Disorders of Temperature Control: Hyperthermia
Saef Izzy
Susanne Muehlschlegel
Mark M. Wilson
I. HEAT STROKE
A. General principles.
1. Heat stroke is a syndrome of acute thermoregulatory failure in warm environments caused by increased heat production and/or impaired heat loss. It is characterized by central nervous system (CNS) depression, core temperatures over 40°C, and typical biochemical and physiologic abnormalities.
2. Mortality may reach 70%. About 4,000 deaths occur annually in the United States.
B. Etiology.
1. Exertional heat stroke is typically seen in active younger persons. With thermoregulatory mechanisms intact, it features rapid onset and high core temperatures.
2. Nonexertional (“classic”) heat stroke affects predominantly elderly or sick persons. With some impairment of thermoregulatory control, it develops slowly over several days and presents with minimally elevated core temperatures.
3. Hypothalamic thermoregulation processes (peripheral vasodilatation, thermal sweating, and cardiac changes) are activated by core temperature increases of ≤1°C (1.8°F). Impaired cardiovascular status, damage to anterior group of hypothalamic nuclei, severe dehydration, and vasoconstricting medications (anticholinergics, diuretics, alcohol) can predispose.
4. Deficient voluntary control and poor acclimatization increase the risk when ambient temperatures are high.
C. Pathophysiology.
1. Direct cellular toxicity results from temperatures >42°C (the critical thermal maximum); mitochondrial activity and enzymatic reactions become dysfunctional, and there is destabilization of cell membrane integrity.
2. Metabolic changes: Dehydration, metabolic acidosis, and local hypoxia potentiate the damage from severe heat stress. Significant muscle enzyme elevation and rhabdomyolysis occur commonly in exertional but rarely in classic heat stroke. Hyperglycemia and elevated serum cortisol have been reported in mild heat stroke. However, hypoglycemia occurs in severe exertional heat stroke due to metabolic exhaustion. Serum potassium levels may be extremely elevated from cell lysis.
3. CNS: Direct thermal toxicity to the brain and spinal cord can rapidly produce cell death, cerebral edema, and local hemorrhage. Stupor or coma is almost universal, while seizures are common.
4. Cardiovascular: Hypotension results from high-output cardiac failure or temperature-induced myocardial hemorrhage and necrosis.
5. Renal: Acute renal failure occurs in 5% of patients with classic, and in up to 35% of cases of exertional heat stroke. Renal damage is potentiated by dehydration, cardiac failure, and rhabdomyolysis.
6. Gastroenterology: Hepatic necrosis and cholestasis occur in nearly every case (mortality 5% to 10%).
7. Hematology: Leukocytosis, anemia, and bleeding diathesis are frequently present. Disseminated intravascular coagulation is present in most cases of fatal hyperthermia and usually appears on the second or third day.
8. Pulmonary: Direct thermal injury to the pulmonary vascular endothelium may lead to cor pulmonale or the acute respiratory distress syndrome.
D. Diagnosis.
1. Heat stroke should be expected in any patient exercising in ambient temperatures >25°C or in susceptible persons during heat waves (ambient peak temperatures >32°C and minimum temperatures ≤27°C).
2. Diagnostic criteria for heat stroke include a core temperature >40°C, severely depressed mental status or coma, elevated serum creatine kinase (CK) levels, and a compatible history.
3. Profuse sweating is typical in exertional heat stroke. Lack of sweating is typical in classic heat stroke, but is not a requirement of diagnosis.
4. Arterial blood gas analysis should be done early in treatment, and values should be corrected for temperature due to altered solubilities of O2 and CO2. The net effect is that the patient is more acidotic and less hypoxemic than uncorrected values imply. For each 1°C the patient’s temperature >37°C, one should increase the O2 tension by 7.2%, increase the CO2 tension by 4.4%, and lower the pH by 0.015.
E. Treatment.
1. Primary therapy includes immediate cooling by either evaporative or direct external methods (ice water or ice packs). A comparative study of the two methods is lacking.
2. Most cooling methods trigger cutaneous vasoconstriction and shivering. To overcome this response, simultaneous peripheral warming (while cooling the core) should be performed, using warm air or a warming blanket over the extremities.
3. External methods, such as cooling blankets, are extremely ineffective and are not recommended as the sole means of cooling.
