Trauma, Sepsis, and Immune Defects

Traumatic injury and burns remain a major cause of morbidity and mortality in the United States and despite modern techniques of resuscitation and intensive care and an ever increasing number of powerful and effective antibiotics nearly 80% of deaths that occur in trauma and burn patients more than 7 days after injury are caused by sepsis [1]. During the past 10 years the longstanding clinical assumption that host defenses against invading microorganisms were impaired following severe injury has become grounded in fact through the study of injured patients and appropriate animal models. Abnormalities in both specific and nonspecific mechanisms of defense against microorganisms have been described by a number of laboratories, including our own. Nonspecific mechanisms include function of polymorphonuclear [2–4] and mononuclear phagocytes [5–6], natural killer cells [7–9], and products of complement activation [10–13]. Specific defense mechanisms include antibody formation by B lymphocytes [14–16], direct microbial killing by T lymphocytes, and T lymphocyte activation of mononuclear phagocytes [17–19].