Hyponatraemia occurs in 14% of hospitalised patients. Our data shows that plasma sodium concentrations < 130 mmol/l occur in 8% of patients with traumatic brain injury (TBI) and in 6% of patients undergoing hypophysectomy. The causes of hyponatraemia in neurosurgical patients include SIADH, cerebral salt wasting (CSW), diuretic therapy, intravenous fluids, and glucocorticoid deficiency.
The greatest diagnostic challenge is to distinguish between SIADH and the syndrome of CSW. In contrast to SIADH, which occurs in the setting of euvolaemia and antidiuresis, CSW is characterised by hypovolaemic hyponatraemia with a marked diuresis and natriuresis. To distinguish between the two syndromes, careful documentation of indices of blood volume is essential. Direct measurement of central venous pressure, which is normal in SIADH but low in CSW, is occasionally required.
Elevated plasma concentrations of natriuretic peptides have been reported in CSW, suggesting that cerebral insults may cause the release of natriuretic peptides, causing natriuresis and diuresis, and the development of hypovolaemic hyponatraemia. This hypothesis has been challenged, on the grounds of insufficient evidence of volume depletion and renal salt wasting in the literature, though in clinical practice there is no doubt that hypovolaemic hyponatraemia developing secondary to profound natriuresis, is a real entity. The syndrome typically resolves within 3-5 days of the onset of hyponatraemia. Although the pathogenesis of CSW requires further elucidation, recognition of the syndrome is crucial, as the treatment of SIADH remains fluid restriction, whereas CSW needs vigorous intravenous saline therapy. Accurate diagnosis is therefore essential for the institution of appropriate treatment.
22 - 24 Mar 2004
British Endocrine Societies