1640
BRITISH MEDICAL JOURNAL
warning to us all properly to weigh the evidence both for and against an established and provenly useful treatment before publicly decrying it. W H HAYES Mevagissey,
St Austell, Cornwall
Treating stroke: home or hospital? SIR,-Dr Graham Mulley and Professor T Arie (11 November, p 1321) rightly draw attention to the need to evaluate claims for the effectiveness of stroke rehabilitation in hospital. However, I would challenge their statement that stroke rehabilitation units "make great demands on the health service in both money and staff." It is at least arguable that the demands arise not from the units but from the needs of the severely disabled patients, who require a great deal of care wherever they are located. Indeed, these needs may well be met more economically and more effectively when the patients are grouped in a unit dedicated to multidisciplinary rehabilitation than when they are scattered throughout the hospital. The 30-bedded stroke rehabilitation ward at Lightburn Hospital, Glasgow, obtained good results' in the rehabilitation of severely disabled stroke patients with no more medical and nursing staff than in the geriatric wards of the hospital and with the part-time services of only two physiotherapists, one occupational therapist, one speech therapist, and one social worker. The costs were less than those of a general medical ward. A similar unit in Edinburgh2 is nearing completion of a comparative trial of its effectiveness with that of general medical wards. Many intangible benefits are excluded from such objective assessments, such as the heightened awareness by all grades of staff of the complexity of the patients' needs and the reassurance given to caring relatives by the insight and understanding of the staff. I don't know how one "assesses objectively" whether stroke rehabilitation units "offer good value for money." I would have thought that that requires a subjective judgment; and my view is that if I were myself to suffer a stroke I should prefer to be in a stroke rehabilitation unit. BERNARD ISAACS University Department of Medicine, Queen Elizabeth Hospital, Birmingham Isaacs, B, Health Bulletin, 1977, 35, 94. 2Garraway, M, and Akhtar, A J, in Recent Advances in Geriatric Medicine (1) ed B Isaacs, p 7. Edinburgh, Churchill Livingstone, 1978.
I
Severe hyponatraemia in hospital inpatients SIR,-We were disappointed that in their article on this subject (4 November, p 1251) Dr P G E Kennedy and his colleagues ignore much relevant literature. We endorse their main conclusions: that the so-called syndrome of inappropriate secretion antidiuretic hormone is not a common cause of severe hyponatraemia, that there is rarely any need to restrict water intake, and that urine analysis is of little practical value. Flear and Singh' said the same and also showed hyponatraemia to be common in a variety of clinical conditions, its incidence and extent varying with the severity of the illness. They showed that an abrupt fall in sodium con-
9 DECEMBER 1978
centration was often caused by a widespread increase in membrane permeability. Membrane permeability is increased by many factors: hypoxia, increased catecholamines, viral infection, endotoxins, and malnutrition. As a result of such an increase some normally non-diffusible solutes "leak" from cells, taking with them water. The resulting hyponatraemia persists for as long as these solutes remain in the extracellular fluid2 and during this time the abnormality is reflected in an increase in the ratio between osmolality (corrected for urea and glucose) and plasma sodium concentration. At the same time cells tend to gain sodium despite increased "sodium pump" activity. This gain accounts for the net fall in extracellular volume usually seen but does not lower the concentration of sodium.2 Hyponatraemia may also develop insidiously when cells show a sustained inability to maintain, by metabolic activity, their normal quantity of non-diffusible solutes. Dr Kennedy and his colleagues ignore these possibilities. We suggest that the so-called "sick cell syndrome" was probably a factor in most of their 44 cases and may entirely explain their four "severely ill" patients in whom hyponatraemia had "no recognised cause." Hyponatraemia due to either of the cell