Anaesthesia, 1979, Volume 34, pages 250-256 REVIEW ARTICLE
Accidental hypothermia
S.W.C O N I A M
Accidental hypothermia may result from exposure to a cold environment or from inadequate heat conservation. Impairment of normal body temperature control may be due to old age, immaturity of temperature regulation as in neonates, or to a hypothalamic or thyroid disorder. An uncommon cause is the condition of erythroderma. Accidental hypothermia can result indirectly from immobility due to cerebrovascular accident, myocardial infarction, neurological disease or from self poisoning with drugs or alcohol. Exposure on mountain sides or immersion in cold water are common causes of hypothermia even in young, healthy persons. Most authorities would consider any person with a rectal temperature below 35°C to be suffering from hypothermia, but it is difficult to give a precise definition. A General Practice survey of septuagenarians in Orkney,' found that 8% had temperatures of 35°C or less, without obvious cause. A survey2 of geriatric hospital admissions found 3.6% to be hypothermic and it was noted that there was a high mortality (45%) when this condition was associated with old age. There appears to be a decrease in the thermoregulatory response with increasing age.3 There is a smaller corelperipheral temperature gradient, lower peripheral blood flow and an inadequate vasomotor response to cold. Physiology
Laboratory animals differ from man in their mechanisms of temperature regulation and
therefore make poor models in the study of accidental hypothermia. Man relies heavily on behavioural adaptation in control of body temperature. Some of the few experiments on hypothermia in humans were carried out on prisoners in Dachau in 1942. The human responses to temperature change include sweating, changes in vasomotor tone and shivering. Vasomotor control alone can probably adjust heat conservation from 0.15 to 0.75 clo units.' Body contour and fat distribution vary between individuals, but the Perth geriatric unit5 found an equal distribution of body types among hypothermic admissions. Shivering increases heat production by about five times, but it also increases the rate of heat loss. Loss of body heat increases in a linear fashion, whereas heat production rises geometrically with increasing temperature. In the range 33-38"C, the body can balance heat loss with increased heat production. However, below about 33°C the body cannot produce enough heat to compensate for losses, and below about 22"C,when survival is unlikely, the body temperature responds to the environmental temperature in a poikilothermic manner.
Cardiovascular system In the range of erective response to cold (approximately down to 33°C) pulse rate increases along with shivering and increased sympathetic stimulation. Below this range, the pulse rate falls, rapidly at first and then
S.W.Coniam, MB, BChir, Registrar, Department of Anaesthetics, Hallamshire Hospital, Sheffield S10 2RX.
250
0003-2409/79/03~250$02.0001978 Blackwall Scienti5c Publications
Accidental hypothermia
more gradually, unless dysrhythmias occur due to depression of intracardiac conductivity, inhibition of normal centres of impulse formation and increased myocardial irritability. The electrocardiograph (ECC)
The QRS segment lengthens, followed by lengthening and depression of the ST interval and a variety of inconstant T wave changes occur in hypothermia. Slowing results from prolongation of systole but the widening of the QRS complex and ST interval is greater than can be attributed simply to slowing of the heart rate. Often a Q wave (abnormal initial negative deflection) or an R’ wave (abnormal second positive deflection) is present.6 The P wave decreases in amplitude. Particularly characteristic of hypothermia is the J wave, described by Osborn in 1953.’ This is a positive-negative deflection following the QRS complex. Its aetiology is unknown, although it has been suggested that it is due to a current of injury. As the temperature falls, dysrhythmias frequently develop. These may start as an atrial ectopic focus or wandering pacemaker, atrial fibrillation (resulting in an abrupt increase in heart rate), ventricular extrasystoles or tachycardia. Ventricular fibrillation may develop without any previous changes of rhythm, especially in the range 2628°C and may appear as groups of waveform complexes.* Young patients maintain sinus rhythm for longer than older patients. Ventricular fibrillation seems to be the commonest cause of death in hypothermia but no single precipitating cause has been isolated. A fine muscle tremor, often present, may produce artefactual changes on the ECG. The initial reaction to cold is peripheral vasoconstriction, resulting in an increased volume of blood in the capacitance vessels, especially in the lungs and liver, producing an increased load on the heart. Stimulation of central volume receptors may be one cause of the diuresis associated with cold. Vasoconstriction may alternate with vasodilatation, known as ‘Lewis’ hunting r e f l e ~ ’There . ~ is a progressive fall in blood pressure.
Blood An initially high haematocrit (up to 60% has
251
been reported) and raised haemoglobin content is due to the movement of plasma out of the peripheral circulation into the tissues. Another factor involved in producing a raised haematocrit is the considerable diuresis which often occurs in the early stages due to decreased renal tubular function. However, with rewarming and the administration of intravenous fluids, the haemoglobin gradually falls over the subsequent few days. This is due to dilution, as the red cell mass does not change. Slight haemolysis with haemoglobinuria is only rarely seen. The oxygen dissociation curve for haemoglobin shifts to the left as temperature falls, decreasing oxygen release to tissues. However, the increased solubility of oxygen and the decreased metabolic rate may partially compensate for this effect. It is thought that hypothermia has little effect on total body oxygen stores.’O There is usually a fall in blood pH, partly due to increased solubility of carbon dioxide, resulting in carbon dioxide retention. It is important to remember that unless results are corrected for temperature, blood gas results can be misleading, masking the degree of hypoxia. The methods suggested by Severinghausll or Marshall & Gunning1* can be used to correct measurements made at 37°C to values which are correct for the temperature of the patient. When measured at 37”C, pH readings are falsely low for the hypothermic patient. The Rosenthal formula suggests adding 0.15 pH units to the reading for each 10°C below normothermia. Respiration
Respiratory rate usually increases initially, particularly in sudden hypothermia following immersion. This may result in tetany. However, as the vital centres become depressed, respiration progressively decreases until eventually apnoea occurs. Renal function
Cold depresses enzyme activity in the distal renal tubule, resulting in decreased reabsorption (especially of glucose) and decreased secretion. A fall in glomerular filtration rate, independently of the fall in systolic blood pressure, results in azotaemia. Failure of tubular reabsorption is
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S. W. Coniam
probably the main cause of the ‘cold diuresis’. An oliguric phase often follows during rewarming.
become progressively depressed as body temperature falls. Pathological changes
Metabolism
As mentioned above, shivering greatly increases the metabolic rate but also increases heat loss, and as the temperature falls, metabolism becomes depressed. The Van? Hoff Arrhenius law14 states that the metabolic rate halves for every fall of 10°C. A respiratory alkalosis may occur initially, but this usually progresses to a mixed acidosis. There is decreased uptake of glucose by cells, either due to inhibition of insulin activity or inhibition of hexokinase, the latter being particularly temperature sensitive.15Plasma glucose levels may be well above 12 mmol/litre without ketoacidosis. This resolves spontaneously and the patient usually has a normal glucose tolerance test following recovery. Glucose administered during hypothermia tends to stay in the extracellular compartment and draws water from the cells to dilute the extracellular fluid. Plasma sodium and protein fall by predicted amounts.16 This presents an argument against giving large quantities of dextrose in hypothermia. A fall of plasma pH causes potassium to move out of cells and as diuresis proceeds, much of this may be lost in the urine. Liver function tests are usually normal except for a low plasma protein. In one s e r i e ~eleven ,~ out of fifteen patients had a raised serum amylase. Five of these had autopsy evidence of pancreatic necrosis. The observed increase in morbidity when hypothermia is associated with physical exhaustion may be due to lack of glycogen storage in muscles. In cases of exhaustion, a raised serum nitrogen, creatinine, creatine phosphokinase, lactate dehydrogenase and serum glutamate oxaloacetate transaminase may be found, along with haemoglobinuria and myoglobinuria. Central nervous system
Below 31°C there is progressive paralysis of the central nervous system, and most patients are unconscious at temperatures below 28°C. Reflexes are lost at much lower temperatures. The respiratory and cardiovascular centres
Specific pathology is difficult to interpret as many hypothermic patients are elderly with a variety of coincidental disease. All cases develop fatty change in the myocardium, liver, renal tubules and zona reticularis of the adrenals. Changes compatible with shock or hypoxia are found in the gut, pancreas, parotids and brain, with perivascular haemorrhages in the third ventricle, and petechiae in the leptomeninges. Multiple infarcts found in many organs are caused by stagnation of blood and sludging of red cells. Pancreatitis is common.17
Diagnosis
If a cold patient is found in a cold environment the diagnosis is usually self evident, but it may be difficult to separate the severely hypothermic from the dead. An unconscious patient who is cold and rigid with fixed dilated pupils and undetectable pulse or respiration is worth resuscitation attempts if hypothermia is suspected. A euthyroid individual may give the appearance of severe hypothyroidism when suffering from prolonged hypothermia. The body is remarkably well preserved at low temperatures and prolonged absence of circulation is not a contraindication to resuscitation. Following experimental coronary artery occlusion in dogs, cooling to 32°C resulted in a three-fold increase in survival, compared with normothermic dogs. Hypothermia was found to have a positive inotropic effect on the myocardium.18 In a Canadian report a young man with apparent cardiac arrest for l t h at a temperature of 252°C made an eventual complete recovery.1g A similar case is reported from Denmark,’O and the difference in mortality between children in drowning accidents in Norway and California suggests a protective effect of cold in the former.21 Fixed dilated pupils or a flat electroencephalograph are not reliable signs of death in hypothermia and resuscitative attempts should not be abandoned until the patient has been adequately rewarmed. It is notable that both hypothermia and alcohol prolong hypoxic survival of neurones, although alcohol also increases heat loss by vasodilatation.
Accidental hypothermia Management The patient should be removed from the adverse environment with a minimum of handling and covered with a blanket. External cardiac massage, tracheal intubation or insertion of oesophageal temperature probes may precipitate ventricular fibrillation.2 Attempts at electrical defibrillation or the use of antiarrhythmic drugs are usually ineffective whilst the temperature is below 28°C and are best avoided. Defibrillation is advisable if ventricular fibrillation develops during warming, when the temperature is between 28-30°C. In many cases reported, ventricular fibrillation has only developed following admission to hospital. The patient is best managed in an intensive care unit. Initial investigations should include measurement of pH and blood gases, haemoglobin level and white cell count, urea and electrolytes, glucose, blood culture, amylase, and screening for barbiturates and salicylates. A chest X-ray and ECG are taken and at some stage, thyroid function must be assessed. Observations can be limited to pulse rate, blood pressure, rectal temperature, fluid balance, conscious level and ECG monitoring. Although oesophageal temperature gives a more accurate measurement of cardiac temperature, a rectal temperature probe results in less disturbance to the patient at a time when dysrhythmias are likely to develop. There are two much debated approaches to rewarming, slow passive, and rapid active. Also warming may be external or internal. There is general agreement that the victim of sudden immersion with rapidly produced hypothermia is best warmed rapidly by immersion of the trunk in a warm bath (40-42°C). The limbs should be kept out of the bath, because warming the periphery before the core results in a rapid return of cold blood to the heart. Even if this precaution is observed, core temperature usually falls 2-3°C after immersion in the warm bath. This is called the ‘afterdrop’.4.5.24 Rewarming of the patient who has suffered from prolonged hypothermia presents a greater problem. Fernandez2 used rapid external warming with a hyperthermic mattress and points to the failure of some previous series which used a less active approach, and the
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success of rapid rewarming in the Dachau experiments. Rapid surface rewarming has been recommended by others.26 Meriwether & Goodman14 advocate immersion in a warm bath. Most authors who have used surface warming advise against warming the limbs, as a rapid return of cold stagnant blood to the heart seems likely to precipitate dangerous arrhythmias, results in a further fall in core temperature and a catastrophic fall in blood pressure due to loss of peripheral resistance. External warming does, however, result in an increase in the metabolic needs of peripheral tissues, further reducing the oxygen available to essential organs. Skin warming may also inhibit endogenous heat production. Many methods of central rewarming have been used. Kugelberg et at.’’ report the use of iliac artery to iliac vein bypass using a heart lung machine with a heat exchanger. They used this method to raise the temperature of one patient from 21.4 to 35°C over a period of 72 min. At 22.5”C atrial fibrillation reverted spontaneously to sinus rhythm. The advantages claimed for the method are that the temperature can be raised rapidly above the critical level of 28°C and that the heart receives warm blood directly and is therefore less likely to fibrillate. If ventricular fibrillation does develop, then the circulation can be maintained until normal rhythm is restored. Wickstrom el aLZ8report a similar technique and add that their cases showed no response to cardiac massage or defibrillation until a temperature of 32°C had been reached. They stress that the threshold for ventricular fibrillation is decreased by acidosis and increased by alkalosis. In hypothermia the oxygen dissociation curve shifts to the left and this is increased by alkalosis, making tissues more hypoxic. Some authors have recommended the use of hydrochloric acid to produce a shift of the curve to the right, but this is not generally accepted.28It is suggested that over treatment with bicarbonate ions may add to the difficulty of defibrillating the heart. Pickering et aLZ2used peritoneal irrigation in a patient with a rectal temperature of 26-4”C following unsuccessful resuscitation with surface warming, warmed intravenous infusion and gastric lavage. Irrigation of the peritoneal cavity with an isotonic dialysis fluid at 38°C was successful with eventual complete recovery
