PLEURAL EFFUSIONS | Malignant Pleural Effusions

PLEURAL EFFUSIONS | Malignant Pleural Effusions

372 PLEURAL EFFUSIONS / Malignant Pleural Effusions Further Reading Introduction Antony VB and Mohammed KA (1999) Pathophysiology of pleural space ...

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372 PLEURAL EFFUSIONS / Malignant Pleural Effusions

Further Reading


Antony VB and Mohammed KA (1999) Pathophysiology of pleural space infections. Seminars in Respiratory Infections 14(1): 9–17. Colice GL, Curtis A, Deslauriers J, et al. (2000) Medical and surgical treatment of parapneumonic effusions. An evidence-based guideline. Chest 18: 1158–1171. Davies CW, Kearney SE, Gleeson FV, and Davies RJ (1999) Predictors of outcome and long-term survival in patients with pleural infection. American Journal of Respiratory and Critical Care Medicine 160: 1682–1687. Davies CWH, Gleeson FV, and Davies RJO (2003) On behalf of the BTS Pleural Disease Group, a sub-group of the BTS Standards of Care Committee. BTS guidelines for the management of pleural infection. Thorax 58(supplement II): ii18–ii28. Ferguson AD, Prescott RJ, Selkon JB, Watson D, and Swinburn CR (1996) Empyema subcommittee of the Research Committee of the British Thoracic Society. The clinical course and management of thoracic empyema. Quarterly Journal of Medicine 89: 285–289. Heffner JE, Brown LK, Barbieri C, and DeLeo JM (1995) Pleural fluid chemical analysis in parapneumonic effusions. A metaanalysis. American Journal of Respiratory and Critical Care Medicine 151: 1700–1708. Maskell NA, Davies CW, Nunn AJ, et al. (2005) U.K. Controlled trial of intrapleural streptokinase for pleural infection. New England Journal of Medicine 352(9): 865–874. Matchaba PT and Volmink J (2003) Steroids for treating tuberculous pleurisy (Cochrane review). In: The Cochrane Library, issue 3. Oxford: Update Software. Valdes L, Pose A, San Jose E, and Martinez-Vazquez JM (2003) Tuberculous pleural effusions. European Journal of Internal Medicine 14: 77–88.

Malignant pleural effusions are effusions that arise from neoplastic involvement of the pleural surface. Malignant pleural effusions are a common clinical problem in patients with various malignancies and produce significant morbidity in the majority of affected patients. The worldwide incidence of malignant pleural effusions is unknown, but the incidence in the US is estimated to be greater than 200 000 cases per year. Malignant pleural effusions are one of the leading causes of exudative effusions. Between 42% and 77% of exudative effusions are secondary to malignancy. The diagnosis of a malignant pleural effusion is the first indication of a malignancy in 13% of patients with a malignant pleural effusion. The majority of patients with malignant pleural effusion will experience dyspnea. Dyspnea may cause limitations in ability to perform activities of daily living in a substantial proportion of patients. In addition, patients may have symptoms of cough and chest pain.

Malignant Pleural Effusions V B Antony and M A Jantz, University of Florida, Gainesville, FL, USA & 2006 Elsevier Ltd. All rights reserved.

Abstract Malignant pleural effusions result from neoplastic infiltration of the pleural surface. Malignant pleural effusions most commonly arise from lung carcinoma, breast carcinoma, and lymphoma. The true incidence of malignant pleural effusion is unknown but up to 15% of patients with lung cancer and 11% of patients with breast cancer will have a malignant effusion at some time during the course of disease. Most patients will have varying degrees of dyspnea at presentation, which is the main symptom related to the effusion. On chest radiograph and computed tomography, there will be evidence of an effusion as well as potential parenchymal lesions consistent with a lung primary tumor or parenchymal metastases. Diagnosis is established by demonstration of malignant cells in the pleural fluid or pleural tissue. Malignant pleural effusions result from metastases to the visceral pleural surface with secondary seeding of the partial pleural surface. In addition to treatment of the primary tumor, management consists primarily of palliation of dyspnea via pleurodesis by means of a chest tube-administered sclerosant agent or talc poudrage by way of medical thoracoscopy.

