Severe nonexertional hyperthermia (classic heat stroke) in adults
- C Crawford Mechem, MD, FACEP
C Crawford Mechem, MD, FACEP
- Professor of Emergency Medicine
- Perelman School of Medicine, University of Pennsylvania
- Section Editor
- Daniel F Danzl, MD
Daniel F Danzl, MD
- Section Editor — Environmental Emergencies
- Professor of Emergency Medicine
- University of Louisville School of Medicine
- Deputy Editor
- Jonathan Grayzel, MD, FAAEM
Jonathan Grayzel, MD, FAAEM
- Senior Deputy Editor — UpToDate
- Deputy Editor — Adult and Pediatric Emergency Medicine
- Deputy Editor — Primary Care Sports Medicine (Adolescents and Adults)
- Assistant Professor of Emergency Medicine
- University of Massachusetts Medical School
Hyperthermia is defined as elevation of core body temperature above the normal diurnal range of 36 to 37.5ºC due to failure of thermoregulation. Hyperthermia is not synonymous with the more common sign of fever, which is induced by cytokine activation during inflammation and regulated at the level of the hypothalamus. A temperature above 40ºC (or 104ºF) is generally considered to be consistent with severe hyperthermia.
The evaluation of severe hyperthermia in adults and the management of nonexertional heat stroke will be reviewed here. Exertional heat illness (including exertional heat stroke), fever in adults, malignant hyperthermia, and neuroleptic malignant syndrome are discussed in detail separately. (See "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis" and "Exertional heat illness in adolescents and adults: Management and prevention" and "Pathophysiology and treatment of fever in adults" and "Malignant hyperthermia: Clinical diagnosis and management of acute crisis" and "Neuroleptic malignant syndrome".)
Body temperature is maintained within a narrow range by balancing heat load with heat dissipation [1,2]. The body's heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation.
Evaporation is the principal mechanism of heat loss in a hot environment, but this becomes ineffective above a relative humidity of 75 percent . The other major methods of heat dissipation—radiation (emission of infrared electromagnetic energy), conduction (direct transfer of heat to an adjacent, cooler object), and convection (direct transfer of heat to convective air currents)—cannot efficiently transfer heat when environmental temperature exceeds skin temperature. The normal regulation of body temperature is discussed separately. (See "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis", section on 'Thermoregulation in the heat'.)
Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. Above 42ºC (108ºF), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function. A cytokine-mediated systemic inflammatory response develops, and production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ system failure and disseminated intravascular coagulation (DIC) [2,4,5].
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- DEFINITIONS AND CLINICAL FINDINGS
- RISK FACTORS FOR INCREASED MORTALITY
- DIAGNOSTIC EVALUATION
- DIFFERENTIAL DIAGNOSIS
- Initial treatment and monitoring
- Cooling measures
- Pharmacologic therapy
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS