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A 43-year-old Caucasian woman presented to her primary care physician for a retirement physical exam. She endorsed mild dyspnoea on exertion, but denied chest pain, cough or shortness of breath at rest. On physical exam, lungs were clear bilaterally with good air movement in all fields. Chest radiograph was normal except for a 6 mm nodular density noted in the right lower lobe. A non-contrast CT scan of the chest was performed revealing a 2 mm calcified granuloma. In addition, there were global, mild and uniform paraseptal emphysematous changes throughout the pleural surfaces of the lungs and the fissures (figures 1 and 2). Pulmonary work-up including spirometry, carbon monoxide diffusing capacity and testing for alpha-1 antitrypsin deficiency was normal. Further investigation revealed a history of premature birth, supported with mechanical ventilation (MV). We attributed her radiographic findings and symptoms to sequelae of bronchopulmonary dysplasia (BPD).
BPD is a pulmonary complication of premature birth.1 BPD occurs in premature infants experiencing respiratory distress syndrome (RDS) treated with MV, resulting in an inflammatory condition characterised by diverse radiographic findings and histologically by fibrosis and smooth muscle hypertrophy in the pulmonary tissues.1 2 The long-term sequelae of BPD are heterogeneous and depend on the initial degree of insult. MV of the premature infant in the setting of RDS is the predominant risk factor. Mild to moderate BPD may have no long-term effects with normal to only mildly obstructed spirometry; these patients typically go on to have normal chest radiographs by adolescence.2 More severe cases may demonstrate bronchial wall thickening, air trapping, lung cysts, linear interstitial opacities and emphysema.1 Case series suggest infants with BPD have more frequent airway hyper-reactivity in adulthood and may have increased susceptibility to respiratory infections.2
Our patient presented with minimal symptoms, a history of MV during premature infancy and a novel, bilateral paraseptal emphysematous pattern without other underlying aetiology suggesting BPD as the cause. Prevention in premature infants is key to management of this disease and centres on minimising airway pressures during MV, antenatal glucocorticoids and exogenous surfactant therapy. The sequela of BPD infrequently persists into adulthood. We postulate that the diffuse and symmetric paraseptal emphysema in this adult patient with no other pulmonary risk factors is a previously undescribed manifestation of BPD as a premature infant.
Bronchopulmonary dysplasia (BPD) is a pulmonary complication of premature birth. BPD occurs in premature infants treated with mechanical ventilation, resulting in inflammation leading to fibrosis and smooth muscle hypertrophy.
Mild to moderate BPD may have no long-term effects with normal to only mildly obstructed spirometry; these patients typically go on to have normal chest radiographs by adolescence.
Contributors All of the authors had direct role in the care of the presented patient. The manuscript was written by TC and KK. Mentorship and editing was performed by WW and JS.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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