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following a 311 h cardiac arrest. They suggest this as the method of choice as it is almost universally available, even in small units, and is a simple technique with low morbidity compared with bypass methods. In the Canadian report mentioned above,I9 the patient suffering exposure with physical exhaustion, was treated with hot, wet towels, hot water bottles, warm enemas and gastric lavage. Ventricular fibrillation developed during warming, but this responded to electrical defibrillation. After 24 weeks recovery was complete, except for a ‘Simian’ deformity of the hands, thought to be due to a peripheral neuropathy. Central rewarming through the airway is often used. The author has treated a patient with a rectal temperature of 22~8°Cwho was successfully managed by very slow central rewarming. He was covered with a ‘spacerescue’ blanket, given a warmed (37°C) intravenous infusion, and allowed to breath oxygen enriched air warmed in an East Radcliffe humidifier containing water at 60°C. A more active approach is recommended by Lloyd24-29 using carbon dioxide from a ‘sparklets’ bulb in conjunction with soda lime in a modified Water’s system. This exothermic reaction heats the inspired gas and the simple portable apparatus can be used at the scene of accidents and provides core rewarming. Lloyd also uses a conventional humidifier with water at 60°C and reports only one case of laryngeal oedema and mild airway scalding. He found no ECG abnormalities following tracheal intubation, and no ‘afterdrop’ using these methods. The lungs are a very efficient heat exchange system. Apart from actively supplying a small amount of heat through the lungs in this way, normal heat loss via the lungs is minimised, thus making 25-30% more metabolic heat available (30 kcal/m2/h at 30°C). The effectiveness of rewarming through the airway is confirmed by a series of experiments on human volunteers by Collis et Hudson & Conn3’ stress that the underlying condition is probably more important in determining survival than the method of rewarming. They suggest that slow passive rewarming can be expected to be suceessful in patients with intoxication or mental abnormalities, but is less so following shock, infections or myocardial infarction. They also stress that
it is a waste of time treating underlying conditions prior to rewarming. Respiratory support
Problems associated with tracheal intubation have already been mentioned and it would seem reasonable to avoid this in the early stages, if possible. However, many hypothermic patients are apnoeic or unable to maintain an adequate airway and the majority of cases described in the literature have been intubated, with or without intermittent positive pressure ventilation (IPPV). Even though the arterial oxygen tension is apparently satisfactory, correction for measurement at the patient’s temperature may reveal considerable hypoxia. Oxygen enrichment of the inspired air is desirable, although in a patient breathing spontaneously there is a danger of carbon dioxide narcosis because an unsuspected hypoxic drive is removed. Some casesL9have been reported to develop pulmonary oedema during rewarming, but this has responded to treatment with IPPV and diuretics. Cardiovascular system
Dysrhythmias commonly revert spontaneously above 28-30°C and should probably be ignored at lower temperatures. Electrical defibrillation may be necessary in this range, but antiarrhythmic drugs should be avoided. Atropine is often used to treat profound bradycardia during rewarming. Renal
The cold diuresis may have several causes, but fluid balance should be maintained with a warmed infusion of dextrose/saline. Following rewarming oliguria may occur, but this generally responds to diuretics. During the diuretic phase, potassium replacement is necessary. Drug therapy
Corticosteroids (hydrocortisone 200 mg or methyl prednisolone 30 mg/kg 4 hourly intravenously) are usually given for a variety of reasons. The effect of stabilising lysosomal membranes in tissues damaged by a stagnant circulation may be important. Another ex-
Accidental hypothermia planation for the use of hydrocortisone is that normal output of corticotrophin and adrenal hormones are depressed in hypothermia. Hypoadrenalism may be partly responsible for the ‘shock’ seen occasionally during rewarming. Some workers have used vasoconstrictors to raise the blood pressure and maintain vasoconstriction during rewarming. The Canadian team used an infusion of dopamine to maintain cardiac output. Cerebral oedema has been suggested as a cause of deathz4 and this may justify the use of steroids. Triiodothyronine (10 pg twice daily) has a place where hypothyroidism is the cause of hypothermia, but it should be administered after rewarming. Most authors2z*27*z8 quote a high rate of respiratory tract infection during recovery, and for this reason, the patient should be started on prophylactic antibiotics at an early stage. It may be better to wait for definitive diagnosis before this line of treatment is started, and more specific drugs should be used in conjunction with physiotherapy. Conclusions
From this review of the literature, certain main recommendations in the management of hypothermia seem to be agreed. Minimal handling and movement of the patient must be the aim. Rewarming of the trunk in a warm bath in cases of sudden hypothermia following cold water immersion is indicated. In other cases, gradual rewarming via the airway or peritoneum, together with adequate thermal insulation should be undertaken. A rate, of temperature rise of 4-1 “Cper hour is suggested. Fluid overloading should be avoided, especially with dextrose. The ECG should be monitored and antiarrhythmic drugs avoided, but electrical defibrillation may be necessary if ventricular fibrillation develops around 28°C. Added oxygen, airway support and mechanical ventilation may be necessary. A cuffed tracheal tube may be of benefit in reducing the high incidence of aspiration pneumonia. The administration of corticosteroids and antibiotics, if specifically indicated, may be thought necessary. Summary The physiological changes associated with accidental hypothermia are considered. Current
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methods of management of the hypothermic patient are reviewed. Key words HYPOTHERMIA; physiology, treatment. Acknowledgments The author wishes to thank Dr H.G. Schroeder for his advice in the preparation of this review, and Mrs J. Gosney for her secretarial assistance. References 1. COLLACOTT, R.A. (1975) Screening for hypothermia in Orkney. Journal of the Royal College of General Practitioners, 25, 647. A,, EXTON-SMITH, A.N., FRANCIS, 2. GOLDMAN, G.& O’BRIEN,A. (1977) A pilot study of low body
temperature in old people admitted to hospital. Journal of the Royal College of Physicians, 11, 291. 3. EDITORIAL(1977) The old in the cold. British Medical Journal, 1, 336.
