Preterm Factors Influencing Surfactant Deficiency

Abstract

Surfactant deficiency has come to be understood as equivalent clinically to lung immaturity, except in situations of extreme prematurity or lung hypoplasia. Thus, surfactant deficiency and the diagnosis respiratory distress syndrome (RDS) have been applied quite uniformly to preterm infants with respiratory distress who have no other identifiable problems. While the diagnosis can be made more specific by assay of surfactant phospholipid composition (12), such measurements are seldom made in clinical practice. Perinatal discussions of the premature with respiratory distress also have been focused toward surfactant by the availability of multiple tests of “lung maturation” based on the assay of surfactant components in amniotic fluid (19). While surfactant is necessary for normal lung function, adequate surfactant is not sufficient to assure normal gas exchange in the preterm. There are no simple ways to separate surfactant deficiency states clearly from other aspects of lung development, such as airway development, alveolarization, and the development of the pulmonary vasculature in the preterm infant. The anatomic data of Hislop et al. (13) and Langston et al. (22) indicate a considerable variability in the number of alveoli in the preterm infant at each gestational age, resulting in large differences in potential gas exchange surfaces in different infants. Airway development also differs between infants of comparable gestational ages, as is evident clinically by susceptibility to the development of pulmonary interstitial emphysema. Assuming that surfactant treatments for RDS fully correct the surfactant deficiency, a realistic expectation based on animal studies (16), surfactant treatments should be useful in the near future to eliminate the surfactant deficiency component of lung immaturity syndromes. Any residual lung disease can then be better characterized.