Hyperbaric oxygen therapy (HBOT) is another intervention used in early prophylactic treatment of TBI. HBOT encompasses the inhalation of 100% oxygen at environmental pressures above one atmosphere. As spoken to earlier, deregulation of CBF produces an oxygen deficit causing metabolic modifications and ischemia. By increasing the partial pressure of oxygen in blood, independent of that bound to hemoglobin in erythrocytes, HBOT increases oxygen saturation reaching the brain and attempts to decrease tissue damage secondary to ischemia and hypoxia [56]. Yet, since most O2 is hemoglobin-bound, HBOT-mediated O2 saturation increase is limited to up to 10%; a clinically significant amount in many cases. Small scale, early research proved treatment with 100% oxygen for six hours reduced lactate and increased brain tissue oxygenation [57]. More extensive evidence from an early systematic review deemed HBOT’s therapeutic benefit inconclusive [58]. Yet, a recent retrospective study found TBI patients treated with HBOT have improved outcomes when compared to control counterparts [59]. Additionally, prospective studies administering HBOT after patients’ conditions stabilized also demonstrated improved outcomes based on GCS and GOS [60]. One large clinical trial examined the efficacy of HBOT followed by normobaric hyperoxia treatment (NBH) for three days and found the treatment group had reductions in ICP, mortality, and cerebral toxicity with improved favorable GOS outcomes [61]. In an earlier study, Rockswold et al. (2010) compared HBOT to NBH and demonstrated the effects of both to be very similar compared to a standard care control group