Produced by Ron Swanson A SYSTEM OF PRACTICAL MEDICINE BY AMERICAN AUTHORS. EDITED BY WILLIAM PEPPER, M.D., LL.D., PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA. ASSISTED BY LOUIS STARR, M.D., CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE UNIVERSITY OF PENNSYLVANIA. VOLUME II. GENERAL DISEASES (CONTINUED) AND DISEASES OF THE DIGESTIVE SYSTEM. PHILADELPHIA: LEA BROTHERS & CO. 1885. Entered according to Act of Congress, in the year 1885, by LEA BROTHERS & CO., in the Office of the Librarian of Congress at Washington. All rights reserved. WESTCOTT & THOMSON, _Stereotypers and Electrotypers, Philada._ WILLIAM J. DORNAN, _Printer, Philada._ CONTENTS OF VOLUME II. GENERAL DISEASES (CONTINUED). PAGE RHEUMATISM. By R. PALMER HOWARD, M.D. . . . . . . . . . . . . . 19 GOUT. By W. H. DRAPER, M.D. . . . . . . . . . . . . . . . . . . 108 RACHITIS. By ABRAHAM JACOBI, M.D. . . . . . . . . . . . . . . . 137 SCURVY. By PHILIP S. WALES, M.D. . . . . . . . . . . . . . . . . 167 PURPURA. By I. EDMONDSON ATKINSON, M.D. . . . . . . . . . . . . 186 DIABETES MELLITUS. By JAMES TYSON, A.M., M.D. . . . . . . . . . 195 SCROFULA. By JOHN S. LYNCH, M.D. . . . . . . . . . . . . . . . . 231 HEREDITARY SYPHILIS. By J. WILLIAM WHITE, M.D. . . . . . . . . . 254 DISEASES OF THE DIGESTIVE SYSTEM. DISEASES OF THE MOUTH AND TONGUE. By J. SOLIS COHEN, M.D. . . . 321 DISEASES OF THE TONSILS. By J. SOLIS COHEN, M.D. . . . . . . . . 379 DISEASES OF THE PHARYNX. By J. SOLIS COHEN, M.D. . . . . . . . . 390 DISEASES OF THE OESOPHAGUS. By J. SOLIS COHEN, M.D. . . . . . . 409 FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH. By SAMUEL G. ARMOR, M.D., LL.D. . . . . . . . . . . . . . . . . . . . . 436 SIMPLE ULCER OF THE STOMACH. By W. H. WELCH, M.D. . . . . . . . 480 CANCER OF THE STOMACH. By W. H. WELCH, M.D. . . . . . . . . . . 530 HEMORRHAGE FROM THE STOMACH. By W. H. WELCH, M.D. . . . . . . . 580 DILATATION OF THE STOMACH. By W. H. WELCH, M.D. . . . . . . . . 586 MINOR ORGANIC AFFECTIONS OF THE STOMACH (Cirrhosis; Hypertrophic Stenosis of Pylorus; Atrophy; Anomalies in the Form and the Position of the Stomach; Rupture; Gastromalacia). By W. H. WELCH, M.D. . . . . . . . . . . . . . . . . . . . . . . . . . 611 INTESTINAL INDIGESTION. By W. W. JOHNSTON, M.D. . . . . . . . . 620 CONSTIPATION. By W. W. JOHNSTON, M.D. . . . . . . . . . . . . . 638 ENTERALGIA (INTESTINAL COLIC). By W. W. JOHNSTON, M.D. . . . . . 658 ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS, COLITIS, PROCTITIS). By W. W. JOHNSTON, M.D. . . . . . . . . . 667 CHRONIC INTESTINAL CATARRH. By W. W. JOHNSTON, M.D. . . . . . . 699 CHOLERA MORBUS. By W. W. JOHNSTON, M.D. . . . . . . . . . . . . 719 INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER. By J. LEWIS SMITH, M.D. . . . . . . . . . . . . . . . . . . . . . . . . . 726 PSEUDO-MEMBRANOUS ENTERITIS. By PHILIP S. WALES, M.D. . . . . . 763 DYSENTERY. By JAMES T. WHITTAKER, A.M., M.D. . . . . . . . . . . 777 TYPHLITIS, PERITYPHLITIS, AND PARATYPHLITIS. By JAMES T. WHITTAKER, A.M., M.D. . . . . . . . . . . . . . . . . . . . . 814 INTESTINAL ULCER. By JAMES T. WHITTAKER, A.M., M.D. . . . . . . 823 HEMORRHAGE OF THE BOWELS. By JAMES T. WHITTAKER, A.M., M.D. . . 830 INTESTINAL OBSTRUCTION. By HUNTER MCGUIRE, M.D. . . . . . . . . 835 CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES. By I. EDMONSON ATKINSON, M.D. . . . . . . . . . . . . . . . . . . . 868 DISEASES OF THE RECTUM AND ANUS. By THOMAS G. MORTON, M.D., and HENRY M. WETHERILL, JR., M.D., PH.G. . . . . . . . . . . . . . 877 INTESTINAL WORMS. By JOSEPH LEIDY, M.D., LL.D. . . . . . . . . . 930 DISEASES OF THE LIVER. By ROBERTS BARTHOLOW, A.M., M.D., LL.D. . 965 DISEASES OF THE PANCREAS. By LOUIS STARR, M.D. . . . . . . . . . 1112 PERITONITIS. By ALONZO CLARK, M.D., LL.D. . . . . . . . . . . . 1132 DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA). By SAMUEL C. BUSEY, M.D. . . . . . . . . . . . . . . . . . . . . . . . . 1182 INDEX. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1195 CONTRIBUTORS TO VOLUME II. ARMOR, SAMUEL G., M.D., LL.D., Brooklyn. ATKINSON, I. EDMONDSON, M.D., Professor of Pathology and Clinical Medicine and Clinical Professor of Dermatology in the University of Maryland, Baltimore. BARTHOLOW, ROBERTS, A.M., M.D., LL.D., Professor of Materia Medica, General Therapeutics, and Hygiene in the Jefferson Medical College, Philadelphia. BUSEY, SAMUEL C., M.D., An Attending Physician and Chairman of the Board of Hospital Administration of the Children's Hospital, Washington, D.C. CLARK, ALONZO, M.D., LL.D., Late Professor of Pathology and Practical Medicine in the College of Physicians and Surgeons, New