That such increased metabolism as occurs in muscle during work occurs also during the course of rheumatic fever is demonstrated by one of the essential phenomena of that disease, increased formation of lactic acid; and the very large extent to which this acid is formed is indicative of the very large increase of the muscle metabolism to which it owes its formation. Rheumatic fever is the only form of fever in which this occurs, because it is the only one whose poison finds its nidus in muscle. The propagation of this poison in muscle gives rise there to the same increased metabolism which would result from natural stimulation.
Muscle being the chief seat of the formation of heat, and the meta bolism of muscle being the chief source of heat, it follows that the disease in which such metabolism is most active is also that in which most heat will be formed. That disease is acute rheumatisM. Theo retically, there is thus reason to believe that heat-production is more active in acute rheumatism than in any other disease. There is also practical' evidence that such is the case. The natural result of in creased formation of heat is its increased elimination. The skin is the channel by which heat is eliminated. Profuse perspiration, the evidence of excessive action of the skin, forms one of the characteris tic features of rheumatic fever. Excessive production is thus met by excessive elimination of heat, and no undue rise of temperature occurs.
But another result of such increased activity of the heat-produc ing process must be stimulation of heat-inhibition. The function of the heat-inhibiting centre is to restrain excessive formation of heat— this excessive formation of heat, though common to all fevers, is most marked in acute rheumatism ; that function is, therefore, likely to be called into more active operation in acute rheumatism than in any other disease. It might happen either from want of vigor, or from unusual susceptibility of the nerve centres, aided possibly by more or less failure in the beat-eliminating action of the skin, that heat-pro duction was in excess of heat-elimination. Under such circumstances heat would accumulate in the system. As a result of this the heat inhibiting centre would be first stimulated to excessive effort, then fatigued, and finally paralyzed, as in heat apoplexy, and hyperpyrexia would result. That is a sequence. of events which might occur in any form of fever or in any ailment, accompanied by increased activity of the heat-producing process. The more active that process the more likely is it to happen. Acute rheumatism, being the ailment in which heat is most abundantly and rapidly formed, is also the one in which inhibition is most likely to be overmatched. Hyperpyrexia is, therefore, more common in it than in any other form of fever.
Though for convenience' sake we refer to paralysis of heat-inhibi tion as the immediate cause of the very high temperature, it is evident that it is not only heat-inhibition, but inhibition of metabol ism iu general that is paralyzed. Hyperpyrexia may be defined as
paralysis of inhibition of metabolism, heat-inhibition being only part of it. It is not the high temperature that causes the nervous symp toms, but disturbance of an important part of the nervous centres that causes the high temperature. In accordance with this we find that, both in heat apoplexy and in rheumatic hyperpyrexia, the occur rence of the high temperature is generally preceded by headache, giddiness, restlessness, or other indication of disturbance of the ner vous centres. All Indian authorities refer to these premonitory indications in the case of heat-apoplexy. In cases of acute rheu matism which become hyperpyretic, there will generally be found evidence of disturbance of the nervous system preceding the pyrexia; and such disturbance should put us on the watch for graver symptoms.
Hyperpyrexia as it occurs in rheumatic fever is not a part of the rheumatic process, but an accidental complication. It is not clue, like the joint inflammation and heart complications, to the direct ac tion of the rheumatic poison, and is not to be treated in the same way. The salicyl compounds put a stop to the rheumatic process by destroying the rheumatic poison. They have no controlling influence in rheumatic hyperpyrexia because it is not part of the rheumatic process but an accidental complication of the febrile state which, for the reasons already given, is more common in rheumatic than in other fevers.
Hyperpyrexia essentially consists in paralysis of inhibition of metabolism. Such paralysis may result from either organic lesion or functional disturbance of the nervous centres. The very high tem perature to which the condition owes its name is the special indica tion that the function of heat-inhibition is impaired; just as the very rapid pulse (150 to 160) and the very frequent and hurried respiration indicate that inhibition of the cardiac and respiratory functions is also impaired. When hyperpyrexia is due to organic lesion treatment is of no avail. When due to functional disorder, as is the case in rheu matic hyperpyrexia, it may be cured. In the treatment of this condi tion the external application of cold is the remedy on which we chiefly depend. How does the cold act The opinion generally _held is that the cold allays the disturbance by lowering the temperature. But to say that mere lowering of the body heat is sufficient to allay the alarming symptoms, is equivalent to saying that these symptoms are caused by the high temperature, and that we have seen is not the case. In hyperpyrexia the external application of cold not only lowers the temperature but arrests the whole morbid process and cures the patient.