4. HERVEY, G.R. (1973) Physiological changes encountered in hypothermia. Proceedings of the Royal Society of Medicine, 66, 1053. 5 . DUGUID,H.,SIMPSON, R.G. &STOWERS, J.M.(1961) Accidental hypothermia. Lancet, 2. 1213. 6. MICKS, C.E., MCCORD, M.C. & BLOUNT,S.G. (1956) Electrocardiographic changes during hypothermia and circulatory occlusion. Circulation, 13, 21.
7. OSBORN,J.J. (1953) Experimental hypothermia: respiratory and blood p H changes in relation to cardiac function. American Journal of Physiology, 175, 389. 8. ROLLASON,W.N. (1975) Electrocardiography for the Anaesthetist. 3rd edn, p. 99. Blackwell Scientific Publications, Oxford. 9. LEWIS, T. & HAYNAL,I . (1930) Observations relating to the tone of the minute vessels of the human skin. Heart, 15, 177. 10. RAVIN,M.B.& SULLIVAN, S.F. (1971) Effects in dogs of hyperventilation and hypothermia on body oxygen stores. British Journal of Anaesthesia, 43, 732. 11. SEVERINGHAUS, J. (1958) Oxyhemoglobin dissociation curve correction for temperature and pH variation in human blood. Journal of Applied Physiology, 12,485. A.J. (1962) Measure12. MARSHALL, R. & GUNNING, ment of blood gas tensions in profound hypothermia. Journal of Surgical Research, 11. 351. 13. ROSENTHAL, T.B. (1948) The effect of temperature on the pH of blood and plasma in vitro. Journal of Biological Chemistry, 173, 25. 14. MERIWETHER, W. & GOODMAN, R. (1972) Severe accidental hypothermia and survival after rapid rewarming. American Journal of Medicine, 53, 505. 15. HENNEMAN, D.H., BUNKER, J.P. & BREWSTER, W.R. (1958) Immediate metabolic response to hypo-
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24. LLOYD, E. L. (1973) Accidental hypothermia treated by central rewarming through the airway. British Journal of Anaesthesia, 45.41. V. (1954) Electrolyte disturbances associated 16. WYNN, 25. FERNANDEZ, J.P., O'ROURKE,R.A. & EWY,G.A. with failure to metabolise glucose during hypo(1970) Rapid active external warming in accidental thermia. Lancet, 2, 575. hypothermia. Journal of the American Medical D., GOUGH,K.R. & 17. READ,A.E., EMSLIE-SMITH, Association, 212, 153. HOLMES,R. (1961) Pancreatitis and accidental 26. LEADING ARTICLE(1 972) Accidental hypothermia. hypothermia. Lancet, 2, 1219. Scottish Medical Journal, 17, 81. 18. BOYER,N.H. & GERSTEIN, M.M.(1977) Induced 27. KUGELBERG, J., SCHOLLER, H., BERG,B. & KALLUM, hypothermia in dogs with acute myocardial B. (1967) Treatment of accidental hypothermia. infarction and shock. Journal of Thoracic and ScandinavianJournal of Thoracic and Cardiovascular Cardiovascular Surgery, 74, 286. Surgery, 1, 142. 19. BRISTOW, G., SMITH,R., LEE,J., AUTY,A. & TWEED, 28. WICKSTROM, P., RUM.E., LILJA,G.P., HINTERKOPF, W.A. (1977) Resuscitation from cardiopulmonary J.P. & HAGLIN, J.J. (1976) Accidental hypothermia: arrest during accidental hypothermia due to corn rewarming with partial bypass. American exhaustion and exposure. Canadian Medical AssociJournal of Surgery, 131,622. ation Journal, 117, 247. N.A., ORGEL, H. & 29. LLOYD, E.L., CONLIFFE, 20. THEILADE, D. (1977) The danger of fatal misjudgement in hypothermia after immersion: WALKER,P.N.(1972) Accidental hypothermia: an apparatus for central re-warming as a first aid successful resuscitation following immersion for measure. Scottish Medical Journal, 17, 83. 25 minutes. Anaesthesia, 32, 889. 30. COLLIS, M.L., STEINMAN, A.M. & CHANEY, R.D. 21. LEADING ARTICLE (1977) Immersion and drowning (1977) Accidental hypothermia: an experimental in children. British Medical Journal, 2, 146. study of practical rewarming methods. Aviation, B.G., BRISTOW, G.K. & CRAIG,D.B. 22. PICKERING, (1977) Core rewarming by peritoneal irrigation in Space and Environmental Medicine, 48, 625. 31. HUDSON,L.D. & CONN,R.D. (1974) Accidental accidental hypothermia with cardiac arrest. hypothermia: associated diagnoses and prognosis Anesthesia and Analgesia; Current Researches, 56, in a common problem. Journal of the American 574. Medical Association, 227, 37. 23. LEADING ARTICLE(1972) Severe accidental hypothermia. Lancet, 1,237.
thermia in man. Journal of Applied Physiology 12,
164.