causes outlined (abrupt or insidious) reflects the severity of the illness and impending threat to renal, cerebral, and myocardial function. In neither situation is hyponatraemia itself dangerous. Indeed, it may be helpful. Lowering the plasma sodium level reduces the rate at which sodium ions enter cells and lessens the electrochemical gradient against which "sodium pumps" have to operate. Both effects limit the rise in cellular energy expenditure observed in the critically ill.4 The therapeutic use of saline solutions in such situations may overwhelm the sodium pumps, causing sodium to accumulate rapidly in cells and thus further impairing tissue function. Dextran 70 is a preferable volume expander. Insulin reduces cell membrane permeability to sodium and facilitates "sodium pump" activity. Infused with glucose, it has reversed hyponatraemia in burns,5 trauma,6 heart failure,7 and fulminant hepatic failure.`
urinary sodium concentration and urine osmolality are shown and even then we are not told whether these were made on spot or timed urinary collections. Urinary sodium concentrations and osmolalities are dependent on many factors and a very wide range of values occurs even in the normal individual. If the authors had hoped to be able to distinguish "depletional" from "dilutional" causes of hyponatraemia using these measurements alone, then they predictably did not obtain what they expected. Previous studies' 2 have shown that in assessing hyponatraemia biochemical results are much more meaningful if comparisons of urine and plasma osmolality are made. In the second of the studies cited,' for example, the patients were all in the "dilutional" group of hyponatraemics and showed marked variation of urinary sodium concentrations and osmolalities, yet the results became much more meaningful when plasma and urine osmolalities were compared. Secondly, the authors include in their "depletional" group of hyponatraemics all the patients on diuretics. It has been reported:' that patients on thiazides or frusamide have increased levels of circulating antidiuretic hormone (ADH) in the presence of a low plasma osmolality and may therefore have "dilution" as a cause of hyponatraemia. Only in three of their eight patients on diuretics was there clinical evidence of dehydration, so on what other evidence the authors placed this whole group of patients in the "depletional" category of hyponatraemia is unclear. Thirdly, it is also unclear what the authors mean by "emergencies"-whether the emergency was due to hyponatraemia per se or whether the hyponatraemia was an epiphenomenon in otherwise critically ill patients. The authors state that "although 12 deaths occurred among the 44 patients hyponatraemia did not play a part in any." As a result of widespread use of biochemical screening hyponatraemia of varying severity remains a commonly encountered biochemical abnormality. Infrequently hyponatraemia results in encephalopathy and, as the results of other studies2 1 have shown, correct therapeutic intervention on the basis of analysing the most appropriate biochemical parameters CECIL T G FLEAR -namely, comparison of plasma and urine J BURN osmolalities, on spot samples initially and on G V GILL a 24-h urine specimen later, and plasma ADH levels when available-has often led to the University Department of Clinical Biochemistry and reversal of cerebral problems. Royal Victoria Infirmary, As they have used inappropriate biochemical Newcastle upon Tyne parameters in their ill-defined clinical context Flear, C T G, and Singh, C M, British Jouirnal of of "emergencies" Dr Kennedy and his Anaesthesia, 1973, 45, 976. colleagues cannot be justified in their final 2Flear, C T G, Lancet, 1974, 2, 164. 3Leaf, A, Lancet, 1974, 1, 119. conclusion. 4Flear, C T G, Bhattacharya, S S, and Nandra, G S, in S JAVED IQBAL Nuttritional Aspects of the Critically Ill, ed J R Richards and J M Kinney, p 195. Edinburgh, P J OJWANG Churchill Livingstone, 1977. 5Hinton, P, et al, Lancet, 1973, 2, 218. 6Woolfson, A M J, Heatley, R V, and Allison, S P, in Ntutritional Aspects of the Critically Ill, ed J R Richards and J M Kinney, p 367. Edinburgh, Churchill Livingstone, 1977. 7Majid, P A, et al, Lancet, 1972, 2, 937. Burn, J, and Williams, W D C, Itntensive Care Medicine, 1978, 4, 133.
