Bronchopulmonary dysplasia (BPD) is a chronic lung disease that remains one of the most prevalent long-term sequelae of premature birth. Northway and colleagues first described the condition in 1967, after 32 preterm infants (mean gestational age 34 weeks) with respiratory distress syndrome developed characteristic radiographic changes following the initiation of positive pressure mechanical ventilation . Four stages of lung injury were described in “classic” BPD: exudative (age 1–3 days); necrosis and early repair (age 4–10 days); microcyst formation and pulmonary fibrosis (age 10–12 days); and severe cystic changes and cor pulmonale (after 30 days of age) . The clinical definition of BPD has evolved with time and advancements in neonatal care including surfactant therapy, antenatal steroid administration, and improved ventilator strategies [3,4]. Most infants currently developing BPD are born between 24-28 weeks gestational age, during the time of canalicular and saccular development. “New” BPD is characterised by a uniform arrest of lung development, with simplified alveolar structures and dysmorphic capillaries. These infants are more likely to present with a mild respiratory distress syndrome and a continued need for supplemental oxygen . Three levels of BPD severity (mild, moderate, or severe) are determined by the gestational age of the infant, oxygen dependency at 36 weeks post-conceptual age, total duration of oxygen supplementation, and positive pressure requirements . Long-term BPD survivors may experience persistent airway obstruction and pulmonary hypertension, complicating anaesthetic management.