Understanding the mechanisms of infant respiratory distress and chronic lung disease.

Abstract

Respiratory distress syndrome in newborn infants (IRDS) is the most frequent respiratory cause of death and morbidity in children � 1 yr of age (1). Therapy for IRDS has been increasingly effective in reducing mortality at the expense of an increasing number of preterm survivors with chronic lung disease. This is particularly evident in extremely low birth weight (0.5‐1.0 kg) infants, born between 24 and 28 wk (2). The lungs of these infants are structurally immature, often surfactant-deficient, fluid filled, and not supported by a stiff chest wall (3), which enhances their susceptibility to lung injury. Recent pathology of chronic lung disease (CLD) differs from that described previously by Northway and colleagues (4) in that the lungs are more uniformly inflated and have minimal airway injury, but demonstrate alveolar hypoplasia (5). CLD is a heterogeneous condition, with a variety of spectra; however, a cardinal event, which appears to be common to all types of CLD, is an inflammatory response. Inflammation can interfere with normal anatomic development of the airways and alveoli, and can lead to lung tissue damage. This tissue damage is exacerbated by the fact that the healing process is generally abnormal in the premature infant due to immaturity. Consequently, excessive inflammation and abnormal healing can result in dysplasia and metaplasia of the respiratory system. Genetic Risk of Developing IRDS