SIR,-The report of Dr P G E Kennedy and others (4 November, p 1251) on their patients with plasma sodium concentrations below 125 mmol/l cannot go without comment with regard to their conclusion that "analysis of blood and urine was of no value in distinguishing the different diagnostic groups in an emergency." Firstly, only the results of estimations of
Department of Biochemical Medicine, Ninewells Hospital, Dundee I
Thomas, T H, et al, Lancet, 1978, 1, 621. De Trayner, A, and Domenet, J C, Quarterly J7ournal of Medicine, 1976, 45, 521. 3Scheiner, E, Advances in Clinical Chemistry, 1975, 17, 1. 4Ashton, M G, et al, British Medical Journal, 1977, 1, 1134. 5 Ruby, R J, and Burton, J R, Lancet, 1977, 1, 1212. 2
Dexamethasone in acute stroke SIR,-In a recent article by Dr Graham Mulley and others (7 October, p 994) and subsequent discussion there has been no reference to the interval between the onset of stroke and the
BRITISH MEDICAL JOURNAL
9 DECEMBER 1978
first dose of steroid. There has been this same surprising omission in most of the otherwise well-controlled studies reported in the literature, the highly significant interval being seldom mentioned, rarely considered, and never stressed. Yet timing is the most important factor in achieving success in the treatment of stroke so that in every case the aim must be to cut the interval to minutes from the hours and days that it is at present. Unfortunately, until cerebral stroke is regarded as an acute medical emergency comparable with coronary thrombosis, with clearcut first aid, the clinical approach will continue to be leisurely. It is customary to regard the motor cells of a hemiplegic patient as having been destroyed by stroke, but this would clearly be impossible if the paralysis were to clear. The explanation of a recovered stroke must be that the motor cells were temporarily non-functioning. Some strokes do cause immediate untreatable neuronal destruction, but the majority present the gradual picture of a stroke in evolution brought about by an underlying process. This cornsists of progressive arterial flow failure, anoxia, and oedema which so involve the neurones that they become functionless though they are, for a while, still viable. Immediate treatment in this early stage may restore normal flow and with this a return of neuronal function. Experience under intensive-care conditions shows that immediate dexamethasone is of value in the treatment of strokes which start in hospital. It is important to use large doses of dexamethasone, the initial dose being at least 10 mg intravenously and then continuing with 4 mg six-hourly for three days. Rubinstein' first reported the importance of giving steroid early after cerebral stroke. Two of his patients were remarkable. They were unconscious hemiplegics who were given intravenous steroid within four hours of the commencement of the strokes. They recovered rapidly and six months later were both free of any neurological deficit. At the present time the only therapeutic first aid available for acute stroke is a large dose of steroid. Dexamethasone is safe and if given immediately after the onset, before the patient is sent to hospital, is often effective. The current practice of giving too little dexamethasone too late will continue to disappoint. GERALD PARSONS-SMITH Bletchinglcy, Surrey Rubinstein, M 1K, ourwnal of IDisease, 1965, 141, 291.
Nervouis anid Menital
SIR,-The article on this subject by Dr Graham Mulley and others (7 October, p 994) contains a type II statistical error. Because they failed to find statistical significance in the difference in mortality rates between the treated and placebo groups the authors conclude that there was no significant difference. Their sample was too small for the conclusion. Had the ratio of mortality rates been maintained, one-tailed significance (POC=0 05) would have been reached when each group totalled 104 and two-tailed significance (PY=0 025) would have been reached when each group totalled 148. On the other hand to be 95 " certain that there was no 10-O difference between the two groups would require 417 members per group for one-tailed significance and 500 members per group for two-tailed significance.
1641
A similar error is to be found in the article by Dr K B Thomas on consultation time in general practice (7 October, p 1000). To demonstrate negative findings is not equivalent to failure to demonstrate positive findings. Feinstein' has published a review of this subject including the details of the calculations for sample size determination.
