This is an important issue, so I present this discussion from, which is a good overview of heat related injuries.

Background: Heat illness may be viewed as a continuum of illnesses relating to the body's inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.

Two forms of heatstroke exist. Exertional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heatstroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed.

With the influence of global warming, it is predicted that the incidence of heatstroke cases and fatalities will also become more prevalent. Because behavioral responses are important in the management of temperature elevations, heatstroke may be entirely preventable.

Pathophysiology: Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body's mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

Heat may be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold to levels exceeding 1000 kcal/h. Similarly, fever, shivering, tremors, convulsions, thyrotoxicosis, sepsis, sympathomimetic drugs, and many other conditions can increase heat production, thereby increasing body temperature.

The body also can acquire heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses. Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body's surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the angle of the sun, the season, and the presence of clouds, among other factors. For example, during summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.

Under normal physiologic conditions, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range. In a simplified model, thermosensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in the blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.

As the major heat-dissipating organ, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.

The efficacy of evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the threshold at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.

When heat gain exceeds heat loss, the body temperature rises. Classic heatstroke occurs in individuals who lack the capacity to modulate the environment (eg, infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heatstroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.

Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.

On a cellular level, many theories have been hypothesized and clinically scrutinized. Generally speaking, heat directly influences the body on a cellular level by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines and heat shock proteins (HSPs) (HSP-70 in particular, which allows the cell to endure the stress of its environment), are produced. If the stress continues, the cell will succumb to the stress (apoptosis) and die. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heatstroke, multiorgan-dysfunction syndrome (MODS), and ultimately death. Progression to heatstroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.


* In the US: According to the National Centers for Health Statistics (NCHS), 7046 deaths were attributed to excessive heat exposure from 1979-1997, or an average of 371 deaths occurred per year. Heatstroke and deaths from excessive heat exposure are more common during summers with prolonged heat waves. For example, during the heat wave of 1980 (a record year for heat), 1700 deaths were attributed to heat, compared to only 148 deaths attributed to heat the previous year. Persons older than 65 years accounted for at least 44% of cases. The numbers published by the NCHS are believed to grossly underestimate the true incidence of heat-related deaths because death rates from other causes (eg, cardiovascular disease, respiratory disease) also increase during the summer, and especially during heat waves.

* Internationally: Heatstroke is uncommon in subtropical climates. The condition is recognized increasingly in countries that experience heat waves rarely (eg, Japan), and it commonly affects people who undertake a pilgrimage to Mecca, especially when the pilgrims arrive from a cold environment. In 1998, one of the worst heat waves to strike India in 50 years resulted in more than 2600 deaths in 10 weeks. Unofficial reports described the number of deaths as almost double that figure.

Mortality/Morbidity: Morbidity and mortality from heatstroke are related to the duration of the temperature elevation. When therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%. Mortality is highest among the elderly population, patients with preexisting disease, those confined to a bed, and those who are socially isolated.

Race: With the same risk factors and under the same environmental conditions, heatstroke affects all races equally. However, because of differences in social advantages, the annual death rate due to environmental conditions is more than 3 times higher in blacks than in whites.

Sex: With the same risk factors and under the same environmental conditions, heatstroke affects both genders equally. However, because of gender differences in the workforce, the annual death rate due to environmental conditions is 2 times higher in men than in women.

Age: Infants, children, and elderly persons have a higher incidence of heatstroke than young, healthy adults.

* Infants and children are at risk for heat illness due to inefficient sweating, a higher metabolic rate, and their inability to care for themselves and control their environment.

* Elderly persons also are at increased risk for heat-related illnesses because of their limited cardiovascular reserves, preexisting illness, and use of many medications that may affect their volume status or sweating ability. In addition, elderly people who are unable to care for themselves are at increased risk for heatstroke, presumably because of their inability to control their environment.

* EHS is the second most common cause of death among high school athletes, surpassed only by spinal cord injury. Unacclimatization is a major risk factor for EHS in young adults.