York. COHEN, J. SOLIS, M.D., Professor in Diseases of the Throat and Chest in the Philadelphia Polyclinic; Physician to the German Hospital, Philadelphia. DRAPER, W. H., M.D., Attending Physician to the New York and Roosevelt Hospitals, New York. HOWARD, R. PALMER, M.D., Professor of Theory and Practice of Medicine in McGill University, Montreal; Consulting Physician to Montreal General Hospital, Canada. JACOBI, ABRAHAM, M.D., Clinical Professor of Diseases of Children in the College of Physicians and Surgeons, New York, etc. JOHNSTON, W. W., M.D., Professor of Theory and Practice of Medicine in the Columbian University, Washington. LEIDY, JOSEPH, M.D., LL.D., Professor of Anatomy in the University of Pennsylvania, Philadelphia. LYNCH, JOHN S., M.D., Professor of Principles and Practice of Medicine in the College of Physicians and Surgeons, Baltimore. MORTON, THOMAS G., M.D., Surgeon to the Pennsylvania Hospital, Philadelphia. MCGUIRE, HUNTER, M.D., Richmond, Va. SMITH, J. LEWIS, M.D., Clinical Professor of Diseases of Children in the Bellevue Hospital Medical College, New York. STARR, LOUIS, M.D., Clinical Professor of Diseases of Children in the Hospital of the University of Pennsylvania, Philadelphia. TYSON, JAMES, A.M., M.D., Professor of General Pathology and Morbid Anatomy in the University of Pennsylvania, Philadelphia. WALES, PHILIP S., M.D., Washington. WELCH, WILLIAM H., M.D., Professor of Pathology in Johns Hopkins University, Baltimore. WETHERILL, HENRY M., JR., M.D., Assistant Physician to the Pennsylvania Hospital for the Insane, Philadelphia. WHITE, J. WILLIAM, M.D., Surgeon to the Philadelphia Hospital; Assistant Surgeon to the University Hospital; Demonstrator of Surgery and Lecturer on Venereal Diseases and Operative Surgery in the University of Pennsylvania, Philadelphia. WHITTAKER, JAMES T., M.D., Professor of Theory and Practice of Medicine in the Medical College of Ohio, Cincinnati. ILLUSTRATIONS TO VOLUME II. FIGURE PAGE 1. POSITION OF PUNCTURES IN DIABETIC AREA OF MEDULLA OBLONGATA NECESSARY TO PRODUCE GLYCOSURIA . . . . . . . . . . . . . . 195 2. THE LAST CERVICAL AND FIRST THORACIC GANGLIA, WITH CIRCLE OF VIEUSSENS, IN THE RABBIT, LEFT SIDE . . . . . . . . . . . . 196 3. DIAGRAM SHOWING COURSE OF THE VASO-MOTOR NERVES OF THE LIVER, ACCORDING TO CYON AND ALADOFF . . . . . . . . . . . . 197 4. DIAGRAM SHOWING ANOTHER COURSE WHICH THE VASO-MOTOR NERVES OF THE LIVER MAY TAKE . . . . . . . . . . . . . . . . . . . 197 5. JOHNSON'S PICRO-SACCHARIMETER . . . . . . . . . . . . . . . 214 6. PEMPHIGUS BULLA FROM A NEW-BORN SYPHILITIC CHILD . . . . . . 276 7. SECTION OF RETE MUCOSUM AND PAPILLAE FROM SAME CASE OF PEMPHIGUS AS FIG. 6 . . . . . . . . . . . . . . . . . . . . 276 8. SECTION OF AN OLD GUMMA OF THE LIVER . . . . . . . . . . . . 284 9. SYPHILITIC DACTYLITIS, FROM BUMSTEAD . . . . . . . . . . . . 292 10. THE SAME AS FIG. 9 . . . . . . . . . . . . . . . . . . . . . 292 11. SERRATIONS OF NORMAL INCISOR TEETH . . . . . . . . . . . . . 297 12. NOTCHING OF SYPHILITIC INCISOR TEETH . . . . . . . . . . . . 297 13. OIDIUM ALBICANS FROM THE MOUTH IN A CASE OF THRUSH . . . . . 331 14. CHRONIC INTUMESCENCE OF THE TONGUE (HARRIS) . . . . . . . . 351 15. HYPERTROPHY OF TONGUE (HARRIS), BEFORE OPERATION AND AFTER . 352 16. GLOSSITIS (LISTON) . . . . . . . . . . . . . . . . . . . . . 361 17. INCISION FOR A CUSPID TOOTH (WHITE) . . . . . . . . . . . . 378 18. INCISION FOR A MOLAR TOOTH (WHITE) . . . . . . . . . . . . . 378 19. FUSIFORM DILATATION OF OESOPHAGUS (LUSCHKA) . . . . . . . . 433 20. and 21. FAUCHER'S TUBE FOR WASHING OUT THE STOMACH . . . . . 605 22. ROSENTHAL'S METHOD OF WASHING OUT THE STOMACH . . . . . . . 606 23. ANTERIOR VIEW OF A STRANGLUATED INTESTINE AND STRICTURE . . 842 24. POSTERIOR VIEW OF A STRANGULATED INTESTINE AND STRICTURE . . 842 25. APPEARANCE OF THE NATURAL RELATIONS OF THE DIVERTICULUM TO THE INTESTINE . . . . . . . . . . . . . . . . . . . . . . . 843 26. SIMPLE INVAGINATION OF THE ILEUM . . . . . . . . . . . . . . 844 27. SIMPLE INVAGINATION, WITH OCCLUSION OF BOWEL, FROM INFLAMMATORY CHANGES . . . . . . . . . . . . . . . . . . . . 844 {17} GENERAL DISEASES (_CONTINUED_). FROM DERANGEMENTS OF THE NORMAL PROCESSES OF NUTRITION. RHEUMATISM. | PURPURA. | GOUT. | DIABETES MELLITUS. | RACHITIS. | SCROFULA. | SCURVY. | HEREDITARY SYPHILIS. {19} RHEUMATISM. BY R. P. HOWARD, M.D. Acute Articular Rheumatism. SYNONYMS AND DEFINITION.