Heat Exhaustion and Heat Stroke

Article about heat disorders, including heat exhaustion and heat stroke.

Heat disorders

The body functions most efficiently at a temperature of about 37°C, and any major deviation from this temperature disrupts body processes. The body has special mechanisms for keeping its internal temperature constant; any malfunctioning or overloading of these mechanisms may cause a heat disorder. The mechanisms by which the body loses excess heat are controlled by the part of the brain known as the hypothalamus.

When blood temperature rises, the hypothalamus sends out nerve impulses to stimulate the sweat glands and dilate blood vessels in the skin. These changes in the skin cool the body down, but excessive sweating may result in an imbalance of salts and fluids in the body, leading to heat cramps or heat exhaustion. When the hypothalamus is disrupted (for example, by fever), the body may overheat, leading to heatstroke. Excessive external heat may cause prickly heat. Most heat disorders can be prevented by gradual acclimatization to hot conditions and taking salt tablets or solution. A light diet and frequent cool baths or showers may also help. Alcohol and strenuous exercise should be avoided.

Heat exhaustion

Heat exhaustion is fatigue, leading to collapse, that is caused by overexposure to heat. The principal causes of heat exhaustion are insufficient water intake, insufficient salt intake, and a deficiency in sweat production. In addition to fatigue, symptoms may include faintness, dizziness, nausea and vomiting, headache, and, when salt loss is heavy, heat cramps. The skin is usually pale and clammy, breathing is fast and shallow, and the pulse is rapid and weak. Unless it is treated, heat exhaustion may develop into heatstroke.

Treatment of heat exhaustion involves rest and replenishing lost water and salt. Prevention is usually by gradual acclimatization to hot conditions. heatstroke A life-threatening condition in which overexposure to heat, coupled with a breakdown of the body’s mechanisms for regulating temperature, cause the body to become overheated. A common cause is prolonged, unaccustomed exposure to the sun in a hot climate. Unsuitable clothing, strenuous activity, overeating, and overconsumption of alcohol can also be contributory factors.

Heat stroke

Heatstroke is often preceded by heat exhaustion, which consists of fatigue and profuse sweating.With the onset of heatstroke, the sweating diminishes and may stop entirely. The skin becomes hot and dry, breathing is shallow, and the pulse is rapid and weak. Body temperature rises dramatically and, without treatment, the victim may lose consciousness and even die.

Heatstroke can be prevented by gradual acclimatization to hot conditions (see heat disorders). If it does develop, emergency treatment is needed. This consists of cooling the victim by wrapping him or her in a cold, wet sheet, fanning the body, sponging with water, and giving the person a salt solution to drink.

Heat disorders in more detail -technical

Essentials

Rising body temperature triggers behavioural and physiological responses including reduction in physical activity, alterations of clothing, skin vasodilatation, and sweating. Heat-related illness is relatively common, especially with high humidity or prolonged physical activity. Risk can be reduced by acclimatization with repeated heat exposure, but some individuals seem to be particularly susceptible.

Clinical presentations of heat-related illness include (1) ‘heat exhaustion’—the commonest manifestation, with symptoms including nausea, weakness, headache, and thirst. Patients appear dehydrated, complain of being hot, and are flushed and sweaty. Treatment requires rest and fluids, given orally or (in severe cases) intravenously. (2) ‘heat stroke’—victims often complain of headache, may be drowsy or irritable, and may claim to feel cold. Core temperature is usually 38 to 41 °C, but the patient is shivering with dry, vasoconstricted skin. Treatment requires (a) aggressive rapid cooling—tepid water and fan-assisted evaporation in the first instance, with more invasive measures, e.g. intraperitoneal fluids, if required; (b) close biochemical monitoring; (c) supportive care for organ failure. There is significant mortality.

Thermoregulation in the heat

Most of human evolution took place in Africa and hence all humans are heat tolerant. We try to maintain a near-tropical microclimate against our skin, by using clothing to reduce heat loss to our surroundings. Thermal balance is regulated by the hypothalamus, which integrates information from skin temperature sensors with core temperature data from receptors within walls of large blood vessels and the brain. Rising temperatures trigger both behavioural and physiological responses.