History: Heatstroke is defined typically as hyperthermia exceeding 41°C and anhidrosis associated with an altered sensorium. However, when a patient is allowed to cool down prior to measurement of the temperature (as may occur during transportation in a cool ambulance or evaluation in an emergency department), the measured temperature may be much lower than 41°C, making the temperature criterion relative. Similarly, some patients may retain the ability to sweat, removing anhidrosis as a criterion for the diagnosis of heatstroke. Therefore, strict adherence to the definition is not advised because it may result in dangerous delays in diagnosis and therapy.

Clinically, 2 forms of heatstroke are differentiated. Classic heatstroke, which occurs during environmental heat waves, is more common in very young persons and in the elderly population and should be suspected in children, elderly persons, and individuals who are chronically ill who present with an altered sensorium. Classic heatstroke occurs because of failure of the body's heat dissipating mechanisms.

On the other hand, EHS affects young, healthy individuals who engage in strenuous physical activity, and EHS should be suspected in all individuals with bizarre irrational behavior or a history of syncope during strenuous exercise. EHS results from increased heat production, which overwhelms the body's ability to dissipate heat.

* Exertional heatstroke

o EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment.

o A number of symptoms (eg, abdominal and muscular cramping, nausea, vomiting, diarrhea, headache, dizziness, dyspnea, weakness) commonly precede the heatstroke and may remain unrecognized. Syncope and loss of consciousness also are observed commonly before the development of EHS.

o EHS commonly is observed in young, healthy individuals (eg, athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory system and become hyperthermic. Because their ability to sweat remains intact, patients with EHS are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C.

o Risk factors that increase the likelihood of heat-related illnesses include a preceding viral infection, dehydration, fatigue, obesity, lack of sleep, poor physical fitness, and unacclimatization. While unacclimatization is a risk factor for heatstroke, EHS also can occur in acclimatized individuals who are subjected to moderately intense exercise.

o EHS also may occur because of increased motor activity due to drug use, such as cocaine and amphetamines, and as a complication of status epilepticus.

* Nonexertional heatstroke

o Classic NEHS is characterized by hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic, although heatstroke may occur with lower core body temperatures.

o Numerous CNS symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma have been described.

o Anhidrosis due to cessation of sweating is a late occurrence in heatstroke and may not be present when patients are examined.

o Other CNS symptoms include hallucinations, seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos.

o Patients with NEHS initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted.

o Classic heatstroke most commonly occurs during episodes of prolonged elevations in ambient temperatures. It affects people who are unable to control their environment and water intake (eg, infants, elderly persons, individuals who are chronically ill), people with reduced cardiovascular reserve (eg, elderly persons, patients with chronic cardiovascular illnesses), and people with impaired sweating (eg, patients with skin disease, patients ingesting anticholinergic and psychiatric drugs). In addition, infants have an immature thermoregulatory system, and elderly persons have impaired perception of changes in body and ambient temperatures and a decreased capacity to sweat.


* Vital signs

o Temperature: Typically, the patient's temperature exceeds 41°C, but, in the presence of sweating, evaporating mechanisms, and the initiation of cooling methods, body temperatures lower than 41°C are common.

o Pulse: Tachycardia to rates exceeding 130 beats per minute is common.

o Blood pressure: Patients commonly are normotensive, with a wide pulse pressure; however, hypotension is common and is due to a number of factors, including vasodilation of the cutaneous vessels, pooling of the blood in the venous system, and dehydration. Hypotension also may be due to myocardial damage and may signal cardiovascular collapse.

* Central nervous system

o Symptoms of CNS dysfunction are present universally in persons with heatstroke. Symptoms may range from irritability to coma.

o Patients may present with delirium, confusion, delusions, convulsions, hallucinations, ataxia, tremors, dysarthria, and other cerebellar findings, as well as cranial nerve abnormalities and tonic and dystonic contractions of the muscles.

o Patients also may exhibit decerebrate posturing, decorticate posturing, or they may be limp.

o Coma also may be caused by electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, uremic encephalopathy, and acute structural abnormalities, such as intracerebral hemorrhage due to trauma or coagulation disorders.

o Cerebral edema and herniation also may occur during the course of heatstroke.

* Eyes

o Examination of the eyes may reveal nystagmus and oculogyric episodes due to cerebellar injury.

o The pupils may be fixed, dilated, pinpoint, or normal.

