CHAPTER 24 HYPOTHERMIA AND HYPERTHERMIA
Practice of Geriatrics
CHAPTER 24 HYPOTHERMIA AND HYPERTHERMIA
Calvin H. Hirsch, M.D.
For this relief much thanks, ’tis bitter cold,
And I am sick of heart.
Fear no more the heat o’ the sun,
Nor the furious winter’s rages …
— William Shakespeare
The human organism, like other mammals, is a homeotherm that generates its body temperature principally through metabolism (endothermia) and is capable of maintaining a body temperature that is very close to 37°C (98.6°F) through a wide range of ambient temperatures. Arbitrarily, hypothermia has been defined as a core body temperature (rectal, esophageal, tympanic, or urine) of below 35°C (95°F) and hyperthermia as a core temperature of above 40.6°C (105°F).* As a group, the elderly share with infants a greater vulnerability to the effects of thermal stress and are disproportionately represented among case fatalities due to hypothermia and hyperthermia.
The failure to recognize the contribution of hypothermia and hyperthermia to death and illness has obscured their true incidence. Among susceptible older persons, morbidity from thermoregulatory failure may result from chronic exposure to cold or heat that would not be considered extreme and commonly occurs inside the older person’s dwelling. In the United Kingdom, where fuel costs traditionally have been high, it has been estimated that one to five older persons out of 2500 die from illnesses related to hypothermia each year. Between 1979 and 1991, an average of 770 persons died per year in the United States from hypothermia, for an age-adjusted death rate of 0.2 per million. Over half of these fatalities were in persons aged 65 and older. Neonates and persons over age 65 constituted 64% and 17%, respectively, of the 1815 hospital admissions attributable to hypothermia in New Zealand between 1979 and 1986; nearly all of these patients were admitted from home. Persons over age 65 accounted for 67% of the documented hypothermia-related fatalities in this report. In a survey of British hospitals conducted in the mid 1970s, 3.6% of all patients 65 and older were found to be hypothermic at admission. Average mortality rates from hypothermia increase with age and are nearly 12 times greater in those 75 and over compared to persons aged 15 to 34. Although basal body temperature does not change with healthy aging, surveys conducted in the United Kingdom have revealed a prevalence of 10% to 11.4% of persons with body temperatures at or near hypothermic levels among older persons living at home.
Heat casualty statistics likewise disproportionately represent the elderly. During the summer of 1966 in St. Louis, Missouri, the average temperature exceeded 32°C for nearly 1 month. Of the 246 certified heat-related deaths, 136 (55%) were people 69 years of age and older. That same summer, New York City experienced 200 documented heat-related casualties, among whom the average age was 78. During a heat wave in Memphis, Tennessee, in 1980, the average age of the 483 patients admitted to hospital with a heat-related disorder was 69. Of 28 patients presenting at Parkland Memorial Hospital in Dallas with classic heat stroke in 1978, 89% were over age 64.
Although socioeconomic conditions, such as poverty, poorly heated or ventilated housing, and undernutrition, may have played a role in these statistics, they demonstrate that older individuals are more likely to present with life-threatening thermoregulatory dysfunction. This increased susceptibility is due to a combination of agerelated changes in physiology, a greater prevalence of co-morbid conditions, and a greater likelihood of using medications that affect thermoregulation. The adult human maintains a fine balance between heat gain and heat loss in order to produce a constant optimum temperature that permits intracellular biochemical reactions. Conservation of body heat occurs through the insulating effect of the body’s shell (skin, subcutaneous fat, and muscle), basal metabolism, muscular work (including involuntary shivering), and vasoconstriction. About 80% of caloric intake goes into the maintenance of body temperature. When the body’s temperature exceeds that of the surrounding air, roughly two thirds of the heat lost occurs by radiation, with variable contributions from conduction and insensible evaporation. Conduction plays a relatively greater role during cold water immersion, since water has 32 times the thermal conductivity of air. Convection (the transfer of heat to currents of passing air or liquid) greatly enhances evaporative and conductive losses.
AGE-ASSOCIATED RISK FACTORS FOR HYPOTHERMIA
In the presence of impaired thermostasis, hypothermia may result from prolonged exposure to an environment that is considered warm yet is cooler than 35°C. Perhaps the most important response of the human organism to cold is behavioral—for example, donning a sweater or moving to a warmer room. An appropriate behavioral response first requires the perception that the environment is too cold. In contrast to young people, healthy older individuals may have difficulty in detecting a 2°C or greater drop in ambient temperature (Table 24-1). In winter, among 72 community-dwelling volunteers in Britain (mean age 77), the average urine temperature was only 36.4°C, yet no subject felt too cold. Seven out of nine subjects with borderline or actual hypothermia claimed they were “comfortable.”1 Peripheral neuropathies, such as those encountered in longstanding or suboptimally controlled diabetes mellitus, may also contribute to diminished thermal sensation.
