eMedicine Specialties > Emergency Medicine > Pulmonary

Pleural Effusion: Differential Diagnoses & Workup

Author: Fredrick Melik Abrahamian, DO, FACEP, Associate Professor of Medicine, University of California at Los Angeles School of Medicine; Director of Education for Emergency Medicine Residency Program, Consulting Staff, Department of Emergency Medicine, Olive View-University of California at Los Angeles Medical Center
Contributor Information and Disclosures

Updated: Jan 14, 2008

Differential Diagnoses

Other Problems to Be Considered

Transudative pleural effusion

Congestive heart failure (most common transudative effusion)
Hepatic cirrhosis with and without ascites
Nephrotic syndrome
Peritoneal dialysis/continuous ambulatory peritoneal
dialysis
Hypoproteinemia (eg, severe starvation)
Glomerulonephritis
Superior vena cava obstruction
Fontan procedure
Urinothorax

Exudative pleural effusion

Malignant disorders - Metastatic disease to the pleura or lungs, primary lung cancer, mesothelioma, Kaposi sarcoma, lymphoma, leukemia

Infectious diseases - Bacterial, fungal, parasitic, and viral infections; infection with atypical organisms such as Mycoplasma, Rickettsiae, Chlamydia, Legionella

GI diseases and conditions - Pancreatic disease (acute or chronic disease, pseudocyst, pancreatic abscess), Whipple disease, intraabdominal abscess (eg, subphrenic, intrasplenic, intrahepatic), esophageal perforation (spontaneous/iatrogenic), abdominal surgery, diaphragmatic hernia, endoscopic variceal sclerotherapy

Collagen vascular diseases - Rheumatoid arthritis, systemic lupus erythematosus, drug-induced lupus syndrome (procainamide, hydralazine, quinidine, isoniazid, phenytoin, tetracycline, penicillin, chlorpromazine), immunoblastic lymphadenopathy (angioimmunoblastic lymphadenopathy), Sjögren syndrome, familial Mediterranean fever, Churg-Strauss syndrome, Wegener granulomatosis

Benign asbestos effusion

Meigs syndrome - Benign solid ovarian neoplasm associated with ascites and pleural effusion

Drug-induced primary pleural disease - Nitrofurantoin, dantrolene, methysergide, bromocriptine, amiodarone, procarbazine, methotrexate, ergonovine, ergotamine, oxprenolol, maleate, practolol, minoxidil, bleomycin, interleukin-2, propylthiouracil, isotretinoin, metronidazole, mitomycin

Injury after cardiac surgery (Dressler syndrome) - Injury reported after cardiac surgery, pacemaker implantation, myocardial infarction, blunt chest trauma, angioplasty

Uremic pleuritis

Yellow nail syndrome

Ruptured ectopic pregnancy

Electrical burns

Conditions causing pleural fluid with exudative or transudative characteristics

Pulmonary embolism
Hypothyroidism
Diuresed transudate
Pericardial disease (inflammatory or constrictive)
Atelectasis
Trapped lung (usually a borderline exudate)
Sarcoidosis (usually an exudate)
Amyloidosis

Miscellaneous conditions

Hemothorax

Following coronary artery bypass graft surgery

After lung or liver transplant

Milk of calcium pleural effusion - Colloidal suspension of precipitated calcium salts

Acute respiratory distress syndrome

Systemic cholesterol emboli

Iatrogenic misplacement of lines or tubes into the mediastinum or the pleural space - Insertion or reinsertion of percutaneous central venous catheter, infusion of enteral formula through misplaced nasogastric or nasoenteric feeding tubes, translumbar aortography

Radiation pleuritis

Necrotizing sarcoid granulomatosis

Ovarian hyperstimulation syndrome

Postpartum pleural effusion (immediate or delayed)

Rupture of a silicone bag mammary prosthesis

Rupture of a benign germ cell tumor into the pleural space (eg, benign mediastinal teratoma)

