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Heat emergencies comprise a range of disorders from minor (heat edema, prickly heat, heat cramps, and heat exhaustion) to major (heat stroke).


Heat Edema Heat edema is a self-limited process manifested by mild swelling of the feet, ankles, and hands that appears within the first few days of exposure to a hot environment. Heat edema is due to the cutaneous vasodilatation and orthostatic pooling of interstitial fluid in gravity-dependent extremities. An increase in the secretion of aldosterone and antidiuretic hormone in response to the heat stress contributes to the mild edema. In general, heat edema is found in elderly nonacclimatized individuals who are physically active after a period of sitting while traveling in a vehicle or airplane. Occasionally, heat edema occurs after prolonged standing. It is commonly seen in healthy travelers just arriving from a colder climate. The edema is mild and does not impair or interfere with normal activities. Very rarely, pitting edema of the ankles may develop but does not progress to the pretibial region.

History and physical examination are usually sufficient to exclude systemic causes of edema, and no further testing or treatment except removal from heat source is needed. In the elderly, new pedal edema from heat should be differentiated from early congestive heart failure or deep venous thrombosis. Heat edema usually resolves spontaneously in a few days. No special treatment is necessary, but elevation of the legs and the use of support hose facilitate removal of the interstitial fluid. Diuretics are not effective and can predispose to volume depletion, electrolyte abnormalities, or more serious heat emergencies.8

Prickly Heat

Prickly heat is a pruritic, maculopapular, and erythematous rash over normally clothed areas of the body. Also known as lichen tropicus, miliaria rubra, or heat rash, it is an acute inflammation of the sweat ducts caused by blockage of the sweat pores by macerated stratum corneum (Figure 210-1). The sweat ducts become dilated under pressure and ultimately rupture, producing superficial vesicles in the malpighian layer of the skin on a red base. Itching is the predominant clinical feature during this phase and can be treated successfully with antihistamines. Wearing clean, light, and loose-fitting clothing and avoiding sweat-generating situations can prevent prickly heat. Calamine lotion or topical steroids can be of benefit. Chlorhexidine in a light cream or salicylic acid cleaning may provide some relief.19

FIGURE 210-1.

Miliaria rubra (prickly heat). [Image used with permission of Peter Lio, MD.]

With prolonged or repeated heat exposure, a keratin plug fills the sweat duct, causing obstruction in the stratum malpighian layer. When the duct ruptures a second time, the resultant vesicle will be driven deeper into the dermis. This vesicle simulates the white papules of piloerection and is not pruritic. This is known as the profunda stage of prickly heat (miliaria profunda) and can readily advance into a chronic dermatitis. Infection with Staphylococcus aureus or methicillin-resistant S. aureus is a common complication. The skin can be desquamated by applying 1% salicylic acid to the affected area three times a day.

Heat Cramps

Heat cramps are painful, involuntary, spasmodic contractions of skeletal muscles, usually those of the calves, although they may involve the thighs and shoulders. These cramps usually occur in individuals who are sweating profusely and replace fluid losses with water or other hypotonic solutions. Heat cramps may occasionally occur during exercise or, more commonly, during a rest period after several hours of vigorous physical activity. Nonacclimated or unconditioned individuals who are just starting manual labor in a hot environment are at risk for heat cramps. Although heat cramps are self-limited and do not cause significant morbidity, the pain associated with them can precipitate an ED visit. In general, heat cramps are short in duration, are limited to a definitive group of muscles, and almost never involve enough muscle mass to cause rhabdomyolysis.

