Accidental hypothermia

Pharmac. Ther. Vol. 22, pp. 331 to 377, 1983

0163-7258/83 $0.00+0.00 Copyright © 1983 Pergamon Press Ltd

Printed in Great Britain. All rights reserved

Specialist Subject Editors: E. SCHONBAUMand P. LOMAX

ACCIDENTAL HYPOTHERMIA BRUCE C. PATON

Clinical Professor of Surgery, University of Colorado Health Sciences Center, and Porter Memorial Hospital, Denver, Colorado, U.S.A.

1. HISTORY Scientific understanding of the effects of cold began towards the end of the eighteenth century. Before then cold had been used therapeutically for centuries, especially for treating fevers and inflammation, and even for controlling epileptic seizures. Accidental hypothermia must have been common, if misunderstood. As the Roman legions trudged through Gaul and weathered the winter storms of the Alps, many a legionnaire must have succumbed to the insidious onset of hypothermia. Alexander the Great, during his campaign into India is said to have become unconscious from cold. Perhaps one of the earliest references to the hypothermia of old age is in the Bible. "Now King David was old and stricken in years; and they covered him with clothes, but he got no heat. Wherefore his servants said unto him, "Let there be sought for my lord the king a young virgin: and let her stand before the king, and let her cherish him, and let her be in thy bosom, that my lord the king may get heat. So they sought for a fair damsel throughout all the coasts of Israel and found Abishag a Shunammite, and brought her to the king. And the damsel was very fair, and cherished the king, and ministered to him: but the king knew her not." (I. Kings i, v. 1-4)

But in spite of the common man's experience with cold (perhaps because of it) there seem to be few early accounts of accidental hypothermia. In 1574 Josias Simler published a guide book to mountain travel entitled 'De Alpibus Commentarius' in which all the dangers of mountaineering were described including hypothermia (Houston, 1980). In 1786 Jonathan Williams, writing to his great uncle Benjamin Franklin, recalled that when a boy he had fallen into a mill creek and was taken out with 'not the smallest sign of life remaining.' Had it not been for the energetic efforts of his mother to rewarm and revive him he would not have survived because when the doctor arrived he 'poured down three Pukes successively, but without effect'. After three hours of active rewarming he began to show signs of life. He lived to become the first Superintendent of West Point (Williams, 1786). In 1786 John Hunter, the insatiable investigator, froze two carp~hoping to find out that it would be possible to revive them after they were completely frozen. When thawed, however, they regained no life. John Hunter commented wryly on his experiment: "Like other schemers I thought I should make may fortune by it; but this experiment undeceived me." Napoleon's surgeon, Baron Larrey (1817), was well aware of the devastasting effects of hypothermia on physical and mental effectiveness--following his troops to and from the gates of Moscow he must have acquired an unenviably great experience. Hypothermia, like frostbite, has been a major influence on the outcome of military campaigns. From the campaigns of Alexander the Great to the ruins of Stalingrad and the hills of Italy and Korea, cold has bitten into the core of armies, slowing thought and action and turning the tide of the battle. Because of the high mortality amongst U-boat crews and downed pilots in the North Atlantic during World War II the Nazis carried out experiments on concentration camp prisoners, attempting to find the best methods for J.Pr. 22/3 A

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rewarming and to develop protective clothing, These inhuman experiments probably did little to save the lives of any of the 30,000 men of the U-boat service who lost their lives in the cold Atlantic waters and contributed little to general knowledge of hypothermia (Alexander, 1945). Mountain and arctic expeditions have been the scenes of many heroic and often tragic cases of hypothermia. Captain Oates sacrificed himself by a hypothermic death in a vain attempt to help Captain Scott and his companions return safely from the Pole. The North Face of the Eiger and Mt McKinley have both claimed their chilling toll. In 1974, eight Soviet women climbers died on the stormy summit of Peak Lenin, their last weak words monitored over a radio, "Now we are two. And now we will all die. We are very sorry. We tried but we could n o t . . . Please forgive us. We love you. Goodbye." (Craig, 1980). In recent years there have been numerous individual cases reported both in the medical literature and the general press: alcoholics found in alleys, hunters lost, climbers stranded, sailors overturned and floating for hours in frigid lakes. Some lived, some died. All have been witnesses to man's constant conflict with his environment. 2. PHYSIOLOGIC CHANGES Hypothermia is a physiologic deceleration. If there is any doubt about the effect of hypothermia upon a physiologic function it may, in most instances, be assumed that the function is diminished or slowed so long as hypothermia persists. When euthermia is restored the function returns to normal. 2.1. CARDIOVASCULAR During the initial phases of hypothermia core temperature is maintained by an increase in heat production by shivering which may produce as much as 250 kcal/hr of energy. Heart rate, blood pressure and oxygen consumption increase. If shivering is prolonged energy reserves are seriously depleted. When heat loss begins to exceed heat production shivering stops and heart rate, blood pressure and oxygen consumption start to fall progressively with decreasing temperature. Oxygen consumption decreases by about 7~o per degree (°C) (Blair, 1956). At 30°C consumption is about 50~ of normal, about 20~ of normal at 20°C and 10~ of normal at 10-15°C. The reduction in oxygen consumption is not linear at temperatures below 20°C and is affected by several variables including blood flow and changes in oxyhemoglobin dissociation (Swan, 1974). Because the reduction in cardiovascular performance is more rapid than the reduction in oxygen consumption a metabolic acidosis slowly develops, which may become even more marked during rewarming. Myocardial depolarization is slowed. The P - R interval is prolonged and the QRS complex widens. T waves are sometimes inverted and a characteristic J wave on the downstroke of the QRS has been described (Emslie-Smith, 1958). Cardiac arrhythmias are common at temperatures below 29°C (Badeer, 1958). Atrial fibrillation/flutter occurs frequently and usually disappears spontaneously during rewarming. Ventricular fibrillation is a major hazard in both accidental and induced hypothermia. Many different causes for the induction of ventricular fibrillation have been postulated (Badeer, 1958; Lloyd, 1974). The direct effect of cold is probably not one of them. Thousands of observations in operating rooms indicate that direct rapid myocardial cooling usually causes asystole, not ventricular fibrillation. High potassium content of blood, changes in H + ion concentration (Swan et al., 1953; Malamos et al., 1962), elevation or depression of pCO2 (Brown and Miller, 1952), mechanical stimulation by movement, intubation, or the passage of an intracardiac catheter (Hegnauer et al., 195 l) have all been incriminated. It is difficult to single out any specific cause. Although mechanical stimuli have long been thought to be important there is little evidence that intubation, or the passage of intracardiac catheters constitutes a true danger (Ledingham and Mone 1972; Harari et aL, 1975; Miller et al., 1980). None of these procedures should be avoided merely because of their supposed danger.

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Lloyd (1974) has postulated that as cooling progresses neuromuscular transmission in the subendocardial conducting network is slowed to a greater extent than direct transmyocardial conduction, resulting in a re-routing of stimuli through the muscle, thereby precipitating ventricular fibrillation. 2.2. NERVOUS SYSTEM 2.2.1. High Cortical Function The effects are variable as is the temperature range within which they occur. Disori. entation, an inability to indulge in rational thought and discussion, forgetfulness, argumentativeness and hallucinations may all occur (Freeman and Pugh, 1969). These changes start about 35°C. As temperature falls consciousness becomes dulled with a final lapse into coma. The temperatures at which these changes occur are a range rather than a fixed point. Most patients are semiconscious by 30°C; but some remain confused but conscious as low as 26°C. Convulsions may occur and seem to be commoner in patients with profound exposure hypothermia than in older patients with 'urban' hypothermia (Pugh, 1966). 2.2.2. Nerve Conduction This is slowed from about 30 m/sec at 35°C, to 26 m/sec at 23°C and 12 m/sec at 21°C. As a result of these changes the patient becomes discoordinated and loses manual dexterity. Reflexes are abolished between 26-27°C including the pupillary reflexes. The pupils appear to be fixed, dilated, and unreponsive to light, so that the patient may be mistaken for dead. Central nervous system electrical activity ceases at 18°C. Cold induced anesthesia starts at about 28°C. As a result a hypothermic accident victim, if conscious, may be unaware of injuries which would be sensed while euthermic. Prolonged exposure of peripheral nerves to temperatures below 10°C may cause both motor and sensory damage (Stephens, 1955). 2.2.3. Protection of the Nervous System Surgical experience has shown that hypothermia protects the central nervous system from ischemic damage. At 30°C cerebral circulation may be shut off for 6-8 min (Swan and Zeavin, 1954). At 15-20°C cerebral circulation may safely be stopped for 60min, especially in small infants. The spinal cord is also protected by cold; and being more resistant to ischemic damage than the brain is protected for even longer periods by hypothermia (Owens et al., 1955). 2.3. RESPIRATORYSYSTEM Respiratory rate falls to 7-15 per minute at 30°C, and 4-7 per minute when core temperature is in the mid 20's. Both airway dead space and physiologic dead space increase. Pulmonary circulation time is prolonged, unless there is intrapulmonary shunting. Pulmonary edema not associated with cardiac failure is a common finding in patients hypothermic for a long time (Ledingham and Mone, 1980; O'Keefe, 1980). The ciliary function of bronchial epithelium is reduced which probably increases the likelihood of bacterial invasion. Bronchitis and pneumonia are common findings. 2.4. GASTROINTESTINALTRACT Gastrointestinal motility slows and finally ceases. Stress ulcers are occasionally found in the stomach. Acute hemorrhagic pancreatitis is commonly found in fatal cases

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(Coopwood, 1971; Hudson and Conn, 1974). Whether this lesion is a cause or an effect is not always clear. 2.5. KIDNEYS Cold induces a diuresis of both water and nitrogen, which appears to be due to a diminution in reabsorption. The environmental temperature does not need to be very cold to initiate this diuresis which may start at an ambient temperature of only 15°C. After prolonged hypotherrnia and low cardiac output acute tubular necrosis may develop, in spite of the protective effect of hypothermia. Renal transplantation research has demonstrated that kidneys kept at 4-10°C for 72 hr outside the body maintain an ability to perform normally after rewarming (Simmons et al., 1979). During hypothermia urine output is low and complete renal shutdown with acute tubular necrosis may occur. An elevation of BUN and creatinine is more likely to be due to underlying renal disease than to hypothermia per se. 2.6. BLOOD The hematocrit rises, in part due to hemoconcentration secondary to cold diuresis and in part due to loss of plasma water into subcutaneous edema. This hemoconcentration and rise in hematocrit causes an increase in blood viscosity which may, in turn, place an added workload on the heart. There are many changes in blood concentrations of electrolytes and plasma constitutents. Glucose is often high, occasionally dangerously low (Stoner et al., 1980). Free fatty acids increase. Eosinophils decrease in numbers while the white cell count is often elevated. Serum sodium falls, as sodium passes into the cells. At the same time potassium is driven out of the cells so that serum levels of potassium may increase dramatically. The coagulation cascade is slowed, but no specific changes or defects occur resulting in a coagulation deficiency. Upon rewarming coagulation becomes normal. An occasional patient may develop DIC, but this complication has been more commonly reported in infants and children than in adults (Mahajan, 1981). Thrombotic complications are quite common especially in fatal cases (Duguid et al., 1961; Tolman and Cohen, 1970). 2.7. ENDOCRINE 2.7.1. A d r e n a l Steroids Corticosteroids are elevated (MacLean and Browning, 1974; Stoner et al., 1980) and there may be an inverse relationship between the duration and severity of hypothermia and the level of l l-hydroxycorticosteroids. MacLean (1974) found a mean plasma level of 68.2 #g/100 ml in 84 hypothermic patients. But when subsets of this group were analyzed it was found that the mean plasma level was 96.4 #g/100 ml in patients who died while still hypothermic, 91.0 # g/100 ml in patients who died within 24 hr, 87.1 # g/100 ml in those who died within three days, and 62.9pg/100ml in those with outdoor or immersion exposure who survived. The conclusion was that adrenal insufficiency did not contribute to the deaths. Mclnnes et al. (1971) measured plasma 11-hydroxysteroid levels in climbers and found that in most the level was elevated and there appeared to be some correlation between physical fitness, stress and plasma levels. In two exhausted climbers unexpectedly low levels were found, possibly a reflection of adrenocortical exhaustion. Body temperatures were not measured in these people so no correlation could be drawn between temperature, exhaustion and steroid levels. In a group of 23 hypothermic patients admitted to a city hospital Woolf et al. (1972) found plasma cortisol levels rose from a baseline level of 22.9/~g/100 ml to a maximum level of 32.4#g/100ml after 7hr of rewarming. Although the correlation was not statistically significant the trend, when plotted, suggested that cortisol levels rose during rewarming. Plasma cortisol levels were measured in 15 patients studied by Stoner (1980) and were found to be high in every patient--the levels were related neither to temperature nor to outcome.

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From these observations there is no reason to believe that adrenocortical function is seriously depleted during hypothermia. Although Duguid (1961) advocated the administration of large doses of steroids, others (MacLean and Browning, 1974; Tolman and Cohen, 1970) do not believe there is objective backing for this view except perhaps in people subjected to prolonged exposure. 2.7.2. Thyroid Woolf et al. (1972) measured TSH and thyroid hormone levels in 12 patients. TSH was normal in all, and there was no correlation between TSH levels and body temperature. Thyroid hormone values were normal (8.2 vg/100 ml) when the patients were first seen, but in 11/12 patients T4 levels fell during rewarming to 7.0 #g/100 ml. T 3 levels were slightly elevated to start with (155 #g/100 ml) and also fell (138/~g/100 ml) when euthermia was reached. Two of three patients responded appropriately to administration of TSH. Other investigators have found that TSH rises after exposure to cold but, in general, there seems to be little or no change in TSH levels. Levels of protein bound iodine were found to range between 3.6-10.9 pg/100 ml (mean 5.8 #g/100 ml) in euthyroid patients and 0.5-3.5 #g/100 ml (mean 2.4 #g/100 ml) in hypothyroid patients. 2.7.3. Insulin Woolf et al. (1972) found no consistent changes in immunoreactive insulin. Insulin is not active below 31°C and in hypothermic diabetics administered insulin may not be effective if the body temperature is below 30°C. Diabetics should therefore be warmed to 30°C, or higher, before insulin is given. Blood glucose levels are variable in hypothermic patients but frequently the level may be very low, especially in alcoholic patients. Some patients may be hyperglycemic (>200mg/100ml) (Prescott et al., 1962). The blood glucose level should always be measured, and if there is any clinical doubt about hypoglycemia the patients should receive a bolus of 10~ glucose intravenously. Diabetes is a common predisposing condition, especially severe ketoacidosis. In diabetic patients the blood glucose level depends upon the metabolic state of the patient and not on the hypothermia. Weyman et al. (1974) found a mean blood glucose level of 161 mg/dl in 31 cases of uncomplicated hypothermia (59-324 mg/dl). Fitzgerald (1980)observed that 419/o of 22 alcoholic hypothermics had low blood sugar levels and advocated giving intravenous glucose to all victims of hypothermia. But Altus et al. (1980) found only one patient in a group of 39 who had a blood sugar less than 58 mg/100 ml. Pancreatitis (Duguid et al., 1961; Savides and Hoffbrand, 1974) is a common finding at autopsy in patients who die from hypothermia and may in individual cases affect blood sugar levels. 2.8. ENZYME LEVELS In a detailed study of creatine kinase (CK), x-hydroxybutyrate dehydrogenase (HBD) and aspartate aminotransferase (GOT) in 75 patients including 18 with myxedema, MacLean et al. (1974) found high levels of all three enzymes. But there was no correlation between the enzyme levels and the severity of hypotension, acid-base changes, hypoxia, or with the duration or severity of hypothermia. It was found, however, that low PBI levels correlated with high concentrations of HBD, and the correlation may reflect the cardiomyopathy of myxedema. 2.9. CHANGES IN THERMOREGULATIONWITH AGE As age increases several important physiologic changes occur which influence the ability to maintain an optimal body temperature. It has been found that many elderly people have a lower than normal body temperature. Collins (1977) found a mean morning oral

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temperature of 35.92°C in 47 people aged from 69-90 years. Afternoon temperatures in the same group averaged 36.39°C. Wagner et al. (1974) also found rectal temperatures to be lower in people aged 46--67 than in younger age groups. In a survey in Britain of elderly patients in their homes Fox (1973) found 11.4~o to have temperatures below 35°C. Almost 25~o had low temperatures, without being categorically hypothermic. In the same study of 77 people in Portsmouth, England, the mean oral temperature was 36.0°C in men and 36.2°C in women. Urine temperatures in the same groups were 36.3°C and 36.4°C respectively. The frequency with which such temperatures are found must depend to a great extent on the environment in which the elderly are living. Primrose and Smith (1981) found that in Glasgow 96~ of elderly surveyed were living in homes with temperatures below a recommended level of 21°C. Eighty-four percent were living exposed to temperatures below a minimally acceptable level of 18.3°C and 61~ were living below the absolutely minimal level of 16°C. Most reports of body temperature in elderly people have originated in Great Britain and have alerted the medical profession to the magnitude, or potential magnitude, of the problem. It may not be wise, however, to extrapolate this information to other populations living in different climates and under different social circumstances. There are a number of mechanisms responsible for lowered temperatures in the elderly, these are discussed below. 2.9.1. Reduction in Metabolic Rate The metabolic rate in the elderly is less than in younger people. In a protected environment this may be of little importance: but in environments such as those described by Primrose (1981), an adequate metabolic rate is obviously essential to the maintenance of body temperature. Stoner et al. (1980) studied metabolism in elderly hypothermic patients and found that body fuels are mobilized, possibly under the influence of adrenal activity. As a result, plasma concentrations of lactate and lipid metabolites are high. Plasma glucose levels are also high because of the peripheral release of glucose, without an increase in peripheral glucose uptake. 2.9.2. Reduction in Peripheral Blood Flow This is probably due to two factors: a reduction in cardiac output and a change in peripheral vascular reactivity. Finger temperatures in a thermoneutral atmosphere are higher in the young than the old. But in a cold atmosphere (15°C) the finger temperatures of the young became lower than those of the old, because they are more able to constrict their peripheral vessels and conserve heat (Wagner et al., 1974). Collins et al. (1977) studied vascular reactivity in old people and found three types of reaction to cold. The participants in the study were exposed to three temperatures, 29°C--15°C 45°C, in that order. Normal people react with a reduction in skin temperature in the 15°C atmosphere, and a rise in temperature when exposed to warmth. Another group (nonconstrictors) stabilized at an initial temperature lower than the normal group, did not constrict in the cold, but dilated upon exposure to warmth. Fourteen (14) out of 43 people studied reacted in this way. The third group neither constricted in the cold, nor dilated in the warmth. Wagner et al. (1974) also found finger blood flow to be reduced in the elderly under most circumstances but changed little upon exposure to cold. Lack of reactivity is an obvious breakdown in thermoregulatory defense mechanisms. 2.9.3. Changes in Temperature Perception Collins et al. (1977, 1981) have demonstrated in two studies that temperature discrimination is reduced in the elderly. Young subjects can detect ambient temperature changes of 0.8°C while a change of 2.5°C is necessary before being noticeable to many old people.