--Acute Rheumatism, Acute Rheumatic Polyarthritis, Rheumarthritis, Rheumatic Fever, Polyarthritis Synovialis Acuta (Heuter). Acute articular rheumatism is a general non-contagious, febrile affection, attended with multiple inflammations, pre-eminently of the large joints and very frequently of the heart, but also of many other organs; these inflammations observing no order in their invasion, succession, or localization, but when affecting the articulations tending to be temporary, erratic, and non-suppurating; when involving the internal organs proving more abiding, and often producing suppuration in serous membranes. It is probably connected with a diathesis--the arthritic--which may be inherited or acquired. It may present such modifications of its ordinary characters as to justify being called (2d) subacute articular rheumatism, and it may sometimes pass into the (3d) chronic form. ETIOLOGY.--There is a general consensus of opinion that acute articular rheumatism belongs especially to temperate climates, and that it is exceedingly rare in polar regions; but respecting its prevalence in the tropics contradictory statements are made. Saint-Vel declares that it is not a disease of hot climates; Rufz de Levison saw only four cases of acute articular rheumatism, and not one of chorea, in Martinique during twenty years' practice; while Pruner Bey says it is common in Egypt, and Webb remarks the same for the East Indies. Even in temperate climates, like those of the Isle of Wight, Guernsey, Cornwall, some parts of Belgium (Hirsch), the disease is very rare--a circumstance not to be satisfactorily explained at present. Acute articular rheumatism is never absent; it occurs at all seasons of the year, although subject to moderate variations depending mainly upon atmospheric conditions. It is the general opinion that it prevails most during the cold and variable months of spring, but this is not true of every place, nor invariably of the same place. Indeed, Besnier,[1] after a long and special observation of the disease in Paris, concludes that there it is most frequent in summer and in spring. In Montreal, during ten years, the largest number of cases of acute rheumatism admitted to the General Hospital obtained in the spring months (March to June {20} inclusive), when they averaged 51 a month; 33 was the average for all the other months, except October and November, when 26-1/2 was the average. The statistics of Copenhagen, Berlin, and Zurich show a minimum prevalence in summer or in summer and autumn. [Footnote 1: _Dictionnaire Encyclopedique des Sciences Med._, Troisieme Serie, t. iv.] Occupations involving muscular fatigue or exposure to sudden and extreme changes of temperature, especially during active bodily exertion, predispose to acute articular rheumatism; hence its frequency amongst cooks, maid-servants, washerwomen, smiths, coachmen, bakers, soldiers, sailors, and laborers generally. While no age is exempt from acute articular rheumatism, it is, par excellence, an affection of early adult life, the largest number of cases occurring between fifteen and twenty-five years of age, and the next probably between twenty-five and thirty-five. A marked decline in its frequency takes place after the age of thirty-five, and a still greater after forty-five. It is not uncommon in children between five and ten, and especially between ten and fifteen, but is very rare under five, although now and then one meets with an example of the disease in children three or four years of age. While the acute articular affections observed in sucklings are, as a general rule, either syphilitic or pyaemic, some authentic instances of rheumatic polyarthritis are recorded. Kauchfuss's two cases among 15,000 infants at the breast, Widerhofer's case, only twenty-three days old, Stager's, four weeks old, and others, are cited by Senator.[2] [Footnote 2: _Ziemssen's Cyclop. of Pract. Med._, xvi. 17.] An analysis of 4908 cases of acute rheumatism admitted to St. Bartholomew's Hospital, London,[3] during fifteen years, and of 456 treated in the Montreal General Hospital during ten years,[4] gives the following percentages at given periods of life: London. Montreal. Under 10 years, 1.79 % | Under 15 years, 4.38 % From 10 to 15 " , 8.1 % | From 15 to 25 " , 48.68 % " 15 to 25 " , 41.8 % | " 25 to 35 " , 25.87 % " 25 to 35 " , 24.5 % | " 35 to 45 " , 13.6 % " 35 to 45 " , 14.2 % | Above 45 " , 7.4 % Above 45 " , 9.5 % | The close correspondence existing in the two tables for all the periods of life above fifteen is very striking: the disparity between them below the age of fifteen may, I believe, be explained by the circumstance that the pauper population of Montreal is, when compared with that of London, relatively very small, and by the further fact that the practice of sending children into hospitals hardly obtains here. [Footnote 3: _St. Bartholomew's Hospital