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Hyponatraemia after orthopaedic surgery

BMJ 1999;318:1363-1364 ( 22 May )

Ignorance of the effects of hyponatraemia after surgery is widespreadand damaging

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/lborderline hyponatraemiaattributable 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 disregarded by the orthopaedic doctors as a potential cause of coma until the medical team were called the next day. Sodium concentrations were restored to 134 mmol/l over five days, leaving our friend with mildbut permanentcognitive impairment. The hospital concerned “apologises unreservedly” but confessed ignorance about the risks of hyponatraemia after joint replacement surgery.

Although the literature is full of similar examples, too many orthopaedic surgeons seem unaware of the dangers of hyponatraemia or its characteristic neurological symptoms. Perhaps the reason lies partly in the scatter of relevant publications: most of the articles are published in journals dedicated to neurology, urology, and acute care; only a handful of reports refer specifically to orthopaedic surgery2-4; and neither the Royal College of Surgeons nor the British Orthopaedic Association publishes guidelines. Many articles focus on tightly defined issues, such as the association between thiazide diuretics and hyponatraemia,2 to the exclusion of a more general overview. As a result, four fundamental problems have arisen: clinicians fail to recognise patients at high risk of hyponatraemia; disregard the dangers of routine infusions of hypotonic fluids; confuse early symptoms of hyponatraemia with postoperative sequelae; and attribute the serious neurological symptoms of hyponatraemic encephalopathy to other conditions such as stroke.

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