
acute peritonitis may result from the bursting of an abscess into the
peritoneal cavity. These abscesses also occasionally open into the
duodenum or stomach. Gangrene and peripancreatic sloughing occur very
exceptionally, and are probably due to extensive hemorrhagic changes.

SYMPTOMS AND COURSE.--The disease may be preceded for an indefinite
period by symptoms of impaired gastric or intestinal digestion, but its
onset is usually sudden. The attack begins with colic or continuous
{1119} deep-seated pain, starting in the epigastrium and extending
toward the right shoulder or the back, and quickly becoming very
intense. The pain is attended by pallor of the face, great
restlessness, praecordial anxiety, dyspnoea, and faintness. The tongue
is furred or dry and red; thirst is increased; the appetite is lost;
there are frequent eructations, nausea, and constant vomiting of a
clear, greenish, viscid fluid; the vomiting produces no sense of
relief, and even increases the epigastric pain. The bowels are
obstinately constipated. The epigastric region is tense, tumid, and
excessively tender, so that it is usually impossible to elicit the
physical signs of enlargement of the gland. There is moderate pyrexia,
with evening exacerbations, and the pulse is increased in frequency.
Jaundice does not occur.

These symptoms progressively increase in severity, and reach their
maximum intensity in from three to five days. The pulse then becomes
small, compressible, and irregular, the extremities cold, the face
hippocratic, and death takes place in a state of collapse. The fatal
termination is preceded by the symptoms of acute peritonitis in the
cases which are complicated by an extension of inflammation or the
rupture of an abscess into the peritoneal cavity.

Recovery is quite possible in the early stage of the disease. On the
other hand, the course may be greatly protracted by a change in the
type of the inflammation, resulting in induration and enlargement of
the gland or in the formation of chronic abscesses. Again, when
peritonitis from extension has been confined solely to the portion of
the peritoneum that covers the gland, and has resulted in the formation
of fibrinous bands binding the pancreas to the adjacent viscera, the
symptoms of pancreatitis will on subsiding give place to those of
obstruction of the stomach, duodenum, or bile-duct.

DIAGNOSIS.--The diseases most likely to be confounded with acute
pancreatitis are biliary colic and the catarrhal form of acute
gastritis.

From biliary colic it is distinguished by the absence of rigors,
jaundice, enlargement of the liver, and a tender pyriform tumor
corresponding in situation to the gall-bladder and due to its
distension with accumulated bile. The pain in both affections is sudden
in its onset, and very similar in character and distribution; but when
caused by the passage of a gall-stone it usually begins either after a
heavy meal or after some severe muscular exertion or shaking of the
body--circumstances inoperative in the production of the pain of
pancreatitis. The pain, too, in the former condition is less severe at
first, increases gradually in severity, is more paroxysmal, is at the
outset lessened by pressure, and is often temporarily relieved by the
act of vomiting. The attacks at the same time are rarely isolated, and
all doubt is removed when the pain ceases suddenly and a calculus is
discovered in the feces.

Acute gastric catarrh is almost always traceable to the ingestion of
some irritant substance, usually alcohol or food of bad quality. This
history, together with the liability of the attack to occur during the
course of chronic dyspepsia, the comparatively trifling severity of the
pain, the headache, the irregularity of the bowels, the condition of
the urine, which is either high-colored or deposits lithates
abundantly, and the tendency of the affection to become chronic, are
the points of distinction between this and the pancreatic disease.

{1120} Acute inflammation of the stomach, or gastritis proper,
resulting from corrosive poisons, presents a train of symptoms entirely
different from those of acute pancreatitis.

TREATMENT.--Absolute rest is essential. The diet should consist of milk
guarded by lime-water and of meat-broths, this food being administered
in small quantities--one to two or three fluidounces of the milk and
lime-water or half as much broth--at proper intervals. In the early
stage an effort must be made to reduce the inflammation by the
application of ice to the epigastrium or of leeches to the same region,
or preferably to the anus. The excessive pain demands the free use of
opium. The nausea and vomiting may be relieved to some extent by
directing the patient to swallow small lumps of ice, and by the
employment of iced carbonic-acid water and the effervescing draught;
and the tendency to constipation may be overcome by enemata. Later in
the course of the disease, if the epigastric tenderness permits of it,
light linseed poultices should be placed over the upper abdomen. During
the stage of collapse alcoholic stimulants and the application of heat
to the extremities are necessary. The occurrence of acute peritonitis
or other complications and sequelae demand appropriate treatment.


Acute Secondary Pancreatitis.

In this condition the pancreas may be the seat of either acute
parenchymatous inflammation or of metastatic abscesses.

Acute parenchymatous degeneration of the muscles, kidneys, liver, and
so on is recognized as a frequent lesion in the acute infectious
diseases, particularly typhoid fever; and it is under these
circumstances, and in association always with similar changes in some
of the organs mentioned, that parenchymatous degeneration of the
pancreas takes place.

Metastatic suppurative inflammation is very rare: it has been observed
in cases of disease of the testicles after the operation of extirpation
of these organs, and occasionally in puerperal peritonitis.

ANATOMICAL APPEARANCES.--In parenchymatous inflammation the gland at
first is hardened, swollen, and reddened, and on section presents a
reddish-gray surface, with indistinctness of the glandular structure,
due to the amount of swelling of the acini. Under the microscope the
gland-cells are found to be enlarged; they contain several nuclei,
their protoplasm is infiltrated with fatty granules, obscuring the
nuclei to a certain extent, and their outline is well defined. These
alterations are most marked in the head of the gland. After a time the
hypertrophy of the cells, by pressing upon the blood-vessels, produces
an anaemic condition and the organ becomes pale; in the advanced stages
softening occurs.

Metastatic suppurative inflammation leads to the formation of a single
large abscess or to multiple minute purulent collections.

SYMPTOMS AND COURSE.--Parenchymatous degeneration gives rise to no
distinctive symptoms. Its occurrence in typhoid fever or other
infectious disease may be suspected when after prolonged hyperpyrexia
there are enlargement of the liver and spleen and albuminuria. The
appearance of jaundice (from pressure) increases the probability of
involvement of the pancreas in the general gland-change.

{1121} The development of rigors, alternating with flushing, during the
course of one of the lesions liable to be attended with metastatic
abscesses in the pancreas might suggest the formation of pus in the
gland, but an absolute diagnosis is impossible.

Several cases are on record pointing to the possibility of a metastasis
of mumps from the parotid gland to the pancreas. In these the
disappearance of the parotiditis was followed by symptoms resembling
those of idiopathic pancreatitis--namely, thirst, fever, loss of
appetite, anxiety, and burning in the epigastrium, with deep-seated
pain extending toward the right side; in addition there was diarrhoea,
with numerous, yellowish, watery stools. In one case that resulted
fatally the secondary diarrhoea suddenly ceased and the parotid
swelling reappeared. At the autopsy the pancreas was found to be
swollen, reddened, engorged with blood, and indurated. Such a
metastasis, however, must be very infrequent, and more extended
observations are necessary to establish its course and clinical
features.

The first form of acute secondary pancreatitis may be a comparatively
unimportant complication of the acute infectious diseases, or, together
with the parenchymatous degeneration of other organs, may form a
distinct element in the fatal issue of these diseases.

Metastatic abscesses are prone to be followed by ulceration and the
formation of fistulous communications with the neighboring viscera.

TREATMENT.--The management of secondary inflammation of the pancreas is
regulated solely by the indications derived from the originating
disease.


Chronic Interstitial Pancreatitis.

Inflammation of the connective tissue of the gland usually occurs after
adult life, and depends upon a variety of causes.

The secondary form, due to long-continued venous engorgement resulting
from lesions of the cardiac valves and from chronic disease of the
lungs or liver, is the most frequently observed.

Other causes are closure of the duct of Wirsung, the retained secretion
producing pressure upon the glandular tissue; the extension of
inflammation from adjacent organs, as the bile-duct when there is an
impacted gall-stone, or the stomach and duodenum, especially in cancer
and perforating ulcer, where the floor of the ulcer is formed by the
pancreas; the pressure of tumors, as aneurisms of the abdominal aorta
and coeliac axis; chronic alcoholism; and syphilis.

ANATOMICAL APPEARANCES.--The lesion may be limited to the head or to
isolated portions of the gland, or be uniformly distributed. The
general changes are a hyperplasia of the interacinous connective
tissue, with subsequent contraction and atrophy, or, in extreme
instances, entire destruction of the glandular elements proper, the
organ becoming granular and firmer and tougher than normal. A section
shows a pale surface, studded at intervals with white spots, from which
little cheese-like and fatty masses may be squeezed, and, when there
has been intense hyperaemia, with minute collections of reddish pigment
and small hemorrhagic cysts, indicating previous interstitial
hemorrhages.

{1122} When the contraction causes closure of the small excretory ducts
or of the duct of Wirsung itself, the section shows secondary cysts and
beaded canals.

In exceptional instances of acquired syphilis the pancreas is the seat
of gummata or sclerosis, but in congenital syphilis hyperplasia of the
glandular connective tissue frequently occurs, being usually associated
with specific lesions of the lungs, liver, kidneys, and general
glandular system.

SYMPTOMS AND COURSE.--As chronic pancreatitis rarely attains a
sufficient degree of development to interfere seriously with the
function of the organ, the disease is usually latent, or masked by the
symptoms of the originating lesion in secondary hyperplasia, or by the
associated diseases of the abdominal viscera in alcoholism and acquired
syphilis.

When due to hereditary syphilis, the foetus is stillborn or death takes
place soon after birth, and there are no characteristic symptoms.

Occasionally, however, especially when it depends upon a complete
obstruction of the duct of Wirsung, a diagnosis may be made from the
presence of emaciation, fatty stools, and melituria, with epigastric
pain of a neuralgic character, and the discovery of a deep-seated,
dense tumor extending transversely across the epigastrium.

The duration is indefinite, and varies greatly with the cause. While a
return to the healthy condition is possible during the early stage of
the lesion, the usual course is similar to that of chronic interstitial
inflammation in other organs.

TREATMENT.--The management, when a diagnosis can be made, must be
guided mainly by the etiological indications. The restoration of the
functions of the heart, lungs, or liver when these organs are at fault,
the abstinence from alcohol in the drunkard, and an energetic use of
mercurials or iodide of potassium in syphilis, are of the first
importance in arresting the disease. A persistent course of mild
purgatives and of cathartic mineral waters is serviceable. Pain should
be relieved by belladonna or opium. The diet must be simple and
digestible, and if an arrest of the pancreatic secretion be indicated
by the appearance of fat in the stools, an effort should be made to
supply the deficiency. For this purpose pancreatin, prepared by
precipitation by alcohol from a watery extract of a calf's or pig's
pancreas, may be used.[1] The pancreatin may be given in doses of from
five to fifteen grains, in the form of a pill or in capsules, and at an
interval of two hours after food is taken, or the same quantity of
pancreatin may be added to the food a few moments before it is eaten.
Probably the best substitute is a watery infusion of the gland
containing all its soluble principles. To prepare an active infusion
the pancreas must be taken from the animal during the act of digestion.
It is then freed from its surrounding fat, and macerated for two hours
in four times its weight of water at a temperature ranging between 25
degrees and 30 degrees C. (58.3 degrees and 61.1 degrees F.). Another
plan is to beat a calf's pancreas in a mortar with six fluidounces of
water until a milk-like fluid is obtained, and strain. One-third of the
infusion obtained by either method is administered after each meal, an
entire pancreas being thus used every twenty-four hours.

[Footnote 1: One gramme of pancreatin is sufficient to emulsify fifteen
grammes of fatty substances, to convert eight grammes of starch into
glucose, to digest fifty grammes of fibrin, twenty grammes of
syntonine, and thirty-three grammes of boiled albumen (Raymond).]

{1123} The extractum pancreatis,[2] as it is now furnished to the
profession, is a very useful preparation. It may be employed to
peptonize milk, milk-gruel, and broth, or be given in combination with
bicarbonate of sodium at a fixed interval after each meal, as in the
following formula:

  Rx. Ext. pancreatis,    drachm j;
      Sodii bicarbonatis, drachm ij;
  M. et. ft. Chart No. XII.

S. One powder to be taken two hours after each meal.

[Footnote 2: That prepared by Fairchild Brothers & Foster of New York
has proved the best in my hands.]

Peptonized milk is prepared by putting into a clean quart bottle 5
grains of extractum pancreatis, 15 grains of bicarbonate of sodium, and
a gill of cool water; shake, and add a pint of fresh cool milk. Place
the bottle in water not so hot but that the whole hand can be held in
it without discomfort for a minute, and keep the bottle there for
exactly thirty minutes. At the end of that time put the bottle on ice
to check further digestion and keep the milk from spoiling.

Peptonized milk-gruel is made of equal parts of any farinaceous gruel
and fresh cold milk. To a pint of this combination 5 grains of
extractum pancreatis and 15 grains of bicarbonate of sodium are added,
and the whole allowed to stand in a warm place for thirty minutes, when
the process of digestion must be arrested by placing on ice.

Peptonized broth is made in the following way: Take one-fourth of a
pound of finely-minced raw lean beef or mutton or chicken, and one-half
pint of cold water; cook over a slow fire, stirring constantly, until
it has boiled a few minutes. Then pour off the liquor, beat the meat to
a paste, and put both into a bottle with a half pint of cold water. Add
30 grains of extractum pancreatis and 20 grains of bicarbonate of
sodium; shake well, and set in a warm place (110-115 degrees) for three
hours, shaking occasionally; then boil quickly. Finally, strain or
clarify in the usual way and season to taste.


MORBID GROWTHS OF THE PANCREAS.


Carcinoma.

Cancer is probably the most common of the chronic affections of the
pancreas. It is usually secondary, being due to an extension of
carcinoma of the stomach, duodenum, liver, or abdominal lymphatic
glands, but there are enough cases on record to show that it may be
primary. It has been discovered in the foetus at birth, but the vast
majority of cases occur after the age of forty. Men are more frequently
affected than women. Nothing is known as to the influence of inherited
tendency in the production of the disease, and as little of the
exciting causes, though some authors attach much importance to
prolonged pressure upon the epigastrium and to blows and contusions on
the upper part of the abdomen.

ANATOMICAL APPEARANCES.--Primary carcinoma may be either {1124}
scirrhous, encephaloid, or colloid, the first being the variety most
frequently observed.

The lesion begins in the head of the gland in the form of several small
nodules which gradually coalesce. Sometimes the whole gland becomes
involved in the new formation; again, isolated nodules may be scattered
throughout its substance, and exceptionally the growth is limited to
the tail or middle portion. When the head alone is involved, the
remainder of the gland either remains healthy, undergoes fatty
degeneration, or becomes indurated. The tumor is rounded in outline and
nodular, and varies in size, density, and color according to the form
of carcinoma present. The duct of Wirsung is ordinarily obstructed,
large retention cysts, containing a yellowish-red liquid, are formed,
and the changes already described under the head of Chronic
Interstitial Pancreatitis take place in those portions of the gland
which are free from carcinoma. The disease is very prone to extend to
the surrounding organs, particularly the neighboring lymphatic glands,
the duodenum, and the liver, rarely to the stomach. When the contiguous
organs are not directly implicated in the carcinomatous changes, they
are subjected to pressure by the tumor, and in the case of the stomach
and duodenum adhesions often form, and are followed by perforation.
There seems to be a tendency also to infiltration of the adjacent
subperitoneal connective tissue and to hyperplasia of the fibrous
tissue of the viscera, even when they are not secondarily involved in
the morbid growth, leading to narrowing of the aorta, thickening of the
walls of the stomach and duodenum, and a sclerosis of the liver.
Obstruction of the common bile-duct, with dilatation of the
gall-bladder from retention of bile, is a frequent result of the
disease.

Secondary carcinoma of the pancreas usually first appears in, and is
limited to, the head of the gland. It seldom occurs in isolated
nodules, but the growth is generally continuous with the primary
cancerous mass. The form is either scirrhous or encephaloid. Wagner
records a case of cylindrical-celled epithelioma following a simple
epithelioma of the mucous membrane of the duodenum; and a similar
instance has come under the author's own observation;[3] but this
variety of morbid growth is rare. The primary growth is almost
uniformly situated in the stomach, duodenum, liver, or gall-bladder,
though occasionally it may be seated in some distant organ; in such
cases the pancreatic tumor appears as an isolated nodular mass.

[Footnote 3: _Transactions of the Pathological Society of
Philadelphia_, vol. ix. 13.]

SYMPTOMS AND COURSE.--The symptoms may be divided into two
classes--namely, first, those which arise from the lesion of the gland
itself; and, secondly, those which depend upon the effect of this
lesion on the neighboring viscera.

The features belonging to the first class are general marasmus, pain,
the appearance of fat and perhaps undigested muscular fibres in the
fecal evacuations and of fat in the urine, and the physical signs of an
abdominal tumor.

Loss of flesh is one of the earliest symptoms: it is generally
progressive, and is at times so great that the spine can be distinctly
traced through the abdominal walls. Together with this emaciation there
is debility, often extreme, but sometimes not so marked as might be
expected from the degree of wasting. The skin is commonly pale and dry,
and before jaundice is {1125} developed has the ordinary sallow hue of
cancerous cachexia. The features are pinched, and the face wears an
expression of anxiety and suffering. In cases uncomplicated by
peritoneal inflammation the temperature remains about normal, or it may
be lowered as the general exhaustion increases. The pulse is feeble and
slightly increased in frequency.

Pain is the most uniformly present and the earliest symptom. It is
always situated deep in the epigastrium, and from thence extends to the
back, to the right or left side, downward to the umbilicus or lower
part of the abdomen, and upward into the chest. It is generally
continuous, but is subject to remissions and paroxysmal exacerbations.
During the remissions sensations of distress, of burning, or of dull
pain are experienced at the pit of the stomach; during the
exacerbations, which may last several days, the pain becomes extremely
acute and lancinating and extended in distribution. The ingestion of
food and pressure upon the epigastrium have no constant effect upon the
pain. Quick movements of the body from side to side often increase it
and excite exacerbations. The suffering is greatest in the erect
posture, and on this account the patient bends his body forward so as
to relax the abdominal muscles. The paroxysmal and neuralgic character
of the pain indicates implication of the coeliac plexus.

The appearance of fat in the stools is an important symptom, unless
there be at the same time an obstruction to the passage of bile into
the duodenum, indicated by jaundice. Lipuria has been noticed in a few
cases only.

In many instances (nearly one-half of the number of recorded cases)
physical exploration reveals the signs of enlargement of the organ. At
times there is merely a sense of fulness and resistance to the touch,
and a modified tympanitic percussion note in one of the three regions
of the upper segment of the abdomen. But usually when a tumor is
present it is readily mapped out by palpation. The tumor is seated in
the epigastrium, and may extend into the right or left hypochondrium or
downward into the umbilical region. It varies much in size, is rounded,
nodulated, firm, slightly movable or fixed, and tender, though
sometimes painless, to the touch. Percussion yields dulness or a
dull-tympanitic sound. On auscultation a blowing murmur may be heard
when the tumor presses upon the aorta; and when this murmur is present
there is usually also transmitted pulsation.

The symptoms belonging to the second class arise when the adjacent
viscera become involved in the cancerous disease, or when their
functional activity is disturbed by the encroachment and pressure of
the enlarged pancreas.

From the association of a catarrhal condition of the mucous membrane of
the stomach, particularly when the pyloric orifice is obstructed,
several prominent symptoms of gastric catarrh are frequently
observed--namely, sialorrhoea, pyrosis, acid eructations, flatulence,
abnormal sensations, such as burning, weight and oppression in the
epigastrium after taking food, and increased thirst. The tongue varies
in appearance: it may be dry and covered with a brown or yellow fur,
but when the flow of saliva is increased it is peculiarly clean and
moist; and this condition is rather characteristic. The appetite is
also variable; sometimes it remains good {1126} until the end, and
occasionally it is perverted. Hiccough in some cases is an obstinate
and annoying symptom.

Nausea and vomiting are late but moderately constant features. Their
relation to the ingestion of food is not fixed. The vomited matter may
consist of food, of glairy mucus more or less tinged with bile, of
colorless liquid, or of a fluid resembling a mixture of bran and water.
If there is marked pyloric obstruction with dilatation of the stomach,
large quantities of frothy and fermenting material containing sarcina
ventriculi are rejected at intervals. In the rare cases in which
secondary sarcoma of the viscus is developed the ejecta are bloody or
have the coffee-ground appearance, and the vomiting occurs several
hours after eating, as the new growth is generally situated at the
pylorus. When there is adhesion of the pancreatic tumor to the stomach,
with perforation, both blood and pus are vomited. Dilatation of the
stomach is attended by prominence of the epigastrium and an extended
area of gastric tympany, and in cancer of the pylorus a tumor is often
appreciable on palpation. The bowels are usually constipated. The fecal
evacuations are hard, and when the biliary secretion is absent from the
intestine they are clay-colored, and often contain fat. When there is
ulceration of the mucous membrane of the duodenum following secondary
cancer or adhesion, the stools become black and tar-like from the
presence of altered blood. Complete obstipation occurs in mechanical
obstruction of the gut from direct pressure or from bands of lymph.
Occasionally, just before death there is diarrhoea, and there may be an
alternation of vomiting and diarrhoea.

The symptoms and signs of secondary carcinoma or sclerosis of the liver
may be present, but the most commonly observed indications of impaired
hepatic function depend upon pressure-obstruction of the common
bile-duct. These are jaundice, fatty and clay-colored stools, and the
appearance of a tumor in the region of the gall-bladder. Jaundice is a
very common symptom. It occurs late in the disease as a rule, is
progressive and persistent, resisting all treatment, and is extreme in
degree, the skin becoming deep-yellow or greenish in color. The tumor
of the distended gall-bladder is pyriform in shape, firm and elastic to
the touch, yields a dull percussion sound, and occupies a position
opposite the extremity of the tenth rib on the right side of the
abdomen.

Dropsy occurs in a large proportion of cases (nearly one-half) during
the advanced stages of the disease. It is due to vascular obstruction
occasioned by the pressure of the enlarged pancreas itself or of the
secondarily degenerated coeliac glands, and finally by secondary
lesions of the liver. The dropsy appears either in the form of ascites
or anasarca, is not often extreme in degree, and is subject to
variations, disappearing and reappearing at intervals. Ascites is the
more common form, but both conditions may exist in the same patient.

It is impossible in the majority of instances to definitely fix the
date of onset of a pancreatic cancer, but the average duration of the
disease may be stated to be about one year. The uniformly fatal
termination usually takes place slowly from gradual exhaustion or with
the symptoms of an adynamic fever, but death may occur suddenly from
hemorrhage.

DIAGNOSIS.--The principal features of carcinoma of the pancreas are
extreme emaciation, loss of strength, dyspepsia, pain of a neuralgic
{1127} character in the epigastrium, constipation, obstinate jaundice,
moderate ascites or anasarca, the appearance of fat in the stools,
lipuria, occasional vomiting, and the physical signs of an epigastric
tumor.

These symptoms are not pathognomonic, however, and the diagnosis can be
certainly established only when it is possible to exclude primary
disease of the surrounding organs, especially of the stomach and liver.

Cancer of the stomach may be excluded by the less-marked character of
the functional disturbances of the viscus; by the absence of frequent
vomiting, haematemesis, and the rejection of coffee-ground material; by
the somewhat different situation and greater immobility of the tumor,
by the seat, distribution, and constancy of the pain; and by the
presence of jaundice and of fat in the stools and urine.

Diseases of the liver attended with alterations in the size of the
organ, as cancer, abscess, albuminoid and fatty degeneration, sclerosis
and hydatid tumor, have sufficiently characteristic physical signs and
symptoms to be readily distinguished from cancer of the pancreas. On
the other hand, the tumor of an enlarged gall-bladder is often
confusing. The situation of this tumor opposite the tenth rib and its
pyriform shape are important; other distinguishing points depend upon
the cause of the enlargement. In enlargement from accumulated bile the
tumor is elastic and fluctuating; from accumulation of gall-stones,
hard and nodulated, movable, painless on palpation, and often the seat
of crackling fremitus, produced by manipulation and due to the rubbing
together of several calculi; from cancer, hard, nodular, the size of an
orange, tender on pressure, rapid in growth, preceded by attacks of
biliary colic, and attended by fistulous communications with the
intestines and the passage of gall-stones per anum.

In aneurism of the aorta or coeliac axis the tumor may present in the
epigastrium and produce analogous pressure symptoms. But the pain is
more of the character described as wearing, and is usually augmented at
night: on grasping the tumor a uniform expanding pulsation is felt in
place of the to-and-fro movement appreciable in a tumor resting upon a
healthy blood-vessel and receiving a transmitted impulse, while the
constitutional symptoms and course are quite different.

The tumor of malignant disease of the omentum, although it appears in
the epigastrium or upper part of the umbilical region, is much more
movable, and is accompanied by ill-defined symptoms very dissimilar to
those of pancreatic cancer.

In cancer of the transverse colon the mass may occupy nearly the same
position as a pancreatic growth, but the pain occurs several hours
after food is taken; vomiting is absent, and there is frequently
hemorrhage from the bowels.

Chronic pancreatitis is accompanied by symptoms simulating those of
cancer; the enlargement of the gland, however, is not so great, nor are
the indications of pressure upon adjacent organs so prominent. The pain
is less severe, the general failure in health more gradual, the
progress slower, and constipation less common.

TREATMENT.--The indications are to maintain the strength of the
patient, to provide a diet that is nutritious and at the same time
easily digested, to allay pain by the employment of narcotics, and to
relieve as far as possible the various symptoms as they arise. The plan
of {1128} administering a calf's pancreas or extractum pancreatis will
prove serviceable when the fecal evacuations contain fat. Nutritious
and peptonized enemata may be of service in some cases.


Sarcoma and Tubercle of the Pancreas.

Sarcoma of the pancreas occurs with extreme rarity. It is impossible
during life to distinguish it from carcinoma.

Tubercle of the gland is infrequently met with. Some pathologists deny
its occurrence, and believe that the cases recorded as such are merely
instances of caseous degeneration of the neighboring glands. When it
does occur, it is always secondary, the primary disease being situated
in the lungs or intestines. The alterations in the gland consist in the
development of cheesy masses or of miliary granulations in the
connective tissue between the acini. The condition gives rise to no
definite symptoms, and its diagnosis during life is impossible.


DEGENERATIONS OF THE PANCREAS.


Fatty Disease of the Pancreas.

Two forms of fatty degeneration occur, either separately or
combined--namely, fatty infiltration and fatty metamorphosis.

Fatty infiltration consists of a true hypertrophy of the fat-tissue
normally existing in the gland, or of an increase and extension into
the gland of the peripancreatic adipose tissue. Yellow bands and masses
of fat-tissue appear between the acini, and by constantly increasing in
size lead gradually to a total atrophy of the cells of the acini. The
canal of Wirsung contains a fatty liquid. These changes are found
associated with fatty liver, heart, and omentum, in drunkards
especially.

Fatty metamorphosis of the gland consists of a change analogous to
fatty metamorphosis of other organs. When hyperplasia of the
interstitial connective tissue is absent, the organ is flaccid, soft,
and diminished in size; the acinous structure remains distinct, though
the acini and ducts are filled with a fatty emulsion: after this is
discharged or absorbed the gland appears as a flaccid band, and finally
becomes entirely atrophied. Fatty metamorphosis occurs in drunkards, in
diabetes, in advanced age, in cancer, phthisis, and other wasting
diseases.

Neither form of fatty disease gives rise to symptoms by which it can be
recognized during life.


Albuminoid Degeneration of the Pancreas.

This is only found in combination with amyloid change in other organs
of the body, and a diagnosis cannot be made.


{1129} Hemorrhages into the Pancreas.

Hemorrhages into the pancreas may be divided into three classes.

The most common form depends upon passive hyperaemia, the result of
chronic diseases of the heart, lungs, or liver. In this condition the
effusion of blood coexists with chronic inflammatory changes in the
interstitial connective tissue. The appearance at first is of minute
bloody points scattered throughout the areolar tissue; later, these
change into round or oval pigment masses, or spaces containing reddish
serum and surrounded by thickened, rust-colored, irregular walls.

The second class includes the rare cases of hemorrhage resulting from
the rupture of one of the large blood-vessels of the gland, and due to
some pre-existing change in the vessel walls. In these the pancreas is
enlarged, may be converted into a sac containing blood, either fluid or
coagulated or partially crystallized according to the duration of life
after the hemorrhage has taken place, and a ruptured blood-vessel may
be readily discovered on dissection.

The condition in which, without any evidence of passive hyperaemia or
gross vascular lesion, the entire pancreas become hemorrhagic,
constitutes the third class. The gland is then dark-red or violet in
color, the meshes of the interstitial tissue are filled with recent or
altered blood, and the acini are stained of a dull-gray hue. The
hemorrhage may extend to the connective tissue surrounding the gland.
Finally, the organ becomes soft, the peritoneal covering sloughs, and
fragments of broken-down gland-tissue escape into the peritoneal
cavity. These lesions are so analogous to those which attend thrombosis
occurring in other organs that their dependence upon the same cause
seems probable.

The first form of hemorrhage is unattended by special symptoms. In the
second a pulsating tumor may suddenly appear in the epigastrium, and
the ordinary indications of hemorrhage--vomiting, fainting fits, cold
extremities, feeble pulse, and general exhaustion--are present. Death
may occur suddenly or the patient may linger on for months. In the
third condition death usually occurs very suddenly, probably from
pressure upon the sympathetic ganglia. There are no symptoms, and the
rapid termination prevents the development of general peritonitis,
which would otherwise occur from the sloughing of the peritoneum.

There are no indications for treatment.


OBSTRUCTION OF THE PANCREATIC DUCT.

Obstruction of the excretory duct is a frequent occurrence in
pancreatic disease, and is due to two classes of causes--namely, 1st,
pressure from without; and, 2d, closure of the canal by catarrhal
swelling of its mucous membrane or by calculi.

In the first class may be placed obstruction depending upon contraction
occurring in sclerosis of the gland, upon carcinoma of the head of the
gland, upon peripancreatic adhesions and indurations, upon the {1130}
presence of large gall-stones in the ductus choledochus, and upon
carcinoma of the pylorus and duodenum and enlargement of the
neighboring lymphatic glands.

In catarrh of the canal of Wirsung the obstruction results either from
simple swelling of the mucous membrane or from the presence of a plug
of tough mucus.

The formation of pancreatic concretions is by no means a rare event,
though these calculi are met with far less frequently than either
gall-stones or salivary concretions. They result from precipitation of
the inorganic ingredients of the pancreatic juice, and are usually
seated in the main duct, although they may be situated in the smaller
branches. They may be single or multiple, as many as twenty having been
counted in one gland. In shape they are spherical, oval, or branched,
with sometimes a smooth, at others a spiculated, surface; their size
varies from that of a minute granule to a small walnut; they are
usually white or grayish-white in color, but may be black; and are
composed of the carbonate of lime or of a combination of the carbonate
and phosphate with oxalate of lime. Coincidently with these calculi it
is common to find concretions in the kidneys and gall-bladder.

Concretions composed of insoluble protein substances have also been
found in the pancreatic ducts (Virchow).

The most probable causes of the formation of pancreatic calculi seem to
be catarrhal conditions of the mucous membrane of the ducts and an
alteration in the chemical composition of the secretion.

Whatever the cause, the obstruction, when complete, leads to retention
of the secretion and the formation of retention cysts.

When the obstruction is situated at the duodenal extremity of the duct,
the canal and its secondary branches are either uniformly dilated or
sacculi are formed. These sacculi are round or oval, vary greatly in
size, sometimes reaching the dimensions of the fist or of a child's
head; they may be single, or several of them may be present, differing
in size and causing irregular projections of the outer surface of the
gland. When the obstruction occurs at some point in the course of the
duct, the dilatations and sacculi are found only behind the point of
occlusion. The small cysts contain a fluid resembling the pancreatic
juice; the larger, a whitish, chalky fluid, which in old cases may
contain white friable concretions composed of carbonate and phosphate
of lime, and become purulent, or be stained bright red or
chocolate-colored from the occurrence of hemorrhage. In such instances
haematoidin crystals can be discovered by the microscope. The interior
of the dilated ducts and of the retention cysts is lined by a single
layer of thin flat cells, with irregular edges and with oval flat
nuclei. The walls are thickened, and composed of superimposed layers of
laminated connective tissue separated from one another by flat
nucleated cells. The secreting structure of the gland undergoes atrophy
from pressure, or fatty metamorphosis takes place, and, although the
gland is increased in size from the presence of the cysts, its
functional power is lost.

In addition to causing obstruction of the duct of Wirsung and the
changes mentioned, pancreatic calculi may produce induration, atrophy,
acute inflammation, or even suppuration of the surrounding glandular
tissue.

{1131} SYMPTOMS AND COURSE.--The main feature is the presence in the
epigastrium of a rounded, smooth, fluctuating, painless tumor. There
are also indications of the absence of the pancreatic secretion from
the digestive tract--notably, emaciation, general debility, and the
appearance of fat in the stools. Jaundice resulting from a coincident
obstruction of the bile-duct is a frequent symptom, and melituria has
been noted in some cases. It is probable, too, that the passage of a
calculus along the duct may give rise to pain resembling in character
and distribution the pain of hepatic colic.

The duration is indefinite. Sometimes the termination is sudden from
the rupture of a cyst into the peritoneal cavity or into the stomach or
duodenum, with hemorrhage.

DIAGNOSIS.--The absence of pain, of tenderness, and of cachexia,
together with the physical characters of the tumor, distinguishes it
from carcinoma of the gland.

Though not likely to be confounded with this disease, both hydatid
tumor of the liver and distension of the gall-bladder must be borne in
mind in making the diagnosis of a fluctuating tumor situated in the
upper third of the abdomen.

TREATMENT must be entirely symptomatic. Attention to the general
health, proper regulation of the diet, and the employment of pancreatin
or an infusion of calf's pancreas to supply the place of the deficient
pancreatic juice, are the important steps. Attacks of pancreatic colic
indicate the use of anodynes.

In two reported cases in which the cysts were very large paracentesis
for the removal of the fluid contents was resorted to, and there are
two cases on record in which the cysts were extirpated after abdominal
section. Kulenhampff of Bremen records a case of a man, thirty-nine
years of age, in whom, after a succession of severe blows upon the
abdomen, a tumor appeared in the epigastrium. An exploratory incision
was made, and a few ounces of pancreatic fluid evacuated by aspiration.
Six days afterward the abdomen was opened, the peritoneum united to the
incision, and antiseptic gauze inserted to produce adhesive
inflammation between the sac and the abdominal wall. Adhesion taking
place after four days, the cyst was opened, a liter of fluid evacuated,
a tent inserted, and an antiseptic dressing applied. For sixteen days
fluid constantly escaped in slowly diminishing quantities, and the
tumor disappeared, a fistulous tract remaining. This completely closed
under the use of tincture of iodine and nitrate of silver at the end of
the seventh week. Thiersch opened a pancreatic cyst and evacuated three
liters of chocolate-colored fluid; recovery with a fistula followed.

From a patient supposed to be suffering from ovarian dropsy Rokitansky
partially extirpated a cyst connected with the tail of the pancreas;
death from suppurative peritonitis occurred on the tenth day.

N. Bozeman[4] on December 2, 1880, successfully removed from a woman
forty-one years old a pancreatic cyst weighing, with its contents,
twenty and a half pounds. In this instance also the operation was
undertaken for the removal of a supposed ovarian tumor, the diagnosis
not being established until after the abdomen was opened.

[Footnote 4: _New York Medical Record_, Jan. 14, 1882.]




{1132}

PERITONITIS.

BY ALONZO CLARK, M.D., LL.D.


Italian physicians in the later years of the seventeenth century and in
the early ones of the eighteenth had acquired some knowledge of the
symptoms of the disease we now call peritonitis, but known to them as
inflammation of the intestines. Indeed, it is claimed by some of the
admirers of Hippocrates that there are passages in his writings that
indicate some knowledge of the disease. But this claim will probably be
always received with many doubts as to its validity.

In confirmation of the first statement I will transcribe certain
passages from Morgagni's thirty-fifth letter: In inflammation of the
intestines "Albertini had observed the pulse to be low and rather weak,
such as you will find it to have been in general in the foregoing
letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to
be tense and hard, the face and eyes to have something unusual in their
appearance. "Medical writers, indeed, agree in the tension of the
abdomen, but they add many other symptoms, which prove beyond a doubt
the intestines to be inflamed; yet they mean that evident inflammation
which all may easily ascertain, and not that obscure disorder which we
now speak of, and which few suspect" (gangrene of the intestines). "By
the same writers it is also supposed that there is an obstinate
costiveness and continual vomiting."

Morgagni refers to the assistance rendered by Albertini, Valsala, Van
Swieten, Rosa, and others in elucidating this subject. It is singular,
considering the clearness of his perception of the symptoms of
inflammation of the intestines, that he should be so greatly confused
regarding gangrene and sphacelus of the same parts. He looks on these
as the result of inflammation, and when the two classes of cases are
considered and compared, the result is a contrast and not a
resemblance. Yet he supposes that the differences are to be accounted
for by the different modes in which the same disease may be developed
in different persons.

Another thing obtrudes itself on the attention in these letters: that
while a number of post-mortem examinations are reported of those who
had died of inflammation of the intestines, of gangrene and sphacelus
of the intestines, of hepatic abscess opening into the peritoneal
cavity, there is no record of finding in the abdomen anything
corresponding to what is now known as the inflammatory effusions from
serous membranes.

Sydenham died in 1689. I have searched his works, not for {1133}
peritonitis, for the word was not in use in his day, but for some
account of inflammation of the intestines or of some disease in the
description of which symptoms are named that distinguish or belong to
peritonitis, and with the single exception of pain the search has been
fruitless.

Cullen in 1775 mentions the disease, but says that so little is known
about it that he will not attempt a description of it.

Bichat died in 1802 in the thirty-eighth year of his age. I am not able
at present to lay my hand on his _Pathological Anatomy_; I therefore
quote from Chomel's article on peritonitis in the _Dictionnaire de
Medecine_ to show his claim to important studies regarding that
disease: "For a long time peritonitis was confounded under the name of
inflammation du bas ventre with inflammations of the abdominal viscera;
and it is to Bichat belongs the merit of having proved that
inflammation of the peritoneum is a disease distinct, and that it ought
to be separated from enteritis, gastritis, etc., as pleurisy is
separate from pneumonia. The studies of Gasc and of Laennec soon
confirmed the opinion of Bichat, and assured to peritonitis the
important place which it ought to occupy in all nosological tables. It
has become since then a subject of numerous observations and of
interesting researches regarding the causes de sa marche and the
lesions it causes."

The references are not given by Chomel, but they are probably these:
Laennec, _Histoire des Inflammations du Peritoine_, 1804; and Gasc,
_Dictionnaire des Sciences Med._, p. 490, 1809.

Gasc says that the twenty years next preceding his publication
witnessed the first stage of the true history of peritonitis. Walther
in 1786 had contributed some facts, and S. G. Vogel in 1795, but the
rounding off and completing their work was left for Bichat.


Acute Diffuse Peritonitis.

MORBID ANATOMY.--The first thing that strikes the observer in the
post-mortem examination of a person who has died of this disease is the
tendency of the intestines to protrude through the cut made in the
abdominal wall. This is produced by their dilatation generally, both
small and large, by gas. No gas, under these circumstances, ever
escapes from the peritoneal cavity unless there has been perforation of
the alimentary canal somewhere. While the intestines are in this manner
dilated, the stomach is small and usually empty.

On the surface of the intestines there will be found a layer of
coagulated fibrin, often very thin and delicate, requiring a scraping
of the surface of the peritoneum to demonstrate it, but commonly
obvious enough, and sometimes quite abundant. This same false membrane
can be found on the viscera covered by the peritoneal membrane, on its
anterior extension, and most at the point of contact of one coil of the
intestine with another. Incorporated with this new membrane or lying
under it will often be seen blood-spots, thin, translucent, diffused,
and having ill-defined boundaries.

The blood-vessels themselves are not remarkably congested. Here and
there may be spots where some redness remains, and the vessels are
larger than natural. But the congestion and redness, which analogy
leads us to {1134} believe belong to the active stages of the disease,
have in great degree disappeared after death.

The peritoneal membrane itself has hardly become thickened, certainly
not in marked degree, but it has lost its lustrous surface, is, at
least in parts, of an opaline color, as if it had absorbed diluted
milk, and there is an effusion of serum or slight oedema on its
attached surface. Whatever may be the popular opinion regarding the
termination of inflammation of the bowels in mortification, whatever
the opinion of the older physicians, it is safe to say that gangrene of
the peritoneum has never been the result of uncomplicated, diffuse,
acute peritonitis. Peritonitis from strangulation of the intestine or
analogous causes is of course excepted. But in puerperal peritonitis I
have noticed a fact to which I have nowhere seen an allusion. The
parietal peritoneum is at two points in the abdomen but loosely
attached to the wall. One of these is on the anterior wall, anterior to
and a little above the iliac fossa; the other is above and below the
kidney on each side of the body. In these parts I have seen the
membrane forced off from its attachment to the walls, which with it
made a sac containing pus. Such an abscess, if the patient live long
enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous
effusion, commonly not seen at first on opening the abdomen, for it has
sunk into the pelvis. It is transparent, of a yellowish hue, and
sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by
it is a question that has been much discussed; but it is admitted that
these organs, to a shallow depth on their surface, have an unnatural
color; and when it is remembered that the peritoneum is nourished by
vessels not exclusively its own, but running along its attached
surface, and distributed as well to the surface of the organs it
covers, it is easy to admit that to a very limited depth the organs
partake of the inflammatory disease. This supposition gives an easy
explanation of the constipation which is so prominent a feature among
the symptoms of the disease.

The manner in which the false membrane is disposed of in those who
recover is an interesting question. Forty or more years ago Vogel
described the process by which the new effusion became a living tissue,
and the manner in which blood-corpuscles and blood-vessels were formed
in it; and another author had found that the time needed to complete
this vascularization was twenty days. But now Bauer and most of the
German writers inform us that the coagulated fibrin is converted into
fatty matter and is absorbed, and that when adhesions occur they result
from the coalescence of a new formation of the connective-tissue
elements built up into granules. The question, then, arises, Will the
chemical constitution of fibrin permit its conversion into oil? If it
will, then the further question presents itself, By what chemical
action is the change effected within the body? I do not intend to
discuss these questions, but propose them by way of expressing some
doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was
pushed off by the first of the effusions in peritonitis, and that this
was one of the causes of the lustreless appearance of the membrane.
This {1135} opinion I have never attempted to confirm or correct by the
microscope. Bauer confounds this idea. He says: "The deposition of
fibrin occurs before the endothelium presents any changes. This
fibrinous effusion encloses, primarily, hardly any cellular elements,
and only a few cast-off endothelial cells are to be found in it. The
endothelium itself is swollen and turbid; the cell-body is increased in
size; the contents are granular; multiplication of the nuclei is
apparent; the cells are, in fact, in active division. In the tissue of
the serous membrane itself, soon after the deposition on its surface,
an accumulation of indifferent (?) cells takes place, especially around
the vessels, so that the spaces between the vessels are thus completely
filled up. The fixed connective-tissue corpuscles take part in the
inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death,
we find the entire peritoneum of a bright-red color from congestion of
the blood-vessels; but that is all: there is no fibrin, no serum, no
pus; epithelial cells are increased in size and number." For this kind
of peritonitis he proposes the term cellular. He finds it in cases of
local abscess of the abdominal cavity in which inflammatory action has
extended over the whole membrane, and particularly on the omentum also,
in the first two days of puerperal peritonitis. "The ordinary form of
acute peritonitis is attended with changes in the endothelium and fixed
connective tissue, and with the production of serum, fibrin, and pus."
He describes the migration of white corpuscles of the blood through the
walls of capillaries to become pus-cells, and then says: "Minute
examination shows that two distinct sets of changes are going on at the
same time: first, a production of fibrin, serum, and pus; second,
swelling and multiplication of the endothelial cells. If the
inflammation is very intense, the pus and fibrin are most abundant; if
milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the
inflammatory effusions. In opposition--or, perhaps better, in
correction--of this idea, Delafield says: "There may be a considerable
amount of pus produced, and yet the layer of endothelium remains in
place." "If, however, the pus and fibrin are produced in large amounts,
the endothelium falls off and leaves the surface of the peritoneum
bare." The connective-tissue cells of peritoneum, he says, undergo but
little change in the first three days of the inflammation, "but by the
seventh day these cells are marked by increase in size and number in
all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of
the false membrane and serum of peritoneal inflammation, of which I do
not remember to have seen a description. It is this: the serum is
enclosed or encysted in bladders, the walls of which are the false
membrane. There may be two or three layers of these bladders, one upon
another, all more or less flattened, and each holding from two to six
ounces of fluid. It would seem that in these cases the inflammatory
activity rose and fell in its progress, early reaching the point at
which coagulable lymph was effused, then falling to the stage in which
serum alone escaped. This serum lifted the false membrane irregularly,
so that several pools were formed. After this the inflammation returns
to the fibrous exudation stage, and gives to these bladders a floor
which blends with the {1136} roof at the edges, and thus makes a
complete sac. Once more the inflammatory action is changed in its
intensity, so that the only effusion is serum; and this serum again
raises the new layer of false membrane into bladders--not always or
generally in the exact position of the first series. Still again, the
inflammation may be so changed as to make a fibrinous flow to this
second series of bladders. I am not certain that I have seen a third
series of these rare productions. They have doubtless been seen by
other persons, and may have been described. I have not been an
exhaustive reader on the subject, but I can well understand how they
may have been called hydatids on examination of the sacs without
looking at the contents. The fluid in the cysts is simply serum, with
no echinococcus sacs, and then the number of these inflammatory sacs
greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive
peritonitis, although it is frequently found in that form of the
disease that attends puerperal fever, septicaemia, or erysipelas. Yet I
have seen it a few times. The pus is not generally pure, but is mixed
with serum in different proportions, and there will be seen at the same
time deposits of lymph attached to the peritoneum or scales of it
floating in the fluid effusion, or both. There is reason to believe
that in the cases of this class a very large proportion are fatal in
the acute stages, but in the cases that live for a few weeks the pus is
disposed to collect in pools and become abscesses by adhesions around
them at their borders. These abscesses are disposed to find an exit
from the body. In one case four abscesses that were found in this way
in different parts of the abdominal cavity had each burrowed toward the
umbilicus, and were actually discharging their contents at this point
when I saw the case. In another case one abscess only was formed, and
in four weeks it had perforated the colon. The opening was nearly an
inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric
plexus in persons who had died of acute peritonitis changes which he
regards as inflammatory had occurred, with subsequent opaque swelling
of the nerve-cells, ultimate fatty degeneration, brown pigmentation,
and atrophy. In chronic peritonitis the cells are often converted into
amorphous pigment matter, with increase and sclerosis of the ganglionic
connective tissue. Still, it is worthy of notice that these changes do
not express themselves in symptoms in those that recover.

ETIOLOGY.--Numerous writers have expressed a doubt whether a
spontaneous acute peritonitis ever occurs, or if it is ever primary its
occurrence in this way is very rare. Habershon[1] has presented the
case with more apparent force than any other writer. He studied the
record of five hundred autopsies of peritonitis made at Guy's Hospital
during twenty-five years, but he "cannot find a single case thoroughly
detailed where the disease could be correctly regarded as existing
solely in the peritoneal serous membrane."

[Footnote 1: _Medico-Chirurgical Trans._, vol. xliii. p. 5.]

This statement must be received with some caution. In twenty-five years
the records were probably made by a number of different persons, and
persons of varying views and varying capacity and judgment. It is
possible that the quotation may embrace some of the changes already
referred to as the consequences of peritonitis. It does embrace the
cases {1137} "when inflammation of the serous membrane occurs in the
course of albuminuria, pyaemia, puerperal fever, erysipelas, etc." It
also includes "peritonitis caused by general nutritive changes in the
system," as seen "in struma, cancer, etc.," "comprising also those
cases in which the circulation of the peritoneum has been so altered by
continued hyperaemia (modifying its state of growth) that very slight
existing causes suffice to excite mischief, as in peritonitis with
cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would
seem to mean without them. It is far from saying that peritonitis
always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all
these years the curative treatment of peritonitis, to which the paper
itself gave currency, has enabled us to study our cases after recovery
as well as before the sickness, and it can hardly be doubted that a
much larger proportion of the cases are primary and idiopathic than
either Louis or Habershon found reason to admit. That a large number
are produced by preceding lesions and constitutional conditions no one
will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by
Habershon, he found preceding disease or injury recognizable in the
abdominal cavity in 261. The following is his table, viz.:

  From hernia, of which 19 were internal obstruction . . . . . . . 102
  From injuries or operations  . . . . . . . . . . . . . . . . . .  35
  From perforation of the stomach, ileum, caecum and appendix,
    colon, etc. (other 13 mentioned with hernia, or with caecal
    disease) . . . . . . . . . . . . . . . . . . . . . . . . . . .  43
  And leading to fecal abscess (2 otherwise mentioned) . . . . . .  17
  From typhoid ulceration without perforation  . . . . . . . . . .   5
  From disease or operation on bladder and pelvis, viscera, etc. .  42
  From disease of the liver and gall-bladder . . . . . . . . . . .  11
  From acute disease of the colon (3 others enumerated with
    perforation) . . . . . . . . . . . . . . . . . . . . . . . . .   3
  From disease of the caecum or appendix (9 others previously
    mentioned) . . . . . . . . . . . . . . . . . . . . . . . . . .   3
                                                                   ---
                                                                   261

Habershon says that in the (his) second and third divisions of the
cases the causes were as follows:

  From Bright's disease  . . . . . . . . . . . . . . . . . . . . .  63
  From pyaemia, 13; erysipelas, 5; puerperal fever, 10; with
    pneumonia, 3 . . . . . . . . . . . . . . . . . . . . . . . . .  31
  From strumous disease  . . . . . . . . . . . . . . . . . . . . .  70
  From cancerous disease . . . . . . . . . . . . . . . . . . . . .  40
  From hepatic disease . . . . . . . . . . . . . . . . . . . . . .  27
  From heart disease . . . . . . . . . . . . . . . . . . . . . . .   9
                                                                   ---
                                                                   240

I have drawn thus liberally from Habershon's paper because it is the
only paper that I know, in any language, founded on the analysis of a
large number of cases (for five hundred post-mortem examinations is a
large number for a disease no more frequent than peritonitis), in the
belief that he dealt with facts and that his conclusions must be of
great value. He may differ with other physicians regarding what
constitutes strumous disease and in the agency of heart disease. He may
have mistaken coincidence for consequence, but the paper bears the
marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of
{1138} peritonitis caused by "a changed condition of the blood," he
ascribes 63 to albuminuria. Every physician knows how often meningitis
or pericarditis or pleurisy may occur under these circumstances,
especially in young persons; but, for myself, I cannot but express
surprise at these figures. In one capacity or another I have been
connected with large hospitals for forty-eight years, and have seen
many cases of albuminuria in private practice, and can recall but few
instances in which kidney disease, excepting cancer and other tumors,
has terminated in peritonitis. In modification of this statement,
however, it is proper to add that the hospital physician cannot know
how half the diseases he treats terminate, on account of the American
plan of interrupted service, and even less can he know of the mode of
death in cases which he sees in consultation. Even with this admission,
from my standpoint it is not easy to believe that one-eighth of the
cases of peritonitis are caused by albuminuria.

The word pyaemia used by Habershon, it seems to me, ought to be
replaced by septicaemia, and it has been by many of the profession.
Sedillot many years ago proved that laudable pus injected into the
blood-vessels of the dog produced no signs of disease, but that septic
pus, so used, was followed by grave symptoms, even death. Among the
author's cases thirteen were associated with the septic poison. He also
found five which he thinks were independent of erysipelas. One in one
hundred is a proportion hardly large enough to establish the relation
of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the
October number (1881) of the _American Journal of Medical Sciences_,
whether diphtheria produces peritonitis. When diphtheria became
epidemic among us in 1860 or 1861 for several years, I saw a great deal
of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need
no commentary.

Perforations of the alimentary canal may require some illustrative
statements. These occur most frequently in the vermiform appendix of
the caecum, and are almost invariably caused by some irritating
substance imprisoned in its tube. In some cases it is a seed of some
fruit, as the orange or lemon; in others, a cherry-pit; in one that I
remember it was a small stone, such as is sometimes found in rice; in
others, a hard fecal concretion; in one, a child, a singular formation:
a strawberry-seed was the centre; around this a layer of fecal matter,
around the fecal matter a calcareous layer, on this, again, a fecal
layer, and so on to the number of six layers, the external one being
calcareous. This body was about one-fourth of an inch in diameter, and
may have been years in forming. In this connection I may state, per
contra, that I am informed that in a pathological museum in Boston is
preserved an appendix that contains, and did contain, a large number of
bird-shot, which did no mischief except to enlarge the appendix. This
was from the body of a man who had shot and eaten many birds. My
observation has led me to the belief that a large proportion of the
cases of peritonitis occurring in children are due to perforation of
the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the
foremost, I think, is abscess, single or multiple. The different modes
in which gall-stones may produce it may be illustrated by the following
{1139} cases: (1) A lady died of acute peritonitis. At post-mortem
examination a large abscess was found, bounded above by the liver, in
other directions by adherent intestines; it contained nearly a quart of
pus: at the bottom of the sac was a single gall-stone, very large and
very black; the gall-bladder was perforated and very much shrunken. The
gall-stone had caused an ulceration of the gall-bladder, but none of
the intestines, in this respect differing from the process known as
painless transit of a gall-stone. So the calculus caused the abscess,
and the abscess caused the general peritonitis. (2) A lady between
fifty and sixty years of age had an attack of gall-stone pains; she had
had them before. In a few hours symptoms of peritonitis were manifest,
and she died. The post-mortem examination showed the ductus cysticus
was ulcerated and perforated. Two gall-stones of large size had been
formed in the gall-bladder, and had been pushed forward into the duct
about halfway to the common duct, leaving it enlarged as they advanced.
The foremost one had caused an ulcer on the anterior or lower side of
the duct, and bile had escaped, staining all the right half of the
abdominal cavity, and throughout this half only the parts were covered
with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a
patient, a colored woman sixty-five years of age, who had been
suffering from intermittent fever, gastric disorder, and retching. In
one of the vomiting spells she experienced great pain, which, being
relieved by an opiate, soon returned and was attended by tympanitic and
tender abdomen. Death occurred in collapse about eight hours later. The
cavity of the abdomen was found filled with blood and bile, the
intestines inflamed and gangrenous in spots, and there was general
peritonitis. The gall-bladder was empty; the hepatic duct was
lacerated, and contained pouches in which gall-stones were encysted.
One of these bags was lacerated. This laceration was surrounded by
evidences of recent inflammation, and caused the general
peritonitis.[2]

[Footnote 2: The _Medical Record_, Dec. 9, 1882.]

The perforations of the stomach which I have seen have been attended by
little inflammation of the peritoneum. Death has followed this accident
in twenty to thirty-six hours. There has been little pain, little
tumefaction of the bowels, little tenderness, but a sense of sinking
and a peculiar feeling at the stomach which the patient finds it
difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the
colon, and yet do not with any uniformity cause general peritonitis;
but as the destructive process approaches the outer covering the latter
becomes inflamed, and lymph enough is effused to close the opening and
prevent the escape of the contents of the intestine; so that, while
perforation is not uncommon, I have rarely seen diffuse peritonitis
accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the
intestines caused peritonitis, and 15 from the complete perforation. I
believe that the physicians of this country and those of France have
found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines
produce peritonitis at all general. I did see, years ago, a man of
middle {1140} age in whom fecal impaction in the ascending colon had
caused destruction of all the layers of the abdominal wall on the right
side, so that the contents of the intestine were exposed to view in a
space of three inches by two. This implies that there had been
peritoneal inflammation enough to seal the intestine to the abdominal
wall on all the borders of this extraordinary ulcer. The man recovered
in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian
dropsy has sometimes been followed by acute peritonitis. In the early
part of my professional life I met with several such cases, and have
witnessed the same from time to time since. These were mostly cases of
dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7
in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger
number of cases such rupture, even when the result of violence, has not
led to inflammation; but the kidney secretion has been greatly
augmented and the fluid absorbed, so that the rupture has been
beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to
the surrounding structures by adhesions the result of chronic
inflammation, but now and then they provoke an acute attack which
becomes general. Benign tumors may, in rare instances, do this. In one
case a man died of acute peritonitis, and the examination showed that a
tumor noticed before death, a very large serous cyst standing out of
the left kidney, downward-forward, was the only lesion that antedated
the inflammation.

Infiltration of urine, in any of the several ways in which it can reach
the peritoneum, is a cause of peritonitis. Pelvic cellulitis may also
be a cause, though twenty or thirty cases in succession may run a
favorable course with no secondary lesions; it is still recognized as
one of the occasional causes of peritonitis.

Among the rare causes of diffusive peritonitis is perforation of the
intestine by lumbricoid worms. In such cases the product of the
inflammatory action is apt to be sero-purulent, with but a limited
amount of fibrin. E. Marcus reports such a perforation, and it was
called by Peris ascaridophagie. The worms were apparently not found in
the peritoneal cavity, but in the intestines. The perforation had
bloodless edges, which lay quite close upon one another, as if they had
been separated by a piercing action of the attenuated extremity of the
parasite not eaten through.[3]

[Footnote 3: _N.Y. Med. Journal_, Jan. 27, 1883.]

Lusk finds that certain vaginal injections excite a local peritonitis.
Sentey gives the details of a case in which a midwife undertook to
procure an abortion by the douche. She used a tube that was large with
a spreading mouth or opening, which probably received the neck of the
uterus in such a way as to prevent the return of the water. It was, in
consequence, forced into the uterus and through one of the Fallopian
tubes into the peritoneal cavity. By this a rapidly-fatal peritonitis
was developed. He refers to two other similar cases. It would seem that
this mode of procuring abortion can be frightfully misused, however
safe it may be in skilful hands.

There is a word still to be said regarding the difference between
peritonitis produced by wounds, operations, violence, and internal
growths, or {1141} what, with a little liberty, may be called traumatic
causes, and that which arises spontaneously or without recognizable
cause. The first shows a tendency to limit itself to the immediate
neighborhood of the injury, and more frequently does not become
general; while the latter spreads pretty quickly over the whole extent
of the peritoneum.

SYMPTOMS.--There is, perhaps, no grave disease whose symptomatology is
more easily interpreted, in which the diagnosis is more easily made,
than the average case of acute diffuse peritonitis. Yet there are
obscure cases which it is difficult to recognize.

In a well-marked case the first symptom is pain. Chomel and even some
later writers believe that chill precedes the pain, but to the best of
my recollection it has not generally so occurred to me; and the
question arises, Have they kept the symptoms of puerperal peritonitis
separated from those of simple peritonitis?

The pain is first felt in a somewhat limited space in the abdomen, and
pretty rapidly spreads, so that it is soon felt in every part of the
bowels. It may remain greatest in the part where it first began, but
there are many exceptions to this statement. As the disease advances
the pain and tenderness become more marked, and the patient will try to
diminish the tension of the abdominal walls by lying on his back and by
bending the hip- and knee-joints, often also for the additional purpose
of lifting the bedclothes from his abdomen. Often the patient will
resist the physician's movement to examine his bowel with the hand. In
the last few hours of life the pain ceases.

The pulse in its frequency follows the advances in the disease. At the
onset it is not much accelerated, but in two or three hours it may
reach 100 to 120 in the minute. Besides becoming more frequent, it
becomes smaller in volume and more tense. Toward the end of a fatal
case it may reach 140 to 160 in the minute and be very small.

In the early hours of peritonitis the bowels begin to swell, and
percussion shows that the swelling is caused by gaseous accumulation.
This increases as the disease goes on, so that in some the bowels
become greatly distended--so much, indeed, as to diminish the thoracic
space and interfere with the respiration. As the disease advances the
tympanitic resonance may give place to dulness on percussion on the
sides and lower part of the abdomen. This is due to fluid effusion.

Before the introduction of opium in the treatment of peritonitis the
green vomit was a marked feature of the disease. It occurs in other
conditions, but rarely, and its occurrence in this disease was so
common that it was regarded as almost diagnostic. The fluid vomited is
of a spinach-green color, and the color is probably derived from the
bile; at least, I have examined it repeatedly for the blood-elements,
and have not found them. In these days this symptom of peritonitis is
not often observed.

Constipation is absolute in uncomplicated peritonitis of ordinary
severity, and I believe is caused by a temporary paralysis of the
muscular layer of the intestine. It has already been stated that the
blood-supply of the peritoneum is through vessels whose capillaries are
shared by that membrane and the tissues which it covers. Inflammatory
action in the peritoneum of average severity would naturally extend to
this muscular layer and render it inactive. When the inflammation
abates it recovers its contractile power. Thus, the intestines become
entirely insensitive to {1142} cathartic medicines. This fact is not
observed in puerperal peritonitis, probably because the large share
which the uterus takes of the disease may act, in some degree, as a
derivative; and then, so far as I know, the muscular layer of the
intestines does not undergo the change of color and appearance in the
latter disease that has been observed in the former. This obstinate
constipation has been noticed from the first discovery of the disease,
and during forty years in the first part of this century many
physicians believed that if they could overcome it their patients would
recover. The present interpretation of this conviction is that if
catharsis, which was very rarely effected, did precede recovery, the
disease was not of a grave type--if, indeed, it was peritonitis at all.

Sometimes peritonitis occurs in the course of a diarrhoea; then the
constipation is not at once established, but the symptoms of the two
diseases concur for one or two days, when the diarrhoea ceases.

Abdominal respiration ceases when peritonitis is established, either
because the movements of the diaphragm produce pain or because the
diaphragm is partly paralyzed, as is the muscle of the intestines. Then
the gaseous distension of the bowels obstructs the action of this
muscle. As a clinical fact it is important, and has often helped me in
a diagnosis. Another kindred fact is that all the indications of
peristaltic action cease. I have a great many times placed my hand on
the abdomen and patiently waited for a sensation that would be evidence
of intestinal movements, but did not discover any--have placed my ear
on the surface of the abdomen, and have long listened for the gurgling
which is so constant in healthy bowels, and have listened in vain. In
this respect my observations differ from those of Battey, who reports
that he has heard the friction of the newly-made false membrane in
respiration, while I concur with him in the statement that the
sensation of friction can be felt by pressure of the ends of the
fingers into the abdominal wall so as to produce indentation. It should
be said regarding the friction sound in respiration that Battey has the
support of Chomel, and he in his turn quotes Barth and Roger; so that
there may be in this sign more than I have thus far found. (See case
hereafter related.)

The temperature of the body is not, considering the extent of membrane
involved, remarkably high. I have recently attended a most
carefully-observed case in which the temperature never rose above 104
degrees F. It falls below the temperature of health as the disease
approaches a fatal termination.

From the time this disease was recognized as a separate and distinct
affection the countenance has fixed the attention of writers. The face
is pale and bloodless and the features pinched, and the general
expression is one of anxiety and suffering. I do not remember to have
seen a flushed face in peritonitis, although the degree of paleness
differs in different patients.

The mind is almost always clear, unless disturbed by the medicines used
in the treatment. Yet cases are recorded in which a mild, and still
more rarely a violent, delirium has been noticed. Subsultus tendinum,
and even convulsions, have been witnessed, but whether these symptoms
belong to the peritonitis or to an accompanying uraemia has not
received the attention of those who have witnessed them.

The urine is usually scanty and high-colored, but it does not often
{1143} contain either albumen or casts. This statement is presumably
untrue of the cases in which Bright's disease preceded the peritonitis
and is supposed to be the cause of it--a variety of the disease with
which I have already declared my scanty acquaintance. The urine is
often voided with difficulty, and sometimes retained, so that resort to
a catheter becomes necessary.

The symptoms of this disease are not invariable. In one case the
inflation of the bowels is only enough to be perceptible; in another,
as I have said, it becomes a distressing symptom, while in most the
bowels are obstinately constipated. A case may now and then occur in
which evacuations can be procured by cathartics. Pain is regarded by
all physicians as the most constant symptom, and it has existed in
every case that I have seen, or at least tenderness; but the late
Griscom stated to me that a man once came to his office for advice in
whom he suspected peritonitis; but the man asserted that he had no
pain, and the doctor placed his fist on the abdominal wall and pushed
backward till he was resisted by the spinal column, the man asserting
that the pressure did not hurt him; yet he died the next day, the
doctor declared, of peritonitis. This may be credible in view of the
fact that absence of pain in puerperal peritonitis is not very
uncommon. The green vomit, which was expected in all cases forty years
ago, for the most part, as I have intimated, disappears under the opium
treatment. There are persons in whom peritonitis does not accelerate
the pulse beyond 100 beats in the minute. The pain, in rare cases,
remits and recurs with some degree of regularity, in this respect
resembling intestinal colic. Andral reports such a case; I have also
witnessed it.

MORTALITY.--Up to the time when the opium treatment was adopted,
peritonitis was a fearful word; a large proportion of those attacked by
it died of it. In 1832, I began to visit hospitals as a medical
student, and for eight years, at home or abroad, was almost a daily
attendant. The number of recoveries of those that I saw in that time
can be counted on the fingers of one hand. This may be regarded as its
natural mortality, for the treatment of that day seemed to exercise
little or no control over it. (Farther on this matter will be referred
to again.)

DURATION.--Chomel believed that the disease might prove fatal in
eighteen hours, while he regards its average duration as seven or eight
days. I very much doubt whether peritonitis, not caused by perforation,
violence, or surgical operation, was ever fatal in eighteen hours. I do
not remember any case of shorter duration than two or three days. Then,
on the other hand, the period of seven or eight days in the fatal cases
appears to me too long. In the early part of my professional life I
remember to have looked for death in three or four days. At present, in
the fatal cases, life is prolonged to double or more than double that
time. In the majority of those that recover at present the duration of
the symptoms is from two days to a week; in a few they have continued
fourteen days; and lately I have assisted in the treatment of a case in
which there was little amelioration for forty days, and yet the
peritonitis was cured.

DIAGNOSIS.--When the symptoms are fully developed there are few
diseases that are more easily recognized. It is when these symptoms are
slowly or irregularly manifested, or when some other disease which may
account for many of the symptoms occurs with it or precedes it, that
there {1144} should be any real difficulty. It is customary to regard
the danger of confounding the transit of a renal or hepatic calculus
with peritonitis as worthy of comment. But if the reader will turn to
the articles in this work which relate to these topics, he will find
the symptoms so widely different from those enumerated in this article
as belonging to peritonitis that he will be surprised that this item in
the diagnosis should have occupied so much room.

In a case already referred to, in which peritonitis followed gall-stone
pains, the transition was so marked by the rapid acceleration of the
pulse and swelling of the abdomen that each of the three physicians in
attendance at once appreciated the significance of the change. A
physician who resided in the country called on me to report his own
case. He had a little before had a very painful affection of the
abdomen which continued for three days. The pain was paroxysmal,
confined to the region of the liver, back and front, for one day; after
that there was some tenderness over most of the abdomen, but no
tympanitis. His pulse became frequent and his temperature advanced to
103 degrees. His physicians believed that these symptoms justified them
in treating him for peritonitis. Yet his position in bed was constantly
changed, and no one attitude long continued--a restlessness which never
occurs in peritonitis, but is common in calculus transits. Add to this
the absence of gaseous distension and of the green vomit, the
paroxysmal character of the pain (though I remember one case in which
peritoneal pain increased and diminished somewhat regularly, but only
one), and, finally, the sudden cessation of the pain, such as often
happens in calculus transit when the calculus passes into the
intestine,--it is plain that his sufferings were caused by a
gall-stone. The elevation of temperature was the result of a
long-continued worry of the nervous system, and the abdominal
tenderness came from the many times repeated contraction of the
abdominal muscles which occurs in hepatic colic. And then, to make the
diagnosis more complete, this gentleman, after twelve or fourteen hours
of pain, became jaundiced--in the end very much so. There was no
absolute constipation, and the stools were of the color of clay from
the absence of bile.

The points of difference between renal colic and peritonitis are even
better defined and easier recognized than those between it and hepatic
colic.

In intestinal colic there may be some inflation of the bowels, and if
it continues a day or two there may be some tenderness; but it is for
the most part distinguished from peritonitis by the intermittent or
remittent character of the pain, by its greater severity while it
lasts, by its courting, rather than repulsing, pressure, by the
moderate acceleration of the pulse, by no or only slight elevation of
temperature (exception being made for long continuance), by the absence
of the green vomit, by the absence of the fixed position of
peritonitis, etc.

There does not seem to me any need of spending time to distinguish
gastritis or enteritis or neuralgia from peritonitis, their symptoms
are so wholly different; and if, as is said, the mucous inflammation
can penetrate all the coats of the stomach or intestine, and so cause
inflammation of the peritoneal layer, that is peritonitis, and will be
distinguished by the proper symptoms of peritonitis.

TREATMENT.--Chomel[4] says: "If general peritonitis is intense, it
{1145} should be attacked by the most powerful therapeutic agents. One
should immediately prescribe a large bleeding from the arm--from 500 to
600 grammes, for example--and repeat according to the need once or even
twice in the first twenty-four hours; apply to the abdomen, and
particularly to the part of it where the pain was first felt, leeches
in large number--fifty, even a hundred--as the violence of the disease
may demand and the strength of the patient will permit." He recommends
baths, presumably tepid, and describes an apparatus by which the
patient can be put into the bath and lifted out of it without pain;
prescribes a fixed posture, gentle laxatives, mercurial frictions,
blisters; conditionally and doubtfully, paracentesis, emetics under
certain circumstances--musk, etc. under others. In the treatment of
general peritonitis there is no reference to opium. The word does not
occur, but it does in the treatment of peritonitis following
perforation. In this condition he would, among other things, give opium
a haute dose, but he does not prescribe any repetition or give any
details. It is probable that the idea was obtained from Graves, whose
first use of opium in this accident was in 1821, although its first
publication appears to have been by Stokes in 1832.

[Footnote 4: _Dictionnaire de Medecine_, 1841.]

Wardell,[5] who has written the latest treatise on the disease we are
considering, relies greatly on bloodletting, but falls short of Chomel
in the quantity of blood he would take--would bleed, not to withdraw a
certain number of ounces, but to produce certain effects. The
venesection is to be followed by the application of leeches--twenty,
thirty, or forty--to the abdomen; after this turpentine applications to
the bowels. After depletion, he says, opium should be given at once:
"two or three grains may be given in urgent cases." Vesication he calls
"another of our aids." He disapproves of cathartics, but when there is
accumulation in the colon would use injections. "Opium in the asthenic
form is the chief agent, and Graves and Stokes were among the first
physicians who gave it very largely." "Two or three grains may at first
be prescribed, and a grain every four or three, or even two, hours
afterward." "In perforation there is sometimes great toleration of the
drug. Murchison has known so large a quantity as sixty grains to be
given in three days with impunity." Mercurials, he thinks, are of
doubtful efficacy. In the paragraph devoted to the treatment of
puerperal peritonitis the word opium does not occur, and it is only by
a very doubtful inference that we can assume that he would ever use it.
Chomel makes no allusion to the use of opium in the same disease.

[Footnote 5: _Reynolds's System of Medicine_.]

For two years (1834-36) I was connected with the New York Hospital as
house-physician or in positions by which that office is reached. The
treatment of acute diffuse peritonitis then and there was formulated as
follows: First, a full bleeding from the arm, commonly sixteen ounces,
then a dozen or more leeches to the abdomen; following this, another
bleeding or not, in the discretion of the physician. Meantime, the
patient would take half a grain to a grain of calomel every two hours,
with a little opium "to prevent the calomel acting on the bowels," of
which there was no danger, in truth. Mercurial inunction was used at
the same time. The belief was that after depletion the most important
thing was "to establish mercurial action in the system;" in other
words, {1146} "to diminish the plasticity of the blood." Under this
plan I saw one recovery in these two years.

In 1840, I went to Vermont to give a course of lectures in the Vermont
Medical College, and while there was called by the physicians to see
with them several cases of peritonitis. I found that they were treating
the disease on the Armstrong plan; that is, bleeding freely, and then
administering a full dose of opium, as they said, "to prolong the
effects of the bleeding." In most cases there was a second bleeding and
a second administration of opium. Leeches were also used, and
irritating applications to the abdomen, and in some cases purges. I
found they were getting better results than we were in New York, and I
studied their cases as closely as I could, and reached the conclusion
that opium was the curative agent, and that it would be safe to omit
the abstraction of blood. This conviction grew in strength with every
new case, and I saw, with different physicians, several cases, the
disease being more prevalent among the mountains there than in the
city--at least that year. The idea then formed was that to establish
the narcotic effects of opium within safe limits, and continue them by
repeated administration of the drug, would cure uncomplicated
peritonitis--that a kind of saturation of the system with opium would
be inconsistent with the progress of the inflammation, and would subdue
it. There was no theory to build the treatment on, and no explanation
of the action of the drug in my mind. What I saw of the action of two
full doses of opium was the only foundation for the idea. I had in the
course of two years after those observations in Vermont 9 cases of
general acute peritonitis, 8 of which were cured. All these were
reported in succession, as they occurred, to the medical societies and
in my college lectures. The plan was adopted by many members of these
societies and by others with whom I had opportunity of conversing on
the subject, so that soon there were several--I may say many--workers
in the field; and in all instances where the practitioner had the
courage to carry out the treatment favorable reports were returned. Not
that every case of peritonitis was cured, but the recoveries generally
exceeded those that followed any other plan ever before used. No
physician tried it with a proper understanding of its details, and with
courage to execute them, who if living does not practise it to-day.

The treatment of puerperal peritonitis is not allotted to me, and I am
very reluctent to encroach in any degree on the province of the very
competent and highly-esteemed gentleman to whom that disease was
assigned. But the history of the opium treatment is very incomplete
without the statement I am about to make, and I trust to his generosity
to forgive this encroachment; and all the more confidently because he
was not at the time acquainted with the manner in which opium was first
introduced into the treatment of puerperal fever.

After the curative action of the drug was demonstrated in general
peritonitis, I was anxious to try it in puerperal fever, of which
peritonitis forms a part. But I had no hospital and no obstetrical
practice. In 1847, I was appointed one of the physicians to Bellevue
Hospital, to which an obstetrical department was attached. After one or
two years a single case occurred and was sent to my division. I gave
her 100 grains of opium in four days, with more or less of calomel--I
have {1147} forgotten how much. She recovered, but after the symptoms
of puerperal fever passed away she had secondary abscesses of the
lungs. These kept her ill for several weeks. At length her recovery was
complete.

In 1840 there was a very fatal visitation of puerperal fever in this
hospital, and on invitation of Vache, who then had charge of the whole
institution, I was a daily visitor and took notes of all the cases. It
was from these notes that Vache compiled his report of the epidemic
published in the _Medical and Surgical Journal_. The disease was
fearfully fatal, although every known mode of treatment was tried in
different cases, including Brenan's plan by turpentine, but all, with
one or two exceptions, with the same result. At this time the opium
plan was on its trial, and I had not acquired a confidence in it that
authorized me to try it in these cases. The time for it came in 1851.
Then a sudden, vigorous attack occurred. One woman was sent to me in
whom the disease was well advanced. I instructed my house-physician not
how much opium to give, but what effects to produce by it. I found this
woman dying the next day, and that she had taken only three grains of
opium in three doses. In three or four days seven cases were sent me
from the lying-in wards. One was returned for error in diagnosis, and
six put under treatment. Having found that prudence in my
house-physician was so much more conspicuous than courage, another
house-officer, who combined them both, was selected to be in almost
constant attendance. The instruction I gave him was in these words: "I
want you to narcotize those women to within an inch of their lives." He
did it, and saved every one of them. This gentleman is now known over
the whole land as a learned and distinguished surgeon. I feel called
upon to give his name in this connection, that he may be a witness to
the facts I state, and for the admiration with which his nerve and
prudence impressed me. One of these patients took first two grains,
then three grains, then four, and so on till she took twelve grains of
opium at a dose, the intervals being two hours. The state into which
the patient was to be brought I have denominated a state of
semi-narcotism. The quantity of the drug necessary to produce this
state varied surprisingly in different persons. One of these women was
pretty fully narcotized by four grains every two hours. She was watched
with anxiety; restoratives were kept in readiness, but nothing was done
but to suspend the administration of the medicine and to wait. In seven
hours the consciousness was fully restored, and the improvement in her
condition was wonderful. The disease seemed to be cured. But in a few
hours more the symptoms recurred, and the same medicine was again given
in three-grain doses, and again narcotism was produced. Taught by the
experience of the day before, we waited, and when she recovered from
this second narcotism her disease was completely cured. She took no
more medicine of any sort. This case was very instructive, as it taught
me that over certain cases of puerperal fever opium has absolute
control.

From the time here referred to, so long as the obstetrical service was
maintained at Bellevue Hospital, a large proportion of cases of this
fever, as they occurred, were sent to my wards, and in all these years
I have not lost faith in opium. This statement, however, requires an
explanation. Puerperal fever is a compound disease. Its great
inflammatory lesions are found in the uterus and its appendages and in
the peritoneum. {1148} When the inflammation of the uterus is the
dominant lesion, and is purulent, opium has little or perhaps no
control over its fatality; but in the cases in which peritonitis is the
ruling lesion, if begun early, it will show its power. In this
connection I will only add that in private practice the drug has been
perhaps more curative than in the hospital. I have seen many cases in
consultation, and a decided majority have recovered. In some instances
the patient has fallen into a pleasant sleep, only broken by some
administration, and ending with her recovery. In one instance a very
eminent physician had undertaken to treat a case by the opium plan, but
he had administered the drug so timidly that for fourteen days he had
done no more than hold the disease in check. After trial, I found that
I could not induce him to give the drug in my way, and I asked him to
give me sole charge of the patient for twenty-four hours. To this he
assented, remarking, "If you cure her, doctor, I will have it announced
to the profession that she was the sickest person I ever saw get well."
In half the time allowed me I was able to establish the opium symptoms
as given farther on, and the lady slowly recovered.

The treatment of any form of peritonitis by opium permits the use of
the drug itself, or of any extract or preparation of it which contains
its narcotic qualities, but it is wise to persevere with that one first
chosen unless there is strong reason for a change. This caution is
based on the fact that we cannot change from one to another and be
certain to obtain the same drug activity. For example, we begin with
laudanum, and find what it will do. We cannot take in its place the
sulphate of morphia with the certainty that we can so graduate it as to
get precisely the same effects. Then the quantity which will be
effectual in one case may be quite inadequate for the next. The
tolerance of opium in different persons varies remarkably, and probably
the disease itself increases the tolerance in all. This will be
illustrated by some of the details of this paper.

The drug symptoms to be produced are as follows: Subsidence or marked
diminution of the pain; some or considerable tendency to sleep;
contraction of the pupils; reduction of the breathing to twelve
respirations in the minute; in the favorable cases a considerable
reduction in the frequency of the pulse; a gentle perspiration; an
itchy state of skin, or oftener of the nose; absolute inactivity of the
bowels, and after a time a subsidence of the tumor and tenderness in
them; some suffusion of the eyes.

Of these several signs of opiumism there is none more easily observed
and none more valuable than the frequency of the respiration; and while
the physician aims to reduce it to twelve in a minute, there are
chances that he will see it fall to something below that. I have often
counted it at seven, and in perhaps two cases it fell to seven in two
minutes; and yet these cases of marked oppression from opium all
recovered. In the cases in which the respiration has fallen so low
there has been considerable obtuseness of the mind; but in no case
except in the hospital patient already referred to have I seen
unconsciousness. Then the sleepiness, so long as the patient is easily
awakened, is wholly within the limits of safety.

As to the quantity of opium to be given, I have known two grains every
two hours do the work, and in other cases many times this {1149}
quantity was necessary to produce this condition of semi-narcotism. The
plan is to begin with a dose that is safe--say two or three grains of
opium or its equivalent of sulphate of morphia--and in two hours notice
its effects. If any of the opium symptoms have appeared, repeat the
dose; if none, increase by one grain, and so on at intervals of two
hours till the degree of tolerance in the patient is ascertained. After
that the case can be treated by a diminished occupation of the
physician's time--two or three visits a day. The dose is to be
increased if the opium symptoms diminish before the disease yields, but
always to be diminished or discontinued if narcotism is approaching.
The duration of the treatment will be sometimes no more than two or
three days; it may be a week, or even a fortnight, and in one case
already mentioned the symptoms persisted mildly for forty days, and
then yielded. In this case the medicine used was the sulphate of
morphia, and the enormous dose reached by steady and graduated increase
was one grain and a quarter every forty minutes in a boy ten years old.

In some puerperal cases the doses have been so large as to require
witnesses to make the statement of them credible, and the
administration of them criminal had not the effect of each dose been
carefully studied and the amount of each measured by the action or
inadequate action of the next preceding one.

Here are the doses given a woman who fell sick October 13, 1857; the
record was made by C. H. Rawson during the treatment, and was kindly
given me two or three years ago: On the first appearance of her
disease, while the diagnosis was uncertain, 10 grains of Dover's powder
gave her a quiet night. The next day the disease was more manifest, and
she took of Magendie's solution (2 grains of sulphate of morphine to a
drachm of water) x minims every hour; growing worse, at night she took
xxx minims every hour; the next day, xl minims every hour, and no
change of symptoms. She took in twenty-four hours 32 grains of sulphate
of morphia; slept, but was awakened by the slightest noise. On the
fourth day 3-1/3 drachms of the solution, and opium as follows: at 4
P.M., 3 gr.; at 5 P.M., 4 gr.; at 6 P.M., 5 gr.; at 7 P.M., 6 gr., and
6 gr. hourly after 7 P.M. Sleep light. Fifth day, in twenty-six hours
took in opium and morphine the equivalent of 208 gr. of opium. The
sixth day, 212 gr. of opium; on the seventh day, 221 gr. of opium; on
the eighth, 224 gr.; on the ninth, the same quantity; on the tenth, the
same; on the eleventh, 247 gr., pulse subsiding; on the twelfth, 261
gr., other symptoms better; on the thirteenth, 144 gr.; fourteenth day,
4 gr. hourly; slept for the first time heavily, all other symptoms
improving, bowels moved freely, ate well, tympanites subsiding;
fifteenth day, 1 gr. of opium every two hours, and at night the last
dose. Recovery was complete. The woman denied the opium habit, and the
medicines were tested by the apothecary. Such doses can only find their
justification in the demonstrated fact that smaller doses will not
produce the degree of narcotism desired.

In Keating's edition of Ramsbotham's _Midwifery_ a case is reported by
myself in which a woman, by pretty rapidly increasing doses, reached
forty-eight grain doses of opium, with the effect of curing her disease
and substituting a temporary active delirium.

A word of caution is probably necessary regarding the use of opium in
high doses when peritonitis and Bright's disease coexist. I have {1150}
already said that I have but scanty personal knowledge of such a
concurrence, but in Bright's disease alone I have known a large,
non-heroic dose of an opiate fatal. For example: A young man had a
felon on his finger, and did not sleep, so great was his pain. His
physician prescribed 40 drops of laudanum at bedtime. Not sleeping on
this, he took another portion of 40 drops, and in the morning he was
found in a comatose condition, and in the course of the day he died. A
post-mortem examination revealed Bright's disease, which was not before
suspected. A woman took half a grain of the sulphate of morphine--for
what reason I do not know. I was called to see her when she was in a
semi-comatose state. The time between my seeing her and that of taking
the morphine was fourteen or fifteen hours; its removal from the body
was therefore hopeless. Her limbs were swollen with oedema, and the
urine contained albumen and casts. Although the usual means of opposing
the poisonous effects of opium were resorted to, they were of little
use, and the patient died in the course of the day. These are selected
from a considerable number of similar cases that show a similarity in
their action on the brain of opium and urea. It seems that opium
precipitates the uraemic coma, yet the coma produced by these agents
combined is not so profound as that produced by opium alone. There is
in it some movement of the limbs or body or some imperfect utterances,
yet it seems to be more fatal than the coma of opium unaided.
Notwithstanding all this, I have met with several cases of cardiac
disease combined with Bright's--perhaps I should say many--in which
half a grain of morphia sulphate has been taken every night to procure
sleep with only beneficial results. This has been observed several
times when physicians have been the patients.

