Heatstroke Treatment & Management

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 patients to an emergency department for further evaluation and treatment.^[3] Controversy still exists over what therapeutic modality is most effective in the treatment of heatstroke; however, the basic premise of rapidly lowering the core temperature to about 39°C (avoid overshooting and rebound hyperthermia) remains the primary goal.

Some recent studies have shown that promptly reducing the exposure time to excessive heat can dramatically improve long-term outcomes and decrease irreversible injury. 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 effect on the overall outcome of the patient.^[4]

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 preferred treatment found for classical or NEHS and no temperature endpoint to prevent overcooling.^[5] 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.

• 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 0.2°C/min to approximately 39°C. Active external cooling generally is halted at 39°C to prevent overshooting, which can result in iatrogenic hypothermia.

• 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.

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

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

• 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.

• 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.

• 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.

• 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 low-dose isoproterenol; however, its arrhythmogenicity has raised questions about its continued use. Dobutamine, which is less arrhythmogenic than isoproterenol and more cardioselective, may be the inotrope of choice in these patients.
• 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.

• 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.

Metabolic support

• 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.

• 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.

• 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.

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

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

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

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

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

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.