Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Radiologic patterns in interstitial lung disease diagnosis

  Interstitial lung disease (ILD) describes a broad group of disorders that damage the lung interstitium, air sacs, and small airways. Because symptoms such as exertional breathlessness and persistent cough are nonspecific, imaging is central to identifying the likely disease process, estimating severity, and guiding further testing.

  High-resolution computed tomography (HRCT) has transformed ILD assessment. It can reveal the distribution, morphology, and chronicity of abnormalities with far greater detail than a standard chest radiograph. For clinicians attending respiratory medicine programs associated with APSR and KATRD, a structured approach to these findings is essential for accurate diagnosis and timely treatment.

  Why imaging matters in interstitial lung disease

  Chest radiography may show reticular opacities, reduced lung volumes, or basal fibrosis, but early disease can be subtle or invisible. HRCT demonstrates fine reticulation, ground-glass opacity, traction bronchiectasis, honeycombing, nodules, cysts, and air trapping. These signs are interpreted together rather than in isolation.

  The radiologist also considers where abnormalities occur: near the pleura, around the bronchovascular bundles, in the upper or lower lungs, or throughout the respiratory lobule. Symmetry, the degree of fibrosis, and the presence of acute features such as consolidation or diffuse ground-glass change help narrow the differential diagnosis.

  Recognizing the usual interstitial pneumonia pattern

  A usual interstitial pneumonia (UIP) pattern is characterized by basal and subpleural-predominant reticulation, architectural distortion, traction bronchiectasis, and honeycombing. Honeycombing consists of clustered, thick-walled cystic spaces, usually several millimeters in diameter and often arranged in multiple layers near the pleura.

  A definite UIP pattern on HRCT strongly supports a diagnosis of idiopathic pulmonary fibrosis (IPF) when alternative causes have been excluded. However, UIP is a radiologic pattern rather than a disease name. It may also occur in connective tissue disease-associated ILD, chronic hypersensitivity pneumonitis, asbestosis, and other fibrotic conditions. Clinical history and multidisciplinary discussion remain indispensable.

  Distinguishing NSIP, organizing pneumonia, and hypersensitivity pneumonitis

  Nonspecific interstitial pneumonia (NSIP) commonly produces bilateral, symmetric ground-glass opacity and fine reticulation with a lower-lung predominance. Subpleural sparing, in which a thin layer of lung beneath the pleura remains relatively normal, can be a useful clue. NSIP is frequently associated with systemic sclerosis, polymyositis, dermatomyositis, and other autoimmune disorders.

  Organizing pneumonia usually appears as patchy consolidation or ground-glass opacity, often in a perilobular or peripheral distribution. The opacities may migrate over time, and an inflammatory rather than densely fibrotic process is often suspected. In hypersensitivity pneumonitis, mosaic attenuation, lobular air trapping, centrilobular nodules, and a three-density pattern can point toward repeated exposure to birds, mold, agricultural material, or other inhaled antigens.

  Reading distribution, density, and associated signs

  The distribution of disease can be as informative as its appearance. Upper-lung fibrosis may suggest sarcoidosis, chronic hypersensitivity pneumonitis, smoking-related disease, or certain occupational exposures. Lower-lung and peripheral fibrosis is more typical of UIP, while peribronchovascular disease can occur in sarcoidosis, organizing pneumonia, and some connective tissue disease patterns.

  Ground-glass opacity may represent inflammation, infection, edema, hemorrhage, or fine fibrosis, so it should not automatically be labeled “early ILD.” Features such as bronchial dilation within abnormal lung, volume loss, architectural distortion, and persistent subpleural reticulation help distinguish fibrotic disease from a reversible inflammatory process. Expiratory CT is particularly valuable when small-airway involvement or air trapping is suspected.

