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  • 1. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 1 4 PLEURAL EFFUSION Rafael S. Andrade, M.D., and Michael Maddaus, M.D., F.A.C.S. Approach to the Patient with a Pleural Effusion Pleural effusion is a common problem in surgical practice. It cer) can raise the index of suspicion for an effusion and provide results from perturbations of normal pleural fluid transport, which guidance regarding possible causes. Careful physical examination are produced by three main mechanisms—abnormalities in of the chest can detect an effusion, and many physical signs may Starling’s equilibrium, increased capillary and mesothelial perme- provide clues to the cause. Physical signs that are particularly useful ability, and interference with lymphatic drainage. These mecha- for diagnostic purposes include jugular venous distention and tachy- nisms are associated with a variety of different causes [see Table cardia (suggestive of congestive heart failure); lymphadenopathy, 1].1,2 Often, more than one mechanism is involved. An inflamma- digital clubbing, and localized bone tenderness (suggestive of lung tory effusion, for instance, is marked by increases in capillary and cancer); and ascites (suggestive of ovarian tumors or cirrhosis). mesothelial permeability, which lead to elevated intrapleural on- Pleural effusion can occur in a wide variety of clinical situations, cotic pressure. however, and it often evades clinical detection by history and phys- Pleural effusion is classified as either transudative or exudative, ical examination. Consequently, imaging tests are indispensable in depending on the chemical composition of the fluid. A transudate the workup of a patient with a possible pleural effusion. Pleural is an ultrafiltrate of serum and has a low total protein content (≤ 3 fluid analysis, pleural biopsy, and thoracoscopy may also be re- g/dl); an exudate is the result of increased permeability and has a quired for evaluation. high total protein content. Increased pleural permeability results from complex inflammatory mediator interactions between the mesothelium (whose cells play an active role in inflammation, Investigative Studies phagocytosis, leukocyte migration, tissue repair, antigen presenta- IMAGING tion, coagulation, and fibrinolysis3,4) and the capillary endotheli- um. The distinction between transudative and exudative pleural effusion is clinically significant in that the two types of effusion Chest Radiography have different causes [see Table 2].1,4 To be detectable on a standard upright posteroanterior chest radiograph, an effusion must have a volume greater than 150 ml. If the volume is 150 to 500 ml, the lateral costophrenic angle will Clinical Evaluation be blunted; if the volume is greater than 500 ml, a meniscus will A complete history, phys- be created.5,6 A lateral decubitus chest radiograph can detect an ical examination, and clini- effusion as small as 5 ml. As a general rule, a layering effusion that cal acuity are the initial tools is at least 1 cm thick is accessible to thoracentesis.6,7 A loculated used for diagnosing pleural effusion may appear as a so-called pseudotumor on a chest radi- effusion. Important facts ograph and typically will not layer freely on a lateral decubitus from a patient’s history (e.g., radiograph. Subtle changes on an upright chest radiograph (e.g., respiratory symptoms, pain, accentuation of a fissure, elevation of a hemidiaphragm [see 4:6 extrathoracic symptoms, duration of symptoms, previous medical Paralyzed Diaphragm], or increased separation between the lung conditions, and risk factors for cardiopulmonary diseases or can- and subdiaphragmatic gas [see Figure 1]) may also signal an effu- Table 1 Pathophysiologic Mechanisms of Pleural Effusion Mechanism Specific Alteration Cause Increased capillary and lymphatic hydrostatic Increased venous pressure (e.g., biventricular pressure heart failure, renal failure) Decreased capillary oncotic pressure Hypoproteinemia (e.g., nephrotic syndrome) Abnormality in Starling’s equilibrium Decreased intrapleural hydrostatic pressure Ex vacuo effusion (e.g., atelectasis) Inflammation (e.g., infection, cancer, autoim- Increased intrapleural oncotic pressure mune disease) Increase in capillary and mesothelial Inflammation (e.g., infection, cancer, autoim- Increased filtration permeability mune disease) Interference with lymphatic drainage Obstruction Cancer, structural abnormalities
  • 2. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 2 Approach to the Patient with a Pleural Effusion Findings are adequate for diagnosis Assess respiratory status. Patient is not in respiratory distress Patient is in respiratory distress Transudative effusion is Exudative effusion is Nature of effusion is unclear suspected suspected Treat underlying cause. Suspected cause is PSI (PPE) Suspected cause is other Suspected cause is malignancy, condition esophageal perforation, hemothorax, or chylothorax [See Table 3.] Treat underlying cause. Patient’s condition improves Patient’s condition does not mprove Provide clinical and radiologic Treat with pleurodesis or long-term follow-up. drainage.