Syphilis

Echinococcosis

Workup

Laboratory Studies

• The initial step in analyzing pleural fluid is to determine whether the effusion is a transudate or an exudate. For the purpose, the following Light criteria are most accurate: Pleural fluid is exudative if one or more of the following conditions is met; it is transudative if none are met: ratio of pleural fluid and serum protein levels is greater than 0.5, ratio of pleural fluid and serum LDH levels is greater than 0.6, and pleural fluid LDH level is more than two thirds of the upper limit for serum LDH levels.
• The criteria are less accurate for transudates caused by congestive heart failure, especially in patients who have undergone diuresis. The longer diuretic therapy lasts, the more likely the fluid will have exudative characteristics. Diuretic therapy less than 48 hours rarely changes the characteristics of pleural fluid to those of exudative effusion. If the criteria are not satisfied despite of high suspicion that congestive heart failure is the cause of the pleural effusion, examine the serum-to–pleural fluid albumin gradient (serum level minus pleural fluid level). A gradient of less than 1.2 g/dL indicates exudative effusion; one greater than 1.2 g/dL, transudative effusion.
• The clinical presentation should direct the biochemical and microbiological studies of pleural fluid. The minimal amount of pleural fluid needed for basic diagnostic purposes is 20 mL; if possible, 60 mL should be obtained for potential diagnostic studies.
  • If the clinical presentation is highly suggestive of transudative effusion, protein and LDH levels should be determined initially. If the patient has undergone diuretic therapy, the pleural albumin level should be determined simultaneously. Concomitant serum total protein; LDH; and, if indicated, serum albumin levels should be measured. If transudative effusion is diagnosed, no further tests are needed.
  • Exudative effusions require further laboratory investigation. In the ED, the pleural fluid should be analyzed for the following:
    • Cell count with differential
    • Total protein level
    • Glucose level
    • LDH level
    • Amylase level
    • pH
    • Cytologic analysis (strongly recommended for patients with history of undiagnosed exudative effusions, suspected malignancy or Pneumocystis carinii infection, or exudative effusions with normal fluid glucose and amylase levels)
    • In the appropriate clinical setting the following may be helpful: Gram staining, acid-fast bacilli staining, fungal (KOH) staining, culturing and sensitivity testing for aerobic and anaerobic organisms and fungi
    • Blood culturing (2 tests, preferably from different sites and one-half hour apart)
    • Determinations of serum total protein, glucose, LDH, and amylase levels; determination of arterial pH (especially if acidemia is suspected)
• Additional studies should be requested on the basis of the gross appearance of the pleural fluid or when a specific condition is suspected.
  • When chylothorax or pseudochylothorax is suspected or when pleural fluid has a distinctive white, turbid, and milky appearance (especially if the supernatant of the pleural fluid remains opaque after centrifugation), assess triglyceride and cholesterol levels and total lipid content, and microscopically examine the sediment. The diagnosis of chylothorax is made by means of lipoprotein analysis, which demonstrates chylomicrons in the pleural fluid.
  • Centrifugation should be performed if the pleural fluid is turbid, milky, bloody, or brown. If the supernatant remains turbid, the triglyceride level should be determined and other lipid studies should be performed. Straw-colored pleural effusion with an ammonia (urine) odor suggests urinothorax; serum and pleural fluid creatinine levels should be determined. A ratio of pleural fluid to serum creatinine level of more than 1 confirms urinothorax.
  • Blood-tinged pleural fluid has no diagnostic value, since a small amount of blood can change a serous effusion into a serosanguineous one. Serum and pleural hematocrit should be assessed with any grossly bloody effusion. If the pleural fluid hematocrit level is higher than 50% of the serum hematocrit level, a hemothorax is present. The following findings suggest traumatic thoracentesis: nonuniform red discoloration of fluid during aspiration, clotting of the fluid within minutes (presence of platelets), and absence of hemosiderin-laden macrophages.
  • Immunologic studies of the pleural fluid, such as evaluation of the rheumatoid factor titer and antinuclear antibody level, are the most useful tests for suspected rheumatoid and lupus pleuritis, respectively. Additional tests of the pleural fluid, such as amylase isoenzyme determination or immunohistochemical studies, can be performed. The pulmonologist almost always orders these tests after the initial evaluation of the pleural fluid is completed, but they have no role in the ED treatment of patients with pleural effusions.
  • The containers necessary for pleural fluid tests are listed in Table 1.
    Table 1. Containers for Pleural Fluid Collection

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    Table

    Container	Primary Study
    Plain red-top tube	Determination of protein, LDH, amylase, and glucose levels (if needed, determine triglyceride cholesterol level)
    Ethylenediaminetetraacetic acid–treated, lavender-top tube	Cell count and differential
    Heparin-treated blood gas syringe	Determination of pH
    Sterile container	Gram staining and culturing (for aerobic and anaerobic organisms, mycobacteria, fungi)
    50-mL heparin-treated container (eg, 5 green-top tubes)	Cytologic analysis

