title: Normobaric hyperoxia in traumatic brain injury: does brain metabolic state influence the response to hyperoxic challenge?
abstract: This study sought to investigate whether normobaric hyperoxia (NH) improves brain oxygenation and brain metabolism in the early phase of severe and moderate traumatic brain injury (TBI) and whether this effect occurs uniformly in all TBI patients. Thirty patients (9 women and 21 men) with a median initial Glasgow Coma Score (GCS) of 6 (range, 3-12) were monitored using a brain microdialysis (MD) catheter with a brain tissue oxygen sensor (PtiO(2)) placed in the least-injured hemisphere. The inspired oxygen fraction was increased to 100% for 2 h. Patients were divided into two groups: Group 1: patients with baseline brain lactate ≤3 mmol/L and Group 2: patients with baseline brain lactate >3 mmol/L, and therefore increased anaerobic metabolism in the brain. In Group 1, no significant changes in brain metabolic parameters were found after hyperoxic challenge, whereas a significant increase in glucose and a decrease in the lactate-pyruvate ratio (LPR) were found in Group 2. In this latter group of patients, brain glucose increased on average by 17.9% (95% CI, +9.2% to +26.6%, p<0.001) and LPR decreased by 11.6% (95% CI, -16.2% to -6.9%, p<0.001). The results of our study show that moderate and severe TBI may induce metabolic alterations in the brain, even in macroscopically normal brain tissue. We observed that NH increased PaO(2) and PtiO(2) and significantly decreased LPR in patients in whom baseline brain lactate levels were increased, suggesting that NH improved the brain redox state. In patients with normal baseline brain lactate levels, we did not find any significant changes in the metabolic variables after NH. This suggests that the baseline metabolic state should be taken into account when applying NH to patients with TBI. This maneuver may only be effective in a specific group of patients.
authors.affiliation: Neurotraumatology and Neurosurgery Research Unit, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Paseo Vall d'Hebron 119-129, Barcelona, Spain.
authors.forename: Anna
authors.initials: A
authors.lastname: Vilalta
authors.forename: Juan
authors.initials: J
authors.lastname: Sahuquillo
authors.forename: Maria-Angels
authors.initials: MA
authors.lastname: Merino
authors.forename: Maria-Antonia
authors.initials: MA
authors.lastname: Poca
authors.forename: Angel
authors.initials: A
authors.lastname: Garnacho
authors.forename: Tamara
authors.initials: T
authors.lastname: Martínez-Valverde
authors.forename: Mithilesh
authors.initials: M
authors.lastname: Dronavalli
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D015331:Cohort Studies; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D006801:Humans; D018496:Hyperoxia / Q000150:complications* / Q000378:metabolism; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D010102:Oxygen Inhalation Therapy / Q000379:methods*; D011446:Prospective Studies; D055815:Young Adult