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Fibrotic hypersensitivity pneumonitis — SCE Respiratory MCQ

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HardHigh-Resolution CTFibrotic hypersensitivity pneumonitisSCE Respiratory

A 67-year-old man is referred with 2 years of progressive exertional dyspnoea and dry cough. He has bred pigeons for 30 years, cleaning an attached loft daily, and has an 18-pack-year smoking history but stopped 12 years ago. Connective-tissue disease review and autoimmune serology are negative. FVC is 74% predicted and TLCO is 42% predicted. Volumetric HRCT at full inspiration shows coarse reticulation, traction bronchiectasis and limited honeycombing involving both peribronchovascular and subpleural lung, without a dominant basal gradient. Superimposed sharply demarcated lobules have three different appearances: normal attenuation, ground-glass attenuation through which vessels remain visible, and reduced attenuation with diminished vessel calibre. On expiratory imaging, the low-attenuation lobules remain lucent and fail to reduce in volume, affecting four lobes. Bronchoalveolar lavage contains 12% lymphocytes; microbiological investigations are negative. Echocardiography suggests significant pulmonary hypertension, and the multidisciplinary team considers lung biopsy to carry disproportionate risk. Which diagnosis should the team regard as most likely?

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Correct answer: D — Fibrotic hypersensitivity pneumonitis

The decisive HRCT finding is the three-density pattern: juxtaposed normal lung, infiltrated ground-glass lung and lucent lobules caused by small-airway obstruction. Expiratory failure of the lucent lobules to increase in attenuation or decrease in volume confirms air trapping rather than simple heterogeneity of inspiratory attenuation. When this accompanies fibrosis, particularly without a classic basal UIP distribution, it is highly specific for fibrotic hypersensitivity pneumonitis. The substantial pigeon exposure provides the relevant clinical context. A low BAL lymphocyte percentage reduces diagnostic confidence but does not exclude fibrotic hypersensitivity pneumonitis; lymphocytosis is less consistently present once fibrosis is established. Given the characteristic imaging, exposure and excessive biopsy risk, multidisciplinary acceptance of this diagnosis is appropriate. Idiopathic pulmonary fibrosis can produce honeycombing and traction bronchiectasis, but does not adequately explain the three-density pattern and extensive lobular air trapping. Fibrotic NSIP may produce ground-glass opacity and traction bronchiectasis but usually lacks this combination of geographically distinct densities and small-airway obstruction. The lucent lobules are air-trapped, not emphysematous, arguing against combined pulmonary fibrosis and emphysema. Chronic thromboembolic disease may cause mosaic perfusion and pulmonary hypertension, but it does not explain the established interstitial fibrosis, and expiratory imaging demonstrates air trapping rather than perfusion-related lucency.

Reference: Diagnosis, course and management of hypersensitivity pneumonitis (2022) — https://publications.ersnet.org/content/errev/31/163/210169 Imaging in the diagnosis and management of fibrosing interstitial lung diseases (2024) — https://publications.ersnet.org/lookup/doi/10.1183/20734735.0006-2024 Diagnosis of Hypersensitivity Pneumonitis in Adults: An Official ATS/JRS/ALAT Clinical Practice Guideline (2020) — https://pubmed.ncbi.nlm.nih.gov/32706311/