Exertional Heat Illness

Dehydration and heat exposure can impair exercise performance and contribute to various illnesses. Exertional heat illnesses are comprised of minor and serious disorders. Minor heat and dehydration-related illnesses include heat cramps, erythromelalgia, and heat syncope. Heat cramps are characterized by intense muscle spasms, typically in the legs, arms, and abdomen. Heat cramps result from fluid and electrolyte deficits and occur most often in persons who have not been fully acclimated to a combination of intense muscular activity and environmental heat. Individuals who are susceptible to heat cramps are often believed to be profuse sweaters who sustain large sweat sodium losses.^13,¹⁰⁶ Heat syncope (fainting) is characterized by dizziness and weakness during or after prolonged standing or after rapidly standing up from a lying or sitting position during heat exposure. Heat syncope results from blood pooling in the cutaneous and skeletal vasculature, and it occurs most commonly in dehydrated and inactive persons who are not acclimated.⁹³ Erythromelalgia is characterized by pain and swelling in the feet and hands that is triggered by exposure to elevated temperatures.⁶⁴

Serious illnesses include exertional heat injury (EHI) and EHS. These illnesses have many overlapping diagnostic features; it has been suggested that they exist along a continuum on the severity scale.¹⁷ Heat exhaustion is characterized by inability to sustain cardiac output in the presence of moderate (>38.5° C [101° F]) to high (>40° C [104° F]) body temperatures, and is frequently accompanied by hot skin and dehydration. EHI is a moderate to severe illness characterized by injury to an organ (e.g., liver, kidneys, gut, muscle) and that usually (but not always) involves a high T_co of more than 40° C (104° F). EHS is a severe illness that is characterized by central nervous system dysfunction (e.g., confusion, disorientation, impaired judgment) and that is usually accompanied by a T_co of more than 40.5° C (105° F). EHI and EHS can be complicated by cardiac arrhythmia, liver damage, rhabdomyolysis, coagulopathy, fluid and electrolyte imbalances, and kidney failure. Rhabdomyolysis is most often observed with novel and strenuous overexertion. Clinical evidence suggests that dehydration increases the likelihood or severity of acute renal failure associated with rhabdomyolysis.^19,⁹¹ Among U.S. soldiers who have been hospitalized for serious heat illness, 25% had rhabdomyolysis, and 13% had acute renal failure.²²

EHS is usually associated with prolonged exertion in a warm climate; however, in many instances, EHS occurs within the first 2 hours of exercise and not necessarily at high ambient temperatures.^17,³⁷ This is because exertion and environmental heat stress during the 72 hours that precede such an event strongly influence the individual’s susceptibility to heat illness.⁴⁰ Using a T_co of 40.5° C (104.9° F) as a critical temperature to initially diagnose EHS is arbitrary. Mental status changes in an individual who is performing exertion in the heat should be the defining characteristic of heat stroke unless the individual has sustained head trauma. At the stage of collapse, profuse sweating is still likely to be present unless heatstroke develops in an already anhidrotic individual. Dry skin may be evident either in situations in which the climate is very dry and sweat evaporates easily or when heatstroke coincides with a severe degree of dehydration.³⁶

Heat stroke is often categorized as either “classic” or “exertional,” with the former primarily observed in elderly individuals or otherwise sick or compromised populations and the latter in apparently healthy and physically fit persons.

On-Site Emergency Medical Treatment

The early diagnosis of heat illness can be critical to therapeutic success. Early warning signs include flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion.⁷⁴ If the patient is alert and has no mental status changes, he or she can rest in the shade or indoors, and oral rehydration can be instituted with cold water or an electrolyte-replacement beverage. The concentration of carbohydrates in such a beverage should not exceed 6%; otherwise, gastric emptying and fluid absorption by the intestines may be delayed. Responders should target an intake of 1 to 2 L (0.9 to 1.8 qt) over 1 hour. If the patient does not improve or in fact worsens, he or she should be evaluated by a medical provider. All persons with suspected heat injuries should be observed to ensure that decompensation does not occur. The victim should continue to rest and drink over the next 24 hours. As a general rule, for every pound of weight lost by sweating, 0.5 qt (2 cups or 500 mL) of fluid should be consumed. It may require 36 hours to completely restore lost electrolytes and fluid volume to all body compartments via oral intake. After the acute episode, a medical provider should determine any possible host risk factors for heat illness and review with the victim the signs of heat illness and preventive measures to consider.

