Disorders of the Pleural Space

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[edit] Disorders of the Pleural Space

Basil Varkey

Ralph M. Schapira

Pleural effusion is an abnormal accumulation of fluid in the pleural space caused by either an intrinsic abnormality of the pleura (exudative effusion) or an imbalance in oncotic or hydrostatic pressures (transudative effusion) (Box 79-1). Other pleural disorders discussed in this chapter are fibrothorax, asbestos-related pleural disease, and pneumothorax.

[edit] PLEURAL EFFUSION

[edit] Pathophysiology

The pleura is a serous membrane made of a single layer of mesothelial cells. The visceral pleura covers the lung parenchyma, and the parietal pleura covers the remaining structures of the thoracic cavity. The airless space between the parietal and visceral pleurae is the pleural space. Because of a net gradient favoring movement of fluid through the parietal pleura into the pleural space, a nearly undetectable amount of clear, colorless pleural fluid with a low protein concentration (less than 1.5 gm/dl) is normally present, estimated at 10 ml in humans. The fluid in the pleural space is believed to be removed by the lymphatics of the parietal pleura, which normally maintain an equilibrium between the physiologic formation of pleural fluid and the removal of pleural fluid. (The visceral pleural lymphatics are poorly developed and do not contribute significantly to the removal of pleural fluid.) The parietal pleura receives its blood supply from systemic arteries of the adjacent chest wall, and the visceral pleura is supplied by the bronchial circulation. Much of the venous drainage of the visceral pleura is into the pulmonary veins; the parietal pleura drains into the bronchial veins and inferior vena cava.

Pleural effusions are caused by increased pleural fluid formation, decreased pleural fluid lymphatic drainage, or a combination of the two mechanisms. Transudative pleural effusions are caused by oncotic or hydrostatic factors that favor increased formation of pleural fluid, the most common cause being congestive heart failure. Exudative pleural effusions are caused by an increase in the permeability of the pleura; examples include malignant pleural effusions (usually caused by tumor invasion of the pleura) and bacterial pneumonia (parapneumonic effusion).

The presence of a pleural effusion limits expansion of the lung and may cause diaphragmatic dysfunction. Consequently, a restrictive ventilatory impairment can be noted on pulmonary function testing. The dyspnea associated with some pleural effusions, particularly those of large size, is believed to result from the mechanical disadvantage of the diaphragm. Hypoxemia associated with a pleural effusion results from intrapulmonary shunt caused by compression of the lung, ventilation/perfusion mismatch, and underlying lung disease. The drainage of a pleural effusion does not always improve gas exchange.^[1]

[edit] Patient Evaluation

[edit] History.

The three cardinal symptoms of a pleural effusion are dyspnea, chest pain (pleuritic or nonpleuritic), and a nonproductive cough. However, even large pleural effusions can be asymptomatic. The underlying disease producing the pleural effusion may play a role in the symptoms. For example, a patient with effusions from left ventricular failure may have symptoms from pulmonary edema rather than from the effusions. The history and physical examination can provide clues as to the cause of the effusion (Box 79-2).

[edit] Physical Examination.

The findings on physical examination usually correlate with the size of the pleural effusion. Inspection of the thorax in a patient with a large pleural effusion may reveal bulging intercostal spaces on the side of the effusion and a shift of the trachea away from the side of the effusion. Palpation reveals a decrease in tactile fremitus over the effusion. The percussion note is dull. Auscultation over the pleural effusion reveals decreased or absent breath sounds. Palpation, percussion, and auscultation are useful in delineating the superior border of the effusion, since the physical signs are normal above this level.

[edit] Diagnosis

[edit] Laboratory Studies and Diagnostic Procedures.

The presence of an effusion is confirmed by chest radiographs. A small effusion (about 200 ml) obliterates the normally sharp costophrenic angle on a lateral view, and a decubitus film can detect as little as 100 ml of pleural fluid. A moderate effusion (about 500 ml) typically reveals a meniscus-shaped border laterally on a posteroanterior (PA) view. Subpulmonic effusions, loculated effusions, and underlying lung disease may alter the typical radiographic pattern. An ultrasonogram is more sensitive than chest radiographs in detecting pleural fluid and in differentiating a pleural effusion from pleural thickening.^[2] When a pleural effusion is suggested on a radiograph, the physician must decide whether to obtain pleural fluid for analysis. If the cause of a pleural effusion is clearly evident, such as bilateral effusions in a patient with heart failure or asymptomatic effusions within 48 hours of parturition or abdominal surgery, the effusions may be observed and resolution documented on serial radiographs during treatment. If a pleural effusion is of unknown cause, however, an evaluation is mandatory. A diagnostic thoracentesis with removal of a small volume of pleural fluid (50 to 100 ml) is needed to define the effusion as a transudate or an exudate and for other tests.

