Pleuritis may exhibit fibrinous exudates on the visceral and/or parietal pleural surfaces. Over time, the fibrinous exudates are often organized by granulation tissue. Fibrinous and fibrous pleuritis may be accompanied by inflammation, particularly lymphoid aggregates in the pleura and subpleural tissues. The granulation tissue of the organizing fibrous pleuritis may mature into fibrous tissue, resulting in a thickened, fibrotic pleura. A variety of conditions may cause fibrinous pleuritis, including pneumonia, pericarditis, hepatitis, peritonitis, pancreatitis, collagen-vascular disease, drug reactions, and cancer.

In some cases, the fibrous tissue may organize into pleural plaque. Grossly, pleural plaque is a thick, firm, yellow-tan to off-white tissue on the surface of the parietal or visceral pleura. Microscopically, pleural plaque consists of virtually acellular collagen bundles in a characteristic basket-weave pattern. Pleural plaques, especially when bilateral, lower zone, and symmetrical, may be markers of asbestos exposure. Pleural plaques may also be seen as a result of infections, surgery, trauma, and apical caps (see Chapter 33). Pleural plaques may undergo calcification or ossification.

Sarcomatous or desmoplastic mesothelioma may sometimes enter into the differential diagnosis of fibrous pleuritis. Fibrous pleuritis is generally limited to or oriented along the pleural surface, whereas sarcomatoid mesothelioma tends to involve the full thickness of the pleura. Keratin immunostains may assist in this differential diagnosis by indicating the location of the mesothelial cells within a thickened pleura; keratin-positive reactive mesothelial cells are generally found toward the pleural surface, whereas keratin-positive mesothelioma cells may be found in the full thickness of the pleura and invade underlying tissues. Another feature of benign reactive pleuritis is that the blood vessels in the granulation tissue tend to be parallel to one another and perpendicular to the pleural surface.