Term newborns are susceptible to a wide spectrum of illnesses. In many instances, clinical manifestations of these disorders are extensions of pathological effects already incurred by the fetus. A common example is the newborn who is depressed and acidotic because of intrapartum septicemia. Because many of these disorders are differently manifested, those more common in term newborns are considered here, whereas those more frequent in preterm neonates are discussed in Chapter 34. Specific disorders that are the direct consequence of maternal diseases are discussed in pertinent chapters.
Respiratory Distress Syndrome
At the time of delivery, the newborn must convert rapidly to air breathing as described in Chapter 7 (Urinary System). With inspiration, there is alveolar expansion, fluid clearance, and surfactant secretion by type II pneumocytes to prevent lung collapse. Interference with these functions can create respiratory insufficiency with hypoxemia and compensatory tachypnea, which is generally referred to as neonatal respiratory distress syndrome or simply RDS. In preterm infants, this is caused by lung immaturity and insufficient surfactant, and variants may be seen in severely ill older children and adults (Chap. 47, Acute Respiratory Distress Syndrome). All of these have some element of surfactant deficiency because the inciting agent damages alveolar epithelium. As fetuses approach term, surfactant deficiency as a cause of RDS diminishes. 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).
Inadequate surfactant secretion that leads to respiratory distress syndrome becomes less frequent with increasing gestational age. That said, even with a low incidence in term infants, RDS from surfactant deficiency is not rare (Berthelot-Ricou, 2012). Male gender and white race are independent risk factors (Anadkat, 2012). Also, mutations of genes that encode for surfactant protein synthesis may augment the deficiency (Garmany, 2008; 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 by insufflation (Chap. 34, Pathology). There is no evidence that antenatal maternal corticosteroid treatment will enhance surfactant synthesis in late preterm fetuses (Gyamfi-Bannerman, 2012). The prognosis in term newborns largely depends on the cause, severity, and response to treatment.
Meconium Aspiration Syndrome
The physiology of meconium passage and amnionic fluid contamination is considered in detail in Chapter 24 (Meconium in the Amnionic Fluid). 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 (Swarnam, 2012). If severe, hypoxemia may ...