674

CorrespondenCe
3. Movig KLL, Leufkens HGM, Lenderink AW, van den Akker VGA, Hodiamont PPG, Goldschmidt HMJ et al. Association between antidepressant drug use and hyponatraemia: a case control study. Br J Clin Pharmacol 2002; 53:363-369. 4. Oh YJ, Lee JH, Nam SB, Shim JK, Song JH, Kwak YL. Effects of chronic angiotensin II receptor antagonist and angiotensinconverting enzyme inhibitor treatments on neurohormonal levels and haemodynamics during cardiopulmonary bypass. Br J Anaesth 2006; 97:792-798. 5. Colson P, Ribstein J, Mimran A Grolleau D, Chaptal PA, Roquefeuil B. Effect of angiotensin converting enzyme inhibition on blood pressure and renal function during open heart surgery. Anaesthesiology 1990; 72:23-27. 6. Shiba S, Sugiura K, Ebata A, Kagaya T, Tomori G, Marumo F et al. Hyponatremia with consciousness disturbance caused by omeprazole administration. A case report and literature review. Dig Dis Sci 1996; 41:1615-1617.

on his regular medications as above, except enalapril. He was treated with 2 units of blood as his haemoglobin was 7.3 g/dl. By postoperative day five his sodium increased to 138 mmol/l (corrected by 17 mmol over 48 hours), and haemoglobin improved to 10.8 gm/dl. His blood pressure was 140 mmHg systolic and his enalapril was restarted at 10 mg bd. He remained in hospital until postoperative day nine and his sodium remained at 136 to 138 mmol/l during this time. He made a full recovery with no residual neurological deficit and was discharged home. Hyponatraemia reflects relative excess of free water to solute and is usually accompanied by a decrease in plasma osmolality. Mild hyponatraemia (sodium <136 mmol/l) is recognised as an adverse effect of therapy with carbamazepine, laxatives, diuretics and angiotensin converting enzyme (ACE) inhibitors with an incidence of 9.4% in the elderly population1. Severe hyponatraemia (<126 mmol/l) can occur due to combination therapy of an ACE inhibitors, selective serotonin reuptake inhibitor and/ or diuretics2,3. ACE inhibited patients have increased vasopressin levels in the perioperative period4 and they also cause increased sodium excretion in urine5. These effects can complement each other in causing severe perioperative hyponatraemia. Our patient was euvolaemic and normotensive with hypoosmolar hyponatraemia, all suggestive of a syndrome of inappropriate antidiuretic hormone as the most probable explanation for his low sodium. Omeprazole has been reported to cause hyponatraemia6, but this patient had been on omeprazole for years with no adverse effect and was continued during the episode of severe hyponatraemia without any apparent implications. We hypothesise that severe hyponatraemia in our patient was due to a syndrome of inappropriate antidiuretic hormone associated with ACE inhibitor therapy in the postoperative period. Hence it may be recommended not to restart ACE inhibitor therapy in postoperative patients if their serum sodium is <136 mmol/l. s. ChAKithAndy r. evAns p. vyAKArnAm Dartford, United Kingdom
References 1. Passare G, Viitanen M, Torring O, Winbald B, Fastbom J. Sodium and potassium disturbance in the elderly: prevalence and association with drug use. Clin Drug Investig 2004; 24:535544. 2. Izzedine H, Fardet L, Launay-Vacher V, Dorent R, Petitclerc T, Deray G. Angiotensin-converting enzyme inhibitor induced syndrome of inappropriate secretion of antidiuretic hormone: case report and review of the literature. Clin Pharmacol Ther 2002; 71:503-507.

Dose of magnesium sulphate for severe acute asthma Several studies have been published, looking at the efficacy of intravenous (IV) magnesium sulphate for severe acute asthma1-3. Theses studies have used doses of magnesium sulphate in the range of 1.2 to 2 g IV over 20 minutes. No benefits were observed in patients with mild to moderate asthma, though there is some evidence magnesium sulphate may be beneficial in severe asthma. A 35-year-old woman was admitted to our accident and emergency department suffering from severe acute asthma. She became critically hypoxic and required tracheal intubation and ventilation there. She was treated with nebulised salbutamol, nebulised ipratropium bromide, hydrocortisone IV and an aminophylline intravenous infusion. After 12 hours of ventilation on our intensive care unit using remifentanil and propofol for sedation, her bronchospasm had resolved and she was extubated. She immediately developed severe bronchospasm again with rapidly worsening hypoxia. She was given a 5 g bolus of magnesium sulphate IV over five minutes and her bronchospasm rapidly resolved. Re-intubation of the trachea was avoided. During infusion of the magnesium sulphate, no bradycardia, no arrhythmias and no muscle weakness occurred. Serum magnesium level was measured 10 minutes after the magnesium sulphate bolus and the level was reported as 1.8 mmol/l. The author has personal experience of using high doses of magnesium sulphate, to induce deliberate hypotension without patients experiencing any cardiac arrhythmias or muscle weakness, despite having serum magnesium levels greater than 4 mmol/ l4. The British National Formulary lists the magnesium sulphate loading dose for eclampsia as 4 g IV over five to 15 minutes5.
Anaesthesia and Intensive Care, Vol. 37, No. 4, July 2009

CorrespondenCe
The author postulates that the dose of magnesium sulphate used in earlier trials in acute asthma was inadequate (1.2 to 2 g IV over 20 minutes) and that 5 g IV over five minutes would be more efficacious. Magnesium sulphate is a safe drug when used at this dose and has the added benefit of its effects being immediately reversible by injecting calcium intravenously6. A prospective, randomised clinical trial using this higher dose of magnesium sulphate is planned. g. sAnders Kent, United Kingdom
References 1. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CA Jr. Intravenous magnesium sulfate treatment for acute asthma in the emergency department: a systematic review of the literature. Ann Emerg Med 2000; 36:181-190.

675

2. Silverman RA, Osborn H, Runge J, Gallagher EJ, Chiang W, Feldman J et al. IV magnesium sulfate in the treatment of acute severe asthma: a multicenter randomized controlled trial. Chest 2002; 122:489-497. 3. Porter RS, Braitman LE, Geary U, Dalsey WC. Intravenous magnesium is ineffective in adult asthma, a randomized trial. Eur J Emerg Med 2001; 8:9-15. 4. Sanders GM, Sim KM. Is it feasible to use magnesium sulphate as a hypotensive agent in oral and maxillofacial surgery? Ann Acad Med Singapore 1999; 27:780-785. 5. British National Formulary. From http://www.bnf.org/bnf/ Accessed April 2009 6. Mordes JP, Wacker WE. Excess magnesium. Pharmacol Rev 1979; 29:273-300.

Anaesthesia and Intensive Care, Vol. 37, No. 4, July 2009