Reports_, xiv. 4.] [Footnote 4: Dr. James Bell, in _Montreal General Hospital Reports_, i. 350.] No doubt the above tables do not correctly represent the liability of children to acute articular rheumatism, but they are probably a fair statement of the relative frequency of the disease in the adult hospital populations of London and Montreal. If primary attacks of the disease only were tabulated, the influence of youth would be more evident, for it is scarcely possible to find on record an authentic instance of the disease showing itself for the first time after sixty. Dr. Pye-Smith[5] has done {21} this in 365 cases, and the results prove the great proclivity of very young persons to acute rheumatism: Between five and ten years, 6 per cent. occurred; between eleven and twenty, 49 per cent.; from twenty-one to thirty, 32.3 per cent.; from thirty-one to forty, 9.5 per cent.; from forty-one to fifty, 2.2 per cent.; and from fifty-one to sixty-one, 1.1 per cent. The same author has also shown that secondary attacks are most common in the young; so that advancing age not only renders a first attack of the disease improbable, but lessens the risk of a recurrence of it. The influence of age upon acute rheumatism is further shown in the fact that the disease is less severe, and less apt to invade the heart, in elderly than in young persons. [Footnote 5: _Guy's Hospital Reports_, 3d Series, xix. 317.] The general opinion that sex exercises no direct influence beyond exposing males more than females to some of the predisposing and exciting causes of acute rheumatism is perhaps true if the statement be confined to adults, to whom, indeed, most of the available statistics apply; but it should be borne in mind that a larger proportion of men than of women resort to hospitals, and there is some reason to believe that in childhood the greater liability to the disease is on the part of the female sex. Thus, the number of cases of rheumatism treated at the Children's Hospital in London from 1852 to 1868 was 478, of whom 226 were males and 252 females.[6] Of Goodhardt's 44 cases of acute rheumatism in children, 26 were girls and 18 were boys.[7] Of 57 examples of rheumatism in connection with chorea observed by Roger in children under fourteen, 33 were girls and 24 were boys.[8] [Footnote 6: Vide Dr. Tuckwell's "Contributions to the Pathology of Chorea," in _St. Bartholomew's Hospital Reports_, v. 102.] [Footnote 7: _Guy's Hospital Reports_, 3d Series, xxv. 106.] [Footnote 8: _Arch. Gen._, vol. ii. 641, 1866, and vol. i. 54, 1867, quoted by Tuckwell.] That heredity predisposes to acute articular rheumatism is admitted by nearly all modern authorities, even Senator, while speaking of it as "a traditional belief," not venturing to deny it. The frequency of the inherited predisposition Fuller placed at 34 per cent.; Beneke, quoted by Homolle,[9] at 34.6 per cent; Pye-Smith at 23 per cent.[10] Such predisposition favors the occurrence of the disease in early life, but does not necessarily determine an attack of acute rheumatism in the absence of the other predisposing or exciting causes. That the inherited bias or mode of vital action or condition of tissue-health may be so great as, per se, to induce an attack of the disease, is held by some authorities. It is probable that not only acute articular rheumatism in the parents, but simple chronic articular rheumatism and those forms grouped under the epithet rheumatoid arthritis, may impart a predisposition to the acute as well as to the chronic varieties of articular disease just mentioned. But owing to the obscurity which still surrounds the relations existing between acute articular rheumatism and rheumatoid arthritis this point needs further investigation. In what the inherited predisposition to acute articular rheumatism consists we are ignorant; to say that it imparts to the tissues or organs a disposition to react or act according to a fixed morbid type, or that some of the nutritive processes are perverted by it, is merely to state a theory, not to explain the nature of the predisposition. [Footnote 9: _Nouv. Dict. de Med. et de Chir._, t. 31, 557.] [Footnote 10: _Guy's Hospital Reports_, 3d Series, xix. 320.] No type of bodily conformation or temperament can be described that {22} certainly indicates a proclivity to acute articular rheumatism; nor is there any change in the constitution of the tissues or fluids of the body by which the proclivity may be recognized. We infer the existence of the inherited predisposition--the innate bias--when rheumatism is found in the family history; when acute rheumatism or cardiac disease, or chorea not produced by mental causes, occurs in childhood; when the first attack of acute articular rheumatism is succeeded by subsequent attacks; and especially when the intervals between the attacks are short. Goodhardt has recently furnished valuable, but not conclusive, evidence to prove that in children obstinate headaches, night-terrors, severe anaemia, various neuro-muscular derangements, such as torticollis, tetany, muscular tremors, stammering, incontinence of urine, recurring attacks of abdominal pain, with looseness of the bowels quickly succeeding a meal, the cutaneous affection erythema nodosum, are indications of a rheumatic bias or predisposition.