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高氧治疗对中重度创伤性脑损伤患者神经学转归及死亡率的影响

The Impact of Hyperoxia Treatment on Neurological Outcomes and Mortality in Moderate to Severe Traumatic Brain Injured Patients.

作者信息

Khan Raymond, Alromaih Sarah, Alshabanat Hind, Alshanqiti Nosaiba, Aldhuwaihy Almaha, Almohanna Sarah Abdullah, Alqasem Muna, Al-Dorzi Hasan

机构信息

King Saud bin Abdulaziz University for Health Sciences College of Medicine, Riyadh, Saudi Arabia.

出版信息

J Crit Care Med (Targu Mures). 2021 Aug 5;7(3):227-236. doi: 10.2478/jccm-2021-0014. eCollection 2021 Jul.

DOI:10.2478/jccm-2021-0014
PMID:34722926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8519380/
Abstract

BACKGROUND

Traumatic brain injury is a leading cause of morbidity and mortality worldwide. The relationship between hyperoxia and outcomes in patients with TBI remains controversial. We assessed the effect of persistent hyperoxia on the neurological outcomes and survival of critically ill patients with moderate-severe TBI.

METHOD

This was a retrospective cohort study of all adults with moderate-severe TBI admitted to the ICU between 1st January 2016 and 31st December 2019 and who required invasive mechanical ventilation. Arterial blood gas data was recorded within the first 3 hours of intubation and then after 6-12 hours and 24-48 hours. The patients were divided into two categories: Group I had a PaO2 < 120mmHg on at least two ABGs undertaken in the first twelve hours post intubation and Group II had a PaO2 ≥ 120mmHg on at least two ABGs in the same period. Multivariable logistic regression was performed to assess predictors of hospital mortality and good neurologic outcome (Glasgow outcome score ≥ 4).

RESULTS

The study included 309 patients: 54.7% (n=169) in Group I and 45.3% (n=140) in Group II. Hyperoxia was not associated with increased mortality in the ICU (20.1% vs. 17.9%, p=0.62) or hospital (20.7% vs. 17.9%, p=0.53), moreover, the hospital discharge mean (SD) Glasgow Coma Scale (11.0(5.1) vs. 11.2(4.9), p=0.70) and mean (SD) Glasgow Outcome Score (3.1(1.3) vs. 3.1(1.2), p=0.47) were similar. In multivariable logistic regression analysis, persistent hyperoxia was not associated with increased mortality (adjusted odds ratio [aOR] 0.71, 95% CI 0.34-1.35, p=0.29). PaO2 within the first 3 hours was also not associated with mortality: 121-200mmHg: aOR 0.58, 95% CI 0.23-1.49, p=0.26; 201-300mmHg: aOR 0.66, 95% CI 0.27-1.59, p=0.35; 301-400mmHg: aOR 0.85, 95% CI 0.31-2.35, p=0.75 and >400mmHg: aOR 0.51, 95% CI 0.18-1.44, p=0.20; reference: PaO2 60-120mmHg within 3 hours. However, hyperoxia >400mmHg was associated with being less likely to have good neurological (GOS ≥4) outcome on hospital discharge (aOR 0.36, 95% CI 0.13-0.98, p=0.046; reference: PaO2 60-120mmHg within 3 hours.

CONCLUSION

In intubated patients with moderate-severe TBI, hyperoxia in the first 48 hours was not independently associated with hospital mortality. However, PaO2 >400mmHg may be associated with a worse neurological outcome on hospital discharge.

摘要

背景

创伤性脑损伤是全球发病和死亡的主要原因。高氧与创伤性脑损伤患者预后之间的关系仍存在争议。我们评估了持续性高氧对中重度创伤性脑损伤重症患者神经功能预后和生存率的影响。

方法

这是一项回顾性队列研究,研究对象为2016年1月1日至2019年12月31日入住重症监护病房(ICU)且需要有创机械通气的所有中重度创伤性脑损伤成年患者。在插管后的前3小时内记录动脉血气数据,然后在6 - 12小时和24 - 48小时后记录。患者分为两类:第一组在插管后12小时内至少两次动脉血气分析中动脉血氧分压(PaO₂)<120mmHg,第二组在同一时期至少两次动脉血气分析中PaO₂≥120mmHg。进行多变量逻辑回归分析以评估医院死亡率和良好神经功能预后(格拉斯哥预后评分≥4)的预测因素。

结果

该研究纳入了309例患者:第一组54.7%(n = 169),第二组45.3%(n = 140)。高氧与ICU死亡率增加(20.1%对17.9%,p = 0.62)或医院死亡率增加(20.7%对17.9%,p = 0.53)无关,此外,出院时的平均(标准差)格拉斯哥昏迷量表评分(11.0(5.1)对11.2(4.9),p = 0.70)和平均(标准差)格拉斯哥预后评分(3.1(1.3)对3.1(1.2),p = 0.47)相似。在多变量逻辑回归分析中,持续性高氧与死亡率增加无关(调整后的优势比[aOR]为0.71,95%置信区间[CI]为0.34 - 1.35,p = 0.29)。插管后3小时内的PaO₂也与死亡率无关:121 - 200mmHg:aOR为0.58,95%CI为0.23 - 1.49,p = 0.26;201 - 300mmHg:aOR为0.66,95%CI为0.27 - 1.59,p = 0.35;301 - 400mmHg:aOR为0.85,95%CI为0.31 - 2.35,p = 0.75;>400mmHg:aOR为0.51,95%CI为0.18 - 1.44,p = 0.20;参考:插管后3小时内PaO₂为60 - 120mmHg。然而,PaO₂>400mmHg与出院时神经功能良好(格拉斯哥预后评分≥4)的可能性降低相关(aOR为0.36,95%CI为0.13 - 0.98,p = 0.046;参考:插管后3小时内PaO₂为60 - 120mmHg)。

结论

在插管的中重度创伤性脑损伤患者中,最初48小时的高氧与医院死亡率无独立相关性。然而,PaO₂>400mmHg可能与出院时较差的神经功能预后相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3312/8519380/b0bb65fe7849/jccm-07-227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3312/8519380/b0bb65fe7849/jccm-07-227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3312/8519380/b0bb65fe7849/jccm-07-227-g001.jpg

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