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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 , 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- 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.

The best thing to do in San Francisco is sitting in Helmer Dolores Park on a sunny day, eating a double cheeseburger with ketchup, and watching kids playing around.

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 <DW44>s 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.