T. Paul Tran
EPIDEMIOLOGY
Heat-related illnesses cause approximately 400 deaths annually in the United States.
Risks for heat-related deaths are highest among children and the elderly, those with predisposing medical conditions, and those on medications that interfere with the thermoregulatory response.
Heat-related illnesses and deaths are preventable and are closely correlated with high environmental temperature and urban heat waves, which are defined as three or more consecutive days with ambient temperatures >32.2°C.
PATHOPHYSIOLOGY
Body heat generated by metabolism and heat gained from the hot environment must be dissipated to maintain body temperature at or near 37°C.
Externally, body heat is thermodynamically dissipated through radiation, convection, evaporation, and conduction.
While radiation is the primary mechanism for heat loss in a cold environment (accounting for 65% of total heat loss), evaporation becomes the primary mechanism for heat dissipation in a hot environment.
Internally, thermoregulatory homeostasis is accomplished via the body’s thermoregulatory response, acute phase response, and heat shock protein response.
Upon exposure to heat stress, cardiac output is augmented, core blood circulation is shifted to the peripheral circulation, vasodilatation occurs, and thermal sweating is augmented.
Several inflammatory cytokines and heat shock proteins are released to improve tissue repair and protect against tissue injury and protein denaturation.
Heat stroke is a life-threatening injury pathogeneti-cally characterized by thermoregulatory breakdown, endothelial injury, coagulation disorder, microcir-culatory derangement, and multiorgan failure. It is the final result of interplay among thermoregulatory response failure, exaggerated acute phase response, and altered heat shock protein response.
Clinically heat stroke is characterized by hyperther-mia and central nervous system (CNS) dysfunction.
CLINICAL FEATURES
Patients with heat stroke usually present with a history of environmental or occupational heat exposure.
On physical examination, patients usually have altered mental status and an elevated body temperature. Core temperature ranges from 40°C to 47°C.
Neurologic abnormalities include ataxia, confusion, bizarre behavior, agitation, seizures, obtundation, and coma. Anhidrosis is not invariably present.
Risk factors for heat-related injuries include extremes of age (<4 years and >75 years), predisposing conditions (heart failure, psychiatric illnesses, alcohol abuse, dehydration, poverty, social isolation), medications (anticholinergics, β-blockers, calcium channel blockers), and host-environment factors (lacking access to air conditioning, poor physical fitness, inadequate acclimatization to hot weather).
DIAGNOSIS AND DIFFERENTIAL
Heat stroke is a true time-dependent medical emergency. It should be considered in the clinical context of environmental heat stress, hyperthermia, and altered mental status.
Patients are tachycardic, are hyperventilating, and have respiratory alkalosis.
About 20% of heat stroke patients are hypotensive.
In contrast to classic heat stroke, patients with exer-tional heat stroke may have both respiratory alkalosis and lactic acidosis.
Exertional heat stroke patients may present with rhab-domyolysis, hyperkalemia, hyperphosphatemia, and hypocalcemia.
Neuroimaging studies and other evaluation (eg, septic workup) can be individualized as clinically indicated.
Differential diagnosis includes infection (sepsis, meningitis, encephalitis, malaria, typhoid fever), toxins (serotonin syndrome, anticholinergics, phenothiazine, salicylate, phencyclidine (PCP), sympathomimetic abuse, alcohol withdrawal), metabolic and endocrinologic emergencies (thyrotoxicosis, diabetic ketoac-idosis), CNS disorders (status epilepticus, stroke syndrome), neuroleptic malignant syndrome, and malignant hyperthermia.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Emergent priorities remain airway, breathing, and circulation. Cardiac monitoring and an IV line should be established.
Along with the ABC, immediate cooling measures must be immediately instituted. The goal in the treatment of heat stroke is to bring the core temperature down by 0.2°C/min, to a core temperature <39°C.
Cooling measures should be stopped when core temperature reaches 39°C to avoid overcooling and hypothermia.
Patients should have clothes removed. Ice packs are placed on neck, axillae, and groins of patient. Tepid or ice water can be sprayed on patients. Fans are positioned near the completely disrobed patient.
High-flow supplemental oxygen should be administered. Patients with significantly altered mental status, diminished gag reflex, and hypoxia are candidates for definitive airway management (eg, endotracheal intubation).
Core temperature should immediately be obtained with a rectal (or bladder) probe and continuously monitored.
