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Resolution of Pleural Effusions* FREE TO VIEW

Mark Cohen, MD; Steven A. Sahn, MD, FCCP
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*From the Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston, SC.

Correspondence to: Steven A. Sahn, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, 96 Jonathan Lucas St, PO Box 250623, Charleston, SC 29425; e-mail: sahnsa@musc.edu

Chest. 2001;119(5):1547-1562. doi:10.1378/chest.119.5.1547
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Pulmonologists, internists, surgeons, and other medical specialists frequently encounter patients with pleural effusions. A plethora of articles have been written about the pathophysiology and pleural fluid (PF) characteristics that assist the physician in establishing a diagnosis and therapeutic plan for pleural diseases associated with effusions. In contrast, there is a paucity of information regarding the resolution time of a pleural effusion.

The purpose of this review is to present the available published data regarding the time course of resolution for nonmalignant pleural effusions in the most commonly encountered pleural diseases (empyema, pus in the pleural space, was excluded). A MEDLINE search from 1966 to 1999 of the English-language literature was instituted, matching pleural effusion with each of the specific diseases most commonly associated with pleural effusions. The search included case reports and retrospective and prospective case series of pleural effusions that resolved spontaneously or with medical management, excluding pleural space manipulation. Of the 393 articles retrieved, only 110 specified a time course of resolution. With the available information, an estimated time course of resolution was determined for the specific pleural process (Table 1 ).

This review should provide the physician with clinically useful information that should narrow the differential diagnosis and focus the diagnostic evaluation.

The annual incidence of bacterial pneumonia in the United States is estimated at 4 million.1Parapneumonic effusions develop in 36 to 66% of hospitalized patients with bacterial pneumonia.25 When both ambulatory and hospitalized patients are studied, the incidence decreases to 9% (168 of 1,906).6 The vast majority of parapneumonic effusions resolve with antibiotic therapy alone, with only a small percentage of patients requiring operative intervention for resolution. The following paragraphs discuss the time course of resolution of parapneumonic effusions associated with specific etiologic agents (Table 2 ).

Streptococcus pneumoniae

The incidence of parapneumonic effusions in pneumococcal pneumonia is reported to be 29 to 57%.34,79 Most effusions are small to moderate in size, even in the presence of positive blood culture results. The effusion is ipsilateral to the pneumonic process, and PF culture results are positive in < 6% of the cases.24 The incidence of parapneumonic effusions increases if medical attention is delayed for > 48 h after the onset of symptoms.3

Despite the high incidence of pneumococcal pneumonia, few studies have delineated the time course of resolution of the associated effusion. Jay and coworkers7 reported that pleural disease occurred in 34% (27 of 80) of cases of S pneumoniae pneumonia, including nine sterile pleural effusions. Pleural changes on radiograph tended to resolve between 8 weeks and 14 weeks, but no time course is mentioned for pleural effusions. Macfarlane and colleagues,9also report complete clearing of infiltrates in bacteremic and nonbacteremic pneumococcal pneumonia at 16 to 20 weeks and 12 to 16 weeks, respectively. After resolution of pulmonary infiltrates, residual pleural thickening was present in 37% and 9%, respectively. More recently, Trejo and associates10 reported a 14% (9 of 65) incidence of pleural effusion in a non-HIV population with S pneumoniae pneumonia. These effusions tended to resolve in 2 to 4 weeks.

Mycoplasma pneumoniae

M pneumonia typically occurs in the 5- to 25-year age group, but can occur in adults of all ages.11 The incidence of parapneumonic effusions is 4 to 20% with the use of lateral decubitus radiographs.9,1215 The effusions are usually small and ipsilateral to the pulmonary infiltrate but may be massive and bilateral.13,1516 It appears that patients with sickle cell disease have a higher incidence of effusions and larger volumes of PF.17

Macrolides or tetracyclines will help resolve the febrile course, reduce the duration of cough, and hasten the radiographic resolution of the pulmonary infiltrates18 and effusions. The resolution of the pleural effusions ranges from 5 days to 8 weeks, with the majority resolving in 2 to 3 weeks.9,1215,1921 Residual pleural thickening is unusual.15,20

Legionella pneumophila

Community-acquired pneumonia (CAP) caused by Legionella has a varied severity without unique clinical features.22The prevalence of this pathogen in CAP ranges from 2% (8 of 456) when ambulatory and hospitalized patients are studied,23to 12% (47 of 392)24and 16% (55 of 346)25 when only hospitalized patients are included. Pleural effusions have been described in 12 to 35% of patients, and may precede the parenchymal infiltrate.9,2529 Effusions are typically small and unilateral but may be large and bilateral. Once macrolide therapy is begun, resolution occurs in 5 days to 4 months, with the majority resolving within 4 weeks.2529 The presence of pleural effusions tends not to affect outcome.30 However, empyemas occur3031 warranting a thoracentesis if clinically indicated.