Etiology Nearly all neoplasms have been reported to involve the pleura. Malignant pleural effusions most commonly arise from metastatic carcinomas outside the pleura, but can also develop from primary pleural neoplasms such as mesothelioma. Lung carcinoma is the most common malignancy causing a malignant pleural effusion in most studies and accounts for approximately one-third of all malignant effusions. Malignant pleural effusions are present in 7–15% of patients with lung cancer at some time during the course of disease. Breast carcinoma is the second most common neoplasm producing a malignant effusion with about 25% of malignant effusions being due to breast cancer. Between 7% and 11% of patients with breast carcinoma will develop a malignant pleural effusion during the course of their disease. Lymphomas, including Hodgkin’s disease and non-Hodgkin’s lymphoma, account for approximately 10% of malignant pleural effusions. In some cases, pleural effusion may be the only evidence of malignancy in a patient. Adenocarcinoma is the most common histological type for malignant pleural effusion with an unknown primary tumor. In some cases the patient will have a known malignancy and a pleural effusion but malignant cells in the pleural fluid or pleural tissue cannot be demonstrated. These effusions, termed ‘paramalignant effusions’ by Sahn, are not the direct result of pleural involvement with tumor but are related to effects of the primary tumor or complications of therapy for

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the primary tumor. Unlike patients with malignant pleural involvement, some patients with lung carcinoma and paramalignant effusions may still be candidates for surgical resection. The pathogenesis of paramalignant effusions is discussed below.

Pathology The pathology of malignant pleural effusions will be similar to the underlying malignancy causing the pleural effusion.

Clinical Features Dyspnea is the most common presenting symptom in patients with malignant pleural effusions. More than half of patients will have some degree of dyspnea. The pathogenesis of dyspnea from a pleural effusion has not been completely elucidated, but several factors may be involved including decreased chest wall compliance, decreased ipsilateral lung volume, contralateral shifting of the mediastinum, and reflex stimulation from the lung parenchyma and chest wall. Cough is the second most common symptom related to malignant pleural effusions. Because malignant pleural effusions represent an advanced stage of the malignancy, patients may also have systemic manifestations such as weight loss, anorexia, and malaise. Some patients may experience chest pain, which is described as dull and aching. Chest pain is more common in patients with malignant mesothelioma than other types of malignant effusions. The presence of chest pain usually signifies parietal pleural infiltration and possible chest wall involvement. On examination, patients with a moderate to large malignant pleural effusion will have findings consisting of decreased breath sounds and dullness to percussion over the effusion. Adenopathy and cachexia may also be noted. Radiological Findings

At presentation, most patients with malignant pleural effusions have moderate to large effusions on chest radiograph. These effusions will have volumes ranging from 500 to 2000 ml (Figure 1). About 10% of patients will have massive pleural effusions, defined as producing total or near-total opacification of the hemithorax. It should be noted that malignancy is the most common cause of a massive pleural effusion. About 15% of patients will have effusions o500 ml in volume, and most of these patients will be relatively asymptomatic. When evaluating the chest radiograph of a patient with a malignant pleural effusion, particular attention

Figure 1 Chest radiograph of patient with moderate pleural effusion due to breast carcinoma.

