Heat Stroke

Heat Stroke

INTRODUCTION

Background: Heat illness may be viewed as a continuum of illnesses relating to the body’s inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heat stroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.

Two forms of heat stroke exist. Exertional heat stroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heat stroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heat stroke are associated with a high morbidity and mortality, especially when therapy is delayed.

Because behavioral responses are important in the management of temperature elevations, heat stroke may be entirely preventable.

Pathophysiology: Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

Heat may be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold to levels exceeding 1000 kcal/h. Similarly, fever, shivering, tremors, convulsions, thyrotoxicosis, sepsis, sympathomimetic drugs, and many other conditions can increase heat production, thereby increasing body temperature.

The body also can acquire heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses. Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body’s surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the angle of the sun, the season, and the presence of clouds, among other factors. For example, during summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.

Under normal physiologic conditions, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range. In a simplified model, thermosensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in the blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.

As the major heat-dissipating organ, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.

The efficacy of evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the threshold at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.

When heat gain exceeds heat loss, the body temperature rises. Classic heat stroke occurs in individuals who lack the capacity to modulate the environment (eg, infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heat stroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heat stroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.

Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.

Frequency:

Mortality/Morbidity: Morbidity and mortality from heat stroke are related to the duration of the temperature elevation. When therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%. Mortality is highest among the elderly population, patients with preexisting disease, those confined to a bed, and those who are socially isolated.

Race: With the same risk factors and under the same environmental conditions, heat stroke affects all races equally. However, because of differences in social advantages, the annual death rate due to environmental conditions is more than 3 times higher in blacks than in whites.

Sex: With the same risk factors and under the same environmental conditions, heat stroke affects both genders equally. However, because of gender differences in the workforce, the annual death rate due to environmental conditions is 2 times higher in men than in women.

Age: Infants, children, and elderly persons have a higher incidence of heat stroke than young, healthy adults.

CLINICAL

History: Heat stroke is defined typically as hyperthermia exceeding 41°C and anhidrosis associated with an altered sensorium. However, when a patient is allowed to cool down prior to measurement of the temperature (as may occur during transportation in a cool ambulance or evaluation in an emergency department), the measured temperature may be much lower than 41°C, making the temperature criterion relative. Similarly, some patients may retain the ability to sweat, removing anhidrosis as a criterion for the diagnosis of heat stroke. Therefore, strict adherence to the definition is not advised because it may result in dangerous delays in diagnosis and therapy.

Clinically, 2 forms of heat stroke are differentiated. Classic heat stroke, which occurs during environmental heat waves, is more common in very young persons and in the elderly population and should be suspected in children, elderly persons, and individuals who are chronically ill who present with an altered sensorium. Classic heat stroke occurs because of failure of the body’s heat dissipating mechanisms.

On the other hand, EHS affects young, healthy individuals who engage in strenuous physical activity, and EHS should be suspected in all individuals with bizarre irrational behavior or a history of syncope during strenuous exercise. EHS results from increased heat production, which overwhelms the body’s ability to dissipate heat.

Physical:

Causes:

DIFFERENTIALS

Delirium
Delirium Tremens
Diabetic Ketoacidosis
Encephalopathy, Hepatic
Encephalopathy, Uremic
Hyperthyroidism
Meningitis
Neuroleptic Malignant Syndrome
Tetanus
Toxicity, Cocaine
Toxicity, Phencyclidine
Toxicity, Salicylate


Other Problems to be Considered:

Closed head trauma
Malignant hyperthermia
Encephalitis
Cerebral malaria
Cerebral hemorrhage
Amphetamine and cocaine toxicity
Strychnine poisoning

WORKUP

Lab Studies:

Imaging Studies:

Other Tests:

Procedures:

TREATMENT

Medical Care: Heat stroke 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 heat stroke is suspected, cooling must begin immediately and must be continued during the patient’s resuscitation. 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.

Surgical Care: 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.

Consultations:

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

Activity: 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.

