By William Brady, MD, FACEP, FAAEM, Professor of Emergency Medicine and Internal Medicine, Vice Chair, Emergency Medicine, University of Virginia, Charlottesville.
Heat illness includes several distinct syndromes, presenting across a range of severity; two distinct syndromes include heat exhaustion and heat stroke. Heat exhaustion, the least concerning of these illnesses, is seen in patients who have been exposed excessively to high ambient temperatures for prolonged time periods. Heat exhaustion is seen in persons working in high heat conditions as well as recreational athletes. Heat exhaustion is associated with a favorable outcome, usually with removal of the patient from the high heat environment. Heat stroke results from an inability to control one’s body temperature, essentially, a failure of the body’s thermoregulatory mechanism. Heat stroke, if not rapidly diagnosed and appropriately managed, can result in death as well as significant long-term disability.
Two different varieties of heat stroke are seen in clinical medicine: classical and exertional.1 Classical heat stroke is seen in the older patient with significant long-term medical problems; the exertional subtype is encountered in the younger, healthier population after intense physical activity.2 Classical heat stroke tends to occur in epidemic fashion during periods of high heat index, a function of both ambient temperature and humidity (e.g., the summer heat wave). Affected patients are usually older with poor conditioning, have significant comorbidity, and have an absence of cooling systems. Psychiatric syndromes with related medications (e.g., anticholinergic drugs, including neuroleptic medications) greatly increase the risk of heat stroke in affected individuals.
Exertional heat stroke commonly occurs in younger, healthy individuals when endogenous heat production overwhelms the thermoregulatory mechanisms. This homeostatic failure typically occurs when the patient is physically active in a warm, humid setting. Military personnel, athletes, and industrial workers are typical patients. Exertional heat stroke occurs sporadically throughout the summer.
Numerous factors—both endogenous and exogenous—can predispose an individual to heat stroke, including patient characteristics (e.g., advanced age, lack of acclimatization, physical activity, obesity, or poor conditioning), medical issues (e.g., substance abuse, dehydration, cardiovascular disease, and history of heat illness), concurrent medication use (e.g., antipsychotic, antidepressant, and cardioactive agents) and environmental factors (e.g., high humidity, high ambient temperature, or inadequate ventilation).3,4
The pathophysiology of heat stroke is linked to methods of bodily heat dissipation. Heat can be removed from the body by convection, radiation, conduction, and/or evaporation. Convection is the transfer of heat to a circulating fluid or gas while radiation is the transfer of heat to a portion of the environment that is not directly in contact with the object. Conduction is direct transfer of heat from the body to another object; evaporation is the transfer of heat by vaporization of liquid. Convection, radiation, and conduction require a thermal gradient between the transferring body and the environment; therefore, as the ambient temperature approaches 99º F, the mechanisms of heat loss become less effective; evaporation then assumes the major responsibility for heat dissipation.3 Furthermore, as humidity levels approach 90%, evaporation becomes much less effective in dissipating heat.1 Thus, a high heat index (both elevated ambient temperature and humidity) is a particularly likely risk scenario for heat stroke.
Heat stroke usually presents as an acute illness; the initial manifestations are altered mentation, high temperature, and ineffective diaphoresis. A minority of patients, however, can present with a transient, prodromal syndrome similar to heat exhaustion. These patients will manifest nausea, weakness, headache, and confusion; such patients then progress onto the typical heat stroke. The classic triad of symptoms includes central nervous system (CNS) dysfunction, hyperthermia, and hypohydrosis; as is true with most classic triads, this complete constellation of findings is encountered less often. CNS dysfunction is a universal finding in heat stroke victims; in fact, the clinical onset of heat stroke often is marked by either a loss of or alteration in consciousness. Any form of CNS dysfunction can be encountered, yet confusion progressing to extreme irritability followed by unresponsiveness is the norm. Convulsions (both focal and generalized), papilledema, muscular rigidity, and dystonic movements are other manifestations of neurologic dysfunction.
Hyperpyrexia is an important finding in the patient with heat stroke. It is difficult, however, to pinpoint an exact temperature at which heat stroke occurs. Prehospital cooling as well as the potential inaccuracies of peripherally obtained body temperatures further complicate the notation of specific temperatures as a criterion for the diagnosis. In fact, a lower temperature does not preclude the diagnosis.
