High-Resolution CT (HRCT) for Diffuse Interstitial Lung Disease

Acquisition settings and contrast timings below are illustrative adult protocol examples. Select the authorized protocol for the indication, scanner, body size, access device, and clinical condition. Treatment decisions belong to the responsible clinical team.

Purpose & Clinical Role of High-Resolution CT

Diffuse parenchymal lung diseases (DPLDs)—collectively known as interstitial lung diseases (ILDs)—comprise a vast spectrum of non-neoplastic inflammatory, granulomatous, and fibrotic disorders affecting the alveolar walls, peribronchovascular interstitium, and peripheral subpleural connective tissues. Conventional thick-section ($3\text{ to }5\text{ mm}$) chest computed tomography is less suitable for fine interstitial assessment for evaluating ILD because volume averaging obscures microscopic architectural distortion, subtle reticular lines, and fine cyst walls.

High-Resolution Computed Tomography (HRCT) is a specialized imaging technique optimized to achieve fine spatial detail of the pulmonary parenchyma. HRCT helps characterize disease distribution and patterns. Imaging findings are interpreted with clinical, exposure and laboratory information; they do not independently determine reversibility or treatment.

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Microscopic Anatomy: The Secondary Pulmonary Lobule (SPL)

Understanding HRCT interpretation requires mastering the microscopic cross-sectional architecture of the Secondary Pulmonary Lobule (SPL). The secondary pulmonary lobule is the smallest anatomical unit of pulmonary parenchyma surrounded by macroscopic connective tissue septa:

1. Dimensions & Lobular Boundaries: The SPL is polygonal or polyhedral in shape, measuring approximately $1.0\text{ to }2.5\text{ cm}$ in diameter. It is best developed and most prominent in the peripheral, anterior, and lateral subpleural regions of the lower and middle lobes.
2. The Interlobular Septa (Peripheral Margins): The boundaries of each lobule are delineated by interlobular septa composed of fibrous connective tissue continuous with the visceral subpleural interstitium. Crucially, the interlobular septa contain pulmonary venules and lymphatic vessels. In healthy individuals, these septa are extremely thin ($<0.1\text{ mm}$) and are largely invisible on HRCT. Pathological processes that infiltrate the septa produce visible linear thickening: smooth septal thickening in hydrostatic pulmonary edema or alveolar proteinosis, and nodular ("beaded") septal thickening in lymphangitic carcinomatosis or sarcoidosis.
3. The Centrilobular Core (Bronchovascular Bundle): At the geometric center of each lobule lies the centrilobular core, containing a terminal or respiratory bronchiole (luminal diameter $\sim 1\text{ mm}$, wall thickness $\sim 0.1\text{ mm}$) and an accompanying pulmonary arteriole ($0.5\text{ to }1.0\text{ mm}$ diameter). While the small normal bronchiole has walls too thin to be seen on HRCT, the accompanying arteriole is normally visualized as a distinct centrilobular dot or branching linear structure approximately $5\text{ to }10\text{ mm}$ from the pleural surface.
4. The Lobular Parenchyma (Acini): Each secondary pulmonary lobule contains 3 to 12 pulmonary acini, which house the functional respiratory bronchioles, alveolar ducts, and alveolar sacs supported by a delicate intra-lobular interstitial network.

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High-resolution technique and complementary acquisitions

Use thin sections and an appropriate high-spatial-frequency reconstruction to evaluate the pulmonary interstitium. Acquisition and reconstructed thickness depend on the scanner and validated task; commonly thin images are around 1 mm, but no single thickness applies to every system. A sharp lung kernel increases noise compared with a smooth soft-tissue kernel. Review a soft-tissue series as appropriate for other thoracic structures.

Routine interstitial lung assessment is usually unenhanced. Contrast is not absolutely contraindicated: a separate vascular, mediastinal or other question may justify enhancement while thin lung data remain available. Match technique to the indication instead of declaring enhanced images intrinsically incapable of showing the interstitium.

Inspiratory supine data establish the main parenchymal assessment. Expiratory imaging can show air trapping, particularly in small-airway disease. Prone imaging can distinguish dependent posterior opacity from persistent abnormality. The latter acquisitions are selected according to the clinical task and protocol; they are not mandatory full-chest scans for every patient. Coach breathing and inspect the result before deciding that a physiologic expiration is pathological.

HRCT Parenchymal Patterns & Pathological Correlations

Radiological interpretation of diffuse lung disease relies on categorizing abnormal attenuation into several useful, highly reproducible parenchymal patterns:

1. Ground-Glass Opacity (GGO)

• Definition: An area of hazy, amorphous increased parenchymal attenuation through which the underlying pulmonary vessels and bronchial wall margins remain clearly visible.
• Pathological Substrate: Partial replacement of alveolar air by transudate, pus, blood, or neoplastic cells, or partial alveolar collapse, combined with active inflammatory cellular thickening of the delicate alveolar interstitium.
• Clinical significance: GGO is nonspecific and can reflect inflammation, edema, hemorrhage, partial filling or fibrosis. Treatment cannot be selected from this pattern alone.

