Pathophysiology of respiratory distress syndrome

Respiratory distress syndrome (RDS) is a major cause of neonatal mortality and morbidity, especially in preterm infants. Its aetiology includes developmental immaturity of the lungs, particularly of the surfactant synthesizing system. Surfactant is produced, stored and recycled by type II pneumocytes and is detectable from about 24 weeks’ gestation. It is a mixture of phospholipids, neutral lipids and proteins and is spread as a film over the alveolar surface to lower surface tension and to prevent alveolar collapse. The resulting clinical correlates of RDS can be predicted from the immature lung structure and atelectasis which occur due to surfactant deficiency. Various clinical factors are known to dysregulate surfactant production and function, leading to the development of RDS. Apart from preventing the incidence of prematurity, antenatal steroids and prophylactic surfactant are of proven benefit in reducing the incidence of RDS.