Michael N Diringer1. 1. Neurology/Neurosurgery Intensive Care Unit, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA. diringerm@neuro.wustl.edu
Abstract
PURPOSE OF REVIEW: For 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 FINDINGS: Previous 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. SUMMARY: Despite 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.
PURPOSE OF REVIEW: For 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 FINDINGS: Previous 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. SUMMARY: Despite 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.
Authors: Alexios A Adamides; Craig D Winter; Philip M Lewis; D James Cooper; Thomas Kossmann; Jeffrey V Rosenfeld Journal: ANZ J Surg Date: 2006-03 Impact factor: 1.872
Authors: Marta Biagioli; Milena Pinto; Daniela Cesselli; Marta Zaninello; Dejan Lazarevic; Paola Roncaglia; Roberto Simone; Christina Vlachouli; Charles Plessy; Nicolas Bertin; Antonio Beltrami; Kazuto Kobayashi; Vittorio Gallo; Claudio Santoro; Isidro Ferrer; Stefano Rivella; Carlo Alberto Beltrami; Piero Carninci; Elio Raviola; Stefano Gustincich Journal: Proc Natl Acad Sci U S A Date: 2009-08-26 Impact factor: 11.205