The pathogenesis of heat cramps is believed to involve a relative deficiency of sodium, potassium, or magnesium and fluid at muscle level. The production of large amounts of sweat, which has a high sodium content, coupled with inadequate sodium replacement results in cellular hyponatremia. This in turn produces muscle cramps with calcium-dependent muscle relaxation. Patients with severe heat cramps may have hyponatremia and hypochloremia.20 Rhabdomyolysis is rare and occurs secondary to diffuse and protracted muscle spasm.15

Treatment consists of fluid and salt replacement (PO or IV) and rest in a cool environment. For mild cases, or if an overwhelming number of patients require treatment, a 0.1% to 0.2% saline solution can be given PO. Two 650 milligram salt tablets dissolved in a quart of water provide a 0.1% saline solution.13,20 Many electrolyte solution drinks (sports drinks) are commercially available and are much more palatable. Patients with more severe symptoms require IV rehydration with normal saline. Heat cramps can be prevented by maintaining adequate dietary salt intake or by drinking commercial electrolyte beverages. Salt tablets by themselves should not be used, because the tablets are a gastric irritant and cause nausea and vomiting.

Heat Stress

Heat stress occurs in two different ways, through water depletion and through sodium depletion, but often is characterized by a combination of both. Water depletion tends to occur in the elderly and in persons working in hot environments with inadequate water replacement. Salt depletion heat exhaustion tends to occur in unacclimatized individuals who replace fluid losses with large amounts of hypotonic solutions.

Heat stress presents with symptoms that include headache, nausea, vomiting, malaise, dizziness, and muscle cramps as well as signs of dehydration, such as tachycardia and orthostatic hypotension or near–syncope. Heat cramps and/or rhabdomyolysis are present on rare occasions. Because of the ill-defined and nonspecific symptoms, heat stress is often a diagnosis of exclusion.

On physical examination, the temperature may be normal or elevated, usually not above 40°C (104°F). Patients with heat exhaustion do not manifest signs of CNS impairment.

Laboratory studies almost universally demonstrate hemoconcentration, although the specific electrolyte abnormalities seen depend on the ratio of fluid and electrolyte losses to intake. Patients who have had no fluid intake of any kind exhibit hypernatremia, whereas those who partly rehydrate with salt-containing fluids develop isotonic hypovolemia with normal sodium and chloride levels. Serum potassium and magnesium levels are variable.

Heat stress is treated with volume and electrolyte replacement and rest. Removal from the heat-stressed environment is essential. Patients with mild heat stress may be treated with oral electrolyte solutions. Rapid infusion of moderate amounts of IV fluids (1 to 2 L of normal saline) may be necessary in patients who demonstrate significant tissue hypoperfusion. Ideally, the choice of IV solution should be guided by laboratory determinations, but isotonic salt solutions may be used until specific electrolyte abnormalities are identified. In general, hospitalization is not required. Patients with congestive heart failure or severe electrolyte disturbances may require admission, because of the time needed to correct their fluid and/or electrolyte deficits.

Heat stress can progress to heat stroke even after the patient is removed from the hot environment. Therefore, patients with heat stress who do not respond to approximately 30 minutes of fluid replacement and removal from the hot environment should be cooled until the core temperature drops to 39°C (102°F).


Heat stroke is an acute life-threatening emergency with high mortality and is fatal if left untreated (Table 210-1).

Table 210-1Signs and Symptoms of Heat Emergencies

The cardinal features of heat stroke are hyperthermia (>40°C [>104°F]) and altered mental status. Although patients presenting with classic (nonexertional) heat stroke may exhibit anhidrosis, the absence of sweat is not considered a diagnostic criterion because sweat is present in over half of patients with heat stroke.15

The CNS is particularly vulnerable in heat stroke. The cerebellum is highly sensitive to heat, and ataxia can be an early neurologic finding. Virtually any neurologic abnormality may be present in heat stroke, including irritability, confusion, bizarre behavior, combativeness, hallucinations, plantar responses, decorticate and decerebrate posturing, hemiplegia, status epilepticus, and coma. Seizures are quite common, especially during cooling. Neurologic injury is a function of the maximum temperature reached and the duration of exposure.15

The distinction between exertional and classic (nonexertional) heat stroke is not clinically important, because immediate cooling and support of organ system function is the therapeutic goal for both. A delay in cooling increases the mortality rate.

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