1434
adult health and on mental and physical development in childhood. Iodine supplementation will eradicate the main clinical effects of iodine deficiency; several large studies have shown that iodine prophylaxis, given by iodisation of salt, water, or bread or by administration of iodised oil, leads to a pronounced reduction in the prevalence of iodine deficiency disorders, including goitre and cretinism, within a few years.3 However, iodine supplementation has its drawbacks. Allergic reactions may follow injection of iodised oil, and outbreaks of hyperthyroidism have been documented after iodine supplementation of salt or bread, mostly in patients with longstanding goitre in whom autonomously functioning thyroid nodules have developed.4 Iodineinduced hypothyroidism is much less common, but administration of iodised oil may sometimes lead to a transient fall in circulating T4 with a rise in thyrotropin.
The value of iodine
treatment
of established iodine
deficiency disorders, especially the reversal of developmental consequences of thyroid hormone deficiency in childhood and later life, is much less clear than that of iodine prophylaxis. Although iodine crosses the placenta, it was long believed that maternal thyroid hormones do not, so T4 and T3 were thought to be important in fetal development only after the appearance of the fetal thyroid in the second trimester.5 There is now persuasive evidence both from animal studies6 and from studies of infants with thyroid agenesis or related conditions7 that substantial amounts of T4 may be transferred from mother to fetus during gestation. This realisation, and the demonstration of specific receptors for thyroid hormones in human fetal brain during the early weeks of development before appearance of a functioning thyroid gland,8 have encouraged the view that a reduction in maternal T4 levels in early pregnancy, as a result of maternal iodine deficiency, can lead to profound
neurological damage (neurological cretinism). By contrast, iodine deficiency in later pregnancy and infancy resulting in fetal or neonatal hypothyroidism exerts predominant effects on somatic development (myxoedematous cretinism).3 This view is supported by the observation that prevention of the neurological consequences of iodine deficiency requires antenatal iodine supplementation,9 whereas in areas where myxoedematous cretinism predominates, supplementation during pregnancy can be effective in preventing the disorder.10 Since the neurological damage associated with maternal iodine deficiency is likely to arise in early pregnancy, it is not surprising that treatment in infancy or later life has little to offer. Similarly, while iodised oil has been reported to reverse the clinical consequences of myxoedematous cretinism when it is administered to children aged less than 4 years, treatment is only partly successful in older children." A
study of supplemental iodine in the treatment of myxoedematous cretinism in patients aged over 14 years has lately shown that signs of hypothyroidism, mental retardation, and other signs of neurological damage are not improved.12 A surprising observation in this study was that iodine treatment, rather than improving the biochemical picture of thyroid hormone deficiency, led to a fall in circulating T4 and T3 and a paradoxical fall in thyrotropin. The explanation for these adverse biochemical effects of iodine is not clear; the researchers’ explanations included direct effects of iodine on pituitary responsiveness to thyroid hormones, effects on thyrotropin secretion, and progressive thyroid atrophy leading to an inability to respond to
iodine supplementation. The occurrence of thyroid atrophy in myxoedematous cretins has been confirmed by ultrasound measurement of thyroid size -133 various aetiologies have been proposed, including selenium deficiency, thiocyanate poisoning, and autoimmune destruction. The autoimmune theory arose from the observation that patients with iodine-deficient goitre have an increased prevalence of thyroid autoantibodies. Whatever the cause of failure to respond to iodine supplementation, thyroxine treatment represents a more logical approach to the management of such cases. Recognition of the failure of iodine supplementation to correct established iodine deficiency disorders effectively and without complications adds to the urgency of programmes for iodine supplementation and abolition of these disorders through adequate prophylaxis. 1. Hetzel BS. Iodine-deficiency disorders. Lancet 1988; i: 1386-87. 2. Delange F, Burgi H. Iodine deficiency disorders in Europe. Bull WHO 1989; 67: 317—25. 3. Eastman CJ, Phillips DIW. Endemic goitre and iodine deficiency
disorders—aetiology, epidemiology and
