Ahn Jungeun, Mastorakos Panagiotis, Sokolowski Jennifer D, Chen Ching-Jen, Kellogg Ryan, Park Min S
1School of Medicine, University of Virginia, Charlottesville, Virginia.
2Department of Neurosurgery, University of Virginia Health System, Charlottesville, Virginia; and.
Neurosurg Focus. 2022 Mar;52(3):E7. doi: 10.3171/2021.12.FOCUS21660.
In recent years, hyperoxemia in the intensive care unit has received attention as potentially contributing to negative outcomes in the setting of cardiac arrest, ischemic stroke, and traumatic brain injury. The authors sought to evaluate whether hyperoxemia contributes to worse outcomes in the setting of aneurysmal subarachnoid hemorrhage (aSAH) and to summarize suggested pathophysiological mechanisms.
A systematic literature review was conducted without date restrictions on the PubMed and Web of Science databases on September 15, 2021. All studies that assessed the relationship between patients treated for aSAH and hyperoxemia were eligible independent of the criteria used to define hyperoxemia. All nonclinical studies and studies that did not report outcome data specific to patients with aSAH were excluded. A total of 102 records were found and screened, resulting in assessment of 10 full-text studies, of which 7 met eligibility criteria. Risk of bias was assessed using the Downs and Black checklist. A meta-analysis on the pooled 2602 patients was performed, and forest plots were constructed. Additionally, a review of the literature was performed to summarize available data regarding the pathophysiology of hyperoxemia.
The included studies demonstrated an association between hyperoxemia and increased morbidity and mortality following aSAH. The criteria used to determine hyperoxemia varied among studies. Pooling of univariate data showed hyperoxemia to be associated with poor neurological outcome (OR 2.26, 95% CI 1.66-3.07; p < 0.001), delayed cerebral ischemia (DCI) (OR 1.91, 95% CI 1.31-2.78; p < 0.001), and increased incidence of poor neurological outcome or mortality as a combined endpoint (OR 2.36, 95% CI 1.87-2.97; p < 0.001). Pooling of multivariable effect sizes showed the same relationship for poor neurological outcome (OR 1.28, 95% CI 1.07-1.55; p = 0.01) and poor neurological outcome and mortality as a combined endpoint (OR 1.17, 95% CI 1.11-1.23; p < 0.001). Additionally, review of preclinical studies underlined the contribution of oxidative stress due to hyperoxemia to acute secondary brain injury and DCI.
Reported outcomes from the available studies have indicated that hyperoxemia is associated with worse neurological outcome, mortality, and DCI. These findings provide a general guideline toward avoiding hyperoxemia in the acute setting of aSAH. Further studies are needed to determine the optimal ventilation and oxygenation parameters for acute management of this patient population.
近年来，重症监护病房中的高氧血症作为心脏骤停、缺血性卒中和创伤性脑损伤等情况下潜在导致不良后果的因素受到关注。作者试图评估高氧血症是否会导致动脉瘤性蛛网膜下腔出血（aSAH）患者出现更差的预后，并总结提出的病理生理机制。
2021年9月15日，在PubMed和Web of Science数据库上进行了无日期限制的系统文献综述。所有评估aSAH治疗患者与高氧血症之间关系的研究均符合条件，无论用于定义高氧血症的标准如何。所有非临床研究以及未报告aSAH患者特定结局数据的研究均被排除。共检索到102条记录并进行筛选，最终评估了10篇全文研究，其中7篇符合纳入标准。使用Downs和Black清单评估偏倚风险。对汇总的2602例患者进行了荟萃分析，并绘制了森林图。此外，还对文献进行了综述，以总结关于高氧血症病理生理学的现有数据。
纳入的研究表明，高氧血症与aSAH后发病率和死亡率增加之间存在关联。不同研究中用于确定高氧血症的标准各不相同。单变量数据汇总显示，高氧血症与不良神经功能结局（比值比2.26，95%置信区间1.66 - 3.07；p < 0.001）、迟发性脑缺血（DCI）（比值比1.91，95%置信区间1.31 - 2.78；p < 0.001）以及不良神经功能结局或死亡率作为综合终点的发生率增加相关（比值比2.36，95%置信区间1.87 - 2.97；p < 0.001）。多变量效应量汇总显示，不良神经功能结局（比值比1.28，95%置信区间1.07 - 1.55；p = 0.01）以及不良神经功能结局和死亡率作为综合终点（比值比1.17，95%置信区间1.11 - 1.23；p < 0.001）也存在相同关系。此外，临床前研究综述强调了高氧血症引起的氧化应激对急性继发性脑损伤和DCI的作用。
现有研究报告的结果表明，高氧血症与更差的神经功能结局、死亡率和DCI相关。这些发现为在aSAH急性发作时避免高氧血症提供了一般指导原则。需要进一步研究以确定该患者群体急性管理的最佳通气和氧合参数。
