The role of the lung in postinjury multiple organ failure

Background. Postinjury multiple organ failure (MOF) is a result of a dysfunctional inflammatory response to severe injury and shock. Acute lung injury is thought to promote further organ dysfunction by the systemic release of inflammatory mediators from injured lung tissue. Although clinical evidence supports this model, a clear understanding of the relationship between lung dysfunction and multiple organ failure has yet to be defined. We hypothesized that respiratory dysfunction is an early obligate event in the progression of postinjury MOF. Methods. Data were collected prospectively on 1, 344 trauma patients at risk for postinjury MOF Inclusion criteria were age greater than 16 years, trauma intensive care unit admission, Injury Severity Score greater than 15, and survival longer than 48 hours. Isolated head injuries and head injuries with an extracranial abbreviated injury score of less than 2 were excluded. Daily physiologic and laboratory data were collected through surgical intensive care unit day 28 and clinical events were recorded thereafter until death or hospital discharge. Organ failure was characterized using the Denver MOF scale. Results. Organ dysfunction was observed in 1, 011 (75%) of 1,344 patients. Lung dysfunction was observed in 951 (94%) patients with 1 or more organ dysfunctions and 598 (99%) of 605 patients with 2 or more organ dysfunctions. Lung dysfunction preceded heart, liver, and kidney dysfunction by an average of 0.6 +/- 0.2 days, 4.8 +/- 0.2 days, and 5.5 +/- 0.5 days, respectively. The severity of lung dysfunction correlated with the severity of heart, liver, and kidney dysfunction, and the number of other dysfunctional organ systems. Conclusions. Postinjury respiratory dysfunction is an obligate event that precedes heart, liver, and kidney failure. The severity of other organ dysfunction is related directly to the severity of respiratory dysfunction. These data implicate lung dysfunction as central to the Promotion of pathogenic inflammation and the development of postinjury MOF.