Pleural Effusion

Henri G. Colt

Pleural fluid serves as a lubricating film between the visceral and parietal pleural surfaces. A few milliliters of pleural fluid are present normally within the pleural space. In normal individuals, thoracentesis may yield less than 1 mL of fluid, although quantities of 3 to 20 mL have been obtained in as many as 10% of healthy individuals in some series. The protein content of pleural fluid is below 1.5 g/dL, and the protein electrophoretic pattern is qualitatively similar to plasma, although the content of albumin is slightly higher and that of fibrinogen slightly lower.

The volume and composition of pleural fluid are maintained virtually constant in healthy individuals by an intricate balance of hydrostatic and oncotic pressures and by the relative permeabilities of the pleural capillaries and lymphatics. Systemic arteries supply the parietal pleura and bronchial arteries do the same for the visceral pleura. Fluid and protein exchange in the pleural space is almost exclusively achieved through the parietal pleura. Fluid may accumulate as a result of any process that obstructs lymphatic drainage.

Pleural effusion is defined as the abnormal accumulation of fluid within the pleural space. It may be caused by either excess fluid production or decreased absorption; in some conditions, both mechanisms may be operative. Effusions are a common manifestation of both systemic and intrathoracic diseases. Factors that determine whether pleural fluid accumulates include (1) oncotic pressure in the pleural fluid, pleural microcirculation, and lymphatics; (2) permeability of the pleural microcirculation; and (3) pressures in the systemic and pulmonary veins. The most common cause of a pleural effusion is congestive heart failure with elevation of the pulmonary venous pressure. Whether elevation of systemic venous pressure alone (pure right heart failure) prompts pleural effusions remains controversial, but elevations of both systemic and pulmonary venous pressures appear to result in larger effusions.

Peritoneal fluid can gain access to the pleural space via diaphragmatic defects and transdiaphragmatic lymphatics. Simple transfer of ascitic fluid across diaphragmatic defects has been invoked as a mechanism for pleural effusions that accompany ascites, as occurs in cirrhosis and Meig syndrome (i.e., benign ovarian fibroma, ascites, and pleural effusion). A similar mechanism has been proposed for fluid accumulation in pancreatitis or subdiaphragmatic abscess, although enhanced transdiaphragmatic lymph flow also can play a role.

From a pathophysiolgic perspective, increased negative pressure in the pleural space enhances fluid accumulation (as occurs in patients with atelectasis). While decreased plasma oncotic pressure favors pleural fluid accumulation, it is unlikely to be sufficient, since effusions are rare in congenitally hypoalbuminemic individuals. Increased capillary permeability caused by local inflammation, circulating toxins, or vasoactive substances play a role in pleural fluid accumulation associated with collagen-vascular diseases, pancreatitis, pulmonary emboli, and pneumonitis. Furthermore, as pleural space oncotic pressure approaches that of plasma (32 cm H₂O), fluid resorption is impaired. An increase in pleural oncotic pressure also contributes to some effusions. This occurs as a consequence of (1) enhanced capillary protein leak, (2) protein exudation from local pleural inflammation or tumor, or (3) defective lymphatic resorption.

On physical examination, patients may have dullness to percussion, diminished breath sounds, and reduced tactile and vocal fremitus over the involved hemithorax. Altering the patient’s position will occasionally shift these physical findings to dependent regions. Large effusions (>1,500 mL) are frequently associated with an appreciable inspiratory lag, bulging intercostal margins, contralateral mediastinal shift, or atelectasis (e.g., egophony, bronchial breath sounds). Nonthoracic signs might suggest the cause of the effusion; pedal edema, distended neck veins, and an S₃ gallop, for example indicate possible congestive heart failure.

