Surfactant therapy in the newborn

Abstract

In 1959 Avery and Mead demonstrated that surfactant deficiency was a key feature in the pathogenesis of respiratory distress syndrome (RDS).’ Pulmonary surfactant is a complex mixture of phospholipids, neutral lipids and specific proteins which spread as a monolayer at the air-liquid interfaces of the lung and lower surface tension at end-expiration thus preventing alveolar collapse. Phosphatidylcholine is the major component, constituting about 60% of total phospholipids and dipalmitoylphosphatidylcholine (DPPC) is the primary surface-tension lowering phospholipid. The physical effects of surfactant depend on the interaction between phospholipids and surfactant-associated proteins, for which at least four have been identified SP-A, SP-B, SP-C and SP-D. These apoproteins are synthesized and secreted by type II alveolar cells. The hydrophilic protein SP-A (MW 28-36 kDa) improves surface properties and regulates secretion and recycling of surfactant constituents by alveolar cells. The hydrophobic proteins SP-B and SP-C (3.5-8.4 kDa) facilitate the adsorption and spreading of lipids.2 In addition SP-A and SP-D seem to play a role in host defence mechanisms of the lung. The pool size of endogenous alveolar surfactant lipids in healthy neonates is at least 100 mg/kg; in preterm infants with RDS, however, it is usually less than about 10 mg/kg.3 Surfactant deficiency causes alveolar collapse, increased work of breathing and progressive respiratory failure in babies with RDS. As a consequence of lung injury during the course of the disease or its treatment, serum proteins leak into the air spaces and inhibit the surfactant function.