Interstitial Diseas e • pathogenesis: pathological process involving the interlobular connective tissue (i.e. “scaffolding of the lung”) • findings ■ septal thickening: fine lines caused by thickened connective tissue septae (most commonly due to pulmonary edema or lymphangitis carcinomatosis) ◆ these manifest on CXR as: – Kerley A: long thin lines in upper lobes – Kerley B: short horizontal lines extending from lateral lung margin – Kerley C: diffuse linear pattern throughout lung ■ nodular: 1-5 mm well-defined nodules distributed evenly throughout lung ◆ seen in malignancy, pneumoconiosis, and granulomatous disease (e.g. sarcoidosis, miliary TB) ■ reticular: fine curvilinear opacities ◆ seen in interstitial lung diseases (pulmonary fibrosis) ◆ watch for pneumothorax as a complication ■ reticulonodular: combination of reticular and nodular patterns ■ may also see signs of airspace disease (atelectasis, consolidation) • differential diagnosis ■ occupational/environmental exposure ◆ inorganic: asbestosis, coal miner’s pneumoconiosis, silicosis, berylliosis, talc pneumoconiosis ◆ organic: hypersensitivity pneumonitis, bird fancier’s lung, farmer’s lung ( mouldy hay), and other organic dust ■ autoimmune: connective tissue diseases (e.g. rheumatoid arthritis, scleroderma, SLE, polymyositis, mixed connective tissue disease), IBD, celiac disease, vasculitis ■ drug-related: antibiotics (cephalosporins, nitrofurantoin), NSAIDs, phenytoin, carbamazepine, fluoxetine, amiodarone, chemotherapy (e.g. methotrexate), heroin, cocaine, methadone ■ infections: non-tuberculous mycobacteria, certain fungal infections ■ idiopathic: hypersensitivity pneumonitis, IPF ■ for causes of Interstitial Lung Disease classified by distribution, see Respirology, R13 ■ management: high-resolution CT thorax and ± open lung biopsy