Health Articles

Most episodes of hypothermia are initiated by ambient temperatures near 15.5° C (60°
F), but older persons may become hypothermic while at home in mildly cool
environments.Current prevalence, incidence, and mortality data for accidental hypothermia are scanty, particularly in the USA. In one study, temperatures of elderly patients admitted to two London hospitals during three winter months revealed a 3.6% incidence of hypothermia in those > 65 yr of age. In a large community survey conducted in Great Britain during the winter of 1972, 10% of the elderly population had early morning core temperatures of s 35.5° C (96° F). There was no correlation between low body temperature and living alone, being housebound, or being without central heating or indoor plumbing. The only available US data are from a study done in Maine, in which 97 elderly persons (average age, 74 yr) from an internal medicine clinic were surveyed. Many persons were poor or lived in subsidized housing; none had a basal body temperature < 35.5° C (96° F).
Estimates of deaths due to hypothermia are difficult to calculate, since no definitive clinical or pathologic findings are available. Also, since most corpses are cold when discovered, attributing the death to hypothermia is difficult.
Accordingly, figures indicating that only a few hundred deaths each year in the USA are caused by hypothermia probably underestimate the problem.
In the USA, about 75,000 "excess winter deaths" occur among the elderly, including deaths from hypothermia and deaths associated with many other winter risks, such as influenza and pneumonia. Among identified cases of hypothermia, the mortality rate is disturbingly high at 50%. Persons > 75 yr of age are five times more likely to die from hypothermia than are those < 75 yr. Mortality correlates more closely with the presence and severity of associated illness than with the degree of hypothermia.
Hypothermia may also result in substantial morbidity. One British study showed a midwinter peak in the incidence of hip fracture in malnourished patients and a higher mortality rate after hip fracture. Malnourished patients were frequently hypothermic on admission to the hospital, whereas well-nourished patients had normal body temperatures. Malnutrition presumably led to impaired heat generation and retention, which caused hypothermia; the hypothermia resulted in lack of coordination and subsequent injury. Additionally, elderly patients with diabetes have a sixfold greater risk of hypothermia, probably due to vascular disease that alters thermoregulatory mechanisms.
Etiology and Pathophysiology
The factors usually implicated in the genesis of accidental hypothermia are a cold environment, age-related physiologic changes in thermoregulation, drugs, and the diseases that decrease heat production, increase heat loss, or impair thermoregulation
Ambient temperature only a few degrees cooler than body temperature can cause hypothermia in severely debilitated elderly persons. Also, a number of physiologic changes predispose elderly persons to hypothermia, including a diminished perception of cold. Changes in response to endogenous catecholamines reduce the vasoconstrictor and shivering responses to cold. A decrease in lean body mass reduces the efficiency of shivering for heat production. Less physical activity and reduced caloric intake affect the ability to generate heat.
Pathologic conditions in older patients add to the physiologic risks. Decreased heat production occurs with hypopituitarism, hypoglycemia, starvation, and malnutrition.
Forced or involuntary inactivity (eg, as in Parkinson's disease, arthritis,paralysis, and dementia) decreases heat production and increases the risk of hypothermia. Increased heat loss can occur secondary to inflammatory skin disease, Paget's disease, alcohol-induced vasodilation, cold exposure, and reduction in insulating subcutaneous fat. Central hypothalamic temperature regulation can be disturbed by stroke, subarachnoid hemorrhage, subdural hematoma, and brain tumor.
Uremia and carbon monoxide poisoning may also affect thermoregulation.Many drugs, including phenothiazines, tricyclic antidepressants, benzodiazepines,barbiturates, reserpine, and narcotics, depress central thermoregulation and predispose patients to accidental hypothermia. Chlorpromazine, which inhibits shivering, is the best-known offender.

Symptoms and Signs
The symptoms of hypothermia are insidious and may be transient. Although elderly people with body temperatures between 35° C (95° F) and 36.1° C (97° F) often complain of being cold, patients with established hypothermia usually do not.
Clinical findings are nonspecific; they can suggest stroke or metabolic disorder.
The patient feels cool to the touch and has a history of confusion and sleepiness,which may progress to coma.Neurologic findings include thick, slow speech; ataxic gait; and depressed deep tendon reflexes. Pathologic reflexes and plantar responses may be present, and pupils may be dilated and sluggishly reactive. Focal signs, seizures, paralysis, and sensory loss may also occur.Although shivering may occur at temperatures > 35° C (> 95° F), it is absent in most hypothermic elderly patients. Instead, marked rigidity accompanied by a generalized increase in muscle tone and, occasionally, a fine tremor may be found.Although many people have cold hands or feet in winter, hypothermic patients also have cold abdomens and backs. The skin has a cadaveric pallor and chill, and pressure points show erythematous, bullous, or purpuric patches. Subcutaneous tissues are firm, probably from edema, which also produces a puffy appearance,especially of the face.