Figure 2 Chest radiograph of patient with large pleural effusion due to lung carcinoma. Note the contralateral shift of the mediastinum.

should be given to the presence or absence of mediastinal shift. In the patient with a large or massive effusion, contralateral mediastinal shift would be expected (Figure 2). If the mediastinum is midline or is shifted ipsilaterally, involvement of the ipsilateral mainstem bronchus by endobronchial tumor producing concurrent atelectasis should be suspected (Figure 3). Other causes for a lack of contralateral mediastinal shift include fixation of the mediastinum by tumor or lymph node involvement, malignant mesothelioma with extensive pleural involvement, extensive visceral pleural involvement by a primary lung carcinoma or metastatic malignancy, and extensive tumor infiltration of the ipsilateral

374 PLEURAL EFFUSIONS / Malignant Pleural Effusions

Figure 3 Chest radiograph of patient with massive pleural effusion due to lung carcinoma. Note the lack of mediastinal shift due to mainstem bronchial obstruction.

involvement by endobronchial tumor. The presence of pleural plaques suggests prior asbestos exposure and possible mesothelioma as the etiology of the effusion. As part of the evaluation of a patient with a suspected or known malignancy, a chest CT scan may demonstrate pleural effusions that are too small to be detected on chest radiographs. Ultrasonography may aid in identifying pleural lesions in patients with malignant effusions and is also useful in guiding thoracentesis in patients with small effusions and thus reducing complications of thoracentesis such as pneumothorax. Magnetic resonance imaging (MRI) has a limited role in the evaluation of malignant pleural effusions. MRI may be helpful in evaluating the presence of and extent of chest wall involvement by tumor. The utility of positron emission tomography (PET) in the evaluation of malignant pleural effusions has yet to be clearly defined. Malignant pleural effusions may show abnormal uptake on PET imaging although the accuracy of PET in diagnosing an effusion as malignant is unknown. PET has been reported to be helpful in evaluating the extent of disease in malignant mesothelioma. Pleural Fluid Analysis

Figure 4 Chest radiograph of patient with trapped lung due to lung carcinoma. Note the lack of lung expansion following chest tube placement and apparent pneumothorax.

lung parenchyma, which radiographically mimics a large effusion. With ipsilateral mediastinal shift in the setting of a large effusion, the possibility of trapped lung should be considered. The diagnosis is confirmed when there is lack of radiographic expansion following large volume thoracentesis or chest tube thoracostomy (Figure 4). Computed tomography (CT) is usually performed in the evaluation of a patient with a potential malignant pleural effusion. In addition to providing further evaluation of the pleural space, CT scans also provide information about mediastinal lymph node involvement, pulmonary parenchymal involvement by the primary tumor or metastases, and airway

Malignancy should be considered and a diagnostic thoracentesis performed in any patient with a unilateral effusion or bilateral effusions, with a normal heart size on chest radiograph. Thirty to fifty milliliters of pleural fluid is adequate for diagnostic studies. The pleural fluid should be sent for the following studies: nucleated cell count and differential, total protein, glucose, lactate dehydrogenase (LDH), pH, and cytology. The utility of measurement of pleural fluid amylase is debatable. Malignant pleural effusions can be serous, hemorrhagic, and grossly bloody in appearance. The malignant pleural effusion is almost always an exudate. A small number, however, may be transudates and are usually paramalignant effusions rather than true malignant effusions. The LDH criterion for an exudate is almost always present in malignant effusions while the pleural fluid protein to serum ratio may be o0.5 in some effusions. The nucleated cell count is typically low (o3000 cells ml 1) and is composed mainly of lymphocytes, macrophages, and mesothelial cells. About half the time the cell count will be lymphocyte predominant with a differential of 50–70% lymphocytes. In lymphomatous pleural effusions, the lymphocytes are typically 480% of the nucleated cells. The presence of neutrophils or eosinophils is much less common but does not exclude a malignant pleural effusion.