To perform a thoracentesis safely, a lateral decubitus chest film with the effusion dependent should be taken to determine whether the suspected pleural fluid is free flowing. If the fluid layers along the inner chest wall, and if the distance between the inner chest wall and the superior surface of the effusion is at least 10 mm, a diagnostic thoracentesis can be performed on the location of the effusion as determined by physical examination. If the pleural effusion does not layer on the lateral decubitus film, however, or if the distance is less than 10 mm, three possibilities exist: (1) the effusion is small in volume, (2) the effusion is loculated, or (3) the radiographic abnormalities represent pleural thickening and not a pleural effusion. An ultrasound of the pleural space can differentiate among these possibilities and, if pleural fluid is present, can guide a diagnostic thoracentesis. A common error is for a patient's chest wall to be marked by the ultrasonographer for subsequent thoracentesis. Unless the patient is in precisely the same position as at the time of marking, the effusion may have shifted, making thoracentesis unsuccessful. Computed tomography (CT) scan of the chest is usually not necessary to identify a pleural effusion but does provide additional information on the underlying lung parenchyma and mediastinum, such as the presence of a mass or lymphadenopathy. Magnetic resonance imaging (MRI) of the chest has less utility than CT scan or ultrasound.

The major complications of thoracentesis are pneumothorax, pleural space infection, hemothorax, and reexpansion pulmonary edema. An end-expiratory PA chest radiograph should be performed after thoracentesis to check for a pneumothorax. Pleural fluid in patients with suspected or confirmed infections, such as human immunodeficiency virus (HIV) or hepatitis B, should be handled with special precautions to avoid transmission of these agents.

Invasive procedures are selectively employed to determine the cause of a pleural effusion if thoracentesis fails to provide a definitive answer. These invasive procedures include percutaneous parietal pleural biopsy (PPB), thoracoscopy (pleuroscopy), fiberoptic bronchoscopy (FOB), and thoracotomy with pleural biopsy.

[edit] Differential Diagnosis.

To define an effusion as a transudate or an exudate, the total protein and lactate dehydrogenase (LDH) concentrations of the pleural fluid must be compared with those of simultaneously obtained serum. An exudative effusion has at least one of the following three criteria (Light's criteria): (1) a pleural fluid/serum protein ratio greater than 0.5, (2) a pleural fluid/serum LDH ratio greater than 0.6, or (3) an absolute LDH greater than two-thirds the upper limits of normal for the serum LDH. Transudative pleural effusions meet none of these three criteria. A study found that new criteria were not superior to Light's criteria in the differentiation of a transudative from an exudative effusion.^[3] A meta-analysis determined that each of Light's three criteria had a similar diagnostic accuracy; paired or triplet combinations increased the diagnostic accuracy compared with any one of the criteria alone, but no combination of tests was found to be superior.^[4]

[edit] Transudative Pleural Effusions.

Congestive heart failure is the most common cause of pleural effusions. Typically the effusion is bilateral, the pleural fluid is serous in appearance, and chemical analysis reveals a transudate. Recent evidence suggests that biventricular failure is a requirement for the development of a pleural effusion and that right ventricular failure alone does not cause a pleural effusion. Diuresis usually does not convert a transudative pleural effusion from cardiac failure into an exudate. A patient who presents with typical clinical features of left-sided cardiac failure, a radiograph demonstrating cardiomegaly, and bilateral effusions usually does not require pleural effusion analysis. Patients with cardiac failure, however, may be at risk for pulmonary embolism; if a patient with cardiac failure presents with a unilateral pleural effusion or atypical features such as a fever or pleuritic chest pain, pulmonary embolism or pneumonia should be considered.

Another common cause of a transudative pleural effusion is hepatic cirrhosis. The pleural effusion of cirrhosis arises by movement of ascitic fluid from the peritoneal cavity through the diaphragm. The chemical characteristics of the pleural and ascitic fluid are usually similar. The chest radiograph typically shows a right-sided pleural effusion (70%) and a normal-sized heart. The patient usually has evidence of chronic liver disease and ascites, although if enough of the fluid in the peritoneum has traversed the diaphragm, clinical evidence of ascites may be lacking.

Although frequently associated with an exudative bloody pleural effusion, pulmonary thromboembolism can cause a typically unilateral pleural effusion, which can be a transudate in 20% of patients. Thus a transudative pleural effusion does not rule out a pulmonary embolism, and further diagnostic evaluation may be necessary.

