Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury

Citation: Bennett M, Trytko B, Jonker B. Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury. (Cochrane Review) In: The Cochrane Library, Issue 4, 2004. Chichester, UK: John Wiley & Sons, Ltd.

Background

Traumatic brain injury is common and presents a health problem with significant effect on quality of life. Hyperbaric oxygen therapy (HBOT) has been suggested to improve oxygen supply to the injured brain and therefore to reduce the volume of brain that will ultimately perish. It is postulated that the addition of HBOT to the standard intensive care regimen may result in a reduction in patient death and disability as a result of these addtional brain-preserving effects.

  Objectives

To assess the benefits and harms of adjunctive HBOT for treating traumatic brain injury.

 Search strategy

We searched CENTRAL (The Cochrane Library Issue 4, 2003), Medline (1966 - 2003), EMBASE (1974 - 2003), CINAHL (1982 - 2003), DORCTHIM (1996 - 2003), and reference lists of articles. Relevant journals were handsearched and researchers in the field were contacted.

 Selection criteria

Randomised studies comparing the effect on traumatic brain injury of therapeutic regimens which include HBOT with those that exclude HBOT (with or without sham therapy).

 Data collection & analysis

Three reviewers independently evaluated the quality of the relevant trials using the validated Oxford-Scale (Jadad 1996) and extracted the data from the included trials.

 Main results

Four trials contributed to this review (382 patients, 199 receiving HBOT and 183 control). There was a trend towards, but no significant increase in, the chance of a favourable outcome when defined as full recovery, Glasgow Outcome Score 1 or 2, or return to normal activities of daily living (RR for good outcome with HBOT 1.94, 95%CI 0.92 to 4.08, P=0.08). Pooled data from the three trials with 327 patients that reported mortality, showed a significant reduction in the risk of dying when HBOT was added to the treatment regimen (RR 0.69, 95%CI 0.54 to 0.88, P=0.003). Heterogeneity between studies was low (I2 =0%), and sensitivity analysis for the allocation of dropouts did not affect that result. This analysis suggests we would have to treat seven patients to avoid one extra death (NNT 7, 95%CI 4 to 22). 

One trial suggested intracranial pressure was favourably lower in those patients receiving HBOT in whom myringotomies had been performed (WMD with myringotomy -8.2mmHg, 95%CI -14.7mmHg to -1.7mmHg, P=0.01), while in two trials there was a reported incidence of 13% for significant pulmonary impairment in the group receiving HBOT versus 0% in the non-HBOT group (P=0.007).

 Reviewers' conclusions

In people with traumatic brain injury, the addition of HBOT significantly reduced the risk of death but not of favourable clinical outcome. The routine application of HBOT to these patients cannot be justified from this review. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT.