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Oddo, Mauro MD; Nduom, Edjah MD; Frangos, Suzanne RN; MacKenzie, Larami MD; Chen, Isaac MD; Maloney-Wilensky, Eileen MSN; Kofke, W. Andrew MD; Levine, Joshua M. MD; LeRoux, Peter D. MD

BACKGROUND: 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.

OBJECTIVE: We examined the association between lung function and brain tissue oxygen tension (PbtO 2 ) in patients with severe TBI.

METHODS: We analyzed data from 78 patients with severe, nonpenetrating TBI who underwent continuous PbtO 2 and intracranial pressure monitoring. Acute lung injury was defined by the presence of pulmonary infiltrates with a PaO 2 /FiO 2 (PF) ratio less than 300 and the absence of left ventricular failure. A total of 587 simultaneous measurements of PbtO 2 and PF ratio were examined using longitudinal data analysis.

RESULTS: PbtO 2 correlated strongly with PaO 2 and PF ratio (P < .05) independent of PaCO 2 , brain temperature, cerebral perfusion pressure, and hemoglobin. Acute lung injury was associated with lower PbtO 2 (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 PbtO 2 (PbtO 2 <20 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21–3.77; P < .01).

CONCLUSION: After severe TBI, PbtO 2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO 2 , independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.

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