Neonatal respiratory distress syndrome

NRDS results from insufficient production of pulmonary surfactant by type II pneumocytes, typically due to lung immaturity in premature infants. Surfactant, composed primarily of dipalmitoylphosphatidylcholine (DPPC) and surfactant proteins, reduces surface tension and prevents alveolar collapse during expiration. Without adequate surfactant, alveoli collapse (atelectasis), leading to ventilation-perfusion mismatch, hypoxemia, and increased work of breathing. Risk factors include prematurity (<34 weeks), maternal diabetes (delayed lung maturity), cesarean delivery without labor, and male sex. Clinical presentation includes onset within 2-6 hours of birth with progressive respiratory distress, characterized by tachypnea (>60/min), expiratory grunting, intercostal retractions, nasal flaring, and central cyanosis. Chest X-ray shows a characteristic 'ground glass' appearance with air bronchograms. Complications include pneumothorax, bronchopulmonary dysplasia, and patent ductus arteriosus. Treatment includes exogenous surfactant administration, mechanical ventilation or CPAP, and supportive care. Prevention involves antenatal corticosteroids (betamethasone) given to mothers 24-48 hours before delivery to accelerate fetal lung maturation.