A Prospective Randomized Clinical Trial to Compare the Effect of Hyperbaric to Normobaric Oxygenation on Cerebral Metabolism and Intracranial Pressure in Severe Traumatic Brain Injury

Abstract

INTRODUCTION: Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain both under normobaric (NBO) as well as hyperbaric (HBO) conditions. This study is a direct comparison. METHODS: Sixty-nine patients sustaining severe TBI (mean GCS, 5.8) were prospectively randomized to one of three groups: 1) HBO: 60 minutes of HBO at 1.5 ATA; 2) NBO: 3 hours of 100% FiO2 at 1 ATA; and 3) control. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue oxygen tension (PtO2), microdialysis, and intracranial pressure (ICP) were continuously monitored. Cerebral blood flow (CBF); cerebral metabolic rate of oxygen (CMRO2); CSF lactate and F2-isoprostane; bronchial alveolar lavage fluid (BAL) IL-8 and IL-6 assays were obtained pretreatment, during treatment, and 1 and 6 hours posttreatment. Linear random-effects mixed modeling was used. RESULTS: Brain PtO2 levels were significantly increased during treatment in both the HBO (223 mmHg) and NBO (86 mmHg) groups (P < 0.0001) and after HBO treatments (P = 0.003) compared with the control group (29 mmHg). HBO significantly increased CBF and CMRO2 for 6 hours (P < 0.01). CSF lactate decreased posttreatment with both HBO and NBO groups (P < 0.05). HBO patients' dialysate lactate decreased posttreatment for 5 hours (P = 0.017). Microdialysis lactate/pyruvate ratios were significantly decreased posttreatment with both HBO and NBO (P < 0.05). ICP was significantly lower after HBO until the next treatment session (P < 0.001). No increase was seen in CSF F2-isprostane levels, microdialysate glycerol, and BAL inflammatory markers which were used to monitor potential oxygen toxicity. CONCLUSION: HBO clearly has a more robust posttreatment effect than NBO on oxidative cerebral metabolism and ICP. However, it appears that oxygen treatment for severe TBI is not an all or none phenomena but represents a graduated effect. No signs of oxygen toxicity were present.