The investigation and management of severe hyponatraemia.

yponatraemia is probably the most common electrolyte disturbance encountered in clinical practice. Despite this, the best way to manage this condition is debated and not always fully appreciated. Indeed, there may be problems in both the investigation and its treatment, as is highlighted in the paper by Saeed and colleagues in this month's edition. 1 One problem would seem to be that some clinicians experience difficulties in investigating the causes of hypo-natraemia. It is here where the clinical biochemistry laboratory and chemical pathologist can play an important role in facilitating optimal patient care. Interestingly , Saeed and colleagues showed that rarely did patients with severe hyponatraemia have their urine osmola-lity or sodium checked. 1 In such cases, it is difficult to see how the cause of the hyponatraemia could be clearly established. This of course is of fundamental importance, because the management of hyponatraemia should differ according to its aetiology. 2–4 Indeed, in the paper by Saeed et al it is reported that some cases of hyponatraemia may incorrectly be attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) because the diagnostic criteria had not been fulfilled. 1 This confirms earlier hospital studies and suggests that the problem could be widespread. 5 SIADH may be over diagnosed and the diagnosis is usually made by finding a urine sodium concentration of greater than 20 mmol/litre in the presence of euvolaemic hyponatraemia or low plasma osmolality and in the absence of hypovolaemia, oedema, impaired renal function, the use of diuretics, adrenal insufficiency, or hypothyroidism. According to the Barter and Schwartz criteria for SIADH, the urine osmolality is inappropriately concentrated in relation to the plasma osmolality—that is, in the hypo-osmal state the urine is not maximally dilute. 6 The clinical biochemistry laboratory also has a role in excluding pseudohy-ponatraemia, where an increase in the non-aqueous phase of plasma gives a spuriously low sodium concentration if assayed by techniques that rely on plasma dilution. This has been described in severe hypertriglyceridaemic or hyper-proteinaemic samples. Translocational hyponatraemia also needs excluding, as can be seen with hyperglycaemia or mannitol administration. Here, translo-cation of water from the intracellular fluid space occurs or the prevention of water entry into cells is associated with increased plasma osmolality. 2–4 " Iatrogenic postoperative hyponatr-aemia, as a result of the injudicious use of isotonic dextrose, is still tragically encountered, and can result in neurological damage or death " Ignorance of the effects …