Heat Stroke Treatment & Management

Updated: Jul 20, 2022
  • Author: Robert S Helman, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Treatment

Medical Care

Heat stroke is a medical emergency and continues to be one of the leading causes of preventable death in sports. [13] Rapid reduction of the core body temperature is the cornerstone of treatment because the duration of hyperthermia is the primary determinant of outcome. Patients diagnosed with exertional heat stroke (EHS) or nonexertional heat stroke (NEHS) should be admitted to the hospital for at least 48 hours to monitor for complications.

Once heat stroke is suspected, cooling must begin immediately and must be continued during the patient's resuscitation. The American College of Sports Medicine recommends that cooling be initiated at the scene, before transporting the patient to an emergency department for further evaluation and treatment. [14] Despite extensive education and training, delays are still reported due to trepidation by athletic trainers to accurately diagnose and rapidly initiate treatment for EHS. [15]

Controversy still exists over what therapeutic modality is most effective in the treatment of heat stroke. However, the basic premise of rapidly lowering the core temperature to about 39°C (to avoid overshooting and rebound hyperthermia) remains the primary goal. Rehydration therapy alone is insufficient for heat stroke patients and should be combined with active cooling. [16]

According to 1 study, oral temperature assessments consistently reflected inaccurate core body temperatures, which delayed the diagnosis and ultimate treatment of patients with heat stroke. Rectal temperatures are still the preferred method of accurately obtaining core body temperatures. [17]

Some 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 the patient may have a much better prognosis. [18]

In a review of 19 clinical trials and observational studies involving 556 patients, the conduction method of cooling was found to be more efficacious in young, active adults with EHS. Unfortunately, this review did not identify a preferred treatment found for NEHS, or a temperature endpoint to prevent overcooling. [19]

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 heat stroke.

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. Interventions to enable monitoring include the following:

  • Insert a thermistor probe or temperature-sensing Foley catheter to monitor temperature continuously

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

  • Place a Foley catheter to monitor urine output and/or monitor body temperature

The goal of treatment is to reduce the temperature by at least 0.2°C/min to approximately 39°C. A flexible indwelling thermistor rectally or an esophageal probe can be placed to monitor core body temperature during treatment; alternatively, a more modern method is to use a temperature-sensing Foley catheter. Because thermal instability may persist for a few days after the onset of heat stroke, the temperature must be monitored continuously until it is stable.

Pharmacologic measures

Antipyretics (eg, acetaminophen, aspirin, other nonsteroidal anti-inflammatory drugs) have no role in the treatment of heat stroke 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 heat stroke. 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 pharmacologic option in the treatment of hyperthermia and heat stroke. To date, however, it has not proved efficacious in clinical trials.

Immediate administration of benzodiazepines is indicated in patients with agitation and shivering, to stop excessive production of heat. In addition, benzodiazepines are the sedatives of choice in patients with sympathomimetic-induced delirium as well as alcohol and sedative drug withdrawals.

Neuroleptics (eg, 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.

Benzodiazepines and, if necessary, barbiturates are the recommended agents for treatment of patients who are having convulsions. 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.

Fluid resuscitation

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 heat stroke 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 heat stroke.

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) historically 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.

Rhabdomyolysis

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 acute kidney injury (AKI). 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 best guided by invasive hemodynamic parameters, and urine output should be maintained at 3 mL/kg/h to minimize the risk of renal failure.

Alkalinization of the urine (to a pH of 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 occur so rapidly 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.

Calcium should be used judiciously 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 heat stroke 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 heat stroke, 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.

Hepatic injury

Heat stroke 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 disseminated intravascular coagulation (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 following:

  • Infusion of dextrose solutions to correct hypoglycemia

  • Early recognition and treatment of DIC, with replacement of clotting factors, fresh frozen plasma, platelets, and blood

  • Meticulous respiratory support

Pulmonary injury

Pulmonary edema is a common complication of heat stroke and may be due to a number of factors, including fluid overload from aggressive rehydration, 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).

Renal injury

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

AKI 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.