Small-airway disease is the signature: poorly defined centrilobular nodules and mosaic attenuation with air trapping on expiration; fibrotic HP adds fibrosis without the basal-subpleural predominance of UIP. Then ask for the exposure.
Orient first
- HP is an immune reaction to an inhaled antigen (birds, moulds, humidifiers) centred on the small airways — hence centrilobular nodules and air trapping.
- Current guidelines classify HP as NON-FIBROTIC or FIBROTIC, each "typical", "compatible" or "indeterminate" on CT (verify the current ATS/JRS/ALAT categories).
- The three-density pattern ("headcheese"): lobules of ground glass, normal lung and air-trapped low attenuation side by side — highly suggestive of fibrotic HP.
Acquire the study
- Volumetric non-contrast thin-section CT at full inspiration AND end-expiration; prone images if dependent opacity is present.
The manoeuvre
- Inspiratory axial images, lung window: ground glass and poorly defined centrilobular nodules, diffuse or upper/mid-zone.
- Expiratory: lobular air trapping — normal lung gains attenuation, trapped lobules stay dark.
- Fibrosis: reticulation, traction bronchiectasis, honeycombing — note the zonal distribution (mid/upper or no predominance; relative basal sparing).
- Three-density pattern across adjacent lobules.
- Assign the category against the current guideline criteria (typical / compatible / indeterminate, non-fibrotic or fibrotic) and ask for the antigen exposure.
What confirms it
- A typical CT pattern plus an identified exposure (± BAL lymphocytosis) — in multidisciplinary discussion.
What licenses you to exclude it
- No air trapping, no centrilobular nodules and no mosaic attenuation on a proper inspiratory/expiratory CT argue strongly against HP.
The classic misread
- Reading mosaic attenuation from vascular disease (chronic PE) as HP — check the vessels and whether it changes on expiration.