The innovation of surfactant replacement therapy in the treatment of respiratory distress syndrome has proven to increase the survival and minimize the complications of the premature neonate. Replacing surfactant has lessened time on ventilators, and allowing the neonate and parents an opportunity to grow together earlier outside of intensive care. This paper will discuss the etiology of respiratory distress syndrome type I, the treatment options and nursing care of the neonate during surfactant replacement. Respiratory distress syndrome type I is a decrease production of surfactant, a noncelluar chemical produced in the type II alveolar in the lungs that’s primary function is to decrease the surface tensions and attraction between the type I alveolar walls. Respiration requires the alveolar walls to inflate and deflate continuously, while ventilating the alveoli are exposed to moisture causing an attraction between the alveolar walls. (Kenner, Lott, & Flandermeyer, 271) Surfactant primary function is to neutralize the attraction to prevent alveolar collapse during deflation. The fetus begins to develop the type II alveoli at 22nd to 24th week of gestation, however these immature alveoli are incapable of supplying enough surfactant to meet the infant’s respiratory needs. The fetus surfactant production begins to become adequate at the middle terminal stage of alveoli development and production becomes optimal at the 34th-to-36th week. (Porth, 1306) There are four types of surfactant produced by the type 2 alveoli known as primary surfactant proteins SP-A, SP-B, SP-C, and SP-D. SP-A and SP-D roles are inhibiting production of surfactant influencing cleansing and phagocytosis in the alveoli. (Hartshorn, 959) SP-B and SP-C surfactants are the hydrophobic molecules that relieve the alveolar surface tension (Hartshorn, 963)Risk factors for developing RDS prenatally are conditions that compromise fetal development and gesta...
