As of the late 1969s, there were no interventions to reduce the respiratory morbidity associated with preterm birth. In the late 1960s, animal studies in lambs and rabbits demonstrated that fetal lung maturity was accelerated in animal fetuses whose mothers received glucocorticoids prior to preterm delivery. These studies stimulated obstetricians and scientists to test whether fetal lung maturity might be similarly improved in humans. Unlike some other animals (. cows), the human placenta is relatively permeable to glucocorticoids, suggesting that maternal administration of steroids would allow transfer of these medicines to the preterm fetus. In the present work, authors randomized women at risk of preterm delivery to receive antenatal steroids or placebo and compared the incidence of RDS between groups.
Delicate physiologic mechanisms allow for circulatory transition after birth with a resultant decrease in pulmonary vascular resistance. Failure of these mechanisms causes increased pulmonary pressures and right-to-left shunting, resulting in hypoxemia. This failure can be caused by meconium aspiration syndrome, pneumonia or sepsis, severe RDS, diaphragmatic hernia, and pulmonary hypoplasia. Severe persistent pulmonary hypertension of the newborn (PPHN) occurs in two out of 1,000 live births. 50 Risk factors include maternal diabetes, cesarean delivery, maternal obesity, and black race. Maternal use of a selective serotonin reuptake inhibitor is associated with the condition. Data show only a small absolute risk. 51