高氧对三级护理中心重症监护室创伤性脑损伤患者的影响

Sarah Alromaih, Hind Alshabanat, Nosaiba Alshanqiti, Almaha Aldhuwaihy, Sarah Abdullah Almohanna, Muna Alqasem, F. Othman, R. Khan
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Multivariable logistic regression was performed to assess predictors of hospital mortality and good neurologic outcome (Glasgow outcome score [GOS] ≥ 4). In a second analysis the patients were divided into survivors and non-survivors. Results: The study included 308 patients: 23.4% (n=72) in normoxia group and 76.6% (n=236) in hyeroxia group. Hyperoxia was not associated with increased hospital (43% vs. 18%, p=0.20) mortality. Further, the hospital discharge GCS (10 ± 5 vs. 11 ± 4, p=0.10) and GOS (3 ± 1 vs. 3 ± 1, p=0.35) were similar. In multivariable logistic regression analysis, hyperoxia was not associated with increased mortality (adjusted odds ratio [aOR] 0.99, 95% CI 0.99-1.00, p=0.11). PaO2 within different ranges was also not associated with mortality: 100-200 mmHg: aOR 0.60, 95% CI 0.29-1.52; 201-300 mmHg: aOR 0.66, 95% CI 0.29-1.52; 301-400 mmHg: aOR 0.80, 95% CI 0.31-2.09; and >400 mmHg: aOR 0.39, 95% CI 0.14-1.08; reference: PaO2 60-99 mmHg. 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摘要

背景:外伤性脑损伤(TBI)是全球发病率和死亡率的主要原因。目前,高氧与TBI患者预后之间的关系仍存在争议。我们评估了高氧对中重度TBI危重患者的神经预后和生存的影响。方法:这是一项回顾性队列研究,纳入了2016年1月1日至2019年12月31日期间入住ICU并需要有创机械通气的所有中度TBI成人患者。我们注意到在插管前3小时,然后是6-12小时和24-48小时进行ABGs。患者分为常氧组(PaO2 60 ~ 99 mmHg)和缺氧组(PaO2 60 ~ 100 mmHg)。采用多变量logistic回归来评估医院死亡率和良好神经系统预后(格拉斯哥预后评分[GOS]≥4)的预测因素。在第二次分析中,将患者分为幸存者和非幸存者。结果:308例患者中,常氧组72例(23.4%),高氧组236例(76.6%)。高氧与住院死亡率增加无关(43%对18%,p=0.20)。出院GCS(10±5比11±4,p=0.10)和GOS(3±1比3±1,p=0.35)相似。在多变量logistic回归分析中,高氧与死亡率增加无关(校正优势比[aOR] 0.99, 95% CI 0.99-1.00, p=0.11)。不同范围内的PaO2也与死亡率无关:100-200 mmHg: aOR 0.60, 95% CI 0.29-1.52;201-300 mmHg: aOR 0.66, 95% CI 0.29-1.52;301-400 mmHg: aOR 0.80, 95% CI 0.31-2.09;400 mmHg: aOR 0.39, 95% CI 0.14-1.08;参考:PaO2 60-99 mmHg。正常氧和高氧的Kaplan-Meier生存曲线显示全因死亡率无显著差异。在幸存者与非幸存者分析中,PaO2(中位,IQT)分别为199 mmHg(111-329)和165 mmHg(84-252)。结论:在中度TBI患者中,高氧(PaO2 >100 mmHg)与死亡率增加或神经预后不良(由GOS确定)无关。
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The Effect of Hyperoxia in Traumatic Brain Injury Patients in the Intensive Care Unit of a Tertiary Care Center
Background: Traumatic brain injury (TBI) is a leading cause of morbidity and mortality globally. Currently, the association between hyperoxia and outcomes in patients with TBI remains debatable. We assessed the effect of hyperoxia on the neurological outcomes and survival of critically ill patients with moderate-severe TBI. Methods: This was a retrospective cohort study of all adults with moderatesevere TBI admitted to the ICU between 1st January 2016 and 31st December 2019 who required invasive mechanical ventilation. We noted ABGs performed with the first 3 hours of intubation, then 6-12 hours and 24-48 hours. The patients were divided into two categories: normoxia (PaO2 60-99 mmHg) and hyeroxia (PaO2 >100 mmHg). Multivariable logistic regression was performed to assess predictors of hospital mortality and good neurologic outcome (Glasgow outcome score [GOS] ≥ 4). In a second analysis the patients were divided into survivors and non-survivors. Results: The study included 308 patients: 23.4% (n=72) in normoxia group and 76.6% (n=236) in hyeroxia group. Hyperoxia was not associated with increased hospital (43% vs. 18%, p=0.20) mortality. Further, the hospital discharge GCS (10 ± 5 vs. 11 ± 4, p=0.10) and GOS (3 ± 1 vs. 3 ± 1, p=0.35) were similar. In multivariable logistic regression analysis, hyperoxia was not associated with increased mortality (adjusted odds ratio [aOR] 0.99, 95% CI 0.99-1.00, p=0.11). PaO2 within different ranges was also not associated with mortality: 100-200 mmHg: aOR 0.60, 95% CI 0.29-1.52; 201-300 mmHg: aOR 0.66, 95% CI 0.29-1.52; 301-400 mmHg: aOR 0.80, 95% CI 0.31-2.09; and >400 mmHg: aOR 0.39, 95% CI 0.14-1.08; reference: PaO2 60-99 mmHg. The Kaplan-Meier survival curve for normoxia verses hyperoxia showed no significant difference for all-cause mortality. In the survivors verse nonsurvivors analysis, the PaO2 were (median, IQT) 199 mmHg (111-329) and 165 mmHg (84-252), respectively. Conclusion: Hyperoxia (PaO2 >100 mmHg) was not associated with increased mortality or poor neurological outcomes (determined by GOS) in moderatesevere TBI patients.
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