St. Martin's Hospital, Canterbury, Kent and
1 Kent Institute of Medicine and Health Sciences, University of Kent at Canterbury, Canterbury, Kent CT2 7PD, UK
Received 12 April 1999; in revised form 28 August 1999; accepted 10 September 1999
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ABSTRACT |
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INTRODUCTION |
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The case presented here shows that the combination of vomiting, malnutrition and alcohol withdrawal can cause a potentially dangerous drop in serum potassium level.
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CASE HISTORY |
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When he contacted our service on the Monday afternoon, he was complaining of weakness and suffered from nausea again; he had not been vomiting since his discharge from hospital. Blood tests were repeated. His potassium level had dropped to 2.2 mmol/l. An urgent referral to the Accident and Emergency Department had to be arranged. He was immediately treated with an intravenous saline infusion (1 l) with 40 mmol potassium chloride in it and intravenous thiamine (Pabrinex: ascorbic acid 500 mg, anhydrous glucose 1 g, nicotinamide 160 mg, pyridoxine hydrochloride 50 mg, riboflavin 4 mg, thiamine hydrochloride 250 mg). Oral diazepam, 10 mg three times daily, was recommenced and oral potassium supplementation was given (Sando-K: potassium 470 mg, chloride 285 mg, four tablets). The next day, his potassium level rose to 2.8 mmol/l. Potassium replacement and thiamine were continued orally (Sando-K, four tablets three times daily, thiamine 100 mg three times daily) and diazepam was reduced to 5 mg three times daily. He was discharged on the Wednesday with a potassium level of 4.3 mmol/l. Potassium supplements were stopped on discharge. No other clinical cause of hypokalaemia was revealed. Continued monitoring of potassium until 1 week after his discharge revealed no abnormalities.
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DISCUSSION |
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Wadstein and Skude (1978) described 26 patients in whom a steady decrease in serum potassium led to hypokalaemia when delirium tremens started. Serum potassium returned to normal with recovery from delirium tremens, and potassium remained unchanged in patients who did not develop delirium tremens. Wetterling et al. (1994) also reported that a decreased serum potassium and chloride indicate a higher risk for the development of delirium tremens. Nanji and Blank (1984), however, reported no significant difference in serum potassium between patients with and without delirium tremens.
Carl and Holzbach (1994) found that the more pronounced the alcohol withdrawal, the sharper the decline in the levels of potassium and magnesium. In each of their cases, the decline in serum magnesium level preceded that of potassium level by 1 day. Laso et al. (1990) also showed a close negative correlation between intensity of withdrawal and serum potassium. Meyer and Urban (1977) revealed a significant decrease of potassium in their group of alcoholics with withdrawal seizures. Serum potassium remained within the normal range (although low) in their control group (withdrawing alcoholics without seizures).
Watson et al. (1984) reported significantly lower total body potassium in alcoholics, compared to non-alcoholics. They found no correlation between total body potassium and day 1 serum potassium levels. However, there was a significant positive correlation between total body potassium and the minimum serum potassium level recorded during the withdrawal period.
The mechanism behind serum electrolyte disturbances during alcohol withdrawal is still poorly understood. As alcoholics are already at higher risk of developing hypokalaemia due to vomiting, diarrhoea and malnutrition whilst drinking, it is clear that during alcohol withdrawal, even in a community setting, careful monitoring of electrolyte concentrations is necessary. This should be conducted, as in the case described, even where symptoms of vomiting and diarrhoea are mild. Further research is needed in order to identify whether or not it would be wise to monitor some or all patients in whom vomiting and diarrhoea are absent. During potassium supplementation, close monitoring is needed to follow normalization of the potassium level and after discontinuation monitoring should be continued in order to exclude relapse.
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FOOTNOTES |
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REFERENCES |
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Laso, F. J., Gonzalez-Buitrago, J. M., Martin-Ruiz, C., Vicens, E. and Moyano, J. C. (1990) Inter-relationship between serum potassium and plasma catecholamines and 3',5' cyclic monophosphate in alcohol withdrawal. Drug and Alcohol Dependence 26, 183188.[ISI][Medline]
Meyer, J. G. and Urban, K. (1977) Electrolyte changes and acid base balance after alcohol withdrawal. Journal of Neurology 215, 135140.[ISI][Medline]
Nanji, A. A. and Blank, D. W. (1984) Usefulness of serum potassium levels in the diagnosis of delirium tremens. Intensive Care Medicine 10, 112.[ISI][Medline]
Wadstein, J. and Skude, G. (1978) Does hypokalaemia precede delirium tremens Lancet ii, 549550.
Watson, W. S., Lawson, P. N. and Beattie, H. D. (1984) The effect of acute alcohol withdrawal on the serum potassium and total body potassium in heavy drinkers. Scottish Medical Journal 29, 222226.[ISI][Medline]
Wetterling, T., Kanitz, R. D., Veltrup, C. and Driessen, M. (1994) Clinical predictors of alcohol withdrawal delirium. Alcoholism: Clinical and Experimental Research 18, 11001102.[ISI][Medline]