  • 3. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 3 Clinical evaluation and chest x-ray suggest pleural effusion Findings are inadequate for diagnosis Perform US or CT. Pleural pathology is not complex Pleural pathology is complex Perform VATS. Perform thoracentesis (with or without imaging guidance) or tube thoracostomy. Drainage is successful Drainage is unsuccessful Analyze pleural fluid sample (total protein Perform VATS. concentration, with or without LDH concentration). Effusion is transudative Effusion is exudative Treat underlying cause. Suspected cause is PSI (PPE) Suspected cause is malignancy Suspected cause is nonmalignant condition other than PSI (PPE) [See Table 3.] Perform cytologic tests. Perform cell count with differential. Assess levels of triglycerides, cholesterol, amylase, chylomicrons, rheumatoid factor, and antinuclear antibodies. Cytology is positive Cytology is negative Treat malignancy (with or without Perform pleural biopsy. pleurodesis or long-term drainage). Test results are positive Test results are negative Treat underlying cause Treat with pleurodesis or (with or without pleurodesis long-term drainage. Biopsy is positive Biopsy is negative or long-term drainage). Treat malignancy (with or without pleurodesis or long-term drainage).
  • 4. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 4 Table 2 Causes of Transudative tween effusion and lung abscess, and for guiding and monitoring and Exudative Pleural Effusion closed drainage of effusions.6,10,12,13 Magnetic Resonance Imaging Type of Effusion Cause Magnetic resonance imaging of the chest provides no useful Congestive heart failure information beyond what can be obtained with CT scanning. Cirrhosis MRI is neither efficient nor cost-effective in standard evaluation Nephrotic syndrome of pleural effusion.12,14 Acute atelectasis Transudative Renal failure THORACENTESIS Peritoneal dialysis If the cause of a pleural Postoperative state Myxedema effusion cannot be explained Postpartum state by the clinical circumstances (e.g., congestive heart failure Pneumonia or a recent surgical proce- Malignancy dure), diagnostic thoracen- Infection tesis [see Sidebar Techniques Esophageal perforation Hemothorax of Bedside Thoracentesis and Tube Thoracostomy] is indicated. Chylothorax Thoracentesis may also have therapeutic value, in that drainage of Pseudochylothorax fluid may relieve dyspnea. Absolute contraindications to thoracen- Connective tissue diseases tesis include lack of cooperation on the patient’s part, clinical insta- Exudative Drug-induced pleuritis bility with hemodynamic or respiratory compromise, severe coag- Pancreatitis ulopathy, and high-pressure ventilation. Relative contraindications Uremia to thoracentesis include a nonlayering effusion, loculations, and Postmyocardial infarction (Dressler syndrome) previous thoracic trauma, chest tube placement, or surgery. Chronic atelectasis A large effusion can be drained without any special imaging Radiation therapy guidance other than an upright lateral chest radiograph. Thora- Asbestos exposure Meigs syndrome centesis for a small or loculated effusion is best done with ultra- Ovarian hyperstimulation sound guidance; success rates are as high as 97%.15 Transudative or exudative Pulmonary embolus sion. Additional findings on a standard chest radiograph (e.g., lat- erality, the size of the cardiac silhouette, the position of the medi- astinum, pulmonary parenchymal changes, pleural calcifications, and osseous abnormalities) may point to a specific cause. Supine chest radiographs are less sensitive than other chest radiographs. With these images, suspicion of an effusion is trig- gered by increased homogeneous density of the lower hemithorax, loss of normal diaphragmatic silhouette, blunting of the lateral costophrenic angle, or apical capping [see Figure 2].8 Ultrasonography Chest ultrasonograms are more reliable for detecting and local- izing small (5 to 100 ml) or loculated pleural effusions than chest radiographs are.5,9,10 Ultrasonography is particularly helpful for guiding thoracentesis for small-volume effusions and for assessing pleural effusions in critically ill patients.6,11 Computed Tomography of the Chest Computed tomography of the chest is a very sensitive tool for evaluating pleural effusion. Free-flowing fluid causes a sickle- shaped opacity in the most dependent portion of the thorax, and even small effusions are readily detected [see Figure 3]. CT may also reveal clues to the cause of the effusion, such as a fluid-fluid level (suggestive of acute hemorrhage), pleural thickening and enhancement (suggestive of pleural space infection [see Figure 4]), calcified pleural plaques (suggestive of asbestosis), and diffuse irregular nodularity and pleural thickening (suggestive of pleural metastases or mesothelioma). CT is especially useful for charac- Figure 1 Posteroanterior chest radiograph of a patient with bilat- terizing loculated effusions, for differentiating pleural thickening eral pleural effusion reveals costophrenic blunting and increased or pleural masses from pleural effusion, for distinguishing be- separation between the left lung and subdiaphragmatic gas.