TABLE 24-1 SUMMARY OF RISK FACTORS FOR THERMOREGULATORY DYSFUNCTION IN THE ELDERLY
Second, the individual must be capable of influencing his or her environment. Among the elderly, physical barriers, such as impaired mobility, may impede an appropriate response to being cold. In addition, mobility impairment usually is associated with reduced muscle activity and hence diminished thermogenesis. Cognitive barriers are likewise common; 5% of those over age 65 suffer from dementia and may not know what to do or be able to communicate their discomfort to others. Finally, many older persons on fixed incomes may not be able to afford the cost of heating their homes.
When behavioral responses are insufficient to protect thermostasis, the body must rely on physiologic defenses, which may be impaired by age-associated physiologic changes, chronic illness, and certain medications. The body’s first line of defense is its insulation—principally clothing and subcutaneous fat. Normal aging is associated with a loss of subcutaneous fat. When insulation is insufficient to prevent peripheral cooling, local reflex vasoconstriction reduces the surface area of contact of blood with the environment. Using volume plethysmography of the hand, Collins and colleagues2 observed that in 14% of elderly volunteers (average age 70) vasoconstriction failed to occur upon cooling. In the same volunteers 4 years later, the proportion in whom vasoconstriction failed had increased to one third. Co-morbid conditions and medications that might have influenced vasomotor responses in the subjects unfortunately were not reported. Forty-three percent of those with abnormal vasoconstrictor responses displayed postural hypotension compared with 10% of those with normal vasoconstriction,3 suggesting that autonomic dysfunction plays a role in increasing susceptibility to hypothermia.
After local vasoconstriction, the body attempts to maintain thermostasis by increasing thermogenesis. The posterior hypothalamus senses cerebral blood temperature and receives input from thermoreceptors via the spinothalamic tract. In response to cooling, the hypothalamus stimulates the sympathetic nervous system to release catecholamines, resulting in further peripheral vasoconstriction and an increase in heart rate, cardiac output, respiratory rate, and blood pressure. Direct stimulation through the extrapyramidal tracts increases muscle tone, which may increase heat production by 50%. When this neuronal stimulation produces rhythmic contraction of the muscles (shivering), heat production may increase fivefold in the healthy adult. Although the ability to shiver is retained at least through the ninth decade, the latency of shivering in response to environmental cooling may be longer in older people compared to that in young people, and lower peaks of contraction are attained. It is possible that reconditioning, by restoring muscle mass and the efficiency of muscle work, may reduce or eliminate these age-associated changes in shivering.
Other Conditions Predisposing to Hypothermia
The basal metabolic rate and therefore thermogenesis decrease with aging, related in part to decreasing lean body mass. Metabolic abnormalities, such as hypothyroidism, hypoadrenalism, hypopituitarism, and malnutrition, predispose the body to hypothermia by decreasing thermogenesis. The prevalence of malnutrition among the elderly living in the community approaches 16% for whites and 18% for blacks but may reach 35% or higher among hospitalized older patients and may exceed 50% among nursing home residents. Protein-calorie malnutrition can easily be overlooked because it may occur without a change in total body weight as a result of replacement of muscle mass by fat. It is diagnosed by finding a serum albumin level of less than 3.5 g/dL in the absence of proteinuria or acute illness. Hypoglycemia, a hazard among alcoholics and the many older patients taking long-acting hypoglycemic medications, may cause hypothermia directly by affecting the hypothalamic thermostat. Hypothermia may also result from diabetic ketoacidosis, presumably due to glucose deprivation of the hypothalamus. Other central nervous system lesions affecting the hypothalamus similarly may induce varying degrees of hypothermia. Wernicke’s encephalopathy has been associated with coma, hypotension, and hypothermia. Patients with anorexia nervosa and Parkinson’s disease often fail to shiver in the presence of decreasing core temperatures and have defective vasoconstriction, consistent with autonomic dysfunction. Burns and erythrodermas (e.g., severe psoriasis) cause massive radiation of body heat to the environment and impair reflex vasoconstriction to cold. Drugs constitute another important class of contributors to hypothermia. Barbiturates and ethanol interfere with central body temperature regulation, while the latter also induces heat loss through vasodilation. Centrally acting sympatholytic antihypertensive agents, such as clonidine, reserpine, and guanabenz, inhibit reflex vasoconstriction in response to a lowered temperature. Phenothiazines can potentiate hypothermia by inhibiting the shivering response through central mechanisms as well as through alpha-adrenergic blockade. The atypical antipsychotic agent clozapine acts directly on the hypothalamus to induce hypothermia. Even caffeine (as well as other methylxanthines) can predispose to hypothermia, especially when taken in combination with a central or peripherally acting alpha-adrenergic blocking agent.4
