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. 1996 Nov;46(5):500-7; discussion 507-8.
doi: 10.1016/s0090-3019(96)00034-1.

Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm

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Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm

Y Kurokawa et al. Surg Neurol. 1996 Nov.

Abstract

Background: Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states.

Methods: To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH.

Results: Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume.

Conclusion: Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.

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