1. Rapid correction of hyponatraemia in humans has been reported to be associated with central pontine myelinolysis (CPM). In patients with hyponatraemia related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) we have rapidly corrected hyponatraemia by using urea, without observing clinical CPM. This led us to analyse the brain damage induced by hypertonic saline and by urea when used for the correction of hyponatraemia in a rat model of SIADH.

2. Severe hyponatraemia (serum Na+ < 115 mmol/l) was produced in 28 rats. Seven rats were excluded from statistical analysis because they died during the correction of hyponatraemia, or because they were under- or over-corrected. Normalization of serum Na+ (135–146 mmol/l) was obtained in 48 h by hypertonic saline (group I, n = 7) or urea (group II, n = 8).

3. Despite similar correction of serum Na+ at 24 h and 48 h, all the rats treated with hypertonic saline presented severe brain damage, whereas those treated with urea were free of any brain damage. A third group of rats (n = 6) who spontaneously corrected their serum sodium level and presented mild hyponatraemia at 48 h (129 ± 5.2 mmol/l) were also free of any brain damage.

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