Any athlete who is performing exercise in warm weather and who develops mental status changes in the absence of trauma should be treated as an EHS victim until proved otherwise.³⁶ EHS is a medical emergency. Rapid reduction of elevated T_co is the cornerstone of EHS management; the duration of hyperthermia may be the primary determinant of outcome.^59,¹⁰⁰ Cooling should not be delayed so that a temperature measurement can be obtained. Cooling measures should only be minimally delayed for vital resuscitation measures. Nevertheless, it is important to follow the ABCs (airway, breathing, and circulation) of stabilization while cooling efforts are initiated; see Box 11-1 for basic first aid information. Before 1950, the mortality rate with EHS was 40% to 75%.^6,³⁵ Long-term survival is directly related to rapid institution of resuscitative measures.⁴⁹

In the field, the sick individual should be placed in the shade, and any restrictive clothing should be removed. There are multiple ways to cool victims in the field, with cold-water immersion (CWI) being the most effective modality.^24,⁸⁶ In a remote setting, this can be accomplished by using a small children’s pool filled with iced water. The victim should be submerged up to the shoulders and kept under immediate hands-on supervision at all times. Another expedient method in the field is to keep bed sheets soaked in a cooler full of iced water; the victim can then be wrapped in the cold sheets. Particular care should be given to covering the head and to resubmerging the sheets every few minutes to recool them.⁷⁹ Ice packs can be applied to the groin, axillae, sides of the neck, and head to augment iced-sheet cooling. Cooling should continue until emergency medical services providers arrive. Nonmedical first responders should not attempt to evacuate heat stroke patients themselves, because this may distract from cooling efforts. If CWI or iced sheets are not available, the victim should be kept wet by applying large quantities (20 to 30 L [5.3 to 7.9 gal]) of tap water or water from any source, and the victim’s body should be constantly fanned. Cooling blankets are generally ineffective as a single modality for inducing the rapid lowering of body temperature required for treating heatstroke.

Emergency Medical Services Treatment

During evacuation, CWI is often not a viable method for treatment. Iced sheets and ice packs can be easily used en route during transport. Many EMS vehicles now carry refrigerated intravenous (IV) fluid to initiate induction of therapeutic hypothermia in cardiovascular emergencies. When used, chilled IV fluid (4° C [39° F]) should be peripherally administered.⁶³ Vascular access should be established without delay by inserting a 12- or 14-gauge IV catheter. Administration of normal saline or lactated Ringer’s solution should be started. Recommendations vary regarding administration rate of fluids. Some clinicians advise a rate of 1200 mL (1.26 qt) over 4 hours,⁷⁸ whereas others encourage a 2-L (2.11-qt) bolus over the first hour and an additional liter of fluid per hour for the next 3 hours.⁹⁸ Patients should be placed on a cardiac monitor. Administration of supplemental oxygen may help to meet the victim’s increased metabolic demands, and it may also be used to treat hypoxia that is commonly associated with aspiration, pulmonary hemorrhage, pulmonary infarction, pneumonitis, or pulmonary edema.^34,⁶⁷ A blood glucose determination should be performed, and adults with blood sugar level less than 60 mg/dL should be treated with 1 ampule of 50% IV dextrose solution. Children should be treated with 2 to 4 cc/kg of 25% IV dextrose solution.

The use of antipyretics is not effective and may potentially be harmful to heatstroke victims. Aspirin and acetaminophen lower T_co by normalizing the elevated hypothalamic set point that is caused by pyrogens; in heatstroke, the set point is normal, with T_co elevation reflecting a failure of normal cooling mechanisms. Furthermore, acetaminophen may induce additional hepatic damage, and administration of aspirin may aggravate bleeding tendencies. Alcohol sponge baths are inappropriate under any circumstances, because transcutaneous absorption of alcohol may lead to poisoning and coma.

In a comatose victim, airway control should be established by inserting a cuffed endotracheal tube. Positive-pressure ventilation is indicated if hypoxia persists despite supplemental oxygen administration.

The victim’s altered mental status may adversely affect the ability of emergency department personnel to obtain a detailed history of precipitating events. Lack of such information may also delay diagnosis. Emergency medical transport personnel should attempt to obtain this history before evacuating the victim and should communicate the information to medical staff. Of particular importance is the duration—and, when available, the maximum degree—of hyperthermia.