which you mention, in a serious case rapid evacuation for the hot bath treatment is usually precluded. Only when helicopter evacuation direct to a hospital is available could one justify attempting this form of treatment. We feel that in these severe cases the victims should if possible be allowed to rewarm "on the hill" in sleeping bags or RONALD A BLATTEL casualty bags in a warm tent until they are fit enough to be carried off the hill or conditions Ottawa, Ontario are suitable for helicopter evacuation. Feinstein, A R, Clinical Pharmacology and Therapeutics, 1975, 18, 491. P J ANDREW Chairman,
Peak District Mountain Rescue Organisation
Treating accidental hypothermia SIR,-In your leading article (18 November, p 1383), while giving an excellent discussion of the subject of accidental hypothermia as a whole, you would appear to us to misunderstand the problem as it usually occurs in young people on the mountains and moors in Britain. Last winter during the severe weather conditions in Scotland a considerable number of climbers survived whole nights on exposed mountain tops by following the advice to "go to ground" in a sheltered place or snow hole out of the wind in order to conserve their body heat and energy reserves. During the same period in the Peak District a hill walker died in a snowstorm during which, it would appear, he had continued to walk, presumably in an attempt to reach shelter. He had set off for a day's walking with a minimum of food. One of us (RSP) performed the necropsy (approximately 30 h after death), when his blood glucose concentration was reported by the laboratory as 0-0 mmol/l. It has frequently been observed that "exposure" develops in walkers who have missed their breakfast or restricted their food intake for various reasons. It is now beginning to appear that the majority of exposure hypothermia cases occurring in the British hills are in reality a combination of exhaustion (presumably with low blood glucose) and hypothermia. As the body core temperature drops it is to be expected that the release of glucose and regeneration of glycogen reserves will be greatly slowed, thus setting up a vicious circle. This has been well described by Dr James Ogilvie in the mountaineering press.' These findings affect our views on treatment in the mountain rescue service in this area. We feel that unless he is close to a habitation the victim must stop walking and "go to ground" as soon as the condition is suspected. He should be taken to the nearest sheltered spot and, after putting on all available spare clothing, he should be put into a heavy-gauge polyethylene exposure bag to minimise loss of heat by evaporation from wet clothing. This is to be preferred to removing wet clothing unless a tent is available, as the wind chill when undressed can be very severe even in a sheltered spot. These measures will ensure that all available energy is used for heat production and not for physical exertion. If conscious he should be given glucose or other sugar-containing food. Most of these cases occur several miles from the nearest habitation in rough and steep country. Stretcher evacuation is always slow and gives an uneven ride with the risk of the patient losing more body heat. Because of the need for gentle handling owing to the risk of ventricular fibrillation,
R S PARKER County Pathologist New Mills via Stockport, Greater Manchester
Ogilvie, J, Climnber and Rambler, September and October 1977.
Heart valve replacement in the elderly SIR,-Mr A H B de Bono and his colleagues (30 September, p 917) are to be congratulated both on a succinct communication and an excellent set of results for valve replacement in the elderly patient. I was very interested to note that in none of the 68 patients was it necessary to combine valve replacement with coronary bypass graft. At the present time cardiologists are being urged to include coronary angiography, a by no means harmless procedure, as part of the investigation of all patients of middle age or over referred for aortic valve replacement, on the grounds that a concomitant coronary graft may improve the short- and long-term results. I would be interested to know whether coronary angiography played any part in the assessment of the Cambridge patients; in particular were any patients turned down on the grounds of extensive coronary artery disease so demonstrated ? J S WRIGHT Department of Cardiology, Victoria Hospital, Blackpool, Lancs
***A copy of this letter was sent to Mr de Bono and his colleagues, whose reply is printed below.-ED, BMJ. SIR,-Thank you for allowing us to reply to the important issues raised by Dr Wright. We believe that the necessity for including coronary arteriography as part of the routine assessment of patients with aortic valve disease is not yet proved. Reasons for this include our belief that the coexistence of important coronary disease with symptomatically severe aortic valve disease is uncommon and that there is as yet no evidence that grafting noncritically stenosed vessels in this group of patients improves either symptomatic relief or long-term prognosis. What is known, however, is that operative risk is increased when aortic valve replacement is associated with concomitant coronary bypass grafting.' Coronary arteriography played no part in the assessment of the elderly group of patients reported by us. Indeed, we had no facilities for this during the first half of the period covered by our review. Although some patients had symptoms from impaired left ventricular function after operation, none experienced angina postoperatively.