* Cardiovascular

o Heat stress places a tremendous burden on the heart. Patients with preexisting myocardial dysfunction do not tolerate heat stress for prolonged periods.

o Patients commonly exhibit a hyperdynamic state, with tachycardia, low systemic vascular resistance, and a high cardiac index.

o A hypodynamic state, with a high systemic vascular resistance and a low cardiac index, may occur in patients with preexisting cardiovascular disease and low intravascular volume. A hypodynamic state also may signal cardiovascular collapse.

o The central venous pressure generally is within the reference range or elevated unless the patient is severely volume depleted.

o High-output cardiac failure and low-output cardiac failure may occur.

* Pulmonary

o Patients with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct CNS stimulation, acidosis, or hypoxia.

o Hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, and pulmonary edema.

* Gastrointestinal hemorrhage occurs frequently in patients with heatstroke.

* Hepatic

o Patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes.

o Rarely, fulminant hepatic failure occurs, accompanied by encephalopathy, hypoglycemia, and disseminated intravascular coagulation (DIC) and bleeding.

* Musculoskeletal

o Muscle tenderness and cramping are common; rhabdomyolysis is a common complication of EHS.

o The patient's muscles may be rigid or limp.

* Renal

o Acute renal failure (ARF) is a common complication of heatstroke and may be due to hypovolemia, low cardiac output, and myoglobinuria (due to rhabdomyolysis).

o Patients may exhibit oliguria and a change in the color of urine.


* Increased heat production

o Increased metabolism

+ Infections

+ Sepsis

+ Encephalitis

+ Stimulant drugs

+ Thyroid storm

+ Drug withdrawal

o Increased muscular activity

+ Exercise

+ Convulsions

+ Tetanus

+ Strychnine poisoning

+ Sympathomimetics

+ Drug withdrawal

+ Thyroid storm

o Moderate physical exercise, convulsions, and shivering can double heat production and result in temperature elevations that generally are self-limited and resolve with discontinuation of the activity.

o Strenuous exercise and status epilepticus can increase heat production 10-fold and, when uninterrupted, can overwhelm the body's heat-dissipating mechanisms, leading to dangerous rises in body temperature.

o Stimulant drugs, including cocaine and amphetamines, can generate excessive amounts of heat by increasing metabolism and motor activity through the stimulatory effects of dopamine, serotonin, and norepinephrine. The development of heatstroke in individuals intoxicated with stimulants is multifactorial and may involve a complex interaction between dopamine and serotonin in the hypothalamus and the brain stem.

o Neuroleptic agents also may elevate body temperature by increasing muscle activity, but, occasionally, these agents may cause neuroleptic malignant syndrome (NMS). NMS is an idiosyncratic reaction characterized by hyperthermia, altered mental status, muscle rigidity, and autonomic instability and appears to be due to excessive contraction of muscles.

o Certain drugs, such as inhaled volatile anesthetics and succinylcholine, may result in malignant hyperthermia. In contrast to heatstroke, malignant hyperthermia is believed to be induced by a decreased ability of the sarcoplasmic reticulum to retain calcium, resulting in sustained muscle contraction.

* Decreased heat loss

o Reduced sweating

+ Dermatologic diseases

+ Drugs

+ Burns

o Reduced CNS responses

+ Advanced age

+ Toddlers and infants

+ Alcohol

+ Barbiturates

+ Other sedatives

o Reduced cardiovascular reserve

+ Elderly persons

+ Beta-blockers

+ Calcium channel blockers

+ Diuretics

+ Cardiovascular drugs - Interfere with the cardiovascular responses to heat and, therefore, can interfere with heat loss

o Drugs

+ Anticholinergics

+ Neuroleptics

+ Antihistamines

o Exogenous factors

+ High ambient temperatures

+ High ambient humidity

* Reduced ability to acclimatize

o Children and toddlers

o Elderly persons

o Diuretic use

o Hypokalemia

* Reduced behavioral responsiveness: Infants, patients who are bedridden, and patients who are chronically ill are at risk for heatstroke because they are unable to control their environment and water intake.