Other less common causes of transudative effusions include the nephrotic syndrome (from decreased oncotic pressure), urinothorax (from retroperitoneal urinary leakage associated with urinary obstruction), and peritoneal dialysis (from movement of dialysate from the peritoneal to pleural space). Collapse of an entire lobe or lung by an endobronchial tumor or foreign body can cause a transudative pleural effusion because of a decrease in the negative pleural pressure, which favors an increase in pleural fluid formation. The cause of transudative effusions is usually apparent from the clinical history.

[edit] Exudative Pleural Effusions.

A pleural effusion associated with bacterial pneumonia, termed a parapneumonic effusion, is the most common cause of an exudative pleural effusion. Parapneumonic effusions occur in about 40% of cases of bacterial pneumonia and are ipsilateral to the pneumonia; pleural fluids have leukocyte counts greater than 10,000 cells/mm³, with a predominance of polymorphonuclear neutrophils (PMNs). A parapneumonic effusion is termed uncomplicated if it resolves with appropriate antibiotic therapy alone without sequelae and complicated if it requires chest tube drainage to avoid persistent pleural space infection, bronchopleural fistula, or pleural adhesions. A loculated parapneumonic effusion suggests a complicated form.

The differentiation between a complicated and an uncomplicated parapneumonic effusion is based on the gross characteristics of the pleural fluid, a Gram's stain and culture of the pleural fluid, and biochemical characteristics of the pleural fluid. Complicated parapneumonic effusions consist of empyemas (gross pus, Gram's stain demonstrating bacteria, or positive culture) or effusions with a pH less than 7.0 or glucose concentration less than 40 mg/dl. The pleural fluid LDH concentration alone does not define a parapneumonic effusion as complicated, although effusions with a pH value under 7.0 or glucose under 40 mg/dl are frequently associated with an LDH greater than 1000 IU/L. Bacteria vary greatly in their potential to cause complicated parapneumonic effusions. Streptococcus pneumoniae, although a common cause of pneumonia, seldom causes complicated parapneumonic effusion. In contrast, anaerobic bacteria, gram-negative bacteria, Staphylococcus aureus, and Streptococcus pyogenes are often associated with complicated parapneumonic effusions.

Malignant pleural effusions, usually caused by pleural invasion by malignant cells, are the second major cause of exudative pleural effusions. Carcinomas of the lung and breast are the leading causes of malignant effusions and, along with lymphomas, account for about 75% of cases. A malignant pleural effusion may be the presenting clinical evidence of cancer and implies an advanced stage and poor prognosis. Although most often caused by direct metastatic involvement of the pleura, pleural effusion may be caused by tumor invasion of mediastinal lymph nodes, atelectasis, or pneumonia rather than direct pleural involvement. These effusions are termed paramalignant by some authorities. Cytopathologic analysis of pleural fluid shows malignant cells in 60% to 80% of malignant effusions. The differentiation of a true malignant effusion (an effusion containing malignant cells) from a paramalignant effusion can be very important clinically. For example, lung cancer with a malignant effusion is surgically unresectable, whereas lung cancer with a paramalignant effusion (no malignant cells in the effusion) may be resectable.

The third most common type of pleural effusion is caused by pulmonary embolism (PE), which is an exudate about 80% of the time. Pleural effusions occur in up to 50% of patients with PE. The effusion usually is unilateral and may be bloody. An underlying pulmonary infiltrate may be present, but the history, physical examination, pleural fluid analysis, and chest radiographs are nonspecific in PE. Therefore the physician should always consider PE in the differential diagnosis of a patient who has a pleural effusion with symptoms or signs suggestive of a PE or risk factors for PE.

Disease caused by Mycobacterium tuberculosis can cause pleuritis with an associated unilateral exudative pleural effusion and should always be considered in the patient with a lymphocyte-predominant exudative pleural effusion (see Chapter 74 ). Glucose concentrations are frequently normal.

Upper abdominal disease (e.g., subphrenic abscess) resulting from perforation of an abdominal structure, a hepatic or splenic abscess, or viral hepatitis may cause upper abdominal or lower thoracic pain, fever, and a pleural effusion. Amebic abscess of the liver may cause right-sided pleural effusions as an inflammatory response to the abscess or, more often, as a result of rupture of the abscess through the diaphragm into the pleural cavity. These illnesses may mislead the physician into looking for pleuropulmonary disease, delaying early recognition of an intraabdominal problem. Acute and chronic pancreatitis may result in a high-amylase exudative pleural effusion, which is usually left sided. A pleural effusion with or without an associated pneumomediastinum or pneumothorax in a patient with a history of vomiting, chest pain, and dyspnea should lead the physician to consider esophageal rupture. The exudative effusion in esophageal rupture typically has a high salivary amylase level and a pH in the range of 6.0. In addition, the pleural space may be infected with oropharyngeal anaerobes. Early diagnosis and management are essential.

