Burn sepsis

Abstract

Sepsis in the burned individual can arise from multiple causes. However, the unique source is the burn wound itself. It is clear that health is association with maintenance of a bacterial equilibrium in the wound and that infection is a result of an imbalance in favor of the bacteria. The primary host defense mechanism, an intact epithelial barrier, has been lost at the time of burning. A portal of entry has been created, and the bactericidal defenses have been neutralized. All of the host defense mechanisms associated with inflammation are evoked but may be limited by the avascular isolation of much of the wound. In addition to alteration in vascular response associated with the burns, there are adverse changes in the neutrophils themselves. The alterations in nutrition that may follow burn injury further reduce systemic host resistance. Associated diseases, such as diabetes, may present a further hazard. All of the local factors influencing host resistance are adversely affected in the burn wound. There is necrotic tissue, decreased local tissue perfusion, and loss of the mechanical barrier. Quantitative techniques have demonstrated that bacteria are present in the depths of the wound from the time of injury. Infection and burn wound sepsis are clearly represented by the quantitative increase in bacteria to numbers exceeding 10(5) per gram of tissue. In no other instance has the importance of the "amphibiont" organisms been more clearly demonstrated than in the burn wound. Today's nonpathogen has all too often become tomorrow's killer. As therapeutic control becomes effective against the current organism, the ecologic void is filled by another, which, by definition, is resistant to the treatment being employed.