Hospital Emergency Medical Treatment

Patients with suspected heat stroke should be placed in a large treatment room to accommodate the needed number of staff. Patients are often combative and disoriented before reestablishing their baseline mental status. Aggressive cooling measures should continue until mental status returns to normal and T_co is 39° C (102° F).²⁴ After discontinuation of cooling, T_co should be monitored every 5 minutes to ensure that it does not increase.

The T_co reported in the field for heatstroke victims may be significantly higher (e.g., 41.1° C [106.9° F]), than those documented in the hospital emergency department (e.g., 37.8° C [100° F]), because T_co may fall during transport to the hospital.⁹⁹ Documenting only a mild elevation in T_co on arrival does not exclude the diagnosis of heatstroke. Central nervous system (CNS) disturbances (i.e., coma, convulsions, confusion, or agitation) that accompany hyperthermia may also result from CNS infections, sepsis, or other disease processes. Other diagnoses should be considered when the patient does not regain normal mental status when the T_co is normalized in less than 30 minutes. When T_co remains elevated for a longer time, there is a decreased likelihood that mental status will normalize with euthermia.¹⁷

T_co can be measured at several anatomic sites, but oral, tympanic, esophageal, and rectal temperatures show regional variations as a result of differences in tissue metabolic activity, local blood supply, and temperature gradients between neighboring tissues. During exercise, active skeletal muscle temperature differs dramatically from that of other areas of the body that are not directly involved in the activity. Oral temperature is considered to be similar to blood temperature as a result of the rich blood supply of the tongue, but it is also influenced by hyperventilation and drinking fluids. Rectal temperature is a highly reliable indicator of body temperature, but it has a slower response rate and gives slightly higher readings than do other sites in the body.

The comparison of oral and rectal temperature values in heat-stressed underground miners showed a difference of approximately 1° C (2° F), with oral temperatures underestimating rectal values.¹⁰⁸ Tympanic temperature responds more rapidly to cooling or heating than does rectal temperature, but it is influenced by changes in the skin temperature of the head and neck.^44,⁶⁸ The ear should be insulated from the environment to prevent cool ambient temperatures (<30° C [86 ° F]) from affecting this measurement. Esophageal temperature is the most accurate and responsive to changes in blood temperature, but its instrumentation is impractical in severely injured or unresponsive patients.

If airway control was not previously established and if the patient is still unconscious, a cuffed endotracheal tube should be inserted to protect against aspiration of oral secretions. Supplemental oxygen—and, when hypoxia (PaO₂ <55 mm Hg) or hypotension is present, positive-pressure ventilation—should be provided. Overly vigorous fluid resuscitation may precipitate pulmonary edema, so careful monitoring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid should be administered during the first hour after collapse, and additional fluids should be administered until satisfactory urine output (0.5 cc/kg/hr in an adult and 1.0 cc/kg/hr in a child) is established.³⁸ Most heatstroke victims arrive with a high cardiac index, low peripheral vascular resistance, and mild right-sided heart failure with elevated central venous pressure. Only moderate fluid replacement is indicated if effective cooling results in vasoconstriction and increased blood pressure. Providers should consider noninvasive intravascular volume monitoring or the minimally invasive monitoring of systolic volume variation and pulse pressure variation. If these methods are not adequate, a Swan-Ganz pulmonary artery catheter may be necessary to assess appropriate fluid supplementation. Some victims have a low cardiac index, hypotension, and elevated central venous pressure. These persons have been successfully treated with an isoproterenol drip (1 mg/min).⁷⁸ Patients with a low cardiac index, low central venous pressure, hypotension, and low pulmonary capillary wedge pressure should receive fluid. Unless the patient has rhabdomyolysis, aggressive fluid hydration is seldom required after initial treatment.

Cardiac monitoring should be maintained during at least the first 24 hours of hospitalization. Arrhythmia is most likely to occur during hyperthermia, but it may also occur as a result of electrolyte abnormalities. The use of norepinephrine and other α-adrenergic drugs should be avoided because they cause vasoconstriction, thereby reducing heat exchange through the skin. Anticholinergic drugs that inhibit sweating (e.g., atropine) should also be avoided.

