- David S. Jardine, MD*
After completing this article, readers should be able to:
Describe the laboratory abnormalities that accompany heat stroke.
Understand the relationship between core temperature and injury.
Discuss strategies to reduce the risk of heat stroke during athletic events.
Describe the physical findings of patients suffering from heat stroke.
List the most common sequelae of heat stroke.
Identify the body temperature above which heat injury begins to occur.
Explain the differences between malignant hyperthermia and heat stroke.
Discuss the differences between heat stress, heat exhaustion, and heat stroke.
Heat illness is caused by an inability to maintain normal body temperature because of excess heat production or decreased heat transfer to the environment. Heat stroke arises when cellular injury is caused by excess body temperature. If the core temperature rises above 105.8°F (41°C) for more than a short time, thermal injury results. Proteins are denatured, and injured cells undergo apoptosis (programmed cell death) or necrosis. Even before injury takes place, an individual may suffer transient mental and physical impairment, which is called heat exhaustion. Heat stroke is a medical emergency that is associated with a mortality of approximately 12% in adult patients. Treatment requires aggressive supportive care to minimize mortality.
It is important to recognize the difference between fever and heat stroke. Fever is a normal response, during which the core temperature remains under the control of the central thermoregulatory centers that reside in the hypothalamus and brainstem. When a pyrogenic stimulus is received, core temperature is elevated rapidly to a new set point that is regulated by normal mechanisms. Maximum febrile temperatures rarely exceed 105.8°F (41°C). (1) In contrast, during heat illness, normal heat transfer mechanisms are overwhelmed and central thermoregulatory control is ineffective. Consequently, the core temperature can rise quickly to injurious levels.
Forms of Heat Illness
Before heat stroke occurs, lesser degrees of dysfunction result from the stress of responding to a thermal load. A patient may be thermally challenged because of excess heat production, typically caused by exercise in a warm environment. Alternatively, patients who are exposed to excessively warm environments even without exercise may develop heat stress. This effect characteristically occurs during heat waves in the summertime. Heat stress is the feeling of discomfort and physiologic strain that results from exposure to a hot environment. Although the individual is uncomfortable, core temperature remains within the normal range. (2) Patients suffering from heat stress show decreased exercise performance but usually no other symptoms.
Elevation of core body temperature is characteristic of heat exhaustion and heat stroke. Heat exhaustion is defined as mild dehydration with or without sodium abnormalities, which can include hypernatremia or hyponatremia. As with heat stress, heat exhaustion usually follows periods of strenuous exercise or exposure to high environmental temperatures. In heat exhaustion, core temperatures are between 100.4°F (38°C) and 104°F (40°C). Symptoms include intense discomfort, confusion, thirst, nausea, and vomiting. (2) The absence of severe neurologic symptoms frequently is used to differentiate heat exhaustion from heat stroke (Table 1).
|Heat Exhaustion||Heat Stroke|
|• Mild dehydration||• Usually severe dehydration|
|• Core temperature 100.4° to 104°F (38° to 40°C)*||• Core temperature may be >104°F (40°C)*|
|• Profuse sweating||• Flushed with hot, dry skin|
|• Thirst, nausea, vomiting, confusion, headache||• Dizziness, vertigo, syncope, confusion, delirium|
|• Feels faint or has collapsed||• May be unconscious|
↵* Core temperature may have fallen substantially by the time the patient reaches a medical facility.
Heat stroke is defined as a core temperature greater than 104°F (40°C), an exposure to heat (exertional or nonexertional), and neurologic dysfunction. Frequently divided into nonexertional (classic) heat stroke and exertional heat stroke, the dangers to the patient and therapeutic measures are similar.
Nonexertional heat stroke occurs in warm, often humid, environments. Affected patients become overheated without engaging in strenuous exercise. As the patient becomes more ill, anhydrosis frequently develops, accelerating the rate of temperature rise and worsening the injury. Nonexertional heat stroke occurs during the summer, frequently during heat waves.