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The clinical observation has been made on many occasions that old people will sit in an uncomfortably cool room without apparent discomfort. This may be partly behavioral as well as physiologic, but with prolonged exposure a tendency towards hypothermia would be increased. 2.9.4. Shivering With increasing age the ability to shiver diminishes. The mechanism for this diminution is not clear. Collins et al. (1977) found that only 4 out of 43 subjects exposed to a cold environment shivered. All were in the nonconstrictor response category. Impairment or abolition of shivering, combined with low basal metabolism further increases the chances of hypothermia. 2.9.5. Changes in Heat Conductance. Heat conductance is increased, accelerating heat loss, and is higher in a cold than in a thermoneutral environment. 2.9.6. Summary of Mechanisms The thermoregulatory homeostatic mechanisms of the elderly are impaired by changes in both heat production and heat conservation. A low metabolic rate and a poor shivering response affect heat production. Reduced vascular reactivity and increased heat conductance impair the ability to retain body heat. In addition an inability to distinguish changes in temperature also reflects a dulling of afferent neurosensory responses. 3. DIAGNOSIS 3.1. HISTORY Hypothermia patients may be classified: 1. 2. 3. 4.

Young healthy victims of exposure Otherwise healthy, but intoxicated by drugs or alcohol. Those with predisposing diseases, but not intoxicated. Elderly patients without a serious illness, and not intoxicated.

This classification forms a logical basis for obtaining a history from, or about, a hypothermic patient. The following questions should be answered: 1. 2. 3. 4. 5. 6. 7.

Under what circumstances was the victim found? What was the probable duration of exposure? Any known pre-existing conditions? Any history of intoxication or drug addiction? Neuropsychiatric history, especially suicidal tendencies? Associated injuries, or frostbite? Has the state of consciousness improved, deteriorated, or remained constant?

3.1.1. Circumstances It is not difficult to diagnose hypothermia in a stranded cross-country skier who had to camp out for two nights without adequate shelter before rescue. The diagnosis may be more difficult in an elderly woman found unconscious in a city apartment. The possibility of hypothermia must be considered in every victim of near drowning, in every victim exposed to a wet and windy environment even in midsummer, and in all elderly people found unconscious or disoriented in their homes during the winter. Cases of hypothermia have been reported from the tropics and from warm areas in the United

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States. It is worth remembering that if body temperature falls to 29°C, the temperature of a hot summer day, the chances of survival are poor (Duckworth and Cooper, 1964; Sadikali and Owor, 1974; Altus et al., 1980). The sequence of events leading to discovery of the patient may or may not be known. The usual story in most nonimmersion cases is that the person became increasingly confused, ataxic, clumsy and finally unresponsive. In the field the person may have gone through a phase of lucidity with shivering and then became combative, disoriented and confused after shivering stopped; or the person may express a great desire to lie down and sleep until the weather improves or circumstances change, although it is obvious to a rational person that it is neither the time nor place for rest. In the elderly cooling may be progressive over several days. As the person becomes colder they become less able to care for themselves and, especially if they live alone, may slowly drift into hypothermia. Most elderly hypothermics are discovered in the morning. Whether this is because they become hypothermic at night when basal metabolism is lowest, or whether it is because neighbors most commonly check on each other early in the day is not known. In Maclean and Emslie-Smith's (1977) experience nearly half their patients (48/100) were found lying on the floor of their homes.

3.1.2. Duration of Exposure The severity of tissue damage in frostbite is related to the duration of exposure and the lowest temperature reached (Sjostrom et al., 1964). Although this correlation has not been made as precisely in hypothermic patients the same principles of heat loss apply in hypothermia as in frostbite. The longer the duration of exposure and the lower the environmental temperature the greater the chances for severe heat loss and the development of hypothermia. The lower the patient's temperature the higher the mortality rate. If longer exposure leads to a lower temperature, then, to that extent, the longer the exposure, the higher the mortality rate. Duration of exposure also affects other important factors such as dehydration, nutrition, blood volume, electrolyte balance and, possibly, endocrine balance. If a hiker is stranded for several days without food, slowly becoming unconscious and hypothermic, not only will there be problems related to hypothermia but the patient will probably be dehydrated with a low blood volume, which requires correction. If, however, the person is cold because of an acute short immersion in very cold water dehydration should not be a problem and fluid replacement will not be as important during rewarming. Elderly patients may not be found for a day or two until neighbors become alerted to a possible problem. If the patient is diabetic, 24 hr without insulin or food accentuates a potentially fatal problem; or if the patient has had a stroke and aspirated, a long delay in discovery may cause irreversible pulmonary damage. Ascertaining the duration of exposure, therefore, is of great importance in determining what may have happened, how severe may be the overall problem, what the prognosis is likely to be and what treatment will be needed.

3.1.3. Predisposing Conditions Diseases likely to cause or predispose to hypothermia are classifiable as (a) those which decrease heat production and (b) those which cause derangements of thermoregulation.

3.1.3.1. Diseases causing decreased heat production (a) Myxedema. Severe hypothyroidism may cause such a reduction in metabolic rate that maintenance of body temperature is not possible. The characteristic facies, husky speech and edema of myxedema may or may not be present. If present, the diagnosis is simplified; but so many clinical features of myxedemic coma are similar to those of simple hypothermic coma that the diagnosis may be confusing. Slow speech, disorientation,

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hypotension, atrial fibrillation, pleural effusions and pulmonary congestion are common in myxedema but also occur in euthyroid hypothermic patients. Renal failure and anemia frequently occur, complicating treatment and fluid replacement. Laboratory confirmation of hypothyroidism includes a decrease in T 4 (thyroxine) levels, serum cholesterol greater than 300 mg/100 ml, increased concentrations of creatine phosphokinase, SGOT and LDH. Serum protein bound iodine (PBI) levels are not always an accurate measurement of hypothyroidism and 20~ of euthyroid elderly people may have low circulating PBI. Because the diagnosis of myxedema is difficult in a normothermic patient and even more so in a hypothermic patient, a combination of clinical and laboratory factors must be correlated in coming to a correct diagnosis. (b) Hypopituitarism. If untreated this results in episodic coma which may also be hypothermic. Hypoglycemia with blood glucose levels of 15-30mg/100ml is common; electrolyte imbalances secondary to acute hypoadrenalism and water retention add to the overall physiologic derangement. Temperatures as low as 30.5°C have been recorded and usually respond to simple rewarming, with a simultaneous improvement in consciousness. Hypopituitarism is often unsuspected because of its slow onset and the diagnosis may only be made when the patient develops a severe infection or becomes comatose. Laboratory confirmation is made by a rise in 17-ketosteroids following stimulation with metopirone and ACTH. But as this test takes 48 hr the results are not available for the management of acute hypothermia. (c) Malnutrition. Undernourished people with poor fat insulation readily become cold (Duckworth and Cooper, 1964). In addition their metabolic activity may be reduced so that they cannot produce sufficient metabolic heat to keep warm. Anemia of malnutrition may enhance the problem. (d) Muscular inactivity. Reduction or abolition of muscular activity because of paralysis, weakness, muscular dystrophy, arthritis or psychiatric depression are possible predisposing factors (Pledger, 1962; Branch et al., 1971). Similarly, an accident such as a fractured femoral neck in an elderly person who lives alone could lead to immobility, hypothermia and coma. There is evidence that shivering is naturally impaired in the elderly, reducing their ability to produce heat and increasing their likelihood of becoming hypothermic (Wollner, 1967). (e) Hypoglycemia. Whether this condition is due to insulin overdosage in a diabetic or as a result of hypopituitarism, it may also contribute to hypothermia. The estimation of serum glucose levels is an essential diagnostic test in evaluating all hypothermic patients.

3.1.3.2. Derangements of thermoregulation (a) Age. Temperature regulation is poor in infants and the elderly. The newborn and infants, especially premature infants, have greatly limited capabilities for maintaining body temperature, and the deficiencies in the elderly have been discussed above. (b) Neurologic diseases. Many central neurologic diseases and localized lesions cause or predispose to hypothermia because they interfere directly with hypothalamic function, or disturb motor function and reduce the production of metabolic heat (Pledger, 1962; Fox et al., 1970; Branch et al., 1971). If peripheral sensory perception is diminished there may be no central reaction to a cold environment: protective mechanisms are not called into action. Such a sequence of physiologic events is probably particularly common in elderly patients after a stroke. A cerebrovascular accident causes relative immobility or even unconsciousness; and the accident may occur where the person is alone so that hours or even days may elapse before the victim is found hypothermic. Cerebral neoplasms, subdural hematomata and encephalopathies have all been implicated, especially if they involve the hypothalamus. Psychiatric disturbances, whether due to organic or nonorganic brain syndromes, are frequently found in elderly hypothermics who may become confused, walk outside in winter in inadequate clothing, become more confused, lost and cold (Hudson and Conn, 1974).

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(c) Drugs. (Lee and Ames, 1965; Linton and Ledingham, 1966; Lash et al., 1967; Tolman and Cohen, 1970; Weyman et al., 1974). Intoxication by drugs or alcohol is a very frequent cause of urban hypothermia. Several mechanisms are involved. An alcoholic becomes drunk and, inadequately dressed, lies down in an alley to sleep in the middle of winter. His insulation (clothing and shelter) is minimal; his sensory perception and vasomotor control are impaired. Muscular activity is minimal and his ability to shiver is inhibited; and he is lying on a cold, perhaps wet, pavement. Heat production is minimal, heat loss maximal, and protective reactions are obtunded. Alcohol, barbiturates, phenothiazines, reserpine and narcotics act directly on the hypothalamus and inhibit or interfere with normal temperature control. When taken in usual therapeutic doses, there is little danger but when self administered in large doses for 'kicks' or suicide attempts hypothermia may develop. The patient is comatose and cold with clinical signs due in part to intoxication, in part to cold. Cyanosis, rigidity and a corpse-like appearance may be due to cold alone and many of these patients are found with core temperatures well below 30°C. Cardiac output is low, peripheral resistance high; responses which could be due either to drug action or hypothermia. With rewarming and removal of the toxic agent by metabolism or dialysis, cardiac output and peripheral resistance return to normal. The prognosis in hypothermic drug intoxication is not as poor as the clinical appearance of the patient might suggest; hypothermia may, in fact, afford some protection against hypoxic damage. The outcome depends more upon the extent of intoxication and the intoxicating agent than upon the hypothermia. (d) Loss of peripheral sensory control. Neurologic lesions such as high spinal cord injuries (Pledger, 1962) which involve loss of peripheral sensation and vasomotor control can frequently be associated with mild hypothermia. Severe hypothermia is avoided in most such patients because they are treated in a protected environment. The losses of motor activity, shivering and central perception of skin temperature are responsible for the inability to maintain temperature. Vasomotor control eventually returns after most spinal cord injuries reducing the chances of hypothermia as a permanent risk to these patients.

3.1.3.3. Other diseases. Severe cardiovascular disease, especially when associated with low cardiac output as after myocardial infarction, terminal diseases and massive invasive infections may be associated with hypothermia (Hudson and Conn, 1974; Miller et al., 1980). Because cardiovascular function is so important in the maintenance of body temperature, any situation in which cardiac output is diminished makes hypothermia possible, especially if the heart cannot respond appropriately to increased demands. In some instances the failure may be due to central pump failure--myocardial injury--and in others to a low circulating blood volume or a loss of vasomotor control. In each individual case it is important to analyze the precise cause so that appropriate corrective action may be taken. For practical purposes cardiac function is dependent upon three factors--pre-load, after-load and myocardial integrity. One or all of these factors may be implicated in any instance, and it may only be after measurement of intracardiac pressures, cardiac output and peripheral and pulmonary resistances that the causative factors can be separated from each other. Maclean and Emslie-Smith (1977) reported their experience with 100 patients: 30% were anemic, 16~o in congestive failure, 17~o had bronchopneumonia, 10~o had taken drugs. Myxedema was diagnosed in 19~ and hypoglycemia in 19~. Weyman et al. (1974), in a report on hypothermia in an alcoholic population, found eight out of 39 patients to have underlying diseases, three with infections and one each with myocardial infarction, cerebral tumor, gastro-intestinal hemorrhage and pulmonary embolism. Seven of these eight patients died. Hudson and Conn (1974) reported a similarly lethal outcome in seven of eight patients with severe underlying diseases. The diagnoses in their patients were pancreatitis, acute

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tubular necrosis, severe anemia due to hemorrhage in four patients, myocardial infarction, pulmonary tuberculosis. Analysis of these series suggests that severe gastro-intestinal bleeding with anemia and shock is a relatively common cause of hypothermia, and has a poor prognosis. Septicemia, anemia and pancreatitis are also common. In many patients several predisposing factors co-exist.

13.1.4. Intoxication The likelihood that drug or alcohol intoxication has contributed to a patient's hypothermia has been discussed above. If intoxication is suspected a search should be made of the patient's house for empty medicine containers, liquor bottles, etc. Blood samples are drawn and gastric contents aspirated for appropriate analysis. Keep vomitus for examination. A hypothermic intoxicated patient without underlying disease such as gastro-intestional hemorrhage, liver dysfunction or broncho-pneumonia has an excellent chance for recovery. Weyman et al. (1974) found that the mortality rate was 6.25~ in patients without underlying disease and 75~ in patients with a concomitant major disease.

3.1.5. Associated Injuries Unconscious hypothermic patients are very difficult to evaluate. Injuries may not be immediately obvious because the patient cannot complain, there may be no external evidence of injury, and hypothermia is analgesic, reducing complaints of pain. A careful examination must be made, taking into account the circumstances under which the person has been found (Yates and Little, 1979). Hypothermic patients may have frostbite (Laufman, 1951); but not everyone with frostbite is hypothermic. Frostbite is difficult to evaluate when first seen and the full extent of damage is seldom obvious until after rewarming. Failure of a part to rewarm and become pink, and the development of blisters within a few hours are diagnostic of frostbite. If the part remains anesthetic, then becomes swollen frostbite should be strongly suspected. If the diagnosis is not made until the digits become obviously discolored, then a serious error has been made.

3.2. PHYSICALEXAMINATION Physical examination must be as complete as circumstances permit; but certain special points relate to the examination of hypothermic patients. 3.2.1. Measurement of Body Temperature (Vale, 1981) There are many considerations in the choice of the optimal method for measuring body temperature. A core temperature less than 35°C is, by definition, hypothermic. It is, therefore, important that readings obtained be accurate. 3.2.1.1. Choice of thermometer. Several types of thermometer are available but some general attributes apply to any choice. (i) Accuracy. The thermometer should be accurate to within 0.2°C. (ii) Range. The thermometer should measure between 0-50°C, although the majority of temperatures to be measured will be between 25 ° and 40°C. (iii) Ease of reading. The thermometer should be easy to read because temperatures may have to be taken very frequently, there may be many staff around the bed reducing accessibility. Mercury-glass thermometers are not easy to read from a distance, have to be shaken down between readings and are not suitable for constant monitoring of temperature. Electronic thermometers or thermocouples are preferable.

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(iv) Speed of equilibration: Frequent readings require that the thermometer equilibrate quickly with the body temperature. Mercury thermometers take 2-3 min to equilibrate: electronic probes equilibrate within a few seconds. (v) Suitability for different areas of body. It may be desirable or necessary to take the temperature in several anatomic areas simultaneously, e.g. rectal and esophageal. Mercury-glass thermometers are not suitable for measuring esophageal temperatures, and the rectal temperature measured by a mercury-glass thermometer may not be deep enough within the body to reflect true core temperature. Electronic probes are available for many areas--rectal, esophageal, subcutaneous--and can be used in these areas without danger of breaking. (vi) Effect of ambient temperature: The temperature of a hypothermic victim of an accident may have to be taken outdoors in wind, snow or rain. The thermometer should not be affected by ambient temperatures. (vii) Energy source. Mercury glass thermometers require no special power source and are, therefore, convenient for use in the field. Electronic probes are usually battery operated. A weak battery will affect both accuracy and speed of equilibration between body and probe. In extreme cold conditions battery operated thermometers may be inaccurate because of the effect of cold on battery function. (viii) General features. The thermometer should be robust, portable, and suitable for use in the field. Price may be a consideration. The two most commonly available thermometers may be assessed with these characteristics in mind. (ix) Mercury-glass. These thermometers are small, portable, easily taken into the field and accurate. But most clinical thermometers will not read below 35°C and special low reading thermometers are required. They are suitable only for reading rectal, oral or axillary temperatures. Equilibration time is relatively long (2-3 rain) and the thermometer has to be re-set (shaken down) between each reading. (x) Electric. These are of two types---electronic probes and thermocouples. Both have the advantage of being useable in anatomic areas inaccessible to other thermometers, and they equilibrate quickly, but have to be calibrated before taking readings. Reaction time is short and they can be converted to a digital read-out system which make continuous temperature monitoring very simple. They require batteries, but are potentially portable. Without batteries or with dead batteries they are useless! 3.2.1.2. Where to measure temperature (i) Oral--Inaccurate and susceptible to too many variabilities. If this site is the only one accessible place the thermometer under the tongue and keep the mouth closed. (ii) Axillary--Skin temperatures are unreliable in hypothermic patients because of the great differences between skin and core temperatures. (iii) Rectal--A deep (15cm) rectal temperature is a good measurement of core temperature. During cooling rectal temperatures lag behind esophageal temperatures by 1-2°C, and also during rewarming the rectal temperature may be slowest to return to normal. Taking a rectal temperature in the field may not be very practical, but in hospital it is the easiest temperature to record, especially continuously and in a Conscious or semiconscious patient. (iv) Esophageal--The upper third of the esophagus lies in close proximity to the trachea, and a thermistor in this area is affected by the temperature of intratracheal air. If warmed air is being used to rewarm the patient a fallaciously high reading could be obtained. The middle third of the esophagus lies behind the left atrium and a thermistor in this site is affected by blood temperature. Myocardial temperature is very close to that of blood and, therefore, esophageal temperature approximates myocardial temperature. In the management of a hypothermic patient knowledge of both myocardial and other core temperatures is valuable and therefore, especially in an unconscious patient undergoing active rewarming, esophageal temperature provides valuable information about the patient's state. (v) Nasopharynx--Nasopharyngeal temperatures are close to those of the brain, but if the patient's mouth is open the reading may be inaccurate.

