The leading cause of death in patients with ARDS is multiorgan failure (MOF) caused by a systemic inflammatory response. This finding has led to a great evolution in our understanding of ARDS since it was first reported in 1967.1 We have struggled over the last number of years to find the molecular basis for the changes we see in the gross pathology of the lung and other end organs.
Many investigators have begun to develop the relationship between cytokine modulation and cytokine levels in the physiology of ARDS and how this syndrome relates to the systemic inflammatory response and end-organ dysfunction. Donnelly and colleagues2– found that patients at risk for ARDS who had higher levels of interleukin (IL)-8 in BAL fluid subsequently progressed to ARDS, thus providing a potential early marker for the development of this syndrome and some clues as to pathogenesis. The clinical importance of this developing understanding of cytokine modulation has led to studies looking at how the simplest treatment for respiratory failure and ARDS, mechanical ventilation, contributes to MOF through the spread of inflammatory mediators.3–4