These facts are stated to show the hesitation and prudence that should
control the administration of opium when there is urea in the blood,
whether there is peritonitis or not; but a case in which one form of
Bright's disease preceded, and perhaps caused, peritonitis will be more
instructive: A gentleman sixty-eight years of age was attacked by
peritonitis on Thursday evening. There was a moderate chill at the
onset (this being one of the few cases in which I have witnessed this
occurrence). The diagnosis was then uncertain, and he took quieting
doses of Dover's powder, which gave him sleep. The next day the
diagnosis was easily made. The urine was examined for albumen, and none
found. It was, however, scanty. He took only six-eighths of a grain of
sulphate of morphine in the first twenty hours. It was then increased,
so that in the next twenty-four hours he took two grains of the
sulphate in divided doses--a quantity which has been greatly exceeded
in hundreds of cases with the best results; but in this case coma was
the result. At 10 A.M. on Sunday he was comatose, but not profoundly;
he could be aroused. The breaths were five in the minute, the pulse
increasing in frequency; secretion of urine next to none. The galvanic
battery was used. After seven hours, while the respiration was growing
more natural, the pulse grew more frequent and the stupor increased. At
8.30 P.M. the breathing was fifteen in the minute, and full and
perfectly easy, but the pulse was running at 140, and the coma
unbroken, and the pupils of good size. The effects of the opiate had
passed off, but those of uraemia were profound. He died at 11 P.M.
After the alarming symptoms occurred we tried to procure another
specimen of the urine for fuller examination, but {1151} could not. It
was only after his death that we procured the evidences that he had
shown symptoms of contracted kidney for months. The urine contained no
albumen at the time of our examination, as very often happens in that
disease.

Regarding other points in the opium treatment there is little to be
said. Purgatives are entirely inadmissible. The bowels should be left
entirely at rest till they recover their muscular tone; then they will
expel first the gas, and then the feces; or if, after the inflammation
is subdued, they do not move of their own accord, injections are
admissible. I have often left the bowels absolutely inactive for
fourteen days without any recognizable consequences. If I meet a
physician who believes that leeches are essential, I yield him his
point, but never advise them. I do this because a moderate bloodletting
will do no harm, and little if any good. The same rule I apply to
irritating applications to the surface of the abdomen. Mercurials, I
think, are harmful, and therefore I object to them. As to food, it
should be milk, fresh eggs beaten up with water and pleasantly
flavored, peptones, etc. selected from among those that leave no
refuse.

The testimony of physicians who have adopted this plan within my own
circle is unanimously in favor of it. B. R. Palmer of Woodstock, Vt.,
afterward of Louisville, Ky., who was the first to test it, told me
after a few years' trial that he used to dread peritonitis as he would
dread the plague, but with opium in his pocket he met it cheerfully and
hopefully, as he did a pneumonia. Chalmers of New York, who is known by
many readers of this article, has a very extensive practice, and he
told me lately that he had not had a fatal case of peritonitis in
twenty-two years. He embraced the plan early.

Now, how did this treatment originate? From whom did the profession
adopt it? In 1836-37, I visited daily the hospitals of London,
Edinburgh, and Paris, was in frequent intercourse with the physicians
of those cities, and never saw a patient anywhere treated by opium, and
never heard the least allusion to it. I can safely appeal to any
physician who was familiar with the history of the profession before
the year 1840, or for two or three years later perhaps, to inquire
whether anything was generally known regarding this treatment of
peritonitis, or whether he himself ever heard of it. Let the inquiry be
made of Willard Parker of New York or Alfred Stille of
Philadelphia--men of a degree of intelligence and learning that has
made them leaders in the profession--and of all the profession at that
time. I venture to assume that they were as ignorant as I was of what
Graves and Stokes had done.

The following fact is significant: In 1843, Graves published _A System
of Clinical Medicine_, the preface of which is dated January, 1843. In
this he says he had previously published essays, lectures, and articles
in several medical journals. In this volume he intends, he says, "to
revise what I have written, and to compress the whole within the limits
of a single volume." There is nothing in the table of contents or
explanatory headings of the several chapters of this volume which
alludes to treating peritonitis by opium. It is fair to infer that the
cases treated in 1823 had made little impression on his mind, and that
he did not think his treatment could take rank as a discovery; and yet
Stokes had made favorable mention of it eleven years before this
publication. Graves, then, did not {1152} publish his cases, and the
first knowledge which the profession could have of them was through
Stokes's paper, published in the _Dublin Journal of Medical and
Chemical Science_, No. 1, in 1832. Perhaps the reason why Stokes's
paper produced so little impression on the profession may be found in
the fact that first numbers of journals of every sort have few readers.
Anyway, it was not till after the opium treatment had attracted much
attention in this country that anybody here knew that Graves or Stokes
had ever had anything to do with it. Besides, Graves and Stokes had
only used opium in cases of perforation, and they had no plan or
symptomatic guide in the use of the drug.

There is something new and strange in the following case copied from
the _Medical Record_ of May 12, 1883, under the heading, "Operative
Measures in Acute Peritonitis:" "Dr. Reibel relates the case of a
child, eight years old, suffering from acute idiopathic peritonitis.
The disease had resisted all treatment, and the child being,
apparently, about to die, it was determined to open the abdomen with a
view to removing the fluid and washing out the peritoneal cavity with a
solution of carbolic acid. The meteorism was intense. No fluid was
found in the abdominal cavity. In prolonging the incision a loop of the
intestine was punctured, as evidenced by the escape of gas and
intestinal fluid. The wound was washed with carbolic acid and covered
with a layer of antiseptic cotton. The following day the little patient
was nearly free from pain, and was able to retain a little milk. The
temperature had fallen from 104 degrees to 101 degrees, and the
tympanitis was almost entirely gone. The (wounded) loop of intestine
was adherent to the abdominal wall, and there had been no escape of
fluid into the peritoneal cavity. The patient made an excellent
recovery."

If the statements of this abstract are true, and the future supports
the practice pursued in this case, acute peritonitis is likely to
become a surgical rather than a medical disease. Reibel thinks that
opening the intestine in the way he did is a better plan than the
punctures with the exploring-needle to relieve the patient of the
tympanitis. But it will require more facts than one to persuade the
profession that this mishap of the scalpel can grow into a rule of
practice. (The _Record_ finds this report in the _Journal de Medecine
de Paris_.)

I cannot say that I see the value of a distinction made in 1877 by
Gubler between peritonitis and peritonism. By the latter term is meant
the total of nervous and other symptoms that arise in the course of
peritonitis. Trasour has lately revived this distinction, and thinks it
important, and that a light peritonitis may be attended by a grave
peritonism. He holds that the distinction is important, because "the
treatment of peritonism consists in the administration of alcohol,
chloral, and especially of opium in large doses. Of the latter fifteen
grains may be given in twenty-four hours." "The symptoms [of
peritonism] are produced through the agency of the great
sympathetic."[6]

[Footnote 6: _Med. Record_, Aug. 28, 1883.]

I cannot say that I have seen great effects follow small causes, but
think that, in general, the effects of peritonitis on the pulse,
strength, nervous tone, etc. are, to some extent at least, a measure of
its severity.

CONSEQUENCES OF PERITONITIS.--These are usually nothing. When recovery
takes place it is commonly complete, but cases have been known {1153}
in which the intestines have been left bound to the abdominal wall and
to each other, and so made incapable of their natural action. The
results of this are a swollen, tympanitic abdomen and impaction of the
bowels, but the general health may be very good. A woman at Bellevue
was left in this condition, yet she performed the duties of nurse in
one of the wards for some years, and finally disappeared from the
institution, and I do not know how it ended with her--probably by the
breaking up of the adhesions and a return of the bowels to their
natural condition.

In some few cases there remains new tissue, which in time is partly
broken up and remains partly attached. In this manner strings and bands
of considerable strength can be formed, and into these loops the
intestine may pass, so as to form an internal hernia of a very
dangerous character. In some bands are formed across the intestine,
which by contraction flatten the tube and obstruct the fecal movement.
There is reason to believe that such bands and bridles are formed by
local inflammation of such imperfect manifestation by symptoms that the
patient knows nothing about it. A very striking case illustrating the
possible sequence of this inflammation came under my observation early
in my professional life: A colored woman about twenty-five years of age
gave a very clear history of a peritonitis from the consequences of
which she had suffered two years before I saw her. About six months
after recovery she began to have constipation and to suffer from small
and frequent discharges of urine. The latter gradually grew milky and
to have a bad odor; the constipation grew more and more, and at length
came to be absolute for many days; then would come a diarrhoea of some
hours' continuance, after which she would have a feeling of relief.
This was her state when I saw her. She was emaciated, and so feeble as
hardly able to leave her bed. She vomited occasionally, and her
appetite for food was all gone. The urine was heavily loaded with pus,
and was ammoniacal. She died after a few weeks. At post-mortem
examination a firm membrane was found strained across the upper strait
of the pelvis, wholly separating the abdominal cavity from the pelvic.
It looked like a drum-head. The left posterior border was drawn very
tensely over the colon where it passed into the pelvic cavity,
flattening it down completely and making stricture. To the under or
lower surface the fundus of the uterus and the base of the bladder were
firmly adherent, and in this way both were suspended. The effect of
this unnatural suspension of the inactive uterus did not seem to be
noticeable, but with the bladder it was very different: it contained
three to four ounces of water, ammoniacal and full of pus, and it could
never have emptied itself. The explanation is very simple. During the
peritonitis a false membrane was effused on the pelvic viscera in situ.
When the period of contraction which is common to all such structures
came, the new membrane was separated from the greater part of these two
organs, but not from their bases. The firm attachment to the brim of
the pelvis did the rest. So unusual a sequel of peritonitis I think
deserves a record. I should add there were no adhesions above the
pelvis. Such a structure as this, found long after the active symptoms
of peritonitis have passed, as also the bands and cords before spoken
of, does not give support to the doctrine that the false membranes are
broken down into fatty matter, and in this condition absorbed.

{1154} The possible remote effects of peritonitis are shown in a case
reported by E. A. Mearns to the _Medical Record_, published Sept. 15,
1883: A young man, aged nineteen, four years after he had had acute
general peritonitis was attacked with constipation, which was absolute.
He had had before occasional attacks of pain in the bowels and
constipation, which were overcome. But this was invincible. He had the
train of symptoms usual in intestinal obstruction. There was no fever
or tympanitis, and this time but little pain. He lived eight days.
There was a tangle and a constriction of the intestines at the middle
of the ileum, caused by the contraction and hardening of the effusion
of the old peritonitis, and the intestine was very much softened.

H. B. Sands reports in another number of the same journal: "The patient
was a man about thirty who had suffered from acute obstruction for a
week. No exact diagnosis was made. When the abdomen was opened the
intestinal coils were found extremely adherent one to another in
consequence of a former peritonitis. A careful search failed to
discover the nature or seat of the obstruction. The abdominal wound was
closed, and the patient died soon after."


Peritonitis from Perforation.

There is no part of the gastro-intestinal canal that may not, from one
cause or another, become the seat of ulceration. The jejunum is the
part of the tube long supposed to be an exception to this rule, but
even in it one or two observers have found ulcers. These ulcers often
exist without distinctive symptoms, and may go on to cicatrization
without announcing themselves. In the stomach, however, there are
commonly indications which will admit a conjecture of their existence,
and perhaps a diagnosis. Sometimes these ulcers penetrate all the
tissues of the tube and allow the contents of the intestine to escape
into the peritoneal cavity, or they may have destroyed all but the
external layer, and some succussion, as in coughing, sneezing,
laughing, or perhaps straining at stool, may make the opening complete,
with the same results. In these cases it seems to be inevitable that
inflammation should follow, unless it has preceded, the complete
opening and sealed it up by adhesions. The tendency of such an
inflammation is to be local and limited, but when the contents of
intestines escape into the peritoneal cavity it usually becomes
general. These accidents are usually attended by the sudden development
of local pain, by rapid increase in the frequency of the pulse,
paleness, and prostration. The perforation of the vermiform appendix is
often a partial exception to this statement, for, while the local
symptoms are marked, the sympathy of the general system is not so
quickly awakened. The same can be said of perityphlitis. The symptoms
are often local for some time--a day or more; sometimes subside, as if
the disease were cured, and then return in full form. This is produced
by the tendency of the inflammation to limit itself to the immediate
neighborhood of its cause. Lymph is effused at a short distance from
the point of irritation, and seals the parts together, so as to shut in
the offending substance; and though this substance may produce pus in
contact with intestine or appendix, that {1155} fluid is held for a
time, as in abscess. It may be permanently held in its new-made sac
till it burrows into some near part, as the intestine or bladder, or
remain an abscess till opened by Willard Parker's puncture. On the
other hand, the contents of this sac may be increased till it breaks
bounds and causes extension of the peritoneal inflammation or general
peritonitis. In one particular case this process of setting limits and
breaking through them occurred in a young lady four times at intervals
of from one to two days. When the limiting adhesions were established
symptoms would subside, so as to encourage in her physicians the hope,
even the expectation, of recovery; but again and again the fire was
rekindled, and she died eight days after the first attack. In the
greater number of cases the first breaking of the adhesions is followed
by full peritonitis, and this often by death.

The perforations of the stomach which I have seen have not been
attended by the severe pain described by most authors, but by a sudden
prostration of strength and a feeling of disquiet and sinking at the
stomach; more of collapse than of inflammation in the symptoms; no
tumefaction of the bowels; almost nothing to indicate the nature of the
accident, but a sudden new sensation in the bowels, a rapid increase in
the frequency of the pulse, it growing small as it increases in
rapidity, and a pale and shrunken countenance, and death in from twelve
to thirty hours. Then, on inspection, hardly any signs of peritonitis
are found. The peritoneal vessels are fuller and the membrane redder
than in health, and its surface covered with the thinnest possible film
of lymphy exudation, and some serum in the deeper parts of the cavity.

These ulcerations of the stomach are not always fatal by peritonitis. A
few instances are recorded in which adhesions of the outer surface of
the organ to adjoining organs have taken place, so as to protect the
peritoneum almost wholly from the fatal contact with the gastric
fluids, and death has occurred in some other way. I have a remarkable
specimen illustrating this fact. It was taken from the body of a woman
of about middle age who had long had symptoms of dyspepsia, and had
from time to time vomited a little blood. It was not difficult to
recognize ulcer, but the extent and peculiarities of it could be
learned only by inspection. She died suddenly of copious haematemesis.
On examination an ulcer two and a half to three inches in its several
diameters was found, beginning near the pylorus and extending toward
the left, which in this large space had destroyed all the coats of the
stomach and exposed an inch and more of the right extremity of the
pancreas and about the same extent of the liver. The liver and pancreas
were both perceptibly eroded when exposed, and in the latter an artery
that would admit the head of a large pin was opened. The stomach,
outside of this extraordinary ulcer, was strongly attached to the
adjacent organs.

The ulcerations of typhoid fever penetrate the intestine about three
times in a hundred cases of the fever. This result is reached by the
study of a large number of cases, and appears to be pretty generally
admitted. The point where this perforation occurs is in the ileum, near
the ileo-caecal valve--within a foot or eighteen inches of it in the
great majority of cases, although it has been known to occur
seventy-two inches above the valve, and it has been seen very rarely in
the caecum. The fever itself may be either severe or mild. Suddenly
severe pain {1156} sets in, oftenest in the lower part of the abdomen,
and spreads rapidly; the pulse is quickly accelerated and becomes
small; and it has been lately stated that in this and other intestinal
perforations the gases of the bowels, escaping into the peritoneal
cavity, will give resonance to percussion over the lower part of the
liver. Fetid gas found in this cavity after death is not without
importance; for example, a distinguished Senator at Washington died not
long ago of a very painful abdominal disease which his physicians
declined to relieve with opium, though the patient pleaded for it. His
family physician at home was summoned. Although the distance he had to
travel was many hundred miles, he found the patient alive and still
suffering. He at once gave morphine for the relief of the pain, but the
patient died. Now, this gentleman had diabetes a year or more before
his death, recognized by his physician at home and also by myself.
While under my observation the urine ceased to contain sugar and its
quantity became normal, but soon after this albumen was occasionally
found in it. The quantity was generally small, and casts were only
found now and then. This new disease was mild, and seemed to be, within
certain limits, manageable. He went to Washington under injunction that
he was not to let official and professional labors bear with any weight
upon him. This last sickness and the death would naturally enough be
supposed to be some new phase or consequence of the previous illness.
But, while a post-mortem examination was not permitted, the family
wished to have the body embalmed. The family physician accompanied the
embalmer, and as the latter made a cut through the abdominal walls
there was a gush of air laden with fecal odor, and he through this
opening saw the intestines covered with false membrane. He satisfied
himself that the intestine was not opened. This fetid gas came from the
peritoneal cavity. An ulcer had perforated the intestine somewhere, and
caused the death. The final disease could be only remotely dependent on
the patient's previous illness, if at all. His impaired health may have
made the ulcer possible.

All kinds of perforations in the bowels, except those of the stomach,
caecum, and appendix, even the cancerous, have one history and the same
symptoms; and if treatment is ever successful in such occurrences it
must all be based on one set of rules--absolute rest, no pressure on
the bowels, and no movements of the muscles that will aggravate it;
food that will be wholly digested and absorbed by the stomach; complete
abstinence from cathartic and laxative medicines, and the free
administration of opium or morphine. By these means, I fully believe,
numbers have already been saved from the fatal consequences of
peritonitis caused by perityphlitis and perforation of the vermiform
appendix--some under my own observation and others under that of my
friends. A boy fourteen years of age was brought to bed by a pain in
the right iliac fossa. After a few hours his father, a physician,
desired me to see him. There was already a perceptible fulness, with
dulness on percussion, in the fossa, and some febrile excitement. I
gave a portion of morphine, and promised to call the next morning. In
the morning a message came from the father stating that the boy was
better and there was no need of further attendance. In the evening I
was recalled. The pain had returned, and had spread over most of the
bowels. He had general peritonitis. He took tincture of opium, of which
I believe the largest dose was 100 {1157} drops, reached after three or
four days of gradual but steady increase of dose. From that point the
patient got better, and the quantity of the medicine was
correspondingly reduced. There were a relapse and a repetition of the
treatment, and again the disease yielded. During convalescence, about
fourteen days from the attack, the boy, after emptying his bladder, was
suddenly pressed to continue the discharge. Now he voided what appeared
to be blood, two or three tablespoonfuls. It was, however, pus with
blood enough to color it. This purulent discharge from the bladder
continued for about three weeks, the boy steadily recovering his
health. This occurred twenty or more years ago, and that boy is now a
well-known physician. Similar cases could be recited.

In 1850, or thereabout, I attended a physician through an attack of
typhoid fever. In the third week there was a sudden outbreak of
peritonitis. The opium treatment was resorted to, and he recovered, and
had good health for twenty years after. Peritonitis occurs rarely in
typhoid fever from any other cause than perforation, and its occurrence
in this case at this time, when perforation is more likely to occur,
renders it probable, at least, that this attack was produced by that
cause.

March 3, 1883, autopsy of Wm. Fletcher, age 59, iron-worker. On Friday
last, Feb. 23d, he was attacked with pain in the region of the right
iliac fossa; it was severe. There was no chill, but little fever, and
only slight acceleration of the pulse. His stomach was a good deal
disturbed, and the bowels were soon distended with flatus. I saw him on
the Tuesday following, with James D. Elliott. The bowels were a good
deal swollen and very resonant on percussion; pulse 84. His stomach was
still greatly disturbed, so that he retained no food, yet there was no
green vomit, but much flatulency. The movements in respiration were
particularly noticeable, being nearly or quite as much abdominal as in
health. There was a short friction sound in inspiration, but an entire
absence of the sound produced by peristaltic action. There was no
dulness on percussing over the iliac fossa, and no pain on pressure
over any part of the abdomen. I was careful in examining the right
fossa, for the first pain was there, and it was severe; but there was
no physical sign by which the perforation could be ascertained. Still,
my mind dwelt on the probability of perforation, and I expressed my
fears to Elliott regarding it. The respiration was of natural
frequency. The bowels had not moved for two or three days.

The next day Flint was added to the consultation. The symptoms had
changed but little; the pulse was 102; no pain, no tenderness, no
peristaltic action; slight friction at one point only; the abdominal
respiration was as marked as before. Frequency of respiration, 18;
patient sleepy; pupils only slightly contracted. When we were in
consultation I again expressed my fear of perforation, but Flint
expressed the most decided opinion as to its absence, because there was
dulness to percussion over the liver. I had read his paper on the
intrusion of gas between the ribs and liver in cases of intestinal
perforation, and felt as if I were almost reproved for entertaining the
thought without this physical corroboration.

Thursday, March 1st, the stomach had become much more retentive; there
were no pain and no tenderness on pressure; pulse 109; no friction
sound, no sound of peristaltic action, no dulness on percussion over
right iliac fossa, but resonance over the whole abdomen, excepting over
the {1158} pubes; there the resonance was not clear; over a small space
there was dulness; this was ascribed to moderate fulness of the
bladder, and, as there had been no difficulty in emptying it, nothing
was said of it. The abdominal respiratory movements were the same as
before.

Friday morning, at 3 A.M., no marked change had occurred in the
symptoms, but from this time onward there was a steady sinking of the
vital powers. The pulse grew small and frequent, the hands became cool,
the breathing more frequent, and without any sudden change or new
symptom he died early in the morning. At the last visit there was no
resonance on percussion over the liver.

Autopsy, Saturday, March 3d, 2 P.M. The bowels were distended, as they
mostly are in peritonitis, but not extraordinarily. There was now
pretty free resonance over the liver. The section to open the abdominal
cavity was carefully made, with the aim of ascertaining whether there
was air or gas in the peritoneal cavity. When a half-inch opening was
made through the peritoneum, gas was forced out through it for some
seconds with an unmistakable noise. The bowels were not opened by this
cut. The bowels exposed, a very thin film of false membrane was found
on all the middle and upper portions of the intestines, with a fringe
of injection where the folds came in contact. But two or three inches
above the symphysis pubis the section opened a collection of pus which
extended downward into the pelvis. Somewhere hereabout--neither of us
could say exactly where--was found a lump of fecal matter, not
indurated, as large as a marrowfat pea, the intestine still unopened.
Search was made for the vermiform appendix. At first it was not
recognized on account of its remarkable shortness. It was found,
however, pointing directly toward the median line of the body, and was
short because a part had been separated from the rest by slough. The
end of what remained was marked by a border, one-eighth of an inch
deep, of a very dark-green gangrenous color. We did not attempt to
measure the quantity of pus. It was six ounces or more. It was
completely bounded and shut in by adhesions.

At no time during life was there resonance over the liver, but there
was some at the time of post-mortem examination before the bowels were
opened, due perhaps to the fact that at death the relaxation of the
muscles allowed the gas to rise higher than it did during life. The
unusual median position of the abscess is important in accounting for
absence of dulness, when it is usually found in slough or ulcer of the
vermiform appendix.

"A Fatal Case of Typhlitis without Recognizable Symptoms." Under this
title Jose M. Fisser published a case of inflammation of the vermiform
appendix causing general peritonitis in a young woman nineteen years of
age. The peculiarities of the case were that the appendix was not
perforated, and consequently there was no tumor in the right iliac
fossa--that the symptoms were all referred to the epigastrium, without
even tenderness in the fossa. She walked the floor and tossed about in
bed; the highest temperature was 103 degrees, and the most frequent
pulse was 120, and these continued but a short time. Of tympanitis
there was none till near death, and then but little. The obscurity in
diagnosis led to the publication of the case. The cause of this disease
was fecal matter, not very hard, in the appendix.[7]

[Footnote 7: _Med. Record_, Sept. 1, 1883.]

{1159} As much has been said in this article on the diagnosis of
peritonitis, it may be well to introduce a case where that diagnosis
was conjectural, and yet quite another state existed. I visited Mrs.
H----, when her disease was advanced, twice. My impression was that she
had peritonitis, but this opinion was held with grave doubt. After her
death, Smith sent me the following record of the autopsy: "Mrs. H----
died Friday evening at ten o'clock; next day, at three in the
afternoon, we made an autopsy. No gas or fluid in the peritoneal
cavity; the small intestines inflated almost to bursting, with
injection of the capillaries. In the left iliac region we at once
discovered a portion of the intestine almost black, and on examination
found a firm white band encircling and constricting that portion. Upon
liberating the gas the intestines collapsed, and the constricted
portion was released and easily removed. A further examination showed
that two of the epiploic appendages, coming off from the colon above
the sigmoid flexure, had united at their extreme points and formed a
loop two and a half to three inches long, and through this loop or ring
a portion of the ileum had passed, and was there constricted. The
constricted intestine was about four feet in length. This examination
has been gratifying to me. There was a small quantity of bloody serum
in the peritoneal cavity low down in the pelvis. The dark grumous blood
that passed the bowels on the second and third days can now be
accounted for, and corroborates your remark that the hemorrhage looked
like strangulation. This was at your first visit. This must be a new
cause of strangulation, and one that we could not anticipate."

There was, before I saw her, a single vomit of a suspicious fluid, but
the evidence was not strong enough to enable us to pronounce it
stercoraceous. Some of the observers noticed bloody serum in the
peritoneal cavity, and perhaps some shreds of lymph, but that was in
consequence of the strangulation.


Local Peritonitis.

This may occur anywhere in the broad extent of the peritoneum, and will
be more or less limited in different cases, or may be limited for a
time, and then become general. It is either acute or chronic. The
product of the diseased action may be serum or lymph or pus, or all of
them. The cause of this local inflammation is sometimes very obvious,
in other cases wholly unknown. The consequences vary all the way from
harmlessness to death; the symptoms are as variable as the
consequences, making the diagnosis easy in some cases, in others
impossible. Some cases in which it was not difficult to recognize it
have already been recorded--those caused by perityphlitis and
perforation of the vermiform appendix, for example. In such cases the
local pain, the swelling, the dulness or resonance on percussion,
depending on whether the tumor is made by inflammatory exudation or
gas, together with the general symptoms and the history, leave but
little ground for doubt regarding the character of the disease. Perhaps
one-half the local abscesses which form between the folds of the
peritoneum are recognizable during life by the local, associated with
the general, symptoms. When situated in the posterior and upper part of
the abdominal cavity, the hand gives little, {1160} perhaps no,
assistance, as in the most widely-known case of abscess that has been
recorded in all time. While the physicians were giving to the country
hopeful reports day by day, thousands of medical men shook their heads
and spoke sadly of the prospects. The illustrious patient was losing
rather than gaining strength and flesh, his appetite poor, his
digestion poor--a strong man growing helpless--and, above all, a pulse
that for months never fell below 100. With an adequate cause of
abscess, whether there were chills or not, what else could it be? Thus,
in peritoneal abscesses that cannot be felt the general symptoms are of
great importance to the diagnosis. When abscesses tend to discharge
their contents soon or late--sometimes into the intestine, sometimes
into the bladder, sometimes externally: in such cases there is a fair
chance. Sometimes they burst into the peritoneum: such cases are almost
inevitably fatal; even opium will not cure them. The pus of these
abscesses often has the fecal odor, which it acquires by the
transmission of the intestinal gases through the intestinal walls. I
was attending, with the late James R. Wood, a young lady in whom
peritoneal abscess had been recognized. It was anterior to the
intestines. In the consultation, while we were discussing the propriety
of using the trocar, the mother became alarmed at the odor and
appearance of the urine just passed, and summoned the doctors back to
the chamber. The abscess had opened into the bladder. The urine
contained pus which gave off the fecal odor strongly. This patient
recovered. It should be added that these abscesses, as well as those of
the convex surface of the liver and those that are post-peritoneal,
sometimes pierce the diaphragm and produce empyema, or by previous
adhesion of the lung to its upper surface find a way into a bronchial
tube, and so the pus is expectorated.

The history of local fibrinous exudations is not as easily told as that
of the purulent. We find from time to time, on the peritoneum, bands,
patches, or cords of false membrane, which were produced in so quiet a
way that we can get no information regarding the time when they were
formed, and perhaps the subject of them was not aware that anything was
wrong with the bowels till he began to have the symptoms of
obstruction. These unnatural structures are formed in great variety.
The omentum is found thickened and contracted. The mesentery and
mesocolon are seen in a similar condition, causing wrinkling and
shortening of the bowels. The spleen has on its surface patches or even
plates, or one great plate, of firm fibrinous deposit, often
cartilaginous in density, sometimes calcareous; and we can rarely fix
the time of these occurrences by any symptoms. It is not always so with
the liver. We are acquainted with a perihepatitis which is acute,
attended by pain in the right side, a febrile movement, and, if the
inflammation reaches the under surface of the organ, by jaundice, and
have learned to combat this with cups and opiates, the latter in rather
free but not heroic doses, and to expect recovery in a few days. This
may leave the liver wholly or partly invested with a layer of false
membrane which may have a sequel of importance. Then, again, we find
the organ invested with a thick contractile membrane, but cannot learn
that the symptoms of perihepatitis have ever occurred. The diseased
action which produced this bad investment appears to be analogous to
that which not only covers the organ with a thinner coat of similar new
tissue, but inlays it everywhere with the same material in cirrhosis.
This also is {1161} unattended by local pain. The effects that may
result from this encasing of the liver in a strong contractile capsule
may be illustrated by the following case (the late Buck was the
physician): The patient was an unmarried lady of middle age who had
consecrated her life to charitable works. In searching for the
suffering poor she often had to ascend several flights of stairs. The
time came when she found this fatiguing and a tax on her respiration.
She observed at the same time that the bowels were enlarged. She called
Buck, and he had no difficulty in discovering ascitic fluid. He was
surprised, as he knew that her habits were perfectly good, and she had
very little the appearance of an invalid. Notwithstanding the proper
use of the usual remedies for dropsy, the fluid slowly increased, and
at length he was obliged to draw it off. He found it to be a clear,
yellowish serum. In the course of about two years she was tapped four
times. I saw her, with Buck, after these tappings, when the fluid had
again been effused in quantity that half filled the peritoneal cavity.
The emaciation was not considerable; there was nothing of the
semi-bronzed color of the skin so common in cirrhosis of similar
duration; her appetite and digestion were not materially impaired; the
temperature was natural; the pulse was increased in frequency only a
few beats. The skin over the abdomen was in a soft, natural state, and
there was nothing that suggested a hyperaemic or inflammatory dropsy.
The liver on percussion appeared to be reduced in size. Taking all
things into account, and especially the patient's habits and the
absence cancerous cachexia, it seemed probable that the dropsy arose
from atrophy of the liver, and that the atrophy was caused by an
adventitious capsule of the organ, although the patient had never had
symptoms of perihepatitis. From this point the fluid did not increase
or diminish, but remained stationary till she died, perhaps two years
after, of some other disease. Meanwhile, the lady resumed her favorite
charity-work to a limited extent. At the post-mortem examination the
capsule was found investing nearly the whole liver, but not materially
obstructing the gall-duct. The new membrane was thick and strong,
having a thickness of at least one-twentieth of an inch. The remaining
liver structure was of natural appearance. The organ was reduced to
one-half its natural size. No other cause of dropsy was found.


Chronic Peritonitis.

I have doubted whether any disease deserving this name really exists
independent of such low inflammatory action as may arise from the
irritations of tumors or heterologous deposits. This statement refers
to general not local peritonitis. I have never seen anything that would
lead me to believe that acute diffuse peritonitis can be deprived of
its acute character and still continue an inflammation. With me it has
always been death or cure. I have already referred to a case in which
after recovery the bowels were greatly disturbed by tympanitis for
years. But this came from adhesions: her general health was good. I
have at long intervals met with cases of ascites in which the
peritoneal membrane was redder than natural, and in which no
obstruction to the portal {1162} circulation was discovered. This,
however, I have regarded as hyperaemia rather than inflammation.

Bauer,[8] however, gives to these cases the title latent general
peritonitis, especially when after death an abnormal adhesion is found
here and there. In the cases that I have seen there was a peculiar
state of the surface of the abdomen. The skin there was more or less
scaly and dry, but I do not remember whether there were internal
adhesions. Bauer regards the diagnosis of this form of disease as
difficult, but refers to the constantly present meteorism as well as
serous fluid. I have met with three or four instances in which at the
time of puberty an abdominal dropsy has rather suddenly occurred,
lasting one to three months, and disappearing on the use of diuretics.
I have had no reason to attribute this effusion to inflammatory action,
except in one case. A lady of extraordinary symmetry and beauty of
form, in excellent health, whom I had treated for this disorder twelve
years before, applied to know whether there was anything in that
disease that would prevent her having children. She had been married
seven or eight years, and had not been pregnant. The question then
occurred to me, At the time of the dropsy could there have been lymphy
exudation that has since confined the ovaries in an unnatural position?
The question I could not answer. The treatment which Bauer prefers for
his latent peritonitis consists in "painting with iodine, the use of
diuretics, and the regulation of diaphoresis by means of Turkish
baths."

[Footnote 8: _Cyclopaedia of the Practice, etc._, vol. viii. pp.
297-302.]

Another form of general chronic peritonitis is, according to Bauer,
that which follows acute peritonitis. He quotes several authorities in
support of his views. I must draw on him for a description of it, for,
as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all
disappear. Vomiting occurs occasionally; tenderness is diminished, but
is quite perceptible; meteorism diminishes, but fluctuates greatly;
appetite is poor or variable; constipation alternates with diarrhoea or
is followed by dysentery; now there is a febrile heat, and then the
temperature is normal--this fever is most likely to come in the
evening; the pulse is frequent and varying; ultimately extreme
emaciation and anaemia. The most striking feature of this condition
appears to be sacculation of the fluid in the abdomen, wholly or
partially; this fluid then is not freely movable, but will give dulness
on percussion, which may contrast well with intestinal resonance in its
immediate neighborhood. When the tension of the abdominal wall is
diminished these sacs can be felt by the hand as uneven tumors. Colicky
pains occur, and in a case cited it was at one time very severe, at
another only slight. The majority of the cases terminate, after a
protracted course, fatally. Recovery may occur by absorption or
external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis--those
arising in the course of old ascites; he, however, does not make much
out of it. He thinks the cases of this kind occur with cardiac and
hepatic disease, and particularly with the nutmeg liver. The symptoms,
he admits, are neither well defined nor severe, and the anatomical
changes consist "in thickening of the serous membrane by a slight
deposit of fibrin, {1163} slight turbidity of the ascitic fluid, and a
few flakes of fibrin suspended in it." He then, strangely, gives, as if
they were illustrations of such a disease, two cases in which death by
acute peritonitis followed the last of many tappings, in one of which a
pool of pus was found encysted in front of the intestines. Both are
borrowed.

Probably most practitioners who are in the habit of making post-mortem
examinations have seen the flakes of lymph in the ascitic fluid, etc.,
but the German physicians have been the first, I believe, to regard
such cases as belonging to separate forms of disease.

William Pepper has published[9] a case observed by himself and G. A.
Rex which shows non-malignant chronic peritonitis better than any I can
recall to mind. The report forms the sequel to the case of the young
woman on whom he successfully performed paracentesis of the
pericardium.

[Footnote 9: _Am. Journ. of Med. Sci._, April, 1874.]

This young woman began to have double pleuritic effusion, and this was
soon followed by ascites three and a half months after the operation.
From that time the ascites was better or worse, but did not wholly
leave her, and became considerable before her death. This was sudden,
she having some convulsive movements in extremis. Lesions were found in
the thoracic cavity like those discovered in the abdominal, showing, it
was believed, a special tendency in this person to plastic exudation on
the serous membranes. "The lower part of the abdomen was found occupied
by an extensive effusion. The intestines were floated upward. There
were few if any signs of inflammation of the intestinal peritoneum, but
marked changes were observed in the parietal peritoneum and in the
capsules of the liver and spleen. The peritonitis was most marked in
the upper segment of the abdomen, while the parietal membrane presented
large patches of irregular thickening. No tubercles were found on any
part of the peritoneum. The capsules of the liver and spleen were
greatly thickened, whitish, opaque, and densely fibrous. The liver was
enlarged and heavy, and so tightly bound by its thickened capsule that
its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial
sacs, had undergone marked fibroid degeneration. The muscular tissue
was much atrophied; many fasciculi had evidently disappeared, while
many others were markedly narrowed, some of them shading off to a width
of less than 1/3000 of an inch, and finally disappearing altogether.
They retained, however, even in their narrowest dimensions, their
transverse striae."

(It may be remarked, in passing, that this substitution of fibrous for
muscular tissue follows the same law that it does in the heart when
that organ is the seat of fibrosis or fibrous degeneration. Here it was
supposed to be the consequence of a low grade of inflammatory action.
Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the
possibility of tubercles or any obscure form of cancer. In the
pericardium, on the heart side, were found numerous small nodular
roughnesses. Irregularities of the pericardial false membrane are so
common that nothing but the close and universal adhesions would raise
any question of these relations. But tubercles would hardly be here and
nowhere else.

{1164} Delafield says that one form of the chronic disease is the
continuance of his cellular peritonitis. In this, he says, the surface
of the omentum is covered with cells which look as if they were derived
from the endothelium and connective-tissue cells, although they differ
from the normal shape of these. The new cells are for the most part
polygonal, of different size, with one or several nuclei, and
giant-cells--large granular masses filled with nuclei. Although these
new cells are produced over the entire surface of the peritoneum, yet,
as a rule, they are more numerous in little patches here and there.
These little patches may be heaped together in such numbers as to form
nodules visible to the naked eye. There is never any stroma between
these cells.

This form of peritonitis occurs most frequently with organic heart
disease, with cirrhosis of the liver, with chronic pulmonary phthisis,
and with acute general tuberculosis. In the two latter diseases he
thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that
occurs without the intervention of fibrin, but, as he supposes, by
coalescence of the branching cells and a production from them of a
fibrillated basement substance, the fibrils crossing in all directions.
In the midst of these fibrils he finds the nuclei of these cells. He
finds also in the immediate neighborhood of these adhesions thousands
of branching cells that are attached one to another and float free in
the water, the fixed end being attached to the peritoneum. He regards
such a peritonitis with adhesions as a more advanced stage of the forms
of cellular peritonitis already described, and the new cells are
changed into membrane.

Sayre has published an extraordinary case in the _Transactions of the
Pathological Society_. He calls it chronic proliferative peritonitis;
it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his
shoulders, and felt a severe pain in his stomach, and soon developed
symptoms of peritonitis. This pain never entirely subsided. The
peritonitis was recognized. About one month after he was tapped, and
240 ounces of serum were drawn. He was tapped one hundred and
eighty-seven times, and 1203-5/16 pounds of fluid were taken from him
during the remainder of his life. At post-mortem examination 3000 cc.
of yellow serum were found. The liver and spleen were covered by a
thick layer of false membrane, intestines were glued together in the
upper part of the abdomen, and the stomach was adherent to the lower
surface of the liver. The portal vein was contracted by this membranous
coating. There were numerous other lesions in the heart and pleura, but
these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an
attack of double pleuro-pneumonia, and in 1878 he slipped on the front
steps and fell, but seemed to recover from the effects of this. The
fall from the swing occurred in July, 1879. He died in February,
1884.[10]

[Footnote 10: _Med. Record_, April 19, 1884.]


{1165} Tubercular Peritonitis.

This form of disease is by no means uniform in its first symptoms or in
its progress. The only things uniformly attending it are tubercles on
the peritoneum and more or less of inflammatory effusion, chiefly lymph
and serum; tumor and hardness of the bowels, general or local; deranged
function of the stomach and intestines; emaciation; and extreme
fatality.

In some cases the invasion is acute and marked--a chill followed by
fever, vomiting, early development of meteorism, and in a few days a
point or points of resistance to pressure, but not necessarily dulness
on percussion. In a few days the febrile action and the meteorism may
subside, leaving the symptoms of local peritonitis. But we have not
long to wait for a renewal of them and an evident extension of the
inflammatory action. Remission and relapse alternate at varying
intervals, until the whole extent of the peritoneal surface seems to be
involved in inflammation. With this mode of development meteorism may
not be renewed in the most common way. The lymphy product of
inflammation may so bind the intestines to the posterior walls of the
abdomen that they cannot extend forward, but are pushed upward against
the liver and diaphragm, and so encroach on the thoracic space. But
then the anterior parietes are tense and hard, and do not move in
respiration. The febrile heat may not continue more than two or three
months, but the pulse will be frequent to the end. There will be a
thinning of bowel walls, and here and there a knuckle of adherent
intestines may cause some prominence and give some resonance on
percussion. There will be also occasional vomiting, and the dejections
will be irregular--maybe only deficient or thin; there may be an
alternation of constipation and diarrhoea.

Tuberculous ulcerations of the mucous layer of the bowels is not
uncommon in tubercular peritonitis, and these ulcers have in rare cases
perforated and allowed the fecal matter to accumulate in considerable
quantity in a sac limited by previous adhesions. In all forms of
tubercular peritonitis death is caused as often by grave complications
as by what appears to be the primary disease. The affection occurs in
probably every instance in those who had at the beginning, or had
acquired in its progress, what we call the tubercular diathesis. We are
not surprised, therefore, to find on inspection a wide diffusion of
tubercles in the body, particularly on other serous membranes, and in
the lungs. Death may occur, then, from phthisis pulmonalis or from
pleurisy or meningitis, as well as from the exhaustion and accidents of
the peritoneal disease. The effusion serum or turbid serum is very
common in tubercular peritonitis, and can be recognized by the dulness
it produces in part of the cavity, and sometimes by fluctuation. It is
often sacculated, but it is not constantly found after death, it having
been absorbed before, and perhaps long before, that event.

In other cases the invasion of the disease is stealthy and deceiving.
It comes so quietly that the patient is not conscious of any local
disorder beyond a dyspepsia and irregular action of the bowels. He has
a pulse of growing frequency, but if he knows it he ascribes it to his
dyspepsia. He is slowly losing flesh and strength; this he accounts for
in the same way. At length a perceptible swelling of the bowels
attracts his attention. At this stage the physician finds that the
swollen bowels are tympanitic everywhere or only in the upper, while
there is evidence of fluid {1166} effusion in the more depending,
parts. He discovers some, it may be little, tenderness on pressure, and
a pulse of 85, or maybe 90, increasing in frequency toward evening. The
appetite is poor, the digestion slow, and occasionally there is
vomiting; the complexion is pale and a little dingy; the skin of the
abdomen may be dry and rough or may be natural; some colicky pains have
been or soon will be felt. From this point the disease gradually
advances. The distension of the bowels slowly increases or they are
firmly retracted; the emaciation increases; the strength diminishes;
there is often cough, which is generally dry; the bowels are slow or
diarrhoea alternates with constipation; with the distended bowels there
is always more than natural resonance on percussion, except when there
is fluid effusion, though not often the full tympanitic sound observed
in acute diffuse peritonitis. This resonance is not equal, always, in
different parts of the abdomen; the respiration is embarrassed and
almost wholly thoracic. The abdomen is often as large as that of a
female at full term of pregnancy, and indeed the condition has been
mistaken for pregnancy. This is an inexcusable blunder in a case like
that which I have in mind--a young unmarried woman. She had no dulness
on percussion in the space that would be occupied by the gravid uterus,
but rather resonance. The case might have been a little less clear if
there had been fluid effusion in the abdominal cavity, but if this were
not encysted it would flow from one side of the abdomen to the other
when the patient turned correspondingly in bed; if it was encysted,
there would be small chances that it would have the shape and position
of the gravid uterus; if it had, there would be no chance of hearing in
it the foetal heart or feeling the foetal movements; and after all this
there remains the experimentum crucis--a vaginal examination.

At first the diagnosis is unavoidably uncertain. Some aid is found,
possibly, in the medical history of the family, in tuberculous
antecedents, yet I remember cases in which no phthisis could be found
in any living or dead member of the family on the paternal or maternal
side as far back as it could be traced. Some aid is found if the
patient himself has any of the physical or rational indications of
pulmonary phthisis, and yet there are recorded cases in which the
abdominal symptoms were the first to appear. The prominent German
physicians attach great importance to the pre-existence of a cheesy
mass or degeneration somewhere in the body as the real parent of
tubercles wherever they appear. The truth of this doctrine, I do not
think, has received anything like universal recognition; and if it had,
as this cheesy degeneration is often, perhaps commonly, only
discoverable after death, it could rarely give any assistance in
diagnosis, so that the early diagnosis is always difficult, and a very
early one often impossible. But as time goes on, and the symptoms are
better defined and show themselves one after another as they are above
described, it seems as if a careful observer could not confound it with
anything except perhaps one of the other forms of chronic peritonitis
or cancerous peritonitis. As to the latter, the cough which exists in
most cases of tubercular peritonitis will assist in the distinction,
but a physical examination much more; for a cough does not always
attend phthisis when this disease exists; for example, I visited a
daughter of one of the distinguished gentlemen of Vermont. She had had
the bowel symptoms that indicated tubercular peritonitis for eight or
ten months, and the diagnosis was not {1167} difficult. Remembering
Louis's opinion that if tubercles invade any other part of the body,
they are likely to be found at the same time in the lungs and in a more
advanced condition, I examined the lungs, and found in the upper part
of the right a cavity so large that it could have received a fist. I
was only surprised by the fact that she did not cough, and had not
coughed. She herself assured me of that (she was twenty-one years old);
her physician, who was present at the visit, had never heard her cough,
and had no suspicion of any pulmonary complication; but, more than all,
her mother, who had walked with her, slept with her, eaten with her,
travelled with her, and from the beginning of the illness had not been
out of her company more than twenty minutes in any twenty-four hours
since the disease began, had never heard her cough. Here, then, the
nervous deviation to the abdomen, or whatever else it may have been,
had so benumbed the sensibility of the pulmonary nerves that the
alarm-bell of phthisis had never been sounded; but the cavity, had
there been any doubt whether the bowel disease was cancerous or
tuberculous, would have almost fully settled the question. But more of
the peculiarities of cancerous peritonitis a little farther on.

The lesions of this disease (or its pathological anatomy) differ
considerably, but the differences are in the amount of tuberculous
deposit and the secondary results, not in the real nature of the
disease. Lebert has published among his plates of pathological anatomy
one which shows the peritoneum thickly sprinkled over with small
tuberculous grains, and represents each particular grain surrounded by
a little zone of inflammatory injection. There is yet no exudation, but
that would soon follow. A fibrinous exudation will soon come over this
primary deposit, and undergo a kind of organization, or at least get
blood-vessels, which in their turn can furnish the material for a new
crop of tubercles. These again provoke a new layer of fibrous tissue,
which also becomes studded with tubercles, and so on, till a thick
covering is formed over the intestines. But the same material is
interposed between their folds, separating one from another and
compressing them and diminishing their calibre; at the same time this
agglomerated mass is firmly adherent to the abdominal walls everywhere.
The new material may have a thickness of half an inch or even more. I
remember how surprised and confused I was when I made my first
inspection of such a case. The abdominal walls were cut through, but
they could not be lifted from the intestines, but were firmly adherent
to something. They were carefully dissected off and the bowel cavity
(?) exposed; there was apparently an immense tumor filling the whole
space: no intestines, no viscera, could be seen. A section was made
through this mass from above downward, and another parallel with it and
an inch distant from it, and this part removed. It appeared like a
large, hard tumor, through which the intestine made several
perforations. The new material appeared to be fibrous, with
grayish-white tubercles sprinkled in through it everywhere, and pretty
abundantly. In another case this fibro-tubercular material may occupy
one part of the abdomen, and a large serous cyst or serous cysts
another. The tuberculo-fibrous material may be found in markedly less
quantity than is so far described, till there will be no more than in a
case from Ziemssen's clinique, quoted by Bauer: "In the peritoneal
cavity about four liters of yellowish-brown, slightly turbid fluid.
Omentum {1168} thickened, stretched, adherent to the anterior wall of
the abdomen and beset with hemorrhages; the same was true of the
parietal peritoneum; between the hemorrhages whitish-yellow and
entirely white tubercles occur, varying in size from the head of a pin
to a lentil. The intestinal serous membrane was similarly invaded. The
intestines intensely inflated; a number of ulcers on the mucous
membrane, one approaching perforation. Covering of the liver thickened
by fibrinous deposition."

The lungs and serous membranes generally will, in all probability, show
more or less of tubercular deposit, the pericardium less frequently
than the others.

The result in this affection, after it is fully established, is
believed to be uniformly fatal, and at its commencement the difficulty
of diagnosis may lead one to doubt whether his apparent success is
anything better than apparent. Still, a plan which I have relied on is,
I believe, worth announcing. As soon as the disease is recognized the
patient is put upon the use of the iodide of potassium and the iodide
of iron, in full average doses, and a solution of iodine in olive oil
is applied to the whole surface of the abdomen by such gentle friction
as will produce no pain; and after a minute or two of such friction the
oil is brushed thinly over the surface and the whole covered with oiled
silk. This dressing is repeated twice a day. The quantity of iodine to
an ounce of oil will vary considerably in different persons; for some,
seven to ten grains will be enough; for others, thirty will be needed.
The iron is to make the application moderately irritating, and if it
produce pinhead blisters or blisters a little larger, all the better.
When the application becomes painful the oil is washed off, and the
application is not renewed for two or three days. In this manner it may
be continued for two or three months. Meantime, the patient is put upon
the diet and regimen of the consumptive, the appetite encouraged; he
takes sustaining food, with plenty of milk and cream, or cod-liver oil,
as much fresh air as possible, and friction is applied to other parts
of the body with dry flannel.


Cancerous Peritonitis.

Benign tumors of the abdomen are not frequently the cause of general
peritonitis, and when they are, the grade of the disease is acute
rather than chronic. They very often provoke local inflammation and
become adherent to the neighboring structures. The same is true of
malignant growths in the abdominal cavity, except that the adhesions
are earlier formed and more likely to occur. Localized cancer, of
whatever variety, is not very prone to produce general peritonitis,
even though there be multiple developments of it. But when the disease
takes the disseminated form, and is sprinkled over the whole extent of
the peritoneum, then inflammation is almost certain to occur--not of
high grade, and yet deserving the name subacute rather than chronic. A
case which illustrates this statement has come under my observation
within the last year. I will recite it with sufficient detail to make
it intelligible.

A lady about forty years of age had, up to the summer of 1881, enjoyed
very good health, though she was never robust. At that time she felt
her strength abating and her stomach disordered. She sought {1169}
health in various places, and took professional advice in September. It
availed her little; the bowels were gradually swelling and fluctuation
could be felt. She was losing strength and flesh. There was not a
cachectic countenance, but the features were growing sharp. She had
suffered but little from pain till October. At that time she was at the
family country home. Then she began to suffer from a severe pain in the
left thigh; and this, it was noticed, increased as the accumulation in
the bowels increased, and at length her physician felt compelled to tap
her--not so much on account of great distension of the bowel as in the
hope of relieving the pain. He drew off nine quarts of gluey, viscid
fluid, and her pain was wholly relieved. Twelve or fifteen days after
this she was brought to her city home, and her city physician, seeing
that her case was a grave one, sought the aid of a distinguished
gynaecologist. She was then again tapped to give him a more
satisfactory examination. He found the ovaries considerably enlarged
and hard. They could not, however, be felt by pressing the fingers into
the pelvis from above--only by the vagina. I saw her on the 10th of
November. The fluid had again made considerable tumefaction of the
bowels, and she was again suffering great pain in the region of the
right kidney and in the leg of the same side, together with cramps. The
relief given by the first tapping induced us to propose its repetition.
It was, however, delayed till the 14th, that the physician who had
tapped her before might be present and assist. The quantity of water
drawn was again nine quarts, and again the pains and spasms were
quieted. The examination of the abdominal fluid was interesting. It was
nearly clear, reddish, of syrupy flow and consistence, and so viscid
that while a portion of it had remained on the slide of the microscope
long enough for the examination of its constituents the thin cover
became so firmly attached to the slide that it could not be removed
without breaking or long maceration. The albumen was so abundant that
the fluid was completely consolidated on boiling. Fibrinous threads
were running through it in great numbers, and here and there was a cell
of large size, round, granular, but not plumped up with granules, with
a nucleus barely less in size than the cell itself; its outer border
within, but only just within, the boundary or wall of the cell. It was
the nucleus that was granular, for there was little room for granules
between the nucleus and the cell wall. The vial containing the fluid
had been standing three or four hours for a sediment. This in a vial
four inches high occupied the lower half, and gave nothing to the
dropping-tube till the sedimentary matter was drawn into it by suction.
This matter consisted of fibrillated fibrin in large quantity; a great
number of the cells just described, some grouped, but most separate or
single. There were pus-cells in moderate quantity, each having the
amoeboid movements, and a considerable number of red blood-corpuscles,
some of natural form, some crenate.

Immediately after the tapping the flaccid condition of the abdominal
walls admitted an examination. A solid, hard mass was found running
across the upper part of the bowels, a nodule of which was lying on the
stomach at the point of the ensiform cartilage. A harder mass of
irregular shape was also found just above the pelvis on the right side,
extending upward and to the right. This was in extent two by three
inches. The ovary, however, could not be detected by pressure from
above {1170} downward. The diagnosis up to this time was hardly
doubtful, but these revelations made it complete, and crushed any
lingering hope of the patient's recovery.

While the pain and spasm ceased after the tapping, the oedema of the
left leg, which came on some time before the last tapping, did not
diminish. The hard spot near the right iliac fossa was tender on
pressure, but otherwise hardly painful. While the fluid did not exceed
six quarts or so, she had little pain anywhere. There were no external
glandular swellings. Her appetite was poor, and she took but little
food. She vomited very little till the end was approaching. The urine
contained a few globules of pus, some pigment matter, two or three
hyaline casts, but no trace of albumen. For sixteen days following
November 14th the patient was comfortable, but the fluid was slowly
filling the bowels again. At that time the pains already referred to
began to return. On December 5th they required another tapping, and
preparations were made for it, but vomiting, rather severe, led to its
postponement to the next day. The quantity of fluid drawn was nine and
a half quarts. It was of the same syrupy consistence as that previously
drawn, and under the microscope showed exactly the same constituents
and gave the same quantity of albumen. The next day stercoraceous
vomiting commenced, with no movement of the bowels, except what was
produced by 10 grains of calomel given on the second day of this
vomiting. That acted well and produced a temporary relief. She after
this took no food by the mouth, but milk and beef-tea were injected
into the rectum. Still, the fecal vomiting returned, and she died on
the 15th.

The post-mortem examination was made on the 17th by William H. Welch. I
could not attend it. His report is complete as to the main features of
the case, though it does not furnish an explanation of the spasms and
the oedema of the left leg, regarding which Welch was not informed. The
pain and spasm were doubtless due to backward pressure of a diseased
part on a nerve or nerves, and the oedema to a narrowing of the iliac
vein by pressure or constriction by fibro-cancerous matter on its outer
sides. "The peritoneal cavity," he says, "contained somewhat over a
gallon of clear, yellow serum. Both the visceral and parietal layers of
the peritoneum were thickened, in some places more than in others; this
was especially marked on the anterior of the stomach and on the lower
part of the ileum and in the left iliac region. The omentum was greatly
thickened and retracted into a firm mass (or roll), which extended
somewhat obliquely across the body, more to the left than to the right.
The mesentery was much thickened and contracted, drawing the intestines
backward. In a few places only was the peritoneal surface coated with
fibrin, and the intestines were mostly free from adhesions. The coils
of the lower part of the ileum, however, were firmly matted together by
organized connective tissue in such a way that they were twisted, often
at a sharp angle, so as greatly to constrict the calibre of the gut.
The serous and muscular layers of the intestine at this point were
greatly thickened. By these causes there appeared to be a complete
obstruction at a point about six inches above the ileo-caecal valve. By
careful dissection these coils were straightened out, so as to remove
the main cause of obstruction. The peritoneal covering of the liver was
adherent to the parietal layer.

{1171} "The surface of both the visceral and parietal peritoneum was
studded over with hundreds of small, firm, whitish nodules, generally
not larger than a pea, and often not larger than a pin's head. In some
places they had coalesced and made firm patches an inch in extent. This
same material was found in the contracted omentum in considerable
quantity. In a few places, particularly on the uterus, a blackish
pigmented deposit appeared.

"The ovaries were not adherent, but both were enlarged to the size of a
hen's egg. The outer surface of each was rough and corrugated. The new
growth was deposited on the exterior and penetrated each a quarter to
half an inch. It was of uniform white color and of firm consistence.

"The stomach wall was thickened nearly throughout its extent, but
particularly in the anterior part, where it amounted to thrice the
normal thickness. This consisted wholly of hypertrophy of the muscular
coat and increase of fibrous tissue in the peritoneal layer. This new
growth was traced, in the interlacing bands, from the surface into the
muscular coat. In the outer layer of the stomach were found three small
white nodules. The mucous membrane of the organ was healthy or a little
pale.

"The retro-peritoneal glands along the aorta were enlarged, soft, and
of a reddish-gray color. A nodule was found in the wall of the duodenum
outside the mucous membrane, and one in the Fallopian tube."

Every organ in the abdomen and chest was examined, but nothing
important found except what is here recorded. Welch concludes his
record with the following diagnosis: "Primary scirrhous carcinoma of
the ovaries. Secondary deposits in the peritoneum, in the outer layer
of the right Fallopian tube, of the stomach and duodenum, and in the
retro-peritoneal glands. Chronic peritonitis, intestinal obstruction."

This case presents to the reader so accurately the usual course of
cancerous peritonitis, and the inspection its lesions, that a treatise
on the subject is hardly called for. It often happens that cancerous
antecedents in the patient or his relatives will lend an aid to the
diagnosis, which this case did not present. To distinguish this disease
from tubercular peritonitis no question can arise except in its
dropsical form, and then the lungs in every case of the latter that I
have met with have the physical signs of tubercles, though not always
the rational indications. The pulse is much more accelerated in the
tuberculous variety. I omitted to state that the temperature of this
patient was often taken, and till the closing scene was never found
more than one or two degrees above the healthy standard, and the
morning and evening heat did not materially vary; the opposite of both,
then, would be expected in a tuberculous case. The existence of
meteorism is much more common in the tubercular disease; indeed, in the
cancerous case recited there was none of it. The duration of the two is
different--that of the cancerous kind is recorded in months, while the
tuberculous variety may continue two years. The cancerous is more
likely to be attended by alarming accidents, like the complete
obstruction of the bowels, large hemorrhages, and a sudden lighting up
of acute peritonitis. Finally, in the light of the case here recorded,
it seems probable that the examination of the abdominal fluid will
become of great importance. I have never carefully examined the fluid
of tubercular dropsy, but it does not seem probable that it will have
the syrupy {1172} appearance, the large amount of albumen, the
abundance of fibrin-fibres, and the granular large cells with nuclei
only perceptibly less in size than the cells themselves, that were
repeatedly found in this case--found by two observers, and at every
tapping after the first.

TREATMENT cannot be curative; it therefore consists of such
administrations as will relieve pain, give sleep, improve the appetite,
increase the flow of urine if it be scanty, and relieve the bowels if
there is a tendency to constipation. It is as much the duty of the
physician to put off the fatal day, when he can, in incurable
affections as it is to cure those that will yield to his prescription
and advice. In the case just narrated opium or an opiate alone produced
such unpleasant after-effects that she was unwilling to take it, but
when the extract of belladonna was given with it she slept pleasantly,
and could take her food the next day.


Infantile Peritonitis, or Peritonitis of Childhood.

Bauer, in _Ziemssen's Cyclopaedia of Practice of Medicine_, and
Wardell, in _Reynolds's System of Medicine_, have each devoted a
chapter to this form of disease. They refer to the fact that the foetus
may have peritonitis before birth or be born with it, or may have it
when a few days old. They say that this form of the disease occurs most
frequently in lying-in asylums or foundling hospitals, and that it has
been supposed to depend on a syphilitic taint. They say, too, that it
follows erysipelas, scarlet fever, measles, etc. I do not perceive that
the description of either of these authors makes any marked distinction
between this and the same disease in adults, except what may arise from
the inability of the infant to describe its sensations, and the more
rapid course of the disease to a fatal result--in some cases
twenty-four hours. Having myself had no obstetrical practice, or next
to none, I have nothing to add to their statements, and can from my own
knowledge abate nothing. I therefore refer the reader to these
chapters, and to the references given by the first of these authors,
for a fuller knowledge of the matter.

Regarding the comparative exemption of children, after the first few
weeks of life, from spontaneous peritonitis, referred to by one of
these authors, I can fully confirm his statement. Though I have
assisted in the treatment of many children suffering from peritonitis,
I have difficulty in recalling to mind a single case in which the
disease was not caused by perforation of the intestine or vermiform
appendix of the caecum, and in much the greatest frequency perforation
of the appendix.

B. F. Dawson,[11] after reciting a case in which the liver had
undergone a peculiar degeneration and was attended by peritonitis
before birth, states that Sir J. Y. Simpson observed nine cases in his
own practice "and notes more than a dozen from different sources."
These cases seemed to have been caused by the ill-health of the mother
during gestation, or excessive labor, injuries, venereal disease, and
were mostly attended by grave disease; the viscera often, the liver;
but sometimes the mother was perfectly healthy, and the peritonitis was
the primary disease. Death almost always occurred in utero or shortly
after birth. In one instance the child recovered.

[Footnote 11: _N.Y. Med. Journ._, Dec., 1882.]

{1173} The _Med. Record_ takes the following from _Schmidt's
Jahrbucher_ for Jan. 7, 1883: "Dr. Oscar Silbermann recognizes two
varieties of peritonitis in the new-born. The non-septic or chronic is
developed usually in the first third of foetal life, and is generally
syphilitic in origin. If the peritoneum covering the intestines be
involved, as well as that over the liver and spleen, various forms of
intestinal obstruction may result. Most frequently there is occlusion
of the anus, less often stenosis or complete stricture of the small
intestine. Of a number of cases of congenital occlusion of the
intestine collected by the author, all ended fatally, only one living
beyond twelve days.

"The second, acute or septic, form of peritonitis in the new-born the
author divides into two varieties, according as the peritonitis is only
a part of general infection or is the sole manifestation of the septic
poison. In either case the point of entrance of the poison is always
the navel wound. The symptoms, which need not all be present in a given
case, are vomiting, watery stools, meteorism, ascites, abdominal
tenderness, icterus, etc. The pulse and temperature may vary in degree
in different cases. A cure of the septic form is possible; therefore
the treatment should be carefully considered. The navel wound should be
cleansed, and the child is to be isolated from its mother. To control
the fever quinine may be given. Priessnitz's sheet is of value;
vomiting may be checked by chloral (one-half to one grain in water).
The strength should of course be maintained by stimulants if
necessary."


Ascites.

The accumulation of fluid indicated by this name has already been
referred to in its relations to several causes. There are, however,
conditions producing it which have not been considered or only
considered partially.

The most prolific source of abdominal dropsy is obstruction of the
portal circulation on its way to or through the liver. Condensation of
the liver structure in cirrhosis, with destruction of many of the
portal capillaries and compression of many more, is prominent in this
connection. The compression of the liver caused by an adventitious
external covering, referred to under the head of Local Peritonitis,
acts similarly, whether it compresses the vein at its entrance into the
liver or not, although it is not known to produce any destruction of
the portal capillaries. Some enlargements of the organ are attended by
the same result, but they are always associated with a hardening of its
structure. The disease lately called waxy liver, now often denominated
lardaceous, belongs to this class, as does that condition in which the
organ is enlarged, hardened, and fissured, regarded as syphilitic
liver. That both these diseases may have a syphilitic and mercurial
origin is not a point now under consideration. They both harden the
hepatic structure and obstruct the portal circulation, while they may
not in equal degree hinder the progress of arterial blood. This is
explained when we remember the diminished force that propels the portal
blood. Neither of these diseases produces dropsy early in its progress,
but, as I have seen it, always before it reaches its fatal termination.
Fatty liver has not, in my observation, produced dropsy, {1174}
although I have seen livers made very large by that disease, and the
absence of dropsy when the liver has been large has aided me in
distinguishing it from the waxy disease. Cancer of the liver in some
instances does, and in others does not, produce dropsy of the bowels.
It is only certain to have this result when a tumor is in position to
press upon and obstruct the portal. Hypertrophy of the liver, caused by
mitral regurgitation or other disease of the heart, does not generally
produce dropsy, but, aided by anaemia or watery condition of the blood,
such a result is possible. In children, however, it is not very rare to
see the bowels distended by dropsy, and to discover that the liver is
enlarged at the same time. It is common in such cases that the dropsy
and the hypertrophy disappear after a few weeks of treatment. This may
occur in a child that is anaemic, but without any disease of the heart.
Such a case was brought to me two or three months ago, and after four
weeks of treatment by tonics and diuretics the health was
re-established. There is one point in these cases of some importance.
When the child lies on his back, if the abdomen is much distended, the
liver cannot be felt. It has sunk away into the fluid, and in this
position ordinary percussion cannot ascertain its dimensions. In the
July number (1840) of a quarterly journal edited by Swett and Watson, I
published an article in which I reported the conjoined labors of the
late Camman and myself on a new method of combining auscultation and
percussion, with its results, under the heading "Auscultatory
Percussion." By the method described in that article--viz. by placing a
solid stethoscope, or for that Laennec's first stethoscope, a rolled-up
pamphlet, on the chest at a point where the liver has not fallen away
from its walls, and percussing on the abdomen from below upward--a
point is reached whence the percussion sound is brought sharply to the
ear, while half an inch below the sound is dull and distant. The lower
edge of the liver is thus easily recognized, and its upper boundary is
found in a similar manner or by ordinary percussion, so the difficulty
of measurement disappears.

In such case, when the dropsy disappears and the liver recovers its
natural dimensions at the same time, the inference is that the
hypertrophy caused the dropsy, and that the hypertrophy was of the kind
called simple. The nutmeg liver is thought to have an agency in
producing dropsy, but as it is for the most part associated with
diseases that have been called dropsy-producing, its bearing on this
effusion may yet be regarded as uncertain.

It is common to speak of heart dropsy in such a way as to imply that
disease of the heart alone can produce abdominal effusion. I doubt it.
I even doubt whether the heart alone can cause the anasarca that is so
often attributed to it. In following a great multitude of heart
diseases from the time they were recognized to their termination, I
have been struck with the ease with which the patients attend to their
business, sometimes even laborious business, for years--in one instance
fifty years--with almost no complaint, and how rapidly their condition
changes as soon as albumen and casts appear in the urine. I have been
compelled by these observations to ascribe the anasarca and oedema that
makes this last stage of heart disease so distressing to the kidneys,
and not to the heart. Double pleuritic effusion is not uncommon under
these circumstances, but every physician must have noticed the rareness
of troublesome abdominal {1175} dropsy, while there is
sometimes--perhaps often--a little effusion; and when in the
exceptional cases there has been much, it was almost always accounted
for by a dropsy-producing change in the abdominal organs, not, perhaps,
discovered during life; so that for me, while they produce overwhelming
effusions in other parts of the system, they are minor agents in the
production of ascites. Phthisis is occasionally attended, toward its
close, by oedematous legs and albuminous urine, but I cannot report any
important relation between these and peritoneal effusion. I can say the
same of chronic bronchitis. I record this negative testimony regarding
the two last-named diseases, because I find them enumerated among the
causes of abdominal dropsy.

Cancer may invade the portal vein, tumors of adjacent parts other than
those of the liver, or an aneurism may compress it and cause dropsy.
Hydatid tumors may do this. Diseases of the pelvic organs, both acute
and chronic, may produce it, but then the disease would fall into the
class of those produced by chronic or subacute peritonitis.

DaCosta thinks he has lately had a case of chronic peritonitis attended
by ascites. It was in a woman thirty years of age, who had been thrown
with force upon the frame of an iron bedstead, striking the lower part
of the bowels. Pain and tenderness followed. These were not confined to
the injured part, but extended to the whole abdomen; and there was
menorrhagia. After a time there was fluid effusion in the peritoneal
cavity, which slowly increased till her state demanded relief from
tapping. The fluid after this operation did not return. The pain and
tenderness were constant symptoms all through. She slowly improved, and
at the time the case was reported it was believed that she would soon
be discharged from the hospital. The only doubt which DaCosta finds
regarding the diagnosis is in the facts that the liver was diminished
in size and that the spleen was moderately enlarged, and he admits the
possibility that an adventitious capsule of the liver may have caused
the ascites, but believes that it was dependent on chronic peritonitis.

Acute peritonitis subsiding into chronic, with increase of fluid
effusion, as I have already said, I am not familiar with. That
occurring in cancerous and tuberculous peritonitis has already been
considered. But in relation to these some facts regarding frequency of
occurrence, collected by Bristowe, are worth quoting. He says that in
48 cases of tubercular peritonitis, dropsy was found in 12, and that in
22 of peritoneal cancer, 12 had more or less ascites. He further adds,
regarding cirrhosis, that of 46 cases observed post-mortem, there was
dropsy in only 20. This is not surprising, as in all the diseased
conditions of the liver that produce dropsy the anatomical changes must
reach the point at which there is considerable portal obstruction
before the effusion will occur.

The amount of fluid found in ascites varies greatly. In some it may
remain for a long time stationary at four or five quarts; in others the
suffering caused by an accumulation of nine or ten quarts will demand
its removal; and in a few cases twenty quarts have been removed in one
operation. It is in cirrhosis that the largest quantity is found, and
it is in this disease and in cancerous peritonitis that the most
frequent tappings are required. The quality of the fluid also varies
markedly: from being almost as clear and thin as spring-water it may be
almost ropy, or in color greenish or yellowish or slightly red; it is
very likely to contain {1176} albumen; and it is probable that a
further study of its microscopic elements may enable us to resolve
doubts regarding the cause of the effusion. It very often contains
blood-corpuscles.

Bristowe finds from hospital records that ascites occurs in about equal
frequency in males and females, but, as everybody has noticed, that
hepatic dropsy is much more frequent in men than in women. Ascites, he
says, is most frequent between the ages of thirty and fifty, and next
between twenty and thirty and between fifty and sixty, but is not
uncommon above the latter age; and it occurs in children.

SYMPTOMS.--In general, ascites is easily recognized by the swollen
state of the bowels: a well-rounded swelling when the patient stands or
sits, but spread out in the flanks when he lies on his back; the
fulness of the side on which the patient may be lying, and the
flattened condition of the opposite side,--belong to this disease, and
as a group to no other. The results of percussion are significant in
the movement it causes in the fluid, and for the resonance or flatness
it produces. When the patient lies on his back, tapping with the
finger-ends on one side of the abdomen sends a wave of the fluid across
to the other side, where it is perceived as a gentle blow by the
applied fingers of the other hand. If the abdomen is not full, this
wave will be produced at the upper level of the fluid, but not above
that. If this wave cannot be sent across the body, it may be found on
either side by percussing above and feeling for it below; percussion
also teaches where the fluid is, and where it is not, by the dull sound
it produces. It is rare in ascites that the intestines do not float on
the surface of the fluid, at least from the umbilicus upward, and there
give a loud percussion sound, while toward the back, and often toward
the pelvis, it is dull, or even flat; changing the position of the
body, the resonance will be uppermost and the dulness in the most
dependent part. Then the softness or impressibility of the abdomen till
the tension becomes great is noticeable. The changed position of the
fluid as the body is turned from side to side is important. A very
small quantity of fluid can be detected in this manner. The patient is
placed on his right side and percussion is made in the right flank:
there is dulness, while in the left flank there is resonance. The
patient turns on to the left side: dulness now changes position, and is
on the left, and on the right resonance. If it is feared that some
undetected fluid remains in the pelvic cavity, the pelvis may be raised
by pillows and the same examination repeated, or he may be placed in
the knee-and-elbow position referred to by Bristowe, and the percussion
will then be made upward in the umbilical region. In some cases the
contraction of the mesentery will not allow the intestines to rise
through a large amount of fluid and float on it; but such cases are
almost confined to the cancerous and the tuberculous varieties of the
disease; and as in these the symptoms are grave, the physician will
probably have visited his patient many times before this contraction
will embarrass him. Besides, when mesenteric contraction occurs there
is a very strong probability that the omentum will also be contracted,
be rolled up, and lumpy; as this can almost always be felt above the
level of the umbilicus, he has in it an explanation of the absence of
resonance on the fluid. It has happened that oedema of the abdominal
walls or fatty accumulations there have given a delusive though feeble
fluctuation on percussion. In such cases, if the patient make moderate
pressure with the back of a small book in {1177} the course of the
median line, that kind of wave will be broken, while a wave in the
abdominal cavity will not be prevented. When there is considerable
distension of the abdomen by fluid, weak spots in the abdominal wall
often yield and make a tumor. This is very common at the umbilicus,
where a little bladder is lifted half an inch or more above the general
curve of the abdomen. The fluid frequently follows the track of
hernias. In females it has been known to press the anterior wall of the
vagina backward and downward, so as to make it protrude at the vulva.
It has, in one of my own cases, by downward pressure caused complete
prolapse of the uterus. It is very often attended by oedema of the
lower limbs. This is accounted for by the pressure of the abdominal
fluid on the veins that return the blood from these parts, or in
cirrhosis by contraction of the ring or notch through which the vena
cava passes in the liver. If there is general oedema, the cause will
probably be found in disease of the kidneys; or if in one limb, in
pressure or thrombosis of one iliac vein. As the disease advances the
accumulating fluid forces the diaphragm upward, diminishes the
breathing room, and threatens the life still more. Then the patient
cannot lie down in bed, but spends his nights as well as days in an
easy-chair, and sleeps leaning forward on a support for his forehead.
The veins on the abdominal surface will fix attention. With almost any
large tumor in the cavity they become more or less enlarged. But in
cirrhotic dropsy this becomes more striking than in any other
affection. The enlargement is attended by a reversion of the
blood-current on the lower half of the abdomen. This is early shown by
emptying an inch or two of a vein with the finger, drawing it either
upward or downward, and noticing from which direction it is refilled
when the pressure is removed. The pelvic veins do not readily discharge
their blood by the natural channels, and by anastomosing branches it is
forced over the surface of the abdomen and into the thoracic veins,
these latter becoming in turn greatly enlarged. The appetite is
commonly poor, the digestion flatulent, the pulse accelerated.
Emaciation is gradual or rapid. The urine is commonly scanty, and in
cirrhosis of a reddish hue. The skin is apt to be dry, particularly so
in simple chronic peritonitis. The tongue has no characteristic fur,
and is often, almost always toward the close, dry. The mind is not
affected till near the end; then often the patient is delirious,
commonly mildly. Diarrhoea is not uncommon, and even dysentery has been
observed. The result is almost always unfavorable, or, as has been
said, lethal.

The diagnosis is not often difficult. When, as in chronic peritonitis
and in tuberculous peritonitis, the fluid is confined in a sac or sacs,
each particular pool will be yielding to pressure, but elastic, and
will give the percussion wave, though it may extend but a short
distance. To distinguish ovarian dropsy--ovarian cysts, as it is now
called--from ascites may require a few words. Ovarian tumors of all
kinds are found to be more prominent on one side when they rise from
the pelvis than on the other. This is not the case with ascites. The
uterus and its appendages lie in front of the pelvic intestine, and
when any of them ascend above the pelvis they must occupy the same
relative position. In other words, a large ovarian cyst must lie in
front of the intestines, while intestinal resonance should be found
behind and in the sides. But if the ovarian cyst does not occupy the
whole height of the bowels, intestinal resonance {1178} may exist above
it, and the dulness may be found below, bounded by a portion of a
circle, and sometimes the cyst walls are resisting enough to allow its
boundaries to be ascertained by the fingers. This cyst can also be felt
in the vagina; and the uterus, instead of being pressed down, is
sometimes lifted upward, so that it cannot be reached in the vagina,
but can be felt through the abdominal walls just above the pelvic
bones. A condition more troublesome than this is when ovarian cyst and
ascites occur together. Then the posterior or lateral resonance is lost
when the patient lies on her back, but can be found on one side when
she lies on the other. In that concurrence, in dorsal decubitus it is
possible by pressure or a little blow to send a wave of the ascitic
fluid over the front of the cyst. This can be seen as well as felt.
Should the patient take the knee-and-elbow position, the intestinal
resonance may be restored in both flanks.

TREATMENT.--In opening the chapter on the treatment of ascites it is
usually said, Give principal consideration to the diseased conditions
that have caused the dropsy; in other words, cure cirrhosis, cancerous
peritonitis, tubercular peritonitis, heart disease, and the secondary
affections of the abdominal organs, release the liver from the
dangerous compression to which it is subjected, and all will go well.
But they do not inform us how these impossibilities--at least in most
cases impossibilities--are to be achieved. It is true that the
physician would not shrink hopelessly from the treatment of simple
chronic peritonitis. But this is one of the rarest causes of ascites. A
physician in a long lifetime may not have seen a case. It is true,
ascites is a symptom, always a secondary, or even a tertiary,
affection; and theoretically there can be no better advice, but
practically it cannot amount to much. Then, if the cause cannot be
removed, it remains to do our best to relieve the patient of his load
and strive to prolong his life to its utmost possible limit. In doing
this the physician will often find himself able to give gratifying
relief, and once in a great while to rejoice in a cure.

The three great emunctories, the skin, the bowels, and the kidneys, are
chiefly appealed to for relief in this as in other serous
accumulations. Most physicians prefer to use the diuretics--first,
because if they will act at all, they act so quietly and produce so
little debility that whatever can be gained by them is obtained at
small cost to the system. The form of ascites that most resists
diuretics is that which originates in cirrhosis. Often a full trial of
them, with suitable changes from time to time, is of no avail, yet now
and then the kidneys yield to persuasion and act freely. The saline
diuretics and digitalis are most in favor with some. In the early part
of the present century a pill composed of squill and digitalis in
powder, and calomel, each one grain, given three times a day, was
almost universally chosen. In place of the calomel the blue mass was
often preferred. When this prescription had produced a little ptyalism
the mercurial was omitted and the squill and digitalis continued. It
has often been observed in dropsies of all kinds that diuretics act
better after a little mercurial action is set up in the system. The
diuretic that I most frequently prescribe is made of the carbonate of
potass. ounce ss and water ounce vj; to a tablespoonful of this a
tablespoonful of fresh lemon-juice is added. This is taken every two
hours, and at the same time a dessertspoonful of the infusion of
digitalis or more is taken three times a day. This is an {1179} old
prescription. Sometimes the old sal diureticus is used. This is the
acetate of potassium. It is not always kindly received by the stomach.
At Bellevue Hospital the following is much used: viz. infusion of
digitalis, ounce iv; bitartrate of potash, ounce j; simple syrup, ounce
ss; and water added to make a pint. This is taken pretty freely. But it
would require many pages to exhaust the diuretics. I will only add that
I have more confidence in the salts of potash and soda, singly or
combined, aided by digitalis and a mercurial, than in any others.

The diaphoretics that are most efficient are warm water and steam. A
foot-bath long continued and frequently repeated, the patient covered
with blankets, and the water kept at 90 degrees or warmer, are very
effectual in producing perspiration. Bricks heated or hot water in
bottles, or potatoes heated, and enveloped in damp cloths and laid
alongside of the body and limbs, form an extemporaneous vapor-bath of
considerable efficiency. A vapor-bath can be easily extemporized in the
following way: Have a kitchen vessel furnished by the tinman with a
cover which has an inch tube fitted to this and bent so as reach the
floor six feet from the fire. The pot should have a capacity of a
gallon or more, and should be kept boiling briskly. Meantime, the
patient, in his night-dress, has a double blanket brought over his
shoulders from behind, and another from before, and fastened. Now he
takes a chair (wooden), under which the steam is delivered. The blanket
from behind is kept off his body by the back of the chair, and the
front one by his knees. The steam, shut in in this way, soon brings on
a sweat, and when it is sufficiently active the front blanket is thrown
off, and the patient wrapped in the rear one and put to bed, when the
sweating can be regulated by blankets. This is better than what is
called the alcohol sweat, for in that the patient is bathed in carbonic
acid gas as well as heat. A patient is sometimes enveloped in a hot,
wet blanket with good effect. Pilocarpine has come into use lately as a
sudorific. I have witnessed its effects many times and can testify to
its certainty as a sudorific; but it is too debilitating for common
use. Digitalis has sometimes acted with extraordinary power in this
way, but there are grave risks in administering large doses.

Among the cathartics that may be used in ascites, it has seemed to me
that the milder hydragogues are safest. One ounce of Epsom salts with a
drachm of the fluid extract of senna can be taken every second or third
day for months, if need be, with little reduction of strength, and
sometimes with an increase of it. I had charge of a young man in the
hospital in whom cirrhosis was unquestionable, and dropsy at one time
extreme, in whom the abdominal veins had made furrows that would
receive the little finger, who was wholly relieved by a drastic dose of
elaterium every second day. I saw him three years after his discharge,
and then his health was good. Notwithstanding this, I prefer the milder
medicines.

Bristowe has seen no cures from either sudorifics, diuretics, or
purgatives. I have seen one or more from each of those agents, all
cirrhotic. He "has seen cures occasionally from mercury, iodide and
bromide of potash, copaiba, and a combination of fresh squills and
crude mercury." I agree with him in his statement that
counter-irritants are useless, making exception for chronic peritonitis
and the early stage of the tubercular variety. He thinks quinia, iron,
and cod-liver oil are useful.

{1180} Paracentesis in almost every case will at length become
necessary, and the question comes whether it should be practised early
or late. If it be delayed till the oppression of the breathing makes it
imperative, the walls of the abdomen will be so stretched as to present
little resistance to the reaccumulation of the fluid, and a second
tapping will be required in fifteen to twenty-five days. A bandage is a
poor substitute for muscular contraction. If, on the other hand, the
fluid is withdrawn before the muscularity is not stretched out of the
muscles, then accumulation will be less rapid and the patient will be
spared the suffering which large accumulations cause. But tapping is
not always an innocent operation. It is sometimes followed by acute
peritonitis. By the early tapping this risk is oftener taken. Reginald
Smith suggests the use of a small canula by which only ten or twenty
ounces of the fluid can escape each hour. This mode, he thinks, removes
the danger of syncope and makes the bandage needless.


Hemorrhagic Effusion

in the peritoneum is a topic on which there is little to be said. A
primary effusion of this kind probably does not occur. In
haematophilia, where the mucous membrane of the nose and wounds bleed
dangerously, there is no record of spontaneous bleeding into the
peritoneal cavity. The same thing can be said of that very rare disease
which has been called bloody sweat. An unmarried lady applied to me
fifteen years ago with this disorder. The blood would ooze out at
hundreds of points on the inner face of the arm; these would run
together and drop off the arm, or the same thing would occur on the
chest and in the bend of the knee. This would continue for two or three
minutes, and then cease of itself, but to recur in one or more, rarely
several, places. For years this habit continued. There was no
irregularity of the menses. I could find no visceral disease; there was
no nose-bleed. She lost strength, but only moderately. This kind of
bleeding continued for several years. She is now approaching fifty
years of age, and for the last two or three years has had no recurrence
of the bleeding. There was never anything in this case to lead to the
suspicion of peritoneal or other serous hemorrhage. In the few similar
cases on record there is the same absence of all evidence of internal
bleeding.

It has already been said that a certain amount of blood, as shown by
its corpuscles, is to be expected in cancerous ascites, and with less
uniformity in tubercular ascites, and not unfrequently in hepatic
dropsy, as well as in acute peritonitis. This may not deserve to be
called hemorrhage, on account of the moderate quantity of blood that is
effused; but aside from that which results from rupture of
blood-vessels it is about the only kind of it with which we are
familiar.

Scurvy, and conditions of the blood analogous to those produced by that
disease, make it almost certain that if pleurisy or pericarditis occurs
while these conditions exist, it will be hemorrhagic. I am not,
personally, acquainted with a single instance in which peritonitis in
this condition has occurred. Copeland, however, says that hemorrhage in
peritonitis has been noticed by Broussais and others. The blood is
mixed {1181} with the serum and stains the surface of the false
membrane, as in hemorrhagic pleurisy and pericarditis, and the disease
is of an asthenic type, "occurring in the hemorrhagic diathesis." "The
symptoms are inflammatory from the beginning, and rapidly pass into
those indicating great depression; the pulse becomes rapid, small, and
soft, death quickly supervening, with convulsions, cold and damp
extremities and surface," etc.