Accidental hypothermia
S.W.C O N I A M
Accidental hypothermia may result from exposure to a cold environment or from inadequate heat conservation. Impairment of normal body temperature control may be due to old age, immaturity of temperature regulation as in neonates, or to a hypothalamic or thyroid disorder. An uncommon cause is the condition of erythroderma. Accidental hypothermia can result indirectly from immobility due to cerebrovascular accident, myocardial infarction, neurological disease or from self poisoning with drugs or alcohol. Exposure on mountain sides or immersion in cold water are common causes of hypothermia even in young, healthy persons. Most authorities would consider any person with a rectal temperature below 35°C to be suffering from hypothermia, but it is difficult to give a precise definition. A General Practice survey of septuagenarians in Orkney,' found that 8% had temperatures of 35°C or less, without obvious cause. A survey2 of geriatric hospital admissions found 3.6% to be hypothermic and it was noted that there was a high mortality (45%) when this condition was associated with old age. There appears to be a decrease in the thermoregulatory response with increasing age.3 There is a smaller corelperipheral temperature gradient, lower peripheral blood flow and an inadequate vasomotor response to cold. Physiology
Laboratory animals differ from man in their mechanisms of temperature regulation and
therefore make poor models in the study of accidental hypothermia. Man relies heavily on behavioural adaptation in control of body temperature. Some of the few experiments on hypothermia in humans were carried out on prisoners in Dachau in 1942. The human responses to temperature change include sweating, changes in vasomotor tone and shivering. Vasomotor control alone can probably adjust heat conservation from 0.15 to 0.75 clo units.' Body contour and fat distribution vary between individuals, but the Perth geriatric unit5 found an equal distribution of body types among hypothermic admissions. Shivering increases heat production by about five times, but it also increases the rate of heat loss. Loss of body heat increases in a linear fashion, whereas heat production rises geometrically with increasing temperature. In the range 33-38"C, the body can balance heat loss with increased heat production. However, below about 33°C the body cannot produce enough heat to compensate for losses, and below about 22"C,when survival is unlikely, the body temperature responds to the environmental temperature in a poikilothermic manner.
Cardiovascular system In the range of erective response to cold (approximately down to 33°C) pulse rate increases along with shivering and increased sympathetic stimulation. Below this range, the pulse rate falls, rapidly at first and then
S.W.Coniam, MB, BChir, Registrar, Department of Anaesthetics, Hallamshire Hospital, Sheffield S10 2RX.
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Accidental hypothermia
more gradually, unless dysrhythmias occur due to depression of intracardiac conductivity, inhibition of normal centres of impulse formation and increased myocardial irritability. The electrocardiograph (ECC)
The QRS segment lengthens, followed by lengthening and depression of the ST interval and a variety of inconstant T wave changes occur in hypothermia. Slowing results from prolongation of systole but the widening of the QRS complex and ST interval is greater than can be attributed simply to slowing of the heart rate. Often a Q wave (abnormal initial negative deflection) or an R’ wave (abnormal second positive deflection) is present.6 The P wave decreases in amplitude. Particularly characteristic of hypothermia is the J wave, described by Osborn in 1953.’ This is a positive-negative deflection following the QRS complex. Its aetiology is unknown, although it has been suggested that it is due to a current of injury. As the temperature falls, dysrhythmias frequently develop. These may start as an atrial ectopic focus or wandering pacemaker, atrial fibrillation (resulting in an abrupt increase in heart rate), ventricular extrasystoles or tachycardia. Ventricular fibrillation may develop without any previous changes of rhythm, especially in the range 2628°C and may appear as groups of waveform complexes.* Young patients maintain sinus rhythm for longer than older patients. Ventricular fibrillation seems to be the commonest cause of death in hypothermia but no single precipitating cause has been isolated. A fine muscle tremor, often present, may produce artefactual changes on the ECG. The initial reaction to cold is peripheral vasoconstriction, resulting in an increased volume of blood in the capacitance vessels, especially in the lungs and liver, producing an increased load on the heart. Stimulation of central volume receptors may be one cause of the diuresis associated with cold. Vasoconstriction may alternate with vasodilatation, known as ‘Lewis’ hunting r e f l e ~ ’There . ~ is a progressive fall in blood pressure.
Blood An initially high haematocrit (up to 60% has
251
been reported) and raised haemoglobin content is due to the movement of plasma out of the peripheral circulation into the tissues. Another factor involved in producing a raised haematocrit is the considerable diuresis which often occurs in the early stages due to decreased renal tubular function. However, with rewarming and the administration of intravenous fluids, the haemoglobin gradually falls over the subsequent few days. This is due to dilution, as the red cell mass does not change. Slight haemolysis with haemoglobinuria is only rarely seen. The oxygen dissociation curve for haemoglobin shifts to the left as temperature falls, decreasing oxygen release to tissues. However, the increased solubility of oxygen and the decreased metabolic rate may partially compensate for this effect. It is thought that hypothermia has little effect on total body oxygen stores.’O There is usually a fall in blood pH, partly due to increased solubility of carbon dioxide, resulting in carbon dioxide retention. It is important to remember that unless results are corrected for temperature, blood gas results can be misleading, masking the degree of hypoxia. The methods suggested by Severinghausll or Marshall & Gunning1* can be used to correct measurements made at 37°C to values which are correct for the temperature of the patient. When measured at 37”C, pH readings are falsely low for the hypothermic patient. The Rosenthal formula suggests adding 0.15 pH units to the reading for each 10°C below normothermia. Respiration
Respiratory rate usually increases initially, particularly in sudden hypothermia following immersion. This may result in tetany. However, as the vital centres become depressed, respiration progressively decreases until eventually apnoea occurs. Renal function
Cold depresses enzyme activity in the distal renal tubule, resulting in decreased reabsorption (especially of glucose) and decreased secretion. A fall in glomerular filtration rate, independently of the fall in systolic blood pressure, results in azotaemia. Failure of tubular reabsorption is
252
S. W. Coniam
probably the main cause of the ‘cold diuresis’. An oliguric phase often follows during rewarming.
