Pneumothorax refers to presence of air or other gas in the pleural sac. It may occur in young, apparently healthy adults, usually men without any known pulmonary disease (simple or spontaneous pneumothorax), or as a result of some thoracic or lung disorder (secondary pneumothorax), such as emphysema or a fractured rib. Secondary pneumothorax is the consequence of rupture of any pulmonary lesion situated close to the pleural surface that allows inspired air to gain access to the pleural cavity. Responsible pulmonary lesions include emphysema, lung abscess, tuberculosis, carcinoma, and many other, less common processes. Mechanical ventilatory support with high pressure also may trigger secondary pneumothorax.
There are several possible complications of pneumothorax. A ball-valve leak may create a tension pneumothorax that shifts the mediastinum. Compromise of the pulmonary circulation may follow and may even be fatal. If the leak seals and the lung is not reexpanded within a few weeks (either spontaneously or through medical or surgical intervention), so much scarring may occur that it can never be fully reexpanded. In these cases, serous fluid collects in the pleural cavity, creating hydropneumothorax. With prolonged collapse, the lung becomes vulnerable to infection, as does the pleural cavity when communication between it and the lung persists. Empyema is thus an important complication of pneumothorax (pyopneumothorax).
Hemothorax, the collection of whole blood (in contrast with bloody effusion) in the pleural cavity, may be a complication of a ruptured intrathoracic aortic aneurysm, an event that is almost always fatal. With hemothorax, in contrast with bloody pleural effusions, the blood clots within the pleural cavity.
Chylothorax is a pleural collection of a milky lymphatic fluid containing microglobules of lipid. The total volume of fluid may not be large, but chylothorax is always significant because it implies obstruction of the major lymph ducts, usually by an intrathoracic cancer (e.g., a primary or secondary mediastinal neoplasm, such as a lymphoma).
Malignant mesothelioma has assumed great importance because it is highly related to exposure to airborne asbestos. It is a rare cancer of mesothelial cells, usually arising in the parietal or visceral pleura; it also occurs much less commonly in the peritoneum and pericardium. Approximately 80% to 90% of individuals with this cancer have a history of exposure to asbestos. Those who work directly with asbestos (shipyard workers, miners, insulators) are at greatest risk, but malignant mesotheliomas have appeared in individuals whose only exposure was living in proximity to an asbestos factory or being a relative of an asbestos worker. The latent period for developing malignant mesothelioma after the initial exposure is long, often 25 to 40 years, suggesting that causative driver mutations are acquired slowly, over a long period of time. As stated earlier, the combination of cigarette smoking and asbestos exposure greatly increases the risk for developing lung carcinoma, but it does not increase the risk for developing malignant mesothelioma.
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Once inhaled, asbestos fibers remain in the body for life. Thus, the lifetime risk after exposure does not diminish over time (unlike with smoking, in which the risk decreases after cessation). It has been hypothesized that asbestos fibers preferentially gather near the mesothelial cell layer, where they generate reactive oxygen species that cause DNA damage and mutations. Sequencing of mesothelioma genomes has revealed multiple driver mutations, many of which cluster in pathways involved in DNA repair, cell cycle control, and growth factor signaling. Of interest, one of the most commonly mutated genes in sporadic mesothelioma, BAP1, encodes a tumor suppressor involved in DNA repair that also is affected by germ line mutations in families showing a high incidence of mesothelioma.