Adult Respiratory Distress Syndrome

Abstract

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 . . .