Bronchopulmonary dysplasia (BPD) is the most common chronic complication associated with preterm birth. In the United States, it affects between 10,000 and 15,000 infants annually, including as many as 50% of extremely low–birth-weight (ELBW; birth weight < 1000 g) infants. BPD is a leading cause of mortality after the first month of life in extremely preterm infants and is a strong predictor of chronic respiratory and cardiovascular impairments, growth failure, and neurodevelopmental delay.
The first descriptions of BPD appeared in the literature soon after the advent of modern day neonatology. In the late 1950s and early 1960s, infant respiratory distress syndrome (RDS) was a leading cause of neonatal death among preterm infants. Increased use of mechanical ventilation improved survival rates for infants with severe RDS. However, prolonged treatment with invasive respiratory support and supplemental oxygen therapy was often necessary. These exposures contributed to chronic lung injury in surviving moderate preterm infants and the development of what Northway and colleagues first termed bronchopulmonary dysplasia in 1967.
As the use of antenatal corticosteroids, noninvasive continuous positive airway pressure (CPAP), and exogenous surfactant therapy increased during the subsequent decades, the epidemiology and pathophysiology of BPD evolved. It is now an infrequent complication among infants born with birth weights greater than 1500 g and gestational ages exceeding 32 weeks. In the presurfactant era, prominent airway injury, epithelial metaplasia, smooth muscle hypertrophy, and alternating parenchymal fibrosis and emphysema were the most common histological findings. This disease phenotype is often termed “old” BPD. The most common lung histology in BPD now commonly displays a homogenous disease pattern marked by reduced numbers of alveoli and pulmonary capillaries, and minimal areas of hyperinflation and focal collapse. This is termed “new” BPD. Importantly, the pathologic characteristics of both old and new BPD can develop in extremely preterm infants who require prolonged intubation and mechanical ventilation. Old and new BPD therefore likely represent a continuum of disease severity and may not be fully distinct disease entities.
The incidence of BPD is highest among infants born with the lowest gestational ages and birth weights. The National Institutes of Child Health and Human Development’s (NICHD) Neonatal Research Network (NRN) reported rates of supplemental oxygen use at 36 weeks postmenstrual age (PMA) among infants who survived to that time point. BPD rates ranged from 85% for those born at 22 weeks’ gestation to 23% for those born at 28 weeks’ gestation (Fig. 62-1). Among preterm infants born in Israel between 2000 and 2010, 31% of surviving ELBW infants received supplemental oxygen at 36 weeks PMA compared to 13.7% of very low–birth-weight (VLBW; birth weight < 1500 g) infants. BPD severity is also inversely proportional to gestational age and birth weight. Fifty-six percent of infants born at 22 weeks’ gestation in the NRN cohort were diagnosed with severe BPD based on the National Institutes of Health (NIH) consensus ...