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(vi) Tympanic--This site also reflects intracranial temperature, but extreme care must be taken not to damage the tympanic membrane. The thermometer tip must be insulated from ambient air in a servo controlled constant temperature environment (Keatinge and Sloan, 1973; Yates and Little, 1979). (vii) Urine--A method for measuring the temperature of freshly voided urine was described by Fox (1971). The reliability of this method was demonstrated, as was the close correlation between urine and rectal temperature, under some circumstances the measurement of rectal temperature may be impractical and the measurement of urine temperature may be as accurate and useful. More recently Lilly et al. (1980) have described a similar technique, but using a thermistor probe incorporated into an indwelling urinary catheter. (viii) Other sites--Skin and muscle temperatures can be measured with needle electrodes; but readings from many sites have to be taken in order to obtain a satisfactory mean reading. 2..2.2. Physical Findings If the patient is conscious speech is slurred, mental reactions are slow and muscular movements are uncoordinated and clumsy. Shivering may or may not be present. The patients may be cadaveric, pale, pink or cyanosed depending upon the degree of peripheral-vasoconstriction. At about 32-30°C vasodilatation occurs and the skin becomes a bright pink. Below 26°C the patient appears cadaveric and may, indeed, be thought to be dead. The skin is cyanosed, breathing is shallow and barely discernible, pupils are dilated and may not react to light. At: higher temperatures the pupils are reactive but sluggish. The skin is often puffy and the face may resemble severe myxedema, even in a euthyroid patient. As the patient rewarms and edema recedes the facial appearance returns to normal. The skin is cold, not only on the extremities but even over the trunk in areas protected by clothing, and the subcutaneous tissues have an unnatural, doughy feel. A low central temperature is confirmed by rectal examination. The pulse may not be palpable; the heart rate is slowed in proportion to the decreased temperature. Arrhythmias, especially atrial fibrillation, are common. The blood pressure, if obtainable, is lower than normal. Neurological reflexes are diminished, and completely absent at lower temperatures. Gastrointestinal function ceases and there are no bowel sounds. Most physiologic functions are slowed but return to normal when the patient is rewarmed. Coagulation is prolonged but there is seldom an intrinsic defect of clotting. With rewarming coagulation returns to normal. Blood viscosity increases with cold, diminishing peripheral circulation but the diminished extraction of oxygen results in very little reduced hemoglobin and a bright pink periphery. 3.2.3. State of Consciousness The state of consciousness is of prognostic as well as diagnostic value. Almost all patients who are admitted hypothermic but fully conscious should survive, unless they die from the disease which precipitated hypothermia. Hypothermia seldom causes loss of consciousness when the core temperature is above 28°C, even though there may be some impairment of mentation or slowing of speech. If, therefore, a patient is admitted unconscious with a rectal temperature of 33°C it is unlikely that hypothermia is the cause of unconsciousness. The state of consciousness should be correlated with temperature, and nonhypothermic causes considered when there is a discrepancy between temperature and consciousness. Rapid and appropriate return of consciousness as a patient is rewarmed is a good prognostic sign. Persistence of unconsciousness when the core temperature has risen to a

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point at which unconsciousness would not be expected is a bad prognostic sign and suggests either that brain damage occurred during the period of hypothermic coma or that hypothermia was secondary to some other cause such as a cerebrovascular accident. Coma due to hypothermia, per se, does not leave residual cerebral damage and a lowered temperature may protect the brain from ischemic damage (Siebke et al., 1975).

4. CLINICAL MANAGEMENT 4.1. INITIAL EVALUATION

Assessment of the severity of the problem depends upon the following factors. (a) Body temperature (b) Consciousness (c) Cardio-respiratory status (d) Metabolic status (e) Associated diseases (f) Associated injuries (g) Age (h) Etiology of hypothermia (i) Duration of hypothermia. Assessment of these factors will enable the physician to classify the patient as severely, moderately, or mildly affected, and may enable a prognosis to be given. The more severe the condition the greater the need for detailed monitoring and close observation. 4.2. LABORATORY EVALUATION No single test will diagnose the severity of the condition, but laboratory evaluation is essential for detecting abnormalities which require correction. The following tests should be made: (a) In all cases--Complete blood count, biochemistry survey, including blood sugar, BUN, electrolytes, amylase, urine analysis. (b) Severe cases--Coagulation screen, including prothrombin time, platelets, APTT, arterial blood gases, pH, base excess. (c) Special cases--Alcohol and drug levels in blood and gastric contents, cultures of blood, sputum, obvious septic foci, protein bound iodine (PBI). 4.3. PATIENT MONITORING All but the mildest cases should be treated where close observation can be maintained, preferably with facilities for constant monitoring of cardiovascular function. Severe cases should be treated in an intensive care unit and managed in the same way as other acutely ill patients. Complete monitoring of physiologic functions should be carried out. Some or all of the following methods should be used. (a) Constant monitoring of cardiac rate and rhythm , (b) Intra-arterial line for pressure and sampling of arterial blood for gases and pH. (c) Central venous line for measurement of venous pressure and administration of fluids. (d) Swan-Ganz thermodilution pulmonary artery catheter for measurement of pressures and cardiac output. (e) Additional peripheral venous catheters for administration of fluids, antibiotics, etc. (f) Indwelling urinary bladder catheter. Measurement of fluid intake and output. (g) Temperature probes in esophagus, rectum, nasopharynx, or external auditory canal. (h) Endotracheal tube for assisted ventillation.

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TABLE1. Correction Factorsfor p02, pCO 2 and pH to be Applied to Measurements Made at 37°C to Obtain Correct Values at Temperature of Patient

Temperature Correction (F) (C) pCO2 pO2 pH 108 42.2 1.25 1.35 -0.08 106 41.1 1.19 1.26 -0.06 104 40.0 1.14 1.19 -0.04 102 38.9 1.08 1.11 -0.03 98.6 37.0 1.00 1.00 0 95 35.0 0.92 0.89 +0.03 90 32.2 0.82 0.76 +0.07 88 31.1 0.78 0.72 +0.09 86 30.0 0.74 0.67 +0.10 84 28.9 0.71 0.63 +0.12 82 27.8 0.68 0.59 +0.14 80 26.7 0.64 0.56 +0.15 78 25.6 0.61 0.52 +0.17 76 24.4 0.59 0.49 + 0.18 74 23.3 0.56 0.46 +0.20 72 22.2 0.53 0.43 +0.22 pH increases 0.008 units per degree F fall in temperature. pO2 decreases 3.3% per degree F fall in temperature. pCO2 decreases 2.4% per degree F fall in temperature.

4.4. SPECIFIC TREATMENT Therapeutic measures should be started as indicated, but special attention should be paid to the following problems.

4.4. I. Correction o f A c i d - B a s e Deficiencies All PO2, pCO2 and pH values should be measured at 37°C. Correction factors are then applied depending upon the patient's temperature (Wears, 1979) (Table 1). If these correction factors are not used a false evaluation may be made of the magnitude of metabolic and respiratory changes. Metabolic acidosis may be corrected by giving sodium bicarbonate according to the following formula. Dose of NaHCO3 (mEq) =

Wt (kg) x Base Excess (mEq) 3

4.4.2. Correction o f Blood Volume The patient may be severely depleted of volume and as rewarming and peripheral vasodilatation occur cardiac output will be deleteriously affected if volume is not restored. The volume required may be considerable, i.e. several liters. If the hematocrit is adequate lactate Ringer's solution is satisfactory initial replacement. The hematocrit may be high because of dehydration; if so, dilutional reduction of hematocrit will reduce blood viscosity and improve peripheral circulation. Theoretically low molecular weight dextran would be a suitable replacement agent provided not more than 500 ml were used in each 24 hr period. The volume to be given should depend upon an assessment of cardiovascular function based on measurements of central venous pressure, pulmonary artery wedge or diastolic pressure, cardiac output and peripheral vascular resistance. All intravenous fluids should be warmed to 37°C, and blood should be passed through a blood warmer.

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4.4.3. Maintain Cardiac Output and Blood Pressure Pressor agents may be used cautiously and if possible their effects should be evaluated by repeated calculations of cardiac output and other cardiovascular parameters. All the pressor agents are arrhythmogenic and their use may have to be stopped if they cause ventricular ectopy. Because hypothermia reduces oxygen consumption, the physiological required cardiac output is not as high as at normal temperature. This protective mechanism should be remembered when attempting to achieve preconceived goals of pressure or cardiac output. 4.4.4. Maintain Adequate Ventilation and Arterial Gases This should be done with or without endotracheal intubation. Do not hyperventilate because a sudden fall in pCO2 may increase the likelihood of ventricular fibrillation (Brown and Miller, 1952). 4.4.5. Antibiotics These should be given in accordance with standard indications. Pneumonia is such a common complication that giving a broad spectrum antibiotic intravenously at the start of treatment may be of value.

4.4.6. Blood Sugar Levels These levels vary widely and the patient may be hypo- or hyperglycemic. Because the danger of hypoglycemia is greater than that of hyperglycemia, draw a blood sample for measurement of blood glucose then give 20 ml 50% glucose intravenously. Insulin is not effective if body temperature is below 30°C. Hypothermic diabetic patients should, therefore, be rewarmed before giving insulin. 4.4.7. Myxedema The treatment of myxedematous hypothermic coma is difficult and uncertain, and no matter what treatment is given the mortality rate is very high. In myxedematous patients with a temperature under 32°C the mortality rate is over 909/0, and about 509/o in those whose temperature is 32°-35°C (Hausman, 1970). There has been much discussion about the importance of thyroid replacement therapy. Thyroid hormone replacement increases endogenous thermogenesis, assisting in rewarming; but it also increases heart rate, myocardial oxygen consumption and overall oxygen utilization. The metabolic demands are, therefore, considerably increased and may result in angina, myocardial infarction, congestive heart failure and pulmonary edema. Current therapy is to use triiodothyronine (50-100/~g i.v.) every 12 hr until the patient is warm, then to reduce the dose. Thyroxine is slow acting, and does not achieve maximal thermogenesis for 6-8 days. Triiodothyronine will, however, significantly stimulate thermogenesis in the first 24 hr (MacDonald, 1958). 4.4.8. Steroids Although Duguid et al. (1961) advocated giving steroids to all hypothermics, subsequent research (MacLean and Browning, 1974; Tolman and Cohen, 1970) has demonstrated that most hypothermics have elevated concentrations of 11-hydroxycorticosteroids and, therefore, steroid replacement is not necessary. There is some evidence that steroids may be of value in hypothermics who are also exhausted from prolonged outdoor exposure (McInnes et al., 1971).

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4.4.9. Cardiac Drugs 4.4.9.1. Arrhythmias. Most atrial arrhythmias will revert spontaneously to normal sinus rhythm as the patient rewarms. Treatment with digoxin or quinidine is, therefore, not usually necessary unless there is a preexisting cardiac condition for which these drugs would be appropriate treatment. 4.4.9.2. Ventricular arrhythmias. These should be treated with great urgency, as they are of serious portent. Surprisingly little is known about the effects of hypothermia on the actions of propanolol, lidocaine, and bretylium all of which are powerful suppressors of ventricular ectopy at normal temperatures. These drugs should be used as they would be in euthermic patients. Multifocal premature ventricular contractions (PVC) may presage the development of ventricular fibrillation and should be treated immediately with lidocaine (50-100 mg i.v.), followed by an infusion of 1-4 mg/min if PVC's continue. If lidocaine is ineffective give propanolol (1-3.0 mg i.v.), at a rate of 1-0 mg/min. A second dose may be given after 2 min, but a third dose should not be given for 3-4 hr. As it slows heart rate and decreases cardiac output it should be used intravenously with caution and only if other drugs are ineffective. Bretylium tosylate is the most powerful inhibitor of ventricular fibrillation available, and is effective in hypothermic patients. In a life saving situation give 5.0 mg by rapid i.v. injection, repeated at 15-30 min intervals to a total dosage of 30 mg/kg. Bretylium is excreted unchanged in the urine so hypothermia should not slow down its excretion except to the extent that renal function is diminished. 4.4.10. Drug Intoxication Patients who are hypothermic because of drug intoxication should be treated for intoxication by whatever means are appropriate. If the drug is dialysable hemodialysis is an excellent method both for removing the drug and simultaneously rewarming the patient. 4.4.11. Cardiorespiratory Resuscitation The decision to start cardiopulmonary resuscitation may be difficult to make. But once the decision has been made resuscitation should be prolonged and energetic and should be continued until the patient recovers or it is certain that the patient is dead. Many cold patients with impalpable peripheral pulses appear to be dead: should resuscitation be started? In the field, much depends upon circumstances. If the patient is a long way from help and transportation is limited resuscitation may not be practical. If, however, the patient is only a short distance from hospital and emergency services are available then resuscitation should be started and continued until the patient is in hospital where a definitive decision is possible. In hospital, do not start resuscitation if the E K G shows cardiac action, if there is regular respiration, even although the pulse may be impalpable. If there is no pulse, no respiration and the E K G shows ventricular fibrillation or cardiac standstill resuscitation should be started at once. The usual principles of cardiopulmonary resuscitation apply. Establish an airway with a mask or an endotracheal tube. Ventilate adequately, but do not hyperventilate. External cardiac compression is done at the usual rate of about 70/min. Insert a central venous line and, if possible, an arterial line. Ascertain the state of oxygenation and metabolic status: correct acidosis. If the patient's temperature is below 30°C the chances of restoring normal sinus rhythm are poor. Rewarming the heart is essential if a stable circulation is to be achieved. Use warmed intravenous fluids. Ventilate with warm (7-13°C) humidified oxygen. Rewarm by the most effective means available (peritoneal dialysis, hemodialysis, extracorporeal circulation: see Rewarming). Continue efforts at resuscitation for a long time, and at least until body temperature is 32°C. Successful resuscitation has been reported after several hours of external cardiac massage (Southwick, 1980; Schissler, 1981). JPT

22/3

B

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BRUCEC. PATON 5. R E W A R M I N G 5.1. CLASSIFICATION

M e t h o d s for rewarming are passive or active, external or internal (Table 2). TABLE2. Rewarming Methods A. Passive

Removal of wet clothing Protection from wind Increasing insulation B. Active--External

Hot water tub/shower Forced warm air Hot water bottles Electric blanket Hydraulic blanket, piped suit Radiant heat Microwaves, diathermy Charcoal heater Hibler technique C. Active--Internal

Hot food, drink Warmed i.v. fluids Gastric lavage Thoracic lavage Inhaled warm oxygen Peritoneal dialysis Hemodialysis Extracorporeal circulation

5.2. CRITERIA A n ideal m e t h o d for rewarming should c o n f o r m to certain criteria (Table 3). 5.2.1. Non-invasive As a general principle in all medical practice if two m e t h o d s o f treatment are equally effective and one is invasive, the other non-invasive, the non-invasive m e t h o d is preferable. M o s t methods for treating h y p o t h e r m i a are non-invasive, but peritoneal dialysis and the use o f extracorporeal circulation are invasive. Sometimes, however, invasive m e t h o d s are the best means for rewarming and the disadvantages o f their invasiveness are outweighted by their effectiveness.

5.2.2. Non-injurious Invasive m e t h o d s are m o r e likely to cause injury than non-invasive. But even noninvasive methods m a y cause injury. Cold patients are particularly easily burned and care must be taken that methods o f external warming do n o t result in burns. Diathermy, no longer used with any frequency, is capable o f producing severe, deep and slow-healing burns.

TABLE3. Criteriafor Ideal Rewarming Method 1. Non-invasive: non-injurious 2. Rapid 3. Permits access to patient 4. Allows access for resuscitation 5. Allows continued rewarming during resuscitation 6. Appropriate to problem

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5.2.3. Rapid There have been more arguments over the advantages and disadvantages of rapid rewarming than over any other single point in the therapy of hypothermia (Duguid et al., 1961; Fernandez et al., 1970; Meriwether and Goodman, 1972; Lloyd, 1973; Gregory and Doolittle, 1973; Marcus, 1978; Ledingham and Mone, 1980; Miller, 1980). Although many patients are rewarmed slowly and recover satisfactorily theoretical considerations would indicate that the more rapidly a patient's temperature is restored to normal the better. But rapid restoration of normal temperature must be accomplished without the imposition of other problems such as cardiovascular shock. The literature is replete with advice about slow rewarming backed by statistics to show that patients rewarmed slowly had better survival rates than those rewarmed quickly (Duguid et al., 1961; Hudson and Conn, 1974; Tolman and Cohen, 1970). But in several of these series very little control was maintained of the patients cardiovascular status, partly because modern techniques for monitoring cardiovascular function were not available when the patients were studied. With the ready availability of accurate means for measuring cardiac output, intracardiac pressures, peripheral resistance, and other parameters by which cardiovascular function, and volume requirements may be adjusted (Harari, 1975) the arguments for slow rewarming have lost much of their validity. To maintain that the persistence of an abnormal physiologic state (hypothermia) is better than its correction does not conform to therapeutic logic. There is no necessity that the most rapid means for warming, extracorporeal circulation, be used in every case, but the slowest methods for passive rewarming should only be used if better methods and means for monitoring the patient are not available. 5.2.4. Permit Access to the Patient Access to the patient for making observations, taking measurements, drawing blood samples is essential. Not all methods provide equal access. Immersion in a bath of hot water provides an excellent means for rewarming but access to the patient may be difficult and during resuscitation the patient may have to be removed from the tub, and, therefore, rewarming temporarily stopped. Warming boxes, piped suits and other similar encircling techniques also limit access. 5.2.5. Access for Resuscitation If the patient is unconscious the possibility of a cardiac arrest and the need for resuscitation is a constant threat. Optimally, not only should there be access to the patient, but rewarming should not have to stop while resusciation is being carried out. If the patient is being rewarmed by warm blankets in a bed, access for resuscitation may be excellent. External cardiac massage could be immediately started and the patient readily intubated. It is feasible to place an unconscious intubated patient in a tub while continuous EKG monitoring provides visual evidence of cardiac action, supplemented by use of an esophageal stethoscope. But cardiopulmonary resuscitation is very difficult, if not impossible in a tub and the patient has to be removed from the tub, dried and placed on a hard surface before defibrillation is possible. Femoral vein-femoral artery perfusion with an extracorporeal pump and heat exchanger not only provides space on the chest for external massage, but insures mechanical support of the circulation and rewarming of the blood even if the patient's own circulation ceases. 5.2.6. Appropriate to Problem (Table 4) There is no single method suitable for all situations. If the patient is conscious, with a core temperature of 34°C, walking and reasonably cooperative, a simple method of rewarming will be satisfactory.

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BRUCEC. PATON TABLE 4. Comparison of Rewarming Methods Showing Differences in Features and Suitability for Different Circumstances

Method Passive

Features Simple: v. slow Good access: warms periphery.

Mild, mod. H.

Active--External

Electric blanket Piped suit (Sarong) Hot tub

Suitability Mild H.

Simple: slow Access OK: peripheral Specialequipment Slow: peripheral: used in field Mod fast: simple Access poor: peripheral

Mild, mod. H. All types in field All types

Active--Internal

Gastric lavage Thoracic lavage

Special knowledge needed Hosp. treatment: s l o w Access good: core Complicated:in O.R. only: rood. fast: c o r e

Peritoneal dialysis

Hospital, invasive, mod fast: core Access fair Hot inhalation Hospital or field: Mod fast: good access: core Extracorp circulation Special hospital: very fast: invasive: Good access

Mod, severe H. Supplemental treatment Severe H. not respondingto other methods Severe H. Mod, severe H. Most severe H.

