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COOLING TECHNIQUE FOR MALIGNANT HYPERTHERMIA
97 for artifactual acetaldehyde formation during treatment of the blood. Schuckit and Rayses’ analytical procedure involved freezing and thawing whole blood, which causes haemolysis and results in acetaldehyde formation; so it is likely that most of what they were measuring was artifactual. The case for raised acetaldehyde levels in relatives of alcoholics in response to alcohol is therefore unproven. University Department of Medicine, Bristol Royal Infirmary, Bristol BS2 8HW
ANDREW WILLIAMS
MA, Rayses V Ethanol ingestion. Differences in blood acetaldehyde in relatives of alcoholics and controls. Science 1979; 203: 54-55. Bardsley ME, Tipton KF. Metabolic aspects of ethanol dependence and tissue damage. In: Richter D, ed. Addiction and brain damage. London: Croom Helm, 1980:
1. Schuckit
concentrations
2.
75-93. 3 Lieber CS. Alcohol and the liver: 1984 update. Hepatology 1984, 4: 1243-60. 4. Erickson CJ. Elevated blood acetaldehyde levels in alcoholics and their relatives: evaluation. Science 1980; 207: 1383-84.
a re-
Actuarial
COOLING TECHNIQUE FOR MALIGNANT HYPERTHERMIA
SIR,-Your May 25 editorial on drug reactions during anaesthesia mentions malignant hyperthermia and recommends, as part of the clinical management of this complication, "enthusiastic cooling". This usually means packing the body with ice to promote removal of heat from the body. However, in malignant hyperthermia the high temperature is due to a combination of increased heat production from the muscles and a decreased heat loss secondary to peripheral vasospasm.The use of ice may be counterproductive since not only does cold on the skin cause vasoconstriction, which will reduce the ability of the skin to dissipate heat,2 but also the cold will stimulate further heat production, including possible shivering. 3,4 Warming 500 ml of cold water from 4°C to 40°C removes 18 kcal of heat. If 500 ml of ice is used the heat removed rises to 60 kcal, but if 500 ml water is evaporated 290 kcal is removed. The aim therefore should be to evaporate as much water from the skin surface as possible, while avoiding vasoconstriction. In heatstroke there is a similar need to dissipate excess heat, and again the traditional method of cooling used to be ice or very cold water. Research and clinical experience has led to the abandonment of ice, and a new technique has been developed.4This involves spraying the patient with a fine spray of warm water and blowing hot air over his body. The hot air maintains vasodilatation by perceived warmth on the skin, while the very low thermal capacity of air means that there is negligible heat input. As an added refinement, the victim is placed on a net stretcher suspended over a bath, to expose the maximum surface area for evaporation. It would seem logical to adopt a similar method to the treatment of
malignant hyperthermia. Department of Anaesthetics, Royal Infirmary, Edinburgh
E. LL. LLOYD D. H. T. SCOTT
1. Britt BA
Malignant hyperthermia. a review. In: Milton AS, ed. Pyretics and antipyretics. Berlin: Springer, 1982 547-615. 2. Maclean D, Emslie-Smith D. Accidental hypothermia. Oxford: Blackwell, 1977. 3. Benzinger TH Mechanisms of human thermoregulation In: Khogali M, Hales JRS, eds. Heat stroke and temperature regulation London: Academic Press, 1983: 53-64 4. Khogali M. The Makkah body cooling unit In Khogali M, Hales JRS, eds. Heat stroke and temperature regulation. London: Academic Press, 1983: 139-48.
SCLEROTHERAPY VERSUS PROPRANOLOL AFTER FIRST VARICEAL HAEMORRHAGE IN ALCOHOLIC CIRRHOSIS
SIR,-Interest in the medical prevention of recurrent haemorrhage in cirrhotic patients stems from the near certainty of early recurrence and the high risk of death within a year if no is given.1 surgery is not a proven solution often because of the poor condition of patients. Variceal sclerotherapy2 and betablocking agents3 seem to help to prevent recurrent bleeding but their effect on survival is disputed. Only one short-term study has compared the two,4and the conclusion was that sclerotherapy was superior to metoprolol, although Child C cases were excluded. However, a (31-selective adrenoreceptor antagonist may not be as effective as propranolol, a non-selective adrenoreceptor antagonist. treatment
curves.
———=sclerotherapy; — — —= propranolol. Left: cumulative percentage chance of remaining free from recurrent variceal bleeding (S=26, P=20). Right: cumulative percentage of survival (S = 24, P== 18). Neither pair of curves significantly different (log-rank test).
