Exogenous surfactant in acute respiratory distress syndrome: more is better

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Abstract
Pulmonary-surfactant dysfunction can lead to acute lung injury and is characterized by alveolar instability, floating, and collapse. These abnormalities have been shown to occur in acute respiratory distress syndrome (ARDS) 5, 6 and infant respiratory distress syndrome (IRDS) 7. Since the initial report of ARDS by Ashbaugh et al. 5, abnormalities of the surfactant system have been recognized. Petty and co-workers 8, 9, later reported both qualitative and quantitative abnormalities in the surfactant content of ARDS patients. It is now known that surfactant dysfunction plays a major role in the pathophysiology of ARDS 6, 10, and functional changes have been described not only in patients with established ARDS, but also in patients at risk 10–12. The main biochemical abnormalities include an 80% fall in the total phospholipid content, decline in the fractional content of DPPC and phosphatidylglycerol and other fractions, and loss of apoproteins (90% of surfactant protein (SP)-A and SP-B) 6, 7. This loss of alveolar surfactant is due to several factors including the presence of plasma proteins 13, cleavage of phospholipids by serum phospholipases 14, formation of free radical species (including nitrates, lipid peroxidation, etc.) 15–17, and conversion to nonfunctional surfactant with more phospholipid aggregates 14.