Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury.Cochrane Database Syst Rev. 2012 Dec 12; 12:CD004609.CD
Traumatic brain injury is a common health problem with significant effect on quality of life. Each year in the USA approximately 0.56% of the population suffer a head injury, with a case fatality rate of about 40% for severe injuries. These account for a high proportion of deaths in young adults. In the USA, 2% of the population live with long-term disabilities following head injuries. The major causes are motor vehicle crashes, falls, and violence (including attempted suicide). Hyperbaric oxygen therapy (HBOT) is the therapeutic administration of 100% oxygen at environmental pressures greater than 1 atmosphere absolute (ATA). This involves placing the patient in an airtight vessel, increasing the pressure within that vessel, and administering 100% oxygen for respiration. In this way, it is possible to deliver a greatly increased partial pressure of oxygen to the tissues. HBOT can improve oxygen supply to the injured brain, reduce the swelling associated with low oxygen levels and reduce the volume of brain that will ultimately perish. It is, therefore, possible that adding HBOT to the standard intensive care regimen may reduce patient death and disability. However, a concern for patients and families is that using HBOT may result in preventing a patient from dying only to leave them in a vegetative state, entirely dependent on medical care. There are also some potential adverse effects of the therapy, including damage to the ears, sinuses and lungs from the effects of the pressure and oxygen poisoning, so the benefits and risks of the therapy need to be carefully evaluated.
To assess the effects of adjunctive HBOT for traumatic brain injury.
We searched CENTRAL, MEDLINE, EMBASE, CINAHL and DORCTHIM electronic databases. We also searched the reference lists of eligible articles, handsearched relevant journals and contacted researchers. All searches were updated to March 2012.
Randomised studies comparing the effect of therapeutic regimens which included HBOT with those that did not, for people with traumatic brain injury.
DATA COLLECTION AND ANALYSIS
Three authors independently evaluated trial quality and extracted data.
Seven studies are included in this review, involving 571 people (285 receiving HBOT and 286 in the control group). The results of two studies indicate use of HBOT results in a statistically significant decrease in the proportion of people with an unfavourable outcome one month after treatment using the Glasgow Outcome Scale (GOS) (relative risk (RR) for unfavourable outcome with HBOT 0.74, 95% CI 0.61 to 0.88, P = 0.001). This five-point scale rates the outcome from one (dead) to five (good recovery); an 'unfavourable' outcome was considered as a score of one, two or three. Pooled data from final follow-up showed a significant reduction in the risk of dying when HBOT was used (RR 0.69, 95% CI 0.54 to 0.88, P = 0.003) and suggests we would have to treat seven patients to avoid one extra death (number needed to treat (NNT) 7, 95% CI 4 to 22). Two trials suggested favourably lower intracranial pressure in people receiving HBOT and in whom myringotomies had been performed. The results from one study suggested a mean difference (MD) with myringotomy of -8.2 mmHg (95% CI -14.7 to -1.7 mmHg, P = 0.01). The Glasgow Coma Scale (GCS) has a total of 15 points, and two small trials reported a significant improvement in GCS for patients treated with HBOT (MD 2.68 points, 95%CI 1.84 to 3.52, P < 0.0001), although these two trials showed considerable heterogeneity (I(2) = 83%). Two studies reported an incidence of 13% for significant pulmonary impairment in the HBOT group versus 0% in the non-HBOT group (P = 0.007).In general, the studies were small and carried a significant risk of bias. None described adequate randomisation procedures or allocation concealment, and none of the patients or treating staff were blinded to treatment.