Chlamydia Pneumonias

The prevalence of Chlamydia pneumoniae as an etiologic pathogen in CAP typically ranges from 3 to 22%,2325,32 but can be as high as 43% during seasonal epidemics.33 Pleural effusion has been reported in 20% to 55% of Chlamydia psittaci pneumonia,36 are extremely rare in Chlamydia trachomatis pneumonia,39 and have been found in 8 to 53% of pneumonias caused by C pneumoniae.44 Most effusions by any of the Chlamydia organisms are small to moderate in size, with large effusions being uncommon. The time of resolution of C psittaci or C pneumoniae pneumonic infiltrates has been reported, but the resolution of pleural effusions has not been commented on previously. The clearance of pneumonic infiltrates was observed in 75 to 100% by 6 to 9 weeks,,3435,42,45 with pleural adhesions or thickening observed in 4 to 20% after > 12 weeks.36,42

Francisella tularensis

Although tularemia has declined in incidence since first described by Francis in 1925,46it continues to occur both sporadically and in epidemics in the United States. Pleuropulmonary disease has occurred in up to 80% of hospitalized patients.47 Pleural involvement is more likely to occur when parenchymal abnormalities are present, and has been described in 13 to 64% of patients.4750 The incidence of pleural effusions increases as untreated diseases progresses, although PF has been found as early as 3 days after the onset of symptoms.47,51 Streptomycin is the drug of choice, with resolution of the pleural effusion in 6 to 7 weeks.49,52

Coccidioides immitis

C immitis is endemic in southwestern United States, northern Mexico, and certain areas of Central and South America. Pleural effusions may occur during either acute primary or chronic progressive disease,53with the reported incidence ranging from 7 to 19%.5456 Effusions tend to develop within a week after the onset of symptoms. The effusions are usually small, but occasionally may be massive. The natural history of acute coccidioidal effusions is self-limited, with radiographic resolution in 1 to 8 weeks.5657 No specific therapy is warranted unless there is evidence of dissemination. Therapeutic thoracentesis may be beneficial to relieve the dyspnea with large effusions.

Pleural effusion in the chronic form of coccidioidomycosis occurs with cavity rupture into the pleura space, with the development of a bronchopleural fistula and empyema. These patients require early drainage and systemic antifungal therapy.

Histoplasma capsulatum

Histoplasmosis is encountered worldwide, with the highest endemic area in the United States being along the Ohio-Mississippi River valleys. Pleural effusion with histoplasmosis is an unusual occurrence in HIV-negative patients.58In a severe epidemic, the incidence of pleural effusions was 5% (21 of 435),59 while nonepidemic histoplasmosis has an incidence of < 1% (1 of 269).60Even with disseminated histoplasmosis in AIDS patients, pleural effusions are uncommon (0 of 72), despite abnormal radiographic findings in > 50% of cases.61

Based on the limited number of cases in the literature, the presence of a pleural effusion associated with histoplasmosis does not influence the prognosis. Specific therapy should be dictated by the underlying condition of the host. In a normal host, spontaneous resolution of the pleural effusion can be expected in 2 to 4 weeks.53,62 Amphotericin B should be initiated if the effusion persists > 4 weeks, the patient is immunosuppressed, or the chronic pulmonary form is present.53 Residual pleural thickening and extensive pleural fibrosis requiring pleurectomy has been reported.63

Viral lower-respiratory-tract infections have been associated with pleural effusion. The incidence of pleural effusions in viral pneumonia is reported to be 2% (2 of 123)64 to 9% (2 of 23)12of cases. When pleural effusions are specifically targeted with lateral decubitus chest views, 18% (2 of 11) with viral pneumonia revealed an effusion.13 A variety of viral infections, including influenza,13,64 parainfluenza,64 respiratory syncytial virus,6466 herpes simplex virus,67 cytomegalovirus,6869 and adenovirus1213,66,7071 have been associated with pleural effusions. Many of these patients were immunocompromised. In general, these effusions are small, transient, and asymptomatic. They tend to resolve within 2 weeks and require no pleural space drainage.1213,72

Eight million people developed tuberculosis in 1990 worldwide, with 95% occurring in underdeveloped countries.73The frequency of pleural effusion in tuberculosis varies from country to country. In the United States, tuberculous pleural effusions represent 4% (905 of 22,764) of all cases of tuberculosis74; in Spain, it affects 23% (146 of 637).75

Radiographs typically show small-to-moderate, unilateral effusions, although massive effusions are seen in 14 to 29% of those with primary disease.7679 Bilateral effusions occur in approximately 10% of cases, and appear to be more common in HIV-positive patients.77,7980

