Congestive heart failure is the most common condition to produce a transudative pleural effusion. The effusions are typically bilateral and larger on the right (4). An isolated right effusion is twice as common as an isolated left effusion.

Parapneumonic Effusion and Empyema. A parapneumonic effusion is defined as an effusion associated with pneumonia. Peripheral parenchymal infection produces an exudative pleural effusion by causing visceral pleural inflammation that increases pleural capillary permeability. Inflammatory thickening of the pleural membranes with lymphatic obstruction may also be a contributing factor. Empyema results when the parenchymal infection extends into the pleural space. Parenchymal infections that typically result in empyema formation are bacterial pneumonia, septic emboli, and lung abscess, whereas fungal, viral, and parasitic infections are uncommon causes. Less commonly, infection may extend into the pleural space from the spine, mediastinum, and chest wall.

Forty percent of bacterial pneumonias have an associated pleural effusion. Staphylococcus aureus and gram-negative pneumonias are the most common cause of parapneumonic effusion and empyema. The natural history of parapneumonic effusions may be divided into three stages (5,6,7). Stage 1 is an exudative stage; visceral pleural inflammation causes increased capillary permeability and pleural fluid accumulation. Most of these sterile exudative effusions resolve with appropriate antibiotic therapy. A stage 2 parapneumonic effusion is a fibrinopurulent pleural fluid collection containing bacteria and neutrophils. Fibrin deposition on the visceral and parietal pleura impairs fluid resorption and produces loculations. If the infection is not treated, the loculations will impair attempts at closed pleural fluid drainage. A stage 3 parapneumonic effusion develops 2 to 3 weeks after initial pleural fluid formation and is characterized by the ingrowth of fibroblasts over the pleura, which produces pleural fibrosis and entraps the lung. Dystrophic calcification of the pleura may develop following resolution of the pleural infection. Tuberculous pleural effusion or empyema resulting from the rupture of subpleural caseating granulomas may complicate pulmonary infection or occur as the primary manifestation of disease. Effusions in tuberculosis (TB) are more common in young adults with pulmonary disease and in HIV-positive individuals with severe immunodeficiency. The pleural fluid is characteristically straw colored, with greater than 70% lymphocytes and a low glucose concentration.

Radiographically, empyema most often appears as a loculated pleural fluid collection. On CT, it is elliptic in shape and is seen most often within the posterior (costal pleura) and inferior (subpulmonic) pleural space. The collection conforms to and maintains a broad area of contact with the chest wall (Fig. 19.2). The distinction of empyema from peripheral lung abscess has important therapeutic implications; empyemas require external drainage, whereas lung abscesses usually respond to postural drainage and antibiotic therapy. Contrast-enhanced chest CT is most useful in making this distinction (Table 19.4) (8). Detection of an empyema may be difficult when there is extensive parenchymal consolidation. In these cases, CT and US are useful in detecting parapneumonic fluid collections and guiding diagnostic thoracentesis and pleural drainage. Findings on CT that are fairly specific for the presence of an exudative pleural effusion include thickening and enhancement of the parietal pleura, the presence of loculations, and the detection of discrete soft tissue lesions along the parietal pleura outlined by low-attenuation pleural fluid. Hemorrhagic effusions can occasionally be recognized on CT by their intrinsic high attenuation or the presence of a fluid–fluid level caused by dependent cellular blood elements.

Neoplasms. Pleural effusion may be seen with benign or malignant intrathoracic tumors. The tumors most commonly associated with pleural effusion are, in order of frequency, lung carcinoma, breast carcinoma, pelvic tumors, gastric carcinoma, and lymphoma. Pleural fluid may result from pleural involvement by tumor or from lymphatic obstruction anywhere from the parietal pleura to the mediastinal nodes. The effusions are exudative and may be bloody. Demonstration of malignant cells on cytologic examination of pleural fluid obtained at thoracentesis is necessary for the diagnosis of a malignant effusion. Image-guided closed or thoracoscopic biopsy is reserved for patients with negative cytologic examination. Clues to the presence of a malignant pleural effusion include smooth or nodular pleural thickening, mediastinal or hilar lymph node enlargement or mass, and solitary or multiple parenchymal nodules. CT is useful in demonstrating pleural masses or underlying parenchymal lesions in those with large effusions (Fig. 19.3).