In contrast, if the patient is unconscious with a temperature of 23°C and in imminent danger of ventricular fibrillation the method used must be rapid and provide excellent control over all available factors. Under these circumstances femoral-femoral extracorporeal circulation is the best available method. The choice of method to be used is, therefore, governed by two factors: availability and suitability. 5.3. METHODS 5.3.1. Passive Whenever a patient is permitted to rewarm at his own metabolic pace without help from any outside heat source, the method is passive. The patient is removed from the cold environment, stripped of wet clothing, sheltered from wind, wrapped in blankets or warm dry clothing and allowed to rewarm, depending solely upon metabolic activity to increase body temperature. In terms of suitability, this method is slow, resulting in a temperature elevation of perhaps 0.5-1.0°C per hour. Periphery and core rewarm at roughly the same speed. The method is suitable for mild hypothermia in conscious patients. It is simple, atraumatic and permits good access to the patient. 5.3.2. A c t i v e - - E x t e r n a l Any non-invasive method which involves use of an external heat source is both active and external. M a n y heat sources have been u s e d - - w a r m e d blankets, hot water bottles, electric blankets, hot water showers and tubs, piped suits ('sarong'), circulated hot air. Although all these methods involve the same principle there are great variations in their effectiveness (Lloyd et al., 1976; Marcus, 1978; Myers et al., 1979). 5.3.2.1. Immersion in hot water. This is the m o s t efficient method enabling the transfer of 600-2400 kcal/hr; depending upon the size of patient and the temperature gradient between patient and water. Water temperature should not exceed 45°C, and in m a n y instances

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water at 45°C will be perceived by the patient as too hot. An unconscious patient can be managed in a hot water tub. For ease of handling a canvas sling should be available to place under the patient to aid in lifting the patient into and out of the water. The head is supported on a waterproof pillow and if the patient is intubated extra-long ventilation lines may be necessary. Arterial and intravenous lines and E K G leads may be waterproofed by plastic drapes before the patient is immersed. Rectal and esophageal continuous readout thermistors permit accurate monitoring of the rising temperature. The water temperature should be measured frequently, and kept constant. By the time the rectal temperature is 33°C the patient will usually be increasingly awake and can be removed from the water and allowed to rewarm further spontaneously. If the patient's temperature is 33°C, yet there are no signs of returning consciousness, cerebral disease or damage or intoxication should be strongly suspected. Access to a patient in a tub is limited. All lines for the withdrawal of blood samples, Foley catheter, etc should be inserted before immersion. If the patient has a cardiac arrest, he has to be removed from the water, and therefore from the rewarming environment before resuscitation can start. The patient should be dried as quickly as possible to avoid cooling by evaporation. Defibrillation of a wet patient, or of a patient in a tub is extremely hazardous and should never be attempted. 5.3.2.2. Hot water bottles. These are a simple means of providing additional heat and are available under most circumstances. Even in the field water bottles filled with hot water are readily available. The bottles should be placed in area where arteries come close to the surface--axillae, groins, abdomen, side of neck, hands. Heat transference is slow and depends upon the temperature gradient between skin and bottle, and the adequacy of peripheral circulation. Cold skin is easily burned and the bottle temperature should not exceed 45 °. Access to the patient is good, and minimal rewarming is possible during resuscitation. :5.3.2.3. Piped-suit ('sarong'). Various types of blankets containing pipes through which hot water can be circulated have been designed. For use in hospital the Thermorite blanket, or equivalent, is best. The blanket is about six feet long and can be used as a single blanket behind or on top of the patient, or two blankets can be zipped together to form a bag covering both sides of the patient. Hot water is provided by a self-contained unit which heats and circulates the water. Water temperature can be regulated to a maximum of 40°C (104°F). Similar piped blankets are made in different sizes suitable for children and babies. A model for use in the field has been described by Dayton and Arnold (1975), and has proved to be effective. The blanket is piped by 3/8" (0.95 cm) I.D. vinyl tubing which is thickwalled enough not be compressed by the weight of the patient. The outer blanket is made from rip-stop nylon. Water is heated by a camp stove and circulated through the pipes by a modified bilge pump. The blanket is long enough to cover the trunk, but is capable of providing 2.5 kcal/min and successfully rewarmed a patient from 25.5°C. The weight of the blanket is only 1.5 kg (3.3 lbs) and adds little to the pack weight of a rescuer. Piped suits are a moderately efficient method of rewarming, suitable for use in all but the most severe cases (Marcus, 1978). If the patient is only lying on a single blanket access is good. If two blankets are joined together the upper blanket may have to be removed: but rewarming is not totally stopped because of continued heating from the lower half. The method is applicable both in the field and in hospital. 5.3.2.4. Hot air. (a) Radiant heat. External radiant heaters are efficient means of maintaining body temperature. For purposes of rewarming, air must be warmed to a temperature greater than that of the patient, e.g. greater than 30°C, which is much warmer than the ambient temperature in most buildings.

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Radiant heaters (electric or kerosene) can provide intense local heat and could easily cause burns in a cold patient. The best method of using a radiant heater is first to place a blanket over the patient. In this way, a burn is less likely and a pocket of warmed air will gradually be trapped between patient and blanket. The method is applicable in hospital and home, requires special but readily available equipment, is only moderately efficient, allows good access to the patient, but does not allow continued rewarming during resuscitation. (b) Charcoal burner. The Norwegian Defense Research Establishment has developed a carbon monoxide-free charcoal fueled heater that can be laid on the abdomen and thorax of a stretcher-borne victim, and which circulates warm air through his clothing and coverings. (c) Hibler technique. The Bavarian Mountain Rescue Service designed a simple method of applying wet heat to the chest. A linen sheet is folded 32 times and 1 liter of very hot water poured into the folds. The hot, wet pack thus formed is placed on the thorax of the victim who is carefully wrapped in blankets and an aluminum sheet. Heating lasts about two hours. The method is suitable for short-term warming during resuce transportation. 5.3.2.5. Suitability. Active external methods are appropriate for all degrees of hypothermia. Some methods are more efficient than others, and access to the patient varies with the complexity of the method. These methods are the most frequently used. 5.3.3. Active--Internal Internal methods make use of large internal surfaces such as the peritoneum, the lung or the blood stream (inspired hot air, extracorporeal circulation). They have the theoretical advantage of heating the internal core. They tend to be more efficient than external methods, but mostly require equipment and techniques available only in hospitals (with the exception of heated inspired air). 5.3.3.1. Gastric lavage. The stomach can be filled with warmed electrolyte solutions through a large bore nasogastric tube. The warm solution is allowed to remain in the stomach for 15 min and is then aspirated and replaced. This method has not been used frequently because of several obvious disadvantages. The surface area available for heat exchange is small. Much of the fluid may pass into the duodenum and intestine so that the patient can receive large volumes of fluid. In an unconscious patient lying flat with a gastric cardia made incompetent by a large tube there is considerable danger of regurgitation of fluid up the esophagus and aspiration into the lungs. The method should only be used in hospital, it is not very efficient and has clearly defined hazards. Access to the patient is good: but external cardiac compression should not be done with the stomach full because of the danger of emptying the stomach causing regurgitation and aspiration. An intragastric balloon through which warmed water is circulated performs the same function but less efficiently, and with the need for special equipment. 5.3.3.2. Thoracic lavage. The chest may be opened and irrigated with large volumes of warmed electrolyte solution (Lintton and Ledingham, 1966; Coughlin, 1973). Cardiac massage may be instituted at the same time. A less invasive means of achieving the same end is to insert one or two pleural chest tubes and use them for continuous or intermittent thoracic irrigation. This method could only be used in hospital. As with any open method there is a risk of infection. Large volumes of fluid may compress the lung reducing ventilation. Because a pleural cavity has a greater surface area than a stomach, the method is probably more efficient than gastric lavage. The heart is also heated directly by the warm fluid.

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5.3.3.3. Peritoneal dialysis. The peritoneum has a large surface area which is an efficient heat exchanger and peritoneal dialysis has been shown to be an effective method for rewarming severly hypothermic patients (Lash et al., 1967; Grossheim, 1973; Picketing et al., 1977). According to the method of Bangs (1980), two peritoneal catheters are inserted into the peritoneum, one through each lower quadrant. Isotonic dialysate fluid at room temperature is perfused under pressure through a plastic blood heating coil immersed in a bucket of tap water at 48-54°C (120-130°F). The dialysate leaves the heating coil at 40-43°C and enters the peritoneum through one of the catheters at a rate of 2.0 liters in 10-15 min. The dialysate may be allowed to circulate in the peritoneum for a few minutes, then is drained by gravity into a collecting receptacle. Body temperature may be raised by 5-10°C/hr by this method. Isotonicity of the dialysate is very important in order to avoid fluid and electrolyte shifts. Under special circumstances, however, rewarming could be combined with correction of electrolyte or volume problems by appropriately modifying concentrations in the dialysate. The advantages of this method are (i) applicability to severely hypothermic patients, (ii) efficiency and rapidity of rewarming, especially of the body core, (iii) relative technical simplicity permitting availability of the method in most hospitals, (iv) good access to the patient with a possibility for continuing rewarming while conducting resuscitation. The disadvantages of the methods are (i) possibility of injury. If the patient has previously undergone abdominal surgery peritoneal adhesions are likely and blind insertion of cannulas can perforate intestine. In dire circumstances and with appropriate surgical help cannulas could be inserted under direct vision through small muscle-splitting incisions. Extensive adhesions would, however, greatly diminish the surface area available, and reduce the efficiency of the technique. (ii) Peritonitis is possible but unlikely if good sterile technique is used. (iii) Electrolyte and fluid exchanges are unavoidable, but can be minimized by measuring blood electrolyte concentrations before, during and after dialysis.

5.3.3.4. Inhaled warm oxygen. The internal surface of the lung is huge and offers great opportunities for heat exchange. There are two methods by which oxygen may be heated. By the first oxygen is passed through hot soda lime: by the second the oxygen is passed directly through a heated humidifier. Oxygen from a tank or wall outlet is passed through a CO2 soda lime absorber which has been heated by being saturated with CO2. The 02 is then passed through a heated humidifier and administered to the patient through a mask or endotracheal tube as circumstances demand. The temperature of the oxygen should be about 46°C (115°F). Heating is more efficient if the 02 is given by endotracheal tube because less heat is dissipated in the nasopharynx. It is essential that the oxygen be fully humidified, because the administration of dry oxygen would cause heat loss from the body as moisturization occurred in the nasopharynx. Experiments and clinical experience have shown that body temperature can be raised by 0.2-1.5°C/hr (Lloyd, 1973; Hayward and Steinman, 1975). However, the rate of temperature elevation differs greatly in different areas of the body. Esophageal temperature rises most rapidly (Hayward and Steinman, 1975). As esophageal temperature is close to cardiac temperature it can be assumed that the latter rises with equal rapidity. The first organ through which the blood warmed by passage through the lungs passes is the heart. The myocardium may receive some heat directly from the blood within the cardiac chambers, but the maximum cardiac rewarming probably comes from circulation of warmed blood through the coronary arteries. The claim has been made that this method reduces or eliminates 'after-drop' (Lloyd et al., 1976) but experiments in human volunteers have not confirmed this view (Marcus, 1978). The apparatus necessary for this method is available in most hospitals and has been adapted for use in the field. A portable system for providing heated moistened oxygen is available and has been used in the rescue of hypothermic accident victims. While this

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system makes available a simple reliable method for slowly rewarming an accident victim it is bulky to carry and adds several pounds to the weight of a rescuer's pack. The advantages of this method are (i) relative simplicity and ease of application, (ii) non-invasive, and non-injurious within wide limits of 02 temperature, (iii) provides 02 as well as heat, (iv) heats the heart and central organs, (v) is well tolerated by a patient even when fully conscious, (vi) permits good access to patient during resuscitation. The disadvantages are: (i) need for special equipment. Although this equipment is available in most hospitals, it is not available in the field unless specially provided. (ii) Rate of rewarming is slow, and while the technique may be excellent in moderately and mildly hypothermic patients it is only useful as an adjunctive method in severely hypothermic patients. 5.3.3.5. Warmed intravenous fluids. The volume of warmed intravenous fluid necessary to rewarm a hypothermic patient is so large that a patient would be seriously overloaded with fluid if this method were solely relied upon for rewarming. Intravenous fluids should be warmed to 37°C before administration to a hypothermic patient to prevent additional heat loss by the administration of fluids at room temperature (20-24°C) to a patient with a temperature of 28-30°C. 5.3.3.6. Extracorporeal circulation. Since the advent of open heart surgery in the mid 1950's extracorporeal circulation with inclusion of a heat exchanger in the circuit has been available for rewarming patients. The first report of the use of this technique in accidental hypothermia was not described until 1967 (Davies, 1967), although it was suggested by Fruehan (1960). Under local anesthesia a femoral artery and vein are exposed through a short vertical incision. The artery and vein are both cannulated and connected to an extracorporeal circuit which contains a heat exchanger and oxygenator. Venous blood is withdrawn, oxygenated, warmed and returned through the femoral artery. Rewarming is rapid, circulation can be maintained even if ventricular fibrillation occurs, correction of electrolyte and volume distrubances is readily achieved, and for the patient admitted in extremis this is the best technique for rewarming. If a rescue group has the choice of taking a severely hypothermic victim to a hospital with open-heart facilities, then the patient should always be taken to such a hospital in preference to one without those facilities. The advantages of this method are: (i) rapid rewarming with excellent physiologic control of the patient. (ii) Ability to support the circulation over a prolonged time, and allow simultaneous rewarming and resuscitation. (iii) Ability to rewarm severely hypothermic patients who could not otherwise be rewarmed because of inadequate circulation. The disadvantages of this method are: (i) requirement for specialized equipment and personnel: only possible in hospital with cardiac surgical service. (ii) Invasive and potentially injurious--the need to cannulate major limb vessels carries a small risk of damaging the vessels and impairing circulation to the leg. Total anticoagulation with heparin is necessary during perfusion and, therefore, this technique would be contraindicated or hazardous in a patient with cerebral or other major injuries. The technique would also be contraindicated if the patient were hypothermic because of a cerebrovascular accident or intracranial disease that might bleed.

6. CLINICAL RESULTS--A CHRONOLOGIC REVIEW Although hypothermia has been recognized for more than 50 years and was used clinically as a means of treatment, an active interest in the recognition, management and treatment is only discernible since the mid 1950's. In 1951 Laufman described profound hypothermia of 18°C in a 23 year old woman who

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was found in an alcoholic hypothermic coma in an alley in Chicago. The patient eventually recovered, although she lost all fingers except one thumb and both legs below the knees. She lived for many years. Between 1951 and 1960 hypothermia and extracorporeal circulation were being developed for use in cardiac surgery and much fundamental information was obtained about the physiology and pathology of hypothermia in humans, although the periods of hypothermia were short and the patients anesthetized and carefully monitored. Posthypothermic circulatory failure (Blair, 1956), and ventricular fibrillation (Badeer, 1958) were recognized as important and potentially lethal complications. Blair described acute circulatory collapse in dogs cooled to 30°C for about an hour and rapidly rewarmed in hot water. The animals developed low cardiac outputs and left ventricular stroke work, hypotension and an increased arterio-venous oxygen difference, compared with their prehypothermic state; although the posthypothermic state was physiologically improved over the hypothermic state. Cardiac index was 4.261iters/min/m2 before cooling, 1.62 liter/min/m2 while 30°C and 2.15 liters/min/m2 when rewarmed to 35°C. Peripheral resistance was 2600 dynes/cmS/m2, 5900 dynes while 30°C and 5200 dynes at 35°C after rewarming. The reduction in cardiac output, therefore, could not be ascribed to peripheral vasodilatation, and as the right atrial pressures remained constant throughout at 2 mm, the right sided filling pressure did not change. The most likely cause of failure in those dogs was a primary myocardial malfunction. Similar accounts of cardiovascular collapse after rewarming were subsequently given in numerous clinical reports leading to possibly erroneous conclusions which will be discussed later. In 1958 Emslie-Smith, in a paper describing electrocardiographic changes and a pathognomonic J wave, also described the clinical courses of eight patients all of whom died. Details of rewarming were not specifically given, although several of the patients were warmed. They died from four hours to one week after admission, and all had severe associated medical problems. Fruehan (1960) treated eight patients of whom one survived. Their ages ranged from 53-80 years and seven, including the survivor, had known disease: three were alcoholics. Therapy included stimulants (caffeine) in three, heparin in six (including two patients with frostbite). Five received steroids, four antibiotics, three blood or plasma and one levarterenol. Two received digitalis and two insulin. It was noted all patients who received heparin had a much greater prolongation of clotting time than is usual in euthermic patients. All patients received intravenous fluids in excess of usual daily requirements. Four patients were actively rewarmed with hot water bottles, warm water, warm drinks, gastric lavage or warm enemas and electric heaters. Four, including the survivor, were passively rewarmed by being covered with blankets and allowed to rewarm. The 'actively' rewarmed patients raised their temperatures at 0.5-0.75°C/hr: the 'passive' group rewarmed at 0.1-0.9°C/hr. There was therefore no difference in rate of rewarming between the groups. It is interesting to note, in retrospect, that this author was probably the first to suggest that the pump oxygenator be used to rewarm patients--'It would seem logical to extend this same therapy to resuscitation of human beings although, to my knowledge, this has not been done.' One of the earliest reports of a group of patients with accidental hypothermia came from the tropics. Morley (1960) from University College, Ibadan, Nigeria took the temperatures of all children with Kwashiorkor who felt cold, and found 19 hypothermic patients in three months. Nine children died. Poor nutrition and separation of the children from the mothers were considered to be important contributing factors. Although the possibility of hypothermia in myxedema had been recognized for some years it was not a complication frequently described or considered. Angel and Sash (1960) described three cases. One patient developed hypothermic myxedematous coma while in hospital receiving treatment: she died. A second patient also died, in spite of thyroid replacement therapy. The third patient died in myxedema coma after voluntarily stopping her treatment. All cases published since 1953 were reviewed, including the author's own patient. Twenty-six patients with 27 admissions were described: only six recovered, and

