Mediators Affecting IL₂ Function in Burn Immunosuppression

Abstract

Thermal injury induces the most complex array of physiological dysfunction known. Extensive research effort has led to an understanding of some of the changes occurring following a major burn, yet early pathological changes have been documented to be different from those of later phases and great difficulties have arisen in determining cause-and-effect relationships in these changes. For example, intensive first treatment using specific, systemic and local therapy successfully delays mortality in the early phase of very severe burns but has little relationship to the outcome. This was observed where burn victims, treated early, survived initially in greater numbers than those devoid of early treatment (48% greater at day 4, 32% at day 12), whereas the difference was only 7.3% at 2 months¹. The fatal outcome of the late phase is ascribed to multiple organ system failure (MOSF) but not always to concomitant sepsis, for often bacteria cannot be detected in up to half the patients who die².Where sepsis had been well controlled and was not confirmed at death, it had been surmised that infection was not the primary cause of death. In this situation, devitalized tissue and/or circulating endotoxin have been thought to perpetuate some mediator-induced response which lead to MOSF². Evidence in animal models suggests, however, that endotoxic shock and burn shock are two different pathologies. Whereas endotoxin mediates its effects through lipid peroxidation via the production of oxygen free radicals, and catalase and superoxide dismutase can reverse these effects, burn shock is not protected by these enzymes³. Thus endotoxin, when present, may not be the main mediator of late death in burns.