MEDICATION

In treating heat stroke, benzodiazepines play a major role in sedating patients, controlling convulsions, and controlling shivering. Barbiturates (eg, phenobarbital) may be used to control convulsions if benzodiazepines are not effective. Hypotension is treated first with cooling and intravenous crystalloid fluids; dobutamine is considered if patients are hypodynamic. Treatment of rhabdomyolysis involves infusing large amounts of intravenous fluids (may require as much as 10 L), alkalinization of urine, and mannitol infusion.

Drug Category: Benzodiazepines -- Safe and effective in controlling agitation, convulsions, and shivering.
Drug Name
 Lorazepam (Ativan) -- Predictability and ease of use make it DOC in most cases. May be used IV and is well absorbed after IM injection. Onset of action is within minutes, effects peak in 15-20 min, and duration of action is 6-8 h.
Adult Dose 0.044 mg/kg IV; maximum rate 2 mg/min; may repeat q15min until desired effect obtained or total of 8 mg administered
Pediatric Dose 0.1 mg/kg IV; maximum rate 2 mg/min
Contraindications Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma
Interactions Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs; metabolism may be reduced by cimetidine or nicotine
Pregnancy D - Unsafe in pregnancy
Precautions Caution in patients with renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, elderly patients, or cardiac disease
Drug Name
 Midazolam (Versed) -- Rapidly acting benzodiazepine with short duration. Ideal for sedation during short procedures and may be effective in convulsions.
Adult Dose 0.01-0.05 mg/kg IV; may repeat q15min until desired effect or total of 10 mg administered
Pediatric Dose 0.05-0.2 mg/kg IV
Contraindications Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (the diluent)
Interactions Sedative effects may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects due to decreased clearance; alcohol, other CNS depressants, cimetidine, and nicotine may reduce metabolism, prolonging duration of effects
Pregnancy D - Unsafe in pregnancy
Precautions Caution in patients with congestive heart failure, pulmonary disease, renal impairment, hepatic failure, and in elderly patients
Drug Category: Alkalinizing agents -- Indicated for severe acidosis and rhabdomyolysis.
Drug Name
 Sodium bicarbonate (Neut) -- Useful in alkalization of urine to prevent acute myoglobinuric renal failure. May be administered as a bolus injection or as an infusion. The ideal solution to which sodium bicarbonate is added should be hypotonic.
Adult Dose Bolus: 1 mEq/kg IV
Infusion: Add 2-3 amp of sodium bicarbonate to 1000 cc of D5W and infuse at 200 cc/h; maintain urine pH between 7.5-8.0
Pediatric Dose Bolus: Administer as in adults, use cautiously in children aged <2 y
Contraindications Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain
Interactions Urinary alkalinization induced by increased sodium bicarbonate concentrations may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances such as patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because tissue necrosis can result
Drug Category: Diuretics (osmotic) -- Osmotic effects retain water during urine formation and dilute electrolytes in the urine, making resorption less efficient.
Drug Name
 Mannitol (Osmitrol) -- DOC for forced diuresis in patients with rhabdomyolysis because of a number of beneficial effects on the kidneys, including an antioxidant effect.
Adult Dose 25-100 g IV infused over 1-2 h
Pediatric Dose Not established
Contraindications Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure
Interactions May decrease serum lithium levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Carefully evaluate cardiovascular status before rapid administration of mannitol because a sudden increase in extracellular fluid may lead to fulminating CHF
Drug Category: Adrenergic agonist agents -- Produce vasodilation and increase inotropic state.
Drug Name
 Dobutamine (Dobutrex) -- Synthetic compound structurally similar to catecholamines. DOC for circulatory support in heat stroke.
Adult Dose 2-20 mcg/kg/min IV infusion
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter
Interactions Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Following a myocardial infarction, use with extreme caution; correct hypovolemic state before using

FOLLOW-UP

Further Inpatient Care:

Further Outpatient Care:

Deterrence/Prevention:

Complications:

Prognosis:

Patient Education:

MISCELLANEOUS

Medical/Legal Pitfalls:

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Constructed by Dr N.A. Nematallah Consultant in perioperative medicine and intensive therapy, Al Razi Orthopedic Hospital , State of Kuwait, email : razianesth@freeservers.com