Hyponatraemia after orthopaedic surgery

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 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 mild—but permanent—cognitive 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 surgery^2–4; 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.

Postoperative hyponatraemia is provoked by surgical stress, which causes a syndrome of inappropriate antidiuretic hormone in almost everyone, often promoting water retention for several days. ^{5 6} Women are more affected than men, as a result of their smaller fluid volume and other sex related hormonal factors.⁵ Premenopausal women and children are prone to brain damage at sodium concentrations as high as 128 mmol/l. Postmenopausal women do not usually become symptomatic until sodium concentrations have fallen below 120 mmol/l, although normal symptoms can occur at higher levels if the rate of change is rapid.^5–7 Importantly, normal ageing impairs fluid homoeostasis and therefore increases the risk of major perturbations in sodium and water balance, especially severe hyponatraemia.⁷ The risk of hyponatraemia among elderly people is compounded by chronic diseases and long term medications. In particular, many women requiring orthopaedic surgery also take thiazide diuretics to control hypertension.² Thiazides are well known to induce mild hyponatraemia and have been linked to the rapid onset of serious postoperative complications.²,³

Women at risk of hyponatraemia are imperilled by routine infusions of isotonic dextrose. Patients recovering from surgery metabolise glucose almost immediately, so “isotonic” dextrose infusions are in effect hypotonic. Since the 1950s numerous reports have linked hypotonic infusions with death or permanent brain damage in postoperative patients.¹ Recent authoritative reviews warn against routine infusions of dextrose,¹,⁶,⁸ even stating explicitly: “the rationale for using hypotonic fluids in postoperative patients is difficult to discern and has no place in the modern practice of medicine.”¹ Volumes as low as 3-4 litres over two days may cause convulsions, respiratory arrest, permanent brain damage, and death in women who were healthy before admission.⁵,⁸ Most of these cases go unrecognised and are ascribed to conditions such as stroke, arteriovenous malformation, subarachnoid haemorrhage, or herpes encephalopathy, even when blood sodium concentrations are known.⁸

Early symptoms of hyponatraemia (such as weakness, nausea, vomiting, and headache) can be distinguished from postoperative sequelae on the basis of sodium concentrations. Timing also helps discrimination: many patients tolerate surgery without complications, being able to talk, walk, and eat before symptoms of hyponatraemic encephalopathy develop.¹ Treatment is simple and should be prompt: the risk of not treating acute cerebral oedema far exceeds the small risk of osmotic demyelination from treatment.¹,⁶ Fluid infusions should be restricted to normal or hypertonic saline and sodium concentrations monitored every two hours.¹,⁵,⁶ The aim is to raise serum sodium by 1-2 mmol/l per hour (depending on the severity of neurological symptoms) until symptoms resolve.¹,⁶ A loop diuretic such as frusemide (furosemide) may be used to enhance free water excretion and hasten the restoration of normal sodium concentrations. ^{1 6} Iatrogenic hyponatraemia is inexcusable. It is time that doctors woke up to the risks.