2. Consolidation

• Definition: A dense, homogeneous increase in parenchymal attenuation that completely effaces and obscures underlying pulmonary vessel margins and airway walls.
• Hallmark Feature: Air Bronchograms—patent, air-filled, branching bronchial tree structures outlined in stark relief against the surrounding dense, non-aerated alveolar exuded fluid.
• Pathological Substrate: Complete replacement of alveolar gas by fluid (pulmonary edema), purulent inflammatory exudate (bacterial pneumonia), hemorrhage (diffuse alveolar hemorrhage), or tumor cells (for example, invasive mucinous adenocarcinoma). Organizing pneumonia is another cause and is not a tumor.

3. Reticulation & Interlobular Septal Thickening

• Definition: A fine meshwork of linear opacities representing interstitial expansion.
• Classification:
  • Smooth Interlobular Septal Thickening: Outlines intact polygonal secondary pulmonary lobules with straight, uniform borders. Classically seen in hydrostatic pulmonary edema (Kerley B lines on CT) and pulmonary veno-occlusive disease.
  • Nodular ("Beaded") Septal Thickening: Interlobular septa studded with discrete focal granulomatous or neoplastic nodules. Classic characteristic sign of lymphangitic carcinomatosis (retrograde lymphatic tumor infiltration) and sarcoidosis.
  • Irregular Reticular Thickening: Disrupted, jagged fibrous lines associated with architectural distortion, indicating established parenchymal fibrosis.

4. Honeycombing (The Hallmark of UIP/IPF)

• Definition: Clustered, thick-walled ($1.0\text{ to }3.0\text{ mm}$), cystic airspaces ranging from $3\text{ to }10\text{ mm}$ in diameter (occasionally up to $25\text{ mm}$), characteristically arranged in contiguous, multi-layered rows that share common fibrous walls abutting the visceral subpleural pleural surface.
• Pathological Significance: Represents end-stage, complete histological destruction of lung parenchyma, where collapsed alveolar spaces are replaced by dense fibrous scar tissue and dilated bronchiolar cysts lined by bronchiolar epithelium. Honeycombing is completely irreversible.
• Interpretation: Basal subpleural honeycombing with the appropriate associated findings can support a UIP pattern. IPF requires the appropriate clinical assessment and exclusion of other causes; UIP is not synonymous with IPF.

5. Traction Bronchiectasis & Bronchiolectasis

• Definition: Irregular, non-tapering, distorted dilatation of bronchial and bronchiolar lumens occurring within areas of surrounding interstitial thickening or reticulation.
• Pathophysiology: Unlike infectious cylindrical bronchiectasis, traction bronchiectasis is caused by the outward mechanical pulling forces exerted by adjacent retractile fibrotic scar tissue as it contracts. When seen within areas of ground-glass opacity, traction bronchiectasis indicates that the "GGO" is not active reversible cellular inflammation, but rather fine interstitial "fibrotic GGO."

6. The Tree-in-Bud Pattern

• Definition: Small centrilobular nodular opacities connected to branching V- and Y-shaped linear structures, resembling the budding branch of a blooming tree.
• Pathological Significance: Reflects dilated, impacted terminal and respiratory bronchioles plugged with mucus, pus, or granulomatous debris, surrounded by peribronchiolar inflammation. Represents endobronchial spread of infection, classically seen in active tuberculosis, non-tuberculous mycobacterial (NTM) infection (Mycobacterium avium-intracellulare), aspiration bronchiolitis, and bacterial bronchopneumonia.

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Describe patterns without promising reversibility

Ground-glass opacity is increased attenuation through which vessels remain visible. It can reflect inflammation, edema, hemorrhage, partial air-space filling or fine fibrosis. It does not guarantee steroid-responsive disease. Consolidation obscures underlying vessels and can have many causes. Reticulation, traction bronchiectasis and honeycombing support fibrotic architectural change, but their meaning depends on distribution and the clinical setting.

A usual interstitial pneumonia (UIP) imaging pattern is not automatically idiopathic pulmonary fibrosis (IPF). Other diseases can produce a UIP pattern, and diagnosis requires exclusion of relevant exposures, connective-tissue disease and other causes through the appropriate clinical assessment. The technologist helps by obtaining the required inspiratory, selected expiratory/prone and reconstruction data and documenting breathing limitations; treatment cannot be assigned from one image descriptor.

Reference: ATS/ERS/JRS/ALAT 2022 guideline.