treatment. Baillières Clin Endocrinol Metab 1988; 2: 719-35. 4. Studer H, Peter HJ, Gerber H. Toxic nodular goitre. Clin Endocrinol Metab 1985; 14: 351-72. 5. Bachrach LK, Burrow GN. Thyroid function in pregnancy-fetal maternal relationships. In: Delange F, Fisher DA, Malvaux P, eds. Pediatric and adolescent endocrinology. Basel: Karger, 1985: 1-18. 6. Obregon MJ, Mallol J, Pastor R, Morealle de Escobar G, Escobar del Rey F. L-thyroxine and 3,5,3’ tri-iodothyronine in rat embryos before onset of fetal thyroid function. Endocrinology 1984; 114: 305-07. 7. Vulsma T, Gons MH, Vijlder LLM. Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis. N Engl J Med 1989; 321: 13-16. 8. Ferreiro B, Bernal J, Goodyer CG, Branchard CL. Estimation of nuclear thyroid hormone receptor saturation in human fetal brain and lung during early development. J Clin Endocrinol Metab 1988; 67: 853-56. 9. Pharoah POD, Buttfield IH, Hetzel BS. Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Lancet 1971; i: 308-10. 10. Thilly CH, Delange F, Lagasse R. Fetal hypothyroidism and maternal thyroid status in severe endemic goiter. J Clin Endocrinol Metab 1978; 47: 354-60. 11. Vanderpas JB, Rivera-Vanderpas MT, Bourdoux P, et al. Reversibility of severe hypothyroidism with supplementary iodine in patients with endemic cretinism. N Engl J Med 1986; 315: 791-95. 12. Boyages SC, Halpern J-P, Maberly GF, et al. Supplementary iodine fails to reverse hypothyroidism in adolescents and adults with endemic cretinism. J Clin Endocrinol Metab 1990; 70: 336-41. 13. Boyages SC, Halpem J-P, Maberly GF, et al. A comparative study of neurological and myxedematous cretinism in Western China. J Clin Endocrinol Metab 1988; 67: 1262-71.
RESEARCH AND OPHTHALMOLOGY IN THE UK These are hard times for those responsible for studies of the eye in health and disease. Fanfares announced the launch of a new eye research institute in Manchester in the mid-1980s, but their echoes have now died away with less than a whimper. Research efforts in ophthalmology made at the Manchester Royal Eye Hospital have not been paralleled at university level, and an institute there that had been seen as competitor for Glasgow’s Tennent Institute and for London’s Institute of Ophthalmology has failed to materialise. Even the world-renowned institute in London, at Moorfields, has fallen on hard times. Victim to the financial retrenchment that has bedevilled academic life during the past decade, it has been able to benefit so far from the generous support of the charity Fight for Sight. As if that were not painful enough, during the latest quinquennium a management crisis has threatened to change the tenor of the
1435
Institute’s research programme
to
such
an extent
that
even
avant-garde researchers are uneasy. More recently, a peer review by an ad hoc body (on which eye experts numbered two of eight), convened by the Director of the British Postgraduate Medical Federation, assessed the various strands of research pursued by the staff, and examined overall performance levels. It can be only to an institution’s advantage if its progress is monitored from time to time. Quinquennial visitations by the University Grants Committee Medical Subcommittee helped to concentrate minds wonderfully. Their inspections have been replaced by procedures sometimes reminiscent of those of the star chamber--criteria of judgment tend to be as secret as is the route whereby the ultimate decisions are reached. However, monitoring progress is one thing; making (possibly ultra vires) decisions affecting people’s careers without giving reasonable notice is another. It is not in academe’s interest to be mealy-mouthed about its dead wood, if any, but the judgment passed on the Institute of Ophthalmology by the peer reviewers is damaging to the morale of most of its staff, and a threat to ophthalmological research in the UK. The modifications proposed for the departments of pathology and of clinical ophthalmology, not to mention the WHO Collaborative Centre of Preventive Ophthalmology, would bolster neurobiology, unrelated to ophthalmology, to the exclusion of basic studies on glaucoma, the crystalline lens, neurophysiology, neurochemistry, and other areas on which the institute had built its enviable reputation during the first four decades of its existence. The manner in which some decisions have been reached may well prompt Prof Stewart Sutherland, the Vice-Chancellor elect of the University of London, to lay down during the next academic session guidelines along which reorganisations might
proceed. Meanwhile one asks: eye research, quo vadis? It has been a commendable opinion of more than one review body, set up for example by the University of London, that schools do not exist primarily to make up the shortfall of resources outside the university sector. But without flexibility
specialist training, research, and-ultimately- patients are going to suffer. The Institute of Ophthalmology of yesteryear has served as a model for multidisciplinary training and research establishments worldwide, and many of their voices are whispering expressions of concern over its apparent future. Some might say that the projected change of character from a many-sided ophthalmological research centre to a virtually monodisciplinary island of basic research is a parochial event, but the consequences could be far-reaching. With an ageing ,UK population, demonstrably and progressively beset by ophthalmological hazards and even impairment, far-sighted vision should focus on an issue which, if ignored now, will take years to resolve.
