The advocates of the lactic-acid theory of rheumatism have taken one of the phenomena of the disease, and have raised it from its nor mal and subordinate position of a symptom, to the rank and dignity of an exciting cause. In so doing they have necessarily fallen into error. Excess of acid may cause joint pains, but what causes the excess of acid? That has to be explained, no less than the phenom ena which combine with it to form the symptoms of acute rheumatism.
And herein we see the inadequacy of Dr. Foster's observations to throw light on the ultimate pathology of the disease; and the short sightedness of the view which regards them as doing so. In his cases the lactic acid was given to the patient, and its presence in excess was readily accounted for. In acute rheumatism the excess of lactic acid is the phenomenon which, of all others, it is at once most essen tial and most difficult to explain. If the first requisite to the pro duction of rheumatism be an excess of lactic acid, the first requisite to a satisfactory theory of rheumatism is that it should account for this excess. An attempt to do so has been made by some of the ad vocates of the lactic-acid theory, notably by Corrigan and Senator. Lactic acid, they say, is formed during muscular exercise. Under ordinary circumstances it is partly oxidized and got rid of as carbonic. acid and water; partly, when there is a great deal of it, excreted Un altered in the sweat. Should the cutaneous surface be chilled, the elimination of the acid will be checked, and it will accumulate in the system.
That chilling of the surface when heated by exercise may be fol lowed by a rheumatic attack there is no doubt. But to be heated by exercise is so common at the age at which acute rheumatism chiefly occurs, and to he exposed to cold so common in the climate in which it most prevails, that great allowance has to be made for the elements -of chance and accidental coincidence. But making allowance for these, there can be no doubt that overheating and subsequent ex posure to cold, and even such exposure without previous overheating, do in some cases seem to determine a rheumatic attack. But it does not follow that the determining agent is the checking of the action of the skin. Overheating and subsequent chilling are not the only effects of exercise and subsequent exposure ; they are not even the most common. A more constant and more important one is exhaus tion, and the probable explanation of the connection -which obtains between the exercise and the rheumatism is that the exhaustion con sequent on the exercise renders the system more susceptible to the action of the rheumatic poison. The depressing influence of cold by
lowering the whole vitality would lead to the same result.
A greater liability to the action of certain morbific agencies, when the system is exhausted or depressed from any cause, has been noted in connection with many diseases. Referring to malarial fevers, with which, as we shall by and by see, rheumatic fever has many analogies, Niemeyer says : " Exhausting exercises and other debilitating in flu ences, errors of diet, and particularly catching cold, increase the pre disposition so much, that persons who have long been exposed to malaria with impunity are not affected by it till one of these causes has acted on them." In the case of acute rheumatism it is not so much the exercise as the exhaustion which follows it; it is not so much the chilling of the surface as the depressing action of the cold on the system which are the disturbing agencies. They do not themselves produce the dis ease, but they render the system more liable to the action of the rheu matic poison.
There are other cogent reasons for rejecting the view that chill ing of the surface plays the part attributed to it in the production of acute rheumatism. In the first place, it is to be noted that chilling of the surface when heated by exercise is frequently had recourse to with impunity, if not with actual benefit. Then again, if we regard sudden chilling of the surface as a danger, and as a cause of acute rheumatism, how are we to explain the beneficial action of the cold bath in the hyperpyrexia of malignant cases of that disease? Here we have the malady presenting itself in the most distinct form, lactic acid is being freely thrown off by the skin, the patient is in imminent danger, and yet the only thing which does him good—the only thing which seems to give him a chance of recovering—is to apply cold to the surface, thereby not only lowering the temperature, but checking also the action of the skin. The same agency which is blamed for causing the patient's illness is applied in a more decided manner to get him out of it, and is really the only reliable means of attaining. this end.