  Imaging pattern	Common distribution or signs	Diagnostic associations
  UIP	Basal, subpleural reticulation; traction bronchiectasis; honeycombing	IPF, autoimmune ILD, chronic hypersensitivity pneumonitis, asbestosis
  NSIP	Symmetric lower-lung ground-glass opacity and fine reticulation; possible subpleural sparing	Systemic sclerosis, inflammatory myopathy, autoimmune ILD
  Organizing pneumonia	Patchy consolidation, ground-glass opacity, perilobular opacities	Infection, drugs, autoimmune disease, cryptogenic organizing pneumonia
  Fibrotic hypersensitivity pneumonitis	Mosaic attenuation, air trapping, centrilobular nodules, fibrosis	Repeated exposure to birds, mold, farming, or occupational antigens
  Sarcoid pattern	Perilymphatic nodules, upper-lung fibrosis, hilar or mediastinal lymphadenopathy	Sarcoidosis
  Smoking-related pattern	Centrilobular nodules, upper-lung emphysema, ground-glass change	Respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia

  Using clinical context to refine the diagnosis

  Radiology cannot be separated from the patient’s story. Age, smoking history, medication exposure, occupational environment, domestic animals, humid buildings, and symptoms of connective tissue disease can change the meaning of the same HRCT finding. Raynaud phenomenon, inflammatory joint pain, mechanic’s hands, skin thickening, or muscle weakness may indicate an autoimmune cause.

  Pulmonary function tests provide complementary information. A restrictive pattern and reduced diffusing capacity for carbon monoxide may support clinically significant ILD, while serial measurements help determine progression. Blood tests, bronchoalveolar lavage, and lung biopsy are selected selectively because a confident radiologic diagnosis can sometimes avoid invasive procedures.

  Avoiding common interpretation errors

  A major error is equating every reticular abnormality with pulmonary fibrosis. Dependent atelectasis, suboptimal inspiration, prior infection, and age-related changes can mimic ILD. Prone imaging may clarify whether posterior basal opacity persists when the patient is repositioned.

  Another pitfall is overlooking combined pulmonary fibrosis and emphysema, in which lung volumes may appear deceptively preserved despite severe gas-transfer impairment. Radiologists should also distinguish honeycombing from emphysematous spaces, paraseptal emphysema, and traction-related bronchiolectasis. Comparing prior scans is often the fastest way to identify meaningful progression.

  Building a multidisciplinary diagnostic pathway

  The most reliable ILD diagnosis comes from collaboration among thoracic radiologists, pulmonologists, pathologists, rheumatologists, and specialist nurses. A radiology report should describe the dominant pattern, distribution, confidence level, relevant alternative diagnoses, and any features that warrant urgent attention.

  Useful reporting also includes pulmonary hypertension clues, acute exacerbation features, suspicious nodules, and the extent of fibrosis. In a conference setting, reviewing representative HRCT cases alongside clinical and pathological data helps clinicians understand why pattern recognition must be combined with exposure assessment and longitudinal follow-up.

  Practical priorities for clinicians

  A consistent imaging workflow can improve diagnostic accuracy:

  • Confirm that HRCT images are technically adequate, including thin sections and appropriate inspiratory views.
  • Describe the dominant abnormality before assigning a named disease.
  • Record the axial and craniocaudal distribution, symmetry, and degree of fibrosis.
  • Search specifically for air trapping, honeycombing, emphysema, lymphadenopathy, and pleural disease.
  • Present uncertain cases at an ILD multidisciplinary meeting before recommending invasive testing.

  Radiologic expertise becomes most valuable when it communicates uncertainty clearly. Terms such as “probable UIP,” “indeterminate for UIP,” or “alternative diagnosis” should be linked to the imaging features that support them, allowing the wider team to integrate the report responsibly.

  Respiratory professionals can deepen this approach through case-based learning, expert lectures, and multidisciplinary discussion at APSR and KATRD congress activities. Explore the conference program and invited-speaker sessions to connect imaging patterns with current advances in ILD diagnosis, classification, and patient care.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)