In our long-term randomised study we are comparing sclerotherapy with oral propranolol. No selection was made as a function of the severity of liver disease (Child’s classification); however, we excluded patients in whom traditional emergency treatment with balloon tamponade and/or vasopressin infusion had not achieved a haemodynamically stable state. Our preliminary results, after a maximum follow-up of 90 weeks, are presented. The sclerotherapy group (S) included 24 patients (51-336 SEMJ years); the propranolol group (P) numbered 20 (56’11 (2 . 2] years). Sclerotherapy was by intravariceal and perivariceal injection of 107o polydocanol (’Aetoxysclerol’, Lab Dexo). No severe complications were noted and sclerotherapy was repeated until varices had disappeared on endoscopy. The propranolol used was ’AvlocardylRetard’ (Lab ICI-Pharma); average daily dose was 160 mg to obtain
diminution of 25% in the heart rate at rest. 8 recurrent bleeding episodes were noted (33%) after initial disappearance of varices in groups, as opposed to 3 (15%), including 1 fatal case, in group P. The difference is not significant. Actuarial curves (figure, left) show a non-significant difference in recurrent bleeding in favour of sclerotherapy between the 15th and 66th weeks (log-rank test). There is no difference in total deaths (6 in group S, 4 in group P) even when stratification into three Child’s subgroups was done (Cochran test). The causes of death differed (3 deaths from gastric variceal haemorrhage in group S and 3 deaths from hepatocellular insufficiency in group P). Actuarial survival curves (figure, right) show a similar decrease for both groups. Days in hospital expressed as a percentage of total survival (in days) averaged 9 - 4 in group S and 7 -7in group P (not a
significant). Long-term, the two treatments do not seem to differ in respect of recurrence of haemorrhage, survival, or number of days in hospital. We recommend the use of sclerotherapy combined with propranolol, as suggested by O’Connor, et al.5 J. M. DOLLET Hepatogastroenterology Service, CHU de Nancy-Brabois, 54 511 Vandoeuvre lès Nancy, France
B. CHAMPIGNEULLE M. EVANGELISTA M. A. BIGARD P. GAUCHER
1. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology 1981; 80: 800-09. 2. The Copenhagen Esophageal Sclerotherapy Project. Sclerotherapy after variceal hemorrhage in cirrhosis. N Engl J Med 1984; 311: 1594-600. 3. Lebrec D, Poynard T, Bernuau J, Bercoff J, et al. A randomized controlled study of propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a final report. Hepatology 1984, 115: 476-80. 4. Westaby D, Melia WM, MacDougall BRD, Hegarty JE, et al. B, selective adrenoreceptor blockade for long term management of variceal bleeding: a prospective randomized trial to compare oral metoprolol with sclerotherapy in cirrhosis Gut 1985, 26: 421-25. 5. O’Connor KW, Lehman GA, Christiansen PA, Lumeng L, et al. Propranolol therapy versus two forms of sclerotherapy for variceal bleeding Preliminary results of a randomized prospective trial Gastroint Endosc 1984; 30: 148A.
ANDREW WILLIAMS
MA, Rayses V Ethanol ingestion. Differences in blood acetaldehyde in relatives of alcoholics and controls. Science 1979; 203: 54-55. Bardsley ME, Tipton KF. Metabolic aspects of ethanol dependence and tissue damage. In: Richter D, ed. Addiction and brain damage. London: Croom Helm, 1980:
1. Schuckit
concentrations
2.
75-93. 3 Lieber CS. Alcohol and the liver: 1984 update. Hepatology 1984, 4: 1243-60. 4. Erickson CJ. Elevated blood acetaldehyde levels in alcoholics and their relatives: evaluation. Science 1980; 207: 1383-84.
a re-
Actuarial
COOLING TECHNIQUE FOR MALIGNANT HYPERTHERMIA
SIR,-Your May 25 editorial on drug reactions during anaesthesia mentions malignant hyperthermia and recommends, as part of the clinical management of this complication, "enthusiastic cooling". This usually means packing the body with ice to promote removal of heat from the body. However, in malignant hyperthermia the high temperature is due to a combination of increased heat production from the muscles and a decreased heat loss secondary to peripheral vasospasm.The use of ice may be counterproductive since not only does cold on the skin cause vasoconstriction, which will reduce the ability of the skin to dissipate heat,2 but also the cold will stimulate further heat production, including possible shivering. 3,4 Warming 500 ml of cold water from 4°C to 40°C removes 18 kcal of heat. If 500 ml of ice is used the heat removed rises to 60 kcal, but if 500 ml water is evaporated 290 kcal is removed. The aim therefore should be to evaporate as much water from the skin surface as possible, while avoiding vasoconstriction. In heatstroke there is a similar need to dissipate excess heat, and again the traditional method of cooling used to be ice or very cold water. Research and clinical experience has led to the abandonment of ice, and a new technique has been developed.4This involves spraying the patient with a fine spray of warm water and blowing hot air over his body. The hot air maintains vasodilatation by perceived warmth on the skin, while the very low thermal capacity of air means that there is negligible heat input. As an added refinement, the victim is placed on a net stretcher suspended over a bath, to expose the maximum surface area for evaporation. It would seem logical to adopt a similar method to the treatment of
malignant hyperthermia. Department of Anaesthetics, Royal Infirmary, Edinburgh
E. LL. LLOYD D. H. T. SCOTT
1. Britt BA
Malignant hyperthermia. a review. In: Milton AS, ed. Pyretics and antipyretics. Berlin: Springer, 1982 547-615. 2. Maclean D, Emslie-Smith D. Accidental hypothermia. Oxford: Blackwell, 1977. 3. Benzinger TH Mechanisms of human thermoregulation In: Khogali M, Hales JRS, eds. Heat stroke and temperature regulation London: Academic Press, 1983: 53-64 4. Khogali M. The Makkah body cooling unit In Khogali M, Hales JRS, eds. Heat stroke and temperature regulation. London: Academic Press, 1983: 139-48.
