It is now clearly established that respiratory distress syndrome (RDS) is associated with prematurity-related surfactant deficiency. Since its discovery,1 there has been a considerable amount of research defining the biochemical composition of surfactant and its relationship to pulmonary function. A considerable amount of research has also been performed on animals to formulate the scientific basis for surfactant replacement therapy in premature infants to prevent or reduce the severity of RDS.
Clinical trials began with the rescue therapy by Fujiwara et al2 and were followed by several single institution or multicenter trials using bovine, human, or synthetic surfactants. Many of these clinical trials have been published,3-11 and others have been submitted for publication. Many of these trials were randomized, and the form of surfactant therapy was either prevention (endotracheal instillation of surfactant at birth) or rescue (treatment after RDS is diagnosed). Based on the published data, it appears that in both prevention and rescue trials, there is early improvement in respiratory status as evidenced by decreased inspired oxygen concentration and mean airway pressure requirements during the first 3 days of life. Some, but not all, published series suggest a reduction in mortality rates and incidence of pulmonary air leaks3,7 during the first 28 days of life, but none of the published series appear to show an improvement in the incidence of such morbidities as bronchopulmonary dysplasia, necrotizing enterocolitis (NEC), infections, patent ductus arteriosus (PDA), and intraventricular hemorrhage (IVH). In fact, one series showed increased incidence of NEC in the surfactant-treated group,6 the European trial showed an increased incidence of IVH,12 and one series showed an increased incidence in PDA9 in the surfactant-treated group.
Closure of the Ductus Arteriosus and Mechanics of Breathing in Preterm Infants after Surfactant Replacement Therapy
