The preterm infant is susceptible to various serious medical complications during the newborn period as well as morbidities extending later into life (Table 34-1). These complications are primarily the consequence of immature organs that result from abbreviated gestation. A less commonly cited cause of morbidity and mortality is congenital malformations, which are much more prevalent in preterm births. For example, between 2010 and 2013 at Parkland Hospital, major malformations were diagnosed in 67 per 1000 singleton births < 37 weeks’ gestation. This compared with 15 per 1000 in those ≥ 38 weeks—an almost fivefold excess. The pivotal complication, however, is respiratory distress syndrome (RDS). This results from immature lungs that are unable to sustain necessary oxygenation. Resulting hypoxia is an underlying associated cause of neurological damage such as cerebral palsy. In addition, hyperoxia, a side effect of RDS treatment, causes bronchopulmonary dysplasia and retinopathy of prematurity. These complications of prematurity can be placed in perspective in terms of the human consequences. In 2009, two thirds of all infant deaths in the United States were in the 12 percent of infants who were born < 37 weeks (Mathews, 2013).
TABLE 34-1Complications of Prematurity |Favorite Table|Download (.pdf) TABLE 34-1 Complications of Prematurity
|Respiratory distress syndrome (RDS, HMD) |
|Bronchopulmonary dysplasia (BPD) |
|Patent ductus arteriosus (PDA) |
|Necrotizing enterocolitis (NEC) |
|Retinopathy of prematurity (ROP) |
|Intraventricular hemorrhage (IVH) |
|Periventricular leukomalacia (PVL) |
|Cerebral palsy (CP) |
Respiratory Distress Syndrome
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 increase remarkably. Some of the fluid is expressed as the chest is compressed during vaginal delivery, and the remainder is absorbed through the pulmonary lymphatics. Sufficient surfactant, synthesized by type II pneumocytes, is essential to stabilize the air-expanded alveoli. It lowers surface tension and thereby prevents lung collapse during expiration (Chap. 7, Urinary System). If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, and RDS develops. Although respiratory insufficiency is generally a disease of preterm neonates, it does develop in term newborns, especially with sepsis or meconium aspiration.
In typical RDS, tachypnea develops, the chest wall retracts, and expiration is accompanied by grunting and nostril flaring. Shunting of blood through nonventilated lung contributes to hypoxemia and metabolic and respiratory acidosis. Poor peripheral circulation and systemic hypotension may be evident. The chest radiograph shows a diffuse reticulogranular infiltrate and an air-filled tracheobronchial tree—air bronchogram.
As discussed further in Chapter 33 (Respiratory Distress Syndrome), respiratory insufficiency can also be caused by sepsis, pneumonia, meconium aspiration, pneumothorax, persistent fetal circulation, heart failure, and malformations involving thoracic structures, such as diaphragmatic hernia. Evidence is also accruing that common mutations in surfactant protein production may cause RDS (Garmany, 2008; Shulenin, 2004).