Tuberculous effusions resolve spontaneously within 2 to 4 months in most healthy individuals; however, if untreated, 65% (92 of 141) of patients will develop pulmonary or extrapulmonary tuberculosis within 5 years.76 Therefore, it is important to start antituberculous therapy in patients with tuberculous pleurisy. Therapy with isoniazid and rifampin for 6 months is effective; two studies in non-HIV patients documented a relapse rate of zero, with a mean follow-up of > 3 years.8182 Complete resolution of the radiograph was seen at the end of 6 months, but no specific data are provided on the resolution rate of the pleural effusion.8182 With a 9-month course of isoniazid and rifampin, resolution of pleural effusion occurred within 6 weeks; pleural thickening may persist for years.53 Before the standardization of therapy, several studies8385 administering different drug regimens reported resolution of effusions from 3 to 9 months, with the majority clearing at 3 to 6 months. The current recommendation for tuberculous effusions consists of isoniazid, rifampin, and pyrazinamide for 2 months, followed by isoniazid and rifampin for the next 4 months.86This standard regimen was administered without supervision to 65 patients, with complete resolution of effusion by 14 months; 75% had resolved by 6 months of therapy.87The relapse rate was 0% at 20 months. During the initial weeks of therapy, effusions may enlarge in a small minority; but this does not imply treatment failure.88

Corticosteroids have been advocated as an adjunct to hasten the resolution of symptoms and absorption of PF and to prevent residual pleural thickening. Three randomized, double-blind, placebo-controlled trials8991 have been completed, but all had important methodologic differences. Lee and coworkers89administered isoniazid, rifampin, and ethambutol for the initial 3 months, and isoniazid and rifampin for the subsequent 6 to 9 months and either prednisolone, 0.75 mg/kg/d, or placebo. Diagnostic thoracentesis (< 50 mL) was done on the first day of hospitalization. PF in the steroid group (21 patients) resolved in a mean of 55 days, and in the placebo group (19 patients) in 123 days (p < 0.01). No significant difference was observed in residual pleural thickening. Galarza and associates90administered isoniazid and rifampin for 6 months and either prednisone, 1 mg/kg/d, or placebo; all effusions were drained to equal amounts (a third the hemithorax). The reabsorption rate at 1 month was 93% (53 of 57) and 89% (53 of 60; p = 0.01) in the steroid and placebo groups, respectively. However, the difference between groups disappears thereafter. No difference was observed between groups with respect to residual pleural thickening. In contrast, Wyser and colleagues91 administered isoniazid, rifampin, and pyrazinamide for 6 months, prednisone (0.75 mg/kg/d; 34 patients) or placebo (36 patients), and complete drainage of effusion via thoracoscopy. No difference in symptoms, recurrence of effusion after drainage, or residual pleural thickening was observed in either treatment group.

Based on these data, routine use of corticosteroids cannot be recommended and should only be used if acute symptoms, such as fever, chest pain, or dyspnea, are disturbing to the patient.

A reasonable management strategy for tuberculous effusions would be to perform a diagnostic and therapeutic thoracentesis, especially in those with large effusions, attempting to evacuate as much fluid as possible and initiate antituberculous chemotherapy.

The incidence of pleural effusion in patients with AIDS varies in different populations and geographic areas. In a large series of 4,511 HIV-positive patients admitted to a New York hospital, pleural effusions were seen in only 1.7% of cases; however, the stage of these cases is not commented on in this abstract.92In a series from South Carolina,93 the prevalence of pleural effusion was 17% in 350 HIV-positive hospitalized patients, but there was a significant difference in CD4 counts in those with (72 ± 12 cells/L) and without (274 ± 26 cells/L) pleural effusion (p < 0.001).

The three most common causes of AIDS-related pleural effusions are parapneumonic effusions or empyemas, tuberculosis, and Kaposi’s sarcoma. The frequency of these conditions varies depending on regional variability, HIV risk factors (ie, IV drug use, homosexuality), and stage of the disease.9295

Parapneumonic Effusions

Bacterial pneumonia is more frequent in HIV-positive individuals than in seronegative control subjects. In a large multicenter, prospective study,96the prevalence of bacterial pneumonia was 5.5/100 person-years and 0.9/100 person-years in HIV-positive and HIV-negative patients, respectively. The course of CAP in AIDS is often complicated, as reflected by higher rates of bacteremia (58% [11 of 19] vs 18% [17 of 96]; p < 0.001), parapneumonic effusions (21%[ 21 of 99] vs 13% [116 of 884]; p < 0.05), and empyemas requiring chest tube drainage (71% [15 of 21] vs 44% [51 of 116]; p < 0.05) in HIV-positive patients compared to HIV-negative patients.97

The management of HIV-positive patients with a parapneumonic effusion is similar to that of the immunocompetent patient. However, because of a higher incidence of infection with Staphylococcus aureus in HIV-positive patients, appropriate antibiotics must be chosen to cover this organism. Trejo and colleagues10 found no significant difference in morbidity or mortality between HIV-positive and HIV-negative patients with uncomplicated parapneumonic effusions. In their study,10 pleural effusions resolved in 17 ± 11 days and 24 ± 22 days (mean ± SD) in the HIV-positive patients and HIV-negative patients, respectively.