Copeland has himself not seen a case, and regards its occurrence as
very rare. Delafield states that "Friedreich describes two cases
occurring in patients with ascites who had been frequently tapped. He
says that both the parietal and visceral peritoneum was covered with a
continuous membrane of a diffuse, yellowish-brown color, mottled with
small and large extravasations of blood. The membrane was thickest over
the anterior abdominal wall. It could be separated into a number of
layers. These layers were composed of blood-vessels, masses of pigment,
branching cells, and fibrillated basement substance. In many places the
extravasated blood was coagulated in the shape of round, hard, black
nodules. The new membrane could be readily stripped off from the
peritoneum, and there were no adhesions between the visceral and
parietal portions of the peritoneum."

The erosions of abdominal cancer sometimes open vessels of considerable
size, causing large hemorrhage into this cavity and sudden death.

When aneurisms of the abdominal aorta rupture, they sometimes flood the
abdominal cavity; oftener they open into the structures under the
peritoneum on the left side, and make a large flat tumor extending from
the point of rupture downward to the brim of the pelvis, and even
beyond it.

A gentleman whose health was usually good, thirty-five years of age,
felt an unwonted exhaustion and feebleness creeping over him. His
countenance became pale, his pulse rapid, growing smaller and smaller.
It seemed certain that there was hemorrhage somewhere, but until it was
noticed that the bowels were growing tumid and hard there was nothing
to guide us to its seat. Even then we were left to conjecture regarding
the bleeding vessel. This sinking continued for thirty-six hours. After
death it was found that a small aneurism had been formed on one of the
vessels of the omentum, not larger than a small walnut, and had
ruptured by a very small opening, and that it was by this small opening
that life had oozed away.

Bleedings from stabs and other wounds of the bowels, from lacerations
of the liver, spleen, uterus, and sometimes of the kidneys, should be
mentioned in this connection; but as they, for the most part, fall into
the hands of the surgeons, this is not the place to give the details
regarding them.




{1182}

DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA).

BY SAMUEL C. BUSEY, M.D.


DEFINITION.--Tabes mesenterica may be briefly defined to be
tuberculosis of the mesenteric glands. This definition may seem too
limited, because it recognizes the identity of tuberculosis and
scrofulosis of the lymph-glands, and excludes those hyperplastic
conditions which do not certainly undergo the cheesy degeneration. It
is supported, however, by the absence of any essential difference in
the histological changes which take place in tuberculous and scrofulous
(Wagner) lymph-glands; by the frequent simultaneous occurrence of each
in the same subject; by the secondary development of tubercles during
the course of scrofulous affections; and by the fact that the cheesy
transformation is alike common to both these conditions of new
formations. Schuppel maintains that the presence of tubercles is
necessary to the production of the cheesy metamorphosis of
lymph-glands, and that "scrofulous glands are always tuberculous
glands." In this view Rindfleisch coincides, and expresses the belief
that the inflammatory and hyperplastic changes are secondary to the
formation of the tubercles. Birch-Hirschfeld asserts that cheesy
degeneration of the mesenteric glands is always accompanied by
tubercular formations.

This definition is therefore adopted as the expression of the result of
the most recent investigations. It must, nevertheless, be admitted that
a few equally competent observers deny the identity of the tuberculous
and scrofulous new formations in lymph-glands. It must also be conceded
that occasionally hyperplastic processes in the lymph-glands undergo
the cheesy metamorphosis independent of tubercular development.

SYNONYMS.--The differences of opinion, especially among the older
authors, in regard to the nature of this disease are very distinctly
indicated in the varying significance of the numerous synonyms, of
which the following list is only a part: Atrophia mesenterica; Atrophia
infantum (Hoffmann); Febris hectica infantum (Sydenham); Scrofula
mesenterica (Sauvages); Paralysma mesentericum (Good); Physconia
mesenterica (Baumes); Mesenteritis chronica (Stewart); Mesenteric
fever, Hectic fever, Marasmus (Underwood); Carreau, Entero-mesenterite
of the French; Darrsucht der Kinder and Gekroschwindsucht of the
Germans; Tubercles of the mesentery; Tuberculous disease of the
abdomen; Phthisis mesenterica; Tabes glandularis; Tabes scrofulosa;
Macies infantum; Paedatrophia; and Rachialgia mesenterica.

{1183} Some of these synonyms indicate the theoretical and unsupported
opinions of their authors, and others refer merely to a symptom. The
name carreau refers to a hardness of the abdomen; physconia, to the
presence of a non-fluctuating and non-sonorous abdominal tumor; and
that of entero-mesenterite presupposes a secondary origin from a
primary enteritis. Good classes it among his numerous varieties of
mesenteric turgescence, but characterizes this special form as a
scrofulous turgescence always associated with the strumous diathesis.
The terms tabes and atrophy originated when the nomenclature of disease
was derived from symptoms, and not from pathology.

HISTORY AND PATHOLOGY.--The history of tabes mesenterica is coeval with
that of scrofula and pulmonary consumption. The ancient authors
recognized the existence of a chronic disease of the mesenteric glands,
characterized by enlargement and induration, followed by destruction of
the gland-parenchyma, which was associated with digestive disturbances,
emaciation, hectic fever, and usually terminated in death. At first,
the degenerative process was regarded as suppurative. But as the study
of scrofula progressed, and frequent observations were made of the
occurrence of disease of the external lymphatics and of the mesenteric
glands in the same subject, disputes arose as to the identity of the
two affections. These controversies led to the general acceptance of
the belief that the scrofulous degeneration of lymph-glands and the
process of destruction in tabes mesenterica were identical.
Consentaneous with these investigations, and for a long time
subsequent, even down to a very late period, which is, perhaps, not yet
concluded, the relation of scrofulous disease of the lymph-glands to
pulmonary consumption was discussed and studied with great assiduity.
As the knowledge concerning these diseases advanced, and the results of
investigations were accepted, the doctrine of the identity of the
morbid processes in scrofulous disease of the external glands and
mesenteric phthisis became firmly established. The history of
scrofulosis and tuberculosis cannot be separated. The connection and
identification of the two processes have been subjects of constant
discussion from the discovery of tubercle to the present time.
Occasionally, the dividing-line seemed definitely fixed. Then would
follow the general acceptance of the doctrine of identity. With the
discovery of miliary tubercle a determined reaction took place against
this view, and for a while many regarded scrofulosis merely as a form
or stage of tuberculosis. As the conclusions in regard to these
questions changed, so did the opinions concerning the true nature of
tabes mesenterica change, until, finally, the investigations of
Rindfleisch, Schuppel, and others seem to have established the
tuberculous nature of the disease. Many authors of a comparatively
recent date have applied the term tuberculosis to this condition, not
because they knew or believed the development of true tubercle was a
constant or essential characteristic, but because they regarded the
words scrofulosis and tuberculosis as synonymous.

Notwithstanding the obscurity in which, for so long a time, the
pathology of this disease was involved, certain facts well known to the
earliest writers have been confirmed by continuous observation down to
the present. Its secondary character has been so uniformly recognized
that some of the older authors based its origin upon the absorption and
conveyance along the lymphatic vessels to the glands of some peccant
material originating {1184} in a primary focus of disease. The constant
coexistence with scrofulous affections and pulmonary consumption had
long ago established the direct and primary relation of these diseases
to tabes mesenterica, and authors of recent date, though not so
generally holding the opinion that it is always an intercurrent
complication of these maladies, yet maintain its secondary development.
Even Schuppel, whose investigations and conclusions lead in the
direction of an idiopathic origin, admits that the only primary element
is the tuberculosis, which finds its cause in some peripheral
irritation.

In the earlier times, as now, tuberculosis of the mesenteric glands has
been observed during every period of life from birth to advanced old
age, but then, as at the present time, the greater number of cases were
known to occur during infancy and childhood. But few cases have been
observed during the earlier months of life or before weaning. Between
the ages of two and eight years is the period of greatest frequency.
Though rarer during the later years of childhood, the older the child
the more rapid its progress to a fatal termination. Nursing infants are
not exempt, but those nursed by healthy mothers are much less liable
than the wet-nursed. Among hand-fed infants it is not an uncommon
disease, but it is much more common among the farmed-out children.
While, as has been stated, the greatest number of cases occur in those
between two and eight years of age, statistics show that the liability
to it increases from the age of two and a half years up to the eighth,
and, according to some authors, up to the tenth year. At the latter age
there is a remarkable diminution in the number of cases. This fact is
probably due to the greater prevalence of the acute diseases of the
respiratory organs and of the exanthematous diseases among children
during this period of life. Some have attributed it to the more rapid
development and increased functional activity of the mesenteric glands.
This circumstance might afford a plausible explanation for the apparent
sudden increase in frequency after the completion of the second year
because of the independent subsistence of children at that age, and the
additional duties imposed upon the alimentary tract and its
dependencies; still, if this were so, the period of greatest frequency
ought to begin at an earlier age and more nearly correspond with the
time of weaning. It is, however, a fact that tubercularization of the
mesenteric glands is more frequently associated with chronic intestinal
inflammation in those over one year than in those under that age. This
fact, together with the greater liability of artificially-fed infants,
would seem to connect, at least in such cases, its secondary origin
with some primary irritation of the intestinal canal.

Authors are not yet agreed in regard to the relative frequency of this
disease in boys and girls, though opinions predominate in favor of the
greater number among the males. The statistics of Rilliet and Barthez
and Schmalz show a decidedly greater prevalence among boys.

The comparative frequency of tuberculosis of the mesenteric glands
cannot be determined. Louis found disease of the mesenteric glands in
one-fourth of the autopsies of persons dying of phthisis; in 100 adults
dying of the same disease Lombard found tuberculosis of these glands in
10; and in the bodies of 100 tuberculous children he found the glands
tuberculous in 34 cases. In the Hopital des Enfants Maladies tubercles
were found in the mesentery of one-half of the children dying of {1185}
tuberculous affections. In the bodies of children dying of tuberculous
disease in the Children's Hospital of Washington tuberculous
degeneration of the mesenteric glands has been found in two-thirds of
the cases, and without a single exception in those dying of rickets.
Authors differ also, and the statistics are equally unreliable, in
regard to the relative frequency of tubercularization of the bronchial
and mesenteric glands. The general opinion seems to be in favor of the
greater frequency in the bronchial glands. In a majority of cases both
sets of glands are found diseased.

The geographical distribution of tabes mesenterica is as universal as
that of scrofula and pulmonary phthisis. No country or climate is
exempt, yet there is no locality in which it is endemic. It has been
observed among all civilized nations, in the cold regions as well as in
the tropical countries. Wherever scrofulous and phthisical diseases are
known, there also are found cases of tabes mesenterica. Livingstone has
stated that scrofula is unknown in some regions in Central Africa, and
other travellers have made similar statements in regard to some Indian
tribes. The statistics of the Children's Hospital of Washington show a
far greater frequency among the African race than among the whites. It
belongs to no class or condition of life, but occurs more frequently
among the children of the squalid than among the children of the
affluent and well-to-do.

ETIOLOGY.--Predisposing Causes.--Modern as well as the older authors
have very generally accepted the conclusion that a constitutional
tendency or liability to this disease is its most frequent and
potential etiological factor. This predisposition may be either
inherited or acquired. The ancients called it the strumous, and the
more recent writers the scrofulous or tuberculous, diathesis. Lugol
maintained that this diathesis is begotten of old and syphilitic
fathers, and others state that children of parents nearly related and
of those broken down by disease and excesses may inherit it. That it is
transmitted by scrofulous and phthisical parents no one can doubt, but
as yet it cannot be defined to be anything more than a peculiarity of
the constitution which may exhibit abnormal reactions against
irritating influences. The scrofulous habit is believed to be indicated
by physical appearances which represent two extremes. The erethic form
is characterized by a feeble and delicate frame; deficient muscular
development; transparent, smooth, and florid skin; light hair and blue
eyes, large pupils; precocious intellect and sanguine temperament; the
torpid form, by a large head; large and tumid upper lip; soft and
flaccid flesh, bloated appearance; short and thick neck; muscular
incapacity, tumid abdomen, and sluggish intellect. Some of these
features are more frequently symptoms of the actual disease than of the
existence of a predisposition to it, and, except so far as they may
refer to a primary scrofulous or pulmonary disease, cannot be accepted
as indicative of the presence of a constitutional tendency to
tuberculosis of the mesenteric glands. A tumid abdomen, rapid
emaciation, and anaemia are far more valuable signs of the disease of
these glands.

Bad air and bad food are also important predisposing causes. They are
conditions to which the children of the poor, especially in large
cities, are constantly exposed. Insufficient protection from climatic
influences, neglect of person, and unhygienic surroundings must be
classed in the same category. It is claimed that vitiated air,
unwholesome habitation, {1186} insufficient or improper food, squalor
and filth may cause the constitutional tendency, as they will certainly
precipitate the development of the disease in those predisposed to it.

Exciting Causes.--The border-line between the predisposing and exciting
causes cannot be positively fixed. The presence of tuberculosis or of
some form of scrofulous disease in some other part of the body so
constantly precedes the development of tuberculosis of the mesenteric
glands, even in those who have not exhibited the characteristic
phenomena of the scrofulous diathesis, that such affections must be
regarded as exciting as well as predisposing causes. No one can doubt
the frequent infection of the mesenteric glands in cases of pulmonary
tuberculosis. The probability of systemic infection from a single focus
is universally admitted. These facts and circumstances do not exclude
the possibility of localized tuberculosis of the mesenteric glands.
Whether such exclusively local development of tubercles ever occurs
independent of the scrofulous diathesis cannot be determined, but that
the disease does find its exciting cause in inflammatory conditions of
the intestinal mucous membrane cannot be doubted. Schuppel, who asserts
the primary development of the tubercle-formation in lymphatic glands,
does not claim an idiopathic origin, but admits the necessity of a
primary peripheral irritation in direct connection with the affected
gland. The intimate connection between diseases of the intestinal
mucous membrane and of the mesenteric glands is established beyond a
doubt. Vogel and Steiner assert that tabes mesenterica is a common
result of enteritis folliculosa. A primary inflammatory process may not
contain any element which could be classed as tubercle, yet it may
excite secondary tuberculosis of the glands. Whether such a result only
occurs in those who may have acquired or inherited the predisposition
is yet undecided. In many of the cases of tabes mesenterica tuberculous
ulcers are found in the intestines, but it cannot be claimed that such
ulcers are always the primary foci of tuberculous development. If
primary, it is not difficult to understand how the virus may be
transmitted to the glands.

It has been claimed that certain articles of food will produce the
disease. Potatoes and rye bread in large quantities and a coarse
vegetable diet have been mentioned among the exciting causes.
Deficiency in the quantity of food is a much more frequent cause than
inferiority in quality, yet there can be no doubt that any and every
article of diet that will set up catarrhal inflammation of the
intestinal mucous membrane may become a cause. Irritation of the mucous
membrane of the alimentary tract, induced by coarse, stimulating, or
imperfectly-digested food, or by the improper and frequent use of
purgative medicines, may give rise to disease of the glands; and, even
though the irritation may in itself be trivial, its long continuance or
frequent renewal may prove sufficient, especially in those in whom the
predisposition is present. Malarial and exanthematous diseases have
also been considered exciting causes, and among the latter class
measles and scarlet fever, because of the inflamed condition of the
intestinal mucous membrane which they leave, are the most frequent.
Difficult dentition and whooping cough must also be classed in this
category.

Recently attention has been called to the probable transmission of the
disease through the milk of diseased cows, but further investigation
and {1187} more reliable data are necessary to establish this
connection. Klebs has deduced the conclusion from recent experiments
that the use of the milk of cows in advanced phthisis will always
produce tuberculosis, which begins as an intestinal catarrh and extends
to the mesenteric glands.

Some of the older authors believed that the cure of some chronic
diseases of the skin and mucous membranes and the suppression of
chronic discharges might induce tuberculosis of the mesenteric glands;
but these conditions are now known to be most frequently the initial
manifestations of the scrofulous diathesis, and the mesenteric
complications are far more likely to occur when these primary foci are
neglected and the patient is left to suffer the unabated progress of
the disease.

MORBID ANATOMY.--It is not usual to find all the glands of the
mesentery affected at once, nor of those affected all in the same stage
of disease. Newly-affected glands may be found alongside of others in
an advanced condition. In the first stage the glands are enlarged, but
rarely exceeding the size of a filbert; they are firm, but not
inelastic. This change consists in hyperplasia of the
gland-constituents. Microscopic examination shows abundant
cell-proliferation, but the cells are badly constructed and prone to
undergo retrogressive metamorphosis. The cells accumulate in clusters
without any intercellular substance, and compress the lymph-sinuses and
blood-vessels.

The second stage is characterized by the commencement of the cheesy
degeneration. The glands enlarge and coalesce in clusters, sometimes
forming large masses of hardened and inelastic glands. On section they
exhibit in the beginning foci of cheesy material imbedded in the
gland-parenchyma. In the further progress of the change the whole gland
is transformed into a homogeneous yellowish substance. In this
condition there are found on microscopic examination globular
corpuscles, nuclei, shrivelled cells, sometimes giant-cells, and most
frequently tubercles. The tubercles are usually found in the follicular
substance. Birch-Hirschfield says the cheesy formations in secondary
tuberculous mesenteric glands are only found in discrete foci, and the
tubercles occur in the follicular substance imbedded in relatively
normal tissue. The cheesy transformation is, according to Virchow, a
necrobiosis of the hyperplastic gland-elements, but Schuppel insists
that it is the result of tubercular development. After a time the
cheesy masses soften, and the glands are converted into sacs containing
a purulent fluid mixed with debris. In this condition they are most
frequently coalesced in bunches, sometimes forming large tumors. The
intervening walls may break down and the whole bunch be transformed
into one large sac filled with purulent fluid and debris. Occasionally
these masses of agglutinated glands become adherent to the abdominal
parietes or to the intestines. Rupture of their walls may occur, and
the contents may be emptied into either the peritoneal cavity or the
intestines. When communication with the intestines takes place, it is
usually through an ulcer on the mucous surface. It is probable that the
cheesy substance may sometimes be absorbed, as Virchow thinks, by
gradual softening proceeding from the surface toward the centre.

It is believed that these degenerated glands sometimes undergo the
cretaceous transformation. Such an instance has been reported by
Carswell: "The patient, who when a child had been affected with tabes
{1188} mesenterica and also with swellings of the cervical glands, some
of which ulcerated, died at the age of twenty-one years of inflammation
of the uterus seven days after delivery. Several of the mesenteric
glands contained a dry cheesy matter mixed with a chalky-looking
substance; others were composed of a cretaceous substance; and a tumor
as large as a hen's egg, included within the folds of the peritoneum,
and which appeared to be the remains of a large agglomerated mass of
glands, was filled with a substance resembling a mixture of putty and
dried mortar, moistened with a small quantity of serosity. In the neck,
and immediately behind an old cicatrix in the skin, there were two
glands containing, in several points of their substance, small masses
of hard cretaceous matter." Calcareous concretions have been observed
by Andral and others in the mesenteric glands in cases of chronic
pulmonary disease; and Soemmering records several observations of a
tartar-like substance found in devastated mesenteric glands in cases of
rickets.

The morbid appearances in tabes mesenterica are not usually confined to
the changes in the glands. In very many cases the evidences of disease
of the peripheral glands are quite manifest, and in much the larger
number of cases pulmonary phthisis and disease of the bronchial glands
are present. The adjacent abdominal organs may also be involved. These
consecutive morbid changes are succinctly set forth in the following
notes of an autopsy taken from the records of the Children's Hospital
of Washington, D.C. The subject was a negro boy aged ten, who had been
taken sick a year previous to his death with a bad cold and cough,
followed several months afterward by enlargement and suppuration of the
cervical glands on both sides: "The body was greatly emaciated, the
lips and teeth covered with sordes. Cheesy masses were scattered
throughout the substance of both lungs. The right lung was firmly
adherent to the thoracic walls, the left adherent at apex. The liver
was enlarged and adherent to all adjacent tissues, and contained many
cheesy nodules scattered throughout its substance and over the surface.
The gall-bladder was distended with bile. The spleen was normal in
size, very dark, and filled with cheesy masses. The pancreas contained
many similar masses. The peritoneal cavity contained a quantity of
muddy fluid. The peritoneum was dark in color, studded with tubercles,
and ulcerated in a few places. The stomach and intestines were
distended with gas; the walls of stomach thickened, the inner surface
covered with a shiny mucus; in its lower wall was one large ulcer,
penetrating to the peritoneal coat and measuring three-fourths of an
inch in diameter. The peritoneal coat was thickly studded with nodules
resembling tubercles. The small intestines were gangrenous in a few
places; on the inner surface were found fourteen ulcers, varying in
size from one-fourth to one and one-fourth inches in diameter, with
elevated edges and red bases; two penetrated the peritoneal coat. This
coat contained very many tubercles. On the mucous surface of the large
intestines there were seven large ulcers, similar in appearance to
those found in the small intestines. Some of Peyer's patches were
ulcerated. The mesenteric glands, some as large as walnuts, were filled
with cheesy material, and the mesentery was dotted over with small
masses of similar matter."

In two of the reported cases of chylous effusion into the peritoneal
cavity the rupture of the lacteals was caused by degeneration of the
{1189} mesenteric glands; and in several other cases the rupture was
produced by the presence of tumors, apparently formed by the
agglomeration of numerous degenerated glands.

Several cases of fatty diarrhoea from mesenteric phthisis have been
reported. Of these the most conclusive is the case of Hall.[1] The
clinical history of the case and the detection of enlarged mesenteric
glands in the umbilical and hypogastric regions placed the diagnosis
beyond a doubt. It was, however, verified by the discovery of several
vomicae in the lungs, and of mesenteric glands "universally enlarged
and affected with strumous disease. The intestinal mucous membrane was
dotted with patches of ulceration, with here and there prominent masses
of strumous deposit on the surface."

[Footnote 1: _Guy's Hospital Reports_, vol. i., 3d Series, 1855, p.
371.]

SYMPTOMATOLOGY.--It is not possible to describe a definite and uniform
clinical history of this disease. As a secondary complication of
pulmonary phthisis and scrofulous affections the preliminary symptoms
are so constantly identified with the development and progress of these
maladies that, as a rule, the initial stage cannot be recognized by any
special assemblage of symptoms. In any tuberculous or scrofulous child
the possible implication of the mesenteric glands may be predicated
upon any array of symptoms that would establish the presence of these
classes of disease. And even in the absence of the rational and direct
signs of such affections, in those exhibiting the physical evidences of
the strumous diathesis, more especially when it is inherited, the
symptoms of any trivial departure from health, such as the catching of
cold, irritation of the alimentary tract, or protracted convalescence
from any of the exanthematous or intestinal diseases, may constitute
the initial history of tabes mesenterica. In such subjects debility and
anaemia, from whatsoever cause they may apparently result--and, in
fact, any manifest lowering of the standard of health, whether gradual
or precipitate, and without assignable cause--may mark the beginning of
the process of change in the parenchyma of the glands that will
terminate in tuberculosis. The later as well as the earlier history may
be completely masked by the symptomatology of other diseases belonging
to the tuberculous class; and so grave, as a rule, are such primary and
coexisting affections that definite recognition of this complication or
localized extension of the systemic infection becomes more a matter of
skilful diagnosis than of practical utility.

But in those cases where disease of the respiratory organs and of the
bronchial glands can be excluded the general symptomatology becomes of
paramount importance. And in view of the value of prophylactic measures
which may be employed to arrest, limit, or delay the localized
tuberculosis of these glands, the precursory symptoms may be of special
significance. This condition may be characterized by languor and
dulness or marked debility and anaemia, with loss of color, attended
with flatulence, stomachal disturbance, frequent eructations consisting
mainly of mucus, a sense of uneasiness in the abdomen after the
ingestion of food, a variable appetite, sometimes voracious and
occasionally depraved. Sometimes a dislike for fatty foods is a
prominent symptom. The tongue may be coated, the breath is usually
foul, and some have said the body emits an acid odor. If these symptoms
occur in a child of the {1190} scrofulous diathesis, or be directly or
remotely associated with a previous gastro-intestinal disease, or occur
or persist during the convalescence of some of the acute affections of
infancy and childhood which stand in etiological relation to this
disease, they may justify a reasonable presumption of commencing change
in the mesenteric glands. This presumption will be strengthened by
emaciation, a more marked disturbance of the digestive function,
attended with fetid and occasionally whitish stools, a tumid belly, and
deep, lancinating abdominal pains of short duration, recurring at long
intervals and neither relieved nor aggravated by pressure or an
evacuation. Some have attributed special importance to a chalky
appearance and loss of consistency of the stools, indicating the
suspension of absorption by the lacteals. There may also be slight
evening fever. Later, the enlargement of the belly increases, the
emaciation becomes more marked and rapid, the appetite more variable,
sometimes very voracious, the alvine discharges more fetid or less
consistent, sometimes putty-like, and generally irregular or
constipated. The febrile exacerbations are more decided, and sometimes
chills may occur at irregular intervals. When, in addition to these
symptoms, either during the earlier or later stages, the enlargement of
the glands can be detected, the clinical picture is complete. In
consequence of the tympanitic distension of the abdomen, which usually
increases with the progress of the disease, it is impossible in a
majority of cases to detect the glandular enlargement; especially is
this true when the affected glands are separate; but, as frequently
happens during the last stage, when large tumors are formed by the
coalescence of a number of diseased glands the diagnosis may be easily
determined. In the absence of the discovery of enlarged glands the
diagnosis cannot be considered positive. They are usually most readily
found in the region of the umbilicus, and may in some cases, even when
the tension of the abdomen is very great, be detected by grasping the
abdomen with the hand and compressing it between the fingers and thumb
so that the enlarged glands will be brought in close contiguity to the
walls and be felt immediately under the fingers. If a tumor should be
present and the peritoneal cavity be free from fluid, its locality may
be recognized by a sense of resistance and circumscribed area of
diminished resonance, and then definitely outlined by palpation.
Underwood says: "Indigestion, costiveness or purging, irregular
appetite, flushed cheeks or a total loss of color, impaired strength
and spirits, remitting fever, and a hard and tumid belly, with
emaciated limbs, are amongst the more common symptoms, attending at one
period or other, of this disease."

When the diagnosis has been made out, it is not impossible to determine
the stage of the disease. The progressive intensity of the symptoms,
with rapid emaciation as a rule, bears a definite relation to the
progress of the morbid changes taking place in the glands. It must,
however, be borne in mind that children have died of tabes mesenterica
who had enjoyed excellent health up to the moment of death, and the
autopsy disclosed the condition of the glands, which had not been
suspected during life. In the case previously cited, in which the
autopsy exhibited such grave lesions of the stomach, liver, spleen,
pancreas, and intestinal mucous membrane, the clinical phenomena were
at no time commensurate with the gravity of the morbid changes.

{1191} DIAGNOSIS.--In the absence of the proof of the presence of
enlarged glands or of a tumor the diagnosis cannot be positively
determined. The enlargement and tympanitic distension of the abdomen do
not necessarily establish the existence of glandular disease, for they
are present in a great many conditions of ill-health in children. Nor
is the coexistence of a tumid belly, emaciation, and fever sufficient,
for they are found in other tuberculous and in gastro-intestinal
diseases. The discovery of enlarged discrete glands by palpation, as
before described, in connection with such disturbances of nutrition as
have been set forth, constitute the strongest presumption in favor of
tabes mesenterica. The presence of enlarged glands unaccompanied by the
ordinary symptoms of the tuberculous or scrofulous processes is
inconclusive, because the glandular hypertrophy may be a simple
hyperplasia, entirely independent of any tendency to retrogressive
metamorphosis. There is usually some tenderness on pressure, but this
may be present in any disease of the abdominal viscera. When the glands
are of sufficient size, they may, by pressure, produce secondary
derangements. Cramps in the legs may be caused by pressure on nerves.
Oedema of the legs and dilatation of the superficial abdominal veins
may result from compression of venous trunks. "If," says Eustace Smith,
"these veins are seen to ramify on the abdominal surface and to join
the veins on the thoracic walls, tabes may be suspected in the absence
of chronic peritonitis and enlargement of the liver." Ascites may be
present, but is not a necessary result of disease of the glands.

When a tumor has been discovered by palpation, it is necessary to
determine its glandular nature. If situated about the umbilicus, in
front of the spinal column, if irregular, hard, and feeling like a
congeries of irregularly-rounded nodules, the evidence is very decided
in favor of its glandular origin. But care must be taken to exclude
tumors formed by fecal accumulations and masses attached to the
omentum. Omental tumors are usually more movable, better defined, more
superficial, and regular in form. Cancerous masses sometimes simulate
glandular tumors. The general history of the case and the age of the
patient are usually sufficient to make a diagnosis by exclusion.
Rilliet and Barthez distinguished a cancerous pancreas by the presence
of vomiting, jaundice, and abdominal pains.

The writer has many times based a conjectural diagnosis--which was
verified by a post-mortem examination--upon the presence of a tumid
abdomen, increasing emaciation, with the history of a protracted
gastro-intestinal catarrh, and an irregular febrile curve characterized
by frequent subnormal temperatures. He has also observed a number of
cases of protracted diarrhoea in children, accompanied with extreme
emaciation, notwithstanding the appetite was good, sometimes even
voracious, and the food taken was ample, nutritious, and easily
digested, in which the stools, varying from two to three, or twice as
many, daily, were whitish, leaden, or slate-colored, sometimes
semi-fluid, at other times containing lumps or masses of putty
consistence, presenting to the naked eye a greasy appearance and to the
touch a fatty feel, and at the autopsy has found only thinness and
transparency of the coat of the small intestines and degenerated
mesenteric glands.

PROGNOSIS.--The prognosis is decidedly unfavorable. So far as is known
to the writer, there is but one recorded case of recovery in which the
{1192} diagnosis was indisputable and the fact of a cure was
established by an autopsy. This was the case reported by Carswell,
before referred to. The older and some of the modern authors have
claimed many recoveries, but it must be manifest to every student of
pathological anatomy that the mistaken diagnoses must have been nearly
if not quite as numerous as the cases of cure. The writer has not
witnessed a single case of recovery, but he has observed very many
cured cases of disease which exhibited all the subjective and objective
symptoms of tuberculosis of the mesenteric glands, save and except
those by which its existence can alone be definitely and positively
established. The case of Carswell demonstrates a remote possibility of
cure by the cretaceous metamorphosis of the degenerated glands in a
subject exhibiting the scrofulous diathesis. In view of this isolated
observation, one cannot refuse to accept a similar possibility in cases
in which the disease may be localized and confined to a few of the
glands. In such cases, if recognized previous to the formation of
cheesy foci, the possibility of staying, limiting, and perhaps
occasionally curing, the disease should not be regarded as absolutely
hopeless; yet the opportunities of examining the glands in the first
stage of change has so rarely occurred that no one is authorized to
assert that the hyperplasia is the true picture of the condition in
which those in the advanced stage had its beginning; nor has any one
claimed to have witnessed the progressive stages of resolution taking
place in such glands.

The cretaceous transformation is an accepted though remote possibility,
and absorption by means of gradual softening of the cheesy masses is
perhaps a reasonable hypothesis. But even if either of these processes
was an occasional termination of the disease, it could only lessen its
gravity and prolong life, with an incomplete recovery, in those few
cases in which the tuberculous or scrofulous changes were confined to a
less number of glands than was necessary to maintain the nutrition of
the body. For while there is no serious obstacle to the flow of chyle
through the glands in the condition of simple hyperplasia, it is
completely obstructed in those transformed into cheesy masses or
purulent collections. The channels through the glands must sooner or
later be obliterated by the presence of the abundant cell-proliferation
which characterizes the initial stage of change in this disease. For if
the compression is sufficient to cut off the supply of blood, it must
prove equally destructive to the complex system of lymph-paths. To the
impermeability of the glands must the emaciation and exhaustion which
mark the course of the disease, to a greater or less degree according
to the number of glands involved, be due.

If the investigations of Schuppel should be verified, and the primary
tubercle-formations be accepted as the initial stage of change, the
prognosis will be less favorable, but a distinct line of demarcation
may be established between two classes of cases in each of which cheesy
transformation may occur, but in one the tubercle-formations may be
primary, and in the other secondary. In the latter class the prognosis
may be more favorable, because treatment may be effective if commenced
prior to the beginning of the retrogressive metamorphosis.

COURSE, DURATION, AND COMPLICATIONS.--When tabes is a complication of
pulmonary or bronchial phthisis, or when either of the latter {1193}
diseases appears as an intercurrent affection during the course of a
primary localized tuberculosis of these glands, the glandular
degeneration runs a more rapid course. When it appears as an extension
of external scrofulous affections or finds its cause in
gastro-intestinal irritation, its course is usually less rapid. The
number of glands involved greatly influences its duration. The
mechanical impediment to nutrition offered by a large number of
impermeable glands promotes rapid emaciation and exhaustion. The
condition of the mucous coat of the alimentary tract offers many
considerations that affect its course and duration. Follicular
enteritis hastens, and tuberculous ulceration of the mucous membrane
speedily brings, the case to a fatal termination.

Some of the older authors refer to the frequent complication of rickets
with tabes mesenterica, and the writer in numerous post-mortem
examinations of the bodies of children dying of rickets has invariably
found cheesy mesenteric glands. In view of the fact that rickets is
constantly associated with disturbance of the alimentary tract, it
should not be a surprise to find the glands in such close contiguity
to, and having vascular communication with, the diseased mucous surface
in a condition of hyperplasia. Simple hypertrophy is probably a common
complication in cases which terminate by recovery, but there must be
some element of cause, other than inflammation of the mucous membrane
of the intestines, that determines the retrogressive metamorphosis.
Several of the older authors have classed rickets in the category of
strumous diseases, and it may be that in the fatal cases tuberculosis
of the mesenteric glands is a local expression of this diathesis.

TREATMENT.--The treatment consists, for the most part, in methods of
prevention and palliation. The tendency to disease of the lymphatic
glands in scrofulous children is so constant that it is important to
remove all sources of irritation and to combat all influences likely to
hasten or promote the localization of the constitutional condition. All
chronic discharges and diseases of the skin and mucous membrane, the
continuance of which might produce glandular complications, should be
cured as speedily as possible, slight colds should receive prompt
attention, and catarrhal inflammations of the respiratory organs should
be arrested as quickly as the resources of science will permit. The
alimentary tract demands constant and careful observation. Trivial
disorders should not be neglected: the causes should be ascertained and
removed. Digestion and nutrition should be maintained at a healthy
standard. The hygiene of person, dwelling, and sleeping apartments
merits constant and intelligent supervision.

As stated above, tabes of the mesenteric glands is so frequently
secondary to other diseases of a scrofulous nature that the danger lies
in the failure to arrest or cure such affections. It is unfortunately
too true that some of them are often beyond the resources of medical
skill, but in many cases the initial manifestations of the strumous
diathesis are either entirely neglected or inappropriately treated. In
many such cases the final and fatal complication of mesenteric phthisis
could be prevented. The treatment of these affections belongs properly
to the subjects of tuberculosis and scrofula, to be found in other
parts of this System of Medicine.

Localized tuberculosis of the mesenteric glands is so often, either
{1194} directly or indirectly, connected with catarrhal inflammations
of the gastro-intestinal mucous membrane that the cure of these
affections cannot be too strongly insisted upon as an effective method
of prevention. This is especially true with children exhibiting the
physical signs of the strumous diathesis. When it is inherited from a
diseased mother, it may be necessary to resort to artificial feeding
before the proper time for weaning has been reached. In such cases no
uniform rule can be arbitrarily followed. The condition of both mother
and child must be considered, and cases will occur which will demand
the exercise of the most cautious discretion and diligent observation.

When the disease has become established but little can be accomplished.
In such cases the treatment refers to the palliation of symptoms and
the maintenance of nutrition. Pain, when present, must be relieved--if
necessary by anodynes, either given internally or applied in the form
of cataplasms. Most often it is due to the coexisting disease of the
intestinal mucous membrane or to the ingestion of unsuitable foods. The
diet should be regulated and limited to nutritious and easily-digested
articles. Sometimes, even in cases of advanced degeneration of the
glands, great benefit may be temporarily obtained by attention to the
diet. Diarrhoea should be controlled, but when dependent upon
tuberculous ulcerations of the intestinal mucous membrane but little
can be done toward delaying the fatal termination. When a large number
of glands are affected, it will be necessary to limit the diet to such
nutrient fluids as may be absorbed from the stomach.

The medical treatment is confined to a few remedies. Faulty nutrition
is the predominant factor, and the drugs employed should be directed to
the improvement of the assimilative functions. The lacto-phosphate of
iron in the form of syrup, or the phosphates in the form of the
compound syrup, sometimes prove valuable tonics. The lacto-phosphate
may be given in combination with cod-liver oil. This latter, either
internally or by inunction, is the most valuable and universally
applicable of all remedies. The mistake is very frequently made of
giving too large quantities. Few children can digest as much as a
drachm administered three times a day. In Washington it is usually
given in the form of the phosphatic emulsion, and has proved in the
service of the Children's Hospital a valuable and effective remedy in
the nutritional disorders of children. Of the chalybeates, the syrup of
the iodide of iron is by far the most valuable; this may be given alone
or in combination with cod-liver oil. It is specially indicated when
anaemia is a marked characteristic. Some recent reports favor the
employment of pancreatized foods. The ointment of the iodide of lead
has been highly extolled as a local application to the belly. The
nature of the disease should be constantly borne in mind, and all
depressing agencies should be sedulously avoided.




{1195}

INDEX TO VOLUME II.


A.

Abdomen, enlargement of, in rachitis, 153
  state of, in ascites, 1176
    in cancerous peritonitis, 1169
    in cirrhosis of liver, 994
    in cholera morbus, 722
    in chronic peritonitis, 1162
    in dysentery, 796, 804
    in enteralgia, 661
    in intestinal catarrh, 679, 706, 707
    in tabes mesenterica, 1190
    in tape-worm, 940
  tetanic spasm of, in dilatation of stomach, 595
  tenderness of, in tubercular peritonitis, 1165, 1166

Abdominal bandage, use of, in dilatation of stomach, 609
  belt, use of, in constipation, 654
  distension, in acute peritonitis, 1141
  glands, disease of, 1182
  swelling, in intestinal indigestion, 627
  tenderness, in intussusception, 848
  veins, abnormal anastomoses of, in thrombosis and embolism of portal
        vein, 1096
    prominence of, in ascites, 1177

Abortions, frequent, significance, in diagnosis of hereditary
        syphilis, 310

Abortive treatment of acute gout, 134

Abscess in acute pancreatitis, 1118
  in local peritonitis, 1159, 1160
  of joints in gout, 116
  of liver, 1002
    discharge of, into neighboring organs, 1007
    influence on causation of acute peritonitis, 1138
    in dysentery, 801
  of rectum, a cause of fistula in ano, 897
  of tonsils, 383
  peri-anal and peri-rectal, 703, 895

Abscesses, number, in suppurative hepatitis, 1006
  peritoneal, in perforation of simple ulcer of stomach, 499
  seat of, in acute peritonitis, 1136
    in typhlitis and perityphlitis, 817

Acanthocephali, the, 949

Acaris autumnalis of anus, 892

Acetate of lead, use of, in hemorrhage from bowels, 834
    in purpura, 193
    in simple ulcer of stomach, 526

Acetonaemia in diabetes mellitus, 205, 206

Acetone and alcohol in diabetic urine, 209

Acid, lactic, theory of origin of acute rheumatism, 23
  nitrate of mercury, use of, in anal fissure and ulcer of rectum, 912
      in cancrum oris, 343
  salicylic, use of, in acute rheumatism, 51-59
  uric, theory of origin of gout from, 112, 113

Acini of pancreas, anatomy, 1113

Acne complicating gout, 121

Aconite, use of, in acute intestinal catarrh, 689
    in acute pharyngitis, 397, 398
    in acute rheumatism, 64
    in parenchymatous glossitis, 364
    in tonsillitis, 388

Actual cautery, use of, in cancrum oris, 343

Acupuncture in hydatids of liver, 1109

Acute yellow atrophy of liver, 1023

Addison's disease, influence on causation of chronic intestinal
        catarrh, 700

Adenomata of stomach, 578

Adhesions, formation of, in abscess of liver, 1007
  in gastric cancers, 566
  peritoneal, in chronic intestinal catarrh, 703

Age, influence of, on causation of abscess of liver, 1003
      of acute yellow atrophy of liver, 1024
      of amyloid liver, 1041
      of ascites, 1176
      of biliary calculi, 1063
      of cancrum oris, 339
      of carcinoma of liver, 1034
      of catarrhal stomatitis, 322
      of cholera morbus, 720
      of cirrhosis of liver, 990
      of cirrhosis of stomach, 612
      of constipation, 639
      of diabetes mellitus, 203
      of dilatation of stomach, 592
      of functional dyspepsia, 438, 439
      of entero-colitis, 732
      of fatty liver, 1047
      of fistula in ano, 897
      of gastric cancer, 534
      of gout, 110
      of intestinal cancer, 869
      of acute intestinal catarrh, 670
      of chronic intestinal catarrh, 699
      of intestinal indigestion, 623
      of intestinal obstruction, 847
      of macroglossia, 350
      of muscular rheumatism, 74, 75
      of organic stricture of oesophagus, 423
      of diseases of pancreas, 1114
      of parenchymatous glossitis, 360
      of phosphorus-poisoning, 1030
      of prolapse of rectum, 881
      of pseudo-membranous enteritis, 764
      of rachitis, 141
      of rheumatism, 20
      of rheumatoid arthritis, 141
      of scrofula, 233
      of scurvy, 169
      of simple ulcer of stomach, 483
      of spasmodic stricture of oesophagus, 419
      of aphthous stomatitis, 326
      of stomatitis ulcerosa, 336
      of tabes mesenterica, 1184
      of thrush, 332
      of tonsillitis, 380
      of typhlitis, 815

Agnew's rectal chemise in hemorrhage from rectum, 927

Air, impure, influence on causation of acute intestinal catarrh, 670
      of rachitis, 143
      of scurvy, 170
      of scrofula, 232
  vitiated, influence on causation of entero-colitis, 728-730
      of tabes mesenterica, 1185, 1186

Albumen in urine of jaundice, 978

Albuminoid degeneration of pancreas, 1128

Albuminuria complicating gout, 123
  in diabetes mellitus, 208
  in intestinal indigestion, 628
  in gastric cancer, 551
  influence of, on causation of acute peritonitis, 1138

Alcohol, abuse of, influence on causation of enteralgia, 660
      of gout, 111
      of gastric cirrhosis, 612
      of acute chronic gastritis, 470
      of intestinal indigestion, 625
      of chronic oesophagitis, 416
      of diseases of pancreas, 1114, 1121
      of simple gastric ulcer, 488
  influence on causation of abscess of liver, 1005
    of biliousness, 966
    of cirrhosis of liver, 991
    of lithaemia, 969
    of acute oesophagitis, 410
    of organic stricture of oesophagus, 423
    of chronic pharyngitis, 402
    of acute and chronic intestinal catarrh, 671, 672, 700
  use of, in acute yellow atrophy of liver, 1030
    in cholera morbus, 725
    in cholera infantum, 761
    in dysentery, 810
    in functional dyspepsia, 439
    in entero-colitis, 761
    in hemorrhage from bowels, 834
    in intestinal ulcerations, 829
    in acute pancreatitis, 1120
    in acute pharyngitis, 398
    in acute rheumatism, 69

Alcoholism, influence on causation of fatty liver, 1047

Alimentation, hypodermatic, in simple ulcer of stomach, 525
  rectal, 928
    in organic stricture of oesophagus, 425

Alkalies, use of, in amyloid liver, 1045
    in diabetes mellitus, 229
    in functional dyspepsia, 458
    in enteralgia, 666
    in fatty liver, 1050
    in gout, 132
    in intestinal disorders of rachitis, 161
    in acute intestinal catarrh, 693
    in lithaemia, 972
    in muscular rheumatism, 77
    in acute oesophagitis, 416
    in acute rheumatism, 60
    in scrofula, 252
    in simple ulcer of stomach, 527
  and salicylates, combined use of, in acute rheumatism, 61

Alkaline carbonates, use of, in chronic gastritis, 477

Almond food, use of, in rickets, 223

Aloes, use of, in constipation, 655
    in functional dyspepsia, 458
    in hemorrhoids, 923

Alopecia, circumscribed, in rachitis, 156

Alum, use of, in constipation, 656
    in enteralgia, 665
    in hemorrhage from bowels, 834
    in acute intestinal catarrh, 696

Alvine discharges of cholera morbus, 722

Amenorrhoea, in simple ulcer of stomach, 495

Ammonia, use of, in suppurative pylephlebitis, 1101

Ammonium chloride, use of, in chronic pharyngitis, 406

Amphistomum hominis, 949

Amyloid degeneration, gastric, influence on causation of dilatation of
        stomach, 590

Amyloid degeneration of mucous membrane in chronic intestinal catarrh,
        705

Amyloid liver, 1040

Anaemia in chronic articular rheumatism, 71
  in chronic intestinal catarrh, 709
  in gastric cancer, 552
  in intestinal indigestion, 629
  in tabes mesenterica, 1189
  influence of, on causation of chronic gastritis, 471
      of functional dyspepsia, 439
      of gastralgia, 460
      of gastric hemorrhage, 582
      of intestinal indigestion, 623
      of simple ulcer of stomach, 487
  pernicious, influence of, on causation of hemorrhage from bowels,
        832

Anaemic murmurs in acute rheumatism, 36

Anasarca, in cirrhosis of liver, 995

Anastomoses of veins, abnormal, in cirrhosis of liver, 996
  of abdominal veins, abnormal, in embolism and thrombosis of portal
        vein, 1096

Anatomy of pancreas, 1112
  of rectum and anus, 879

Anatomical peculiarities of scrofulous tissue, 238

Anchylostomum duodenale, 955

Aneurism of gastric vessels in simple ulcer of stomach, 511

Aneurisms, miliary, of stomach, 579

Angina, 390

Angiocholitis from biliary concretions, 1077

Ankylosis following gonorrhoeal rheumatism, 106
  from chronic articular rheumatism, 71
  in general rheumatoid arthritis, 81

Annular form of dilatation of oesophagus, 431, 432
    of gastric cancer, 562

Anomalies in form and position of stomach, 617

Anodyne applications in rheumatoid arthritis, 100

Antimony-poisoning, as a cause of cirrhosis of the liver, 991
  influence of, on causation of fatty liver, 1047

Antiphlogistic treatment of acute gout, 133

Antiseptics, use of, in stomatitis ulcerosa, 338

Antispasmodics, use of, in enteralgia, 665

Anal fissure as a cause of hemorrhage from bowels, 830
  fistula, 897
  openings, abnormal, 880

Anus, abscess of, 880
  imperforate, 877
  and rectum, cancer of, 902
    fissure of, 888
    scrofulous and tuberculous affections of, 901
    spasm of, 909
    syphilis of, 900
    ulceration of, 893

Aorta, aneurismal dilatation from pressure in pancreatic diseases,
        1116

Aperient, mineral waters, use of, in functional dyspepsia, 458

Appendix vermiformis, lesions of, in entero-colitis, 738

Appetite, capricious, in cirrhosis of liver, 993
    in tabes mesenterica, 1189
  impaired, in carcinoma of liver, 1038
    in catarrh of bile-ducts, 1053
    in catarrhal stomatitis, 323
    in cholera infantum, 742
    in cirrhosis of stomach, 613
    in constipation, 646, 647, 853
    in dilatation of stomach, 543
    in dysentery, 796, 804
    in chronic gastritis, 473
    in gastric cancer, 538
    in chronic intestinal catarrh, 707
    in intestinal ulcer, 826
    in simple ulcer of stomach, 494
    in stomatitis ulcerosa, 339
    in typhlitis and perityphlitis, 818, 819
  state of, in diabetes mellitus, 204
    in acute rheumatism, 27
    in muscular rheumatism, 76
    in rheumatoid arthritis, 83
    in scurvy, 177

Aphthous stomatitis, 325
  ulcerations in morbid dentition, 373

Armies, prevalence of dysentery among, 785, 786

Arseniate of sodium, use of, in jaundice, 982

Arsenic, effect of, on rectum, 910
  use of, in amyloid liver, 1046
    in catarrh of bile-ducts, 1057
    in constipation, 654
    in diabetes mellitus, 227
    in dilatation of stomach, 609
    in enteralgia, 665
    in functional dyspepsia, 457
    in gastralgia, 462
    in hepatic glycosuria, 975
    in chronic intestinal catarrh, 715
    in lithaemia, 973
    in organic stricture of oesophagus, 425
    in pseudo-membranous enteritis, 775
    in chronic articular rheumatism, 74
    in rheumatoid arthritis, 98

Arsenic-poisoning as a cause of cirrhosis of liver, 991
  influence of, on causation of fatty liver, 1067

Arteries, increased width of, in rachitis, 139

Arthritis deformans, 84
  gonorrhoeal, 102
  rheumatoid, 78

Articular symptoms of chronic gout, 121

Articulations, lesions of, in acute rheumatism, 46
  condition of, in scurvy, 179

Artificial feeding, influence of, on causation of entero-colitis, 731
  production of gastric ulcer, 514

Ascaris lumbricoides, 952
  mystax, 954
  vermicularis, 950

Ascites, 1173
  in cancerous peritonitis, 1169
  in carcinoma of liver, 1037
  in carcinoma of pancreas, 1126
  in cirrhosis of liver, 995
  in cirrhosis of liver, treatment, 1001
  in echinococcus of liver, 1104
  in Filaria sanguinis, 964
  in gastric cancer, 553
  in hyperaemia of liver, 987
  in local peritonitis, 1161
  frequency in amyloid liver, 1044
  sudden development of, in thrombosis and embolism of portal vein,
        1096

Aspirator, use of, in abscess of liver, 1022
    in hydatids of liver, 1107

Astringents, use of, in mercurial stomatitis, 348
    in stomatitis ulcerosa, 338

Atmospheric changes, influence of, on causation of tonsillitis, 380

Atonic dyspepsia, 436

Atrophy, acute yellow, of liver, 1023
  of abdominal viscera in dilatation of stomach, 600
  of gastric walls in dilatation of stomach, 599
  of hepatic cells in cirrhosis, 992, 993
  of intestinal walls in chronic intestinal catarrh, 704
  of kidneys in cirrhosis of liver, 999
  of liver in hydatids of, 1102
  of liver from occlusion of biliary passages, 1088
  of nerve, as a cause of paralysis of oesophagus, 429
  of oesophagus in organic stricture, 424
  of stomach, 566, 616
  of testes in diabetes mellitus, 202
  of tongue in chronic parenchymatous glossitis, 367

Auscultatory percussion in ascites, 1174


B.

Bacteria and micrococci in deposits of tonsillitis, 384
  influence of, on causation of acute intestinal catarrh, 673
  significance of, in cholera infantum, 744

Bandage, use of, in perihepatitis, 990

Bands and loops, formation of, in acute peritonitis, 1153

Bathing in biliary calculus state, 1079
  in treatment of constipation, 651, 653
  necessity of, in lithaemia, 971
  value of, in scrofula, 250

Baths, use of, in diabetes mellitus, 225
    in chronic intestinal catarrh, 714, 716
    in intestinal indigestion, 632
    in gout, 130
    in gonorrhoeal rheumatism, 107
  cold, use of, in acute gastritis, 470
  hot, use of, in hepatic colic, 1082
    in muscular rheumatism, 77
    in rachitis, 163
    in rheumatoid arthritis, 99
  hot sand, use of, in local treatment of rheumatoid arthritis, 101
  local vapor, use of, in rheumatoid arthritis, 100
  mineral, use of, in rheumatoid arthritis, 99
  mud, in rheumatoid arthritis, 100
  warm and cold, use of, in acute intestinal catarrh, 692
  salt, in rachitis, 163

Beading of ribs in rachitis, 152

Beef-essences, use of, in intestinal indigestion, 633

Beef-tea, use of, in entero-colitis and cholera infantum, 754
    in rachitis, 161

Beef tape-worm, 933

Belladonna, use of, in cancerous peritonitis, 1122
    in constipation, 458, 654
    in enteralgia, 665
    in spasmodic stricture of oesophagus, 421

Benzoate of sodium, use of, in intestinal indigestion, 636

Benzoic acid, use of, in acute rheumatism, 62

Bifid tongue, 349

Bile, action of, in digestion, 621
  composition of, 1062
  in pus of hepatic abscesses, 1007
  in urine, tests for, 978

Bile-ducts, catarrh of, 1051

Biliary calculi, 1058
    seat, 1066
    origin and development, 1061-1063
    number, shape, and composition, 1059-1061
    impaction of, 1074
    treatment of, 1079
  fistulae, 1068, 1074
  form of intestinal indigestion, diagnosis, 631
  passages, affections of. See _Liver, Diseases of_.
    occlusion of, 1082

Biliousness, 965

Bill of fare for diabetics, 221

Bilharzia haematobia, 948

Bismuth subnitrate, use of, in entero-colitis and cholera infantum,
        759
    in acute yellow atrophy of liver, 1030
    in cancer of stomach, 576
    in cholera morbus, 725
    in functional dyspepsia, 457
    in gastralgia, 463
    in chronic gastritis, 478
    in acute intestinal catarrh, 693
    in vomiting of abscess of liver, 1021
    in simple ulcer of stomach, 523

Bitartrate of potassium, use of, in ascites, 1179

Bitter waters, use of, in intestinal indigestion, 636

Black pepper, use of, in hemorrhoids, 923
    in proctitis, 919
    in intestinal ulcer, 827
  stools in cancer of stomach, 550
  tongue. See _Glossitis parasitica_.

Bladder and kidneys, influence of, on causation of gastralgia, 460

Bleeding, use of, in intestinal obstruction, 864

Blindness in scurvy, 181

Blisters, use of, in acute rheumatism, 63, 68
    in cirrhosis of liver, 1002
    in rheumatoid arthritis, 100, 101

Blood, alterations of, in diabetes mellitus, 206
  coagulable state of, as a cause of thrombosis and embolism of portal
        vein, 1095
  lesions, in acute yellow atrophy of liver, 1029
    in cholera morbus, 721
    in gout, 115
    in acute rheumatism, 31
    in scurvy, 173
  extravasation of, into skin in scurvy, 178
  presence of fat in, in diabetes mellitus, 206, 207
  watery condition of, in cirrhosis of liver, 995

Bloodletting, use of, in acute intestinal catarrh, 690
  in acute peritonitis, 1145

Blood-vessels, disease of, as a cause of hemorrhage from bowels, 832
  lesions of, in diabetes mellitus, 200
    in gout, 117
    in acute peritonitis, 1133

Bloody stools in chronic intestinal catarrh, 708

Boiled-sago matter in stools of dysentery, 803

Boils, complicating diabetes mellitus, 205
  and carbuncles in jaundice, 980

Bones, disease of, in hereditary syphilis, 286
  lesions of, in rheumatoid arthritis, 87
    in scurvy, 172, 179
  of extremities, curvature of, in rachitis, 155
  of face, alterations of, in rachitis, 150
  rachitic, composition of, 138

Borborygmi in chronic intestinal catarrh, 706
  in intestinal indigestion, 627

Bothriocephalus cordatus, 939
  cristatus, 939
  latus, 938

Bougies, use of, in cancer of rectum, 914
    in non-malignant rectal stricture, 917
    in organic stricture of oesophagus, 425
    in spasmodic stricture of oesophagus, 422
    in sphincterismus, 916

Bowels, compression and contraction of, as a cause of intestinal
        obstruction, 857
  hemorrhage from, 830
  increased weight of, as a cause of acute intestinal strangulation,
        841
  irregular, in cancer of intestines, 869
    in pseudo-membranous enteritis, 765
    in suppurative pylephlebitis, 1100
  state of, in biliousness, 966
    in catarrh of bile-ducts, 1054, 1055
    in cirrhosis of liver, 993
    in enteralgia, 661
    in lithaemia, 970
    in chronic intestinal catarrh, 706

Brain, condition of, in dysentery, 804
  disease, organic, distinguished from lithaemia, 917
  lesions of, in acute yellow atrophy of liver, 1026
    in entero-colitis, 740
    in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 706
    in scurvy, 172
  and membranes, lesions of, in acute rheumatism, 39
  and meninges, condition of, in rachitis, 148, 149
  and spinal cord, organic disease of, influence on causation of
        enteralgia, 658

Bran bread, use of, in diabetes mellitus, 223

Breast-milk, poor, influence of, on causation of entero-colitis, 731

Breath, in cancrum oris, 340
  in scurvy, 177
  fetor of, in catarrhal stomatitis, 323

Bright's disease, as a cause of chronic intestinal catarrh, 699
    complicating chronic intestinal catarrh, 710

Bromide of ammonium, use of, in acute rheumatism, 62
  of arsenic, use of, in diabetes mellitus, 247
  of lithium, use of, in chronic articular rheumatism, 74
  of potassium, use of, in cholera infantum and entero-colitis, 759
      in diabetes mellitus, 227
      in enteralgia, 665
      in spasmodic stricture of oesophagus, 421
    and sodium, use of, in rachitis, 163
  of sodium, use of, in cholera morbus, 725
      in gastralgia, 463
      in acute intestinal catarrh, 698

Bronchial catarrh in trichinosis, 960
  and tracheal catarrh, frequency of, in rachitis, 152

Bronchitis complicating gout, 122
  chronic, complicating chronic intestinal catarrh, 709

Broncho-pneumonia, frequency of, in rachitis, 153

Bronzing of skin in diseases of pancreas, 1117

Buboes, in Filaria sanguinis, 963

Burning in gullet in phosphorus-poisoning, 1031
  sensation in epigastrium in chronic gastritis, 473

Burns, external, influence on causation of acute intestinal catarrh,
        670
  of skin, influence on causation of intestinal ulcers, 824
      of simple ulcer of stomach, 488

Bursitis, gonorrhoeal, symptoms of, 105

Buttermilk, use of, in treatment of acute intestinal catarrh, 691


C.

Cachexia in gastric cancer, 552
  in intestinal cancer, 871
  of scurvy, 176
  influence on causation of fatty liver, 1047

Caecum, suppuration of, as a cause of suppurative pylephlebitis, 1098

Calcification, defective, in rachitis, causes of, 138, 139
  of gastric vessels, in simple ulcer of stomach, 511

Calculi, biliary, 1058
  passage of, as a cause of occlusion of biliary passages, 1083
  pancreatic, 1130

Calf's pancreas, infusion of, preparation, 1122

Calibre of intestines, alteration of, in chronic catarrh, 700

Calomel, use of, in Anchylostomum duodenale, 956
    in catarrh of bile-ducts, 1056
    in cholera morbus, 725
    in entero-colitis and cholera infantum, 760
    in acute gastritis, 469
    in acute intestinal catarrh, 695
    in jaundice, 982

Camphor, use of, in cholera morbus, 725
    in acute intestinal catarrh, 698
    in spasmodic stricture of oesophagus, 421

Cancer as a cause of stricture of bowels, 855
  of bile-ducts, relation to biliary concretions, 1077
  of gall-bladder as a cause of occlusion of common biliary duct, 1085
  of intestines, 868
  of liver, 1033
  of oesophagus, 426
  of rectum and anus, 902
  of stomach, 530
  and ulcer of stomach, influence on causation of chronic intestinal
        pancreatitis, 1121

Cancrum oris, 338

Capillary congestion in acute intestinal catarrh, 677

Carbohydrates, avoidance of, in dietetic treatment of gout, 128

Carbolic acid, use of, in cholera infantum, 761
    in cholera morbus, 725
    in entero-colitis, 761
    in functional dyspepsia, 459
    in acute intestinal catarrh, 696
    in pruritus ani, 917
    in tuberculous pharyngitis, 402

Carbonate of potassium with lemon-juice, in ascites, 1178

Carbonic acid, distension of stomach by, in diagnosis of gastric
        dilatation, 596, 601
  water, use of, in chronic oesophagitis, 417

Carbuncle of tongue, 368

Carbuncles complicating diabetes mellitus, 205

Carcinoma, of pancreas, 1123
  influence of, on causation of dilatation of stomach, 587
      of organic stricture of oesophagus, 423
  of pylorus and duodenum, as a cause of obstruction of pancreatic
        duct, 1130
  ventriculi, 530

Cardiac affections complicating gonorrhoeal rheumatism, 106
    in acute rheumatism, 28, 31
  disease, chronic influence of, on causation of chronic oesophagitis,
        416
      of functional dyspepsia, 448
  murmurs in purpura rheumatica, 189
  orifice, obstruction of, in gastric cancer, 566
  palpitation in constipation, 647

Cardialgia, 459
  in functional dyspepsia, 449

Caries of vertebrae, influence of, on causation of chronic
        oesophagitis, 416

Carlsbad water, artificial, mode of preparing, 522
  use of, in chronic gastritis, 477
    in dilatation of stomach, 609
    in simple ulcer of stomach, 522

Cartilages, lesions of, in gout, 115
    in acute rheumatism, 47
    in chronic articular rheumatism, 70
  of joints, lesions of, in gonorrhoeal rheumatism, 103
      in rheumatoid arthritis, 87

Cascara sagrada, use of, in constipation, 656

Caseation of cells in scrofula, 239

Castor oil, use of, in pseudo-membranous enteritis, 774

Casts, epithelial, in acute oesophagitis, 412

Catarrh, acute gastric, 463
  chronic gastric, 470
  of middle ear in hereditary syphilis, 282
  tendency to, in scrofula, 245

Catarrhal gastritis, complicating simple ulcer of stomach, 502
  pneumonia, frequency of, in rachitis, 153
  stomatitis, 321
  ulcers in acute intestinal catarrh, 676
  ulcers of stomach, 529

Cathartics, abuse of, influence on causation of pseudo-membranous
        enteritis, 765
  use of, in ascites, 1179
    in enteralgia, 665
    in gout, 131

Caustic drinks, influence of, on causation of organic stricture of
        oesophagus, 422
  potash, use of, in hemorrhoids, 926

Cauterization, use of, in prolapsus ani, 919
  in ulceration of oesophagus, 418
  value of, in cancrum oris, 343

Cautery, actual, use of, in cancrum oris, 343

Cell-degeneration in acute yellow atrophy of liver, 1025
  hepatic, in phosphorus-poisoning, 1031

Cell-growth, excessive, in scrofula, 238

Cell-proliferation, increased, in chronic intestinal catarrh, 703

Cells, caseation of, in scrofula, 239
  fatty degeneration of, in scrofula, 239
  of liver, atrophy of, in cirrhosis, 992, 993

Cellular growth, increased, in acute intestinal catarrh, 677

Cerebral disease, influence of, on causation of constipation, 641
  hemorrhage complicating constipation, 648
  inflammation, tendency to, from gastric irritation, 474
  sclerosis in cirrhosis of liver, 999
  symptoms of entero-colitis and cholera infantum, treatment, 759
    of acute gastritis, 467
  syphilis, hereditary, 304

Cerebro-spinal axis, disease of, influence on causation of oesophageal
        paralysis, 429

Cerium oxalate, use of, in cancer of stomach, 576

Cestodes, 931

Chancroids as a cause of follicular ulceration of rectum and anus, 895

Change of air, in cholera infantum and entero-colitis, 746, 756
    value of, in dysentery, 813
  of climate, benefit from, in rheumatoid arthritis, 102
    value of, in acute intestinal catarrh, 688
      in intestinal indigestion, 632
  of residence, value of, in chronic intestinal catarrh, 715, 716

Charcoal, use of, in chronic gastritis, 478
    in gastric cancer, 576

Cheek, perforation of, in cancrum oris, 341, 342

Cheesy degeneration of mesenteric glands in tabes mesenterica, 1187

Chemical theory of origin of gout, 112

Chemise, Agnew's rectal, in rectal hemorrhage, 927

Chest, alterations of, in rachitis, 152

Chilblains, tendency of scrofulous persons to, 245

Children, constipation in, treatment, 656
  acute rheumatism in, peculiarities, 49

Chills in acute pharyngitis, 395
  in hepatic abscess, 1008
  in hepatic colic, 1071, 1072
  in peri-rectal and anal abscesses, 896
  in suppurative pylephlebitis, 1099
  in typhlitis and perityphlitis, 818

Chloasma cachecticorum, 552

Chloral, use of, in acute rheumatism, 65
    in hepatic colic, 1082
    in rachitis, 163
  hypodermatically, use of, in cholera morbus, 725

Chloride of gold, use of, in amyloid liver, 1046
    and sodium, use of, in cirrhosis of liver, 1001

Chlorodyne, use of, in hepatic colic, 1082

Chloroform, use of, in cholera morbus, 725
    in enteralgia, 665
    in hepatic colic, 1082
    in pruritus ani, 917
    as a solvent of biliary calculi, 1081

Chlorosis, influence of, on causation of simple ulcer of stomach, 487

Cholaemia in abscess of liver, 1010
  in occlusion of biliary passages, 1091

Cholagogues, use of, in lithaemia, 972
    in fatty liver, 1050
    in hyperaemia of liver, 988

Cholate of sodium, use of, in biliary calculi, 1081

Cholera, effect of, on rectum, 910

Choleraic diarrhoea in acute intestinal catarrh, 682
  form of acute intestinal catarrh, treatment, 698

Cholera infantum, 744

CHOLERA MORBUS, 719
  Synonyms, 719
  Definition, 719
  History, 719
  Nature, 720
    Niemeyer's views of, 720
    Nervous origin, 720
    Specific origin, 720
    Relation to cholera infantum, 720
  Etiology, 720
    Predisposing causes, 720
    Climate, 720
    Geographical distribution, 720
    Age, 720
    Sex, 720
    Exhaustion of nervous system, 720
    Extreme heat, 720
    Mental anxiety, 721
    Exciting causes, 721
    Septic material from fermentation of food, 721
    Improper food, 721
    Unripe fruit, 721
    Ice-water, 721
    Deficient gastric juice, 721
    Offensive exhalations, 721
    Nervous disturbance from other diseases, 721
    Malaria, 721
    Sewer-gas, 721
  Morbid anatomy, 721
    Signs of gastro-intestinal catarrh, 721
    Mucous membrane, lesions, 721
    Solitary glands, swelling of, 721
    Peyer's patches, swelling of, 721
    Blood, lesions of, 721
    Kidneys, lesions of, 722
    Muscular degeneration, 722
  Symptoms, 722
    Mode of onset, 722
    Vomiting, 722
    Vomit, characters, 722
    Borborygmi, 722
    Alvine discharges, 722
    Stools, character of, 722
    Pain, 722
    Cramps, 722
    Abdomen, state of, 722
    Skin, state of, 722
    Physiognomy, 722
    Collapse, 722
    Mental state, 722
    Pulse, 723
    Urine, condition of, 723
    Temperature, 723
  Progress and termination, 723
    Tendency to recovery, 723
    Mode of death, 723
    Duration, 723
  Diagnosis, 723
    From epidemic cholera, 723
    From irritant poisoning, 723
    From uraemic choleriform attacks, 724
    From acute peritonitis, 724
  Prognosis, 724
  Mortality, 724
  Treatment, 724
    Preventive, 724
      of vomiting, 725
      of heart-weakness, 725
      of thirst, 725
    Use of emetics, 724
      of morphia, hypodermatically, 724
      of friction, 724
      of alcohol, 725
      of ice, 725
      of chloroform, 725
      of opium, 725
      of camphor, 725
      of chloral, hypodermatically, 725
      of carbolic acid, 725
      of bromide of sodium, 725
      of hydrocyanic acid, 725
      of bismuth, 725
      of calomel, 725
    Diet, 725

Choleriform diarrhoea, 741

Chordo-tympani nerve, relation to causation of parenchymatous
        glossitis, 363

Chorea following acute rheumatism, 38
    from Oxyuris vermicularis, 951

Chromic acid, use of, in syphilitic pharyngitis, 408

Chronic articular rheumatism, 69
  hydrarthrosis of gonorrhoeal rheumatism, 105
  gastritis, 470
  glossitis, 366
  gout, 120
  intestinal pancreatitis, 1121
    catarrh, 699
  oesophagitis, 416
  peritonitis, complicating simple ulcer of stomach, 502
  pharyngitis, 402
  form of catarrhal stomatitis, 323
    of dysentery, 800
    of peri-rectal and anal abscess, 896
  variety of general progressive form of rheumatoid arthritis, 81

Chyluria in Filaria sanguinis, 963

Chyme, composition of, 621

Cicatricial contraction a cause of organic stricture of oesophagus,
        422

Cicatrization in simple ulcer of stomach, 506
  in syphilitic pharyngitis, 407
  of gastric ulcer as a cause of hypertrophic stenosis of pylorus, 615
  of ulcers as a cause of stricture of bowel, 855
    in chronic intestinal catarrh, 703
    influence on causation of occlusion of common biliary duct, 1083
  of gastric cancer, 563

Cider, influence of, on causation of gout, 111

Circulation, deficient, in scrofula, 245

Cirrhosis of kidneys in gout, 117
  of liver. See _Liver, Diseases of_.
  of stomach, 611
    influence on causation of dilatation of stomach, 590

Clamp and cautery, removal of hemorrhoids by, 925
    use of, in rectal polypi, 921

Cleanliness, want of, influence on causation of thrush, 332

Clergyman's sore throat, 402

Climate, change of, in entero-colitis and cholera infantum, 756
  influence on causation of abscess of liver, 1002
      of catarrh of bile-ducts, 1051
      of cholera morbus, 720
      of dysentery, 786
      of hyperaemia of liver, 983
      of acute intestinal catarrh, 669
      of rachitis, 143
      of rheumatism, acute, 19
      of scrofula, 233
      of simple ulcer of stomach, 485
  warm, in treatment of gout, 131

Closure of hepatic vein as a cause of cirrhosis of liver, 991

Clothing, importance of proper, for prevention of chronic articular
        rheumatism, 73
  proper, necessity of, for prevention of muscular rheumatism, 77

Clubbing of fingers in scrofula, 246

Codeia, use of, in diabetes mellitus, 226
    in simple ulcer of stomach, 524

Cod-liver oil, use of, in diabetes mellitus, 228
    in intestinal indigestion, 637
    in chronic intestinal catarrh, 718
    in pseudo-membranous enteritis, 776
    in rachitis, 162
    in chronic articular rheumatism, 74
    in rheumatoid arthritis, 98
    in scrofula, 252
    in tabes mesenterica, 1194

Coffee, iced, use of, in intestinal catarrh of children, 698

Coffee-grounds vomit in gastric cancer, 546
    in simple ulcer of stomach, 493

Colchicum, use of, in acute gout, 134

Cold, influence of, on causation of oesophageal paralysis, 429
      of enteralgia, 658
      of dysentery, 789, 790
      of acute intestinal catarrh, 670
  use of, in enteralgia, 665
    in acute rheumatism, 66
    in hemorrhage from bowels, 834
  and damp, influence on causation of acute pharyngitis, 390
      of catarrh of bile-ducts, 1051
      of jaundice, 977
      of parenchymatous glossitis, 359
      of pseudo-membranous enteritis, 765
      of acute oesophagitis, 410
      of rheumatism, acute, 22
      of chronic rheumatism, 70
      of muscular rheumatism, 75
      of gonorrhoeal rheumatism, 103
      of rheumatoid arthritis, 88, 90, 91
  baths, in acute gastritis, 470

Cold-water injections, in hemorrhoids, 924

Colic, dry, 662
  hepatic, 1058, 1070
  intestinal. See _Enteralgia_.
  nervous, 662
  in acute intestinal catarrh, 679, 682

Colitis, 667, 683

Collapse in acute pancreatitis, 1119
  in acute intestinal catarrh, 682
  in cholera morbus, 722
  in enteralgia, 662
  in hemorrhage from bowels, 833
  in hemorrhage into pancreas, 1129
  in hepatic colic, 1071
  in perforation of simple gastric ulcer, 498

Colles' law of infection of mother by syphilitic children, 263

Colloid cancer of intestine, 868
  degeneration of gastric walls, in dilatation of stomach, 600
  form of gastric cancer, 564
    of cancer of oesophagus, 426

Colocynth, use of, in constipation, 655
    in functional dyspepsia, 458

Colon, congenital stricture of, 836
  dilatation of, in constipation, 644
  displacement of, in constipation, 643
  increased length of, in constipation, 644
  lesions, in entero-colitis, 738
  ulcers of, in chronic intestinal catarrh, 702
  and rectum, dilatation of, from fecal impaction, 852

Colotomy, lumbar, for cancer of rectum, 915, 916

Coma, dyspnoeic, in gastric cancer, 554
  in acute yellow atrophy of liver, 1027
  in acute rheumatism, 38
  in cirrhosis of liver, 999
  in diabetes mellitus, 204, 205
  in dilatation of stomach, 596

Complications of biliary concretions, 1076
  of cancrum oris, 341
  of constipation, 648
  of diabetes mellitus, 210
  of gastric cancer, 560
  of gout, 121
  in chronic intestinal catarrh, 709
  of mercurial stomatitis, 346
  of acute oesophagitis, 414
  of chronic oesophagitis, 417
  of parenchymatous glossitis, 362
  of syphilitic pharyngitis, 407
  of purpura, 190
  of acute rheumatism, 31
  of gonorrhoeal rheumatism, 106
  of rheumatoid arthritis, 83-86
  of Heberden's nodosities of rheumatoid arthritis, 86
  of simple ulcer of stomach, 502
  of tonsillitis, 383
  of tabes mesenterica, 1193
  and sequelae of aphthous stomatitis, 329
    of dysentery, 805

Compression, use of, in hypertrophy of tongue, 353
  and contraction of bowel as a cause of intestinal obstruction, 857

Conception, infection of child with syphilis at moment of, 262, 267

Condensed milk, use of, in cholera infantum, 754
    in entero-colitis, 754

Condurango, use of, in gastric cancer, 576

Condylomata in hereditary syphilis, 279
  of rectum and anus, 901

Confluent form of aphthous stomatitis, 329

Congenital deficiency of tongue, 348, 349
  nature of macroglossia, 350
  malformations of rectum and anus, 879
  origin of dilatation of oesophagus, 430
    of organic stricture of oesophagus, 422
  rachitis, 141-143

Congestion of lungs in acute rheumatism, 37
  passive and active, as a cause of hemorrhage from stomach, 581

Conium, use of, in spasmodic stricture of oesophagus, 421

Connective tissue, hyperplasia of, in chronic intestinal pancreatitis,
        1122
    increase of, in acute yellow atrophy of liver, 1025
    new, development of, in cirrhosis of liver, 992

Consanguineous marriages, influence on causation of scrofula, 234

Consistence of liver in amyloid disease of, 1042

CONSTIPATION, 638
  Synonyms, 638
  Nature, 638, 639
  Definition, 638, 639
  Etiology, 639
    Age, 639
    Female sex, 639, 640
    Heredity, 640
    Habit, 640
    Occupation, 640
      sedentary, 640
    Acute and chronic brain disease, 641
    Abuse of aperients, 641
      opium, 641
    Lead-poisoning, 641
    Tobacco, 641
    Chronic pulmonary disease, 641
      heart disease, 641
      liver disease, 641
    Painful disease of rectum, 642
    Chronic cachexiae, 642
    Wasting diseases, 642
    Disorders of digestion, 642
    Pancreatic disease, 642
    Loss of fluids, 642
      by perspiration, 642
      by diuresis, 642
      by diabetes, 642
      by exercise, 643
    Food, 643
    Intestinal worms, 643
  Morbid anatomy, 643
    Displacement of colon, 643
    Dilatation of intestines, 643
      of sigmoid flexure, 643
      of colon, 644
    Increased length of colon, 644
    Mucous membrane, intestinal, lesions of, 644
    Ulcers of intestines, 644
    Thinning of intestinal walls, 644
    Hypertrophy of intestinal walls, 644
    Fecal accumulations, 644
      character, 645
    Scybalae, formation of, 645
    Hemorrhoidal tumors, 645
    Peri-rectal abscesses, 645
    Fistulae, 645
  Symptoms, 645
    Fulness and heat of rectum, 645
    Appetite, impaired, 646, 647
    Tongue, state, 646, 647
    Flatulence, 646, 647
    Abdominal distension, 646, 647
      pain, 646
    Stools, character, 646
    Cold feet, 646
    Pain in groin, 646
    Varicocele, 646
    Seminal emissions, 646
    Urinary retention, 646
    Jaundice, 646
    Uterine displacements, 647
    Nervous symptoms, 647
    Vertigo, 647
    Headache, 646, 647
    Visual disorders, 647
    Disorders of hearing, 647
    Heart-palpitation, 647
    Chilliness, 647
    Menstrual disorders, 647
    Anaemia and chlorosis, 647
    Mental depression, 647
    Hallucinations, 647
    Relation of displacements of colon to suicide, 647
    Fever, 647, 648
    Urine, state of, 648
    Skin disorders, 648
  Complications and results, 648
    Ulceration of intestinal mucous membrane, 648
    Abscess, peri-rectal, 648
    Fistulae, 648
    Hemorrhoids, 648
    Intussusception, 648
    Typhlitis and perityphlitis, 648
    Haemoptysis, 648
    Cerebral hemorrhage, 648
    Hernia, 648
    Death, cause of, 649
  Diagnosis, 649
    From secondary constipation, 649
    From rectal growths and tumors, 649
    From stricture, 649
    From abdominal tumors, 649, 650
    From obstruction by gall-stones, 649
    Of stercoral tumors, 649, 650
        physical signs, 650
  Prognosis, 650
  Treatment, 651
    Prophylactic, 651
    Exercise, 651, 653
    Bathing, 651
    Acute form, 651
      Use of purgatives, 651
        enemata, 651
    Chronic form, 652
      Diet, 652
      Use of milk, 652
    Of atony of colon, 653
    Use of bathing, 653
      of massage, 653
      of cold douche, 653
      of electricity, 653
      of abdominal belt, 654
      of diet, 654
      of mineral waters, 652, 653, 655
      of strychnia, 654
      of iron, 654
      of belladonna, 654
      of arsenic, 654
      of ipecacuanha, 654
      of zinc salts, 655
      of enemata, 655
        of cold water, 655
      of water, 655
      of podophyllin, 655
      of rhubarb, 655
      of aloes, 655
      of colocynth, 655
      of ox-gall, 655
      of salines, 655
      of Epsom salts, 655
      of Rochelle salts, 655
      of purgatives, mode, 656
      of cascara sagrada, 656
      of alum, 656
      of sulphur, 656
      of guaiacum, 656
      of colchicum, 656
      of senna, 656
      of tonics, 657
    In children and infants, 656
    Diet, 656
      Objections to vegetables, 654
    Use of soap suppository, tonics, 656, 657

Constipation due to disease of spinal cord, 906
  in cancer of intestine, 891
  in dilatation of stomach, 594
  in fissure of anus and rectum, 888
  in functional dyspepsia, 450
  in gastric cancer, 550
  in chronic gastritis, 475
  in gout, 118
  in hepatic colic, 1072
  in chronic intestinal catarrh, 706
  in intestinal indigestion, 627
  in acute pancreatitis, 1119
  in acute peritonitis, 1141
  in acute rheumatism, 27
  in rheumatoid arthritis, 83
  in simple ulcer of stomach, 494, 495
  in tabes mesenterica, 1190
  in typhlitis and perityphlitis, 819
  significance of, in rachitis, 154
  influence on causation of enteralgia, 658
      of functional dyspepsia, 447
      of hemorrhage from bowels, 830
      of internal hemorrhoids, 884
      of acute intestinal catarrh, 671
      of intestinal indigestion, 625
      of rectal prolapse, 881
      of typhlitis, 814
  as a cause of intestinal obstruction, 850
  as a cause of torsion of caecum, 853

Constitutional peculiarity, influence on causation of catarrh of
        bile-ducts, 1051
  treatment of cancer of oesophagus, 428
    of cancrum oris, 343
    of enteralgia, 665
    of mercurial stomatitis, 348

Contagiousness of dysentery, 793, 794
  of scurvy, 169
  of stomatitis ulcerosa, 336
  of thrush, 332

Contraction of stomach in gastric cirrhosis, 613

Convalescence in entero-colitis, 736
  in acute gastritis, treatment of, 470
  in acute rheumatism, treatment of, 169
  of simple ulcer of stomach, treatment of, 529
  of typhlitis, treatment of, 822

Convulsions in enteralgia, 662
  in chronic gastritis, 474
  in hepatic colic, 1071
  in acute yellow atrophy of liver, 1027
  in morbid dentition, 374
  in occlusion of biliary ducts, 1092
  in acute oesophagitis, 414
  in rachitis, 149
  in rachitis, treatment of, 163, 164
  in acute rheumatism, 38
  in scurvy, 180
  relation of, to macroglossia, 350

Cooking, defective, influence on causation of functional dyspepsia,
        445
  necessity of thorough, in trichinosis, 962

Co-ordination of muscles of defecation, loss of, treatment of, 916

Copaiba, use of, in hemorrhoids, 923
    in chronic intestinal catarrh, 718
    in cirrhosis of liver, 1001
    in proctitis, 919
    in pseudo-membranous enteritis, 775

Copper sulphate, use of, in pseudo-membranous enteritis, 775
    in phosphorus-poisoning, 1033

Cornea in interstitial keratitis of hereditary syphilis, 299
  lesions of, in chronic intestinal catarrh, 706

Corneal ulceration complicating chronic intestinal catarrh, 710

Cornil and Ranvier on causes of scrofulous inflammation, 239

Corrosive poisons, influence on causation of acute gastritis, 465
        of simple ulcer of stomach, 486
  sublimate, use of, in chronic intestinal catarrh, 717
      in pseudo-membranous enteritis, 775
      in suppurative pylephlebitis, 1101

Coryza of hereditary syphilis, 277

Cough in functional dyspepsia, 451
  in acute pharyngitis, 394
  in chronic pharyngitis, 404
  in tuberculous pharyngitis, 401

Coughing, influence on causation of prolapse of rectum, 881

Counter-irritation, use of, in cirrhosis of liver, 1002
  in acute and chronic gastritis, 469, 479
  in acute intestinal catarrh, 688, 690, 698
  in spasmodic stricture of oesophagus, 422
  in pseudo-membranous enteritis, 776
  in simple ulcer of stomach, 524

Course of biliary concretions, 1076
  of acute yellow atrophy of liver, 1029
  of amyloid liver, 1044
  of carcinoma of liver, 1039
  of cirrhosis of liver, 998
  of functional diseases of liver, 967, 970, 974, 981
  of hyperaemia of liver, 987
  of occlusion of biliary passages, 1092
  of phosphorus-poisoning, 1032
  of perihepatitis, 989
  of suppurative pylephlebitis, 1101
  of hereditary syphilis, 273
  of intestinal indigestion, 630
  of cancer of stomach, 538
  of dilatation of stomach, 603
  of simple ulcer of stomach, 500
  of acute rheumatism, 44
  of gonorrhoeal rheumatism, 106

Cow's milk, impure, influence on causation of entero-colitis, 731
  composition, 749, 750

Cramps in cholera morbus, 722
  in diabetes mellitus, 206
  muscular, in muscular rheumatism, 75

Craniotabes, occurrence of, in rachitis, 147

Creasote, use of, in enteralgia, 666
    in vomiting of abscess of liver, 1021
    in treatment of liver-flukes, 1110

Cretaceous degeneration of mesenteric glands in tabes mesenterica,
        1189

Croton oil, effect on rectum, 910

Croupous nature of pseudo-membranous enteritis, 767, 768

Cry, peculiarity of, in thrush, 334

Cryptogam as a cause of mycotic tonsillitis, 381

Cubebs, use of, in chronic pharyngitis, 406
    in pseudo-membranous enteritis, 775

Cutaneous affections complicating acute rheumatism, 42
      rheumatoid arthritis, 84
  eruptions of anus, 892

Cyanotic atrophy of liver, 985

Cylinder-cell epithelioma, common form of intestinal cancer, 871

Cylindrical-celled epithelial form of gastric cancer, 564

Cynanche tonsillaris, 379

Cysts of echinococci of liver (description), 1102
  of hydatids of liver, contents, 1103
  of mucous membrane of stomach, 579
  of false membrane, in acute peritonitis, 1135
  of Taenia echinococcus, character, 944
  formation and origin of, in chronic intestinal catarrh, 704
  formation of, from obstruction of pancreatic ducts, 1130

Cystic duct, occlusion of, effects of, 1085

Cystitis and orchitis complicating acute rheumatism, 42


D.

