Normobaric Hyperoxia is Associated with Increased Cerebral Excitotoxicity After Severe Traumatic Brain Injury

作者：Quintard Herve; Patet Camille; Suys Tamarah; Marques Vidal Pedro; Oddo Mauro^*

来源：Neurocritical Care, 2015, 22(2): 243-250.

DOI：10.1007/s12028-014-0062-0

• Oxygen
• Hyperoxia
• Brain
• Traumatic brain injury
• Glutamate
• Cerebral microdialysis
• Excitotoxicity

Normobaric oxygen therapy is frequently applied in neurocritical care, however, whether supplemental FiO(2) has beneficial cerebral effects is still controversial. We examined in patients with severe traumatic brain injury (TBI) the effect of incremental FiO(2) on cerebral excitotoxicity, quantified by cerebral microdialysis (CMD) glutamate.
This was a retrospective analysis of a database of severe TBI patients monitored with CMD and brain tissue oxygen (PbtO(2)). The relationship of FiO(2)-categorized into four separate ranges (< 40, 41-60, 61-80, and > 80 %)-with CMD glutamate was examined using ANOVA with Tukey's post hoc test.
A total of 1,130 CMD samples from 36 patients-monitored for a median of 4 days-were examined. After adjusting for brain (PbtO(2), intracranial pressure, cerebral perfusion pressure, lactate/pyruvate ratio, Marshall CT score) and systemic (PaCO2, PaO2, hemoglobin, APACHE score) covariates, high FiO(2) was associated with a progressive increase in CMD glutamate [8.8 (95 % confidence interval 7.4-10.2) A mu mol/L at FiO(2) < 40 % vs. 12.8 (10.9-14.7) A mu mol/L at 41-60 % FiO(2), 19.3 (15.6-23) A mu mol/L at 61-80 % FiO(2), and 22.6 (16.7-28.5) A mu mol/L at FiO(2) > 80 %; multivariate-adjusted p < 0.05]. The threshold of FiO(2)-related increase in CMD glutamate was lower for samples with normal versus low PbtO(2) < 20 mmHg (FiO(2) > 40 % vs. FiO(2) > 60 %). Hyperoxia (PaO2 > 150 mmHg) was also associated with increased CMD glutamate (adjusted p < 0.001).
Incremental normobaric FiO(2) levels were associated with increased cerebral excitotoxicity in patients with severe TBI, independent from PbtO(2) and other important cerebral and systemic determinants. These data suggest that supra-normal oxygen may aggravate secondary brain damage after severe TBI.

• 出版日期2015-4