Volume-depleted patients should be rehydrated with IV normal saline or lactated Ringer’s solution to maintain mean arterial pressure >60 mm Hg or a urine output of ≥0.5mL/kg/h. Inotropic support and pres-sors may be required. Care should be exercised not to volume overload the patient.
Spraying with ice water may cause shivering, which induces thermogenesis. Excessive shivering can be treated with short-acting benzodiazepines (mida-zolam 2 milligrams IV).
Other methods of cooling such as immersion cooling, cold water gastric and urinary bladder lavage, peritoneal or thoracostomy lavage, cold IV fluid infusion, cooling blanket, and cardiopulmonary bypass may be considered as clinically indicated and logistically feasible.
Seizures can be treated with benzodiazepines.
Treat rhabdomyolysis with IV hydration. To date, no prospective control studies have shown improved outcomes from alkalinization of the urine or forced diuresis with mannitol or loop diuretics.
Hyperkalemia should be treated with standard regimens. The patient’s electrolytes should be monitored every hour initially.
Heat stroke patients need to be admitted to an intensive care unit for further observation and monitoring.
OTHER HEAT ILLNESSES
HEAT EXHAUSTION
Heat exhaustion is a clinical syndrome that results from heat exposure in an individual who is volume depleted, sodium depleted, or both.
It is characterized by nonspecific signs and symptoms, including malaise, fatigue, weakness, dizziness, syncope, headache, nausea, vomiting, myalgias, diaphoresis, tachypnea, tachycardia, and orthostatic hypotension.
Core body temperature is frequently elevated, but usually doesn’t exceed 40°C (104°F).
Although patients may complain of neurologic symptoms, patients’ sensorium and neurologic examination should be normal.
Laboratory examination usually demonstrates hemo-concentration. A creatinine kinase level should be checked to exclude rhabdomyolysis.
Treatment consists of rest, evaporative cooling, and administration of IV normal saline or oral electrolyte solution, depending upon the clinical situation.
Since heat exhaustion has the potential to evolve into heat stroke, patients should be aggressively treated and observed until symptoms resolve.
The majority of patients can be discharged home. Those patients with significant comorbid conditions (heart failure, poor social support) or severe electrolyte abnormality may require hospitalization.
HEAT SYNCOPE
Heat syncope results from volume depletion, peripheral vasodilation, and decreased vasomotor tone.
It occurs most commonly in the elderly and poorly acclimatized individuals.
Postural vital signs may or may not be demonstrable on presentation to the ED.
Patients should be evaluated for any trauma resulting from a fall.
Potentially serious causes of syncope (eg, cardiovascular, neurologic, infectious, endocrine, and electrolyte abnormalities) should be investigated, especially in the elderly.
Treatment for heat syncope consists of rest and oral or IV rehydration.
HEAT CRAMPS
Heat cramps are characterized by painful muscle spasms, especially in the calves, thighs, and shoulders.
Common during athletic events, they are thought to result from dilutional hyponatremia as individuals replace evaporative losses with free water but not salt.
Core body temperature may be normal or elevated.
Treatment consists of rest and administration of oral electrolyte solution or IV normal saline. Patients should be instructed to replace future fluid losses with a balanced electrolyte solution.
HEAT TETANY
Heat tetany is due to the effects of respiratory alka-losis that result when an individual hyperventilates in response to an intense heat stress.
Patients may complain of paresthesia of the extremities, circumoral paresthesia, and carpopedal spasm. Muscle cramps are minimal or nonexistent.
Treatment consists of removal from the heat stress and self-rebreathing through a paper bag.
HEAT EDEMA
Heat edema is a self-limited, mild swelling of dependent extremities (hands and feet) that occurs in the first few days of exposure to a new hot environment.
It is due to cutaneous vasodilation and pooling of interstitial fluid in dependent extremities.
Treatment consists of elevation of the extremities, and in severe cases, application of compressive stockings. Administration of diuretics may exacerbate volume depletion and should be avoided.
HEAT RASH
Heat rash (prickly heat) is a maculopapular eruption that is most commonly found over clothed areas of the body.
It results from inflammation and obstruction of sweat ducts.
Early stages present with a pruritic, erythematous rash best treated with antihistamines and chlorhexi-dine cream or lotion.
Continued blockage of pores results in a nonpruritic, nonerythematous, whitish papular rash known as the profunda stage of prickly heat.
This is best treated with antistaphylococcal antibiotics and application of 1% salicylic acid to affected areas three times daily.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 204, “Heat Emergencies,” by Thomas A. Waters and Ma ¡id A. Al-Salamah.