Dactylitis in hereditary syphilis, 291

Daettwyler's and Cohnheim's experiments in artificial production of
        gastric ulcers, 514

Death, cause of, in cancrum oris, 341
    in chronic intestinal catarrh, 709
    in constipation, 649
    in dilatation of oesophagus, 432
    in entero-colitis, 736
    in gastric cancer, 559
    in mercurial stomatitis, 347
    in thrush, 334
  in simple ulcer of stomach, causes of, 502
  mode of, in cholera morbus, 723
    in dilatation of stomach, 603
  sudden, cause of, in acute rheumatism, 50

Debility in gastric cancer, 551
  in tabes mesenterica, 1189
  influence of, on causation of aphthous stomatitis, 326

Defecation, difficult, in cancer of rectum and anus, 904

Definition of ankyloglossia, 349
  of biliousness, 965
  of biliary concretions, 1058
  of catarrh of bile-ducts, 1051
  of occlusion of biliary passages, 1082
  of cancrum oris, 338
  of cholera morbus, 719
  of constipation, 638, 639
  of diabetes mellitus, 195
  of dysentery, 777
  of functional dyspepsia, 436
  of enteralgia, 658
  of gastralgia, 459
  of acute gastric catarrh, 463
  of chronic gastritis, 470
  of glossitis, 354, 355, 357, 359, 367
  of glossanthrax, 368
  of gout, 108
  of hepatic glycosuria, 973
  of cancer of intestines, 868
  of intestinal ulcer, 823
  of jaundice, 975
  of abscess of liver, 1002
  of acute yellow atrophy of liver, 1023
  of amyloid liver, 1040
  of carcinoma of liver, 1033
  of cirrhosis of liver, 990
  of echinococcus of liver, 1101
  of fatty liver, 1046
  of hyperaemia of liver, 983
  of macroglossia, 349
  of morbid dentition, 371
  of oesophagitis, 409
  of chronic oesophagitis, 416
  of carcinoma of oesophagus, 426
  of dilatation of oesophagus, 430
  of stricture of oesophagus, 419, 422
  of ulceration of oesophagus, 418
  of paralysis of oesophagus, 429
  of perihepatitis, 989
  of acute pharyngitis, 390
  of chronic pharyngitis, 402
  of tubercular pharyngitis, 400
  of phosphorus-poisoning, effect on liver, 1030
  of purpura, l86, 187
  of pseudo-membranous enteritis, 763
  of rheumatism, acute, 19
  of chronic articular rheumatism, 69
  of muscular rheumatism, 74
  of rachitis, 137
  of scrofula, 231, 232
  of scurvy, 167
  of cancer of stomach, 530
  of cirrhosis of stomach, 611
  of dilatation of stomach, 586
  of acute dilatation of stomach, 610
  of hemorrhage from stomach, 580
  of simple ulcer of stomach, 480
  of stomatitis, 321
  of aphthous stomatitis, 325
  of catarrhal stomatitis, 321
  of mercurial stomatitis, 344
  of toxic stomatitis, 344
  of stomatitis ulcerosa, 336
  of stomatorrhagia, 370
  of tabes mesenterica, 1182
  of thrombosis and embolism of portal vein, 1095
  of thrush, 331
  of tonsillitis, 379

Deformities in chronic gout, 121
  of rachitis, treatment, 165, 166
  of joints in chronic variety of general rheumatoid arthritis, 81, 82
  in partial form of rheumatoid arthritis, 85, 86

Deformity in gonorrhoeal rheumatism, 104

Degeneration of pancreas, 1128
  of liver, fatty, 1046
  fatty and amyloid, of gastric walls, in functional dyspepsia, 451
  fatty and colloid, of gastric walls, in dilatation of stomach, 600
  lardaceous, of intestine, 874
  of vessels in lardaceous disease of intestines, 876

Deglutition, difficult, in parenchymatous glossitis, 361
    in tuberculous pharyngitis, 401
    in aphthous stomatitis, 329
    in mercurial stomatitis, 345
    in tonsillitis, 381
  impediment to, in organic stricture of oesophagus, 423
  painful, in acute oesophagitis, 413
  slow, in oesophageal paralysis, 429

Dejecta, influence of, on causation of dysentery, 791, 792

Delirium of enteralgia, 662
  in acute intestinal catarrh, 681
  in acute internal strangulation of intestines, 843
  in acute peritonitis, 1142
  in acute rheumatism, 37, 38

Delirium ferox, in acute yellow atrophy of liver, 1027

Demulcent drinks, use of, in acute gastritis, 469

DENTITION, MORBID, 371
  Definition, 371
  Synonyms, 371
  Etiology and symptoms, 371
    Teeth, order of normal eruption of, 372
      precipitate eruption of, 372
      tardy eruption of, 372
      rachitis as a cause of tardy eruption of, 372
    Mild cases, initial symptoms, 373
      increase of saliva, 373
      general, 373
    Ulcerations, aphthous, 373
      at point of eruption, 373
    Stomatitis, catarrhal, 373
    Pain, 373
    Heat and tumefaction of gum, 373
    Constitutional, 374
    Reflex nervous symptoms, 374
    Convulsions, 374
      characters of, 374
      cause of, 374
    Paralyses, 375
    Idiocy, 375
    Gastro-intestinal disorders, 374
      causes, 374
      mechanical, 374
    Otitis media, 375
    Conjunctivitis, 375
    Second dentition, 375
    Teeth, order of eruption, 375
      Symptoms, 375
    Nervous system, 376
    Gastro-intestinal tract, 375
    Wisdom teeth, eruption of, 376
      Symptoms of, 376
  Diagnosis, 376
  Prognosis, 376
  Treatment, 376
    Preventive, 376
    Avoidance of cold, 376
    Diet, 377
    Complications, 377
    Aphthous ulcerations, 377
    Local, 377
    Use of lancet, 377
    Method of incision, 378
      contraindications, 378

Dentition, influence on causation of macroglossia, 350
      of aphthous stomatitis, 326
      of catarrhal stomatitis, 322
      of tabes mesenterica, 1186
  relation to entero-colitis, 733

Deposit of thrush, microscopic appearance of, 333
  in herpetic or membranous form of pharyngitis, nature of, 392

Deposits in tonsillitis, nature of, 384

Depressing emotions, influence of, on causation of scurvy, 169
      of cancer of stomach, 536

Depression, mental, in chronic intestinal catarrh, 706
  of spirits in functional dyspepsia, 451
  of vital powers in pseudo-membranous enteritis, 765, 766

Dermalgia distinguished from enteralgia, 664

Desquamation of tongue in parenchymatous glossitis, 361

Deuteropathic form of tonsillitis, 380

Development of gastric ulcer, influence of digestive action of gastric
        juice upon, 512

Diabetes, influence on causation of constipation, 642

DIABETES MELLITUS, 195
  Definition, 195
  Etiology, 203
    Nervous shock, influence on causation, 203
    Mental anxiety, influence on causation, 203
    Malaria, influence on causation, 203
    Injury, influence on causation, 203
    Heredity, influence on causation, 203
    Sexual excess, influence on causation, 203
    Age, influence on causation, 203
    Sex, influence on causation, 203
    Race, influence on causation, 204
  Geographical distribution, 203
  Pathology and pathogenesis, 195
    Hyperaemia of liver, relation of, to, 195
      causes of, 195-199
    Diabetic area of medulla oblongata, result of puncture, 195
    Glycosuria, artificial methods of production, 195-199
    Glycogenic influence, pathology of, 196
    Sympathetic nerve, relation of, to production of glycosuria, 196
    Glycosuria, artificial, irritative nature of, 198
    Vaso-motor nerves, influence on production of glycosuria, 196-199
    Glycosuria, production of, from medicinal substances, 198
    Pavy's chemical theory of production of glycosuria, 199
  Morbid anatomy, 199
    Nervous system, lesions of, 200
    Dickinson's alterations of nervous centres, 200
    Blood-vessels, lesions of, 200
    Pancreas, lesions of, 200
      nature of lesions, 200
      disease of, relation to causation, 201
    Liver, enlargement of, 201
      lesions of, 201
    Kidneys, lesions of, 202
    Testes, atrophy of, 202
    Lungs, lesions of, 202
    Phthisis, complicating nature of, 202
  Symptoms, 204
    Initial, 204
    Thirst, 204
    Dryness of skin, 204
    Loss of weight, 204
    Pruritus of genitalia, 204
    Muscular weakness, 204
    Sexual appetite, loss of, 204
    Appetite, 204
    Dyspepsia, 204
    Vision, disorders of, 204
    Hearing, disorders of, 205
    Temperature, 204
    Carbuncles and boils, 205
    Ulcerated surfaces, 205
    Eczema of genitalia, 205
    Urethritis, 205
    Coma, 204, 205
      causes of, 205, 206
      mode of onset, 205
    Acetonaemia, 205, 206
    Nervous symptoms, 205, 206
    Cramps, 206
    Facial paralysis, 206
    Neuralgia, 206
    Blood, alterations of, 206
      presence of fat in, 206, 207
      source of fat in, 207
      corpuscles, diminution of, 207
    Urine, changes in, 207
      amount of sugar in, 207
      effect of diet and exercise on amount of sugar in, 207, 208
      presence of inosite in, 208
      specific gravity of, 208
      color of, 208
      odor of, 208
      acetone and alcohol, presence of, 209
    Albuminuria, 208
  Duration, 210
  Complications, 210
    Phthisis, 210
    Duodenal catarrh, 210
    Boils and abscesses, 205, 210
    Jaundice, 210
    Pancreatic disease, 210
  Diagnosis, 210
    Tests for sugar, 211
    Fehling's test, 211
      quantitative, 212
    Fermentation test, 212
      quantitative, 213
    Picric acid and potash test, 213
      quantitative, 214
    Indigo-carmine test, 216
      quantitative, 216
      precautions, 217
    Test for inosite, 217
  Prognosis, 217
    Influence of pancreatic disease upon, 218
      of age upon, 218
      of phthisis upon, 218
  Treatment, 218
    Dietetic, 218
      By skim-milk, 218
        mode of administering, 219
      Peptonized milk, 219, 220
      Saccharine foods admissible in, 220
      Foods and drinks admissible in, 220, 221
      Bill of fare for diabetics, 221
      Alcoholic beverages admissible, 222, 225
      Gluten bread, use of, 222
      Bran bread, use of, 223
      Almond food, use of, 223, 224
      Substitutes for sugar in food, 224
      Use of bicarbonate of sodium and potassium in place of sugar,
        224
    Hygienic, 225
      Use of mineral waters, 225, 226
      Ventilation, 225
      Use of baths, 225
    Medicinal, 226
      Use of codeia, 226
        of opium, 226, 227
        of ergot, 227
        of bromide of potassium, 227
        of bromide of arsenic, 227
        of arsenic, 227
        of strychnia, 227
        of phosphates, 227
        of iodide of potassium, 228
        of tincture of iodine, 228
        of nitrate of uranium, 230
        of lactic acid, 228
        of cod-liver oil, 228
        of soap, 228
        of iodoform, 229
        of salicylate of sodium and salicylic acid, 229, 230
        of alkalies, 229
      Transfusion of blood, 229
      Of neuralgia, 229

Diabetes mellitus, influence on causation of pruritus ani, 909
    simple gastric ulcer, 488
  relation to disease of pancreas, 1117

Diabetic area of medulla oblongata, effects of puncture, 195

Diagnosis of ascites, 1177
  of biliary calculi, 1078
  of catarrh of bile-ducts, 1055
  of occlusion of biliary passages, 1092
  of cancrum oris, 342
  in cholera infantum, 745
  of cholera morbus, 723
  of constipation, 648
  of diabetes mellitus, 210
  of dysentery, 806
  of functional dyspepsia, 452
  of enteralgia, 663
  of entero-colitis, 740
  of fistula in ano, 898
  of gastralgia, 461
  of acute gastritis, 468
  of chronic gastritis, 475
  of simple gastric ulcer, 514
  of superficial glossitis, 357
  of chronic superficial glossitis, 367
  of parenchymatous glossitis, 363
  of chronic parenchymatous glossitis, 368
  of glossitis parasitica, 359
  of gout, 124
  of hemorrhage from bowels, 833
  of hepatic colic, 1078
  of hepatic glycosuria, 974
  of ileo-colitis, 685
  of acute intestinal catarrh, 684
  of chronic intestinal catarrh, 710
  of ulcerations in acute intestinal catarrh, 685
  of intestinal cancer, 873
  of indigestion, 630
  of obstruction, 858
    by fecal accumulations, 860
    by internal hernia, 860
    by gall-stones, 860
  of seat of intestinal obstruction, 861
  of intestinal ulcer, 828
  of lardaceous degeneration of intestines, 876
  of torsion of intestines, 860
  of jaundice, 981
  of lithaemia, 970
  of abscess of liver, 1018
  of acute yellow atrophy of liver, 1029
  of amyloid liver, 1045
  of carcinoma of liver, 1039
  of cirrhosis of liver, 999
  of fatty liver, 1049
  of hydatids of liver, 1104
  of hyperaemia of liver, 988
  of liver-flukes, 1110
  of lumbago, 77
  of macroglossia, 353
  of morbid dentition, 376
  of acute oesophagitis, 414
  of chronic oesophagitis, 417
  of dilatation of oesophagus, 433
  of paralysis of oesophagus, 429
  of organic stricture of oesophagus, 424
  of spasmodic stricture of oesophagus, 420
  of ulceration of oesophagus, 418
  of acute pancreatitis, 1119
  of carcinoma of pancreas, 1126
  of obstruction of pancreatic ducts, 1131
  of perihepatitis, 989
  of acute peritonitis, 1143
  of tubercular peritonitis, 1167
  of acute pharyngitis, 396
  of chronic pharyngitis, 404
  of syphilitic pharyngitis, 408
  of tuberculous pharyngitis, 401
  of phosphorus-poisoning, 1032
  of pleurodynia, 77
  of pseudo-membranous enteritis, 773
  of purpura, 190
  of suppurative pylephlebitis, 1101
  of hypertrophic stenosis of pylorus, 615
  of acute rheumatism, 47
  of chronic articular rheumatism, 73
  of gonorrhoeal rheumatism, 107
  of muscular rheumatism, 76
  of rheumatoid arthritis, 92
  of scrofula, 248
  of scurvy, 182
  of cancer of stomach, 569
  of cirrhosis of stomach, 613
  of dilatation of stomach, 600
  of hemorrhage from stomach, 584
  of simple ulcer of stomach, 514
  of aphthous stomatitis, 329
  of catarrhal stomatitis, 325
  of mercurial stomatitis, 347
  of stomatitis ulcerosa, 337
  of stomatorrhagia, 371
  of hereditary syphilis, 309
  of bone disease of hereditary syphilis, 289, 290
  of erythema of hereditary syphilis, 278
  of interstitial keratitis in hereditary syphilis, 299
  of nervous disease in hereditary syphilis, 304
  of pemphigus in hereditary syphilis, 276
  of pustular syphilides in hereditary syphilis, 279
  of roseola in hereditary syphilis, 278
  of tabes mesenterica, 1191
  of thrombosis and embolism of portal vein, 1096
  of thrush, 334
  of tonsillitis, 386
  of tongue-tie, 349
  of tubercular ulceration of tongue, 369
  of torticollis, 78
  of trichinosis, 961
  of typhlitis and perityphlitis, 820

Diaphoretics, use of, in ascites, 1179
    in muscular rheumatism, 77

Diaphragmatic hernia, 843

Diarrhoea, in acute gastritis, 467
  in chronic gastritis, 475
  in gout, 118
  in acute intestinal catarrh, 679, 681
  in chronic intestinal catarrh, 706
  in intestinal indigestion, 627
  in lardaceous degeneration of intestines, 874
  in intussusception, 848
  in amyloid liver, 1044
  in diseases of pancreas, 1115
  in acute secondary pancreatitis, 1121
  in carcinoma of pancreas, 1126
  in tabes mesenterica, 1190
  in cancer of stomach, 550
  in dilatation of stomach, 594
  in aphthous stomatitis, 329
  in catarrhal stomatitis, 323
  in trichinosis, 960
  influence on causation of prolapse of rectum, 881
  and dysentery complicating acute rheumatism, 42

Diarrhoeal diseases of children, mortality in, 726, 727

Diet in biliousness, 967
  in catarrh of bile-ducts, 1056
  in biliary concretions and hepatic colic, 1079
  in cholera morbus, 725
  in constipation, 652, 654
  in constipation of children, 656
  in diabetes mellitus, 218-224
  in functional dyspepsia, 452
  in dysentery, 809, 812
  in enteralgia, 666
  in pseudo-membranous enteritis, 776
  in acute gastritis, 468
  in chronic gastritis, 476
  in chronic superficial glossitis, 367
  in parenchymatous glossitis, 365
  in gout, 127, 133
  in hemorrhage from bowels, 834
  in hepatic glycosuria, 975
  in intestinal cancer, 874
  in acute intestinal catarrh, 687, 688, 690, 692
  in chronic intestinal catarrh, 714, 716
  in intestinal indigestion, 633, 634
  in intestinal ulcer, 829
  in lardaceous degeneration of intestines, 876
  in jaundice, 983
  in abscess of liver, 1021
  in amyloid liver, 1046
  in cirrhosis of liver, 1000
  in fatty liver, 1050
  in hyperaemia of liver, 988
  in lithaemia, 971
  in morbid dentition, 376
  in acute oesophagitis, 416
  in chronic oesophagitis, 417
  in dilatation of oesophagus, 434
  in oesophageal paralysis, 430
  in acute pancreatitis, 1120
  in carcinoma of pancreas, 1127
  in acute peritonitis, 1151
  in tubercular peritonitis, 1168
  in acute pharyngitis, 398, 399
  in phosphorus-poisoning, 1033
  in purpura, 193
  in rachitis, 159
  in acute rheumatism, 69
  in chronic articular rheumatism, 74
  in gonorrhoeal rheumatism, 107
  in rheumatoid arthritis, 102
  in scrofula, 249
  in scurvy, 183
  in cancer of stomach, 576
  in dilatation of stomach, 603, 608
  in simple ulcer of stomach, 519-522
  in aphthous stomatitis, 330
  in catarrhal stomatitis, 325
  in syphilitic children, 315
  in thrush, 335
  in tonsillitis, 388
  in trichinosis, 962

Digestion, disturbances of, in Anchylostomum duodenale, 956
    in Ascaris lumbricoides, 953
    in ascites, 1177
    in constipation, 853
    in pseudo-membranous enteritis, 765
    from presence of gall-stones, 1070
    in gout, 118
    in hepatic glycosuria, 974
    in intestinal hepatitis, 993
    in intestinal ulcer, 826
    in lithaemia, 969
    in abscess of liver, 1013
    in echinococci of liver, 1104
    in fatty liver, 1048
    in carcinoma of pancreas, 1125
    in tubercular peritonitis, 1166
    in suppurative pylephlebitis, 1100
    in non-malignant stricture of rectum, 886
    in acute rheumatism, 27
    in gonorrheal rheumatism, 104
    in muscular rheumatism, 76
    in scurvy, 173
    in tabes mesenterica, 1189
    in tape-worm, 940
    in trichinosis, 960
    in typhlitis and perityphlitis, 819

Digitalis, use of, in ascites, 1179
  stupes, use of, in cirrhosis of liver, 1001

Dilatation of bowel in dysentery, 812
  of oesophagus, 430
    in organic stricture, 424
  forcible, in organic stricture of oesophagus, 426
  of stomach, 586
  acute, of stomach, 610
  of stomach in chronic gastritis, 472
    in gastric cancer, 566
  in simple ulcer of stomach, 503
  in anal fissure and rectal ulceration, 912
  of rectal pouches, 885
  in non-malignant rectal stricture, 917
  and incision of rectum for sphincterismus, 916

Dilators, use of, in cancer of oesophagus, 428

Diluents, use of, in chronic gastritis, 477

Diphtheria distinguished from acute pharyngitis, 396
  influence of, on causation of acute peritonitis, 438
  distinguished from tonsillitis, 387

Discharges, characters of, in dysentery, 796, 803
  of fistula in ano, 898
  mucous, in non-malignant stricture of rectum, 886
    and purulent, in ulceration of rectum and anus, 894

Disinfectants, use of, in cancrum oris, 343

Disinfection in acute intestinal catarrh, 688
  of discharges of dysentery, 808

Dislocation of intestine as a cause of obstruction, 851

Displacements of stomach, 617

Dissemination of echinococcus, 944

Distomum conjunctum, 947
  crassum, 948
  hepaticum, 946, 1109
  heterophyes, 948
  lanceolatum, 947, 1109
  ophthalmobium, 948
  ringeri, 948
  sinense, 947

Diuresis, influence on causation of constipation, 642

Diuretics, use of, in ascites, 1178

Diverticula of stomach, 617

Dogs, infection of Taenia echinococcus, liability to, from association
        with, 945

Douche, cold, use of, in constipation, 653

Drinking-water, dissemination of Ascaris lumbricoides by, 952
  necessity of pure, in prevention of dysentery, 808

Dropsy, general, in amyloid liver, 1044
    in chronic intestinal catarrh, 709
  of gall-bladder from biliary calculi, 1077

Drowsiness in entero-colitis, 735, 736

Dry colic, 662

Dryness, influence on causation of dysentery, 788

Ductus communis choledochus, stenosis of, 1082
      seat of occlusion of, 1083, 1084
  pancreaticus, obstruction, 1129

Duodenal catarrh complicating diabetes mellitus, 210
  form of gastric ulcer, etiology, 825
    of intestinal cancer, symptoms, 870
    of chronic intestinal catarrh, diagnosis, 711
  ulcers, in chronic intestinal catarrh, 703, 713

Duodenitis, 667, 682
  acute, relation to integumental burns, 682

Duodenum, congenital stricture of, 836
  lesions of, in entero-colitis, 737
    in acute intestinal catarrh, 674
  perforation of, by gall-stones, 1068-1074

Durande's solvent for biliary calculi, 1080

Duration of catarrh of bile-ducts, 1055
  of biliousness, 967
  of occlusion of biliary passages, 1092
  of cholera infantum, 723
  of cholera morbus, 746
  of diabetes mellitus, 210
  of enteralgia, 660
  of pseudo-membranous enteritis, 774
  of parenchymatous glossitis, 362
  of acute gout, 119
  of paroxysms of hepatic colic, 1071
  of hepatic glycosuria, 974
  of cancer of intestines, 871-873
  of acute intestinal catarrh, 682
  of intestinal indigestion, 630
  of intestinal obstruction, 862
  of intestinal ulcer, 827
  of acute internal strangulation of intestines, 843
  of intussusception, 849
  of jaundice, 981
  of abscess of liver, 1017
  of acute yellow atrophy of liver, 1029
  of amyloid liver, 1044
  of carcinoma of liver, 1039
  of cirrhosis of liver, 999
  of fatty liver, 1049
  of hydatids of liver, 1105
  of hyperaemia of liver, 987
  of lithaemia, 970
  of acute oesophagitis, 414
  of spasmodic stricture of oesophagus, 420, 421
  of carcinoma of pancreas, 1126
  of obstruction of pancreatic ducts, 1131
  of chronic interstitial pancreatitis, 1122
  of perihepatitis, 989
  of acute peritonitis, 1143
  of acute pharyngitis, 395, 396
  of syphilitic pharyngitis, 407
  of phosphorus-poisoning, 1032
  of suppurative pylephlebitis, 1101
  of acute rheumatism, 44
  of chronic articular rheumatism, 72
  of gonorrhoeal rheumatism, 106
  of muscular rheumatism, 76
  of acute variety of general rheumatoid arthritis, 80
  of chronic variety of general rheumatoid arthritis, 82
  of aphthous stomatitis, 329
  of catarrhal stomatitis, 323
  of mercurial stomatitis, 346
  of stomatitis ulcerosa, 337
  of cancer of stomach, 559
  of simple ulcer of stomach, 501
  of transmission power of syphilis, 257-260
  of tabes mesenterica, 1193
  of thrush, 334
  of trichinosis, 960
  of typhlitis and paratyphlitis, 820

Dyscrasia, gouty, symptoms of, 120

Dysenteric ulceration, influence on causation of abscess of liver,
        1004

DYSENTERY, 777
  Definition, 777
  Etymology, 777
  History, 777
    Ancient, 777-780
    Modern, 780-784
  General remarks, 784
    Nature, 784
    Primary nature, 784
    Secondary nature, 784
    Periodicity of recurrence, 784, 786
    Tendency to circumscription, 785
    A disease of armies, 785, 786
  Etiology, 786
    Climate, influence on causation, 786
    Hot seasons, influence on causation, 787
    Moisture, influence on causation, 788
    Dryness, influence on causation, 788
    Decay of animal and vegetable matter, 787, 789
    Atmospheric changes, 789
    Taking cold, influence on causation, 789, 790
    Nervous influence, 790
    Food, irritating and improper, 791
    Water, impure, 791
    Dejecta, influence on causation, 791
      mechanical irritation of colon by, 791
      propagation of the disease by, 792
    Specific nature, 792
    Micro-organism, influence on causation, 792
    Contagiousness, 793, 794
    Poison, duration of activity of, 794, 795
  Pathology, 796
    Local nature, 796
    Discharges, characters of, 796, 803
  Morbid anatomy, 797
    Mucous membrane, an inflammation of, 797
    Lesions of catarrhal form, 797
    Mucous membrane, state of, 798
    Cells, desquamation of, 798
    Follicles, intestinal, alterations in, 798
    Protuberances of mucosa, 798, 799
    Tenesmus, cause of, 799
    Of pseudo-membranous form, 799
    False membranes, formation, 799
    Ulcers, character and seat of, 799
    Perforation, 799
      date of occurrence, 800
    Perityphlitis, lesions of, 800
    Of chronic form, 800
    Ulceration, seat and character, 800
    Cicatrization in, 800
    Mesenteric glands, lesions of, 801
    Kidneys, lesions of, 801
    Joints, lesions of, 801
    Liver, lesions of, 801
      abscess of, 801
  Symptoms, 802
    Onset, 796, 802
      Pains of, 796, 802
        seat and character, 802
        physiognomy during, 802
    Tenesmus, 796, 802
    Heat of rectum, 796, 802
    Vomiting, 803, 804
    Strangury, 803
    Prolapsus ani, 797, 803
    Stools, 796, 803
      character, 796, 803
      bloody, 796, 803
      boiled-sago matter in, 803
    Fever, 796
    Skin, state, 796, 804
    Abdomen, state, 796, 804
    Typhoid state, occurrence of, 797, 804
    Tongue, state, 804
    Pulse, 804
    Physiognomy, 796
    Appetite impaired, 796, 804
    Brain, condition, 804
    Pyaemia, occurrence of, 797, 804
    Gangrene of intestine, 804
  Complications and sequelae, 805
    Rheumatism, 805
    Paralysis, 805
      seat, 805, 806
    Hepatic abscess, 806
    Kidney disease, 806
    Parotitis, 806
    Hyperaesthesia of intestinal mucous membrane, 806
  Diagnosis, 806
    From intestinal catarrh, 807
      Typhoid fever, 807
      Cholera morbus, 807
      Cancer of rectum, 807
      Intussusception, 807
  Prognosis, 807
  Mortality, 807
  Prophylaxis, 808
    Prevention of over-crowding, 808
    Cleanliness, 808
    Ventilation, 808
    Drinking-water, necessity of good, 808
    Disinfection of discharges, 808
    Food, improper, avoidance of, 808
    Cold, avoidance of, 808
  Treatment, 809
    Rest, 809
    Diet, 809, 812
    Local, 809
    Of ulcers, 812
    Of paralysis, 813
    Of abscess of liver, 813
    Of rheumatism, 813
    Change of air, 813
    Laxatives, use of, 809
    Enemata, use of, 809
    Irrigation of bowel, 809
        method, 809, 810
      by ice-water, 810
    Nitrate of silver, use of, 809, 812
    Salicylic acid, use of, 809
    Corrosive sublimate, use of, 809
    Ipecacuanha, use of, 810
      mode of administering, 811
    Opium, use of, 811
    Alum, use of, 810
    Stimulants, use of, 812
    Ergotin, use of, 812
    Carbolic acid, use of, 810
    Dilatation of bowel, 812
    Electricity, use of, 813

Dysentery as a cause of intestinal ulcer, 824
    of hemorrhage from bowels, 831

DYSPEPSIA, FUNCTIONAL, 436
  Definition, 436
  Synonyms, 436
  Etiology, 438
    Predisposing causes, 438
    Depressed vitality, 438
    Heredity, 438
    Age, 438, 439
    Anaemia, 439
    Febrile states, 440
    Exhaustion of nerves of organic life, 440
    Mental state, influence on digestion, 437
    Nervous system, influence on digestion, 437
    Gastric juice, action of, 437
    Privation and want, 441
    Deficient gastric secretion, 441
    Gastric juice, analysis of, 442
    Exciting causes, 442
    Errors of diet, 442
    Excess of nitrogenous food, 443
    Unwholesome food, 443
    Over-eating, 444
    Restricted regimen, 444
    Defective cookery, 445
    Hasty eating, 445
    Imperfect mastication, 445
    Irregularity in meals, 446
    Spirit-drinking, 446
    Hepatic disturbance, 447
    Pancreatic disease, 447
    Constipation, 447
    Nervous sympathy, 448
    Pregnancy, 448
    Menstruation, 448
    Uterine disease, 448
    Cardiac disease, 448
    Pulmonary disease, 448
  Symptoms, 448
    Fulness after meals, 448
    Pain, seat and character, 448
    Flatulence, 449
    Nature of eructations, 449
    Regurgitation, 449
    Nature of liquids regurgitated, 449
    Cardialgia, 449
    Nausea and vomiting, 449
    Vomiting, time of, 450
    Vomit, character of, 450
    Tongue, condition of, 450
    Constipation, 450
    Urine, condition of, 451
    Gastric vertigo, 451
    Skin diseases, 451
    Disturbed innervation, 451
    Languor and drowsiness, 451
    Palpitation and cough, 451
    Hypochondriasis, 451
    Depression of spirits, 451
    Sleeplessness, 451
  Pathology, 451
    Atrophy of mucous membrane of stomach, 451
    Fatty and amyloid degeneration of stomachal walls, 451
  Diagnosis, 452
    From subacute or chronic gastritis, 452
    From gastric ulcer, 452
    From gastric carcinoma, 452
  Treatment, 452
    Removal of cause, 452
    Improvement of general health, 452
    Diet, 452
      kinds of, 453
    Use of peptonized food, 453
    Exercise, 454
    Fresh air, 454
    Mental and moral means, 454
    Travel, 455
    Pain, gastric, 459
    Anaemia, 457
    Hepatic form, 457
    Constipation, 458
    Nausea and vomiting, 458
    Use of bitters, 455
      of nerve-tonics, 455
      of nux vomica and strychnia, 455
      of mineral acids, 456
      of ipecacuanha, 456
      of pepsin, 456
      of bismuth, 457
      of iron, 457
        form of, 457
      of silver salts, 457
      of arsenic, 457
      of mercury in hepatic forms, 457
      of aperient mineral waters, 458
      of belladonna in constipation, 458
      of nux vomica in constipation, 458
      of aloes in constipation, 458
      of tincture of colocynth, 458
      of hydrocyanic acid, 458, 459
      of creasote, 458
      of carbolic acid, 459
      of ice, 458
      of lime-water, 458
      of sulphurous acid, 459
      of alkalies, 458
      of alcohol, 459
      of hydrotherapy, 457
      of electricity, 457

Dyspepsia in diabetes mellitus, 204
  in gout, 118

Dysphagia, in acute oesophagitis, 413
  in cancer of oesophagus, 427
  in dilatation of oesophagus, 431
  in organic stricture of oesophagus, 423
  in oesophageal paralysis, 429
  in acute pharyngitis, 394
  in cancer of stomach, 546

Dysphonia, in cancer of oesophagus, 427
  in organic stricture of oesophagus, 423

Dyspnoea in enteralgia, 661
  in acute gastritis, 467
  in chronic gastritis, 475
  in dilatation of stomach, 595

Dyspnoeic coma, in gastric cancer, 555

Dysuria, complicating gout, 124
  in paratyphlitis, 819
  in peri-rectal and anal abscesses, 896


E.

Early life, influence on causation of rachitis, 141, 142
    cause of tendency to scrofula in, 242

Ear disorders in hereditary syphilis, 282

Eating, hasty, influence on causation of functional dyspepsia, 445

Echinococci, seat of deposit in liver, 1102
  mode of growth in liver, 1102, 1103

Echinococcus of liver, 1101

Echinorhynchus gigas, 949

Ecraseur, use of, in hemorrhoids, 925

Eczema of anus, 892
  of genitalia in diabetes mellitus, 205
  complicating gout, 121

Eczemas, tendency to, in scrofula, 245
  influence on causation of scrofula, 237

Effusions, pericardial, in acute rheumatism, treatment, 64

Elaterium, use of, in ascites, 1179

Electricity, use of, in catarrh of bile-ducts, 1057
    in constipation, 653
    in dysentery, 813
    in functional dyspepsia, 457
    in impaction of feces, 919
    in gastralgia, 463
    in jaundice, 983
    in lithaemia, 973
    in intestinal obstruction, 864
    in dilatation of oesophagus, 435
    in oesophageal paralysis, 430
    in spasmodic stricture of oesophagus, 422
    in dilatation of stomach, 608
    in rheumatoid arthritis, 101

Electrolysis in hydatids of liver, 1108

Elephantiasis in Filaria sanguinis, 964

Emaciation in cholera infantum, 742
  in chronic gastritis, 475
  in acute intestinal catarrh, 682
  progressive, in chronic intestinal catarrh, 709
  in amyloid liver, 1044
  in carcinoma of liver, 1038
  in cirrhosis of liver, 999
  in cancer of oesophagus, 427
  in pancreatic diseases, 1114
  in carcinoma of pancreas, 1124
  in chronic intestinal pancreatitis, 1122
  in obstruction of pancreatic ducts, 1131
  in tubercular peritonitis, 1166
  in cancer of stomach, 551

Emboli, influence of, on causation of phlegmonous form of acute
        oesophagitis, 411
      of suppurative pylephlebitis, 1097

Embolism as a cause of hemorrhage from bowels, 831
    of duodenal ulcers in chronic intestinal catarrh, 703
  complicating cancer of stomach, 560
  in simple ulcer of stomach, 510
  of portal vein, 1095
  of cerebral arteries in acute rheumatism, 39
  of lungs and spleen, in scurvy, 181
  influence on causation of abscess of liver, 1004

Embryo of Trichina spiralis, migration of, 959

Emetics, use of, in jaundice, 982
    in cholera morbus, 724
    in hepatic colic, 1082
    in phosphorus-poisoning, 1033

Emotions, influence of, on production of jaundice, 976

Emphysema, diagnosis of, from abscess of liver, 1020
    from perforation, in simple gastric ulcer, 509

Encephaloid carcinoma of rectum and anus, 904

Endarteritis in chronic articular rheumatism, 72

Endocarditis in acute rheumatism, 28, 33, 34
  complicating gonorrhoeal rheumatism, 106

Endo- and pericarditis complicating rheumatic arthritis, 83

Enemata, anodyne, use of, in irritable rectum, 919
  in impaction of feces, 918
  in pseudo-membranous enteritis, 774
  in carcinoma of pancreas, 1128
  in rectal alimentation, amount of, 928
    substances employed, 929
  medicated, use of, in chronic intestinal catarrh, 714, 717, 718
  nutrient, in abscess of liver, 1021
    in cancer of oesophagus, 428
  of tobacco, use of, in enteralgia, 666
  use of, in catarrh of bile-ducts, 1057
    in constipation, 655
    in dysentery, 809
    in enteralgia, 666
    in entero-colitis, 760
    in hemorrhoids, 923
    in acute intestinal catarrh, 697
    in intestinal ulcer, 823
    in pruritus ani, 917
    in seat-worms, 951

ENTERALGIA (INTESTINAL COLIC), 658
  Synonyms, 658
  History, 658
  Nature, 658, 659
  Definition, 658, 659
  Etiology, 659
    Heredity, 659
    Sex, 659
    Cachexiae of chronic disease, 659
    Morbid blood-conditions, 659
    Syphilis, 660
    Malaria, 660
    Lead, copper, and arsenic poisoning, 660
    Venereal excess, 660
    Abuse of tobacco and alcohol, 660
    Idiosyncrasy, 660
    Reflex and sympathetic causes, 660
    Ovarian and uterine irritation, 660
    Disease of abdominal viscera, 660
    Organic disease of brain and spinal cord, 660
    Cold, 660
    Indigestion, 660
    Food, 660
    Constipation, 660
    Foreign bodies, 660
    Cathartics, 660
  Symptoms, 660
    Pain, 660, 661
      character and seat of, 660, 661
      duration of paroxysms of, 660
      effect of pressure on, 661
    Eructations and borborygmi, 661
    Nausea and vomiting, 661
    Tongue, condition of, 661
    Physiognomy, 661
    Pulse, 661
    Dyspnoea, 661
    Muscular cramps, 661
    Bowels, state of, 661
    Abdomen, state of, 661
    Micturition, painful, 661
    Collapse, 662
    Nervous, 662
    Delirium, 662
    Convulsions, 662
    Vertigo, 662
  Duration, 660
  Varieties, 662
    Alcoholic form, 662
    From opium-eating, 662
    Neurotic form, 662, 663
      symptoms, 663
      pain, 663
      duration, 663
      paralysis, 663
  Diagnosis, 663
    A true neuralgia, 663
    From lumbo-abdominal neuralgia, 663
      dermalgia, 664
      gastralgia, 664
      rheumatic pains, 664
      ileus, 664
      hepatic colic, 664
      renal colic, 664
      syphilitic colic, 664
      intestinal catarrh, 664
  Prognosis, 664
  Termination, 664
    in death, 664
    in recovery, 664
  Treatment, 664
    Removal of cause, 664, 665
    Of nervous form, 665
    Flatulent form, 665
    Hysterical form, 664
    Preventive, 665, 666
    Constitutional, 665
    Local, 665
    Use of bromides, 665
      of iodide of potassium, 665
      of iron, 665
      of alum, 665
      of arsenic, 665
      of nitrate of silver, 665
      of belladonna, 665
      of valerianate of zinc, 665
      of antispasmodics, 665
      of opium, 665
      of heat, 665
      of cold, 665
      of sinapisms, 665
      of spinal applications, 664, 665
      of cathartics, 665
      of chloroform, 665
      of puncturing of colon, 665
      of alkalies, 666
      of creasote, 666
      of enemata, 666
      of tobacco, 666
      of phosphate of sodium as preventive, 666
    Diet, 666
      milk, 666

Enteritis, catarrhal, complicating gastric cancer, 560

ENTERITIS, PSEUDO-MEMBRANOUS, 763
  Synonyms, 763
  Definition, 763
  History, 763
  Etiology, 764
    Age, influence on causation, 764
    Sex, influence on causation, 764
    Temperament, influence on causation, 764
    Determinative causes, 765
    Perversion of nutrition and innervation, 765
    Wet and cold, 765
    Food, improper, 765
    Fecal impaction, 765
    Cathartics, abuse, 765
    Parasitic growths, relation to causation, 765
    Ovarian disease, relation to causation, 765
    Menstrual disorders, relation to causation, 765
    Prostatic disease, relation to causation, 765
  Symptoms, 765
    Digestive derangements, 765
    Obscurity of early, 765
    Initial, 765
    Irregularity of bowels, 765
    Abdominal soreness, 765
    Vomiting of mucus and blood, 765
    Heat in rectum, 765
    Depression of vital powers, 765, 766
    Loss of strength, 765, 766
    Pulse, state of, 766
    Tongue, state of, 766
    Mouth, state of, 766
    Ulceration of tonsils, 766
    Physiognomy, 766
    Skin, state of, 766
    Urine, condition of, 766
    Of paroxysms, 766
    Stools, character of, 766
      mucous exudates in, 766
      frequency of, 766
      painful, 766
    Pain, character and seat of, 766
    Appetite, loss of, 766
    Nervous disturbances, 766, 767
    Hysterical, 767
    Perversions of sensation, 767
    Headache, 767
    Special senses, perversion of, 767
    Uterine disorders, 767
  Pathology, 767
    Views as to nature of, 767
    Croupous nature of, 767, 768
    Inflammatory nature of, 768
  Morbid anatomy, 769
    Mucous membrane, lesions of, 769
    Restriction of false membrane to large intestine, 769
    False membrane, characters, 769, 770
      chemical characters, 772
      microscopic appearance of, 770
      origin from muciparous glands, 772
  Diagnosis, 773
    From mucous discharges of chronic diarrhoea, 773
      enteritis, 773
      fatty discharges of chronic hepatic and duodenal disease, 773
      discharges of cholera, 773
  Prognosis, 774
    Cause of death, 774
  Duration, 774
  Treatment, 774
    Of paroxysms, 774
    Of intervals, 775
    Local, 775
    General, 775
    Hygienic, 776
    Diet, 776
    Exercise, 776
    Use of enemata, 774
      of castor oil, 774
      of mercury, 774
      of rhubarb, 774
      of sodium bicarbonate, 774
      of ipecacuanha, 775
      of sulphur, 775
      of Plummer's pill, 775
      of morphia, hypodermically, 775
      of opium, 775
      of nitrate of silver, 775
      of sulphate of zinc, 775
      of sulphate of copper, 775
      of iron, 775
      of nitro-muriatic acid, hot solutions locally, 775
      of copaiba and cubebs, 775
      of tar, 775
      of arsenic, 775
      of corrosive sublimate, 775
      of iodide of potassium, 775
      of cod-liver oil, 776
      of counter-irritation, 776
      of mineral waters, 776

Enteroliths, influence on causation of intestinal obstruction, 838

Enterotomy in intestinal obstruction, 867

Entorectomy in intestinal obstruction, 866

Epigastric prominence, in dilatation of stomach, 596
  fulness in catarrh of bile-ducts, 1053
  tenderness, in jaundice, 979
    in pancreatic diseases, 1116, 1119

Epileptic attacks from Ascaris lumbricoides, 953
    from tape-worm, 940

Epistaxis in occlusion of bile-ducts, 1089
  in acute yellow atrophy of liver, 1028
  in purpura haemorrhagica, 188
  in scurvy, 179, 180

Epithelial form, flat and cylindrical-celled, of gastric cancer, 564,
        565
  desquamation in acute intestinal catarrh, 677

Epithelium, detachment of, in superficial glossitis, 355
  changes in, in acute oesophagitis, 411
    in acute peritonitis, 1134, 1135
    in chronic pharyngitis, 403
    in tonsillitis, 384

Epsom salts, use of, in constipation, 655
  and senna, use of, in ascites, 1179
    in Oxyuris vermicularis, 951

Erethistic form of scrofulous habit, 243

Ergot, local use of, in chronic pharyngitis, 405
  Use of, in diabetes mellitus, 227
    in chronic intestinal catarrh, 718
    in ulceration of oesophagus, 418
    in purpura, 193
    in stomatorrhagia, 371

Ergotin, local use, in prolapsus ani, 921
  Use of, in dysentery, 812
    in hemorrhage from bowels, 834
    in hemorrhages of hepatic cirrhosis, 1002
    in hemorrhoids, 923, 924
    in intestinal ulcer, 829
    in acute yellow atrophy of liver, 1030
    in simple ulcer of stomach, 525

Erosions, hemorrhagic, of stomach, 529
  of teeth in hereditary syphilis, 298

Errors in diet, influence on causation of functional dyspepsia, 442
      of chronic gastritis, 470
      of gout, 112
    as a cause of jaundice, 977

Eructations in functional dyspepsia, 449
  in chronic gastritis, 473
  in cancer of stomach, 540
  in dilatation of stomach, 593
  and borborygmi in enteralgia, 661

Eruption of purpura haemorrhagica, 188
    rheumatica, 189
    simplex, 187

Eruptive diseases, influence on causation of acute gastritis, 464
  fevers, influence on causation of chronic gastritis, 470
        of acute intestinal catarrh, 671
        of scrofula, 237

Erysipelas as a cause of infantile peritonitis, 1172
  complicating mercurial stomatitis, 346

Erysipelatous form of acute pharyngitis, nature, 393
    of acute pharyngitis, symptoms, 396
    of acute pharyngitis, treatment, 399

Erythema intertrigo, 892
  of hereditary syphilis, 277
  complicating gonorrhoeal rheumatism, 106

Erythematous form of acute pharyngitis, symptoms, 394

Eschar in cancrum oris, characters of, 340

Ether, use of, in hepatic colic, 1082

Etiology of ascites, 1173
  of catarrh of bile-ducts, 1051
  of biliary calculi, 1063
  of cancrum oris, 339
  of cholera morbus, 720
  of constipation, 639, 850
  of diabetes mellitus, 203
  of dysentery, 786
  of functional dyspepsia, 438
  of enteralgia, 659
  of pseudo-membranous enteritis, 764
  of entero-colitis, 726
  of fistula in ano, 897
  of gastralgia, 459
  of acute gastritis, 464
  of catarrhal form of acute gastritis, 464
  of erythematous form of acute gastritis, 465
  of chronic gastritis, 470
  of superficial glossitis, 355
  of chronic superficial glossitis, 366
  of parenchymatous glossitis, 359
  of glossitis parasitica, 358
  of glossanthrax, 368
  of gout, 109
  of hemorrhoids, 882
  of internal hemorrhoids, 884
  of hemorrhage from bowels, 830
  of acute intestinal catarrh, 669
  of chronic intestinal catarrh, 699
  of intestinal indigestion, 623
  of intestinal ulcer, 823
  of cancer of intestines, 868
  of jaundice, 975
  of abscess of liver, 1002
  of acute yellow atrophy of liver, 1023
  of amyloid liver, 1040
  of carcinoma of liver, 1033
  of cirrhosis of liver, 990
  of fatty liver, 1046
  of hydatids of liver, 1101
  of hyperaemia of liver, 983
  of macroglossia, 350
  of morbid dentition, 371
  of cancer of oesophagus, 429
  of dilatation of oesophagus, 430
  of spasmodic stricture of oesophagus, 419
  of organic stricture of oesophagus, 422
  of ulceration of oesophagus, 418
  of acute oesophagitis, 409
  of chronic oesophagitis, 416
  of pancreatic diseases, 1114
  of acute secondary pancreatitis, 1128
  of carcinoma of pancreas, 1123
  of chronic intestinal pancreatitis, 1121
  of obstruction of pancreatic duct, 1129
  of acute diffuse peritonitis, 1136
  of infantile peritonitis, 1172
  of acute pharyngitis, 390
  of chronic pharyngitis, 402
  of tuberculous pharyngitis, 400
  of syphilitic pharyngitis, 406
  of proctitis, 887
  of pruritus ani, 909
  of purpura, 190
  of hypertrophic stenosis of pylorus, 615
  of rachitis, 137
  of dilatation of rectal pouches, 885
  of fissure of anus and rectum, 888
  of neuralgia of rectum, 909
  of non-malignant rectal stricture, 885
  of obstruction of rectum, 889
  of prolapse of rectum, 881
  of ulceration of rectum and anus, 894
  of peri-rectal and anal abscesses, 895
  of rheumatism, acute, 19
  of chronic articular rheumatism, 69
  of gonorrhoeal rheumatism, 102
  of muscular rheumatism, 74
  of rheumatoid arthritis, 88
  of atrophy of stomach, 616
  of cancer of stomach, 531
  of cirrhosis of stomach, 612
  of dilatation of stomach, 587
  of acute dilatation of stomach, 610
  of hemorrhage from stomach, 580
  of rupture of stomach, 618
  of simple ulcer of stomach, 481
  of stomatorrhagia, 370
  of aphthous stomatitis, 325
  of catarrhal stomatitis, 321
  of mercurial stomatitis, 344
  of stomatitis ulcerosa, 336
  of scrofula, 232
  of scurvy, 169
  of tabes mesenterica, 1185
  of thrombosis and embolism of portal vein, 1095
  of thrush, 331
  of tonsillitis, 380
  of tuberculous ulceration of tongue, 369
  of typhlitis, 814

Etymology of dysentery, 777

Euonymin, use of, in biliousness, 968
    in intestinal indigestion, 636
    in jaundice, 982
    in acute yellow atrophy of liver, 1030
    in hepatic colic, 1082

Eustrongylus gigas, 957

Evacuation of abscess of liver, 1021

Exacerbations, frequency of, in chronic gout, 121

Exanthemata, acute, influence on causation of tabes mesenterica, 1186

Exanthematous form of acute pharyngitis, nature, 393

Excision, in prolapsus ani, 919
  in hypertrophy of tongue, 354
  of rodent ulcer of rectum, 913
  of cancer of rectum, 914, 915

Exercise, importance of, in biliary calculus state, 1079
  in lithaemia, 971
  in pseudo-membranous enteritis, 776
  necessity of, in functional dyspepsia, 454
    in hyperaemia of liver, 988
    in treatment of gout, 130, 131
    in scrofula, 252
  value of, in treatment of constipation, 651, 653
    in chronic intestinal catarrh, 714, 716
    in intestinal indigestion, 632

Expectoration in chronic pharyngitis, 404

Extractum pancreatis, in carcinoma of pancreas, 1128
    use of, in entero-colitis, 752
      in chronic interstitial pancreatitis, 1122, 1123

Extravasations of blood into hepatic tissues, in hyperaemia of liver,
        988

Extremities, appearance of, in rachitis, 155

Exudates in stools of pseudo-membranous enteritis, 766

Exudations, characters of, in gout, 115
  fibrinous, in local peritonitis, 1160
  thickness of, in tubercular peritonitis, 1167

Eye affections, complicating gonorrhoeal rheumatism, 106
  diseases, complicating rheumatoid arthritis, 84


F.

Facial paralysis in diabetes mellitus, 206

False membranes, cysts of, in acute peritonitis, 1134
    disposition of, in acute peritonitis, 1134
    in pseudo-membranous enteritis, 766
    characters of, in pseudo-membranous enteritis, 769-772
    thickness of, in tubercular peritonitis, 1167

Farinaceous foods, analysis of, 750, 751
    use of, in cholera infantum, 754
      in entero-colitis, 753, 754

Fatigue, influence of, on causation of gonorrhoeal rheumatism, 103
  and exhaustion, influence of, on causation of acute rheumatism, 22
  and strain, muscular, influence of, on causation of muscular
        rheumatism, 75

Fat in blood of diabetes mellitus, 207
  seat of deposit, in fatty liver, 1047, 1048

Fats and oils, absorption of, in digestion, 623

Fatty degeneration of pancreas, 1128
    of cells in scrofulous inflammation, 239
    of gastric walls in dilatation of stomach, 600
    of gastric vessels, in simple ulcer of stomach, 511
    gastric, influence on causation of dilatation of stomach, 590
    of heart, complicating cancer of stomach, 560
  infiltration of pancreas, 1128
  liver, 1046
  metamorphosis of pancreas, 1128
  stools in diseases of pancreas, 1115, 1122, 1125, 1131

Febrile states, influence of, on causation of functional dyspepsia,
        440
  affections, influence of, on causation of superficial glossitis, 355
  diseases, influence of, on causation of intestinal indigestion, 623

Fecal accumulations, in constipation, 644
  tumor, characters of, 852
  impaction, influence of, on causation of pseudo-membranous
        enteritis, 765
    in intestinal obstruction, treatment, 863
  vomiting, in gastric cancer, significance, 558
    in stricture of bowel, 856, 858
    in intestinal obstruction, 840, 843, 848

Feces, color, in jaundice, 978
  collection of, in vermiform appendix, as a cause of typhlitis, 814
  impaction of, treatment, 918
  wire-drawn, in non-malignant rectal stricture, 886

Feet, deformities of, in general rheumatoid arthritis, 82

Fehling's test for sugar in urine, 212

Fermentation test for sugar in urine, 212

Fetid secretions, in gangrenous form of acute pharyngitis, 396

Fever, in catarrh of bile-ducts, 1054
  in occlusion of biliary passages, 1090
  in constipation, 648
  in dysentery, 796
  in entero-colitis, 734, 736
  in acute gout, 119
  in hepatic colic, 1072
  in acute intestinal catarrh, 681
  in chronic intestinal catarrh, 709
  in jaundice, 980
  in acute secondary pancreatitis, 1121
  in suppurative pylephlebitis, 1099
  in tabes mesenterica, 1190
  in trichinosis, 960
  in typhlitis and perityphlitis, 818, 819

Fibrin, amount of, in blood of scurvy, 174

Fibrinous exudations in acute peritonitis, 1133, 1134
    in local peritonitis, 1160

Fibromata of stomach, 579

Filaria lentis, 964
  loa, 964
  medinensis, 962
  restiformis, 964
  sanguinis, 963
  trachealis, 964

Filth, influence of, on causation of entero-colitis, 730
      of tabes mesenterica, 1186

Fingers, clubbing of, in scrofula, 246

Fish as a source of Bothriocephalus latus, 939

Fissure of anus in cirrhosis of liver, 994
  of anus and rectum, 888

Fistula in ano, 897

Fistulae, biliary, 1068, 1074
  in constipation, 645, 648
  formation of, by gall-stones, 1068
    in chronic intestinal catarrh, 703
  gastro-colic, in simple ulcer of stomach, 508
  gastro-cutaneous, in simple ulcer of stomach, 500
  gastro-duodenal, in simple ulcer of stomach, 508
  gastro-pleural, in simple ulcer of stomach, 508
  in cancer of stomach, formation of, 558
  in ulceration of oesophagus, 418

Fistulous openings into viscera in acute pancreatitis, 1121

Flat-celled epithelial form of gastric cancer, 565

Flatulence in constipation, 646, 647
  in functional dyspepsia, 449
  in acute intestinal catarrh, treatment, 693
  in simple ulcer of stomach, 494
  and colic in intestinal indigestion, treatment, 636

Flatulent form of enteralgia, treatment, 665

Flesh-worm, 957

Flexure of thigh upon leg in paratyphlitis, 819

Flour-ball, use of, in infant feeding, 754, 755

Fluctuation in abscess of liver, 1011

Flukes, liver, 1109

Fluke-worms, 946

Foetus in utero, syphilitic infection of mother by, 262

Follicles, changes in, in acute oesophagitis, 412
  enlargement of, in chronic pharyngitis, 403
  intestinal, lesions of, in dysentery, 798

Follicular pharyngitis, 402
  ulcers in acute intestinal catarrh, 676
    of stomach, 529
  ulceration of chronic intestinal catarrh, treatment, 718
    of rectum and anus, 894

Fomentations, hot, in hepatic colic, 1082

Fontanels, condition of, in rachitis, 146

Food, amount of, ingested by healthy infants, 746
  certain, influence of, on causation of gastralgia, 460
  improper, influence of, on causation of biliary calculi, 1065
        of catarrh of bile-ducts, 1052
        of cholera morbus, 721
        of constipation, 643, 851
        of dysentery, 791
        of functional dyspepsia, 442, 443
        of enteralgia, 660
        of pseudo-membranous enteritis, 765
        of entero-colitis, 726
        of acute gastritis, 465
        of parenchymatous glossitis, 360
        of chronic intestinal catarrh, 700
        of intestinal indigestion, 625
        of diseases of pancreas, 1114
        of chronic pharyngitis, 402
        of rachitis, 144
        of aphthous stomatitis, 326
        of catarrhal stomatitis, 322
        of stomatitis ulcerosa, 336
        of scrofula, 232
        of tabes mesenterica, 1185, 1186
  inability to ingest large quantities of, in cirrhosis of stomach,
        613
  peptonized, use of, in functional dyspepsia, 453
      in chronic interstitial pancreatitis, 1122, 1123
  retention of, in dilatation of oesophagus, 431
  uncooked, as a cause of intestinal worms, 931

Foods, saccharine, use of, in diabetes mellitus, 220
  and drinks, admissible in diabetes mellitus, 220, 221
  certain, as a cause of spasmodic stricture of oesophagus, 420
  farinaceous, for infants, analyses, 750, 751
    use of, in cholera infantum and entero-colitis, 753

Foreign bodies, influence of, on causation of occlusion of biliary
        passages, 1084
        of enteralgia, 660
        of chronic intestinal catarrh, 700
        of typhlitis, 816, 817
    as a cause of hemorrhage of bowels, 830
      of chronic oesophagitis, 416

Formad on scrofulous peculiarity, 232

Formication of right leg in typhlitis and perityphlitis, 818

Frequency of stricture of bowel, 854
  of intestinal ulcer, 823
  of acute yellow atrophy of liver, 1023
  of cancer of stomach, 532
  of simple ulcer of stomach, 481, 482
  of tabes mesenterica, 1184

Friction sound in perihepatitis, 989

Frictions, use of, in cholera morbus, 724

Friedrichshall water, use of, in intestinal indigestion, 636

Fruit, necessity of, for prevention of scurvy, 183

Fulness after eating in functional dyspepsia, 448
  and weight in dilatation of stomach, 593

Functional dyspepsia, 436
  disorders of liver, 965
  diseases of stomach, 436
  obstruction of bowel, diagnosed from organic, 859

Furuncular eruptions in hereditary syphilis, 280

Furunculi of anus, 892


G.

Gall-bladder, changes in, from biliary calculi, 1066
  distension of, from occlusion of biliary ducts, 1085
  dropsy of, from biliary concretions, 1077
    from occlusion of biliary ducts, 1086
  lesions of, in chronic intestinal catarrh, 705
  puncture of, for relief of biliary calculi, 1081
      of occlusion of biliary passages, 1094
  and hepatic tubes, character of contents of, in occlusion of biliary
        ducts, 1085

Gallic acid, use of, in acute intestinal catarrh, 695
    in chronic intestinal catarrh, 717

Gall-stones, 1058
  diagnosis of presence of, 1078
  impaction of, 1074
  influence of, on causation of acute peritonitis, 1139
  as a cause of intestinal obstruction, 839
  migration of, 1067
    by artificial routes, 1068, 1074
    symptoms due to, 1070
  passage of, a cause of perihepatitis, 989
  presence of, as a cause of obstruction of pancreatic duct, 1130
    symptoms due to, 1069
  treatment, 1079

Galvanism, use of, in muscular rheumatism, 76

Gangrene in cancrum oris, date of appearance, 342
  of tongue in parenchymatous glossitis, 362
  of bowel in intussusception, 845, 849
  in acute oesophagitis, 413
  in acute pancreatitis, 1118
  occurrence of, in tonsillitis, 383

Gangrenous form of acute pharyngitis, 395

Gas in arteries from perforation in simple gastric ulcer, 510
  source of, in intestinal indigestion, 627

Gaseous distension of gut, in intestinal obstruction, tapping in, 865
  eructations in dilatation of stomach, nature of, 593

Gastralgia in cirrhosis of stomach, 613
  in acute rheumatism, 42

GASTRALGIA (CARDIALGIA, SPASM OF STOMACH), 459
  Definition, 459
  Varieties, 459
  Etiology, 459
    Predisposing causes, 460
    Depressed vitality, 460
    Nervous excitability, 460
    Female sex, 460
    Menstruation, 460
    Anaemia, 460
    Blood-poisons, 460
    Malaria, 460
    Gout and rheumatism, 460
    Certain foods, 460
    Disease of nerve-centres, 460
    Exciting causes, 460
    Venereal excesses, 460
    Abuse of narcotics, 460
    Reflex causes, 460
    Affections of bladder and kidneys, 460
      of uterus, 460
      of ovaries, 460
  Symptoms, 460
    Pain, 460
      character of, 460
      seat of, 460, 461
      hysterical phenomena, 461
      tongue, 461
      vomiting, 461
  Diagnosis, 461
    From inflammation of stomach, 461
      organic gastric affections, 461
      gastric ulcer and cancer, 461
      rheumatism of abdominal muscles, 462
      hepatic colic, 462
  Prognosis, 462
  Treatment, 462
    Radical, 462
    Palliative, 463
      of chlorosis and anaemia, 462
      of irritable nervous system, 463
      of hysterical phenomena, 463
      of pain, 463
    Use of iron, form, 462
      of quinine, 462
      of arsenic, 462
      of nux vomica and strychnia, 463
      of silver salts, 463
      of valerianate of zinc, 463
      of bromides, 463
      of electricity, 463
      of bismuth, 463
      of hydrocyanic acid, 463
      of morphia, 463
      of spirits of chloroform, 463
      of hot water, 463
    Travel, 463
    Change of air, 463

Gastralgia distinguished from enteralgia, 664

Gastrectasia. See _Dilatation of Stomach_.

Gastric catarrh of phthisis, treatment of, 478
  disease, chronic, influence on causation of atrophy of stomach, 616
  fluids of cancer of stomach, absence of free hydrochloric acid in,
        543
  glands, alterations in chronic gastritis, 472
  juice, action of, 437, 620, 621
    excess of, influence on causation of intestinal indigestion, 626
    erosion by, as a cause of intestinal ulcer, 824, 825
  secretion, deficient, as a cause of functional dyspepsia, 441
  tubules, alterations in chronic gastritis, 472
    atrophy of, in atrophy of stomach, 616
      in cirrhosis of stomach, 614
    degeneration of, in atrophy of stomach, 616
    origin of cancer of stomach from, 563, 564
  ulcer, artificial production of, 514
  vertigo, in functional dyspepsia, 451
  walls, thickening of, in cirrhosis of stomach, 614

GASTRITIS, ACUTE (ACUTE GASTRIC CATARRH), 463
  Definition, 463
  Varieties, 464
  Etiology, 464
    Predisposing causes, 464
    Of catarrhal form, 464
    Mechanical, 464
    Weak heart-action, 464
    Organic disease of heart and lungs, 464
        of liver, 464
    Gout and rheumatism, 464
    Malarious fevers, 464
    Passive gastric hyperaemia, 465
    Erythematous form, 465, 466
    Frequency in children, 465
    Eruptive disorders, 464
      fevers, 464
    Relation to brain disorders, 465
    Exciting causes, 465
    Catarrhal form, 465
    Improper food, 465
    Acrid and corrosive poisons, 465
    Alcohol, excessive use of, 465
    Scarlatina, 466
  Morbid anatomy, 466
    Difficulty in determining post-mortem changes, 466
    Catarrhal form, state of mucous membrane, 466
    Erythematous form, state of mucous membrane, 466
    Acute form, state of mucous membrane, 466
    Toxic form, state of mucous membrane, 466
  Symptoms, 467
    Acute toxic form, 467
    Erythematous form, 467
    Cholera infantum, 467
    In infants, 467
    Catarrhal form, 467
    Pain, 467
    Thirst, 467
    Vomiting, 467
    Vomit, character of, 467
    Physiognomy, 467
    Coldness of surface, 467
    Prostration, 467
    Pulse, 467
    Temperature, 467
    Hiccough, 467
    Tongue, state of, 467
    Urine, state of, 467
    Cerebral symptoms, 467
    Headache, 467
    Vertigo, 467
    Mental depression, 467
    Dyspnoea, 467
    Diarrhoea, 467
    Pain after eating, 467
  Diagnosis, 468
    From brain disease, 468
    Remittent or typhoid fevers, 468
    Meningitis, 468
    Peritonitis, 468
  Prognosis, 468
  Treatment, 468
    Severe forms, 468
    Rest of inflamed organ, 468
    Diet, 468
    Of thirst, 468
    Of vomiting, 469
    Mild forms, 469
    Rest, 469
    Diarrhoea, 469
    Pyrexia, 469, 470
    Pain, 469
    In children, 469
    Convalescence, 470
    Use of ice, 468
      stimulants, 469
      ipecacuanha, 469
      calomel, 469
      sod. bicarbonate, 469
      bismuth, 469
        salicylate, 469
      demulcent drinks, 469
      hydrocyanic acid, 469
      counter-irritation, 469
      baths, cold, 470

GASTRITIS, CHRONIC (CHRONIC GASTRIC CATARRH), 470
  Definition, 470
  Etiology, 470
    Functional gastric disorders, 470
    Interference with portal circulation, 470, 471
    Rheumatism and gout, 470, 471
    Phthisis, 470, 471
    Renal disease, 470
    Eruptive diseases, 470
    Malarious fevers, 470, 471
    Alcohol, excessive use of, 470
    Errors of diet, 470
    Decomposition of ingested aliment, 470
    Weak digestive power, 470
    Injudicious medication, 470
    Disease of heart and lungs, 471
    Anaemia, 471
  Anatomical characters, 471
    Lesions of mucous membrane, 471, 472
    Softening of mucous membrane, 471
    Thinning of gastric walls, 471
    Scirrhous state of pyloric orifice, 471
    Ulceration of pyloric orifice, 472
    Hypertrophy of pyloric orifice, 472
    Dilatation of stomach, 472
    Hypertrophy of interstitial tissue, 472
    Glands, gastric, alterations in, 472
    Tubules, gastric, alterations in, 472
  Symptoms, 472
    Of difficult digestion, 473
    Pain, 473
    Burning sensation in epigastrium, 473
    Tenderness on pressure of epigastrium, 473
    Appetite, impaired, 473
    Nausea and vomiting, 473
    Vomiting, time of, 473
    Vomit, nature of, 473
    Tongue, condition of, 473
    Breath, condition of, 473
    Thirst, 473
    Jaundice, 474
    Sympathetic nervous symptoms, 474
    Mucous membranes, freedom from pain in disorders of, 474
      sympathetic phenomenon in disorders of, 474
    Gastric irritation, tendency to terminate in cerebral
        inflammation, 474
    Convulsion, 474
    Headache, 474
    Vertigo, 474
    Heart, disturbance of, 474
    Dyspnoea, 475
    Constipation, 475
    Piles, 475
    Diarrhoea, 475
    Urine, state of, 475
    Emaciation, 475
  Diagnosis, 475
    From atonic dyspepsia, 475
      Gastric cancer, 476
        ulcer, 476
  Treatment, 476
    Importance of rest, 476
    Diet, 476
    Milk, use of, 476
    Diluents, use of, 477
      mode of administering, 477
    Gum-water, 477
    Use of alkaline carbonates, 477
      Alkaline mineral waters, 477
      Carlsbad water, 477
      Marienbad waters, 477
      Hot water, 477
        mode of administering, 478
      Bismuth, 478
      Charcoal, 478
      Mercurials, 478
      Nitrate of silver, 478
      Astringents, 478
      Stomach-pump, 478
      Counter-irritation, 479
      Mucous vomiting, 478
      Constipation, 478

Gastric catarrh of phthisis, 475

Gastritis, catarrhal, complicating simple ulcer of stomach, 502
  chronic catarrhal, as a cause of cirrhosis of stomach, 612
    complicating gastric cancer, 560
    influence on causation of dilatation of stomach, 590

Gastro-duodenal catarrh, signs of, in acute yellow atrophy of liver,
        1027

Gastrodynia, 459

Gastro-intestinal canal, state of, in cancrum oris, 341
    condition of, in parenchymatous glossitis, 362
      in hereditary syphilis, 306
    catarrh, signs of, in catarrh of bile-ducts, 1053
    in carcinoma of liver, 1038
    of cirrhosis of liver, treatment, 1001
    signs of, in hyperaemia of liver, 986
  catarrhal symptoms in jaundice, 977
  disorders, influence on causation of superficial glossitis, 355
    in morbid dentition, 374
  lesions in tabes mesenterica, 1188

Gastro-colic fistulae, in gastric cancer, 558
    in simple gastric ulcer, 508

Gastro-cutaneous fistulae, in simple ulcer of stomach, 500

Gastromalacia, 618

Gastro-pleural fistulae, in simple ulcer of stomach, 508

Gastrorrhagia, 580

Gastrostomy in cancer of stomach, 578
  in dilatation of stomach, 609
  use of, in cancer of oesophagus, 428
  in dilatation of oesophagus, 435
  in organic stricture of oesophagus, 426

Gargles, use of, in acute pharyngitis, 397
    in tonsillitis, 388

General progressive form of rheumatoid arthritis, symptoms, 80

Genito-urinary affections, complicating gout, 123

Geographical distribution of cholera morbus, 720
    of diabetes mellitus, 203
    of acute intestinal catarrh, 669
    of cancer of stomach, 535
    of simple ulcer of stomach, 485
    of tabes mesenterica, 1184

Germ, infective, origin of acute rheumatism, 26

Glands, abdominal, diseases of, 1182
  bronchial and tracheal, enlargement in rachitis, 153
  changes in, in scrofula, 239, 240
  gastric, alterations, in chronic gastritis, 472
  of Lieberkuhn, elongation of, in chronic intestinal catarrh, 703
  lymphatic, enlargement of, in tuberculous pharyngitis, 401
    swelling of, in acute pharyngitis, 395
  mesenteric change in, in tabes mesenterica, 1187
  pharyngeal, hypertrophy of, in chronic pharyngitis, 403

GLOSSITIS, 354
    Definition, 354
  Glossitis, superficial, 355
    Definition, 355
    Synonyms, 355
    Etiology, 355
      Teeth, irregular and jagged, 355
      Tobacco, 355
      Liquids, hot and acrid, 355
      Nervous irritation, 355
      Stomatitis, 355
      Febrile affections, 355
      Gastro-intestinal disease, 355
    Pathology and morbid anatomy, 355
      Nature, 355
      Lesions, description of, 355
      Epithelium, increase and detachment of, 355
      Papillae, enlargement, 355, 356
      Unilateral, 356
      Psoriasis linguae, 356
      Superficial ulceration, 356
      Microscopic appearance, 356
      Ichthyosis linguae, 356
      Relative frequency of, in smokers and non-smokers, 356
      Termination in epithelioma, 356
    Symptoms, 357
      Local, 357
      General, 357
    Diagnosis, 357
    Treatment, 357
      Importance of treating gastric complications, 557
      Local, 357
      Of ulcers, 357
      Removal of imperfect teeth, 357
  _Glossitis Parasitica_ (_Black tongue_), 357
    Definition, 357
    Synonyms, 357
    History, 357
    Etiology, 358
      Faulty nutrition, 358
      Chlorate of potash, use of, 358
      Syphilis, 358
    Pathology and morbid anatomy, 358
      Discoloration of tongue, 358
      Papillae, enlargement of, 358
      Parasitic growth, 358
        microscopic appearance, 358
        mode of development, 358
        seat of, 358
    Symptoms, 359
    Diagnosis, 359
    Prognosis, 359
    Treatment, 359
      Indications, 359
      Local, 359
      Use of potassium chloride, 359
        sodium borate, 359
  _Glossitis, Parenchymatous_, 359
    Definition, 359
    Synonyms, 359
    History, 359
    Etiology, 359
      Impaired health, 359
      Atmospheric changes, 359
      Cold and damp, 359
      Age, 360
      Influenza, 360
      Improper and acrid food, 360
      Certain plants, 360
      Tobacco, 360
      Acute exanthemata, 360
      Disease of mucous membranes, 360
      Endemic and epidemic nature, 360
      Traumatic form, 360
      Teeth, irregular, 360
      Injuries, 360
      Acrid and irritant poisons, 360
      Saliva of the toad, 360
    Symptoms, 360
      Mode of onset, 360
      Tongue, condition of, 361
        enlargement of, 361
        pain in, 361
        desquamation of, 361
        chronic induration of, 361
        gangrene of, 361
      Lymphatic glands, swelling of, 361
      Respiration, laborious, 361
      Deglutition, difficult, 361
      Physiognomy, 361
      Saliva, dribbling, 361
      Thirst, 362
      Cough, 362
      Pyrexia, 362
      Pulse, 362
      Skin, condition of, 362
      Gastro-intestinal canal, condition of, 362
      Nervous system, 362
      Resolution, 362
      Suppuration, 362
      Gangrene of tongue, 362
    Duration, 362
    Complications, 362
      Diffused inflammation of areolar tissue between genio-hyo-glossi
        muscles, 362
    Pathology and morbid anatomy, 363
      Chordo-tympani and glosso-pharyngeal nerve, relation to
        causation, 363
      Tongue, infiltration of, by fibrin and serum, 363
      Epithelium, changes in, 363
      Suppuration, nature of, 363
        seat of pointing, 363
      Gangrene of tongue, cause of, 363
      Muscles, condition of, in diffuse inter-connective tissue
        inflammation, 363
    Diagnosis, 363
      From hypertrophy of tongue, 364
        cystoma of tongue, 364
    Prognosis, 364
    Mortality, 364
    Treatment, 364
      Of mild cases, 364
      Antiphlogistic, 364
      Of debility, 364
      Of severe cases, 365
      Of localized form, 365
      Diet, 365
      Enemata, nutrient, 365
      Abscesses, 365
      Of tumefaction of tongue, 365
      Of gangrene of tongue, 366
      Local, 365
      Use of aconite, 364
        of tartar emetic, 364
        of leeching, 364
        of venesection, 364
        of iron and quinia, 365
        of deep incisions, 365
        of astringents, 365
        of detergent washes, 365
        of spray of ammonium chloride, 365
  _Glossitis, Chronic_, 366
  _Glossitis, Chronic Superficial_, 366
    Etiology, 366
      Dyspepsia, 366
      Chronic alcoholism, 366
    Symptoms, 366
      Pain in taking acid food, 366
      Sensation of enlarged tongue, 366
      Tongue, appearance of, 366
        furrows of, 366
      Papillae, enlarged, 366
      Ulcers, superficial, 366
    Pathology, 367
    Diagnosis, 367
      From syphilis, 367
        epithelioma, 367
    Prognosis, 367
    Treatment, 367
      Cleanliness, necessity of, 367
      Diet, 367
      Exercise, 367
      Avoidance of alcohol, 367
      Local, 367
  _Glossitis, Chronic Parenchymatous_, 367
    Definition, 367
    Pathology, 368
      Connective-tissue hyperplasia, 368
    Symptoms, 368
      Tongue, induration of, 367, 368
        circumscribed tumefaction of, 367, 368
        loss of sensibility of, 367, 368
        enlargement or atrophy of, 367, 368
        chronic abscess of, 368
      Pain in taking arid and sapid food, 368
      Difficult articulation and deglutition, 368
    Diagnosis, 368
      From cystic tumor, 368
    Prognosis, 368
    Treatment, 368
      Local, 368
      General, 368
  _Glossanthrax_ (_Carbuncle of Tongue_, _Malignant Pustule of
        Tongue_), 368
    Definition, 368
    Etiology, 368
    Symptoms, 368
    Prognosis, 368
    Treatment, 368

Gluten bread, use of, in diabetes mellitus, 222

Glycosuria, artificial, methods of production, 195-199
  influence of vaso-motor nerves on production, 196-199
  relation of sympathetic nerve to, 196
  complicating gout, 123
  hepatic, 973

Gold and silver, use of, in acute yellow atrophy of liver, 1030

Gold and sodium chloride, use of, in amyloid liver, 1046
    in cirrhosis of liver, 1001

Gonorrhoea complicating gout, 123
  of rectum, treatment of, 918

Gonorrhoeal bursitis, symptoms of, 105
  poison, influence on causation of proctitis, 888
  rheumatism, 102

GOUT, 108
  Definition, 108
  Synonyms, 108
  Classification, 108
  History, 109
  Etiology, 109
    Predisposing causes, 109
    Heredity, 109
    Sex, 109
    Age, 110
    Temperament, 110
    Vicious hygiene, influence of, on causation, 110
    Luxurious living, influence of, on causation, 110
    Poverty, influence of, on causation, 110, 111
    Alcoholic liquors, influence of, on causation, 111
    Fermented liquors, influence of, on causation, 111
    Malt liquors, influence of, on causation, 111
    Cider, influence of, on causation, 111
    Lead-poisoning, relation of, to causation, 111
    Exciting causes, 112
    Errors in diet, 112
    Sudden changes in temperature, 112
    Traumatism, 112
    Nervous exhaustion, 112
    Overwork, 112
    Sexual excess, 112
  Pathology, 112
    Theories regarding, 112
    Lithaemic theory, 112
    Chemical theory, 112
    Defective oxidation, origin of, from, 112, 113
    Uric-acid theory, 112, 113
        objections to, 113, 114
    Nervous theory of origin, 114
  Morbid anatomy, 115
    Changes in blood, 115
    Uric acid, excess of, in blood, 115
    Urates, deposits of, 115
    Exudations, composition of, 115
      location, 115
    Joints, changes in, 116
    Cartilages, changes in, 115
      necrosis of, 116
        relation of, to uratic deposits, 116
    Synovial membranes, changes in, 115
    Joints, hyperplasia of connective tissue of, 116
      abscesses of, 116
      metatarso-phalangeal, frequency of disease of, 116
      most affected, 116
    Blood-vessels, changes in, 117
    Heart, changes in, 117
    Nerves, changes in, 117
    Kidneys, changes in, 117
      cirrhosis of, 117
      deposits in, 117
        seat and character, 117
      uratic deposits in, 117
    Liver, changes in, 117, 118
  Symptoms, 118
    Prodromal, 118
    Derangements of primary digestion, 118
    Dyspepsia, 118
      Constipation, 118
      Diarrhoea, 118
      Nervous symptoms accompanying, 118
    Derangements of nutrition, 118
    Catarrhal affections of skin, 118
        mucous membranes, 118
    Debility, 118
    Irritability of temper, 118
    Hypochondriasis, 118
    Acute articular form, 119
      attack, 119
    Onset, 119
    Fever, 119
    Sleeplessness, 119
    Pain, 119
    Local, 119
    Condition of joint, 119
    Reflex muscular spasm, 119
    Urine, changes in, 119
      amount of uric acid in, during attack, 119
    Duration, 119
    Improved health following, 119
    Atonic or irregular forms, 120
    General symptoms, 120
    Dyspepsia, 120
    Urine, changes in, 120
      specific gravity, 120
      amount of urea, uric acid, and urates, 120
    Polyuria, 120, 123
    Articular symptoms, 121
    Joints most affected, 121
    Pain, 121
    Deformities, 121
    Exacerbations, frequency of, 121
  Complications, 121
    Skin affections, 121
    Perspirations, local, 121
    Seborrhoea, 121
    Eczema, 121
      relation of, to, 121, 122
      seat and character, 122
    Acne, 121
    Erythematous affections, 121
    Affections of mucous membranes, 122
    Pharyngeal and laryngeal catarrh, 122
    Bronchitis, 122
    Gastro-duodenal catarrh, 122
    Intestinal catarrh, 122
    Genito-urinary affections, 123
    Vesical catarrh, 123
    Gonorrhoea, 123
    Granular kidney, 123
    Albuminuria, 123
      importance of, 123
    Glycosuria, 123
    Gravel, 124
    Renal colic, 124
    Dysuria, 124
  Diagnosis, 124
    Relation of, to acute and chronic rheumatic diseases, 124
      to gonorrhoeal rheumatism, 124
    Importance of heredity in, 125
    From acute rheumatism, 125
      rheumatoid arthritis, 125
      traumatic joint affections, 126
      nervous arthropathies, 126
    Of irregular gout, 126
  Prognosis, 126
    Effects of renal affections on, 127
      treatment on, 127
  Treatment, 127
    Indications, 127
    Dietetic, 127
    Necessity of avoidance of carbohydrates, 128
        of fermented alcoholic liquors, 128
        of beer and wine, 128
        of saccharine and amylaceous foods, 128, 129
    Use of fatty foods, 129
      of succulent vegetables, 129
      of milk, 129
    Proper amount of food, 129
    Necessity of exercise, 130, 131
    Active and passive exercise, 130
    Bathing, 130
    Baths, use of, 130
    Climate, 130
    Medicinal, 131
    Of the dyspepsia, 131
    Gastro-intestinal catarrh, 131
    Use of pepsin and pancreatin, 131
      of hydragogue cathartics, 131
      of natural mineral waters, 131
      of iron, 132
        and potash, 132
      of alkalies, 132
      of lithia salts, 132
      of potassium salts, 132
      of sodium salts, 132
    Modes of administering alkaline salts, 132, 133
    Use of iodine salts, 132
      of water, 133
    Of acute articular gout, 133
    Antiphlogistic method, 133
    Expectant method, 133
    By diet, 133
    Local, 134
    Abortive method, 134
    Use of colchicum, 134
        action of, 134
        objections to, 134
        method of administration, 135
      salicylic acid and salicylates, 135
      oil of wintergreen, 136

Gout, influence on causation of chronic intestinal catarrh, 699
      of rachitis, 144
      of rheumatoid arthritis, 89
  and rheumatism, influence on causation of acute gastritis, 464

Gravel complicating gout, 124

Guaiacum, use of, in chronic articular rheumatism, 74
    in tonsillitis, 388
  and colchicum, use of, in constipation, 656

Guinea-worm, 962

Gummata of lungs in hereditary syphilis, 307
  of rectum and anus, 900

Gummatous infiltration in syphilitic pharyngitis, 407

Gums, state of, in morbid dentition, 373
    in scurvy, 177

Gum-water, use of, in chronic gastritis, 477

Gymnastic exercises, use of, in rachitis, 166


H.

Habit, influence on causation of constipation, 640
  scrofulous, peculiarities of, 243, 244

Haematemesis in lardaceous degeneration of intestines, 875
  in acute yellow atrophy of liver, 1028
  in purpura haemorrhagica, 188
  in scurvy, 180
  in cancer of stomach, treatment of, 577
  in dilatation of stomach, 594
  in hemorrhage from stomach, 586
  in simple ulcer of stomach, 493

Haematogenous jaundice, 975

Haematuria in Bilharzia haematobia, 948
  in Filaria sanguinis, 963
  in purpura haemorrhagica, 188
  in scurvy, 180

Haemophilia, influence on causation of stomatorrhagia, 370
      of hemorrhage from bowels, 830
      of hemorrhage from stomach, 582

Hair, growth on forehead and shoulders, in scrofula, 246

Hairs on mucous membrane of anus, 892

Hallucinations in constipation, 647

Hamamelis virginica, use of, in hemorrhoids, 923

Hand, deformities of in general rheumatoid arthritis, 82

Head, changes in, in rachitis, 146
  of Taenia saginata, 934
  of tape-worm, description of, 932

Headache in biliousness, 966
  in catarrh of bile-ducts, 1054, 1055
  in constipation, 646, 647, 853
  in pseudo-membranous enteritis, 767
  in chronic intestinal catarrh, 708
  in intestinal indigestion, 628
  in jaundice, 980
  in lithaemia, 970
  in acute gastritis, 467
  in chronic gastritis, 475
  in scurvy, 180
  in simple ulcer of stomach, 494
  in trichinosis, 960
  and vertigo, in cancer of stomach, 554

Hearing, disorders of, in constipation, 647
    in diabetes mellitus, 205
    in scurvy, 181

Heart-action, cause of slowing of, in jaundice, 979

Heart affections in acute rheumatism, 28, 31
    complicating chronic articular rheumatism, 72
  disease, influence on causation of chronic intestinal catarrh, 700
        of intestinal indigestion, 626
        of simple ulcer of stomach, 487
    organic, influence on causation of constipation, 641
      as a cause of hyperaemia of liver, 984
  disease of, as a cause of ascites, 1174
    complicating simple ulcer of stomach, 503
  disturbance in biliary concretions, 1077
    in chronic gastritis, 474
    in intestinal indigestion, 628
    in rachitis, 152
  lesions of, in gout, 117
    in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 705
    in acute yellow atrophy of liver, 1026
  weak, as a cause of thrombosis and embolism of portal vein, 1095
  and blood-vessels, lesions of, in scurvy, 172
  and circulation, condition of, in scurvy, 179
  and lungs, disease of, influence on causation of acute gastritis,
        464
      of chronic gastritis, 471
      of gastric hemorrhage, 581
  and membranes, lesions of, in acute rheumatism, 31-36

Heartburn in functional dyspepsia, 449
  in dilatation of stomach, 593

Heat, extreme, influence on causation of cholera morbus, 720
      of aphthous stomatitis, 326
  of mouth, in aphthous stomatitis, 329
    in stomatitis ulcerosa, 337
  in rectum in pseudo-membranous enteritis, 765
  use of, in enteralgia, 665
    in hemorrhage from bowels, 834

Heberden's nodosities of rheumatoid arthritis, 86

Hectic in chronic intestinal catarrh, 709
  in chronic form of peri-rectal and anal abscesses, 896

Hemiplegia following chronic intestinal catarrh, 710

Hemorrhage, frequency of, in scurvy, 179, 180

HEMORRHAGE FROM BOWELS, 830
  General remarks, 830
  Etiology, 830
    Constipation, 830
    Scybalous masses, 830
    Hemorrhoids, 830
    Anal fissure, 830
    Foreign bodies, 830
    Abuse of cathartics, 830
    Parasites, 831
    Anomalies in intestinal walls, 831
    Dysentery, 831
    Typhoid fever, 831
    Embolism, 831
    Tuberculous and syphilitic ulceration, 831
    Invagination, 831
    Polypi, 831
    Tumors, 831
    Diseases of blood-vessels, 832
    Acute infectious diseases, 832
    Haemophilia, 832
    Leuchaemia, 832
    Anaemia, pernicious, 832
    Of melaena neonatorum, 832
  Morbid anatomy, 832
  Symptoms, 832
    Pains and borborygmi, 833
    Blood, appearance of, 833
    Stools, tarry, 833
    Concealed form, 833
    Collapse, 833
    Syncope, 833
    Anaemia, progressive, 833
  Diagnosis, 833
    of seat, 833
      importance of examination of rectum in, 834
  Treatment, 834
    Rest, 834
    Of collapse, 834
    Of anaemia, 834
    Diet, 834
    Cold, use of, 834
    Ice-water injections, 834
    Ergotin, use of, 834
    Opium, use of, 834
    Tannic acid, 834
    Tincture of iron, 834
    Acetate of lead, 834
    Alum, 834
    Turpentine, 834
    Alcohol, 834
    Heat for collapse, 834
    Transfusion of blood, 834
    Milk, use of, 834

Hemorrhage from bowels, in intestinal ulcer, 827
    mucous surfaces in acute yellow atrophy of liver, 1028
    mouth. See _Stomatorrhagia_.
    occlusion of biliary passages, 1089
    stomach, 580
    rectum, 899
  in cancrum oris, 341
  in internal hemorrhoids, 884
  in acute yellow atrophy of liver, 1030

Hemorrhages in cirrhosis of liver, 994
  into pancreas, 1129
  in purpura haemorrhagica, 188
  in cancer of stomach, 545
  in simple ulcer of stomach, 492
  in suppurative pylephlebitis, 1100
  in cancer of rectum and anus, 904
  in polypi of rectum, 882
  sudden suppression of, as a cause of hyperaemia of liver, 984

Hemorrhagic diathesis, tendency to, in jaundice, 981
  effusion into peritoneum, 1180
  extravasations in acute pancreatitis, 1118
    in liver tissue in acute yellow atrophy of, 1025
  form of acute intestinal catarrh, treatment, 698

Hemorrhoids, 882
  complicating constipation, 645, 648
  external, 883
  internal, 883
  in chronic intestinal catarrh, 706
  in intestinal indigestion, 627
  in amyloid liver, 1044
  in cirrhosis of liver, 994
  influence on causation of hemorrhage from bowels, 830

Hepar adiposum, 1046

Hepatic calculi, 1058
  colic, 1058, 1070
    distinguished from enteralgia, 664
    relation to malaria, 1071, 1072
  disease, as a cause of hemorrhoids, 884
    complicating chronic intestinal catarrh, 710
    influence on causation of chronic intestinal catarrh, 700
  disturbance, influence on causation of functional dyspepsia, 447
  duct, cause of occlusion of, 1084
    effects of occlusion of, 1085
  dulness, increased, in hyperaemia of liver, 986
  form of functional dyspepsia, treatment, 457
  glycosuria, 973
  resonance on percussion, significance, 1156
  secretion, deficient, in intestinal indigestion, treatment, 635

Hepatogenous jaundice, 976

Hereditary nature of rachitis, 144
  syphilis. See _Syphilis, Hereditary_.