    Container	Primary Study
    Plain red-top tube	Determination of protein, LDH, amylase, and glucose levels (if needed, determine triglyceride cholesterol level)
    Ethylenediaminetetraacetic acid–treated, lavender-top tube	Cell count and differential
    Heparin-treated blood gas syringe	Determination of pH
    Sterile container	Gram staining and culturing (for aerobic and anaerobic organisms, mycobacteria, fungi)
    50-mL heparin-treated container (eg, 5 green-top tubes)	Cytologic analysis

• The gross appearance of the pleural fluid, as well as results of certain laboratory studies, may provide useful diagnostic information. The color, turbidity, viscosity, and odor are essential characteristics of any fluid. Table 2 lists the clinical significance of the gross characteristics of pleural fluid.
  Table 2. Clinical Significance of Pleural Fluid Characteristics

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  Table

  Characteristic	Significance
  Bloody	Most likely an indication of malignancy in the absence of trauma; can also indicate pulmonary embolism, infection, pancreatitis, tuberculosis, mesothelioma, or spontaneous pneumothorax
  Turbid	Possible increased cellular content or lipid content
  Yellow or whitish, turbid	Presence of chyle, cholesterol or empyema
  Brown (similar to chocolate sauce or anchovy paste)	Rupture of amebic liver abscess into the pleural space (amebiasis with a hepatopleural fistula)
  Black	Aspergillus involvement of pleura
  Yellow-green with debris	Rheumatoid pleurisy
  Highly viscous	Malignant mesothelioma (due to increased levels of hyaluronic acid) long-standing pyothorax
  Putrid odor	Anaerobic infection of pleural space
  Ammonia odor	Urinothorax
  Purulent	Empyema
  Yellow and thick, with metallic (stainlike) sheen	Effusions rich in cholesterol (longstanding chyliform effusion, eg, tuberculous or rheumatoid pleuritis)

  Characteristic	Significance
  Bloody	Most likely an indication of malignancy in the absence of trauma; can also indicate pulmonary embolism, infection, pancreatitis, tuberculosis, mesothelioma, or spontaneous pneumothorax
  Turbid	Possible increased cellular content or lipid content
  Yellow or whitish, turbid	Presence of chyle, cholesterol or empyema
  Brown (similar to chocolate sauce or anchovy paste)	Rupture of amebic liver abscess into the pleural space (amebiasis with a hepatopleural fistula)
  Black	Aspergillus involvement of pleura
  Yellow-green with debris	Rheumatoid pleurisy
  Highly viscous	Malignant mesothelioma (due to increased levels of hyaluronic acid) long-standing pyothorax
  Putrid odor	Anaerobic infection of pleural space
  Ammonia odor	Urinothorax
  Purulent	Empyema
  Yellow and thick, with metallic (stainlike) sheen	Effusions rich in cholesterol (longstanding chyliform effusion, eg, tuberculous or rheumatoid pleuritis)