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Approximately one-third of malignant effusions have a pleural fluid pHo7.30 and glucose o60 mg dl 1 at presentation. The cause of these low-pH, low-glucose malignant effusions appear to be increased tumor mass within the pleural space. The increased tumor burden results in decreased glucose transfer into the pleural space and decreased efflux of acidic byproducts of glucose metabolism out of the pleural space. Malignant effusions with a low pH and low glucose concentration have been noted to have higher diagnostic yields on cytology and to be associated with worse survival and lower response to pleurodesis. A recent meta-analysis by Heffner and colleagues found that, while pleural fluid pH was an independent predictor of survival, it had insufficient predictive accuracy for selecting patients for pleurodesis procedures on the basis of estimated survival. Diagnosis

Pleural fluid cytology Pleural fluid cytology is the least invasive method for obtaining a diagnosis of a malignant pleural effusion. Diagnostic yields for pleural fluid cytology range from 60% to 90%. Pleural fluid cytology is most often positive with adenocarcinomas and is positive less often with squamous cell carcinoma, sarcoma, and mesothelioma. It does not appear that sending a large volume of pleural fluid for analysis increases the yield of diagnosis compared with sending just 20–50 ml. Some clinicians have recommended the routine use of cell blocks plus cytology smears while others suggest this is not cost effective. The use of current tumor markers for the diagnosis of malignant pleural effusion does not appear to be helpful although some tumor markers such as carcinoembryonic antigen (CEA), Leu-1, mucin, and surfactant protein may be helpful in distinguishing between adenocarcinomas and reactive mesothelial cells or mesothelioma. In cases where non-Hodgkin’s lymphoma is suspected, flow cytometry analysis of the pleural fluid may be helpful in establishing a diagnosis. Closed pleural biopsy Closed pleural biopsies are less sensitive than pleural fluid cytology for the diagnosis of malignant pleural effusion. Diagnostic yields range from 40% to 75%. Studies have shown that 7–12% of patients with malignant effusion may be diagnosed with closed pleural biopsy when fluid cytology is negative. The reasons for the low yield of closed pleural biopsy include the blind nature of the procedure, early stage of disease with minimal pleural involvement, initial lesions being located along the mediastinal and diaphragmatic pleura which is not sampled during blind biopsy, and operator inexperience.

Recently, there has been interest in the use of CTguided cutting-needle biopsy for diagnosis of malignant pleural effusions with one study demonstrating higher yields than blind closed pleural biopsies. Thoracoscopy and video-assisted thoracic surgery The diagnostic yields for thoracoscopy and video-assisted thoracic surgery (VATS) range from 95% to 100%. Medical thoracoscopy has an advantage over VATS in that it can be performed in an endoscopy suite under local anesthesia and conscious sedation. By allowing direct visualization of the pleural cavity, biopsies can be obtained from suspicious areas under direct view (Figures 5–7). This is particularly advantageous in earlier disease when there is patchy pleural involvement by the malignancy. The reasons for false-negative thoracoscopies include presence of adhesions (often a consequence of repeated

Figure 5 Thoracoscopic view of patient with patchy pleural involvement by metastatic breast carcinoma.

Figure 6 Thoracoscopic view of patient with patchy pleural involvement by metastatic sarcoma. A large parenchymal lung mass due to sarcoma is also visible superiorly.

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removing 500 ml of fluid are highly suggestive of a trapped lung.

Pathogenesis Malignant Pleural Effusions

Figure 7 Thoracoscopic view of patient with extensive pleural involvement by lung carcinoma. Diaphragmatic involvement at the left aspect of the image and lung involvement at the superior aspect of the image is also visible.

thoracenteses) that prevent complete examination, insufficient and nonrepresentative tissue samples, and operator inexperience. Pleurodesis via talc poudrage may be performed at the time of thoracoscopy when the diagnosis of malignancy has been established. In addition, thoracoscopy is helpful in distinguishing malignant from paramalignant effusions and identifying those patients with lung carcinoma that may be candidates for surgical resection. VATS procedures usually require general anesthesia and single lung ventilation. VATS may be necessary if the pleural space contains multiple adhesions that would make performing medical thoracoscopy unsafe. Pleurodesis procedures may also be performed following the diagnostic portion of the VATS procedure. Bronchoscopy The diagnostic yield of bronchoscopy is low in patients with undiagnosed pleural effusions and is not routinely recommended. Bronchoscopy may be helpful when there is a large effusion with ipsilateral mediastinal shift or if the patient has hemoptysis suggesting an endobronchial lesion. Bronchoscopy should be considered to exclude endobronchial obstruction when there is absence of lung expansion after therapeutic thoracentesis. Trapped lung A trapped lung is suggested by failure of the lung to expand completely after removal of the majority of fluid via thoracentesis. Although not widely performed, pleural manometry may also suggest the diagnosis of trapped lung. An initial pleural fluid pressure o 5 cmH2O, a decrease in pleural fluid pressure to o 20 cmH2O after 1 l is removed, or a pleural fluid elastance of 419 cmH2O while

Autopsy studies suggest that most pleural metastases arise from tumor emboli to the visceral pleural surface followed by secondary seeding of the parietal pleura. In the case of mesothelioma, the tumor originates on the parietal pleural surface and then spreads to the visceral pleural surface. With lung carcinoma, breast carcinoma, and chest wall neoplasms, there may be direct tumor invasion into the pleural space. There can also be hematogenous spread to the parietal pleura from extrapulmonary primaries as well as lymphatic involvement. Interference with the lymphatic drainage system anywhere between the parietal pleura and the mediastinal lymph nodes can result in pleural effusion formation. Pleural effusions from malignancy develop primarily due to increased pleural membrane and vascular permeability with resultant plasma leakage. Reduced pleural fluid outflow results from tumor blockage of parietal pleural stomas or lymphatic obstruction due to mediastinal node involvement. The mechanisms of pleural metastasis have not been clearly defined but include processes such as cell adhesion, migration, propagation, and angiogenesis. Angiogenesis is critical for the ability of malignant cells to develop blood vessel formation to provide substrate for tumor growth. Malignant cells can produce multiple cytokines including vascular endothelial growth factor (VEGF) and basic-fibroblast growth factor (bFGF). These cytokines are angiogenic and increase the permeability of the pleural tissue allowing for development of new capillaries and tumor growth. In addition, malignant cells can produce a variety of autocrine growth factors. Paramalignant Pleural Effusions

As noted, a paramalignant pleural effusion is an effusion that is related to effects of the tumor or complications of therapy, but malignant cells are not present in the pleural fluid or pleural tissue. The local effects of tumor producing a paramalignant effusion include lymphatic obstruction, endobronchial obstruction with pneumonia, endobronchial obstruction with atelectasis, trapped lung, chylothorax, superior vena cava syndrome, and malignant pericardial effusion. Systemic effects of the malignancy may cause an effusion via pulmonary embolism related to a hypercoagulable state as well as hypoalbuminemia due to anorexia and cachexia. Complications of

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radiation therapy, including radiation pleuritis, mediastinal fibrosis, and constrictive pericarditis, may also produce an effusion. Lastly, certain chemotherapeutic agents, such as methotrexate, procarbazine, cyclophosphamide, and docetaxel, may cause pleural effusions.

lack of lung expansion suggests trapped lung due to extensive pleural tumor infiltration or mainstem bronchial obstruction. In some patients with significant dyspnea and a large effusion with contralateral mediastinal shift, some clinicians may elect to proceed directly to chest tube drainage and chemical pleurodesis or thoracoscopy with talc poudrage.

Trapped Lung

In the setting of malignancy, a trapped lung occurs when the visceral pleura becomes encased with tumor or a fibrous peel. This prevents lung expansion to the chest wall, and in the area where the lung cannot expand, the pleural pressure becomes more negative. The negative pleural pressure results in fluid movement from the interstitium into the pleural space to produce a volume of fluid that reflects the steady state of fluid formation and resorption. If pleural fluid is removed, the same volume will accumulate within 48–72 h. A similar pathophysiology occurs when there is endobronchial obstruction by tumor.


