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 push¹⁰³ 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.

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

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.