ABSTRACT
Pulmonary edema is a consistent pathological feature of both the acute and chronic respiratory distress syndromes that occur after premature birth. In acute respiratory distress syndrome, or hyaline membrane disease (HMD), the lungs typically are heavy and have a widened interstitium between airspaces and blood vessels; accumulation of fluid within dilated lymphatic channels and the connective tissue space surrounding large pulmonary blood vessels and airways; and abundant deposits of plasma proteins within the terminal respiratory units (1). These signs of abnormal vascular and epithelial permeability usually disappear as the respiratory distress resolves, either spontaneously or after treatment with surfactant and assisted ventilation. Sometimes, however, the need for prolonged mechanical ventilation persists because of continuing respiratory failure, either from residual lung disease, chest wall instability, apnea, or infection. Long-term exposure to repetitive lung inflation with positive pressure and supplemental oxygen often leads to chronic lung disease (CLD). This condition was described by Northway et al. (2) as bronchopulmonary dysplasia (BPD), the pathology of which includes edema, prominent lymphatics, inflammation, and subsequent fibrosis (Fig. 1) (3).
