Department of Intensive Care and Hyperbaric Medicine, The Alfred, 55 Commercial Road, Melbourne, VIC, 3004, Australia.
Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, 553 St Kilda Road, Melbourne, VIC, 3004, Australia.
Neurocrit Care. 2021 Apr;34(2):441-448. doi: 10.1007/s12028-020-01033-y.
Supplemental oxygen administration to critically ill patients is ubiquitous in the intensive care unit (ICU). Uncertainty persists as to whether hyperoxia is benign in patients with traumatic brain injury (TBI), particularly in regard to their long-term functional neurological outcomes.
We conducted a retrospective multicenter cohort study of invasively ventilated patients with TBI admitted to the ICU. A database linkage between the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS-APD) and the Victorian State Trauma Registry (VSTR) was utilized. The primary exposure variable was minimum acute physiology and chronic health evaluation (APACHE) III PO in the first 24 h of ICU. We defined hypoxia as PO < 60 mmHg, normoxia as 60-299 mmHg, and hyperoxia as ≥ 300 mmHg. The primary outcome was a Glasgow Outcome Scale-Extended (GOSE) < 5 at 6 months while secondary outcomes included 12 and 24 months GOSE and mortality at each of these timepoints. Additional sensitivity analyses were undertaken in the following subgroups: isolated head injury, patients with operative intervention, head injury severity, and PO either subcategorized by increments of 60 mmHg or treated as a continuous variable.
A total of 3699 patients met the inclusion criteria. The mean age was 42.8 years, 77.7% were male and the mean acute physiology and chronic health evaluation (APACHE) III score was 60.1 (26.3). 2842 patients experienced normoxia, and 783 hyperoxia. The primary outcome occurred in 1470 (47.1%) of patients overall with 1123 (47.1%) from the normoxia group and 312 (45.9%) from the hyperoxia group-odds ratio 0.99 (0.78-1.25). No significant differences in outcomes between groups at 6, 12, and 24 months were observed. Sensitivity analyses did not identify subgroups that were adversely affected by exposure to hyperoxia.
No associations were observed between hyperoxia in ICU during the first 24 h and adverse neurological outcome at 6 months in ventilated TBI patients.
在重症监护病房（ICU），给危重症患者补充氧气的做法非常普遍。目前仍不确定对于创伤性脑损伤（TBI）患者，高氧血症是否是良性的，特别是在长期神经功能预后方面。
我们对 ICU 收治的接受有创通气的 TBI 患者进行了回顾性多中心队列研究。我们利用了澳大利亚和新西兰重症监护学会成人患者数据库（ANZICS-APD）和维多利亚州创伤登记处（VSTR）之间的数据库链接。主要暴露变量是 ICU 第 1 天 24 小时内的急性生理学和慢性健康评估（APACHE）III 最低动脉血氧分压（PO）。我们将缺氧定义为 PO＜60mmHg，氧合正常定义为 60-299mmHg，高氧血症定义为≥300mmHg。主要结局是 6 个月时格拉斯哥预后量表-扩展版（GOSE）评分＜5，次要结局包括 12 个月和 24 个月时的 GOSE 评分和各时间点的死亡率。在以下亚组中进行了额外的敏感性分析：单纯性头部损伤、有手术干预的患者、头部损伤严重程度以及将 PO 按每 60mmHg 的增量亚分类或作为连续变量处理。
共有 3699 名患者符合纳入标准。平均年龄为 42.8 岁，77.7%为男性，急性生理学和慢性健康评估（APACHE）III 评分平均为 60.1（26.3）。2842 名患者氧合正常，783 名患者高氧血症。总体上，1470 名（47.1%）患者发生主要结局，其中 1123 名（47.1%）来自氧合正常组，312 名（45.9%）来自高氧血症组-比值比为 0.99（0.78-1.25）。在 6、12 和 24 个月时，两组之间的结果没有明显差异。敏感性分析未发现亚组因暴露于高氧血症而受到不利影响。
在 ICU 接受有创通气的 TBI 患者中，在第 1 天 24 小时内的高氧血症与 6 个月时的不良神经结局之间没有观察到关联。
