Purpose of review: Currently, no neuroprotective therapies have been shown to reduce the secondary neuronal damage occurring after traumatic brain injury. Recent studies have addressed the potentiality of hyperoxia to ameliorate brain metabolism after traumatic brain injury. In this article, we present the principles of oxygen transport to the brain, the effects of hyperoxia on cerebral metabolism, and the role of lactate in brain metabolism after traumatic brain injury.
Recent findings: It has been shown that hyperoxia obtained by increasing the inspired fraction of oxygen results in a decreased cerebral lactate concentration measured in the extracellular space using the microdialysis. However, the brain oxygen delivery is not substantially improved by eubaric hyperoxia and the ratio between lactate and pyruvate (a better indicator of the cellular redox state than lactate alone) is not changed by hyperoxia. In addition, it has been shown the lactate might be an alternative fuel for neurons during the acute postinjury phase.
Summary: At present, there is no evidence supporting any clinical benefit of hyperoxia in brain-injured patients, and the meaning of posttraumatic brain extracellular lactate accumulation should be further investigated.