Behavioural changes include reducing physical activity, altering clothing, and seeking shade or cool shelter. Cold drinks are also helpful. Although these responses seem simplistic, decisions may not be straightforward. If physical activity is low and water is in short supply, it is better to increase clothing cover and protect yourself from high radiant heat inputs. If activity must be continued and water is freely available, minimal clothing to permit maximal sweat evaporation is preferable. Immediate physiological responses involve vasodilatation of skin and subcutaneous blood vessels to enhance surface heat loss from radiation, conduction, and convection. The vasodilatation is triggered by a sympathetic cholinergic reflex in response to skin warming, with additional direct effects of heat on arteriolar tone. In a resting person, skin vasodilatation can maintain thermal equilibrium in environmental temperatures up to 32 °C, but with higher temperatures or heat production from activity, core temperatures will rise. This will trigger sweating to promote evaporative cooling.

Heat acclimatization

Repeated heat exposure can increase our capacity to lose heat by about 20-fold. This is partly due to greater skin blood flow from increases in circulating volume and improved vasodilatory responses, but changes in sweating responses are more important. In the nonacclimatized, sweating is triggered by a rise in core temperature of about 1 °C and maximum rates are limited to about 0.5 litre/h. Following acclimatization, a 0.5 °C core rise will trigger the response and sweat rates may exceed 2.0 litres/h. Acclimatization also leads to aldosterone-mediated reductions in sodium loss in both sweat and urine. The acclimatized individual therefore requires no sodium supplementation and giving supplements can delay the acclimatative process. Avoiding them altogether, however, risks salt depletion in nonacclimatized persons during prolonged heat stress. Acclimatization develops swiftly and around 90% of maximum heat tolerance is present after 7 to 10 days on which core temperature has risen by more than 1 °C for more than 1 h. Physical exertion combined with heat makes the changes even more rapid. After returning to cool environments, adaptation is lost in 20 to 40 days.

Susceptibility to heat-related illness

Although we are generally heat tolerant, heat-related illness is relatively common, and a number of factors increase vulnerability. Above an environmental temperature of about 35 °C, we tend to gain heat from our surroundings, and this, along with metabolic heat production, can only be lost via evaporation of sweat. Hot environments with high humidity are therefore the greatest threat. Acclimatization status has a marked influence on heat-related risks, the unacclimatized being prone to hyperthermia and salt depletion, while the fully acclimatized are vulnerable to dehydration from high sweat rates. Dehydration in itself limits sweating capacity and skin blood flow and hence increases risks. It can occur easily since thirst is a poor trigger for adequate drinking. Sweat rates in the acclimatized can also exceed gut capacity for water absorption.

Prolonged physical activity can cause heat illness under quite modest environmental conditions. This is particularly common when individuals are obliged to wear clothing that is insulative or vapour-impermeable. Military heat casualties are sometimes due to these factors, but there have also been fatalities in soldiers who have been susceptible to heat for no obvious cause. Such genetic or constitutional vulnerability should be suspected whenever a heat-related problem occurs following relatively modest heat stress. These people should be strongly advised to avoid similar circumstances in future. Obesity and poor physical fitness are further risk factors in the heat, as is diabetic autonomic dysfunction. Older people are generally heat sensitive and, in addition, are prone to problems from the increased circulatory demands of vasodilatation. Drugs can also induce heat illness (see following paragraphs).

Heat exhaustion

Most casualties in hot environments suffer from heat exhaustion. There is usually a history of prolonged heat stress followed by nausea, weakness, headache, thirst, and sometimes collapse. Patients appear dehydrated with a tachycardia and low blood pressure. If hyperthermic, the casualty should be complaining of feeling hot and should appear flushed and sweaty. The absence of these symptoms and signs, especially with a very high core temperature, suggests heat stroke. Heat exhaustion is ascribable to sodium and/or water depletion, but discriminating between these can be difficult. Sodium depletion tends to be greater if the casualty was poorly acclimatized and hence sweated relatively more sodium than water. Conversely, water depletion is more common in acclimatized individuals. Muscle cramps or whole-body dehydration without marked changes in haematocrit or serum proteins are suggestive of excessive sodium loss, but serum sodium tends to be normal in such cases unless enthusiastic fluid replacement without salt has led to hyponatraemia. This sometimes occurs in runners after completing marathons in hot environments. In predominantly water-depleted heat exhaustion, haematocrit, serum proteins, and serum sodium tend to be high. Renal impairment occurs in either form of heat exhaustion and the treatment of both types often requires 5 to 10 litres of oral or intravenous fluids in the first 24 h. Sodium supplementation is given as appropriate, but if sodium status is uncertain, it is usually safer to provide some than to precipitate acute hyponatraemia.

Heat stroke

Mild heat stroke has occurred when a hot environment or high activity levels have led to pyrexia with cerebral disturbance. Core temperature is usually 38 to 41 °C. The condition frequently follows heat exhaustion but temperature may have risen rapidly allowing no time for salt or water depletion. Sufferers have headaches and may be either drowsy or irritable. They often hyperventilate. The great danger is progression to more severe heat stroke, in which core temperature reaches levels that cause irreversible denaturing of proteins. This usually occurs at above 41.5 °C. Damage is widespread and particularly affects brain, liver, kidney, and muscle. Furthermore, the hypothalamic thermoregulatory centre may fail, switching off vasodilatation and sweating, and switching on cold defences inappropriately. Patients may therefore claim to feel cold and on examination may be shivering with a dry, vasoconstricted skin. A disastrous vicious cycle of increasing temperatures can then ensue.

Treatment for all heat stroke requires early recognition and rapid cooling. Tepid water and fan-assisted evaporation may be more effective than immersion in cold water, which can limit heat loss by stimulating intense peripheral vasoconstriction. Intraperitoneal fluids, paralysis, and ventilation may be needed and, in extreme circiumstances, cooling by cardiac bypass should be considered. Hyperkalaemia, hypocalcaemia, acidosis, rhabdomyolysis, disseminated intravascular coagulation, and hepatic or renal failure are common complications. Ventricular fibrillation is a frequent terminal event. Even if apparently resuscitated and cooled successfully, a 12- to 24-h ‘lucid interval’ may precede major deterioration. Permanent neurological damage is common.

Drug-induced heat illness

Many drugs can cause mild degrees of pyrexia by inducing local or systemic inflammation or hypersensitivity. Some also increase susceptibility to environmental heat by inhibiting central thermoregulation (e.g. barbiturates and phenothiazines) or reducing sweating capacity (e.g. anticholinergics). Salicylate overdose can generate heat stroke by increasing metabolic heat production while impairing hypothalamic regulation. There are two types of heat-related drug reactions, however, which are particularly dangerous.

Malignant hyperpyrexia

This is usually a dominantly inherited condition, although different gene defects may affect families. Administration of a variety of anaesthetic agents, including halothane and suxamethonium, leads to rapid, massive heat production from generalized increases in skeletal muscle tone. Contraction is triggered at the muscle cell membrane and hence neuromuscular blocking agents are ineffective. Intravenous dantrolene, an inhibitor of muscle calcium flux, is helpful and can be used along with ventilation and cooling/supportive measures. Fatalities are common, and it is therefore important to avoid risks whenever possible. In patients with a relevant personal or family history, in whom an anaesthetic is unavoidable, oral dantrolene should be given prior to the use of low-risk agents.

Neuroleptic malignant syndrome

This condition has similarities to malignant hyperpyrexia but is induced by idiosyncratic reactions to normal doses of antidopaminergic drugs, including phenothiazines and butyrophenones. The onset is less rapid than malignant hyperpyrexia, occurring over a few days. The increased muscle tone is also induced presynaptically and hence neuromuscular blocking agents help. Some recreational drugs, such as ecstasy, may induce this type of response, although most cases of ecstasy-induced hyperthermia are probably cases of heat stroke induced by enthusiastic dancing with limited fluid intake in hot, humid environments.

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Further reading

Bouchama A, Knochel JP (2002). Heat stroke. N Engl J Med, 346, 1978–88.

Hodgson P (1991). Malignant hyperthermia and the neuroleptic malignant syndrome. In: Swash M, Oxbury J (eds) Clinical neurology, pp. 1344–5. Churchill Livingstone, Edinburgh.

Hubbard RW, Armstrong LE (1988). The heat illnesses: biochemical, ultrastructural, and fluid-electrolyte considerations. In: Pandolf KB, Sawka MN, Gonzalez R (eds) Human performance physiology and environmental medicine at terrestrial extremes, pp. 305–59. Benchmark, Indianapolis, IN.