and when the heart finally stops the brain’s requirement for oxygen is greatly reduced. The time between cessation of heart beat and brain damage is increased to as much as 30 minutes at a body temperature of25°C. A case-report from Canada1 highlights the clinical lesson that flows from these physiological considerations. At eight o’clock one morning in March, 1989, beside a highway in Manitoba, police found a young woman apparently dead in a car, having been there all night. There was no pulse or respiration. An ambulance was called and one of the crew thought he saw a twitch in a neck muscle so CPR was started 25 minutes after she had first been found. On arrival in hospital examination showed fixed dilated pupils and cold, stiff, and areflexive extremities. Cardiac monitoring confirmed asystole. Rewarming was started and when a rectal temperature was obtained an hour later it was 26°C. As the patient was rewarmed the heart started to beat, blood pressure came up, respirations returned, and later the same day she regained consciousness. She was discharged after three days in hospital with no neurological abnormalities except that she could not remember any events during the 24 hours before she regained consciousness. There were no details as to how the patient became hypothermic. Presumably she went to sleep in her car in freezing conditions. Often such cases are associated with alcohol excess which, by its vasodilatory effect, may hasten the rate of cooling and deaden the victim to the usual protective discomfort of cold. Overdose with other sedative drugs may be another factor. Cardiac arrest due to hypothermia is also encountered with cold water immersion and with mountaineering incidents (exposure, avalanche, and crevasse incidents). Hypothermia develops much faster in such circumstances and respiration is impeded. In cases of water immersion (in ice cold water) resuscitation has been successful even after 25-40 minutes.2,3 Apart from cooling the body rapidly, the very cold water may trigger the diving reflex, causing breathholding and bradycardia and thereby protecting the victim from water inhalation and rapid asphyxia. In avalanche victims it is important to know whether the patients have been able to breathe or not. Wet snow tends to encompass the chest whereas very fine snow may be inhaled. In either case respiration stops while the victim is still warm and resuscitation is unlikely to be successful if it is started more than a few minutes after cardiac arrest. However, even in the unfavourable setting of a wet snow avalanche resuscitation may be worthwhile,’ and similarly in cases of cold exposure in mountain or wilderness environments.5 The lesson from these cases is that even when there is no sign of life in a victim of hypothermic cardiac arrest, resuscitation should be attempted. The aphorism "No one is dead until warm and dead"6 still applies. Kristjanson MR, Bristow GK. Resuscitation from hypothermia-induced cardiac arrest. Can Med Assoc J 1990; 142: 741-42. 2. Siebke H, Breivik H, Rod T, Lind B. Survival after 40 minutes submersion without cerebral sequelae. Lancet 1975; i: 1275-77. 3. Sekar TS, MacDonnell F, Namsirikul P, Herman RS. Survival after prolonged submersion in cold water without neurological sequelae. 1.
KISS OF LIFE FOR A COLD CORPSE
Cardiopulmonary resuscitation (CPR) is usually undertaken in patients who have had a cardiac arrest after a myocardial infarction. Since brain oxygen requirements are normal when cerebral perfusion stops, the time between cessation of heart beat and irreversible brain damage is about 5 minutes. Not so in cardiac arrest from hypothermia. As the body cools, the heart continues to pump ever cooling blood to the brain, which also cools. Cerebral metabolism slows
Arch Intern Med 1980; 140: 775-79. burial in an avalanche. Br Med J 1987; 294: 611-12. 5. Bristow G, Smith R, Lee J, Auty A, Tweed WA. Resuscitation from cardiopulmonary arrest during accidental hypothermia due to exhaustion and exposure. Can Med Assoc J 1977; 117: 247-49. 6. Southwick FS, Dalglish PH. Recovery after prolonged asystolic cardiac arrest in profound hypothermia. JAMA 1980; 243: 1250-53.
4.
Grey D. Survival after
adult health and on mental and physical development in childhood. Iodine supplementation will eradicate the main clinical effects of iodine deficiency; several large studies have shown that iodine prophylaxis, given by iodisation of salt, water, or bread or by administration of iodised oil, leads to a pronounced reduction in the prevalence of iodine deficiency disorders, including goitre and cretinism, within a few years.3 However, iodine supplementation has its drawbacks. Allergic reactions may follow injection of iodised oil, and outbreaks of hyperthyroidism have been documented after iodine supplementation of salt or bread, mostly in patients with longstanding goitre in whom autonomously functioning thyroid nodules have developed.4 Iodineinduced hypothyroidism is much less common, but administration of iodised oil may sometimes lead to a transient fall in circulating T4 with a rise in thyrotropin.
The value of iodine
treatment
of established iodine
deficiency disorders, especially the reversal of developmental consequences of thyroid hormone deficiency in childhood and later life, is much less clear than that of iodine prophylaxis. Although iodine crosses the placenta, it was long believed that maternal thyroid hormones do not, so T4 and T3 were thought to be important in fetal development only after the appearance of the fetal thyroid in the second trimester.5 There is now persuasive evidence both from animal studies6 and from studies of infants with thyroid agenesis or related conditions7 that substantial amounts of T4 may be transferred from mother to fetus during gestation. This realisation, and the demonstration of specific receptors for thyroid hormones in human fetal brain during the early weeks of development before appearance of a functioning thyroid gland,8 have encouraged the view that a reduction in maternal T4 levels in early pregnancy, as a result of maternal iodine deficiency, can lead to profound
neurological damage (neurological cretinism). By contrast, iodine deficiency in later pregnancy and infancy resulting in fetal or neonatal hypothyroidism exerts predominant effects on somatic development (myxoedematous cretinism).3 This view is supported by the observation that prevention of the neurological consequences of iodine deficiency requires antenatal iodine supplementation,9 whereas in areas where myxoedematous cretinism predominates, supplementation during pregnancy can be effective in preventing the disorder.10 Since the neurological damage associated with maternal iodine deficiency is likely to arise in early pregnancy, it is not surprising that treatment in infancy or later life has little to offer. Similarly, while iodised oil has been reported to reverse the clinical consequences of myxoedematous cretinism when it is administered to children aged less than 4 years, treatment is only partly successful in older children." A
study of supplemental iodine in the treatment of myxoedematous cretinism in patients aged over 14 years has lately shown that signs of hypothyroidism, mental retardation, and other signs of neurological damage are not improved.12 A surprising observation in this study was that iodine treatment, rather than improving the biochemical picture of thyroid hormone deficiency, led to a fall in circulating T4 and T3 and a paradoxical fall in thyrotropin. The explanation for these adverse biochemical effects of iodine is not clear; the researchers’ explanations included direct effects of iodine on pituitary responsiveness to thyroid hormones, effects on thyrotropin secretion, and progressive thyroid atrophy leading to an inability to respond to
iodine supplementation. The occurrence of thyroid atrophy in myxoedematous cretins has been confirmed by ultrasound measurement of thyroid size -133 various aetiologies have been proposed, including selenium deficiency, thiocyanate poisoning, and autoimmune destruction. The autoimmune theory arose from the observation that patients with iodine-deficient goitre have an increased prevalence of thyroid autoantibodies. Whatever the cause of failure to respond to iodine supplementation, thyroxine treatment represents a more logical approach to the management of such cases. Recognition of the failure of iodine supplementation to correct established iodine deficiency disorders effectively and without complications adds to the urgency of programmes for iodine supplementation and abolition of these disorders through adequate prophylaxis. 1. Hetzel BS. Iodine-deficiency disorders. Lancet 1988; i: 1386-87. 2. Delange F, Burgi H. Iodine deficiency disorders in Europe. Bull WHO 1989; 67: 317—25. 3. Eastman CJ, Phillips DIW. Endemic goitre and iodine deficiency
disorders—aetiology, epidemiology and
