Adult Respiratory Distress Syndrome

In 1982, we reviewed current concepts of the pathogenesis of the adult respiratory distress syndrome (ARDS).1 At that time, the role of the intravascular activation of circulating blood leukocytes, especially granulocytes, was a topic of burgeoning interest. Observations that hemodialysis caused neutropenia, hypoxemia, and sequestration of granulocytes in the lung,2 that complement activation accounted for the phenomenon,3 and that complement activation predicted the onset of ARDS in patients4 had recently been reported. These reports suggested a unifying hypothesis for the pathogenesis of ARDS: that complement activation caused activated granulocytes to adhere to and damage pulmonary microvascular endothelial cells, resulting in . . .