In a small number of cases fractures of the skull are met with. This accident usually follows violent attempts at delivery, though occasionally it may occur spontaneously.
—J. Whitridge Williams (1903)
In the first edition of this book, Williams wrote very little of the disorders of the term newborn. That said, it is well known that these neonates are susceptible to a wide variety of illnesses and injuries. 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 manifest differently, those more common in term newborns are considered here. 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.
At the time of delivery, the newborn must convert rapidly to air breathing as described in Chapter 32 (Transition to Air Breathing). With inspiration, there is alveolar expansion, fluid clearance, and surfactant secretion by type II pneumocytes to prevent alveolar collapse. Interference with these functions can create respiratory insufficiency with hypoxemia and compensatory tachypnea, nasal flaring, retractions, and grunting (Reuter, 2014). In preterm infants, this is caused by lung immaturity and insufficient surfactant—respiratory distress syndrome (RDS)—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 respiratory distress diminishes. The leading causes in term newborns are transient tachypnea of the newborn, RDS, meconium aspiration syndrome, pneumonia, persistent pulmonary hypertension, and hypoxic-ischemic encephalopathy (Lin, 2015).
Respiratory Distress Syndrome
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 deficiency is not rare (Berthelot-Ricou, 2012). Chorioamnionitis, male gender, and white race are independent risks (Anadkat, 2012; Higgins, 2016). Also, mutations of genes that encode for surfactant protein synthesis may augment the deficiency (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, Clinical Course). Evidence now supports that antenatal maternal corticosteroid treatment will enhance surfactant synthesis in late-preterm fetuses, that is, those 34 to 37 weeks’ gestation (Gyamfi-Bannerman, 2016). At Parkland Hospital, corticosteroids are ...