Unintentional hypothermia occurs in approximately half of patients undergoing surgery and is more likely to occur in patients who are older or who receive general anesthesia. General anesthesia transforms the patient into a poikilotherm whose body temperature varies directly with the temperature of the environment. During mild perioperative hypothermia, catecholamine production increases dramatically; there is a 100% to 500% rise in norepinephrine concentration for each 1° to 2°C reduction in core temperature, resulting in vasoconstriction and frequently in hypertension.5 Older hypothermic surgical patients generally take longer to return to a temperature of 36°C (often 5 hours or more) unless rewarming procedures are administered. In the immediate postoperative period, Frank and colleagues6 reported the presence of myocardial ischemia on continuous electrocardiographic monitoring in 36% of hypothermic patients but in only 13% of euthermic patients. Among patients without a preoperative history of coronary artery disease, perioperative hypothermia was associated with a fourfold greater incidence of myocardial ischemia.6 The shivering that occurs in postoperative older patients produces a 30% to 40% increase in oxygen consumption; narcotic analgesia appears to blunt the shivering response. However, perioperative coronary ischemia is more likely to be related to the catecholamine rise than to the metabolic demands of shivering.7
In the elderly, hypothermia often develops insidiously, and subnormal temperatures may be maintained for days or weeks before they finally drop below 35°C. The clinical presentation of hypothermia between 32° and 35°C (“mild hypothermia”) mimics that of severe hypothyroidism, with coarse facies, slow, husky speech, impaired mentation, and lethargy. Heterogeneous neurologic symptoms emerge, including confusion, dysarthria, ataxia, focal weakness, sensory loss, depression or loss of the deep tendon reflexes, frontal-release signs, and hallucinations. Hypothermia therefore must be distinguished from other causes of delirium. Pupillary reflexes may be irregular and sluggish, and miosis, mydriasis, or anisocoria may be present. The skin usually is cold to the touch unless external warming has been applied and may appear either pale and corpse-like or show blotchy patches of erythema and purpura. Bullae over pressure-dependent areas have been reported, and the examiner should be alert to signs of frostbite if outside temperatures have been below freezing. A generalized edema may be present owing to the cold-induced shift of intravascular fluid into the interstitium.
Blood pressure, cardiac output, and respiratory rate are characteristically elevated during this phase. Vasoconstriction shunts blood centrally, resulting in increased alveolar and interstitial pulmonary fluid and increased urine output. Hypothermia causes renal tubular glycosuria and a renal concentrating defect, the latter predisposing the individual to hypovolemia. Cold also induces copious bronchial secretions—so-called cold bronchorrhea, which, together with suppression of the cough reflex and increasing lethargy as hypothermia progresses, predisposes the individual to bronchopneumonia. Inspiration of cold air causes an increase in airway resistance owing to increased mucus production, vascular congestion, decreased mucociliary clearance, and bronchial smooth muscle contraction. As the core temperature descends to 32°C, cardiac output along with blood pressure, pulse, and respiratory rate begin to drop. Increasing atrial ectopy occurs, and the electrocardiogram may show inversion of T waves and lengthening of the PR, QT, and QRS intervals. A slowly inscribed terminal force in the QRS (J or Osborn wave [Fig. 24-1]) may appear. Once thought to be pathognomonic for hypothermia, Osborn waves have been reported in patients with massive cerebral injury, hypercalcemia, and interruption of cervical sympathetic pathways.8 Intestinal motility decreases at a temperature of about 34°C and gradually progresses to ileus. Initially, pancreatic function is undisturbed, but with further cooling, insulin secretion decreases, resulting in hyperglycemia. Hepatic metabolism similarly declines with decreasing core temperature, prolonging the half-life of drugs metabolized by the liver.
Figure 24-1 Upper panel: Electrocardiogram (ECG) taken during hypothermia showing characteristic terminal J-point elevation of QRS complex (Osborn wave). Lower panel: ECG after normalization of temperature.
Leakage of plasma from the intravascular space and the cold-induced diuresis result in prerenal azotemia and hemoconcentration. The hematocrit increases roughly 2% for each 1 degree drop in core temperature.9 Hypothermia inhibits platelet function and the enzymes of the clotting cascade, resulting in a coagulopathy that can lead to persistent bleeding or oozing from venipuncture sites and wounds. Hypothermia-related ventilation-perfusion mismatching, increased blood viscosity, and a leftward shift of the oxyhemoglobin curve contribute to hypoxemia. The reduced clearance of lactate produced by shivering muscle and the decreased renal excretion of acid may result in a metabolic acidosis. Serum glucose concentration rises because of decreased insulin secretion. Alcoholics, however, may present with hypoglycemia because of a preexposure depletion of glycogen. Serum potassium levels may be depressed owing to decreased tubular resorption.
At a temperature of between 30° and 31.5°C the last remaining defenses against the cold—shivering and consciousness—cease. At this temperature atrial ectopy gives way to atrial fibrillation with a slow ventricular response. Hypoventilation sets in, and respiratory acidosis augments the metabolic acidosis. As core cooling continues, ventricular irritability increases, leading to a high risk of ventricular fibrillation at 28°C and below. Below 28°C the patient may appear dead—cold to the touch, the pulse absent, respirations agonal or undetectable, and the pupils fixed and dilated. Cardiac output drops by 50% at 25°C and by 75% at 22°C, but a parallel reduction in oxidative metabolism spares the vital organs from cell death until extreme hypothermia or prolonged cardiac arrest occurs. At 19° to 20°C the heart stops, and the electroencephalogram becomes flat.