Tuberculous Pleural Effusions

The incidence of tuberculous pleurisy in HIV-positive patients has been reported as higher,9899 lower,10 or the same100103 as in HIV-negative patients. Among patients with AIDS, the percentage of tuberculous effusions is higher in patients with CD4+ counts > 200 cells than in those with CD4+ counts< 200 cells.104

Therapy for tuberculous effusions in HIV-positive patients does not differ from the standard treatment but should be prolonged if there is evidence of a slow or suboptimal response.86 No significant difference in morbidity and mortality was seen between the HIV-positive and HIV-negative patients.10 As shown by Trejo and coworkers10 tuberculous effusions resolved in 79 ± 81 days in the HIV-positive patients and 69 ± 61 days (mean ± SD) in HIV-negative patients.

Congestive heart failure (CHF) is the most common cause of a transudative pleural effusion, and is probably the most common cause of all pleural effusions. Defining the precise incidence of pleural effusion with CHF is problematic, because there is variance between techniques used to detect the effusion and the stage and degree of heart failure at the time of the evaluation. Earlier literature reports an incidence of 38% (136 of 356) clinically and radiographically,105and as high as 72% (290 of 402) at autopsy.106More recently, a large epidemiologic study from Czechoslovakia demonstrated pleural effusions in 46% (65 of 142) of CHF patients.107 Radiographically, these effusions are usually bilateral, right greater than left, with associated cardiomegaly; however, if unilateral, there is a right-sided predominance.106,108109

It is believed that PF accumulates in patients with CHF when they have left, but not right, ventricular failure.110111 Therefore, treatment should consist of decreasing pulmonary venous hypertension and improving cardiac output. When heart failure is treated successfully, effusions tend to resolve in < 1 month.106,112113 Occasionally, refractory cases may require repeated thoracentesis or chemical pleurodesis for symptomatic relief.114Pleuroperitoneal shunt is also an option.115

The postcardiac injury syndrome (PCIS) occurs days, weeks, or months after a variety of myocardial or pericardial injuries. The syndrome has been described after cardiac surgery (postpericardiotomy syndrome),116121 myocardial infarction (postmyocardial infarction or Dressler’s syndrome),122125 blunt chest trauma,126127 pacemaker implantation (postpericardial trauma syndrome),128131 and angioplasty.132133 This autoimmune syndrome is manifested by pericarditis, with variable features of fever, leukocytosis, high erythrocyte sedimentation rate, and pulmonary infiltrates and/or pleural effusion. The incidence of PCIS varies with the sustained injury. PCIS after myocardial infarction has been reported in 1 to 7%,122123,125 with pleural effusion occurring in 40% (16 of 40)123 to 68% (30 of 44) of patients.122 The PCIS occurs more frequently after cardiac surgery, with an incidence ranging from 17 to 31%,116,118119,121 with the incidence of pleural effusion ranging from 47% (16 of 34)134 to 68% (26 of 38).119

Pleural effusions resolve over a variable period, modulated by the response to anti-inflammatory drugs. For most postmyocardial infarction patients, the effusions resolved 1 to 5 weeks after nonsteroidal anti-inflammatory drugs (NSAIDS) or prednisone were initiated.122123 After cardiac surgery, the effusions tend to resolve spontaneously by 2 months; some cases resolve in a few days to 3 weeks with anti-inflammatory drugs.119 Salicylates, other NSAIDS, or corticosteroids should be used for the symptomatic patient or those with large-to-moderate symptomatic pleural effusion.

Pleural effusions are common after coronary artery bypass graft surgery. The reported incidence ranges from 40 to 90%, depending on the diagnostic modality used to detect the presence of PF.135139 The majority of pleural effusions are small and usually left sided; however, large and bilateral effusions have been reported.

These effusions have multiple causes. They could be related to CHF, PCIS, atelectasis, chest tubes, pleural lymphatic injury from the pleurotomy, injury to the internal mammary artery bed, or pericardial inflammation.137 Despite conflicting data, the incidence of pleural effusions in patients receiving internal mammary artery grafts appears to be higher (70 to 85%) than those receiving saphenous vein grafts (30 to 50%).135136,138There is no difference between bilateral mammary artery and left internal mammary artery grafting in the incidence or severity of postoperative pleural effusions.139

