Trauma, inflammatory cells and ARDS.

Abstract

The adult respiratory distress syndrome (ARDS) was initially described by Ashbaugh as comprising profound hypoxia refractory to oxygen therapy, loss of lung compliance and diffuse radiographic alveolar infiltration (Ashbaugh et al., 1967). The pathophysiological features of ARDS are well established and include reduced functional residual capacity and lung compliance, increased airway resistance, microvascular permeability and severe ventilation/perfusion mismatch (Petty & Fowler 1982; Lloyd et al., 1984; Repine et al., 1992). It is now considered that the process is initiated by a provoking combination of insults, most often distant to the lung, which results in mediator release. This, in turn, initiates a complex sequence of cellular events culminating in breakdown of alveolar/capillary integrity in the lung, leakage of protein-rich fluid into the airspaces, and the clinical manifestations as outlined above.