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Disorders due to Heat

Four medical disorders comprise a spectrum of illness that can result from excessive exposure to hot environments: heat syncope, hear cramps, heat exhaustion, and heat stroke. A stable internal temperature requires a balance between heat production and heat loss, which the hypothalamus regulates in initiating changes in muscle tone, vascular tone, and sweat gland function.

Etiology

Sweat production and evaporation is a major mechanism of heat removal. Conduction - the direct transfer of heat from the skin to the surrounding air - also occurs, but with diminished efficiency as the ambient temperature rises. The passive transfer of heat from a warmer to a cooler object by radiation accounts for 65% of body heat loss decreases as the temperature of the surrounding environment increases up to 37.2, the point at which heat transfer reverses direction. At normal temperatures, evaporation accounts for approximately 20% of the body's heat loss, but at high temperature is becomes the major mechanism for dissipation of heat; with vigorous exertion, sweat loss can be as much as 2.5 L/h. This mechanism is also limited as humidity increases.

Health conditions that inhibit sweat production or evaporation and increase susceptibility to heat disorders include obesity, generalized skin diseases, diminished cutaneous blood flow, dehydration, malnutrition, hypotension, and reduced cardiac output. Medications that impair the sweating mechanism are the anticholinergics, antihistamines, phenothiazines, tricyclic antidepressants, monoamine oxidase inhibitors, and diuretics; reduced cutaneous blood flow results from use of vasoconstrictors and - adrenergic blocking agents; and dehydration results from use of alcohol. Illicit drugs eg, phencyclidine, LSD, amphetamines, and cocaine - can cause increased muscle activity and thus generate increased body heat. Drug withdrawal syndromes may have the same effect, as may prolonged seizures.

The risk of heat disorder also increased with age, impaired cognition, concurrent illness, reduced physical fitness, and insufficient acclimatization.

Prevention

Medical evaluation and monitoring should be used to identify individuals at increased risk of heat disorders. The exposed public should be made aware of the early symptoms and signs of heat disorders. It is not recommended to make salt tablets available for use without medical supervision; close monitoring of fluid and electrolyte intake may be necessary in situations necessitating activity in hot environments. Athletic events should be organized and managed with attention to thermoregulation: the WBGT Index should be encouraged, and medical support should be immediately accessible. Competition is not recommended when the WBGT exceeds 28 C. Workers should not begin work in hot temperatures without proper acclimatization and should be encouraged to drink water or balanced electrolyte fluids frequently.

Protective cooled suits have been used successfully in industry for prolonged work in environment up to 60 C.

Acclimatization is achieved by scheduled regulated exposure to hot environments and by gradually increasing the duration of exposure and the work load until the body adjusts by starting to produce sweat of lower salt content in greater amounts at later ambient temperatures. Acclimatization is accompained by increased plasma volume, cardiac output, and cardiac stroke volume and a slower heart rate.

SPECIFIC SYNDROMES DUE TO HEAT EXPOSURE

1. Heat Syncope

Sudden unconsciousness can result from cutaneous vasodilation with consequent systemic and cerebral hypotension. Systolic blood pressure is usually less than 100 mm Hg, and there is typically a history of vigorous physical activity for 2 hours or more just preceding the episode. The skin is typically cool and moist and the pulse is weak.

Treatment consist of rest and recumbency in a cool place, with fluids by mouth

2. Heat Cramps

Fluid and electrolyte depletion can result in slow, painful skeletal muscle contractions and even severe muscle spasms lasting 1 - 3 minutes, usually of the muscles most heavily used. Cramping results from salt depletion as sweat losses are replaced with water alone. The skin is moist and cool, and the muscles are tender. There may be muscle twitching. The victim is alert, with stable vital signs, but may be agitated and complaining of pain. The body temperature may be normal or slightly increased. Involved muscle groups are hard and lumpy. There is almost always a history of vigorous activity just preceding the onset of symptoms. Laboratory evaluation may show low serum sodium, hemoconcentration, and elevated urea and creatinine.

The patient should be moved to a cool environment and given oral saline solution to replace both salt and water. Because of their slower absorption, salt tablets are not recommended. The victim may have to rest for 1 - 3 days with continued dietary salt supplementation before returning to work or resuming strenuous activity in the heat.

3. Heat Exhaustion

Heat exhaustion results from prolonged heavy activity with inadequate salt intake in a hot environment and is characterized by dehydration, sodium depletion, or isotonic fluid loss with accompanying cardiovascular changes.

The diagnosis is based on prolonged symptoms and a rectal temperature over 37.8 C, increased pulse rare - usually more than half again the patient's normal rate - and moist skin. Symptoms associated with heat syncope and heat cramps may also be present. The patient may be quite thirsty and weak, with central nervous system symptoms such as headache, fatigue, and, in cases due chiefly to water depletion, anxiety, paresthesias, impaired judgment, hysteria, and occasionally psychosis. Hyperventilation secondary to heat exhaustion can lead to respiratory alkalosis. Heat exhaustion may progress to heat stroke if sweating ceases.

Treatment consist of patient location in a shaded, cool environment, providing adequate hydration, salt replenishment - orally, if possible - and active cooling if necessary. Physiologic saline or isotonic glucose solution can be administered intravenously in severe cases or when oral administration is not appropriate. Intravenous 3% saline may be necessary if sodium depletion is severe. At least 24 hours of rest is recommended.

4. Heat Stroke

Heat stroke is a life - threatening medical emergency resulting from failure of the thermoregulatory mechanism. Heat stroke is imminent when the core temperature approaches 41 C. It presents in one of two forms: Classic heat stroke occurs in patients with compromised hoemostatic mechanism: exertional heat stroke occurs in previously healthy persons undergoing strenuous exertion in a thermally stressful environment. Morbidity or even death can result from cerebral , cardiovascular, hepatic, or renal damage.

The hallmarks of heat stroke are cerebral dysfunction with impaired consciousness, high fever, and absence of sweating. Persons at greatest risk are the very young, the elderly or chronically infirm, and patients receiving medications that interfere with heat-dissipating mechanisms.

Exertional heat stroke and exertion - related illnesses, including rhabdomyolysis, are appearing more frequently as including rhabdomyolysis, are appearing more frequently as complications of participation by unconditioned amateurs in strenuous athletic activities such as marathon running and triathlon competition.

Clinical Findings

A. Symptoms and Signs
Failure of the heat dissipation mechanism for any reason result in dizziness, weakness, emotional liability, nausea and vomiting, diarrhea, confusion, delirium, blurred vision, convulsions, collapse, and unconsciousness. The skin is hot and initially covered with perspiration. Later it dries. The pulse is strong initially. Blood pressure may be slightly elevated at first, but hypotension develops later. The core temperature is usually over 41 C. As with heat exhaustion, hyperventilation can occur, leading to respiratory alkalosis.

Exertional heat stroke may present with sudden collapse and loss of consciousness followed by irrational behavior. Anhidrosis may not be present. Twenty-five percent of heat stroke victims have prodromal symptoms for minutes to hours that may include dizziness, weakness, nausea, confusion, disorientation, drowsiness, and irrational behavior.

B. Laboratory Findings :
Laboratory evaluation may reveal dehydration leukocytosis, elevated BUN, hyperuricemia, hemoconcentration, acid-base abnormalities, and decreased serum potassium, sodium, calcium, and phosphorus; urine is concentrated, with elevated protein, tubular casts, and myoglobinuria. Thrombocytopenia, increased bleeding and clotting times, fibrinolysis, and consumption coagulopathy may also be present. Rhabdomyolysis and myocardial, hepatic, or renal damage may be identified by elevated serum creatine kinase and aminotransferase levels and BUN and by the presence of anuria, proteinuria, and hematuria. Electrocardiographic findings may include ST - T changes consistent with myocardial ischemia.

Treatment
Treatment is aimed at reducing the core temperature rapidly and controlling the secondary effects. Evaporative cooling is rapid and effective and is easily performed in most emergency settings. The patient's clothing should be removed and the entire body sprayed with water while cooled or ambient air is passed across the patient's body with large fans or other means at high velocity. The patient should be in the lateral recumbent position or supported in a hands - and - knees position to expose as much skin surface as possible to the air. Other alternatives include use of cold wet sheets accompained by fanning or immersion in chilled water. Cardiopulmonary bypass provides rapid cooling but is often not practical.

Immersion is an ice-water bath as initial treatment is no longer preferred because of its greater potential for complications of hypotension and shivering. However, it should be considered if core temperature is not decreased rapidly in response to other treatment. Alternatives include hand forearm immersion in cold water, ice packs, and iced gastric lavage, though these are much less effective than evaporative cooling.

Treatment should be continued until the rectal temperature drops to 30 C. The temperature remains stable in most cases, but it should continue to be monitored for 24 hours. Chlorpromazine or diazepam can be give initially and then every 4 hours to control shivering and other muscular activity associated with increased heat load. Antipyretics have no effect on environmentally induced hyperthermia and are contraindicated.

Hypovolemic and cardiogenic shock must be carefully distinguished, as either or both may occur. Central venous or pulmonary artery wedge pressure should be monitored. Five percent destrose in half-normal or normal saline should be administered for fluid replacement.

The patient should also be observed for renal failure due to rhabdomyolysis, hypokalemia, cardiac arrhythmias, disseminated intravascular coagulation, and hepatic failure. Hypokalemia frequently accompanies heat stroke but may not appear until rehydration. Maintenance of extracellular hydration and electrolyte balance should reduce the risk of renal failure due to rahbdomyolysis. Fluid administration to ensure a high urine output, mannitol administration , and alkalinizing the urine are recommended. Corticosteroids have not been shown to be of value.

Fluid output should be monitored through the use of an indwelling urinary catheter.

Because sensitivity to high environmental temperature continues in some patients for prolonged periods following an episodes of heat stroke, immediate reexposure should be avoided.