Trauma. Blunt or penetrating trauma to the chest, including iatrogenic trauma from thoracotomy, thoracostomy, or placement of central venous catheters, may result in a hemothorax. Hemothorax results from laceration of vessels within the lung, mediastinum, chest wall, or diaphragm. Intrapleural blood coagulates rapidly, and septations form early. In some individuals, pleural motion causes defibrination, which lyses the clotted blood. In the acute setting, pleural fluid of high
CT attenuation (>80 H) may be seen (Fig. 19.4); associated rib fractures or subcutaneous emphysema should suggest the diagnosis. An acute hemothorax is treated with thoracostomy tube drainage, whereas thoracotomy is generally reserved for persistent bleeding or hypotension.

Esophageal perforation from prolonged vomiting (Boerhaave syndrome) or as a complication of esophageal dilatation may produce a pleural effusion, most commonly on the left side.

Extravascular placement of a central line can result in a hydrothorax when intravenous solution is inadvertently infused into the pleural or extrapleural space.

Collagen Vascular and Autoimmune Disease. Systemic lupus erythematosus has a reported incidence of pleural effusions ranging from 33% to 74% (Fig. 19.5). These exudative effusions are a result of pleural inflammation; patients often present with pleuritic chest pain. In some cases, the nephrotic syndrome associated with systemic lupus erythematosus may produce transudative effusions. Cardiomegaly is a common associated radiographic finding and may be caused by pericardial effusion, hypertension, renal failure, or lupus-associated endocarditis or myocarditis. Pleural effusion is the most common intrathoracic manifestation of rheumatoid arthritis and is most frequently seen in male patients following the onset of joint disease. The effusions occur independent of pulmonary parenchymal involvement, but may develop following intrapleural rupture of peripheral rheumatoid nodules. The effusions of rheumatoid arthritis are exudative, with lymphocytosis, low glucose concentration, and low pH (<7.2). Rheumatoid effusions may persist unchanged for years. Autoimmune syndromes producing pleural and pericardial effusions have been described following myocardial infarction (Dressler syndrome) or cardiac surgery (postpericardiotomy syndrome). Both are characterized by fever, pleuritis, pneumonitis, and pericarditis developing within days to weeks of the precipitating event. The radiographic findings include enlargement of the cardiac silhouette, pleural effusions, and parenchymal airspace opacities. A serosanguineous exudative pleural effusion is seen in over 80% of patients. Treatment with nonsteroidal anti-inflammatory drugs usually results in symptomatic and radiographic improvement.

Abdominal Disease. Radioisotope studies have demonstrated that peritoneal fluid may enter the pleural space via transdiaphragmatic lymphatic channels or through defects in the diaphragm. The lymphatic channels are larger on the right side, accounting for the higher incidence of right-sided effusions associated with ascites or liver failure (hepatic hydrothorax).

Pancreatitis. Acute or chronic pancreatitis can cause pleural effusions that are most often left-sided because of the proximity of the pancreatic tail to the left hemidiaphragm. The effusion associated with acute pancreatitis is typically exudative and may be bloody. Pleural effusion from chronic pancreatitis
may cause pleuritic chest pain and shortness of breath. Rupture of the pancreatic duct can lead to a pancreaticopleural fistula. A high amylase concentration in the pleural fluid should suggest the pancreas as the etiology of the effusion, although elevated amylase may be seen in pleural effusions caused by malignancy or esophageal perforation.

Subphrenic abscess complicating abdominal surgery or perforation of a hollow viscus can cause diaphragmatic paresis, basilar atelectasis, and pleural effusion. Patients with a pleural effusion associated with upper abdominal pain, fever, and leukocytosis should have CT or US examination and when applicable, percutaneous catheter drainage of the abscess.

Pelvic Tumors. An association between benign pleural effusions and pelvic tumors has long been recognized. First described with ovarian fibroma (Meigs syndrome), a number of pelvic and abdominal tumors, including pancreatic and ovarian malignancy, lymphoma, and uterine leiomyomas, have been found to cause pleural effusion. The effusions in Meigs syndrome are usually transudative and resolve after removal of the pelvic tumor.

Chylothorax is a pleural collection containing triglycerides in the form of chylomicrons resulting from extravasation of thoracic duct contents secondary to malignancy, iatrogenic trauma, or TB (Fig. 19.6). The thoracic duct originates from the cisterna chyli at the level of the first lumbar vertebra and ascends along the right paravertebral space, entering the thorax via the aortic hiatus. The duct crosses from right to left at the level of the sixth thoracic vertebra to lie alongside the upper esophagus. A knowledge of this anatomy is useful, as disruption of the upper duct caused by direct trauma or obstruction with rupture produces a left chylothorax, whereas injury to the lower intrathoracic duct produces a right chylothorax. At the level of the left subclavian artery, the duct arches anteriorly to empty into the confluence of the left internal jugular and subclavian veins. The radiographic appearance is indistinguishable on plain radiographs and CT from other causes of free-flowing effusions. The diagnosis is confirmed by triglyceride levels exceeding 110 mg/dL in the pleural fluid.

Pulmonary Embolism. Infarction complicating pulmonary embolism is a well-recognized cause of pleural effusion. The effusion may be associated with elevation of the ipsilateral diaphragm and peripheral wedge-shaped opacities (Hampton hump). The pleural effusion is typically a small, unilateral, serosanguineous exudate.

Drugs may cause pleural effusions as a result of pleural inflammation (methysergide) or by producing a lupus-like syndrome (phenytoin, isoniazid, hydralazine, procainamide). Nitrofurantoin has been associated with an immunologic reaction that causes pleuropulmonary disease with eosinophilia.

Management of Pleural Effusion. Transudative pleural effusions are managed by treatment of the underlying disorder because the pleura is intrinsically normal in these diseases. Management of parapneumonic effusions is best guided by evaluation of the likelihood that the effusion, if not drained, would result in prolonged hospitalization, pleural fibrosis with resultant respiratory impairment, local spread of infection, or death. This likelihood is based on the anatomy, bacteriology, and chemistry (i.e., ABCs) of the fluid collection. In general, larger, loculated collections with positive gram stains or cultures and pH less than 7.20 are associated with a moderate to high risk for poor outcome as detailed above and should be drained if possible (5). The choice of drainage procedure depends on various factors, including patient age and underlying condition, length of illness, and access to image-guided therapy and thoracoscopy. Although intrapleural fibrinolytic therapy with tissue plasminogen activator will help a certain subset of patients with complex parapneumonic effusions (Fig. 19.7), some will require open pleural drainage by video-assisted thoracoscopic surgery (VATS) or thoracotomy with decortication. In contrast, malignant pleural effusions most often require closed drainage and pleural sclerosis, with talc being the current agent of choice. Trials of other pleurodesis agents have not shown superiority while being marred by higher cost. It is notable that talc pleurodesis can cause FDG-18 PET positive nodularity, which is a source of false-negative PET evaluations. Some patients may benefit from VATS drainage and sclerosis. Select patients can be managed as outpatients with indwelling silastic catheters (e.g., PleurX™catheter, CareFusion Corp, San Diego, CA), which allow intermittent patient-directed drainage of fluid. Patients with chylothorax secondary to lymphoma or TB require therapy directed at this underlying, whereas patients with traumatic disruption of the thoracic duct often require surgical ligation of the duct.

Patients with pleural effusions from trauma, pulmonary embolism, autoimmune disorders, and drug reactions often require no specific therapy. Exceptions include the postpericardiotomy
or post-MI patients (Dressler syndrome), who are treated with nonsteroidal anti-inflammatory agents, and patients with large hemothoraces requiring large bore tube drainage to prevent pleural fibrosis and lung entrapment.