treatment. Baillières Clin Endocrinol Metab 1988; 2: 719-35. 4. Studer H, Peter HJ, Gerber H. Toxic nodular goitre. Clin Endocrinol Metab 1985; 14: 351-72. 5. Bachrach LK, Burrow GN. Thyroid function in pregnancy-fetal maternal relationships. In: Delange F, Fisher DA, Malvaux P, eds. Pediatric and adolescent endocrinology. Basel: Karger, 1985: 1-18. 6. Obregon MJ, Mallol J, Pastor R, Morealle de Escobar G, Escobar del Rey F. L-thyroxine and 3,5,3’ tri-iodothyronine in rat embryos before onset of fetal thyroid function. Endocrinology 1984; 114: 305-07. 7. Vulsma T, Gons MH, Vijlder LLM. Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis. N Engl J Med 1989; 321: 13-16. 8. Ferreiro B, Bernal J, Goodyer CG, Branchard CL. Estimation of nuclear thyroid hormone receptor saturation in human fetal brain and lung during early development. J Clin Endocrinol Metab 1988; 67: 853-56. 9. Pharoah POD, Buttfield IH, Hetzel BS. Neurological damage to the fetus resulting from severe iodine deficiency during pregnancy. Lancet 1971; i: 308-10. 10. Thilly CH, Delange F, Lagasse R. Fetal hypothyroidism and maternal thyroid status in severe endemic goiter. J Clin Endocrinol Metab 1978; 47: 354-60. 11. Vanderpas JB, Rivera-Vanderpas MT, Bourdoux P, et al. Reversibility of severe hypothyroidism with supplementary iodine in patients with endemic cretinism. N Engl J Med 1986; 315: 791-95. 12. Boyages SC, Halpern J-P, Maberly GF, et al. Supplementary iodine fails to reverse hypothyroidism in adolescents and adults with endemic cretinism. J Clin Endocrinol Metab 1990; 70: 336-41. 13. Boyages SC, Halpem J-P, Maberly GF, et al. A comparative study of neurological and myxedematous cretinism in Western China. J Clin Endocrinol Metab 1988; 67: 1262-71.
RESEARCH AND OPHTHALMOLOGY IN THE UK These are hard times for those responsible for studies of the eye in health and disease. Fanfares announced the launch of a new eye research institute in Manchester in the mid-1980s, but their echoes have now died away with less than a whimper. Research efforts in ophthalmology made at the Manchester Royal Eye Hospital have not been paralleled at university level, and an institute there that had been seen as competitor for Glasgow’s Tennent Institute and for London’s Institute of Ophthalmology has failed to materialise. Even the world-renowned institute in London, at Moorfields, has fallen on hard times. Victim to the financial retrenchment that has bedevilled academic life during the past decade, it has been able to benefit so far from the generous support of the charity Fight for Sight. As if that were not painful enough, during the latest quinquennium a management crisis has threatened to change the tenor of the
1435
Institute’s research programme
to
such
an extent
that
even
avant-garde researchers are uneasy. More recently, a peer review by an ad hoc body (on which eye experts numbered two of eight), convened by the Director of the British Postgraduate Medical Federation, assessed the various strands of research pursued by the staff, and examined overall performance levels. It can be only to an institution’s advantage if its progress is monitored from time to time. Quinquennial visitations by the University Grants Committee Medical Subcommittee helped to concentrate minds wonderfully. Their inspections have been replaced by procedures sometimes reminiscent of those of the star chamber--criteria of judgment tend to be as secret as is the route whereby the ultimate decisions are reached. However, monitoring progress is one thing; making (possibly ultra vires) decisions affecting people’s careers without giving reasonable notice is another. It is not in academe’s interest to be mealy-mouthed about its dead wood, if any, but the judgment passed on the Institute of Ophthalmology by the peer reviewers is damaging to the morale of most of its staff, and a threat to ophthalmological research in the UK. The modifications proposed for the departments of pathology and of clinical ophthalmology, not to mention the WHO Collaborative Centre of Preventive Ophthalmology, would bolster neurobiology, unrelated to ophthalmology, to the exclusion of basic studies on glaucoma, the crystalline lens, neurophysiology, neurochemistry, and other areas on which the institute had built its enviable reputation during the first four decades of its existence. The manner in which some decisions have been reached may well prompt Prof Stewart Sutherland, the Vice-Chancellor elect of the University of London, to lay down during the next academic session guidelines along which reorganisations might
proceed. Meanwhile one asks: eye research, quo vadis? It has been a commendable opinion of more than one review body, set up for example by the University of London, that schools do not exist primarily to make up the shortfall of resources outside the university sector. But without flexibility
specialist training, research, and-ultimately- patients are going to suffer. The Institute of Ophthalmology of yesteryear has served as a model for multidisciplinary training and research establishments worldwide, and many of their voices are whispering expressions of concern over its apparent future. Some might say that the projected change of character from a many-sided ophthalmological research centre to a virtually monodisciplinary island of basic research is a parochial event, but the consequences could be far-reaching. With an ageing ,UK population, demonstrably and progressively beset by ophthalmological hazards and even impairment, far-sighted vision should focus on an issue which, if ignored now, will take years to resolve.
