Classically, heatstroke is defined as the triad of a core temperature greater than 40.5°C (104.9°F), CNS dysfunction, and anhidrosis. However, anhidrosis, or a lack of sweating may not be present for a variety of reasons and is not considered to be an absolute diagnostic criterion. Subsequently, anyone with hyperpyrexia and CNS dysfunction should be considered to have a heatstroke, which is a medical emergency with multiple organ system involvement and a high mortality rate and requires immediate intervention.

The CNS is particularly vulnerable in heatstroke, manifesting with such symptoms as irritability, bizarre behavior, combativeness, hallucinations, seizures, or coma. The cerebellum is highly sensitive to heat, and ataxia can be an early finding. Virtually any neurologic abnormality may be present in heatstroke, including plantar responses, decorticate and decerebrate posturing, hemiplegia, status epilepticus, and coma. Cerebral edema is a common finding. CNS dysfunction is universal at core temperatures higher than 42°C (107.6°F). However, there is no arbitrary core temperature threshold for heatstroke. Cellular injury is a function of both the maximum temperature reached and the time of exposure. Patients with lower temperatures for longer periods may do worse than patients with higher temperatures for shorter periods.

The presence or absence of sweating has traditionally been one of the important distinctions between true heatstroke and other heat emergencies. The presence of sweating does not exclude the diagnosis of heatstroke. Patients with early heatstroke typically demonstrate marked sweating but eventually develop anhidrosis due to profound volume depletion or sweat gland dysfunction.

Heatstroke is a total breakdown of thermoregulation. Traditionally, two forms of heatstroke have been described: nonexertional and exertional. Nonexertional or "classic" heatstroke usually occurs during summer heat waves. Since physical exertion is not a major component of heat production in classic heatstroke, it tends to be more insidious in onset. Because of this slow evolution, there is sufficient time for fluid and electrolyte abnormalities to develop. The poor, the elderly, infants, and the chronically ill are a greatest risk. The pathophysiology is increased exogenous heat gain and diminished heat dispersion. The specific stressors are lack of air-conditioning, presence of cardiovascular disease, older age, and use of cardiovascular or anticholinergic drugs. Small children are at risk because of the immaturity of their thermoregulatory systems, as well as their dependence on others for fluids.

Exertional heatstroke usually strikes a younger segment of the population as a consequence of vigorous physical activity. The primary cause is increased endogenous heat production. Individuals who perform physical labor or exercise in a hot, humid climate are especially prone to develop exertional heatstroke. The distinction between exertional and nonexertional heatstroke is moot, because signs, symptoms, and management are the same. The primary factor that contributes to the morbidity and mortality of heat illness is the severity of underlying disease and not the absolute height of the core temperature.

The definitive diagnosis of environmental heatstroke is a diagnosis of exclusion. The differential diagnosis for fever and altered mental status is varied and lengthy

(Table 187.-.3,). However, once heatstroke is suspected, efforts to lower the body temperature must be initiated immediately by whatever means available, whether in the prehospital or emergency department setting. A delay in cooling represents a primary reason for the high potential mortality rate associated with heatstroke.

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