Department of Neurosurgery, Nara Medical University, Nara, Japan.
Acta Neurochir (Wien). 2010 Dec;152(12):2147-52. doi: 10.1007/s00701-010-0735-1. Epub 2010 Aug 3.
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.
脑动脉瘤性蛛网膜下腔出血（SAH）后升高的血清心钠肽（ANP）引起利尿和利钠（脑性盐耗综合征），并可能加重迟发性缺血性神经功能缺损（DIND）。我们研究了低钠血症、血清 ANP 升高与 SAH 后 DIND 发病之间的关系。
39 例连续 SAH 患者（女性 15 例，男性 24 例）被分为正常血钠组或 SAH 后发生低钠血症组。在 SAH 后评估血清 ANP 和脑利钠肽。所有患者均保持血容量和血压正常。我们仅在没有其他原因且得到脑血管造影支持的情况下将 DIND 归因于血管痉挛。
11 例患者（28.2%）发生 SAH 后低钠血症，此后第 0 天和第 3 天血清 ANP 浓度显著升高。此外，5 例（45.5%）和 2 例（7.1%）低钠血症和正常血钠血症患者分别发生 DIND（P < 0.05）。SAH 后第 0 天的血清 ANP 水平在 Hunt 和 Kosnik 3-4 级高于 1-2 级，Fisher 3-4 级高于 1-2 级（P < 0.05）。
血清 ANP 浓度升高与导致 DIND 的低钠血症独立相关。早期治疗低钠血症可能预防 SAH 后患者的 DIND。