Medical Care: Heatstroke is a medical emergency. Rapid reduction of the core body temperature is the cornerstone of treatment because the duration of hyperthermia is the primary determinant of outcome. Except for the mildest cases, patients diagnosed with EHS or NEHS should be admitted to the hospital for at least 48 hours to monitor for complications.

Once heatstroke is suspected, cooling must begin immediately and must be continued during the patient's resuscitation. Controversy still exists over what therapeutic modality is most effective in the treatment of heatstroke; however, the basic premise of rapidly lowering the core temperature to about 39°C (avoid overshooting and rebound hyperthermia) remains the primary goal. Some recent studies have shown that promptly reducing the exposure time to excessive heat can dramatically improve long-term outcomes and decrease irreversible injury. However, to date, no controlled studies have compared the efficacy of the various cooling methods on time or outcome.

Removal of restrictive clothing and spraying water on the body, covering the patient with ice water–soaked sheets, or placing ice packs in the axillae and groin may reduce the patient's temperature significantly. Patients who are unable to protect their airway should be intubated. Patients who are awake and responsive should receive supplemental oxygen. Intravenous lines may be placed in anticipation of fluid resuscitation and for the infusion of dextrose and thiamine if indicated. Hypoglycemia is a common occurrence in patients with EHS and may be a manifestation of liver failure; therefore, infusion of dextrose 50% in water solution (D50W) should be considered in all patients with heatstroke.

* Intensive care personnel must pay meticulous attention to the airway, reduce the temperature, limit the production of heat, optimize circulation, and monitor for and treat complications.

o Insert a thermistor probe to monitor temperature continuously.

o Insert a nasogastric tube to monitor for gastrointestinal bleeding and fluid losses.

o Place a Foley catheter to monitor urine output.

* The goal of treatment is to reduce the temperature by at least 0.2°C/min to approximately 39°C. Active external cooling generally is halted at 39°C to prevent overshooting, which can result in iatrogenic hypothermia.

o Place a flexible indwelling thermistor rectally or an esophageal probe to monitor core body temperature during treatment.

o Because thermal instability may persist for a few days after the onset of heatstroke, the temperature must be monitored continuously until it is stable.

* The optimal method of rapidly cooling patients is a matter of debate; each method has its own theoretical advantages and disadvantages.

o Ice-water immersion or an equivalent method is an extremely effective method of rapidly reducing core body temperature and traditionally was the most frequently recommended method. The increased thermal conductivity of ice water can reduce core body temperature to less than 39°C in approximately 20-40 minutes. The practice has been criticized recently. Theoretically, the ice water, which may be extremely uncomfortable to patients who are awake, can cause subcutaneous vasoconstriction, preventing the transfer of heat via conduction. Ice water also increases shivering, which in turn increases internal heat production. Other reasons for the recent criticisms include difficulty monitoring and resuscitating patients.

o Recently, evaporative techniques have been touted to be as effective as immersion techniques without the practical difficulties. However, data on the efficacy of this method are limited. Evaporative body heat loss may be accomplished by removing all of the patient's clothes and intermittently spraying the patient's body with warm water while a powerful fan blows across the body, allowing the heat to evaporate.

o A number of other cooling techniques have been suggested, but none has proven superior to or equal to cold-water immersion or evaporative techniques. These include peritoneal, thoracic, rectal, and gastric lavage with ice water; cold intravenous fluids; cold humidified oxygen; cooling blankets; and wet towels.

o In the most severe cases, cardiopulmonary bypass has been suggested, but this requires highly trained personnel and sophisticated equipment.

o Antipyretics (eg, acetaminophen, aspirin, other nonsteroidal anti-inflammatory agents) have no role in the treatment of heatstroke because antipyretics interrupt the change in the hypothalamic set point caused by pyrogens. They are not expected to work on a healthy hypothalamus that has been overloaded, as in the case of heatstroke. In this situation, antipyretics actually may be harmful in patients who develop hepatic, hematologic, and renal complications because they may aggravate bleeding tendencies.

o Dantrolene has been studied as a possible pharmacological option in the treatment of hyperthermia and heatstroke, but at present, it has not been proven to be efficacious in clinical trials.

* Along with immediate active cooling, steps to stop excessive production of heat must be taken.

o Agitation and shivering should be treated immediately with benzodiazepines.

o Benzodiazepines are the sedatives of choice in patients with sympathomimetic-induced delirium as well as alcohol and sedative drug withdrawals.

o Neuroleptics, such as chlorpromazine, which were the mainstays of therapy in the past, are best avoided because of their deleterious adverse effects, including lowering of the seizure threshold, interference with thermoregulation, anticholinergic properties, hypotension, hepatotoxicity, and other adverse effects.

* Similarly, convulsions must be controlled.

o Benzodiazepines and, if necessary, barbiturates are the recommended agents in this setting. Barbiturates may be used despite their theoretical impedance of sweat production.

o Phenytoin is not effective in controlling convulsions in this situation.

o Patients whose convulsions are refractory to benzodiazepines and barbiturates should be paralyzed and provided mechanical ventilation. Electroencephalographic monitoring is recommended in all such patients, and anticonvulsant medications should be adjusted accordingly.

* Recommendations on the administration of intravenous fluids for circulatory support differ among patient populations and depend on the presence of hypovolemia, preexisting medical conditions, and preexisting cardiovascular disease.

o While patients with heatstroke invariably are volume depleted, cooling alone may improve hypotension and cardiac function by allowing blood to redistribute centrally.

o Aggressive fluid resuscitation generally is not recommended because it may lead to pulmonary edema.

o Cor pulmonale also is a common finding in patients with heatstroke.

* When pulse rate, blood pressure, and urine output do not provide adequate hemodynamic information, fluid administration should be guided by more invasive hemodynamic parameters, such as central venous pressure (CVP), pulmonary capillary wedge pressure, systemic vascular resistance index (SVRI), and cardiac index (CI) measurements.

o Patients who exhibit a hyperdynamic state (ie, high CI, low SVRI) generally respond to cooling and do not require large amounts of intravenous crystalloid infusions.

o Hypotensive patients who exhibit a hypodynamic response (ie, high CVP, low CI) traditionally have been treated with low-dose isoproterenol; however, its arrhythmogenicity has raised questions about its continued use. Dobutamine, which is less arrhythmogenic than isoproterenol and more cardioselective, may be the inotrope of choice in these patients.

o Alpha-adrenergic drugs generally are contraindicated because they cause vasoconstriction and may interfere with heat loss.

* The occurrence of rhabdomyolysis may be heralded by the development of dark, tea-colored urine and tender edematous muscles.

o Rhabdomyolysis releases large amounts of myoglobin, which can precipitate in the kidneys and result in ARF. Renal failure especially is common in patients who develop hypotension or shock during the course of their disease and may occur in as many as 25-30% of patients with EHS.

o Treatment of rhabdomyolysis involves infusion of large amounts of intravenous fluids (fluid requirements may be as high as 10 L), alkalinization of the urine, and infusion of mannitol.

o Fluid administration is guided best by invasive hemodynamic parameters, and urine output should be maintained at 3 cc/kg/h to minimize the risk of renal failure.

o Alkalinization of the urine (urine pH 7.5-8.0) prevents the precipitation of myoglobin in the renal tubules and may control acidosis and hyperkalemia in acute massive muscle necrosis.

o Mannitol may improve renal blood flow and glomerular filtration rate, increase urine output, and prevent fluid accumulation in the interstitial compartment (through its osmotic action). Mannitol also is a free radical scavenger and, therefore, may reduce damage caused by free radicals.

o Once renal failure occurs, dialysis is the only effective therapeutic modality for rhabdomyolysis.