With moderate to severe hypothermia, additional laboratory abnormalities may be found. Signs of pancreatitis are common; pancreatic inflammation and necrosis are seen at autopsy in approximately 50% of patients dying of hypothermia. At or below 20°C leukopenia and thrombocytopenia are commonly observed because of sequestration in the liver and spleen. An elevation in cardiac creatinine phosphokinase (CPK-MB) values to levels suggestive of a myocardial infarction may occur despite the absence of ischemic changes on the electrocardiogram or wall motion abnormalities on the echocardiogram.10 Although an elevated CPK-MB level may be a benign artifact of cold-induced changes in the membrane permeability of heart muscle, it may also represent subendocardial damage or very small transmural infarctions, which have been detected at necropsy in persons succumbing to hypothermia.11
Diagnosis and Management
In hypothermic patients presenting to the emergency department, the lowered body temperature may be a complication of an acute medical condition (for example, overwhelming sepsis or prolonged exposure following a fall and inability to get up). However, hypothermic older patients frequently present with nonspecific symptoms such as shortness of breath, weakness, lightheadedness, confusion, lethargy, or stupor. Overlooking the possible contribution of hypothermia to the patient’s symptoms as well as to the physical and laboratory findings could result in inappropriate treatment. Conventional glass and electronic thermometers do not measure temperature below 34°C. Any patient with a temperature of 35°C or below must have his or her core temperature taken with a low-reading thermometer.
In patients with mild hypothermia (core temperatures of over 32°C), passive rewarming with blankets is effective and is probably the safest method of treatment. When active rewarming by externally applied heat is carried out in carefully controlled settings, the outcomes are similar to those achieved with passive rewarming. However, external rewarming generally should be avoided unless the hospital or emergency department has had extensive experience with this technique. The vasodilation that results from external rewarming (e.g., with an electric blanket or currents of warm air) exacerbates the well-described “after-drop” of core temperature that occurs when sequestered cool blood from the surface returns to the core. The vasodilation also increases the risk of hypotension. The complications of external rewarming can be reduced if the application of heat is limited to the trunk.
Unless they are minimally hypothermic, older patients should be admitted to an intensive care unit and placed on telemetry because of the risk of rhythm disturbances and the need for close attention to vital signs, fluid status, and metabolic parameters. Because of the cold-induced diuresis, most hypothermic patients are hypovolemic and require parenteral rehydration, preferably with normal saline warmed to 37° to 40°C. Lactated Ringer’s solution should be avoided because of the inability of the hypothermic liver to metabolize lactic acid. As the core temperature returns to normal, third-spaced fluid reenters the vascular space. Thus, fluid resuscitation should proceed cautiously to avoid precipitating congestive heart failure. Monitoring of the central venous pressure may help guide fluid management, but right heart catheterization should be avoided because the catheter tip may induce supraventricular or ventricular arrythmias when it touches irritable mycocardium. Unless the patient has underlying chronic obstructive pulmonary disease, the degree of hypoxemia can be assessed by pulse oximetry. Serum electrolytes, blood urea nitrogen, and serum creatine should be checked and abnormalities corrected. Insulin should not be given unless hyperglycemia is severe (more than 350 to 400 mg/dL) because endogenous insulin secretion increases during rewarming, risking hypoglycemia. The patient should have nothing by mouth until his or her core temperature has risen above 35°C. Unless the patient is able to fully cooperate, bladder (or condom) catheterization is necessary to allow accurate monitoring of urine output. Despite the uncertain clinical significance of the elevated CPK-MB fraction commonly found in hypothermic patients, the high prevalence of coronary artery disease in the elderly, coupled with the documented association of perioperative hypothermia with myocardial ischemia, justifies screening the hypothermic patient for myocardial infarction with serial electrocardiograms and CPK-MB measurements. However, empirical treatment with nitrates and beta-blockers is not justified because it may precipitate or worsen hypotension. Aspirin aggravates the coagulopathy associated with hypothermia.
At a temperature of below 28°C the patient has a depressed level of consciousness. Prophylactic intubation is recommended to prevent aspiration, to control the copious bronchial secretions, and to permit ventilation in the event of cardiac arrest. Intubation should be performed gently and, preferably, after preoxygenation through a mask to minimize the risk of inducing ventricular ectopy. If atrial fibrillation occurs, an agent to slow conduction, such as digoxin or diltiazem, generally is not needed. The atrial fibrillation seen in patients with hypothermia has a slow ventricular response and usually converts spontaneously to normal sinus rhythm following rewarming; such agents may thus induce postre-warming bradycardia or even heart block. A nasogastric tube may be required if ileus is present.