Malignant pleural effusions that are likely to be chemotherapy responsive include small cell lung carcinoma, breast carcinoma, and lymphoma. Effusions due to prostate, ovarian, thyroid, and germ-cell tumors may also be chemotherapy responsive. For patients with these malignancies who have no symptoms or mild symptoms, a trial of chemotherapy with observation of the effusion is reasonable. For more symptomatic patients, therapeutic thoracentesis followed by a trial of chemotherapy may be warranted. Malignant pleural effusions due to neoplasms other than those mentioned above are unlikely to be controlled by chemotherapy alone.

Animal Models

Radiation Therapy

Tumor cells are injected, either intravenously or intrapleurally, into animals that usually have immunological deficiencies to induce disseminated malignancy with pleural effusion. Yano and co-workers have developed a model of malignant pleural effusion in athymic BALB/c nude mice. The human lung adenocarcinoma cell line PC14PE6 and the squamous cell line H226 are injected into the lateral tail vein with subsequent development of lung tumors and pleural effusions. Ohta and colleagues have produced a model of malignant pleural effusion in rats. In this model, PC-14 adenocarcinoma cells are injected into the thoracic cavity with resultant disseminated malignancy and pleural effusion.

In general, radiation therapy of the hemithorax is contraindicated for management of malignant pleural effusions. The adverse effects of radiation pneumonitis outweigh the possible benefits of therapy. Radiation therapy to the mediastinum may be helpful in management of pleural effusions due to mediastinal lymph node involvement by lymphoma or small cell carcinoma.

Management and Current Therapy For patients with malignant pleural effusion who are symptomatic, palliative therapy should be considered. Therapeutic thoracentesis should be performed in dyspneic patients with malignant pleural effusions to determine its effects on breathlessness and rate of recurrence. Rapid recurrence of the effusion suggests the need for immediate therapy. In the absence of recurrence, observation may be warranted. If dyspnea is not relieved, other causes such as lymphangitic carcinomatosis, endobronchial obstruction, thromboembolism, and tumor embolism should be considered. Lung expansion following therapeutic thoracentesis should be assessed. The

Therapeutic Thoracentesis

Repeated therapeutic thoracentesis may be appropriate therapy in patients with far advanced disease, poor performance status, and a short life expectancy. For other patients who have recurrence of the effusion and symptoms following initial thoracentesis, we favor chest tube drainage and chemical pleurodesis or thoracoscopy and talc poudrage as repeated thoracentesis may produce multiple adhesions that limit the success of pleurodesis procedures. In addition, a delay in performing a pleurodesis procedure may allow for development of extensive pleural tumor burden, which decreases the effectiveness of a pleurodesis procedure, or the development of a trapped lung, which precludes performing a pleurodesis procedure. The volume of fluid that can be safely removed from the pleural space during a therapeutic thoracentesis is unknown. Monitoring of pleural pressure during thoracentesis may be performed with removal of fluid as long as the pleural fluid pressure does not

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fall below 20 cmH2O. As most clinicians do not measure pleural pressure during therapeutic thoracentesis, it is recommended that only 1–1.5 l be removed at one time and the procedure be terminated if the patient develops significant cough, chest tightness, or dyspnea. In patients without contralateral mediastinal shift, the possibility of a precipitous fall in pleural pressure is increased, and either pleural pressure should be monitored during thoracentesis or a smaller volume of fluid (300–500 ml) should be removed. Chest Tube Drainage and Chemical Pleurodesis