Heredity, influence on causation of constipation, 640
      of diabetes mellitus, 203
      of functional dyspepsia, 438
      of enteralgia, 659
      of gout, 109
      of cancer of intestine, 869
      of chronic intestinal catarrh, 699
      of intestinal indigestion, 623
      of carcinoma of liver, 1033
      of purpura, 191
      of acute rheumatism, 21
      of chronic articular rheumatism, 70
      of gonorrhoeal rheumatism, 103
      of muscular rheumatism, 75
      of rheumatoid arthritis, 88, 91
      of scrofula, 232
      of cancer of stomach, 535
      of tonsillitis, 380
      of tabes mesenterica, 1105

Hernia, complicating constipation, 648
  internal, laparotomy for, 866
    strangulated, forms of, 843

Herniae, weight, influence on causation of dilatation of stomach, 590

Hernial sacs, stomach in, 617

Herpes of anus, 892
  zoster due to biliary calculi, 1078

Herpetic form of acute pharyngitis, nature and course, 392
  tonsillitis, etiology, 380
  form of tonsillitis, treatment of, 388

Hiccough in acute gastritis, 467
  in spasmodic stricture of oesophagus, 420
  in cancer of stomach, 540

Histology of gastric cancer, 563, 564, 565

History of catarrh of bile-ducts, 1051
  of cancrum oris, 338, 339
  of cholera morbus, 719
  of dysentery, 777
  of enteralgia, 658
  of pseudo-membranous enteritis, 763
  of acute yellow atrophy of liver, 1023
  of gout, 109
  of glossitis parasitica, 357
  of parenchymatous glossitis, 359
  of acute intestinal catarrh, 667
  of macroglossia, 349
  of acute oesophagitis, 409
  of organic stricture of oesophagus, 422
  of spasmodic stricture of oesophagus, 419
  of diseases of pancreas, 1112
  of paratyphlitis, 814
  of acute pharyngitis, 400
  of peritonitis, 1132
  of introduction of opium in treatment of acute peritonitis,
        1146-1151
  of rheumatoid arthritis, 78
  of scurvy, 167-169
  of cancer of stomach, 530
  of cirrhosis of stomach, 611
  of dilatation of stomach, 586
  of simple ulcer of stomach, 480
  of tabes mesenterica, 1183
  of thrush, 331
  of tonsillitis, 379
  of typhlitis, 814

Hoarseness in chronic pharyngitis, 404

Hob-nail appearance of hepatic surface in cirrhosis of liver, 992

Hog, Trichina spiralis in, 958

Hooklets, in fluid of hydatids of liver, significance, 1105

Hot climates, influence on causation of intestinal indigestion, 624
  drinks, as a cause of acute oesophagitis, 410
    influence on causation of chronic oesophagitis, 416
  embrocations in typhlitis, 820
  season, influence on causation of dysentery, 787
  weather, intestinal affections of children in, 726

Hot-water injections in pseudo-membranous enteritis, 774
    in intestinal obstruction, 860
    in intestinal ulcer, 829
  use of, in gastralgia, 463
    in chronic gastritis, 477
    in pruritus ani, 917
    in sphincterismus, 916

Hour-glass contraction of stomach, 617
    in gastric cancer, 566

Hutchinson on peculiarities of incisor teeth in hereditary syphilis,
        293, 294

Hunyadi Janos water, use of, in intestinal indigestion, 636

Hydatid tumors, varieties and seat, 944

Hydatids of liver, 1101

Hydrocephalus, spurious, in entero-colitis, 735

Hydrochloric acid, use of, in functional dyspepsia, 456
    free, detection of, in fluids of gastric cancer, 543
    use of, in dilatation of stomach, 609

Hydrocyanic acid, use of, in cholera morbus, 725
      in functional dyspepsia, 458, 459
      in gastralgia, 463
      in acute gastritis, 469

Hydrogen peroxide, use of, in tuberculous pharyngitis, 402

Hydrophobia, influence on causation of spasmodic stricture of
        oesophagus, 419

Hydrotherapy, use of, in functional dyspepsia, 457

Hydrothorax, complicating gastric cancer, 560

Hygiene, bad, influence on causation of scrofula, 232
  improper, influence on causation of chronic intestinal catarrh, 699

Hygienic treatment of diabetes mellitus, 225
    of pseudo-membranous enteritis, 776
    of intestinal indigestion, 632
    of chronic interstitial pancreatitis, 1122
    of obstruction of pancreatic duct, 1131
    of acute rheumatism, 69
    of muscular rheumatism, 77
    of rheumatoid arthritis, 101
    of scurvy, 183
    of tabes mesenterica, 1194

Hyperaemia of liver, 983
    relation to causation of diabetes mellitus, 195

Hyperplasia and atrophy of liver, in phosphorus-poisoning, 1031

Hyperpyrexia in acute rheumatism, 29, 66
  of acute rheumatism, treatment of, 66-68
  treatment, in acute intestinal catarrh, 692

Hypertrophy, of intestinal walls in constipation, 644
  of gastric walls in stenosis of pylorus, 615
      in dilatation of stomach, 599
  of tongue, 349

Hypochondria in fatty liver, 1048

Hypochondriasis in functional dyspepsia, 451
  in gout, 118

Hypochondrium, right, uneasiness in, from gall-stones, 1069

Hypodermatic alimentation in simple ulcer of stomach, 525
  use of iron in simple ulcer of stomach, 528

Hypogastric plexus, lesions, in acute peritonitis, 1136

Hypophosphates, use of, in scrofula, 252

Hypostatic congestion of lungs in entero-colitis, 734
  pneumonia, in entero-colitis, 735

Hysteria in hepatic colic, 1071
  influence on causation of oesophageal paralysis, 429

Hysterical form of enteralgia, treatment, 664
  origin of spasmodic stricture of oesophagus, 767
  phenomena in gastralgia, 461
  symptoms of pseudo-membranous enteritis, 767


I.

Ice, use of, in cholera infantum, 762
    in cholera morbus, 725
    in entero-colitis, 762
    in acute gastritis, 468
    in acute intestinal catarrh, 689, 690, 693, 698
    in intestinal ulceration, 829
    in acute pancreatitis, 1120
    in acute pharyngitis, 397
    in acute oesophagitis, 416
    in rectal hemorrhage, 927
    in cancer of stomach, 576
    in simple ulcer of stomach, 525
    in aphthous stomatitis, 330
    in catarrhal stomatitis, 325
    in tonsillitis, 388
  local use of, in intestinal obstruction, 864
  locally, in proctitis, 919

Ice-bag, use of, in typhlitis and perityphlitis, 822

Ice-water, influence on causation of cholera morbus, 721
  injections in dysentery, 810
    in hemorrhage from bowels, 834
    in hemorrhage from rectum, 927

Icterus, 925

Icthyosis linguae, 356

Idiocy and cretinism, relation to macroglossia, 350

Idiopathic causes of gastric hemorrhage, 582
  pancreatitis, acute, 1118
  tonsillitis, 379

Idiosyncrasy, influence on causation of enteralgia, 660
      of acute intestinal catarrh, 671
      of intestinal indigestion, 623

Ignipuncture, use of, in hypertrophy of tongue, 354

Ileitis, 667, 683

Ileo-caecal valve, lesions of, in entero-colitis, 737
  variety of intussusception, 846

Ileo-colitis of acute intestinal catarrh, lesions of, 674

Ileum, lesions of, in entero-colitis, 737

Ileus, distinguished from enteralgia, 664

Impacted feces, influence on causation of ulceration of rectum and
        anus, 894

Impaction of biliary calculi, 1074
  of foreign bodies, as a cause of intestinal obstruction, 837

Impurities of air, influence on causation of entero-colitis, 728-730

Incision, deep in parenchymatous glossitis, 365
  in fissure of anus, 912
  in fistula in ano, 922

Incisions, use of, in acute pharyngitis, 397

Incisor teeth, Hutchinson on peculiarities of, in hereditary syphilis,
        293, 294

Indigestion. See _Functional Dyspepsia_.
  influence on causation of constipation, 642
      of enteralgia, 660
  in atrophy of stomach, 616

Indigo-carmine test for sugar in urine, 216

Individual predisposition, influence on causation of gastric cancer,
        537

Induration of tongue in chronic parenchymatous glossitis, 367
    in tubercular ulceration of tongue, 369

Infants, treatment of constipation in, 656

Infants' foods, farinaceous, analysis of, 750, 751

Infantile peritonitis, 1172

Infection, syphilitic, of child at moment of conception, 262, 267
      during birth, 269
      during utero-gestation, 267
    of mother by foetus in utero, 262

Infectious diseases, acute, as a cause of hemorrhage from stomach, 581

Infiltration, fatty, of pancreas, 1128

Infiltrating form of carcinoma of liver, 1034

Inflammation, scrofulous, Cornil and Ranvier on causes of, 239

Inflammatory affections of pancreas, 1118
  diseases of stomach, 436
  nature of syphilitic pharyngitis, 406
  nature of rachitis, 137, 138
  theory of origin of gastric ulcer, 512

Inflation of stomach, value, in diagnosis of gastric cancer, 549

Ingluvin, use of, in simple ulcer of stomach, 525

Inhalations, steam, use of, in acute pharyngitis, 397, 398

Injection of bowel in intestinal obstruction, 864
  of ice-water in hemorrhage from rectum, 927
  subcutaneous, of oil, in simple ulcer of stomach, 525

Injections of hot water, in intestinal ulcer, 829
  uterine, influence on causation of acute peritonitis, 1140

Injury, influence on causation of acute intestinal catarrh, 673
      of acute oesophagitis, 411
      of diseases of pancreas, 1114
      of acute peritonitis, 1140
      of acute pharyngitis, 391
      of rheumatoid arthritis, 91
      of scrofula, 236
      of cirrhosis of stomach, 612
      of rupture of stomach, 618
      of simple ulcer of stomach, 486

Injuries, influence on causation of diabetes mellitus, 203
      of parenchymatous glossitis, 360

Inosite in diabetic urine, 208
  test for, in diabetic urine, 217

Inspissated bile, 1058
    treatment of, 1079

Intellect, state of, in rachitis, 149

Intermarriage of scrofulous persons, 249

Intermittence of pain in simple ulcer of stomach, 491

Intermittent fever, complicating chronic intestinal catarrh, 710
    influence on causation of simple gastric ulcer, 488

Internal hemorrhoids, symptoms of, 883
  strangulated hernia, forms of, 843

Interstitial hepatitis, 990
  keratitis in hereditary syphilis, 299
  pancreatitis, chronic, 1121

INTESTINES, CANCER OF, 868
  Definition, 868
  Etiology, 868
    Forms of, 868
    Scirrhous, 868
    Lympho-sarcoma, 868
    Cylinder-cell, 868
    Colloid, 868
    Primary, 868
    Secondary, 868
    Relative frequency, 868
    Seat, 869
      of secondary form, 869
    Age, influence of, on causation, 869
    Sex, influence of, on causation, 869
    Heredity, influence of, on causation, 869
    Exciting causes, 869
  Symptoms, 869
    Vagueness of early symptoms, 869
    Irregular bowels, 869
    Undefined pains, 869
    Physiognomy, 869
    Tumor, presence of, 869
      character of, 870
      pain in, 870
      pulsation of, 870
    Of duodenal form, 870
      pain in, 870
      vomiting in, 870
    Of lower intestine, 870
      constipation, 871
      stools, bloody and mucous, 871
      sudden disappearance of symptoms from softening of tumor, 871
    Oedema, 871
    Wasting, 871
    Cachexia, 871
    Duration, 871, 873
  Morbid anatomy, 871
    Cylinder-cell epithelioma most common form, 871
    Method of growth, 872
    Scirrhous form, method of growth of, 872
    Ulceration in, 872
    Colloid form, method of growth of, 872
    Invasion of neighboring parts, 873
    Secondary to hepatic cancer, 873
    Melanotic sarcoma, secondary to tumor of eye or skin, 873
  Diagnosis, 873
    Of duodenal form, 873
        from pyloric cancer, 873
    Tumor, significance of, 873
      from fecal tumor, 873
    Significance of cancerous fragments in stools, 873
  Prognosis, 873
    Death, cause of, 873
  Treatment, 874
    Diet, 874

INTESTINES, LARDACEOUS DEGENERATION OF, 874
  Synonyms, 874
  Frequency, 874
  Symptoms, absence of specific, 874
    Diarrhoea, 874
    Hemorrhage from bowels, 874
    Haematemesis, 875
    General condition, 875
    Death, cause, 875
  Morbid anatomy, 875
    Seat of degeneration, 875
    Mucous membrane, lesions of, 875
    Iodine test, 875
    Methyl-aniline-violet test, 875
    Method of testing, 876
    Ulceration and enlargement of mucous surface, 876
    Microscopic appearance of lardaceous materials, 876
    Degeneration of the vessels, 876
  Diagnosis, 876
  Prognosis, 876
  Treatment, 876
    Incurability of, 876
    Diet, 876
    Of diarrhoea, 876
    Bismuth subnitrate, use of, in large doses, 876
    Of hemorrhage, 876

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER, 726
  _Entero-colitis_, 726
    Etiology, 727
      Summer heats, 727
      Season, 727, 728
      Vitiated air, 728-730
        nature of impurities in, 729
        gases, 729
        organic matter, 729
      Over-crowding, 730
      Filth, 730
      Improper food, 731, 732
      Artificial feeding, 731
      Poor breast-milk, 731
      Impure cow's milk, 731
      Age, influence on causation, 732
      Relation of dentition to, 733
    Symptoms, 733
      Onset, 733
      Stools, characters of, 733, 734, 736
      Tongue, state, 733
      Vomiting, 733
        significance of date of appearance of, 733, 734
      Vomit, characters, 733
      Pulse, state of, 734, 736
      Fever, 734, 736
      Skin, state of, 734, 736
      Kidneys, state of, 734
      Skin eruptions, 734
      Hypostatic congestion of lungs, 734
        pneumonia, 735
      Spurious hydrocephalus, 735
          symptoms, 735
      Convalescence, 736
      Death, cause of, 736
      Wasting, 736
      Drowsiness, 735, 736
      Morbid anatomy, 736
      Hyperaemia of mucous membrane, 737
      Duodenum, lesions of, 737
      Jejunum, lesions of, 737
      Ileum, lesions of, 737
      Ileo-caecal valve, thickening of, 737
      Ulcers, 737, 738
        seat of, 737, 738
      Mucous membrane, softening of, 737
      Colon, lesions of, 738
      Solitary glands, enlargement of, 738
      Peyer's patches, enlargement of, 738
      Appendix vermiformis, lesions of, 738
      Mesenteric glands, enlargement of, 739
      Stomach, lesions of, 739
      Mouth, lesions of, 739
      Liver, lesions of, 739
      Lungs, lesions of, 740
      Brain, lesions of, 740
    Diagnosis, 740
      Significance of abdominal tenderness, 740
    Prognosis, 741
    Mortality, 726, 727
  _Cholera Infantum, or Choleriform Diarrhoea_, 741
    Nature, 744
      Relation to thermic fever, 745
    Symptoms, 741
      Onset, 741
      Stools, 741
        characters of, 741
      Vomiting, 742
      Appetite, impaired, 742
      Thirst, 742
      Tongue, state of, 742
      Temperature, 742
      Restlessness, 742
      Loss of strength, 742
      Emaciation, 742
      Urine, state of, 742
      Pulse, state of, 742
      Stupor, 742
    Morbid anatomy, 742
      Rilliet and Barthez on lesions, 742
      Stomach, lesions of, 743, 744
      Intestinal canal, lesions of, 743, 744
      Bacteria, significance of, 744
    Diagnosis, 745
    Prognosis, 745
    Duration, 746
    Treatment, 746
      Preventive, 746
      Weaning, time for, 746
      Change of air, 746, 756
      Amount of food ingested by healthy infants, 746
      Curative, 747
      Diet, 746, 748
      Milk, use of, 749
      Woman's milk, composition of, 749, 750
      Cow's milk, composition of, 749, 750
      Farinaceous foods, analyses of, 750, 751
      Cow's milk, objections to, 749, 751
      Peptonized milk, use of, 751, 753
      Mode of peptonizing, 752
      Oatmeal and barley as diluents, 753
      Farinaceous foods, use of, 753
      Flour-ball, use of, 754, 755
      Liebig's foods, use of, 754
      Nestle's food, use of, 754
      Ridge's food, use of, 754
      Condensed milk, use of, 754
      Beef-, mutton-, and chicken-tea, use of, 755
      Necessity of cleanliness, 756
      Change of climate, 756
      Medicinal, 757
      Of first stage, 757
      Purgatives, use of, 757
      Sodium benzoate, use of, 757, 761
      Sodium bicarbonate, 757
      Opium, use of, 758, 759
      Mist. cretae, use of, 758
      Bismuth subnitrate, use of, 758
      Of cholera infantum, 759
      Of cerebral symptoms, 759
      Bromide of potassium, use of, 759
      Of second stage, 759
      Pepsin, use of, 760
      Calomel, use of, 760
      Lactopeptin, use of, 760
      Enemata, use of, 760
      Argenti nitratis, use of, 761
      Alcohol, use of, 761
      Of vomiting, 761
      Lime-water, use of, 762
      Carbolic acid, use of, 761
      Ipecacuanha, use of, 762
      Ice, use of, 762
      Liquor ferri nitratis, use of, 762

Intestinal canal, lesions of, in cholera infantum, 743, 744
    state of, in catarrh of bile-duct, 1054

INTESTINAL CATARRH, ACUTE, 667
  Synonyms, 667
  History, 667
  Nature and classification, 668
    Inflammatory nature, 668
  Etiology, 669
    Geographical distribution, 669
    Race, 669
    Sex, 669
    Age, 670
    Climate, 669
    Summer heats, 669
    Sudden changes of temperature, 670
    Cold, 670
    External burns, 670
    Impure air, 670
    Sewer gas, 670
    Temperament and idiosyncrasy, 671
    Previous attacks, 671
    Sedentary, life, 671
    Abuse of tobacco and alcohol, 671, 672
    Constipation, 671
    Eruptive fevers, 671
    Uraemia, 671
    Malaria, 671
    Chronic wasting diseases, 671
    Phthisis, 671
    Improper and excessive food, 671, 672
    Irritant and caustic poisons, 672
    Drastic purgatives, 672
    Foreign bodies, 672
    Impure water, 672, 673
    Injury, 673
    Emotional influence, 673
    Lesions of nerve-centres, 673
    Micro-organisms, 673
    Bacteria, 673
  Morbid anatomy, 673
    External appearance of intestines, 673
    Distension of colon and caecum, 673
      of small intestines, 673
    Color of intestines, 673
    Serous membrane of intestines, lesions of, 674
    Appearance of intestinal contents, 674
    Intestinal mucous membrane, lesions of, 674
    Mucous membrane, seat of inflammation of, 674
    Ileo-colitis, 674
    Duodenal mucous membrane, lesions of, 674
    Hyperaemia of mucous membrane, 674
    Swelling and softening of, 675
    Villi, lesions of, 675
    Solitary glands, lesions of, 675
    Peyer's patches, tumefaction of, 675
    Ulcers, catarrhal, 676
      follicular, 676
      seat of, 676
    Mucous collections, 676
    Vibrios and bacteria, 676
    Mesenteric glands, enlargement of, 677
    Liver, lesions of, 677
    Spleen, lesions of, 677
    Kidneys, lesions of, 677
    Lungs, lesions of, 677
    Heart, lesions of, 677
    Brain, lesions of, 677
  Pathological histology, 677
    Congestion of capillaries, 677
    Transudation of serum, 677
    Rupture of small vessels, 677
    Increase of mucus, 677
    Origin of mucus, 677
    Increased cellular growth, 677
    Formation of ulcers, 677
    Desquamation of epithelium, 677
  Symptoms, 677
    Mild forms of, 678
    Onset of, 678
    Pain, 678
    Stools, character of, 678
    Tongue, dryness of, 678
    Duration of, 678, 681
    Severe forms of, 678
    Pain and colics, 679, 682
    Borborygmi, 679
    Tympanites, 679
    Abdomen, intumescence of, 679
      tenderness of, 679
      soreness on moving, 679
      pain in, 679, 682
    Diarrhoea, 679, 681
    Number of stools, 679
    Character of stools, 680, 681, 682
    Color of stools, 680, 681, 682
    Blood in stools, 680, 681, 682
    Odor of stools, 680
    Tongue, condition of, 680, 681
    Thirst, 680, 681
    Nausea and vomiting, 681
    Fever, 681
    Urine, condition of, 681
    Paraplegia and muscular contraction, 681
    Delirium, 681
    Physiognomy, 681
    Emaciation, 682
    Collapse, 682
    Pulse, 682
    Duration, 682
    In children, 682
    Loss of strength, 682
    Choleriform diarrhoea, 682
  Varieties due to seat, 682
    Acute duodenitis, 682
        relation to integumental burns, 682
        symptoms, 682
      ileitis, 683
      jejunitis, 683
        symptoms, 683
      colitis, 683
        symptoms, 684
        bloody stools, 684
        tenesmus, 684
    Proctitis, 684
      symptoms, 684
      burning in rectum, 684
      tenesmus, 684
      mucous stools, 684
  Diagnosis, 684
    Of ileo-colitis, 685
    Of follicular ulceration, 685
    In children, 686
    From typhoid fever, 676, 685, 686
      dysentery, 686
      enteralgia, 686
      abdominal rheumatism, 686
      lead colic, 686
      peritonitis, 686
  Prognosis, 687
  Treatment, 687
    Prophylactic, 687
    Change of climate, 688
    Disinfection, 688
    Proper clothing, 688
    When arising from cold, 688
      heat, 688
      undigested food, 689
      Bright's disease, 689
      phthisis, 689
    Value of rest, 690
      of counter-irritation, 688, 690, 698
    Of thirst, 690
    Of hyperpyrexia, 692
    Of flatulence, 693
    Of diarrhoea, 693
    Of ulcers, 698
    Of hemorrhagic form, 698
    Of choleraic form in children, 698
        in adults, 698
    Of duodenitis, 698
    By rectum, 697
    Diet, 687, 688, 690
      in children, 692
      of convalescence, 692
    Use of blood-letting, 690
      of milk, 690, 691
      of buttermilk, 691
      of koumiss, 691
      of eggs, 691
      of beef-tea, 691
      of raw-beef, 691
      of milk, 690, 691
      of poultices, 688, 690
      of sinapisms, 688, 690
      of ice, 689, 690, 693, 698
      of warm and cold baths, 692
      of aconite, 689
      of quinia, 692
      of jaborandi, 688
      of bismuth, 693
      of alkalies, 693
      of mineral acids, 693, 694, 695
      of opium, 689, 693, 698
      of oxide of zinc, 694
      of chalk mixture, 694
      of lime-water, 694
      of cassava-water, 694
      of sugar of lead, 694
      of calomel, 695
      of bichloride of mercury, 695
      of vegetable astringents, 695
      of gallic acid, 695
      of tannic acid, 695
      of ipecacuanha, 695
      of coto-bark, 696
      of alum, 696
      of sulphate of copper, 696
      of nitrate of silver, 696, 698
      of oxide of silver, 696
      of iron, 696
      of carbolic acid, 696
      of creasote, 696
      of salicylic acid, 696
      of sulpho-carbolate of calcium, 696
      of enemata, 697
      of irrigation of large intestine, 697
      of iced coffee in children, 698
      of bromides, 698
      of spirits of camphor, 698

INTESTINAL CATARRH, CHRONIC, 699
  Etiology, 699
    Age, 699
    Sex, 699
    Heredity, 699
    Bad hygiene, 699
    Overwork, 699
    Chronic wasting diseases, 699
    Phthisis, 699
    Bright's disease, 699
    Gout, 699
    Addison's disease, 700
    Syphilis, 700
    Malaria, 700
    Disease of heart and lungs, 700
      liver, 700
    Improper food, 700
    Alcohol, 700
    Foreign bodies, 700
    Chronic lesions of bowels, 700
  Morbid anatomy, 700
    Intestines, seat of lesions, 700, 701
      alteration in calibre, 700
    Intestinal walls, hypertrophy, 700
    Mucous membrane, lesions of, 700
      alteration in color, 701
      of ileum, swelling of, 701
        hypertrophy of villi, 701
    Solitary glands, alterations in, 702
    Peyer's patches, alterations in, 702
    Colon, ulcers of, 702
        seat and character, 702
        perforating, 702
    Presence of pseudo-membrane, 702
    Veins, varicose condition, 702
    Duodenal ulcer from external burns and chronic Bright's disease,
        703
      from embolism, 703
    Adhesions, peritoneal, 703
    Suppuration of duodenum, 703
    Chronic proctitis, lesions, 703
    Mucous membrane, condition, 703
    Inflammation of peri-rectal tissue, 703
    Abscesses, 703
    Fistulae, 703
  Pathological histology, 703
    Increased cell-proliferation, 703
    Hypertrophy of tissue, 703
    Glands of Lieberkuhn, elongation of, 703
    Mode of formation of ulcers, 703
      cicatrization of ulcers, 703
    Formation of cysts, 704
        origin, 704
      polypoid growths, 704
        seat, 704
    Atrophy of intestinal walls, 704
        seat, 704
        mucous membrane in, 705
    Amyloid degeneration of mucous membrane, 705
    Peritoneum, lesions, 705
    Mesenteric glands, enlargement, 705
    Liver, lesions of, 705
      abscess of, 705
    Gall-bladder, lesions of, 705
    Spleen, lesions of, 705
    Pancreas, lesions of, 705
    Kidneys, lesions of, 705
    Heart, lesions of, 705
    Lungs, lesions of, 706
    Pleura, lesions of, 706
    Cornea, lesions of, 706
    Brain, lesions of, 706
  Symptoms, 706
    Mild forms, 706
    State of bowels, 706
    Signs of intestinal indigestion, 706
    Time of appearance, 706
    Fulness, 706
    Colicky pains and borborygmi, 706
    Constipation, 706
    Diarrhoea, 706
    Abdomen, state of, 706
    Depression of spirits, 706
    Hemorrhoids, 706
    Severe forms, 707
    Tongue, state, 707
    Appetite impaired, 707
    Time of appearance, 707
    Pain, 707
    Abdomen, state, 707
    Tympanites, 707
    Diarrhoea, 707
      quantity, 707
    Stools, appearance, 707
      bloody, 707
      mucous, 708
      composition, 708
      micrococci and bacteria in, 708
      unaltered food (lientery), 708
    Headache, 708
    Depression, 708
    Vertigo, 708
    Sleeplessness, 708
    Palpitation, 708
    Urine, state, 708
  Progress and termination, 709
    Progressive emaciation, 709
    Anaemia, 709
    Cuticle, dryness of, 709
    Fever, 709
    Hectic, 709
    Pulse, 709
    Death, cause, 709
  Complications, 709
    Dropsy, general, 709
    Oedema of one extremity, 709
    Chronic bronchitis, 709
    Phthisis, 709
    Pneumonia, 709
    Peritonitis, 710
    Tuberculosis, 710
    Bright's disease, 710
    Intermittent and remittent fever, 710
    Hepatic disease, 710
    Ulceration of cornea, 710
  Sequelae, 710
    Chronic intestinal indigestion, 710
    Tabes mesenterica, 710
    Constipation, 710
    Stricture, intestinal, 710
    Paralysis, 710
    Para- and hemiplegia, 710
  Diagnosis, 710
    Of primary from secondary diarrhoea, 711
    From chronic dysentery, 711
    Of locality of lesion, 711
    Of duodenal form, 711
    Of catarrh of jejunum and ileum, 712
    Of catarrh of colon, 712
    Of stage of inflammatory process, 712
    Of follicular ulceration, 712, 713
    Of duodenal ulcer, 713
    From tuberculous ulceration, 713
    From cancerous ulceration, 713
  Prognosis, 713
  Treatment, 714
    Preventive, 714, 715
    Of cause, 714
    Mild forms, 714
    Diarrhoea, 715
    Constipation, 714
    Of follicular form, 715
        ulceration, 718
    Rest, 716
    Change of residence, 715, 716
    Baths, 714, 716
    Sitz baths, 716
    Permanent baths, 716
    Exercise, 714, 716
    Diet, 714, 716
    Milk, 716
    Use of stimulants, 716
      wines, 716
      purgatives, 714, 715
      mineral waters, 714, 715
      Rockbridge alum water, 714, 717
      iron, 714, 715, 717
      bitter tonics, 715
      quinia, 715
      mineral acids, 715
      strychnia, 714, 715
      medicated enemata, 714, 717, 718
      rectal irrigation, cold water, 717
      arsenic, 715
      bismuth, 715, 717
      liquor pancreaticus, 714
      mineral astringents, 717
      nitrate of silver, 717, 718
      opium, 715, 718
      turpentine and copaiba, 718
      ergot, 718
      cod-liver oil, 718
      corrosive sublimate, 717
      gallic acid, 717

Intestinal catarrh, complicating gout, 122
    influence on causation of tabes mesenterica, 1186
  colic. See _Enteralgia_.
  contents, in acute intestinal catarrh, 674
  dilatation, in constipation, 643
  disorders, influence on causation of catarrhal stomatitis, 322
      of thrush, 332

INTESTINAL INDIGESTION, 620
  Nature, 620
    Physiology of intestinal digestion, 620
    Action of saliva, 620, 621
      of gastric juice, 621
    Chyme, composition of, 621
    Action of bile, 621
      of pancreatic juice, 622
      of trypsin, 622
    Peristalsis, cause of, 622, 623
    Action of liver, 623
    Absorption of peptones and sugar, 623
      of oils and fats, 623
  Etiology, 623
    Sex, 623
    Age, 623
    Heredity, 623
    Idiosyncrasy, 623
    Anaemia, 623
    Rachitis, 623
    Syphilis, 623
    Febrile diseases, 623
    Strumous diathesis and phthisis, 624
    Want of exercise, 624
    Sexual excess, 624
    Impure air, 624
    Mental overwork, 624
    Worry and anxiety, 624
    Wealth, 624
    Sedentary occupations, 624
    Tight-lacing, 624
    Hot climates, 624
    Over-eating, 624
    Indigestible food, 625
    Excess of starchy food, 625
    Alcohol, abuse of, 625
    Condiments, abuse of, 625
    Irregularity in meals, 625
    Imperfect mastication, 625
    Tobacco, abuse of, 625
    Constipation, 625
    Excess of gastric acid, 626
    Obstruction of bile-ducts, 626
    Pancreatic disease, 626
    Disease of heart and lungs, 626
      of intestines, 626
  Symptoms, 626
    Forms, 626
    Acute form, 626
    Chronic form, 627
    Time of appearance after eating, 627
    Pain, 627
      character and seat of, 627
    Tympanites and borborygmi, 627
    Fulness after eating, 627
    Gas, source of, 627
    Abdominal swelling, 627
    Constipation, 627
    Stools, character of, 627
    Diarrhoea, 627
    Hemorrhoids, 627
    Tongue, state of, 628
    Nervous system, state of, 628
    Depression of spirits, 628
    Sleeplessness, 628
    Headache, 628
    Vertigo, 628
    Anxiety and worry, 628
    Mental power, impaired, 628
    Paralysis, 628
    Sensibility, modifications of, 628
    Faintings, 628
    Heart disturbance, 628
    Palpitation, 628
    Circulation, languid, 628
    Cold extremities, 628
    Urine, state of, 628
      lithates in, 628
      albuminuria, 628
    Perversion of sexual function, 629
    Anaemia, 629
    Skin eruptions, 629
    Liver, functional disorder of, 629
  Course, 630
  Duration, 630
  Termination, 630
    In deterioration of health, 630
    In organic disease, 630
    In phthisis, 630
  Diagnosis, 630
    From gastric dyspepsia, 631
    Of varieties of, 631
    Of pancreatic form, 631
    Of biliary form, 631
  Prognosis, 631
  Treatment, 632
    Of acute form, 632
    Of chronic form, 632
    Hygienic, 632
    Change of climate, 632
    Exercise, 632
    Thorough mastication, 632
    Swedish movements, 632
    Bathing, 632
      salt-water, 632
      Russian, 633
    Regularity in eating, 633
    Diet, 633, 634
    Milk, use of, 633
    Koumiss, use of, 633
    Beef-essences, 633
    Foods to be avoided, 635
    Use of wine, 634
    Mineral waters, 634, 636
    Use of pre-digested foods, 635
      of pancreatic extract, 635
        mode of administering, 635
    Of deficient hepatic secretion, 635
    Of flatulence and colics, 636
    Of constipation, 636
    Of strumous form, 636
    Use of ipecacuanha, 636
      of euonymin, 636
      of sanguinarin, 636
      of podophyllin, 636
      of sulphate of sodium, 636
      of benzoate of sodium, 636
      of iron, 636
      of quinia, 636
      of strychnia, 636
      of mineral acids, 636
      of bitter waters, 636
      of Friedrichshall waters, 636
      of Hunyadi Janos, 636
      of cod-liver oil, 637

INTESTINAL OBSTRUCTION, 835
  Classification, 835
  Congenital strictures and malformations, 836
    Strictures, 836
      seat, 836
      of colon, 836
        sigmoid flexure, 836
        duodenum, 836
      malformations, 837
      of anus and rectum, 837
  _Impaction of Foreign Bodies_, 837
    Nature of substances found in intestines, 837, 838
      Stony concretions (enteroliths), 838
      Gall-stones, 838
    Symptoms, 839
      Modes of discharge of, 839
      By vomiting, 839
      By ulceration, 839
      Peritonitis from, 839
      Of inflammation, 839
      Remote results of, 840
      Impaired health, 840
      Emaciation, 840
      Of impaction from gall-stones, 840
      Pains, colicky, 840
      Vomiting, 840
      Prostration, 840
      Signs of disordered liver, 840
  _Acute Internal Strangulation, Twisting, etc._, 840
    Seat of twisting, 840
    Conditions necessary to production, 841
    Elongated mesentery, 841
    Increased weight of bowel, 841
    Inflammation of elongated bowel, 841
    Symptoms, 841
      Prodromal, 841
      Signs of intestinal disorder, 841
      Actual attack, 841
    Other modes of strangulation and twisting, 841, 842
    Forms of internal strangulated hernia, 843
    Diaphragmatic hernia, 843
      Symptoms, 843
      Suddenness of onset, 843
      Nausea and vomiting, 843
      Pains, 843
      Tympanites, 843
      Of peritonitis, 843
      Delirium, 843
      Duration, 841, 843
  _Intussusception, Invagination_, 844
      Without symptoms, 844
    Morbid anatomy of, 844
      Diminished lumen of bowel, 845
      Inflammation, changes produced by, 845
      Sloughing of invaginated parts, 845
      Gangrene and ulceration in, 845
      Seat, 846
      Ileo-caecal variety, 846
      Method of production, 846
      Frequency in relation to sex, 847
        in relation to age, 847
      Mechanism of, 847
      Local paresis and tenesmus of bowel, 847
      Length of, 848
    Symptoms, 848
      Onset of, 848
      Pain, characters of, 848
        effect of pressure upon, 848
      Vomiting, 848
      Vomit, fecal, 848
      Diarrhoea, 848
      Stools, characters of, 848
      Abdominal tenderness, 848
      Tumor, presence of, 848
      Tympanites, 848
      Urgency of symptoms, relation to locality and degree of
        constriction, 848
      Suddenness of acute cases, 848
      Gangrene of invaginated portion, 849
      Date of separation of sequestrum, 849
      Of chronic cases, 849
      Duration, 849
      Abatement of symptoms before death, 849
  _Constipation_, 850
    Number of fecal evacuations in health, 850
    Etiology, 850
      Sex, 850
      Sedentary life, 850
      Rapid loss of fluid, 851
      By kidneys, 851
        lungs, 851
        skin, 851
      Food, improper, 851
      Bile, deficiency of, 851
      Dislocations of intestines, 851
      Nervous diseases, 851
      Hysteria, 851
      Paralysis of muscular coat of intestine, 851
      Chronic debilitating diseases, 852
      Loss of sensibility of colon and rectum, 852
      Fecal impaction, 852
      Tumor, fecal, characters of, 852
      Dilatation of colon and rectum, 852
    Symptoms, 853
      Torsion of caecum, 853
      Internal strangulation from, 853
      Digestive disturbances, 853
      Appetite, impaired, 853
      Headache, 853
      Pain, colicky, 853
      Diarrhoea, 853
      Evolution of gases, 853
      Mental depression, 854
      Nervous symptoms, 854
      Pain in legs, 854
        in back, 854
      Strength, loss of, 854
          of obstruction from, 854
  _Stricture of bowel_, 854
      Frequency of, 854
      Seat of, 855
      From cicatrization of ulcers, 855
        cancer, 855
    Symptoms, 856
      Intestinal disorders, 856
      Colicky pains, 856
      Paroxysmal pain, 856
      Of rectum, 856
      Determination of, by digital examination, 856
  _Compression and Contraction of Bowel_, 857
      From abdominal tumors and cysts, 857
      From adhesions of chronic peritonitis, 857
      Seat of, 857
    Symptoms, 857
      Insidiousness of onset of, 858
      Intestinal disorders, 858
      Exhaustion, 858
      Distinguished from stricture, 858
    Differential diagnosis, 858
      From external strangulated hernia, 858
        functional obstruction of bowel, 859
      Of congenital occlusion, 859
      Of obstruction by foreign bodies, 859
        by gall-stones, 860
        by internal hernia, 860
        by torsion, 860
        uneven distension of abdomen in torsion, 860
        fecal accumulation, 860
        abdominal tumors, 861
      Of seat of obstruction, 861
      Of pain, significance of, 861
      Significance of constipation, 862
        of vomiting, stercoraceous, 862
    Duration, 862
    Mortality, 862
      Relative frequency of deaths by different forms, 862
    Treatment, 862
      Purgatives, uselessness and danger, 862, 863
      Quicksilver, use of, 863
      Opium, use of, 863
        method of administration, 863
      Of fecal impaction, 863
        Castor oil, use of, in, 863
      Of invagination low in rectum, 864
      Ice, locally, use of, 864
      Bleeding, use of, 864
      Electricity, use of, 864
      Abdominal taxis, 864
      Injection of warm water, 864
      Replacement of pressing tumors or organs, 864
      Stimulants, use of, 865
      Quinia, use of, 865
      Tapping of gut, in gaseous distension, 865
      Surgical, 865
      Laparotomy, 865
        in invagination, 866
        mortality, 866, 867
        in internal hernia, volvulus, etc., 866
      Entorectomy, 866
      Enterotomy, 867
        method of performing, 867

Intestinal tract, condition in rachitis, 153
  trichina, 959
  tube, ulceration and suppuration of, as a cause of suppurative
        pylephlebitis, 1097, 1098

INTESTINAL ULCER, 823
  Synonyms, 823
  Definition, 823
  Etiology, 823
    Frequency, 823
    Toxic form, 823
    Mineral acids, 823
    Syphilis, 823
    Traumatic form, 823
    From hardened feces and foreign bodies, 823
      intestinal parasites, 823
      use of enemata, 823
      burns of skin, 824
      dysentery, 824
      tuberculosis, 824
      typhoid fever, 824
      arrest of circulation, 824
      erosion of gastric juice, 824, 825
    Of duodenal form, 825
      frequency, 825
      tendency to perforation, 825
          cicatrization, 825
  Symptoms, 825
    Indefinite nature of, 825
    Pain, 826
      character, 826
    Appetite, loss, 826
    Failure of general health, 826
    Digestive disturbances, 826
    Nausea and vomiting, 826
    Diarrhoea, 827
    Stools, character, 827
      effect of seat of ulcers upon, 827
    Hemorrhage of bowel, 827
      black and tarry stools in, 827
  Duration, 827
  Diagnosis, 828
    From intestinal catarrh, 828
        carcinoma, 828
      enteralgia, 828
      hemorrhage of gastric ulcer, 828
  Prognosis, 828
  Treatment, 828
    Diet, 829
    Of vomiting, 829
    Of pain, 829
    Of hemorrhage, 829
    Of peritonitis, 829
    Of constipation, 829
    Alcohol, use of, 829
    Bismuth, use of, 829
    Sodium bicarbonate, use of, 829
    Oxide of zinc, use of, 829
    Purgatives, use of, 829
    Ice, use of, 829
    Hot-water injections, use of, 829
    Cataplasms, use of, 829
    Opium, use of, 829
    Ergotin, use of, 829
    Turpentine, use of, 829
    Prophylaxis against recurrence, 829

Intestinal ulcers, in hereditary syphilis, 306

INTESTINAL WORMS, 930
  Varieties, 930
  Mode of access to body, 931
  Frequency in relation to uncooked food, 931
      unfiltered waters, 931
      uncleanliness, 931
  _Cestodes, or Tape-worms_, 931
    Description of mature worm, 931
      head, 932
    Sexual apparatus of, 932
    Description of embryo or proscolex, 932
    Mode of dissemination, 932, 933
    Species, 933
    Taenia saginata, 933
      Synonyms, 933
      Characteristics, 934
      Length, 934
      Head, 934
      Sexual organs, 934
      Rapidity of growth, 934
      Number of eggs, 934
      Sources, 934
      Eating of underdone beef, 935
    Taenia solium, 935
      Synonyms, 935
      Characteristics, 935
      Sexual organs, 934, 935
      Head, 935
      Source, 936
      Rapidity of growth, 936
    Taenia cucumerina, 937
      elliptica, 937
      nana, 937
      tenella, 938
      flavopunctata, 938
      madagascariensis, 938
    Bothriocephalus latus, 939
      Synonyms, 938
      Countries where most prevalent, 938
      Characteristics, 939
      Sexual organs, 939
      Sources, 939
      From fish, 939
    Bothriocephalus cordatus, 939
      cristatus, 939
    Symptoms of tape-worms, 939
      Local, 940
      Pruritus ani, 940
      Dyspeptic, 940
      Headache, 940
      Nausea, 940
      Abdomen, queer sensation in, 940
      Colicky pains, 940
      Vertigo, 940
      Tongue, state, 940
      Fainting, 940
      Chorea, 940
      Epileptic fits, 940
      Uterine disorders, 940
    Treatment, 941
      Importance of removal of head, 940
      Method of examining evacuations, 940
      Preliminary, 941
      Oil of turpentine, use of, 941
          mode, 941
      Male fern, use of, 941
          mode of, 941
      Pomegranate-bark, use of, 941
          mode, 941
      Pelletierin, use of, 942
      Kousso, use of, 942
      Koussin, use of, 942
      Pumpkin-seeds, use of, 942
      Santonin, use of, 942
      Quinia, use of, 942
      Prophylaxis, 942, 943
    Taenia echinococcus, 943
      Synonyms, 943
      Description of, 943
        head, 943
        sexual organs, 943
      Shortness of life, 943
      Mode of dissemination, 944
      Migration from intestinal canal, 944
      Hydatid tumors, seat, 944
          varieties of, 944
      Cysts, forms of, 944
        characters of, 944
        contents of, 944
        effects of, 945
      Infection, liability to, proportioned to association with dogs,
        945
      Treatment, 945
    Taenia acanthotrias, 945
  _Trematodes, or Fluke-worms_, 946
    Varieties, 946
    Distomum hepaticum, 946
        Synonyms, 946
        Tendency to inhabit liver, 946
        Physical characters, 946
        Snail as a home during youth, 947
        Rarity in man, 947
        Animals most affected, 946, 947
      lanceolatum, 947
        Synonym, 947
        Physical characters, 947
      sinense, 947
      conjunctum, 947
        Symptoms of fluke-worms, 947
        Signs of obstruction of bile-ducts, 947
        Treatment, 948
      heterophyes, 948
      crassum, 948
      ringeri, 948
      ophthalmobium, 948
    Bilharzia haematobia, 948
        Synonyms, 948
        Geographical distribution, 948
        Mode of introduction to body, 948
          by water, 948
          by vegetables, 948
        Symptoms, 948
          Haematuria, 948
        Treatment, 949
    Amphistomum hominis, 949
  _The Acanthocephali, or Thorn-head Worms_, 949
    Echinorhynchus gigas, 949
      Limited to hog, 949
  _The Nematodes, or Thread-worms_, 949
    General description of, 949, 950
    Varieties, 950
    Oxyuris vermicularis, 950
      Synonyms, 950
      Physical characters, 950
        of female, 950
        of male, 950
      Number of eggs, 950
      Description of eggs, 950
      Modes of dissemination, 951
        of introduction to body, 951
      Symptoms, 951
        Itching of anus, 951
          periodic, nature of, 951
        Onanism from, 951
        Nervous disturbances, 951
        Intestinal catarrh, 951
        Epileptic fits from, 951
        Chorea from, 951
      Treatment, 951
        Purgatives, use of, 951
        Epsom salts and senna, 951
        Tincture of aloes, 951
        Enemata, 951
        Suppositories, medicated, 951
    Ascaris lumbricoides, 952
      Synonyms, 952
      Physical characters, 952
        of female, 952
        of male, 952
      Number of eggs, 952
      Mode of infection, 952
        by drinking-water, 952
      Geographical distribution, 953
      Small intestine, most frequent habitat, 953
      Migrations of, 953
      Symptoms, 953
        Digestive disorders, 953
        Flatulence, 953
        Abdominal pains, 953
        Tongue, state of, 953
        Appetite, impaired, 953
        Nervous disorders, 953
        Epileptic fits, 953
      Treatment, 953
        Wormseed, 954
          oil, 954
        Santonin, 954
    Ascaris mystax, 954
    Triocephalus dispar, 954
      Synonyms, 954
      Physical characters, 954
      Symptoms, 954
      Treatment, 954
    Leptodera stercoralis, 954
      Synonyms, 954
      Physical characters, 955
      Mode of infection, 955
      Treatment, 955
    Anchylostomum duodenale, 955
      Synonyms, 955
      Geographical distribution, 955
      Physical characters, 955
      Mode of introduction to body, 955
      Symptoms, 955
      A source of wasting diseases, 955
      Mode of onset, 955
      Debility, 956
      Palpitation, 956
      Digestive disorders, 956
      Emaciation, 956
      Prognosis, 956
      Treatment, 956
        Calomel and turpentine, 956
      Prophylaxis, 956
    Strongylus longevaginatus, 956
    Eustrongylus gigas, 957
      Physical characters, 957
      Animals infested by, 957
    Trichina spiralis, 957
      Mode of infection, 958
      Date of discovery in muscles, 958
      Animals most frequent in, 958
        Hog, 958
        Rat and mouse, 958
        Cats, 958
      Muscular trichinae, 958
      Appearance of infected meat, 959
        of trichinae in muscle, 959
      Muscular trichinae, decay of, 959
          size of, 959
          duration of life of, 959
      Intestinal trichinae, 959
        Physical characters, 959
        Embryos, method of migration to muscles, 959
      Symptoms, 959
        Initial, 960
        Appetite impaired, 960
        Thirst, 960
        Diarrhoea, 960
        Vomiting, 960
        Headache, 960
        Prostration, 960
        Constipation, 960
        Muscular, 960
          swellings, 960
        Muscles, pain in, 960
          painful and difficult motion of, 960
        Bronchial catarrh, 960
        Fever, 960
        Sweating, 960
        Insomnia, 961
        Formication, 961
        Oedema, 961
        Peritonitis, 961
        Pleuritis, 961
        In children, 961
          mildness of, 961
      Duration, 960
      Diagnosis, 961
        From gastro-intestinal catarrh, 961
        From cholera, 961
        From rheumatism, 961
      Prognosis, 961
      Treatment, 961
        Purgatives, 962
        Diet, 962
        Prophylaxis, 962
        Necessity of thorough cooking, 962
    Filaria medinensis, 962
      Synonyms, 962
      Geographical distribution, 962
      Physical characters, 962
      Mode of introduction to body, 963
      Symptoms, 963
        abscesses, 963
      Treatment, 963
    Filaria sanguinis, 963
      Synonyms, 963
      Geographical distribution, 963
      Physical characters, 963
      Mode of entrance to blood, 963
      Habitat in lymphatic vessels, 963
      Symptoms, 963
        Haematuria, 963
        Chyluria, 963
        Buboes, 963
        Ascites, 964
        Elephantiasis, 964
        Lymphangiectasis, 963
      Treatment, 964
        Prophylaxis, 964
    Filaria loa, 964
      restiformis, 964
      oculi humani, Filaria lentis 964
      trachealis, 964

Intestinal worms, influence on causation of constipation, 643
        of acute peritonitis, 1140
        of proctitis, 887

Intra-uterine rachitis, 141-143

Intussusception. See _Intestinal Obstruction_.
  complicating constipation, 648
  and invagination as a cause of intestinal obstruction, 844

Inunctions of mercury in hereditary syphilis, 316
  of oil in simple ulcer of stomach, 527

Invagination. See _Intestinal Obstruction_.
  as a cause of hemorrhage from bowels, 831
  intestinal, laparotomy in, 866

Invasion, order of, in gonorrhoeal rheumatism, 104

Iodide of iron, in tubercular peritonitis, 1168
    use of, in rheumatoid arthritis, 98
      in scrofula, 251
      in tabes mesenterica, 1194
  of mercury, ointment, in lithaemia, 973
      in amyloid liver, 1046
      in cirrhosis of liver, 1002
  of potassium, use of, in diabetes mellitus, 228
      in enteralgia, 665
      in pseudo-membranous enteritis, 775
      in amyloid liver, 1045
      in chronic oesophagitis, 417
      in organic stricture of oesophagus, 425
      in tubercular peritonitis, 1168
      in syphilitic pharyngitis, 408
      in acute rheumatism, 62
      in chronic articular rheumatism, 74
      in muscular rheumatism, 77
      in gonorrhoeal rheumatism, 107
      in rheumatoid arthritis, 98
      in hereditary syphilis, 316

Iodine, injection of, in hydatids of liver, 1108
  use of, in diabetes mellitus, 228
    in hepatic glycosuria, 975
    in chronic pharyngitis, 405
    in rheumatoid arthritis, 100
    in scrofula, 251
    in typhlitis and perityphlitis, 822
  test for amyloid liver, 1043
    for lardaceous degeneration, 875
  and olive oil, locally, in tubercular peritonitis, 1168
  salts, use of, in gout, 132

Iodoform, use of, in diabetes mellitus, 229
    in tuberculous pharyngitis, 402
    in aphthous stomatitis, 330

Ipecacuanha, use of, in biliousness, 968
    in constipation, 654
    in dysentery, 810
    in functional dyspepsia, 456
    as antiemetic, in entero-colitis and cholera infantum, 762
    in pseudo-membranous enteritis, 775
    in acute gastritis, 469
    in hepatic colic, 1082
    in acute intestinal catarrh, 695
    in intestinal indigestion, 636
    in jaundice, 982
    in biliousness, 968

Iridin, use of, in hepatic colic, 1082
    in acute yellow atrophy of liver, 1030
    in hyperaemia of liver, 988

Iritis, complicating gonorrhoeal rheumatism, 106
  in hereditary syphilis, 281

Iron, use of, in catarrh of bile-ducts, 1057
    in constipation, 654
    in functional dyspepsia, 457
    in enteralgia, 665
    in pseudo-membranous enteritis, 775
    in gastralgia, 462
    in parenchymatous glossitis, 365
    in acute intestinal catarrh, 696
    in chronic intestinal catarrh, 714, 715, 717
    in intestinal indigestion, 636
    in acute yellow atrophy of liver, 1030
    in amyloid liver, 1046
    in cirrhosis of liver, 1002
    in fatty liver, 1051
    in acute pharyngitis, 398
    in purpura, 194
    in pruritus ani, 917
    in acute rheumatism, 63
    in chronic articular rheumatism, 74
    in gonorrhoeal rheumatism, 107
    in rachitis, 162
    in dilatation of stomach, 609
    in simple ulcer of stomach, 528
  and potash, use of, in gout, 132
  tinct. of chloride, use of, in hemorrhage from bowels, 834
      in pain of simple gastric ulcer, 524

Irrigation of bowel in dysentery, 809
    in jaundice, 983
    in typhlitis, 821
  intestinal, in acute catarrh of intestines, 697
    in intestinal obstruction, 863, 864

Irritable rectum, treatment, 919

Irritant poisoning, diagnosis from cholera morbus, 723

Irritating medicines as a cause of acute oesophagitis, 410

Itching of anus in seat-worms, 951
  at extremities of alimentary canal in tape-worm, 940


J.

Jaborandi, use of, in acute intestinal catarrh, 688
    in chronic pharyngitis, 406
  effect on rectum, 911

Jaundice. See _Liver, Diseases of_.
  in biliousness, 966
  in catarrh of bile-ducts, 1054
  in occlusion of biliary passages, 1087, 1089
  from constipation, 646
  complicating diabetes mellitus, 210
  in chronic gastritis, 474
  in hepatic abscess, 1009, 1013
  in hepatic colic, 1073
  in acute yellow atrophy of liver, 1027
  frequency, in amyloid liver, 1044
  in carcinoma of liver, 1038
  in cirrhosis of liver, 993
  in fatty liver, 1049
  in hydatids of liver, 1102, 1104
  in hyperaemia of liver, 986, 987
  in disease of pancreas, 1116
  in obstruction of pancreatic duct, 1131
  in carcinoma of pancreas, 1125, 1126
  in perihepatitis, 989
  in phosphorus-poisoning, 1032
  in suppurative pylephlebitis, 1100
  complicating gastric cancer, 560

Jejunitis, 667, 683
  and ileitis of chronic intestinal catarrh, diagnosis, 712

Jejunum, lesions of, in entero-colitis, 737

Joint, condition of, in acute gonorrhoeal arthritis, 105
    in acute gout, 119

Joints, abscesses of, in gout, 116
  alterations of, in chronic articular rheumatism, 71
  condition of, in purpura rheumatica, 189
    in acute rheumatism, 27
    in chronic articular rheumatism, 71
    in acute variety of general rheumatoid arthritis, 80
    in chronic variety of general rheumatoid arthritis, 81
    in partial form of rheumatoid arthritis, 85
  lesions of, in dysentery, 801
    in gout, 116
    in acute rheumatism, 46
    in chronic articular rheumatism, 70
    in gonorrhoeal rheumatism, 103
    in rheumatoid arthritis, 86
    in scurvy, 172
  most affected in gout, 116, 121
    in acute rheumatism, 27
    in chronic articular rheumatism, 72
    in gonorrhoeal rheumatism, 104


K.

Keratitis, interstitial, in hereditary syphilis, 299

Kibbie's cot, use of, in acute rheumatism, 67

Kidneys, amyloid degeneration of, in rachitis, 153
  condition of, in occlusion of biliary passages, 1090
    in entero-colitis, 734
    in acute rheumatism, 42
    in hereditary syphilis, 308
  enlargement of, in amyloid liver, 1044
    in rachitis, 140
  diseases of, as a cause of ascites, 1174
    complicating dysentery, 806
    influence on causation of hemorrhage from stomach, 582
  lesions, in cholera morbus, 722
    in diabetes mellitus, 202
    in dysentery, 801
    in gout, 117
    in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 705
    in acute yellow atrophy of liver, 1026
    in phosphorus-poisoning, 1031
    in rachitis, 154
    in scurvy, 173
  uratic deposits in, in gout, 117

Kidney-worm, 957

Koumiss, use of, in treatment of acute intestinal catarrh, 691
    in intestinal indigestion, 633

Kousso and koussin, use of, in tape-worm, 942

Kyphosis in rachitis, nature of, 151


L.

Lactic acid, use of, in diabetes mellitus, 228
    origin of acute rheumatism, 23

Lacto-peptin, use of, in cholera infantum and entero-colitis, 760

Lacto-phosphate of iron, in tabes mesenterica, 1194

Lacto-phosphates, use of, in scrofula, 252

Lancing, in morbid dentition, method of, 378

Languor and drowsiness, in functional dyspepsia, 451

Laparotomy in intestinal obstruction, 865
  in perforating form of typhlitis, 822
  question of, in perforation of gastric ulcer, 527

Lardaceous degeneration of intestine, 874

Laryngismus stridulus in rachitis, 149

Larynx, disease of, in hereditary syphilis, 308
  displacement of, from hypertrophy of tongue, 351
  oedema of, in mercurial stomatitis, 346
  and pharynx, lesions of, in mercurial stomatitis, 347
    gangrene of, complicating cancrum oris, 341

Latham's hyperoxidation theory of origin of acute rheumatism, 24

Laxatives, use of, in dysentery, 809
    in pseudo-membranous enteritis, 774

Lead colic distinguished from acute intestinal catarrh, 686

Lead-poisoning, influence on causation of constipation, 641
      of oesophageal paralysis, 429

Lead, sugar of, use of, in acute intestinal catarrh, 694
  copper, and arsenic poisoning, as a cause of enteralgia, 660

Leeches to epigastrium in acute pancreatitis, 1120

Leeching, in parenchymatous glossitis, 364
  in perihepatitis, 990
  in acute pharyngitis, 398

Lemon-juice, use of, in acute rheumatism, 63

Leptodera stercoralis, 954

Leube's beef-solution, use of, in simple ulcer of stomach, 520

Leuchaemia, influence on causation of hemorrhage from bowels, 832

Liebig's foods for infants, 754

Lienteric stools, in chronic intestinal catarrh, 708

Ligaments, lesions of, in rheumatoid arthritis, 87

Ligation in fistula in ano, 922
  in polypi of rectum, 921
  in hypertrophy of tongue, 354
  of hemorrhoids, 924

Ligature of upper extremities, in hemorrhage of simple gastric ulcer,
        526

Lime, elimination of, in rachitis, 138

Lime-juice, use, in scurvy, 183, 184
  salts, use of, in rachitis, 162
  water, local use, in hemorrhoids, 923
    use in entero-colitis and cholera infantum, 762
    in acute intestinal catarrh, 694

Lip, upper, thickness of, in scrofula, 246

Lipaemia in diabetes mellitus, 207

Lipomata of stomach, 579

Lipuria, in diseases of pancreas, 1115
  in carcinoma of pancreas, 1125

Liquor ferri nitratis, use of, in entero-colitis, 762

Lithaemia, 968

Lithaemic theory of origin of gout, 112

Lithia salts, use of, in gout, 132

Lithium bromide, use of, in chronic articular rheumatism, 74

Liver, action of, in process of digestion, 623
  amyloid degeneration of, in rachitis, 153
  changes in, from occlusion of biliary ducts, 1086
  condition of, in catarrh of bile-ducts, 1053
  degeneration of, complicating simple ulcer of stomach, 503

LIVER, DISEASES OF, 965
  Functional Disorders, 965
    _Biliousness_, 965
      Definition, 965
      Pathogeny, 965
        Malarial poison, effect on functions of liver, 965
        Metals, effect on functions of liver, 965
        Food, improper, influence of, on causation, 966
        Alcoholic and malt liquors, 966
      Symptoms, 966
        Physiognomy, 966
        Tongue, state of, 966
        Breath, state of, 966
        Appetite, impaired, 966
        Nausea, 966
        Bowels, state of, 966
        Headache, 966
        Vertigo, 966
        Conjunctivae, yellow, 966
        Jaundice, 966
      Course, 967
      Duration, 967
      Termination, 967
      Treatment, 967
        Prophylaxis, 967
        Diet, 967
        Skimmed milk, use of, 967
        Blue-pill, 967
        Rochelle and Epsom salts, 967
        Euonymin, use of, 968
        Ipecacuanha, 968
        Podophyllin, 968
        Calomel, dose of, 968
        Phosphate of sodium, 968
        Mineral waters, 968
    _Lithaemia_, 968
      Definition, 968
      Pathogeny, 968
        Hepatic action in formation of uric acid, 969
        Albuminoid food, over-consumption of, 969
        Luxurious habits, 969
        Sedentary life, 969
        Alcoholic and malt liquors, 969
      Symptoms, 969
        Digestive disturbances, 969
        Appetite, capricious, 969
        Tongue, state of, 969
        Bowels, state of, 970
        Oxaluria, 970
        Nervous symptoms, 970
        Headache, 970
        Nausea, 970
        Mental depression, 970
        Vertigo, 970
        Skin, state of, 970
        Urticaria, 970
        Urine, state of, 970
        Pain in back, 970
      Course, 970
      Duration, 970
      Termination, 970
      Prognosis, 970
      Diagnosis, 970
        from gastro-duodenal catarrh, 970
        from organic brain disease, 971
      Treatment, 971
        Diet, 971
        Avoidance of fatty, starchy, and saccharine articles, 971
          of wine and malt liquors, 971
        Food, allowable, 971
        Exercise, 971
        Sea-bathing, 971
        Nitric acid, use of, 972
        Alkalies, use of, 972
        Purgative mineral waters, 972
        Phosphate of sodium, 972
        Mercurials, 972
        Podophyllin, 972
        Euonymin, 972
        Arsenic, 973
        Quinine, 973
        Sponge-baths, 973
        Iodide of mercury, locally to hepatic region, 973
        Electricity, 973
        Of hypochondriasis, 973
    _Hepatic Glycosuria_, 973
      Definition, 973
      Pathogeny, 973
      Symptoms, 973
        Digestive disturbances, 974
        Increased urination, 974
        Urine, condition of, 974
          specific gravity of, 974
          tests for sugar in, 974
      Course, 974
      Duration, 974
      Termination, 974
      Prognosis, 974
      Diagnosis, 974
        From gastro-duodenal catarrh, 974
        From lithaemia, 974
        From diabetes, 974
      Treatment, 974
        Diet, 975
        Exercise, 975
        Medicinal, 975
        Nux vomica, 975
        Fowler's solution, dose, 975
        Phosphate of sodium, 975
        Carbolic acid, 975
        Bismuth, 975
        Tr. iodine, 975
    _Jaundice_ (_Icterus_), 975
      Definition, 975
      Etiology, 975
        Disorganization of the blood, 975
        Non-disposal by liver of biliary material, 976
        Absorption of biliary material by blood, 976
        Emotions, influence of, on causation, 976
        Obstruction from hyperaemia of bile-ducts, 977
            from spasm of muscular fibre of ducts, 977
          gastro-duodenal catarrh, 977
          errors in diet, 977
          rich food, 977
          cold and wet, 977
          malaria, 977
      Symptoms, 977
        Premonitory, 977
        Signs of gastro-duodenal catarrh, 977
        Yellowness, seat of appearance, 977
          mode of extension, 978
        Feces, discoloration of, 978
        Urine, condition of, 978
          color of, 978
          tests for bile, 978
          albumen in, 978
          urea in, 979
        Liver, condition of, 979
        Epigastrium, tenderness of, 979
        Pulse, state of, 979
        Heart, slowing of, 979
            cause, 979
        Temperature, 980
        Fever, 980
        Nervous disturbances, 980
        Nutrition, disturbances of, 980
        Vision, modifications of, 980
        Xanthopsy in, 980
        Headache and vertigo, 980
        Mental depression, 980
        Wakefulness, 980
        Pruritus of skin, 980
        Boils and carbuncles, occurrence of, 980
        Xanthelasma vitiligoidea of skin, 980
          plane form, 980
          tuberose form, 981
        Hemorrhagic diathesis, 981
      Course, 981
      Duration, 981
      Prognosis, 981
      Diagnosis, 981
        Importance of ascertaining condition of gall-bladder, 982
      Treatment, 982
        Of nausea, 982
        Diet, 983
        Rectal irrigation, 983
        Emetics, use of, 982
        Ipecacuanha, 982
        Calomel, 982
        Cholagogues, use of, 982
        Podophyllin, 982
        Euonymin, 982
        Phosphate of sodium, 982
        Arseniate of sodium, 982
        Mineral waters, 982
        Nitric acid, 983
        Nitro-muriatic acid, 983
            locally, 983
        Electricity, use of, 983
  Structural diseases of liver, 983
    _Hyperaemia of Liver_, 983
      Definition, 983
      Etiology, 983
        Digestive process, 984
        Food, over-indulgence in, 984
        Sedentary life, 984
        Sudden suppression of hemorrhages, 984
        Menstrual period, 984
        Mechanical, 984
        Heart disease, organic, 984
        Pulmonary disease, chronic, 984
        Climate, 984
        Malaria, 984
      Pathological anatomy, 985
        Enlargement of liver, 985
        Portal vein, changes in, 985
        Extravasations of blood in hepatic tissue, 985
        Mechanical form, 985
        Nutmeg liver, 985
        Cyanotic atrophy of, 985
        Atrophy of hepatic cells, 985
        Sclerosis of central vein, 985
      Symptoms, 986
        Signs of gastro-intestinal catarrh, 986
        Hypochondrium, right, fulness of, 986, 987
          pain in, 986, 987
        Increased hepatic dulness, 986
          method of determining, 986
        Urine, state of, 986, 987
        Jaundice, 986, 987
        Stools, condition of, 986, 987
        Ascites in nutmeg liver, 987
        Mental depression, 987
      Course, 987
      Duration, 987
      Termination, 987
      Prognosis, 988
      Diagnosis, 988
      Treatment, 988
        Diet, 988
        Skim-milk, 988
        Exercise, 988
        Bathing, 988
        Mineral waters, saline laxative, 988
        Phosphate of sodium, 988
        Cholagogues, 988
        Digitalis, use of, when due to organic heart disease, 988
    _Perihepatitis_, 989
      Definition, 989
      Pathogeny, 989
        As an extension from other parts, 989
        Passage of gall-stones, 989
        Traumatic causes, 989
        Tight-lacing, 989
      Symptoms, 989
        Pain in right hypochondrium, 989
        Hepatic colic, 989
        Jaundice, 989
        Friction sound, 989
      Course, 989
      Duration, 989
      Termination, 989
      Diagnosis, 989
        From pleuritis, 990
      Treatment, 990
        Leeching, 990
        Turpentine stupes, 990
        Bandage, use of, 990
        Morphia for pain, 990
    _Interstitial Hepatitis--Sclerosis of Liver: Cirrhosis_, 990
      Definition, 990
      Etiology, 990
        Age, influence of, on causation, 990
        Sex, influence of, on causation, 991
        Alcohol, influence of, on causation, 991
        Syphilis, influence of, on causation, 991
        Malaria, influence of, on causation, 991
        Obstruction of bile-ducts, 991
        Closure of hepatic vein, 991
            portal vein, 991
        Arsenic and antimony, 991
        Phosphorus, 991, 992
        Extension of inflammation in perihepatitis, 992
      Pathological anatomy, 992
        Increased size of liver, 992
        Development of new connective tissue, 992
        Monolobular form, 992
        Multilobular form, 992
        Contraction of connective tissue, 992
        Decreased size of liver, 992
        Hobnail appearance of surface, 992
        Portal veins, lesions of, 992
        Atrophy of hepatic cells, 992, 993
      Symptoms, 993
        Insidious development, 993
        Digestive disturbances, 993
        Jaundice, 997
        Appetite, capricious, 993
        Nausea and vomiting, 993
        Bowels, state of, 993
        Stools, state of, 994
        Hemorrhoids, 993
        Fissure of anus, 994
        Abdomen, state of, 994
        Flatus, accumulation of, 994
        Hemorrhages, 994
        Spleen, enlargement of, 994
        Ascites, 995
        Blood, watery condition of, 995
        Anasarca, 995
        Oedema, general, 995
        Anastomoses of veins, 996
        Physical signs, 996
        Auscultation, 996
        Mode of examining liver, 996, 997
        Size of area of dulness, 997
        Physiognomy, 997
        Skin, color and state of, 997, 998
        Urine, state of, 998
        Ulcers of stomach and intestine, 999
        Thrombosis of portal vein, 999
        Nervous disturbances, 999
        Cerebral symptoms, 999
        Coma in, 999
        Emaciation, 999
        Kidneys, atrophy of, 999
        Cerebral sclerosis, 999
      Course, 998
      Duration, 999
      Terminations, 999
      Prognosis, 999
      Diagnosis, 999
        From amyloid disease, 1000
          hydatids, 1000
          cancer, 1000
          acute yellow atrophy, 1000
      Treatment, 1000
        Prophylaxis, 1000
        Diet, 1000
        Of malarial cause, 1000
        Of overgrowth of connective tissue, 1000
        Of gastro-intestinal catarrh, 1002
        Of dropsical effusions, 1001
        Of ascites, 1001
        Of diarrhoea, 1002
        Local, 1002
        Of hemorrhage, 1002
        Chloride of gold and sodium, 1001
          of mercury, 1001
        Phosphate of sodium, 1001
        Vapor bath, 1001
        Digitalis stupes, 1001
        Copaiba, 1001
        Pilocarpine, 1001
        Hydragogue cathartics, 1001
        Tapping, 1002
        Bismuth, 1002
        Opium, 1002
        Ergotin, 1002
        Iron, 1002
        Counter-irritation, 1002
        Dry cups, 1002
        Blisters, 1002
        Ung. hydrarg. iod. rubri, 1002
    _Suppurative Hepatitis--Abscess of Liver_, 1002
      Definition, 1002
      Etiology, 1002
        Climate, influence on causation, 1002
        Sex, influence on causation, 1003
        Age, influence on causation, 1003
        Temperament, influence on causation, 1003
        Traumatism, 1003
        Wounds, 1003
        State of portal and hepatic veins, 1004
            embolism, 1004
          Source of emboli, 1004
        Ulceration and dilatation of bile-ducts, 1005
        Proctitis, 1004
        Dysenteric ulceration, 1004
        Food, improper, 1005
        Alcohol, 1005
        Malarial influence, 1005
      Pathological anatomy, 1005
        Initial lesions, 1005
            in cells, 1005
            in vessels, 1005
        From embolism, lesions of, 1005
        Tropical form, lesions of, 1006
          development of, 1006
        Size of purulent collections, 1006
        Formation of limiting membrane, 1006
        Number of abscesses, 1006
        Seat of abscesses, 1006
        Contents of abscesses, 1007
        Presence of bile in pus, 1007
        Absence of limiting membrane, 1007
        Pointing of abscesses, 1007
            method of, 1007
        Formation of adhesions, 1007
        Pus, modes of escape, 1007
          escape into neighboring organs, 1007
        Processes of healing, 1008
        Condition of liver outside of abscess, 1008
      Symptoms, 1008
        Systemic, 1008
        Onset of, 1008
        Chills, 1008
        Temperature, 1008
        Pulse, 1009
        Fever, type of, 1008
          typhoid form of, 1009
        Sweating, 1009, 1010
        General malaise, 1009
        Flesh, loss of, 1009
        Skin, color of, 1009
        Jaundice, 1009, 1013
        Mental condition, 1009
        Cholaemia, 1010
        Stupor, 1010
        Wakefulness, 1009
        Hypochondria, 1010
        Urine, state of, 1010, 1014
        Absence of general, 1010
        Local, 1010
        Change in size of liver, frequency of, 1010
        Enlargement, 1010
        Seat of purulent collection, 1011
        Tumor of epigastrium, 1011
        Fluctuation, 1011
        Pain, 1011, 1012
          seat of, 1011
          character of, 1012
          in right shoulder, 1012
        Decubitus, characteristic, 1012
        Nausea and vomiting, 1013
        Tongue, state of, 1013
        Relation to dysentery, 1014
        Cough, 1014
        Respiration, 1014
        Pleuritis, 1014
        Pleuro-pneumonia, 1014
        Singultus, 1015
        Pericarditis, 1015
      Course, 1014
        Usual point of discharge, 1016
        Discharge into pleural cavity, 1016
          pericardium, 1016
          peritoneal cavity, 1016
          intestines, 1016
      Duration, 1017
      Termination, 1017
        Effect of mode of discharge upon, 1017
        Recovery by absorption of pus, 1018
        Fatty degeneration of pus, 1018
      Mortality, 1017
      Prognosis, 1018
      Diagnosis, 1018
        From echinococcus, 1018
          dropsy of gall-bladder, 1019
          cancer of liver, 1019
          abscess of abdominal wall, 1019
          empyema, 1020
          intermittent fever of hepatic colic, 1020
        Value of puncture of right lobe in, 1020
      Treatment, 1020
        Aborting, 1020
          use of quinia in, 1020
        Of septicaemic fever, 1020
        Of dysentery in, 1020
        Of vomiting, 1021
        Local, 1021
        Evacuation of pus, 1021
        Puncture, exploratory, 1021
          harmlessness of, 1021
          effects of, 1022
          mode of, 1022
        Aspirator, use of, 1022
          mode of using, 1022
        Poultices, use of, 1023
        Quinia, use of, 1020
        Ipecacuanha, 1020
        Soda powders, 1020
        Bismuth, 1021
        Creasote, 1021
        Diet, 1021
        Stimulants, 1021
        Nutrient enemata, 1021
    _Acute Yellow Atrophy_, 1023
      Definition, 1023
      History, 1023
      Etiology, 1023
        Frequency, 1023
        Age, influence on causation, 1024
        Sex, influence on causation, 1024
        Pregnancy, influence on causation, 1024
        Depressing emotions, 1024
        Syphilis, 1024
      Pathological anatomy, 1025
        Change in size, 1025
        Capsule, state of, 1025
        Hemorrhagic extravasations in liver-tissue, 1025
        Bile-ducts, lesions of, 1025
        Microscopic appearance of hepatic tissue, 1025
        Cell-degeneration, 1025
        Connective tissue, increase of, 1025
        Spleen, lesions of, 1026
        Peritoneum, lesions of, 1026
        Mesenteric glands, swelling of, 1026
        Stomach and intestines, lesions of, 1026
        Kidneys, lesions of, 1026
        Heart, lesions of, 1026
        Brain, lesions of, 1026
      Symptoms, 1026
        Prodromata, 1026
        Duration of, 1027
        Signs of gastro-duodenal catarrh, 1027
        Jaundice, 1027
        Toxaemic period, 1027
        Dilatation of pupil, 1027
        Excitement with delirium, 1027
        Coma, 1027
        Convulsions, 1027
        Sensibility, disturbances of, 1028
        Motility, disturbances of, 1028
        Hemorrhages from mucous surfaces, 1028
        Epistaxis, 1028
        Haematemesis, 1028
        Temperature, 1028
        Pulse, condition of, 1028
        Tongue, condition of, 1028
        Nausea and vomiting, 1026, 1027, 1028
        Constipation, 1028
        Skin disorders, 1028
        Urine, state of, 1027, 1028
        Blood, changes in, 1029
      Course, 1029
      Duration, 1029
      Termination, 1029
      Diagnosis, 1029
        From catarrhal jaundice, 1029
        Acute phosphorus-poisoning, 1029
      Treatment, 1030
        Quinia, use of, 1030
        Phosphate of sodium, 1030
        Euonymin, use of, 1030
        Iridin, use of, 1030
        Purgatives, 1030
        Bismuth, 1030
          and carbolic acid, 1030
        Ergotin, use of, 1030
        Alcohol, use of, 1030
        Iron, 1030
        Phosphorus, 1030
        Gold and silver, chloride of, 1030
        Of nausea and vomiting, 1030
        Of hemorrhage, 1030
    _The Liver in Phosphorus-poisoning_, 1030
      Definition, 1030
      Pathogeny, 1030
        Age, 1030
        Women, frequency in, 1030
        Tissues, biliary staining of, 1031
        Extravasation of blood in mucous and serous membranes, 1031
        Spleen, enlargement of, 1031
        Liver, hyperplasia and atrophy of, 1031
          cell-degeneration, 1031
        Bile-ducts, lesions of, 1031
        Mucous membrane of stomach, lesions of, 1031
        Kidneys, lesions of, 1031
      Symptoms, 1031
        Resemblance to acute yellow atrophy, 1031
        Of local irritation of poison, 1031
        Burning in gullet, 1031
        Nausea and vomiting, 1031
        Systemic, 1031
        Vomiting, 1031
        Vomit, characters of, 1031
        Stools, characters of, 1031
          phosphorescent, 1031
        Hepatic dulness, increase of, 1032
        Jaundice, 1032
        Liver, enlargement of, 1032
        Nervous disorders, 1032
          drowsiness, 1032
          delirium, 1032
          convulsions, 1032
        Temperature, 1032
        Pulse, state of, 1032
        Urine, state of, 1032
      Course, 1032
      Duration, 1032
      Termination, 1032
      Diagnosis, 1032
        From acute yellow atrophy, 1032
      Treatment, 1033
        Emetics, 1033
        Decoction of flaxseed, 1033
        Slippery elm, 1033
        Oil of turpentine, 1033
        Sulphate of copper, 1033
        Transfusion, 1033
        Diet, 1033
        Of inflammatory symptoms, 1033
    _Carcinoma of Liver_, 1033
      Definition, 1033
      Etiology, 1033
        Heredity, 1033
        Age, 1034
        Sex, 1034
      Morbid anatomy, 1034
        Primary form, 1034
        Hepatic enlargement, 1034
        Microscopic appearances, 1035
        Secondary form, 1034, 1035
          frequency of, 1035
        Metastasis in, 1035
          forms of, 1035
          from face, 1035
            stomach, 1035
            intestines, 1035
          nodes, number of, 1035
            size, 1035
            changes in, 1036
        Atrophy of hepatic structure, 1035
        Infiltrating form, 1034
        Pigment form, 1035
        Tumors, shape and size, 1034
        Sarcomas, 1036
      Symptoms, 1036
        General history of, 1036
        Liver, condition, 1037
          mode of examining, 1037
        Ascites, 1037
        Peritonitis in, 1037
        Pain, seat and character, 1038
        Vomiting in secondary form, 1038
        Jaundice, frequency, 1038
        Skin, state, 1038
        Physiognomy, 1038
        Emaciation, 1038
        Strength, loss, 1038
        Urine, condition, 1038
        Signs of gastro-intestinal catarrh, 1038
        Appetite, impaired, 1038
      Course, 1039
      Duration, 1039
      Termination, 1039
      Diagnosis, 1039
        From amyloid disease, 1040
        From echinococcus, 1040
        From cirrhosis, 1040
        From syphilis, 1040
      Treatment, 1040
    _Amyloid Liver_, 1040
      Definition, 1040
      Etiology, 1040
        Suppuration of bone, 1041
        Syphilis, 1041
        Chronic malarial infection, 1041
        Pulmonary cavities, 1041
        Age, 1041
        Sex, 1041
        Cachexia from development of new formations, 1041
        Temperament, 1041
        Frequency in lymphatic individuals, 1041
      Pathological anatomy, 1041
        Origin of amyloid deposit, 1042
        Mode and order of deposit, 1042
        Size and shape of liver, 1042
        Consistence of, 1042
        Iodine test for, 1043
          Mode, 1043
        Condition of hepatic tissues not invaded, 1043
      Symptoms, 1043
        Liver enlargement, 1043
        Cachexia, 1043
        Jaundice, frequency, 1044
        Ascites, frequency, 1044
        Hemorrhoids, 1044
        Diarrhoea, 1044
        Stools, 1044
          black, 1044
        Vomiting in, 1044
        Vomit, bloody, 1044
        Spleen, enlarged, 1044
        Kidney, enlarged, 1044
        General dropsy, 1044
        Hydraemia, 1044
        Urine, state, 1044
        Emaciation, 1044
      Course, 1044
      Duration, 1044
      Prognosis, 1045
      Diagnosis, 1045
        From fatty liver, 1045
          hydatid disease, 1045
          cancer, 1045
      Treatment, 1045
        Of cause, 1045
        Alkalies, use of, 1045
        Iodides, use of, 1046
        Ung. hydrarg. iod. rubri, 1046
        Chloride of gold and sodium, 1046
          silver, 1046
          arsenic, 1046
          iron, 1046
        Diet, 1046
        Of nausea and vomiting, 1046
    _Fatty Liver--Fatty Degeneration of Liver_ (_Hepar Adiposum_),
        1046
      Definition, 1046
      Etiology, 1046
        Sex, 1047
        Phthisis, 1047
        Cachexiae, 1047
        Alcoholism, 1047
        Poisoning by phosphorus, 1047
          arsenic, 1047
          antimony, 1047
        Pregnancy, 1047
        Deficient oxidation of fat, 1046, 1047
        Sedentary life, 1047
      Pathological anatomy, 1047
        Liver, enlargement of, 1047
          shape and size, 1047
          anaemic condition of, 1047
          seat of fatty deposit, 1047, 1048
      Symptoms, 1048
        Dyspeptic disturbances, 1048
        Stools, character, 1048
        Circulation, feeble, 1048
        Pulse, condition, 1048
        Sleeplessness, 1048
        Mental depression, 1048
        Hypochondria, 1048
        Jaundice, 1049
        Urine, state, 1049
        Area of hepatic dulness, 1049
      Course, 1049
      Duration, 1049
      Termination, 1049
      Prognosis, 1049
      Diagnosis, 1049
        From amyloid liver, 1049
          cancer, 1050
        Treatment, 1050
          Of digestive disturbances, 1050
          Diet, 1050
          Cholagogues, 1050
          Phosphate of sodium, 1050
          Sulphate of manganese, 1050
            quinia, 1051
            iron, 1051
          Tinct. nux vomicae, 1050
          Nitric acid, 1050
          Alkalies, 1050
          Permanganate of potassium, 1051
  Affections of Biliary Passages, 1051
    _Catarrh of Bile-ducts_, 1051
      History, 1051
      Definition, 1051
      Etiology, 1051
        Peculiarity of constitution, 1051
        Climate, 1051
        Malaria, 1051
        Cold and wet, 1051
        Disturbances of portal circulation, 1052
        Extension from duodenum, 1052
        Food, improper, 1052
        Condiments and sauces, 1052
        Alcoholic and malt liquors, abuse, 1052
      Pathological anatomy, 1052
        Seat of catarrh, 1052
        Mucous membrane of ducts, lesions of, 1053
          swelling of, 1053
        Finer ducts, lesions of, 1053
        Liver, condition of, 1053
      Symptoms, 1053
        Signs of gastro-duodenal catarrh, 1053
        Tongue, state of, 1053
        Appetite impaired, 1053
        Epigastrium, fulness of, 1053
        Abdomen, state of, 1054
        Intestinal canal, state of, 1054
        Diarrhoea and constipation, 1054, 1055
        Stools, characters of, 1054, 1055
        Urine, state of, 1054, 1055
        Nervous disturbances, 1054, 1055
        Headache, 1054, 1055
        Vertigo, 1054, 1055
        Febrile movement, 1054
        Jaundice, 1054
      Course, 1055
      Duration, 1055
      Termination, 1055
      Diagnosis, 1055
      Treatment, 1056
        Diet, 1056
        Diarrhoea, 1056
        Constipation, 1056
        Mercury, use of, 1056
        Calomel, use of, 1056
        Phosphate of sodium, 1057
        Silver and zinc salts, 1057
        Arsenic, 1057
        Iron, 1057
        Quinia, 1057
        Permanganate of potassium, 1057
        Mineral acids, 1057
        Enemata, 1057
        Electricity, 1057
    _Biliary Concretions, Gall-stones, Hepatic Calculi, etc._, 1058
      Definition, 1058
      Formation, 1058
        From inspissated bile, 1058
        Of calculi, 1059
          shape, 1059
          number, 1059
          color, 1059
          size, 1059
          composition, 1060
          nucleus, 1060
          body of, 1061
          rind, 1061
          specific gravity, 1061
          origin and formation, 1061-1063
          composition of bile, 1062
          reaction, 1062
      Etiology, 1063
        Age, 1063
        Sex, 1064
        Social state, 1064
        Malarial influence, 1064
        Season, 1065
        Obesity, 1065
        Starchy, fatty, and saccharine foods, 1065
        Irregular meals, 1065
        Retardation to flow of bile, 1066
        Mental emotion, 1066
        Situation and destiny of gall-stones, 1066
        Spontaneous disintegration of, 1066
        Gall-ducts, dilatation of, from, 1067
          -bladder, changes in, from, 1066
            dilatation of, 1067
            adhesions, 1067
            cancer of, 1067
            hypertrophy of, 1067
          -stones, migrations of, 1067, 1068
            ulceration into neighboring organs by, 1068
        Formation of fistulae, 1068
      Symptoms due to presence of gall-stones at their original site,
        1069
        Uneasiness in hypochondrium, 1069
        Pain, 1069
          in shoulder, 1069
          in right side of neck, 1069
        Gastralgia, 1069
        Vertigo, 1070
        Migraine, 1069
        Headache, 1070
        Digestive disturbances, 1070
      Symptoms due to migration by natural channels (hepatic colic),
        1070
        Time of occurrence of paroxysms, 1070
        Paroxysm, onset of, 1070, 1071
        Pain, seat and characters of, 1070
        Physiognomy, 1071
        Nausea and vomiting, 1071, 1072
        Pulse, state of, 1071
        Collapse, 1071
        Duration, 1071
        Nervous disturbances, 1071
        Hysteria, 1071
        Convulsions, 1071
        Chills, 1071, 1072
        Periodicity of paroxysms, 1071
        Relation to malaria, 1071, 1072
        Fever, 1072
        Constipation, 1072
        Jaundice, 1072
          duration of, 1073
        After paroxysm, 1073
        Stools, 1073
          search for calculi in, 1073
            method, 1073
        Passage of inspissated bile, 1073, 1074
        Recurrence of attacks, 1074
      Impaction of calculi, 1074
          point of, 1074
          peritonitis from, 1074
          adhesions, 1074
      Migration by artificial routes, 1074
          into neighboring organs, 1074
          into stomach, 1074
          into intestines, 1074
          into duodenum, 1074
        Biliary fistulae, formation of, 1075
      Course, 1075
        Migration without symptoms, 1075
        Obstruction of bowels from, 1075
        Symptoms of presence in intestinal canal, 1076
        Vomiting of gall-stones, 1076
      Complications, 1076
        Local inflammation, 1076
        Dropsy of gall-bladder, 1077
        Angiocholitis, 1077
        Relation to cancer of ducts, 1077
        Heart disturbance, 1077
        Initial murmurs, 1077
        Reflex nervous disorders, 1078
        Herpes zoster, 1078
        Death from lodgment of calculus in Vater's diverticulum, 1078
          from vomiting, 1078
      Diagnosis, 1078
        From gastralgia, 1078
          hepatalgia, 1079
          flatulent colic, 1079
          renal colic, 1079
      Treatment, 1079
        Of calculus state, 1079
        Of inspissated bile, 1079
          by sulphate of soda, 1079
        Diet, 1079
        Exercise, 1079
        Bathing, 1079
        Alkaline mineral waters, 1079
        Phosphate of sodium, 1080
        Of biliary calculi in situ, 1080
        Manipulation of gall-bladder, 1080
        Faradization, 1080
        Ether and turpentine (Durande's remedy), 1080
        Chloroform, 1081
        Cholate of sodium, 1081
        Ox-gall, 1081
        Puncture of gall-bladder, 1081
        Removal of contents of gall-bladder by puncturing, 1081
        Of paroxysms of hepatic colic, 1081
        Of pain, 1081
        Morphia and atropia, hypodermically, 1082
          dose of, 1082
        Emetics, 1082
        Hot fomentations, 1082
        Hot baths, 1082
        Chloroform, 1082
        Ether, 1082
        Chlorodyne, 1082
        Chloral, 1082
        Purgatives, 1082
        Cholagogues, 1082
        Ipecacuanha, 1082
        Euonymin, 1082
        Iridin, 1082
    _Occlusion of Biliary Passages--Stenosis of Ductus Communis
        Choledochus_, 1082
      Definition, 1082
      Pathogeny, 1082
        Of cystic duct, 1083
        Of common duct, 1083
        Passage of calculi, 1083
        Catarrhal inflammation, 1083
        Cicatrization of ulcers, 1083
        Impaction of biliary calculi, 1084
        Foreign bodies, 1084
        Of hepatic duct, 1084
        Seat and cause of occlusion in common duct, 1083, 1084
        Pressure of tumors, 1085
        Cancer of gall-bladder, 1085
          of pylorus, 1085
        Enlarged lymphatic glands, 1085
        Effects of occlusion of cystic duct, 1085
        Retention of secretion in gall-bladder, 1085
        Effects of occlusion of hepatic duct, 1085
        Catarrhal state, 1085
        Distension of hepatic tubes with sero-mucus, 1085
        Dilatation of ducts, 1086
        Rupture of ducts, 1086
        Changes in liver, 1086
        Cell-degeneration, 1086
      Symptoms, 1086
        Of cystic duct, 1086
        Dropsy of gall-bladder, 1086
        Of hepatic duct, 1086
        Jaundice, 1086, 1087
          sudden disappearance of, 1087
        Pruritus, 1087
        Eczema, 1087
        Xanthelasma, 1087
        Increased area of hepatic dulness, 1087
        Tenderness of hypochondrium, 1087
        Enlargement of liver, 1087
        Hepatic secretion, state of, 1087
        Atrophy of liver, 1088
        Enlargement of gall-bladder, 1087
        Digestive disturbances, 1088
        Appetite, state of, 1088
        Tongue, state of, 1088
        Thirst, 1088
        Nausea and vomiting, 1088
        Vomit, characters of, 1088
        Bowels, irregular, 1088
        Stools, characters of, 1088
          color of, 1088
        Kidneys, state of, 1090
        Urine, state of, 1089, 1090
        Albuminuria, 1090
        Casts, 1090
        Pulse, state of, 1089
        Hemorrhages, 1089
        Epistaxis, 1089
        Haematemesis, 1089
        Fever, 1090
          intermittent form, 1090
          distinguished from malaria, 1090
          temperature, 1091
          duration, 1091
        Cholaemia, 1091
        Nervous disturbances, 1092
        Headache, 1092
        Mental depression, 1092
        Xanthopsia, 1092
        Paralysis, 1092
        Convulsions, 1092
      Course, 1092
      Duration, 1092
      Termination, 1092
      Prognosis, 1092
      Diagnosis, 1092
        Puncture of gall-bladder in, 1092
        Exploration of gall-bladder, 1093
        Mode of puncture, 1093
        Of dilated gall-bladder from aneurism, 1093
            from hypertrophic cirrhosis, 1093
      Treatment, 1094
        Fracture of impacted calculus, 1094
            mode of, 1094
        Solution of impacted calculi by puncture of gall-bladder, 1094
  Diseases of Portal Vein, 1095
    _Thrombosis and Embolism of Portal Vein; Stenosis; Pylephlebitis_,
        1095
      Definition, 1095
      Causes, 1095
        Coagulable state of blood, 1095
        Weak heart-action, 1095
        Impeded circulation from external pressure, 1095
        Of adhesive pylephlebitis, 1095
      Symptoms, 1096
        Sudden formation of ascites, 1096
          enlargement of spleen, 1096
          passive congestion of gastro-intestinal mucous membrane,
            1096
        Catarrh of gastro-intestinal mucous membrane, 1096
        Nausea and vomiting, 1096
        Hemorrhages, 1096
        Abdominal veins, abnormal anastomoses of, 1096
      Course and termination, 1097
      Diagnosis, 1097
      Treatment, 1097
        Copaiba, 1097
        Pilocarpine, 1097
        Leeches, 1097
    _Suppurative Pylephlebitis_, 1097
      Pathogeny, 1097
        Ulceration and suppuration of intestinal tube, 1097, 1098
        Multiple abscess of liver, 1097, 1098
        Typhlitis, 1097, 1098
        Traumatic injuries of intestine, 1097
        Formation of emboli, 1097, 1098
        Changes in vein-wall, 1098
        Production of thrombi, 1098
        Formation of secondary hepatic abscesses, 1098
        Suppuration of caecum, 1098
          of rectum, 1098
      Symptoms, 1099
        Of primary lesion, 1099
        Of secondary result, 1099
        Chills, 1099
        Pain, seat and character, 1099
        Fever, 1099
          periodic form, 1099
        Temperature, 1100
        Digestive disturbances, 1100
        Vomiting, 1100
        Hemorrhages, 1100
        Tongue, condition of, 1100
        Irregular bowels, 1100
        Jaundice, 1100
      Course, 1101
      Duration, 1101
      Termination, 1101
      Diagnosis, 1101
      Treatment, 1101
        Ammonia, use of, 1101
        Quinine, 1101
        Corrosive sublimate, 1101
  Parasites of the Liver, 1101
    _Echinococcus of Liver_, 1101
      Definition, 1101
      Etiology, 1101
        Migration of embryo from intestine, 1102
      Pathology, 1102
      Symptoms, 1102
        Number of, 1102
        Seat of, 1102
        Atrophy of liver, 1102
        Jaundice, 1102, 1104
        Growth, mode of, 1102, 1103
        Characters of vesicles, 1103
        Contents of vesicles, 1103
        Multilocular form, 1103
        Hydatid tumor, characteristics of, 1104
        Ascites, 1104
        Enlargement of spleen, 1104
        Digestive disturbances, 1104
      Diagnosis, 1104
        Characters of fluid, 1105
        Hooklets in fluid, 1105
        From abscess of liver, 1105
      Duration, 1105
      Termination, 1106
      Treatment, 1106
        Prophylaxis, 1106
        Boiling and filtering of water, 1106
        Therapeutical, 1106
        Removal of vesicle, 1107
          by incision, 1107
        Puncture, 1107
        Aspirator, use of, 1107
        Injection of iodine, 1108
        Electrolysis, 1108
        Acupuncture, 1109
    _Distomum hepaticum_ (_liver-flukes_), 1109
      Description, 1110
      Mode of access to man, 1110
      Diagnosis, 1110
      Symptoms, 1110
      Treatment, 1110
        Parasiticides, use of, 1110
        Creasote, 1110
        Bichloride of mercury, 1110
        Thymol, 1110
    Parasites in Portal Vein, 1111