[11] [Footnote 11: _Guy's Hospital Reports_, 3d Series, xxv.] There is some basis for the opinion that residence in damp, cold dwellings predisposes somewhat to acute articular rheumatism, although not at all to the same degree that it does to the chronic articular and muscular forms. Chomel and Jaccoud especially have insisted that it will gradually create a predisposition to the disease, even if it has not been inherited. All pathologists agree that cold is the most frequent exciting cause of acute articular rheumatism, and that it is especially effective when applied while the body is perspiring freely or is overheated or fatigued by exercise. There is no necessary ratio between the degree of cold or its duration and the severity of the resulting rheumatism. A slight chilling or a momentary exposure to a current of cold air will in some act as powerfully and as certainly as a prolonged immersion in cold water or a night spent sleeping on the damp grass. This circumstance, together with the fact that cold applied in the same way may also produce a pharyngitis or a bronchitis, a pneumonia or a nephritis, etc., is held to indicate that the cold acts according to individual predisposition; and Jaccoud, Flint, and others maintain that unless a rheumatic proclivity exists cold will not produce an attack of the disease under consideration. I doubt that we are yet in a position to assert that absolutely, although the weight of argument is in its favor. Let it suffice to say, that while a prolonged residence in a cold, damp dwelling may gradually develop a predisposition to rheumatism, a short exposure to cold will be likely to induce an attack of rheumatism if the predisposition exist. There are other influences which may be regarded as auxiliaries to cold in exciting an attack, as they seem to increase the susceptibility of the patient to its operation: they establish what has been felicitously called a state of morbid opportunity. Such are all influences that reduce the resisting powers of the organs and organism, as bodily fatigue, mental exhaustion, the depressing passions, excessive venery, prolonged lactation, losses of blood, etc. It is probably in such a manner that local injuries (traumatism) sometimes appear to induce an attack of rheumatism. A blow on a finger (Cotain), the extraction of a tooth (Homolle), a hypodermic injection (ibid.), etc., may act powerfully in some persons upon and through the nervous system, and by lessening their resisting power {23} may favor the overt manifestation of the rheumatic predisposition. But doubtless some such cases have been examples of mere coincidence. There are certain pathological and even physiological conditions during or after which an inflammatory affection of one or several joints closely resembling acute articular rheumatism more or less frequently arises. Thus, during the early desquamating stage of scarlatina a mild inflammation of the joints of the hands and feet, and frequently of the large articulations as well, is very often seen, and it is attended with profuse perspiration, with a condition of urine like that of ordinary acute rheumatism, and occasionally with inflammation of the heart or pleura. During convalescence from dysentery an affection of a single or of several articulations resembling rheumatism has been noticed, and the two affections have even alternated in the same patient. That singular epidemic disease dengue is attended with a polyarticular affection closely resembling acute articular rheumatism, occasionally pursuing a protracted course, and not seldom leaving after it a cardiac lesion. In haemophilia polyarticular and muscular disorders frequently arise which closely resemble, and appear to be sometimes identical with, ordinary acute articular and muscular rheumatism. Gonorrhoea too is often associated with a febrile polyarthritis, and rarely with an endocarditis at the same time. In the puerperal state an inflammation of one or several articulations is not unfrequently observed (puerperal