Bronchopulmonary Dysplasia: Strategies for Therapeutic Intervention

Abstract

Bronchopulmonary dysplasia (BPD), or chronic neonatal lung injury, is a chronic pneumopathy most commonly seen in preterm newborn infants requiring prolonged respiratory support. It was first described in the mid-1960’s, following the introduction of effective and commercially available neonatal ventilators which allowed the extended survival of infants with severe pulmonary insufficiency. Bronchopulmonary dysplasia has become the commonest chronic lung disease seen in infancy, with there being some 7000 new cases per year in the USA in the early 1980s [1]. The increased survival of extremely low birth weight infants over the last decade is likely to have increased this number significantly. The increased representation of extremely low birth weight infants in the overall pool of infants developing BPD has also been associated with a change in the expected radiological and pathological features associated with evolving BPD. When first described, there appeared to be a fairly clear, and well correlated, sequence of changes on X-ray (XR) and in lung histology occurring in the relatively large infants surviving with BPD in that era. The XR changes were divided into four stages, with stage I having the characteristic features of neonatal respiratory distress syndrome (RDS), followed by an opacification of the lung fields in stage II, which was associated with thick airway exudates, necrosis of respiratory epithelium and evidence of early repair. Survival into stage III represented a transition stage into chronic lung injury with areas of emphysematous alveoli being adjacent to patches of alveolar atelectasis and fibrosis reflected in the XR by rounded areas of radiolucency superimposed on lung fields of increased radiodensity.