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SURVIVING WITHOUT BRONCHOPULMONARY DYSPLASIA
Forty years after its initial description, the clinical definition of bronchopulmonary dysplasia (BPD) has changed but its aetiology and treatment are still debated.1 2 The incidence of BPD is greatest in very low birth weight (VLBW) infants of <28 weeks’ gestation.1 The severity of BPD has decreased with advances in care, including surfactant treatment, but primary prevention of BPD by avoiding premature birth remains elusive. Targets for decreasing the incidence of BPD include reducing oxygen exposure, avoiding lung infection/inflammation and avoiding ventilator-induced lung injury.
Oxygen exposure is linked to the occurrence of BPD.3 Preterm human neonates have oxidant stress from birth, and animal data demonstrate poor antioxidant defences.4 5 Thus avoidance of unnecessary oxygen exposure from birth is recommended.6 7 However, BPD can develop when continuous supplemental oxygen is not administered.1
Fetal/neonatal inflammation, infectious and non-infectious, has been causally linked to BPD,1 2 but treatment with postnatal steroids is problematic. A reduction in BPD with inhaled nitric oxide may be limited to neonates with birth weights >1000 g.8–10
Although some neonates can develop BPD despite minimal mechanical ventilation, a significant association exists between invasive artificial ventilation and BPD.1 Indeed, room air artificial ventilation of the fetal lamb results in lung injury similar to BPD.11 Measures to minimise ventilator-induced lung injury must begin from birth.6 12–14 Reducing the duration of artificial ventilation by early extubation to nasal continuous positive airway pressure (NCPAP) can minimise lung injury in immature baboons.15 However, extubation failure occurs with NCPAP mainly owing to apnoea,16 despite caffeine treatment that is associated with decreased BPD.17 Non-invasive positive pressure ventilation (NIPPV) increases successful extubation by ∼30%.18–20 Although no strong evidence confirms that NIPPV reduces the occurrence of BPD, …
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