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 41.1C (106F) 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 46C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106F or 41.1C 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 1.1C/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. An index used by some, including the American College of Sports Medicine, is the Wet Bulb Globe Temperature (WBGT). It is an environmental heat stress index used to evaluate the risk of heat of heat-related illness on an individual. It is calculated using 3 parameters: temperature, humidity, and radiant heat. There is low risk if the WBGT is < 65 F, moderate risk if it is between 65-73 F, high risk if between 73-82 F, and very high risk >82 F. Epidemiology Frequency United States In the United States, heat waves claim more lives each year than all other weather-related exposures combined (hurricanes, [1] tornadoes, floods, and earthquakes). According to the Centers for Disease Control and Prevention, 8,015 deaths were attributed to excessive heat exposure from 1979-2003, or an average of approximately 334 deaths per year.[2] 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. International 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. Lack of acclimatization is a major risk factor for EHS in young adults. History Heatstroke is defined typically as hyperthermia exceeding 41C 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 41C, 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 EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment. 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. 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 41C. Despite education and preventative measures, EHS is still the third most common cause of death among high school students. 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 lack of acclimatization. Although lack of acclimatization is a risk factor for heatstroke, EHS also can occur in acclimatized individuals who are subjected to moderately intense exercise. 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 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 41C are diagnostic, although heatstroke may occur with lower core body temperatures. Numerous CNS symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma have been described. Anhidrosis due to cessation of sweating is a late occurrence in heatstroke and may not be present when patients are examined. Other CNS symptoms include hallucinations, seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos. Patients with NEHS initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted. 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. Physical Vital signs Temperature: Typically, the patient's temperature exceeds 41C, but, in the presence of sweating, evaporating mechanisms, and the initiation of cooling methods, body temperatures lower than 41C are common. Pulse: Tachycardia to rates exceeding 130 beats per minute is common. 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. This will usually correct with normalization of the body temperature. Central nervous system Symptoms of CNS dysfunction are present universally in persons with heatstroke. Symptoms may range from irritability to coma. 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. Patients also may exhibit decerebrate posturing, decorticate posturing, or they may be limp. 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. Cerebral edema and herniation also may occur during the course of heatstroke. Eyes Examination of the eyes may reveal nystagmus and oculogyric episodes due to cerebellar injury. The pupils may be fixed, dilated, pinpoint, or normal. Cardiovascular Heat stress places a tremendous burden on the heart. Patients with preexisting myocardial dysfunction do not tolerate heat stress for prolonged periods. Patients commonly exhibit a hyperdynamic state, with tachycardia, low systemic vascular resistance, and a high cardiac index. 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. The central venous pressure generally is within the reference range or elevated unless the patient is severely volume depleted. High-output cardiac failure and low-output cardiac failure may occur.

Pulmonary Patients with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct CNS stimulation, acidosis, or hypoxia. Hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, and pulmonary edema. Gastrointestinal Gastrointestinal hemorrhage occurs frequently in patients with heatstroke. Hepatic Patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes. Rarely, fulminant hepatic failure occurs, accompanied by encephalopathy, hypoglycemia, and disseminated intravascular coagulation (DIC) and bleeding. Musculoskeletal Muscle tenderness and cramping are common; rhabdomyolysis is a common complication of EHS. The patient's muscles may be rigid or limp. Renal Acute renal failure (ARF) is a common complication of heatstroke and may be due to hypovolemia, low cardiac output, and myoglobinuria (due to rhabdomyolysis). Patients may exhibit oliguria and a change in the color of urine. Causes Increased heat production Increased metabolism Increased muscular activity y y y y y y y Exercise Convulsions Tetanus Strychnine poisoning Sympathomimetics Drug withdrawal Thyroid storm

y Infections y Sepsis y Encephalitis y Stimulant drugs y Thyroid storm y Drug withdrawal 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. 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. 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 brainstem. 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. 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 Reduced sweating y Dermatologic diseases y Drugs y Burns

Reduced CNS responses y Advanced age y Toddlers and infants y Alcohol y Barbiturates y Other sedatives Reduced cardiovascular reserve y Elderly persons y Beta-blockers y Calcium channel blockers y Diuretics y Cardiovascular drugs - Interfere with the cardiovascular responses to heat and, therefore, can interfere with heat loss Drugs y Anticholinergics y Neuroleptics y Antihistamines Exogenous factors y High ambient temperatures y High ambient humidity Reduced ability to acclimatize y Children and toddlers y Elderly persons y Diuretic use y 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. To compound matters, comorbidities and polypharmacy in the elderly can compromise their recovery. 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. According to the American College of Sports Medicine, the current recommendation is to initiate cooling immediately before transferring these [3] patients to an emergency department for further evaluation and treatment. 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 39C (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. If treatment is initiated within this so-called golden hour and is aggressive enough to rapidly reduce the core body temperature, complications (including multisystem organ failure) may be averted and have a positive [4] effect on the overall outcome of the patient. Recently, a review of 19 past clinical trials and observational studies (involving 556 patients) was performed, and the conduction method of cooling was found to be more efficacious in young, active adults with EHS. Unfortunately from this review, there was no [5] preferred treatment found for classical or NEHS and no temperature endpoint to prevent overcooling. 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. y y y Insert a thermistor probe to monitor temperature continuously. Insert a nasogastric tube to monitor for gastrointestinal bleeding and fluid losses. Place a Foley catheter to monitor urine output.

The goal of treatment is to reduce the temperature by at least 0.2C/min to approximately 39C. Active external cooling generally is halted at 39C to prevent overshooting, which can result in iatrogenic hypothermia. y y Place a flexible indwelling thermistor rectally or an esophageal probe to monitor core body temperature during treatment.[6] 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. y 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 39C 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. 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. 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. In the most severe cases, cardiopulmonary bypass has been suggested, but this requires highly trained personnel and sophisticated equipment. 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. 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.

y y

Along with immediate active cooling, steps to stop excessive production of heat must be taken. y y y Agitation and shivering should be treated immediately with benzodiazepines. Benzodiazepines are the sedatives of choice in patients with sympathomimetic-induced delirium as well as alcohol and sedative drug withdrawals. 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. y y Benzodiazepines and, if necessary, barbiturates are the recommended agents in this setting. Barbiturates may be used despite their theoretical impedance of sweat production. Phenytoin is not effective in controlling convulsions in this situation.

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. y y y While patients with heatstroke invariably are volume depleted, cooling alone may improve hypotension and cardiac function by allowing blood to redistribute centrally. Aggressive fluid resuscitation generally is not recommended because it may lead to pulmonary edema. 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. y y 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. Hypotensive patients who exhibit a hypodynamic response (ie, high CVP, low CI) traditionally have been treated with lowdose 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. 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. y 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. 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. 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. 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. 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. Once renal failure occurs, dialysis is the only effective therapeutic modality for rhabdomyolysis.

y y y y

Metabolic support y y y y y y Muscle necrosis may be so rapid that hyperkalemia, hypocalcemia, and hyperphosphatemia become significant enough to cause cardiac arrhythmias and require immediate therapy. In the presence of renal failure, hemodialysis may be necessary. 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. 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. 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. 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. y y 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. 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. 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. y y y y ARF initially is treated with intravenous fluids, diuretics, and correction of associated acid-base and electrolyte abnormalities. 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. Furosemide may cause tubular acidosis and, therefore, may promote myoglobin deposition within the renal tubules. 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. Consultations 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. Medication Summary In treating heatstroke, benzodiazepines play a major role in sedating patients, controlling convulsions, and controlling shivering. Barbiturates (eg, phenobarbital) may be used to control convulsions if benzodiazepines are not effective. Hypotension is treated first

with cooling and intravenous crystalloid fluids; dobutamine is considered if patients are hypodynamic. Treatment of rhabdomyolysis involves infusing large amounts of intravenous fluids (may require as much as 10 L), alkalinization of urine, and mannitol infusion. Benzodiazepines Class Summary Safe and effective in controlling agitation, convulsions, and shivering. View full drug information Lorazepam (Ativan) Predictability and ease of use make it DOC in most cases. May be used IV and is well absorbed after IM injection. Onset of action is within minutes, effects peak in 15-20 min, and duration of action is 6-8 h. View full drug information Midazolam (Versed) Rapidly acting benzodiazepine with short duration. Ideal for sedation during short procedures and may be effective in convulsions. Alkalinizing agents Class Summary Indicated for severe acidosis and rhabdomyolysis. View full drug information Sodium bicarbonate (Neut) Useful in alkalization of urine to prevent acute myoglobinuric renal failure. May be administered as a bolus injection or as an infusion. The ideal solution to which sodium bicarbonate is added should be hypotonic. Diuretics (osmotic) Class Summary Osmotic effects retain water during urine formation and dilute electrolytes in the urine, making resorption less efficient. View full drug information Mannitol (Osmitrol) DOC for forced diuresis in patients with rhabdomyolysis because of a number of beneficial effects on the kidneys, including an antioxidant effect. Adrenergic agonist agents Class Summary Produce vasodilation and increase inotropic state. View full drug information Dobutamine (Dobutrex) Synthetic compound structurally similar to catecholamines. DOC for circulatory support in heatstroke. Further Inpatient Care Once the acute phase is stabilized, further inpatient care may be necessary to address the complications of heatstroke. Further Outpatient Care

Long-term outpatient therapy may be required when chronic renal failure develops and when irreversible damage to the CNS, lungs, heart, and liver occurs. Deterrence/Prevention Heatstroke is a preventable illness, and education is the single most important tool for its prevention. Recognition of host risk factors and modification of behavior (eg, limiting alcohol and drug intake, avoiding use of medications and drugs that interfere with heat dissipation) and physical activity also can prevent heatstroke. Complications Heatstroke is a multisystem insult that potentially can affect almost every organ system. The CNS is especially sensitive to the damaging effects of hyperthermia. Widespread cell death occurs but is more evident in the region of the cerebellum (Purkinje cells). Heatstroke related long-term CNS sequelae include cerebellar deficits, dementia, hemiplegia, quadriparesis, and personality changes. In one study, rhabdomyolysis was observed in almost all patients with EHS and in as many as 86% of patients with NEHS. Compartment syndrome is observed most commonly in patients with severe rhabdomyolysis and in patients who are immobilized. ARF may occur in as many as 25-30% of patients who have heatstroke (especially EHS). Acute liver failure due to centrilobular hepatic necrosis and cholestasis generally occurs in the first 48 hours, but it can peak as long as 2 weeks after the onset of heatstroke. In rare instances, liver failure may be complicated by a fulminant course requiring liver transplantation. Patients who survive generally have a complete return of hepatic function. DIC is a rare complication and caries a poor prognosis when it occurs. Electron microscopy studies have shown that direct thermal injury to the vascular endothelium is the primary trigger of platelet aggregation and, possibly, DIC. ARDS may be due to direct thermal injury to the lung, or it may complicate liver failure, infection, or aspiration. When associated with liver failure, the patient prognosis is much worse. Prognosis Indicators of poor prognosis during acute episodes include the following: y y y y y y y Initial temperature measurement higher than 41C or a temperature higher than 108F or a temperature persisting above 102F despite aggressive cooling measures Coma duration longer than 2 hours Severe pulmonary edema Delayed or prolonged hypotension Lactic acidosis in patients with classic heatstroke ARF and hyperkalemia Aminotransferase levels greater than 1000 IU/L during the first 24 hours

Patient Education Education is the single most important tool for the prevention of heatstroke. The media, public education, public health programs, and athlete safety programs can play a pivotal role in increasing the public's awareness of the dangers of heat during heat waves and advising the public on methods of remaining cool. Similarly, drinking fluids on schedule (and not based only on thirst), frequent cooling breaks, and frequent visits to air-conditioned places are very important because even short stays in an air-conditioned environment may drastically reduce the incidence of heatstroke. Recognition of host risk factors and modification of behavior (eg, limiting alcohol and drug intake and the use of medications and drugs that interfere with heat dissipation) and physical activity also will prevent heatstroke.

Heat stroke facts y Heat stroke is a form of hyperthermia in which the body temperature is elevated dramatically. y Heat stroke is a medical emergency and can be fatal if not promptly and properly treated. y Cooling the victim is a critical step in the treatment of heat stroke. y The most important measures to prevent heat strokes are to avoid becoming dehydrated and to avoid vigorous physical activities in hot and humid weather. y Infants, the elderly, athletes, and outdoor workers are the groups at greatest risk for heat stroke. What is, and who is at risk for heat stroke? Heat stroke is a form of hyperthermia, an abnormally elevated body temperature with accompanying physical symptoms including changes in the nervous system function. Unlike heat cramps and heat exhaustion, two other forms of hyperthermia that are less severe, heat stroke is a true medical emergency that is often fatal if not properly and promptly treated. Heat stroke is also sometimes referred to as heatstroke or sun stroke. Severe hyperthermia is defined as a body temperature of 104 F (40 C) or higher. The body normally generates heat as a result of metabolism, and is usually able to dissipate the heat by radiation of heat through the skin or by evaporation of sweat. However, in extreme heat, high humidity, or vigorous physical exertion under the sun, the body may not be able to dissipate the heat and the body temperature rises, sometimes up to 106 F (41.1 C) or higher. Another cause of heat stroke is dehydration. A dehydrated person may not be able to sweat fast enough to dissipate heat, which causes the body temperature to rise. Those most susceptible (at risk) individuals to heart strokes include: y infants, y the elderly (often with associated heart diseases, lung diseases, kidney diseases, or who are taking medications that make them vulnerable to dehydration and heat strokes), y athletes, and y individuals who work outside and physically exert themselves under the sun. What are heat stroke symptoms and signs? Symptoms of heat stroke can sometimes mimic those of heart attack or other conditions. Sometimes a person experiences symptoms of heat exhaustion before progressing to heat strokes. Signs and symptoms of heat exhaustion include: y headache, y nausea, y muscle cramps and aches, and y vomiting, y dizziness. y fatigue, y weakness, However, some individuals can develop symptoms of heat stroke suddenly and rapidly without warning. Different people may have different symptoms and signs of heatstroke. Common symptoms and signs of heat stroke include: y high body temperature, y confusion, y the absence of sweating, with hot red or flushed dry y agitation, skin, y disorientation, y rapid pulse, y seizure, and/or y difficulty breathing, y coma. y strange behavior, y hallucinations, What about heat stroke in children? While the elderly are at greatest risk for heat stroke, infants and children are also at risk. In particular, infants or young children who are unattended in locked cars may suffer heat-related illness quickly, since the indoor temperature of a locked care can rise to dangerous levels even in moderate weather. Rarely, infants have died of heat stroke when overly bundled in their cribs. It is critically important that parents understand the medical dangers inherent in leaving children unattended in cars in addition to the obvious safety risks. Further, cars should always be kept locked when not in use so that children may not enter them and become trapped. Among older children and teens, heat stroke or heat-related illness is a risk for athletes who train in hot environmental conditions. Among reported heat-related illnesses in U.S. high school athletes, the majority of cases occur in football players during the month of August. How do you treat a heat stroke victim? Victims of heat stroke must receive immediate treatment to avoid permanent organ damage. First and foremost, cool the victim. y Get the victim to a shady area, remove clothing, apply cool or tepid water to the skin (for example you may spray the victim with cool water from a garden hose), fan the victim to promote sweating and evaporation, and place ice packs under armpits and groin. y If the person is able to drink liquids, have them drink cool water or other cool beverages that do not contain alcohol or caffeine. y Monitor body temperature with a thermometer and continue cooling efforts until the body temperature drops to 101 to 102 F (38.3 to 38.8 C).

Always notify emergency services (911) immediately. If their arrival is delayed, they can give you further instructions for treatment of the victim. How can heat stroke be prevented? y The most important measures to prevent heat strokes are to avoid becoming dehydrated and to avoid vigorous physical activities in hot and humid weather. y If you have to perform physical activities in hot weather, drink plenty of fluids (such as water and sports drinks), but avoid alcohol, caffeine (including soft drinks and tea), and tea which may lead to dehydration. y Your body will need replenishment of electrolytes (such as sodium) as well as fluids if you sweat excessively or perform vigorous activity in the sunlight for prolonged periods. y Take frequent breaks to hydrate yourself. Wear hats and light-colored, lightweight, loose clothes. y Keep cars locked when not in use and never, ever, leave infants or children unattended in a locked car. y Heat stroke is the most severe of the three forms of heat-related illness. In heat stroke, a person s body temperature rises to 104F (40C) or higher. Unlike heat cramps and heat exhaustion, however, heat stroke is a life-threatening condition. It has two forms: exertional heat stroke (EHS), related to work or exercise in the heat; and nonexertional heat stroke (NEHS), which is not caused by working or exercising outside and primarily affects the elderly, chronically ill persons, and infants during heat waves. y Heat stroke is a medical emergency that develops when a person s body can no longer get rid of excess heat through sweating and evaporation of the sweat. As a result, the body s core temperature rises, damaging the proteins and cell membranes in the body tissues and leading to organ failure, destruction of muscle tissue, the collapse of the cardiovascular system, and eventually death. According to the CDC, over 8,000 people died in the United States from heat-related illness between 1979 and 2003. People over the age of sixtyfive account for 44 percent of heat-related deaths. Heat stroke affects people from all races and ethnic groups. Men and women are equally affected by heat stroke; however, men are twice as likely as women to die from heat stroke because more men than women are employed in occupations that require working outdoors in hot weather. y Some groups of people have a greater risk of heat stroke: Newborn infants. The body of a baby cannot adjust to changes in temperature as efficiently as an adult s. In addition, babies have a limited ability to exit a hot environment. Elderly people. As with infants, the bodies of elderly people do not regulate internal temperature as effectively as those of younger adults. In addition, elderly people may have underlying illnesses or take medications that make them more vulnerable to heat stress. Workers whose jobs require working outdoors in hot weather or near ovens, blast furnaces, or other sources of heat. People who are not physically fit or have not undergone a conditioning program to get their bodies used to work or exercise in the heat. People who take certain types of medications, including diuretics, drugs that regulate blood pressure, tranquilizers, antihistamines, and drugs given to treat people with schizophrenia. Homeless people. Obese people. Nursing Care Plan Signs and Symptoms Like heat exhaustion, heat stroke is caused by the loss of water and salt from the body due to sweating during exposure to heat or vigorous physical exercise in hot conditions. High humidity makes it harder for the body to regulate its internal temperature through sweating, which is its normal way to get rid of heat when the outside temperature is 95F (35C) or higher. As sweat evaporates, it carries body heat with it. In addition to losing water through sweating, however, the body also loses electrolytes, which are minerals that are necessary to proper body functioning. In heat stroke, the body s cooling mechanisms are overwhelmed, and the body s internal temperature starts to rise uncontrollably. Other factors that can impair the body s ability to regulate its temperature in hot, humid weather include drinking alcohol, which leads to losing more water through the urine, and wearing tight clothes or clothes made of fabrics that do not allow sweat to evaporate easily. Heat stroke is often preceded by the symptoms of heat exhaustion, which include nausea and vomiting, headache, muscle cramps, dizziness, and difficulty breathing. The symptoms of heat stroke itself usually include: Hot, flushed, dry skin Changes in level of consciousness, including hallucinations, confusion, and irrational behavior Rapid heartbeat, sometimes as high as 130 beats per minute

y y

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Rapid, shallow breathing Blood pressure may be either normal or low Body temperature above 104F (40C) or rectal temperature above 106F (41.1C). Nursing Care Plan Diagnosis The diagnosis of heat stroke is usually obvious from the patient s situation and previous activities. In addition to taking the patient s temperature, doctors in the emergency room may also take a urine sample to check kidney function or a blood sample to check the level of the patient s electrolytes and blood sugar. A blood test can also be used to evaluate whether the patient s liver has been damaged. In addition to these laboratory tests, the doctor may also order a muscle function test to see whether the patient s muscle tissue has begun to break down. Nursing Care Plan Treatment Immediate treatment for heat stroke is essential as death or permanent brain damage can occur within minutes. Emergency treatment is focused on cooling the patient as quickly as possible to a core body temperature of 102F (38.9C). Cooling may be done by spraying water on the body, covering the patient with sheets soaked in ice water, or placing ice packs in the patient s armpits and groin area. The patient s temperature is not lowered further because they may start to shiver, and shivering will raise their internal temperature again. If the patient is conscious, they may be given additional oxygen to breathe and intravenous fluids to restore their blood volume. In most cases these fluids will contain sugar in order to lower the risk of liver failure. Patients who are having muscle cramps or convulsions are usually given benzodiazepine tranquilizers, which relax the muscles and reduce the risk of damage to muscle tissue. The patient will be kept in the hospital for at least forty-eight hours after emergency treatment and monitored for brain damage, signs of liver failure, or other complications. This period of observation is necessary because heat stroke can damage almost all major body systems. Nursing Care Plan Prognosis Although people have survived body temperatures as high as 114.8F (46C), any temperature above 106F (41.1C) is potentially fatal. People who receive prompt treatment for heat stroke have a 90 percent chance of survival; without prompt treatment, 80 percent will die. Nursing Care Plan Prevention Heat stroke is largely preventable by taking time to adjust to hot weather and dressing sensibly for local weather conditions: Most people in temperate climates need time to acclimate to seasonal temperature changes. People should work up gradually to sports and other outdoor activities during the first few warm days of summer rather than overdoing. The same is true of visiting a country with a tropical or hot climate; it is best to keep one s activity level moderate for a few days rather than crowding in too many activities. It can take people between seven and fourteen days to adjust to a hot climate; marathon runners generally take two weeks to acclimate to training in the heat. Wear loose-fitting and light-colored clothing; choose fabrics that absorb sweat, such as cotton; wear a hat outdoors. Drink fluids before exercising or working outside in hot weather. The American College of Sports Medicine recommends drinking about 20 ounces (0.6 liter) of water or sports drink two to three hours prior to exercise, and 10 ounces (0.3 liter) of water or a sports drink ten to twenty minutes before exercise. Do not use thirst as a guide to fluid intake; a person can become dehydrated before feeling thirsty enough to want a drink. Use sunscreen generously, as sunburn lowers the body s ability to get rid of excess heat. Avoid caffeinated beverages and alcohol; they cause the body to lose additional fluid through the urine. People who must take prescription medications for allergies, high blood pressure, heart conditions, or certain types of mental disorders should ask their doctor whether any of their medications affect their response to hot weather. Exercise during the early morning or late evening, when the temperature is cooler and the humidity lower. Workers in occupations that require them to work in hot environments should take rest breaks during periods of hot weather. Some companies also provide rest areas where workers can cool off. Consult a heat stress index like the one printed in the American Council on Exercise fact sheet listed below or the National Weather Service s heat index to help decide whether it is safe to exercise outdoors. There are times when the heat and humidity are so high that exercise should be avoided. Heat stroke is likely to occur when the heat stress index (the apparent temperature) is over 105F (40.5C) and the person is exposed to it for a long period of time; if the heat index is 130F (54.4C) or higher, heat stroke is highly likely even with short exposure. People with elderly friends or relatives should check on them during summer heat waves. Heat waves that last longer than two days put the elderly at risk of heat exhaustion. People who do not have air conditioning in their homes should go to a library, shopping mall, or other public building that is air-conditioned during a heat wave. Even a few hours in a cooler location can help to lower the risk of heat stroke.

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The Future Heat stroke is a common hot-weather disorder; it is often a consequence of exercising or working outdoors without proper conditioning or precautions. Heat stroke can be prevented in normally healthy individuals by dressing appropriately for hot weather, drinking enough fluids, consulting the local heat index before outdoor activity, and knowing when to slow down and cool off. It is possible that heat stroke may become more common in some parts of the United States in the summer time because of the growing size of the elderly population and others who do not tolerate heat well because of chronic illness. One problem is geography: most parts of the United States have uncomfortably high temperatures for at least part of the summer, and some areas have temperatures at or above 90F (32.2C) for weeks on end. In addition, large cities tend to be hotter than the surrounding areas G. alert: the majority of heat-related deaths occur in the aged because their CV systems are unable to compensate for stresses imposed byheat. NURSING ALERT: a seizure may be followed by recurrence of hyperthermia