Liver, diseases of, as a cause of ascites, 1173
      of pancreatic hemorrhage, 1129
    influence on causation of constipation, 641
        of functional dyspepsia, 447
        of acute gastritis, 464
  enlargement of, in rachitis, 139
    in hereditary syphilis, 283
  functional disturbance of, in intestinal indigestion, 629
  hyperaemia of, relation to causation of diabetes mellitus, 195
  lesions of, in diabetes mellitus, 201
    in dysentery, 801
    in entero-colitis, 739
    in gout, 117, 118
    in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 705
    in scurvy, 173
    in tabes mesenterica, 1188
  secondary growths of, in gastric cancer, 556

Lobe of ear, ulceration of, in scrofula, 246

Local causes of gastric cancer, 537
  nature of dysentery, 796
  peritonitis, 1159
  symptoms, of superficial glossitis, 357
    of abscess of liver, 1010
    of chronic articular rheumatism, 71
    of rheumatoid arthritis, 80, 81, 85
    of thrush, 334
  treatment of cancrum oris, 343
    of enteralgia, 665
    of parenchymatous glossitis, 365
    of chronic parenchymatous glossitis, 368
    of superficial glossitis, 357
    of chronic superficial glossitis, 367
    of glossitis parasitica, 359
    of acute gout, 134
    of intestinal obstruction, 864
    of abscess of liver, 1021
    of cirrhosis of liver, 1002
    of morbid dentition, 376
    of chronic oesophagitis, 417
    of cancer of oesophagus, 428
    of organic stricture of oesophagus, 425
    of spasmodic stricture of oesophagus, 421
    of ulceration of oesophagus, 418
    of perihepatitis, 990
    of acute peritonitis, 1151
    of acute pharyngitis, 397
    of syphilitic pharyngitis, 408
    of purpura rheumatica, 194
    of acute rheumatism, 68
    of chronic articular rheumatism, 74
    of muscular rheumatism, 76, 77
    of gonorrhoeal rheumatism, 107
    of rheumatoid arthritis, 100
    of aphthous stomatitis, 330
    of mercurial stomatitis, 348
    of stomatitis ulcerosa, 338
    of hereditary syphilis, 317
    of thrush, 335
    of tonsillitis, 387
    of typhlitis and perityphlitis, 822

Locality, influence on causation of scrofula, 233

Loop-shaped form of stomach, 617

Lumbago, 77

Lumbar colotomy for cancer of rectum, 915

Lumbo-abdominal neuralgia, distinguished from enteralgia, 663

Lung disease, chronic, influence on causation of constipation, 641

Lungs, condition of, in rachitis, 152
    in hereditary syphilis, 307
  gangrene of, complicating cancrum oris, 341
  gummata of, in hereditary syphilis, 307
  hypostatic congestion and pneumonia of, in entero-colitis, 734
  lesions of, in diabetes mellitus, 202
    in entero-colitis, 740
    in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 706
    in scurvy, 172
    in tabes mesenterica, 1188

Lupoid ulcer of rectum, 889

Luxurious living, influence of, on causation of gout, 110

Lymphangiectasis in Filaria sanguinis, 963

Lymphatic glands, caseation of, in scrofula, 239, 240
    changes of, in scrofula, 239, 240
      in tabes mesenterica, 1187
    swelling of, in cancrum oris, 342
      in parenchymatous glossitis, 361
      in catarrhal stomatitis, 323
      in mercurial stomatitis, 346
      in tonsillitis, 382

Lympho-sarcoma of intestine, 868


M.

Macroglossia, 349

Magnesium sulphate, use of, typhlitis and perityphlitis, 822

Malaria, influence on causation of biliary calculi, 1064
      of catarrh of bile-ducts, 1051
      of cholera morbus, 721
      of diabetes mellitus, 203
      of enteralgia, 660
      of gastralgia, 460
      of gastric hemorrhage, 582
      of acute intestinal catarrh, 671
      of chronic intestinal catarrh, 700
      of jaundice, 977
      of abscess of liver, 1005
      of amyloid liver, 1041
      of cirrhosis of liver, 991
      of hyperaemia of liver, 984
      of tabes mesenterica, 1186
  relation to hepatic colic, 1072
    to causation of rachitis, 145

Malarial form of acute pharyngitis, symptoms, 395
  poison, influence on causation of biliousness, 965
        of acute pharyngitis, 391

Malarious fevers, influence on causation of acute and chronic
        gastritis, 464, 470

Male fern, use of, in tape-worm, 941

Malformations, congenital, of anus and rectum, 837, 879

Malignant pustule of tongue, 368
  stricture and ulceration of rectum and anus, 902

Malt extracts, use of, in rachitis, 162
  liquors, influence on causation of biliousness, 966
        of catarrh of bile-ducts, 1052
        of gout, 111
        of lithaemia, 969

Manganese sulphate, use of, in fatty liver, 1050

Manipulation of gall-bladder to dissolve biliary calculi, 1080

Marasmus, influence on causation of atrophy of stomach, 616

Marriage of syphilitics, 255, 265, 269

Marriages, consanguineous, influence on causation of scrofula, 234

Massage, use of, in constipation, 653
    in rheumatoid arthritis, 101

Mastication, imperfect, influence on causation of functional
        dyspepsia, 445
      of intestinal indigestion, 625

Maternal ill-health, influence on causation of infantile peritonitis,
        1172

Maxillary bones, alterations of, in rachitis, 150

Meals, irregular, influence on causation of functional dyspepsia, 446

Measles of tape-worm, 932

Mechanism of intussusception, 847

Medina-worm, 962

Medulla oblongata, effects of puncture of diabetic area, 195

Medullary form of gastric cancer, 563
    of gastric cancer, histology, 563

Melaena, in simple ulcer of stomach, 492, 493
  neonatorum, etiology, 832

Melaenamesis in gastric cancer, 545

Melanotic sarcoma of intestines, secondary to tumor of eye or skin,
        873

Melituria in chronic intestinal pancreatitis, 1122
  in obstruction of pancreatic ducts, 1131

Membranous form of acute pharyngitis, symptoms, 395
    of acute pharyngitis, treatment, 399

Meningitis, distinguished from acute gastritis, 468
  in acute rheumatism, 39

Menstrual disease, influence on causation of pseudo-membranous
        enteritis, 765
  disorders from constipation, 647
    influence of, on causation of rheumatoid arthritis, 90
        of aphthous stomatitis, 326
        of simple ulcer of stomach, 487

Menstruation, influence on causation of functional dyspepsia, 448
      of gastralgia, 460
  scanty, in scrofula, 245
  suppression of, influence on causation of disease of pancreas, 1114

Mental anxiety, influence on causation of cholera morbus, 721
    and shock, influence on causation of diabetes mellitus, 203
  condition, in hepatic abscess, 1009
    in acute peritonitis, 1142
    in scurvy, 176
    in scrofula, 245
  depression in occlusion of biliary ducts, 1092
    in constipation, 647, 854
    in chronic intestinal catarrh, 708
    in intestinal indigestion, 628
    in jaundice, 980
    in fatty liver, 1048
    in hyperaemia of liver, 987
    in lithaemia, 970
    influence on causation of chronic pharyngitis, 403
  emotion, influence on causation of biliary calculi, 1066
        spasmodic stricture of oesophagus, 419
  state, in cancrum oris, 341
    in cholera morbus, 722
    influence on digestion, 437
      on causation of functional dyspepsia, 437
  overwork, influence on causation of intestinal indigestion, 624
  power, impaired, in intestinal indigestion, 628

Mercuric chloride, use of, in tonsillitis, 388
      in acute yellow atrophy of liver, 1030

Mercury, use of, in biliousness, 967
    in catarrh of bile-ducts, 1056
    in functional dyspepsia, 457
    in pseudo-membranous enteritis, 774
    in entero-colitis and cholera infantum, 760
    in scrofula, 251
    in hereditary syphilis, 315
    in syphilitic pharyngitis, 408
  bichloride, effect on rectum, 911
    use of, in acute intestinal catarrh, 695
      in dysentery, 809
      in cirrhosis of liver, 1001
      in amyloid liver, 1046
      in treatment of liver-flukes, 1110
      in chronic pharyngitis, 406

Mercurial ointments, use of, in pruritus ani, 917
      in typhlitis and perityphlitis, 822
  stomatitis, 344

Mercurials, use of, in ascites, 1178, 1179
    in hyperaemia of liver, 988
    in chronic gastritis, 478
    in jaundice, 982
    in lithaemia, 972
    in acute peritonitis, 1151

Mesenteric glands, changes in, in tabes mesenterica, 1187
    cheesy degeneration of, in tabes mesenterica, 1187
    enlargement of, in entero-colitis, 739
      in acute intestinal catarrh, 677
      in chronic intestinal catarrh, 705
      in acute yellow atrophy of liver, 1026
    lesions of, in dysentery, 801

Mesentery, elongated, as a cause of acute intestinal strangulation,
        841

Metals, certain, influence on causation of biliousness, 966

Metamorphosis, fatty, of pancreas, 1128

Methyl-aniline-violet test for lardaceous degeneration, 875

Metastasis in gastric cancer, frequency of, 567
  in carcinoma of liver, 1035
  occurrence of, in tonsillitis, 383
  secondary pancreatitis from, 1120
  tendency to, in medullary form of gastric cancer, 563

Metastatic abscesses, complicating mercurial stomatitis, 346

Miasmatic origin of acute rheumatism, 26

Micturition, painful, in enteralgia, 661

Micro-organisms, influence on causation of dysentery, 792
      of acute intestinal catarrh, 673

Micrococci and bacteria in stools in chronic intestinal catarrh, 708

Migraine complicating rheumatoid arthritis, 84

Migration of embryo from intestinal canal, in hydatids of liver, 1102
  of biliary calculi by artificial routes, 1068, 1074
  of echinococcus, 944
  of gall-stones by artificial routes, 1068, 1074
    symptoms due to, 1070

Migrations of Ascaris lumbricoides, 953
  of gall-stones, 1067

Miliary aneurisms of stomach, 579

Milk of diseased cows as a cause of tabes mesenterica, 1186
  condensed, use of, in cholera infantum and entero-colitis, 754
  peptonized, use of, in entero-colitis and cholera infantum, 751, 753
      in functional dyspepsia, 453
      in chronic interstitial pancreatitis, 1123
    mode of preparing, 1123
  use of, in constipation, 652
    in diabetes mellitus, 218
    in dysentery, 809
    in functional dyspepsia, 453
    in enteralgia, 666
    in entero-colitis, 749
    in acute and chronic gastritis, 468, 476
    in treatment of gout, 129
    in hemorrhage from bowels, 834
    in acute intestinal catarrh, 690, 691
    in chronic intestinal catarrh, 716
    in intestinal indigestion, 633
    in jaundice, 983
    in amyloid liver, 1046
    in cirrhosis of liver, 1000
    in rachitis, 159
    in cancer of stomach, 576
    in dilatation of stomach, 608
    in simple ulcer of stomach, 519

Milk-leg in paratyphlitis, 820

Mineral acids, use of, in catarrh of bile-ducts, 1057
      in chronic intestinal catarrh, 715
      in intestinal indigestion, 636
      in scurvy, 184
      in acute intestinal catarrh, 693, 694, 695
  baths, use of, in rheumatoid arthritis, 99
  poisoning, influence on causation of atrophy of stomach, 616
  waters, alkaline, use of, in biliary calculus state, 1079
      in chronic gastritis, 477
    natural, use of, in gout, 131
    saline laxative, use of, in hyperaemia of liver, 988
    use of, in biliousness, 968
      in constipation, 652, 653, 655
      in diabetes mellitus, 225, 226
      in pseudo-membranous enteritis, 776
      in chronic intestinal catarrh, 714, 715
      in intestinal indigestion, 634, 636
      in jaundice, 982
      in lithaemia, 972
      in rheumatoid arthritis, 99
      in typhlitis, 822

Mist. cretae, use of, in entero-colitis and cholera infantum, 758

Mitral murmurs due to biliary calculi, 1077

Moisture, influence on causation of dysentery, 788

Monolobular form of interstitial hepatitis, 992

Mono- or uniarticular rheumatism, 49

Morbid anatomy of catarrh of bile-ducts, 1052
    of cancrum oris, 341
    of cholera infantum, 742
    of cholera morbus, 721
    of constipation, 643
    of diabetes mellitus, 199
    of dysentery, 797
    of pseudo-membranous enteritis, 769
    of entero-colitis, 736
    of acute gastritis, 466
    of chronic gastritis, 471
    of parenchymatous glossitis, 363
    of superficial glossitis, 355
    of glossitis parasitica, 358
    of gout, 115
    of hemorrhage from bowels, 832
    of interstitial hepatitis, 992
    of acute intestinal catarrh, 673
    of chronic intestinal catarrh, 700
    of cancer of intestine, 871
    in lardaceous degeneration of intestine, 875
    of intussusception, 844
    of abscess of liver, 1005
    of amyloid liver, 1041
    of carcinoma of liver, 1034
    of fatty liver, 1047
    of hyperaemia of liver, 985
    of macroglossia, 352
    of acute oesophagitis, 411
    of chronic oesophagitis, 416
    of cancer of oesophagus, 427
    of dilatation of oesophagus, 432
    of paralysis of oesophagus, 429
    of organic stricture of oesophagus, 424
    of spasmodic stricture of oesophagus, 420
    of ulceration of oesophagus, 418
    of carcinoma of pancreas, 1123
    of acute pancreatitis, 1118
    of chronic interstitial pancreatitis, 1121
    of acute diffuse peritonitis, 1133
    of tubercular peritonitis, 1167
    of acute pharyngitis, 391
    of chronic pharyngitis, 403
    of syphilitic pharyngitis, 406
    of tuberculous pharyngitis, 400
    of hypertrophic stenosis of pylorus, 615
    of acute rheumatism, 46
    of chronic articular rheumatism, 70
    of gonorrhoeal rheumatism, 103
    of muscular rheumatism, 74
    of rheumatoid arthritis, 86
    of atrophy of stomach, 616
    of cancer of stomach, 560
    of cirrhosis of stomach, 613
    of dilatation of stomach, 599
    of hemorrhage from stomach, 583
    of simple ulcer of stomach, 503
    of aphthous stomatitis, 326
    of catarrhal stomatitis, 323
    of mercurial stomatitis, 346
    of stomatitis ulcerosa, 336
    of scrofula, 238
    of scurvy, 171
    of tabes mesenterica, 1187
    of thrush, 332
    of tonsillitis, 383
    of typhlitis, 814
  dentition, 371
  growths of pancreas, 1123
    influence on causation of organic stricture of oesophagus, 423

Morbus maculosus Werlhofii, 188

Morning vomiting in chronic gastritis, 473
    in cirrhosis of liver, 993

Morphia, effect on rectum, 911
  use of, in cholera morbus, 724
    in dysentery, 811
    in enteralgia, 665
    hypodermatically, in pseudo-membranous enteritis, 775
    in gastralgia, 463
    in acute intestinal catarrh, 693
    in intestinal obstruction, 863
    in organic stricture of oesophagus, 425
    in perihepatitis, 990
    in tuberculous pharyngitis, 402
    in acute rheumatism, 65
    in muscular rheumatism, 76
    in typhlitis, 822
  and atropia, hypodermic use of, in hepatic colic, 1082

Mortality of cholera morbus, 724
  of dysentery, 807
  of entero-colitis, 726, 727
  of hereditary syphilis, 272, 273
  of parenchymatous glossitis, 364
  of abscess of liver, 1017
  of intestinal obstruction, 862
  of acute peritonitis, 1143
  of acute rheumatism, 50
  of cancer of stomach, 532, 535
  of simple ulcer of stomach, 502
  of typhlitis and perityphlitis, 820, 821

Mouth, diseases of, 321
  hemorrhage from, 370
  lesions of, in entero-colitis, 739
  state of, in pseudo-membranous enteritis, 766
    in aphthous stomatitis, 329
    in gangrenous stomatitis, 340
    in mercurial stomatitis, 345
    in ulcerous stomatitis, 337

Movements, passive, in chronic forms of rheumatoid arthritis, 100

Mucous collections in acute intestinal catarrh, 676
  discharges in non-malignant stricture of rectum, 886
  membranes, affections of, in gout, 118
    atrophy of, in functional dyspepsia, 451
    condition of, in proctitis of chronic intestinal catarrh, 703
      in thrush, 333
    hypertrophy of, in chronic oesophagitis, 416
    of bile-ducts, lesions of catarrh of, 1053
    intestinal, lesions of, in cholera morbus, 721
      in constipation, 644
    gastric, lesions of, in acute gastritis, 466
    lesions of, in pseudo-membranous enteritis, 769
      in chronic gastritis, 471
      in acute intestinal catarrh, 674
      in chronic intestinal catarrh, 700
      in lardaceous degeneration of intestines, 875
      in catarrhal stomatitis, 324
      in mercurial stomatitis, 347
      in cirrhosis of stomach, 614
      in organic stricture of oesophagus, 424
      in typhlitis, perityphlitis, 814
    miliary infiltration of, in tubercular pharyngitis, 400
    softening of, in chronic gastritis, 471
    state of, in dilatation of stomach, 600
      in dysentery, 798
    of anus, hairs on, 892
    of ileum, swelling of, in chronic intestinal catarrh, 701
    of stomach, microscopic appearance of, in gastric cirrhosis, 614
  patches, appearance of, in syphilitic pharyngitis, 407
    of hereditary syphilis, 278
  stools, in chronic intestinal catarrh, 708
    in proctitis, 684
  vomiting of chronic gastritis, 478

Mud-baths, use of, in rheumatoid arthritis, 100

Multilobular form of interstitial hepatitis, 992
    of hydatid tumor of liver, 1103

Mumps, acute secondary pancreatitis metastasic of, 1121

Muriatic acid, use of, in cancrum oris, 343
    dilute, in functional dyspepsia, 456
      in acute intestinal catarrh, 693, 694
      in chronic intestinal catarrh, 715
      in intestinal indigestion, 636

Murmurs, haemic, in gastric cancer, 553
  heart, in purpura rheumatica, 189
    in acute rheumatism, 28, 35

Muscles, discovery of Trichina spiralis in, 958
  fatty degeneration of, in tuberculous pharyngitis, 401
  lesions of, in chronic articular rheumatism, 71
    in rheumatoid arthritis, 88
    in scurvy, 172
  pain of, in trichinosis, 960
  swelling of, in trichinosis, 960
  wasting of, in acute variety of general rheumatoid arthritis, 80

Muscular coat, hypertrophy of, in chronic oesophagitis, 417
    of stomach, hypertrophy of, in gastric cirrhosis, 614
  contraction in acute intestinal catarrh, 681
  cramps in enteralgia, 661
  degeneration, lesions, in cholera morbus, 722
  hypertrophy in dilatation of oesophagus, 432
  rheumatism, 74
  spasm in acute variety of general rheumatoid arthritis, 80
  trichinae, 958
  weakness in diabetes mellitus, 204

Musk and asafoetida, in spasmodic stricture of oesophagus, 421

Mutton-tea, use of, in entero-colitis and cholera infantum, 755

Myalgia complicating gonorrhoeal rheumatism, 106

Mycotic form of tonsillitis, 381, 386
  theory of origin of simple ulcer of stomach, 513
      parasite of, 386

Myocarditis in acute rheumatism, 34

Myomata of stomach, 578

Myo-sarcomatous tumors of stomach, 578


N.

Narcotics, abuse of, influence on causation of gastralgia, 460
  use of, in cancer of oesophagus, 428

Natiform skull, significance of, in hereditary syphilis, 312

Nature of cholera infantum, 744
  of cholera morbus, 720
  of constipation, 638, 639
  of dysentery, 784
  of enteralgia, 658, 659
  of pseudo-membranous enteritis, 767, 768
  of growth in glossitis parasitica, 358
  of acute intestinal catarrh, 668
  of intestinal indigestion, 620
  of acute pharyngitis, 391
  of rachitis, 137 _et seq._
  essential, of syphilis, 256

Nausea, in Ascaris lumbricoides, 953
  in biliousness, 966
  in catarrh of bile-ducts, 1053
  in acute gastritis, 467
  in chronic gastritis, 473
  in simple ulcer of stomach, 494
  in dysentery, 803
  in cancer of stomach, 540
  and vomiting in functional dyspepsia, 448, 449
    in pseudo-membranous enteritis, 765
    in enteralgia, 661
    in acute intestinal catarrh, 681
    in intestinal obstruction, 843, 854
    in intestinal ulcer, 826
    in jaundice, 977
    in acute yellow atrophy of liver, 1026, 1027, 1028
    in cancer of liver, 1038
    in cirrhosis of liver, 993
    in acute pancreatitis, 1119
    in phosphorus-poisoning, 1031
    in tape-worm, 940
    in thrombosis and embolism of portal vein, 1096
    in trichinosis, 960

Necrosis of cartilages in gout, 116
  of inferior maxilla in mercurial stomatitis, 346

Necrotic ulcers of stomach, 529

Nematodes, the, or thread-worms, 949

Nephritis, chronic, complicating gastric cancer, 560
  parenchymatous, in hereditary syphilis, 308

Nerve, atrophy of, as a cause of cancer of oesophagus, 429
  disease of, influence on causation of oesophageal paralysis, 429

Nerve-centres and nerves, disease of, in hereditary syphilis, 302

Nerves, lesions of, in gout, 117
  of organic life, exhaustion of, as a cause of functional dyspepsia,
        440

Nervous affections in acute rheumatism, 37
        treatment, 65
    complicating rheumatoid arthritis, 84
  centres, hemorrhagic extravasations into, in scurvy, 180
  colic, 662
  disease in hereditary syphilis, diagnosis of, 304
  disorders in Ascaris lumbricoides, 953
    in constipation, 647
    in phosphorus-poisoning, 1032
  disturbances in catarrh of bile-ducts, 1054, 1055
    due to biliary calculi, 1078
    from occlusion of biliary passages, 1092
    as a cause of cholera morbus, 721
    of pseudo-membranous enteritis, 766, 777
    of hepatic colic, 1071
    in jaundice, 980
    in lithaemia, 970
    in cirrhosis of liver, 999
    in Oxyuris vermicularis, 951
    in tape-worm, 940
  excitability, influence on causation of gastralgia, 460
  exhaustion, influence of causation of cholera morbus, 720
        of gout, 112
  form of enteralgia, treatment of, 665
  influence on causation of dysentery, 790
  origin of acute rheumatism, 24
    of rheumatoid arthritis, 92
  symptoms from constipation, 854
    of diabetes mellitus, 205, 206
    of enteralgia, 662
    reflex, in morbid dentition, 374
    sympathetic, in chronic gastritis, 474
  system, condition of, in parenchymatous glossitis, 362
    influence on digestion, 437
    lesions of, in diabetes mellitus, 200
    state, in intestinal indigestion, 628
  theory of origin of gout, 114

Nestle's food for infants, 754

Neuralgia in diabetes mellitus, 206
      treatment, 229
  complicating chronic articular rheumatism, 72
    gonorrhoeal rheumatism, 106
  of rectum, 909

Neurotic form of enteralgia, 662, 663
  origin of pruritus ani, 909
    of spasmodic stricture of oesophagus, 419
  theory of origin of gastric ulcer, 512

Niemeyer's views of origin of cholera morbus, 720

Nitrate of uranium, use of, in diabetes mellitus, 230

Nitric acid, cauterization with, in irritable rectum, 919
    use of, in cancrum oris, 343
      in fatty liver, 1050
      in jaundice, 982
      in lithaemia, 972
      in prolapsus ani, 920
      in anal fissure and rectal ulceration, 912
    local use of, in hemorrhoids, 926

Nitro-muriatic acid, local use of, in jaundice, 983
    in pseudo-membranous enteritis, 775

Nitrogen, elimination of, in rachitis, 130

Nitrogenous food, excess of, as a cause of functional dyspepsia, 443

Nodes, periosteal, in gonorrhoeal rheumatism, 105

Nodosities in acute rheumatism, 43
  Heberden's, of rheumatoid arthritis, 86

Nodular tubercular infiltration of tongue, 369

Nodules, number and size of, in carcinoma of liver, 1035

Non-cancerous tumors of stomach, 578

Non-malignant tumors of stomach, 578
    of stomach, distinguished from malignant, 572
  stricture of rectum, 885

Nose, flattening of, in hereditary syphilis, 277

Nostalgia, influence of, on causation of scurvy, 169, 170

Nursing of syphilitic children, necessity of maternal, 315

Nutmeg liver, 985

Nutrient enemata, use of, in simple ulcer of stomach, 519
  suppositories, 929

Nutrition, defective, in mother, a cause of rachitis, 143

Nutritive enemata in organic stricture of oesophagus, 425

Nux vomica, use of, in functional dyspepsia, 455, 458
    in constipation of functional dyspepsia, 458
    in gastralgia, 463
    in hepatic glycosuria, 976
    in jaundice, 975
    in fatty liver, 1050
    in paralysis of oesophagus, 430
    in acute pharyngitis, 399
    in dilatation of stomach, 609


O.

Oatmeal and barley as diluents of milk for infants, 753

Obesity, influence on causation of biliary calculi, 1065

Obstruction, intestinal, 835
  of bile-ducts, as a cause of jaundice, 977
    as a cause of cirrhosis of liver, 991
    in carcinoma of pancreas, 1124
  to flow of bile as a cause of biliary calculi, 1066
  intestinal from bands and loops of acute peritonitis, 1153, 1154
  of orifices of stomach in gastric cancer, 566
  of pancreatic duct, symptoms of, 1129
  of pylorus and duodenum following acute pancreatitis, 1119
  of rectum, 889

Occlusion of biliary passages, 1082
  of cystic duct, pathogeny, 1082

Occupation, influence on causation of constipation, 640
      of acute rheumatism, 20
      of mercurial stomatitis, 344
      of simple ulcer of stomach, 486

Odor of diabetic urine, 208
  of mouth in stomatitis catarrhalis, 323
  of stools, in acute intestinal catarrh, 680
    in chronic intestinal catarrh, 708

Oedema, in gastric cancer, 553
  in cancer of intestines, 871
  in diseases of pancreas, 1116
  in trichinosis, 961
  of glottis, in tonsillitis, 383
  of larynx in mercurial stomatitis, 346
      treatment, 348
  of lung, complicating gastric cancer, 560
  of one extremity in chronic intestinal catarrh, 709
  of skin in scurvy, 178
  of vulva in cirrhosis of liver, 995
  general, in cirrhosis of liver, 995

OESOPHAGUS, DISEASES OF, 409
  _Oesophagitis_, 409
    Definition, 409
    Synonyms, 409
  _Oesophagitis, Acute_, 409
    Definition, 409
    Synonyms, 409
    History, 409
    Etiology, 409
      Of idiopathic catarrhal form, 410
      Predisposing causes, 410
      Cold and moisture, 410
      Rheumatism, 410
      Hot drinks, 410
      Tobacco and alcohol, 410
      Irritating medicines, 410
      Of deuteropathic catarrhal form, 410
      As an extension of catarrhal pharyngitis, 410
      Pseudo-membraniform, 410
      Traumatic form, 410
        from injury, 411
      Phlegmonous form, 411
        from disease, 411
        from injury, 411
        from emboli, 411
        from fits of anger, 411
    Pathology and morbid anatomy, 411
      Nature of inflammatory process, 411
      Epithelium, changes in, 411
        thickening and desquamation of, 411
      Epithelial casts of tube, 412
      Follicles, swelling and hypertrophy of, 412
        ulceration of, 412
      Pseudo-membranous form, 412
      Seat and character of pseudo-membrane, 412
      Variolous pustules, 412
      Phlegmonous form, 412
      Purulent infiltration in submucous connective tissue, 412
      Diffuse form, 413
      Mode of escape of pus, 413
      Gangrene, 413
    Symptoms, 413
      Painful deglutition, 413
      Substernal pain, 413
      Pain over vertebrae, 413
      Dysphagia, amount and character of, 413
      Of pseudo-membranous form, 414
      Expulsion of shreds of membrane, 414
      Of phlegmonous form, 414
      Convulsions from pressure on pneumogastric nerve, 414
    Duration, 414
    Complications and sequelae, 414
    Diagnosis, 414
      From dorsal myelitis, 414
      Value of auscultation, 414
        of catheterism, 415
      From spasm and stricture, 415
      From carcinoma, 415
    Prognosis, 415
    Treatment, 415
      Of mild form, 415
      Of severe cases, 416
      Of pyrexia, 416
      Of traumatic form, 416
      Use of anodynes, 416
        of ice, 416
      Diet, 416
      Alkalies, 416
  _Oesophagitis, Chronic_, 416
    Definition, 416
    Synonym, 416
    Etiology, 416
      Sequel of acute form, 416
      Abuse of alcohol, 416
      Hot drinks, 416
      Chronic pulmonary and cardiac disease, 416
      Foreign bodies, 416
      Caries of vertebrae, 416
      Pressure of tumors, 416
    Pathology and morbid anatomy, 416
      Hypertrophy of mucous membrane, 416
        of muscular coat, 417
      Abscess and ulceration, 417
      Diffuse inflammation of connective tissue, 417
    Symptoms, 417
    Complications and sequelae, 417
      Stricture, 417
    Diagnosis, 417
      From spasm and stricture, 417
      From carcinoma, 417
    Prognosis, 417
    Treatment, 417
      Constitutional, 417
      Diet, 417
      Abstinence from alcohol, 417
      Sinapisms and revulsives, 417
      Use of iodides, 417
        of carbonic acid waters, 417
      Of pain, 418
      Local, 417
      Use of astringents, 417
      Mode of applying astringents, 418
      Cauterization of painful spots, 418
  _Oesophagus, Ulceration of_, 418
    Definition, 418
    Etiology, 418
      Sequel of inflammation, 418
    Symptoms, 418
      Sanguinolent products, expulsion of, 418
      Perforation into trachea, 418
        into mediastinum, 418
    Pathology and morbid anatomy, 418
      Deep-seated ulcers, 418
      Fistulae, 418
    Diagnosis, 418
    Prognosis, 418
    Treatment, 418
      Constitutional, 418
      Of hemorrhage, 418
      Cauterization of ulcers, 418
      Use of ergot and turpentine, 418
  _Oesophagus, Stricture of_, 419
      Definition, 419
    _Spasmodic Stricture_, 419
      Definition, 419
      Synonyms, 419
      History, 419
      Etiology, 419
        Neurotic origin, 419
        Hysterical origin, 419
        Sex, 419
        Age, 419
        Mental emotion, 419
        Organic diseases, relation of, to, 419
        Pregnancy, 419
        Gout and rheumatism, 419
        Hydrophobia, 419
      Symptoms, 419
        Spasm, seat of, 419, 420
        Inability to swallow, 420
        Spasm, relaxation of, 420
          causes of, 420
          certain foods as a cause, 420
        Dysphagia not complete, 420
        Pain, 420
        Hiccough, 420
        Time of regurgitation of food, 420
        Duration, 420, 421
      Pathology and morbid anatomy, 420
      Diagnosis, 420
        From organic spasm, 421
      Prognosis, 421
        Frequency of recurrence, 421
      Treatment, 421
        Causal, 421
        General, 421
        Use of valerian, 421
          of oxide of zinc, 421
          of bromide of potassium, 421
          of camphor, 421
          of musk and asafoetida, 421
          of belladonna and conium, 421
        Local, 421
        Bougie, use of, 421
          mode of using, 421
        Use of counter-irritation, 422
          of electricity, 422
    _Organic Stricture_, 422
      Definition, 422
      Synonym, 422
      History, 422
      Etiology, 422
        Congenital, 422
        Cicatricial contraction, 422
        Injury, 423
        Scalds, 422
        Caustic drinks, 422
        Syphilis, 423
        Morbid growths, 423
        Carcinoma, 423
        Spirituous liquors, 423
        Sex, 423
        Age, 423
      Symptoms, 423
        Impediment in deglutition, 423
        Regurgitation of food, 423
        Pain, 423
        Dysphonia, 423
        Suffocative symptoms, 423
      Pathology and morbid anatomy, 424
        Lesions of mucous membrane, 424
        Thickening of mucous membrane, 424
        Lesions of muscular tissue, 424
        Seat of strictures, 424
        Number of strictures, 424
        Forms of strictures, 424
        Dilatation of oesophagus, 424
        Atrophy of oesophagus, 424
      Diagnosis, 424
        Auscultation in, 424
        Value of bougies, 424, 425
        Necessity of excluding aneurism, 425
      Prognosis, 425
      Treatment, 425
        General, 425
        Use of iodides, 425
        Nutrient enema, 425
        Malignant form, 425
        Use of arsenic, 425
          of morphia, 425
        Pain, 425
        Local, 425
        Bougies, use of, 425
          mode of applying, 425, 426
        Forcible dilatation, 426
        Oesophagotomy, 426
  _Oesophagus, Carcinoma of_, 426
    Definition, 426
    Synonym, 426
    Etiology, 426
      Varieties, 426
      Spheroidal-celled, 426
      Squamous-celled, 426
      Colloid, 426
    Symptoms, 427
      Dysphagia, 427
      Regurgitation of food, 427
      Vomiting, 427
        character of, 427
      Emaciation, 427
      Pain, 427
        character of, 427
        seat of, 427
      Dyspnoea, 427
      Perforation of larynx, 427
        of lungs, 427
        of pleura, 427
        of large vessels, 427
    Pathology and morbid anatomy, 427
      Seat, 427
      Involvement of adjacent structures, 427
    Diagnosis, 428
    Prognosis, 428
    Treatment, 428
      Constitutional, 428
      Local, 428
      Use of stomach-tube, 428
        of opium, 428
        of nutrient enemata, 428
        of dilators, 428
      Gastrostomy, 428
  _Oesophagus, Paralysis of_, 429
    Definition, 429
    Synonyms, 429
    Etiology, 429
      Impairment of nerve-function 429
      From atrophy of nerve, 429
      Pressure from tumors, etc., 429
      Disease of nerves, 429
        of cerebro-spinal axis, 429
      Syphilis, 429
      Plumbism, 429
      Shock and fright, 429
      Cold, 429
      Hysteria, 429
    Symptoms, 429
      Dysphagia, 429
      Slow deglutition, 429
      Pain, 429
      Salivation, excessive, 429
    Pathology and morbid anatomy, 429
    Diagnosis, 429
      From paralysis of pharynx, 430
      Value of auscultation, 430
    Prognosis, 430
    Treatment, 430
      Diet, 430
      Mode of feeding, 430
      Use of strychnia, 430
        ignatia amara, 430
        electricity, 430
  _Oesophagus, Dilatation of_, 430
    Definition, 430
    Synonyms, 430
    Etiology, 430
      Congenital origin, 430
      Mechanical origin, 430
      Paralysis of muscular coat, 430
      General form, 431
      Annular form, 431
      Pouched form, 431
      Retention of food, 431
    Symptoms, 431
      Dyspepsia, 431
      Presence of a tumor, 431
      Regurgitation, 431
        time of, 432
      Of annular form, 432
      Odor of breath, 432
      Perforation, 432
      Death, cause of, 432
    Pathology and morbid anatomy, 432
      General form, 432
      Muscular hypertrophy, 432
      Size of dilatation, 432
      Annular form, 432
        seat, 432
      Pouched form, 432
        nature, 433
        seat, 433
        size, 433
    Diagnosis, 433
      Value of auscultation, 434
    Prognosis, 434
    Treatment, 434
      Use of stomach-tube, 434
      Diet, 434
      Constitutional, 435
      Use of stimulants, 435
        strychnia, 435
        electricity, 435
      Operative measures, 435
      Gastrostomy, 435

Oesophageal stenosis in atrophy of stomach, 616

Oesophagoscope, use of, in diagnosis of gastric hemorrhage, 584

Offensive exhalations, influence on causation of cholera morbus, 721

Oidium albicans of thrush, nature, 333

Oil of amber, locally, in hemorrhoids, 923
  of turpentine, use of, in tape-worm, 941
  of wintergreen, use of, in acute gout, 136
    in acute rheumatism, 59
  of wormseed, use of, in Ascaris lumbricoides, 954

Oils and fats, absorption of, in digestion, 623

Ointment of iodide of lead, use of, in tabes mesenterica, 1194
  of red iodide of mercury in amyloid liver, 1046
      in cirrhosis of liver, 1002

Oleum gaultheria, use of, in acute rheumatism, 59

Oligo-articular form of rheumatoid arthritis, 84

Olive oil and iodine, locally, in tubercular peritonitis, 1168

Onanism from Oxyuris vermicularis, 951

Onset of cholera infantum, 741
  of cholera morbus, 722
  of entero-colitis, 733
  of acute gout, 119
  of intestinal catarrh, 678
  of acute variety of general rheumatoid arthritis, 80
  of chronic variety of general form of rheumatoid arthritis, 81
  of partial form of rheumatoid arthritis, 85
  of tubercular peritonitis, 1165
  of typhlitis and perityphlitis, 818
  mode of, in acute pharyngitis, 394
    in tonsillitis, 381

Operative measures in tonsillitis, 388
    in dilatation of oesophagus, 435
    in cancer of stomach, 577
    in stenosis of pylorus, 609

Opium, abuse of, influence on causation of constipation, 641
  -eating as a cause of enteralgia, 662
  use of, in cholera morbus, 725
    in diabetes mellitus, 226, 227
    in dysentery, 811
    in enteralgia, 665
    in pseudo-membranous enteritis, 775
    in entero-colitis and cholera infantum, 758, 759
    in hemorrhage from bowels, 834
    in acute intestinal catarrh, 689, 693, 698
    in chronic intestinal catarrh, 715, 718
    in intestinal obstruction, 863
    in intestinal ulcers, 829
    in cirrhosis of liver, 1002
    in cancer of oesophagus, 428
    in acute pancreatitis, 1120
    in chronic interstitial pancreatitis, 1122
    in acute peritonitis, 1146
    in cancerous peritonitis, 1172
    in perforative peritonitis, 1156
    in acute pharyngitis, 397, 398, 399
    in cancer of stomach, 576
    in simple ulcer of stomach, 524, 527
    in mercurial stomatitis, 348
    in typhlitis and perityphlitis, 822

Ophthalmia, influence on causation of scrofula, 237

Organic changes, minor, in stomach, 611
  disease, influence on causation of acute gastritis, 464
    influence on causation of gastric hemorrhage, 580
    of thoracic and abdominal viscera, a cause of ascites, 1173
    of stomach, 480
  stricture of oesophagus, 422

Origin of biliary calculi, 1061-1063
  of cholera morbus, 720
  of false membranes, in pseudo-membranous enteritis, 772
  of gastric ulcer, hemorrhagic infiltration theory of, 512
  of gastric ulcer, inflammatory theory of, 512
      mycotic theory of, 513
  of simple gastric ulcer, neurotic theory of, 512
  nervous, of rheumatoid arthritis, 92
  specific, of rheumatoid arthritis, 92
  spontaneous, of acute peritonitis, 1136, 1137

Osteo-chondritis in hereditary syphilis, 288

Osteo-periostitis in hereditary syphilis, 291

Osteophytes in hereditary syphilis, 289
  formation of, in rheumatoid arthritis, 87

Otitis, influence on causation of scrofula, 237
  media, in morbid dentition, 375

Otorrhoea in hereditary syphilis, 282, 283

Ovarian cysts, distinguished from ascites, 1177
    rupture of, influence on causation of acute peritonitis, 1140
  disease, influence on causation of pseudo-membranous enteritis, 765
  disorders, influence on causation of gastralgia, 460
  and uterine irritation, influence on causation of enteralgia, 658

Over-crowding, influence on causation of entero-colitis, 730

Over-distension, as a cause of rupture of stomach, 618

Over-eating, as a cause of functional dyspepsia, 444
  influence on causation of intestinal indigestion, 624

Overwork, influence on causation of chronic intestinal catarrh, 699
      of functional dyspepsia, 444

Oxaluria, 970

Ox-gall, use of, in biliary calculi, 1081
    in constipation, 655

Oxidation, deficient, in hepatic disease, 1051, 1057
    as a cause of fatty liver, 1047
  defective, origin of gout from, 112, 113

Oxyuris vermicularis, 950


P.

Pain, abdominal, in Ascaris lumbricoides, 953
  colicky, in stricture of bowel, 856
  from presence of biliary calculi, 1069
  in cholera morbus, 722
  in constipation, seat, 646
  seat and character of, in dysentery, 802
  in functional dyspepsia, 448
  in enteralgia, 660, 661
    effect of pressure upon, 661
  in pseudo-membranous enteritis, 766
  in fistula in ano, 898
  in gastralgia, 460
  of gastralgia, treatment of, 463
  in acute gastritis, 467
  in chronic gastritis, 473
  in parenchymatous glossitis, 361
  in chronic parenchymatous glossitis, 368
  in acute gout, 119
  in chronic gout, 121
  in acute gonorrhoeal arthritis, 105
  in hepatic colic, seat and character, 1070
      treatment of, 1081
  in acute intestinal catarrh, 678, 679, 682
  in chronic intestinal catarrh, 706, 707
  in cancer of intestines, 870
  in intestinal indigestion, 627
  in acute internal strangulation of intestines, 843
  abdominal, in obstruction of intestines by gall-stones, 840
  in intestinal ulcers, 826
      treatment, 829
  in intussusception, 848
  in legs, from constipation, 854
  in abscess of liver, 1011, 1012
  in carcinoma of liver, seat and character, 1038
  in right hypochondrium, in hyperaemia of liver, 986, 987
  in back, in lithaemia, 970
  in morbid dentition, 373
  seat of, in acute oesophagitis, 413
  in cancer of oesophagus, 427
  in organic stricture of oesophagus, 423
  in spasmodic stricture of oesophagus, 420
  in oesophageal paralysis, 429
  in diseases of pancreas, 1116
  seat and character of, in carcinoma of pancreas, 1125
  in acute pancreatitis, 1119
  in chronic interstitial pancreatitis, 1122
  in obstruction of pancreatic ducts, 1131
  in acute pharyngitis, 394, 395
  seat of, in perihepatitis, 989
  in cancerous peritonitis, 1169
  character and seat of, in acute peritonitis, 1141
  in chronic peritonitis, 1162
  in proctitis, 887
  in suppurative pylephlebitis, seat and character of, 1099
  in non-malignant stricture of rectum, 886
  in cancer of rectum and anus, 903
  characters of, in fissure of rectum and anus, 888
  in peri-rectal and anal abscesses, 896
  in ulceration of rectum and anus, 893
  in acute rheumatism, 27
  in chronic articular rheumatism, 71
  in arthralgic form of gonorrhoeal rheumatism, 104
  in rheumatic form of gonorrhoeal rheumatism, 104
  in muscular rheumatism, 75
  in chronic articular form of gonorrhoeal rheumatism, 105
  in chronic variety of general rheumatoid arthritis, 81
  in Heberden's nodosities of rheumatoid arthritis, 86
  seat and character of, in cancer of stomach, 539
  in cancer of stomach, treatment of, 576
  in dilatation of stomach, 593
  in acute dilatation of stomach, 610
  in simple ulcer of stomach, 488
  treatment, in simple ulcer of stomach, 524
  muscular, in scurvy, 177
  abdominal, in tapeworm, 940
  in tonsillitis, 381, 382
  in tubercular ulceration of tongue, 369
  in typhlitis and perityphlitis, 818

Palate, soft, appearance of, in acute pharyngitis, 391-395
      in tonsillitis, 381
    paralysis of, in acute pharyngitis, 395
      in tonsillitis, 383

Palpitation, in functional dyspepsia, 451
  in chronic intestinal catarrh, 708
  in intestinal indigestion, 628
  in dilatation of stomach, 595

Pancreas, condition of, in hereditary syphilis, 306
  disease of, relation to diabetes mellitus 201

PANCREAS, DISEASES OF, 1112
  History, 1112
  Anatomy and physiology, 1112
    Position, 1112
    Wirsung, canal of, 1113
    Acini, 1113
    Relation of head to ductus choledochus, 1113
    Pancreatic juice, properties of, 1113
  Etiology, general, 1114
    Sex, 1114
    Age, 1114
    Alcohol, 1114
    Tobacco, 1114
    Food, improper, 1114
    Suppression of menstruation, 1114
    Injury, 1114
    Secondary organic disease of thoracic abdominal viscera, 1114
  Symptomatology, general, 1114
    Objective, 1114
    Emaciation, 1114
    Excessive salivation, 1114
    Diarrhoea, 1115
    Fatty stools, 1115
    Stools, undigested striped muscular fibres in, 1116
    Subjective, 1116
    Epigastrium, abnormal sensations in, 1116
    Pain, seat and character, 1116
    From pressure, 1116
    Of ductus choledochus, 1116
    Jaundice, 1116
    Of portal vein, 1116
    Oedema, 1116
    Aneurismal dilatation of aorta, 1116
    Of stomach, 1116
    Vomiting, 1116
    Of duodenum, 1116
    Relation to diabetes mellitus, 1117
    Of solar plexus, 1117
    Bronzing of skin, 1117
  Physical signs, 1117
    Method of examination, 1117
    Palpation, 1117
    Percussion, 1118
    Auscultation, 1118
  Inflammatory Affections of Pancreas, 1118
    _Acute Idiopathic Pancreatitis_, 1118
      Morbid anatomy, 1118
        Hemorrhagic extravasations in, 1118
        Abscesses of, 1118
        Pus, character of, 1118
        Secondary peritonitis, 1118
        Gangrene, 1118
      Symptoms, 1118
        Onset, 1118
        Tongue, 1119
        Constipation, 1119
        Appetite, impaired, 1118
        Physiognomy, 1119
        Vomiting, 1119
        Temperature, 1119
        Pain, 1119
        Pulse, 1119
        Collapse, 1119
        Epigastrium, tenderness of, 1119
        Peritonitis, 1119
        Obstruction of stomach, duodenum, and bile-duct, following,
            1119
      Diagnosis, 1119
        From biliary colic, 1119
          acute gastric catarrh, 1119
            gastritis, 1120
      Treatment, 1120
        Rest, necessity, 1120
        Diet, 1120
        Ice and leeches to epigastrium, 1120
        Opium, 1120
        Of pain, 1120
        Of vomiting, 1120
        Alcohol, 1120
    _Acute Secondary Pancreatitis_, 1120
      Etiology, acute infectious diseases, 1120
        Metastasis, 1120
      Morbid anatomy, 1120
        Cells, changes in, 1120
      Symptoms and course, 1120
        Rigors, 1121
        Metastatic of mumps, 1121
        Fever, 1121
        Pain, 1121
        Diarrhoea, 1121
        Fistulous openings into viscera, 1121
      Treatment, 1121
    _Chronic Interstitial Pancreatitis_, 1121
      Etiology, 1121
        Closure of duct of Wirsung, 1121
        Extension from other organs, 1121
        Cancer and ulcer of stomach, 1121
        Alcoholism, 1121
        Syphilis, 1121
        Pressure of tumors, 1121
      Morbid anatomy, 1121
        Hyperplasia of connective tissue, 1121
        Atrophy of connective tissue, 1121
        Of syphilitic hyperplasia, 1122
      Symptoms and course, 1122
        Emaciation, 1122
        Fatty stools, 1122
        Melituria, 1122
        Pain, 1122
        Presence of a tumor, 1122
      Duration, 1122
      Treatment, 1122
        Hygienic, 1122
        Of pain, 1122
        Diet, 1122
        Peptonized milk, use of, 1123
            mode of preparing, 1123
          gruel, 1123
          broth, 1123
        Ext. pancreatis, use of, 1122, 1123
        Watery infusion of pancreas, use of, 1122
        Purgatives, use of, 1122
        Opium, 1122
  Morbid Growths of Pancreas, 1123
    _Carcinoma of Pancreas_, 1123
      Etiology, 1123
      Morbid anatomy, 1123
        Primary forms, 1123
        Method of growth, 1124
        Wirsung's duct, obstruction of, 1124
        Tumor, shape and seat of, 1124
        Extension to other organs, 1124
        Common bile-duct, obstruction of, 1124
        Secondary forms, 1124
        Limitation to head of gland, 1124
        Seat of primary growth, 1124
      Symptoms and course, 1124
        Emaciation, 1124
        Debility, 1124
        Physiognomy, 1124, 1125
        Temperature, 1125
        Pulse, 1125
        Pain, 1125
          seat and character of, 1125
        Stools, fat in, 1125
        Jaundice, 1126
        Urine, fat in, 1125
        Tumor, presence of, 1125
        Salivation, 1125
        Pyrosis, 1125
        Eructations, 1125
        Epigastrium, burning and weight in, 1125
        Thirst, 1125
        Tongue, state of, 1125
        Appetite, impaired, 1125
        Nausea and vomiting, 1125
        Vomit, characters of, 1126
        Stools, bloody, 1126
        Diarrhoea, 1126
        Of secondary carcinoma of liver, 1126
        Dropsy, 1126
        Ascites, 1126
      Duration, 1126
      Prognosis, 1126
      Diagnosis, 1126
        From gastric cancer, 1127
        From hepatic disease, 1127
        From tumor of enlarged gall-bladder, 1127
        From aneurism of aorta, 1127
        From carcinoma of omentum, 1127
            of transverse colon, 1127
        From chronic pancreatitis, 1127
      Treatment, 1127
        Diet, 1127
        Ext. pancreatis, use of, 1128
        Enemata, 1128
    _Sarcoma and Tubercle of Pancreas_, 1128
  Degenerations of Pancreas, 1128
    _Fatty Degeneration of Pancreas_, 1128
        Fatty infiltration, 1128
        Fatty metamorphosis, 1128
    _Albuminoid Degeneration of Pancreas_, 1128
    _Hemorrhages into Pancreas_, 1129
        From chronic disease of liver, 1129
            of heart and lungs, 1129
        From rupture of vessels of gland, 1129
        Appearance of gland, 1129
      Symptoms, 1129
        Vomiting, 1129
        Collapse, 1129
        Pulse, feeble, 1129
        Pulsating tumor, presence of, 1129
      Treatment, 1129
    _Obstruction of Pancreatic Duct_, 1129
      Etiology, 1129
        From pressure from without, 1129
        Sclerosis and carcinoma of head, 1129
        Of gland, 1129
        Gall-stones, 1130
        Carcinoma of pylorus and duodenum, 1130
        Canal of Wirsung, catarrh of, 1130
        Pancreatic calculi, 1130
            causes of, 1130
            size and shape, 1130
            composition, 1130
            seat of, 1130
        Dilatation of canal from, 1130
        Cysts of canal, 1130
            contents of, 1130
        Cell-structure, changes in, 1130
      Symptoms and course, 1131
        Presence of a tumor, 1131
        Emaciation, 1131
        Stools, fatty, 1131
        Jaundice, 1131
        Melituria, 1131
        Pain, 1131
      Duration, 1131
      Diagnosis, 1131
        From hydatid of liver, 1131
        From distension of gall-bladder, 1131
      Treatment, 1131
        Hygienic, 1131
        Diet, 1131
        Anodynes, use of, 1131
        Paracentesis of cysts, 1131

Pancreas, lesions of, in diabetes mellitus, 200
    in chronic intestinal catarrh, 705
    in scurvy, 173
    in tabes mesenterica, 1188

Pancreatic calculi, composition of, 1130
    size and shape, 1130
  disease complicating diabetes mellitus, 210, 1117
    influence of, on causation of constipation, 642
        of functional dyspepsia, 447
  extract, use of, in entero-colitis and cholera infantum, 752
      in functional dyspepsia, 453
      in intestinal indigestion, 633, 635
  form of intestinal indigestion, diagnosis, 631
  juice, properties of, 1114
    in diseases of pancreas, 1122, 1123, 1128

Pancreatin, use of, in chronic interstitial pancreatitis, 1122, 1123

Papillae, enlargement of, in glossitis parasitica, 358
    in superficial glossitis, 355, 356

Papular eruption of hereditary syphilis, 278

Paracentesis in ascites, 1180
  in obstruction of pancreatic duct, 1131

Paralyses in morbid dentition, 375

Paralysis, facial, in diabetes mellitus, 206
  complicating dysentery, 805
  following chronic intestinal catarrh, 710
  in intestinal indigestion, 628
  of muscular coat as a cause of intestinal obstruction, 851
      in dilatation of oesophagus, 430
  of oesophagus, 429
  of palate in acute pharyngitis, 395
    in tonsillitis, 383
  of rectum in chronic heart disease, 908
    in spinal meningitis, 908
  of rectum in vertebral fracture, 908
  in scurvy, 180

Paraplegia in acute intestinal catarrh, 681
  following chronic intestinal catarrh, 710

Parasite of thrush, nature of, 333
  of mycotic form of tonsillitis, 386

Parasites as a cause of hemorrhage from bowels, 831
  in portal vein, 1111
  influence on causation of intestinal ulcer, 823
  of the liver, 1101

Parasitic conditions of anus, 892
  growths, influence on causation of pseudo-membranous enteritis, 765

Parasiticides, use of, in treatment of liver-flukes, 1110

Paratyphlitis, 814

Parenchymatous glossitis, 35

Parents, syphilitic, treatment of, 260, 261, 314, 315

Paresis, influence on causation of dilatation of stomach, 590

Parotitis complicating dysentery, 806

Paroxysms of hepatic colic, date of appearance, 1070
    treatment of, 1081
  of pseudo-membranous enteritis, symptoms of, 766

Partial form of rheumatoid arthritis, symptoms of, 84

Passive movements in chronic forms of rheumatoid arthritis, 100

Pathenogenesis of cancer of stomach, 568
  of simple ulcer of stomach, 512

Pathogenesis of diabetes mellitus, 195
  of rheumatoid arthritis, 92

Pathogeny of biliousness, 965
  of occlusion of biliary passages, 1082
  of hepatic glycosuria, 973
  of lithaemia, 968
  of perihepatitis, 989
  of the liver in phosphorus-poisoning, 1030
  of suppurative pylephlebitis, 1097

Pathological anatomy of acute yellow atrophy of liver, 1025
  histology of acute intestinal catarrh, 677
    of chronic intestinal catarrh, 703

Pathology of cancrum oris, 341
  of diabetes mellitus, 195
  of dysentery, 796
  of functional dyspepsia, 451
  of pseudo-membranous enteritis, 767
  of superficial glossitis, 355
  of chronic superficial glossitis, 367
  of parenchymatous glossitis, 363
  of chronic parenchymatous glossitis, 368
  of glossitis parasitica, 358
  of gout, 112
  of hydatids of liver, 1102
  of macroglossia, 352
  of acute oesophagitis, 411
  of chronic oesophagitis, 416
  of cancer of oesophagus, 427
  of dilatation of oesophagus, 432
  of organic stricture of oesophagus, 424
  of spasmodic stricture of oesophagus, 420
  of oesophageal paralysis, 429
  of ulceration of oesophagus, 418
  of acute pharyngitis, 391
  of chronic pharyngitis, 403
  of syphilitic pharyngitis, 406
  of tuberculous pharyngitis, 400
  of purpura, 191
  of acute rheumatism, 23
  of rachitis, 137
  of aphthous stomatitis, 326
  of catarrhal stomatitis, 323
  of stomatitis ulcerosa, 336
  of mercurial stomatitis, 346
  of bone disease, in hereditary syphilis, 286-288
  of enlarged liver in hereditary syphilis, 283, 284
  of scrofula, 238
  of scurvy, 173
  of tabes mesenterica, 1183
  of thrush, 332
  of tuberculous ulceration of tongue, 369
  of tonsillitis, 383

Pavy's chemical theory of production of glycosuria, 199

Peliosis rheumatica, 189

Pelletierin, use of, in tape-worm, 942

Pelvic inflammations, influence on causation of acute peritonitis,
        1140

Pelvis, deformities of, in rachitis, 153

Pemphigus in hereditary syphilis, 274
    diagnosis of, 276

Pepsin, use of, in functional dyspepsia, 456
    in entero-colitis, 760
    in dilatation of stomach, 609
  and pancreatin, use of, in gout, 131

Peptones and sugar, absorption of, in digestion, 623

Peptonized food, use of, in functional dyspepsia, 453, 454
  milk, use of, in entero-colitis and cholera infantum, 751, 752
      in acute intestinal catarrh, 691
      in intestinal indigestion, 633
      in chronic gastritis, 476
      in chronic interstitial pancreatitis, 1123
      in simple ulcer of stomach, 520
    preparation of, 1123

Perchloride of iron in hemorrhage from rectum, 927

Percussion in diseases of pancreas, 1118
  in dilatation of stomach, 598
  in cancer of stomach, 572
  auscultatory, in ascites, 1174

Perforation in dysentery, 799
  in cancer of oesophagus, 427
  in dilatation of oesophagus, 432
  in cancer of stomach, 558
      frequency of, 558
  in simple ulcer of stomach, 496
      treatment of, 527
  in typhlitis and perityphlitis, 819
    treatment of, 822
  into mediastinum in ulceration of oesophagus, 418
  into trachea in ulceration of oesophagus, 418
  of cheek in cancrum oris, 341, 342
  of pericardium in simple ulcer of stomach, 500
  of stomach and intestines by gall-stones, 1068, 1074
  of transverse colon in simple ulcer of stomach, 500

Perforations of intestinal canal as a cause of peritonitis, 1138

Perforative form of peritonitis, 1154

Peri-anal and peri-rectal abscesses, 895
      treatment of, 918

Peri-articular form of gonorrhoeal rheumatism, symptoms of, 105
  tissue, lesions of, in acute rheumatism, 47

Pericarditis, complicating gastric cancer, 560
  in abscess of liver, 1015
  in acute rheumatism, 28, 33, 34

Peri- and endocarditis in acute rheumatism, treatment of, 63, 64

Perihepatitis, 989
  as a cause of cirrhosis of liver, 992

Periodicity of recurrence of dysentery, 785

Peristalsis, cessation of, in acute peritonitis, 1142
  intestinal, cause of, 622, 623

Peristaltic movements of stomach in gastric dilatation, 596

Peritoneal abscesses, in simple ulcer of stomach, 507
  adhesions as a cause of compression and contraction of bowel, 857

Peritoneum, condition of, in hereditary syphilis, 307
  lesions of, in chronic intestinal catarrh, 705
    in cirrhosis of stomach, 614
    in simple ulcer of stomach, 506
  secondary growths of, in gastric cancer, 557

Peritonism, relation to peritonitis, 1152

PERITONITIS, 1131
    History, 1131
  _Peritonitis, Acute Diffuse_, 1133
    Morbid anatomy, 1133
      Collections of fibrin on intestines, 1133
      Blood-vessels, lesions, 1133
      Peritoneum, thickening of, 1134
      Serous effusions, 1134
      False membrane, disposition of, 1134
          fatty degeneration of, 1134
          cysts of, 1135
      Epithelium, changes in, 1134, 1135
      Pus, character of, 1136
      Abscesses, seat, 1136
      Solar plexus, lesions, 1136
      Hypogastric plexus, lesions, 1136
    Etiology, 1136
      Spontaneous origin, 1136, 1137
      Albuminuria, influence on causation, 1138
      Pyaemia, influence on causation, 1138
      Diphtheria, influence on causation, 1138
      Perforations of intestinal canal, 1138
        of appendix, 1138
      Abscess of liver, 1138
      Gall-stones, 1138, 1139
      Ulcers of stomach, 1139
        of dysentery, 1139
        of typhoid fever, 1139
      Fecal accumulations, 1139
      Injury from operations, 1140
      Rupture of ovarian cysts, 1140
      Tumors, presence of, 1140
      Urine, infiltration of, 1140
      Pelvic inflammations, 1140
      Intestinal worms, 1140
      Vaginal and uterine injections, 1140
      Traumatism, 1141
    Symptoms, 1141
      Pain, 1141
        characters and seat, 1141
        absence of, 1143
      Pulse, 1141
      Respirations, 1141, 1142
      Abdominal distension, 1141
      Tympanites, 1141
      Constipation, 1141
      Vomiting, 1141
      Vomit, green, 1141
      Peristalsis, cessation of, 1142
      Temperature, 1142
      Physiognomy, 1142
      Mental condition, 1142
      Delirium, 1142
      Urine, condition, 1142
      Relation to peritonism, 1152
    Consequences, 1152
      Formations of bands and loops, 1153
      Constipation from, 1153
      Obstruction, intestinal, from, 1153, 1154
    Mortality, 1143
    Duration, 1143
    Diagnosis, 1143
      From hepatic colic, 1144
        renal colic, 1144
        intestinal colic, 1144
    Treatment, 1144
      History of, 1145
      Bloodletting, 1145
      Opium, 1146
        history of introduction of, 1146
        method of administration, 1148
        amount necessary, 1148, 1149
        cautions in using, 1150
        use of, in Bright's disease, 1150
          origin of, 1151
      Purgatives, use of, 1151
      Mercurials, use of, 1151
      Diet, 1151
      Operative measures, 1152
      Puncture of intestine, 1152
      Of puerperal form, 1146, 1149
      Peritonism, 1152
  _Peritonitis from Perforation_, 1154
    Seat of, 1154
    From perforation of stomach, 1155
    Symptoms, 1155
      in typhoid fever, 1155
      seat, 1155
    Of intestines, 1155, 1156
    Hepatic resonance of percussion, significance in, 1156
    Treatment, 1156
      Rest, 1156
      Opium, 1156
  _Local Peritonitis_, 1159
    Seat, 1159
    Purulent form, 1159
    Symptoms, 1159, 1160
    Diagnosis, 1159
      Of abscesses, 1159, 1160
        pus, fecal odor of, 1160
        discharge of, mode, 1160
      Fibrinous exudations, 1160
          seat, 1160
      Formation of contractile capsule on liver, 1160, 1161
      Ascites from, 1161
  _Chronic Peritonitis_, 1161
    Possibility of, 1161
    Symptoms, 1162
      Vomiting, 1162
      Pain, 1162
      Temperature, 1162
      Pulse, 1162
      Constipation and diarrhoea, 1162
      Abdominal tenderness, 1162
      Abdomen, sacculation of fluid in, 1162
  _Tubercular Peritonitis_, 1165
    Symptoms, 1165
      Onset, 1165
      Remissions in, 1165
      Fever, 1165
      Temperature, 1165
      Pulse, 1165, 1166
      Tympanites, 1165, 1166
      Digestion, disturbances of, 1166
      Abdomen, tenderness of, 1165, 1166
      Emaciation, 1166
    Diagnosis, 1166
      Significance of cough, 1167
    Morbid anatomy, 1167
      False membranes, thickness of, 1167
      Lungs, lesions of, 1168
    Prognosis, 1168
      Fatality of, 1168
    Treatment, 1168
      Iodide of potassium, 1168
      Iodine and olive oil, locally, 1168
      Iodide of iron, 1168
      Diet, 1168
  _Cancerous Peritonitis_, 1168
    Etiology, 1168
      Disseminated carcinoma, most frequent cause, 1168
      Case illustrating, 1168, 1171
      Vomiting, 1170
      Pain, 1169
      Urine, condition of, 1170
      Physiognomy, 1169
      Ascites, 1169
        fluid, characters of, 1169
      Abdomen, state of, 1169
    Diagnosis, 1171
      From tubercular peritonitis, 1171
    Treatment, 1172
      Opium, 1172
      Belladonna, 1172
  _Infantile Peritonitis_, 1172
    Etiology, 1172
      Scarlet fever, 1172
      Erysipelas, 1172
      Age, 1172
      Syphilis, 1172
      Ill-health of mother, 1172
      Visceral disease, 1172
    Symptoms, 1173
    Treatment, 1173
  _Ascites_, 1173
    Etiology, obstruction to portal circulation, 1173
      Liver disease, 1173
      Heart disease, 1174
      Kidney disease, 1174
      Phthisis disease, 1175
      Chronic peritonitis, 1175
      Acute peritonitis, 1175
      Sex, 1176
      Age, 1176
    Symptoms, 1175
      Amount of fluid, 1175
      Abdomen, state of, 1176
        effect of position on, 1176
      Respiration in, 1177
      Abdominal veins, prominence of, 1177
      Digestion, derangements of, 1177
      Appetite, impaired, 1177
      Emaciation, 1177
      Urine, condition of, 1177
      Skin, condition of, 1177
      Tongue, condition of, 1177
      Mental state, 1177
    Diagnosis, 1177
      From ovarian cysts, 1177
      Auscultatory percussion in, 1174
    Treatment, 1178
      Diuretics, use of, 1178
      Carbonate of potash and lemon-juice, 1178
      Bitartrate of potash, 1179
      Digitalis, 1179
      Diaphoretics, 1179
      Vapor bath, 1179
      Pilocarpine, 1179
      Cathartics, 1179
      Epsom salts, 1179
      Ext. senna, 1179
      Elaterium, 1179
      Mercurials, 1178, 1179
      Paracentesis, 1180
        method, 1180
  Hemorrhagic effusion of peritoneum, 1180
      Scurvy as a cause of, 1180
      Erosions of abdominal vessels, 1181
      Aneurisms, 1181
      Traumatism, 1181
    Symptoms, 1181

Peritonitis, chronic, influence on causation of dilatation of stomach,
        590
  complicating chronic intestinal catarrh, 710
    acute rheumatism, 42
    cancer of stomach, 560
    simple ulcer of stomach, 502
  acute, distinguished from cholera morbus, 724
  distinguished from acute intestinal catarrh, 686
    from acute gastritis, 468
  in acute intestinal strangulation of intestines, 843
  in intestinal ulcer, treatment, 829
  in perforation of simple gastric ulcer, 499
  in trichinosis, 961
  secondary, in acute pancreatitis, 1118, 1119

Perityphlitis. See _Typhlitis_.

