Predisposition of infants with chronic lung disease to respiratory syncytial virus-induced respiratory failure: a vascular hypothesis.

BACKGROUND

Respiratory syncytial virus (RSV) causes the highest rate of severe respiratory infections and mortality in infants and children worldwide. Preterm infants with underlying chronic lung disease (CLD), including bronchopulmonary dysplasia (BPD), are among those at high risk for severe morbidity, long term sequelae and mortality postinfection. The definition of CLD/BPD has evolved and is currently described as a disease of restricted lung development (i.e. impaired alveolar and pulmonary vascular development). This article describes potential mechanisms by which RSV infection causes respiratory failure in the infant with BPD.

METHODS AND RESULTS

The opinions expressed in this article are based on a review of recent investigations into the mechanisms through which RSV infections could cause excessive pulmonary edema formation and subsequent respiratory failure in the infant with CLD. Although alveolar overinflation and atelectasis are well-described patterns of RSV-induced respiratory illness in this infant population, the finding of pulmonary edema is a complex, multifactorial process that is less well understood. Experimental evidence suggests that RSV infection in infants with CLD/BPD not only causes increases in pulmonary vascular reactivity but also precipitates pulmonary edema formation via multiple mechanisms (e.g. nonuniform elevations in pulmonary artery pressure, endothelial injury, alveolar epithelial damage and impairments of native alveolar liquid clearance mechanisms).

CONCLUSIONS

Novel therapies for managing RSV-induced respiratory failure in the infant with CLD/BPD must consider factors responsible for the substantial pulmonary vascular component of this illness.