Infants of Ͻ30 wk gestation often require respiratory support for several weeks and may develop bronchopulmonary dysplasia (BPD), which is associated with long-term pulmonary disability or death in severe cases. To examine the status of surfactant in infants at high risk for BPD, this prospective study analyzed 247 tracheal aspirate samples from 68 infants of 23-30 wk gestation who remained intubated for 7-84 d. Seventy-five percent of the infants had one or more surfactant samples with abnormal function (minimum surface tension 5.1-21.7 mN/m by pulsating bubble surfactometer), which were temporally associated with episodes of infection (p ϭ 0.01) and respiratory deterioration (p ϭ 0.005). Comparing normal and abnormal surfactant samples, there were no differences in amount of surfactant phospholipid, normalized to total protein that was recovered from tracheal aspirate, or in relative content of phosphatidylcholine and phosphatidylglycerol. Contents of surfactant proteins (SP) A, B, and C, measured in the surfactant pellet by immunoassay, were reduced by 50%, 80%, and 72%, respectively, in samples with abnormal surface tension (p Յ 0.001). On multivariable analysis of all samples, SP-B content (r ϭ Ϫ0.58, p Ͻ 0.0001) and SP-C content (r ϭ Ϫ0.32, p Ͻ 0.001) were correlated with surfactant function. We conclude that most premature infants requiring continued respiratory support after 7 d of age experience transient episodes of dysfunctional surfactant that are associated with a deficiency of SP-B and SP-C. Infants born prematurely, particularly those of Յ30 wk gestation, are at high risk for lung disease. Although the incidence and severity of respiratory distress syndrome has been reduced with antenatal corticosteroid therapy, which hastens lung development, and postnatal replacement surfactant treatment, newborn respiratory distress remains a frequent occurrence in very low birth weight infants and a requirement for respiratory support often continues for many weeks (1, 2). The clinical pattern after the first week of life frequently includes episodes of respiratory deterioration necessitating increased inspired oxygen or ventilatory support (3). In some infants, lung disease progresses to BPD, which is defined as a continuing requirement for supplemental oxygen and/or positive pressure ventilatory support at 36 wk postmenstrual age (4). BPD occurs in approximately 30% of infants with birth weights Ͻ1000 g and is associated with long-term pulmonary and/or neurodevelopmental disability or death in severe cases (4, 5). The etiology of this progressive respiratory insufficiency is likely multifactorial, including oxygen toxicity, volutrauma associated with mechanical ventilation, infection, patent ductus arteriosus, and inflammation, and results in arrest of alveolar development and interstitial fibrosis (4).Pulmonary surfactant is a mixture of lipids and proteins produced by alveolar type II cells. The major phospholipid component, saturated phosphatidylcholine, forms a highly surface-active film in lung alveoli ...