Permanent teeth, disease of, in hereditary syphilis, 293

Permanganate of potassium, use of, in catarrh of bile-ducts, 1057
      in fatty liver, 1051

Perspiration, excessive, as a cause of constipation, 642
  in acute rheumatism, 27, 30
  in rheumatic form of gonorrhoeal rheumatism, 104
  of head in rachitis, 146

Perspirations, local, complicating gout, 121

Perverted nutrition, the essential character of scurvy, 173

Pessary, dilated gum, in prolapsus ani, 920

Peyer's patches, degeneration of, in hereditary syphilis, 306
    lesions of, in cholera morbus, 721
      in entero-colitis, 738
      in acute intestinal catarrh, 675
      in chronic intestinal catarrh, 702

PHARYNX, DISEASES OF, 390
  _Pharyngitis, Acute_, 390
    Definition, 390
    Synonyms, 390
    Etiology, 390
      Diathetic cause of, 390
      Scrofula, 390
      Rheumatism and gout, 390
      Syphilis, 390
      Age, 390
      Cold and damp, 390
      Malarial poison, 391
      The exanthemata, 391
      Drugs, 391
      Injury, 391
    Pathology and morbid anatomy, 391
      Acute form, nature of, 391
      Phlegmonous form, nature of, 391
          course of suppurative process, 301
      Ulcerative form, nature of, 392
      Membranous or herpetic form, nature and course, 392
          deposit, nature of, 392
          vesicles of, 392
      Gangrenous form, nature of, 392
          course of, 392
          description of ulcerative process, 393
      Erysipelatous form, nature of, 393
          extension from lips and skin, 393
      Exanthematous form, 393
          of variola, 393
          of measles, 394
          of scarlatina, 394
    Symptoms, 394
      Erythematous form, 394
        Mode of onset, 394
        Pain, 394
        Dysphagia, 394
        Skin, state of, 394
        Pulse, 394
        Temperature, 394
        Cough, 394
        Glands, swelling of, 395
        Localization of inflammatory process, 395
      Rheumatic form, 394
      Malarial form, 395
      Phlegmonous form, 395
        Constitutional, 395
        Local, 395
        Paralysis of palate, 395
      Ulcerative form, 395
        Constitutional, 395
        Headache, 395
        Local, 395
      Membranous form, 395
        Constitutional, 395
        Chills, 395
        Pain, 395
        Local, 395
        Duration, 395
      Gangrenous form, 395
        Constitutional, 395
        Temperature, 395
        Pulse, 395
        Pain, 395
        Local, 395
        Fetid secretions, 395
        Odor of breath, 396
        Diarrhoea, 396
        Mode of death, 396
      Erysipelatous form, 396
        Constitutional, 396
        Local, 396
        Duration, 396
    Diagnosis, 396
      From scarlatina, 396
        diphtheria, 396
    Prognosis, 396
    Treatment, 397
      Of simple form, 397
        General, 397
        Local, 397
      Phlegmonous form, 397
        General, 397
        Local, 397
        Gargles, 397
        Medicated sprays, 398
        Leeching, 398
      Rheumatic form, 398
      Ulcerative form, 398
      Gangrenous form, 398
        Diet, 398
      Traumatic form, 399
        Diet, 399
      Erysipelatous form, 399
        Diet, 399
      Membranous form, 399
        Diet, 399
      Exanthematous form, 399
      Use of aconite, 397, 398
        of astringents, 397, 398
        of steam inhalations, 397, 398, 399
        of ice, 397
        of medicated powders, 398
        of iron and quinia, 398
        of alcohol, 398
        of opium, 397, 398, 399
      Incisions and scarification, 397
      Tracheotomy, 398, 399
  _Pharyngitis, Tuberculous_, 400
    Definition, 400
    Synonyms, 400
    History, 400
    Etiology, 400
    Pathology and morbid anatomy, 400
      Nature of ulcerative process, 400
      Ulcers, description of, 401
      Mucous membrane, miliary infiltration of, 400
      Extension to oesophagus, 401
      Muscles, fatty degeneration, 401
      Lymphatic glands, enlargement of, 401
    Symptoms, 401
      Pain in swallowing, 401
      Cough, 401
      Pyrexia, 401
      Wasting, 401
    Diagnosis, 401
      Significance of intense pain in swallowing, 401
    Prognosis, 401
    Death, cause of, 402
    Treatment, 402
      Iodoform and morphine, insufflations of, 402
      Hydrogen peroxide, locally, 402
      Carbolic acid, use of, 402
      General, 402
      Rectal alimentation, 402
  _Pharyngitis, Chronic_, 402
    Definition, 402
    Synonyms, 402
    Etiology, 402
      Predisposing causes, 402
      Overcrowding, 402
      Sedentary occupation, 402
      Food, improper, 402
      Tobacco, 402
      Alcohol, 402
      Voice, improper use of, 402
      Relation to chronic inflammations of other mucous membranes,
        402, 403
      Uterine disturbances, 403
      Mental depression, 403
      Exciting causes, 402
    Pathology and morbid anatomy, 403
      Nature of, 403
      Structures involved, 403
      Epithelium, desquamation of, 403
      Glands of pharynx, dilated and hypertrophied, 403
      Follicles, enlargement, 403
      Papillae of base of tongue, enlargement of, 403
      Of folliculous variety, 403
      Involvement of glands, 403
      Projections on mucous membrane, 403
        nature of, 403, 404
        engorgement of capillaries at base of, 404
      Viscid mucus, secretion of, 404
      Dry catarrh, atrophic form, 404
    Symptoms, 404
      Cough, 404
      Expectoration, 404
      Hoarseness, 404
      Hemming, 404
      Sensations of throat uncomfortable, 404
      Absence of symptoms, 404
    Diagnosis, 404
    Prognosis, 404
    Treatment, 405
      Of catarrhal form, 405
      Constitutional, necessity of, 405
      Use of mild astringents, 405
        of sprays, medicated, 405
      Mode of making applications, 405
      Of folliculous form, 405
      Constitutional, 405
      Strong solutions of silver nitrate, 405
        of iodine, 405
      Use of ergot, locally, 405
      Destruction of enlarged follicles, 405
      Use of medicated sprays, 406
        of mercuric chloride, 406
          local, 406
      Counter-irritation, 406
      Chronic atrophic form, 406
      Use of cubebs, 406
        of jaborandi, 406
        ammon. chloride, 406
        pyrethrum, 406
  _Pharyngitis, Syphilitic_, 406
    Definition, 406
    Synonyms, 406
    Etiology, 406
    Pathology and morbid anatomy, 406
      Varieties of, 406
      Secondary manifestations, 406
      Inflammatory nature of, 406
      Mode of spread, 406
      Mucous patches, 407
          microscopic appearance of, 407
      Ulceration, occurrence of, 407
      Tertiary manifestations, 407
      Gummatous infiltration, 407
          seat of, 407
      Course of the process, 407
      Ulcerations, nature and seat of, 407
      Cicatrization, 407
      Hereditary manifestations, 407
    Symptoms, 407
      Course of, 407
      Duration of, 407
    Complications, 407
    Sequelae, 407
      Cicatricial stricture, 407
    Diagnosis, 408
    Prognosis, 408
    Treatment, 408
      Use of mercury, 408
        potassium iodide, 408
            necessity of large doses, 408
      Local, 408
      Use of sulphate of copper, 408
        of chromic acid, 408

Pharyngeal nerve, relation to causation of parenchymatous glossitis,
        363
  phthisis, 400
  and laryngeal catarrh in gout, 122

Pharyngitis in acute rheumatism, 42

Phlegmasia alba dolens complicating gastric cancer, 560

Phlegmatic form of scrofulous habit, 243

Phlegmonous form of acute oesophagitis, 414
    of acute pharyngitis, 395
        treatment of, 397

Phosphate of sodium, use of, in biliary calculi, 1080, 1081
      in biliary calculus state, 1080
      in catarrh of bile-ducts, 1057
      in biliousness, 968
      as a preventive of enteralgia, 666
      in jaundice, 982
      in lithaemia, 972
      in acute yellow atrophy of liver, 1030
      in cirrhosis of liver, 1001
      in fatty liver, 1050
    in hyperaemia of liver, 988

Phosphates, use of, in diabetes mellitus, 227

Phosphoric acid, elimination of, in rachitis, 138

Phosphorus, use of, in acute yellow atrophy of liver, 1030
    in cirrhosis of liver, 1001
    in rachitis, 165

Phosphorus-poisoning as a cause of cirrhosis of liver, 991, 992
  influence on causation of fatty liver, 1047
  the liver in, 1030
  resemblance to symptoms of acute yellow atrophy of liver, 1031

Phthisis as a consequence of intestinal indigestion, 630
  complicating diabetes mellitus, 210
    chronic intestinal catarrh, 709
  influence on causation of ascites, 1175
      of fistula in ano, 897
      of chronic gastritis, 470, 471
      of acute intestinal catarrh, 671
      of chronic intestinal catarrh, 699
      of intestinal indigestion, 624
      of fatty liver, 1047
      of rheumatoid arthritis, 90
      of simple ulcer of stomach, 487
  nature of, complicating diabetes mellitus, 202
  pharyngeal, 400

Physical signs of pancreatic disease, 1117

Physick's encysted rectum, 885

Physiognomy in cholera morbus, 722
  in dysentery, 796
  in enteralgia, 661
  in pseudo-membranous enteritis, 766
  in hepatic colic, 1071
  in cancer of intestines, 869
  in acute intestinal catarrh, 681
  in acute gastritis, 467
  in parenchymatous glossitis, 361
  in carcinoma of liver, 1038
  in cirrhosis of liver, 997
  in carcinoma of pancreas, 1124, 1125
  in acute peritonitis, 1142
  in cancerous peritonitis, 1169
  in scrofula, 243, 244
  in scurvy, 176
  in gastric cancer, 552
  in simple ulcer of stomach, 496
  of syphilitic children, peculiarities of, 313

Physiology of intestinal digestion, 620
  of pancreas, 1112

Physostigma, use of, in lithaemia, 973
    in constipation, 655

Picric acid and potash test for sugar in urine, 214

Pigment form of carcinoma of liver, 1035

Piles. See _Rectum and Anus, Diseases of_.
  in chronic gastritis, 475

Pilocarpine, use of, in ascites, 1179
    in acute intestinal catarrh, 688
    in cirrhosis of liver, 1001
    in chronic articular rheumatism, 74

Placental syphilis, pathology of, 271, 272

Plane vitiligoidea of skin in jaundice, 980

Pleura, lesions of, in chronic intestinal catarrh, 706

Pleurae, lesions of, in scurvy, 173

Pleural cavities, perforation of, in simple ulcer of stomach, 500

Pleuritis, complicating gastric cancer, 560
  distinguished from perihepatitis, 990
  in hepatic abscess, 1014
  in acute rheumatism, 37
  in trichinosis, 961

Pleurodynia, 77

Pleuro-pneumonia in hepatic abscess, 1014

Plumbism, relation of, to gout, 111

Pneumonia, complicating cancrum oris, 341
    chronic intestinal catarrh, 709
    gastric cancer, 560
  embolic, complicating simple ulcer of stomach, 503
  frequency of, in rachitis, 153
  hypostatic, in entero-colitis, 735
  in acute rheumatism, 37
  in hereditary syphilis, 307

Pneumo-pericardium, in simple gastric ulcer, 508

Podophyllin, use of, in biliousness, 968
    in constipation, 655
    in functional dyspepsia, 458
    in intestinal indigestion, 636
    in jaundice, 982
    in lithaemia, 972
    in hyperaemia of liver, 988
    in fatty liver, 1050

Point of discharge in hepatic abscess, 1015, 1016

Pointing of hepatic abscesses, 1007

Poison of dysentery, duration of activity, 794, 795

Poisoning, phosphorus, influence on causation of fatty liver, 1047

Polyarticular form of rheumatoid arthritis, 80
  inflammations of acute diseases, relation of, to acute rheumatism,
        23

Polyphagia, in dilatation of stomach, 593

Polypi, as a cause of hemorrhage from bowels, 831
  influence on causation of prolapse of rectum, 881
  of rectum, 882
    treatment, 921
  of stomach, 578

Polypoid growths, formation and origin of, in chronic intestinal
        catarrh, 704

Polyuria in irregular gout or gouty dyscrasia, 120, 123

Pomegranate-bark, use of, in tape-worm, 941

Pork measle-worm, 935

Portal circulation, obstructed, influence on causation of chronic
        gastritis, 470
    obstruction of, a cause of ascites, 1173
  vein, changes in, in hepatic hyperaemia, 985
    congestion of, as a cause of hemorrhage from stomach, 581
    diseases of, 1095
    parasites in, 1111
    stenosis of, 1095
    symptoms of pressure of, in disease of pancreas, 1116
    thrombosis and embolism of, 1075
    lesions of, in cirrhosis of liver, 992

Post-mortem, nature of gastromalacia, 618

Potassium bromide, in acute intestinal catarrh of children, 698
    in diabetes, 227
    in laryngismus stridulus, 163
  chlorate, influence on causation of glossitis parasitica, 358
    local use of, in hemorrhoids, 923
        in morbid dentition, 376
        in acute pharyngitis, 397-399
    use of, in aphthous stomatitis, 330, 331
        in mercurial stomatitis, 348
        in stomatitis ulcerosa, 338
        in glossitis parasitica, 359
  citrate, use of, in muscular rheumatism, 77
  iodide, in pseudo-membranous enteritis, 775
    in scrofula, 252
    in syphilis, hereditary, 316
    in syphilitic pharyngitis, 408
  salts, use of, in gout, 132
      in acute rheumatism, 60

Pouched form of dilatation of oesophagus, 431

Pouches, rectal, dilatation of, 885

Poultices, use of, in acute intestinal catarrh, 688, 690
    in abscess of liver, 1023
    in acute rheumatism, 68
    in muscular rheumatism, 76
    in rheumatoid arthritis, 100
    in tonsillitis, 388
    in simple ulcer of stomach, 527
    in typhlitis, 822

Poverty, influence of, on causation of gout, 110, 111
      of rheumatoid arthritis, 91
      of simple ulcer of stomach, 486
      of tabes mesenterica, 1186

Pre-digested foods, use of, in intestinal indigestion, 635

Predisposing causes of cholera morbus, 720
    of functional dyspepsia, 438
    of gout, 109
    of scrofula, 232

Pregnancy, influence on causation of functional dyspepsia, 448
      of acute yellow atrophy of liver, 1024
      of fatty liver, 1047
      of spasmodic stricture of oesophagus, 419
      of rheumatoid arthritis, 90
      of aphthous stomatitis, 326
  and lactation, influence on causation of scrofula, 237

Preliminary treatment of tape-worm, 941

Premonitory symptoms of jaundice, 977

Pre-natal treatment of rachitis, 158

Prevention of hereditary syphilis by treatment of parents, 260, 261

Preventive treatment of cholera morbus, 724
    of enteralgia, 665
    of entero-colitis and cholera infantum, 746
    of chronic intestinal catarrh, 714, 715
    of morbid dentition, 376
    of rachitis, 158
    of hereditary syphilis, 314
    of scrofula, 249
    of mercurial stomatitis, 347
    of tabes mesenterica, 1193
    of thrush, 335

Primary disease of rectum and anus, 881
  form of cancer of liver, 1034

Privation and want, influence on causation of functional dyspepsia,
        441

Procidentia of rectum, 881

Proctitis, 667, 684. See _Rectum and Anus, Diseases of_.
  influence on causation of abscess of liver, 1004

Prodromal symptoms of gout, 118

Prodromata of typhlitis and perityphlitis, 818

Prognosis of Anchylostomum duodenale, 956
  of occlusion of biliary passages, 1092
  of cancrum oris, 342
  of cholera infantum, 745
  of cholera morbus, 724
  of constipation, 650
  of diabetes mellitus, 217
  of dysentery, 807
  of enteralgia, 664
  of pseudo-membranous enteritis, 774
  of entero-colitis, 741
  of gastralgia, 462
  in acute gastritis, 468
  of parenchymatous glossitis, 364
  of chronic parenchymatous glossitis, 368
  of glossitis parasitica, 359
  of chronic superficial glossitis, 367
  of glossanthrax, 368
  of gout, 126
  of hepatic glycosuria, 974
  of acute intestinal catarrh, 687
  of chronic intestinal catarrh, 713
  of lardaceous degeneration of intestines, 876
  of intestinal cancer, 873
  of intestinal indigestion, 631
  of intestinal ulcer, 828
  of jaundice, 981
  of lithaemia, 970
  of abscess of liver, 1018
  of acute yellow atrophy of liver, 1029
  of amyloid liver, 1045
  of cancer of liver, 1039
  of cirrhosis of liver, 999
  of fatty liver, 1049
  of hyperaemia of liver, 988
  of macroglossia, 353
  of morbid dentition, 376
  of oesophageal paralysis, 430
  of acute oesophagitis, 415
  of chronic oesophagitis, 417
  of cancer of oesophagus, 428
  of dilatation of oesophagus, 434
  of organic stricture of oesophagus, 425
  of spasmodic stricture of oesophagus, 421
  of ulceration of oesophagus, 418
  of carcinoma of pancreas, 1126
  of tubercular peritonitis, 1168
  of acute pharyngitis, 396
  of chronic pharyngitis, 404
  of syphilitic pharyngitis, 408
  in tuberculous pharyngitis, 401
  of purpura, 193
  of hypertrophic stenosis of pylorus, 615
  of rachitis, 157
  of congenital malformations of rectum and anus, 880
  of acute rheumatism, 50
  of chronic articular rheumatism, 73
  of gonorrhoeal rheumatism, 106
  of rheumatoid arthritis, 95
  of scrofula, 248
  of scurvy, 182
  of cancer of stomach, 575
  of cirrhosis of stomach, 614
  of acute dilatation of stomach, 610
  of dilatation of stomach, 603
  of hemorrhage from stomach, 585
  of rupture of stomach, 618
  of simple ulcer of stomach, 518
  of aphthous stomatitis, 330
  of catarrhal stomatitis, 325
  of mercurial stomatitis, 347
  of stomatitis ulcerosa, 338
  of stomatorrhagia, 371
  of hereditary syphilis, 309
  of iritis in hereditary syphilis, 281
  of nervous disease in hereditary syphilis, 304
  of tabes mesenterica, 1191
  of tongue-tie, 349
  of syphilitic ulceration of tongue, 370
  of tonsillitis, 387
  of trichinosis, 961
  of typhlitis and perityphlitis, 820

Progress and termination of chronic intestinal catarrh, 709

Prolapse of rectum, 881

Prolapsed hemorrhoids, treatment of, 924

Prolapsus ani, in dysentery, 797, 803
    treatment of, 919

Propagation of dysentery by dejecta, 791

Prophylactic treatment of acute intestinal catarrh, 687

Prophylaxis in biliousness, 967
  of dysentery, 808
  of Filaria sanguinis, 194
  of cirrhosis of liver, 1000
  of tape-worm, 942, 943
  of trichinosis, 962

Propylamine, use of, in acute articular rheumatism, 62
    in chronic articular rheumatism, 74

Proscolex of tape-worm, 932

Prostatic disease, influence on causation of pseudo-membranous
        enteritis, 765

Prostration in acute gastritis, 467
  in obstruction of intestines by gall-stones, 840
  in trichinosis, 960

Prurigo podicis of anus, 892

Pruritus in jaundice, 980
  in occlusion of biliary passages, 1087
  of genitalia in diabetes mellitus, 204
  ani, 909
    treatment, 917
    in Oxyuris vermicularis, 951
    in tape-worm, 940

Pseudo-membrane, seat and character, in acute oesophagitis, 412

Pseudo-membranous enteritis, 763
    form, of dysentery, lesions of, 799
      of acute oesophagitis, etiology, 410
        symptoms, 414

Pseudo-paralysis in hereditary syphilis, 289, 312

Psoriasis linguae, 356

Puerperal form of acute peritonitis, treatment, 1146, 1149

Pullna water, use of, in intestinal indigestion, 636

Pulmonary affections in acute rheumatism, 36
    complicating gonorrhoeal rheumatism, 106
      rheumatoid arthritis, 84
  artery, enlargement of, in rachitis, 139
  cavities, influence on causation of amyloid liver, 1041
  congestion in acute rheumatism, 37
  disease, influence on causation of functional dyspepsia, 448
        of chronic intestinal catarrh, 700
        of intestinal indigestion, 626
    chronic, influence on causation of chronic oesophagitis, 416
    influence on causation of hyperaemia of liver, 984

Pulsating tumor of epigastrium, in hemorrhage into pancreas, 1129

Pulsation, epigastric, in cancer of stomach, 553

Pulse, characters of, in acute peritonitis, 1141
    in tubercular peritonitis, 1165, 1166
  state of, in occlusion of biliary passages, 1089
    in cancrum oris, 341
    in cholera infantum, 742
    in cholera morbus, 723
    in dysentery, 804
    in enteralgia, 661
    in pseudo-membranous enteritis, 766
    in entero-colitis, 734, 736
    in acute gastritis, 467
    in parenchymatous glossitis, 362
    in hepatic abscess, 1009
    in hepatic colic, 1071
    in acute intestinal catarrh, 682
    in chronic intestinal catarrh, 709
    in jaundice, 979
    in acute yellow atrophy of liver, 1028
    in fatty liver, 1048
    in acute pancreatitis, 1119
    in carcinoma of pancreas, 1125
    in acute pharyngitis, 394, 395
    in phosphorus-poisoning, 1032
    in cancer of stomach, 553
    in tonsillitis, 381
    in typhlitis and perityphlitis, 819

Pumpkin-seeds, use of, in tape-worm, 942

Puncture, exploratory, in abscess of liver, 1021
  in hydatids of liver, 1107
  of colon, in enteralgia, 665
  of gall-bladder as a means of diagnosis of occlusion of biliary
        passages, 1092
    for relief of biliary calculi, 1081
      of impacted calculus, 1094
  of intestine in acute peritonitis, 1152
  of right lobe, value of, in diagnosis of abscess of liver, 1020,
        1021

Pupil, dilatation of, in acute yellow atrophy of liver, 1027

Purgatives, abuse of, influence on causation of acute intestinal
        catarrh, 672
  use of, in constipation, 651, 656
    in entero-colitis and cholera infantum, 757
    in hepatic colic, 1082
    in impaction of feces, 918
    in chronic intestinal catarrh, 714, 715
    in intestinal ulcer, 829
    in acute yellow atrophy of liver, 1030
    in acute peritonitis, 1151
    in chronic interstitial pancreatitis, 1122
    in seat-worms, 951
    in trichinosis, 962
  uselessness of, in intestinal obstruction, 862, 863

PURPURA, 186
    Definition, 186, 187
    Etiology, 190
      Heredity, influence on causation, 190
      Hereditary predisposition to, 191
      Specific nature, 191
    Pathology, 191
    Forms, 187
    Symptoms, 187
  _Purpura Simplex_, 187
    Mode of onset, 187
    Eruption, character, 187
      duration, 187
    General condition, 187
  _Purpura Haemorrhagica_ (_Morbus Maculosus Werlhofii_), 188
    Mode of onset, 188
    Eruption, character and seat, 188
    Epistaxis, occurrence of, 188
    Haematemesis, occurrence of, 188
    Haematuria, occurrence of, 188
    General condition, 188
    Duration, 189
    Temperature, 189
  _Purpura Rheumatica_ (_Peliosis Rheumatica_), 189
    Mode of onset, 189
    Joints, condition of, 189
    Pains in joints, 189
    Eruption, character and seat, 189
      duration, 189
    Cardiac murmurs, 189
  _Sub-varieties_, 189
      In children, 190
      Purpura urticaria, 190
      Purpura papulosa, 190
    Complications, 190
      Gangrene of intestines, 190
    Diagnosis, 192
      From scurvy, 192
      From haemophilia, 192
      From effusions and ecchymoses of acute exanthemata, 192
      From erythema nodosum, 192
      From erythema multiforme, 192
    Prognosis, 193
    Treatment, 193
      Of mild cases, 193
      Diet, 193
      Necessity of quiet, 193
      Of complications, 194
      Of purpura rheumatica, local, 194
      Use of sulphuric acid, 193
        of acetate of lead, 193
        of ergotin, 193
        of turpentine, 193
        of iron, 194
      Transfusion of blood, 194

Purpura haemorrhagica, complicating gastric cancer, 560
    in children, 190
  papulosa, 190
  urticaria, 190

Purulent form of local peritonitis, 1159
  infiltration, in phlegmonous form of acute oesophagitis, 413

Pus, characters of, in acute peritonitis, 1136
  evacuation of, in abscess of liver, 1021
  mode of escape, in phlegmonous form of acute oesophagitis, 413
  of acute pancreatitis, character of, 1118
  of hepatic abscesses, 1007

Pustular syphilides in hereditary syphilis, 279
    diagnosis of, 279, 280

Putrefaction, influence on causation of dysentery, 787, 789

Pyaemia complicating mercurial stomatitis, 346
  influence on causation of acute peritonitis, 1138
  occurrence of, in dysentery, 797, 804

Pylephlebitis, 1095
  in simple ulcer of stomach, 502
  suppurative, 1097

Pylethrombosis, in gastric cancer, 560

Pylorus, cancer of, influence on causation of occlusion of common
        biliary duct, 1085
  distortion of, as cause of dilatation of stomach, 588
  hypertrophic stenosis of, 615
    Synonyms, 615
    Etiology, 615
      Cicatrization of gastric ulcer, 615
    Morbid anatomy, 615
      Hypertrophy of gastric walls, 615
      Fibrous tissue, new growth of, 615
    Symptoms, 615
      Of chronic gastritis, 615
      Presence of a tumor, 615
    Diagnosis, 615
    Prognosis, 615
    Treatment, 615
  hypertrophy and ulceration of, in chronic gastritis, 472
  obstruction of, in gastric cancer, 566
    influence on causation of dilatation of stomach, 587
  resection of, in dilatation of stomach, 609
  scirrhous state of, in chronic gastritis, 471
  spasm of, influence on causation of dilatation of stomach, 588
  stenosis of, in simple ulcer of stomach, 503
    influence on causation of dilatation of stomach, 587

Pyo-pneumothorax subphrenicus in perforation of simple ulcer of
        stomach, 499

Pyrethrum, use, in chronic pharyngitis, 406

Pyrexia in acute gastritis, treatment of, 469, 470
  in parenchymatous glossitis, 362
  in acute oesophagitis, treatment of, 416
  in tuberculous pharyngitis, 401
  in catarrhal stomatitis, 323
  in mercurial stomatitis, 346

Pyrosis in functional dyspepsia, 449


Q.

Quicksilver, use of, in intestinal obstruction, 863

Quiet, necessity of, in purpura, 193

Quinia, use of, in ascites, 1179
    in catarrh of bile-ducts, 1057
    in dysentery, 812
    in functional dyspepsia, 457
    in gastralgia, 462
    in parenchymatous glossitis, 365
    in gout, 135
    in acute intestinal catarrh, 689, 692
    in chronic intestinal catarrh, 715
    in intestinal indigestion, 636
      obstruction, 865
    in lithaemia, 973
    in acute yellow atrophy of liver, 1030
    in abscess of liver, 1020
    in aborting abscess of liver, 1020
    in amyloid liver, 1045
    in cirrhosis of liver, 1000
    in fatty liver, 1051
    in acute pharyngitis, 398
    in pruritus ani, 917
    in purpura, 194
    in suppurative pylephlebitis, 1101
    in rectal paralysis of malarial origin, 908
    in acute rheumatism, 61
    in chronic articular rheumatism, 74
    in gonorrhoeal rheumatism, 107
    in rheumatoid arthritis, 98
    in gangrenous stomatitis, 344
    in tape-worm, 942
    in tonsillitis, 388

Quinsy, 379


R.

Race, influence on causation of diabetes mellitus, 204
      of cancer of stomach, 535
      of acute intestinal catarrh, 669
      of scrofula, 235

RACHITIS, 137
  Definition, 137
  Etiology and pathology, 137
    Inflammatory nature of, 137, 138
    Defective calcification, causes of, 138, 139
    Lime, method of elimination, 138
    Phosphoric acid, method of elimination, 139
    Nitrogen, method of elimination, 139
    Anatomical causes, 139
    Arteries, increased width of, influence on causation, 139
    Artery, pulmonary, enlargement of, influence on causation, 139
    Thoracic and abdominal viscera, relation to causation, 140
    Liver, enlargement of, 139
    Spleen, enlargement of, 140
    Kidneys, enlargement of, 140
    Direct causes, 140
    Early life, influence on causation, 141, 142
    Climate, influence of, on causation, 143
    Air, bad, influence of, on causation, 143
    Defective maternal nutrition, influence of, on causation, 143
    Intestinal catarrh, influence of, on causation, 144
    Improper food, influence of, on causation, 144
    Pulmonary diseases, influence of, on causation, 144
    Hereditary nature of, 144
    Gout, influence of, on causation, 144
    Syphilis, influence of, on causation, 144
    Malaria, influence of, on causation, 145
    Intra-uterine and congenital forms, causes and symptoms, 141-143
  Symptoms, 146
    Mode of development in infants, 146
        in older infants, 146
    Head, appearance of, 146
      sweating of, 146
      condition of sutures, 147
        of fontanels, 147
        of cranial bones, 147
    Craniotabes, 147
    Cranial sclerosis, 148
    Brain and meninges, condition of, 148, 149
    Brain compression, 149
    Intellect, state of, 149
    Convulsions, 149
    Laryngismus stridulus, 149
    Face, alterations in, 150
    Maxillary bone, lower, changes in, 150
    Teething, anomalies of, 150, 151
    Vertebral columns, changes in, 151
    Kyphosis, occurrence of, 151
    Ribs, changes in, 152
      tenderness of, 152
      beading of, 152
    Chest, alterations in shape, 152
    Heart and lungs, condition of, 152
    Pneumonia, catarrhal, frequency of, 153
    Bronchial and tracheal catarrh, tendency to, 152
        glands, enlargement of, 152
    Abdomen, enlargement of, 153
    Pelvis, deformities of, 153
    Liver, changes in, 153
      degeneration, amyloid, 153
    Spleen and kidneys, degeneration, amyloid, 153
    Tonsils, enlargement of, 153
    Tongue, condition of, 153
    Stomach, condition of, 153
    Intestinal tract, condition of, 153
    Constipation, significance of, 154
    Kidneys, changes in, 154
    Extremities, appearance of, 155
      bones of, changes in, 155
    Bones, curvatures of, 155
        causes of, 155
    Skin, disorders of, 156
    Alopecia, circumscribed, 156
    Of rachitis, acute, 156
      Nature, 156
  Prognosis, favorable nature of, 157
    Influence of complications on, 158
  Treatment, 158
    Preventive, 158
    Pre-natal, 158
    Of intestinal disorders, 158
    Diet, 159
    Milk, use of, 159
      mode of administration, 159, 160
    Weaning, proper time for, 160
    Of craniotabes, 162
      perspiration, 162
      laryngismus stridulus, 163
      convulsions, 163, 164
      complications, 164
      constipation, 164
        by diet, 164
        by strychnia, 164
      deformities, 165, 166
        by gymnastic exercises, 166
        by mechanical apparatus, 166
    Use of alkalies, 161
      of acids, 161
      of baths, salt, 163
        hot, 163
          mode of applying, 163
      of beef-tea, 161
        mode of preparation, 161
      of bromides of potassium and sodium, 163
      of chloral hydrate, 163
      of cod-liver oil, 162
      of iron, 162
      of lime, 162
      of lime-water, proper dose, 161
      of malt extracts, 162
      of phosphate of lime, 162
      of phosphorus, 165
    Fresh air, value of, 163
    Sea-bathing, value of, 163

Ranvier and Cornil on causes of scrofulous inflammation, 239

Rat and mouse, Trichina spiralis in, 958

Raw beef, use of, in acute intestinal catarrh, 691

Rectal alimentation, 928
  conditions necessary to success, 928
    emptiness of bowel, 928
    time of administering, 928
    syringe, variety of, 928
    amount of enemata, 928
    frequency of enemata, 928
    substance employed, 929
    contraindications, 929
    use of nutrient suppositories, 929
    in gastric cancer, 576
    in organic stricture of oesophagus, 425
  heat and fulness, in constipation, 645
  inflammation, 887
  irrigation in dysentery, 809
    in chronic intestinal catarrh, 717
    in jaundice, 983
  pouches, dilatation of, 885
  treatment in acute intestinal catarrh, 697

RECTUM AND ANUS, DISEASES OF, 877
    Forms of, 877
    Anatomy of, 877-879
  _Congenital Malformations_, 879
      Imperforate anus, 879
      Abnormal anal openings, 880
      Absence of anus, 880
      Greater liability of males to, 880
    Prognosis, 880
    Treatment, 880
  _Primary Diseases of Rectum and Anus_, 881
    _Prolapse and Procidentia of Rectum_, 881
      Etiology, 881
        Age, infancy and senility, 881
        Worms, 881
        Diarrhoea, 881
        Constipation, 881
        Coughing and crying, 881
        Loss of tone of anus and rectum, 881
        Abuse of cathartics, 881
        Urethral stricture, 881
        Polypi, 881
        Tumors, 881
      Symptoms, 881
        Size, 881
        Appearance of mucous membrane, 881
    _Polypi of Rectum_, 882
      Varieties, 882
        Gelatinoid form, 882
        Fibroid form, 882
        Nature, 882
        Physical characters, 882
      Symptoms, 882
        Frequent desire to stool, 882
        Heat and tenesmus, 882
        Hemorrhage, 882
        Number, 882
        Seat, 882
    _Hemorrhoids or Piles_, 882
      Etiology, 882
        Abnormal state of blood-vessels, 882
      External, 883
        Sex, influence of, on causation, 883
        Age, influence of, on causation, 883
        Exciting causes, 883
        Tendency to inflammation, 883
        Obliteration of vessels in, 883
        Structure of, 883
        Symptoms, 883
          Pain, 883
          Tenesmus, 883
          Inability to urinate, 883
        Suppuration of, 883
      Internal, 883
        Physical characters, 883
        Structure of, 883
        Color, 883
        Etiology, 884
          Constipation, 884
          Diseases of liver, 884
          Abdominal tumors, 884
          Horseback riding, 884
          Dysentery, 884
          Diarrhoea, 884
          Sedentary life, 884
          Age, 884
          Sex, 884
          Rich food, 884
        Symptoms, 884
          Pain, 884
          Tenesmus, 884
          Spasm of sphincters, 884
          Hemorrhage, 884
          Weight and fulness, 884
    _Dilatation of the Rectal Pouches_, 885
      Rarity of, 885
      Causes, 885
      Symptoms, 885
        Weight and uneasiness of rectum, 885
        Pain, 885
        Mucus, increased secretion of, 885
        Exploration of bowel with blunt hook, 885
    _Non-malignant Stricture of Rectum_, 885
      Nature, 885
      Etiology, 885
        Traumatism, 885
        Following operations, 885
        Secondary of pelvic inflammation, 885
          of syphilis, 885
        Constipation, 886
        Sex, influence of, on causation, 886
      Symptoms, 886
        Physical characters, 886
        Violent straining at stool, 886
        Wire-drawn feces, 886
        Irregular bowels, 886
        Appetite, impaired, 886
        Digestive disturbances, 886
        Pain, 886
        Mucous discharges, 886
        Seat, 886
          of syphilitic, 886
        Characters of syphilitic, 886
    _Proctitis_, 887
      Frequency, 887
      Etiology, 887
        Intestinal worms, 887
        Rhus toxicodendron, 887
        Gonorrhoeal poison, 888
        Unnatural intercourse, 888
      Symptoms, 887
        Pain, 887
        Tenesmus, 887
        Mucous and bloody discharges, 887
    _Fissure of Anus and Rectum_, 888
      Frequency, 888
      Character, 888
      Position, 888
      Etiology, 888
        Uterine disease, 888
        Frequency in women, 888
        Constipation, 888
        Syphilis, 888
      Symptoms, 888
        Pain, 888
        Spasm of sphincters, 888
        Mental depression, 889
    _Rodent or Lupoid Ulcer of Rectum_, 889
      Frequency, 889
      Seat, 889
      Characters, 889
      Symptoms, 889
        Pain, 889
        Spasm of sphincters, 889
    _Obstruction of Rectum_, 889
      Etiology, 889
        Foreign bodies, 889, 890
        Sex, 889
        Loss of nervous and muscular tone, 889
        Impaction of feces, 889
        Concretions, 890
        Enteroliths, 890
          composition, 890
        Gall-stones, 891
        Intestinal worms, 891
        Tumors, pelvic, 891
      Symptoms, 891
        Appetite impaired, 890
        Digestive disturbances, 890
        Melancholia, 890
        Vomiting, 890
        Tenesmus, etc., 890
        Sloughing of rectum, 891
    _Cutaneous Eruptions and Parasitic Conditions of Anus_, 892
      Eczema, 892
      Erythema intertrigo, 892
      Prurigo podicis, 892
      Herpes, 892
      Furunculi, 892
      Hairs on mucous membrane, 892
      Sarcoptes hominis, 892
      Acarus autumnalis, 892
      Rhus toxicodendron, 892
    _Ulceration of Rectum and Anus_, 893
      Frequency, 893
      Etiology, 894
        Syphilis, 894
        Struma, 894
        Traumatic, 894
        Foreign bodies, 894
        Impacted feces, 894
      Symptoms, 893
        Initial, 893
        Diarrhoea, 893
        Stools, character, 893
        Pains, 893
        Muco-purulent discharges, 894
        Sphincters, loss of power in, 893
        Abscesses, formation, 893
        Ulcers, physical character, 893
        Enlargement of rectal glands, 893
    _Follicular Ulcerations_, 894
      Etiology, 894
      Origin, 894
        From chancroidal invasion, 895
      Symptoms, 895
    _Peri-anal and Peri-rectal Abscess_, 895
        Etiology, 895
      Acute form, 895
          Anatomical causes, 895, 896
          Sex, influence on causation, 896
          Cold and wet, 896
          General debility, 896
          Hepatic disorders, 896
        Symptoms, 896
          Sudden onset, 896
          Chills, 896
          Heat and fulness, 896
          Pain, 896
          Dysuria, 896
          Appetite impaired, 896
          Malaise, 896
      Chronic form, 896
        Etiology, 896
          From traumatic causes, 896
            ulceration of rectum, 896
        Seat, 896
        Symptoms, 896
          Hectic, 896
          Emaciation, 896
          Slow formation, 896
          Difficult to heal, 897
    _Fistula in Ano_, 897
      Great frequency, 897
      Etiology, 897
        Abscesses, 897
        From traumatic causes, 897
        Age, 897
        Male sex, 897
        Phthisis, 897
      Forms, 897
        complete, 897
        incomplete, 897
      Multiple, 897
      Seat of external opening, 897
        internal opening, 898
      Course, 898
      Discharges, character of, 898
      Pain in, 899
      Diagnosis, 898
        Use of probe, 898
    _Hemorrhage from Rectum_, 899
      Primary and Secondary, 899
  _Secondary Diseases of Rectum and Anus_, 900
    _Syphilis of Rectum and Anus_, 900
      Frequency, 900
        relative, in the sexes, 900
      Seat and character, 900, 901
      Mucous patches, 900
      Gummatous deposits, 900
      Condylomata, 901
    _Scrofulous and Tuberculous Affections_, 901
      Pathology of tubercular form, 901
      Description and course, 901
      Causation from ingestion of morbid products of tuberculous
          lungs, 902
      Seat, 902
    _Cancer, Malignant Stricture and Malignant Ulceration_, 902
      Forms, 902
      Relative frequency of forms, 903
      Sex, influence on causation, 903
      Age, influence on causation, 903
      Scirrhous, method of growth, 903
        Pain in, 903
        Difficult defecation, 904
        Odor of patient, 904
        Exhaustion, 904
      Encephaloid, rapid growth of, 904
        hemorrhage in, 904
      Lymphatic glands, enlargement of, 904
      Disease of rectum, by extension from colon, 904
      Ulceration of rectum following typhoid fever and dysentery, 905
      Ulceration from mechanical causes, 906
    _Effects of Abnormal Conditions of Spinal Cord and Membranes on
          Rectum and Anus_, 906
      Constipation in, 906
      Loss of control, 907
      Paralysis of rectum in pressure myelitis, 907
        rectal, in spinal meningitis, 907
        in fracture of vertebrae, 908
      Sphincters, condition of, in convulsions of epilepsy, 908
      Paralysis, in chronic heart disease, 908
        in malaria, 908
    _Spasm of Rectum and Anus_, 909
    _Pruritus Ani_, 909
      Etiology, 909
        Neurotic origin, 909
        Digestive derangements as causes, 909
        Overwork, 909
        Spinal irritation, 909
        Worms, 909
        Rheumatism, 909
        Diabetes mellitus, 909
    _Neuralgia of Rectum_, 909
      Frequency of, 910
      Causes of, 910
      Malaria, 910
      Reflex, 910
      Uterine disease, 910
      Symptoms, 910
    _Effect of Cholera and Certain Poisons and Remedies on Rectum_,
          910
      Of cholera, 910
      Of arsenic, 910
      Of corrosive sublimate, 910
      Of croton oil, 910
      Of strychnia, 911
      Of morphia, 911
      Of jaborandi, pain in rectum, from, 911
      Of mineral acids, 911
  Treatment, therapeutical and surgical, 911
    Of anal fissure, 911
      Cauterization with nitrate of silver, 912
      Incision and dilatation, 912
    Of rectal ulcer and deep anal fissure, 912
      Cleanliness, 912
      Bougies of soap, 912
      Cauterization, 912
      Glycerite of tannin, 912
      Astringent, 912
      Red precipitate ointment, 912
      Use of acid nitrate of mercury, 912
      Nitric acid, 912
      Incision, 912
        method of, 913
      Dilatation, method of, 912
    Of tuberculous ulcer of rectum, 913
    Of chronic ulcer of rectum, 913
        use of Ward's paste, 913
    Of rodent ulcer, 913
        excision in, 913
    Of cancer of rectum, 913
        use of anodynes, 913
        enemata of warm water, 914
        bougies, use of, 914
        excision, 914, 915
          method of, 915
        lumbar colotomy, 915
          method of, 916
    Of dilatation and inflammation of rectal pouches, 916
        incision, 916
    Of loss of co-ordination in muscles of defecation, 916
    Of sphincterismus, 916
      Use of purgatives, 916
        of hot hip-baths, 916
        of bougies, 916
        of incision and dilatation, 916
    Of pruritus ani, 917
      Use of enemata, 917
        of carbolic acid, 917
        of turpentine, 917
        of hot water, 917
        of sulphate of zinc and alum, 917
        of chloroform, 917
        of iron and quinine, 917
        of mercurial ointment, 917
        of tincture gelsemium, 917
    Of non-malignant rectal stricture, 917
      Use of bougies, 917
        of dilatation, 917
      Of syphilitic form, 917
    Of peri-anal and peri-rectal abscess, 918
      Use of poultices, 918
        of incision, 918
    Of gonorrhoea of rectum, 918
      Astringent injections, 918
    Of impaction of feces, 918
      Use of dilatation of sphincter, 918
        of enemata, 918
        of purgatives, 918
        of iron and quinine, 919
        of electricity, 919
    Of irritable rectum, 919
        Anodyne enemata, 919
        Cauterization with nitric acid, 919
    Of concretions of rectum, 919
    Of proctitis, 919
      Use of copaiba, 919
        of black pepper, 919
        of ice, locally, 919
    Of prolapsus ani and procidentia, 919
      Use of astringent solutions, 919
        of anal pad and T-bandage, 920
        of cauterization, 920
          method, 920
        of excision, 920
          method, 920
        of dilated gum pessary, 920
        of ergotin, locally, 920, 921
        of strychnia, locally, 921
        of nitric acid, locally, 920
        of nitrate of silver, 920
    Of polypus, 921
      Ligation, 921
      Clamp and cautery, 921
    Of fistula in ano, 921
      Palliative, 921
      Operative, 921
        by incision, 922
        by ligation, 922
          methods, 922
        question of operation in phthisical cases, 922
    Of hemorrhoids, 923
      Palliative, 923
      Astringent ointments, 923
      Enemata of potassium chlorate, 923
        of lime-water, 923
      Use of copaiba, 923
        of black pepper, 923
      Oil of amber, locally, 923
      Use of hamamelis virginica, 923
        of ergotin, 923, 924
        of aloes, 923
        of cold water, 924
      Rest after defecation, 924
      Of prolapsing, 924
      Operative, 924
      Of external, 924
      Of internal, 924
        by strangulation, 924
          method, 925
        by clamp and cautery, 925
        by ecraseur, 925
        by caustics, 926
        by nitric acid, 926
        by caustic potash, 926
    Of hemorrhage from rectum, 926
      Ice, use of, 927
      Injections of ice-water, 927
        of perchloride of iron, 927
      Use of tampon, 927
          method, 927
        of Agnew's rectal chemise, 927
        of ligature, 927

Rectum, heat of, in dysentery, 802
    in pseudo-membranous enteritis, 765
  painful disease of, influence on causation of constipation, 642
  suppuration of, as a cause of suppurative pylephlebitis, 1098
  stricture of, symptoms, 856

Recurrence of spasmodic stricture of oesophagus, frequency of, 421
  of tonsillitis, frequency of, 387

Reflex causes of enteralgia, 660
  nervous disturbance, due to biliary concretions, 1078
    symptoms in morbid dentition, 374
  spasm of muscles in general form of rheumatoid arthritis, 80

Regimen, restricted, influence on causation of functional dyspepsia,
        444

Regurgitation, in functional dyspepsia, 449
  of food in cancer of oesophagus, 427
    in dilatation of oesophagus, 432
    in organic stricture of oesophagus, 423
    time of, in spasmodic stricture of oesophagus, 420
    in ulceration of oesophagus, 418
    in acute oesophagitis, 413
    in cancer of cardiac orifice of stomach, 542

Relapses, frequency of, in typhlitis and peri- and paratyphlitis, 820
  influence of salicyl treatment on frequency of, in acute rheumatism,
        52
  tendency to, in acute rheumatism, 44, 45

Remissions in chronic variety of general rheumatoid arthritis, 82
  in tubercular peritonitis, 1165

Remittent and typhoid fever, distinguished from acute gastritis, 468

Renal affections complicating acute rheumatism, 42
  colic complicating gout, 124
    distinguished from enteralgia, 664
  disease, influence on causation of chronic gastritis, 470
    influence on causation of simple ulcer of stomach, 488

Resection, in gastric cancer, 577
  of pylorus, in dilatation of stomach, 609

Respiration, in ascites, 1177
  in acute peritonitis, 1141
  difficult, in tonsillitis, 382
  laborious, in parenchymatous glossitis, 361

Rest after defecation, in hemorrhoids, 924
  in hemorrhage from bowels, 834
  in perforative peritonitis, 1156
  importance of, in dysentery, 809
    in chronic gastritis, 476
    in treatment of simple ulcer of stomach, 519
  local, importance in rheumatoid arthritis, 100
  necessity of, in acute gastritis, 469
    in treatment of heart, complications of acute rheumatism, 64
  value of, in treatment of acute intestinal catarrh, 690
    in chronic intestinal catarrh, 716

Restlessness in cholera infantum, 742

Results of chronic articular rheumatism, 71, 72

Retention of food in dilatation of oesophagus, 431

Rhamnus, fl. ext., use in constipation, 656

Rheumatic and arthritic diathesis, relation of, to causation of
        gonorrhoeal rheumatism, 103
  form of acute pharyngitis, symptoms, 394
      treatment, 398
    of gonorrhoeal rheumatism, symptoms, 104
    of tonsillitis, treatment, 388, 389

RHEUMATISM--_Acute_, 19
    Synonyms, 19
    Definition, 19
    Etiology, 19
      Climate, influence of, on causation, 19
      Season, influence of, on causation, 19
      Occupation, influence of, on causation, 20
      Age, influence of, on causation, 20
      Sex, influence of, on causation, 21
      Heredity, influence of, on causation, 21
      Temperament, influence of, on causation, 21
      Cold and damp, influence of, on causation, 22
      Fatigue and exhaustion, influence of, on causation, 22
      Depressing passions, influence of, on causation, 22
      Traumatism, influence of, on causation, 22
      Polyarticular inflammation of acute diseases, relation of, to,
          23
    Pathology, 23
      Theories regarding origin, 23
      Lactic-acid theory, 23
      Latham's theory of hyperoxidation, 24
      Nervous theory, 24
      Miasmatic theory, 26
      Infective-germ theory, 26
    Symptoms, 26
      Invasion, 26
      General description, 27
      Local, 27
        date of appearance of, 27
      Joints, condition of, 27
        most affected, 27
      Pain, character of, 27
      Tendency to invade fresh joints, 27
      Description of special symptoms, 29
      Temperature, 27, 29
      Hyperpyrexia, 29, 66
      Defervescence, mode of, 29
      Digestive tract, 27
      Tongue, 27
      Appetite, 27
      Constipation, 27
      Thirst, 27
      Urine, condition of, 30
        amount of urea and uric acid in, 30
        during convalescence, 30
      Albuminuria in, 30
      Saliva, condition of, 30
      Perspiration in, 27, 30
      Blood, condition of, 31
    Complications, 31
      Cardiac affections in, 28, 31
        frequency of, 32
        causes of, 32
          occupation, 33
          age, 32
        date of appearance of, 28, 33
        forms of, 32
        relative frequency of forms of, 33
        endocarditis and pericarditis, symptoms, 28, 33, 34
        ulcerative endocarditis, 33
        myocarditis, 34
          symptoms of, 34
          subacute, 35
        murmurs in, 28, 35
        relative frequency of different murmurs, 35
        anaemic murmurs, 36
      Pulmonary affections, 36
        frequency of, 36
        relation of, to cardiac complications, 36
        pneumonia and pleuritis, 36, 37
        congestion of lungs, 37
      Nervous affections, 37
        delirium, 37, 38
        coma, 38
        convulsions, 38
        chorea, 38
        meningitis, 39
        embolism of cerebral arteries, 39
        spinal inflammation, 40
        causes of, 40
        hyperpyrexia as a cause of, 41
        intemperance, 40
        rheumatic poison as a cause of, 41
      Renal affections, 42
      Pharyngitis, 42
      Gastralgia, 42
      Diarrhoea and dysentery, 42
      Peritonitis, 42
      Cystitis and orchitis, 42
      Cutaneous affections, 42
      Nodosities, 43
        Position, 43
        Duration, 43
        Pathology of, 44
    Course and duration, 44
      Average duration of acute symptoms, 45
      Relapses, tendency to, 44, 45
    Morbid anatomy, 46
      Articulations, changes in, 46
      Synovial membrane, changes in, 46
      Microscopic appearance of effusion, 47
      Cartilages, changes in, 47
      Soft parts about joints, changes in, 47
      Brain and membranes, changes in, 39
      Spinal cord and membranes, changes in, 40
      Blood, changes in, 31
      Heart and membranes, changes in, 31-36
    Diagnosis, 47
      From pyaemia, 47
        acute glanders, 48
          periostitis, 48
        articular enlargements of rickets, 48
            of hereditary syphilis, 48
          inflammation of cerebral softening and hemorrhage, 49
            of spinal disease, 49
    Prognosis, 50
    Mortality, 50
      Cause of sudden death in, 50
    Rheumatism, acute articular, in children, 49
        Peculiarities of, 49
    Treatment, 51
      Use of salicylic acid and salicylates, 51-59
          Influence of, upon joint-pains, 51, 52
            on pyrexia and hyperpyrexia, 52, 55
            on frequency of relapses, 52
            on frequency of heart complications, 53-55
            on duration, 55
          Unpleasant effects of, 56
          Effects of, upon the heart, 57
          Heart-failure from, 57
          Delirium from, 57
          Albuminuria and haematuria from, 58
          Doses of, 58
          Mode of administration, 59
      Use of salicine, advantages of, 58
          Dose of, 58
        of oil of wintergreen, 59
        of alkalies, 60
          Method of administration, 60
          Influence of, on pain and pyrexia, 60
            on duration, 60
            on heart complications, 60, 61
          and salicylates, relative power of, 60, 61
            combined use of, 61
        of quinia, 61
        of potassium iodide, 62
        of ammonium bromide, 62
        of cold, 66
        of trimethylamine, 62
        of benzoic acid, 62
        of chloral and morphia, 65
        of lemon-juice, 63
        of perchloride of iron, 63
        of alcohol, 69
        of blisters, 63, 68
        of aconite, 64
      Of complications, 63
      Of peri- and endocarditis, 63, 64
      Of pericardial effusions, 64
      Of myocarditis, 64
      Necessity of rest in heart complications, 64
      Of meningitis, 65
      Of nervous affections, 65
      Of delirium, 65
      Of sleeplessness, 65
      Of hyperpyrexia, 66
        by cold, 66
          modes of applying, 67
      Summary of treatment, 68
      Diet in, 69
      Hygienic management, 69
      Convalescence, 69
  _Subacute Articular_, 46
    Symptoms of, 46
  _Mono- or Uni-articular Acute and Subacute_, 49
  _Chronic Articular_, 69
    Synonyms, 69
    Definition, 69
    Etiology, 69
      Primary nature, 70
      Predisposing causes, 70
      Heredity, 70
      Acute rheumatism, 70
      Cold and damp, 70
      Exciting causes, 70
    Symptoms and course, 71
      Mild forms, 71
      Pain, character of, 71
      Local, 71
      Creaking of joints, 71
      Alteration of joints, 71
      Anaemia and debility, 71
      Tendency to exacerbation, 71
      Influence of weather on, 71
      Joints most affected, 72
      General condition of, 71
    Complications, 72
      Cardiac disease, 72
      Endarteritis, 72
      Asthma, 72
      Bronchitis, 72
      Neuralgia, 72
      Dyspepsia, 72
    Results, 71, 72
      Ankylosis from, 71
      Thickening, 71, 72
    Duration, 72
    Termination, 72
    Morbid anatomy, 70
      Of simple form, 70
      Changes in joints, 70
        synovial membrane, 70
      Capsule and ligaments, 70
      Cartilages, 70
      Muscles, 71
    Diagnosis, 73
      From rheumatoid arthritis, 73
      From articular enlargement of spinal diseases, 73
          of syphilis and struma, 73
          of tubercular disease, 73
      From chronic articular gout, 73
    Prognosis, 73
    Treatment, 73
      Hygienic, 73
      Importance of proper clothing, 73
      Therapeutic, 73
      Use of salicylates in, 73, 74
        of salicylate of quinia, 74
        of propylamine, 74
        of trimethylamine, 74
        of potassium iodide, 74
        of arsenic, 74
        of cod-liver oil, 74
        of quinia, 74
        of guiaiac, 74
        of bromide of lithium, 74
        of pilocarpine, 74
        of iron, 74
      Local, 74
      Diet, 74
  _Muscular_, 74
    Synonyms, 74
    Definition, 74
    Etiology, 74
      Age, influence of, on causation, 74
      Sex, influence of, on causation, 75
      Cold, influence of, on causation, 75
      Fatigue and strain, influence of, on causation, 75
      Heredity, 75
    Symptoms, 75
      Pain, character of, 75
        effect of pressure upon, 75
      Cramp, muscular, 75
      Spasm, muscular, in, 75
      Muscles most affected, 76
      Digestive tract, 76
      Appetite, 76
      Constipation, 76
      General, 76
    Duration, 76
    Diagnosis, 76
      Tendency to error, 76
      From organic spinal disease, 76
        functional spinal disease, 76
        lead and mercurial poisoning, 76
        neuralgia, 76
    Morbid anatomy, 74
    Varieties, 77
      Lumbago, 77
        Symptoms, 77
        Diagnosis, 77
      Pleurodynia, 77
        Symptoms, 77
        Diagnosis, 77
          from intercostal neuralgia, 77
      Torticollis, 78
        Symptoms, 78
        Diagnosis, 78
    Treatment, 76
      Indications, 76
      Relief of pain, 76
      Use of morphia, 76
        of diaphoretics, 77
        of potassium iodide, 77
        of alkalies, 77
        of citrate of potassium, 77
        of salicylates, 77
        of baths, hot, 77
        of galvanism, 76
      Local, 76, 77
      Heat, 76
      Poultices, 76
      Hygienic, 77
        necessity of proper clothing, 77
      Of lumbago, 77
      Of pleurodynia, 78
      Of torticollis, 78
  _Rheumatoid Arthritis_, 78
    Synonyms, 78
    History, 78
    Etiology, 88
      Of general progressive form, 88
        Influence of age on causation, 88
          of sex on causation, 88
          of cold and damp on causation, 88, 90
          of heredity on causation, 88
          of rheumatism on causation, 88, 89
          of gout on causation, 89
          of diseases of pregnancy on causation, 90
          of disorders of menstruation, 90
          of scrofula on causation, 90
          of phthisis on causation, 90
          of poverty on causation, 91
          of injury on causation, 91
      Of partial form, 91
        Advanced age, influence of, on causation, 91
        Sex, influence of, on causation, 91
        Local irritation of joint, influence of, on causation, 91
        Cold and damp, influence of, on causation, 91
      Of Heberden's nodosities, 91
        Advanced age, influence of, on causation, 91
        Female sex, influence of, on causation, 91
        Poverty, influence of, on causation, 91
        Heredity, influence of, on causation, 91
    Varieties, 79
    Symptoms, 80
      Of general progressive or polyarticular form, 80
        Acute variety, 80
        Resemblance to acute rheumatism, 80
        Mode of onset, 80
        General, 80
        Local, 80
        Wasting of muscles, 80
        Reflex muscular spasm, 80
        Duration, 80
      Of chronic variety, 81
        Mode of onset, 81
        Local, 81
        Pain, character of, 81
        Position and shape of joints, 81
        Creaking of joints, 81
        Ankylosis, 81
        Course and duration, 82
        Remissions, 82
        Deformities of upper extremities, description, 82
          of hand, description, 82
          of lower extremities, description, 82
          of feet, description, 82
        General condition, 82
        Digestive symptoms, 82
        Loss of appetite, 83
        Constipation, 83
        Skin, condition of, 83
        Urine, condition of, 83
      Of partial or oligo-articular form (arthritis deformans), 84
        Mode of onset, 85
        Local, 85
        Condition of joint, 85
        Deformities of special joints, description, 85, 86
        Remissions, 85
        Duration, 85
      Of Heberden's nodosities, 86
        Seat and nature, 86
        Pain in, 86
        Exacerbations, acute, in, 86
    Complications, 83-86
      Of progressive form, 83
        Endo- and pericarditis, 83
        Pulmonary affections, 84
        Nervous affections, 84
        Cutaneous affections, 84
        Migraine, 84
        Eye diseases, 84
        Rheumatic nodules, 84
      Of partial form, 84, 85
      Of Heberden's nodosities, 86
    Morbid anatomy, 86
      Changes in the joints, 86
        in synovial membranes, 86
          fluid, 86
        in cartilages, 87
        in bones, 87
        in ligaments, 87
        in muscles, 88
      Formation of osteophytes, 87
      Frequency of ankylosis, 87
    Pathogenesis, 92
      Relation of, to rheumatism, 92
      Nervous origin of, 92
      Specific origin, 92
    Diagnosis, 92
      Of acute form, from subacute or chronic rheumarthritis, 92
      Of chronic form, from chronic articular rheumatism, 93
      Of partial form, from chronic articular rheumatism, 93
        from chronic traumatic arthritis, 93
        from chronic periarthritis of shoulder-joint, 93
        from articular affection of locomotor ataxia, 94
        from articular affections of progressive muscular atrophy, 94
      From chronic gout, 94, 95
        arthritis of late syphilis, 95
    Prognosis, 95
      Of progressive or polyarticular form, 95, 96
      Of partial form, 96
      Of Heberden's nodosities, 96
    Treatment, 96
      Unsatisfactory, 96
      Indications, 96
      Removal of causation, 96
      Use of salicylic acid and salicylates, 97
        of salicylate of quinia, 97
          of sodium, 97
        of potassium iodide, 98
        of cod-liver oil, 98
        of iodine, 98
        of quinia, 98
        of iodide of iron, 98
        of iron, 98
        of arsenic, 98
        of baths, hot, 99
          mineral, 99
            selection of, 99
            indications for, 99
          mud, 100
          local, 100
        of anodyne applications, 100
        of poultices, 100
        of tinct. iodine, 100
        of rest in acute forms, 100
        of blisters, 100, 101
        of passive movements in chronic forms, 100
        of mercurial ointment, 100
        of iodine ointment, 100
        of vapor baths, 100
        of sand baths, 101
        of electricity, 101
          mode of applying, 101
        of massage, 100, 101
        of compression by rubber bandage, 101
      Hygienic, 101
      Use of flannel clothing, 102
      Change of climate, 102
      Diet, 102
      Duration of, 102
  _Gonorrhoeal Rheumatism, or Gonorrhoeal Arthritis_, 102
    Synonyms, 102
    Etiology, 102
      Non-gonorrhoeal origin, 102
      Stage of gonorrhoea at which most frequent, 102
      Predisposing causes, 103
        Cold and damp, 103
        Fatigue, 103
        Rheumatic and arthritic diathesis, 103
        Heredity, 103
      Sex, 103
    Morbid anatomy, 103
      Changes in joints, 103
        in synovial membrane, 103
            fluid, 103
        in cartilages, 103
    Symptoms, 104
      Joints most affected, 104
      Order of invasion, 104
      Arthralgic form, 104
        pain in, 104
      Rheumatic form, 104
        mode of invasion, 104
        local, 104
        temperature, 104
        perspiration, 104
        pain, 104
        digestion, 104
        deformity in, 104
      Acute gonorrhoeal arthritis, 105
        pain in, 105
        condition of joint in, 105
        general, 105
      Chronic hydrarthrosis, 105
          joints most affected, 105
            condition of, 105
        formation of pus, 105
      Involvement of tendons and sheaths, 105
      Periarticular form, 105
        pain in, 105
      Gonorrhoeal bursitis, 105
      Nodes in periosteum, 105
    Complications, 106
      Neuralgia, 106
      Sciatica, 106
      Myalgia, 106
      Affections of the eye, 106
      Iritis, 106
      Erythema, 106
      Cardiac affections, 106
      Endocarditis, 106
      Pulmonary affections, 106
    Termination, 106
      Followed by ankylosis, 106
        spondylitis, 106
        rheumatoid arthritis, 106
        strumous articular disease, 106
    Course and duration, 106
    Prognosis, 106
    Mortality, 106
    Diagnosis, 107
    Treatment, 107
      Local, 107
      General, 107
      Use of iron, 107
        of quinia, 107
        of potassium iodide, 107
        of sodium salicylate, 107
        of baths, 107
      Diet in, 107

Rheumatism complicating dysentery, 805
  influence on causation of acute oesophagitis, 410
      of pruritus ani, 909
      of tonsillitis, 380
  acute and chronic, influence of, on causation of rheumatoid
        arthritis, 88, 89
  and gout, influence on causation of gastralgia, 460
      of chronic gastritis, 470, 471
      of acute pharyngitis, 390

Rheumatoid arthritis following gonorrhoeal rheumatism, 106

Rhubarb, use of, in constipation, 655, 656
    in functional dyspepsia, 458
    in pseudo-membranous enteritis, 774
    in jaundice, 982

Rhus toxicodendron, eruption of anus from, 892
  influence on causation of proctitis, 887

Ribs, changes in, in rachitis, 152

Rickets, as a cause of tardy eruption of teeth, 372
  complicating tabes mesenterica, 1193
  influence on causation of intestinal indigestion, 623

Ridge's foods for infants, 754

Rigors in hepatic abscess, 1008
  in acute secondary pancreatitis, 1121

Rilliet and Barthez on lesions of cholera infantum, 742

Rochelle salts in biliousness, 967
    use of, in constipation, 655

Rockbridge alum water, use of, in chronic intestinal catarrh, 714, 717

Rodent ulcer of rectum, 889
      treatment of, 913

Roseola of hereditary syphilis, 277
    diagnosis of, 278

Round-worms, 952

Rubeolous form of acute pharyngitis, 394

Rubber bandage, compression by, in treatment of rheumatoid arthritis,
        101

Rupture of stomach, 618

Russian baths, use of, in intestinal indigestion, 633


S.

Saccharine foods, use of, in diabetes mellitus, 220

Sacculation of ductus pancreaticus, from obstruction, 1130
  of fluid, in chronic peritonitis, 1162

Salicine, advantages of, in treatment of acute rheumatism, 58

Salicylate of quinia, use of in chronic articular rheumatism, 74
      in rheumatoid arthritis, 97
  of sodium, use of, in gonorrhoeal rheumatism, 107
      in thrush, 335
    and salicylic acid, use of, in diabetes mellitus, 229, 230

Salicylates, use of, in muscular rheumatism, 77
  and alkalies, combined use of, in acute rheumatism, 61
    relative power of, in acute rheumatism, 60, 61

Salicylic acid, use of, in acute intestinal catarrh, 696
    in catarrhal stomatitis, 325
    in rheumatism of dysentery, 809
  and salicylates, influence of, on duration of acute rheumatism, 55
      on frequency of relapses in acute rheumatism, 52
      on heart complications of acute rheumatism, 53-55
    use of, in acute rheumatism, 51-59
      in acute gout, 135
      in chronic articular rheumatism, 73, 74
      in rheumatoid arthritis, 97

Saliva, action of, in digestion, 620
  condition of, in acute rheumatism, 30
  dribbling of, in parenchymatous glossitis, 361

Salivary glands, condition of, in scurvy, 177

Salivation, excessive, in morbid dentition, 373
    in pancreatic carcinoma, 1125
        diseases, 1114
    in aphthous stomatitis, 329
    in catarrhal stomatitis, 323
    in mercurial stomatitis, 345
    in stomatitis ulcerosa, 337
    in tonsillitis, 382

Salted meats, influence of, on causation of scurvy, 171

Sanguinarin, use of, in intestinal indigestion, 636
    in constipation, 665

Sanguine form of scrofulous habit, 243

Santonin, use of, in Ascaris lumbricoides, 954
    in tape-worms, 942

Sarcinae and bacteria in vomit of dilatation of stomach, 594

Sarcoma of pancreas, 1128
  of stomach, 578
  of liver, 1036

Sarcoptes hominis of anus, 892

Scalds, influence on causation of organic stricture of oesophagus, 422

Scarification in acute pharyngitis, 397

Scarlatina, influence on causation of acute gastritis, 466

Scarlatinous form of pharyngitis, 394

Scarlet fever, influence on causation of infantile peritonitis, 1172

Sciatica complicating gonorrhoeal rheumatism, 106

Scirrhous carcinoma of pancreas, secondary nature of, 1124
  form of gastric cancer, 564
    of intestinal cancer, 868
        method of growth, 872
  state of pylorus in chronic gastritis, 471
  of rectum and anus, 903

Sclerosis, cranial, in rachitis, 148
  of central vein, in hepatic hyperaemia, 985
  of liver. See _Liver, Diseases of_.

Scolex of tape-worm, 932

SCROFULA, 231
  Synonyms, 231
  Definition, 231, 232
  Etiology, 232
    Predisposing causes, 232
    Formad on the scrofulous peculiarity, 232
    Heredity, influence on causation of, 232
    Bad hygienic surroundings, influence on causation of, 232
    Food, improper, influence on causation of, 232
    Air, impure, influence on causation of, 232
    Locality and climate, 233
    Season, 233
    Age, 233
    Sex, 234
    Social position, 234
    Consanguineous marriages, 234
    Complexion and temperament, 235
    Race and nationality, 235
    Acquired scrofula, 236
  Exciting causes, 236
    Injury, 236
    The eruptive fevers, 237
    Vaccination, 237
    Pregnancy and lactation, 237
    Eczemas, 237
    Catarrhs, 237
    Ophthalmia and otitis, 237
  Pathology and morbid anatomy, 238
    Anatomical peculiarity of tissue, 238
    Excessive cell-growth in, 238
    Low vitality of cells in, 239
    Cornil and Ranvier on causes of scrofulous inflammation, 239
    Fatty degeneration of cells in scrofulous infiltration, 239
    Caseation of cells, 239
    Glands, changes in, 239, 240
      caseation of, 239, 240
    Relation of, to tuberculosis, 240, 241, 242
    Causes of tendency to appear in early life, 242
  Symptoms, 243
    Physiognomy of, 243, 244
    Scrofulous habits, 243, 244
      forms of, 243
    Phlegmatic form, description of, 243
    Erethistic form, description of, 243
    Torpid form, description of, 243
    Sanguine form, description of, 243
    Features peculiar to, 245
    Deficient circulation, 245
    Tendency to chilblains, 245
      to catarrhs and eczema, 245
    Low temperature, 245
    Scanty menstruation, 245
    Mental condition, 245
    Downy hair, growth on forehead and shoulders, 246
    Cutting and ulceration of lobe of ear from ear-rings, 246
    Thick upper lip, 246
    Teeth, condition of, 246
    Clubbing of fingers, 246
    General manifestations, 246
    Influence upon other diseases, 246
    Modification of measles by, 247
      of boils by, 247
      ordinary injuries by, 247
      conjunctivitis by, 248
    No such disease per se, 248
  Diagnosis, 248
    From syphilis, 248
      lupus, 248
  Prognosis, 248
  Treatment, 249
    Preventive, 249
    Intermarriage, danger from, 249
    Diet, 249
    Importance of breast-milk, 249
    Starchy food, danger from, 249
    Weaning, proper time for, 250
    Air, pure, importance of, 250
    Bathing, value, 250
    Therapeutic, 251
      Necessity of exercise, 252
      Use of iodine, 251
        of iodide of iron, 251
        of mercury, 251
        of cod-liver oil, 252
        of alkalies, 252
        of hypophosphites and lactophosphates, 252
      Of enlarged glands, 252

Scrofula, influence on causation of acute pharyngitis, 390
      of rheumatoid arthritis, 90
      of tonsillitis, 380
  acquired, 236
  and tuberculosis, relation to tabes mesenterica, 1183, 1185

Scrofulous affections of rectum and anus, 901

SCURVY, 167
  Synonyms, 167
  Definition, 167
  History, 167, 168, 169
  Etiology, 169
    Sex, influence on causation, 169
    Age, influence on causation, 169
    Contagiousness of, 169
    Depressing emotions, influence on causation, 169
    Nostalgia, influence on causation, 169, 170
    Atmospheric changes, influence on causation, 170
    Air, impure, influence on causation, 170
    Personal habits, influence on causation, 170
    Tobacco, influence on causation, 170
    Drink and food, influence on causation, 170, 171
    Salted food, influence on causation, 171
  Morbid anatomy, 171
    Post-mortem appearance of body, 171, 172
    Skin, lesions of, 172
    Muscles, lesions of, 172
    Bones, lesions of, 172
    Joints, lesions of, 172
    Brain, lesions of, 172
    Heart and pericardium, lesions of, 172
    Blood-vessels, lesions of, 172
    Lungs, lesions of, 172
    Pleurae, lesions of, 173
    Digestive tract, lesions of, 173
    Pancreas, lesions of, 173
    Kidneys, lesions of, 173
    Liver, lesions of, 173
    Bladder, lesions of, 173
    Spleen, lesions of, 173
  Pathology, 173
    Essential characters, 173
    Perverted nutrition, 173
    Blood, condition of, 173
      amount of fibrin in, 174
        of albumen, 174
        of red corpuscles, 174
        of salines in, 174, 175
        of water, 175
      alkalinity of, 175
      analyses of, 175
  Symptoms, 176
    Mode of development, 176
    Cachexia of, 176
    Initial, 176
    Mental condition, 176
    Physiognomy, 176
    Pains, muscular, 177
    Appetite, 177
    Breath, 177
    Tongue, condition of, 177
    Gums, condition of, 177
    Salivary glands, condition of, 177
    Skin, condition of, 176, 178
      extravasations of blood in, 178
      oedema of, 178
      ulceration of, 178
    Bones, condition of, 179
    Articulations, condition of, 179
    Heart, condition of, 179
    Hemorrhages, frequency of, 179
    Epistaxis, 179, 180
    Haematemesis, 180
    Hemorrhage from bowels, 180
    Haematuria, 180
    Serous inflammations, 180
    Pericarditis, 180
    Pleuritis, 180
    Nervous centres, hemorrhagic extravasations into, 180
    Convulsions, 180
    Headache, 180
    Paralysis, 180
    Embolism of lungs and spleen, 181
    Urine, condition of, 181
    Spleen, enlargement of, 181
    Visual disorders, 181
    Blindness, 181
    Conjunctiva, hemorrhage under, 181
    Hearing, disorders of, 181
    Temperature, 182
  Diagnosis, 182
    From skin disorders, 182
      rheumatism, 182
  Prognosis, 182
  Treatment, 183
    Preventive, 183
    Hygienic, 183
    Diet, 183
    Necessity of fruit, 183
      of milk, 183
    Lime-juice, 183, 184
      preparation of, 184
    Ventilation, 184
    Air, pure, 184
    Therapeutic, 184
    Use of vegetable bitters, 184
      of mineral acids, 184
      of haemostatics, 185
    Of stomatitis, 185
        local, 185
    Of hemorrhages, 185

Scurvy as a cause of hemorrhagic effusion of peritoneum, 1180

Scybalae, formation of, in constipation, 645

Sea-bathing, value of, in rachitis, 163

Season, hot, influence on causation of dysentery, 787
      of biliary calculi, 1065
      of entero-colitis, 727, 728
      of rheumatism, acute, 19
      of scrofula, 233
      of stomatitis ulcerosa, 336
      of thrush, 332

Seat of abscesses in suppurative hepatitis, 1006, 1011
  of deposit in lardaceous degeneration of intestines, 875
  of cancer of intestine, 869
  of intussusception, 846
  of local forms of peritonitis, 1159
  of stricture of bowel, 855

Seat-worms, 950
  symptoms of, 951
  treatment of, 951

Seborrhoea complicating gout, 121

Second dentition, 375

Secondary causes of disease of pancreas, 1114
  character of tabes mesenterica, 1183, 1186
  disease of liver in carcinoma of pancreas, 1126
    of rectum and anus, 900
  form of intestinal cancer, 869
    of carcinoma of liver, 1034, 1035
  growths, in gastric cancer, 556
  pancreatitis, acute, 1120
  period of hereditary syphilis, 274
  ulcers of tongue, 370

Secretions in tonsillitis, character of, 385
  fetid, in gangrenous form of acute pharyngitis, 396

Sedentary life, influence on causation of constipation, 640
      of acute intestinal catarrh, 671
      of dilatation of stomach, 592
    and occupation, influence on causation of intestinal indigestion,
        624
  occupation as a cause of chronic pharyngitis, 402

Seminal emissions in constipation, 646

Senna, use of, in constipation, 656

Sensations, perversions of, in pseudo-membranous enteritis, 767

Sensibility, modifications of, in intestinal indigestion, 628

Septic material from fermentation of food, influence on causation of
        cholera morbus, 721

Septicaemic fever, in abscess of liver, treatment of, 1020

Sequelae of cancrum oris, 341
  of chronic intestinal catarrh, 710
  of acute oesophagitis, 414
  of chronic oesophagitis, 417
  of syphilitic pharyngitis, 407
  of simple ulcer of stomach, 500, 503
  of tonsillitis, 383

Serous effusion in acute peritonitis, 1134
  inflammations in scurvy, 180

Severe forms of chronic intestinal catarrh, 707

Sewer-gas, influence on causation of cholera morbus, 721

Sex, influence on causation of ascites, 1175
      of biliary calculi, 1064
      of cholera morbus, 720
      of constipation, 639, 640, 850
      of diabetes mellitus, 203
      of enteralgia, 659
      of pseudo-membranous enteritis, 764
      of fistula in ano, 897
      of gastralgia, 460
      of gout, 109
      of hemorrhoids, 883
      of acute intestinal catarrh, 669
      of chronic intestinal catarrh, 699
      of cancer of intestine, 869
      of intestinal indigestion, 623
      of intussusception, 847
      of abscess of liver, 1003
      of acute yellow atrophy of liver, 1024
      of amyloid liver, 1041
      of carcinoma of liver, 1034
      of cirrhosis of liver, 990
      of fatty liver, 1047
      of organic stricture of oesophagus, 423
      of spasmodic stricture of oesophagus, 419
      of diseases of pancreas, 1114
      of peri-rectal and -anal abscesses, 896
      of phosphorus-poisoning, 1030
      of cancer of rectum and anus, 903
      of non-malignant rectal stricture, 886
      of acute rheumatism, 21
      of gonorrhoeal rheumatism, 103
      of rheumatoid arthritis, 88, 91
      of tabes mesenterica, 1184
      of typhlitis, 815
      of scrofula, 234
      of scurvy, 169
      of cancer of stomach, 533
      of cirrhosis of stomach, 612
      of simple ulcer of stomach, 483

Sexual apparatus of the various species of tape-worm, 932, 934, 935,
        939
  appetite, loss of, in diabetes mellitus, 204
  excess, influence of, on causation of diabetes mellitus, 203
        of gout, 112
        of intestinal indigestion, 624
  functions, perversion of intestinal indigestion, 629
  organs of Taenia echinococcus, 943

Shingles, occurrence of, in gall-stones, 1069

Shock and fright, influence of, on causation of paralysis of
        oesophagus, 429

Sialorrhoea in carcinoma of pancreas, 1125
  in diseases of pancreas, 1114

Sigmoid flexure, dilatation of, in constipation, 643
    stricture of, 836

Silver, chloride of, use of, in amyloid liver, 1046
  nitrate, use of, in dysentery, 809, 812
      in enteralgia, 665
      in pseudo-membranous enteritis, 775
      in entero-colitis, 761
      in chronic gastritis, 478
      in chronic intestinal catarrh, 717, 718
      in spasmodic stricture of oesophagus, 422
      in ulcer of oesophagus, 418
      in chronic oesophagitis, 418
      in prolapsus ani, 920
      in acute and chronic pharyngitis, 399, 405
      in simple ulcer of stomach, 523, 524
      in aphthous stomatitis, 330
      in mercurial stomatitis, 348
      in ulcerative stomatitis, 338
  salts, use of, in catarrh of bile-ducts, 1057
      in functional dyspepsia, 457
      in gastralgia, 463
      in acute intestinal catarrh, 696, 698
      in acute yellow atrophy of liver, 1030

Sinapisms, use of, in cholera infantum, 762
    in cholera morbus, 724
    in enteralgia, 665
    in acute intestinal catarrh, 688, 690

Singultus, in hepatic abscess, 1015

Siphon process for washing out of stomach in gastric dilatation, 604

Situation of biliary calculi, 1066

Sitz-baths, use of, in chronic intestinal catarrh, 716

Size of purulent collections in abscess of liver, 1006

Skim-milk, use of, in biliousness, 967
    in diabetes mellitus, 218
    in hyperaemia of liver, 988

Skin affections complicating gout, 118, 121
  appearance of, in cancrum oris, 342
  bronzing of, in diseases of pancreas, 1117
  burns of, influence of, on causation of ulcer of intestine, 824
        of simple ulcer of stomach, 488
  condition of, in ascites, 1177
    in chronic variety of general rheumatoid arthritis, 83
    in scurvy, 176, 178
  diseases, chronic, cure of, as a cause of tabes mesenterica, 1187
  disorders, in constipation, 648
    in functional dyspepsia, 451
    in intestinal indigestion, 629
    in jaundice, 980
    in cirrhosis of liver, 995, 998
    in acute yellow atrophy of liver, 1028
    in rachitis, 156
  dryness of, in diabetes mellitus, 204
    in chronic intestinal catarrh, 709
  eruptions in entero-colitis, 734
  lesions of, in scurvy, 172
  state of, in cholera morbus, 722
    in dysentery, 796, 804
    in pseudo-membranous enteritis, 766
    in entero-colitis, 734, 736
    in hepatic abscess, 1009
    in lithaemia, 970
    in carcinoma of liver, 1038
    in acute pharyngitis, 394

Sleeplessness, in functional dyspepsia, 451
  in chronic intestinal catarrh, 708
  in intestinal indigestion, 628

Sloughing of intestine in invagination, 845

Soap, use of, in diabetes mellitus, 228

Social position, influence of, on causation of scrofula, 234
  state, influence of, on causation of biliary calculi, 1064

Sodium arseniate, use of, in catarrh of bile-ducts, 1057
      in fatty liver, 1050
      in lithaemia, 972
  benzoate, use of, in entero-colitis and cholera infantum, 757, 761
      in intestinal indigestion, 636
      in acute rheumatism, 62
  bicarbonate, use of, in diabetes, 230
      in pseudo-membranous enteritis, 774
      in acute gastritis, 469
      in acute and chronic intestinal catarrh, 693, 714
      in chronic gastritis, 478
      in intestinal ulcer, 829
      in scrofula, 252
      in dilatation of stomach, 609
      in cancer of stomach, 576
      in thrush, 335
      in tonsillitis, 388
  borate, use of, in glossitis parasitica, 359
  chloride of gold and, in amyloid liver, 1046
      in cirrhosis of liver, 1001
  salts, use of, in gout, 132
  sulphite and hyposulphite in aphthous stomatitis, 330

Solar plexus, lesions of, in acute peritonitis, 1136
    symptoms of pressure upon, in diseases of pancreas, 1117

Solitary glands, lesions of, in cholera morbus, 721
      in entero-colitis, 738
      in acute intestinal catarrh, 675
      in chronic intestinal catarrh, 702

Solvent treatment of biliary calculi, 1080

Sore throat, 390

Sour-smelling perspiration in acute rheumatism, 30, 31

Spasm, muscular, in muscular rheumatism, 75
    in acute variety of general rheumatoid arthritis, 80
  of rectum and anus, 909
  reflex muscular, in acute gout, 119
  seat of, in spasmodic stricture of oesophagus, 419, 420

Spasmodic stricture of oesophagus, 419

Spasms, tetanic, in dilatation of stomach, 595

Specific nature of dysentery, 792
  origin of purpura, 191
    of rheumatoid arthritis, 92

Sphincter ani, loss of power in, in ulceration of rectum and anus, 893
    paralysis of, in diseases of spinal cord, 907
    spasm, in fissure of anus, 888

Sphincterismus, treatment of, 916

Spinal applications, use of, in enteralgia, 664, 665
  cord, effects of abnormal condition of, on rectum and anus, 906
    and membranes, lesions of, in acute rheumatism, 40
  inflammation complicating acute rheumatism, 40
  irritation, influence of, on causation of pruritus ani, 909

Spirit-drinking, influence of, on causation of functional dyspepsia,
        446

Splashing sound on palpation in dilatation of stomach, 597

Spleen, amyloid degeneration in rachitis, 153
  lesions of, in acute intestinal catarrh, 677
    in chronic intestinal catarrh, 705
    in scurvy, 173
    in tabes mesenterica, 1188
    in acute yellow atrophy of liver, 1026
  enlargement of, in amyloid liver, 1044
    in cirrhosis of liver, 994
    in hydatids of liver, 1104
    in phosphorus-poisoning, 1031
    in thrombosis and embolism of portal vein, 1096
    in rachitis, 140
    in hereditary syphilis, 305

Spondylitis following gonorrhoeal rheumatism, 106

Spontaneous disintegration of biliary calculi, 1066
  origin of acute peritonitis, 1136, 1137

Sprays, medicated, use of, in acute pharyngitis, 398
      in chronic pharyngitis, 405, 406

Squamous-celled form of cancer of oesophagus, 426

Starchy food, influence on causation of intestinal indigestion, 625

Steam inhalations, use of, in acute pharyngitis, 397, 398

Stenosis, influence on causation of dilatation of stomach, 587
  of cardia as a cause of atrophy of stomach, 616
  of ductus communis choledochus, 1082
  of portal vein, 1095
  of oesophagus, as a cause of atrophy of stomach, 616
  of orifices of stomach in gastric cancer, 566
  of pylorus in carcinoma of stomach, treatment, 578
    in simple ulcer of stomach, 503
    hypertrophic, 615

Stercoraceous vomit, in acute internal strangulation of intestines,
        843
    in intussusception, 848, 849
  vomiting, in enteralgia, 662
    significance of, in intestinal obstruction, 862
      in stricture of bowel, 856

Stimulants, use of, in cancrum oris, 344
    in cholera morbus, 725
    in dysentery, 812
    in entero-colitis and cholera infantum, 761
    in acute gastritis, 469
    in chronic intestinal catarrh, 716
    in intestinal obstruction, 865
    in abscess of liver, 1021
    in aphthous stomatitis, 331
    in gangrenous stomatitis, 344

STOMACH, ATROPHY OF, 616
    Etiology, 616
      General inanition and marasmus, 616
      Result of stenosis of oesophagus or cardia, 616
      Anaemia, 616
      Secondary nature, 616
      Acute infectious diseases, 616
      Mineral poisoning, 616
      Chronic gastric disease, 616
    Morbid anatomy, 616
      Gastric tubules, degeneration of, 616
          atrophy of, 616
    Symptoms, 616
      Digestive disturbances, 616
      Anorexia, 616
      Vomiting, 616
      Anaemia, 616
  _Anomalies of Form and Position_, 617
    Hour-glass contraction, 617
    Diverticula, from ingestion of foreign substances, 617
    Loop-shaped form, 617
    In hernial sacs, 617
    In diaphragmatic hernias, 617
      umbilical hernias, 617
    Displacements, 617
      by tumors, 617
      by tight-lacing, 617
    Twisting of, 617

STOMACH, CANCER OF, 530
  Definition, 530
  Synonyms, 530
  History, 530
  Etiology, 531
    Frequency, 532
    Sex, 533
    Age, 534
    Geographical distribution, 535
    Race, 535
    Heredity, 535
    Simple ulcer of stomach, 536
    Chronic gastritis, 536
    Depressing emotions, 536
    Individual predisposition, 537
    Local predisposition, 537
  Symptoms, 537
    Course of typical cases, 538
    Loss of appetite, 538
    Pain, 539
      Seat, 539
      Effect of food on, 539
      Character of, 539
      Absence of, 539
    Functional disturbance of stomach, 540
    Eructations, 540
    Breath, fetid, 540
    Hiccough, 540
    Tongue, appearance, 540
    Vomiting, 541
      Character, 541
      Effect of situation of cancer on, 541
      Time of, 541
      In pyloric form, 541
        cardiac form, 541
      Frequency, 542
      Cause of, 542
    Vomit, characters of, 542
    Gastric fluids, detection of cancerous fragments in, 542
        absence of free hydrochloric acid in, 543
      tests for hydrochloric acid in, 543, 544
    Vomit, bloody, 545
      detection of blood in, 545
      coffee-grounds, 546
    Hemorrhages, frequency, 545
    Dysphagia, 546
    Tumor, presence of, 546
      frequency of, 546
      method of examining for, 546-549
      seat of, 548, 561
      size of, 548
      consistence of, 548
      inflation of stomach with carbonic acid gas in diagnosis of, 549
    Constipation, 550
    Diarrhoea, 550
    Black stools, 550
    Urine, state of, 550
    Albuminuria, 551
    Emaciation, 551
    Debility, 551
    Depression of spirits, 552, 554
    Anaemia, 552
    Cachexia, 552
    Physiognomy, 552
    Oedema, 553
    Ascites, 553
    Pulse, 553
    Epigastric pulsation, 553
    Haemic murmurs, 553
    Venous thrombosis, 553
    Temperature, 554
    Dyspnoea, 554
    Headache and vertigo, 554
    Intelligence, 554
    Coma, 554
      dyspnoeic, 555
      cause of, 555
    Secondary growths, 556
        of liver, 556
          diagnosis of, 556, 557
      growth of peritoneum, 557
    Enlargement of supra-clavicular glands, 557
    Perforation, 558
      frequency of, 558
      formation of fistulae, 558
      gastro-colic fistula, 558
    Fecal vomiting in gastro-colic fistulae, 558
    Death, cause of, 559
  Duration, 559
    In early life, 559
  Complications, 560
    Jaundice, 560
    Pylethrombosis, 560
    Peritonitis, 560
    Catarrhal enteritis, 560
    Chronic diffuse nephritis, 560
    Pleuritis, 560
    Pericarditis, 560
    Hydrothorax, 560
    Pyo-pneumothorax, 560
    Oedema of lung, 560
    Pneumonia, 560
    Embolism, 560
    Aphthae, 560
    Fatty degeneration of heart, 560
    Phlegmasia alba dolens, 560
    Insanity, 560
    Purpura haemorrhagica, 560
    Chronic catarrhal gastritis, 560
  Morbid anatomy, 560
    Varieties, 561
      relative frequency of, 561
    Method of growth, 562
    Of annular form, 562
    Of diffuse form, 562
    Relation to coats of stomach, 562
    Ulceration, 562
      causes of, 562
      cicatrization of, 563
    Suppuration, 563
    Medullary form, 563
        peculiarities of, 563
        histology of, 563
        tendency to metastasis, 563
        origin in gastric tubules, 563
    Cylindrical-celled epithelioma, 564
        histology of, 564
        origin from gastric tubules, 564
    Scirrhous form, 564
        histology of, 564
    Colloid form, 564
        histology of, 564
    Flat-celled epithelioma, 565
    Secondary form, 565
        peculiarities of, 565
        seat of, 565
    Changes, secondary, in stomach, 566
    Hypertrophy of gastric wall, 566
    Obstruction of orifices of stomach, 566
    Atrophy of stomach, 566
    Dilatation of stomach, 566
    Hour-glass contraction of stomach, 566
    Adhesions to adjacent organs, 566
    Metastasis, 567
      relative frequency of, 567
      causes of, 568
    Wasting of various organs, 568
  Pathenogenesis, 568
    Theories regarding origin, 569
  Diagnosis, 569
    Presence of a tumor, value in, 569
    Detection of fragments of cancer in vomit, 569
    Absence of free hydrochloric acid in gastric fluid, 569
    Value of coffee-ground vomit, 569
    From gastric ulcer, 569-571
      chronic gastric catarrh, 569-571
      gastralgia, 571
      nervous dyspepsia, 571
      fibroid induration of stomach, 571
      chronic interstitial gastritis, 571
      non-malignant stenosis, 571
      non-malignant tumors, 572
      tumors of adjacent organs, 572
        of liver, 572
      cancer of pancreas, 572
      tumors of omentum and intestines, 573
      aneurism of aorta, 573
      spasm of rectus muscle, 573
      pernicious anaemia, etc., 574
      cirrhosis of liver, 574
    of position of growth, 574
    of form of growth, 574
  Mortality, 574
  Prognosis, 575
  Treatment, 576
    Diet, 576
    Pain, 576
    Vomiting, 576
    Acid eructations and heartburn, 576
    Constipation, 577
    Diarrhoea, 577
    Haematemesis, 577
    Stenosis of pylorus, 578
    Use of condurango, 576
      of opium, 576
      of ice, 576
      of hydrocyanic acid, 576
      of bismuth, 576
      of oxalate of cerium, 576
      of rectal alimentation, 576
      of antacids, 576
      of charcoal, 576
      of washing out of stomach, 577
    Surgical measures, 577
    Resection, 577
    Gastrostomy for stenosis, 578
  _Non-cancerous Tumors of_, 578
    Polypi of, 578
    Adenomata, 578
    Myomata, 578
    Myosarcomata, 578
    Sarcoma, 578
    Miliary aneurisms, 579
    Cysts of mucous membrane, 579
    Fibromata and lipomata, 579

STOMACH, CIRRHOSIS OF, 611
  Definition, 611
  Synonyms, 611
  History, 611
  Etiology, 612
    Sex, influence on causation, 612
    Age, influence on causation, 612
    Alcohol, abuse of, 612
    Syphilis, 612
    Injury, 612
    Chronic catarrhal gastritis, 612
  Symptoms, 612
    Of chronic dyspepsia, 613
    Appetite, impaired, 613
    Gastralgia, 613
    Inability to ingest large quantities of food, 613
    Loss of flesh and strength, 613
    Vomiting, 613
    Vomit, characters of, 613
  Diagnosis, 613
    Significance of long duration of dyspepsia, 613
    Value of physical examination, 613
    Presence of a tumor, 613
    Stomach-tube, use of, 613
    From cancer, 613
  Morbid anatomy, 613
    Contraction of stomach, 613
    Cavity of stomach, size of, 613
    Thickening of gastric walls, 614
    Mucous membrane, lesions, 614
    Muscular coat, hypertrophy of, 614
    Fibrous tissue, increase of, 614
    Microscopical appearances of mucous membrane, 614
    Gastric tubules, atrophy of, 614
    Formation of adhesions, 614
    Peritoneum, lesions of, 614
  Prognosis, 614
    grave nature of, 614
  Treatment, 615

Stomach, condition of, in rachitis, 153

STOMACH, DILATATION OF, 586
  Definition, 586
  Synonyms, 586
  History, 586
  Etiology, 587
    Stenosis of pyloric orifice, 587
    Carcinoma, 587
    Cicatricial growths from simple ulcer, 587
      from corrosive poisons, 587
    Hypertrophy of pyloric orifice, 587
    Obstruction of pylorus by polypi, 587
    Narrowing of pylorus by tumors of adjacent organs, 587
    Congenital stenosis, 588
    Spasm of pylorus, 588
    Obstruction from distortion and displacement, 588
    Without obstruction (atonic form), 589
    Abnormal gastric contents, 589
    Excessive eating and drinking, 589
      use of beer, 589
    Abuse of condiments, 589
      of tobacco, 589
    Fermentation of contents of stomach, 589
    Impairment of gastric muscular force, 590
    Organic changes in muscular coat, 590
    Destruction by ulcers and cancers, 590
    Chronic catarrhal gastritis, 590
      peritonitis, 590
    Degenerations (fatty, colloid, and amyloid), 590
    Oedema of coats of stomach, 590
    Cirrhosis of stomach, 590
    Mechanical restraint of gastric movements, 590
    Adhesions, 590
    Weight of herniae, 590
    Impaired general nutrition, 590
    Paresis from neuropathic causes, 590
    Frequency of, in its causal relation, 592
    Age, 592
    Infrequency of atonic form among the poor, 592
    Sedentary life, 592
  Symptoms, 592
    Disturbance of gastric functions, 592
    Impaired appetite, 593
    Increased appetite (polyphagia), 593
    Thirst, 593
    Pain, 593
    Fulness and weight, 593
    Eructations and heartburn, 593
    Gases, nature of, 593
      inflammability of, 593
    Vomiting, 593
      time of, 593
    Vomited matters, abundance of, 593
        amount of, 593
        fermentation of, 594
        odor of, 594
        presence of micro-organisms in, 594
        sarcinae, bacteria, etc. in, 594
        absence of free hydrochloric acid in, 594
        presence of blood in, 594
    Constipation, 594
    Diarrhoea, 594
    Urine, state of, 594
    Dyspnoea and cardiac palpitation, 595
    General condition, 595
    Tetanic spasms, 595
        seat of, 595
        muscles of calves and abdomen, 595
        of flexors of hand and forearm, 595
    Coma, 596
    Temperature, 596
    Physical signs, 596
    Prominence of epigastric region, 596
    Peristaltic movements, 596
    Splashing sound on palpation, 597
      method of producing, 597
    Percussion, 598
    Auscultation, 598
    Displacement of adjacent organs, 599
  Morbid anatomy, 599
    Degrees of, 599
    Capacity, 599
    Fundus, size of, 599
    Oesophagus, dilatation of, 599
    Hypertrophy of gastric walls, 599
    Atrophy of gastric walls, 599
    Fatty and colloid degeneration of muscular coats, 600
    Mucous membrane, state of, 600
    Atrophy of abdominal viscera, 600
  Diagnosis, 600
    Distension of stomach with carbonic acid gas in, 596, 601
    Ingestion of water to aid, 598, 602
    Stomach-tube, use of, 597, 602
    Determination of lower gastric border, 598, 602
    From chronic catarrhal gastritis, 603
      atonic dyspepsia, 603
  Prognosis and course, 603
    Death, mode of, 603
  Treatment, 603
    Prophylactic, 603
    Diet, 603, 608
    Washing of stomach, 603
        object of, 604
        modes of, 604
        apparatus used in, 604-607
        siphon process, 604-606
        stomach-pump, 604
        frequency of, 607
        objections to, 607
      contraindications, 608
    Of heartburn, 609
    Of anaemia, 609
    Of constipation, 609
    Use of electricity, 608
      of nux vomica, 609
      of strychnia, 609
      of abdominal bandage, 609
      of hydrochloric acid, 609
      of pepsin, 609
      of sodium bicarbonate, 609
      of Carlsbad water, 609
      of iron and arsenic, 609
      of resection of pylorus, 609
      of gastrotomy, 609
  _Acute Dilatation of_, 610
    Definition, 610
    Etiology, 610
    Symptoms, 610
      Pain, 610
      Tympanites, 610
      Vomiting, cessation of, 610
    Prognosis, 610
    Treatment, 610
      Use of stomach-tube, 610

Stomach, functional and inflammatory diseases of, 436

STOMACH, HEMORRHAGE FROM, 580
  Definition, 580
  Synonyms, 580
  Etiology, 580
    Ulcer of stomach, 580
    Cancer, 580
    Traumatism, 580
    Corrosive poisons, 580
    Diseases of gastric vessels, 580
    Aneurism of gastric arteries, 580
    Varices of veins, 580
    Degenerations of vessels, 581
    Congestion, active, 581
      passive, 581
    Portal vein, 581
    Pulmonary blood-vessels, 581
    Heart disease, 581
    Violent vomiting, 581
    Acute infectious diseases, 581
    Hemorrhagic diathesis, 582
    Malaria, 582
    Anaemia, 582
    Cholaemia, 582
    Bright's disease, 582
    Neuropathic conditions, 582
    Melaena neonatorum, 582
    Bursting aneurisms, 582
    Idiopathic causes, 582
    Hemorrhage from nose, mouth, lungs, etc., 583
  Symptoms. See _Gastric Ulcer_.
  Morbid anatomy, 583
    Source of, 583
    From diapedesis, 583
    From rupture of blood-vessels (rhexis), 583
  Diagnosis, 584
    Significance of black stools, 584
    Examination of vomit, 584
    From hysterical vomiting, 584
    Examination of nose and throat, 584
    From oesophageal hemorrhage, 584
    Use of oesophagoscope in, 584
    From haemoptysis, 584, 585
    Of causes, 585
  Prognosis, 585
  Treatment. See _Gastric Ulcer_.