The cardiovascular system is initially stimulated by cold, resulting in peripheral vasoconstriction, tachycardia, and elevation of blood pressure. As hypothermia progresses, the myocardium is depressed, producing hypotension and progressive sinus bradycardia. Severe hypothermia can reduce blood pressure and heart beat to barely detectable levels, sometimes leading to an erroneous pronouncement of death. Various other cardiac arrhythmias are associated with cold temperatures, including atrial fibrillation and flutter, premature ventricular beats, and idioventricular rhythm.Cardiac arrest, from either ventricular fibrillation or asystole, is increasingly likely as body temperature falls below 30° C (86° F).
The gastrointestinal response to hypothermia consists of decreased peristalsis or even ileus, producing abdominal distention and diminished or absent bowel sounds.
Less often, acute gastric dilation occurs with vomiting. Pancreatitis may also occur but is usually not apparent until rewarming has been achieved. Because hepatic metabolism is depressed, drug metabolism may be sharply reduced.
Pulmonary findings include depression of respiration and cough reflex. Atelectasis is almost universal, and pneumonia is common. Pulmonary edema during recovery may be related to increased vascular permeability as well as to heart failure.
Early in hypothermia, there is an increase in heart rate, cardiac output, and renal blood flow with diuresis. In addition, cold suppresses antidiuretic hormone secretion and diminishes tubular responsiveness to its action, further increasing diuresis. As volume depletion reduces glomerular filtration and renal blood flow,oliguria and tubular necrosis follow.
Diagnosis
Hypothermia is often missed; the usual clinical practice is to search for and exclude fever, not to search for and exclude hypothermia. Hypothermia should be suspected if the history or physical examination is suggestive, and core temperature should be recorded using a low-reading thermometer. The diagnosis of accidental hypothermia depends on the ability to measure body temperature < 34.4° C (94° F).
Standard clinical thermometers are calibrated from 34.4° to 42.2° C (94° to 108° F), and hypothermic patients have temperatures < 34.4° C. Since these thermometers are usually shaken down to only between 35° and 35.5° C (95° and 96° F) before measuring temperature, they probably will not detect hypothermia. Rectal thermometers calibrated from 28.9° to 42.2° C (84° to 108° F) are available from most hospital suppliers, although they are not commonly used. A special low-reading thermometer can be obtained from Becton Dickinson, 1 Becton Drive, Franklin Lakes, NJ 07417 (201-847-4000). If a low-reading thermometer is unavailable, more expensive thermistors or thermocouples can be used.
Most clinical laboratory data are not specific for hypothermia. Hemoconcentration,leukocytosis, lactic acidosis, and thrombocytopenia are all common. The ECG can provide a major diagnostic clue. A junctional (J), or Osborn, wave is a small
deflection early in the ST segment, positive in the left ventricular leads and negative in the right ones. Although present in only about '/? of hypothermic patients, this finding always indicates hypothermia. Another, more common ECG finding frequently seen in the nonshivering patient is a fine regular oscillation of the baseline produced by increased muscle tone with an imperceptible tremor.
Blood glucose findings in hypothermia can be confusing. Usually, hyperglycemia is found. Hypothermia triggers hyperglycemia by corticosteroid- and catecholamine-induced gluconeogenesis. Although insulin secretion is also stimulated, cold interferes with its action, further raising blood glucose levels.Less commonly, hypothermic patients are hypoglycemic, in which case it is the hypoglycemia, usually drug-induced, that produces the hypothermia.
Prevention
Preventing accidental hypothermia is preferable to treating it. Older persons with identifiable predisposing problems should have their household thermostats set at>
18.3° C i≥ 65° F) and should keep a reliable thermometer available (separate from the thermostat) for determining room temperature. This should be checked daily,especially during very cold weather. Extra clothing, particularly for hands,feet,and head, should be worn indoors. Frequent periods of exercise can increase heat production, and adequate caloric intake is of primary importance. Drugs that may alter thermoregulatory mechanisms should be discontinued whenever possible.Treatment An elderly patient with accidental hypothermia usually is treated initially for some other disorder—either a cause or complication of hypothermia is the exclusive focus,or the symptoms and signs of hypothermia are erroneously attributed to some disease common in the elderly. In either case therapy is delayed.Once the temperature falls into the hypothermic range, thermoregulation becomes progressively impaired; indeed, early during the temperature fall, regulatory mechanisms fail altogether and the patient reacts like a poikilotherm. Accordingly,even mild accidental hypothermia should be considered a medical emergency, and patients should be monitored under hospital conditions (usually in an intensive care setting) until recovery is complete.Therapy can be divided into two foci: (1) primary treatment by rewarming and (2) secondary treatment of the direct effects and complications of hypothermia. General medical care demands comprehensive evaluation, close monitoring, and anticipation of likely complications. Laboratory evaluation should include CBC count; platelet count; clotting studies; measurements of BUN, creatinine, electrolytes, blood glucose, and serum and urine amylase levels; thyroid and liver function tests;arterial blood gas studies; ECG with constant monitoring; chest and abdominal
x-rays; and constant monitoring and recording of core temperature.
