Pulmonary disease is the most important cause of morbidity in preterm neonates, whose lungs are often physiologically and morphologically immature. Surfactant deficiency in immature lungs triggers a cascade of alveolar instability and collapse, capillary leak edema, and hyaline membrane formation. The term respiratory distress syndrome (RDS) has come to represent the clinical expression of surfactant deficiency and its nonspecific histologic counterpart, hyaline membrane disease. Historically, chest radiographs of infants with RDS predictably demonstrated decreased pulmonary expansion, symmetric generalized reticulogranular lung opacities, and air bronchograms. Refinements in perinatal medicine, including antenatal glucocorticoid administration, surfactant replacement therapy, and increasingly sophisticated ventilatory strategies have decreased the prevalence of RDS and air leak, altered familiar radiographic features, and lowered the threshold of potential viability to a gestational age of approximately 23 weeks. Alveolar paucity and pulmonary interstitial thickness in these profoundly premature neonates impair normal gas exchange and may necessitate prolonged mechanical ventilation, increasing the risk of lung injury. Bronchopulmonary dysplasia (BPD), alternatively termed chronic lung disease of infancy, is a disorder of lung injury and repair originally ascribed to positive-pressure mechanical ventilation and oxygen toxicity. Before the advent of surfactant replacement therapy, chest radiographs of infants with classic BPD demonstrated coarse reticular lung opacities, cystic lucencies, and markedly disordered lung aeration that reflected alternating regions of alveolar septal fibrosis and hyperinflated normal lung parenchyma. In the current era of surfactant replacement, BPD is increasingly a disorder of very low-birth-weight neonates with arrested alveolar and pulmonary vascular development, minimal alveolar septal fibrosis and inflammation, and more subtle radiographic abnormalities.
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