Pleural effusions after coronary artery bypass graft surgery should be treated conservatively. Other causes for these effusions should be sought only if the patient is febrile, the effusion is large, or if it fails to resolve in the appropriate time frame. These effusions tend to resolve within 8 weeks,136 but long-term effusions have persisted for 3 to 20 months.140142 Some long-term effusions result from prolonged oozing of blood and serum into the pleural space at the site of harvest of the internal mammary artery,140 while others are the result of trapped lung.143

Pleural involvement appears to be the most common intrathoracic manifestation of rheumatoid arthritis (RA), occurring in approximately 5% of patients.144145 However, based on autopsy findings, clinical presence of pleural effusion and pleurisy significantly underestimates pleural involvement in RA patients. Postmortem series146report a 40 to 70% incidence of pleuritis; this clinicopathology discrepancy suggests that many patients are asymptomatic or that anti-inflammatory drugs mask minimal symptoms. In two large series, the incidence of rheumatoid pleurisy with effusion was 4% (21 of 516)147 and 5% (9 of 180),144 with a striking predominance in men; other predisposing factors for the development of effusion in RA include age> 45 years and subcutaneous nodules.144,147148 Pleural effusion may occur at any time during the course of RA, with 20% preceding or occurring at the onset of arthritis, and 50% developing within 5 years of onset of articular manifestations.147

The clinical presentation may mimic bacterial pneumonia or be asymptomatic.149Radiographs usually reveal a small-to-moderate unilateral pleural effusion; however, large and occasionally massive pleural effusions have been documented.150151 A rheumatoid pleural effusion can be transient, long-term, or relapsing.147,152 It is uncommon for the effusion to resolve in < 4 weeks; most effusions resolve in 3 to 4 months.144,147149,153155 Fifty percent of the patients have a protracted course that lasts from 7 months to 5 years,144,147149,153156 with occasional progression to marked pleural thickening and trapped lung requiring decortication.144,157160

There are no controlled studies evaluating the efficacy of corticosteroids or NSAIDS in the treatment of rheumatoid pleural effusion. Both systemic and intrapleural corticosteroids have been used, with variable results.144,147148,153156,161163 If the main goal of therapy is the prevention of progressive pleural fibrosis, anti-inflammatory drugs should be considered. A reasonable strategy would be to institute therapy with aspirin, other NSAIDS,164) or prednisone165 early in the disease process. If at 8 to 12 weeks the effusion resolves, therapy could be discontinued. If the effusion does not resolve, therapeutic thoracentesis and intrapleural corticosteroids should be considered.

Pleurisy (pleural inflammation), a common feature of systemic lupus erythematosus (SLE), is usually associated with chest pain with or without pleural effusion, and occurs in 45 to 56% of patients during the course of the disease.166167 Radiographic evidence of pleural effusion is less common, with an incidence of 16 to 37%.166168 Pleural effusions occur more frequently in female patients and usually are a late manifestation of the disease but may be the presenting feature in 5% of cases.166,168169 The most common radiographic presentation of lupus pleuritis is small-to-moderate bilateral pleural effusions, although unilateral and massive effusions has been reported.168,170172

In contrast to rheumatoid pleuritis, the majority of lupus pleural effusions resolve rapidly with corticosteroid therapy. Hunder and associates156 reported that in five of six patients, pleural effusions resolved “quickly” once corticosteroids were initiated; the sixth patient’s effusion gradually resolved after 6 months. In the series of Winslow and colleagues,168 11 patients received corticosteroid and the effusions cleared in < 2 weeks; in contrast, only 10 of 16 effusions cleared without corticosteroid therapy at 2 weeks. Other researchers173175 have reported clearing of the effusion in 7 days to 6 weeks with prednisone, 20 to 30 mg/d.

Other causes for pleural effusion should be considered when patients with SLE develop effusions, such as nephrotic syndrome, CHF, pulmonary embolism, parapneumonic effusion, uremia, and drug-induced SLE pleuritis. In the latter, therapy consists of withdrawing the offending drug. Once other causes of the effusion have been excluded, therapy with prednisone, 60 to 80 mg/d, should be initiated and rapidly tapered once the acute pleurisy has subsided.165 Rarely, lupus pleuritis can be massive and refractory to steroid therapy. Adding a second immunosuppressive drug, such as cyclophosphamide or azathioprine, may be successful. Alternative treatments for refractory cases include chemical pleurodesis with tetracyclines176177 or talc,178IV immunoglobulins,179and pleurectomy.180181

Although the lung is affected in > 90% of patients with sarcoidosis, pleural involvement is an uncommon manifestation. The incidence of pleural effusion with sarcoidosis ranges from 0 to 5%182184 but has been reported to be as high as 7.5%.185 Patients with sarcoid pleural effusion usually have extensive parenchymal disease (stage 2 or stage 3) and frequently have extrathoracic sarcoidosis.182185 Chest radiographs usually show unilateral, small-to-moderate effusions, but bilateral and massive effusions have been noted.182,184190 Pleural sarcoidosis is a diagnosis of exclusion in the proper clinical setting when tuberculosis and fungal disease have been excluded.

