Hyperbaric oxygen as adjuvant therapy in the management of burns: Can evidence guide clinical practice?

Abstract

In 2006, therapy for burns is based on aggressive and appropriatefluid resuscitation; topical agents, including skin substitutes for pain relief, antisepsis and scar reduction; and early debridement of devitalised tissue and surgical wound closure; all measures designed to promote healing and minimise scar formation. Developments over the last two decades have significantly improved outcomes, but burn remains an ongoing source of mortality and long-term morbidity [1]. An active search therefore continues for interventions that will further improve outcomes. Hyperbaric oxygen therapy (HBOT) may be one such intervention. It was first suggested for the treatment of thermal burns more than 40 years ago when Wada et al. [2] serendipitously observed more rapid healing of seconddegree burns in a group of coal miners who were being treated with HBOT for carbon monoxide poisoning In 1969, Gruber et al. [3] demonstrated that the area sub-adjacent to a full-thickness injury was hypoxic and could be raised to normal or supra-normal levels through the administration of oxygen under pressure and this was followed by a series of animal experiments that demonstrated a significant reduction of oedema, improved microcirculation, reduced inflammatory responses, faster epithelialisation, and improved wound healing with HBOT [4,5]. The apparent effectiveness of HBOT in these animal models is attributed to the grossly increased partial pressure of oxygen in the arterial blood, and a consequent modest increase in the ability of HBOT to deliver a greatly increased partial pressure of oxygen in the tissues. HBOT can achieve improvements in tissue oxygenation, even in the face of significant ischaemia, because very high arterial oxygen tensions (PaO2) can be achieved by oxygen breathing at increased pressure. While the PaO2 of a normal individual breathing air will be approximately 100 mmHg, breathing oxygen at 2 ATA produces a PaO2 of about 1400 mmHg. Such high arterial partial pressures produce steep gradients down which oxygen diffuses into hypoxic tissues. Normalisation of tissue oxygen tensions in hypoxic wounds by this mechanism is achieved in hyperbaric facilities to produce clinically important benefits for those with diabetic foot ulcers and radiation tissue injury [6,7].