We present a prospective study, designed to evaluate surfactant abnormalities In severely injUred patients during the course of post-traumatic pulmonary dysfunction. Serially obtained bronchoalveolar lavage fluids from noncontused lung areaa (in total, 132samples from 17patients) were analyzed fOr alveolar phospholipid composition and surfactant function in vitro during the first 14days after trauma. The data were compared with thosa ot 29 lavage samples obtained trom

10 healthy control subjects and correlated to severity ot respiratory failure. In the traumatized patients, the total lavage phospholipid content was unchanged, but there was a progressive decrease in the relative amounts of phosphatidylcholine (% PC) and phosphatidylglycerol and an increase in phosphatldyllnositol, phosphatldylethanolamlne, and sphingomyelin. These alterations were paralleled by a marked decrease in the hysteresis area ot the surface tension isotherm. The decrease in% PC and reduction ot hysteresis area were significantly correlated. The alterations in alvaolar phospholipid composition and In vitro surfactant function ware more pronounced in patients with severe respiratory failure. There was a significant inverse correlation between severity ot respiratory dysfunction and% PC or hysteresis area fOrall traumatized patients. Protein leakege into the alveolar space was slgnitlcantly higher In patients with severe respiratory failure and appeared to precede surfactant abnormalities in such patients. The neutrophil content In the alveolar space was markedly Increased in all patients with multiple injuries however, no significant correlation with the noted alterations In alveolar phospholipid composition or surfactant function was fOund. Weconcluded that sUrfactant abnormalities occur during the course ot post-traumatic pulmonary dysfunction and are correlated with the severity ot respiratory failure. AM REV RESPIR DIS 1989; 140: 1033-1039 tntroduetlen Multiple trauma and bacterial sepsisare the most consistent factors associated with the development of acute respiratory distress syndrome in adults (ARDS)(1, 2). It has long been speculated that the alveolar surfactant system might be involved in the pathogenesis of this lifethreatening syndrome (3). This hypothesis is supported by similarities in pulmonary dysfunction between patients with ARDS and preterm babies with respiratory distress syndrome (RDS), in which a deficiency of surfactant is the primary cause of the disease (4). Many in vitro and in vivo studies have illustrated that the alveolar lining layer contains surface-active material that prevents alveolar collapse and makes breathing at normal trans pulmonary pressures feasible (5, 6). To fulfill this physiologic role, a calcium-dependent interaction of different phospholipids and surfactant apoproteins is evidently necessary, though not yet fully understood (7-14). Mechanisms of surfactant alteration in the course of ARDS could include not only lack of surface-active compounds, but also changes in the relative composition of its phospholipid or protein components (15). During the last years much attention has been focused on the mechanisms related to increased lung endothelial and epithelial permeability, a typical finding in ARDS states (16-19). Leakage of protein-rich edema into the alveolar space and subsequent alteration in lung surface tension caused by surfactant-protein interaction has been suggested as an important pathophysiologic event under experimental conditions (20-24). Although knowledge and understanding of the lung surfactant system are increasing rapidly (for review, see 6-9), and a variety of successful surfactant replacement studies in …