Pathological Conditions

Pleural disease is either primary or secondary, e.g., to an underlying lung lesion or systemic disorder such as SLE.

Pleural effusions: over 90% of effusions are secondary to one of four conditions - congestive heart failure, pneumonia, malignancy or pulmonary emboli. Transudates are effusions containing low concentrations of proteins (< 3 g/dl) and the majority are due to congestive heart failure. Exudates contain higher concentrations of protein (> 3 g/dl) and over 80% are due to pneumonia, neoplasm or pulmonary emboli. Depending on the aetiology effusions can be serous, fibrinous, serofibrinous, purulent or haemorrhagic.

Empyema is the presence of frank pus in the pleural cavity. Non-infective processes such as pulmonary infarction, rheumatoid disease, SLE and uraemia may present with a pleural effusion.

Asbestos-related pleural effusion develops in 3% of asbestos workers. In most it will resolve in one to two years but 20% progress to massive pleural fibrosis and 5% develop malignant mesothelioma. Carcinoma of the lung is the most common malignancy to invade the pleura and produce pleural effusions, followed by carcinoma of the breast.

Pneumothorax: primary spontaneous pneumothorax occurs most commonly in 30 to 40 year old tall, thin males. They are most often due to rupture of blebs or bullae on the apical parts of the upper lobes. Rate of recurrence is 25%. Secondary pneumothorax occurs in chronic obstructive pulmonary disease, cystic fibrosis, asthma, tuberculosis, idiopathic pulmonary fibrosis, lymphangioleiomyomatosis, Langerhans histiocytosis and pneumocystis carinii pneumonia (PCP). Catamenial pneumothorax is associated with menstruation and may be due to focal endometrial deposits on the pleura. Traumatic pneumothorax can be iatrogenic, e.g., secondary to biopsy or otherwise, e.g., penetrating chest trauma.

Pleural plaques: usually but not always associated with asbestos. Histological examination shows hyalinized fibrous tissue with basket-weave collagen fibres. Usually present on the parietal pleura mainly in the intercostal spaces on the anterior and posterolateral aspects of the chest wall and on the dome of the diaphragm.

Diffuse pleural thickening: involves the visceral pleura and is associated with asbestos exposure.

Asbestos-induced mesothelial hyperplasia: consists of a papillary proliferation of the surface mesothelium with cores of connective tissue and a surface lining of regular mesothelial cells. It may be difficult to distinguish from well-differentiated malignant mesothelioma on pleural biopsy.

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