Exertional heat stroke affects actively exercising individuals. Highly motivated athletes, soldiers, and laborers are at risk for this problem. Dehydration is a common feature. Warm, humid weather increases the risk of this illness, but cases frequently occur during cooler months.
The incidence of heat stroke is greater during periods of unusually high temperatures, but the overall incidence of heat stroke probably is underreported. This problem is compounded for young children and infants because the symptoms of heat stroke in pediatric patients are very similar to those observed in bacterial sepsis. (3)
Hemorrhagic Shock and Encephalopathy Syndrome
Infants are susceptible to a unique form of heat stroke that is termed hemorrhagic shock and encephalopathy syndrome. This illness was described initially in 1983, although the relationship between this illness and heat stroke was not recognized. Subsequently, a large number of cases have been described, many of which clearly were the result of heat stroke. (4) It is important to identify hemorrhagic shock and encephalopathy syndrome correctly because the neurologic sequelae may be severe.
Malignant Hyperthermia is Not Heat Stroke
Heat stroke sometimes is confused with malignant hyperthermia. Although both share the characteristic of injurious elevation of body temperature, they are distinctly different illnesses that have different causes. In heat stroke, the primary abnormality is the patient's inability to transfer normally produced heat (from normal metabolic activity or exercise) to the environment. In contrast, malignant hyperthermia is caused by abnormalities in the ryanodine receptor, a calcium channel receptor in the smooth endoplasmic reticulum. Malignant hyperthermia almost always follows treatment with a known triggering agent (volatile halogenated anesthetics and depolarizing muscle relaxants), causing skeletal muscle rigidity, hypercapnia, and rapid increase in core temperature to injurious levels. Dantrolene, a drug that depresses excitation-contraction coupling in skeletal muscle, has well-demonstrated efficacy in the treatment of malignant hyperthermia, but appears to show little or no benefit in treating heat stroke. Although malignant hyperthermia has been reported in the absence of triggering agents, this occurrence appears to be rare. Thus, malignant hyperthermia is not normally considered in the differential diagnosis of heat stroke.
Exertional heat stroke is caused by increased heat production over a period of sufficient duration to raise core temperature to injurious levels. Vigorous exercise is not a problem if the duration of the exercise is brief or if the environment is cool. The combination of prolonged exertion in a warm, humid environment, however, is dangerous. Among high school athletes, heat stroke is the third leading cause of mortality. (5) Dehydration can contribute significantly to the risk of heat stroke while exercising.
Exertional heat stroke is reported more commonly among adolescents and adults than among young children. The reasons for this discrepancy are unknown, but it may be that the discomfort that precedes heat illness usually causes younger children to decrease their activity level before the onset of injury. Unfortunately, adolescents and adults may be sufficiently motivated to ignore the discomfort until they collapse from heat stroke.
Nonexertional heat stroke occurs in the absence of excessive physical activity among individuals who are exposed to excessively warm, humid environments and are unable to disperse heat produced by basal metabolic processes. Sleeping infants may be at risk if they are covered with excessive bedding. Because of their limited motor skills, infants may be unable to remove the blankets in response to overheating; they depend on their caretakers to provide a safe thermal environment. Both infants and young children are at risk for nonexertional heat during the summer if they are left unattended in an automobile exposed directly to the sun or in hot environments. (6) Measurements of automobile temperatures in the summer show that the temperature can reach 145°F (62.8°C) in as few as 40 minutes, even in a light-colored vehicle that has the windows partly open. Heat stroke occurs rapidly in such an inhospitable environment.
Disabled children and adolescents as well as the elderly may have limited mobility and be unable to leave their dwellings during hot weather. In France, during the heat wave of 2003, an estimated 14,800 deaths were attributed to the hot weather. Despite the obvious public health risk of municipal heat waves, many cities at risk in the United States have inadequate or no plans for managing this problem. (7)
Clinical and Laboratory Abnormalities in Heat Stroke
Heat illness or heat stroke should be considered in any patient whose core temperature is elevated significantly (>104°F [40°C]) and who has mental status changes such as confusion, irritability, or loss of consciousness. Although heat illness may be differentiated from meningitis by the absence of nuchal rigidity, both of these illnesses share the characteristics of depressed blood pressure and elevated body temperature.
Heat stroke is a multisystem illness (Table 2). The signs observed in heat stroke are the result of one or more systems failing. Individuals suffering from heat stroke undergo a characteristic pattern of clinical and laboratory changes.
|Clinical Findings |
|Laboratory Abnormalities |
Patients who present with the signs of heat stroke have been injured by core temperatures greater than 104°F to 105.8°F (40°C to 41°C). The severity of injury is cumulative, so exposure to a very high temperature (109.4°F [43°C]) for a relatively brief time may produce an injury that is similar to one produced by exposure to a lower temperature (106.2°F [41.2°C]) for a longer period of time. Removal of the patient from the offending circumstances often is enough to begin cooling. By the time the patient reaches medical attention, his or her core temperature may be lower than 105.8°F (41°C), even though he or she may have suffered a significant heat injury. Because of this effect, it is important to recognize heat stroke, even in the absence of an elevated core temperature on presentation. In fact, insistence on the temperature being greater than 105.8°F (41°C) leads to significant underdiagnosis of heat stroke and the potential for misdiagnosis as intoxication or serious infection. For this reason, a careful history of the patient's recent exposure to circumstances that can lead to overheating is invaluable. In the absence of elevated core temperature, heat stroke may be diagnosed accurately by the presence of appropriate risk factors, typical clinical signs, and laboratory abnormalities.
Central Nervous System (CNS) Failure
The onset of severe neurologic dysfunction (delirium, coma, seizures) often is identified as one of the features that distinguishes heat stroke from heat exhaustion. In general, severe neurologic dysfunction is not observed until the rectal temperature is greater than 105.8°F (41°C). Confusion or delirium is the first sign of a deteriorating neurologic status. Coma and seizures can follow rapidly and often are associated with a poor outcome.
Hypotension is a common accompaniment of heat stroke and is frequent when the temperature exceeds 107.6°F (42°C). In the early stages of heat stroke, vasodilation leads to a low blood pressure, even though the cardiac index is increased and the central venous pressure is normal. More severe heat stroke produces irreversible myocardial impairment. Electrocardiographic findings that are indistinguishable from coronary ischemia may be observed. In the later stages of heat stroke, patients often become hypovolemic from sweat losses. Hypotension in heat stroke frequently is associated with diminished cerebral perfusion, which causes cerebral ischemia. These effects compound the injurious effects of heat on the CNS and may produce severe and potentially permanent neurologic dysfunction.
Serum lactate concentrations frequently are elevated in heat stroke. (8) Even after the blood pressure has returned to normal and vasopressors no longer are necessary, blood lactate values may remain elevated and only gradually return to normal. This delay is not unique to heat stroke; it is seen following circulatory shock and in patients who have hepatic dysfunction, which commonly accompanies heat stroke. In addition, vasomotor tone may remain abnormally low, even after normal temperature and intravascular volume have been restored. This outcome may be caused by the direct effects of heat on the heart and vascular system, or it may be mediated by the effects of endotoxin released from the heat-injured gastrointestinal (GI) tract or other inflammatory mediators.
GI Abnormalities and Hepatic Injury
Heat stroke causes a number of GI abnormalities. Although mild heat stroke may cause little more than diarrhea, more severe heat stroke produces significant injury to the GI tract, including mucosal swelling, petechiae, and hemorrhages. Even after resuscitation and return to normal temperature, GI tract injury can continue to evolve. As a consequence of these injuries, circulating endotoxin rises and potentially toxic free radicals may be generated. Injury to the GI tract probably contributes significantly to the hypotension and multisystem failure observed in heat stroke.