Collagen vascular diseases, particularly systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), may be complicated by effusions. Although pleural effusions usually complicate previously defined SLE and RA, an effusion may be the presenting clinical manifestation. Glucose levels in the pleural fluid are often greatly reduced in rheumatoid effusions, and physical examination almost invariably shows joint abnormalities. Dressler's syndrome, also known as postcardiac injury syndrome (PCIS), can occur after myocardial injury, such as infarction, trauma, or cardiac surgery. The syndrome includes pericarditis, pleural effusions, and pulmonary infiltrates associated with fever or chest pain, usually a few weeks to several months after myocardial injury. PCIS should be considered in any patient with a pleural effusion, unilateral or bilateral, after a myocardial infarction or cardiac surgery.

Exudative pleural effusions may result from medications, either directly or as a part of the drug-induced lupus syndrome (Box 79-3). Pleural effusion in a patient with a central venous catheter may result from erosion of the venous wall by the catheter tip. This complication most often occurs with left-sided venous catheters and is suggested by a hemothorax or an effusion with a composition similar to that of the infusate.

[edit] Utility of Diagnostic Tests.

The key to ordering the appropriate tests is to form a pretest diagnosis based on integrated clinical information. Pleural fluid tests can be divided into four groups based on their relative usefulness (Table 79-1). Observation of gross characteristics (group A tests) costs nothing but may provide a specific diagnosis or lead to individual tests that are diagnostic. Foul-smelling, yellow-green thick fluid is pus (empyema). Chocolate-colored (anchovy sauce) fluid strongly suggests a ruptured amebic liver abscess. White milky pleural fluid indicates a chylous or chyliform effusion and the need for triglyceride level and cytologic evaluation. A grossly bloody fluid suggests hemothorax, and the pleural fluid hematocrit must be checked. Protein and LDH along with serum protein and LDH separate transudates and exudates with a 95% accuracy. When a transudate is suspected, a two-step approach is appropriate, keeping some fluid in reserve pending protein and LDH determinations. If the effusion is confirmed as a transudate, no further analysis is necessary.

Table 79-1 Diagnostic Utility of Pleural Fluid Tests

Group B tests have the potential to provide a definite diagnosis of empyema or malignant effusion. Although about 40% of bacterial pneumonias may be associated with a parapneumonic effusion, only a small percentage develop into an empyema. In contrast, cytologic examination proves malignancy in most cases of malignant effusions. In either case, negative studies do not exclude the diagnosis of a parapneumonic effusion or a malignancy.

Group C tests have a high specificity for diagnosing uncommon causes of pleural effusion. These tests should be selectively ordered based on clinical suspicion and gross appearance of the pleural fluid. Pleural fluid cultures for mycobacteria and fungi have a low sensitivity but should be obtained if these organisms may be the cause of the exudative effusion. Pleural effusions are present in 16% to 37% of patients with SLE. These patients are symptomatic with pleuritic chest pain, and most have arthralgias or arthritis before the pleuritis. Measurement of the antinuclear antibody (ANA) level in pleural fluid and serum is helpful in diagnosing lupus pleuritis. Pleural fluid ANA titer is usually 1:160 or greater, and the pleural fluid ANA/serum ANA is 1 or greater. The finding of LE cells in pleural fluid is considered to be diagnostic of lupus pleuritis.

Pleural fluid amylase determination is indicated when pancreatitis or esophageal rupture is suspected. Pleural fluid amylase is above the upper limits of normal for serum and above the amylase level of a simultaneously sampled serum in pancreatitis. In chronic effusions caused by pancreatic pseudocyst, abdominal symptoms may be minimal and chest symptoms may predominate. In large left-sided effusions of unknown cause an effusion of pancreatic origin must be considered. Pleural fluid amylase is also elevated in esophageal rupture, but unlike with pancreatitis, the amylase is of salivary origin. Pleural fluid amylase may also be elevated in some malignant effusions, but the levels of amylase usually do not reach the levels seen in pancreatic disease and esophageal rupture, and the amylase is of salivary origin.

A triglyceride level greater than 110 mg/ml in the pleural fluid indicates chylothorax. If the level is indeterminate, 50 to 110, lipoprotein analysis is indicated. The detection of chylomicrons confirms the diagnosis of chylothorax. A chylothorax indicates disruption of the thorax duct, which allows chyle to enter the pleural space. The most common causes are malignancy, particularly lymphoma, and trauma.

The hematocrit of a bloody pleural effusion should be measured. A pleural fluid hematocrit approaching that of blood indicates a hemothorax and suggests trauma as the cause; chest tube drainage should be strongly considered. A hematocrit greater than 1% suggests malignancy, trauma, or pulmonary embolism. A hematocrit less than 1% is a relatively nonspecific finding.