SCLEROTHERAPY VERSUS PROPRANOLOL AFTER FIRST VARICEAL HAEMORRHAGE IN ALCOHOLIC CIRRHOSIS
SIR,-Interest in the medical prevention of recurrent haemorrhage in cirrhotic patients stems from the near certainty of early recurrence and the high risk of death within a year if no is given.1 surgery is not a proven solution often because of the poor condition of patients. Variceal sclerotherapy2 and betablocking agents3 seem to help to prevent recurrent bleeding but their effect on survival is disputed. Only one short-term study has compared the two,4and the conclusion was that sclerotherapy was superior to metoprolol, although Child C cases were excluded. However, a (31-selective adrenoreceptor antagonist may not be as effective as propranolol, a non-selective adrenoreceptor antagonist. treatment
curves.
———=sclerotherapy; — — —= propranolol. Left: cumulative percentage chance of remaining free from recurrent variceal bleeding (S=26, P=20). Right: cumulative percentage of survival (S = 24, P== 18). Neither pair of curves significantly different (log-rank test).
In our long-term randomised study we are comparing sclerotherapy with oral propranolol. No selection was made as a function of the severity of liver disease (Child’s classification); however, we excluded patients in whom traditional emergency treatment with balloon tamponade and/or vasopressin infusion had not achieved a haemodynamically stable state. Our preliminary results, after a maximum follow-up of 90 weeks, are presented. The sclerotherapy group (S) included 24 patients (51-336 SEMJ years); the propranolol group (P) numbered 20 (56’11 (2 . 2] years). Sclerotherapy was by intravariceal and perivariceal injection of 107o polydocanol (’Aetoxysclerol’, Lab Dexo). No severe complications were noted and sclerotherapy was repeated until varices had disappeared on endoscopy. The propranolol used was ’AvlocardylRetard’ (Lab ICI-Pharma); average daily dose was 160 mg to obtain
diminution of 25% in the heart rate at rest. 8 recurrent bleeding episodes were noted (33%) after initial disappearance of varices in groups, as opposed to 3 (15%), including 1 fatal case, in group P. The difference is not significant. Actuarial curves (figure, left) show a non-significant difference in recurrent bleeding in favour of sclerotherapy between the 15th and 66th weeks (log-rank test). There is no difference in total deaths (6 in group S, 4 in group P) even when stratification into three Child’s subgroups was done (Cochran test). The causes of death differed (3 deaths from gastric variceal haemorrhage in group S and 3 deaths from hepatocellular insufficiency in group P). Actuarial survival curves (figure, right) show a similar decrease for both groups. Days in hospital expressed as a percentage of total survival (in days) averaged 9 - 4 in group S and 7 -7in group P (not a
significant). Long-term, the two treatments do not seem to differ in respect of recurrence of haemorrhage, survival, or number of days in hospital. We recommend the use of sclerotherapy combined with propranolol, as suggested by O’Connor, et al.5 J. M. DOLLET Hepatogastroenterology Service, CHU de Nancy-Brabois, 54 511 Vandoeuvre lès Nancy, France
B. CHAMPIGNEULLE M. EVANGELISTA M. A. BIGARD P. GAUCHER
1. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology 1981; 80: 800-09. 2. The Copenhagen Esophageal Sclerotherapy Project. Sclerotherapy after variceal hemorrhage in cirrhosis. N Engl J Med 1984; 311: 1594-600. 3. Lebrec D, Poynard T, Bernuau J, Bercoff J, et al. A randomized controlled study of propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a final report. Hepatology 1984, 115: 476-80. 4. Westaby D, Melia WM, MacDougall BRD, Hegarty JE, et al. B, selective adrenoreceptor blockade for long term management of variceal bleeding: a prospective randomized trial to compare oral metoprolol with sclerotherapy in cirrhosis Gut 1985, 26: 421-25. 5. O’Connor KW, Lehman GA, Christiansen PA, Lumeng L, et al. Propranolol therapy versus two forms of sclerotherapy for variceal bleeding Preliminary results of a randomized prospective trial Gastroint Endosc 1984; 30: 148A.