• Laboratory results can aid in narrowing the differential diagnosis of exudative pleural effusions. Diagnosis requires an integrative approach involving laboratory and clinical findings. Common laboratory studies of the following may indicate the diagnosis:
  • Amylase: An elevated pleural fluid amylase level is one greater than the upper limit for serum levels or one that results in a pleural fluid–to–serum amylase ratio of more than 1. Pleural fluid amylase levels can be elevated in acute pancreatitis, pancreatic pseudocyst, esophageal rupture, malignancy, and ruptured ectopic pregnancy. Among these, pancreatic pseudocyst has the highest amylase levels (frequently >100,000 U). Determination of the amylase isoenzyme level is useful in distinguishing effusions caused by pancreatic disease (pancreatic isoamylase) from effusions caused by esophageal rupture or nonpancreatic carcinoma (salivary isoamylase).
  • Glucose: A low pleural fluid glucose level is one less than 60 m/dL. The differential diagnosis includes TB, malignancy, rheumatoid pleurisy, complicated parapneumonic effusion, empyema, hemothorax, paragonimiasis, Churg-Strauss syndrome, and occasionally, lupus pleuritis.
  • pH: Pleural fluid pH of less than 7.20 suggests empyema, complicated parapneumonic effusion, esophageal rupture, rheumatoid pleuritis, malignancy, paragonimiasis, hemothorax, tuberculous pleuritis, lupus pleuritis, or urinothorax. Arterial pH influences pleural fluid pH; therefore, acidemia must be ruled out before any of the above causes are considered. With parapneumonic effusions, indications for tube thoracostomy include a pH less than 7.0, glucose level less than 40 m/dL and positive finding with Gram stains or cultures. To use the pH criteria for chest tube placement in systemic acidosis, the pleural fluid pH should be at least 0.30 units less than the arterial pH. Check for possible laboratory errors in measuring pleural fluid pH.
    • Pleural fluid has a low pH, low glucose level, and a high LDH level. Suspect laboratory error when this pattern is not present.
    • Also, determine the pleural fluid pCO₂. A low pleural fluid pH almost always is associated with a high pCO₂.
  • LDH: The LDH level is an indicator of the degree of pleural inflammation. The higher the value, the more inflamed the pleural surface. High concentrations (>1000 IU/L) occur with complicated parapneumonic effusions and paragonimiasis. Rheumatoid pleuritis is associated with moderately high (>700 IU/L) LDH levels.
  • RBC and total WBC counts: RBC counts or more than 100,000 per cubic millimeter suggest trauma, malignancy, pulmonary embolism, injury after cardiac surgery, asbestos pleurisy, esophageal rupture, pancreatitis, tuberculous pleurisy, and catamenial hemothorax (thoracic endometriosis). The total pleural fluid leukocyte count is virtually never diagnostic. Counts exceeding 10,000 per cubic millimeter are most common with parapneumonic effusions; however, other inflammatory diseases are another cause.
  • Neutrophil, eosinophil, and basophil counts: Neutrophilic predominance indicates an acute inflammatory process near the time of thoracentesis. Significant eosinophilia occurs when the ratio of pleural fluid and total pleural fluid counts is more than 10%; the most common cause is air or blood in the pleural space.
  • The differential diagnosis of pleural fluid eosinophilia includes pneumothorax, hemothorax, pulmonary infarction, prior thoracentesis, benign asbestos effusion, drug use (eg, dantrolene, bromocriptine, nitrofurantoin), parasitic diseases (eg, paragonimiasis, hydatid disease, amebiasis, ascariasis), fungal infections (eg, histoplasmosis, coccidioidomycosis), and Churg-Strauss syndrome; in the absence of these, eosinophilia with pneumonia and pleural effusion is a good prognostic sign, because such effusions rarely become infected. Eosinophilia with tuberculous pleurisy or malignancy is rare. Pleural fluid eosinophilia commonly indicates benign disease and a favorable prognosis when it is present in malignant effusions. Significant basophilia (counts >10%) is distinctly uncommon; however, if present, it suggests leukemic pleural infiltration.
  • Lymphocyte count: Lymphocytes indicate a long-standing chronic effusion. Pleural fluid lymphocytosis (>50%) suggests malignant disease, particularly lymphoma or TB; however, other conditions (eg, chronic rheumatoid pleurisy, chronic fungal infection, yellow nail syndrome, chylothorax, trapped lung, benign asbestos pleural effusion, sarcoidosis) must be considered. The presence of an undiagnosed exudative effusion with lymphocytosis is an indication for closed pleural biopsy. Pleural fluid WBC differential findings may reveal neutrophilic predominance in patients with tuberculous pleuritis and symptoms lasting longer than 2 weeks. If serial thoracenteses are performed, the WBC differential reveals a change to lymphocytic predominance.
  • Mesothelial cell count: These cells line the pleural cavities, and their absence simply indicates diffuse pleural injury or fibrosis. Diffuse fibrosis inhibits exfoliation of mesothelial cells into the pleural space. Mesothelial cells are uncommon in tuberculous effusion, except perhaps at the onset of the disease. The finding of more than 5% mesothelial cells in an exudative effusion virtually excludes the tuberculous pleurisy. These cells predominate in transudative effusions. The absence of mesothelial cells also is common in conditions in which the pleurae become coated with fibrin (eg, complicated parapneumonic effusion, chronic rheumatoid pleurisy, chronic malignant effusions). Mesothelial cells, particularly in their activated form, may be confused with malignant cells. Because of their similarity, clinical correlation, evaluation by an experienced pathologist, and further diagnostic studies (such as immunohistochemical tests) are often necessary to make the distinction.
  • Plasma cell and macrophage counts: A large number of plasma cells in the pleural fluid suggests multiple myeloma with pleural involvement. A small number of plasma cells is of no particular diagnostic value. The presence of macrophages has no diagnostic value. A large number of macrophages leads to localized pleural space fibrosis (eg, pleural plaques, granulomas), whereas a small number of macrophages is associated with widespread fibrosis.

Imaging Studies

• After the initial stabilization of the patient, the evaluation of pleural effusion in the ED begins with confirming the presence and then the location of the effusion. This step is the most important in the evaluation of a pleural effusion. Common imaging studies used to confirm pleural effusion are chest radiography, ultrasonography, and CT scan.
• Chest radiography is the primary diagnostic tool because of its availability, accuracy, and low cost. Chest radiographs can be used to determine the cause of the effusion (eg, enlarged cardiac silhouette, underlying lung, parenchymal disease). The most common radiologic appearance is blunting of the costophrenic angle and/or sulci (sharp angle between the diaphragm and rib cage). As fluid accumulates, blunting becomes more pronounced, and an upwardly concave meniscus seems to ascend the lateral chest wall; this is called the meniscus sign. Clues indicating pleural effusion include generalized homogenous opacity and diffuse haziness as the fluid forms layers posteriorly (ground-glass appearance), visibility of pulmonary vessels through the haziness, and an absence of air bronchogram.
  • Upright posteroanterior or anteroposterior radiographs may not show lateral costophrenic angle blunting until 250-500 mL of fluid is present. Haziness is less apparent as it progresses cephalad. Lateral radiographs show blunting of the posterior costophrenic angle and the posterior gutter when as little as 175-200 mL of fluid is present. Bilateral decubitus radiographs are recommended, especially with larger effusions. They provide clues to exclude a loculated effusion and underlying pulmonary lesion or pulmonary thickening and can depict as little as 5-10 mL of fluid. Recumbent (supine views) usually are obtained in critically ill patients. Findings may include costophrenic angle blunting (earliest finding), generalized homogenous opacity, obliteration of the diaphragmatic silhouette, decreased visibility of the lower-lobe vasculature, widened minor fissure, apical capping, and hemidiaphragmatic elevation.
  • Bilateral effusions with enlarged cardiac silhouette most likely are caused by congestive heart failure. In absence of cardiomegaly, malignancy (either carcinoma or lymphoma) is the most common cause of bilateral effusions; however, in this setting, differential diagnoses that must be considered include lupus pleuritis, rheumatoid pleurisy, nephrotic syndrome, cirrhosis with ascites, pulmonary embolism, TB, esophageal rupture, benign asbestos pleural effusion, Meigs syndrome, uremic pleuritis, yellow nail syndrome, and effects of medications.
  • Malignant effusions usually are medium to large (500-2000 mL); however, 10% are less than 500 mL, and another 10% occur with massive effusions in which the hemithorax is completely opacified. The most common cause of massive pleural effusion is malignancy (70%). Other conditions that must be considered with massive pleural effusions include congestive heart failure, TB, hepatic cirrhosis with ascites, transdiaphragmatic rupture of a liver abscess into the pleural space (>90% right sided), paragonimiasis (usually unilateral), peritoneal dialysis or continuous ambulatory peritoneal dialysis (CAPD) (90% right sided), cryptococcosis, pancreatic pseudocyst, chronic pancreatitis, Meigs syndrome, uremic pleuritis, yellow nail syndrome, and effects of medications.
  • Massive effusions usually have an accompanying mediastinal shift to the contralateral side of the pleural effusion. However, when a massive effusion exists without a this shift (midline mediastinum or mediastinum shift toward the side of the effusion), the differential diagnosis is narrowed to carcinoma of the ipsilateral mainstem bronchus with or without ipsilateral lung atelectasis, fixed mediastinum caused by fibrosis or tumor infiltration of mediastinal lymph nodes, tumor infiltration of the ipsilateral lung, malignant mesothelioma, or complete atelectasis of the ipsilateral lung.
  • The location of the pleural effusion can help in differential diagnosis.
    • Isolated right-sided pleural effusions commonly occur with cirrhosis, peritoneal dialysis (CAPD), subphrenic or intrahepatic abscess, amebic liver abscess, Echinococcosis infection, liver transplantation, Meigs syndrome, or catamenial hemothorax (thoracic endometriosis).
    • Isolated left-sided effusions occur with esophageal rupture, pancreatic disease, subphrenic or splenic abscess, splenic infarction, diaphragmatic hernia, pericardial disease, or coronary artery bypass surgery.
    • With exception of lung and breast cancer, most pleural effusions associated with malignancies are bilateral, and no ipsilateral predilection is present. Primary lung carcinoma most commonly occurs with unilateral pleural effusion ipsilateral to the primary lesion. Pleural effusions associated with breast carcinoma typically are ipsilateral to the primary breast cancer (58-70%); however, 20-26% develop effusions contralateral to the primary lesion, and 10-16% develop bilateral effusion.
