16 High-Resolution ComputedTomography of Interstitial and

Occupational Lung Disease

Dr. Muhammad Bin ZulfiqarPGR IV FCPS Services Institute of Medical Sciences / Hospitalradiombz@gmail.comGRAINGER & ALLISON’S DIAGNOSTIC RADIOLOGY

• FIGURE 16-1 Usual interstitial pneumonia. (A) HRCT ■abnormalities predominate in the posterior, subpleural regions of the lower lobes and comprise patchy honeycombing and traction bronchiectasis within the abnormal lung. (B) Sagittal reformation shows the abnormalities creeping up the periphery into the anterior zones of the upper lobes.

FIGURE 16-2 Biopsy proven ■usual interstitial pneumonia. HRCT performed (A) before and (B) after clinical deterioration in a biopsy-proven usual interstitial pneumonia associated with a HRCT pattern more akin with non-specific interstitial pneumonia. HRCT obtained during the accelerated phase of the disease demonstrates a generalised increase in lung attenuation and progression of both the reticular and honeycomb patterns.

• FIGURE 16-3 Tuberculosis on a background of usual ■interstitial pneumonia. Biopsy of the area of consolidation in the right lower lobe confirmed tuberculosis.

• FIGURE 16-4 Nonspecific interstitial pneumonia. (A) ■The predominant abnormality is patchy, bilateral ground-glass opacification, mild reticulation and traction bronchiectasis. (B) In this fibrotic form, reticulation is more extensive and traction bronchiectasis more severe. However, there is no frank honeycombing destruction.

FIGURE 16-5 Respiratory ■bronchiolitis–interstitial lung disease. HRCT shows (A) subtle areas of ground-glass opacification and (B) ill-defined centrilobular nodules.

• FIGURE 16-6 Biopsy proven DIP. Several areas of non-■specific reticulation and ground-glass opacification in both lower lobes.

FIGURE 16-7 Smoking ■related interstitial lung disease. (A) Upper and (B) lower lobes of a 42-year-old man with a 25 pack-year smoking history and dyspnoea. The combination of a fine reticular pattern representing fibrosis and ground-glasso pacification on a background of emphysema suggests a diagnosis of smoking related-interstitial lung disease.

• FIGURE 16-8 Lymphoid interstitial pneumonitis. ■There are patchy ground-glass opacities and a few thin-walled cystic air spaces in the right lung.

• FIGURE 16-9 Idiopathic pleuroparenchymal ■fibroelastosis. HRCT through the upper lobes shows bilateral irregular pleural thickening and a subjacent reticular pattern consistent with fibrosis.

• FIGURE 16-10 Sarcoidosis. Typical HRCT ■features are (A) nodular opacities which (B) may become confluent, and (C) interlobular septal thickening.

• FIGURE 16-11 Fibrotic sarcoidosis. There are areas ■of conglomerate fibrosis in a perihilar distribution with associated bronchial distortion and volume loss. The appearances superficially mimic progressive massive fibrosis seen in the pneumoconiosis.

• FIGURE 16-12 Subacute extrinsic allergic ■alveolitis. HRCT shows numerous poorly defined, relatively low-attenuation nodules and ground-glass opacification in the upper lobes.

FIGURE 16-13 ■Hypersensitivity pneumonitis. (A) Inspiratory image shows patchy density differences, reflecting both the interstitial infiltrate of subacute hypersensitivity pneumonitis and coexisting small airways disease. (B) End-expiratory image enhances the density differences, revealing several secondary pulmonary lobules of decreased attenuation.

• FIGURE 16-14 Chronic hypersensitivity ■pneumonitis. The reticular pattern with distortion of the lung parenchyma indicates established fibrosis in this case of chronic hypersensitivity pneumonitis.

FIGURE 16-15 ■Langerhans cell histiocytosis. (A) The characteristic combination of thin-walled cysts and poorly defined nodules, some of which are just beginning to cavitate. (B) Image from a patient with more advanced disease. There are numerous irregularly shaped cysts bilaterally and a pneumothorax on the right.

• FIGURE 16-16 ■Lymphangioleiomyomatosis. (A) There is a profusion of thin-walled cystic air spaces scattered evenly throughout the lungs. The cysts are relatively uniform in size. (B) In a more advanced case of LAM, note the small left pleural effusion.

• FIGURE 16-17 Rheumatoid arthritis with a usual ■interstitial pneumonia (UIP)type pattern. In this case the HRCT appearances of peripheral reticular abnormality and honeycombing are indistinguishable from that of UIP.

• FIGURE 16-18 Rheumatoid arthritis. HRCT ■demonstrates both mild cylindrical bronchiectasis and constrictive obliterative bronchiolitis (reflected by areas of low attenuation in which there is a reduction in the number of vessels present) in this patient with rheumatoid arthritis.

• FIGURE 16-19 Sjögren’s syndrome. Lymphoid interstitial ■pneumonia and amyloid. There are numerous thin-walled cysts in association with multiple irregular solid nodules, some of which are heavily calcified. Histopathological examination showed marked thickening of the interstitium with an infiltrate of small, mature lymphocytes and plasma cells. Multiple deposits of amyloid were seen throughout the specimen and there was no evidence of malignancy.

FIGURE 16-20 ■Scleroderma. (A) In this case, ground-glass opacification admixed with fine reticular opacities are associated with mild traction bronchiectasis. Note the mild dilatation of the oesophagus. (B) In a more advanced case, reticulation and traction bronchiectasis are more severe but still closest to an NSIP pattern; the oesophagus is also more dilated.

FIGURE 16-21 ■Polymyositis/dermatomyositis. HRCT features include (A) reticular opacities and (B) areas of ground-glass opacification. The appearance of (B) is compatible with organising pneumonia being incorporated as fibrosis.

• FIGURE 16-22 Churg–Strauss syndrome. ■ Spectrum of HRCT features: (A) areas of ground-glass opacification, (B) small cavitating nodules, (C) thickened interlobular septa and (D) an area of air-space opacification, likely to be a peripheral infarct.

• FIGURE 16-22 Churg–Strauss syndrome. ■ Spectrum of HRCT features: (A) areas of ground-glass opacification, (B) small cavitating nodules, (C) thickened interlobular septa and (D) an area of airspace opacification, likely to be a peripheral infarct.

• FIGURE 16-23 Diffuse alveolar damage ■secondary to amiodarone. There is extensive bilateral ground-glass opacification and airspace consolidation.

• FIGURE 16-24 Nonspecific interstitial pneumonia ■secondary to bleomycin. The dominant abnormality is ground-glass opacification in association with a fine reticular pattern. The pattern of fibrosis most closely resembles non-specific interstitial pneumonia.

• FIGURE 16-25 Organising pneumonia secondary to (A, ■B) nitrofurantoin and (C) amiodarone. The HRCT features of ground-glass opacification and consolidation (A, C) and a peri-lobular pattern (B) are in keeping with organising pneumonia. The areas of consolidation in (C) are both peribronchial and perilobular in distribution.

• FIGURE 16-25 Organising pneumonia secondary to ■(A, B) nitrofurantoin and (C) amiodarone. The HRCT features of ground-glass opacification and consolidation (A, C) and a perilobular pattern (B) are in keeping with organising pneumonia. The areas of consolidation in (C) are both peribronchial and perilobular in distribution.

• FIGURE 16-26 Progressive massive fibrosis in coal ■worker's pneumoconiosis. Mass-like opacities are seen bilaterally in the upper lobes in association with multiple small nodules and calcified mediastinal lymphadenopathy.

• FIGURE 16-27 ■Atelectasis. Two examples of rounded atelectasis in association with (A) pleural thickening and (B) a pleural effusion. In both cases, there is evidence of lobar volume loss as evidenced by displacement of fissures. The most common location of rounded atelectasis is in the lower lobes.

• FIGURE 16-28 Asbestosis. ■(A) HRCT features of early asbestosis include subpleural lines (arrowheads) and fine reticulation (arrows). These subtle abnormalities persisted on prone sections. (B) In more advanced disease, a coarse reticular pattern with honeycombing, often indistinguishable from usual interstitial pneumonia on HRCT, is seen in the left lower lobe. Note the calcified pleural plaques in both examples.