Clinical meaning
Respiratory distress syndrome (RDS) results from insufficient pulmonary surfactant production by type II pneumocytes, which typically mature by 34-36 weeks gestation. Surfactant reduces alveolar surface tension, preventing alveolar collapse during expiration. Without adequate surfactant, alveoli collapse with each breath (atelectasis), requiring tremendous work of breathing to re-expand. This creates a cycle of progressive atelectasis, ventilation-perfusion mismatch, hypoxemia, and respiratory acidosis. Damaged alveolar epithelium allows plasma protein leakage, forming hyaline membranes that further impair gas exchange. Exogenous surfactant therapy dramatically improves outcomes when administered early.
Exam relevance
Risk factors: - Prematurity (<34 weeks gestation, highest risk factor) - Maternal diabetes (hyperinsulinemia delays surfactant production) - Cesarean delivery without labor (absence of catecholamine surge) - Perinatal asphyxia - Male sex - Second-born twin - Hypothermia at birth
Diagnostics: - Monitor oxygen saturation continuously via pulse oximetry - Expect chest X-ray showing ground-glass appearance with air bronchograms - Monitor arterial blood gases for hypoxemia and respiratory acidosis - Assess Silverman-Andersen score for respiratory distress severity - Monitor blood glucose (increased metabolic demands) - Expect lecithin-sphingomyelin (L/S) ratio from amniotic fluid prenatally