Pleural Fibrosis (Pleural Thickening)

Pleural fibrosis describes fibrotic thickening of visceral and/or parietal pleura, ranging from focal pleural plaques (asbestos-related, often calcified, predominantly parietal) to diffuse pleural thickening involving large areas of visceral pleura with fusion to parietal pleura, encasing the lung (trapped lung, fibrothorax). Pathogenesis involves persistent pleural inflammation triggering fibroblast proliferation and collagen deposition with disruption of normal pleural fluid clearance and mesothelial regeneration.

Etiologies include asbestos exposure (most common cause of bilateral calcified pleural plaques and diffuse pleural fibrosis), tuberculous pleurisy with delayed or inadequate treatment, post-empyema fibrothorax, post-hemothorax fibrothorax, post-traumatic, autoimmune (rheumatoid pleurisy, lupus), drug-induced (methysergide, ergot, amiodarone, dantrolene), uremia, and idiopathic. Pleural plaques alone are markers of asbestos exposure but rarely cause symptoms; diffuse pleural fibrosis can cause significant restrictive disease.

Imaging: chest radiograph and CT scan show pleural thickening (>3 mm definite, >5 mm marked), calcification (asbestos), costophrenic angle blunting, and trapped lung (atelectasis with curved appearance suggesting visceral pleural restriction). Pulmonary function tests reveal restrictive pattern with reduced lung volumes (FVC, TLC) and reduced DLCO. Pleural biopsy may distinguish causes when malignancy (mesothelioma) or specific etiology is unclear. Treatment: address underlying cause (anti-tuberculous chemotherapy for TB pleurisy, antibiotics and drainage for empyema, removal from asbestos). Surgical decortication (VATS or thoracotomy) is indicated for symptomatic trapped lung with restrictive impairment, removing the fibrotic peel from visceral pleura. Asbestos pleural plaques alone do not require treatment but warrant lung cancer surveillance.