  • 5. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 5 preferable to minimize the chance of edema. Additional potential complications include so-called dry tap, vasovagal reaction, hem- orrhage hypovolemia, and pleural space infection (PSI).10,16-18 PLEURAL FLUID ANALYSIS Assessment of a pleural fluid sample is guided, to some extent, by the clinical context in which the pleural effusion occurs. When the cause of the effusion is un- known, evaluation of a pleu- ral fluid sample typically in- cludes measurement of total protein and lactic dehydrogenase (LDH) concentrations, a cell count with differential, cause-specif- ic testing, and microbiologic and cytologic analysis. Biochemical Analysis of Pleural Fluid A total protein concentration higher than 3 g/dl is generally used as the main criterion for distinguishing a transudate from an exudate; however, the use of this criterion may result in misclassi- Figure 2 Supine chest radiograph of a patient with bilateral fication of as many as 15% of effusions. According to Light’s cri- pleural effusion shows increased homogeneous density of the teria,19 which have a sensitivity of 99% and a specificity of 98% for lower hemithoraces. identifying exudates, an effusion is an exudate if any of the follow- ing three findings is present: 1. A pleural fluid–to–serum protein ratio higher than 0.5 2. A pleural fluid–to–serum LDH ratio higher than 0.6 3. A pleural fluid LDH concentration higher than two thirds of the upper limit of the serum reference range A 1997 meta-analysis of the diagnostic value of tests used to dis- tinguish transudates from exudates did not find any test or com- bination of tests to be clearly superior.20 The choice of a test for this purpose is therefore a matter of individual preference. If only one test is to be performed, measurement of the total protein con- centration is the most practical choice, in view of its accuracy and availability. Figure 3 Chest CT shows a free-flowing, sickle-shaped right- side effusion. The incidence of complications associated with thoracentesis varies, depending on the experience of the operator and on the use of imaging guidance. Pneumothorax occurs in 3% to 20% of patients, of whom approximately 20% require tube thoracostomy [see Sidebar Techniques of Bedside Thoracentesis and Tube Thoracostomy]. Patients commonly experience pain and cough with lung reexpansion during drainage. Reexpansion pulmonary edema is an uncommon complication that can occur with rapid drainage of a large-volume effusion. It is common practice to drain no more than 1 to 1.5 L at a time, even though no evidence sup- ports this practice. Experimental data suggest that active aspira- tion of fluid can cause high negative intrapleural pressures, poten- Figure 4 Chest CT of a patient with right-side empyema shows a tially precipitating edema formation; gravity drainage may be loculated effusion. The pleura is enhanced with I.V. contrast.
  • 6. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 6 Techniques of Bedside Thoracentesis and Tube Thoracostomy Bedside Thoracentesis During preparation for chest tube placement, narcotics and sedatives should be administered intravenously; additional doses should then be Bedside thoracentesis should be performed on a bed or an examination administered at the beginning of and during the procedure. table (as a safeguard if hypotension develops). The patient should be The ideal location for chest tube placement is determined by clinical upright and seated (provided that he or she is awake and cooperative), and radiographic examination. The area is prepared and draped wide- with the arms leaning comfortably on a bedside table and the back fac- ly, and a local anesthetic is used at a near-maximum dosage, with care ing the surgeon. taken to anesthetize skin, subcutaneous tissue, muscle, and perios- The proper intercostal space for catheter insertion is determined teum. A 1.5 cm skin incision is made, a soft tissue tunnel is created with through physical examination and radiologic evaluation of the effusion; blunt instrument and finger dissection, the upper edge of the rib is generally, the ninth or 10th intercostal space in the midscapular line is a identified clearly, and additional local anesthetic is applied to the per- good choice. The area is prepared and anesthetized with 1% lidocaine, iosteum and the intercostal muscles. The subcutaneous tunnel should 3 to 5 mg/kg, with care taken not to injure the intercostal bundle. To con- generally be directed posteriorly so that the chest tube will sit along the firm that the catheter is in the correct location, we recommend drawing a posterior chest wall and will not be trapped in a fissure. The intercostal small amount of pleural fluid at the time of local anesthetic infiltration. muscle is pierced bluntly, and digital examination of the pleural space Several thoracentesis kits with one-way valves are available. To minimize is performed to confirm that an intrapleural location has been reached the risk of reexpansion pulmonary edema, fluid should be allowed to and to search for abnormalities such as adhesions or tumor implants. drain by gravity, and drainage should not exceed 1.5 L. Frequently, a dry The chest tube is then directed to the desired location with the aid of a cough and pleuritic pain develop as drainage approaches its end. To clamp. As with thoracentesis, fluid should be allowed to drain by gravi- minimize anxiety, the patient should be warned about this possibility in ty, but drainage should not exceed 1.5 L. If the effusion exceeds 1.5 L, advance. After the completion of thoracentesis, a chest radiograph the chest tube should be clamped and the remaining fluid allowed to should be obtained. drain intermittently