BRITISH MEDICAL JOURNAL
warning to us all properly to weigh the evidence both for and against an established and provenly useful treatment before publicly decrying it. W H HAYES Mevagissey,
St Austell, Cornwall
Treating stroke: home or hospital? SIR,-Dr Graham Mulley and Professor T Arie (11 November, p 1321) rightly draw attention to the need to evaluate claims for the effectiveness of stroke rehabilitation in hospital. However, I would challenge their statement that stroke rehabilitation units "make great demands on the health service in both money and staff." It is at least arguable that the demands arise not from the units but from the needs of the severely disabled patients, who require a great deal of care wherever they are located. Indeed, these needs may well be met more economically and more effectively when the patients are grouped in a unit dedicated to multidisciplinary rehabilitation than when they are scattered throughout the hospital. The 30-bedded stroke rehabilitation ward at Lightburn Hospital, Glasgow, obtained good results' in the rehabilitation of severely disabled stroke patients with no more medical and nursing staff than in the geriatric wards of the hospital and with the part-time services of only two physiotherapists, one occupational therapist, one speech therapist, and one social worker. The costs were less than those of a general medical ward. A similar unit in Edinburgh2 is nearing completion of a comparative trial of its effectiveness with that of general medical wards. Many intangible benefits are excluded from such objective assessments, such as the heightened awareness by all grades of staff of the complexity of the patients' needs and the reassurance given to caring relatives by the insight and understanding of the staff. I don't know how one "assesses objectively" whether stroke rehabilitation units "offer good value for money." I would have thought that that requires a subjective judgment; and my view is that if I were myself to suffer a stroke I should prefer to be in a stroke rehabilitation unit. BERNARD ISAACS University Department of Medicine, Queen Elizabeth Hospital, Birmingham Isaacs, B, Health Bulletin, 1977, 35, 94. 2Garraway, M, and Akhtar, A J, in Recent Advances in Geriatric Medicine (1) ed B Isaacs, p 7. Edinburgh, Churchill Livingstone, 1978.
I
Severe hyponatraemia in hospital inpatients SIR,-We were disappointed that in their article on this subject (4 November, p 1251) Dr P G E Kennedy and his colleagues ignore much relevant literature. We endorse their main conclusions: that the so-called syndrome of inappropriate secretion antidiuretic hormone is not a common cause of severe hyponatraemia, that there is rarely any need to restrict water intake, and that urine analysis is of little practical value. Flear and Singh' said the same and also showed hyponatraemia to be common in a variety of clinical conditions, its incidence and extent varying with the severity of the illness. They showed that an abrupt fall in sodium con-
9 DECEMBER 1978
centration was often caused by a widespread increase in membrane permeability. Membrane permeability is increased by many factors: hypoxia, increased catecholamines, viral infection, endotoxins, and malnutrition. As a result of such an increase some normally non-diffusible solutes "leak" from cells, taking with them water. The resulting hyponatraemia persists for as long as these solutes remain in the extracellular fluid2 and during this time the abnormality is reflected in an increase in the ratio between osmolality (corrected for urea and glucose) and plasma sodium concentration. At the same time cells tend to gain sodium despite increased "sodium pump" activity. This gain accounts for the net fall in extracellular volume usually seen but does not lower the concentration of sodium.2 Hyponatraemia may also develop insidiously when cells show a sustained inability to maintain, by metabolic activity, their normal quantity of non-diffusible solutes. Dr Kennedy and his colleagues ignore these possibilities. We suggest that the so-called "sick cell syndrome" was probably a factor in most of their 44 cases and may entirely explain their four "severely ill" patients in whom hyponatraemia had "no recognised cause." Hyponatraemia due to either of the cell causes