Neonatal respiratory distress syndrome (RDS) results from developmental deficiency of pulmonary surfactant in premature infants, predominantly those born before 34 weeks gestation when type II alveolar pneumocytes have not yet produced adequate surfactant. Surfactant is a complex mixture of phospholipids (primarily dipalmitoylphosphatidylcholine/DPPC, comprising 80% of surfactant mass) and surfactant-associated proteins (SP-A, SP-B, SP-C, SP-D) that reduces alveolar surface tension at the air-liquid interface according to the LaPlace law (P = 2T/r, where decreasing radius increases collapsing pressure). Without surfactant, alveoli collapse during expiration (atelectasis), and the high opening pressures required for each breath cause progressive respiratory failure, ventilation-perfusion mismatch, intrapulmonary shunting, and hypoxemic respiratory failure. The lecithin-to-sphingomyelin (L/S) ratio in amniotic fluid predicts fetal lung maturity: a ratio greater than or equal to 2:1 indicates mature surfactant production, while the presence of phosphatidylglycerol (PG) confirms lung maturity. Antenatal corticosteroids (betamethasone 12 mg IM x 2 doses 24 hours apart, or dexamethasone 6 mg IM x 4 doses 12 hours apart) given to mothers at risk for preterm delivery between 24-34 weeks accelerate fetal lung maturation by inducing type II pneumocyte...