Often, the chest roentgenogram is the only clue to the presence of an effusion. It also may suggest its cause (e.g., cardiomegaly and redistribution of pulmonary veins in heart failure, lung or pleural-based masses, atelectasis, rib erosions signifying metastatic carcinoma, or an elevated hemidiaphragm suggesting subdiaphragmatic abscess, volume loss, or bronchial obstruction). At least 150 mL of fluid is required to detect an effusion on a standard posteroanterior and lateral chest roentgenogram. Today, pleural ultrasonography is increasingly used to image both large and small effusions. Typically, fluid initially collects between the anteroinferior lung surface and the diaphragm. It then obliterates the costophrenic angle on the frontal view of the chest radiograph, or creates a triangular density that obscures the ipsilateral diaphragm and posterior costophrenic sulcus on a lateral film. Further accumulation obliterates the hemidiaphragm and opacifies the hemithorax with an upward concavity that extends higher laterally than medially. On the lateral view, pleural fluid ascends obliquely along the posterior chest wall. Significantly smaller quantities of pleural fluid are detectable on lateral decubitus views. On lateral decubitus films, fluid layers along the dependent chest wall. On the opposite decubitus view, fluid shift allows examination of underlying parenchyma. However, decubitus films often are not necessary because both loculated and free flowing fluid are detected by pleural ultrasonography before thoracentesis. A very large effusion should cause a contralateral mediastinal shift. When this shift does not occur, parenchymal collapse or mediastinal fixation, often from a tumor, may be present.

When underlying parenchymal abnormalities or adhesions between pleural layers exist, atypical patterns of fluid accumulation result. A subpulmonic effusion can harbor more than 1,000 mL of fluid and may resemble merely an elevated hemidiaphragm. However, the “diaphragmatic” contour is often more horizontal than usual, with a steep angulation laterally that creates a shallow costophrenic angle. A lateral decubitus film may layer the fluid and reveal the true diaphragmatic shadow. When pleural fluid becomes loculated (or entrapped) within an interlobar fissure, it can create the appearance of an elliptic opacity, or pseudotumor, on the posteroanterior film and a spindle-shaped opacity tapering into fissure lines on the lateral film. For unknown reasons, this appearance is especially common with congestive heart failure and resolves as hemodynamics improve. Fluid that is loculated laterally can result in a smooth, contoured, semicircular opacity abutting a pleural surface, which can simulate a mass lesion on a posteroanterior film. Loculations are frequently seen in patients with evolving parapneumonic effusions or empyema after either thoracic surgery or pleurodesis. It is noteworthy that computed tomography (CT) scans often exaggerate the amount of fluid actually present.

The information from chest radiographs can be supplemented by pleural ultrasonography and CT scans. Bedside ultrasound, which is now commonplace, visualizes the effusion as well as loculations, diaphragmatic movements, and the underlying lung. CT scans should be performed in the investigation of unexplained exudative effusions, and can be useful in distinguishing malignant from benign pleural thickening. CT scans should be performed with contrast enhancement, and before complete drainage of the effusion. Scans also are performed in cases of complicated pleural infections, especially if initial tube drainage has been unsuccessful, magnetic resonance imaging (MRI) may also help distinguish malignant from benign disease, particularly if chest wall or diaphragmatic involvement is suspected. Positron emission tomography–computed tomography (PET–CT), in combination with MRI may have a role to monitor response to chemotherapy in the treatment of malignant mesothelioma.

The differential diagnosis of pleural effusion should reflect the clinical context and ancillary findings, but thoracentesis and careful examination of the pleural fluid are indicated in nearly every instance. Thoracentesis has low morbidity in experienced hands. Precautions should be used in patients with a bleeding diathesis, a very small effusions, or an obliterated pleural space, as well as in patients taking anticoagulant drugs, those who are uncooperative, and those for whom even a small pneumothorax could be extremely hazardous. Ultrasound guidance increases the likelihood of successful sampling, and reduces the risk of complications. Furthermore, ultrasound has a specificity similar to that of CT in differentiating malignant from benign effusions, and identifies exudative effusions through detection of septations (loculations) or echogenicity. It is traditionally suggested that no more than 1,000 mL of fluid be removed at any one sitting to avoid reexpansion pulmonary edema, but this complication is unusual. The procedure should probably be halted, however, if the patient begins to cough, has chest pain, or other possible signs of increasingly negative pleural pressure. Regardless, fluid should be removed slowly.

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