Group D tests do not provide specific diagnoses, but integrated with clinical information, they often help the physician narrow the range of possible disorders. Red blood cell (RBC) count of pleural fluid should be interpreted with great caution, and RBC counts generated by an automated counter may not be reliable. RBC counts greater than 5000/mm³ may impart a bloodlike color (serosanguineous) to the fluid but are not very helpful, since 40% of exudative effusions and some transudates may be blood tinged. Effusions with RBC counts greater than 100,000 cells/mm³ suggest the same diagnostic possibilities as those with a hematocrit less than 1%.

A white blood cell (WBC) count greater than 10,000/mm³ is most often seen in parapneumonic effusions but also occurs in PE, malignancy, tuberculosis, pancreatitis, Dressler's syndrome, and SLE. Neutrophilic predominance indicates acute pleural inflammation. A predominance of small lymphocytes in an exudative effusion strongly suggests tuberculosis or malignancy. Eosinophilic effusions (more than 10% eosinophils) have a variety of causes. Malignant pleural effusions can be eosinophilic. Pleural effusions after trauma and thoracic surgery, as well as benign asbestos-related effusions, can show eosinophilia. Drug-induced pleural effusions are frequently eosinophilic, as are effusions caused by parasitic and some fungal diseases. Mesothelial cells are sparse (less than 5%) in tuberculous pleural effusions. This finding is not specific, however, since any extensive inflammatory process may diminish the number of mesothelial cells in the pleural fluid.

A low pleural fluid glucose level (less than 60 mg/ml) suggests a short list of possible causes of the effusion, primarily RA and parapneumonic and malignant effusions. Often the pleural fluid glucose in RA pleural effusions is strikingly low; in 80% of patients pleural fluid glucose levels are less than 30 mg/ml.^[5] In comparison, lupus pleuritis is less often associated with low glucose pleural effusions (in one study 21%^[6]), and the levels are not as low as in effusions associated with RA.

Pleural fluid acidosis (pH less than 7.2) can have a variety of causes, including infection, esophageal rupture, rheumatoid effusion, tuberculosis, malignancy, hemothorax, lupus pleuritis, and urinothorax. In combination with high pleural fluid amylase, a low pH (under 6.0) suggests esophageal rupture as a cause. At present the best use of pH testing is for parapneumonic effusions to decide if chest tube drainage is necessary, since effusions with pH under 7.0 generally require tube drainage to avoid serious pleural space complications (e.g., loculations, adhesions). Although helpful in this regard, pleural fluid pH is not foolproof in its predictive value.

[edit] Indications and Utility of Other Invasive Procedures.

Consideration should be given to other invasive procedures when the cause of a pleural effusion remains unknown after thoracentesis and pleural fluid analysis.

Percutaneous pleural biopsy (PPB) is particularly useful in the diagnosis of tuberculous pleuritis or pleural malignancy (see Chapter 74 ). The predominance of lymphocytes in pleural effusion is predictive of a high diagnostic yield by PPB. The diagnostic yield of PPB in tuberculous pleuritis is 87% when two or more pleural samples are obtained and the tissue is analyzed by both histology and culture.^[7] In malignant pleural effusions, the yield of pleural fluid cytopathologic analysis alone is 50% to 60%, and the gain from adding PPB to a negative cytologic study is only 7.1%.^[8][9] The most common complication of PPB is pneumothorax, usually caused by entry of atmospheric air into the pleural space (3% to 15%). An end-expiratory PA chest radiograph should be performed after the procedure. PPB is most safely performed in a cooperative patient when a sufficient amount of pleural fluid is present in the biopsy area to minimize the chance of penetrating the underlying lung during the biopsy.

A PPB that yields a histologic diagnosis of nonspecific pleuritis is not helpful. The physician must then decide whether to observe the effusion without further diagnostic tests or proceed with thoracoscopy or fiberoptic bronchoscopy.

Thoracoscopy has replaced thoracotomy and open pleural biopsy as the preferred procedure in pleural diseases that are difficult to diagnose. In a study of thoracoscopy in 102 patients with undiagnosed pleural disease, a diagnosis of malignancy was established in 38 patients, yielding a sensitivity of 91% and a specificity of 100%. The four cases of malignancy that were missed by thoracoscopy were all malignant mesothelioma. Thoracoscopy is also useful in the diagnosis of tuberculous pleuritis. Some controversy remains on the role of thoracoscopy, however, since it may not add much to the diagnosis of metastatic pleural malignancy or tuberculous pleuritis compared with thoracentesis and PPB. In addition, biopsies from other causes of exudative pleural effusions (e.g., rheumatologic disease or pulmonary embolism) may demonstrate a nonspecific pleuritis. Thus thoracoscopy should be considered when a diagnosis of tuberculous pleuritis has been missed despite negative cultures and nondiagnostic pleural histopathology or if the diagnosis of a malignant pleural effusion has not been established after cytopathologic analysis of at least three pleural fluid samples obtained by thoracentesis. Thoracoscopy is also useful in suspected malignant mesothelioma because of the relatively low yields of PPB and thoracentesis.