• Atypical chest radiographic presentations are possible.
  • Subpulmonic (infrapulmonary) effusions are fluid collections between the inferior pulmonary margin and superior diaphragmatic margin that usually occur with nephrotic syndrome.
  • Posteroanterior radiographs may depict the following:
    • Flattening of the medial diaphragmatic aspect, with gradual upward and lateral inclination from the cardiac shadow; lateral displacement of the diaphragmatic dome apex (middle or inner hemithoracic third to lateral third)
    • Change of the normal, domelike diaphragmatic curve to a hockey-stick shape
    • Sharp diaphragmatic sloping toward the lateral costophrenic angle
    • Hemidiaphragm elevation
    • Increased distance (>2.0 cm) between the gastric fundus air bubble and superior right hemidiaphragmatic margin
    • Absence of lower-lobe vessels normally present below the diaphragm.
  • Lateral radiographs may depict sharp angulation of the anterior diaphragmatic portion (ie, Rock of Gibraltar or middle-lobe step sign).
  • If pleural adhesions are absent, subpulmonary effusion can be confirmed and quantified with lateral decubitus images, which show free infrapulmonary fluid moving from the top of the diaphragm to the dependent chest wall and layering along the lateral chest wall.
  • Pseudotumors represent an accumulation of fluid between interlobar fissures or fluid encapsulated by adhesions. They most commonly occur in the minor fissure and usually occur in patients with congestive heart failure.
  • Diaphragmatic inversion because of the weight of the pleural effusion on the left side. The superior border of the diaphragm become upwardly concave, and paradoxical movement occurs with respiration; the diaphragm rises with respiration and falls with expiration. When the pleural fluid is removed, the diaphragm assumes its normal shape.
  • When an air-fluid level is present in the pleural space, the following must be considered: bronchopleural fistula, pneumothorax, trauma, presence of gas-forming organisms, diaphragmatic hernia, fluid-filled bullae or lung cysts, and rupture of the esophagus into the pleural space. Diaphragmatic hernias can be excluded or confirmed with the administration of GI contrast material.
• Ultrasonography can be used to detect as little as 5-50 mL of pleural fluid, with 100% sensitivity for effusions of 100 mL or more.
  • It aids in the identification of loculated effusions and the differentiation of pleural fluid from pleural fibrosis, thickening, and parenchymal consolidation.
  • It can help localize the diaphragm if pleural or parenchymal disease obscures it. Its major role to provide imaging guidance for identifying a site thoracentesis, pleural biopsy, or pleural drainage (eg, chest tube placement) and to decrease the risk of complications from such procedures.
  • It may aid characterizing the pleural fluid and the exudative nature of the effusion with pleural thickening, loculations, or complicated echogenic patterns. (However, anechoic effusions may be either exudative or transudative.)
  • Unlike CT, ultrasonography is rapid and available bedside.
• Chest CT scanning (including use of lung windows views) permits imaging of the entire pleural space, pulmonary parenchyma, and mediastinum simultaneously.
  • CT scans reveal early-stage pleural abnormalities, and contrast-enhanced scans can depict multiple loculations and localizing effusions; differentiate between lung consolidation versus pleural effusion; cystic lesions versus solid lesions; of necrotic areas; pleural thickening, nodules, masses, or rounded atelectasis; and peripheral lung abscess versus loculated empyema, and tumoral extent.
  • Scans can help in identifying benign or malignant pleural involvement. One or more of the following indicates malignancy (sensitivity, 72%; specificity, 83%): circumferential pleural thickening, nodular pleural thickening, parietal pleural thickening (>1.0 cm), and mediastinal pleural involvement.
  • CT scans are highly sensitive for discrete pleural plaques, but rarely is helpful in differentiating transudates, exudates, and chylous pleural effusions.
• Other imaging studies include MRI and nuclear scanning. MRI has a somewhat limited role, with even less value in the ED workup. It is the imaging modality of choice in evaluating superior sulcus tumors, and it is superior to CT scan in depicting tumor extension to the chest wall, brachial plexus, subclavian vessels, vertebral bodies, and spinal canal. Nuclear scanning with gallium-labeled or indium-labeled leukocytes occasionally is used to rule out infection in lung parenchyma or pleural fluid.

