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

Abstract 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 ten...

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Bibliographic Details
Published in:Neurosurgery Vol. 67; no. 2; pp. 338 - 344
Main Authors: Oddo, Mauro, Nduom, Edjah, Frangos, Suzanne, MacKenzie, Larami, Chen, Isaac, Maloney-Wilensky, Eileen, Kofke, W. Andrew, Levine, Joshua M., LeRoux, Peter D.
Format: Journal Article
Language:English
Published: Hagerstown, MD Oxford University Press 01.08.2010
Lippincott Williams & Wilkins
Wolters Kluwer Health, Inc
Subjects:
Acute Lung Injury - epidemiology
Acute Lung Injury - etiology
Adult
APACHE
Biological and medical sciences
Brain Chemistry - physiology
Brain Injuries - complications
Brain Injuries - epidemiology
Brain Injuries - therapy
Female
Glasgow Coma Scale
Humans
Hypoxia
Hypoxia, Brain - epidemiology
Hypoxia, Brain - etiology
Intracranial Pressure - physiology
Male
Medical sciences
Middle Aged
Monitoring, Physiologic
Neurosurgery
Oxygen Consumption
Respiration, Artificial
Risk Factors
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Tomography, X-Ray Computed
Traumatic brain injury
Acute lung injury
Lung function
Traumatic brain injury
Systemic oxygenation
Brain hypoxia
Brain tissue oxygen tension
Lung disease
Oxygen
Nervous system diseases
Respiratory disease
Encephalon
Surgery
Risk factor
Hypoxia
Head trauma
Oxygenation
ISSN:0148-396X, 1524-4040, 1524-4040
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Summary:Abstract 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 (PbtO2) in patients with severe TBI. METHODS 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. RESULTS 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). CONCLUSION 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.
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ISSN:0148-396X
1524-4040
1524-4040
DOI:10.1227/01.NEU.0000371979.48809.D9