Fiberoptic bronchoscopy (FOB) after nondiagnostic thoracentesis and PPB is indicated only when the chest radiograph or CT scan demonstrates a lung parenchymal abnormality, such as a mass or collapse, or if the patient has a history of hemoptysis. In the absence of these features, FOB has a very low diagnostic yield.

Even after an evaluation that includes invasive procedures, the cause of a pleural effusion remains unknown in about 15% of patients, although the course and outcome are often favorable. In a study of 51 patients, 31 (60.8%) had spontaneous resolution of the effusion. In another study of 40 patients with an undiagnosed pleural effusion, 32 (80%) were not diagnosed even after prolonged follow-up. The remaining eight cases were eventually diagnosed as three asbestos-related effusions and one each of adenocarcinoma, mesothelioma, rheumatoid arthritis, cirrhosis, and heart failure.^[10]

[edit] Management

The many causes of pleural effusions demand that treatment be directed at the specific etiology (see Box 79-1). In some patients, however, the pleural fluid must be drained for therapeutic or palliative reasons. Most transudative pleural effusions are treated by addressing the underlying cause of the effusion, such as heart failure. Video-assisted thoracoscopic surgery has been successfully used to localize and close diaphragmatic defects in select patients with recurrent effusions caused by cirrhosis and ascites.^[11] Although critically ill medical patients frequently develop pleural effusions, 90% are small effusions and do not necessarily require evaluation by thoracentesis. Congestive heart failure, atelectasis, ascites, hypoalbuminemia, and atelectasis account for almost 75% of the effusions in these patients.^[2] Other causes include uncomplicated parapneumonic effusion (11%); rare causes include malignancy, uremic pleurisy, pancreatitis, and empyema.

The appropriate initial method to drain an empyema is by tube thoracostomy using a closed system. Thoracoscopy (preferably with video assistance) is indicated with a loculated or poorly draining empyema to facilitate complete drainage, which may obviate the need for more invasive surgical procedures such as pleurectomy. A similar approach is needed in other types of complicated parapneumonic effusions that have a pH less than 7.0 or a glucose less than 40 mg/ml. Parapneumonic effusions with a pH greater than 7.2 usually respond to an appropriate antibiotic alone; a repeat thoracentesis in 5 to 7 days should be done only if fever or leukocytosis persists or the effusion is unchanged or enlarging. In parapneumonic effusions with pH of 7.0 to 7.2, thoracentesis should be repeated within 12 to 24 hours and chest tube drainage instituted if the pleural fluid pH has dropped further.

The palliation of dyspnea in patients with a recurrent malignant pleural effusion is an important goal. The instillation of agents such as talc, doxycycline, or bleomycin into the pleural space after chest tube drainage is an effective method to fuse the pleura (pleurodesis) and can prevent recurrence of the effusion. A success rate greater than 70% has been reported with talc or bleomycin instillation.^[8] Ambulatory sclerotherapy is a possible alternative to inpatient treatment of malignant effusions.^[12] The decision to perform these interventions depends on the patient's overall condition and life expectancy.

Certain caveats apply to the management of other conditions causing pleural effusions. In PE, neither the bloody character of the pleural fluid nor hemoptysis is a contraindication to anticoagulation treatment. A patient with an undiagnosed lymphocyte-predominant exudative effusion who has a positive intermediate-strength tuberculin skin test (PPD) should be considered for antituberculosis drug therapy. Pleural effusion and pleuritis caused by PCIS respond to nonsteroidal antiinflammatory agents; In severe cases of PCIS, glucocorticoids are also effective. In effusions caused by esophageal rupture or a pancreatic pseudocyst, thoracic surgical consultation should be promptly obtained.

[edit] FIBROTHORAX

Deposition of fibrous tissue results in a thick fibrotic visceral pleura that impairs the mobility of the pleura and the expansion of the underlying lung. This condition, fibrothorax, is often caused by pleural empyema, hemothorax, or tuberculous pleural disease. Other conditions that induce pleural inflammation, including uremia, collagen vascular disease, and pancreatitis, can also cause fibrothorax.

