Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 > or = 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.
T he enormous negative social and economic impact of TBI throughout the world cannot be overemphasized. The major issue is premature death and disability both in civilian and military populations. Conservative estimates of the prevalence of long-term disability due to TBI in the United States are well over 3 million people. The economic toll of TBI exceeds $60 billion per year. 18 Our previous investigations of HBO 2 Object. Preclinical and clinical investigations indicate that the positive effect of hyperbaric oxygen (HBO 2 ) for severe traumatic brain injury (TBI) occurs after rather than during treatment. The brain appears better able to use baseline O 2 levels following HBO 2 treatments. In this study, the authors evaluate the combination of HBO 2 and normobaric hyperoxia (NBH) as a single treatment.Methods. Forty-two patients who sustained severe TBI (mean Glasgow Coma Scale [GCS] score 5.7) were prospectively randomized within 24 hours of injury to either: 1) combined HBO 2 /NBH (60 minutes of HBO 2 at 1.5 atmospheres absolute [ATA] followed by NBH, 3 hours of 100% fraction of inspired oxygen [FiO 2 ] at 1.0 ATA) or 2) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Intracranial pressure, surrogate markers for cerebral metabolism, and O 2 toxicity were monitored. Clinical outcome was assessed at 6 months using the sliding dichotomized Glasgow Outcome Scale (GOS) score. Mixedeffects linear modeling was used to statistically test differences between the treatment and control groups. Functional outcome and mortality rates were compared using chi-square tests.Results. There were no significant differences in demographic characteristics between the 2 groups. In comparison with values in the control group, brain tissue partial pressure of O 2 (PO 2 ) levels were significantly increased during and following combined HBO 2 /NBH treatments in both the noninjured and pericontusional brain (p < 0.0001). Microdialysate lactate/pyruvate ratios were significantly decreased in the noninjured brain in the combined HBO 2 /NBH group as compared with controls (p < 0.0078). The combined HBO 2 /NBH group's intracranial pressure values were significantly lower than those of the control group during treatment, and the improvement continued until the next treatment session (p < 0.0006). The combined HBO 2 /NBH group's levels of microdialysate glycerol were significantly lower than those of the control group in both noninjured and pericontusional brain (p < 0.001). The combined HBO 2 /NBH group's level of CSF F2-isoprostane was decreased at 6 hours after treatment as compared with that of controls, but the difference did not quite reach statistical significance (p = 0.0692). There was an absolute 26% reduction in mortality for the combined HBO 2 /NBH group (p = 0.048) and an absolute 36% improvement in favorable outcome using the sliding dichotomized GOS (p = 0.024) as compared with the control group.Conclusions. In this Phase II clinical trial, in comparison with standard care (control t...
The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.
Hypertonic saline as a single osmotic agent decreased ICP while improving CPP and PbtO2 in patients with severe traumatic brain injury. Patients with higher baseline ICP and lower CPP levels responded to hypertonic saline more significantly.
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