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Hyperthermia and Hypothermia

HYPERTHERMIA AND HYPOTHERMIA
FAITH T. FITZGERALD
Hyperthermia
Hypothermia

Maintenance of body temperature in humans is a balance between heat production and heat loss. The principal source of heat is the oxidation of ingested food. During physical work, including shivering and chilling, muscles generate much additional heat. The loss of body heat occurs through radiation, convection, and evaporation of sweat, with the last of these becoming progressively more important as the surrounding temperature increases. Evaporation of sweat is virtually the sole mode of heat loss at ambient temperatures greater than 35°C (95°F).
Heat sensors through the skin and nervous system send signals to the preoptic nucleus of the anterior hypothalamus, which directs the dissipation of heat by cutaneous vasodilatation (flushing) and sweating, and retention or generation of heat by cutaneous vasoconstriction and muscular activity. Behavioral responses (e.g., seeking shade in the heat or warmth on a cold day) also are important, and impairment of these voluntary actions, as in cognitive dysfunction, can predispose a person to hyperthermia or hypothermia.
Normal body temperatures in healthy adults range from 36.1°C to 37.4°C (97°F to 100.2°F), with the highest readings between 4 p.m. and 8 p.m. and the lowest between 4 a.m. and 6 a.m. This diurnal pattern is maintained (although set at a higher level) in most febrile diseases. The average body temperature is lower in the aged, the cachectic, the neurologically impaired, and those with certain disease states such as uremia. In assessing the clinical significance of body temperature, the underlying condition of the patient must be considered: a sustained temperature of 37.7°C (100°F) might be pathologic in an elderly cachectic man and normal in a young and vigorous one.
HYPERTHERMIA
Fever, discussed in Chapter 266, is the complex physiologic response of most vertebrates to immune challenges. Mediated by the hypothalamus, neurologic, endocrine, and behavioral changes are set in motion to achieve a new, higher hypothalamic temperature set point, which appears to have adaptive advantage to the organism. In contract, hyperthermia results when increased body temperature occurs following the breakdown of thermoregulatory homeostasis caused by an uncontrolled rise in heat production, failure of heat dissipation, extreme environmental heat, or, rarely, hypothalamic malfunction. Therefore, fever results from thermoregulation by the body, whereas hyperthermia is a failure of thermoregulation.
Environmental heat illness is caused by increased muscular activity in warm weather, particularly if volume deficiency limits heat dissipation (Table 62.1). Persons with poor conditioning and higher body mass index are at increased risk of exertional heat illness. Elderly patients risk heat stroke because of exposure and neurologic, vascular, or drug-induced predispositions.

TABLE 62.1. HEAT ILLNESS

Heat stroke, the most severe of environmental heat illnesses, is associated with increased intercellular adhesion molecule–1, endothelin, and von Willebrand factor antigen, which mediate vascular changes. Mortality can be as high as 10%, even with vigorous treatment. Death occurs from shock, arrhythmia, cardiac ischemia, renal failure, and neurologic dysfunction. Poor prognostic indicators are core temperature higher than 42.2°C (108°F), aspartate aminotransferase level greater than 1,000 during the first 24 hours, and coma of more than 2 hours duration. Although core temperature alone is not prognostic, duration and intensity of hyperthermia are.
Nonexertional causes of dramatic hyperthermia are presented in Table 62.2.

TABLE 62.2. NONEXERTIONAL CAUSES OF DRAMATIC HYPERTHERMIA

Neuroleptic malignant syndrome and familial malignant hyperthermia are discussed in Chapter 266.
HYPOTHERMIA
Human hypothermia has been arbitrarily defined as a rectal temperature of less than 35°C (95°F). Although it occurs mainly in winter and in cold climates, it can happen in any season anywhere the environmental temperature is less than 35°C (95°F). Like hyperthermia, it is generated by exposure plus conditions that compromise thermoregulation (Table 62.3). The body’s responses to hypothermia are outlined in Table 62.4.

