Pharmacology Review

Abstract

After completing this article, readers should be able to: 1. Explain the sources of immediate and delayed treatment responses to surfactant. 2. List the factors that affect surfactant distribution in the preterm lung. 3. List the mechanisms that can inhibit surfactant function. 4. Explain why antenatal corticosteroids and surfactant improve lung function and outcomes of preterm infants. Surfactant treatments have been the standard of care for infants who have respiratory distress syndrome (RDS) ever since the United States Food and Drug Administration approved its use in 1990. The development of surfactant is one of the great success stories in neonatal care because the therapy specifically treats the surfactant deficiency and changes the pathophysiology and outcome of RDS. Many clinicians now use surfactant without appreciating the research that was essential to learning how to use it and to understanding why it works so well for most infants. That research history is the basis for interpreting new approaches to the care of infants who have RDS, such as the early use of continuous positive airway pressure (CPAP). Surfactant works because of complicated biophysical and metabolic effects within the preterm lung. These effects are modified by clinical variables such as antenatal steroids, lung injury, and gestational age. The standard diagram of the pathophysiology of RDS developed in the 1980s still holds today (Fig. 1). Infants who have RDS have surfactant lipid pools of less than 10 mg/kg compared with the surfactant lipid pool sizes in term infants of perhaps 100 mg/kg. Further, lung structure is immature at less than 32 weeks’ gestation. The fetal human lung is in the saccular stage of development during the period of viability from 23 weeks’ gestation to the initiation of secondary septation (alveolarization), which begins at about 32 weeks’ gestation. The structure of the preterm lung affected by RDS limits lung …