Febrile State of Infancy

Febrile State of Infancy, elevated body temperature in infants that arises not on the basis of infection but, apparently, in direct connection with changes in the quality and quantity of the food (and drink) introduced; in some cases this connection is undoubted, but in others, for example, in so-called A. toxicoses, it cannot yet be considered fully proven. A. l. can occur both in sick children (acute digestive disorders) and in completely healthy ones; sometimes it can be induced experimentally. The etiology of A. l. is diverse. In some cases A. l. is associated with a disturbance of water metabolism, for example, in so-called salt fever, i.e., in that elevation of body temperature which sometimes occurs in poorly nourished infants (especially those in the convalescent stage after gastrointestinal disorders) if a NaCl solution is administered per os. In this case the main role is played not by the absolute amount of NaCl but rather by its concentration (hypertonic solution, e.g., 3%). The fever of thirst, which has practically greater significance, belongs here as well; this is a symptom complex that develops in approximately 10% of infants if the amount of fluid introduced is sharply limited, namely, giving less than 50 cubic centimeters per kilogram of body weight. The resulting elevation of body temperature can reach 40° and is accompanied by a number of other symptoms of "drying" of the organism (decreased turgor, retracted abdomen, concentrated urine, clouding of consciousness, vomiting, collapse, etc.). The introduction of water rapidly eliminates this severe picture. According to Rietschel, the elevations of temperature observed sometimes in pylorospasm can also be classified here, as well as, probably, the so-called transient fever—a brief (from several hours to 1–2 days) elevation of body temperature in some newborns on the 2nd–4th day after birth, which usually coincides with the moment of maximum weight loss. The causes of this fever are not yet entirely clear, but most agree on recognizing the alimentary nature of it (insufficiency of moisture in the first days of life, when its losses are relatively large); at least, it is sufficient to introduce a small amount of fluid to eliminate or prevent the elevation of body temperature. In other cases, an important role in the etiology of A. l. may belong to protein. According to Finkelstein and others, we encounter pyrogenic protein action in every diarrhea accompanied by an elevation of temperature and associated with an intensification of fermentation in the intestine. This fermentation is a necessary condition for the occurrence of fever; it is especially favored by food rich in sugar and serum. However, the clearest example of pyrogenic protein action we have in the state of relative thirst or so-called concentration fever, which can arise if a small (3–4-month-old) child's fluid intake is limited to approximately 100 grams per kilogram of body weight, and at the same time food rich in milk serum is given in a strongly concentrated form (condensed milk, concentrated protein milk, Mixture Moro) or fat and carbohydrates are replaced by any food mixture with an isodynamic amount of protein. Rietschel considers that the elevation of body temperature is associated in this case with an increase in heat production due to the impossibility of its sufficient excretion because of a lack of water; this is a "dynamic" protein fever. The pathogenesis of A. l. is not yet fully elucidated in many cases. This is especially true of fever in acute (toxic) dyspepsias. The fact that this fever usually disappears after a fasting diet gives Finkelstein and his school grounds to assert that A. l. is caused not by bacterial toxins but by the formation in the intestine of products of incomplete protein breakdown (of a peptide nature) capable of acting pyrogenically. He points out in this connection the experiments of Moro, who succeeded in inducing fever by parenteral administration of peptone. Pyrogenic protein breakdown products arise in the process of disturbed intermediate metabolism caused by pathological fermentation in the intestine; the necessary substrate for the latter is food rich in milk serum and sugar, which is why this type of fever is referred to as A. If these products can sometimes form even in a healthy intestine, then there they are either not absorbed or, upon absorption, are detoxified by the liver. However, damage to the intestinal mucosa during diarrhea can not only cause an increase in the absorption of various colloids but also disturb protein metabolism in the intestinal epithelium; in this case, pyrogenic substances, entering the bloodstream, can no longer be detoxified by the liver, whose function has suffered in the course of the disease, and cause an elevation of body temperature. According to this view, other types of A. l. are also explained by the formation of protein breakdown products due to local disturbances of water metabolism in those organs and tissues where protein metabolism is especially intense (for example, the liver). In salt fever this disturbance of protein metabolism is conditioned by blood hypertension. In contrast to this view, in recent times Rietschel has asserted that any A. l. can be explained by purely physical causes and reduced to phenomena of increased heat production and retention in the organism. Indeed, the introduction of NaCl in a concentrated solution mobilizes colloidal-bound water, extracting it from the tissues; this creates a great deal of work, which leads to hyperproduction of heat. A secondary role is played here by increased muscular work (crying due to thirst) and other conditions. If water is given simultaneously with NaCl, fever does not arise. In the same way, fever after the introduction of sugar and milk serum is explained, since it occurs only in the presence of diarrhea, i.e., in the loss of water; thus, here also a great deal of work is performed in mobilizing water to bind the sugar. In protein fever there is an increase in heat production due to the burning of protein. Therefore, Rietschel calls A. l. hyperthermias, in contrast to true fevers, the basis of which is not hyperproduction of heat but disturbance of heat dissipation or other factors. However, it must be emphasized that the pathogenesis of A. l., at least for some cases, is considered controversial; in particular, after the works of Bessau and others on endogenous ascending invasion of the intestinal bacillus during diarrhea and newer bacteriological works of Adam, the possibility of the participation of bacteria in the pathogenesis of fever in toxic diarrhea in infants can in no way be denied.