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 PAPILLÆ 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. OÏDIUM 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 Encyclopédique des Sciences Méd._, Troisième
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 pyæmic, 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. Gén._, 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 Méd. 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 anæmia, 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 hæmophilia 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 pyæmic 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: _Beiträge 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 rôle
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, fasciæ, 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 rôle 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° F. to 104° 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 Médicale_, 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° F., and while the subsequent evening exacerbations
may reach 104°, 104.4°, or very rarely 105°, yet in the great majority
of cases the maximum temperature does not exceed 103° F., and in a very
considerable number falls short of 102°. 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°; 8, that of 104° to 105°; 15, that
of 103° to 104°; 32, that of 102° to 103°; 17, that of 101° to 102°;
10, that of 100° to 101°; and 1, that of 99.8°; that is, the
temperature was below 103° in five-sevenths, and below 104° 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° 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°, 108°,[29] 109.4°,[30] 110.2°,[31] or even
111°,[32] or 112°. 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.]