The liver may be injured severely in heat stroke. As a metabolically active solid tissue, the liver normally is a major site of heat production in the body. During periods of hyperthermia, the temperature of the liver is among the highest of any site in the body, placing hepatic tissue at high risk of injury. In addition, portal circulation perfuses the liver with a variety of toxic substances generated by the GI tract during heat stroke, including endotoxin and free radicals. Patients who survive heat stroke demonstrate rapidly rising alanine aminotransferase and aspartate aminotransferase concentrations that peak at 48 to 72 hours after injury and gradually return to normal after 10 to 14 days. Bilirubin can be elevated, but severe hyperbilirubinemia is unusual. Prolongation of the prothrombin time is common.
Biopsy of the liver after heat stroke shows few changes in mild heat stroke, although apoptosis can be an early finding. After severe heat stroke, the liver shows widespread abnormalities, including areas of cholestasis and necrosis.
Renal insufficiency is a common finding in heat stroke, affecting at least 50% of the patients who have nonexertional heat stroke and an even higher proportion of patients who suffer from exertional heat stroke. The usual clinical findings are those of prerenal azotemia, with elevation of blood urea nitrogen to a greater extent than creatinine. These abnormalities respond well to rehydration and usually correct within the first few days. Dialysis or other forms of renal support are required infrequently in patients who have no pre-existing renal disease.
Abnormalities in hematologic and coagulation values commonly follow heat stroke. The hematocrit declines rapidly in the first 24 hours following heat stroke. Although a portion of the decrease can be explained by rehydration, the reduction in hematocrit often is much greater than would be caused by rehydration. The cause of this anemia may be multifactorial. Red blood cell half-life is shortened after heat stroke. Further, red blood cells that have been heated in vitro have greater membrane rigidity and increased osmotic fragility, which may contribute to red blood cell damage and ultimately lead to early removal from the circulation. Individuals suffering from heat stroke tend to have a much greater number of spherocytes, which may have a shortened life span.
Thrombocytopenia is common, although the platelet count may remain normal in mild heat stroke. The cause of thrombocytopenia has not been defined. The platelet count often is normal at the time of presentation, but declines steadily for the first 24 hours. (3)
In a recent series, 45% of patients had evidence of disseminated intravascular coagulation. Coagulation abnormalities include prolongation of the prothrombin time and partial thromboplastin time and elevation of the d-dimer. (9) Abnormalities of plasminogen activator inhibitor 1 also have been described. Although bleeding diatheses are reported most commonly, some patients may experience a period of hypercoagulability shortly after the onset of heat stroke. Within 24 hours, these findings are replaced by a picture of disseminated intravascular coagulation. Such abnormalities generally resolve within a few days. (3) In spite of the coagulation abnormalities, clinically significant hemorrhage is uncommon.
Hypersegmented neutrophils frequently are observed in the peripheral circulation for the first few hours after the onset of heat stroke and are cleared rapidly from the blood. These neutrophils, which have five or more nuclear lobes (Fig. 1), are termed “botryoid” nuclei because the morphology resembles a cluster of grapes. Although the cause of this abnormality is not known, probably these cells are undergoing the morphologic changes of apoptosis.
Death from heat stroke does not produce any distinguishing postmortem abnormalities. Nonspecific findings include hepatocellular necrosis, disseminated intravascular coagulation, and in children, intrathoracic petechiae. Such histologic abnormalities are not immediately apparent at the onset of heat stroke; the patient must survive for at least 6 hours for the abnormalities to evolve. If the patient dies rapidly from heat stroke, the histologic abnormalities associated with heat stroke are not observed. In the absence of external evidence that overheating may have been the cause of death, the observed postmortem abnormalities are sufficiently ambiguous that heat stroke may not be considered in the differential diagnosis. For this reason, it is important to search for environmental clues that heat may have been the cause of an otherwise unexplained death.
To prevent injury from heat-related illnesses, it is important to maintain a high index of suspicion. Heat exhaustion should be suspected if an individual is exercising in a warm environment and feels faint or nauseated or is confused or vomiting. Effective treatment requires immediate removal from the heat source, cessation of exercise, and hydration. If the patient has significant CNS symptoms (ataxia, confusion, seizures, coma) or symptoms of heat illness do not resolve within 20 to 30 minutes, the diagnosis of heat stroke should be considered strongly and the patient treated accordingly.
