Other symptoms of the disease, too, this theory not only does not explain, but does not even take cognizance of. In advancing a theory of the causation of acute rheumatism, we have to account, not only for the occurrence of the joint pains, the febrile disturbance, and the acid sweats, but for the occurrence of the symptoms which precede these special and characteristic manifestations of the fully developed. disease ; and precede even the evidence of the existence of an excess of lactic acid. A case of acute rheumatism does not leap at once in medics yes. The characteristic symptoms of the disease are preceded often for two, three, or more days by shivering, malaise, and a sense of weakness accompanied by aching of the limbs. These initial symp toms are as much a part of the ailment as the joint pains which they usher in, and have equally to be accounted for. This the lactic acid theory does not even attempt to do.
But while we reject the view which regards lactic acid as the cause of rheumatic fever, as the morbific agency which originates the disease, we are far from regarding that acid as without action, and as having no share in the production of the phenomena of a rheu matic attack. An excess in the blood of any product of retrograde
tissue metamorphosis could scarcely be without some action. And there can be no reasonable doubt that the profuse perspirations which form a characteristic feature of the disease are mainly clue to the stimulant action on the skin of the excess of lactic acid in the blood. It is probable, too, that should formation exceed elimination, the resulting excess of acid would tend to exaggerate the already existing disturbance of the fibrous tissues, and so aggravate the pains and general symptoms of the malady.
We shall by and by see that there is reason to suppose that cases in which the fibrous tissues have been weakened and rendered irri table by frequently repeated rheumatic attacks may have their con valescence retarded and the ailment prolonged by the action of the acid on the altered fibrous tissues. Such cases may be placed in the same category as that related by Dr. Foster. They tend to show that the presence of an excess of lactic acid in the blood has a dis turbing action on the fibrous tissues ; but they do not show that that acid is the rheumatic poison.