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  Always consider secondary causes of hyperthermia. Heat exhaustion and heat stroke should be diagnoses of exclusion.

  
  
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  Do not fluid overload elderly patients while rehydrating them in the emergency department (ED). Remember that their fluid and electrolyte deficits developed over days, and they do not need to be fully repleted while in the ED.

  
  
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  Begin cooling the severely hyperthermic patient as soon as other life-threatening conditions and airway, breathing, and circulation have been addressed. Delays in treatment can increase morbidity and mortality.

Heat exhaustion and heat stroke are on a continuum of disease severity. Heat exhaustion occurs when the body can no longer dissipate heat adequately, resulting in hyperthermia. Heat stroke is the result of complete thermoregulatory dysfunction. Classic heat injury occurs in the elderly or ill with prolonged exposure to high environmental temperatures. Physical exertion is not required. Elevated temperatures and high humidity overwhelm the body’s normal cooling mechanisms. Exertional heat injury occurs in physically fit individuals who exert themselves during conditions with high heat and humidity. Heat gain from the environment combined with internal heat production overwhelms the body’s normal cooling mechanisms, creating hyperthermia.

There are about 400 deaths from heat-related illness in the United States every year. Extremes in weather conditions can greatly affect these numbers. The Midwest heat wave in July 1995 caused 465 deaths in the city of Chicago alone. The mortality rate in patients with heat stroke can range between 10% and 70% and is affected by a patient’s physical ability to adapt to changes in the ambient temperature and medical comorbidities.

The body normally maintains its core temperature between 36°C (96.8°F) and 38°C (100.4°F). In hyperthermia, as opposed to fever, there is an elevated body temperature without a resetting of the hypothalamic temperature center. The body reacts to a heat stress to decrease body temperature via 3 main mechanisms: increased sweat production, decreased internal heat production, and removal from the hot environment. Any factors that impede these responses can lead to heat exhaustion or heat stroke.

Evaporation of sweat is the main mechanism through which the body dissipates heat. Evaporative mechanisms are impaired by both environmental and physical factors. High humidity, as seen with an elevated heat index, impedes the body’s ability to evaporate sweat and cool. Elderly, infants, and those with chronic illness have decreased ability to adapt to hot conditions. Certain medications including antipsychotics, anticholinergics, beta-blockers, and diuretics also interfere with sweat evaporation and cooling. Alcoholics, those with decreased mobility, and some patients with chronic medical conditions including obesity, poor cardiac function, and scleroderma have impaired abilities to evaporate heat as well.

Radiation, conduction, and convection of heat also allow the body to lose heat, but only when the ambient temperature is lower than body temperature. Utilizing these mechanisms can aid in cooling a hyperthermic patient.

In patients presenting with heat exhaustion, core body temperature is usually normal, but can be elevated to 40°C (104°F). Patients complain of nonspecific symptoms and signs including weakness, dizziness, fatigue, nausea, vomiting, headache, myalgias, tachycardia, tachypnea, hypotension, and diaphoresis. By definition, mental status remains normal. Heat stroke patients present with altered mental status (AMS) ranging from mild confusion to coma. Body temperature is elevated above 40°C (104°F), and they may or may not be sweating. Patients can exhibit a wide range of neurologic symptoms and signs, including ataxia, seizures, and hemiplegia. Multiorgan system failure consisting of hepatic, renal, and cardiac impairment may also be present in severe cases.