Sarcoid pleural effusions may resolve spontaneously or require corticosteroids for resolution. The time of spontaneous resolution is variable, but most resolve in 1 to 3 months.183,185,187,191192 However, there are reports of resolution at 2 weeks with steroid therapy,188,193 and as long as 6 months with or without steroid administration.183,186 Therefore, the management of sarcoid pleural effusion should be guided by the clinical presentation. In the absence of symptoms, the effusion usually resolves spontaneously. If the effusion is symptomatic and recurrent, steroid therapy is recommended for symptomatic relief and to hasten the resolution of the effusion. Incomplete resolution of these effusions has been reported with eventual progression to chronic pleural thickening.185

Pulmonary embolism should be a diagnostic consideration in every patient with an acute, unilateral pleural effusion. Pleural effusion occurs in 10 to 50% of patients with pulmonary embolism194199; an associated ipsilateral parenchymal infiltrate is seen on chest radiography in 50% of patients.195 Effusions secondary to pulmonary embolism generally are small and occupy less than a third of the hemithorax.195,197199 The effusion tends to be larger if an associated infiltrate is present.195 In the absence of complications, pleural effusions tend to reach their maximal size early and should not enlarge after the third day after admission.195 If effusions increase after the third day, recurrent pulmonary embolism, hemothorax from anticoagulation, secondary infection, or an alternate diagnosis should be suspected. On standard chest radiographs, most effusions are unilateral even if bilateral pulmonary emboli are present195; however, using spiral chest CT, bilateral small effusions are present in 75% of cases.199

The course of resolution of these effusions has not been extensively studied. To our knowledge, the study of Bynum and Wilson195 is the only one that has addressed this issue. In their series, pleural effusion without parenchymal infiltrates (infarction) resolved in < 7 days in 72% (18 of 25) of cases, with five effusions resolving within 3 days. Among the 31 patients that completed follow-up at 10 days, all patients with an associated parenchymal infiltrate had a persistent effusion. No data are reported on the time of resolution for those cases that persisted > 7 days.195

Pleural effusion resulting from asbestos exposure is the most common asbestos-related pleuropulmonary abnormality during the first 20 years after exposure; however, it may occur from 1 to 60 years from initial exposure.200202 Benign asbestos pleural effusion (BAPE) is defined as an effusion that occurs in the setting of asbestos exposure, in the absence of other conditions, and is not followed by the development of a malignancy within 3 years. Using this definition, Epler and coworkers200reported an incidence of 9.2 effusions, 3.9 effusions, and 0.7 effusions per 1,000 person-years after heavy, moderate, and mild asbestos exposures, respectively. Cookson and associates201reported an incidence of 8% (24 of 280) in patients with heavy asbestos exposure. Hillerdal andÖ zesmi202 reported an incidence of 4% (60 of 1,500), but only 20% of the patients had moderate or heavy asbestos exposure.

Most patients (46 to 66%) are asymptomatic at the time the pleural effusion is discovered,200,202 usually by screening radiograph. Most effusions are small to moderate in size and unilateral; bilateral or massive effusions occur in approximately 10%.200The natural history of BAPE is one of chronicity with frequent recurrences. Most effusions resolve in 3 to 4 months, with a range of 1 to 17 months.201204 Resolution typically results in a blunted costophrenic angle (80 to 90%), with diffuse pleural thickening occurring in approximately 50% of patients.200,202 Recurrences are frequent (30 to 40%) and usually occur within 3 years of the initial presentation.200,204 A number of patients have developed malignant pleural mesothelioma years after an episode of BAPE,200,205 but large epidemiologic studies are needed to confirm a relationship.

Lung and Heart-Lung Transplantation

Pleural effusions are the rule in the early postoperative period. One series206of heart-lung transplants reported a 100% (10 of 10) incidence of pleural effusions. More parapneumonic effusions have been noted in double-lung transplants than in single-lung transplants (16% [4 of 25] vs 0% [0 of 5]).207 The latter is possibly explained by the greater pretransplant incidence of pulmonary sepsis in double-lung recipients with cystic fibrosis and COPD.

Most of these pleural effusions are small to moderate in size, but rarely may be massive.208In the vast majority of cases, pleural effusions resolve spontaneously within 9 to 14 days after transplantation,209 although a small percentage may increase in size over the first 3 postoperative weeks.206 This correlates with animal studies210212 demonstrating that allograft lymphatics reconstitute and become functional 2 to 4 weeks after transplantation. Failure of resolution by 3 weeks suggests a pathologic process, such as the pulmonary reimplantation response, infection, or acute lung rejection. Therapy targeted to these complications usually is accompanied by clearing of the pleural effusion.

