Bronchopulmonary Dysplasia
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Direct answer
Oxygen dependence at 36 weeks postmenstrual age in an infant born before 32 weeks defines bronchopulmonary dysplasia — the chronic lung disease of prematurity that follows respiratory distress syndrome, volutrauma, oxygen toxicity and inflammation in an immature lung whose alveoli and microvasculature develop abnormally. Severity grades one to three reflect the fraction of oxygen needed at 36 weeks (none, under 30 per cent, 30 per cent or more). Prevention is the most examinable chapter: antenatal corticosteroids, surfactant replacement, gentle non-invasive ventilation from birth and judicious oxygen targeting. Long-term management bundles nutrition for lung growth, immunisation including palivizumab prophylaxis against respiratory syncytial virus, bronchodilator and diuretic trials for symptomatic benefit, and home oxygen for the severely affected.
What you must remember
- Definition and grading: oxygen or respiratory support need at 36 weeks postmenstrual age for infants born under 32 weeks — grade 1 on room air, grade 2 under 30 per cent oxygen, grade 3 at 30 per cent or more or with positive pressure; infants born at 32 weeks or later are assessed at 28-56 days.
- Old versus new BPD: classical Northway disease (barotrauma, fibrosis, hyperinflation) of the pre-surfactant era versus the new BPD of extreme prematurity — a hazy, ground-glass picture with minimal fibrosis but arrested alveolarisation.
- Risk factors: lower gestation and birth weight (the strongest), chorioamnionitis, patent ductus arteriosus, sepsis, high tidal-volume ventilation, prolonged 100 per cent oxygen, and pulmonary interstitial emphysema.
- Prevention with hard evidence: antenatal betamethasone, surfactant, caffeine (the CAP trial reduced BPD), non-invasive CPAP with early extubation, and oxygen saturation targets of 90-95 per cent.
- Postnatal steroids: systemic dexamethasone improves lung function but excess doses raise cerebral palsy risk — reserved for infants over one to two weeks of age who cannot be weaned, at minimal effective dose and duration; early hydrocortisone has been studied for prophylaxis in the most immature infants with sepsis risk.
- Chronic therapy: calories at 140 or more per kg per day, fat-soluble vitamins, bronchodilators and inhaled steroids for reactive symptoms, diuretics only for documented benefit, and home oxygen for saturations at or above 92-94 per cent.
- Infection shield: full immunisation on chronological age plus palivizumab monthly (15 mg/kg intramuscularly) during the respiratory syncytial virus season for infants under one year with significant BPD; influenza vaccination from six months.
- Outcome expectation: most survivors wean oxygen in the first year or two; long-term risks are asthma-like symptoms, recurrent hospitalisation with viral wheeze, poor growth, and neurodevelopmental impairment coupled to the same prematurity.
How to work through it
Follow a 27-week infant through the disease. Day two: intubated for respiratory distress syndrome, surfactant given, antenatal steroids missed — flag this infant as high risk. Week two: still ventilated with a significant ductus; treat the ductus, treat infection, extubate to CPAP early. Week four: oxygen need persists at 30-40 per cent with hazy lungs on radiograph; start caffeine, optimise calorie-dense feeds, and screen for reflux and aspiration contributing to desaturations. At 36 weeks postmenstrual age the infant still needs 32 per cent oxygen — grade 3 BPD is assigned; arrange palivizumab for the winter, teach parents the saturation target, and plan home oxygen with pulse oximeter spot checks if weaning stalls.
The examinable fork in this story is the steroid decision at week three: a candidate who reflexively prescribes dexamethasone loses marks for not weighing cerebral palsy risk against ventilator dependence; the correct answer is the DART-style low-dose, short-course approach only when weaning fails.
How the exam frames it
Questions cluster on the definition (36 weeks postmenstrual age, not 28 days of oxygen — the old definition survives only in older textbooks), the grading percentages, and the evidence-based prevention bundle. The Indian angle: BPD in Indian nurseries is driven less by aggressive ventilation and more by late referral, absent antenatal steroids and nosocomial sepsis in 26-30-week infants who once did not survive; home oxygen programmes are scarce, so discharge often happens on intermittent oxygen with close follow-up. Expect crossover items linking BPD to patent ductus arteriosus and to retinopathy of prematurity, which track the same oxygen-targeting failures.
Frequently asked questions
How is bronchopulmonary dysplasia defined?
Oxygen or respiratory support requirement at 36 weeks postmenstrual age in an infant born before 32 weeks, graded 1-3 by the oxygen fraction needed at that timepoint.
Which interventions prevent BPD?
Antenatal corticosteroids, surfactant therapy, non-invasive CPAP with gentle ventilation, caffeine citrate, targeted oxygen saturations of 90-95 per cent, and avoidance of sepsis and late ductal shunting.
Why is dexamethasone used cautiously in BPD?
Prolonged or high-dose postnatal dexamethasone improves lung function but increases the risk of cerebral palsy and hypertension, so it is reserved for infants who cannot be weaned, at low dose and short duration.
What is the role of palivizumab?
Monthly intramuscular prophylaxis (15 mg/kg) during the respiratory syncytial virus season for infants under one year with significant BPD, alongside routine immunisation on chronological age.
What nutritional strategy supports lung recovery?
High-calorie feeding at 140 or more kcal/kg/day with adequate protein, because these infants have elevated energy expenditure from respiratory work and need substrate for alveolar and somatic growth.