become progressively depressed as body temperature falls. Pathological changes
Metabolism
As mentioned above, shivering greatly increases the metabolic rate but also increases heat loss, and as the temperature falls, metabolism becomes depressed. The Van? Hoff Arrhenius law14 states that the metabolic rate halves for every fall of 10°C. A respiratory alkalosis may occur initially, but this usually progresses to a mixed acidosis. There is decreased uptake of glucose by cells, either due to inhibition of insulin activity or inhibition of hexokinase, the latter being particularly temperature sensitive.15Plasma glucose levels may be well above 12 mmol/litre without ketoacidosis. This resolves spontaneously and the patient usually has a normal glucose tolerance test following recovery. Glucose administered during hypothermia tends to stay in the extracellular compartment and draws water from the cells to dilute the extracellular fluid. Plasma sodium and protein fall by predicted amounts.16 This presents an argument against giving large quantities of dextrose in hypothermia. A fall of plasma pH causes potassium to move out of cells and as diuresis proceeds, much of this may be lost in the urine. Liver function tests are usually normal except for a low plasma protein. In one s e r i e ~eleven ,~ out of fifteen patients had a raised serum amylase. Five of these had autopsy evidence of pancreatic necrosis. The observed increase in morbidity when hypothermia is associated with physical exhaustion may be due to lack of glycogen storage in muscles. In cases of exhaustion, a raised serum nitrogen, creatinine, creatine phosphokinase, lactate dehydrogenase and serum glutamate oxaloacetate transaminase may be found, along with haemoglobinuria and myoglobinuria. Central nervous system
Below 31°C there is progressive paralysis of the central nervous system, and most patients are unconscious at temperatures below 28°C. Reflexes are lost at much lower temperatures. The respiratory and cardiovascular centres
Specific pathology is difficult to interpret as many hypothermic patients are elderly with a variety of coincidental disease. All cases develop fatty change in the myocardium, liver, renal tubules and zona reticularis of the adrenals. Changes compatible with shock or hypoxia are found in the gut, pancreas, parotids and brain, with perivascular haemorrhages in the third ventricle, and petechiae in the leptomeninges. Multiple infarcts found in many organs are caused by stagnation of blood and sludging of red cells. Pancreatitis is common.17
Diagnosis
If a cold patient is found in a cold environment the diagnosis is usually self evident, but it may be difficult to separate the severely hypothermic from the dead. An unconscious patient who is cold and rigid with fixed dilated pupils and undetectable pulse or respiration is worth resuscitation attempts if hypothermia is suspected. A euthyroid individual may give the appearance of severe hypothyroidism when suffering from prolonged hypothermia. The body is remarkably well preserved at low temperatures and prolonged absence of circulation is not a contraindication to resuscitation. Following experimental coronary artery occlusion in dogs, cooling to 32°C resulted in a three-fold increase in survival, compared with normothermic dogs. Hypothermia was found to have a positive inotropic effect on the myocardium.18 In a Canadian report a young man with apparent cardiac arrest for l t h at a temperature of 252°C made an eventual complete recovery.1g A similar case is reported from Denmark,’O and the difference in mortality between children in drowning accidents in Norway and California suggests a protective effect of cold in the former.21 Fixed dilated pupils or a flat electroencephalograph are not reliable signs of death in hypothermia and resuscitative attempts should not be abandoned until the patient has been adequately rewarmed. It is notable that both hypothermia and alcohol prolong hypoxic survival of neurones, although alcohol also increases heat loss by vasodilatation.
Accidental hypothermia Management The patient should be removed from the adverse environment with a minimum of handling and covered with a blanket. External cardiac massage, tracheal intubation or insertion of oesophageal temperature probes may precipitate ventricular fibrillation.2 Attempts at electrical defibrillation or the use of antiarrhythmic drugs are usually ineffective whilst the temperature is below 28°C and are best avoided. Defibrillation is advisable if ventricular fibrillation develops during warming, when the temperature is between 28-30°C. In many cases reported, ventricular fibrillation has only developed following admission to hospital. The patient is best managed in an intensive care unit. Initial investigations should include measurement of pH and blood gases, haemoglobin level and white cell count, urea and electrolytes, glucose, blood culture, amylase, and screening for barbiturates and salicylates. A chest X-ray and ECG are taken and at some stage, thyroid function must be assessed. Observations can be limited to pulse rate, blood pressure, rectal temperature, fluid balance, conscious level and ECG monitoring. Although oesophageal temperature gives a more accurate measurement of cardiac temperature, a rectal temperature probe results in less disturbance to the patient at a time when dysrhythmias are likely to develop. There are two much debated approaches to rewarming, slow passive, and rapid active. Also warming may be external or internal. There is general agreement that the victim of sudden immersion with rapidly produced hypothermia is best warmed rapidly by immersion of the trunk in a warm bath (40-42°C). The limbs should be kept out of the bath, because warming the periphery before the core results in a rapid return of cold blood to the heart. Even if this precaution is observed, core temperature usually falls 2-3°C after immersion in the warm bath. This is called the ‘afterdrop’.4.5.24 Rewarming of the patient who has suffered from prolonged hypothermia presents a greater problem. Fernandez2 used rapid external warming with a hyperthermic mattress and points to the failure of some previous series which used a less active approach, and the
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success of rapid rewarming in the Dachau experiments. Rapid surface rewarming has been recommended by others.26 Meriwether & Goodman14 advocate immersion in a warm bath. Most authors who have used surface warming advise against warming the limbs, as a rapid return of cold stagnant blood to the heart seems likely to precipitate dangerous arrhythmias, results in a further fall in core temperature and a catastrophic fall in blood pressure due to loss of peripheral resistance. External warming does, however, result in an increase in the metabolic needs of peripheral tissues, further reducing the oxygen available to essential organs. Skin warming may also inhibit endogenous heat production. Many methods of central rewarming have been used. Kugelberg et at.’’ report the use of iliac artery to iliac vein bypass using a heart lung machine with a heat exchanger. They used this method to raise the temperature of one patient from 21.4 to 35°C over a period of 72 min. At 22.5”C atrial fibrillation reverted spontaneously to sinus rhythm. The advantages claimed for the method are that the temperature can be raised rapidly above the critical level of 28°C and that the heart receives warm blood directly and is therefore less likely to fibrillate. If ventricular fibrillation does develop, then the circulation can be maintained until normal rhythm is restored. Wickstrom el aLZ8report a similar technique and add that their cases showed no response to cardiac massage or defibrillation until a temperature of 32°C had been reached. They stress that the threshold for ventricular fibrillation is decreased by acidosis and increased by alkalosis. In hypothermia the oxygen dissociation curve shifts to the left and this is increased by alkalosis, making tissues more hypoxic. Some authors have recommended the use of hydrochloric acid to produce a shift of the curve to the right, but this is not generally accepted.28It is suggested that over treatment with bicarbonate ions may add to the difficulty of defibrillating the heart. Pickering et aLZ2used peritoneal irrigation in a patient with a rectal temperature of 26-4”C following unsuccessful resuscitation with surface warming, warmed intravenous infusion and gastric lavage. Irrigation of the peritoneal cavity with an isotonic dialysis fluid at 38°C was successful with eventual complete recovery
