When considering the lactic-acid theory, we saw that one of the most common and constant effects of the internal administration of that acid was increased action of the skin. The dry and branny skin of diabetes becomes under its influence moist and perspiring. If such be the effect of a comparatively small quantity given by the mouth in a disease in which there is great difficulty in getting the skin to act at all, what is likely to be the effect of its formation in large quantity in the system during the course of a malady in which there is no difficulty in getting the skin to act ? Clearly, profuse perspiration. That lactic acid is formed in very large quantity in the course of acute rheumatism is evidenced by the quantity elimi nated by the skin. Normally it is converted in the system into carbonic acid and water, and in that form is thrown off by the lungs and skin. The elimination of the unchanged acid indicates that there has been formed a larger quantity than can be so converted.
The profuse perspirations of acute rheumatism are due, not to an effort of nature to eliminate the rheumatic poison, but to the stimu lant action on the skin of the excess of lactic acid formed during the increased metamorphosis of muscle. These perspirations are to be regarded as neither prejudicial nor beneficial, but as simply one of the essential symptoms of the disease during whose course they occur. They occupy in its symptomatology the same position as increased elimination of urea and bear to the local lesion of rheumatic fever the same relation. The excess of acid is the result of increased meta morphosis of the non-nitrogenous, the excess of urea the result of increased metamorphosis of the nitrogenous elements of muscle.
8. The Shifting Character of t1w Joint Affection.—This is one of the most striking peculiarities of a rheumatic attack. In the history of all forms of the disease, acute, subacute, and chronic, it occupies a prominent place ; and no theory of rheumatism can be regarded as satisfactory which does not recognize and account for it.
It is impossible to explain it on any theory which recognizes only the existence of a poison equally distributed through the blood, act ing like an ordinary medicinal or poisonous agency, and acting, there fore, equally and continuously so long as it exists in adequate quantity; the action of such a poison would be continuous and persistent, not shifting and variable.
The miasmatic theory which regards the rheumatic poison as a parasitic organism requiring for its development and action a second factor or nidus which is localized in fibrous and serous tissues, which exists in varying amount in different parts of these tissues, and which, like the nidus of ordinary malarial fevers, may be exhausted and renewed again, satisfactorily explains this peculiarity of the local lesion of acute rheumatism. Exhaustion of the nidus implies decline of inflammation, its renewal a re-accession to it. Its exhaustion in one joint may coincide in point of time with its renewal in another. In that case the decline of the inflammation in the one will coincide with its onset in the other. In this we have the explanation of the apparent occurrence of metatasis. The inflammation seems to leave one joint and go to another; in reality it is a mere coincidence. The decline of the inflammation in the one has nothing to do with its ap pearance in the other; by mere accident the second factor is ex hausted in the one at the same time that it is renewed in the other. With so many joints liable to disturbance such a coincidence could scarcely fail to occur. Occasionally the metatasis seems to be to the heart; but here too it is a coincidence, for in its tendency to become the seat of rheumatic inflammation the heart is in the same position as a joint.