Abstract

After completing this article, readers should be able to: 1. Explain the difference in clinical course between classic bronchopulmonary dysplasia (BPD) and “new BPD.” 2. Describe the potential role of inflammation in the pathogenesis of BPD. 3. Describe how patent ductus arteriosus may affect the development of BPD. 4. Delineate the role of infection in the pathogenesis of BPD. The classic severe form of bronchopulmonary dysplasia (BPD) described by Northway and colleagues is occurring less frequently, but there is an increasing number of small preterm infants who are surviving with a milder form of chronic lung damage (Fig. 1⇓ ). These two forms of chronic lung disease (CLD) differ not only in their clinical presentation but in pathogenic mechanisms and long-term consequences. Figure 1. Incidence of BPD by birthweight among infants weighing less than 1,500 g born in 1996 through 1998 at the University of Miami/Jackson Memorial Medical Center. Classic BPD was described in infants who had severe respiratory distress syndrome (RDS) and received aggressive ventilation with high positive airway pressures and inspired oxygen concentrations. The new form of BPD occurs in smaller preterm infants, most of whom receive antenatal steroids and postnatal surfactant therapy. Because of this therapy, they experience a mild initial respiratory course and, therefore, are not exposed to aggressive ventilation or high inspired oxygen concentrations. Accordingly, the lung damage they suffer must be caused in part by other factors. Most of these infants have extremely low birthweights and require prolonged ventilator support primarily for management of apnea and poor respiratory effort. They represent more than 75% of all infants diagnosed with CLD in our institution. In contrast to infants who have severe BPD, these patients initially require low concentrations of oxygen for treatment of mild RDS that usually responds favorably to exogenous surfactant. This often is followed by a few days …

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