• Michael N Diringer.
• Neurology/Neurosurgery Intensive Care Unit, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA. diringerm@neuro.wustl.edu
• Curr Opin Crit Care. 2008 Apr 1; 14 (2): 167-71.

Purpose Of ReviewFor decades it was assumed that cerebral ischemia was a major cause of secondary brain injury in traumatic brain injury, and management focused on improving cerebral perfusion and blood flow. Following the observation of mitochondrial dysfunction in traumatic brain injury and the widespread use of brain tissue oxygen tension (P(br)O(2) monitoring, however, recent work has focused on the use of hyperoxia to reduce the impact of traumatic brain injury.Recent FindingsPrevious work on normobaric hyperoxia utilized very indirect measures of cerebral oxygen metabolism (intracranial pressure, brain oxygen tension and microdialysis) as outcome variables. Interpretation of these measures is controversial, making it difficult to determine the impact of hyperoxia. A recent study, however, utilized positron emission tomography to study the impact of hyperoxia on patients with acute severe traumatic brain injury and found no improvement on cerebral metabolic rate for oxygen with this intervention.SummaryDespite suggestive data from microdialysis studies, direct measurement of the ability of the brain to utilize oxygen indicates that hyperoxia does not increase oxygen utilization. This, combined with the real risk of oxygen toxicity, suggests that routine clinical use is not appropriate at this time and should await appropriate prospective outcome studies.

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