Traumatic brain injury (TBI) is an important critical neurologic illness that requires neurocritical care. Traumatic brain injury is an active disease process in which primarily injured tissue manifests as brain hemorrhage and subsequent edema, which can lead to elevated intracranial pressure (ICP). For many years, secondary brain ischemia that resulted from elevated ICP, and a resultant reduction in cerebral perfusion, have been of concern. This concern has led to a number of investigations using brain positron emission tomography and parenchymal brain tissue oxygen monitoring. These investigations have resulted in several reproducible findings. First, cerebral blood flow (CBF) is reduced within and surrounding brain contusions.1 Second, cerebral oxidative metabolism is reduced heterogeneously across the brain and even within normal-appearing brain regions.1 Third, ischemic tissue volume ranges from 5% to 10% of the brain volume after TBI.2 Fourth, nonischemic metabolic crisis can occur in part owing to impaired mitochondrial respiration.3 Fifth, therapeutic hyperventilation can increase the volume of ischemic tissue.4 Sixth, very low levels of brain tissue oxygen can occur in the setting of malignant cerebral edema and correlate with poor outcome.5
Vespa PM. Brain Hypoxia and Ischemia After Traumatic Brain Injury: Is Oxygen the Right Metabolic Target? JAMA Neurol. 2016;73(5):504–505. doi:10.1001/jamaneurol.2016.0251
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