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one of these died of a myocardial infarction three weeks after recovering from hypothermia. The temperatures of these patients were between 23.3-38°C. The temperatures of 10 patients were greater than 35°C and, therefore, by current definitions would not be considered hypothermic. But this paper served to re-introduce the concept that hypothermic coma is a not uncommon complication of myxedema. In 1961 Duguid published a report on 23 patients with 20 deaths. All her patients, except one (aged 56 years), were elderly (63-86 years) and three were over 80. All had concurrent severe medical, or medical and mental problems. The three survivors were aged 68 years--with chronic leg swelling, 73 years--with bronchitis and 63 years--with myxedema. Only seven patients rewarmed sufficiently to become euthermic and one patient remained hypothermic and unconscious for seven days. No details are given of the methods used for active rewarming except to say that six patients were so rewarmed and promptly died. No hemodynamic data were available and it can obviously be assumed because of the time-span within which the patients were treated that none of the methods now used routinely for intensive care were applied to these patients. There was clear recognition that active rewarming abolished peripheral vasoconstriction and that circulatory failure and 'after-drop' might occur. No therapeutic steps were suggested to make active rewarming safer. This paper by Duguid was a milestone report. Because of the care with which the details were provided and because of the numbers and the outcome (20/23 dead) her conclusion-"Elderly patients with accidental hypothermia should not be actively rewarmed"--was, and still is, widely accepted as a therapeutic norm for all cases of hypothermia. Such a conclusion would no longer be justifiable with modern methods for monitoring cardiovascular function including measurements of intracardiac pressures, cardiac output, and pulmonary and peripheral resistances, and with the manipulation of these factors by volume replacement and drugs the cardiovascular effects of rewarming should be controllable. Prescott (1962) described nine patients seen in four months in seven of whom there were obvious predisposing factors. Three patients survived, aged 76, 85, 80 years. All had been poisoned, one by alcohol, one by barbituate and one by coal-gas. All nine patients were treated passively by being well covered with blankets: no active measures were used. All received steroids. With increasing numbers of reports on hypothermia in the elderly, investigators were beginning to take greater interest in the temperature regulating mechanisms of elderly people. Hockaday (1962) investigated temperature control mechanisms in three patients all of whom had been hypothermic on more than one occasion. One patient had no discernible temperature control and relied on insulation and environment to maintain body temperature. In two others the 'set-point' seemed to be low, although normal responses existed. The British Medical Journal ran an editorial in 1963, 'Deadly Cold', in which the dangers of hypothermia in infants and the elderly were emphasized. No therapeutic measures were advised; but that the journal should publish such an editorial indicated an increasing awareness of the problem, and an awareness of its domestic as well as its outdoors importance. Murphy and Faul (1963) described eight cases, the first cases to be reported from Ireland. Five patients died. They advocated moderately rapid rewarming of the trunk with maintenance of blood pressure by fluid infusion to be the best treatment. Four to five liters should be given daily during the first 24-48 hr. McNicol and Smith (1964), from Great Britain, described 15 patients with three long-term survivors. Eight of these patients had broncho-pneumonia found at autopsy and, for the first time, attention was drawn to the respiratory aspects of the problem. Arterial oxygen tensions varied between 55-113 mmHg and the A-a gradients between 25-77 mmHg. The high A-a gradients were presumed to be due to bronchopneumonia, and the possibility was raised of a specific cold injury to the lung. Their results showed evidence of anoxia, respiratory depression, and acidosis. "Good oxygenation by assisted

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respiration and rapid rewarming might improve the chances of survival if the problems of circulatory collapse could be solved." A new understanding of the interplay between respiratory and cardiovascular function in determining survival was developing, not only in the treatment of hypothermia, but in the treatment of all severely ill patients. In the same year Pugh (1964), an eminent physiologist who had been on the first successful ascent of Everest in 1953 and an authority on mountain medicine, published findings based on an inquest following the deaths of three young men involved in a competitive walk in Britain. The course to be covered was 72 km long over moors with a total ascent-descent of 1200 m. Of 240 competitors only 22 finished. Weather conditions were very severe with temperatures between 0-4°C, and wind velocities of at least 25 knots. Those who died were aged 19, 21, 21 years. The most important conclusions were that clothing must be adequate, as it seemed as though the boys' wet clothing was incapable of providing appropriate protection. The speed with which hypothermic victims can be evacuated is also of great importance. Hypothermic collapse can develop in two hours, but in one fatal case evacuation alone took five hours. In response to Duguid's (1961) paper, several authors reported on hypothermic victims. Paulley et al. (1964) treated 22 patients with accidental hypothermia between November 1962 and March 1963 in Ipswich, England. Thirteen (59~) survived. Passive rewarming only was used. Thyroid and steroids were administered, as were antibiotics. The antibiotics were given to counter the almost universal occurrence of broncho-pneumonia, and the use of antibiotics was believed to be important to the high survival rate. Two review articles on cold in the elderly, by Taylor (1964) and an unnamed author (Special Committee, 1964), drew further attention to this major problem, which is as much a social as a medical problem, because it occurs most frequently in old people with limited income, faulty nutrition and inadequate heating. Duckworth (1964) drew attention to another group of patients at risk. In five months he saw five cases of hypothermia amongst the Bantu population of Johannesburg. Post-alcoholic hypoglycemia is common among this population and was thought to be a contributing causative factor. Two of the five patients died. Thyroid function in a group of 32 hypothermic patients was evaluated by Rosin and Exton-Smith (1964). Serum T 3 levels were abnormally high in several patients without a clear explanation for this. They advised that T3 and PBI levels should be measured in all patients but should be interpreted in relation to pH and pCO2 levels measured at the same time. No consistent thyroid abnormalities were found except in patients thought clinically to be myxedematous. With technological improvements in many other fields it was inevitable that some of those improvements would be applied to the treatment of hypothermia victims, especially if the technology could treat more than one condition simultaneously. In 1965 another milestone paper was published. Lee (1965) from King's College, London described the use of hemodialysis for the treatment of the combination of barbiturate poisoning and hypothermia. Within 18 months 181 patients were treated for barbiturate poisoning of whom 15 required hemodialysis for treatment, the primary indication being the barbiturate level in the blood. Of 15 patients, 8 were also hypothermic. Their rectal temperatures were between 28.3 and 35.6°C. All were dialyzed with fluid at 37°C and the usual rate of temperature elevation was 0.55°C/hr. All patients survived. Several advantages of this technique became apparent: (1) it was safe, (2) the technique was not difficult and the instrumentation necessary was readily available, (3) electrolyte and fluid imbalances could be treated concurrently, (4) body core was rewarmed before the periphery. Although the main purpose of this paper was to promote the use of dialysis in the treatment of barbiturate poisoning, it may have been even more important in promoting the use of dialysis in treating hypothermia. Later Linton and Ledingham (1965) described another technique, thoracotomy with internal cardiac massage and mediastinal irrigation with saline at 40°C to rewarm and defibrillate the heart of a 27 year old man with barbiturate poisoining. The treatment saved the patient, but there have been no subsequent reports of the use of a similar technique

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probably because of its drastic nature and uncertain results, added to the possibility of iatrogenic complications. The importance of hypothermia as a cause of death after shipwreck was graphically emphasized by Keatinge (1965) in his analysis of 124 deaths which occurred after the abandonment of the liner Lakonia in 1963. Only four of the known deaths could be accounted for by accident. Virtually everyone, survivors and those who died, wore life jackets which were effective in keeping people afloat. The water temperature was 17.9°C with an air temperature of 15°C. Those who survived seemed to be younger than those who did not and were probably wearing more clothing. The evidence pointed to hypothermia and not drowning as the major cause of death. By 1966 Pugh had had the opportunity to review a more extensive experience with hypothermia in walkers, climbers and campers; and he published his findings in a report to the Medical Commission on Accident Prevention (Pugh, 1966). The report reviewed 23 incidents from Wales, Scotland and England. In these incidents 100 people were at risk, 23 became hypothermic, 25 died and 18 were rescued and treated for exposure. The causes included (1) weather conditions, (2) being benighted without adequate shelter, (3) being wet through without adequate clothing, especially for the legs, (4) exhaustion, (5) unusual thinness of victims, (6) females more resistant than males, (7) inexperience and lack of training, leading to serious errors of judgment. Emphasis was again placed on the short time, 1-2 hr, required to induce hypothermia. Mental impairment caused by reduced body temperature often started a chain of events which eventually led to disaster. It was also concluded that waterproof clothing would prevent most exposure casualties. This paper again accented the many differences between hypothermia in the field and in the home. In the field the victims are young and healthy, hypothermia comes on quickly and often kills with equal speed. In the home the victims are elderly, diseased or intoxicated, hypothermia takes a long time to develop, and even with treatment rewarming is slow, and death frequently occurs many days later because of intercurrent disease. Because an increasing number of cases of hypothermia was being recognized in elderly patients, more attention was being paid to temperature regulation in old people. In 1967 two papers drew attention to changes in temperature regulation in old people, and how these changes make elderly people more likely to become hypothermic. Wollner (1967) reviewed the subject and pointed out that shivering does not occur readily in the elderly, and that vasoconstriction does not occur in response to exposure to cold. As a result heat loss is greater than in younger patients, and endogenous heat production, by shivering, is much less than normal. Natural insulation through weight loss or undernutrition, decreased metabolism sometimes accentuated by hypothyroidism, diminished exercise capabilities, and impaired sensory perception of cold all combine to increase the possibility of hypothermia. MacMillan (1967) studied thermoregulatory responses in eight survivors of hypothermic episodes. Central and superficial temperatures, shivering, hand blood-flow, and other factors were studied in a comfortably warm environment, and after the subjects were cooled. The results confirmed that the responses of elderly controls were normal while those of the hypothermia survivors were abnormal. On exposure to cold the controls vasoconstricted, the posthypothermics did not. Also the posthypothermics vasodilated at a lower body temperature than normal. Shivering developed normally in controls; but posthypothermics did not shiver even though their body temperatures were below 36°C. When hypothermics were exposed to cold they did not vasoconstrict, therefore their skin remained warm and it was postulated that the persistence of warm skin prevented these people from recognizing that they were in a cold environment. While knowledge of temperature regulation was increasing new methods were being tried to rewarm victims of hypothermia. In 1960 Fruehan had suggested the possibility of using the technology of open heart surgery, the pump-oxygenator and the heat exchanger to rewarm hypothermic patients. The first patient treated in that way seems to be a patient treated by Dr Kugelberg in Lund, Sweden on March 22, 1966 (Kugelberg, 1967). A 59 year old man was admitted after an alcoholic binge with a rectal temperature of 21.7°C.

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During the first hours after admission his temperature decreased and it was therefore decided to use the heart-lung machine. During 72min of venoarterial bypass his body temperature was raised to 35.0°C; normal sinus rhythm re-appeared at 29.5°C. On January l, 1967, an 82 year old woman was admitted to Shotley Bridge Hospital, Durham, England. Her rectal temperature was 34°C, blood pressure 1600110. Twenty-four hours later her temperature was 33.3°C, and because she was not responding to treatment a veno-arterial bypass was set up. Within 90 min she had been successfully rewarmed and later left the hospital (Davies, 1967). This case proved several points: (1) age is no bar to the use of extracorporeal circulation; (2) in extreme cases this technique provides excellent controlled rewarming, and at the same time supports the circulation. About five weeks later (February 10, 1967) a third case in which extracorporeal circulation was used was treated and later described by Fell (1968). The patient was 42 years old, a housewife who attempted to commit suicide with phenobarbitone. Her rectal temperature was 22°C and during resuscitation her heart stopped. After about 150 rain of external cardiac massage femoral veno-arterial bypass was started at 3.0°3.5 liters/rain. She was warmed from 25°C to 34°C in 40 rain. After a three-month convalescence she left the hospital. Another example of internal rewarming was described by Lash (1967). On February 21, 1966, a 24 year old woman was discovered in an exposed situation in Tennessee. She seemed to be barely alive. Her rectal temperature was 21°C. Because drug ingestion was a possible cause of her problem peritoneal dialysis seemed to offer two advantages, rewarming and removal of drugs. For one hour after admission no cardiac action was discernible and she received cardiac massage. About 1.5 hr after starting treatment her heart could be defibrillated. Peritoneal dialysis was continued for more than 12 hr with 32 liters of dialysate. The patient eventually left the hospital without discernible sequelae. Mathews (1967), in a review of hypothermia,reflected opinions then current. He pointed out that the treatment of hypothermia does not lend itself to controlled trials, but stated that the older and more infirm the patient and the longer he had been hypothermic the slower he should be rewarmed. Conversely, young patients otherwise fit should be rapidly rewarmed in a hot water bath. Intravenous fluids, oxygen, antibiotics and steroids were advocated as routine treatment. Thyroid replacement in myxedematous patients, and pressors in those who are hypotensive was also suggested. Although several large reports had been published by that time the overall mortality rate quoted was 37.7~, in the Royal College of Physicians of London Report (1966), except in patients with temperatures under 30°C in whom the mortality was 70~o. This seems a low figure to quote in that era when most series reported mortality rates between 40-80~/o. Mant (1969), in describing the post mortem findings in 28 patients drew attention to the frequency of changes in the pancreas (82~o), which varied between small foci of fat necrosis to gross hemorrhagic pancreatitis. Fat necrosis, however, was not seen outside the pancreas possibly because of the inhibitory action of cold on tissue damage. A second common finding (89~o) was submucosal gastric hemorrhage. Most of the hemorrhages were in the stomach, 1-2 mm in diameter, and occasionally in the duodenum or elsewhere in the alimentary tract. If death does not occur soon after the onset of hypothermia the hemorrhages may be converted to superficial ulcerations. Facial and peripheral edema and bullae on pressure areas were also found in about one patient out of four. Microscopically, pancreatic necrosis, fatty changes in the myocardium and gastric hemorrhages or ulceration without inflammatory reaction were seen. It is difficult to distinguish between lesions caused by hypothermia and those caused by predisposing conditions. But for whatever reason, pancreatitis and gastric hemorrhages are found with such frequency that they should be regarded as characteristic of hypothermia; and further evidence of this is the finding of elevated serum amylase levels in survivors. The list of associated conditions is long; in Mant's 28 cases there were 21 pre-existing or co-existing diseases. In some patients hypothermia was believed to be a terminal event in the course of dying. The lowest body temperature from which humans can be resuscitated is not known. A distinction should be made between the lowest temperature from which a patient could

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rewarm spontaneously, and the lowest temperature from which survival would only be possible with the aid of mechanical assistance such as extracorporeal circulation. Individual organs can be cooled to very low temperatures and their structure and function is preserved during periods of anoxia by low temperatures. The heart is commonly cooled to 10°C during surgically induced cold cardioplegia (Barratt-Boyes et al., 1971): the kidney and liver can be preserved intact for many hours if cooled to 4°C, and provide normal function after transportation. The heart also can withstand 2-4 hr at 4°C and function normally (Mendez-Picon et al., 1982). A timely review of hypothermia in mountain accidents was published by Freeman and Pugh (1969). Symptoms, predisposing factors, physiologic changes and treatment were discussed. While advocating rapid rewarming by immersion in hot water the authors listed some of the disadvantages: manhandling is unavoidable, effective cardiorespiratory resuscitation is impossible, and the method is unsuitable if there are other major injuries. The longer the duration of hypothermia the slower the rewarming. Several cases have been reported of patients with body temperatures below 20°C who have survived. Anderson (1970) from Orebro, Sweden treated a three year old boy who wandered from home and was found apparently dead 15 hr later, after being exposed to an ambient temperature of about 0°C for that period. His rectal temperature was 17°C. A cardiogram recorded irregular complexes at 8-10/min; there were no respiratory movements. He was warmed in a hot water bath (37-38°C) and after 130 min had a rectal temperature of 33°C and a normal sinus rhythm. He was discharged home after five days, and one year later seemed to be perfectly normal. The usual environment for hypothermia is imagined to be cold and northern; but several series of patients have been encountered in normally warm climates. This is not surprising as an ambient temperature of 30°C is 5.5°C lower than the upper limits of hypothermia. Tolman and Cohen (1970) managed 11 patients at the Ben Taub Hospital in Houston, Texas. Ten of the 11 patients were either alcoholic or diabetic: five died. Of the six survivors five did not develop any complications; whereas those who died had thrombotic complications such as myocardial or pulmonary infarcts. No patient was actively rewarmed, and all were insulated from further heat loss by light blankets. Plasma steroid levels were measured in five patients and were found to be elevated in all of them. There was therefore no logical reason to give steroids and none was given. In analyzing factors of prognostic value the authors felt that a low platelet or fibrinogen level probably indicated intravascular thrombosis; and as most of their fatal cases had intravascular thrombotic complications, evidence of thrombosis may be important prognostically. The continuing discussion about the optimal rate of rewarming was the topic of a report by Fernandez et al. (1970). They treated three patients aged 36, 53 and 60 years. They were warmed from 28.9, 23.8 and 25.5°C respectively by active rewarming with a hot blanket. The period of rewarming varied from 4-7 hr and all patients survived. In discussing these cases they postulated that core rewarming by extracorporeal circulation or hemodialysis was the optimal treatment, but was impractical because of the lack of facilities and the time delay involved. Hypothermic patients with a central neurological lesion are occasionally seen. One such patient was reported by Fox et al. (1970). A 26 year old man with repeated episodes of hypothermia was found, after his death, to have a severe localized area of degeneration in his anterior hypothalamus, and because of this was unable to maintain a normal body temperature even in a controlled thermoneutral environment. Coopwood and Kennedy (1971) published a series of 11 patients also from the Ben Taub Hospital. Not all these patients were in the previously reported series (Tolman and Cohen, 1970) but some may have been. Nine patients died. Active rewarming with electric blankets was advised, with administration of intravenous fluids and use of pressor amines to maintain blood pressure. Five died while still hypothermic between 9 and 36 hr after admission to hospital. If active rewarming was used in all the patients the rate was very slow if a patient was still hypothermic 36 hr after admission to hospital.

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Accidental hypothermia is not only thought of as a problem of cold climes but also of situations outside hospital. Infants, however, especially premature infants, may become cold in hospital if not adequately protected. Newman (1971) pointed out the dangers of hypothermia in another group of patients, those undergoing vascular surgery. In a group of 33 patients undergoing peripheral vascular operations 33 sustained reductions in body temperature of 0.8-4.6°C. The methods advised to avoid this included the routine use of a hydraulic thermostatically controlled blanket and warmed intravenous fluids. A series of letters in the Lancet were prompted by a recent climbing and exposure disaster in the north of Scotland. Hillman (1971) advised several measures which had not previously been suggested: (1) abdominal 'pumping' or jack-knife procedures to improve circulation; (2) intracarotid centripetal infusions of blood serum or balanced salt solution. The suggestions were based on experimental work with animals. Two weeks later Lloyd (1971) of Edinburgh wrote a short note on the use of warmed gases, a method which he subsequently described in detail and which has found considerable approval. More and more evidence was being found in Great Britain that, in that country at least, many elderly people had body temperatures lower than normal, and lived in homes where the temperatures were consistently lower than desirable. Eddy (1970) found that in a group of homes in London the mean night-time temperature in bedrooms was 8-9°C in homes where the sleeping and living rooms were separate, and 9-13°C where the people slept and lived in the same room. Salvosa (1971) found the same conditions to be true in another similar study, of people believed to be specially at risk because of their social circumstances. Some of the patients were found to have mouth temperatures below 35°C but their urine temperatures were normal. Fox (1971) reported a technique of measuring urine temperature which was not only convenient for use in the homes of elderly people, but which produced measurements that correlated well with rectal temperatures. Urine and rectal tempeatures correlated better than mouth and rectal temperatures. Since Duguid's (1961) paper in which it was suggested that steroids should be given almost routinely to hypothermics, there had been discussions about the validity of this view. Maclnnes et al. (1971) reported on plasma-I 1-hydroxycorticosteroid and growth hormone levels in nine young male climbers undertaking a week long climbing course. These results were compared with those found in the climber's instructor, eleven other men after a day of hiking, and four men and one woman rescued in a state of exhaustion. It was found that the stresses of climbing increased adrenal cortical levels; but in two of five people rescued in an exhausted state plasma hydroxycorticosteroid levels were low (10 and 9 #g/100 ml). It was suggested that steroid therapy might be valuable in hypothermic, exhausted climbers. Endocrine function was studied in 12 hypothermic patients with temperatures below 32°C (Woolf et al., 1971) including measurements of thyrotropin, growth hormone, insulin, T4, T3, cortisol and glucose. The conclusions reached were that the hypothalamic-pituitary-thyroid axis remained intact, that hypothermia is not a stimulus for the release of TSH. Changes in growth hormone and insulin levels were not consistent, nor were plasma glucose concentrations. Plasma cortisol was found to be inappropriately low in some patients. No therapeutic implications were drawn from these results. Several centers around the world have developed a particular interest and skill in the management of hypothermia. The Western Infirmary in Glasgow, Scotland is one of these. In a letter to the Lancet Ledingham and Mone (1972) outlined their experience with 30 patients and this is an excellent capsule report on optimum management. Seven points were emphasized: (1) Oxygen, frequently with intubation and positive-pressure respiration; (2) Insertion of arterial and central venous catheters for monitoring. A special point was made that none of their patients had sustained any deleterious effects from intubation or cannulation; (3) Correction of metabolic acidosis; (4) Rapid rewarming of the torso by external means, at a rate of 0.5-1.0°C/hr; (5) Warmed intravenous fluids; (6) BUN, blood

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sugar, and electrolyte levels; (7) Drugs--steroids, heparin, pressor amines and thyroid-not felt to have any usefulness in initial management. The patient should be treated in an intensive care unit. Alaska would seem to be the archetypical environment for hypothermia. Although there had been much attention given to frostbite in that state Gregory (1971) was the first to review the problem of hypothermia. Fifty-one physicians answered a questionnaire and reported having seen 61 cases in 15 years. No details were given about treatment or mortality; but an important problem was the unavailability of low-reading thermometers for accurate diagnosis. Gregory contacted 21 thermometer manufacturers before he could locate a low-reading clinical thermometer. Early in 1972 the Lancet continued to publish a flurry of letters. Gregory and Patton (1972), who had just reviewed the experience in Alaska, advocated internal or core rewarming, citing the avoidance of rewarming shock and published results that suggested 100~o success for core rewarming. In these letters an increasing awareness of the importance of adequate oxygenation and control of ventilation was apparent (Gregory et al., Editorial Comment, 1972). Whitby (1972) provided an interesting historical comment on Lloyd's proposed use of warmed gases, pointing out that in 1812 Brodie had found that curarized rabbits cooled if ventilated with cold air, and that as early as 1834 a system had been devised for warming air for artificial ventilation. Hypothermia is quite common in neonatal infants, especially if premature. Ten percent of babies admitted to the Cardiff Maternity Hospital, Wales were found to be hypothermic (Chadd and Gray, 1972). In two groups, 19 hypothermic babies and 19 euthermic babies, mortality was seven in the hypothermic group, and one in the euthermic group. Pulmonary and cerebral hemorrhages were common in the hypothermic infants and were caused by derangements of coagulation, thrombocytopenia and a consumption coagulopathy. A brief report in the New England Journal of Medicine by Towne et al. (1972) described another patient, a 581 year old alcoholic with a temperature of 25°C who was rewarmed to 34.4°C in 45 min by the use of partial cardiopulmonary bypass. "We suggest that when profound hypothermia and intractable arrhythmia combine to prevent successful resuscitation, rapid core rewarming using partial cardiopulmonary bypass may prove life-saving." Meriwether and Goodman (1972) from the State University of Ohio described the successful treatment of a 74 year old woman who was admitted with a rectal temperature of 28.9°C. She was submerged in water (40-42°C) for 20 min and was then warmed by a heating blanket. The authors believed that rapid rewarming by immersion in warm water was the best treatment available. By this time, there appeared to be an increasing weight of evidence in favor of rapid rewarming, although this evidence was more anecdotal than statistical and lacked hemodynamic information and control. Although Linton and Ledingham (1966) had reported the use of intrathoracic warmed lavage in 1965 no other reports of this technique had been forthcoming. But Coughlin (1973), in response to the description by Towne (1972) of using cardiopulmonary bypass to rewarm a patient recalled that in 1957 he, Usman and Brunner had resuscitated a cold patient by open chest massage. Initially this was unsuccessful until some warm saline was poured on the heart. Because a few beats occurred 76 liters of warm unsterile tap water were then poured into the pleural space, rewarming the patient who survived without neurologic damage and with only a minor wound infection. Timely reviews of clinical experience are an important means for determining what has been done, and whether changes are necessary. Gregory and Doolittle (1973) reviewed all the available clinical results up to this time. The treatment of 201 patients had been published with 103 (51.2~) survivors. Passive rewarming was used in 121 patients with 44~ mortality; active rewarming was used in 73 patients with 60~ mortality. Internal rewarming, by inhaled gases, peritoneal lavage or dialysis had been used in 14 patients with 0~ mortality. On the basis of these results and their own experience a strong advocacy was made for the use of internal methods to achieve a more rapid result, with better

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restoration of cardiac output to normal and the avoidance of rewarming shock and 'after drop'. Although special equipment is needed for some of these methods, peritoneal dialysis can be effected with little specialized training and with no need for special equipment except the cannulae which are easily obtainable. Another case in which extracorporeal circulation was used for rewarming was described by Truscott et al. (1973). A 23 year old woman was found near her wrecked car. The ambient temperature had been about -20°C. Soon after arriving at the hospital and the insertion of an endotracheal tube and a pacemaker lead she developed ventricular fibrillation. After an hour of external cardiac massage she was taken to the operating room where femoral vein-femoral artery bypass was established. After treatment of tamponade caused by ventricular puncture by the pacemaker lead perfusion was stopped. As the accident had rendered her paraplegic she was in hospital for a long time and died suddenly, in hospital, four months after the accident. Fox et al. (1973) added to their valuable contributions to knowledge of body temperature in elderly people. Two large surveys of body temperature were carried out in Britain during the winter of 1972. One study involved randomly selected people over 65 from all over Britain, the other involved people in one section of London. Hand and urine temperatures were measured, and thermal comfort was assessed. Deep body temperatures below 35°C were found in 10~o of more than 1000 people surveyed. In a similar survey, also by Fox (1973), 81.3~ of rooms in which elderly people lived were found to be below the acceptable temperature standard of 18.2°C, and 57~o were below 16°C. Both studies confirmed that many elderly people in Britain live in the winter in uncomfortably cool environments, and that about 1: 10 of the population at risk has a body temperature at or below 35°C. Lloyd (1973) made an important contribution to the treatment of hypothermia by describing the use of warmed oxygen in 11 patients. He had previously described a technique for warming and humidifying oxygen by passing it through a soda lime container previously saturated with CO2. The apparatus could be used in the field with people breathing spontaneously, or in hospital to be attached to a Waters' anesthetic machine; or a conventional humidifier can be used with the temperature set at 60°C. A group of 11 patients was rewarmed, their ages being between 22 and 86 years. Five recovered. All had underlying disease, or drug intoxication. The rate of temperature elevation varied between 0.2-1.0°C/hr. No respiratory problems were ascribed to the treatment, and no cardiac arrhythmias resulted from the necessary endotracheal intubation. Although this method restores only a small amount of heat to the body (1.2 kcal/m2/hr) the heat is transferred directly to the blood and thence to the heart. It was believed that this was responsible for improvement in cardiac function. Hudson and Robinson (1973) addressed the theoretical considerations involved in airway rewarming, they calculated that ventilation at 81iters/min with 100~ water saturated oxygen at 40°C would provide 13 kcal/hr. Exton-Smith (1973) reviewed the problems of diagnosis and management, especially the question of the best way to rewarm. He pointed out that current therapeutic teaching was to place the patient lightly covered in a room at 21°C and allow the temperature to rise slowly. The disadvantage of this method is that the incidence of complications and mortality rate are related to the duration of hypothermia, and this method prolongs the period of hypothermia. He concluded that better results are obtained by more rapid rewarming with the patient in an intensive care unit. Two important papers were published in January 1974 both of which added to understanding that the outcome from hypothermia did not depend solely upon hypothermia itself. Hudson and Conn (1974) treated 16 patients in one year in Seattle, Washington. Eight of the patients had severe underlying diseases including pancreatitis, acute tubular necrosis, perforated gastric ulcer, peptic ulcer disease with hemorrhage, sepsis and myocardial infarction. Only one patient in this group survived. He had pulmonary ituberculosis and had been exposed to cold immersion. Seven patients were intoxicated with JPT 2 2 / 3 ~

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alcohol or barbiturates, but did not have other diseases. All survived. One patient was admitted with a temperature of 20°C and died without a diagnosis being made. The average admission temperature of the patients with other diseases was 30.7°C (28.3-32.7°C), and the average temperature of those intoxicated was 29.6°C. Nearly all the patients were treated with simple passive rewarming. The determining factor in survival, therefore, was not the depth of hypothermia, nor the rapidity of rewarming, but the presence of a severe and potentially fatal disease. Weyman e t al. (1974) came to the same conclusion from their study of 39 patients admitted to St. Vincent's Hospital, New York. Of 31 patients, mostly alcoholics but without associated disorders, only two died. But in a group of eight patients, also alcoholic but with additional disorders such as septicemia or gastro-intestinal hemorrhage, six died. There were no consistent abnormalities in hematologic or electrolyte values. Blood sugars varied between 40 and 728 mg/100 ml without any relationship to survival. Thirty-two patients were actively rewarmed, with a hot blanket, seven passively rewarmed. All the deaths occurred in those actively rewarmed. The rate of rise of temperature was 1.3°C/hr in those passively rewarmed, 1.0°C/hr in those actively rewarmed who survived, and 0.7°C/hr those actively rewarmed who died. These numbers suggest that those passively rewarmed were not as sick as those actively rewarmed and that those who died were the sickest from the time of admission. But this paper re-emphasized that there is a major difference in the possibility for survival between those with and those without severe underlying disease. Hypothermia associated with intoxication, whether alcoholic or barbiturate is not by itself a severely fatal condition. Additional evidence for the abnormalities of temperature control in older people was provided by Wagner e t al. (1974), Indiana University, who studied responses to cold in young and old people. Four groups of males aged 10-13, 14-16, 20 and 46-67 years. After a period in a thermoneutral environment the volunteers were exposed to a temperature of 16-17°C for 10-15 min. The younger subjects reacted promptly to cold with peripheral vasoconstriction, and an increase in metabolism. The older men exhibited a lesser increase in metabolism and had higher finger blood flows, indicating a decreased vasoconstrictive response to cold. Numerous instances of ventricular fibrillation in hypothermic patients have been reported, but the precise cause of the dysrhythmia is unknown. Lloyd (1974) postulated that hypothermia impairs normal neuro-muscular subendocardial conduction and encourages abnormal myocardial conduction more liable to cause ventricular fibrillation. Duguid (1961) believed that patients with hypothermia had adrenal insufficiency and, therefore, gave steroids to most of her patients: a therapeutic regimen which was followed by many others. MacLean and Browning (1974) found 11-hydroxycorticosteroid levels to be high in patients with accidental hypothermia. There was also a correlation between high corticosteroid levels and mortality. The hypotension in hypothermic patients was due to prolonged hypothermia and not to adrenal insufficiency. The high corticosteroid levels returned to normal after a few days. In a further study of endocrine activity in hypothermic patients MacLean e t al. (1974) measured enzyme activity in 75 patients with accidental hypothermia and 18 patients with hypothermic myxedema. High activity levels of creatine kinase, ~-hydroxybutyrate dehydrogenase and aspartate aminotransferase were related to hypoxia, acid-base disequilibrium and hypotension, and not to hypothermia, p e r se. A postulate was made that the poor prognosis in hypothermic myxedema may be due to a thyroid related cardiomyopathy. A suggestion was also made that prognosis would be most improved by early correction of acid-base disturbances and hypoxia rather than by concentrating solely on temperature correction. Sadikali (1974) from Makerere University, Uganda, reviewed 24 cases of hypothermia seen within two years ranging in age from 17-80 yr. Four patients were hypoglycemic but the response to glucose was disappointing. Malnutrition was present in two-thirds with weights averaging 5 kg below 'normal'. Three patients had acute hemorrhagic pancreatitis and six patients had focal pancreatic lesions. The very low incidence of pancreatitis in

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nonhypothermic patients in the same hospital seems to confirm the specificity of pancreatitis as a complication of hypothermia. Fourteen of the 24 patients died, still hypothermic: four died euthermic. Only two recovered completely. During the roughly 20 yr covered by this review there has been only one paper published which has described detailed hemodynamic data in a group of severely hypothermic patients. Harari et al. (1975) measured cardiac output, peripheral and systemic resistances and the effects of rapid volume expansion and isoproterenol infusion in six patients. The ages of the patients varied between 48-77 yr: the average duration to cold was 30 hr, and the temperatures on admission were 25.3-29°C (mean 26.5°C). Five patients were slowly rewarmed with blankets and one rapidly rewarmed in a bath at 40°C for 40 min. One patient died while being rewarmed, and three patients died from underlying disease 15-40 days after rewarming. Blood volume expansion was achieved by the infusion of 500-2000 ml of fluidified gelatine at 17 ml/min. Isoproterenol was infused at 20 pg/min. Before treatment heart rates were slow (44-80), right sided pressures normal to low, and cardiac indices were low (1.1-2.01iter/min/m 2) with high systemic resistances (1475-2820 dynes/cm-5). The response to volume expansion was a marked reduction in systemic resistance (780-1950dynes/sec/cm -5) and an increase in cardiac index (1.85-3.9 liter/min/m2) and an elevation of pulmonary artery pressure to normal levels. The infusion of isoproterenol also caused an increase in cardiac index from a mean of 2.41iter/min/m2 to 4.3 liter/min/m2. Systemic resistances fell from a mean of 1288 to 802 dynes/sec/cm- 5. The response to rapid volume expansion was also measured 48 hr following restoration of temperature to normal, when a mean pre-expansion cardiac index of 2.8 liter/min/m2 rose to 4.04 liter/min/m2 indicating normal cardiovascular function. Observations were made on one patient who was rapidly rewarmed in a hot water bath, after preliminary blood-volume expansion. There was an immediate decrease in right auricular, pulmonary capillary wedge and aortic pressures with a drop in systemic resistances. The cardiac index was sustained initially, but fell after 40 min of rewarming. After one hour of normothermia the cardiovascular response to further volume expansion was poor; but after 36 hr of normothermia there was considerable improvement in cardiac function. The significant findings were a decrease in power of both right and left sides of the heart, caused by bradycardia and low stroke index. Ventricular filling pressures were low-causing a low stroke work index. And filling pressures in turn were low because of an absolute hypovolemia. The response to volume expansion, although positive, was less than in normothermia. There was, therefore, during hypothermia a primary cardiac deficiency not present in normothermia. The longer the duration of hypothermia, the greater the myocardial dysfunction. Two patients exposed for eight hours or less had normal ventricular function; but three patients with prolonged exposure (more than 48 hr) had impaired ventricular function. The precise nature of this impairment is not clear but could be due to decreased or uncoordinated myocardial contractility. The therapeutic implications of this study are that in prolonged hypothermia hypovolemia is sufficient to impair cardiac function. Hypovolemia should therefore be corrected rapidly, especially if active external rewarming is to be used. Isoproterenol may be used cautiously, but only after restoration of blood volume. This very important paper demonstrated conclusively that with appropriate monitoring and measurements as rational an approach to fluid replacement and pressor administration can be developed in hypothermic patients as in any very sick patient with or without a temperature derangement. In this era increasing attention was being paid to core rewarming. Sereda (1975) suggested that these techniques should be used more frequently, but Hunt (1975), in reply, pointed out that in smaller hospitals some of the equipment was not available and that a warm water tub was a very effective, readily available method.

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Not only are methods necessary for rewarming patients in hospital but also in the field. In a climbing journal, Off Belay, Dayton and Arnold (1975), described a portable hydraulic warming blanket that had been successfully used to rewarm hypothermia victims at the site of their accident. An effective apparatus of this sort could considerably reduce the delay before rewarming some accident victims. Neurological integrity after severe hypothermia and cardiac arrest has been reported on several occasions (Jessen, 1978; Schissler et al., 1981) but no case is more remarkable than that of Siebke et al. (1975) in Norway. A 5 year old boy fell into a partially frozen river and was removed from 3 m of water 40 min later by a rescue squad. On arrival at hospital a few minutes later he appeared to be dead, and his rectal temperature was 24°C. Cardiopulmonary resuscitation which had been started as soon as he was brought out of the water was continued until 105 min after submission a strong pulse was restored. He was discharged after eight days almost completely normal and a year later demonstrated no abnormalities of cerebral or neurologic function. Further evidence became available of the usefulness of extracorporeal circulation for rewarming patients in extremis. Wickstrom et aL (1976) described three patients, two of whom were successfully resuscitated--a 65 year old woman, a 45 year old man, and a 64 year old man. Their respective temperatures were 25°C, below 20°C and 23.8°C. The intervals between admission and onset of bypass were I hr, 1 hr, 2 hr: in each case cardiopulmonary resuscitation was used to maintain life during these waiting periods. The authors urged that that once resuscitative measures are started they should be prolonged and vigorous. From the first description of airway rewarming by Lloyd (1971) there was continuing discussion about the effectiveness of the method. Hayward and Steinman (1975) carried out experiments on 10 volunteers cooled by immersion to about 35°C and rewarmed either by immersion in hot water, or with treated humidified oxygen. There was no difference in the amount of temperature afterdrop (0.38°C with inhalation vs 0.48°C with bath). Inhalation appeared to increase tympanic temperature slightly more rapidly than did the bath. The author concluded that the experiments confirmed the effectiveness of inhalation rewarming. He also felt that the method provided some protection against ventricular fibrillation, by directly rewarming the heart, and improved rewarming of the brain. Two papers by Lloyd (1975) compared the effects of rewarming sheep experimentally cooled to about 3 I°C while anesthetized. In the first paper the cardiovascular effects of rewarming techniques were compared. Rewarming in a hot bath produced a continuing rise in cardiac output but with airway rewarming the cardiac output did not change significantly. The increase in cardiac output was due to an increased stroke volume; with airway rewarming there was tachycardia with a decrease in stroke volume. Peripheral resistance fell with spontaneous rewarming and hot water immersion, but was compensated for by an increase in cardiac output so that blood pressure did not fall. In a second paper Lloyd (1976) described similar experiments in which heat transfer was measured in sheep. Central airway rewarming was found to be three times as fast as spontaneous rewarming with insulation. And warming in a hot bath was three times as fast as central airway rewarming. The importance of adequate insulation to prevent further heat loss was emphasized. Sixty-two cases of hypothermia were seen over a 32 month period by O'Keefe (1977) in Denver; Colorado all with core temperatures below 35°C. Most of the patients were men and 77~ were encountered outdoors; 63~ were alcoholics. Nine patients (15~) had medical problems sufficiently severe to warrant admission without superimposed hypothermia. The mortality rate was 119/o. Sixty percent were admitted to hospital, but 40~ were discharged to nursing homes or other hospitals after being rewarmed in the emergency room. Fifty-six (90~o) patients were treated with warmed blankets; two patients were immersed in hot water. Three patients were warmed with cardiopulmonary bypass. One patient warmed in a tub arrested after becoming normothermic and could not be resuscitated.

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Thirty-five patients were in normal sinus rhythm, 16 had atrial dysrhythmias including 14 with atrial fibrillation. All the atrial dysrhythmias reverted to normal rhythm with rewarming. Profound bradycardia seemed to be a more common precursor of ventricular fibrillation than other rhythm disturbances. Three patients who developed ventricular fibrillation did so after therapeutic manipulations, and caution was expressed about intubating patients, placing intracardiac pacing wires, or passing esophageal temperature probes. Patients with temperatures between 32-35°C may be sufficiently well after rewarming to be discharged; but those with temperatures below 32°C should be admitted. In the discussion mention is made of seven patients rewarmed by cardiopulmonary bypass with three long-term survivors. All these patients had arrested before bypass was started, and the conclusion was that this procedure could be quite successful in such extreme patients. An additional longitudinal study by the London group, Collins et al. (1977) compared body temperature regulation in 47 people in 1971-2 and again in 1975-6. Measurements were made in the subjects home and in hospital. No cases of hypothermia were discovered in either survey. The ability to conserve heat deteriorated slightly during the four year interval. It was possible to categorize responses to cold in three ways: (1) Normal: a rapid reduction of peripheral blood flow followed by vasodilatation on rewarming; (2) No vasoconstrictive phase, but a good vasodilatory phase; (3) No constriction and no dilatation. In the first study 6:43 were nonconstrictors: in the second study 14:43 were nonconstrictors. Shivering only occurred in 4:43, and always in subjects with a nonconstrictor response to cold. Thermal perception was blunted with age. Young controls could distinguish differences of 0.8-0.9°C: elderly people could only distinguish differences of 2.3-2.5°C. The study confirmed 'an age related decline in autonomic nervous function leading to an impairment of thermoregulatory capacity in a high proportion of old people.' Three additional cases were reported in which peritoneal dialysis was used successfully. Johnson (1977) described an alcoholic 38 year old woman with a temperature of 24.4°C who was treated with peritoneal lavage at 43.3°C. Dialysis was stopped when the temperature was 30.5°C and she was warmed thereafter by a warm hydraulic blanket. Picketing et al. (1977) also reported the case of a 20 year old woman who had been consuming alcohol and who was found outdoors (Winnipeg, Canada: temp -36°C). Her rectal temperature was 26.4°C. She had ventricular fibrillation and closed-chest massage was started. Warming was first started with a blanket, but because her temperature continued to fall, peritoneal dialysis was started and continued for 90 min. Her temperature rose from 26°C to 32°C when defibrillation was accomplished. She finally made a full recovery. Soung et al. (1977) treated a 20 year old juvenile diabetic with a temperature of 28°C. Peritoneal dialysis was started, and within one hour the patient was alert. In two hours his temperature was normal. In 1978 both the Lancet (Editorial, 1978) and the British Medical Journal (Editorial, 1978) considered hypothermia to be a topic of sufficient importance to warrant editorials on the subject. The Lancet addressed the causes of death and the management of the patient whose heart has stopped. Although mention was made of peritoneal dialysis and cardiopulmonary bypass the editor stated: 'But even in such extreme cases effective cardiac massage and pulmonary ventilation combined with surface rewarming may have as much chance of success with less trauma to the patient.' Some doubt was cast on the effectiveness of warmed oxygen inhalation, as experiments had shown that there was little effect on deep body temperature. No statistical evidence existed that the death rate is any lower with one method of rewarming than with another, but it was known that rewarming in a hot bath was highly effective. 'Do not use difficult and dangerous treatments when a simple and effective one is already available.' The British Medical Journal (1978) reviewed the whole topic more extensively, and made a few important conclusions. All hypothermic patients should be given coma nursing in intensive care conditions. Assisted ventilation should be available. There may be a case

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for the routine administration of antibiotics, but not of steroids, thyroid replacement, or vasocactive drugs. Mortality was still believed to be about 50~o, but in many elderly patients the cause of death was the precipitating illness, and not hypothermia. About the same time a review of hypothermia, its pathophysiology, clinical settings and management was published by Reuler (1978). This excellent review is probably the most detailed compact review of the subject yet available. Additional evidence of the efficacy of peritoneal dialysis rewarming was given by Jessen (1978), from the Municipal Hospital, Copenhagen, Denmark. Three patients were rewarmed by this technique. The first, a 30 year old woman was found in the harbor and thought to be dead. Initial treatment was in a warm water bath, but she also received cardiac massage. After 2.5 hr peritoneal dialysis was started and her temperature was raised to 30.2°C, but all attempts to restart her heart were unsuccessful. The second and third cases were children 4 and 6 years old. The first had a rectal temperature of 24°C, the second a temperature of 21°C. Both children were victims of cold immersion, and both made complete recoveries. Soung (1978) had the opportunity to comment on peritoneal dialysis and pointed out that the method is not without potential complications, and suggested that a single needle or catheter method of hemodialysis might be as efficient and simpler. Experiments in humans are limited by the temperature to which the subject can be cooled, but do provide valuable comparative data as reported by Marcus (1978). Four subjects were each cooled four times to 35°C. Hot bath, piped suit, inhalation and spontaneous rewarming were carried out on each subject on different occasions. The hot bath and piped suit rewarmed more rapidly than inhalation or spontaneous rewarming. Inhalation rewarming was found to afford little advantage over spontaneous rewarming. There were no differences in 'afterdrop' during rewarming by any of the techniques studied. The conclusion was that in the absence of a technique for central rewarming the most effective method was to apply heat to the skin. Rectal temperature responds slowly to cooling and rewarming, and auditory canal temperature is a more accurate indication of core temperature. Cardiopulmonary resuscitation should be prolonged and energetic especially in the young and healthy. Bristow (1978) reported the story of a 16 year old boy who became exhausted and hypothermic (25.2°C rectal temperature) and was resuscitated after 1.5 hr of cardiac arrest. He sustained some mild peripheral nerve damage which finally resolved. The advice: do not abandon resuscitation until the body temperature is 30°C, or above. A symposium held at the Royal Air Force Institute of Aviation Medicine on the Treatment of Accidental Hypothermia and edited by Marcus (1979) placed most emphasis on the problems of acute outdoor exposure and immersion hypothermia. Air-sea rescue operations of downed airmen involve highly specialized techniques which in peace-time may be used infrequently. In wartime in an area such as the Falkland islands such rescues may be very common. In 10 peace-time years the R.A.F. only rescued three airmen with mild hypothermia. Rewarming on the rescue helicopter is probably not feasible and the best that can be done is to protect the victim from further cooling, and transport him as quickly as possible to a hospital facility whether land or sea-based. Mountain rescue teams commonly encounter three conditions: (1) A climber in early hypothermia who can walk off the mountain; (2) A known accident with one person cold initially, then a delay ending up with several victims; (3) A missing person search which ends either with a body being found or a healthy person who has bivouaced until help arrived. In category (2) the rescuer can provide insulation, and special insulated stretchers may provide better protection than currently available equipment. Field rewarming equipment may be available but considerations such as weight, waterproofing, wind resistance, cost and manipulability with gloved hands make some equipment impractical. Drug therapy is difficult to give; but in mountain rescue steroids may be important. During a major search communications are extremely important, but there is never enough equipment, and patient monitoring equipment for field use is usually not available. In the same symposium Keatinge pointed out the difficulty of distinguishing between

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hypothermia and drowning. Some factors, especially loss of consciousness or confusion coupled with abnormalities of behavior, may be important clues that the victim is hypothermic. Golden questioned the validity of theories that all patients should be actively rewarmed (Golden et al., 1977). The usual reasons given for rewarming are to reduce complications, to provide heat to those incapable of producing it, and to reduce afterdrop. In fact, some of the complications may be due to circulatory complications and hemoconcentration, even down to 29°C some people shiver and produce metabolic heat, and rapid rewarming reduces only the duration, not the magnitude of 'afterdrop'. Golden also argued with the concept that a bolus of cold blood from the periphery causes afterdrop; he believed that afterdrop can be accounted for purely by the laws governing heat flow in solids. 'During rewarming it takes a finite time for the wave of warming to reach the core through the shell, and this defines the afterdrop.' The optimal methods of rewarming were discussed by Norman who carried out animal experiments comparing (1) drying and insulation, (2) the same with airway rewarming, (3) airway rewarming and assisted ventilation with muscular relaxation, (4) water immersion at 42~4°C. Airway heat gain was found to be 10~ of metabolic heat production and was dependent on minute ventilation. Shivering produced the most heat, and airway rewarming in relaxed animals was very slow. Inspired air at 50°C produced no damage. The experiments of Marcus (1979) also showed that airway rewarming was not significantly different from spontaneous rewarming in that all techniques produce afterdrop. Discussion of piped suits, changes in peripheral resistance during rewarming, intravenous fluids and methods of monitoring temperature added to the value of this symposium and drew attention to a number of unsolved problems. Cardiopulmonary resuscitation was reviewed by Merrifield (in Marcus, 1979). Two factors increase the chances of success, the protective effect of low temperature and that the heart is normal in many patients. (This obviously applies only to the young healthy exposure victim). Keatinge felt that the first treatment of an immersion hypothermia victim is rewarming in a hot bath, perhaps even before transportation. Some authorities, however, felt that cold victims should be evacuated cold before attempts at resuscitation are made. Once cardiopulmonary resuscitation is started it must be continued until a hospital is reached. Drugs should be used sparingly; the routine use of steroids is probably wrong. Vasopressors are occasionally indicated. Anti-dysrhythmic drugs may lead to hypotension and, when the heart is warm most of the arrhythmias disappear. The symposium concluded with the hope that an organized effort might be made to collect data in the field, a hope which might have more validity in Britain than in some other larger countries. Yates and Little (1979) from the University of Manchester, England reviewed the numbers of patients admitted to the North-West region of England with a coded diagnosis of hypothermia and found a high incidence (327.8/100,000) between the ages of 0--4 yr. There were few cases until the 60-69 age group is reached when the incidence rose to 43/100,000 with a deathrate of 7/100,000. With each decade increase in age there was a substantial increase in the diagnosis of hypothermia with a peak of 414/100,000 at age 90-99 (probably not a very valid statistic as not very many 90-99 year old patients are admitted!). These authors advocated the use of a 'zero-gradient' aural thermometer. Five of 11 patients described survived. One of their patients demonstrated an unusual but important clinical finding--the delayed development of post-traumatic hematoma, confirming an injury not suspected until the patient became warm. Although much has been written about the treatment of hypothermia and the rates of rewarming achievable or achieved with different techniques few calculations have been made of the amount of heat necessary to rewarm a body, and the potential heat gained through various modalities. Myers et al. (1979) described two patients, one passively and one actively rewarmed. In discussing these patients theoretical values were derived for heat

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gain by both central and peripheral rewarming methods. For instance, it was calculated that a patient with a body temperature of 28°C, ventilated with 20 liters/min watersaturated air at 45°C could gain about 0.5 kcal/min, 30 kcal/hr (about half normal metabolic rate). By comparison, shivering can produce 250 kcal/hr. Assuming that a body contains 60 kg water, at least 60 kcal/hr would be required to raise the temperature by one degree. One liter of fluid at 45°C yields 17 kcal of heat to a body at 28°C. Hemodialysis could yield 300°500 kcal/hr, and cardiopulmonary bypass could deliver even more heat. Calculation of heat transfer by external methods such as immersion in warm water is difficult. Heat is transferred through vasoconstricted hand skin at 6 calories/100 cm2/min°C. By making various assumptions calculations indicate that as much as 2400 kcal/hr might be transferred from a water bath at 45°C to a patient at 28°C. These theoretical considerations confirm the clinical experience of the relative efficacies of these methods. Occasionally victims of hypothermic death are found under circumstances suggesting criminal assault. Wedin (1979) obtained 33 cases from police records in Sweden in which the body was found partially or totally naked. In 67~ of instances there was evidence of alcohol or drug consumption. Frequently the victim's clothes were scattered suggesting that they were removed and dropped over a period of time. A possible mechanism for this occurrence is that loss of hypothalamic control causes a feeling of intense heat sufficient to make the victims remove their clothes. Because of the lack of precise information and knowledge about optimal methods for rewarming, experimental papers comparing one method with another still attempt to solve the riddles. Experiments carried out with animals carry the criticism that results from animals cannot automatically be extrapolated to humans--experiments carried out with human volunteers cannot imitate the situation of deep hypothermia, and the forms of exposure are relatively short lived and in healthy volunteers. Harnett et al. (1980) compared inhalation, heating pads, plumbed garments and combinations of these modalities with trunk immersion and spontaneous rewarming in human volunteers who were cooled to 35°C. The least afterdrop was found with trunk immersion which was also the quickest method of rewarming with a rewarming rate of 4.5°C/hr compared with 0.57°C for spontaneous rewarming and 1.03°C/hr for inhalation. The greatest afterdrop was seen with the use of the plumbed suit. The conclusion reached was that inhalation therapy is the only treatment recommended for use in the field. In an unpublished study Manart reviewed the experience at the Denver General Hospital, Denver, Colorado. There were 69 admissions of 68 patients between January 1972 to April 1980. Mortality was correlated with several factors. The overall mortality was 26~o. Those admitted with a temperature below 30°C had a mortality rate of 29.7~: but those with temperatures between 30-34°C had a 22~ mortality rate. Age made no difference to mortality rates. Ten patients, nine of whom were moribund on admission were rewarmed with cardiopulmonary bypass. Three survived. It was felt that temperature, cardiac arrhythmias and severe associated diseases contributed to an increase in mortality rate. Cardiopulmonary bypass should be considered in all patients with temperatures below 30°C with severe arrhythmias. Between February 1971 and March 1980, 114 patients were treated 135 times at the University of Kentucky by Miller et al. (1980). The methods used for rewarming included passive external, active external and heated oxygen aerosol. There were no differences between rewarming rates for passive external warming (0.71°C/hr) and heated oxygen inhalation (0.74°C/hr). Active external methods rewarmed at 0.9°C/hr. Heated oxygen delivered by intubation rewarmed the patient at 1.22°C/hr, a significantly greater rate than passive external warming. The overall mortality rate was 11.9~, but was 47.9~o in patients with serious underlying disease. The mortality rate in 68 patients treated with passive external rewarming was 5.9~. The greatest mortality was in 14 patients rewarmed with heated blankets or in a warm water whirlpool (64.3~o). The lowest mortality rate (5.0~) was in 40 patients treated with heated oxygen delivered by intubation. Because the patients were assigned to different treatment groups on the basis of medical judgment, conclusions

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about the merits of one treatment over another were not possible. But temperature on admission and the presence of underlying disease were found to be important factors influencing outcome. Of nine patients who died six had serious associated diseases. Mortality rates were 4-5.4~o in those only moderately hypothermic, but were 18.5~ if admission temperature was less than 30°C. Only one prospective clinical study of treatment has been published. The contribution of Ledingham and Mone (1980) in developing a 15 yr prospective study was therefore a major step in answering questions about the optimum methods for treatment. Between 1963 and 1978 44 patients were treated at the Western Infirmary, Glasgow, Scotland, and from 1968 all of them were treated in an intensive care unit. The lowest core temperatures recorded were 20°C and all patients had a temperature less than 34.3°C. The precipitating factors were poisoning (drugs, alcohol, coal-gas) in 25 cases and illness in 19. In most patients (42/44) rewarming was achieved by a heat cradle over the torso. Intravenous fluids were warmed, oxygen was administered, arterial and central venous pressures and urine output were monitored and maintained at satisfactory levels. Twelve patients died, two of them during rewarming. Ten of those who died had serious illnesses, only two were intoxicated one by coal gas, the other with alcohol. The mortality rate, therefore, among those intoxicated was 2/25, a much more favorable figure than 10 deaths in 19 patients with underlying disease. Seventeen (39~) of the patients had respiratory problems, 9 were apnoeic. Hypotension was a major problem during rewarming, which was achieved at a rate of about 1.13°C/hr over an 8 hr period. Hypotension occurred in 14 (32~o) patients, and seven of these patients were treated with inotropic agents. In most patients the effect of isoproterenol or dopamine was beneficial. In a retrospective study of 77 patients reviewed at the same time the mortality was found to be 46 patients (60~o) of whom 78~ died during rewarming. The overall conclusion reached was that carefully controlled and monitored rewarming is safe even in the elderly, but uncontrolled rewarming may carry a high mortality rate. The use of drugs should be restricted early during treatment, and in most instances hypotension responds to volume replacement. Few of the patients in the prospective study died of hypothermia; most died from their associated diseases. In two reviews of therapy Bangs (1980) and Bangs and Hamlet (1980) described detailed methods for peritoneal dialysis and inhalation of warmed oxygen, but did not provide any clinical results. The problem of cardiopulmonary resuscitation in the profoundly hypothermic patient contains several separate points of judgment. Should resuscitation be started? How long should resuscitation be continued? Should an alternative method of rewarming or resuscitation be started? All these matters of judgment were raised by the report of Southwick (1980) on the successful resuscitation, after 135min of cardio-pulmonary resuscitation. Several conclusions were reached. First, that resuscitation should be prolonged and that neurological function may be unimpaired even after several hours of resuscitation. Second, that therapeutic manipulations may induce ventricular fibrillation and, therefore, all instrumental intervention should be started with care, and in the knowledge that ventricular fibrillation may be induced. In subsequent correspondence White (1980), from Bellevue Hospital, New York, disputed the argument that treatment caused ventricular fibrillation. In a subset of 11 patients admitted with temperatures less than 26°C refractory ventricular fibrillation started only after starting passive rewarming and the insertion of a peripheral venous line in four cases. Hypoxia, alkalosis or acidosis could not be implicated in the origin of these episodes. Temperature, per se, (less than 26°C) seemed to be an important factor and, at that temperature, the arrhythmia is extremely refractory to treatment. All four of their patients died. White also considered that sinus bradycardia, far from being a benign rhythm, was the precursor of ventricular fibrillation in several of these patients. Manart, in his unpublished study, also found that all the patients who developed ventricular fibrillation in hospital had previously been in sinus bradycardia. In rebuttal Southwick (1980) quoted from the published literature and referred to seven

