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  1. Definition. 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. 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' postconceptional age (PCA) 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 and is graded 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.

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

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

  2. Incidence. 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 birthweight and affects ~30% of infants with birthweights <1000 g. There is a large variability in rates reported among centers in part related to differences in clinical practices, such as criteria used for the management of mechanical ventilation.

  3. Pathophysiology. 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 is 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.

          1. 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 (NCPAP) and noninvasive ventilatory support (nasal intermittent positive pressure ventilation) has led to lesser rates of BPD.

          1. Oxygen exposure. Classic BPD observed prior to the availability of exogenous surfactant treatment was always associated with prolonged exposure (>150 h) 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, exposure to prolonged high oxygen is limited. Nevertheless, aiming for arterial oxygen saturation in the range 85–93% rather than >92% has led to a decrease in the need for supplemental oxygen at 36 weeks PCA in this postsurfactant era.

      1. Pathologic changes. Compared with the presurfactant era, lungs of infants currently dying from BPD have normal-appearing airways, less fibrosis, and more uniform inflation. However, these lungs have deficient septation, leading to fewer and larger alveoli with possible reduced pulmonary capillarization that may lead to pulmonary hypertension.

  4. Risk factors. Major risk factors are prematurity, white race, male gender, chorioamnionitis, tracheal colonization with ureaplasma, and the increased survival of the extremely low birthweight infant. Other risk factors are RDS, excessive early intravenous fluid administration, symptomatic PDA, ...

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