Patients with recurrence of effusion following initial thoracentesis or highly symptomatic patients with large effusions at presentation should be considered for pleurodesis. Following chest tube drainage, complete lung expansion should be demonstrated, as pleurodesis will not be successful without apposition of the visceral and parietal pleural surfaces. A variety of sclerosant agents aimed at achieving pleurodesis have been utilized. The most studied agents include talc, tetracycline and doxycycline, and bleomycin. Of these, talc is the most effective with success rates reported from 88% to 100% with a mean of 90%. Doxycycline has had success rates varying from 65% to 100% with a mean of 76%. Tetracycline is no longer available as an intravenous preparation and thus is not available in a form suitable for intrapleural administration. Lastly, bleomycin has been reported to have success rates of 58–85% with a mean of 61%. Bleomycin is by far the most expensive of these agents. For talc slurry, the recommended dose is 3–5 g mixed in 50 ml of normal saline with most studies using a dose of 5 g. The most common adverse reactions of talc pleurodesis are fever (16%) and chest pain (7%). Acute pneumonitis and respiratory failure have been noted following talc slurry pleurodesis and talc poudrage with an estimated incidence of 1%. The mechanism of acute pneumonitis is unclear but the dose of talc and physical characteristics of the talc, including size and type, may be important determinants for the development of this complication. To reduce the risk of this reaction, no more than 4 g of talc should be used, the majority of talc particles in the preparation should be 430 mm, and talc pleurodesis should not be performed in patients with severe underlying pulmonary disease. For doxycycline, the recommended dose is 500 mg mixed with 50–100 ml of sterile saline. Chest pain occurs in 40% and fever in 31% of patients treated with doxycycline. With bleomycin, most studies have used 60 IU mixed with 50–100 ml of normal saline.

Chest pain and fever have been noted in 28% and 24% of patients, respectively, following bleomycin pleurodesis. Traditionally, 24–32 French chest tubes have been used for pleurodesis procedures although more recently 10–14 French chest tubes have been successfully utilized. For talc slurry pleurodesis, however, some clinicians still favor larger bore chest tubes due to concern for tube occlusion. Historically, introduction of the sclerosant agent for pleurodesis has been performed when the lung is fully expanded on chest radiograph and there is o150 ml day 1. More recent studies, however, suggest that pleurodesis can be performed as soon as the lung is re-expanded, regardless of chest tube output. Following instillation of sclerosant, the chest tube should be clamped for 1 h. Patient rotation is not necessary after administration of doxycycline but may be considered for talc slurry. The chest tube may be removed 24–48 h after sclerosant administration unless there is excessive chest tube drainage (4250 ml day 1). Repeat pleurodesis may be considered if there is continued high fluid output. Based on animal studies, systemic administration of corticosteroids may decrease the efficacy of pleurodesis and should be discontinued or the dosage reduced if possible. Thoracoscopy and Talc Poudrage

Talc poudrage involves insufflation of talc in the form of a dry powder through the thoracoscope under direct visualization (Figure 8). Talc poudrage can be performed during medical thoracoscopy using conscious sedation and can be performed in the same setting as diagnostic thoracoscopy when the diagnosis of malignancy is established. The success rate for talc poudrage is 490% with a perioperative mortality rate o0.5%. Although the use of thoracoscopy

Figure 8 Thoracoscopic view of pleural surface following talc poudrage for malignant effusion due to lung carcinoma.

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with talc poudrage is strongly favored over chest tube drainage and talc slurry by some clinicians, one small and one large randomized trial suggest that success rates are similar. Long-Term Indwelling Pleural Catheter Drainage

Recently, the use of a long-term tunneled pleural catheter has been described. The catheter may be placed as an outpatient procedure. Through a oneway valve system, the patients connect themselves to a drainage bottle that removes 500–1000 ml of fluid each day or every other day. Spontaneous pleurodesis with the catheter in place has been reported in 21– 46% of patients. Catheter malfunction and pleural space infection has been reported in a small number of patients. The use of tunneled pleural catheters may be helpful in the management of patients with trapped lung who are not candidates for a pleurodesis procedure and for those patients who fail a pleurodesis procedure.

