To determine the effect of normobaric hyperoxia on cerebral metabolism in patients with severe traumatic brain injury.
Prospective clinical investigation.
Neurosciences critical care unit of a university hospital.
Eleven patients with severe traumatic brain injury.
Cerebral microdialysis, brain tissue oximetry (Pbo2), and oxygen-15 positron emission tomography (15O-PET) were undertaken at normoxia and repeated at hyperoxia (Fio2 increase of between 0.35 and 0.50).
Established models were used to image cerebral blood flow, blood volume, oxygen metabolism, and oxygen extraction fraction. Physiology was characterized in a focal region of interest (surrounding the microdialysis catheter) and correlated with microdialysis and oximetry. Physiology was also characterized in a global region of interest (including the whole brain), and a physiologic region of interest (defined using a critical cerebral metabolic rate of oxygen threshold). Hyperoxia increased mean ± sd Pbo2 from 28 ± 21 mm Hg to 57 ± 47 mm Hg (p = .015). Microdialysate lactate and pyruvate were unchanged, but the lactate/pyruvate ratio showed a statistically significant reduction across the study population (34.1 ± 9.5 vs. 32.5 ± 9.0, p = .018). However, the magnitude of reduction was small, and its clinical significance doubtful. The focal region of interest and global 15O-PET variables were unchanged. “At-risk” tissue defined by the physiologic region of interest, however, showed a universal increase in cerebral metabolic rate of oxygen from a median (interquartile range) of 23 (22–25) μmol·100 mL−1·min−1 to 30 (28–36) μmol·100 mL−1·min−1 (p < .01).
In severe traumatic brain injury, hyperoxia increases Pbo2 with a variable effect on lactate and lactate/pyruvate ratio. Microdialysis does not, however, predict the universal increases in cerebral metabolic rate of oxygen in at-risk tissue, which imply preferential metabolic benefit with hyperoxia.
From the University Division of Anaesthesia (JN, JPC, JGO, DAC, AKG, DKM), Academic Neurosurgery Unit (IT, PS, JDP, PJH), and Wolfson Brain Imaging Centre (JN, JPC, IT, TDF, FIA, PS, JGO, DAC, JDP, PJH, DKM), University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
The authors have not disclosed any potential conflicts of interest.
Supported, in part, by a British Journal of Anaesthesia/Royal College of Anaesthetists Research Fellowship (Dr. Nortje), an Academy of Medical Sciences/Health Foundation Clinician Scientist Fellowship (Dr. Coles), by grants from Codman and the Evelyn Trust (Dr. Timofeev), by an Academy of Medical Sciences/Health Foundation Senior Surgical Scientist Fellowship (Dr. Hutchinson), and by grant G9439390 ID65883 from the Medical Research Council.
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