Surfactant deficiency is the primary cause of RDS, often complicated by an overly compliant chest wall. Both factors lead to progressive atelectasis and failure to develop an effective functional residual capacity (FRC). Surfactant is a surface-active material produced by airway epithelial cells called type II pneumocytes. This cell line differentiates, and surfactant synthesis begins at 24–28 weeks' gestation. Type II cells are sensitive to and decreased by asphyxial insults in the perinatal period. The maturation of this cell line is delayed in the presence of fetal hyperinsulinemia. The maturity of type II cells is enhanced by the administration of antenatal corticosteroids and by chronic intrauterine stress such as pregnancy-induced hypertension, intrauterine growth restriction, and twin gestation. Surfactant, composed chiefly of phospholipid (75%) and protein (10%), is produced and stored in the characteristic lamellar bodies of type II pneumocytes. This lipoprotein is released into the airways, where it functions to decrease surface tension and maintain alveolar expansion at physiologic pressures.