outlined (abrupt or insidious) reflects the severity of the illness and impending threat to renal, cerebral, and myocardial function. In neither situation is hyponatraemia itself dangerous. Indeed, it may be helpful. Lowering the plasma sodium level reduces the rate at which sodium ions enter cells and lessens the electrochemical gradient against which "sodium pumps" have to operate. Both effects limit the rise in cellular energy expenditure observed in the critically ill.4 The therapeutic use of saline solutions in such situations may overwhelm the sodium pumps, causing sodium to accumulate rapidly in cells and thus further impairing tissue function. Dextran 70 is a preferable volume expander. Insulin reduces cell membrane permeability to sodium and facilitates "sodium pump" activity. Infused with glucose, it has reversed hyponatraemia in burns,5 trauma,6 heart failure,7 and fulminant hepatic failure.`
urinary sodium concentration and urine osmolality are shown and even then we are not told whether these were made on spot or timed urinary collections. Urinary sodium concentrations and osmolalities are dependent on many factors and a very wide range of values occurs even in the normal individual. If the authors had hoped to be able to distinguish "depletional" from "dilutional" causes of hyponatraemia using these measurements alone, then they predictably did not obtain what they expected. Previous studies' 2 have shown that in assessing hyponatraemia biochemical results are much more meaningful if comparisons of urine and plasma osmolality are made. In the second of the studies cited,' for example, the patients were all in the "dilutional" group of hyponatraemics and showed marked variation of urinary sodium concentrations and osmolalities, yet the results became much more meaningful when plasma and urine osmolalities were compared. Secondly, the authors include in their "depletional" group of hyponatraemics all the patients on diuretics. It has been reported:' that patients on thiazides or frusamide have increased levels of circulating antidiuretic hormone (ADH) in the presence of a low plasma osmolality and may therefore have "dilution" as a cause of hyponatraemia. Only in three of their eight patients on diuretics was there clinical evidence of dehydration, so on what other evidence the authors placed this whole group of patients in the "depletional" category of hyponatraemia is unclear. Thirdly, it is also unclear what the authors mean by "emergencies"-whether the emergency was due to hyponatraemia per se or whether the hyponatraemia was an epiphenomenon in otherwise critically ill patients. The authors state that "although 12 deaths occurred among the 44 patients hyponatraemia did not play a part in any." As a result of widespread use of biochemical screening hyponatraemia of varying severity remains a commonly encountered biochemical abnormality. Infrequently hyponatraemia results in encephalopathy and, as the results of other studies2 1 have shown, correct therapeutic intervention on the basis of analysing the most appropriate biochemical parameters CECIL T G FLEAR -namely, comparison of plasma and urine J BURN osmolalities, on spot samples initially and on G V GILL a 24-h urine specimen later, and plasma ADH levels when available-has often led to the University Department of Clinical Biochemistry and reversal of cerebral problems. Royal Victoria Infirmary, As they have used inappropriate biochemical Newcastle upon Tyne parameters in their ill-defined clinical context Flear, C T G, and Singh, C M, British Jouirnal of of "emergencies" Dr Kennedy and his Anaesthesia, 1973, 45, 976. colleagues cannot be justified in their final 2Flear, C T G, Lancet, 1974, 2, 164. 3Leaf, A, Lancet, 1974, 1, 119. conclusion. 4Flear, C T G, Bhattacharya, S S, and Nandra, G S, in S JAVED IQBAL Nuttritional Aspects of the Critically Ill, ed J R Richards and J M Kinney, p 195. Edinburgh, P J OJWANG Churchill Livingstone, 1977. 5Hinton, P, et al, Lancet, 1973, 2, 218. 6Woolfson, A M J, Heatley, R V, and Allison, S P, in Ntutritional Aspects of the Critically Ill, ed J R Richards and J M Kinney, p 367. Edinburgh, Churchill Livingstone, 1977. 7Majid, P A, et al, Lancet, 1972, 2, 937. Burn, J, and Williams, W D C, Itntensive Care Medicine, 1978, 4, 133.
