Rheumatic hyperpyrexia might be merely an exaggeration of the ordinary pyrexia of rheumatic fever; or it might result from a direct paralyzing action of the rheumatic poison on the heat-inhibiting cen tre; or it might be produced in the same way as heat apoplexy by over-stimulation and consequent paresis of that centre.
The first hypothesis is scarcely adequate, for were the hyper pyrexia of rheumatic fever merely an exaggeration of the ordinary pyrexia of the disease, cases in which it occurs would be characterized by inordinate severity of the rheumatic symptoms. But such is not the case. ' In cases which become hyperpyretic the disease up to the onset of the hyperpyrexia may present no unusual features. The temperature, the joint pains, the acid sweats, the heart complications, may all be such as are met with daily in ordinary rheumatic attacks; and there may be nothing in their symptoms to lead the physician to anticipate so alarming a complication.
The hypothesis that it may result from paralysis of the heat inhibiting centre consequent on the direct toxic action on that centre of the rheumatic poison, or some product of the rheumatic process, is one regarding which no more can be said than that it is possible. Against it may be adduced the argument that were such the mode of production of rheumatic hyperpyrexia, that condition would arise more frequently than it does. The rheumatic poison and the pro ducts of the rheumatic process operate in every case, but, hyper pyrexia is of rare occurrence. Then again hyperpyrexia occurs in other fevers and other morbid states in which the rheumatic poison does not operate.
The third hypothesis is oue for which more may be said, for be tween heat apoplexy and rheumatic hyperpyrexia there are many points of analogy. The symptoms and clinical features of both are very much alike, and the description of the post-mortem appearances observed in the one serves equally to describe those noted in the other. Treatment, too, is the same in both. The main difference between them is in the circumstances which lead up to their occur rence. With so many points of resemblance between them we cannot but look for a common mode of production, some common pathologi cal bond. The question for consideration is the possibility of the rheumatic process, as it exists in acute rheumatism, producing the same results as we find follow exposure to great heat. The latter
acts by over-stimulating, fatiguing, and finally paralyzing the thermic inhibitory centre. The question before us, therefore, narrows itself into a consideration of the point as to whether or not over-stimula tion and consequent fatigue of the heat-inhibiting centre is a possible result of the process of acute rheumatism. Wide as is the difference between that process and great heat, and great as seems the improb ability of two such different agencies producing the same effect on the system, a careful consideration of the facts, nevertheless, leads to the conclusion that such a result is not impossible. Certain it is that if overstimulation and fatigue of the heat-inhibiting centre, and consequent impairment of heat-inhibition, could be a result of any fever, rheumatic fever is the one in which it would most likely occur, and that for the following reasons : In all fevers the rise of temperature results from increased tissue metamorphosis. This is the case in rheumatic fever, as it is in typhus, typhoid, and other fevers. But the circumstances under which that increased metabolism takes place in rheumatic fever are altogether peculiar, and the peculiarity of these circumstances it is which leads up to the phenomenon which we are now considering— the greater tendency to the occurrence of hyperpyrexia,.
Rheumatism is essentially a disease of the motor apparatus of the body. Part of this motor apparatus—the muscles—is the chief seat of heat production. The more active the metabolism of the muscles the greater the amount of potential energy produced. This potential energy may take the form of work or heat. As a matter of fact, it generally assumes the form of work, for it is when mus cles are actively contracting that this potential energy is chiefly formed. But if the same metabolic changes which take place in a contracting muscle were to take place in that muscle when quies cent, the potential energy would take the form, not of work but of heat. This is what occurs in acute rheumatism. The rheumatic poison causes general febrile disturbance accompanied by inflamma tion of the muscles and fibrous textures of the large joints. Inflam mation of these textures is of course accompanied by increased flow of blood to, and increased metamorphosis in them.