Other Tests

• Contrast material–enhanced study of the esophagus
  • Esophageal perforation is a medical emergency that requires rapid diagnosis and treatment.
  • When this condition is suspected, contrast-enhanced studies of the esophagus should be performed with the patient in the lateral decubitus position.
  • The contrast agent of choice should be water soluble; an example is Hexabrix (meglumine and sodium ioxaglate). Although Gastrografin is water-soluble, its use is not recommended because it causes marked bronchospasm when it is aspirated.
  • Because of a high percentage of false-negative findings when water-soluble agents are used, a barium sulfate esophagogram should be obtained after a negative finding. Barium is not used initially because it is not absorbed once it leaks into the mediastinum or pleura. It also elicits a marked inflammatory reaction in the pleura, resulting in subsequent fibrosis and granuloma formation.
  • Upon confirmation of the diagnosis, immediate surgical consultation is needed.
• Ventilation-perfusion scanning
  • Pulmonary embolization should be considered in every patient with a pleural effusion.
  • Obtain a perfusion lung scan when the origin of the effusion is not apparent after initial diagnostic thoracentesis.
  • Also, obtain a lung scan in all patients with nephrotic syndrome and pleural effusion, especially those with unilateral pleural effusion, bilateral effusions of unequal sizes, and renal vein thrombosis.
  • Strongly consider lung scanning in patients with unilateral pleuritic chest pain ipsilateral to the pleural effusion, patients with no preexisting cardiac or pulmonary disease who have dyspnea (out of proportion to the size of the effusion) and tachypnea, and patients with known congestive heart failure and pleuritic chest pain.
  • Lung scans are difficult to interpret in the presence of pleural effusion. Therefore, therapeutic thoracentesis often is indicated prior to lung scanning. Consequently, early pulmonary consultation is indicated when this diagnosis is being considered.

