Department of Neurological Surgery, Vanderbilt University Medical Center, 1161 21st Avenue South, T4224 Medical Center North, Nashville, TN, 37232-2380, USA.
Vanderbilt University School of Medicine, Nashville, TN, USA.
Neurocrit Care. 2021 Aug;35(1):30-38. doi: 10.1007/s12028-020-01136-6. Epub 2020 Nov 4.
Cerebral vasospasm is a major contributor to disability and mortality after aneurysmal subarachnoid hemorrhage. Oxidation of cell-free hemoglobin plays an integral role in neuroinflammation and is a suggested source of tissue injury after aneurysm rupture. This study sought to determine whether patients with subarachnoid hemorrhage and cerebral vasospasm were more likely to have been exposed to early hyperoxemia than those without vasospasm.
This single-center retrospective cohort study included adult patients presenting with aneurysmal subarachnoid hemorrhage to Vanderbilt University Medical Center between January 2007 and December 2017. Patients with an ICD-9/10 diagnosis of aneurysmal subarachnoid hemorrhage were initially identified (N = 441) and subsequently excluded if they did not have intracranial imaging, arterial PaO values or died within 96 h post-rupture (N = 96). The final cohort was 345 subjects. The degree of hyperoxemia was defined by the highest PaO measured within 72 h after aneurysmal rupture. The primary outcome was development of cerebral vasospasm, which included asymptomatic vasospasm and delayed cerebral ischemia (DCI). Secondary outcomes were mortality and modified Rankin Scale.
Three hundred and forty five patients met inclusion criteria; 218 patients (63%) developed vasospasm. Of those that developed vasospasm, 85 were diagnosed with delayed cerebral ischemia (DCI, 39%). The average patient age of the cohort was 55 ± 13 years, and 68% were female. Ninety percent presented with Fisher grade 3 or 4 hemorrhage (N = 310), while 42% presented as Hunt-Hess grade 4 or 5 (N = 146). In univariable analysis, patients exposed to higher levels of PaO by quintile of exposure had a higher mortality rate and were more likely to develop vasospasm in a dose-dependent fashion (P = 0.015 and P = 0.019, respectively). There were no statistically significant predictors that differentiated asymptomatic vasospasm from DCI and no significant difference in maximum PaO between these two groups. In multivariable analysis, early hyperoxemia was independently associated with vasospasm (OR = 1.15 per 50 mmHg increase in PaO2 [1.03, 1.28]; P = 0.013), but not mortality (OR = 1.10 [0.97, 1.25]; P = 0.147) following subarachnoid hemorrhage.
Hyperoxemia within 72 h post-aneurysmal rupture is an independent predictor of cerebral vasospasm, but not mortality in subarachnoid hemorrhage. Hyperoxemia is a variable that can be readily controlled by adjusting the delivered FiO and may represent a modifiable risk factor for vasospasm.
蛛网膜下腔出血后，脑血管痉挛是导致残疾和死亡的主要原因。无细胞血红蛋白的氧化在神经炎症中起着重要作用，并且被认为是动脉瘤破裂后组织损伤的来源。本研究旨在确定蛛网膜下腔出血伴脑血管痉挛患者是否比无血管痉挛患者更有可能早期发生高氧血症。
这项单中心回顾性队列研究纳入了 2007 年 1 月至 2017 年 12 月期间在范德比尔特大学医学中心就诊的成人蛛网膜下腔出血患者。最初确定了具有国际疾病分类第 9 版/第 10 版（ICD-9/10）蛛网膜下腔出血诊断的患者（N=441），但如果他们没有颅内影像学、动脉 PaO 值或在破裂后 96 小时内死亡（N=96），则将其排除在外。最终的队列包括 345 名患者。高氧血症的程度通过在动脉瘤破裂后 72 小时内测量的最高 PaO 值来定义。主要结局是发生脑血管痉挛，包括无症状性血管痉挛和迟发性脑缺血（DCI）。次要结局是死亡率和改良 Rankin 量表。
345 名患者符合纳入标准；218 名患者（63%）发生血管痉挛。在发生血管痉挛的患者中，85 名患者被诊断为迟发性脑缺血（DCI，39%）。该队列的平均患者年龄为 55±13 岁，其中 68%为女性。90%的患者出现 Fisher 分级 3 或 4 级出血（N=310），而 42%的患者出现 Hunt-Hess 分级 4 或 5 级（N=146）。在单变量分析中，按暴露五分位的 PaO 值分层，暴露水平较高的患者死亡率更高，并且更有可能以剂量依赖性方式发生血管痉挛（P=0.015 和 P=0.019）。没有统计学意义的预测因素可以区分无症状性血管痉挛和 DCI，这两组之间的最大 PaO 值没有显著差异。多变量分析显示，早期高氧血症与血管痉挛独立相关（PaO2 每增加 50mmHg，比值比[OR]为 1.15[1.03，1.28]；P=0.013），但与蛛网膜下腔出血后的死亡率无关（OR=1.10[0.97，1.25]；P=0.147）。
动脉瘤破裂后 72 小时内的高氧血症是蛛网膜下腔出血后血管痉挛的独立预测因素，但不是死亡率的预测因素。高氧血症是一个可以通过调整提供的 FiO 来轻松控制的变量，并且可能是血管痉挛的可改变危险因素。
