BOBY HEAT

by Stan Macik.

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In health, the body core temperature is maintained at 37°C by the hypothalamic thermoregulator centre.

Heat is produced by cellular metabolism, and lost through the skin by both vasodilatation and sweating and through the lungs in expired air. Profuse sweating occurs when the ambient temperature is greater than 32.5°C and during exercise. Evaporation of sweat is the vital mechanism cooling the body.

Heat acclimatization

Acclimatization to hot climates takes several weeks. Sweat volume increases and its salt content falls. Increased evaporation cools down the body.

Heat cramps


Painful muscle (usually leg) cramps often occur in well-acclimatized fit young people when they exercise in hot weather. Cramps are probably the result of low extracellular sodium caused by replenishment of water but not salt during prolonged sweating. They can be prevented by increasing dietary salt and respond to combined salt and water replacement.

Heat illness (heat exhaustion)

In high environmental temperatures, particularly with high humidity, vigorous exercise in clothing which inhibits heat loss can provoke a sudden elevation in core temperature. Weakness/exhaustion, dizziness and syncope, with a core temperature > 37°C define heat illness (exertional heat illness after exercise). Temperature elevation is more critical than water and sodium loss. Heat illness may progress to heat injury, a serious medical emergency.

Management

Remove the patient from any heat source. Cool with cold sponging and fans. Give oxygen by mask. Other causes of hyperpyrexia, e.g. malaria, should be considered.

Oral rehydration with both salt and water (25 g of sodium chloride per 5 L of water) is given in the first 24 hours, with adequate replacement thereafter. In severe heat illness, intravenous fluids are needed. Isotonic saline is usually given, depending on serum sodium. Careful monitoring is required. Secondary potassium loss must be corrected.

Heat injury (heat stroke)


Heat injury is an acute life-threatening situation when core temperature rises above 41°C. There is headache, nausea, vomiting and weakness. The skin is hot. Sweating is often absent, but this is not invariable, even in severe heat injury. Brain involvement leads to confusion, delirium and coma.

Heat injury develops in unacclimatized people in hot, humid windless climates, even without exercise. Sweating may be limited by prickly heat. Excessive exercise in inappropriate clothing, e.g. exercising on land in a wetsuit, can lead to heat injury in temperate climates. Old age, diabetes, drugs (e.g. alcohol, antimuscarinics, diuretics and phenothiazines) are all further precipitating factors. The pathogenesis of heat injury is a fall in cardiac output, lactic acidosis and intravascular coagulation. Diagnosis is clinical.

Management

Remove the patient from the hot area immediately.
Cool with sponging and icepacks.
Manage in intensive care (monitor biochemistry, clotting and muscle enzymes).
Give fluids with caution: hypovolaemia is often absent.
Prompt treatment is essential and can lead to rapid and complete recovery. Delay may be fatal. Prevention is by acclimatization, fluids and common sense.

Complications

These are hypovolaemia (shock), intravascular coagulation, cerebral oedema, rhabdomyolysis, and renal and hepatic failure. Their management is described in appropriate chapters.

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