Abstract

Chronic lung disease of prematurity (CLD) is commonly considered to be a consequence of assisted ventilation. However, prior to the description in 1967 of bronchopulmonary dysplasia (BPD), following ventilator therapy for respiratory distress syndrome, Wilson-Mikity syndrome (WMS) had been described in very preterm infants on minimal oxygen supplementation. In the 1970s and 1980s, many infants treated with assisted ventilation required prolonged mechanical ventilation after developing radiographic features of coarse infiltrates, severe hyperinflation, and microcystic changes, associated with hypercarbemia and the need for increased inspired oxygen concentrations. Some infants died and showed evidence of pulmonary fibrosis, obstructive bronchiolitis, and dysplastic change. The role of supplemental oxygen, positive pressure ventilation, and the immaturity of the lung have long been considered important in the etiology of CLD/BPD. More recently, the role of inflammation (particularly antenatal exposure to cytokines) and individual susceptibility (genetic predisposition) have assumed greater etiologic importance. The historical setting into which corticosteroid treatment for BPD was introduced is also discussed. After the licensing of exogenous surfactant to treat RDS in the early 1990s and more widespread use of prenatal corticosteroids in the mid-1990s, severe BPD became an unusual event. Gradually, the diagnosis of CLD, still often referred to as BPD, was based on an oxygen requirement at 36 weeks postmenstrual age. However, it is not clear that this 'new BPD' is substantially different from WMS. It is difficult to make prognostications about long-term lung function of these infants based on oxygen 'requirement' at 36 weeks, since supplemental oxygen is frequently used unnecessarily.

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