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Classic bronchopulmonary dysplasia (BPD) is a neonatal form of chronic pulmonary disorder that follows a primary course of respiratory failure (eg, respiratory distress syndrome [RDS], meconium aspiration syndrome) in the first days of life. It is sometimes referred to as chronic lung disease (CLD) of prematurity. A “new” form of BPD has been described in extremely low birthweight infants. This occurs in infants who initially had none or modest initial ventilatory and oxygen needs. BPD is defined as persistent oxygen dependency up to 28 days of life. The severity of BPD-related pulmonary dysfunction in early childhood is more accurately predicted by an oxygen dependence at 36 weeks' postmenstrual age (PMA) in infants <32 weeks' gestational age (GA) and at 56 days of age in infants with older GA. BPD is thus classified at this later postnatal age according to the type of respiratory support required to maintain a normal arterial oxygen saturation (89%).


  1. Mild BPD. Infants who have been weaned from any supplemental oxygen.

  2. Moderate BPD. Infants who continue to need up to 30% oxygen.

  3. Severe BPD. Infants whose requirements exceed 30% and/or include continuous positive airway pressure or mechanical ventilation.




The incidence of BPD is influenced by many risk factors, the most important of which is lung maturity. The incidence of BPD increases with decreasing birth- weight and affects ∼30% of infants with birthweights <1000 g. The large variability in rates among centers is partly related to differences in clinical practices, such as criteria used for the management of mechanical ventilation.




A primary lung injury is not always evident at birth. The secondary development of a persistent lung injury is associated with an abnormal repair process and leads to structural changes such as arrested alveolarization and pulmonary vascular dysgenesis.


  1. The major factors contributing to BPD are as follows:

    1. Inflammation. Central to the development of BPD. An exaggerated inflammatory response (alveolar influx of numerous proinflammatory cytokines as well as macrophages and leukocytes) occurs in the first few days of life in infants in whom BPD subsequently develops.

    2. Mechanical ventilation. Volutrauma/barotrauma is one of the key risk factors for the development of BPD. Minimizing the use of mechanical ventilation by the use of early nasal continuous positive airway pressure, noninvasive ventilatory support (nasal intermittent positive pressure ventilation), and early use of methylxanthines (caffeine) has led to fewer days of mechanical ventilation and to lesser use of postnatal steroids.

    3. Oxygen exposure. Classic BPD observed before the availability of exogenous surfactant treatment was always associated with prolonged exposure (>150 hours) to an Fio2 >60%. Hyperoxia can have major effects on lung tissue, such as proliferation of alveolar type II cells and fibroblast, alterations in the surfactant system, increases in inflammatory cells and cytokines, increased collagen deposition, and decreased alveolarization and microvascular density. Today, in the postsurfactant era, exposure to prolonged high oxygen is limited, and a new form of BPD is being observed. For this “new” BPD, the association between persistent need for mechanical ventilation and supplemental oxygen in the first 2 weeks of life is not as dominant as in the past. For instance, a third of the preterm infants receiving either supplemental oxygen or intermittent positive pressure ventilation at 14 days did not ...

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