SIR,-The report of Dr P G E Kennedy and others (4 November, p 1251) on their patients with plasma sodium concentrations below 125 mmol/l cannot go without comment with regard to their conclusion that "analysis of blood and urine was of no value in distinguishing the different diagnostic groups in an emergency." Firstly, only the results of estimations of
Department of Biochemical Medicine, Ninewells Hospital, Dundee I
Thomas, T H, et al, Lancet, 1978, 1, 621. De Trayner, A, and Domenet, J C, Quarterly J7ournal of Medicine, 1976, 45, 521. 3Scheiner, E, Advances in Clinical Chemistry, 1975, 17, 1. 4Ashton, M G, et al, British Medical Journal, 1977, 1, 1134. 5 Ruby, R J, and Burton, J R, Lancet, 1977, 1, 1212. 2
Dexamethasone in acute stroke SIR,-In a recent article by Dr Graham Mulley and others (7 October, p 994) and subsequent discussion there has been no reference to the interval between the onset of stroke and the
BRITISH MEDICAL JOURNAL
9 DECEMBER 1978
first dose of steroid. There has been this same surprising omission in most of the otherwise well-controlled studies reported in the literature, the highly significant interval being seldom mentioned, rarely considered, and never stressed. Yet timing is the most important factor in achieving success in the treatment of stroke so that in every case the aim must be to cut the interval to minutes from the hours and days that it is at present. Unfortunately, until cerebral stroke is regarded as an acute medical emergency comparable with coronary thrombosis, with clearcut first aid, the clinical approach will continue to be leisurely. It is customary to regard the motor cells of a hemiplegic patient as having been destroyed by stroke, but this would clearly be impossible if the paralysis were to clear. The explanation of a recovered stroke must be that the motor cells were temporarily non-functioning. Some strokes do cause immediate untreatable neuronal destruction, but the majority present the gradual picture of a stroke in evolution brought about by an underlying process. This cornsists of progressive arterial flow failure, anoxia, and oedema which so involve the neurones that they become functionless though they are, for a while, still viable. Immediate treatment in this early stage may restore normal flow and with this a return of neuronal function. Experience under intensive-care conditions shows that immediate dexamethasone is of value in the treatment of strokes which start in hospital. It is important to use large doses of dexamethasone, the initial dose being at least 10 mg intravenously and then continuing with 4 mg six-hourly for three days. Rubinstein' first reported the importance of giving steroid early after cerebral stroke. Two of his patients were remarkable. They were unconscious hemiplegics who were given intravenous steroid within four hours of the commencement of the strokes. They recovered rapidly and six months later were both free of any neurological deficit. At the present time the only therapeutic first aid available for acute stroke is a large dose of steroid. Dexamethasone is safe and if given immediately after the onset, before the patient is sent to hospital, is often effective. The current practice of giving too little dexamethasone too late will continue to disappoint. GERALD PARSONS-SMITH Bletchinglcy, Surrey Rubinstein, M 1K, ourwnal of IDisease, 1965, 141, 291.
Nervouis anid Menital
SIR,-The article on this subject by Dr Graham Mulley and others (7 October, p 994) contains a type II statistical error. Because they failed to find statistical significance in the difference in mortality rates between the treated and placebo groups the authors conclude that there was no significant difference. Their sample was too small for the conclusion. Had the ratio of mortality rates been maintained, one-tailed significance (POC=0 05) would have been reached when each group totalled 104 and two-tailed significance (PY=0 025) would have been reached when each group totalled 148. On the other hand to be 95 " certain that there was no 10-O difference between the two groups would require 417 members per group for one-tailed significance and 500 members per group for two-tailed significance.
1641
A similar error is to be found in the article by Dr K B Thomas on consultation time in general practice (7 October, p 1000). To demonstrate negative findings is not equivalent to failure to demonstrate positive findings. Feinstein' has published a review of this subject including the details of the calculations for sample size determination.