Cooling techniques are ineffective when the victim suffers seizures that increase storage of body heat; therefore, convulsions should be controlled. Intravenous benzodiazepines are preferred for their efficacy and renal clearance. Initial dosing is either 4 to 8 mg of IV lorazepam or 10 mg of IV diazepam. If seizures persist for more than 10 minutes after the first dose, an additional 4 mg of lorazepam or 10 mg of diazepam should be administered.

As a result of drastic cooling, skin temperature may decrease enough to cause shivering. Administration of 12.5 mg of meperidine via slow IV push ¹⁰³ or of 5 mg of diazepam is effective to suppress shivering and to prevent an additional rise in T_co from metabolic heat production. If CWI is used, the increase in metabolic rate as a result of shivering will be more than offset by the high rate of heat transfer. Therefore the presence of shivering should not be a cause for concern when this method of cooling is used.^24,⁸³

Severe muscle cramping may be caused by electrolyte imbalances. Magnesium levels should be obtained. If magnesium levels are low, consideration may be given to the use of 50% IV magnesium sulfate (4 g in 250 mL of 5% dextrose injection at a rate that does not exceed 3 mL per minute).^14,¹⁵

A Foley catheter should be placed to monitor urine output. Renal damage from myoglobinuria and hyperuricemia can be prevented by promoting renal blood flow by administering IV mannitol (0.25 mg/kg) or furosemide (1 mg/kg).⁹⁸ If creatine phosphokinase (CPK) levels exceed 100,000 international units, alkalinize the urine of patients with exertional rhabdomyolysis; there is no advantage to alkalinization when levels are lower. Hemodialysis should be reconsidered if anuria, oliguria (<0.5 mL/kg of urine per hr for >6 hr), uremia, or hyperkalemia develops. Cooling and hydration usually correct acid–base abnormalities; however, serum electrolytes should be monitored and appropriate modifications of IV fluids made. Glucose should be monitored repeatedly, because either hypoglycemia or hyperglycemia may occur after EHS.⁹⁵ Oral and gastric secretions are evacuated via a nasogastric tube that is connected to continuous low suction. Although antacids, proton pump inhibitors, and histamine-2 blockers have been used to prevent gastrointestinal bleeding, no studies to date demonstrate their efficacy for heatstroke victims.

Induced Hypothermia

Induced hypothermia is increasingly being used for many neurologic and cardiovascular emergencies, including acute stroke, neonatal hypoxic–ischemic encephalopathy, and after cardiac arrest.^9,^50,^76,⁹⁴ This therapeutic modality has not been evaluated for effectiveness in individuals with EHS, but may have a role in cooling severe refractory cases of EHS. There may be a role for a period of induced hypothermia after severe EHS.

Dantrolene

No drug has been found to have a significant effect for reducing T_co. Antipyretics are ineffective, because the thermoregulatory set point is not affected in heatstroke. Furthermore, antipyretics might be harmful, because they cannot be readily metabolized in the heat-affected liver. However, dantrolene has been used quite successfully for the treatment of several hypercatabolic syndromes, such as malignant hyperthermia, neuroleptic malignant syndrome, and other conditions that are characterized by muscular rigidity or spasticity.^107,¹¹⁴ Dantrolene stabilizes the calcium (Ca²⁺)-release channel in muscle cells, thereby reducing the amount of Ca²⁺ released from cellular calcium stores. This lowers intracellular Ca²⁺ concentrations, muscle metabolic activity, muscle tone, and thus heat production.^27,⁷⁵ In some studies, dantrolene was claimed to be effective for the treatment of heatstroke, whereas in others it improved neither the rate of cooling nor survival.^25,^31,^66,¹⁰⁹ In six patients with rhabdomyolysis, intramuscular Ca²⁺ concentrations were 11 times higher than in controls, and dantrolene successfully lowered this elevated Ca²⁺.⁶⁵ Collectively, the limited data available are at best inconsistent. Despite growing evidence for a possible benefit of dantrolene treatment in patients with heatstroke, justification for its routine use in such cases is not proved, although future clinical trials may change this assessment.

Moran and colleagues ⁷¹ studied dantrolene in a hyperthermic rat model, and found it to be effective as a prophylactic agent in sedentary animals only. Dantrolene induced more rapid cooling by depressing Ca²⁺ entry into the sarcoplasm; this led to relaxation of peripheral blood vessels with attenuated production of metabolic heat. Dantrolene may also be effective in treating heatstroke by increasing the cooling rate. However, in other animal models, dantrolene was not superior to conventional cooling methods.¹¹⁷ As such, dantrolene is not recommended.