in 200 ml aliquots every 2 hours. Immediately after completion of the procedure, a chest radiograph should be obtained to Bedside Tube Thoracostomy verify lung expansion and confirm the position of the chest tube. When Bedside tube thoracostomy should be performed with the patient chest tube output falls below 200 ml/day and reexpansion of the lung supine. The side on which the thoracostomy will be created should be is verified, pleurodesis should be performed. We recommend that pa- elevated, and the patient’s ipsilateral arm should be abducted. Supple- tient-controlled analgesia be employed while the chest tube remains mental oxygen should be supplied. Monitoring must include, at the in place. least, continuous oxygen saturation plethysmography and intermittent The size of the chest tube is determined by the suspected cause and measurement of blood pressure and heart rate. Tube thoracostomy is by the radiologic characteristics of the effusion. For a free-flowing tran- potentially very painful; accordingly, in a nonemergency situation, every sudative effusion, a small (20 to 24 French) chest tube or even a pigtail effort should be made to minimize pain and anxiety. We usually adminis- catheter usually suffices; for a thick exudative effusion or a hemothorax, ter intravenous ketorolac about 30 to 60 minutes before the procedure. a tube as large as 40 French may be required. Assessment of pleural fluid pH and glucose levels may be used are idiopathic. As a rule, the presence of mesothelial cells is of lit- adjunctively for risk stratification in patients with PSI, but the clin- tle diagnostic value; the exception to this rule is that if such cells ical utility of these measurements is not well established (see account for more than 5% of WBCs, a tuberculous effusion is below).21 unlikely.23,27 There are numerous pleural fluid components whose concen- trations can be measured to help determine the specific cause of a Microbiologic Tests pleural effusion, such as triglycerides, chylomicrons, and choles- If a PSI is suspected, Gram staining and standard bacterial cul- terol (to help diagnose chylothorax); amylase (to help diagnose tures are indicated. If tuberculous pleurisy is a possibility, acid-fast esophageal perforation or pancreatitis); rheumatoid factor (to help stains and mycobacterial cultures should be performed. Fungal, diagnose rheumatoid effusion); antinuclear antibodies (to help viral, and parasitic PSIs are uncommon; accordingly, special stains diagnose lupus pleuritis); carcinoembryonic antigen (to help diag- and cultures for these conditions are indicated only if dictated by nose malignancy); and adenosine deaminase (to help diagnose a specific clinical setting.28 tuberculous pleurisy).3,22-25 Cytologic Tests Cell Counts Cytologic testing of pleural fluid is routinely performed when- Analysis of the number and type of white blood cells (WBCs) ever the cause of an effusion is unclear. The diagnostic yield for present in pleural fluid is often diagnostically useful. Pleural effu- malignancy varies depending on the stage of the disease, but it sions can be categorized according to the type of WBC that is pre- generally is in the range of 50% to 60% (higher in patients with dominant. Generally, pleural fluid neutrophilia points to acute bulky pleural tumors). Repeat cytologic testing may increase the inflammation (e.g., from PSI or pulmonary infarction) as the yield to more than 70%,10,29 and testing of three or more samples underlying cause; however, the presence of a neutrophilic effusion may increase the yield to 90%.30 does not exclude malignancy. Pleural fluid lymphocytosis, in PLEURAL BIOPSY which lymphocytes account for more than 50% of WBCs, most frequently is indicative of malignancy (occurring in 50% of malig- In approximately 25% of patients with exudative effusion, the nant effusions), tuberculosis (occurring in 15% to 20% of tuber- cause remains unknown after clinical evaluation, imaging, and culous effusions), or chylothorax.26 Pleural fluid eosinophilia, in pleural fluid analysis. The next step in the evaluation of such which eosinophils account for more than 10% of WBCs, can be patients is pleural biopsy. caused by a wide variety of benign and malignant conditions— Percutaneous pleural biopsy is an infrequently used tool that even, in some cases, by the mere presence of air or blood in the has a diagnostic yield of 57% for carcinoma. Its low yield for pleural space. Approximately one third of eosinophilic effusions malignant effusion can be explained by the uneven distribution of
  • 7. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 7 pleural metastases. For tuberculous pleurisy, however, the diag- nostic yield of percutaneous pleural biopsy is 75%, and the yield rises to 90% when this procedure is combined with pleural fluid culture. In about 10% to 20% of patients with exudative pleural effusion, laboratory analysis of pleural fluid and percutaneous biopsy fail to produce a specific diagnosis.18 The contraindications and complications associated with percutaneous pleural biopsy are similar to those associated with thoracentesis.31 Video-assisted thoracoscopic surgery (VATS) is also employed for pleural biopsy; its diagnostic yield in this setting is 92% for malignancy and nearly 100% for tuberculous pleurisy. VATS is a therapeutic procedure as well, allowing the surgeon to perform pleurodesis, decortication, or pleurectomy if necessary. VATS pleural biopsy is typically performed with the patient under gen- eral anesthesia, but if the patient is highly debilitated, it can be done with regional and local anesthesia.32 Procedure-specific com- plications include hypoxemia, hemorrhage, prolonged air leakage, subcutaneous emphysema, and