Hyponatraemia is the most common electrolyte abnormality following subarachnoid haemorrhage (SAH). Retrospective data suggests that the Syndrome of Inappropriate Antidiuresis (SIAD) is the most common cause, although glucocorticoid deficiency and rarely cerebral salt wasting may also cause hyponatraemia.
We prospectively studied 100 patients (61% female, median age 53 (range 1682)) with non-traumatic aneurysmal SAH. Each patient had plasma sodium (pNa), urea, osmolality, glucose, 0900 h cortisol (PC) and vasopressin (AVP), and urinary sodium and osmolality measured on days 1, 2, 3, 4, 6, 8, 10 and 12 following SAH. Fluid balance and haemodynamic parameters were recorded daily. A PC <300 nmol/l was regarded clinically as inappropriately low.
49% developed pNa < 35 mmol/l, including 14% with pNa <130 mmol/l. 36/49 (73.4%) developed hyponatraemia between days 1 and 3 post SAH. The median duration of hyponatraemia was 3 days (range 110 days).
In 35/49 (71.4%), hyponatraemia was due to SIAD as defined by standard diagnostic criteria. In 4/49 (8.2%) hyponatraemia was preceded by acute cortisol deficiency and responded to hydrocortisone treatment. Overall, 14/100 patients developed acute cortisol deficiency, of whom 4 developed hyponatraemia due to the cortisol deficiency and 1 developed hyponatraemia due to SIAD. In 5/49 (10.2%) hyponatraemia was due to volume depletion and in 5/49 hyponatraemia was due to inappropriate fluid resuscitation. There were no cases of cerebral salt wasting. Patients with SIAD had a failure of osmoregulation of AVP release, with detectable AVP levels despite hypoosmolality. Patients with SIAD had higher AVP levels than those with hyponatraemia due to acute cortisol deficiency or inappropriate fluid administration (P=0.03).
In the first prospective study of its kind, hyponatraemia occurs in over half of aneurysmal SAH cases, predominantly due to SIAD. Acute glucocorticoid deficiency is a infrequent but treatable cause of hyponatraemia. We found no evidence of cerebral salt wasting syndrome.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology