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  • Heat stroke is distinguished from less severe forms of environmental hyperthermia by higher body temperature and the presence of severe central nervous system dysfunction.
  • Classic (nonexertional) heat stroke affects the elderly and the chronically ill and is associated with high morbidity and mortality rates.
  • Exertional heat stroke affects younger individuals who exercise in hot environments, and it develops over a short period.
  • Immediate conductive or evaporative cooling should be instituted for heat stroke victims with a core temperature above 41°C.
  • Malignant hyperthermia is a rare syndrome of hyperthermia, muscle contractions, and cardiovascular instability triggered by succinyl choline and inhaled anesthetics.
  • Management of malignant hyperthermia includes the prompt recognition of the syndrome, discontinuation of the inciting drug, administration of dantrolene, and supportive care.
  • Neuroleptic malignant syndrome is an idiosyncratic reaction to neuroleptic drugs characterized by hyperthermia, muscle rigidity, alterations in mental status, autonomic dysfunction, and rhabdomyolysis.
  • Treatment of neuroleptic malignant syndrome includes discontinuation of the triggering drug, administration of dantrolene for muscle rigidity and hyperthermia, administration of dopaminergic drugs such as bromocriptine and amantadine, and supportive care.

Hyperthermia is defined as a core body temperature above 38.2°C (101.8°F) and is commonly present in patients in the intensive care unit. In most cases, hyperthermia is a consequence of the presence of pyrogens that reset the hypothalamic thermoregulatory mechanism to a higher temperature.1 This response, referred to as fever, is part of the individual's immune response to infection, malignancy, inflammation, or autoimmune disease.

The disorders discussed in this chapter, environmental hyperthermia, malignant hyperthermia, and the neuroleptic malignant syndrome, are not part of the body's immune response and result from a failure of homeostatic thermoregulatory mechanisms. Prompt recognition and appropriate treatment of these syndromes are critical to prevent irreversible cellular and organ injury.

Pathophysiology

Environmental hyperthermia is related to endogenous heat production, high ambient temperatures, and/or high humidity. Humans produce approximately 50 to 60 kcal/m2 per hour of heat, or approximately 100 kcal/hour.2 Minimal activity can increase heat production two- to fourfold, and strenuous exercise may increase heat production as much as 20 times the baseline level. Normally, most heat loss (50% to 70%) occurs from the skin and lungs through radiation in neutral environments. Conduction of heat through direct contact with cooler objects or loss of heat due to convection accounts for a smaller percentage of heat loss. Evaporation of sweat from the skin is a major mechanism of heat loss in a warm environment.

The preoptic nucleus of the anterior hypothalamus receives information from temperature-sensitive receptors in the skin, viscera, and great vessels and initiates physiologic responses to temperature increases. Increased temperatures result in cutaneous vasodilation, decreased muscle tone, and increase in sweating. As ambient temperature nears 37°C (98.6°F), the body relies primarily on evaporation of sweat as a cooling mechanism. Evaporation can result in the loss of 580 kcal/L of evaporated sweat. Conditions of high humidity (>75%) ...

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