Clinical Manifestations

Clinical manifestations of heatstroke vary, depending on whether the victim suffers from classic heatstroke, which is a common disorder of older adults during heat waves and occurs in the form of epidemics, or EHS,¹ which occurs when excess heat generated by muscular exercise exceeds the body’s ability to dissipate it (Table 11-1). Some overlap in presentation may occur; treatment with a medication (e.g., antihypertensive or antipsychotic) that places an older adult at risk for classic heatstroke also places an exercising individual at risk for EHS. The clinical picture of heatstroke usually follows a distinct pattern of events with three phases: (1) acute, (2) hematologic or enzymatic, and (3) late.³⁸

TABLE 11-1 Comparison of Classic and Exertional Heatstroke

Characteristics	Classic	Exertional
Age group	Young children and older adults	Men between the ages of 15 and 45 yr
Health status	Chronically ill	Healthy
Concurrent activity	Sedentary	Strenuous exercise
Drug use	Diuretics, antidepressants, antihypertensives, anticholinergics, and antipsychotics	Usually none
Sweating	May be absent	Usually present
Lactic acidosis	Usually absent; poor prognosis if present	Common
Hyperkalemia	Usually absent	Often present
Hypocalcemia	Uncommon	Frequent
Hypoglycemia	Uncommon	Common
Creatine phosphokinase	Mildly elevated	Markedly elevated
Rhabdomyolysis	Unusual	Frequently severe
Hyperuricemia	Mild	Severe
Acute renal failure	<5% of patients	25-30% of patients
Disseminated intravascular coagulation	Mild	Marked; poor prognosis
Mechanism	Poor dissipation of environmental heat	Excessive endogenous heat production and overwhelming heat-loss mechanisms

Modified from Knochel JP, Reed G: Disorders of heat regulation. In Kleeman CR, Maxwell MH, Narin RG, editors: Clinical disorders of fluid and electrolyte metabolism, New York, 1987, McGraw-Hill.

Acute Phase

The acute phase of heatstroke is characterized by CNS manifestations. Because brain function is very sensitive to hyperthermia, this phase is present in all heatstroke patients. Early signs of CNS dysfunction are typically cerebellar and include ataxia, poor coordination, and dysarthria.¹¹⁶ Advanced signs of CNS depression include irritability, aggressiveness, stupor, delirium, and coma.^2,^21,¹⁰² Mental status changes usually resolve after return to a normal T_co. After a return to normothermia, persistence of coma is a poor prognostic sign.^57,¹⁰² Other symptoms include fecal incontinence, flaccidity, and hemiplegia. Cerebellar symptoms may persist beyond the acute phase.^69,^102,¹¹⁶

Other common disturbances during the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dysfunction, including diarrhea and vomiting, often occurs. However, the latter may reflect translocation of toxic gram-negative bacterial lipopolysaccharide from the lumen of the intestines because of poor splanchnic perfusion as a result of hypotension caused by increased skin blood flow and from CNS impairment.^18,^41,¹⁰² Hyperventilation and elevation of T_co primarily lead to respiratory alkalosis, which in EHS may be masked by metabolic acidosis as a result of increased glycolysis and hyperlacticacidemia.^26,⁷⁴ Hypoxemia may be present in patients with respiratory complications.^28,^74,¹⁰⁵ It should also be noted that oxygen consumption is elevated during hyperthermia, with a 10% to 13% increase for every ° C above euthermia.³²

EHS shares many common findings with systemic inflammatory response syndrome (SIRS).^17,⁹⁷ Endotoxemia, hyperthermia, and other risk factors (e.g., preexisting infection) and stressors associated with EHS can trigger this exaggerated inflammatory response. Patients should be assessed for SIRS after admission with the use of the following criteria:¹⁶ (1) body temperature of less than 36° C (98.6° F) or of more than 38° C (100.4° F); a heart rate of more than 90 beats per minute, tachypnea, or an arterial partial pressure of carbon dioxide of less than 4.3 kPa (32 mm Hg); and a white blood cell count of less than 4000 cells/mm³ (4 × 10⁹ cells/L) or of more than 12,000 cells/mm³ (12 × 10⁹ cells/L) or the presence of more than 10% immature neutrophils. When two or more of these criteria are met, SIRS can be diagnosed. The presence of systemic inflammatory response markers during the acute phase predicts the severity of subsequent phases.

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