THE INFLAMMATORY BASIS OF TRAUMA SHOCK-ASSOCIATED MULTIPLE ORGAN FAILURE/

Multiple alterations in inflammatory and immunologic function have bee n demonstrated in clinical and experimental situations after trauma an d hemorrhage, in particular the activation of various humoral (e.g. co mplement, coagulation) and cellular systems (neutrophils, endothelial cells, macrophages). As a consequence of this activation process there is synthesis, expression and release of numerous mediators (toxic oxy gen species, proteolytic enzymes, adherence molecules, cytokines), whi ch may produce a generalized inflammation and tissue damage in the bod y. Mediators are responsible for ongoing interactions of different cel l types and for amplification effects through their networks and feedb ack cycles, finally leading to a sustained inflammation and multiple o rgan damage in the body. In the setting of trauma/shock, many activato rs including bacterial as well as non-bacterial factors may be present that will induce local and systemic inflammatory responses. Although the potential role of bacteria/endotoxin translocation and its clinica l relevance remains controversial, many lines of evidence support the concept that the gut may be the reservoir for systemic sepsis and subs equent MOF in a number of pathophysiologic states.