rheumatism). Respecting the real nature of these polyarticular inflammations very much has to be made out; and it must suffice at present to say that while many of them are of a pyaemic nature, as some examples of puerperal and scarlatinal arthritis, in which pus forms in or about the joints and in the serous cavities and viscera, some of them are no doubt examples of genuine rheumatism occurring in persons of rheumatic predisposition, which have either been induced by the lowering influence of the disease upon which they have supervened, or by the accidental coincidence of some of the other causes of acute rheumatism. There remains, however, the ordinary form of scarlatinal arthritis, which so closely resembles true acute articular rheumatism in its symptoms, course, visceral complications, and morbid anatomy that it cannot be said that the two affections are distinct and different. And much the same appears to be true of the articular affection of dengue. Yet so frequently does the articular affection accompany scarlatina and dengue respectively that it cannot logically be referred to a coexisting rheumatic predisposition, and must be a consequence of the disturbing influences of the specific poison of those zymotic affections per se. PATHOLOGY.--The pathology of acute articular rheumatism is a very much debated question, and is not at all satisfactorily known. Hence a mere statement of the most prominent theories now held by different pathologists will be given.[12] [Footnote 12: The reader may consult with advantage Dr. Morris Longstreth's fourth chapter in his recent excellent monograph upon _Rheumatism, Gout, and some Allied Disorders_, New York, 1882.] The latest modification of the lactic-acid theory of Prout is founded upon the modern physiological teaching that during muscular exercise sarcolactic acid and acid phosphate of potassium are formed, and carbon dioxide set free, in the muscular tissue, and that cold, acting on {24} the surface under such circumstances, may check the elimination of these substances and cause their accumulation in the system. This view, it is held, explains why the muscles and their associated organs, the joints and tendons, suffer first and chiefly, because the morbific influence is exerted upon them when exhausted by functional activity; and it further accounts for the visceral manifestations and the apparent excess of acid eliminated during the course of the disease. The circumstance that in three cases of diabetes (Foster,[13] Kuelz[14]) the administration of lactic acid appeared to induce polyarticular rheumatism favors the idea that acid is the materies morbi in rheumatism. [Footnote 13: _Brit. Med, Jour._, ii. 1871.] [Footnote 14: _Beitrage zur Path. und Therapie des Diabetes_, u. s. w., ii. 1875.] Now it must be admitted that, as yet, no sufficient proof is forthcoming that a considerable excess of lactic acid exists in the fluids or solids of the body or in the excretions in rheumatism (it is true the point has not been sufficiently investigated). On the other hand, that acid has been found in the urine of rickets, and its excess in the system is regarded by Heitzmann and Senator[15] as the cause of the peculiar osteoplastic disturbances of that disease--an affection altogether different from rheumatism. It is quite improbable that the amount of sarcolactic acid produced by over-prolonged muscular exertion, and whose elimination has been prevented by a chill or a mental emotion, is sufficient to maintain the excessive acidity of the urine and other fluids during a long rheumatic fever; and arguments can be adduced favorable to the view that excessive formation of acid is an effect rather than the cause of rheumatism: cases of that disease occur in which neither excessive muscular exertion nor exposure to chill have preceded the rheumatic outbreak. Lastly, lactic acid is not the only principle retained when the functions of the skin are arrested by cold, the usual exciting cause of rheumatism; why should not the retained acetic, formic, butyric, and other acids, for example, play their role in the production of the symptoms observed under such conditions? [Footnote 15: _Ziemssen's Cyclop._, xvi. p. 177.] The same objections apply to Latham's[16] hypothesis that hyperoxidation of the muscular tissue is the starting-point of acute rheumatism. He assumes, with other physiologists, the existence of a nervous centre which inhibits the chemical changes that would take place if the tissues were out of the body. If this centre be changed or weakened, the muscle, instead of absorbing and fixing the oxygen and giving out carbonic acid, disintegrates; lactic acid is formed, and, passing into the blood, may be there oxidized and produce the pyrexia of acute rheumatism. It need hardly be remarked that the existence of a chemical inhibitory centre has yet to be proved, although much may be advanced in its favor; and, secondly, the recent investigations of Zuntz render it highly probable that in all febrile affections it is the muscles chiefly, if not solely, which suffer increased oxidation, and that this is due to increased innervation--views not easily reconciled with Latham's theory. [Footnote 16: _Brit. Med. Jour._, ii. 1880, p. 977.] The nervous theory of rheumatism and of articular diseases originated with Dr. J. K. Mitchell of Philadelphia[17] in 1831, and was afterward elaborated by Froriep in 1843,[18] Scott Alison[19] in 1846, Constatt in 1847,[20] {25} Gull in 1858, Weir Mitchell in 1864,[21] Charcot in 1872, and by very many others since. According to present physiological doctrine, the exciting cause of rheumatism, cold, either acts directly upon the vaso-motor or the trophic (?) nerves of the articulations, and excites inflammation of them, or else it irritates the peripheral ends of the centripetal nerves, and through these excites actively the vaso-motor and trophic nerve-centres. The local lesions, on this hypothesis, are of trophic origin; the fever is due to hyperactivity of the centres supposed to control the chemical changes going on in the tissues; the excessive perspiration to stimulation of the sweat-centres; and so on. It is not held that a definite centric lesion of the nervous system exists in rheumatism, analogous to the lesions which in myelitis or locomotor ataxia develop the arthropathies of those affections, but rather a functional disturbance. One of the latest and ablest advocates of the neurosal theory of rheumatism in all its forms (simple, rheumatoid, gonorrhoeal, urethral, etc.), Jonathan Hutchinson, calls it "a catarrhal neurosis, the exposure of some tract of skin or mucous membrane to cold or irritation acting as the incident excitor influence."[22] [Footnote 17: _Am. Jour. Med. Sci._, 1831; _ib._, 1833.] [Footnote 18: _Die Rheumatische Schwiele_, Weimar, 1843.] [Footnote 19: _Lancet_, 1846, i. 227.] [Footnote 20: _Spec. Pathologie und Therapie_, 1847, ii. p. 609.] [Footnote 21: Vide _Am. Jour. Med. Sciences_, April, 1875, vol. lxix. 339-348.] [Footnote 22: _Trans. International Med. Congress_, 1881, ii. 93.] In order that peripheral irritation shall thus induce inflammation of the joints and the other affections of muscles, tendons, fasciae, etc. which are called rheumatic, he holds with the French School that the arthritic diathesis must exist, or that state of tissue-health which involves a tendency to temporary inflammation of many joints or fibrous structures at once, or to repeatedly recurrent attacks of inflammation of one joint or fibrous structure. If I understand Mr. Hutchinson correctly, he also holds that a nerve-tissue peculiarity exists which renders persons liable to rheumatism. He does not indicate either the cause or the nature of the nerve-tissue peculiarity. But modern pathology teaches that the functional conditions of the nervous centres known as neuroses, whether inherited or acquired, reveal themselves as morbid manifestations of nerve-function on the part of special portions of or the entire nervous system, and, as Dr. Dyce Duckworth has well pointed out, these neuroses may be originated, when not inherited, in various ways, as by excessive activity of the nervous system, by prolonged or habitual excesses, etc. "Thus, undue mental labor, gluttony, alcoholic intemperance, debauchery, and other indulged evil propensities in the parent come to be developed into definite neurotic taint and tendency in the offspring." But is there nothing more in acute articular rheumatism than an inflammation of certain structures, articular and visceral, lighted up in an individual of a neuro-arthritic diathesis? What do we learn from that closely-allied affection, gout, which involves especially the same organs as rheumatism, and is held by many of the ablest pathologists to belong to the same basic diathesis as it? Duckworth[23] has very ably advocated a neurotic theory of gout, but it is admitted on all hands--and by Duckworth himself--that in gout a large part of the phenomena is due to perverted relations of uric acid and sodium and to the presence of urate of soda in the blood. May we not from analogy, as well as from other evidence, infer that in that so-called other neurosis, rheumatism, a considerable part of the phenomena is due to perversions of {26} the processes of assimilation and excretion, and