The third classic finding in the heat stroke patient is hot, dry skin. Strict adherence to this criterion will lead to many missed cases; dry skin is a late phenomenon of heat stroke. In fact, most patients with heat stroke will present with continued, profuse sweating. The lack of anhydrosis does not rule out the possibility of heat stroke.1-4
Other organ systems are affected. The cardiovascular system invariably is involved with manifestation ranging from compensatory sinus tachycardia with nonspecific ST-segment changes on the electrocardiogram, to overt cardiac failure with acute coronary syndrome. Hepatic damage is an almost constant feature of heat stroke and is manifested by elevations in the transaminases levels, with jaundice appearing 24-72 hours after heat stroke onset. Hepatic synthetic dysfunction is manifested by coagulation abnormalities. Acute renal failure complicates 30% of exertional heat stroke cases but is much less common in the classical heat stroke patient. Rhabdomyolysis and hypotension are additional stresses placed on the renal system that may precipitate renal failure.1-3
Treatment and Outcome
Heat stroke is a medical emergency; irreversible damage may occur quickly if cooling measures are not started immediately. As abnormalities in the ABCs are addressed, cooling measures must be initiated. Several cooling methods are available, including cool/ice water immersion and evaporative techniques. The most commonly used method—ice water tub immersion—results in a rapid reduction of core body temperature with a cooling rate of up to 16º C/min. Cool water—rather than ice water—immersion also may be used and generally is less uncomfortable with a lower rate of cooling.1,2,4 The evaporative technique uses a combination of aerosolized water and fanning applied to the disrobed patient. Evaporative cooling methods may be employed easily in the ED using aerosolized tepid tap water and a fan over a disrobed patient; this approach likely represents the most appropriate method of core temperature reduction in the heat stroke patient. Other methods of cooling have been used to reduce core temperature (e.g., ice pack application, cooling blankets, peritoneal dialysis, and cardiopulmonary bypass); none of these methods has been proven to be superior to the immersion and evaporative approaches. As cooling occurs, the body temperature must be monitored. When body temperature reaches 38.5º C, cooling measures should be modified to avoid hypothermic overshoot.2
Other management issues include the support and maintenance of an adequate airway with appropriate oxygenation and ventilation; endotracheal intubation with mechanical ventilation often is required due to aspiration and convulsion management. Cardiovascular support most often is accomplished with intravenous fluids; it is uncommon to require vasopressor infusions. Seizures are frequent and are managed in standard also will address agitation and control shivering associated with cooling; older therapies with chlorpromazine should be avoided due to the potential for increased heat production. Surveillance for, and treatment of, rhabdomyolysis and the associated renal failure with appropriate laboratory testing and intravenous fluids is encouraged. Antipyretic agents play no role in the management of heat stroke unless complicated by an infectious syndrome after hospitalization.
The outcome of heat stroke is related to numerous factors including the degree of hyperthermia, the duration of hyperthermia, and co-morbidities. Investigators suggested that mortality in heat stroke is inversely related to the rapidity of effective cooling of the patient; the absolute peak of body temperature elevation is not so important prognostically.5 Duration of hyperthermia is another major factor in the outcome of the heat stroke patient; morbidity and mortality markedly increases with prolonged periods of elevated body temperature.6
1. Zelenak RR, et al. Morning report at Charity Hospital: Heat stroke New Orleans style. Am J Med Sciences 1987;294:268-274.
2. Shapiro Y, et al. Field and clinical observations of exertional heat stroke patients. Med Science Sports Exerc 1990;22:6-14.
3. Barthel HJ. Exertion-induced heat stroke in a military setting. Military Med 1990;155:116-119.
4. Kilbourne EM, et al. Risk Factors for Heatstroke. J Am Med Assoc 1982;247:3332-3336.
5. Hart GR, et al. Epidemic classical heat stroke: Clinical characteristics and course of 28 patients. Medicine 1982;61:189-196.
6. Knochel JP. Environmental heat illnesses — An eclectic review. Arch Int Med 1974;133:841-847.