In patients with moderate hypothermia (28° to 32°C), cardiac instability, manifested by ventricular ectopy, warrants active core rewarming. Ventilation with humidified oxygen warmed to 42°C allows the body temperature to rise 1° to 2°C per hour. A popular method of core rewarming is peritoneal lavage with crystalloid dialysate warmed to 40° to 45°C, which achieves rewarming rates of 2° to 4°C per hour. This technique has the advantage of being able to remove dialyzable drugs like barbiturates. Similar rates of rewarming can be achieved with pleural irrigation using large-bore thoracostomy tubes and saline warmed to 40° to 42°C. Recently, hemodialysis has been used successfully for core rewarming; it achieves rewarming rates comparable to those seen with peritoneal dialysis, offers the advantage of more precise correction of acid base and electrolyte disturbances, and eliminates the risk of iatrogenic peritonitis. Because of its ready availability in most hospitals, hemodialysis may replace peritoneal dialysis as a first-line treatment for moderate hypothermia. Gastric, colonic, or bladder irrigation with warmed saline offers relatively little surface area for heat transfer and consequently remains a second-line therapy that can be used when dialysis and pleural irrigation are not available.
At temperatures of below 28°C (severe hypothermia), ventricular fibrillation, the most common cause of death in patients with accidental hypothermia, occurs frequently and is generally refractory to electrical and pharmacologic cardioversion. However, bretylium tosylate has shown some promise at low core temperatures; it is administered as an infusion of 10 mg/kg during ventricular fibrillation.9 Its efficacy in preventing ventricular fibrillation when given prophylactically is unknown. Extracorporeal rewarming is the most effective method for rapidly raising core temperature and is the treatment of choice in patients with severe hypothermia. Cardiopulmonary bypass can raise core temperature 1° to 2°C every 5 minutes. Femoral vein–femoral artery and atrial-aortic bypass appear to be equally effective, though the the former is less invasive and can be instituted outside the operating room.
A fundamental adage about hypothermia is that the victim is not dead until he or she is warm and dead. The protective effect of hypothermia may permit continued organ survival for many minutes after complete circulatory collapse has occurred. At a core temperature of 25°C, cerebral oxygen requirements are reduced by 70%. Thus, even in the presence of cardiac arrest, cardiopulmonary resuscitation should be continued until the patient has been rewarmed to at least 32°C. The increase in metabolism with rewarming may produce transient hypoxemia that responds to supplemental oxygen. The metabolic acidosis frequently seen in victims of prolonged hypothermia is remarkably well tolerated, and administration of sodium bicarbonate is not generally recommended. In moderate to severe hypothermia, arterial blood gases are useful for monitoring acid base status and oxygenation. Blood gas autoanalyzers warm the blood to 37°C, and the values reported at this temperature should be used for interpretation. For every 1°C drop in temperature, there is a corresponding 0.015 increase in pH and a decrease in the PCO2 due to the direct effect of temperature on the dissociation of hydrogen ions and the partial pressure of dissolved gases. Correcting the blood gas for the patient’s temperature consequently may result in an erroneous diagnosis of respiratory alkalosis and an inappropriate reduction in minute ventilation. Maintaining the uncorrected pH close to 7.4 appears to result in better myocardial function and electrical stability in both experimental animals and humans.12 Occult sepsis may complicate hypothermia and has been seen in up to 41% of hypothermic patients presenting to institutions serving a large alcoholic population.11,13 Empirical administration of broad spectrum antibiotics therefore appears justified once blood for the appropriate cultures has been drawn. Among victims in whom alcohol abuse is suspected, thiamine should be administered empirically because of the association of Wernicke’s encephalopathy with hypothermia.
The published mortality from severe hypothermia ranges from 0% to 80%. Little relationship exists between the core temperature at the time of diagnosis, age, rate of rewarming, and survival. One of the lowest temperatures ever recorded in an elderly patient who fully recovered from accidental hypothermia was 25°C, detected in an 86-year-old man.14 In patients with hypothermia alone, as among some alcoholics and individuals with mental illness, the prognosis is good, whereas the risk of mortality increases with the severity of underlying disease. Taken as a group, older individuals, with their increased prevalence of predisposing conditions (e.g., hypothyroidism, diabetes mellitus, undernutrition, use of medications), predisposing physiologic changes (e.g., decreased subcutaneous fat, diminished temperature perception, decreased shivering), and the presence of other chronic disease, are more likely to experience and suffer complications from accidental hypothermia.