and when the heart finally stops the brain’s requirement for oxygen is greatly reduced. The time between cessation of heart beat and brain damage is increased to as much as 30 minutes at a body temperature of25°C. A case-report from Canada1 highlights the clinical lesson that flows from these physiological considerations. At eight o’clock one morning in March, 1989, beside a highway in Manitoba, police found a young woman apparently dead in a car, having been there all night. There was no pulse or respiration. An ambulance was called and one of the crew thought he saw a twitch in a neck muscle so CPR was started 25 minutes after she had first been found. On arrival in hospital examination showed fixed dilated pupils and cold, stiff, and areflexive extremities. Cardiac monitoring confirmed asystole. Rewarming was started and when a rectal temperature was obtained an hour later it was 26°C. As the patient was rewarmed the heart started to beat, blood pressure came up, respirations returned, and later the same day she regained consciousness. She was discharged after three days in hospital with no neurological abnormalities except that she could not remember any events during the 24 hours before she regained consciousness. There were no details as to how the patient became hypothermic. Presumably she went to sleep in her car in freezing conditions. Often such cases are associated with alcohol excess which, by its vasodilatory effect, may hasten the rate of cooling and deaden the victim to the usual protective discomfort of cold. Overdose with other sedative drugs may be another factor. Cardiac arrest due to hypothermia is also encountered with cold water immersion and with mountaineering incidents (exposure, avalanche, and crevasse incidents). Hypothermia develops much faster in such circumstances and respiration is impeded. In cases of water immersion (in ice cold water) resuscitation has been successful even after 25-40 minutes.2,3 Apart from cooling the body rapidly, the very cold water may trigger the diving reflex, causing breathholding and bradycardia and thereby protecting the victim from water inhalation and rapid asphyxia. In avalanche victims it is important to know whether the patients have been able to breathe or not. Wet snow tends to encompass the chest whereas very fine snow may be inhaled. In either case respiration stops while the victim is still warm and resuscitation is unlikely to be successful if it is started more than a few minutes after cardiac arrest. However, even in the unfavourable setting of a wet snow avalanche resuscitation may be worthwhile,’ and similarly in cases of cold exposure in mountain or wilderness environments.5 The lesson from these cases is that even when there is no sign of life in a victim of hypothermic cardiac arrest, resuscitation should be attempted. The aphorism "No one is dead until warm and dead"6 still applies. Kristjanson MR, Bristow GK. Resuscitation from hypothermia-induced cardiac arrest. Can Med Assoc J 1990; 142: 741-42. 2. Siebke H, Breivik H, Rod T, Lind B. Survival after 40 minutes submersion without cerebral sequelae. Lancet 1975; i: 1275-77. 3. Sekar TS, MacDonnell F, Namsirikul P, Herman RS. Survival after prolonged submersion in cold water without neurological sequelae. 1.
KISS OF LIFE FOR A COLD CORPSE
Cardiopulmonary resuscitation (CPR) is usually undertaken in patients who have had a cardiac arrest after a myocardial infarction. Since brain oxygen requirements are normal when cerebral perfusion stops, the time between cessation of heart beat and irreversible brain damage is about 5 minutes. Not so in cardiac arrest from hypothermia. As the body cools, the heart continues to pump ever cooling blood to the brain, which also cools. Cerebral metabolism slows
Arch Intern Med 1980; 140: 775-79. burial in an avalanche. Br Med J 1987; 294: 611-12. 5. Bristow G, Smith R, Lee J, Auty A, Tweed WA. Resuscitation from cardiopulmonary arrest during accidental hypothermia due to exhaustion and exposure. Can Med Assoc J 1977; 117: 247-49. 6. Southwick FS, Dalglish PH. Recovery after prolonged asystolic cardiac arrest in profound hypothermia. JAMA 1980; 243: 1250-53.
4.
Grey D. Survival after
