Heat Illness and Heat Stroke

Abstract

After completing this article, readers should be able to: 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.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 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)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.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)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.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.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.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 few changes in mild heat stroke, although apoptosis can be an early After severe heat stroke, the liver abnormalities, including of and is a common in heat stroke, at of the patients who have nonexertional heat stroke and an even of patients who suffer from exertional heat stroke. The clinical findings are those of with elevation of blood to a greater than These abnormalities well to and usually within the first few days. or other of are in patients who have no in and values commonly follow heat stroke. The rapidly in the first hours following heat stroke. Although a of the decrease can be by the in often is greater than be caused by The cause of this may be blood cell is after heat stroke. blood cells that have been in have greater and increased which may contribute to blood cell and lead to early from the Individuals suffering from heat stroke to have a greater number of which may have a is although the may remain normal in mild heat stroke. The cause of has not been The often is normal at the time of but for the first a recent of patients of intravascular abnormalities include of the prothrombin time and time and elevation of the of have been Although are reported patients may a period of after the onset of heat stroke. these findings are by a of intravascular abnormalities within a few days. In of the abnormalities, significant is frequently are observed in the circulation for the first few hours after the onset of heat stroke and are rapidly from the These which have or more are termed because the a of Although the cause of this abnormality is not probably these cells are the changes of from heat stroke not produce any abnormalities. findings include intravascular and in abnormalities are not at the onset of heat stroke; the patient survive for at hours for the abnormalities to evolve. If the patient rapidly from heat stroke, the abnormalities associated with heat stroke are not observed. In the absence of that overheating may have been the cause of the observed abnormalities are sufficiently that heat stroke may not be considered in the differential For this reason, it is important to for environmental that heat may have been the cause of an injury from it is important to maintain a high index of Heat exhaustion should be if an individual is exercising in a warm environment and or or is confused or vomiting. treatment requires from the heat of and If the patient has significant CNS symptoms confusion, or symptoms of heat illness not within to minutes, the diagnosis of heat stroke should be considered and the patient of heat stroke of the patient be from the circumstances that to heat stroke to of heat and core temperature. the patient has been from the offending the core temperature begin to but it is important to the patient to than 104°F as rapidly as to injury. After the patient's temperature has been under is with the of the produced by the heat injury and the patient from injury caused by hypotension and dysfunction (Table have been described for patients who have heat stroke. of the patient in may be the In circumstances this is not may be as as active and is for the of the the patient may not as rapidly as because those who are in shock may have poor circulation to the heat has no efficacy in treating hyperthermia from heat stroke.The of treating shock are of circulating volume and of If heat exhaustion is not rapidly with and it may to heat stroke. In cases of heat exhaustion and in cases of heat stroke, should be If the patient's core temperature is greater than 104°F (40°C), may be used to cooling. In to abnormalities of sodium and other concentrations may be present and should be during Because cardiac may be diminished in heat stroke, the patient should be for signs of heart failure during the central vascular volume has been of may be because of diminished cardiac or low vascular In pediatric usually is for only to 48 after which cardiac and vascular tone return to of the risk of and of patients who have heat stroke should be with a blood and In cases of severe heat stroke, these should be more frequently because significant abnormalities may develop within the first In mild cases of heat stroke, treatment of the abnormalities usually is not necessary, but in more severe cases of heat stroke, of blood cells may be to within the first 48 Although it is may become a problem and is with and should be to these abnormalities before such as a that may be if by neurologic is one of the of heat stroke. This dysfunction can the form of confusion, coma, or usually can be relatively often with Although any of can be has the of not CNS which may be an important when to the of the patient's is to be common after heat stroke, with of cerebral in both pediatric and adult patients. Although have of sodium concentrations as an to cerebral it is that the cause of is thermal injury to cerebral to general, the are relatively by heat stroke, although failure is common in severe heat stroke. The cause of failure is CNS dysfunction than Because of this patients usually very for a few until they CNS control of During the period of the often are The of severe may of to or the of an elevation of hepatic is so common in heat stroke that the presence of such abnormalities may the clinical In severe heat stroke, transient liver failure with hepatic may Although liver has been in the treatment of severe hepatic failure caused by heat stroke, of hepatic is and is a suffering from heat exhaustion a they are and The outcome is and on the of the injury. the patient is from the circumstances that to hyperthermia, the core temperature to normal and injury The severity of the injury appears to the duration of hyperthermia and to the of the who have mild heat stroke usually are no and neurologic is when who survive heat stroke have a of an but the risk of sequelae is If the core temperatures have been greater than 107.6°F patients have a Patients from the hepatic and injuries, but neurologic injury often is neurologic abnormalities include decreased and poor Among severe cases of heat stroke, one third have permanent impairment, including and syndrome. and initially may show and often is The mortality rate for severe cases appears to be at illness, heat stroke, is potentially and care is Consequently, is of heat stroke in children and adolescents is to occur during so should occur in of these to the of heat are in to the risk of heat The is used by the United States to the risk of heat This takes into temperature and but measures the effect of thermal from the Although this may be the of heat illness, it is to and requires A more of the risk of heat illness is the Heat produced by the The Heat a for the risk of heat illness on the and the temperature. Because the to the risk of overheating can be quickly from the it is for and other to this It should be that the Heat not from the the heat index may be even than is on the as as who young during periods of exercise should for of heat Because the signs and symptoms of heat illness are this may be The presence of excessive confusion, and muscle may the onset of heat If any of these is the individual should be to a environment for and observed for of signs and who not quickly to this should be by a are during periods of hot an individual for the can be should be in the or in the when the risk is should be If this is not the temperature, and of the should be and should be During it may be to and of the may be the only safe is important to be to of and of If sweat are not patients may become which can lead to decreased in of sodium are in so is to hyponatremia. Individuals who be exercising in a hot environment should be to to the risk of hyponatremia. of large of should not be because of the risk of is important for to appropriate of during has that if is left to individuals not sufficient to maintain Although not for pediatric for adults are to of within hours to exercise the patient is During approximately of is to sweat losses. (5) have that individuals are more to to maintain than are those who are not should be to individuals who are not to hot it is important to not heat It is for individuals to suffer heat illness or heat stroke if they continue to exercise at a rate that heat more rapidly than it can be to the should be to to warm for at to before the of heat illness increased sweat rate and decreased exercise of to hours are for adolescents and adults to a longer as many as to 10 exercise should be to heat from the sun and to sweat should be to exercise in that sweat which is dangerous. have when individuals to their increased loss in should be to and adults the risk of heat stroke. The of adults in this can to among those who are in the to the of children and Because the risk for exertional heat stroke is the during the summer, can be for of nonexertional heat stroke of and from environments that at risk of health measures should be at the public the dangers of excessively hot for individuals who have limited the and In general, it is relatively to identify these environments excessively hot in the summer should be their should be that during is a sign and clearly that more of the body should be exposed to heat periods of high temperature and and the of sufficient of is to heat injury. During periods of high periods of and for early signs of heat exhaustion are can of potentially environmental and it to when physical should be limited or care of patients who develop heat stroke is supportive and treating the symptoms of and neurologic impairment. abnormalities should be and medical until the injury caused by excessive body temperature has The outcome after heat stroke can from to neurologic sequelae are the permanent seen of children and those who during physical may to this potentially