Hyponatremia is predictable in patients with aneurysmal subarachnoid hemorrhage—clinical significance of serum atrial natriuretic peptide

Abstract

Serum atrial natriuretic peptide (ANP) that is elevated after aneurysmal subarachnoid hemorrhage (SAH) causes diuresis and natriuresis (cerebral salt wasting) and might exacerbate delayed ischemic neurological deficit (DIND). We investigated relationships among hyponatremia, serum ANP elevation, and the onset of DIND after SAH. Thirty-nine consecutive patients (15 women and 24 men) with SAH were assigned to a normonatremia group or a group that developed hyponatremia after SAH. Serum ANP and brain natriuretic peptide were assessed after SAH. All patients remained normovolemic and normotensive. We attributed DIND to vasospasm only in the absence of other causes and when supported by cerebral angiography. Hyponatremia developed after SAH in 11 patients (28.2%), among whom serum ANP concentrations at 0 and 3 days thereafter were significantly increased. Furthermore, DIND developed in five (45.5%) and two (7.1%) hyponatremic and normonatremic patients, respectively (P < 0.05). The serum ANP levels on day 0 after SAH were higher in Hunt and Kosnik grades 3-4 than in 1-2 and in Fisher groups 3-4 than in 1-2 (P < 0.05). Increasing serum ANP concentrations were independently associated with hyponatremia resulting in DIND. Early treatment of hyponatremia might prevent DIND in patients after SAH.