Dyspnea on exertion is a common symptom, and examination may reveal diminished expansion and narrowed intercostal spaces in the involved side. A tracheal shift toward the involved side may be noted on palpation of the suprasternal notch. Radiographic findings are an ipsilateral mediastinal shift and a dense pleural peel surrounding the lung. Calcification may be noted in the inner peel. Pulmonary function tests show restrictive ventilatory impairment. The only effective treatment is decortication with removal of the fibrous peel from the visceral pleura. The degree of impairment caused by the fibrothorax and the status of the underlying lung are the main factors in deciding whether decortication will be beneficial. In patients without significant lung disease, especially fibrosis, improvement after decortication can be expected.

[edit] ASBESTOS-RELATED PLEURAL DISEASE

Asbestos is a naturally occurring, fibrous silicate that causes a variety of pleural and pulmonary parenchymal diseases (see Chapter 76 ). Asbestos enters the respiratory tract through inhalation. Because of its size and shape, asbestos is only minimally cleared by the normal host defense system of the lungs. The retained fibers are found in both the lung parenchyma and the pleura, where they are believed to generate a chronic inflammatory response that causes tissue injury. Five pleural disorders are associated with asbestos exposure: benign pleural effusions, pleural plaques, pleural fibrosis, rounded atelectasis, and malignant mesothelioma.

Benign pleural effusion (BPE) is the most common asbestos-related disorder, occurring within 10 years of exposure. In some cases the latency period may be longer. BPE may be incidentally discovered on a chest radiograph or may simulate a pneumonia with pleuritic pain and fever. The effusions more often are unilateral, and the natural history is spontaneous resolution with a tendency to recur. The pleural fluid may be blood tinged and often eosinophilic. The diagnosis of BPE is made by excluding other causes in a patient with a history of asbestos exposure.

Pleural plaques, the most common manifestation of asbestos exposure, are discrete areas of the parietal pleura that consist of an abnormal accumulation of mesenchymal cells and connective tissue matrix. They often become calcified. Asbestos can be found in plaques using electron microscopy. Pleural plaques are located on the parietal pleura, usually on the lateral and inferior aspects; frequently involve the diaphragmatic pleura; and may be bilateral. Plaques usually manifest at least 20 years after asbestos exposure, and pleural plaques usually do not cause pulmonary function abnormalities. CT scanning is much more sensitive in demonstrating pleural plaques than conventional chest radiography. No therapy is needed for pleural plaques, and they do not evolve into malignant mesothelioma. In contrast to pleural plaques, diffuse pleural fibrosis (which involves both the visceral and parietal pleura) is a rare manifestation of asbestos exposure than can cause a severe restrictive ventilatory impairment.

Rounded atelectasis is a pleuropulmonary process that usually occurs in patients with asbestos exposure. It is believed that an inflammatory process in the visceral pleura causes underlying lung parenchyma to collapse. On chest radiograph, rounded atelectasis can simulate a lung carcinoma, from which it must be differentiated. The CT scan is helpful in this situation, since the appearance can be diagnostic; a biopsy is necessary if doubt remains.

Patients with malignant pleural mesothelioma frequently complain of chest pain or dyspnea. About 80% of these patients have had asbestos exposure. The latency period from exposure to development of disease is usually 35 to 40 years. Chest radiographs demonstrate a unilateral pleural effusion and thickening. The diagnosis of malignant pleural mesothelioma usually requires thoracoscopy or thoracotomy, since PPB and cytologic specimens do not yield enough material for analysis, so confusion with other malignant or inflammatory processes is possible. Electron microscopy and advanced staining techniques have increased diagnostic accuracy. The prognosis of patients with malignant pleural mesothelioma is poor, although pleuropneumonectomy combined with chemotherapy shows some promise. In contrast to malignant pleural mesothelioma, fibrous mesothelioma is a benign disease unrelated to asbestos exposure.

[edit] PNEUMOTHORAX

A pneumothorax is an accumulation of air in the normally airless pleural space between the lung and chest wall. Pneumothorax can be divided into spontaneous or traumatic causes. Spontaneous pneumothoraces can be further subdivided into primary or secondary types. Primary spontaneous pneumothorax occurs in healthy persons without lung disease, whereas a secondary spontaneous pneumothorax occurs as a complication of underlying pulmonary disease. A primary spontaneous pneumothorax occurs more often in young, tall, asthenic men. A reasonable theory for this predisposition is that, because of the configuration of the thoracic cage, traction on the alveolar walls is increased, causing rupture of subpleural apical blebs. The most common underlying disease responsible for secondary pneumothorax is obstructive airways disease. Infections that cause necrosis (e.g., pulmonary tuberculosis, necrotizing pneumonias, lung abscess) can cause a pneumothorax. Other diseases that predispose to secondary pneumothorax include histiocytosis X, sarcoidosis, tuberous sclerosis, cystic fibrosis, pulmonary infarction, and primary lung carcinoma. Catamenial pneumothorax is an uncommon entity that recurs at menstrual periods. Although the exact pathogenesis of this disorder is unknown, it may be related to pleural and diaphragmatic endometriosis.

