The Development of Hyponatraemia Following Aneurysmal Subarachnoid Haemorrhage Is Mediated By Arginine Vasopressin But Not Brain Natriuretic Peptide

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 130-162-Neuroendocrinology
Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-131
Mark John Hannon*1, Lucy-Ann Behan1, Bairbre Rogers1, Mark Sherlock1, William Tormey1, Stephen G Ball2 and Chris John Thompson1
1Beaumont Hospital / RCSI Medical School, Dublin, Ireland, 2Royal Victoria Infirmary, Newcastle Upon Tyne, United Kingdom
Hyponatraemia following subarachnoid haemorrhage (SAH) is common, but opinion is divided over whether the Syndrome of Inappropriate Antidiuresis (SIAD), glucocorticoid deficiency or cerebral salt wasting syndrome (CSWS) is the key aetiology. To test our hypothesis that SIAD is the most frequent cause of post-SAH hyponatraemia, we prospectively studied 100 patients (61% female, median age 53 (range 16-82)) with non-traumatic aneurysmal SAH. Each patient had plasma sodium (pNa), vasopressin (AVP), brain natriuretic peptide (BNP) and 0900h plasma cortisol (PC), 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<300nmol/L was regarded clinically as inappropriately low. 49% of patients developed hyponatraemia (pNa<135 mmol/L), with 14%<130mmol/L. 36/49 (73.4%) developed hyponatraemia between days 1 and 3 post SAH, 6/49 (12.24%) between days 4 and 7 and 7/49 (14.3%) after day 7. 35/49 (71.4%) hyponatraemic patients were found to have SIAD, 5/49 (10.2%) were hyponatraemic from inappropriate intravenous fluids, 5/49 (10.2%) were volume depleted and 4/49 (8.2%) were hyponatraemic from acute cortisol deficiency. In each patient who developed hyponatraemia which was clinically due to SIAD, AVP was higher before and during the episode of hyponatraemia compared with AVP levels measured once the hyponatraemia had resolved (p=0.03). Plasma BNP levels remained unchanged during their admission (p=0.37). Patients with SIAD had loss of the osmotic relationship between plasma sodium and AVP release, whereas those with normal sodium levels maintained this physiological association (R=0.51, p=0.04). 4/14 developed acute cortisol deficiency (median nadir cortisol 141 nmol/L, range 57 - 251 nmol/L) and consequent hyponatraemia; all were successfully treated with IV hydrocortisone. Patients with SIAD had higher AVP levels than any other hyponatraemic group. Those with hyponatraemia due to inappropriate intravenous fluids and cortisol deficiency had the lowest AVP levels. There was no difference in BNP level between any hyponatraemic group. In the first prospective study of its kind, hyponatraemia following SAH is predominantly due to SIAD, confirmed by sequential AVP measurement. There were no cases of cerebral salt wasting. BNP does not contribute to the development of hyponatraemia following SAH.

Nothing to Disclose: MJH, LAB, BR, MS, WT, SGB, CJT

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: The authors have received an unrestricted educational grant from Novo Nordisk.