Treatment of heat stroke consists of three phases. First, the patient must be removed from the circumstances that led to heat stroke to prevent ongoing accumulation of heat and increasing core temperature. Once the patient has been removed from the offending circumstances, the core temperature will begin to fall, but it is important to cool the patient to less than 104°F (40°C) as rapidly as possible to prevent ongoing injury. After the patient's temperature has been brought under control, therapy is supportive, with the goal of ameliorating the derangements produced by the heat injury and protecting the patient from additional injury caused by untreated hypotension and organ dysfunction (Table 3).
Several techniques have been described for cooling patients who have heat stroke. Immersion of the patient in ice water may be the most effective means. (10) In circumstances where this technique is not practical, simple evaporative cooling may be as effective as some active cooling methods (11) and is less uncomfortable for the patient. Regardless of the method chosen, the patient may not respond as rapidly as expected because those who are in shock may have poor circulation to the peripheral vasculature, thereby reducing heat transfer. Dantrolene has no efficacy in treating hyperthermia from heat stroke.
TREATMENT OF SHOCK.
The mainstays of treating shock are restoration of circulating volume and use of vasopressors. If heat exhaustion is not treated rapidly with cooling and rehydration, it may progress to heat stroke. In most cases of heat exhaustion and in all cases of heat stroke, intravenous rehydration should be undertaken. If the patient's core temperature is greater than 104°F (40°C), chilled intravenous fluids may be used to hasten cooling. In addition to dehydration, abnormalities of sodium and other electrolyte concentrations may be present and should be addressed during resuscitation. Because cardiac function may be diminished in heat stroke, the patient should be monitored for signs of congestive heart failure during rehydration.
Once the central vascular volume has been replenished, initiation of vasopressor therapy may be necessary because of diminished cardiac function or persistently low systemic vascular resistance. In pediatric patients, vasopressor therapy usually is required for only 24 to 48 hours, after which cardiac function and vascular tone return to normal.
TREATMENT OF HEMATOLOGIC AND COAGULATION ABNORMALITIES.
Because of the risk of anemia, thrombocytopenia, and prolongation of coagulation parameters, patients who have heat stroke should be monitored daily with a complete blood count and coagulation studies. In cases of severe heat stroke, these parameters should be monitored more frequently because clinically significant abnormalities may develop within the first 24 hours. In mild cases of heat stroke, treatment of the hematologic abnormalities usually is not necessary, but in more severe cases of heat stroke, transfusion of packed red blood cells may be needed to treat progressive anemia within the first 48 hours. Although it is unusual, bleeding occasionally may become a problem and is treated easily with fresh frozen plasma and platelets. Consideration should be given to correcting these abnormalities before performing procedures such as a lumbar puncture that may be dangerous if accompanied by bleeding.
TREATMENT OF NEUROLOGIC ABNORMALITIES.
Acute neurologic disability is one of the hallmarks of heat stroke. This dysfunction can take the form of confusion, obtundation, coma, or seizures. Seizures usually can be controlled relatively easily, often with anticonvulsant monotherapy. Although any of several anticonvulsants can be effective, phenytoin has the advantage of not producing additional CNS depression, which may be an important consideration when attempting to assess the progress of the patient's condition.
Cerebral edema is believed to be common after heat stroke, with local areas of cerebral infarction possibly occurring in both pediatric and adult patients. Although some have advocated close monitoring of serum sodium concentrations as an approach to avoid cerebral edema, it is probable that the cause of edema is thermal injury to neuronal cells, making cerebral edema difficult to prevent.
TREATMENT OF RESPIRATORY FAILURE.
In general, the lungs are relatively unaffected by heat stroke, although respiratory failure is common in severe heat stroke. The cause of respiratory failure is CNS dysfunction rather than parenchymal lung disease. Because of this mechanism, patients usually require very modest ventilator settings for a few days until they regain CNS control of respiratory activities. During the period of respiratory failure, the chest radiographs often are clear. The development of severe lung disease may indicate aspiration of gastric contents prior to intubation or the development of an intercurrent infection.
TREATMENT OF HEPATIC FAILURE.
Marked elevation of hepatic enzymes is so common in heat stroke that the presence of such abnormalities may help confirm the clinical diagnosis. In severe heat stroke, transient liver failure with widespread hepatic necrosis may occur. Although liver transplantation occasionally has been employed in the treatment of severe hepatic failure caused by heat stroke, spontaneous recovery of hepatic function is likely, and transplantation is a last resort.
Outcome of Heat Stroke and Heat Illness
Patients suffering from heat exhaustion make a full, prompt recovery once they are cooled and rehydrated. The outcome is variable and depends on the extent of the original injury. Typically, once the patient is removed from the circumstances that led to hyperthermia, the core temperature decreases to normal and injury ceases. The severity of the injury appears related to the duration of hyperthermia and to the height of the temperature.
Patients who have mild heat stroke generally recover uneventfully. There usually are no sequelae, and neurologic functioning is intact when tested several months later. Those who survive moderate-to-severe heat stroke have a good chance of making an intact recovery, but the risk of sequelae is higher. If the core temperatures have been greater than 107.6°F (42°C), patients have a poorer prognosis. Patients generally recover from the hepatic and renal injuries, but neurologic injury often is permanent. Persistent neurologic abnormalities include behavioral changes, decreased visual acuity, dysarthria, impaired memory, ataxic gait, and poor coordination. Among severe cases of heat stroke, one third have permanent moderate-to-severe impairment, including spasticity and pancerebellar syndrome. Computed tomography scan and MRI initially may show edema and ischemic changes. Later, atrophy often is noted. The mortality rate for severe cases appears to be at least 10%.
Preventing Heat Illness
Heat illness, especially heat stroke, is potentially devastating, and care is supportive. Consequently, prevention is of utmost importance. Exertional heat stroke in children and adolescents is most likely to occur during athletic activities, so planning should occur in advance of these activities to reduce the likelihood of heat illness.
Two methods are in widespread use to assess the risk of heat illness. The Wet Bulb Globe Temperature Index (http://www.usariem.army.mil/heatill/appendc.htm) is used by the United States Armed Services to assess the risk of heat illness. This measure takes into account temperature and humidity but also measures the effect of radiant thermal energy from the sun. Although this measurement may be the most accurate predictor of heat illness, it is complex to use and requires special equipment. A much more user-friendly measure of the risk of heat illness is the Heat Index Chart (Fig. 2) produced by the National Weather Service (http://www.crh.noaa.gov/jkl/?n=heat_index_calculator). The Heat Index Chart provides a ready means for assessing the risk of heat illness based on the relative humidity and the temperature. Because the information needed to assess the risk of overheating can be obtained quickly from the Weather Service, it is far easier for coaches and other supervisory personnel to employ this method. It should be noted that the Heat Index Chart does not measure radiant energy from the sun. On sunny days, therefore, the heat index may be even higher than is indicated on the chart (by as much as 15°F [9.5°C]).
Those who supervise young people during periods of exercise should monitor them carefully for evidence of heat illness. Because the signs and symptoms of heat illness are nonspecific, this task may be difficult. The presence of excessive fatigue, confusion, and muscle cramps may indicate the onset of heat illness. If any of these is present, the affected individual should be moved to a cool environment for oral rehydration and observed carefully for progression of signs and symptoms. Children who do not respond quickly to this intervention should be evaluated by a physician.
When athletic events are planned during periods of hot weather, designating an individual responsible for determining whether the activities can be conducted safely should be considered. Scheduling events late in the day or in the evening when the risk is less also should be considered. If this scheduling is not possible, the temperature, humidity, and condition of the participants should be monitored. Frequent breaks, shade, and fluids should be provided. During especially adverse conditions, it may be impossible to ensure participant safety, and cancellation of the event may be the only safe option.
