PULMONARY SURFACTANT COMPOSITION EARLY IN DEVELOPMENT OF ACUTE LUNG INJURY AFTER CARDIOPULMONARY BYPASS - PROPHYLACTIC USE OF SURFACTANT THERAPY

Cardiopulmonary bypass surgery (CPB) causes lung injury and at least 2 % of adult patients and more children develop the most severe form acu te respiratory distress syndrome (ARDS). Pulmonary surfactant deficien cy contributes to the pathogenesis of ARDS. It has been proposed that surfactant therapy immediately after CPB might arrest progression to A RDS. However, many patients develop only mild lung injury after CPB. T hus early markers are needed to identify those patients at highest ris k to guide selection for treatment. The aim of this study was to deter mine whether changes in surfactant phospholipids occur, and reflect se verity of lung injury within the first few hours after bypass. Because of the relatively low incidence of ARDS in adult patients, this study was conducted using young pigs highly susceptible to bypass-induced l ung injury. Eight pigs were given 2 hours bypass. Six controls underwe nt 'sham' bypass. At 3 h after bypass pulmonary vascular endothelial p ermeability was assessed by transcapillary leakage of radiolabelled tr ansferrin. A 4 hour broncho-alveolar lavage (BAL) was used to assess i ntra-alveolar levels of surfactant, inflammatory cells and oedema prot ein. Bypass caused falls in arterial oxygenation and lung compliance ( P<0.01), but at this early stage in progression of lung injury BAL sur factant phospholipid and albumin levels were within the control range indicating that the alveolar epithelium had not yet suffered major dam age. The main abnormalities were increases in vascular endothelial per meability (P<0.01), BAL neutrophils (P<0.01), total protein and sphing omyelin (SM) (P<0.05). Lung histology showed that the main damage was interstitial oedema located around the bronchioles and their associate d vessels. A single instilled dose of surfactant phospholipids in 5 an imals caused excess in vivo supplementation and did not reduce the ear ly pathophysiologic changes. Our findings suggest that surfactant phos pholipid deficiency does not make a major contribution in the initial stages of lung injury after CPB, and that excessive phospholipid suppl ementation at this stage can be deleterious.