Liver Transplantation

Pleural effusions unrelated to primary cardiopulmonary disease usually develop after liver transplantation. The reported incidence of pleural effusions is between 48% and 100%,213217 with most reporting a 100% incidence. Injury to the right hemidiaphragm from right-upper-quadrant abdominal dissection and retraction, perioperative infusion of blood products, hypoalbuminemia, and atelectasis all may contribute to the development of pleural effusions.217The most important factor probably is operative transection of hepatic lymphatics, in particular the pulmonary ligament that communicates with the visceral pleural lymphatics, as shown in a swine model.218 These severed lymphatics may leak lymph and result in the immediate development of ascites and subsequent right pleural effusion via congenital or acquired diaphragmatic defects.218

The pleural effusions are bilateral in about a third of patients, but the amount of fluid is always greater on the right.217 These effusions typically develop and enlarge over the first 3 to 7 days after surgery.213,215216 Most effusions resolve within 2 to 3 weeks,213215 although there may be persistence for months.216217 Thoracentesis or tube thoracostomy for symptomatic relief was required in 11 to 30% of cases,213215,217,219 and the fluid had the characteristics of a transudate.213 If accumulation of PF persists after 7 days, a subdiaphragmatic process or pleural infection should be suspected.216,220

In 1836, Bright221reported that only 29% of patients with albuminous urine had healthy pleura at autopsy. Fibrinous pleuritis has been found in 20 to 58% of uremic patients at autopsy.222223 There are several reasons why pleural disease may be common in patients with renal failure: (1) CHF because of tenuous fluid balance, ischemic heart disease, and dilated cardiomyopathy; (2) increased risk of infection224225; (3) diseases associated with renal and pleural manifestations (ie, SLE); (4) uremic pericarditis228; (5) increased risk for certain malignancies229230; (6) pulmonary embolism; and (7) uremic pleurisy from an unknown putative agent.231232 Therefore, uremic pleuritis is a diagnosis of exclusion.

Two retrospective studies have studied the incidence of uremic pleurisy in hospitalized patients receiving long-term dialysis. Berger and coworkers233reported a 4% (14 of 436) incidence of pleural effusion; however, the incidence could have been underestimated because patients who had a small effusion or resolved rapidly after detection were not included. Jarratt and Sahn234 reported a 16% (16 of 100) incidence of pleural effusions secondary to uremia. The chest radiograph usually shows a unilateral, moderate-sized pleural effusion, although massive and bilateral effusions have been described.233,235236 Pleural effusions usually resolve (80%) with continued dialysis in 4 to 6 weeks,233 but recurrences may occur. Effusions may persist despite aggressive hemodialysis, and progress to fibrothorax requiring decortication.235237 Toxins or immune complexes not removed with dialysis may be pathogenic, and possibly other modalities of therapy may be helpful in removal of the substances from the circulation (ie, plasmapheresis).,231232

Pleuropulmonary complications are commonly associated with pancreatic disease. Pleural effusions are no exception, but the clinical presentation, management, and prognosis for effusions in acute and chronic pancreatitis are different.

Acute Pancreatitis

Pleural effusions have been reported to occur in 4 to 20% of patients with acute pancreatitis.238243 Mechanisms that may be involved in the pathogenesis of these effusions include direct contact of pancreatic enzymes with the diaphragm (sympathetic effusion) and movement of pancreatic ascites through diaphragmatic defects into the pleural space.238,241243 This explains why the majority of pleural effusions in acute pancreatitis are small and have a predilection for the left pleural space. However, the effusion may be isolated to the right side (30%) or be bilateral (10%).239 Most patients present with abdominal symptoms and a pleural to serum amylase ratio > 1 (usual PF/serum ratio, 5 to 10:1).

No specific treatment is necessary for the pleural effusions of acute pancreatitis, as they tend to resolve as the pancreatic inflammation subsides. Most effusions will clear within 2 weeks,160,164 and none are present after 2 months.243 Thoracentesis should not be performed unless the patient presents with fever or if effusions do not show regression by 3 weeks. In these cases, pancreatic abscess and pseudocyst need to be excluded.

Chronic Pancreatitis

Chronic pancreatic pleural effusion is less common than effusion from acute pancreatitis, but it appears that this entity is more common than previously appreciated. By 1990, only 96 cases had been reported245in the English-language literature; however, a large series246 from Japan reported 114 cases.