Primary measures aim to restore normal body temperature and to abort the pathophysiologic consequences of hypothermia. In young, physiologically vigorous persons who suffer hypothermia, especially as a result of exposure, rapid active rewarming is carried out by active heating. Elderly persons with accidental hypothermia, when rewarmed actively and rapidly, often develop a syndrome of profound hypotension, new cardiac arrhythmias, and deteriorating metabolic abnormalities, culminating in death. For this reason, slow spontaneous rewarming is
recommended for older victims of hypothermia. By preventing further heat loss and
conserving the heat still being produced by the patient, slow spontaneous rewarming
allows the body temperature to rise slowly, at a rate of about 0.6° C (1° F)/h. A
more rapid rise in core temperature, even when slow spontaneous rewarming is used,
has been associated with rewarming hypotension. The environmental temperature is
kept > 21.1° C (> 70° F), and blankets or more sophisticated insulating materials
are used to retain body heat.
If slow spontaneous rewarming does not produce a rise in body temperature, rapid
active rewarming of the core is necessary. Techniques for core rewarming include the
use of heated, moist inspired air, warmed IV fluids at 37° C (98.6° F), and heated
peritoneal dialysis. If rapid active rewarming of the core or periphery is used in elderly patients, scrupulous, comprehensive intensive care must be taken. When ventricular fibrillation or cardiac standstill occurs at temperatures < 29.4° C (85°F), warming must be accomplished as quickly as possible because the heart is unresponsive to electrical defibrillation at temperatures below this level. Bradycardia resulting from myocardial depression is not influenced by atropine. The need for ventilatory assistance, intracardiac monitoring and pacing, and full circulatory support should be anticipated, since collapse and profound hypotension associated with warming are common under such conditions.
Ventricular arrhythmias, if not rapidly responsive to rewarming, should be suppressed with lidocaine. Both countershock and pacing are less effective at low temperatures; if critical arrhythmias appear, appropriate therapy should be administered while the patient is rewarmed. If cardiac arrest or ventricular fibrillation is unresponsive to usual measures, cardiopulmonary resuscitation should be continued until rewarming has been accomplished; treatment then should be
repeated. All IV fluids should be warmed to normal or slightly above normal body temperature.
Although some studies have recommended the routine use of such drugs as corticosteroids, thyroid hormone, anticoagulants, antibiotics, and digitalis, none of these agents has proved effective unless specifically indicated. Myxedema is, of course, a well-known cause of hypothermia; when hypothermia and hypothyroidism occur
together, they result in a very high mortality rate.
Although hyperglycemia is common in hypothermic patients, insulin is rarely given
unless glucose levels are very high (> 400 mg/dL) because insulin is ineffective at low temperatures. Any previously administered insulin, combined with endogenous insulin, can produce severe hypoglycemia during rewarming. In general, most drugs
are less active during hypothermia but have exaggerated pharmacologic effects as
body temperature rises.
Death usually results from cardiac arrest or ventricular fibrillation. The temperature at which each cardiac event appears varies, but at temperatures < 29.4°C (85° F), risk of death is high, particularly in patients with underlying heart disease. Movement or excessive stimulation of hypothermic patients may provoke
arrhythmias and should be performed cautiously. Resuscitation during rewarming
should be aggressive and prolonged in patients who are profoundly hypothermic;
remarkable recoveries have been reported in such cases. Most authorities agree that patients should not be pronounced dead until cardiopulmonary resuscitation is shown
to be ineffective after body temperature has been raised to at least 35.8° C (96.5°F).

Under usual environmental conditions, convection and radiation account for 65% of heat loss; evaporation from skin and lungs contributes another 30%. The hypothalamus regulates heat loss through neuroendocrine and autonomic mechanisms. Heat causes blood vessels in the skin to dilate, and sweating increases as a result of cholinergic discharge. Vasodilation, in turn, reflexly increases heart rate and cardiac
output.
When environmental temperature exceeds body surface temperature, heat is no longer lost through convection and radiation but begins to be absorbed. Evaporation of sweat becomes the last major mechanism by which to lose heat, but increased humidity can prevent cooling by this mechanism.
Aging appears to reduce the effectiveness of sweating in cooling the body. Many eccrine glands become fibrotic, and surrounding connective tissue becomes less vascular. In addition, the remaining anatomically normal eccrine glands may not function properly. Older persons initiate sweating at higher core temperatures and have less maximal sweat output per gland.
Heart disease increases the risk for heat stress. Under experimental conditions, increased ambient heat and humidity exacerbate heart failure. The greater the degree of cardiac impairment, the less a person is able to withstand the environmental stress. Thus, physiologic changes resulting from normal aging and from diseases more common in the elderly combine to impair optimal heat regulation.

Abnormally high body temperature due to inadequate or inappropriate responses of heat-regulating mechanisms.
Hyperthermia represents an important health risk for older people, because heat exacerbates chronic diseases and because heatstroke causes many pathophysiologic changes. The number of deaths resulting from most diseases increases during hot, humid weather, particularly among elderly persons. About 80% of heatstroke deaths occur in those > 50 yr of age.