Severe thermal injury is one of the most devastating physical and psychological injuries a person can suffer. Over 2 million burn injuries are brought to medical attention in the United States per year. Of these, there are 14 000 deaths and approximately 20 000 sustain injuries requiring admission to a specialised burn unit. About 75 000 patients require hospitalisation each year, and 25 000 of those remain hospitalised for more than 2 months. The most common mechanisms of burn injury are flame and scalding, and the upper extremity, head and neck are the most common body areas involved.
Goals of burn treatment include survival of the patient with rapid wound healing, minimal scarring and abnormal pigmentation, and cost-effectiveness. The optimal outcome is restoration, as nearly as possible, to the pre-burn quality of health and psychological well being.
The burn wound is a complex and dynamic injury characterised by a central zone of coagulation, surrounded by an area of stasis, and bordered by an area of erythema. The zone of coagulation or complete capillary occlusion may progress by a factor of 10 during the first 48 hours after injury; local microcirculation is compromised to the worst extent 12-24 hours post-burn. Burns are in this dynamic state of change for up to 72 hours after injury. Ischaemic necrosis quickly follows. Haematological changes, including platelet micro-thrombi and haemoconcentration, occur in the post-capillary venules. Oedema formation is rapid in the area of the injury; factors include increased capillary permeability, decreased plasma oncotic pressure, increased interstitial oncotic pressure, changes in interstitial space compliance, and lymphatic damage. Oedema is most prominent in directly involved burned tissues, but also develops in distant, uninjured tissue, including muscle, intestine and lung.
Changes occur in the distant micro-vasculature including red cell aggregation, white cell adhesion to venule walls, and platelet thromboemboli. Inflammatory mediators are elaborated locally in part from activated platelets, macrophages, and leukocytes, contribute to local and systemic hyper-permeability of the microcirculation and appear histologically as gaps in the venule and capillary endothelium. This progressive process may extend damage dramatically during the early days after injury. The ongoing tissue damage in thermal injury is due to multiple factors including the failure of the surrounding tissue to supply borderline cells with oxygen and nutrients necessary to sustain viability, capillary or microvascular occlusion in deeper burns leading to decreased perfusion of the burned tissue, and destruction of lymphatics resulting in impaired absorption. The impediment of circulation below the injury leads to desiccation of the wound, as fluid cannot be supplied via the thrombosed or obstructed capillaries. Topical agents and dressings may reduce, but cannot prevent, desiccation of the burn wound and the inexorable progression to deeper layers. Altered permeability is not caused by heat injury alone. Oxidants and other mediators (prostaglandins, kinins and histamine) also contribute to vascular permeability. Neutrophils are a major source of oxidants and injury in the ischaemia-reperfusion mechanism. This complex process may be favourably effected by several interventions.
A decrease in oedema formation has a marked positive proactive impact, especially on the early haemodynamic instability, as well as the later wound conversion from partial to full thickness injury, defining a role for the use of adjunctive hyperbaric oxygen therapy as a modulator of inflammation.
Infection remains the leading overall cause of death from burns. Susceptibility to infection is greatly increased due to the loss of the integumentary barrier to bacterial invasion, the ideal substrate present in the burn wound, and the compromised or obstructed micro-vasculature that prevents humoral and cellular elements from reaching the injured tissue. Additionally, the immune system is seriously affected, demonstrating decreased levels of immunoglobulins and serious perturbations of polymorphonuclear leukocyte (PMNL) function including a reduction in chemotaxis, phagocytosis and diminished killing ability, resulting in increased morbidity and mortality. Patients with specific polymorphisms in the tumour necrosis factor and bacterial recognition genes have a higher incidence of sepsis than the burn injury alone would predict.
Regeneration cannot take place until equilibrium is reached; hence, healing is retarded. Prolongation of the healing process may lead to excessive scarring. Hypertrophic scars are seen in only 4% of cases requiring 10 days to heal, but up to 40% of cases requiring longer than 21 days to heal. Therapy of burns, therefore, must be directed toward minimising oedema, preserving marginally viable tissue, protecting the micro-vasculature, enhancing host defences, and promoting wound closure.
Adjunctive HBO2 therapy can benefit each of these problems directly, and shows promise in the treatment of inhalation injury.