Abstract
BackgroundTraumatic 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.MethodThis 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).ResultsThe 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.ConclusionIn 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.
Highlights
Traumatic Brain Injury (TBI) is the leading cause of mortality and disability worldwide among the young population [1]
There were no significant differences between Group I and II in Injury Severity Score [29.9(6.8) vs. 30.2(8.2), 0.74], Revised Trauma Score [5.3(1.2) vs. 5.4(1.1), 0.63] and IMPACT mortality [29.2(18.7) vs. 26.5(16.8), p=0.19]
We investigated if using the threshold of a PaO2 >100mmHg to define hyperoxia would yield a difference in ICU mortality
Summary
Traumatic Brain Injury (TBI) is the leading cause of mortality and disability worldwide among the young population [1]. Acute management of patients after TBI targets physiologic parameters to minimize secondary brain injury. This secondary injury is precipitated by ischemia resulting from decreased cerebral blood flow (CBF) and is likely to occur in the first twenty-four hours after injury [4]. We assessed the effect of persistent hyperoxia on the neurological outcomes and survival of critically ill patients with moderate-severe TBI. Hyperoxia >400mmHg was associated with being less likely to have good neurological (GOS ≥4) outcome on hospital discharge Conclusion: In intubated patients with moderate-severe TBI, hyperoxia in the first 48 hours was not independently associated with hospital mortality. PaO2 >400mmHg may be associated with a worse neurological outcome on hospital discharge
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