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following a 311 h cardiac arrest. They suggest this as the method of choice as it is almost universally available, even in small units, and is a simple technique with low morbidity compared with bypass methods. In the Canadian report mentioned above,I9 the patient suffering exposure with physical exhaustion, was treated with hot, wet towels, hot water bottles, warm enemas and gastric lavage. Ventricular fibrillation developed during warming, but this responded to electrical defibrillation. After 24 weeks recovery was complete, except for a ‘Simian’ deformity of the hands, thought to be due to a peripheral neuropathy. Central rewarming through the airway is often used. The author has treated a patient with a rectal temperature of 22~8°Cwho was successfully managed by very slow central rewarming. He was covered with a ‘spacerescue’ blanket, given a warmed (37°C) intravenous infusion, and allowed to breath oxygen enriched air warmed in an East Radcliffe humidifier containing water at 60°C. A more active approach is recommended by Lloyd24-29 using carbon dioxide from a ‘sparklets’ bulb in conjunction with soda lime in a modified Water’s system. This exothermic reaction heats the inspired gas and the simple portable apparatus can be used at the scene of accidents and provides core rewarming. Lloyd also uses a conventional humidifier with water at 60°C and reports only one case of laryngeal oedema and mild airway scalding. He found no ECG abnormalities following tracheal intubation, and no ‘afterdrop’ using these methods. The lungs are a very efficient heat exchange system. Apart from actively supplying a small amount of heat through the lungs in this way, normal heat loss via the lungs is minimised, thus making 25-30% more metabolic heat available (30 kcal/m2/h at 30°C). The effectiveness of rewarming through the airway is confirmed by a series of experiments on human volunteers by Collis et Hudson & Conn3’ stress that the underlying condition is probably more important in determining survival than the method of rewarming. They suggest that slow passive rewarming can be expected to be suceessful in patients with intoxication or mental abnormalities, but is less so following shock, infections or myocardial infarction. They also stress that
it is a waste of time treating underlying conditions prior to rewarming. Respiratory support
Problems associated with tracheal intubation have already been mentioned and it would seem reasonable to avoid this in the early stages, if possible. However, many hypothermic patients are apnoeic or unable to maintain an adequate airway and the majority of cases described in the literature have been intubated, with or without intermittent positive pressure ventilation (IPPV). Even though the arterial oxygen tension is apparently satisfactory, correction for measurement at the patient’s temperature may reveal considerable hypoxia. Oxygen enrichment of the inspired air is desirable, although in a patient breathing spontaneously there is a danger of carbon dioxide narcosis because an unsuspected hypoxic drive is removed. Some casesL9have been reported to develop pulmonary oedema during rewarming, but this has responded to treatment with IPPV and diuretics. Cardiovascular system
Dysrhythmias commonly revert spontaneously above 28-30°C and should probably be ignored at lower temperatures. Electrical defibrillation may be necessary in this range, but antiarrhythmic drugs should be avoided. Atropine is often used to treat profound bradycardia during rewarming. Renal
The cold diuresis may have several causes, but fluid balance should be maintained with a warmed infusion of dextrose/saline. Following rewarming oliguria may occur, but this generally responds to diuretics. During the diuretic phase, potassium replacement is necessary. Drug therapy
Corticosteroids (hydrocortisone 200 mg or methyl prednisolone 30 mg/kg 4 hourly intravenously) are usually given for a variety of reasons. The effect of stabilising lysosomal membranes in tissues damaged by a stagnant circulation may be important. Another ex-
Accidental hypothermia planation for the use of hydrocortisone is that normal output of corticotrophin and adrenal hormones are depressed in hypothermia. Hypoadrenalism may be partly responsible for the ‘shock’ seen occasionally during rewarming. Some workers have used vasoconstrictors to raise the blood pressure and maintain vasoconstriction during rewarming. The Canadian team used an infusion of dopamine to maintain cardiac output. Cerebral oedema has been suggested as a cause of deathz4 and this may justify the use of steroids. Triiodothyronine (10 pg twice daily) has a place where hypothyroidism is the cause of hypothermia, but it should be administered after rewarming. Most authors2z*27*z8 quote a high rate of respiratory tract infection during recovery, and for this reason, the patient should be started on prophylactic antibiotics at an early stage. It may be better to wait for definitive diagnosis before this line of treatment is started, and more specific drugs should be used in conjunction with physiotherapy. Conclusions
From this review of the literature, certain main recommendations in the management of hypothermia seem to be agreed. Minimal handling and movement of the patient must be the aim. Rewarming of the trunk in a warm bath in cases of sudden hypothermia following cold water immersion is indicated. In other cases, gradual rewarming via the airway or peritoneum, together with adequate thermal insulation should be undertaken. A rate, of temperature rise of 4-1 “Cper hour is suggested. Fluid overloading should be avoided, especially with dextrose. The ECG should be monitored and antiarrhythmic drugs avoided, but electrical defibrillation may be necessary if ventricular fibrillation develops around 28°C. Added oxygen, airway support and mechanical ventilation may be necessary. A cuffed tracheal tube may be of benefit in reducing the high incidence of aspiration pneumonia. The administration of corticosteroids and antibiotics, if specifically indicated, may be thought necessary. Summary The physiological changes associated with accidental hypothermia are considered. Current
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methods of management of the hypothermic patient are reviewed. Key words HYPOTHERMIA; physiology, treatment. Acknowledgments The author wishes to thank Dr H.G. Schroeder for his advice in the preparation of this review, and Mrs J. Gosney for her secretarial assistance. References 1. COLLACOTT, R.A. (1975) Screening for hypothermia in Orkney. Journal of the Royal College of General Practitioners, 25, 647. A,, EXTON-SMITH, A.N., FRANCIS, 2. GOLDMAN, G.& O’BRIEN,A. (1977) A pilot study of low body
temperature in old people admitted to hospital. Journal of the Royal College of Physicians, 11, 291. 3. EDITORIAL(1977) The old in the cold. British Medical Journal, 1, 336.
