At the time of this textbook’s first edition in 1903, preterm delivery was often followed by neonatal death. However, subsequent scientific innovation has advanced the threshold of viability to 22 to 24 weeks’ gestation (Watkins, 2020). Moreover, the overall survival rate for preterm neonates <29 weeks’ gestation approaches 80 percent (Travers 2018). Still, the preterm newborn is susceptible to many serious medical complications both early and later in life (Table 34-1).
TABLE 34-1Complications of Prematurity ||Download (.pdf) TABLE 34-1Complications of Prematurity
|Respiratory distress syndrome (RDS) |
|Bronchopulmonary dysplasia (BPD) |
|Patent ductus arteriosus (PDA) |
|Necrotizing enterocolitis (NEC) |
|Retinopathy of prematurity (ROP) |
|Intraventricular hemorrhage (IVH) |
|Periventricular leukomalacia (PVL) |
|Cerebral palsy (CP) |
Neurodevelopmental Impairment (NDI)
The complications of prematurity can be serious, and this is reflected in overall neonatal mortality rates. In 2018, two thirds of all infant deaths in the United States were in the 10 percent born before 37 weeks (Ely, 2020; Hamilton, 2021). Fortunately, rates of preterm birth have declined from approximately 12 percent in 2007 to 10 percent in 2020. The rate of early preterm births (<34 weeks’ gestation) declined from 2.77 to 2.69 percent, which is the lowest level reported since 2007 (Hamilton, 2021).
RESPIRATORY DISTRESS SYNDROME
The seminal complication of the preterm newborn is respiratory distress syndrome (RDS). This results from immature lungs that are unable to sustain necessary oxygenation due to surfactant deficiency. The resulting hypoxia can be associated with pulmonary hypertension and neurologic damage such as cerebral palsy. In addition, hyperoxia, a side effect of RDS treatment, contributes to other preterm morbidities including bronchopulmonary dysplasia, necrotizing enterocolitis, periventricular leukomalacia, and retinopathy of prematurity.
To provide blood gas exchange immediately following delivery, the lungs must rapidly fill with air while being cleared of fluid. Concurrently, pulmonary arterial blood flow must rise. Although some of the fluid is expelled as the chest is compressed during vaginal delivery, most is absorbed through the pulmonary lymphatics via complex mechanisms described in Chapter 32 (p. 586). Sufficient surfactant, synthesized by type II pneumocytes, is essential to stabilize the air-expanded alveoli. This lipoprotein lowers surface tension and thereby prevents lung collapse during expiration (Chap. 7, p. 131). If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, and RDS develops. Although RDS is generally a disease of preterm neonates, it can develop in term newborns, especially with sepsis, pneumonia, or meconium aspiration. In these cases, surfactant can be inactivated by inflammation and/or the presence of meconium (Chap. 33, p. 600).
With inadequate surfactant, alveoli are unstable and collapse with the low pressures of end expiration. Pneumocyte nutrition is compromised by hypoxia and systemic hypotension. Partial persistence of the fetal circulation may lead to ...