Hyponatraemia after orthopaedic surgeryBMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7195.1363 (Published 22 May 1999) Cite this as: BMJ 1999;318:1363
Ignorance of the effects of hyponatraemia after surgery is widespreadand damaging
- Nick Lane, Honorary research fellow,
- Kathryn Allen, Honorary research associate
- University Department of Surgery, Royal Free and University College Medical School, London NW3 2QG (firstname.lastname@example.org)
- Department of Neurochemistry, Institute of Neurology, London WC1N 3BG
Iatrogenic injury is an unfortunate reversal of the physician's role. To cause the death or brain damage of a patient has to be the physician's worst transgression, particularly if the causes are well known, simple, and reversible. Each is true of acute postoperative hyponatraemia, but, despite repeated warnings, the condition remains common. According to a recent estimate based on prospective and retrospective studies, 20% of women who develop symptomatic hyponatraemia die or suffer serious brain damage, totalling 10 000-15 0000 cases every year in the United States and Western Europe.1
An elderly female friend of ours is a classic example. Some months ago she underwent a routine knee replacement operation. Before the operation her blood sodium concentration was 134 mmol/l—borderline hyponatraemia—attributable to her long term use of thiazide diuretics. After the operation she vomited frequently and received 6 litres of 5% dextrose saline over two days before passing into a coma. Her blood sodium concentration measured on the second day after surgery was 115 mmol/l, but electrolyte disturbance was …
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