AGE-ASSOCIATED RISK FACTORS FOR HYPERTHERMIA
Under conditions of rest and fasting, an average 70-year-old man produces about 65 kcal of heat per hour, about 5 kcal/hour less than an average 40-year-old. While this may be a disadvantage in a cold environment, it may be the one advantage that age confers for protection against hyperthermia. External warming (e.g., the sun) and muscular work add additional heat. An increase in blood temperature is sensed by the anterior hypothalamus, which in turn mediates increased blood flow to the skin and muscle with compensatory vasoconstriction of the splanchnic bed. Cutaneous vasodilation allows heat to be radiated to the environment when ambient temperatures are below 37°C. The increase in peripheral blood flow is accompanied by an increase in heart rate and cardiac output. Impaired cardiovascular performance is therefore an important risk factor for heat-related illness in older individuals (see Table 24-1). Cardiac output declines with age, although the slope of decline is reduced in physically active individuals such as master athletes. Not surprisingly, persons with congestive heart failure are at particular risk for heat-related illness. These individuals cannot acclimatize to the heat and may show signs of worsening congestive heart failure during prolonged exposure to heat. Similarly, common medications among the elderly that reduce cardiovascular function or reduce vascular volume, such as calcium channel antagonists, beta-blockers, and diuretics, increase the risk of heat intolerance. Peripheral vascular disease reduces heat tolerance by interfering with cutaneous vasodilation. Among healthy unacclimatized volunteers with similar proportions of body fat, older subjects (mean age 66) displayed a significantly lower forearm blood flow and a greater esophageal temperature compared to young subjects in response to dry heat exposure.15 Reduced cardiovascular responsiveness to heat exposure appears to be a concomitant of aging, at least in unacclimatized individuals, and a risk factor for heat intolerance.
When the ambient temperature exceeds 37°C, heat loss from the body depends almost entirely on the evaporation of sweat, which may be enhanced by convective cooling such as that provided by fans. However, as the humidity increases, the ability to lose heat through the evaporation of sweat declines, and fans consequently lose their protective effect. For example, at an ambient temperature of 32.2°C, fans cease to cool when the humidity exceeds 35%. At temperatures of more than 37.8°C, fans may actually contribute to heat stress by increasing the movement of hot air, analogous to the action of a convection oven.
Sweat responses in the elderly have been a subject of controversy. The absolute number of sweat glands per square centimeter of skin does not appear to change with healthy aging, although their function may be altered. Foster and colleagues found a marked reduction in sweating activity in older men compared to younger controls, and an even greater reduction in older women.16 However, virtually all their older subjects were frail and suffering from a variety of chronic diseases. Among healthy subjects, an age-related decrement in sweat rate can be detected in response to dry but not to moist heat. The sweat rate in the elderly thus appears to be related to the initial hydration of the skin. The threshold core temperature at which sweating occurs also appears to be higher in older persons. Conditions that impair sudomotor activity, such as sweat gland injury from prior heat stroke, ichthyosis, and scleroderma, can predispose to heat intolerance. Medications with anticholinergic effects, such as benztropine, oxybutynin, tricyclic antidepressants, phenothiazines, and antihistamines, directly inhibit sweat production. Benzodiazepines, alcohol, and other sedatives can blunt the patient’s awareness of excessive heat and prevent appropriate behavioral responses. Obesity, common in older adults, is associated with an altered sweat gland distribution and results in a decreased surface area to mass ratio and decreased skin blood flow, thus compromising heat loss.
A decrease in the effective arterial volume commonly results from the physiologic response to heat stress. This occurs as a result of loss through sweating, peripheral vasodilation in excess of splanchnic vasoconstriction, and leakage of plasma into myocytes (the latter two occuring during hard muscular work). Although acclimatization reduces the amount of sweat produced for a given amount of work, timely replacement of fluids is a critical behavioral response. After 24 hours of water deprivation, healthy elderly men were less thirsty, drank less water, and failed to dilute their plasma volume to predeprivation osmolality compared to younger subjects.17 Thirst resulting from heat stress and dehydration is also reduced in the elderly.
As with cold exposure, the most important responses to excessive heat are behavioral, such as removing excess clothing or turning on a fan or air conditioner. However, appropriate behavioral responses depend on the perception of discomfort. Crowe and Moore18 tested older and younger subjects in a warm chamber with their right hands immersed in a warm water bath that was hot enough to raise core body temperature. The subjects were allowed to obtain a burst of cool air ad libitum. The older subjects availed themselves of the cool air less often than would have been expected, given that their mean tympanic temperature and the mean rate of rise of temperature were significantly higher than these values in the younger subjects. Elderly diabetics and patients with peripheral neuropathies are at substantially increased risk for inability to detect small or gradual increases in ambient temperature. In addition, elderly diabetics may be unable to generate sufficient vasodilation in response to heat stress because of subcutaneous microvascular disease as well as autonomic dysfunction.
Data suggest that acclimatization can reverse or reduce these age-related changes in heat tolerance. Acclimatization involves an increase in circulating blood volume, increased cardiac output for a given level of exercise, an increase in the efficiency of skeletal muscle, a rise in sweat production, an increase in serum aldosterone levels, and increased conservation of sodium in both urine and sweat. Acclimatization thus resembles aerobic conditioning. Tankersley and colleagues19 compared the responses of seven young men (mean age 29) and 13 older men (mean age 65) to aerobic exercise in a warm environment (30°C, 55% relative humidity). When the young men were compared to the subgroup of older men with comparable levels of physical activity, the older subjects had significantly lower sweat rates and peripheral vasodilation. However, when the younger subjects were compared to seven master athletes who had comparable maximal O2 uptakes (VO2max—a measure of physical conditioning), the sweat rates and degree of peripheral vasodilation were similar in the two groups. Thus, among healthy, functionally independent older persons, aerobically conditioned individuals can be expected to have greater heat tolerance than their sedentary peers. Conversely, elderly persons who have become cardiovascularly deconditioned due to restricted mobility (e.g., from a stroke or arthritis) are at substantially greater risk for heat intolerance.