which you mention, in a serious case rapid evacuation for the hot bath treatment is usually precluded. Only when helicopter evacuation direct to a hospital is available could one justify attempting this form of treatment. We feel that in these severe cases the victims should if possible be allowed to rewarm "on the hill" in sleeping bags or RONALD A BLATTEL casualty bags in a warm tent until they are fit enough to be carried off the hill or conditions Ottawa, Ontario are suitable for helicopter evacuation. Feinstein, A R, Clinical Pharmacology and Therapeutics, 1975, 18, 491. P J ANDREW Chairman,
Peak District Mountain Rescue Organisation
Treating accidental hypothermia SIR,-In your leading article (18 November, p 1383), while giving an excellent discussion of the subject of accidental hypothermia as a whole, you would appear to us to misunderstand the problem as it usually occurs in young people on the mountains and moors in Britain. Last winter during the severe weather conditions in Scotland a considerable number of climbers survived whole nights on exposed mountain tops by following the advice to "go to ground" in a sheltered place or snow hole out of the wind in order to conserve their body heat and energy reserves. During the same period in the Peak District a hill walker died in a snowstorm during which, it would appear, he had continued to walk, presumably in an attempt to reach shelter. He had set off for a day's walking with a minimum of food. One of us (RSP) performed the necropsy (approximately 30 h after death), when his blood glucose concentration was reported by the laboratory as 0-0 mmol/l. It has frequently been observed that "exposure" develops in walkers who have missed their breakfast or restricted their food intake for various reasons. It is now beginning to appear that the majority of exposure hypothermia cases occurring in the British hills are in reality a combination of exhaustion (presumably with low blood glucose) and hypothermia. As the body core temperature drops it is to be expected that the release of glucose and regeneration of glycogen reserves will be greatly slowed, thus setting up a vicious circle. This has been well described by Dr James Ogilvie in the mountaineering press.' These findings affect our views on treatment in the mountain rescue service in this area. We feel that unless he is close to a habitation the victim must stop walking and "go to ground" as soon as the condition is suspected. He should be taken to the nearest sheltered spot and, after putting on all available spare clothing, he should be put into a heavy-gauge polyethylene exposure bag to minimise loss of heat by evaporation from wet clothing. This is to be preferred to removing wet clothing unless a tent is available, as the wind chill when undressed can be very severe even in a sheltered spot. These measures will ensure that all available energy is used for heat production and not for physical exertion. If conscious he should be given glucose or other sugar-containing food. Most of these cases occur several miles from the nearest habitation in rough and steep country. Stretcher evacuation is always slow and gives an uneven ride with the risk of the patient losing more body heat. Because of the need for gentle handling owing to the risk of ventricular fibrillation,
R S PARKER County Pathologist New Mills via Stockport, Greater Manchester
Ogilvie, J, Climnber and Rambler, September and October 1977.
Heart valve replacement in the elderly SIR,-Mr A H B de Bono and his colleagues (30 September, p 917) are to be congratulated both on a succinct communication and an excellent set of results for valve replacement in the elderly patient. I was very interested to note that in none of the 68 patients was it necessary to combine valve replacement with coronary bypass graft. At the present time cardiologists are being urged to include coronary angiography, a by no means harmless procedure, as part of the investigation of all patients of middle age or over referred for aortic valve replacement, on the grounds that a concomitant coronary graft may improve the short- and long-term results. I would be interested to know whether coronary angiography played any part in the assessment of the Cambridge patients; in particular were any patients turned down on the grounds of extensive coronary artery disease so demonstrated ? J S WRIGHT Department of Cardiology, Victoria Hospital, Blackpool, Lancs
***A copy of this letter was sent to Mr de Bono and his colleagues, whose reply is printed below.-ED, BMJ. SIR,-Thank you for allowing us to reply to the important issues raised by Dr Wright. We believe that the necessity for including coronary arteriography as part of the routine assessment of patients with aortic valve disease is not yet proved. Reasons for this include our belief that the coexistence of important coronary disease with symptomatically severe aortic valve disease is uncommon and that there is as yet no evidence that grafting noncritically stenosed vessels in this group of patients improves either symptomatic relief or long-term prognosis. What is known, however, is that operative risk is increased when aortic valve replacement is associated with concomitant coronary bypass grafting.' Coronary arteriography played no part in the assessment of the elderly group of patients reported by us. Indeed, we had no facilities for this during the first half of the period covered by our review. Although some patients had symptoms from impaired left ventricular function after operation, none experienced angina postoperatively.