* Metabolic support

o Muscle necrosis may be so rapid that hyperkalemia, hypocalcemia, and hyperphosphatemia become significant enough to cause cardiac arrhythmias and require immediate therapy.

o In the presence of renal failure, hemodialysis may be necessary.

o Hypertonic dextrose and sodium bicarbonate may be used to shift potassium into the intracellular environment while more definitive measures (eg, intestinal potassium binding, dialysis) are prepared.

o Use of insulin may not be necessary in patients who are not diabetic and may be deleterious for patients with EHS and patients with liver failure, who commonly develop hypoglycemia.

o Use of calcium should be judicious because it may precipitate in and cause additional muscle damage. Use of calcium is reserved for patients with ventricular ectopy, impending convulsions, or electrocardiographic evidence of hyperkalemia.

o Various other electrolyte abnormalities have been reported in patients with heatstroke and must be monitored closely and treated carefully. These abnormalities may be related to solute-altering conditions such as vomiting, diarrhea, and use of diuretics. For example, hypokalemia, which is common in the early phases of heatstroke, may develop in response to respiratory alkalosis, diarrhea, and sweating. Similarly, hyponatremia may be due to sodium losses and/or rehydration with salt-poor solutions (eg, water), and hypernatremia may be due to dehydration.

* Heatstroke commonly leads to severe but reversible hepatic damage.

o Hepatic injury is represented by elevations in transaminase levels and bilirubin. During this phase, hypoglycemia, abnormal coagulation, cerebral edema, and death can occur, although rarely.

o Prolonged coagulation times also may signal the development of DIC, which, when present, carries a poor patient prognosis. Clinical manifestations can range from abnormal laboratory values to generalized bleeding occurring approximately 48 hours after the initial insult. DIC also may predispose patients to development of acute respiratory distress syndrome (ARDS), which also increases mortality.

o Treatment of hepatic failure includes the infusion of dextrose solutions to correct hypoglycemia; the early recognition and treatment of DIC, with replacement of clotting factors, fresh frozen plasma, platelets, and blood; and meticulous respiratory support.

* Pulmonary edema is a common complication of heatstroke and may be due to a number of factors, including fluid overload from aggressive rehydration, fluid overload from renal failure, congestive heart failure, and ARDS. The latter may develop because of multiple insults, including heat-induced pulmonary damage, aspiration pneumonia, and as a complication of liver failure. ARDS should be treated aggressively, with early mechanical ventilation and positive end-expiratory pressure (PEEP).

* ARF may occur because of direct thermal injury of the kidney, myoglobinuria, hypotension, and/or shock (acute tubular necrosis). Early manifestations of renal failure include oliguria, low-grade proteinuria, and granular casts.

o ARF initially is treated with intravenous fluids, diuretics, and correction of associated acid-base and electrolyte abnormalities.

o In the setting of rhabdomyolysis, mannitol may be the diuretic of choice because it does not interfere with the acid-base status of the urine, and it may have antioxidant activity.

o Furosemide may cause tubular acidosis and, therefore, may promote myoglobin deposition within the renal tubules.

o Once renal failure has set in, hemodialysis is the most effective therapy.

Surgical Care: Compartment syndrome must be suspected in all patients who exhibit rhabdomyolysis and muscle edema and tenderness. Intramuscular compartment pressure measurements must be performed when compartment syndrome is suspected, and fasciotomy must be performed when the intramuscular pressure exceeds 50 mm Hg. Fasciotomy also should be considered when intracompartmental pressures are 30-50 mm Hg, especially when they show no tendency to decrease in 6 hours and in patients who are hypotensive.


* Consider consultation with a nephrologist as soon as renal failure occurs.

* Consultation with a surgeon is indicated when compartment syndrome is suspected.

* Consider consultation with a liver transplant service for patients with persistent fulminant liver failure.

Diet: Patients may resume oral feeding when mental status, swallowing, and gastrointestinal tract function are normal.

Activity: During the initial phase of therapy, neuromuscular blockade with muscular paralysis should be considered for patients who are not cooling adequately. Depolarizing agents (eg, succinylcholine) and inhaled anesthetics should be avoided because of the risk of malignant hyperthermia. Patients may resume activity when the temperature has stabilized.

Medical/Legal Pitfalls:

* Relying on the criteria listed in the classic definition for diagnosing heatstroke

* Failure to consider the diagnosis in mildly hyperthermic patients with altered mental status: The diagnosis of heatstroke should be applied liberally to patients with altered mental status during environmental heat waves, even in the absence of severe hyperthermia.

* Failure to measure the temperature, thereby delaying the diagnosis and therapy

* Failure to initiate cooling measures in an expeditious manner

* Overcooling, thus causing iatrogenic hypothermia

* Prescribing antipyretics