Hyperpyrexia supervenes when the body cannot dissipate sufficient heat through radiation, convection, and evaporation. At a core temperature of between 37° and 40°C, the symptoms may appear nonspecific and deceptively flu-like; they include anorexia, nausea, vomiting, diarrhea, lightheadedness, fatigue, headache, myalgias, and muscle cramping. The patient may be confused or display impaired judgment. This type of thermal disorder is termed heat exhaustion or heat prostration, and results from dehydration with varying degrees of salt depletion. Individuals who may have difficulty in gaining access to water, such as patients in nursing homes or those with restricted mobility, are at special risk for heat prostration and characteristically present with hypertonic dehydration. Patients with advanced dementia may not be able to communicate their thirst and may be unable to regulate their environment. Individuals who have lost large quantities of sweat that has been replaced with free water may be eunatremic or hyponatremic. This variant of heat prostration typically occurs in individuals who perform prolonged, intense muscular work in hot environments. The overenthusiastic “weekend gardener” and master athlete are among those prone to this disorder.
Although heat prostration usually responds to simple correction of the fluid-electrolyte imbalance, it can also progress to heat stroke. Heat stroke is defined as a core temperature of over 40.6°C in association with hot, dry skin and functional disturbances of the central nervous system (CNS). At temperatures of over 39° to 40°C, CNS dysfunction occurs, leading to neurogenic hyperventilation, paresthesias, tetany, cerebellar ataxia, agitation, and confusion. As core temperature rises, confusion gives way to lethargy, stupor, and then coma. Sweat gland failure is responsible for the hot, dry skin that is a hallmark of heat stroke.
Heat stroke has two variants: classic and exertional. The latter is the result of large endogenous heat production through intense physical exercise in a hot, usually humid, environment. Clinical and laboratory features of classic and exertional heat stroke are presented in Table 24-2. Hypotension is common in the elderly patient with classic heat stroke (CHS), resulting from dehydration and the inability of cardiac output to maintain a normal blood pressure. Heat stroke induces neurogenic hyperventilation with resulting respiratory alkalosis. However, if hypoperfusion occurs secondary to cardiovascular collapse, lactic acidosis may replace the respiratory alkalosis. Hyperglycemia is observed in up to 60% of patients with CHS, in part due to the stimulation of glycogenolysis and inhibition of insulin secretion by catecholamines, which are elevated during heat stress.20 Patients with CHS frequently present with diarrhea. Less commonly, cerebellar ataxia may be present and the patient may experience convulsions. Renal tubular damage and hepatocellular necrosis, similar to that seen in shock, also may occur. Disseminated intravascular coagulation, though usually milder than in exertional heat stroke, occurs in about 20% of cases and may cause a diffuse hemorrhagic diathesis. Adult respiratory distress syndrome also has been reported in approximately one fifth of cases.20 CHS may mimic septic meningitis with the appearance of confusion, nuchal rigidity, and hyperpyrexia. Although the cerebrospinal fluid may be blood-tinged and show an elevated protein content, pleocytosis is absent.21 Electrocardiographic changes in CHS are heterogeneous and include nonspecific ST-T wave changes, intraventricular conduction defects, prolonged PR and QT intervals, and supraventricular arrythmias, the most common abnormality being sinus tachycardia. Myocardial ischemia and infarction may complicate CHS, especially in older patients and those with preexisting coronary artery disease. In CHS death usually results from irreversible CNS injury, and necropsy usually reveals signs of neuronal injury and petechial hemorrhages scattered throughout the brain. A small percentage of survivors suffer permanent brain injury, particularly cerebellar injury. In general, however, patients with classic heat stroke suffer less tissue damage than victims of the exertional variant.
