Advances in the treatment of burn patients

Abstract

eous tissues. The tissue surrounding the central zone of coagulation has a moderate degree of vascular injury that causes a decrease in tissue perfusion. This zone of stasis can progress to a partial-thickness or a full-thickness injury due to the release of local mediators, such as arachidonic acid, oxidants and cytokines produced by the burn wound. These mediators cause arteriolar and venular dilatation followed by platelet aggregation that causes vascular stasis. Thromboxane A2 (TXA,) is found in high concentrations in the burn wound and is thought to contribute to the decreased blood flow in the zone of stasis. TXA2 increases platelet aggregation and neutrophil migration in the wound microcirculation. TXA2 inhibitors applied locally have been shown to improve blood flow in the zone of ischaemia-'. Increased local vascular permeability may also be attenuated by the use of antioxidants, particularly xanthine oxidase inhibitors, which indicates that an ischaemic-reperfusion injury occurs 3. Many local and systemic physiological alterations are caused by the release of cytokines from the burn wound. The cytokines are involved in haemodynamic changes, tissue inflammation, wound healing, immune .defenses, hypermetabolism and catabolism. The major cytokines that have so far been found to be involved in burn injury are tumour necrosis factor (TNF), interleukin 1 (IL-1), IL-2, IL-4,