Procedures

• After the presence of a pleural effusion is established, the cause should be identified. This step can be critical in evaluating pleural effusions because unnecessary invasive procedures cause morbidity and mortality. When a decision is made to investigate the cause of the pleural effusion, thoracentesis is the first-line invasive diagnostic procedure. Thoracentesis also can be used as a therapeutic modality. Chest tubes serve a solely therapeutic role. They are used for evacuating air or fluid from the pleural space and for administering fibrinolytic (eg, urokinase, streptokinase) or sclerosing agents (eg, doxycycline, bleomycin, talc, minocycline). Other procedures used to diagnosis the cause of a pleural effusion include percutaneous pleural biopsy, thoracoscopy, and open pleural biopsy. However, of all these procedures, thoracentesis and chest tube placement usually suffice for evaluation or treatment of pleural effusions in the ED. Ancillary procedures (eg, bronchoscopy, perfusion lung scanning, pulmonary arteriography) can complement the other invasive procedures.
• Thoracentesis
  • Thoracentesis is the least invasive procedure, and it is relatively safe.
  • For stable and asymptomatic patients in whom effusion most likely is caused by viral pleurisy, manifestation of a systemic disease (eg, congestive heart failure, renal disease, hepatic cirrhosis), thoracic or abdominal surgery, or childbearing, thoracentesis may not be indicated, or it can be deferred. In this situation, therapy for the specific cause should be initiated, and if no improvement occurs after a few days, diagnostic thoracentesis should be performed.
  • Thoracentesis is also indicated in cases in which the specific cause of the effusion is unknown or has never been investigated or when the thickness of the free pleural fluid level is more 10 mm on the lateral decubitus radiograph. In addition, thoracentesis is indicated if the patient has respiratory compromise, hemodynamic instability, or massive effusion with contralateral mediastinal shift.
  • For massive effusions with a midline mediastinum or ipsilateral mediastinal shift, consultation with a pulmonologist is indicated prior to any intervention. In patients with massive effusions, bronchoscopy, rather than thoracentesis, is the initial diagnostic procedure. If more than 1000 mL of fluid is removed, pleural pressures must be monitored. Measurements of pleural pressures with the aspiration of large amounts of fluid not only increase the safety of procedure, but they also aid diagnosis. Negative initial pleural pressures and/or rapid changes in the pressure as fluid is withdrawn can suggest malignancy or a trapped lung.
  • Diagnostic thoracentesis is indicated for patients with obvious or known congestive heart failure if any of the following conditions are present: fever, unequal effusions, pleuritic chest pain, unilateral pleural effusion, or absence of cardiomegaly.
  • If a stable patient has undergone prior thoracentesis and the cause remains unknown, a specialist should perform further thoracentesis, since an indication for closed pleural biopsy or other invasive procedures might exist. If pleural fluid is removed without recognition of the need for pleural biopsy, subsequent biopsy can become difficult and unsafe. Malignancy is strongly suggested in chronic exudative effusions in which the cause remains undiagnosed despite several thoracenteses and one or more closed pleural biopsies.
  • A pulmonologist should aspirate difficult pleural taps, such as small loculated effusions or loculated anterior effusions.
  • If a ruptured diaphragm is suspected ipsilateral to the pleural effusion, thoracentesis should be performed under fluoroscopic or ultrasonic guidance.
  • Thoracentesis safely can be performed in patients receiving mechanical ventilation, even positive pressure ventilation.
  • No absolute contraindications to thoracentesis exist. If the thickness of the free pleural fluid level (distance between the inner border of the chest wall and outer border of the lung) is less than 10 mm on a lateral decubitus radiograph, thoracentesis is not considered safe. These small effusions usually resolve without specific drainage procedures. Relative contraindications include predisposition to hemorrhage (particularly if the prothrombin time [PT] or activated partial thromboplastin time [aPTT] is 2 times the normal value), iatrogenic systemic anticoagulation (particularly with thrombolytic agents), cutaneous disease (eg, herpes zoster infection or pyoderma at the needle entry site), and uncooperative patients.
  • After thoracentesis (regardless of its success), chest radiography is recommended to rule out a subsequent pneumothorax. Pneumothorax is the most common complication and is operator dependent. Its incidence is 3-20% with unguided thoracentesis and 2-7% with ultrasonographic guidance. Therapeutic thoracentesis has a high incidence of pneumothorax, and a chest radiograph should be obtained after the procedure.
  • Other complications include subcutaneous hematoma, infection of the pleural space or soft tissue overlying the thoracentesis site, pain at the site, cough, chest pain, hemothorax, vasovagal reflex, reexpansion (unilateral) pulmonary edema, hypovolemia, hypoxemia, splenic or hepatic laceration, hemoperitoneum, and adverse reactions to the local anesthetic. The risk of complications decreases if careful attention is given to the use of sterile technique, slow removal of less than 1 L of fluid at a time, and proper anesthetization of the patient.
    • Consider reexpansion pulmonary edema in patients with large pneumothoraces or large pleural effusions lasting at least 3 days who are undergoing tube thoracostomy or thoracentesis. The condition is serious and possibly fatal. Pulmonary edema commonly develops in the reexpanding ipsilateral lung. It occurs with the drainage of large amounts (>1000 mL) of pleural fluid when pleural pressures are not monitored and with abnormally negative (below negative 20 cm H₂ O) pleural pressures.
    • Hypoxemia is a common complication and can persist for several hours after the procedure. All patients (certainly those with severe cardiopulmonary disease) should receive oxygen by means of nasal cannula during thoracentesis and for several hours afterwards.
  • Indications for removal of the thoracentesis needle during the procedure include aspiration of air, development of cough, dyspnea, chest pain, and ipsilateral shoulder pain. Referred ipsilateral shoulder pain can indicate injury to the diaphragm. The risk of injuring the diaphragm, spleen, or liver increases when thoracentesis is performed in or below 10th intercostal space.
  • Universal precautions regarding the handling bodily fluids apply to pleural fluid. Proper disposal of needles is essential.
• Tube thoracostomy
  • Definite indications include empyema (presence of pus in the pleural space); hemothorax; large pneumothorax; and parapneumonic effusion with a positive finding with Gram staining of pleural fluid, pH less than 7.0, or a glucose level less than 40 m/dL. A chest tube also might be indicated for parapneumonic effusion with a pH between 7.00 and 7.20 or an LDH level above 1000 IU/L. Patients with these findings should be admitted, and a pulmonologist should decide if chest tube placement is required. A chylothorax can be managed with a chest tube, although placement of a pleuroperitoneal shunt is preferred because it prevents malnourishment and immunologic compromise.
  • Malignant tumors obstructing a mainstem or lobar bronchus are a contraindication for chest tube placement, because the obstruction prevents expansion of the lung underlying the effusion.
  • When chest tubes are inserted in the ED for the treatment of a spontaneous pneumothorax, they initially should be connected to an underwater-seal drainage apparatus or a Heimlich valve rather than to a suction device. Suction can create negative pleural pressures and increase the risk of reexpansion pulmonary edema. A pulmonologist should be consulted when change to a suction device is considered.

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