4. HERVEY, G.R. (1973) Physiological changes encountered in hypothermia. Proceedings of the Royal Society of Medicine, 66, 1053. 5 . DUGUID,H.,SIMPSON, R.G. &STOWERS, J.M.(1961) Accidental hypothermia. Lancet, 2. 1213. 6. MICKS, C.E., MCCORD, M.C. & BLOUNT,S.G. (1956) Electrocardiographic changes during hypothermia and circulatory occlusion. Circulation, 13, 21.
7. OSBORN,J.J. (1953) Experimental hypothermia: respiratory and blood p H changes in relation to cardiac function. American Journal of Physiology, 175, 389. 8. ROLLASON,W.N. (1975) Electrocardiography for the Anaesthetist. 3rd edn, p. 99. Blackwell Scientific Publications, Oxford. 9. LEWIS, T. & HAYNAL,I . (1930) Observations relating to the tone of the minute vessels of the human skin. Heart, 15, 177. 10. RAVIN,M.B.& SULLIVAN, S.F. (1971) Effects in dogs of hyperventilation and hypothermia on body oxygen stores. British Journal of Anaesthesia, 43, 732. 11. SEVERINGHAUS, J. (1958) Oxyhemoglobin dissociation curve correction for temperature and pH variation in human blood. Journal of Applied Physiology, 12,485. A.J. (1962) Measure12. MARSHALL, R. & GUNNING, ment of blood gas tensions in profound hypothermia. Journal of Surgical Research, 11. 351. 13. ROSENTHAL, T.B. (1948) The effect of temperature on the pH of blood and plasma in vitro. Journal of Biological Chemistry, 173, 25. 14. MERIWETHER, W. & GOODMAN, R. (1972) Severe accidental hypothermia and survival after rapid rewarming. American Journal of Medicine, 53, 505. 15. HENNEMAN, D.H., BUNKER, J.P. & BREWSTER, W.R. (1958) Immediate metabolic response to hypo-
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24. LLOYD, E. L. (1973) Accidental hypothermia treated by central rewarming through the airway. British Journal of Anaesthesia, 45.41. V. (1954) Electrolyte disturbances associated 16. WYNN, 25. FERNANDEZ, J.P., O'ROURKE,R.A. & EWY,G.A. with failure to metabolise glucose during hypo(1970) Rapid active external warming in accidental thermia. Lancet, 2, 575. hypothermia. Journal of the American Medical D., GOUGH,K.R. & 17. READ,A.E., EMSLIE-SMITH, Association, 212, 153. HOLMES,R. (1961) Pancreatitis and accidental 26. LEADING ARTICLE(1 972) Accidental hypothermia. hypothermia. Lancet, 2, 1219. Scottish Medical Journal, 17, 81. 18. BOYER,N.H. & GERSTEIN, M.M.(1977) Induced 27. KUGELBERG, J., SCHOLLER, H., BERG,B. & KALLUM, hypothermia in dogs with acute myocardial B. (1967) Treatment of accidental hypothermia. infarction and shock. Journal of Thoracic and ScandinavianJournal of Thoracic and Cardiovascular Cardiovascular Surgery, 74, 286. Surgery, 1, 142. 19. BRISTOW, G., SMITH,R., LEE,J., AUTY,A. & TWEED, 28. WICKSTROM, P., RUM.E., LILJA,G.P., HINTERKOPF, W.A. (1977) Resuscitation from cardiopulmonary J.P. & HAGLIN, J.J. (1976) Accidental hypothermia: arrest during accidental hypothermia due to corn rewarming with partial bypass. American exhaustion and exposure. Canadian Medical AssociJournal of Surgery, 131,622. ation Journal, 117, 247. N.A., ORGEL, H. & 29. LLOYD, E.L., CONLIFFE, 20. THEILADE, D. (1977) The danger of fatal misjudgement in hypothermia after immersion: WALKER,P.N.(1972) Accidental hypothermia: an apparatus for central re-warming as a first aid successful resuscitation following immersion for measure. Scottish Medical Journal, 17, 83. 25 minutes. Anaesthesia, 32, 889. 30. COLLIS, M.L., STEINMAN, A.M. & CHANEY, R.D. 21. LEADING ARTICLE (1977) Immersion and drowning (1977) Accidental hypothermia: an experimental in children. British Medical Journal, 2, 146. study of practical rewarming methods. Aviation, B.G., BRISTOW, G.K. & CRAIG,D.B. 22. PICKERING, (1977) Core rewarming by peritoneal irrigation in Space and Environmental Medicine, 48, 625. 31. HUDSON,L.D. & CONN,R.D. (1974) Accidental accidental hypothermia with cardiac arrest. hypothermia: associated diagnoses and prognosis Anesthesia and Analgesia; Current Researches, 56, in a common problem. Journal of the American 574. Medical Association, 227, 37. 23. LEADING ARTICLE(1972) Severe accidental hypothermia. Lancet, 1,237.
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