LAUSR

Dear Editor, We thank Dr. Wang and colleagues for their interest in our recent review [1]. We agree with them that hyperbaric oxygen may represent a potentially important therapeutic option for post-arrest encephalopathy as well as other forms of brain injury. We also agree that animal studies of global brain ischemia suggest that hyperbaric oxygen may be beneficial with regard to neurologic outcome [2, 3], although not all preclinical studies concur [4]. However, we did not include hyperbaric oxygen in our review on cerebral edema after cardiac arrest for several reasons. Foremost, the preclinical studies mentioned did not specifically evaluate the effects of hyperbaric oxygen on cerebral edema, only on other measures of neurological outcome. To our knowledge, hyperbaric oxygen is not utilized in Western medicine to treat either cardiac arrest or cerebral edema, and American Heart Association guidelines do not list hyperbaric oxygen as part of post-arrest management recommendations [5]. Additionally, although the clinical data referenced by the authors do suggest that hyperbaric oxygen may be beneficial as part of a neuroprotective strategy following cardiac arrest, this study, like the preclinical studies, provides no data specifically on cerebral edema [6]. Given the focus of our review in cerebral edema, and the absence of data demonstrating anti-edema effects of hyperbaric oxygen on post-arrest edema, we elected to exclude hyperbaric oxygen from our discussion of therapeutic options. However, we would enthusiastically welcome future preclinical and clinical studies evaluating the effects of hyperbaric oxygen on cerebral edema in the setting of cardiac arrest.