TABLE 24-2 FEATURES OF CLASSIC AND EXERTIONAL HEAT STROKE
OTHER CAUSES OF HYPERTHERMIA
Adverse drug reactions or interactions must be included in the differential diagnosis of hyperthermia. Hyperpyrexia, changes in mental status, and increased muscle rigidity in a patient taking a neuroleptic medication should alert the clinician to the possibility of neuroleptic malignant syndrome (NMS). Although rare (occurring in 0.5% to 1.0% of patients taking neuroleptics), the syndrome has also been reported during withdrawal of dopamine agonists in patients with Parkinson’s disease and with the use of metoclopramide. NMS can be effectively treated with bromocriptine or dantrolene. Mortality approaches 20%. Malignant hyperthermia (MH) is a rare, genetically determined syndrome precipitated by certain inhaled anesthetic agents, muscle-blocking agents, and stress. Alterations in the permeability of the sarcoplasmic reticulum to ionized calcium characterize this autosomally dominant trait. The treatment of choice is the muscle relaxant dantrolene. Since mortality approaches 60%, contemplated surgery should be preceded by a careful history to search for any prior adverse reactions to anesthetics in the patient or family members. Although the creatinine phosphokinase level is elevated in approximately 70% of persons at risk for MH, a muscle biopsy is required for definitive diagnosis. Administration of meperidine to an individual taking a monoamine oxidase inhibitor (MAO) may precipitate delirium, hypotension, and hyperthermia. This reaction may occur following a single dose of meperidine. It is thought to be due to accumulated serotonin resulting from the monoamine oxidase blockade. The number of half-lives of the MAO inhibitor that must transpire after the last dose before meperidine can safely be given is unknown. However, the manufacturers recommend that meperidine not be administered within 2 to 3 weeks following discontinuation of the drug.
Diagnosis and Management
The symptoms of heat prostration in the elderly may develop insidiously, may persist for days, and may not all be present simultaneously. In frailer individuals, heat prostration may occur in the absence of thirst. Thus, among patients brought to the physician for one or more of these symptoms, the heat stress causing them may be overlooked, risking the development of life-threatening heat stroke. Assessment of flu-like symptoms in the elderly during periods of hot weather should be accompanied by queries about the patient’s living situation. In summer, physicians should educate patients, their families, and caregivers about the symptoms of heat prostration and, for patients living in homes that are poorly ventilated or without air conditioning, encourage them to spend part of the day cooling off in air conditioned public places like shopping malls. When heat prostration is diagnosed, the patient should be placed in a cool room and rehydrated with isotonic or hypotonic saline, depending on the initial sodium and calculated water deficit.
It is important to note that many, if not most, older victims of heat stroke have no prodrome and collapse suddenly. Although heat prostration may progress to heat stroke, it is not a necessary precondition. Heat stroke is a medical emergency, with morbidity and mortality proportional to the delay in recognition and treatment. The presence of sweating should not exclude its diagnosis because the neurologic abnormalities typical of CHS may develop while the patient is still actively sweating. Moreover, generalized sweating may reappear when the victim of CHS is moved to a cool environment. Thus, during hot spells heat stroke should be considered in any patient who presents with a core temperature of over 39°C and mental status changes, even if he or she is sweating.
The cornerstone of therapy is the rapid reduction of core temperature and fluid resuscitation. The patient should be placed in an air conditioned room, if available, and core temperature should be continuously monitored, preferably with a rectal thermistor probe. Acetaminophen and salicylates are ineffective, and the latter paradoxically may increase core temperature. The best method for cooling remains controversial. Chilled intravenuous fluids and gastric, bladder, or colonic lavage with chilled normal saline may produce cooling rates of 0.15°C/minute. Keeping the body wet with cool water applied by wet towels or spray, using a large fan to evaporate the moisture, and placing ice bags in the groin and axillae will cool the patient at a rate of 0.3° to 0.6°C/minute. Rubbing the body with ice bags may expedite cooling, and stimulation of the skin by rubbing reduces reflex vasoconstriction that may delay cooling of the core. Ice water baths should be avoided because they impair access to the patient, especially during cardiopulmonary resuscitation. Intravenous chlorpromazine (25 to 50 mg) can inhibit reflex shivering but may aggravate hypotension and theoretically can lower the seizure threshold at a time when there is a high risk of convulsions. In the older patient, rehydration should proceed cautiously, and consideration should be given to central venous pressure monitoring or right heart catheterization. Peripheral vasoconstriction during cooling will augment the central circulation, and the victim may have underlying cardiovascular disease or may have sustained myocardial injury as a result of the hyperthermia. Seizures frequently complicate the cooling phase and pose a risk of aspiration as well as an increase in core temperature from the muscular activity. In a comatose patient, prophylactic intubation is therefore recommended. External cooling should be continued until the core temperature reaches 40°C, at which point the body temperature usually continues to fall. However, in patients who are unable to sweat, hyperthermia may recur in 3 to 4 hours. Recovery of the ability to sweat may take several weeks or may be permanently impaired.
Mortality from classic heat stroke approaches 70% in untreated cases but may be reduced to around 17% with treatment. Mortality increases with the duration and severity of the hyperthermia and is higher in those presenting in coma or shock.
Hypothermia and hyperthermia disproportionately affect older individuals. Although age-related physiologic changes contribute to thermoregulatory dysfunction in the elderly, the type and severity of underlying chronic diseases, together with the medications used to treat them, confer the greatest risk of morbidity and mortality during periods of thermal stress (see Table 24-1). Physical conditioning has the potential to improve the older person’s adaptation to heat, but its ability to slow or reverse age-associated changes in response to cold stress is unknown.
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* Hereafter, only °C will be used. For those readers more comfortable with the Fahrenheit scale, the following conversion may be used: °F = (9/5 × °C) + 32.