The Metabolic Theory Of Pyrexia

According to this theory the abnormal production of heat is due to the direct action of the fever-producing agents on the living tissues, while the due regulation of the temperature is interfered with.

To the author there are insuperable difficulties in accepting the purely nervous theory of fever. Pyrexia is produced, as we have seen, by a large number of different agents, each of which when present in the blood produces a rise of temperature. They do so also, up to a certain point, in proportion to the amount of the agent present in the blood. It seems inconsistent that such different agents should act in a similar fashion on the nervous system.

Besides, the production of heat is brought about by a process distinct from normal heat-production. In the normal production of heat in muscles, contraction is a constant if not a necessary element, and the production of heat in glands and elsewhere is associated with the performance of their function. In fever, however, the muscles are relaxed and the glands are to a large extent deprived of their function, and the production of heat is due to a destructive combustion of the tissues, and is thus abnormal in its method. It seems more probable that a morbid agent in the blood directly induces this change in the tissues, than that it should be due to a nervous influence.

This also would give us the key to the paralysis of the regulatory apparatus. This apparatus has relations on the one hand with the heat-producing functions, and on the other hand with the heat-discharging, and it is by the mutual regulation of these that the normal balance is maintained. But if heat-production proceeds from an extraneous cause, and is therefore placed outside the influence of the regulating centre, then the latter may reasonably be expected to be at fault. In addition, the fever-producing agent acts on the nervous centres as well as on other organs, and produces a certain paralysis of their functions, just as it paralyzes secretion and muscular contraction. . In most fevers the cerebral functions are abnormal, although the form of disturbance varies considerably in the different fevers.

It may be a question to what extent the increased metabolism of the tissues is a reaction against the morbid agent in the blood. In this sense the rise in temperature may possibly be related to the elimination of the morbid agent, although the view that the rise in temperature in itself inhibits the morbid poison can scarcely be sustained.

Other Phenomena Of Fever

Most of the remaining phenomena of fever are to be brought into relation either with the rise in temperature or the direct action of the fever-producing agent.

Parenchymatous degeneration or Cloudy swelling is a frequent change in the tissues in fever. It affects chiefly the muscles and the secreting glands. Sometimes there is great enlargement of the liver and kidneys from this cause. The weakness of the heart, which is so marked in many fevers and may give rise to dilatation of its cavities, is, partly at least, due to this. The parenchymatous change has been ascribed to the action of the over-heated blood (Liebermeister, Wickham Legg), but this explanation is not sufficient, as it may be absent in cases where the temperature has been high (in cases of acute pneumonia) and is sometimes present without fever (Cohnheim). The action of the altered blood must be taken along with the high temperature.

The increased rate of the pulse is generally referred directly to the action of the rise in temperature on the heart. It is known by experiment that when the heart is artificially raised in temperature by heating the blood which is passing to it or by increasing the temperature of the surrounding air after the heart has been exposed, it beats at an accelerated rate. The increased frequency of respiration is also ascribed to the elevation of temperature of the blood. Goldstein, by heating the blood in the carotid so that the temperature in the medulla oblongata was raised, caused great acceleration of the respiration.

Fall of blood-pressure is a usual concomitant of fever, although it is not always present. It is present as evidenced by Dicrotism of the pulse in typhoid, septic, and puerperal fevers, but absent in the eruptive stages of scarlet fever and small-pox (Recklinghausen). It is to be ascribed to a general relaxation of the arteries due to a paralysis of the muscular coat similar to that of the voluntary muscles, and also to some extent to the weakness of the heart.

The nervous disturbances in fevers vary greatly and are only in part to be ascribed to the high temperature. In relapsing fever and in the rise of temperature which sometimes occurs in simple fractures or under the antiseptic treatment of wounds, there are usually no nervous disturbances. On the other hand, typhus fever is usually accompanied by delirium; typhoid with dulness of mind, etc.; while in children convulsions occasionally accompany fever. These facts indicate that the nervous symptoms are essentially related to the pyrogenic agent, and differ according to the nature of it.

Post-Mortem Appearances In Fever

It will be inferred from what has gone before that there are no constant anatomical changes characteristic of all fevers. The most frequent are the parenchymatous changes already referred to, but even these, as we have seen, are not constant. In the acute specific fevers the blood is usually found after death imperfectly coagulated. As a consequence of this the haemoglobin is readily dissolved out of the corpuscles and stains the internal surfaces of the heart and vessels; the colouring matter frequently penetrates to surrounding parts, producing frequently deep staining of the skin. The spleen is enlarged in most fevers, and it is frequently very soft, especially in typhus. Sometimes there are wedge-shaped infarctions. The liver is commonly enlarged from parenchymatous degeneration, which is frequently associated with a certain amount of fatty degeneration. The kidneys are also commonly enlarged. The muscles are liable to parenchymatous degeneration, but they are also subject to waxy or hyaline degeneration, especially in typhoid fever.

Besides these general changes, many of the individual fevers have specially localized lesions, such as the affection of the intestine and mesenteric glands in typhoid fever, of the throat in scarlet fever, of the skin and mucous membranes in small-pox, and of the soft membranes of the brain in cerebro-spinal meningitis.

Literature

Wunderlich, Temperature in disease, Syd. Soc. transl., 1870; Murchison, The continued fevers, 3rd ed., 1884; Rosenthal, in Hermann's Handb. d. Physiol., 1882, Bd. iv., Heft. 2; Cohnheim, Allg. Path., 1882, ii., 481; Recklinghausen, Allg. Path., 1883, 449; Liebermeister, Handb. des Fiebers, 1875; Jurgensen, Korperwiirme des gesunden Menschen, 1873; Wood, Fever, a study In morbid and normal physiology, Philadelphia, 1880; Senator, Untersuch. liber d. fieberhaften Process, 1873; Hilton Fagge, Medicine, i., 34; Macalister, Gul-stonian lectures, 1887, and Croonian lectures, 1888 (Reports in Brit. Med. Jour.); Bkeschet et Becqderel, Arch. gen. de med., 1835, and Annales d. sc. natur., 1835; Ludwig, Lehrb. d. physiol., 1801; Reincke, Deutsch. Arch. f. klin. Med., xvi., 12; Peter, Gaz. hebd., 1872, Nos. 31 and 32; Stapff, Arch. f. Physiol., 1879; Hale White, Guy's Hosp. Rep., 1884; Ord, Brit. Med. Jour., 1885, vol. ii., 783; Billroth, Langenbeck's Arch., vi., ix., xiii.; Unruh, Virch. Arch., xlviii., 227; Sidney Ringer, Med. Chir. trans., 1859, 361; Goldstein, Wurzb. Verhandl. 1871, p. 156.