Chronic lung disease of prematurity: clinical and pathophysiological correlates

Abstract

Chronic lung disease of prematurity (CLD) is largely confined to preterm infants who require mechanical ventilation in the newborn period. Its development is associated with preterm labour and pulmonary inflammation secondary to oxidant stress, barotrauma of mechanical ventilation and antenatally--or postnatally--acquired respiratory tract infection. Pathological studies have shown that infants dying of established CLD have airway wall thickening secondary to increased airway wall smooth muscle mass, alveolar hypoplasia and pulmonary vascular re-modelling. These structural abnormalities are likely to account for the clinical problems of arterial hypoxemia and hypercapnia, tachypnea, recurrent wheezing and decreased exercise tolerance. Severity of the structural components may account for the clinical variation that is observed in a particular child. Management of CLD is aimed at decreasing the effects of hypoxemia and in maximising somatic, and by implication lung, growth. Low flow domiciliary oxygen and bronchodilators are used for arterial hypoxemia and recurrent wheezing. Systemic and inhaled corticosteroids may be beneficial but it is unclear if such treatment alters the natural history of CLD in the developing lung. Gastro-esophageal reflux should be sought in these infants and they should receive immunizations or immunoprophylaxis against respiratory tract pathogens. There is considerable concern that survivors of CLD may develop respiratory failure in early--or late--middle age.