But potent as cold is in precipitating or aggravating an attack, it cannot be looked on as the sole or essential cause of rheumatism. The great majority exposed to the cold escape. The animal which has stood in the stall, or shed, is less likely to be attacked than the one at work in which the heat production has been more active. Indeed an immunity has been claimed for the Arctic regions, provided the subject is not exerted so as to cause perspiration. One might readily conclude that this apparent immunity, depended on the absence of an essential germ, as is also claimed for catarrhs, yet Nansen after his prolonged bath in the frigid waters seems to have had an attack of rheumatism. Cold appears to be one of the most potent accessory causes, but evidently not in itself the essential cause.
Cold undoubtedly affects profoundly the metabolism of the body and especially when the vital powers have been reduced by severe exertion, fatigue and perspiration. The same applies to many other affections especially such as are associated with an infecting element, which takes occasion of the debility caused by the cold to establish itself in the tissues.
Lactic acid and other metabolic products. Prout long ago claimed that rheumatism was caused by an excess of lactic acid in the system, and this was supported by the fact that an exclusive diet of buttermilk given in diabetes, is likely to produce acute articular rheumatism. Again the production of rachitis in the young can be traced in certain cases to excess of this acid. The strongly acid odor of the sweat in certain rheumatic attacks is thought to support this theory. The excess of lactic acid is variously explained by the overwork of the muscles of which it is the normal product, and by the imperfect oxidation of the muscular tissue and its product into lactic acid (C3H4O(OH)2), instead of carbonic acid (CO(OH)2). But in spite of the perfect theory, there is the fact that as a rule no special increase of lactic acid can be found in blood or urine in acute rheumatism and the improbability that an excess of this acid caused by sudden excessive muscular waste could be kept up during a long attack of acute much less of chronic rheumatism. Again the comparative immunity of sucklings in which there is the greatest opportunity for the production of lactic acid, would imply that that alone cannot be accepted, as the one essential cause of the affection. That its excess in the system will aggravate rheumatism, or even produce it under favorable circumstances must be freely acknowledged; also that acidity of the saliva is a marked feature of rheumatism.
The acid phosphate of soda may be assigned a somewhat similar rôle. In strongly predisposed subjects the ingestion of citric or other organic acid will sometimes precipitate rheumatic articular pains.
Still other products, the result of imperfect oxidation or metabolism must be allowed a place as probable factors in rheumatism. The occurrence of gout in connection with the excess of uric acid in the system is strongly suggestive of this, and the frequency of muscular rheumatism in pampered, overfed dogs with diseased livers and abnormal hepatic products, seems to give further support. Even in man, the subject of acute rheumatism, often leads a luxurious life and suffers from inactive or disordered liver, while in man and animals alike, a low grade of health and imperfect functional activity of important organs, are often precursors and accompaniments of acute rheumatism.
Neuropathic theory. The doctrine of a neurotic cause originated by Dr. Mitchell, of Philadelphia, has considerable basis in theory. The primary chill tends to nervous derangement, which may readily affect the overworked or already diseased and debilitated joints. Similar peripheric disturbance of nutrition occurs in locomotor ataxia in which the central nervous lesion is very evident. There is a strong disposition in rheumatism to show a bilateral symmetry, which points directly to a central nervous control. The frequent violence of the pain, disproportionate to the moderate structural changes, points in the same direction, and the free perspiration present in some severe attacks, points alike to its origin in cutaneous chill and to derangement of the centres presiding over perspiration. It may be added that the development of rheumatic symptoms in the advanced stages of infectious diseases, when the toxins are accumulating in the system, suggests that they are the direct result of a toxic action on the nerve centres. In man the influence of severe nervous shock in developing and maintaining rheumatism is recognized.
Theory of infection. This has been advocated by Cornil and Babes and Friedberger and Fröhner. The former quote the frequent presence of microörganisms and above all of micrococci in the liquids of the affected joints, serosæ and valvular exudates and ulcers, and even in the blood, and the occurrence of rheumatism in the course of various septic affections. The latter quote Auer and others as to the frequent supervention of articular rheumatism on the retention of the afterbirth in the cow. The weak point in these theories is the multiplicity and variety of the microbes found in the exudates. Either we must accept the rheumatic lesions as an occasional result of many microbes, which habitually act differently on the system, or we must look upon them as mere accessory causes or accidental complications. It might even be, that the invasion of these microbes are made possible by the inflammation and debility of the tissues, without being directly chargeable with the rheumatic process. Even then there remains the possibility that a specific microbe is present, which by reason of its infinitesimal size, or other physical property, has as yet escaped recognition. If such specific microbe is present, it manifestly requires a very special predisposition, since it is not seen to advance from one individual to another unless such favoring conditions are present. The symptoms and lesions of rheumatism are not incompatible with the idea of such an essential, specific germ, but as yet no such germ has been satisfactorily demonstrated as present in all cases.
Local injuries. Rheumatism seems to attack by preference parts that have already been debilitated by disease, a disposition which is also true of distinctly microbian infections. A pre-existing sprain, blow, bruise or an inflammation arising from any other cause seems to practically invite the localization of the morbid process at that point, and thus what was at first a purely traumatic lesion becomes the seat of active and perhaps permanent rheumatism. Unusual overwork and fatigue of given joints and muscles induce a similar predisposition, and habitual overexertion, sprain, injury or inflammation affecting repeatedly the rheumatic organ tends to fix the process in chronic form.
Articular lesions. These tend to concentrate as a form of inflammation in the synovial membranes, but usually implicate all the constituent structures of the joint, capsular and binding ligaments, cartilage and fibro-cartilage, articular lamella and osseous tissue. The synovial membrane may show only slight hyperæmia, or in severe cases it may be congested, red, thickened or even extensively infiltrated with a serogelatinoid liquid. These lesions are most marked around the line of attachment on the articular surface and in the synovial fringes. The synovia is usually in excess, distending the capsule and is whitish, opaque, flocculent or more or less deeply colored with red. It contains flakes of fibrine, leucocytes, albumen and it may be red blood globules. Pus cells are usually absent unless in distinctly infective cases. Coagula and false membranes floating from or adherent to the solid tissues, may be present in considerable amount and if these become organized they tend to lay the foundation for future stiffening and rigidity. In and beneath the serosa, cell proliferation may go on actively, especially in the synovial fringes. The synovia is usually neutral or slightly alkaline, though in rare instances it has proved to be acid.
The inflammation of the synovial membrane of the joint often extends to those of the adjacent tendons, implicating at the same time the tendons and their fibrous sheaths. Softening and rupture of the tendons have been noted by different observers (perforans, Oger; gastrocnemii, Trasbot; suspensory ligament, Olivier).