52 - Pleural Effusion

nature) can usually be explained by either increased pleural fluid formation or decreased pleural fluid absorption, or both. Pleural effusions caused by an increase in pleural fluid formation can be further subdivided into elevation in hydrostatic pressure (e.g., congestive heart failure), decreased colloid osmotic pressure (e.g., cirrhosis, nephrotic syndrome), increased capillary permeability (e.g., infection, neoplasm), passage of fluid through openings in the diaphragm (e.g., ascites), or reduction of pleural space pressure (e.g., atelectasis). An effusion caused by decreased pleural fluid absorption can be qualified further as either lymphatic obstruction or elevation of systemic venous pressure resulting in impaired lymphatic drainage (e.g., superior vena cava syndrome). The presence of fluid in the normally negative pressure environment of the pleural space has a number of consequences for respiratory physiology. Pleural effusions produce a restrictive ventilatory defect and also decrease total lung capacity, functional residual capacity, and forced vital capacity. They may cause ventilation-perfusion mismatches and, when large enough, compromise cardiac output. The classic work of Light et al. in 1972 demonstrated that 99% of pleural effusions could be classified into these two general categories, transudative and exudative (Box 52.1). A basic difference is that transudates generally reflect a systemic process whereas exudates usually signify underlying local pleuropulmonary disease.