CHAPTER 31 ■ FEVER TODD A FLORIN, KERI A COHN, ELIZABETH R ALPERN INTRODUCTION Fever, the abnormal elevation of body temperature, has been recognized for centuries by physicians as a sign of disease Fever in a child is one of the most commonly encountered chief complaints in clinical pediatrics, accounting for as many as 20% of pediatric emergency department (ED) visits The problem of appropriate clinical and laboratory evaluation of febrile children, however, remains a major challenge The approach outlined in this chapter helps the physician evaluate and treat a febrile child in the ED, proceeding systematically with the appropriate diagnostic steps and management The principal causes of fever in children include infectious and noninfectious etiologies ( Tables 31.1 and 31.2 ) PATHOPHYSIOLOGY Fever is a complex process, involving the highly coordinated interplay of autonomic, neuroendocrine, and behavioral responses to a variety of infectious and noninfectious inflammatory challenges Fever is believed to be an adaptive response that is ubiquitous in animals Exogenous pyrogens (e.g., toxins, infectious agents, etc.) from many sources produce fever by inducing the production of endogenous pyrogens (e.g., interleukin-B1, interleukin-6, etc.) These pyrogens interact with specialized receptor neurons of the hypothalamus This leads to the production of prostaglandins as the critical mediators of the febrile response, resetting the hypothalamic thermostat to elevate body temperature There is some evidence that increased body temperature impairs replication of microbes and may aid phagocytic bactericidal activity Additionally, the febrile response includes adaptive neuroendocrine and metabolic effects that further enhance the host’s response to microbial invasion Rarely, fever results from central nervous system (CNS) dysfunction (e.g., hypothalamic tumor, infarction) that alters the thermostatic set point directly, rather than via pyrogen induction Finally, sometimes hyperpyrexia is not due to altered hypothalamic regulation, but rather to increased heat production (e.g., stimulant drug overdose; see Chapter 102 Toxicologic Emergencies ) or exposure to excess environmental heat (heat stroke; see Chapter 90 Environmental Emergencies, Radiological Emergencies, Bites and Stings )