Igarashi Takahiro, Moro Nobuhiro, Katayama Yoichi, Mori Tatsuro, Kojima Jun, Kawamata Tatsuro
Department of Neurological Surgery, Nihon University School of Medicine, 30-1 Oyaguchi-kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.
Neurol Res. 2007 Dec;29(8):835-41. doi: 10.1179/016164107X228624.
Symptomatic cerebral vasospasm is a major complication in patients with subarachnoid hemorrhage (SAH). Symptomatic cerebral vasospasm has been reported to be related to the patient's blood volume which is influenced by cerebral salt wasting syndrome (CSWS). We undertook a prospective study to assess whether the onset of symptomatic cerebral vasospasm was predictable or not, by observing the phenomena of CSWS (natriuresis and osmotic diuresis).
Sixty-seven consecutive aneurysmal SAH patients were analysed. After surgery, all patients underwent hypervolemic therapy in order to keep central venous pressure (CVP) within 8-12 cmH(2)O, serum sodium level above 140 mEq/l and a positive water balance. Patients were classified into two groups: those without symptomatic cerebral vasospasm (n=55) and those with symptomatic cerebral vasospasm (n=12). To estimate natriuresis and osmotic diuresis, sodium in/out, water in/out, CVP and other parameters were measured and compared between the two groups.
One day before symptomatic cerebral vasospasm, three factors reached statistical difference in the group that experienced symptomatic cerebral vasospasm: sodium balance, urine volume and water balance. On the day of symptomatic cerebral vasospasm, two factors reached statistical difference: sodium excretion and urine volume. No factor was significantly different 2 days before symptomatic cerebral vasospasm.
Symptomatic cerebral vasospasm has a strong relationship with CSWS. Negative sodium and water balance and increased urine volume indicate a predictor of symptomatic cerebral vasospasm. To predict symptomatic cerebral vasospasm, strict observations are required, because CSWS and symptomatic cerebral vasospasm which follows, develop rapidly.
症状性脑血管痉挛是蛛网膜下腔出血(SAH)患者的主要并发症。据报道,症状性脑血管痉挛与受脑性盐耗综合征(CSWS)影响的患者血容量有关。我们进行了一项前瞻性研究,通过观察CSWS现象(利钠和渗透性利尿)来评估症状性脑血管痉挛的发作是否可预测。
对67例连续性动脉瘤性SAH患者进行分析。术后,所有患者均接受扩容治疗,以使中心静脉压(CVP)维持在8 - 12 cmH₂O,血清钠水平高于140 mEq/l,且水平衡为正值。患者分为两组:无症状性脑血管痉挛组(n = 55)和症状性脑血管痉挛组(n = 12)。为评估利钠和渗透性利尿情况,测量并比较两组的钠出入量、水出入量、CVP及其他参数。
在症状性脑血管痉挛前一天,症状性脑血管痉挛组有三个因素达到统计学差异:钠平衡、尿量和水平衡。在症状性脑血管痉挛当天,有两个因素达到统计学差异:钠排泄和尿量。在症状性脑血管痉挛前两天,无因素有显著差异。
症状性脑血管痉挛与CSWS密切相关。负钠和水平衡以及尿量增加表明是症状性脑血管痉挛的一个预测指标。为预测症状性脑血管痉挛,需要严格观察,因为CSWS及随后发生的症状性脑血管痉挛发展迅速。