Traumatic (noniatrogenic) pneumothorax is caused by penetrating or nonpenetrating chest trauma. Iatrogenic pneumothorax, the most common type of pneumothorax diagnosed in the hospitalized patient, is a complication of procedures such as transthoracic needle aspiration, subclavian vein puncture, thoracentesis, pleural biopsy, and transbronchial lung biopsy. Another iatrogenic cause is positive-pressure mechanical ventilation, particularly with high airway pressures or airway obstruction.

Normally the pressure in the pleural space is negative with reference to atmospheric and alveolar pressures. Therefore, if a communication exists between the pleura and the atmosphere (e.g., after penetrating trauma) or between the pleura and the lung (e.g., after rupture of an emphysematous bulla), air continues to enter the pleural space until pleural pressure becomes atmospheric. This increased pleural pressure collapses the lung. In some cases a ball-valve communication is formed in which air can enter but cannot leave the pleural space. Intrapleural pressure may then exceed atmospheric pressure throughout expiration and often during inspiration. This tension pneumothorax is life threatening because it compromises ventilation by shifting mediastinal structures, impairing venous return, and diminishing cardiac output. Tension pneumothorax more often develops as a complication of mechanical ventilation or other secondary pneumothoraces rather than from primary spontaneous pneumothorax.

The main symptoms of pneumothorax are chest pain and dyspnea, which usually start abruptly. The severity of the symptoms depends on the volume of air in the pleural space and the degree of underlying disease. The physical signs are hyperresonance on percussion and diminished or absent tactile fremitus and breath sounds on the affected side. Patients with tension pneumothorax are in distress, with dyspnea, tachypnea, and tachycardia often accompanied by distended neck veins, thready pulse, and hypotension. Bulging of the ipsilateral intercostal spaces is sometimes observed, and mediastinal shift may be signaled by tracheal deviation to the contralateral side. The chest radiograph is diagnostic because the margin of the collapsed lung is separated from the parietal pleura by air.

The management options are observation only, small-catheter pleural aspiration or chest tube drainage to evacuate the air, and chemical pleurodesis or open thoracotomy or thoracoscopy with pleural abrasion to prevent a recurrence of pneumothorax. The choice depends on severity of the pneumothorax, predisposing state, and underlying disease.

Asymptomatic, unilateral, small (10% to 20% of the lung volume) primary spontaneous pneumothoraces can be observed, since most resolve within 10 days. A repeat chest radiograph in 6 to 12 hours should be done to check for progression of the pneumothorax. Supplemental oxygen is believed to hasten the resorption of air in the pleural space, since supplemental oxygen increases the gradient between nitrogen in the pleural space and nitrogen in the pleural capillary blood, favoring movement of nitrogen out of the pleural space. Progressively increasing spontaneous pneumothorax and large symptomatic pneumothoraces should be treated by evacuation of the pleural air. The preferred method is insertion of a small catheter (7 to 9 French) in the second anterior intercostal space in the midclavicular line using either a trocar or the Seldinger technique. Air is aspirated using a stopcock and a 60-ml syringe until a mild resistance is felt, and a Heimlich valve is attached to permit continued air evacuation. In large symptomatic pneumothoraces, suction can be added through the exhaust port of the Heimlich valve. After the pneumothorax is evacuated, with no evidence of reaccumulation of air on chest radiograph, the catheter can be removed. Chest tube insertion and drainage are indicated in a few cases of primary spontaneous pneumothorax when the initial volume of air evacuated is large (about 4 L) or when there is a persistent pneumothorax after catheter evacuation. Small-catheter pleural aspiration can also be used in iatrogenic pneumothoraces or selectively in patients with minor trauma.

Chest tube drainage is the preferred management in tension pneumothorax, hydropneumothorax, hemopneumothorax, and pneumothorax with underlying pulmonary disease. Tension pneumothorax is a medical emergency; if the diagnosis is suspected, a large-bore needle should be immediately inserted into the second anterior intercostal space to evacuate the air in the pleural space. A large amount of air coming through the needle confirms the diagnosis. The needle should be left in place until a chest tube is inserted and the air drained under water seal.

The recurrence rate of primary spontaneous pneumothorax is about 50% in 2 years. An ipsilateral recurrence should be treated with chest tube drainage and chemical pleurodesis. Open thoracotomy or thoracoscopy with pleural abrasion is indicated for subsequent recurrence.

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