Introduction Pathophysiology aka hyaline membrane disease immature fetal lungs have a deficiency in surfactant reduced surfactant results in low lung compliance and subsequent atelectasis, intrapulmonary shunting, and acute lung injury Causes prematurity (most important) type II pneumocytes not developed normal source of surfactant production Cesarean section lack of vaginal compression stress on the infant during delivery results in reduced fetal cortisol production and resultant reduction in surfactant production maternal diabetes high insulin levels decrease surfactant production increased fetal blood glucose results in increased fetal insulin production Presentation Symptoms dyspnea, tachypnea during first hours of life nasal flaring expiratory grunting, intercostal, subxiphoid retractions Physical exam severe hypoxemia not responsive to 100% O2 atelectasis results in intrapulmonary (right-to-left) shunting perfusion without ventilation Evaluation ABG hypoxemia respiratory acidosis (elevated PCO2) from poor ventilation Histology hyaline membrane surrounds collapsed alveoli CXR "ground-glass" appearance Amniotic fluid lecithin:sphingomyelin ratio < 1.5 Treatment Prevention corticosteroids given to mother between 23 and 34 weeks gestation at increased risk for preterm delivery within 7 days results in increased surfactant production Treatment nasal CPAP surfactant replacement (endotracheal, so intubation is needed) Complications Bronchopulmonary dysplasia still very common Patent ductus arteriosus normally closed by increased O2 tension at birth hypoxia keeps shunt open 100% O2 therapy damage free radical damage of eyes and lungs may result in blindness and pulmonary dysplasia damage also when the neonate is taken off oxygen therapy upregulation of VEGF due to relative hypoxia results in neovascularization in the retina (retinopathy of prematurity)