Bronchopulmonary Dysplasia: The Role of Oxidative Stress

Description of BPD Historical perspectivePrior to the era of mechanical ventilation, few infants of very low birth weight (less than 1500 g) survived, and neonatal mortality for extremely low birth weight infants (less than 1000 g) exceeded 90% (Behrman et al., 1971).Most survivors required little or no oxygen supplementation initially but later deteriorated to requirements of up to 40% in order to prevent cyanosis.On radiography, findings included microcystic changes as well as varying degrees of hyperinflation and flattening of the diaphragm.Some infants recovered spontaneously over weeks to months but others died, with postmortem examination revealing hyperaeration and reduced alveolar septa.Wilson and Mikity in 1960 were the first to describe this chronic pulmonary syndrome, in a case report of five very small preterm survivors (Wilson & Mikity, 1960).At that time, assisted ventilation was not used in preterm infants.An additional 29 babies with Wilson-Mikity syndrome (WMS) were identified at the same medical institution in 1969 (Hodgman et al., 1969), and many other cases worldwide.After the introduction of mechanical ventilation to manage respiratory distress syndrome in the mid-1960s, reports began to appear of radiographic and pathological abnormalities that www.intechopen.comLung Diseases -Selected State of the Art Reviews 486 seemed to result from exposure to high concentrations of oxygen and mechanical ventilation.In 1967, Northway et al. coined the term "bronchopulmonary dysplasia" to describe findings of pulmonary complications following respiratory therapy for hyaline membrane disease (Northway et al., 1967).Northway et al. believed the critical factor to be exposure to an inspired oxygen concentration > 80% for longer than 150 hours.The 1990s saw major changes in both obstetric and neonatal care for preterm labour, with surfactant administration and assisted ventilation.The outcome of most preterm infants improved in the first half of the decade, particularly for infants with very low birth weight, who benefitted from decreased mortality and morbidity (Horbar et al., 2002).Following these changes, classical BPD, which occurred as a result of injury to the immature lung, became less common.Chronic lung disease in preterm infants became increasingly attributable to the response of the immature lung to early air breathing rather than to damage from barotrauma or oxygen toxicity.In 1999, Jobe described the "new" BPD as occurring in immature infants who did not have extensive lung disease soon after birth (Jobe, 1999).Jobe attributed the "new" BPD to pulmonary anomalies resulting from an inhibition of alveolar and vascular development (Jobe, 1999). Clinical definitionsWith the change in clinical presentation over time, a variety of definitions of BPD have been used in the literature.i. Original criteria for BPD: A U.S. National Institutes of Health (NIH) workshop held in 1979 proposed to define BPD as a "continued oxygen dependency during the first 28 days plus compatible clinical and radiographic changes" (Natl Inst Health Consens Dev Conf Summ, 1979).ii.Traditional definition: Instead of the original definition, Shennan et al. (1988) suggested a more accurate predictor of BPD to be, "the requirement for additional oxygen at a corrected postnatal gestational age of 36 weeks in infants born with a birth weight of less than 1,500 g".This definition appears to also predict pulmonary outcome among infants with the "new" BPD (Davis et al., 2002).iii.Severity definition: Participants at a joint U.

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