Current perspectives on the prevention and management of chronic lung disease in preterm infants

Chronic lung disease (CLD) or bronchopulmonary dysplasia is a recognized sequel of preterm birth. With improving survival of infants at lower gestational ages, the incidence is on the rise. Pathological features of CLD include alveolar maldevelopment, with or without areas of pulmonary fibrosis. Assisted ventilation, infection/inflammation, oxygen administration, and fluid overload are the major risk factors in the evolution of CLD.Interventions, including the treatment of maternal infection, administration of prenatal glucocorticoids, and postnatal surfactant replacement therapy, improve the survival of preterm infants; however, their effect on CLD is difficult to determine. Strategies that have been effective in reducing CLD are the administration of retinol (vitamin A), high frequency oscillatory ventilation, and administration of glucocorticoids. Previous concerns regarding neurological problems associated with high frequency ventilation have not been substantiated in recent studies. Current recommendations do not advise the routine use of glucocorticoids due to concerns regarding long-term neurodevelopment. Therapies that were found to be ineffective in reducing the incidence of CLD include prenatal thyrotropin, cromolyn sodium (sodium cromoglycate), alpha-1 antitrypsin, superoxide dismutase, tocopherol (vitamin E), ascorbic acid (vitamin C), allopurinol, ambroxol, inositol, inhaled bronchodilators, and fluid restriction. Strategies that may be effective in reducing lung injury and subsequent CLD include avoiding assisted ventilation, lung protective ventilatory maneuvers, permissive hypercapnia, prevention of infection, early aggressive nutrition, and the treatment of a patent ductus arteriosus. The use of inhaled glucocorticoids improves pulmonary dynamics but long-term effects are unknown. The management of infants with established CLD has not been studied adequately, and the role of various ventilatory strategies for infants with established CLD is not clear. Adequate oxygenation should be maintained to prevent hypoxic episodes. Diuretics are helpful during acute decompensation; however, their long-term impact has not been well studied. Provision of adequate nutrition, immunization (routine and against respiratory syncytial virus), follow-up, and monitoring are the key elements in the long-term management of infants with CLD. Future research priorities should be to identify strategies to prevent/treat inflammation and promote the healing processes in the injured lung. The long-term effects of lung-protective ventilation strategies need to be studied.