In a report from Beijing that described 125 term infants with RDS, the most frequent causes were perinatal infection with sepsis syndrome in 50 percent, elective cesarean delivery in 27 percent, severe asphyxia in 10 percent, and meconium aspiration in 7 percent (Liu, 2010). Notably, even with a low incidence in term infants, RDS from surfactant deiciency is not rare (Berthelot-Ricou, 2012). Chorioamnionitis, male gender, and white race are independent risks (Anadkat, 2012; Higgins, 2016). lso, mutations of genes that encode for surfactant protein synthesis may augment the deiciency (Wambach, 2012). Regardless of etiology, when surfactant secretion is diminished, the pulmonary pathophysiology, clinical course, and management are similar to that for preterm infants. Treatment includes mechanical ventilation and replacement of surfactant (Chap. 34, p. 637). Evidence now supports that antenatal maternal corticosteroid treatment will enhance surfactant synthesis in late-preterm fetuses, that is, those 34 to 37 weeks' gestation (Gyami-Bannerman, 2016). At Parland Hospital, corticosteroids are not given for this indication in the late-preterm period. Neonatal hypoglycemia is a concern with such treatment, and long-term efects are unknown. However, data indicate that hypoglycemia, if promptly treated, creates no adverse sequelae (McKinlay, 2015). he prognosis in term newborns with RDS largely depends on the cause, severity, and response to treatment.
The physiology of meconium passage and amnionic luid contamination is considered in Chapter 24 (p. 474). In some instances, inhalation of meconium-stained fluid at or near delivery causes acute airway obstruction, chemical pneumonitis, surfactant dysfunction or inactivation, and pulmonary hypertension (Lee, 2016; Lindenskov, 2015). If severe, hypoxemia may lead to neonatal death or long-term neurological sequelae in survivors.
Given the high incidence-10 to 20 percent-of meconium-stained amnionic fluid in laboring women at term, one may reasonably assume that meconium aspiration must be relatively common. Fortunately, severe aspiration leading to overt respiratory failure is much less frequent. And although the exact incidence of meconium aspiration syndrome is unknown, Singh and associates (2009) reported it to complicate 1.8 percent of all deliveries. In a French study of nearly 133,000 term newborns, the prevalence of severe aspiration syndrome was 0.07 percent, and this rose progressively from 37 to 43 weeks' gestation (Fischer, 2012). Mortality rates depend on severity.
Fetal morbidity is more often associated with thicker meconium content. Presumably, in most cases, amnionic luid is ample to dilute the meconium to permit prompt clearance by normal fetal physiological mechanisms. Meconium aspiration syndrome still occasionally develops with light staining. Many newborns are afected after a normal labor and uncomplicated delivery. However, some associated obstetrical factors include postterm pregnancy and fetal-growth restriction. hese fetuses are at highest risk because diminished amnionic fluid and labor with cord compression or utero placental insuiciency are often comorbid. These can enhance the likelihood of meconium passage that is thick and undiluted (Leveno, 1984).