Stomach, lesions of, in cholera infantum, 743, 744
    in entero-colitis, 739
  minor organic changes in, 611
  organic diseases of, 480

STOMACH, RUPTURE OF, 618
  Etiology, 618
    Injury, 618
    From over-distension by solids or gas, 618
  Symptoms, 618
  Prognosis, 618
  Treatment, 618

STOMACH, SIMPLE ULCER OF, 480
  Definition, 480
  Synonyms, 480
  History, 480
  Etiology, 481
    Frequency, 481, 482
    Sex, influence on causation, 483
    Age, influence on causation, 483
      when most frequent, 484, 485
    Climate, influence on causation, 485
    Geographical distribution, 485
    Poverty, 486
    Occupation, 486
    Needle-women, cooks, and maid-servants, 486
    Shoemakers and tailors, 486
    Injury, 486
    Corrosive poisons, 486
    Pulmonary phthisis, influence of, on causation, 487
    Menstrual disorders, 487
    Chlorosis and anaemia, 487
    Diseases of heart and blood-vessels, 487
      of kidneys, 487
      of stomach, 488
    Diabetes mellitus, 488
    Intermittent fever, 488
    Abuse of alcohol, 488
    Burns of skin, 488
  Symptoms, 488
    Pain, 488
      Character, 489
      Localized nature of, 489
      Seat, 489
      Effect of food upon, 489
        pressure, 490
        rest, 490
        mental emotion, 490
      Distribution of, 490
      Intermittence of, 491
      Causes of, 491
    Vomiting, 491
      Time of, 491
      Character of, 491, 492
      Causes of, 492
    Hemorrhage, 492
      Quantity, 492
      Voided by bowels, 492
        appearance of stools in, 493
    Haematemesis, 493
      Appearance of blood in, 493
      Causes, 493
    Hemorrhage, effect upon other symptoms, 494
      Relief of pain after, 494
      Sources of, 494
    Of indigestion, 494
    Appetite, loss of, 494
    Thirst, 494
    Constipation, 494, 495
    Flatulence, 494
    Nausea and vomiting, 494
    Headache, dizziness, etc., 494
    Tongue, condition, 495
    Amenorrhoea, 495
    Temperature, 495
    General health, 496
    Physiognomy, 496
    Cachectic dropsy, 496
    Physical signs, 496
    Perforation, 496
      Frequency, 497
        in sexes, 497
      May occur without symptoms, 497
      Cause, 498
      Pain in, 498
      Collapse in, 498
      Physiognomy in, 498
      Temperature, 498
      Pulse, 498
      Vomiting, 498
      Constipation, 498
      Thirst, 498
      Respiration, 498
      Suppression of urine, 498
      Abdomen, state of, 498
      Tympanites, 498
      Retraction of testicle, 498
      Position of patient, 498
      Death in, cause of, 499
      Peritonitis in, 499
      Peritoneal abscesses, 499
      Pyo-pneumothorax subphrenicus of Barlow and Wilks, 499
      Into pleural cavities, 500
        transverse colon, 500
        pericardium, 500
  Sequelae, 500, 503
    Gastro-cutaneous fistulae, 500
    Stenosis of pylorus, and dilatation, 503
  Complications, 502
    Pylephlebitis, 502
    Chronic peritonitis, 502
    Catarrhal gastritis, 502
    Interstitial gastritis, 502
    Extension to pleura, 503
    Fatty degeneration of heart, 503
    Embolic pneumonia, 503
    Pulmonary tuberculosis, 503
    Bright's disease, 503
    Heart disease, 503
    Hepatic degenerations, 503
  Course, 500
    Forms of, 501
      Latent, 501
      Acute perforating, 501
      Hemorrhagic, 501
      Gastralgic-dyspeptic, 501
      Chronic hemorrhagic, 501
      Cachectic, 501
      Recurrent, 501
      Stenotic, 501
  Duration, 501
  Terminations, 501
    Tendency to recovery, 501
    Causes of death, 502
  Mortality, 502
  Morbid anatomy, 503
    Ulcers, number, 503
      Position, 503
      Size, 504
      Shape, 504
        tendency to become conical, 504
      Tendency to transverse extension, 504
      Appearance of edges, 505
        floor, 505
      Microscopic appearance of surrounding tissue, 505
      Cicatrization, 506
        method, 506
        deformities of stomach from, 506
    Peritoneum, lesions of, 506
    Perforations, seat, 509
      Lesions resulting from, 507
        Ulcerations of surrounding viscera, 507
        Circumscribed peritoneal abscess, 507
        Gastro-cutaneous fistulae, 508
          -colic fistulae, 508
          -duodenal fistulae, 508
        Pneumo-pericardium, 508
        Gastro-pleural fistulae, 508
        Emphysema of areolar tissue, 509
          time of appearance, 509
          nature of the gas, 509
        Gas in arteries, 510
        Hemorrhage, source of, 510
    Changes in blood-vessels, 510
    Embolism, 510
    Thrombosis of vessels about ulcer, 510
    Fatty and waxy degeneration and calcification of gastric
        vessels, 511
    Varicosities of veins, 511
    Aneurism of vessels about ulcer, 511
  Pathenogenesis, 512
    Theories regarding development, 512
    Digestive action of gastric juice on development, 512
    Inflammatory theory of origin, 512
    Neurotic theory of origin, 512
    Theory, circumscribed hemorrhagic infiltration, 512
    Disease of gastric blood-vessels, 513
    Bottcher's view of mycotic origin, 513
    Artificial production of, 514
        Daettwyler and Cohnheim's experiments, 514
  Diagnosis, 514
    From nervous gastric disorders, 515
      nervous vomiting, 516
        gastralgia, 516
      gastric crises, 517
        cancer. See _Stomach, Cancer of_.
      chronic catarrhal gastritis, 517
      hepatic colic, 517
  Prognosis, 518
  Treatment, 519
    Removal of sources of irritation, 519
    Importance of rest, 519
    Diet, 519-522
    Use of nutrient enemata, 519
    Milk, 519
      peptonized, 520
    Leube's beef, solution of, 520
    Beef-juice, freshly-expressed, 521
    Avoidance of coarse food and fruits, 521
    Of pain, 524
    Of vomiting, 524
    Of hemorrhage, 525
    Of dyspepsia, 527
    Of perforation, 527
    Importance of maintaining nutrition, 527
    Of anaemia, 528
    Of sequelae, 528
    Of convalescence, 529
    Carlsbad waters, use of, 522
        method of preparing, 522
    Use of stomach-tube, 523, 525
          method of, 523
      of bismuth, 523, 524
      of argentum nitratis, 523, 524
      of opium, 524
      of codeia, 524
      of astringents to relieve pain, 524
      of tr. ferri-chlor. to relieve pain, 524
      of counter-irritation, 524
      of subcutaneous injection of milk, oil, and beef-tea, 525
      of ice, 525
      of antiemetics, 525
      of ingluvin, 525
      of ergotin in hemorrhage, 525
      of dil. sulphuric acid in hemorrhage, 526
      of acetate of lead in hemorrhage, 526
      of ligature of upper extremities in hemorrhage, 526
      of rubber balloon tampon in hemorrhage, 526
      of alkalies in dyspepsia, 527
      of poultices in perforation, 527
      of laparotomy in perforation, 527
      of inunctions of oil, 527
      of iron in anaemia, 528
        hypodermic, 528

Stomach, tubercular ulcers of, 529
  typhoid ulcers of, 529
  syphilitic ulcers of, 529
  necrotic ulcers of, 529
  catarrhal ulcers of, 529
  follicular ulcers of, 529

Stomach and intestines, lesions of, in acute yellow atrophy of liver,
        1026
    perforation of, by gall-stones, 1068, 1074

Stomach-pump, use of, in chronic gastritis, 478

Stomach-tube, use of, in cancer of oesophagus, 428
    in dilatation of oesophagus, 434
    in organic stricture of oesophagus, 426
    in paralysis of oesophagus, 430
    in simple ulcer of stomach, 523, 525
    in washing of stomach in gastric dilatation, 604
  value of, in diagnosis of organic stricture of oesophagus, 424
    in diagnosis of cirrhosis of stomach, 613
    in diagnosis of dilatation of stomach, 597, 602

STOMATITIS, 321
    Definition, 321
    Varieties, 321
  _Stomatitis Catarrhalis_, 321
    Synonyms, 321
    Definition, 321
    Etiology, 321
      Irritation of alimentary canal, 321
      Local causes, 321
      Foreign substances, 321, 322
      Medicines, certain, 322
      Morbid dentition, 322
      Protracted crying, 322
      Distant causes, 322
      Intestinal derangements, 322
      Improper food, 322
      Cold, 322
      Acute exanthemata, 322
      Age, 322
    Symptoms, 322
      Initial, 322
      Heat of mouth, 322
      Unwillingness to nurse, 322
      Painful deglutition, 323
      Increased secretion, 323
      Impaired taste, 323
      Fetor of breath, 323
      Loss of appetite, 323
      Diarrhoea, 323
      Swelling of lymphatic glands, 323
      Pyrexia, 323
      Chronic form, 323
      Vomiting, 323
      Duration, 323
    Pathology and morbid anatomy, 323
      Hyperaemia of tissues, 324
      Mucous membrane, state of, 324
      Tongue, engorgement of, 324
      Ulcerations, 324
      Congestion of palate, 324
      Lips, state of, 324
    Diagnosis, 325
      From gastric catarrh, 325
    Prognosis, 325
    Treatment, 325
      Correction of intestinal disturbances, 325
      Local, 325
      Ice, use of, 325
      Salicylic acid, 325
  _Aphthous Stomatitis_, 325
    Definition, 325
    Synonyms, 326
    Etiology, 326
      Age, 326
      Scrofula, influence on causation, 326
      Heredity, influence on causation, 326
      Improper food, influence on causation, 326
      Excessive heat, influence on causation, 326
      Overwork, influence on causation, 326
      Excessive menstruation, influence on causation, 326
      Pregnancy, influence on causation, 326
      Debility, influence on causation, 326
      Chronic diseases, influence on causation, 326
      Acute exanthemata, influence on causation, 326
      Exciting causes, 326
      Morbid dentition, 326
      Dampness of atmosphere, 326
      Personal habits, 326
      Drugs, 326
    Pathology and morbid anatomy, 326
      Vesicles, nature of, 327
        rarity of their detection, 327
      Lesions, characteristics of, 327
      Ulceration, anatomy of, 328
        cause, 328
        method of repair, 328
      Lesions, seat of, 328
        in confluent, 328
        in discrete, 328
    Symptoms and course, 328
      Discrete form, 328
      Confluent form, 328, 329
      Constitutional, 329
      Diarrhoea, 329
      Vomiting, 329
      In parturient women, 329
      Local, 329
      Heat of mouth, 329
      Increased secretion, 329
      Difficult mastication, 329
    Duration, 329
      Discrete form, 329
      Confluent form, 329
    Complications and sequelae, 329
    Diagnosis, 329
      Of confluent form from ulcerative stomatitis, 330
      Of confluent form from thrush, 330
    Prognosis, 330
      Of confluent form, 330
      In parturient women, 330
    Treatment, 330
      Diet, 330
      Local, 330
      Use of sodium hyposulphite, 330
        of ice, 330
        of astringents, 330
        of iodoform, 330
      Of confluent form, 331
      Necessity of constitutional, 331
      Use of iron and quinia, 331
        of stimulants, 331
        of chlorate of potassium, 331
  _Stomatitis Parasitica_ (_Thrush_), 331
    Definition, 331
    Synonyms, 331
    History, 331
    Etiology, 331
      Innutrition, influence on causation, 332
      Want of cleanliness, influence on causation, 332
      Age, influence on causation, 332
      Season, influence on causation, 332
      Exhausting diseases, influence on causation, 332
      Intestinal disorders, influence on causation, 332
      Contagiousness, 332
    Pathology and morbid anatomy, 332
      Deposit, description of, 332
        microscopic appearance, 333
        seat of, 333
      Parasite of, 333
      Oidium albicans, nature, 333
      Mucous membrane, condition, 333
      Deposit in oesophagus and larynx, 334
        in intestinal canal, 334
    Symptoms, 334
      Initial, 334
      Cry in, 334
      Growth, seat of, 334
      Constitutional, 334
    Duration, 334
    Cause of death, 334
    Diagnosis, 334
      Value of microscopic examination, 335
    Treatment, 335
      Preventive, 335
      Diet, 335
      Local, 335
      Constitutional, 335
      Use of astringents, 335
        of sodium bicarbonate, 335
        of sodium salicylate, 335
  _Stomatitis Ulcerosa_, 336
    Synonyms, 336
    Definition, 336
    Etiology, 336
      Atmosphere, impure, 336
      Uncleanliness, 336
      Food, improper, 336
      Measles, influence on causation, 336
      Age, influence, on causation, 336
      Season, influence on causation, 336
      Sex, influence on causation, 336
      Contagiousness, 336
    Pathology, 336
      Fibro-purulent infiltration of lymph-spaces, 336
      Ulcers, description of, 336, 337
        seat of, 336
        course of, 337
    Symptoms, 337
      Initial, 337
      Mouth, heat of, 337
      Appetite, loss of, 337
      Difficult deglutition, 337
      Lymphatic gland, swelling, 337
      Salivation, excessive, 337
    Duration, 337
    Diagnosis, 337
      From mercurial stomatitis, 338
        cancrum oris, 338
    Prognosis, 338
    Treatment, 338
      Preventive, 338
      Hygienic, 338
      Air, fresh, necessity of, 338
      Constitutional, 338
      Local, 338
      Use of antiseptics, 338
        of astringents, 338
        of potassium chlorate, 338
      Extraction of carious teeth, 338
  _Stomatitis Gangrenosa_ (_Cancrum Oris_), 338
    Definition, 338
    Synonyms, 338
    History, 338, 339
    Etiology, 339
      Hygiene, improper, 339
      Endemic character, 339
      Age, 339
      Sex, 340
      Acute exanthemata, 340
    Symptoms, 340
      Initial, 340
      Tumefaction of cheek, 340
      Ulceration of cheek, 340
      Odor of breath, 340
      State of gums, 340
      Difficult deglutition, 340
      Eschar, characters of, 340
      Constitutional, 341
      Intelligence, 341
      Pulse, 341
      Appetite, 341
      Gastro-intestinal canal, 341
    Death, cause of, 341
    Complications and sequelae, 341
      Pneumonia, 341
      Lungs, gangrene, 341
      Vulva, gangrene, 341
      Larynx and pharynx, gangrene, 341
      Hemorrhage, 341
    Pathology and morbid anatomy, 341
      Nature, 341
      Character and seat of ulceration, 341
      Ulceration, color, 342
        rapidity, 341
        of gums, 342
      Gangrene, date of appearance, 342
      Skin, appearance of, 342
      Perforation of cheek, 341, 342
      Glands, swelling of, 342
    Diagnosis, 342
      From malignant pustule, 342
    Prognosis, 342
    Treatment, 343
      Local, 343
      Cauterization, 343
        by nitric acid, 343
        by muriatic acid, 343
        by acid nitrate of mercury, 343
        by actual cautery, 343
      Use of disinfectants, 343
      Constitutional, 343
      Use of stimulants, 344
  _Stomatitis, Toxic_, 344
    Definition, 344
  _Stomatitis Mercurialis_, 344
    Definition, 344
    Synonyms, 344
    Etiology, 344
      Special vulnerability to toxic influence of mercury, 344
      Difference in susceptibility, 344
      Depraved constitution, 344
      Idiosyncrasy, 344
      Occupation, 344
    Symptoms, 345
      Subjective, 345
      Gums, state of, 345
      Mouth, tenderness of, 345
      Teeth, state of, 345
      Difficult deglutition, 345
      Saliva, increase of, 345
        amount secreted, 345
      Lymphatic glands, enlargement, 346
      Tongue, inflammation of, 346
      Larynx, oedema of, 346
      Gangrene of mucous membranes, 346
      Necrosis of inferior maxilla, 346
      Constitutional, 345, 346
      Fever, 346
      Cachexia, 346
    Duration, 346
    Complications, 346
      Erysipelas, 346
      Pyaemia, 346
      Metastatic abscesses, 346
    Pathology and morbid anatomy, 346
      Nature of, 346
      Microscopic appearance of detritus, 346
      Ulceration of gums, 347
      Characters of ulcers, 347
      Mucous membrane, lesions of, 347
      Tongue, inflammation of, 347
      Tongue and mucous membrane, ulcers of, 347
      Teeth, loosening of, 347
      Larynx and pharynx, lesions of, 347
    Diagnosis, 347
    Prognosis, 347
    Death, cause of, 347
    Treatment, 347
      Preventive, 347
      Use of potassium chlorate, 348
        of opium, 348
        of astringents, 348
        of detergents, 348
        of enemata, nourishing, 348
        of tonics, 348
      Local, 348
      Constitutional, 348
      Of glossitis, 348
      Of oedema of larynx, 348

Stomatitis, catarrhal, in morbid dentition, 373

Stomatorrhagia, 370
  Definition, 370
  Synonym, 370
  Etiology, 370
    Disease or injury, 370
    Haemophilia, 370
    Vicarious of menstruation, 370
  Symptoms, 371
    Gums most frequent source, 371
  Results, 371
  Diagnosis, 371
  Prognosis, 371
  Treatment, 371
    Use of ergot, 371
      of turpentine, 371
      of astringent washes, 371

Stony concretions as a cause of intestinal obstruction, 838

Stools, appearance in hemorrhage from bowels, 833
    and characters of, in chronic intestinal catarrh, 707
  black, in hemorrhage from bowels, 833
    in intestinal ulcer, 827
    in cancer of stomach, 545
    in simple ulcer of stomach, 492, 493
  bloody, in carcinoma of pancreas, 1126
    in intestinal ulcer, 827
    and mucous, in intestinal cancer, 871
  characters of, in catarrh of bile-ducts, 1054, 1055
    in cholera morbus, 722
    in acute colitis, 684
    in constipation, 646
    in dysentery, 796, 803
    in pseudo-membranous enteritis, 766
    in acute intestinal catarrh, 678, 680-682
    in chronic intestinal catarrh, 706-708
    in intestinal indigestion, 627
    in intussusception, 848
    in intestinal ulcer, 827
    in cirrhosis of liver, 994
    in fatty liver, 1048
    in proctitis, 887
    in ulceration of rectum and anus, 893
    in tabes mesenterica, 1190
  condition of, in hyperaemia of liver, 986, 987
  fatty, in diseases of pancreas, 1115, 1122, 1125, 1131
  frequency and characters, in cholera infantum, 741
      in entero-colitis, 733, 734, 736
  in non-malignant rectal stricture, 886
  mucous, in proctitis, 684
  number of, in acute intestinal catarrh, 679
  of hepatic colic, 1073
      mode of searching for calculi in, 1073
  phosphorescent, in phosphorus-poisoning, 1031
  significance of cancerous fragments in, in malignant diseases of
        intestine, 873
  undigested striped muscular fibres in, in pancreatic diseases, 1116

Stramonium ointment, use of, in hemorrhoids, 923
      in acute oesophagitis, 418

Strangulation, acute internal, as a cause of intestinal obstruction,
        840
  of bowels, acute internal, 840
  removal of hemorrhoids by, 924

Strangury in dysentery, 803

Stricture, cicatricial, in syphilitic pharyngitis, 407
  congenital, a cause of intestinal obstruction, 835
  following chronic oesophagitis, 417
  of bowel, 854
    following chronic intestinal catarrh, 710
  of oesophagus, 419
    spasmodic, 419
  seat of, in organic stricture of oesophagus, 424
  of rectum, symptoms, 856
  malignant, of rectum and anus, 902
  non-malignant, of rectum, 885
      treatment, 917

Strongylus longevaginatus, 956

Structural diseases of liver, 983

Struma, See _Scrofula_.
  as a cause of ulceration of rectum and anus, 894

Strumous articular disease, as a sequel of gonorrhoeal rheumatism, 106
  diathesis, influence on causation of intestinal indigestion, 624
  form of intestinal indigestion, treatment, 636

Strychnia, effect on rectum, 911
  use of, in constipation, 654-657
    in diabetes mellitus, 227
    in functional dyspepsia, 455
    in gastralgia, 463
    in chronic intestinal catarrh, 714, 715
    in intestinal indigestion, 636
    in dilatation of oesophagus, 435
    in oesophageal paralysis, 430
    in prolapsus ani, 921
    in rachitis, 164
    in dilatation of stomach, 609

Stupes, digitalis, use of, in cirrhosis of liver, 1001
  turpentine, use of, in perihepatitis, 990

Stupor in abscess of liver, 1010
  in cholera infantum, 742

Subacute articular rheumatism, 46
      symptoms, 46

Substernal pain in acute oesophagitis, 413

Sucking, influence on causation of macroglossia, 350

Suffocation, from hypertrophy of tongue, 350
  sensation of, in organic stricture of oesophagus, 423

Sugar, absorption of, in digestion, 623
  in urine of diabetes mellitus, amount of, 207
  substitutes for, in food of diabetics, 224
  tests for, in diabetic urine, 211-217

Suicide, relation of displacements of colon to, 647

Sulphate of copper, use of, in acute and chronic intestinal catarrh,
          696, 717
      in superficial glossitis, 357
      in syphilitic pharyngitis, 408
  of manganese, use of, in fatty liver, 1050
  of sodium, use of, in biliary concretions, 1079
      in intestinal indigestion, 636
  of zinc, enemata of, in chronic intestinal catarrh, 714, 717
    and alum, use of, in pruritus ani, 917

Sulpho-carbolate of calcium, use of, in acute intestinal catarrh, 696

Sulphur, use of, in constipation, 656
    in pseudo-membranous enteritis, 775

Sulphuric acid, use of, in purpura, 193
      in simple ulcer of stomach, 526

Summer heats, influence on causation of cholera infantum, 727
        of entero-colitis, 727
        of acute intestinal catarrh, 669

Superficial glossitis, 355

Supporting treatment in hereditary syphilis, necessity of, 315

Suppositories, iodoform, use of, in fissure of anus, 912
  medicated, use of, in seat-worms, 951
  nutrient, 929

Suppuration, duodenal, in chronic intestinal catarrh, 703
  of bone, influence on causation of amyloid liver, 1041
  seat of, in parenchymatous glossitis, 363
  symptoms of, in tonsillitis, 383

Suppurative hepatitis, 1002
  pylephlebitis, 1097

Supra-clavicular glands, enlargement, in gastric cancer, 557

Surgical measures in gastric cancer, 577
  treatment of intestinal obstruction, 865

Sutures of head, condition of, in rachitis, 147

Sweating, in acute rheumatism, 30, 31
  in hepatic abscess, 1009, 1010
  in trichinosis, 960
  of head, in rachitis, 146

Swedish movements, value, in intestinal indigestion, 632

Sympathetic nerve, to production of glycosuria, 196
  nervous symptoms, in chronic gastritis, 474

Symptomatology, general, of pancreatic disease, 1114

Symptoms due to migration of gall-stones, 1070
    to presence of gall-stones of original site, 1069
  of Anchylostomum duodenale, 955
  of Ascaris lumbricoides, 953
  of ascites, 1175
  of catarrh of bile-ducts, 1053
  of occlusion of biliary passages, 1086
  of biliousness, 966
  of compression and contraction of bowel, 857
  of hemorrhage from bowels, 830
  of stricture of bowel, 856
  of cancrum oris, 340
  of cholera infantum, 741
  of cholera morbus, 722
  of acute colitis, 684
  of constipation, 645, 853
  of diabetes mellitus, 204
  of acute duodenitis, 682
  of dysentery, 802
  of functional dyspepsia, 448
  of enteralgia, 660
  of entero-colitis, 733
  of pseudo-membranous enteritis, 765
  of Filaria medinensis, 963
    sanguinis, 963
  of fistula in ano, 898
  of fluke-worms, 947
  of gastralgia, 460
  of acute gastritis, 467
  of chronic gastritis, 472
  of superficial glossitis, 357
  of chronic superficial glossitis, 357
  of parenchymatous glossitis, 360
  of chronic parenchymatous glossitis, 368
  of glossitis parasitica, 359
  of glossanthrax, 368
  of gout, 118, 120
  of hemorrhoids, 883
    internal, 884
  of hepatic colic, 1070
  of hepatic glycosuria, 973
  of acute ileitis and jejunitis, 683
  of acute intestinal catarrh, 677
  of chronic intestinal catarrh, 706
  of intestinal indigestion, 626
      time of appearance after eating, 629
    obstruction from foreign bodies, 839
  of acute internal strangulation of intestines, 840
  of intestinal ulcer, 825
  of cancer of intestines, 869
  of lardaceous degeneration of intestine, 874
  of intussusception, 848
  of jaundice, 977
  of lithaemia, 969
  of abscess of liver, 1008
  of acute yellow atrophy of liver, 1026
  of amyloid liver, 1043
  of carcinoma of liver, 1036
  of cirrhosis of liver, 993
  of fatty liver, 1048
  of hydatids of liver, 1102
  of hyperaemia of liver, 986
  of liver-flukes, 1110
  of liver in phosphorus-poisoning, 1031
  of morbid dentition, 371
  of cancer of oesophagus, 427
  of dilatation of oesophagus, 431
  of paralysis of oesophagus, 429
  of organic stricture of oesophagus, 423
  of spasmodic stricture of oesophagus, 419
  of ulceration of oesophagus, 418
  of acute oesophagitis, 413
  of chronic oesophagitis, 417
  of carcinoma of pancreas, 1124
  of hemorrhage into pancreas, 1129
  of acute pancreatitis, 1118
  of acute secondary pancreatitis, 1120
  of chronic interstitial pancreatitis, 1122
  of obstruction of pancreatic ducts, 1131
  of paratyphlitis, 819
  of perihepatitis, 989
  of hemorrhagic effusion of peritoneum, 1181
  of acute diffuse peritonitis, 1141
  of chronic peritonitis, 1162
  of infantile peritonitis, 1173
  of perforative form of peritonitis, 1155, 1156
  of tubercular peritonitis, 1165
  of peri-rectal and anal abscesses, 896
  of acute pharyngitis, 394-396
  of chronic pharyngitis, 404
  of syphilitic pharyngitis, 407
  of tuberculous pharyngitis, 401
  of proctitis, 684, 887
  of thrombosis and embolism of portal vein, 1096
  of purpura, 187
  of purpura haemorrhagica, 188
  of purpura rheumatica, 189
  of purpura simplex, 187
  of suppurative pylephlebitis, 1099
  of hypertrophic stenosis of pylorus, 615
  of rachitis, 146
  of dilatation of rectal pouches, 885
  of neuralgia of rectum, 910
  of non-malignant stricture of rectum, 886
  of obstruction of rectum, 891
  of polypi of rectum, 882
  of prolapse of rectum, 881
  of rodent ulcer of rectum, 889
  of follicular ulceration of rectum and anus, 895
  of ulceration of rectum and anus, 893
  of fissure of rectum and anus, 888
  of acute rheumatism, 26
  of chronic articular rheumatism, 71
  of gonorrhoeal rheumatism, 104
  of muscular rheumatism, 75
  of rheumatoid arthritis, 80
  of general progressive form of rheumatoid arthritis, 80
  of partial form of rheumatoid arthritis, 84
  of seat-worms, 951
  of scrofula, 243
  of scurvy, 176
  of atrophy of stomach, 616
  of cancer of stomach, 530
  of cirrhosis of stomach, 612
  of dilatation of stomach, 592
  of acute dilatation of stomach, 610
  of hemorrhage from stomach, 493
  of simple ulcer of stomach, 488
  of perforation in simple ulcer of stomach, 496
  of rupture of stomach, 618
  of aphthous stomatitis, 328
  of catarrhal stomatitis, 322
  of mercurial stomatitis, 345
  of stomatitis ulcerosa, 337
  of stomatorrhagia, 371
  of hereditary syphilis, 273
  of tabes mesenterica, 1189
  of tape-worm, 939
  of thrush, 334
  of hypertrophy of tongue, 350
  of syphilitic ulceration of tongue, 370
  of tubercular ulceration of tongue, 369
  of tonsillitis, 381
  of trichinosis, 959
  of Triocephalus dispar, 954
  of typhlitis and perityphlitis, 818

Syncope in hemorrhage from bowels, 833

Synonyms of Anchylostomum duodenale, 955
  of Ascaris lumbricoides, 952
  of Bothriocephalus latus, 938
  of cancrum oris, 338
  of cholera morbus, 719
  of constipation, 638
  of Distomum hepaticum, 946
  of functional dyspepsia, 436
  of enteralgia, 658
  of pseudo-membranous enteritis, 763
  of Filaria sanguinis, 963
  of gout, 108
  of superficial glossitis, 355
  of parenchymatous glossitis, 359
  of glossitis parasitica, 357
  of acute intestinal catarrh, 667
  of lardaceous degeneration of intestine 874
  of intestinal ulcers, 823
  of macroglossia, 349
  of morbid dentition, 371
  of cancer of oesophagus, 426
  of dilatation of oesophagus, 430
  of organic stricture of oesophagus, 422
  of spasmodic stricture of oesophagus, 419
  of oesophagitis, 409
  of acute oesophagitis, 409
  of chronic oesophagitis, 416
  of Oxyuris vermicularis, 950
  of acute pharyngitis, 390
  of chronic pharyngitis, 402
  of syphilitic pharyngitis, 406
  of tuberculous pharyngitis, 400
  of hypertrophic stenosis of pylorus, 615
  of rheumatism, acute, 19
  of chronic articular rheumatism, 69
  of gonorrhoeal rheumatism, 102
  of muscular rheumatism, 74
  of rheumatoid arthritis, 78
  of scrofula, 231
  of scurvy, 167
  of cancer of stomach, 530
  of cirrhosis of stomach, 611
  of dilatation of stomach, 586
  of hemorrhage from stomach, 580
  of simple ulcer of stomach, 480
  of aphthous stomatitis, 326
  of catarrhal stomatitis, 321
  of mercurial stomatitis, 344
  of stomatitis ulcerosa, 336
  of stomatorrhagia, 370
  of Taenia echinococcus, 943
  of Taenia saginata, 933
  of Taenia solium, 935
  of tabes mesenterica, 1182
  of thrush, 331
  of tongue-tie, 349
  of tonsillitis, 379

Synovial membranes, lesions of, in gout, 115
      in acute rheumatism, 46
      in chronic articular rheumatism, 70
      in gonorrhoeal rheumatism, 103
      in rheumatoid arthritis, 86

Syphilides, pustular, in hereditary syphilis, 279

Syphilis, distinguished from carcinoma of liver, 1040

SYPHILIS, HEREDITARY, 254
  Marriage of syphilitics, 255-265
    Essential nature of syphilis, 256
        of tertiary syphilis, 257
    Duration of transmissive power, 257-260
    Period when marriage is admissible, 260, 261
    Treatment of married syphilitics, 260, 261, 269
    Methods of infection between parents, 262, 264
    Infection of mother by foetus in utero, 262
          by conception, 264
    Colles' law of infection of mothers of syphilitic children, 263
  Modes of infection of the child, 265
    From the father, 265
    From the mother, 266
      By infection previous to conception, 266
          at moment of conception, 262, 267
          during utero-gestation, 267
          during birth, 269
  Summary of facts in regard to transmission, 269, 270
  Placental, pathology of, 271, 272
  Modes of manifestation, in offspring of syphilitics, 272
    Danger to offspring in untreated syphilitics, 272
    Influence of interval between infection and conception on
        development of, 272
    Mortality of syphilitic children, 272, 273
  Symptoms and course, 273
    Average time of appearance, 273, 274
    Symptoms of secondary period, 274
      Pemphigus, 274
        Objections to specific origin of, 274
        Arguments favoring specific origin of, 275
        Description of eruption, 276
        Diagnosis, 276
      Coryza, 277
        Symptoms of, 277
        Difficulty in suckling from, 277
        Flattening of nose, 277
      Erythema, or Roseola, 277
        Seat and character of, 277, 278
        Diagnosis, 278
      Papules, 278
        Seat and character, 278
      Mucous patches, 278
        Seat and character, 278
        Diagnosis, 278, 279
        Danger of transmission from, 279
          by nursing-bottles, etc., 279
          by caresses and kisses, 279
      Condylomata, 279
        Seat and character, 279
      Pustular syphilides, 279
        Date of appearance, 279
        Seat and character, 279
        Diagnosis, 279, 280
      Furuncular eruption, 280
      Iritis, 280
        Specific character, 280
        Symptoms, 280
        Age when most frequent, 281
        Prognosis, 281
    Symptoms of intermediate period, 281
      Of tertiary period, 282
        Ear disorders, 282
          catarrh of middle, 282
        Deafness, 282, 283
          duration of, 283
        Liver, disease of, 283
          enlargement of, 283
        Pathology, 283, 284
        Diagnosis, 286
      Bones, disease of, 286
        Pathology, 286-288
        Osteo-chondritis, symptoms, 288
        Most attacked, 288
        Pseudo-paralysis, 289, 312
        Formation of osteophytes, 289
        Diagnosis, 289, 290
          from rickets, 289, 290
        Osteo-periostitis, 291
          diagnosis from non-specific form, 291
        Dactylitis, 291
          Varieties, 291
          Diagnosis, 291
          Prognosis, 291
      Teeth, disease of, 292
        Temporary, 292
        Permanent, 293
        Hutchinson on malformation of central upper incisors, 293,
            294
        Diagnosis from non-specific malformations, 293, 297
        Erosions of, 298
      Keratitis, interstitial, 299
        Symptoms, 299
        Complications, 299
        Diagnosis, 299
          from non-specific forms, 299
        Age when most frequent, 300
      Nerve-centres and nerves, disease of, 302
        Resemblance to adult form, 303
        Age and date of appearance, 304
        Pathology, 304
        Diagnosis, 304
        Prognosis, 304
      Spleen, disease of, 305
        enlargement, 305
          cause, 306
      Gastro-intestinal tract, disorders, 306
        Peyer's patches, degeneration of, 306
        Intestinal ulcers, 306
      Pancreas, disease of, 306
      Peritoneum, disease of, 307
      Lungs, disease of, 307
        gummata of, 307
        pneumonia, specific, 307
      Larynx, disease of, 308
      Testicles, disease of, 308
      Kidneys, disease of, 308
        Bright's disease of, 308
        Parenchymatous nephritis, 308
      Thymus gland, disease of, 309
  Diagnosis, 309
    Chief elements of, 310
    Relative importance of a specific parental history, 310
    Appearance of child at birth, 311
    Physiognomy of syphilitics, 313
    Abortions, frequent, significance of, in, 310
  Prognosis, 310
  Treatment, 314
    Preventive, 314
    Of parents, 260, 261, 314, 315
    Necessity of supporting, 315
    Nursing of syphilitic children, necessity of maternal, 315
    Wet-nurses, for syphilitic children, question of, 315
    Diet, 315
    Mercury, use of, 315, 316
      mode of administration, 316
      inunctions of, 316
    Iodide of potassium, use of, 316
    Local, 317

Syphilis as a cause of infantile peritonitis, 1172
  influence on causation of enteralgia, 669
      of glossitis parasitica, 358
      of chronic intestinal catarrh, 700
      of intestinal indigestion, 623
      of acute yellow atrophy of liver, 1024
      of amyloid liver, 1041
      of cirrhosis of liver, 991
      of oesophageal paralysis, 429
      of organic stricture of oesophagus, 423
      of chronic intestinal pancreatitis, 1121
      of acute pharyngitis, 390
      of rachitis, 144, 145
      of fissure of rectum and anus, 888
      of non-malignant rectal stricture, 885
      of ulceration of rectum and anus, 894
      of cirrhosis of stomach, 612
      of rectum and anus, 900

Syphilitic parents, treatment of, 314, 315
  pharyngitis, 406
  ulcers of stomach, 529
  ulceration of tongue, 370
    influence on causation of hemorrhage from bowels, 831

Syphilitics, marriage of, 255-265

Syringe, variety of, in rectal alimentation, 928


T.

TABES MESENTERICA, 1182
  Definition, 1182
  Synonyms, 1182
  History, 1183
  Pathology, 1183
    Secondary character, 1183, 1186
    Tuberculous nature, 1183
    Relation to scrofula and tuberculosis, 1183, 1186
    Age, 1184
    Sex, 1184
    Frequency, 1184
    Geographical distribution, 1185
  Etiology, 1185
    Scrofulous and tuberculous diathesis, 1185
    Heredity, 1185
    Diet and food, improper, 1185, 1186
    Filth and poverty, 1186
    Malaria, 1186
    Inflammation of intestinal mucous membrane, 1186
    Acute exanthemata, 1186
    Dentition, 1186
    Whooping cough, 1186
    Mild of diseased cows, 1186
    Cure of chronic skin disease, 1187
  Morbid anatomy, 1187
    Glands, mesenteric, changes in, 1187
        enlargement, 1187
        cheesy degeneration, 1187
        softening of, 1187
        cretaceous degeneration, 1187
    Spleen, lesions of, 1188
    Lungs, lesions of, 1188
    Liver, lesions of, 1188
    Gastro-intestinal canal, lesions of, 1188
    Pancreas, lesions of, 1188
  Symptoms, 1189
    Precursory, 1189
    Debility and anaemia, 1189
    Digestive disorders, 1189
    Tongue, state of, 1189
    Appetite, state of, 1189
    Stools, characters of, 1190
    Bowels, irregular, 1190
    Pyrexia, 1190
    Abdomen, state of, 1190
    Tympanites, 1190
    Tumor, presence of, 1190
  Diagnosis, 1191
    From fecal accumulation, 1191
      tumors of omentum, 1191
  Prognosis, 1191
  Course, 1192
  Duration, 1193
  Complications, 1193
    Rickets, 1193
  Treatment, 1193
    Preventive, 1193
    Hygienic, 1193
    Pain, 1194
    Diarrhoea, 1194
    Cod-liver oil, 1194
    Iodide of iron, 1194
    Lacto-phosphates, 1194
    Ointment of iodide of lead, 1194

Tabes mesenterica following chronic intestinal catarrh, 710

Taenia acanthotrias, 945
  cucumerina, 937
  echinococcus, 943
    migration of, from intestinal canal, 945
    mode of dissemination of, 944
  elliptica, 937
  flavopunctata, 938
  madagascariensis, 938
  nana, 937
  saginata, 933
  solium, 935
  tenella, 938

Tampon, use of, in hemorrhage from rectum, 927

Tannic acid, use of, in acute intestinal catarrh, 695
      in hemorrhage from bowels, 834

Tape-worms, 131
  method of examining evacuations for, 940

Tapping in cirrhosis of liver, 1002
  of gut in intestinal obstruction, 865

Taraxacum, local use of, in pseudo-membranous enteritis, 775

Tarry stools in hemorrhage from bowels, 833

Taxis, abdominal, in intestinal obstruction, 864

T-bandage, use of, in prolapsus ani, 919

Teeth, condition of, in scrofula, 246
  displacement of, from hypertrophy of tongue, 351
  eruption of, in second dentition, 375
  irregular and jagged, influence on causation of superficial
            glossitis, 355
          of parenchymatous glossitis, 360
  malformation of, in hereditary syphilis, 292
  order of normal eruption, 372
  precipitate eruption of, 372
  state of, in mercurial stomatitis, 345
  tardy eruption of, 372
  wisdom, eruption of, 376

Teething, anomalies of, in rachitis, 150, 151

Temperament, influence on causation of pseudo-membranous enteritis,
        764
      of gout, 110
      of acute intestinal catarrh, 671
      of amyloid liver, 1041
      of acute rheumatism, 21
      of scrofula, 235

Temperature in occlusion of biliary passages, 1091
  in cholera infantum, 742
  in cholera morbus, 723
  in diabetes mellitus, 204
  in entero-colitis, 734, 736
  in acute gastritis, 467
  in jaundice, 980
  in abscess of liver, 1008
  in acute yellow atrophy of liver, 1028
  in carcinoma of pancreas, 1125
  in acute pancreatitis, 1119
  in acute peritonitis, 1142
  in tuberculous peritonitis, 1165
  in acute pharyngitis, 394, 395
  in phosphorus-poisoning, 1032
  in purpura haemorrhagica, 189
  in suppurative pylephlebitis, 1100
  in acute rheumatism, 27, 29
  in rheumatic form of gonorrhoeal rheumatism, 104
  in scrofula, low, 245
  in scurvy, 182
  in cancer of stomach, 554
  in dilatation of stomach, 596
  in simple ulcer of stomach, 495
  in tabes mesenterica, 1190
  in tonsillitis, 381, 382
  sudden changes of, as a cause of gout, 112

Tenderness of epigastrium in chronic gastritis, 473

Tenesmus in acute colitis, 684
  in dysentery, 796, 802
  in polypi of rectum, 882
  in proctitis, 684

Termination of catarrh of bile-duct, 1055
  of occlusion of biliary passages, 1092
  of lithaemia, 970
  of abscess of liver, 1017
  of acute yellow atrophy of liver, 1029
  of carcinoma of liver, 1039
  of cirrhosis of liver, 999
  of fatty liver, 1049
  of hydatids of liver, 1106
  of perihepatitis, 989
  of suppurative pylephlebitis, 1101
  of phosphorus-poisoning, 1032
  of gonorrhoeal rheumatism, 106
  of simple ulcer of stomach, 501

Terminations of cholera morbus, 723
  of enteralgia, 464
  of intestinal indigestion, 630

Tertiary period of hereditary syphilis, 282
  ulcers of tongue, 370

Test, Fehling's, for sugar in urine, 211
  fermentation, for sugar in urine, 212
  indigo-carmine, for sugar in urine, 216
  for inosite in diabetic urine, 217
  iodine, for amyloid liver, 1043
    for lardaceous degeneration of intestines, 875
  picric acid and carmine, for sugar in urine, 213

Testicle, atrophy of, in diabetes mellitus, 202
  retraction of, in paratyphlitis, 819
    in perforation of simple gastric ulcer, 498

Testicles, disease of, in hereditary syphilis, 308

Tests for bile in urine, 978
  for free hydrochloric acid in vomit of gastric cancer, 543, 544
  for sugar in diabetic urine, 211-217

Thermic fever, relation to cholera infantum, 745

Thermo-cautery, use of, in hypertrophy of tongue, 354

Thigh, flexure upon leg, in paratyphlitis, 819

Thirst in cholera infantum, 742
  in cholera morbus, treatment of, 725
  in diabetes mellitus, 204
  in acute gastritis, 467
  in chronic gastritis, 473
  in parenchymatous glossitis, 362
  in acute intestinal catarrh, 680, 681
        treatment of, 690
  in carcinoma of pancreas, 1125
  in acute rheumatism, 27
  in dilatation of stomach, 593
  in simple ulcer of stomach, 494
  in hypertrophy of tongue, 351
  in trichinosis, 960
  in typhlitis and perityphlitis, 818

Thorn-head worms, 949

Thread-worms, 949

Thrombi, as a cause of suppurative pylephlebitis, 1098

Thrombosis in simple ulcer of stomach, 510
  of portal vein, 1095
      in cirrhosis of liver, 999
  venous, in gastric cancer, 533

Thrush. See _Stomatitis Parasitica_.

Thymol, use of, in treatment of Distomum hepaticum, 1110

Thymus gland, disease of, in hereditary syphilis, 309

Tight-lacing, a cause of perihepatitis, 989
  displacement of stomach by, 617
  influence of, on causation of intestinal indigestion, 624

Tincture of aloes, use of, in seat-worms, 951
  of chloride of iron, use of, in simple ulcer of stomach, 524
  of gelsemium, use of, in pruritus ani, 917
  of iodine, use of, in diabetes mellitus, 228
    locally, in rheumatoid arthritis, 100
  of iron, use of, in hemorrhage from bowels, 834

Tobacco, abuse of, influence of, on causation of constipation, 641
        of enteralgia, 660
        of acute intestinal catarrh, 671, 672
        of intestinal indigestion, 625
        of parenchymatous glossitis, 360
        of superficial glossitis, 355
        of acute oesophagitis, 410
        of diseases of pancreas, 1114
        of chronic pharyngitis, 402
        of dilatation of stomach, 589

TONGUE, ABNORMALITIES AND VICES OF CONFORMATION, 348
    Congenital deficiency of, 348, 349
    Bifid, 349
  _Ankyloglossia_ (_Tongue-tie_), 349
    Definition, 349
    Synonyms, 349
    Pathology and morbid anatomy, 349
    Diagnosis, 349
    Prognosis, 349
    Treatment, 349
  _Macroglossia_ (_Hypertrophy of Tongue_), 349
    Definition, 349
    Synonyms, 349
    History, 349
    Etiology, 350
      Congenital nature of, 350
      Age, 350
      Sex, 350
      Sucking, influence of, on causation, 350
      Dentition, influence of, on causation, 350
      Convulsions and epileptic seizures, 350
      Idiocy and cretinism, relation of, to, 350
    Symptoms, 350
      Character of enlargement, 350
      Suffocation from, 350
      Saliva, increase of, 351
      Thirst, 351
      Larynx and hyoid bone, displacement of, 351
      Ulceration of tongue, 351
      Teeth, displacement of, 351
      Difficult mastication, 351
    Pathology and morbid anatomy, 352
      Nature of, 352
      Microscopic changes, 353
      Size of, 353
    Diagnosis, 353
    Prognosis, 353
    Treatment, 353
      Use of bandaging and compression, 353
        of leeching, 353
      Operative measures, 353
        Ligation, 354
        Excision, 354
        Ignipuncture, 354
        Thermo-cautery, 354
      Medication, futility of, 354

TONGUE, ULCERATION OF, 369
  Tuberculous ulceration of, 369
    Etiology, 369
    Pathology, 369
      Epithelium, shedding of, 369
      Ulcer, anatomical characters of, 369
        formation of, 369
      Nodular tubercular infiltration, 369
    Symptoms of, 369
      Seat of, 369
      Course, 369
      Characters, 369
      Induration, 369
      Indolence of, 369
      Saliva, increased secretion, 369
      Pain, 369
    Diagnosis, 369
      From squamous-celled carcinoma, 369
        syphilitic ulcer, 370
    Treatment, 370
  Syphilitic ulceration of, 370
    Symptoms, 370
      Secondary ulcers, 370
        seat, 370
        pain, 370
        characteristics, 370
      Tertiary, 370
        sequelae of gummata, 370
        seat, 370
        characteristics, 370
    Prognosis, 370
    Treatment, 370

Tongue, state of, in catarrh of bile-ducts, 1053
    in biliousness, 966
    in cholera infantum, 742
    in constipation, 646, 647
    in dysentery, 804
    in functional dyspepsia, 450
    in enteralgia, 661
    in pseudo-membranous enteritis, 766
    in gastralgia, 461
    in acute gastritis, 467
    in chronic gastritis, 473
    in parenchymatous glossitis, 361
    in chronic parenchymatous glossitis, 367
    in chronic superficial glossitis, 366
    in acute intestinal catarrh, 678, 680, 681
    in chronic intestinal catarrh, 707
    in intestinal indigestion, 628
    in abscess of liver, 1013
    in acute yellow atrophy of liver, 1028
    in acute pancreatitis, 1119
    in acute rheumatism, 27
    in scurvy, 177
    in cancer of stomach, 540
    in simple ulcer of stomach, 495
    in tonsillitis, 381, 383
    in typhlitis and perityphlitis, 819
  enlargement of, in catarrhal stomatitis, 324
    in parenchymatous glossitis, 361
  inflammation of, in mercurial stomatitis, 346

Tongue-tie, 349

TONSILS, DISEASES OF, 379
  _Tonsillitis_, 379
    Definition, 379
    Varieties, 379
    Synonyms, 379
    History, 379
    Etiology, 380
      Of idiopathic form, 380
      Diathetic causes, 380
      Rheumatism, 380
      Scrofula, 380
      Heredity, 380
      Chronic disease of tonsils, 380
      Age, 380
      Of deuteropathic form, 380
      Of hepatic form, 380
      Of traumatic form, 380
      Of mycotic form, 381
        due to cryptogam, 381
    Symptomatology, 381
      Onset, 381
      Pulse, 381
      Temperature, 381, 382
      Appearance of throat, 381
      Pain, 381, 382
      Ears, noises in, 381
      Involvement of adjacent structures, 381, 382
      Appearance of soft palate, 381
        of uvula, 382
      Deglutition, difficult, 381
      Salivation, excessive, 382
      Regurgitation of liquids, 382
      Glands, lymphatic, swelling, 382
      Voice, alteration of, 382
      Respiration, difficult, 382
      Headache, 383
      Tongue, condition of, 381, 383
      Urine, condition of, 383
      Albuminuria, 383
      Termination, 383
      Resolution, 383
      Suppuration, 383
        symptoms of, 383
      Abscess, point of rupture, 383
      Gangrene, 383
      Metastasis, occurrence, 383
      Ulceration of maxillary and carotid arteries, 383
      Oedema of glottis, 383
      Paralysis of palate, 383
      Hypertrophy of tonsil following, 383
    Complications and sequelae, 383
    Pathology and morbid anatomy, 383
      Of catarrhal form, 384
      Of lacunar form, 384
        condition of epithelium, 384
        deposit, nature of, 384
        presence of micrococci and bacteria, 384
        mode of subsidence, 384
      Of follicular form, 384, 385
      Of parenchymatous form, 385
          result of lacunar form, 385
          mode of subsidence, 385
      Secretion, character of, 385
      Presence of micro-organisms, 385
      Submaxillary glands, lesions of, 385
      Of herpetic form, 386
      Of mycotic form, 386
        nature of parasite, 386
        seat of deposit, 386
        subjective symptoms, 386
    Diagnosis, 386
      From diphtheria, 387
        sore throats of cachectic conditions, 387
    Prognosis, 387
      Recurrence, frequency of, 387
    Treatment, 387
      Mild cases, 387
      Local, 388
      Pyrexia, 388
      Pain, 388
      Severe cases, 388
      Rheumatic form, 388
      Herpetic form, 388
      Mycotic form, 389
      Diet, 388
      Gargles, use of, 388
      Ice, use of, 388
      Tincture of guaiacum, 388
        of aconite, 388
      Sodium bicarbonate, 388
      Poultices, 388
      Sodium salicylate in rheumatic form, 388
      Mercuric chloride in herpetic form, 388
      Operative measures, 388
      Cauterization in mycotic form, 389

Tonsils, hypertrophy of, following tonsillitis, 383
  ulceration of, in pseudo-membranous enteritis, 766

Torsion of caecum from constipation, 853

Torticollis, 78
  treatment, 78

Toxaemic period of acute yellow atrophy of liver, 1027

Toxic form of acute gastritis, 467
    of intestinal ulcer, 823
  stomatitis, 344

Tracheotomy in acute pharyngitis, 398, 399

Transfusion of blood in diabetes mellitus, 229
    in hemorrhage from bowels, 834
    in phosphorus-poisoning, 1033
    in purpura, 194

Transmission of syphilis at moment of conception, 262, 267
    by infection prior to conception, 266
    during utero-gestation, 267

Traumatic causes of perihepatitis, 989
  form of intestinal ulcer, 823

Traumatism, influence on causation of gout, 112
      of hemorrhagic effusion into peritoneum, 1181
      of abscess of liver, 1003
      of non-malignant stricture of the rectum, 885
      of acute rheumatism, 22
      of hemorrhage from stomach, 580

Travel, value of, in functional dyspepsia, 455
    in gastralgia, 463

Treatment of Ascaris lumbricoides, 953
  of ascites, 1178
  of Anchylostomum duodenale, 956
  of Bilharzia haematobia, 949
  of catarrh of bile-ducts, 1056
  of biliary calculi in situ, 1080
      calculus state, 1079
      concretions, 1079
  of occlusion of biliary passages, 1094
  of biliousness, 967
  of cancrum oris, 343
  of cholera infantum, 759
      morbus, 724
  of constipation, 651
      in children, 656
  of diabetes mellitus, 218
  of diarrhoea in chronic intestinal catarrh, 715
  of duodenitis, 698
  of dysentery, 809
  of functional dyspepsia, 452
  of enteralgia, 664
  of nervous form of enteralgia, 665
  of pseudo-membranous enteritis, 774
  of entero-colitis, 746
  of impaction of feces, 918
  of Filaria medinensis, 963
  of Filaria sanguinis, 964
  of fissure of anus, 911
  of fistula in ano, 921
  of fluke-worms, 948
  of gastralgia, 462
  of acute gastritis, 468
  of chronic gastritis, 475
  of parasitic glossitis, 359
  of parenchymatous glossitis, 364
  of chronic parenchymatous glossitis, 368
  of superficial glossitis, 357
  of chronic superficial glossitis, 367
  of glossanthrax, 368
  of gout, 127
  of acute articular gout, 133
  of hemorrhage from bowels, 833
  of hemorrhoids, 923
  of hepatic colic, paroxysms, 1081
  of hepatic glycosuria, 974
  of lardaceous degeneration of intestine, 876
  of acute intestinal catarrh, 687
  of chronic intestinal catarrh, 714
  of intestinal cancer, 874
  of intestinal indigestion, 632
  of intestinal obstruction, 862
      from fecal impaction, 863
      surgical, 865
  of intestinal ulcer, 828
  of invagination, low in rectum, 864
  of intussusception, 864
  of jaundice, 982
  of Leptodera stercoralis, 954
  of lithaemia, 971
  of abscess of liver, 1020
  of acute yellow atrophy of liver, 1030
  of amyloid liver, 1045
  of carcinoma of liver, 1040
  of cirrhosis of liver, 1000
  of fatty liver, 1050
  of hydatids of liver, 1106
  of hyperaemia of liver, 988
  of liver-flukes, 1110
  of lumbago, 77
  of macroglossia, 353
  of cancer of oesophagus, 428
  of dilatation of oesophagus, 434
  of organic stricture of oesophagus, 425
  of spasmodic stricture of oesophagus, 421
  of oesophageal paralysis, 430
  of ulceration of oesophagus, 418
  of acute oesophagitis, 415
  of chronic oesophagitis, 417
  of carcinoma of pancreas, 1127
  of hemorrhage into pancreas, 1129
  of obstruction of pancreatic duct, 1131
  of acute pancreatitis, 1120
      secondary pancreatitis, 1121
  of chronic interstitial pancreatitis, 1122
  of peri-anal and peri-rectal abscess, 918
  of perihepatitis, 990
  of acute peritonitis, 1144
  of cancerous peritonitis, 1172
  of infantile peritonitis, 1173
  of perforative peritonitis, 1156
  of puerperal peritonitis, 1146
  of tubercular peritonitis, 1168
  of peri- and endocarditis in acute rheumatism, 63, 64
  of phosphorus-poisoning, 1033
  of acute pharyngitis, 397
  of phlegmonous form of acute pharyngitis, 397
  of chronic pharyngitis, 404
  of syphilitic pharyngitis, 408
  of tuberculous pharyngitis, 402
  of pleurodynia, 78
  of proctitis, 919
  of prolapsus ani, 919
  of purpura, 193
  of suppurative pylephlebitis, 1101
  of hypertrophic stenosis of pylorus, 615
  of rachitis, 158
  of cancer of rectum, 913
  of dilatation of rectal pouches, 916
  of gonorrhoea of rectum, 918
  of hemorrhage of rectum, 926
  of irritable rectum, 919
  of polypi of rectum, 913
  of rodent ulcer of rectum, 913
  of non-malignant stricture of rectum, 917
  of ulceration of rectum, 912
  of tuberculous ulcer of rectum, 913
  of diseases of rectum and anus, 911
  of congenital malformation of rectum and anus, 880
  of acute rheumatism, 51
  of chronic articular rheumatism, 73
  of gonorrhoeal rheumatism, 107
  of muscular rheumatism, 76
  of rheumatoid arthritis, 96
  local, of rheumatoid arthritis, 100
  of scrofula, 249
  of scurvy, 183
  of seat-worms, 951
  of sphincterismus, 916
  of cancer of stomach, 576
  of cirrhosis of stomach, 615
  of dilatation of stomach, 603
  of acute dilatation of stomach, 603
  of hemorrhage from stomach, 585
  of rupture of stomach, 618
  of simple ulcer of stomach, 519
  of aphthous stomatitis, 330
  of catarrhal stomatitis, 325
  of mercurial stomatitis, 347
  of stomatitis ulcerosa, 338
  of stomatorrhagia, 371
  of tabes mesenterica, 1193
  of Taenia echinococcus, 945
  of tape-worm, 941
  of thrombosis and embolism of portal vein, 1096
  of thrush, 335
  of tongue-tie, 349
  of syphilitic ulceration of tongue, 370
  of tubercular ulceration of tongue, 370
  of tonsillitis, 387
  of torticollis, 77
  of trichinosis, 961
  of Triocephalus dispar, 954
  of typhlitis, peri- and paratyphlitis, 822

Trematodes, 946

Trichina spiralis, 957
    appearance of meat affected with, 959
    discovery of, in muscles, 958
    method of migration to muscles, 959
    symptoms of, 959

Trichinosis. See _Intestinal Worms_.
  in children, 961
  prophylaxis of, 962
  symptoms of, 959
  treatment of, 961

Trimethylamine, use of, in acute rheumatism, 62
    in chronic articular rheumatism, 74

Triocephalus dispar, 954
    symptoms and treatment of, 954

Tropical form of hepatic abscess, lesions of, 1006

Trypsin, action of, in digestion, 622

Tubercle of pancreas, 1128

Tubercular peritonitis, 1165
  ulcers of stomach, 529

Tuberculosis complicating chronic intestinal catarrh, 710
  influence of, on causation of intestinal ulcer, 824
  relation of, to scrofula, 240-242

Tuberculous affections of rectum and anus, 901
  nature of tabes mesenterica, 1183, 1184
  pharyngitis, 400
  ulcer of rectum, treatment of, 913
  ulceration, as a cause of hemorrhage from bowels, 831
    of bowel, distinguished from chronic intestinal catarrh, 713
    of tongue, 369

Tuberose vitiligoidea of skin, in jaundice, 981

Tubules, gastric, alterations in chronic gastritis, 472

Tumefaction of cheek in cancrum oris, 340

Tumor, fecal, characters of, 852
  frequency of, in gastric cancer, 546
  presence of a, in cancer of intestines, 869
    in intussusception, 848
    in hypertrophic stenosis of pylorus, 615
    significance of, in diagnosis of cancer of stomach, 569
      of cirrhosis of stomach, 613
    in tabes mesenterica, 1190
    in typhlitis and paratyphlitis, 819
  of carcinoma of liver, shape and size, 1034
  of epigastrium in abscess of liver, 1011
  pulsating, of epigastrium, in hemorrhage into pancreas, 1129
  significance of a, in diagnosis of intestinal cancer, 873
  seat and character, in carcinoma of pancreas, 1124, 1125
      in cancer of stomach, 548

Tumors, as a cause of hemorrhage from bowels, 831
  of stomach, non-cancerous, 578
  pressure of, as a cause of occlusion of common biliary duct, 1085
      of pancreatic duct, 1129
  and cysts, compression by, as a cause of intestinal obstruction, 857

Turkish baths, use of, in rheumatoid arthritis, 99

Turpentine, use of, in Anchylostomum duodenale, 956
    in chronic intestinal catarrh, 718
    in intestinal ulcer, 829
    in ulceration of oesophagus, 418
    in hemorrhage from bowels, 834
        from mouth, 371
    in phosphorus-poisoning, 1033
    in pruritus ani, 917
    in purpura, 193
    in stomatorrhagia, 371
    in tape-worm, 941
  stupes, use of, in perihepatitis, 990
  and ether, as solvents of biliary calculi, 1080

Twisting of bowels, 840
    seat, 841
  of stomach, 617

Tympanites, in acute internal strangulation of intestines, 843
    intestinal catarrh, 679
  in chronic intestinal catarrh, 707
  in intestinal indigestion, 627
  in intussusception, 848
  in acute peritonitis, 1141
  in acute dilatation of stomach, 610
  in perforation of simple ulcer of stomach, 498
  in tabes mesenterica, 1190

Typhlitis, influence of, on causation of suppurative pylephlebitis,
        1097
  stercoralis, treatment, 821
  and perityphlitis in constipation, 648

TYPHLITIS, PERITYPHLITIS AND PARATYPHLITIS, 814
  History, 814
  General remarks, 814
  Etiology, 815
    Age, influence of, on causation, 815
    Sex, influence of, on causation, 815
    Appendix vermiformis, disease of, 815
        abnormalities of size and position, 815
        ulceration and stricture of, 815
        collection of feces and foreign bodies in, 816
        anatomical peculiarities of, 816
    Constipation, influence of, on causation, 816
    Paresis of muscular tissue of caecum, 817
    Foreign bodies, influence of, on causation, 817
  Morbid anatomy, 817
    Perforative peritonitis, lesions of, 817
    Intestinal walls, thickening, 817
    Mucous membrane, ulceration, 817
    Abscesses, seat, 817
      point of discharge, 818
    Contortions and adhesions of vermiform appendix, 818
    Cicatrix of vermiform process, 818
  Symptoms, 818
    Mode of onset, 818
    Prodromata, 818
    Disinclination to walk, 818
    Formication and paresis of right leg, 818
    Chill, 818
    Collapse of strength, 818
    Fever, 818, 819
    Thirst, 818
    Appetite, loss of, 818, 819
    Pain, 818
      character and seat, 818
    Abdominal tenderness, 818
    Tumor, presence of, 819
      seat and shape, 819
    Disturbance of digestion, 819
    Vomiting, 819
    Constipation, 819
    Tongue, state of, 819
    Pulse, state of, 819
    Urine, state of, 819
    Perforation, occurrence of, 819
      causes of, 819
    Of paratyphlitis, 819
      Insidiousness of, 819
      Flexure of thigh upon leg, 819
      Perversions of sensation in right leg, 819
      Dysuria, 819
      Retraction of testicle, 819
      Priapism, 819
      Milk-leg from thrombosis, 820
      Frequency of relapses, 820
  Diagnosis, 820
    From fecal impaction, 820
      cancer, 820
      invagination, 820
  Duration, 820
  Prognosis, 820
  Mortality, 820, 821
  Prophylaxis, 821
  Treatment, 821
    Of typhlitis stercoralis, 821
    Irrigation of bowel, 821
    Of abscesses, 822
    Of perforative form, 822
    Of indurated tumors, 822
    Of convalescence, 822
    Magnesium sulphate, use of, 822
    Opium, use of, 822
    Hot embrocations, use of, 822
    Ice-bag, use of, 822
    Mineral waters, 822
    Mercurial ointment, 822
    Iodine, 822
    Laparotomy in perforative form, 822

Typhoid fever, as a cause of hemorrhage from bowels, 831
    distinguished from dysentery, 807
    influence of, on causation of intestinal ulcer, 824
  ulcer, as a cause of acute peritonitis, 1139
    of stomach, 529


U.

Ulcer, duodenal, of chronic intestinal catarrh, diagnosis, 713
  gastric, influence on causation of cancer of stomach, 536
  intestinal, 823
  of intestine, prevention of recurrence, 829
  of rectum, treatment, 912
  rodent, of rectum, 889
  simple, of stomach, 480
      position and shape, 504
  tuberculous, of rectum, treatment, 913

Ulcerated surfaces, complicating diabetes mellitus, 205

Ulceration, character and seat, in cancrum oris, 341
  follicular, of chronic intestinal catarrh, 712, 713
  in aphthous stomatitis, 328
  intestinal, in constipation, 644
  of cheek in cancrum oris, 340
  of colon in chronic intestinal catarrh, 702
  of gums, in mercurial stomatitis, 347
  of intestines, complicating constipation, 648
  of maxillary and carotid arteries in tonsillitis, 383
  of oesophagitis, 418
  of rectum, influence on causation of carcinoma of, 904
  of rectum and anus, 893
  of lobe of ear in scrofula, 246
  of skin and muscles in scurvy, 178
  of cancer of stomach, 562
  of tongue, 369
    syphilitic, 370
    tuberculous, 369
  of vermiform appendix, as a cause of typhlitis, 814
  and dilatation of bile-ducts, as a cause of abscess of liver, 1005

Ulcerations, follicular, of rectum and anus, 894
  nature and seat, in syphilitic pharyngitis, 407
  of chronic form of dysentery, seat and characters, 800

Ulcerative endocarditis in acute rheumatism, 34
  form of acute pharyngitis, morbid anatomy, 392
        symptoms, 395
        treatment, 398

Ulcerous stomatitis, 336

Ulcers, in dysentery, characters and seat, 799
  in entero-colitis, seat, 737, 738
  in acute intestinal catarrh, catarrhal and follicular, 676
        seat, 976
        treatment, 698
  in chronic intestinal catarrh, mode of formation, 703
  in simple ulcer of stomach, number, 503
  in stomatitis ulcerosa, seat and character, 336, 337
  of stomach as a cause of acute peritonitis, 1139
  of stomach and intestines in cirrhosis of liver, 999

Uncleanliness, influence on causation of intestinal worms, 931
      of stomatitis ulcerosa, 336

Ung. hydrarg. iod. rubri, in lithaemia, 973
      use of, in amyloid liver, 1046
        in cirrhosis of liver, 1002

Uni-articular rheumatism, 49

Unilateral enlargement of papillae in superficial glossitis, 356

Unripe fruit, influence on causation of cholera morbus, 721

Uraemia, influence on causation of acute intestinal catarrh, 671

Uraemic choleriform attacks, diagnosis from cholera morbus, 724
  coma, complicating cancer of stomach, 556

Uranium nitrate, use of, in diabetes, 230

Uratic deposits in kidneys in gout, 117

Urea, action of liver in formation of, 968, 969
  amount of, in urine of jaundice, 979
  diminished excretion of, in acute yellow atrophy of liver, 1029

Urethral stricture, influence on causation of prolapse of rectum, 881

Urethritis, complicating diabetes mellitus, 205

Uric acid, amount in urine, during paroxysms of gout, 119
    in blood of gouty individuals, 115
    in urine of lithaemia, 970
    theory of origin of gout, 113, 114
    and urates, amount of, in urine of gouty dyscrasia, 120
      urea, amount excreted, in acute rheumatism, 30

Urinary retention in constipation, 646

Urine, state of, in ascites, 1177
    in catarrh of bile-ducts, 1054, 1055
    in occlusion of biliary passages, 1089, 1090
    in biliousness, 966
    in cholera infantum, 742
      morbus, 723
    in constipation, 648
    in diabetes mellitus, 207
    in dysentery, 803
    in functional dyspepsia, 451
    in enteralgia, 661
    in pseudo-membranous enteritis, 766
    in entero-colitis, 734
    in acute gastritis, 467
    in chronic gastritis, 475
    in acute gout, 119
    in gouty dyscrasia, 120
    in hepatic glycosuria, 974
    in acute intestinal catarrh, 681
    in chronic intestinal catarrh, 708
    in intestinal indigestion, 628
    in jaundice, 978
    in lithaemia, 970
    in abscess of liver, 1010, 1014
    in acute yellow atrophy of liver, 1029
    in amyloid liver, 1044
    in carcinoma of liver, 1038
    in cirrhosis of liver, 998
    in fatty liver, 1049
    in hyperaemia of liver, 986, 987
    in chronic interstitial pancreatitis, 1122
    in acute peritonitis, 1142
    in cancerous peritonitis, 1170
    in phosphorus-poisoning, 1032
    in acute rheumatism, 30
    in gonorrhoeal rheumatism, 104
    in chronic general rheumatoid arthritis, 83
    in gastric cancer, 550
    in dilatation of stomach, 595
    in scurvy, 181
    in tonsillitis, 383
    in typhlitis and perityphlitis, 819
  fat in, in carcinoma of pancreas, 1125
  infiltration of, as a cause of acute peritonitis, 1140
  presence of albumen in, in gout, 123
  tests for bile in, 978
    for sugar in, 211

Uterine disorders in pseudo-membranous enteritis, 767
    in tape-worm, 940
    influence on causation of functional dyspepsia, 448
        of fissure of anus, 888
        of gastralgia, 460
        of chronic pharyngitis, 403
  displacements from constipation, 647
  injections as a cause of acute peritonitis, 1140

Utero-gestation, infection of child with syphilis during, 267
  in acute pharyngitis, 391-394

Uvula, appearance of, in tonsillitis, 382


V.

Vaccination, influence on causation of scrofula, 237

Valerian, use of, in spasmodic stricture of oesophagus, 421

Vapor baths, use of, in ascites, 1179
      in cirrhosis of liver, 1001
      in rheumatoid arthritis, 100

Varicocele from constipation, 646

Varieties of enteralgia, 662
  of gastralgia, 459
  of acute gastritis, 464
  of acute intestinal catarrh, 682
  of rheumatoid arthritis, 79
  of seat-worms, 950
  of stomatitis, 321
  of tonsillitis, 379

Variolous form of acute pharyngitis, 393
  pustules in acute oesophagitis, 412

Vaso-motor nerves, influence on production of glycosuria, 196-199

Vater's diverticulum, death from lodgment of biliary calculi in, 1078

Veins, varicose condition of, in chronic intestinal catarrh, 702

Venereal excess, influence on causation of enteralgia, 660
      of gastralgia, 460

Venesection, use of, in parenchymatous glossitis, 364

Venous walls, changes in, influence on causation of pylephlebitis,
        1098

Vermiform appendix, contortions and adhesions of, in typhlitis, etc.,
        814

Vertebral column, changes in, in rachitis, 151
  pain in acute oesophagitis, 413

Vertigo in catarrh of bile-ducts, 1054
  in biliousness, 966
  in constipation, 647
  gastric, in functional dyspepsia, 451
  in enteralgia, 662
  in acute gastritis, 467
  in chronic gastritis, 474
  in hemorrhage from bowels, 833
  in intestinal indigestion, 628
  in lithaemia, 970
  in cirrhosis of liver, 993
  in dilatation of stomach, 595
  in simple ulcer of stomach, 494
  in tape-worm, 940

Vesical catarrh, complicating gout, 123

Vesicles of aphthous stomatitis, nature of, 327

Vibrios and bacteria in acute intestinal catarrh, 676

Villi, lesions of, in acute intestinal catarrh, 675
  hypertrophy of, in chronic intestinal catarrh, 701

Virchow on circumscribed hemorrhagic infiltration as a cause of
        gastric ulcer, 512

Vision, disorders of, in diabetes mellitus, 204
  yellow, in jaundice, 980

Visual disorders in biliousness, 966
    in constipation, 647
    in pseudo-membranous enteritis, 767
    in intestinal indigestion, 628
    in scurvy, 181

Vitiated air, influence on causation of cholera infantum, 728-730
      of entero-colitis, 728-730

Vitiligoidea in jaundice, 980

Voice, alteration of, in parenchymatous glossitis, 361
    in stomatitis parasitica, 334
    in tonsillitis, 382
  characters of, in cholera morbus, 722
  improper use of, as a cause of chronic pharyngitis, 402

Vomit, characters of, in cholera morbus, 722
    in functional dyspepsia, 450
    in enteralgia, 662
    in pseudo-membranous enteritis, 765
    in entero-colitis, 733
    in acute gastritis, 467
    in chronic gastritis, 473
    in hepatic colic, 1072
    in cancer of intestines, 870
    in intestinal obstruction from internal strangulation and
        twisting, 843
      from intussusception, 848, 849
      from impaction of gall-stones, 840
      from stricture of bowel, 856
    in abscess of liver, 1014
    in acute yellow atrophy of liver, 1028
    in cirrhosis of liver, 993
    in carcinoma of pancreas, 1126
    in diseases of pancreas, 1116
    in acute pancreatitis, 1119
    in acute peritonitis, 1141
    in phosphorus-poisoning, 1031
    in suppurative pylephlebitis, 1100
    in dilatation of stomach, 594
    in cancer of stomach, 542
    in cirrhosis of stomach, 613
    in simple ulcer of stomach, 491, 492
  coffee-grounds, in acute yellow atrophy of liver, 1028
    in phosphorus-poisoning, 1031
  detection of blood in, in cancer of stomach, 545
    of cancerous fragments in, in cancer of stomach, 542
  presence of micro-organisms in, in dilatation of stomach, 594
  spinach-colored, in acute peritonitis, 1141
  stercoraceous, in enteralgia, 662
    in intestinal obstruction from internal strangulation and
        twisting, 843
      from impaction of gall-stones, 840
      from intussusception, 848, 849
    in stricture of bowel, 856

Vomiting in Ascaris lumbricoides, 953
  in occlusion of biliary ducts, 1088
  in cholera infantum, 742
        treatment, 761
  in cholera morbus, 722
        treatment, 725
  in dysentery, 803
  in functional dyspepsia, 449
  in enteralgia, 662
  in pseudo-membranous enteritis, 765
  in entero-colitis, 733
        treatment, 761
  in intestinal impaction of gall-stones, 840
  in gastralgia, 461
  in acute gastritis, 467
        treatment, 469
  in chronic gastritis, 473
  in hepatic colic, 1070, 1071, 1072
  in hemorrhage from bowels, 833
  in acute internal strangulation and torsion of intestines, 843
  in acute intestinal catarrh, 681
  in intestinal cancer, 870
  in intestinal obstruction, 843, 848, 849, 854, 856
      from stricture of bowel, 856
    ulcer, 826
      treatment of, 829
  in intussusception, 848, 849
  in impaction of fecal matter, 854
  in abscess of liver, 1013
      treatment of, 1021
  in acute yellow atrophy of liver, 1026, 1028
  in carcinoma of liver, 1038
  in cirrhosis of liver, 993
  in cancer of oesophagus, 427
  in acute oesophagitis, 413
  in carcinoma of pancreas, 1126
  in diseases of pancreas, 1116
  in hemorrhage into pancreas, 1129
  in acute pancreatitis, 1119
    peritonitis, 1141, 1143
  in cancerous peritonitis, 1170
  in tuberculous peritonitis, 1165
  in suppurative pylephlebitis, 1100
  in obstruction of rectum, 890
  in atrophy of stomach, 616
  in cancer of stomach, 541
      time of, 541
      treatment of, 576
  in cirrhosis of stomach, 613
  in dilatation of stomach, 593
      time of appearance, 593
  in simple ulcer of stomach, 491
      treatment of, 524
  in aphthous stomatitis, 329
  in typhlitis and perityphlitis, 818, 819
  in trichinosis, 960
  of blood in hemorrhage from bowels, 833
    in cirrhosis of liver, 833
    in simple ulcer of stomach, 493
  of gall-stones, 1076
  of segments of tape-worm, 940

Von der Velden on absence of free hydrochloric acid in fluids of
        gastric cancer, 543

Vulva, gangrene of, complicating cancrum oris, 341
  oedema of, in cirrhosis of liver, 995


W.

Walls of intestines, hypertrophy of, in chronic catarrh, 700

Ward's paste, use of, in tuberculous ulcer of rectum, 913

Warm baths, use in constipation, 653
    in acute intestinal catarrh, 692

Washing out of stomach in gastric cancer, 577
          dilatation, 603
      objections to, in gastric dilatation, 607
      contraindications of, in gastric dilatation, 608
      in simple ulcer of stomach, 523

Wasting in entero-colitis, 736
  in cancer of intestines, 871
  in tuberculous pharyngitis, 401
  diseases, influence on causation of constipation, 642
      of chronic intestinal catarrh, 699
      in acute intestinal catarrh, 671

Water, impure, influence on causation of dysentery, 791
      acute intestinal catarrh, 672, 673
  unfiltered, influence on causation of intestinal worms, 931
  use of, in constipation, 655
  as a solvent, use of, in gout, 133
  hot, use of, in chronic gastritis, 477

Water-brash in functional dyspepsia, 449

Weak heart-action as a cause of acute gastritis, 464

Weaning, proper time for, 160, 746

Weather, influence of, on exacerbations of chronic articular
        rheumatism, 71

Weight, loss of, in diabetes mellitus, 204

Wet-nurses for syphilitic children, question of, 315

Whip-worm, 954

Whooping cough, influence on causation of tabes mesenterica, 1186

Wine, use of, in intestinal indigestion, 634

Wintergreen, oil of, use in Ascaris lumbricoides, 954
      in gout, 136
      in liver-flukes, 1110
      in Oxyuris vermicularis, 951
      in acute rheumatism, 59

Wire-drawn feces in non-malignant stricture of rectum, 886

Wirsung's canal, anatomy of, 1113
    catarrh of, as a cause of obstruction of pancreatic duct, 1130
    dilatation of, from pancreatic calculi, 1130
  duct, closure of, as a cause of chronic interstitial pancreatitis,
        1121

Wisdom teeth, eruption of, 376

Woman's milk, composition of, 749, 750

Worms, intestinal, 930
    influence on causation of rectal prolapse, 881

Wormseed, use of, in Ascaris lumbricoides, 954

Worry and anxiety, influence on causation intestinal indigestion, 624


X.

Xanthelasma in jaundice, 980

Xanthopsy in jaundice, 980


Y.

Yellow atrophy of liver, acute, 1023
  vision, in jaundice, 980

Yellowness of skin in jaundice, mode of extension of, 977


Z.

Zinc chloride, local use of, in hemorrhoids, 926
  oxide, use of, in catarrh of bile-ducts, 1057
      in acute intestinal catarrh, 694
      in intestinal ulcer, 829
      in spasmodic stricture of oesophagus, 421
  salts, use of, in constipation, 655
      in acute intestinal catarrh, 697
      in chronic intestinal catarrh, 714, 717
  sulphate, use of, in gonorrhoea of rectum, 978
      in pseudo-membranous enteritis, 775
    local use of, in chronic pharyngitis, 405
        in aphthous stomatitis, 330
  valerianate, use of, in constipation, 655
      in enteralgia, 665
      in gastralgia, 463




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