to the presence of some unknown intermediate product of destructive metamorphosis--lactic or other acid? This is admitted by Maclagan and strongly advocated by Senator; and in this way the pathology of the disease may be said to embrace the humoral as well as the solidist doctrines--the resulting theory being a neuro-humoral one. No doubt pathological chemistry and clinical investigation will ere long make important discoveries respecting the pathology of acute rheumatism which shall maintain the close alliance believed to exist between that affection and gout. [Footnote 23: _Brain_, April, 1880.] The miasmatic theory, so ably advocated by Maclagan,[24] assumes that rheumatism is due to the entrance into the system from without of a miasm closely allied to, but quite distinct from, malaria. His argument on this topic is ingenious and elaborate, yet has not been favorably received by pathologists. Opposed to it are the following amongst other considerations: Heredity exercises a marked influence upon the occurrence of rheumatism; unlike malarial disease, no climate or locality is immune from rheumatism; the many indications that a diathesis plays a chief role in rheumatism; the remarkable influence exerted by cold and dampness in the etiology of the disease. [Footnote 24: _Rheumatism: its Nature, Path., etc._, London, 1881, pp. 60-95.] Heuter's[25] infective-germ theory, like the miasmatic, refers rheumatism to a principle not generated in the system, but introduced from without. A micrococcus enters the dilated orifices of the sweat-glands, and, reaching the blood, first sets up an endocarditis, and then capillary emboli produce the articular inflammations. This is a reversal of what really happens, so far as the time of invasion of the endocardium and the synovial membranes is concerned; and Fleischauer's case, in which miliary abscesses were found in the heart, lungs, and kidneys, was probably one of ulcerative endocarditis, which, after all, is a rare complication of acute articular rheumatism. Moreover, it is a gratuitous assertion to say that endocarditis exists in all cases of the disease. If, however, Heuter were content to say that acute articular rheumatism was produced by a specific germ, as held by Recklinghausen and Klebs, which on entering the system acted specially upon the joints and the fibro-serous tissues, as the poison of small-pox does upon the skin, while at the same time it sets up general disturbances of the entire economy as other zymotic poisons do, there would be nothing opposed to general pathological laws. Even the existence of a diathesis capable of favoring the action of the specific germ would be analogous to the tuberculous diathesis, which favors the action of the bacillus of tubercle; and cold, its ordinary exciting cause, might be regarded simply as a condition which renders the system more susceptible to the action of the germ, and the modus operandi of cold in doing this might be variously explained. [Footnote 25: _Klinik der Gelenkkrankheiten_, Leipzig, 1871.] SYMPTOMS.--The disease has no uniform mode of invasion. (_a_) Very frequently slight disorder of health, such as debility, pallor, failure of appetite, unusual sensibility to atmospheric changes, grumbling pains in the joints or limbs, or even in some muscle or fascia, precedes by one or more days the fever and general disturbance. (_b_) Not infrequently a mild rigor or repeated chilliness, accompanied or soon followed by moderate or high fever, ushers in the illness, and in from a few hours to one {27} or at most two days the characteristic articular symptoms ensue. (_c_) In very rare cases febrile disturbance, ushered in by chills, may be followed by inflammation of the endo- or pericardium or pleura before the joints become affected. Whatever the mode of invasion, the symptoms of the established disease are well defined, and marked febrile disturbance, transient inflammation of several of the larger articulations, excessive activity of the cutaneous functions, and a great proclivity to inflammation of the endo- and pericardium constitute the stereotyped features of the disease. As a very general rule, the temperature early in the disease promptly attains its maximum of 102 degrees F. to 104 degrees F., yet the surface does not feel very hot; the pulse ranges from 90 to 100 or 110, and is regular, large, and often bounding; the tongue is moist, but thickly coated with a white fur; there are marked thirst, impaired appetite, and constipation; the stools are usually dark; the urine scanty, high , 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 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.