Changes in the pathogenesis and prevention of chronic lung disease of prematurity

Abstract

With the increasing survival of extremely premature infants there is a large number of them who are developing chronic lung disease (CLD), but the severity of the lung damage is considerably less than that observed in the classic form of bronchopulmonary dysplasia (BPD). Because many of these infants have only a mild initial respiratory distress and therefore do not receive aggressive ventilation, it is clear that factors other than oxygen toxicity and barotrauma are involved in the pathogenesis of this new milder type of CLD. CLD results from the interaction of multiple factors that can injure the immature lung. For this reason the prevention must be based on the elimination of all the factors implicated in its pathogenesis. Clinical and epidemiological data strongly suggest that infections, either prenatal or nosocomial, and the presence of a patent ductus arteriosus (PDA) play a major role in the development of CLD in these infants. For this reason, efforts to prevent CLD in extremely low birth weight infants should include an aggressive approach to the prevention and treatment of prenatal and neonatal infections and an early closure of the PDA.