Postinjury multiple organ failure: role of extrathoracic injury and sepsis in adult respiratory distress syndrome

Abstract

Adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF) occur as a result of an unbridled systemic inflammatory response (i.e., severe systemic inflammatory response syndrome [SIRS]). Early epidemiologic studies concluded that infection with systemic sepsis was the common pathway for the development of ARDS and eventual MOF. As a consequence, research investigation from 1977 to 1987 focused on later clinical events (e.g., immunosuppression, persistent hypercatabolism, and bacterial translocation). Now, it is believed that an initial massive traumatic insult can create severe SIRS independent of infection (one-hit model). Alternatively, a less severe traumatic insult can create an inflammatory environment (i.e., primes the host) such that a later, otherwise innocuous, secondary inflammatory insult precipitates severe SIRS (two-hit model). As a result of these newer inflammatory models, research interest over the last 5 yrs has shifted to investigating earlier clinical events (e.g., unrecognized flow-dependent oxygen consumption, ischemia/reperfusion, and priming/activation of the inflammatory response). The traditional infection models of ARDS and MOF are applicable to current research and patient care efforts. However, the inflammatory models emphasize the pivotal role of the initial traumatic insult. Moreover, while ARDS occurs earlier than other types of overt organ failure, it is now believed that simultaneous organ injury is occurring, presumably via similar inflammatory mechanisms.