ABSTRACT
I. Introduction In the first medical description of the acute respiratory distress syndrome (ARDS) provided in 1967 by Ashbaugh and coworkers (1), the authors postulated that surfactant function might be diminished in patients with ARDS, with resultant alveolar collapse, edema, increased shunt, and hypoxemia. Indeed, using tools available at the time, a loss of surfacetension lowering capacity in fluid from the lungs of ARDS patients was demonstrated (2). Subsequent investigations have firmly established that there is diminished surfactant mass and function in the lungs of patients with ARDS, and have also provided excellent rationale for surfactant replacement in those patients. Although clinical trials have shown modest improvement in gas exchange after surfactant replacement, none has yet to show improved survival. Nevertheless, because of the strong rationale for this intervention and because of the lack of efficacy of any other pharmacologic intervention, efforts to establish a role for the application of exogenous surfactant in the treatment of patients with ARDS continue.