A pancreatic pleural effusion, associated with a pancreaticopleural fistula, is defined as massive fluid accumulation in the thorax with an extremely high amylase content, often in the ten of thousands of international units per liter, and albumin concentration > 3 g/dL, resulting from a disrupted pancreatic duct. Most patients are male, and> 90% have alcohol-induced pancreatic disease.245246 Although pancreatic pleural effusions are caused by pancreatitis, these patients usually do not present with abdominal symptoms. The majority complain of dyspnea and chest pain because of the massive effusion.246247

Initial therapy should be nonoperative, consisting of decreasing pancreatic secretion and promoting serosal apposition. GI rest, nasogastric suction, total parenteral nutrition, and paracentesis and thoracentesis should be done. This medical therapy is successful approximately 50% of the time. Resolution of these effusions range from 9 days to 2 months, with most clearing by 2 to 3 weeks.248252 Reports of octreotide administration have shown that surgical intervention can be avoided in severely ill patients by promoting resolution of the effusions in 3 to 4 weeks.253254 Endoscopic stenting of the disrupted pancreatic duct may also be a promising therapeutic option.255 If recovery does not result within 3 weeks with these therapies, surgical intervention should be considered because of the high rate of complications and mortality. Before surgery, an endoscopic retrograde pancreatogram and abdominal CT should be obtained to better delineate the site of pancreatic disruption and fistulous tract.245246,250,252,256

There are only a few causes of persistent benign pleural effusion. These effusions are because of lymphatic abnormalities or a severe inflammatory process. The lymphatic abnormalities include yellow nail syndrome (YNS),257chylothorax from lymphangioleiomyomatosis258or Noonan’s syndrome, and other causes of lymphangiectasis259260 and trapped lung because of chronic inflammation.

YNS, the triad of yellow, slow-growing nails, lymphedema, and respiratory tract disease, which includes pleural effusion, chronic bronchitis, chronic sinusitis, recurrent pneumonias, or bronchiectasis, results from a paucity of hypoplastic lymphatic vessels.257 The effusion is an exudate that does not have high levels of triglycerides or the presence of chylomicrons. YNS is one of the causes of effusions with > 80% lymphocytes. Other lymphatic abnormalities that can cause a persistent pleural effusion are seen in Noonan’s syndrome,261262 which shares many phenotypic features of Turner’s syndrome, such as short stature, webbed neck, pectus carinatum, and mental retardation. It is distinguished from Turner’s syndrome by having a normal karyotype and frequent cardiovascular anomalies, such as pulmonic stenosis and atrial septal defect. In addition, as many as 20 to 35% of patients with either Turner’s or Noonan’s syndrome have peripheral lymphedema ascribed to hypoplasia or aplasia of the superficial lymphatics. Patients with Noonan’s syndrome also develop abnormalities of the intestinal and pulmonary lymphatics. This pulmonary lymphangiectasia typically presents with chylothorax and lymphangiographic evidence of abnormally dilated and tortuous thoracic lymphatics with occasional absence of the thoracic duct.

A trapped lung occurs when a fibroelastic peel covers all or a portion of the visceral pleura, not allowing the lung to expand to the chest wall. This results in increased intrapleural negative pressure and promotes filling of the space en vacuo until the balance of hydrostatic pressure is restored. Clinically, this results in a variable-sized pleural effusion, depending on the degree of lung trapping, which is borderline between a transudate and an exudate with a low number of mononuclear cells. Causes of trapped lung include inadequately or never-treated empyema, rheumatoid pleurisy, uremic pleuritis, postcardiac surgery, hemothorax, pneumothorax therapy for tuberculosis, and tuberculous pleurisy. Thoracentesis will result in rapid recurrence of the pleural effusion at the prethoracentesis volume. The treatment for patients with significant restriction and symptoms is decortication. Decortication will be effective if the underlying lung parenchyma is normal, regardless when the procedure is performed in relation to the initial insult.

Knowledge of the spontaneous resolution rates of pleural effusions should be of value to the clinician when diagnosis is problematic. With this information, the differential diagnosis can be limited, possibly avoiding unnecessary diagnostic testing, with its inherent morbidity and economic burden. Although the data presented are derived from case series, most of which are retrospective, effusions can be reliably categorized by resolution times (Table 3 ) and, thus, be of clinical value in accepting observation as an appropriate course, pursuing further diagnostic testing, or proceeding with definitive therapy.

Abbreviations: BAPE = benign asbestos pleural effusion; CAP = community-acquired pneumonia; CHF = congestive heart failure; NSAIDS = nonsteroidal anti-inflammatory drugs; PCIS = postcardiac injury syndrome; PF = pleural fluid; RA = rheumatoid arthritis; SLE = systemic lupus erythematosus; YNS = yellow nail syndrome

Table Graphic Jump Location
Table 1. Resolution of Pleural Effusions*

ACE = angiotensin-converting enzyme inhibitor; INH = isoniazid; LMWH = low-molecular-weight heparin; PZA = pyrazinamide; TPN = total parenteral nutrition; unc = uncomplicated; NPO = nothing by mouth.


In 50% of cases.

Table Graphic Jump Location
Table 2. Resolution of Parapneumonic Effusions
Table Graphic Jump Location
Table 3. Pleural Effusion Resolution by Time Interval
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