Acute Lung Injury Is an Independent Risk Factor for Brain Hypoxia After Severe Traumatic Brain Injury

Abstract

Pulmonary complications are frequently observed after severe traumatic brain injury (TBI), but little is known about the consequences of lung injury on brain tissue oxygenation and metabolism. We examined the association between lung function and brain tissue oxygen tension (PbtO2) in patients with severe TBI. We analyzed data from 78 patients with severe, nonpenetrating TBI who underwent continuous PbtO2 and intracranial pressure monitoring. Acute lung injury was defined by the presence of pulmonary infiltrates with a PaO2/FiO2 (PF) ratio less than 300 and the absence of left ventricular failure. A total of 587 simultaneous measurements of PbtO2 and PF ratio were examined using longitudinal data analysis. PbtO2 correlated strongly with PaO2 and PF ratio (P < .05) independent of PaCO2, brain temperature, cerebral perfusion pressure, and hemoglobin. Acute lung injury was associated with lower PbtO2 (34.6 +/- 13.8 mm Hg at PF ratio >300 vs 30.2 +/- 10.8 mm Hg [PF ratio 200-300], 28.9 +/- 9.8 mm Hg [PF ratio 100-199], and 21.1 +/- 7.4 mm Hg [PF ratio <100], all P values <.01). After adjusting for intracranial pressure, Marshall computed tomography score, and APACHE II (Acute Physiology and Chronic Health Evaluation) score, acute lung injury was an independent risk factor for compromised PbtO2 (PbtO2 <20 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21-3.77; P < .01). After severe TBI, PbtO2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO2, independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.