empyema, each of which occurs at a rate of about 2%. The mortality associated with diagnostic tho- Figure 5 Shown is a Pleurx catheter after placement and subcu- racoscopy ranges from 0.01% to 0.09%.29,31 When VATS is per- taneous tunneling. The vacuum container is not connected. formed to remove a suspected malignant lesion, a protective plas- tic device is required to minimize the possibility of tumor seeding. Incisional tumor seeding after a VATS biopsy is rare but can occur at Small-bore subcutaneously tunneled catheters may be em- any time after the procedure (reported range, 2 weeks to 29 months).33 ployed for long-term management of malignant pleural effusions. If mesothelioma is suspected, open lung biopsy (through a 5 to Two options are available: the Pleurx catheter (Denver 7 cm incision) is the preferred diagnostic procedure. Ideally, the Biomedical, Golden, Colorado) [see Figure 5] and the Tenckhoff biopsy incision should be placed at the location of a potential tho- peritoneal dialysis catheter. Regardless of which option is chosen, racotomy incision so that future excision of the biopsy scar can be the procedure is essentially the same: the catheter is inserted with accomplished in a manner that minimizes the risk of local tumor the patient under local or general anesthesia, the patient is dis- recurrence.34 charged on the same day or on the day after insertion, and the pleural fluid is drained either according to a schedule or on an as- needed basis. Small-bore tunneled catheters are comfortable, but Management patients may object to having a permanent catheter or to under- going home-based procedures. In 20% to 58% of patients with a PLEURAL EFFUSION IN THE permanent catheter, pleurodesis develops within 4 to 6 weeks. INTENSIVE CARE UNIT Catheter removal, if desired, is easily done in the office setting. Pleural effusion develops Technical failures and infection may occur in as many as 20% of in as many as 60% of inten- patients with permanent catheters, but such problems are easily sive care unit patients who managed.36-39 are evaluated with ultraso- Pleuroperitoneal shunting has been advocated as an alternative nography.11 When pleural effusion occurs in the ICU, drainage for long-term management of malignant pleural effusions. Ex- should be liberally employed to optimize the patient’s hemody- perience with this mode of drainage is limited, however, and the namic and respiratory status and to detect PSI early.Thoracentesis potential for technical complications is high.40,41 can be done in critically ill ventilator-dependent patients with the Recurrence of malignant pleural effusion is best prevented by help of bedside ultrasonography. Chest tube thoracostomy does using sclerosants to induce pleurodesis. The sclerosant may be not require ultrasonographic guidance and may be a safer choice instilled either via a bedside tube thoracostomy or thoracoscopi- for patients on high-pressure ventilation. cally; a median hospitalization of 6.5 days is required.36 Of the var- ious sclerosants available, talc is the most efficacious, with an over- MALIGNANT PLEURAL EFFUSION all success rate of 80% to 96%.42,43 The ideal talc dose has not Pleural effusion is associated with malignancy in 30% to 65% been determined; the usual dose is 4 or 5 g. Talc pleurodesis with of patients, and approximately 75% of patients with malignant a 5 g dose has generally proved efficient and safe. For obvious rea- effusion have lung or breast cancer.35 The principal aim of thera- sons, simultaneous bilateral talc instillation should be avoided.42 A py is to relieve dyspnea and to limit the number of procedures and phase III intergroup study (CALGB 9334) that compared bedside hospital days that patients with a limited life expectancy must talc slurry pleurodesis with thoracoscopic talc insufflation pleu- endure. rodesis found no difference in outcome at 30 days; however, sub- Drainage can be achieved by means of thoracentesis, chest tube group analysis revealed that thoracoscopic talc insufflation pleu- placement, or VATS. Thoracentesis is a valuable option for initial rodesis was superior in patients with primary lung cancer or breast patient evaluation, particularly in the office setting. Because malig- cancer.44 Thoracoscopically guided talc pleurodesis can be per- nant pleural effusion recurs rapidly unless patients undergo effec- formed with an operative mortality of less than 1%.45,46 tive systemic or local treatment, repeat thoracentesis is generally Pain and fever are frequent side effects of talc pleurodesis, but not recommended for anything other than urgent relief of symp- the main concern is the possible development of acute lung injury toms. Chest tubes are placed primarily with the intention of per- (ALI) and respiratory failure. Respiratory failure occurs in approx- forming bedside pleurodesis. imately 1% to 4% of patients.The cause of respiratory failure sec-