It is important to be attentive to adequacy of hydration and maintenance of proper electrolyte balance. If sweat losses are not replaced, patients may become hypovolemic, which can lead to decreased sweating and, in extreme cases, hypotension. Significant amounts of sodium are lost in sweat, so electrolyte replacement is essential to avoid hyponatremia. Individuals who will be exercising in a hot environment should be encouraged to consume liquids containing electrolyte solutions (ie, “sports drinks”) to avoid the risk of hyponatremia. Consumption of large quantities of hypotonic fluids should not be encouraged because of the risk of electrolyte imbalance.
It is important for supervisory officials to encourage appropriate intake of fluids during activities. Research has shown that if fluid intake is left up to personal preference, most individuals do not drink sufficient quantities to maintain proper hydration. Although figures do not exist for pediatric patients, current recommendations for adults are to consume 500 mL of fluid within 2 hours prior to exercise (assuming the patient is euvolemic). During exercise, approximately 250 mL of fluid every 20 minutes is recommended to offset sweat losses. (5) Studies have shown that acclimated individuals are more likely to consume liquids to maintain hydration than are those who are not acclimated. Therefore, special attention should be paid to individuals who are not yet acclimated to hot weather.
Although it is important to emphasize adequate hydration, hydration alone does not prevent heat illness. It is possible for well-hydrated individuals to suffer heat illness or heat stroke if they continue to exercise at a rate that generates heat more rapidly than it can be transferred to the environment.
Athletes should be encouraged to acclimate to warm conditions for at least 3 to 4 days before competing. Acclimatization reduces the likelihood of heat illness through increased sweat rate and decreased electrolyte loss. At least four exercise sessions of 1 to 4 hours each are necessary for adolescents and adults to acclimate. Children need a longer acclimatization program, requiring as many as 8 to 10 exercise sessions.
Clothing should be light colored to reduce radiant heat absorption from the sun and loose to help sweat evaporate. Athletes never should be allowed to exercise in garments that restrict sweat loss, which is extremely dangerous. Deaths have resulted when individuals trying to reduce their weight through increased fluid loss exercised in waterproof garments.
Consideration should be given to teaching youth and adults about the risk of heat stroke. The involvement of supervising adults in implementing this program can help to disseminate up-to-date information among those who are in the best position to assure the safety of children and adolescents. Because the risk for exertional heat stroke is the greatest during the summer, educational efforts can be timed for maximum impact.
Prevention of nonexertional heat stroke consists of removing vulnerable populations (infants, small children, and disabled individuals) from environments that place them at risk of overheating. Public health measures should be directed at educating the public about the dangers of excessively hot environments, especially for individuals who have limited self-help skills (ie, the young, disabled, and elderly). In general, it is relatively simple to identify these environments (eg, excessively hot rooms, closed cars in the summer sun). Parents should be cautioned against overbundling their infants. They also should be told that sweating during sleep is a dangerous sign and clearly indicates that more of the infant's body surface should be exposed to allow adequate heat loss.
During periods of high temperature and humidity, encouraging hydration and the availability of sufficient quantities of electrolyte-containing fluids is essential to prevent heat injury. During periods of high risk, limiting activity, enforcing periods of rest, and monitoring for early signs of heat exhaustion are important. Using readily available charts can facilitate identification of potentially dangerous environmental conditions and make it easier to determine when physical activities should be limited or rescheduled.
The care of patients who develop heat stroke is supportive and involves treating the symptoms of dehydration, shock, and neurologic impairment. Hematologic abnormalities should be corrected and medical support provided until the injury caused by excessive body temperature has abated. The outcome after heat stroke can range from full recovery to death. Severe neurologic sequelae are the permanent injuries seen most often. Education of children and those who supervise them during physical activities may help to prevent this potentially devastating illness.
Dr Jardine did not disclose any financial relationships relevant to this article.
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