Pollak JS (2002) Malignant pleural effusions: treatment with tunneled long-term drainage catheters. Current Opinion in Pulmonary Medicine 8: 302–307. Rodriguez-Panadero F (2003) Effusions from malignancy. In: Light RW and Lee YCG (eds.) Textbook of Pleural Diseases, pp. 297– 309. London: Arnold. Rodriguez-Panadero F (2004) Pleurodesis. In: Bouros D (ed.) Pleural Disease, pp. 479–503. New York: Dekker. Sahn SA (1998) Malignancy metastatic to the pleura. Clinics in Chest Medicine 19: 351–361. Sahn SA (2004) Malignant pleural effusions. In: Bouros D (ed.) Pleural Disease, pp. 411–438. New York: Dekker. Villanueva AG and Beamis JF Jr (2004) Medical thoracoscopy: diagnosis of pleural pulmonary disorders. In: Beamis JF Jr, Mathur PN, and Mehta AC (eds.) Interventional Pulmonary Medicine, pp. 431–449. New York: Dekker. Wohlrab JL and Read CA (2004) Medical thoracoscopy: therapy for malignant conditions. In: Beamis JF Jr, Mathur PN, and Mehta AC (eds.) Interventional Pulmonary Medicine, pp. 451– 468. New York: Dekker.

Postsurgical Effusions

Pleuroperitoneal Shunts

R W Light, Vanderbilt University, Nashville, TN, USA

Pleuroperitoneal shunts may be considered as an alternative therapy in patients with a trapped lung or who fail pleurodesis. Shunt occlusion rates vary from 12% to 25% and typically require replacement of the shunt. Often the pressure gradient between the pleural and peritoneal space is low, and the shunt requires manual compression of the pump chamber by the patient, sometimes over 400 times per day.

& 2006 Elsevier Ltd. All rights reserved.

Parietal Pleurectomy

Parietal pleurectomy provides an effective method for controlling malignant pleural effusions. The procedure carries significant morbidity and perioperative mortality rates of 10–13%. This therapy should be reserved for patients who have failed pleurodesis, have a good performance status, and have an expected survival of more than 6 months. See also: Mesothelial Cells. Mesothelioma, Malignant. Pleural Effusions: Overview; Pleural Fluid Analysis, Thoracentesis, Biopsy, and Chest Tube.

Further Reading Antony VB, Loddenkemper R, Astoul P, et al. (2000) Management of malignant pleural effusions. American Journal of Respiratory and Critical Care Medicine 162: 1987–2001. Antunes G, Neville E, Duffy J, and Ali N (2003) BTS guidelines for the management of malignant pleural effusions. Thorax 58(supplement II): ii29–ii38. Lee YCG and Light RW (2004) Management of malignant pleural effusions. Respirology 9: 148–156.

Abstract The majority of patients who undergo coronary artery bypass graft surgery develop a pleural effusion that is usually predominantly left sided and small. Approximately 10% of patients develop a pleural effusion that occupies more than 25% of the hemithorax and the main symptom is dyspnea. The pleural effusions usually disappear after one to three therapeutic thoracenteses. The postcardiac injury syndrome occurs after various types of trauma to the heart, including blunt trauma, myocardial infarction, and cardiac surgery. It is characterized by the development of fever, pleuropericarditis, and parenchymal pulmonary infiltrates in the weeks posttrauma. The primary symptoms are chest pain and fever. The primary treatment is the administration of anti-inflammatory agents, and sometimes corticosteroids are required. After abdominal surgery, the incidence of pleural effusion is approximately 50%. Most effusions are small, but approximately 10% of patients develop moderate to large effusions. The majority of patients postliver transplantation develop a pleural effusion. The effusions occupy more than 25% of the hemithorax in one-fourth of patients and usually are right sided or, if bilateral, larger on the right. There is increased pleural fluid production immediately after lung transplant because the lymphatics draining the pulmonary interstitial fluid are transected. Pleural effusions are not apparent immediately postoperatively because chest tubes are in place. Pleural effusions occurring more than a few weeks after lung transplantation are likely to be due to a complication of the transplant, such as acute rejection, chronic rejection, pulmonary infection, or lymphoproliferative disease.

Introduction Increasingly more surgical procedures are being performed. Some of these surgical procedures are