Background: Pleural effusion is defined as an abnormal accumulation of fluid in the pleural space. Excess fluid results from the disruption of the equilibrium that exists across pleural membranes.
In terms of anatomy, the pleural space is bordered by parietal and visceral pleura. Parietal pleurae cover the inner surface of the thoracic cavity, including the mediastinum, diaphragm, and ribs. Visceral pleurae envelop all surfaces of the lungs, including the interlobar fissures. This lining is absent at the hilus, where pulmonary vessels, bronchi, and nerves enter the lung tissue. The mediastinum completely separates the right and left pleural spaces.
Both parietal and visceral membranes are smooth, glistening, and semitransparent. Despite these similarities, the two membranes have unique differences in anatomic architecture, innervation, pain fibers, blood supply, lymphatic drainage, and function. For example, the visceral pleurae contain no pain fibers and have a dual blood supply (bronchial and pulmonary).
Pathophysiology: Pleural effusion is an indicator of a pathologic process that may be of primary pulmonary origin or of an origin related to another organ system or to systemic disease. It may occur in the setting of acute or chronic disease and is not a diagnosis in itself.
Normal pleural fluid has the following characteristics: clear ultrafiltrate of plasma, pH 7.60-7.64, protein content less than 2% (1-2 g/dL), fewer than 1000 WBCs per cubic millimeter, glucose content similar to that of plasma, lactate dehydrogenase (LDH) level less than 50% of plasma and sodium, and potassium and calcium concentration similar to that of the interstitial fluid.
The principal function of pleural fluid is to provide a frictionless surface between the two pleurae in response to changes in lung volume with respiration. The following mechanisms play a role in the formation of pleural effusion:
Altered permeability of the pleural membranes (eg, inflammatory process, neoplastic disease, pulmonary embolus)
Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, hepatic cirrhosis)
Increased capillary permeability or vascular disruption (eg, trauma, neoplastic disease, inflammatory process, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis)
Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena caval syndrome)
Reduction of pressure in pleural space; lung unable to expand (eg, extensive atelectasis, mesothelioma)
Inability of the lung to expand (eg, extensive atelectasis, mesothelioma)
Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma)
Increased fluid in peritoneal cavity, with migration across the diaphragm via the lymphatics (eg, hepatic cirrhosis, peritoneal dialysis)
Movement of fluid from pulmonary edema across the visceral pleura
Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing accumulation of further fluid
Iatrogenic causes (eg, central line misplacement)