TABLE 62.3. FACTORS PREDISPOSING TO HYPOTHERMIA

TABLE 62.4. THE BODY’S RESPONSE TO COOLING

Below 23.9°C (75°F), all responses are so affected by the cold that the patient loses heat as would a poikilotherm and the victim begins to approach a deathlike state. If a patient appears dead but has a history of hypothermic exposure, he or she should be warmed before being pronounced dead because patients with temperatures as low as 10°C (50°F) have survived.
Physical examination is difficult in a very cold patient. The temperature should be taken with a thermometer designed to read below the standard 34.4°C (94°F) lowest marking. The skin usually is cold, dry, and pale, but may show edema even in the face of intravascular volume depletion. Warm skin on a cold patient suggests that the hypothermia is caused by sepsis, skin disease, or vasodilator drugs. Respiratory compromise ranges from cold-induced bronchorrhea and aspiration pneumonia to noncardiogenic pulmonary edema. Blood gases, warmed by the laboratory to 37°C (98.6°F) as the measurements are made, may show hypoxemia, hypercarbia, and acidemia. Even if the blood gases show significant hypoxemia, cold protects the patient by decreasing tissue oxygen requirements. Pulse oximeters may not be accurate in patients with hypothermia and vasoconstriction.
Cardiovascular volume is depleted in most patients with chronic hypothermia as a result of the early diuresis described and a later cold-induced renal tubular concentrating defect. Hemoconcentration plus circulatory slowing may lead to intravascular sludging and microvascular occlusion. This, plus myofibrillar enzyme leaks across the cold cell membranes of skeletal and cardiac muscle, can cause dramatic elevations of creatine kinase (including MB) and lactic dehydrogenase. Electrocardiographic changes in hypothermia include increases in the PR interval, QT prolongation, bradycardia, atrial fibrillation with slow ventricular response, nodal rhythm, asystole, and the classic (although not pathognomonic) camel hump sign of Osborn, also called the J wave, a little “hump” on the down slope of the QRS complex, seen at 32.2°C (90°F) and below (Fig. 62.1).

FIGURE 62.1. The camel hump sign, also called the Osborn wave or J wave (arrow; 81°F; lead V5).

The abdomen may have rigid musculature and decreased bowel sounds. Gastrointestinal submucosal hemorrhage, if present, seldom is of major clinical significance. The amylase level may be increased, the platelet count decreased, and the prothrombin time prolonged. Hepatic and renal clearance of drugs, and their tissue effects, are unpredictable. Renal tubular glycosuria, myoglobinuria, and renal failure may occur.
Consciousness and reflexes are depressed and pupillary reflexes unreliable; the electroencephalogram may be flat below 20°C (68°F), and hypothermia is exclusionary of the diagnosis of brain death by electroencephalography.
Therapy for hypothermia is directed both to discovering and correcting the underlying cause of the hypothermia while rewarming the victim without causing harm. All patients, after blood samples for appropriate laboratory studies have been drawn, should receive 100 mg of thiamine, 50 g of glucose and naloxone (Narcan), 1 to 2 mg intravenously. Other drugs should not be used unless absolutely necessary, given their uncertain effects at the patient’s depressed temperature. Because sepsis is hidden in hypothermia, blood cultures and empirical antibiotics may be needed. Stress level corticosteroids are unnecessary unless adrenal insufficiency is a serious possibility. Patients with temperatures less than 32.2°C (90°F) should be admitted to the intensive care unit.
Appropriate initial and serial laboratory studies include a complete blood cell count; determination of electrolyte, calcium, albumin, amylase, and creatine kinase levels; renal and hepatic function tests; and urinalysis, coagulation studies, blood cultures, chest radiography, electrocardiography, and arterial blood gas analysis. Cardiac monitoring may be sufficient, although seriously ill patients may require right-sided heart catheterization. The latter should be done judiciously because dysrhythmias are common in hypothermia and may be stimulated by the placement of an intracardiac line. Volume replacement should be with normal saline and with dextrose and water. Lactated Ringer’s solution should not be used because the hypothermic liver may not be able to metabolize lactate to bicarbonate. The patient should be reassessed continually because physical examination and laboratory studies will change with rewarming.
The great debate in therapy revolves around rewarming therapy itself. Three major methods exist: external active rewarming, central active rewarming, and passive rewarming. External active rewarming includes immersing the patient in hot water or covering him or her with heating blankets. Although this rarely may be necessary in the profoundly cold, asystolic patient, it usually is not required and can be dangerous, leading to more profound hypothermia (the “afterdrop phenomenon”), cutaneous burns, or death. Central active rewarming involves either the use of warmed peritoneal or gastric lavage, which can be complicated by aspiration or infection, or the safer but more difficult to arrange use of warming hemodialysis or inhaled supplemental oxygen delivered as mist, keeping the inspired oxygen at 40°C (104°F) or less to prevent pulmonary burns. All intravenous fluids should be warmed to 37°C (98.6°F).
There is no proven benefit to more rapid rewarming. In all but the most severe cases, passive rewarming (correcting the underlying pathologic process if possible, removing the patient from the cold, and using warm—not hot—blankets) suffices, although airway warming at temperatures less than 32°C (89.6°F) and aggressive central active rewarming at temperatures less than 28°C (82.4°F) may be necessary, especially if the patient is in cardiac arrest.
BIBLIOGRAPHY
Bouchama A, Hammami MM, Haq A, et al. Evidence for endothelial cell activation/injury in heat stroke. Crit Care Med 1996;24:1173–1178.
Danzl DF, Dozos RS. Accidental hypothermia. N Engl J Med 1994;331:1756–1760.
Dematte JE, O’Mara K, Buescher J, et al. Near fatal heat stroke during the 1995 heat wave in Chicago. Ann Intern Med 1998;129:173–181.
Garners JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male marine corps recruits. Med Sci Sports Exerc 1996;28:939.
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