  • 8. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 8 Table 3 Categorization of PPE by Risk of Poor Outcome Risk of Poor Pleural Space Anatomy Pleural Fluid Bacteriology Category Drainage Outcome Minimal free-flowing effusion (< 10 mm Culture and Gram stain results unknown 1 Very low No on lateral decubitus x-ray) Small to moderate free-flowing effusion (> 10 mm Negative culture and Gram stain 2 Low No but < 50% hemithorax) Large free-flowing effusion (> 50% hemithorax), loc- Positive culture or Gram stain 3 Moderate Yes ulated effusion, or effusion with thickened pari- etal pleura (as seen on contrast-enhanced CT) Pus 4 High Yes ondary to talc pleurodesis is not clear and is probably related to In most patients, PSI is caused by bacteria.The most common multiple factors (e.g., talc dose, talc absorption, underlying lung pathogens are Staphylococcus aureus, Streptococcus pneumoniae, disease, reexpansion pulmonary edema, systemic inflammatory enteric gram-negative bacilli, and anaerobes. Approximately 30% response, tumor burden, and lymphatic obstruction). There is no to 40% of cultures are polymicrobial. In a subgroup of patients, definitive evidence that the talc dose is correlated with the inci- there is sterile pus in the pleural space, as a consequence either of dence of ALI; respiratory failure has been reported even with a 2 previous antimicrobial therapy or of bacterial autolysis. The g talc dose.42,47-51 pathogens identified vary according to the cause of PSI. For Treatment of malignant pleural effusion must be individual- instance, S. aureus and S. pneumoniae predominate in PPE; S. ized. The key factors governing the choice of treatment approach aureus, in postthoracotomy PSI; mixed oropharyngeal organisms, are (1) the patient’s performance status, (2) the prognosis, (3) the in PSI resulting from esophageal perforation28; and acid-fast bac- pleural tumor bulk, and (4) the ability of the lung to reexpand. teria, in tuberculous empyema.55 Patients who have poor performance status (e.g., those with advanced tumors or significant comorbid conditions) or a very Parapneumonic Effusion poor short-term prognosis should undergo the least invasive treat- PPE occurs in as many as 57% of patients hospitalized with ment—namely, drainage only. Patients who have better function- pneumonia, and pneumonia accounts for 42% to 73% of cases of al status and are expected to survive longer should undergo tho- PSI. In most cases, early PPE is effectively treated by timely racoscopically guided talc pleurodesis. Intrathoracic tumor bulk is antibiotic therapy aimed at the underlying pneumonia.21,28 important in that a bulky pleural lesion will interfere with pleu- In 2000, a panel convened by the Health and Science Policy rodesis. The lung’s ability to reexpand after drainage of a malig- Committee of the American College of Chest Physicians (ACCP) nant effusion is significant because if the lung is atelectatic as a reviewed the available literature with the aim of developing an evi- result of airway obstruction or trapped as a result of pleural seed- dence-based clinical practice guideline for the treatment of PPE.21 ing, no agent will be able to induce pleurodesis, and the best treat- The panel formulated a clear and relatively simple classification ment will be long-term drainage. system that used pleural anatomy and bacteriology to stratify patients according to the risk of a poor outcome [see Table 3]. It PLEURAL SPACE INFECTION then made therapeutic recommendations on the basis of this clas- PSI can be caused by a variety of factors, including pneumonia, sification. Some authors have used pleural fluid chemistry test trauma, and intrathoracic procedures. It has a wide clinical spec- results (e.g., pH and glucose concentration) as additional criteria trum, ranging from a small parapneumonic effusion (PPE) to a for categorizing PPE; for example, a pleural fluid pH lower than pus-filled pleural space (empyema) with respiratory compromise 7.20 or a glucose level lower than 60 mg/dl has been considered and sepsis. (The terms PSI and PPE are often used interchange- suggestive of moderate risk. To date, however, the clinical utility ably.) PSI can be classified either according to its pathophysiolog- and decision thresholds of pH and glucose values have not been ic stage (exudative, fibrinopurulent, or organizing) or according to well defined. Accordingly, we prefer to omit pleural fluid chem- its anatomic appearance (nonloculated versus loculated or non- istry from these guidelines. complicated versus complicated). The term empyema is com- The ACCP Health and Science Policy Committee evaluated monly reserved for the most advanced stage of PSI.52 six primary management approaches: no drainage, therapeutic The pathophysiology of PSI or PPE can be divided into three thoracentesis, tube thoracostomy, fibrinolytic therapy, VATS, and stages.The exudative stage is characterized by the development of open surgery. Overall, pooled outcomes favored patients treated an exudative effusion secondary to increased pleural permeability; with fibrinolytics, VATS, and open surgery. However, the success the pleural space is often sterile initially, but if it is left untreated, of an approach is related to the patient’s risk category. The rec- bacterial infection is likely to ensue. The fibrinopurulent stage is ommendations for drainage in relation to risk category are gener- marked by the progressive deposition of fibrin and the increasing al guidelines, based on level C and D evidence (with level C refer- presence of WBCs; gradual angioblastic and fibroblastic prolifera- ring to historically controlled series and case series and level D to tion leads to extensive fibrin deposits, and the effusion becomes expert opinion). With these recommendations (and their limita- loculated (complicated). The organizing stage starts as early as 1 tions) in mind, treatment should be tailored to the specific situa- week after infection, with increasing collagen deposition and lung tion of each patient. entrapment. After 3 or 4 weeks, the organized collagen has formed a peel, and the pleural fluid is grossly purulent. Eventually, dense Category 1 and 2 PPE PPE in categories 1 (very low risk) fibrosis, contraction, and lung entrapment develop.53,54 and 2 (low risk) can be treated with antibiotic therapy directed at