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cases described separately in which patients were admitted with a palpable pulse but developed ventricular fibrillation soon after treatment was started. He was not aware of reports of patients admitted with established ventricular fibrillation. 'All previous evidence suggests that ventricular fibrillation i~a the hypothermic patient is an iatrogenic complication.' There seems little doubt that'manipulation can induce ventricular fibrillation but so many patients have been intubated, handled and examined in many ways without inducing fibrillation, that it would not seem wise to withhold these maneuvers if they are going to be beneficial on the off chance that they may start ventricular fibrillation. Dorsey (1980), in another letter, raised the legitimate point that Southwick did not discuss the use of cardiopulmonary bypass, and quoted a successful experience of his own. Southwick's patient was treated in a large city hospital where cardiopulmonary bypass was available, and it might be argued that immediate use of bypass, under these circumstances, might be better than prolonged external cardiac massage. Hypothermia is known to occur as a complication of hypoglycemia, and hypoglycemia may occur as a complication of hypothermia. Blood sugar levels are unpredictable in hypothermic patients. Fitzgerald (1980) examined the case records of 22 patients, mostly alcoholics, who were admitted because of hypothermia to San Francisco General Hospital between 1975 and 1977. The highest blood sugar level was 314 mg~, and the lowest was 13 mg~. A blood sugar level less than 50 mg~ was taken as hypoglycemia, and 41~o (9 patients) were found to have blood sugar levels below that. Four of these nine patients died. There was no relationship between depth of hypothermia and blood glucose level. Because of the high frequency of hypoglycemia it was suggested that all hypothermic patients should be given 50~o glucose solution after a blood specimen has been drawn for a blood sugar level. Because hypothermia may cause renal tubular glycosuria the presence of sugar in the urine does not guarantee that an adequate blood sugar level exists. Further evidence of the usefulness of urinary bladder temperature measurements was provided by Lilly (1980) who designed a Foley-type urinary catheter which included a temperature probe. A comparison was made, in patients undergoing general anesthesia, of urinary bladder and esophageal, pulmonary arterial and rectal temperatures. A close correlation was found between bladder temperature and temperatures at these other sites. The measurement of urine temperature, as suggested by Fox (1971), is a practical method for obtaining core temperatures when the taking of a rectal temperature might be impractical. The method of Lilly using a specially modified Foley catheter may prove to be a good method for continuous monitoring of temperature in hospital. Cold water drowning is a special problem in many ways. The victim is cooled fairly rapidly, but at the same time is hypoxic. The incidence of neurologic damage is high. Young (1980) described a seven year old boy who was found floating face downwards in icy water after 15 min of immersion. He had neither pulse nor respirations on arrival at hospital, and a pulse was not established for 2.5 hr. His temperature was 27°C. One day later he was stuporous, by four days he was breathing spontaneously and by three weeks he was walking with assistance. By three months his motor skills were almost normal and six months later he followed normal advancement at school. In a search of the literature the author found 14 similar cases with three deaths and 11 complete recoveries. While hypothermia may be protective, it also indicates prolonged immersion and is, therefore, a bad sign. However, the reports of complete recovery should encourage physicians not to give up prematurely, and to use every available means for monitoring and treating such patients. A report of 10 cases of hypothermia from Tampa, Florida, (Altus et al., 1980) confirmed that this problem is not confined to cold climates. Four of his patients had important aspects to their cases. One could not be resuscitated in spite of thoracotomy, open cardiac massage and rewarming with saline irrigation. A second case, an elderly woman was found naked from the waist downwards, and was thought to have been a rape victim. The third patient developed frostbite and the fourth patient had pulmonary emoboli. Metabolic changes in the elderly during and after hypothermia were measured in 43 patients by Stoner et al. (1980). Core temperatures were measured with a zero-gradient

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aural thermometer. Plasma concentrations of glucose, lactate, non-esterified fatty acids, glycerol, ketone bodies, amino acids, cortisol, insulin and ethanol were measured soon after admission to hospital. There was no obvious precipitating illness in half the patients and only 7 of these 22 patients died (32~). In comparison, 16 of 21 (76~) with precipitating illness died. The concentrations of energy yielding substrates were high, suggesting mobilization of body fuel stores. There was also evidence of lipolysis, breakdown of muscle glycogen, and proteolysis. Glucose concentrations were high in patients with hypothermia of short duration and in those with body temperatures below 29°C. Glucose utilization is reduced below 30°C. Cortisol levels were high and, therefore, there is no need to give supplemental steroids. Metabolic disturbances soon returned to normal after the patients were rewarmed. It was concluded that rewarming was more important therapeutically than attempting to intervene metabolically. Abnormalities of coagulation are not usually a major problem in hypothermic patients. If anything, the tendency is towards thrombotic vascular complications. Disseminated intravascular coagulation (DIC) has been described in cold infants and Mahajan (1981) reported its occurrence in a 13 yr old boy. He had drunk an excessive amount of alcohol and passed out while walking home when the ambient temperature was -4°C. He was found unconscious 14 hr later with a rectal temperature of 22°C. His heart stopped shortly after admission to hospital. After resuscitation he started to bleed from his gastrointestinal, genito-urinary and respiratory tracts. He died 4 hr later. Mahajan could find only one other report of DIC in a non-neonatal hypothermic patient, but believes that the condition may be commoner than reported. With an increasing awareness of hypothermia as a problem, and with the increasing use of low reading thermometers or thermistor probes in emergency rooms and hospitals, unusual cases of hypothermia will be increasingly reported. Murray (1981) treated a 49year old woman who was admitted semi-comatose with a rectal temperature of 30.5°C and with the smell of alcohol on the breath. Subsequent investigation demonstrated a pH of 6.67, pO2 91 mmHg, pCO2 13 mmHg, bicarbonate 1.5 mEq/liter and abnormalities of liver function. An arterial lactate level was 180 mg~o. After rewarming and energetic treatment to replace her anion deficiency she recovered. The severity of acidosis with recovery may be unique, and her recovery was probably due to the protective metabolic effect of hypothermia. Schissler (1981) recounted what may be the most prolonged successful resuscitation of a patient. A 67 year old woman was admitted at 18:35 hr with a heart rate of 20/rain and a temperature of 22.2°C. during intubation the patient fibrillated. Because ventricular fibrillation was intractable peritoneal dialysis was started. After 3.5 hr of resuscitation combined with dialysis cardiac action was restored. The patient was eventually discharged after a lengthy hospital stay. As in Southwick's (1980) case the question might be raised about the reasons for not using cardiopulmonary bypass which might have provided greater hemodynamic control and more rapid rewarming. A small but intriguing description was provided by Bowesman (1981) of what might be called the hypothermic's 'snorkel'. Two 36 mm polypropylene tubes are arranged together to enable someone to sleep completely covered by blankets with one end of the apparatus in his mouth, the other end outside the blankets acting as an air inlet, and an outlet for CO 2. This apparatus not only permits breathing in this way, but as the person is completely covered the temperature in the bed increased by 1.1.°C/min for 15 min, and 0.6°C/min for a second 15 min. Another study comparing the response ol~ young and old to cold was carried out by Collins et al. (1981). Seventeen men over 70 years old 13 young adults were studied in a controlled environment room. After a period of stabilization the subjects were asked to manipulate room temperature to maintain it at a level of personal comfort. The mean preferred temperatures were almost the same in both groups: 23.0 +__2.3°C in the old and 22.7 __+1.2°C in the young. Five of the 17 old people were found to have poor temperature discrimination and poor control of ambient temperature, perceiving peripheral temperature changes inaccurately. The evidence supported previous findings that elderly

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people are physiologically impaired in their ability to perceive temperature changes and maintain a constant euthermic body temperature. 7. S U M M A R Y C O M M E N T Knowledge of the effects of hypothermia has increased greatly over the past 25 yr. Thousands of patients have been cooled intentionally in the operating room, and hundreds of thousands of living hearts have been temporarily stopped by cold cardioplegia and restarted without difficulty or apparent ill-effect. Yet in spite of the acquisition of this vast body of clinical experience an aura of mystery stills surrounds the patient who becomes hypothermic accidentally. The best treatment in any particular case is not always clear, and published accounts do not always give the impression that the hypothermic patient is treated with the same rational approach with which other sick and comatose patients are treated. In summarizing, therefore, conclusions that might be reached from reviewing past experience several important points emerge. (1) The severely hypothermic patient should be treated in an intensive care unit where appropriate monitoring of temperature, cardiovascular function and respiratory function are available, and where full respiratory support including assisted ventilation can be given. (2) The final outcome depends upon the etiology. The young healthy victim of exposure has a good chance of suriviving. The patient poisoned by alcohol or barbiturates has a good chance of surviving provided the level of intoxication is not itself lethal. The elderly without severe underlying disease have a good chance of surviving. The patient with severe underlying disease of the endocrine, cardiovascular or neurologic system probably has, at best, a 50~ chance of surviving and, at worst, a chance of only 10-20~, depending upon the associated disease. (3) There is no statistical evidence that any one method of rewarming is significantly better than any other. But there is anecdotal evidence that in the absence of full monitoring and support systems slow rewarming is safer than over-energetic external rewarming. Internal rewarming, peritoneal dialysis, hemodialysis, inhalation of warmed oxygen and extracorporeal circulation are effective in severe cases and can be used with safety. (4) The causes of, and triggering mechanism for, ventricular fibrillation are still largely unknown but the onset of ventricular fibrillation in a very cold patient may often be an irreversible complication. The place of modern anti-arrhythmic drugs in the prevention and management of this complication has yet to be elucidated. (5) Cardiopulmonary resuscitation is difficult in profoundly hypothermic patients but should be maintained until a body temperature of 30°C has been achieved. This is particularly true in the young and healthy. (6) In the asystolic, hypothermic patient the most efficient rewarming method available should be used. In optimum circumstances extracorporeal circulation provides circulatory support, rewarming and metabolic control. (7) Under all circumstances the rewarming method chosen should be appropriate to the clinical problem. REFERENCES ALEXANDERL. (1945) The treatment of shock from prolonged exposure to cold, especially in water. London, Combined Intell. Obj. Subcomm. (Forms file No. XXVI-37, Item No. 24, CIOS report). ALTUS,P., HXCKMAN,J. W., PINAI. and BARRY,P. P. (1980) Hypothermia in the sunny south. South Med. J. 73: 1491-1492. ANDERSON,S., HERBRING,B. D. and WIDMAN,B. (1970) Accidental profound hypothermia. Brit. J. Anaesthes. 42: 653-655. ANGEL,J. H. and SASR,L. (1960) Hypothermia coma in myxedema. Br. reed. J. 1: 1855--1859. BADEER,H. (1958) Ventricular fibrillation in hypothermia. J. Thorac. Surg. 35: 265-273. BANGS,C. (1980) Disturbances due to cold. In: Current Therapy, pp. 910-918, CONN(ed.) W. B. Saunders, Philadelphia. BANGS,C. and HAMLET,M. (1980) Out in the cold. Topics in Emerg. Med. 2: 19-3]. BARRATT-BOYES,B. G., SIMPSON,M. M. and NEUTZE,J. M. (1971) Intracardiac surgery in neonates and infants using deep hypothermia. Circulation 43 (Suppl): 25-30.

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BLAIR, E., MONTGOMERY, A. V. and SWAN, H. (1956) Posthypothermic circulatory failure. I. Physiologic observations on the circulation. Circulation 13: 909-915. BOWESMAN, R. (1981) Urban hypothermia. Dr. reed. J. 1: 474. BRANCH, E. F., BURGER,P. C. and BREWER, D. L. (1971) Hypothermia in a case of hypothalamic infarction and sarcoidosis. Arch. Neurol. 25: 245-255. BRISTOW, G. (1978) Treatment of accidental hypothermia with peritoneal dialysis. Can. reed. Ass. J. 118: 764. BROWN, E. B. and MILLER, F. (1952) Ventricular fibrillation following a rapid fall in alveolar carbon dioxide concentration. Am. J. Physiol. 169: 56-60. CHADD, M. A. and GRAY, O. P. (1972) Hypothermia and coagulation defects in the newborn. Arch. dis. Child. 47: 819-821. COLLINS,K. J., nORl~,C., EXTON-SMITH, A. N., FOX, R. H., MACDONALD, I. C. and WOODWARD,P. M. (1971) Accidental hypothermia and impaired temperature homeostasis in the elderly. Dr. reed. J. i: 353-356. COLLINS, K. J., EXTON-SMITH,A. N. and DORfL C. (1981) Urban hypothermia: preferred temperature and thermal perception in old age. Dr. reed. J. 282: 175-177. COMMITTEE ON ACCIDENTAL HYPOTHERMIA. (1966) Royal College of Physicians, London. COOPWOOD,T. B. and KENNEDY,J. H. (1971) Accidental hypotherma. Cryobiology 7: 243-247. COUGHLIN, F. (1973) Heart warming procedure. N. Engl. J. Ned. 288: 326. CRAIG,R. W. (1980) In: Storm and Sorrow in the High Pamirs, p. 208, Simon and Schuster, New York. DAVIES, D. i . , MILLER, I. A. (1967) Accidental hypothermia treated by extracorporeal blood warming. Lancet i: 1036-1037. DAYTON, L. B. and Arnold, J. W. (1975) Hydraulic sarong. O f f B e l a y 21: 2-4. DORSEY, J. S. (1980) Venoarterial bypass in hypothermia. J. Am reed. Ass. 244: 1900. DUCKWORTH, W. C. and COOPER, B. C. (1964) Accidental hypothermia in the Bantu. S. Afr. reed. J. 38: 295-298. DUGUID, H., SIMPSON, R. G. and STOWERS, J. M. (1961) Accidental hypothermia. Lancet ii: 1213-1219. EDDY, T. P., PAYNE, P. R., SALVOSA,C. and WHEELER, E. F. (1970) Body temperatures in the elderly. Lancet ii: 1088. EDITORIAL (1973) Deadly cold. Dr. med. J. i: 203-204. EDITORIAL COMMENT (1972) Treatment after exposure to cold. Lancet i: 378. EDITORIAL (1978) Rewarming for accidental hypothermia. Lancet i: 251-252. EDITORIAL (1978) Treating accidental hypothermia. Dr. med. J. ii: 1383-1384. EMSLIE-SMITH, D. (1958) Accidental hypothermia: a common condition with a pathognomonic electrocardiogram. Lancet ii: 492-495. EXTON-SMITH, A. N. (1973) Accidental hypothermia (rev.). Dr. reed. J. 4: 727-729. FELL, R. H., GUNNING, A. J., BARDHAN, K. D. and TRIGER, D. R. (1968) Severe hypothermia as a result of barbiturate overdose domplicated by cardiac arrest. Lancet i: 392-394. FERNANDEZ, J. P., O'ROURKE, R. A. and EwY, G. A. (1970) Rapid active external rewarming in accidental hypothermia. J. Am. reed. Ass 212: 153-156. FITZGERALD, F. T. (1980) hypoglycemia and accidental hypothermia in an alcoholic population. West. J. Ned. 133: 105-107. Fox, R. H., DAVIS, T. W., MARSH, F. P. and URICH, H. (1970) Hypothermia in a young man with an anterior hypothalamic lesion. Lancet ii: 185-188. Fox, R. H., WOODWARD, P. M., FRY, A. S., COLLINS, J. C. and MACDONALD K. (1971) Diagnosis of accidental hypothermia of the elderly. Lancet i: 424-427. Fox, R. H., WOODWARD,P. M., EXTON-SMITH,A. N., GREEN, M. F., DONNISON, D. V. and WICKS, M. H. (1973) Body temperatures in the elderly: a national study of physiological, social and environmental conditions. Dr. reed. J. i: 200-206. Fox, R. H., MACGIBBON,R., DAVIESand WOODWARD, P. (1973) Problem of the old and cold. Br. reed. J. i: 21-24. FREEMAN, J. and POGH, L. G. C. E. (1969) Hypothermia in mountain accidents. Int. Anesthesiol. Clin. 7: 997-1007. FRUEHAN, A. E. (1960) Accidental hypothermia. Arch. intern. Ned. 106: 218-229. GOLDEN, F. S., HERVEY, G. R. and WILLIAMS,J. M. (1977) Evidence from computer simulation for a conductive mechanism for the after-drop of body temp after immersion hypothermia. J. PhysioL 271: 66. GREGORY, R. T. (1971) Accidental hypothermia: Part I. An Alaskan problem. Alaska Ned. 13: 134--136. GREGORY, R. T. and PATTON, J. F. (1972) Treatment after exposure to cold. Lancet i: 377. GREGORY, R. T. and DOOLITTLE, W. H. (1973) Accidental hypothermia II: clinical implications of experimental studies. Alaska Ned. 15: 48-52. GROSSHEIM, R. L. (1973) Hypothermia and frostbite treated with peritoneal dialysis. Alsaka Ned. 15: 53-55. HARARI, H., REGNIER, B., RAPIN, i . , LEMAIRE, F. and LE GALL, J. R. (1975) Hemodynamic study of prolonged deep accidental hypothermia. Eur. J. Intensive Care Ned. 1: 65-70. HARNETT, R. M., O'BRIEN, E. M., SIAS, F. R. and PRUITT,J. R. (1980) Initial treatment of profound accidental hypothermia. Aviat. Space environ. Ned. 51: 680--687. HAUSMAN,W. (1970) Myxedema crisis. Hormones 1: 110-128. ]-IAYWARD,J. S. and STEINMAN,A. M. (1975) Accidental hypothermia: an experimental study of inhalation rewarming. Aviat. Space Environ. Ned. 46: 1236-1240. HEGNAUER, A. H., D'AMATO, H. D. and FLYNN, J. (1951) Influence of intraventricular catheters on the course of immersion hypothermia in the dog. Am. J. Physiol. 167: 63-68. HILLMAN, H. (1971) Treatment after exposure to cold. Lancet ii: 1257. HILLMAN, H. (1972) Treatment after exposure to cold. Lancet i: 141, 378. HOCKADAY, T. D. R., CRANSTON, W. I., COOPER, K. E. and MOTTRAM R. F. (1962) Temperature regulation in chronic hypothermia. Lancet ii: 428-432. HOUSTON, C. (1980) In: Going High, p. 29, CHARLES S. HOUSTON and American Alpine Club. HUDSON, L. D. and CONN, R. n . (1974) Accidental hypothermia--associated diagnoses and prognosis in a common problem, d. Am. reed. Ass. 227: 37-40.

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HUDSON, M. C. and ROBINSON, G. J. (1973) Treatment of accidental hypothermia. Med. J. Aust. 1: 410-411. HUNT, P. K. (1975) Treatment of hypothermia. Can. reed. Ass. J. 19: 112-113. HUNTER, JOHN (1786) Experiments and observations on animals with respect to the power of producing heat. In: Observations on Certain Parts o f Animal Oeconomy, London. JESSEN, K. and HAGELSTENJ. O. (1978) Peritoneal dialysis in the treatment of profound accidental hypothermia. Aviat. Space environ. Med. 49: 426-429. JOHNSON, L. A. (1977) Accidental hypothermia: peritoneal dialysis. J.A.C.E.P. 6: 556-561. KEATINGE, W. R. (1965) Death after shipwreck. Br. reed. J. 2: 1537-1540. KEAT1NGE,W. R. and SLOAN,R. E. G. (1973) Measurement of deep body temperature from external auditory canal with servo-controlled heating around ear. J. Physiol. 234: 8P-9P. KUGELBERG, J., SCHULLER, H., BERG, B. and KALLUM, B. (1967) Treatment of accidental hypothermia. Scand. J. thorac, cardiovasc. Surg. 1: 142-146. LARREY, D. J. 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