Abstract
Ischemia and metabolic dysfunction remain important causes of neuronal loss after head injury, and we have shown that normobaric hyperoxia may rescue such metabolic compromise. This study examines the impact of hyperoxia within injured brain using diffusion tensor imaging (DTI). Fourteen patients underwent DTI at baseline and after 1 hour of 80% oxygen. Using the apparent diffusion coefficient (ADC) we assessed the impact of hyperoxia within contusions and a 1 cm border zone of normal appearing pericontusion, and within a rim of perilesional reduced ADC consistent with cytotoxic edema and metabolic compromise. Seven healthy volunteers underwent imaging at 21%, 60%, and 100% oxygen. In volunteers there was no ADC change with hyperoxia, and contusion and pericontusion ADC values were higher than volunteers (P<0.01). There was no ADC change after hyperoxia within contusion, but an increase within pericontusion (P<0.05). We identified a rim of perilesional cytotoxic edema in 13 patients, and hyperoxia resulted in an ADC increase towards normal (P=0.02). We demonstrate that hyperoxia may result in benefit within the perilesional rim of cytotoxic edema. Future studies should address whether a longer period of hyperoxia has a favorable impact on the evolution of tissue injury.
Highlights
Cerebral ischemia and metabolic dysfunction remain important causes of neuronal loss after traumatic brain injury (TBI).[1]
We defined a rim of cytotoxic edema (‘traumatic penumbra’) on apparent diffusion coefficient (ADC) images that we have previously reported around contusions using diffusion tensor imaging (DTI) (Figure 2).[9]
There was no significant change in ADC after hyperoxia within contusional Regions of interest (ROIs) (P 1⁄4 0.16, paired t-test), but an increase within pericontusional ROIs (P 1⁄4 0.02, paired t-test)
Summary
Cerebral ischemia and metabolic dysfunction remain important causes of neuronal loss after traumatic brain injury (TBI).[1]. While previous studies demonstrate a consistent effect of hyperoxia in increasing brain tissue oxygen levels, reports of the impact on brain metabolism have been inconsistent, regionally variant, and dependent on the underlying metabolic state of the tissue concerned.[2,4] Additional concerns have been raised regarding the potential deleterious effects on pulmonary function and worsening of neuronal injury because of oxidative stress.[5,6] Studies within other pathologies such as stroke and myocardial infarction have shown conflicting evidence of benefit and harm.[7,8] Given this background, it is clear that further study of the regional effects of normobaric hyperoxia is warranted before definitive clinical trials of the intervention after TBI
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