  • 9. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 9 the underlying pneumonia. Some patients with category 2 PPE Tuberculous PSI may require drainage for relief of dyspnea through either thora- Pleural effusion is common in patients with clinically evident centesis or tube thoracostomy. pulmonary tuberculosis. Most cases of tuberculous effusion are secondary to hypersensitivity and resolve spontaneously. Tuber- Category 3 and 4 PPE Drainage options for categories 3 culous empyema is relatively rare; it is typically the result of active (moderate risk) and 4 (high risk) PPE include tube thoracostomy pleural infection by acid-fast bacteria.55 alone, tube thoracostomy with intrapleural fibrinolytic therapy, Tuberculous PSI is also treated in accordance with the general VATS drainage, and open surgical drainage. These various ap- treatment guidelines for bacterial PSI. Chronic tuberculous PSI proaches are not mutually exclusive: in some cases, patient out- may present specific problems, such as drug resistance and im- comes may be optimized by combining them.56 paired ability (or even inability) to reexpand the lung. Surgical pro- Tube thoracostomy alone may be appropriate for category 3 cedures performed to manage chronic tuberculous empyema patients with free-flowing effusion.With loculated effusion, howev- include VATS, standard open decortication, thoracoplasty, parietal er, the key to successful therapy is breaking down the fibrin septa- wall collapse, open drainage, myoplasty, and omentopexy.55 tions. Evidence from three small randomized, controlled trials sug- gested that intrapleural fibrinolytic therapy has an advantage over CHYLOTHORAX AND PSEUDOCHYLOTHORAX tube thoracostomy alone for patients with category 3 or 4 PPE; a Chylothorax is the presence of chyle in the pleural space as a large trial is being conducted to address this specific issue.53 To consequence of blockage of or damage to the thoracic duct or one date, only one randomized study, including 20 patients with cate- of its tributaries.The rate at which chyle flows through the thoracic gory 3 or 4 PPE, has compared VATS with fibrinolytic therapy. duct can be higher than 100 ml/hr, and thus, large amounts of The primary treatment success rate was significantly higher in the chyle can leak into the pleural space.61 The principal causes of chy- VATS treatment group, the duration of chest tube drainage was lothorax are surgical trauma and malignancy (70% to 80% are less, and the total hospital stay was shorter.57 VATS allows not only adequate drainage and visualization of the pleural space but also caused by non-Hodgkin lymphoma).46,61,62 Congenital chylotho- decortication of the lung if required; however, if decortication can- rax is more often due to malformation of the thoracic duct than to not be thoroughly accomplished by means of VATS and satisfac- birth trauma.24 tory lung expansion cannot be achieved, a thoracotomy should be The diagnosis of chylothorax is made by measuring triglyceride performed.58 levels in pleural fluid. Levels higher than 110 mg/dl are highly sug- The principles of PPE treatment can be applied to PSI from any gestive of chylothorax; levels between 50 and 100 mg/dl are equiv- cause, but in view of the paucity of reliable data, caution should be ocal; and levels lower than 50 mg/dl rule out chylothorax.24 exercised. A pleura-to-serum triglyceride ratio higher than 1 can be a useful indicator63; the presence of chylomicrons is synonymous with Posttraumatic PSI chylothorax.25 PSI occurs in about 1% to 5% of patients who have sustained Treatment of chylothorax depends on its cause and severity. blunt or penetrating thoracic injury. The incidence of PSI in the Postoperative chylothorax may be treated initially with conserva- setting of trauma increases with the number of chest tubes placed tive measures (e.g., with a nihil per os [NPO] regimen, total par- and with the duration of chest tube drainage. The effect of an enteral nutrition, and administration of octreotide). However, undrained hemothorax on the risk of PSI has not been complete- drainage totaling more than 500 ml/day is considered to predict ly defined, and prophylactic antibiotics have not been shown to failure of conservative management. Thoracic duct ligation is the reduce the incidence of PSI.52 surgical treatment of choice and can often be performed thoraco- As noted (see above), the general guidelines for the treatment of scopically. To help identify the leak intraoperatively, it may be PPE apply to the treatment of posttraumatic PSI. helpful to administer 100 to 200 ml of heavy cream or olive oil orally 2 to 3 hours before the operation.64,65 Early surgical inter- Iatrogenic PSI vention is important because the ongoing loss of lymph has sig- Iatrogenic PSI develops when a preexisting pleural effusion is nificant effects on fluid homeostasis, nutrition, and immunocom- inoculated with bacteria during an invasive procedure (e.g., thora- petence (secondary to lymphocyte loss). In the early postligation centesis or tube thoracostomy). The presence of fluid in the pleu- period, medical management should be continued to allow any ral space appears to be a prerequisite for infection.52 small leaks to seal. An alternative to surgical ligation that has A bronchopleural fistula (BPF) is by definition a PSI and there- evoked some interest is transabdominal percutaneous emboliza- fore has a similarly broad spectrum of clinical presentation. The tion of the thoracic duct. This technique requires significant overall incidence of BPF after lobar resection is approximately 1%; expertise.66 it is somewhat higher after resections for inflammatory diseases Lymphoma-related chylothorax is caused principally by obstruc- than after resections for cancer. The incidence of BPF after pneu- tion and usually develops on the left side [see Figure 6]. In a stiff and monectomy varies, depending on the side on which the pneu- infiltrated duct, minor triggers (e.g., a