Diringer Michael N
Neurology/Neurosurgery Intensive Care Unit, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Curr Opin Crit Care. 2008 Apr;14(2):167-71. doi: 10.1097/MCC.0b013e3282f57552.
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.
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.
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.
几十年来，人们一直认为脑缺血是创伤性脑损伤继发性脑损伤的主要原因，治疗重点是改善脑灌注和血流量。然而，在观察到创伤性脑损伤中的线粒体功能障碍以及广泛使用脑组织氧分压（P(br)O(2)）监测之后，最近的研究工作集中在使用高氧来减轻创伤性脑损伤的影响。
以往关于常压高氧的研究将非常间接的脑氧代谢指标（颅内压、脑氧分压和微透析）用作结果变量。这些指标的解读存在争议，难以确定高氧的影响。然而，最近一项研究利用正电子发射断层扫描研究高氧对急性重型创伤性脑损伤患者的影响，发现该干预措施并未改善脑氧代谢率。
尽管微透析研究有提示性数据，但对大脑利用氧气能力的直接测量表明，高氧并不会增加氧利用。这一点，再加上氧中毒的实际风险，表明目前常规临床使用并不合适，应等待适当的前瞻性结果研究。