Valsalva maneuver) can lead monectomy was done, the indications for surgery, the extent of to duct rupture. Although patients with chylothorax often have preoperative irradiation, and the comorbid conditions present. In extensive disease, supradiaphragmatic disease is not always present. a report encompassing 464 pneumonectomies for cancer, the inci- Lymphoma-related chylothorax is best managed with thoracentesis dence of BPF was 8.6% after right pneumonectomy and 2.3% and with therapy directed at the underlying cause. If first-line ther- after left pneumonectomy. The overall incidence of postpneu- apy fails, thoracoscopic talc pleurodesis is recommended; a small monectomy empyema (generally but not always secondary to a series reported 100% resolution of lymphoma-related chylothorax BPF) is 1% to 3%.59,60 with thoracoscopic talc pleurodesis. If the chylothorax does not PSI that is not associated with a BPF is treated in accordance respond to any of these approaches, it may respond to thoracic duct with the treatment guidelines for PPE, but if a BPF is present, ligation or pleuroperitoneal shunting. Chylothorax in the presence operative management is required. of lymphoma-related chylous ascites is a difficult problem that is
  • 10. © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 4 THORAX 4 PLEURAL EFFUSION — 10 generally refractory to most forms of therapy (though pleurodesis is occasionally successful).46,61,62,67,68 Pseudochylothorax is a rare disorder associated with the forma- tion of persistent exudates that last for months or years. The most common cause is tuberculosis; the second most common cause is rheumatoid arthritis. Biochemical analysis of pleural fluid from patients with pseudochylothorax reveals very high cholesterol lev- els (> 200 mg/dl) and the presence of cholesterol crystals. Treat- ment is generally conservative.24,25 IDIOPATHIC PERSISTENT PLEURAL EFFUSION In a small percentage of patients, the cause of pleural effusion remains unknown despite extensive diagnostic evaluation. Tuber- culosis and other granulomatous diseases, malignancy, and pulmon- ary embolism account for most cases of idiopathic effusion; those causes are identified later in the course of the disease or at autopsy. Other causes include constrictive pericarditis, subphrenic abscess, connective tissue diseases, drug-induced pleuritis, peritoneal dial- Figure 6 Chest CT shows left-side chylothorax secondary to ysis, and cirrhosis.23 In the management of persistent benign or lymphoma. Subtle mediastinal lymphadenopathy obstructing the idiopathic effusion, talc pleurodesis has a high success rate and thoracic duct (arrow) is apparent. minimal long-term implications.69,70 Discussion Pleural Anatomy of the venules, which suggests that the pleural mesothelial cell The pleura is a continuous membrane that covers the parietal layer may be as leaky as the venular endothelium.3,4,72 and visceral surfaces of the thorax. In adults, it has an estimated surface area of 2,000 cm2.71 Light microscopy shows the pleura to have five layers: (1) a mesothelial cell layer; (2) a mesothelial con- Pleural Fluid Physiology nective tissue layer with basal lamina; (3) a superficial elastic layer; The amount of pleural fluid in an adult is 1 to 10 ml and forms (4) a loose connective tissue layer with adipose tissue, blood ves- a 10 µm–thick layer.1,3,71,72 Fluid exchange across the pleural sur- sels, nerves, and lymphatic vessels; and (5) a deep fibroelastic face depends on three mechanisms: (1) passive filtration following layer.The parietal pleura establishes a pleurolymphatic communi- Starling’s equilibrium, (2) active solute transport, and (3) lym- cation on the diaphragm to allow clearance of large (> 1,000 nm) phatic clearance. In the normal pleura, Starling’s equilibrium particles and cells from the normal pleural space.The structure of favors the flow of fluid in a parietal-to-visceral direction.71 The rate this pleurolymphatic communication consists of stomata 2 to 12 at which fluid traverses the pleura ranges from 20 to 160 ml/day µm in diameter, which overlie bulblike lymphatic channels (lacu- in adults; maximal lymphatic clearance is believed to be approxi- nae) separated by a layer of loose connective tissue (the mem- mately 700 ml/day.2,71,73-76 brana cribriformis). The chemical composition of normal pleural fluid is similar to Electron microscopy reveals microvilli on the mesothelial cell that of interstitial fluid.The protein concentration is typically 1 to surface of the pleura. The main function of these microvilli is to 2 g/dl.The concentration of high-molecular-weight proteins (e.g., enmesh glycoproteins rich in hyaluronic acid for purposes of LDH) is approximately half that seen in serum. Cell counts in lubrication.The structure of the intercellular junction in the meso- normal pleural fluid range from 1,400 to 4,500 cells/mm3; macro- thelial cells of the pleura is similar to that in the endothelial cells phages account for the majority of the cells.3,72 References 1. Tran AC, Lapworth RL: Biochemical analysis of sions: how should you go about finding the cause? sus radiography. Radiology 191:681, 1994 pleural fluid: what should we measure? Clin Bio- Postgrad Med 105:39, 1999 10. Bartter T, Santarelli R, Akers SM, et al:The evalu- chem 38:311, 2001 6. Levin DL, Klein JS: Imaging techniques for pleu- ation of pleural effusion. Chest 106:1209, 1994 2. Jaker SA: Pleural anatomy, physiology and diag- ral space infections. Semin Respir Infect 14:31, 11. Azoulay E: Pleural effusions in the intensive care nostic procedures. Textbook of Pulmonary Dis- 1999 unit. Curr Opin Pulm Med 9:291, 2003 eases, 6th ed, Vol 1. Baum GL, Crapo JD, Celli 7. 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