Figure 32.1. Indications for performing an initial thoracentesis.

    Complications from thoracentesis include pain at the puncture site, cutaneous or internal bleeding, pneumothorax, empyema, and spleen/liver puncture. Pneumothorax may complicate as many as 12–30% of thoracenteses in some series but requires treatment with a chest tube in <5% of cases. The frequency of complications from thoracentesis is lower when a more experienced clinician performs the procedure and when performed with ultrasound guidance. Postprocedure expiratory chest radiographs to exclude pneumothorax are not needed in asymptomatic patients after uncomplicated procedures (single needle pass without aspiration of air). However, postprocedure inspiratory chest radiographs are recommended to establish a new baseline for patients likely to have recurrent symptomatic effusions. Symptomatic reexpansion pulmonary edema complicates only 0.5% of therapeutic thoracenteses and some believe results from removing large volumes (>1.5 liters) of pleural fluid from the chest. Other studies suggest that reexpansion pulmonary edema after thoracentesis does not correlate with the volume of fluid removed, the change in pleural pressures during the procedure, or with patient symptoms in a more recent large series of patients undergoing a therapeutic thoracentesis. Therefore, there are no strong data to support limiting a thoracentesis to 1.5 liters. The consensus is that removing larger volumes of a free flowing pleural effusion should be individualized and is reasonable if there are no other risk factors for pulmonary edema (e.g., pre-procedure vascular volume overload or decompensated congestive heart failure).

Pleural Fluid Analysis

The gross appearance and even odor of pleural fluid can sometimes be very informative; for example, frankly purulent-appearing or putrid-smelling pleural fluid indicates a likely empyema, whereas a milky, opalescent fluid suggests a chylothorax or pseudochylothorax. Grossly bloody fluid may result from trauma, malignancy, postpericardiotomy syndrome, and asbestos-related effusion.

    An initial chemical analysis is critical in distinguishing a pleural transudate from an exudate. Exudates have a protein level of >3 g/dL, and transudates a protein level of <3 g/dL. However, if the patient’s serum protein level is abnormal or the pleural protein level is close to the 3 g/dL cutoff point, using the criteria by Light is recommended. This requires measurement of serum and pleural fluid total protein and lactate dehydrogenase (LDH) levels. Light’s criteria are used for differentiating a transudate from an exudate. The fluid is considered an exudate if any of the following apply:

•  Ratio of pleural fluid to serum total protein >0.5

•  Ratio of pleural fluid to serum LDH >0.6

•  Pleural fluid LDH greater than two-thirds of the upper limits of normal serum value.

Light’s criteria identify nearly all exudates correctly (i.e., very sensitive at detecting exudates), but they misclassify approximately 20% of transudates as exudates (i.e., not specific)—usually in patients on long-term diuretic therapy for CHF, because of the concentration of protein and LDH within the pleural space. Using the criterion of serum minus pleural fluid albumin concentration of ≤1.2 g/dL to classify exudates is more specific than Light’s criteria and often is helpful at identifying a “true transudate” when a pleural effusion was classified as a false exudate by Light’s criteria (see table 32.3 for the sensitivity and specificity of these criteria).

    The pleural fluid, usually only when exudative, can be tested for other chemical markers, cellular analysis, cytologic examination, and microbiologic cultures to help identify its underlying etiology:

•  Differential cell counts on the pleural fluid. Pleural lymphocytosis is common in malignancy and tuberculosis. An eosinophilic pleural effusion is defined as the presence of 10% or more eosinophils in the pleural fluid. The presence of pleural fluid eosinophilia is disappointingly nonspecific and may be found in parapneumonic effusions, tuberculosis, drug-induced pleurisy, benign asbestos pleural effusions, Churg Strauss syndrome (also known as eosinophilic granulomatosis with polyangiitis), pulmonary infarction, parasitic disease, and malignancy. Air or blood in the pleural space can also elicit an eosinophilic response.

•  Cytology. Consideration of a malignant etiology for pleural effusion should prompt cytologic evaluation. Cytology alone has an approximate sensitivity of 60%. If there is clinical suspicion of a malignancy, and if the first pleural fluid cytology specimen is negative, then it should be repeated a second time. Both cell blocks and fluid smears should be prepared for examination and, if the fluid has clotted, it needs to be fixed and sectioned as a histological section. Immunocytochemistry, as an adjunct to cell morphology, is becoming increasingly helpful in distinguishing benign from malignant mesothelial cells and mesothelioma from adenocarcinoma. Epithelial membrane antigen (EMA) is widely used to confirm a cytologic diagnosis of epithelial malignancy. When malignant cells are identified, the glandular markers for CEA, B72.3, and Leu-M1 together with calretinin and cytokeratin 5/6 will often help to distinguish adenocarcinoma from mesothelioma.

•  Pleural fluid amylase. Amylase may be elevated in esophageal rupture (Boerhaave syndrome), pancreatitis, or pancreatic cancer. Amylase isoenzymes can be used to differentiate esophageal rupture (salivary isoenzymes) from a pancreatic source.

•  Pleural fluid glucose. The glucose is characteristically decreased with malignancy, SLE, esophageal rupture, tuberculosis, empyema, and rheumatoid pleuritis. (The lowest glucose concentrations are found in rheumatoid effusions and empyema.)

•  Pleural fluid pH. The pH of the normal pleural fluid is approximately 7.64 because of active transport of bicarbonate into the pleural space. Typically the pH is <7.2 with an empyema and indicates the need for drainage. Urinothorax is the only transudative effusion that can present with a low pleural fluid pH and a physiologically normal serum pH.

•  Pleural fluid Gram staining and culture. The pleural space is normally sterile. The finding of bacteria on Gram stain or culture raises concern for empyema. The yield of mycobacteria on culture of pleural fluid in patients with tuberculous pleurisy is low (approximately 30%). If there is suspicion of tuberculosis, additional analysis can include measurement of pleural fluid adenosine deaminase and interferon-γ (markers for tuberculous pleurisy) and polymerase chain reaction (PCR) for tuberculous DNA (see below).

    If pleural fluid analysis does not reveal the cause of a pleural effusion, additional investigation may be required including sampling of pleural tissue (thoracoscopic biopsy) as reviewed in table 32.4.

CHARACTERISTICS AND MANAGEMENT OF COMMON TRANSUDATIVE AND EXUDATIVE PLEURAL EFFUSIONS

Transudative Effusions

Congestive Heart Failure

    Congestive heart failure (CHF) is the most common cause for a transudative pleural effusion. Over 80% of effusions from CHF are bilateral. Other causes of bilateral pleural effusions are shown in box 32.1. The most likely mechanism is pulmonary venous hypertension. Patients present with clinical features of CHF. The chest radiograph shows cardiomegaly and bilateral effusions of relatively equal size with evidence of vascular congestion. Treatment is directed at the underlying heart failure. Removal of a modest amount of fluid, 500–1000 mL, should be considered in patients who are refractory to medical therapy or are dyspneic because of large effusions. If therapeutic thoracentesis relieves the dyspnea but the effusion cannot be controlled with medical therapy, chemical pleurodesis with doxycycline or talc is a therapeutic consideration.

Box 32.1 CAUSES OF BILATERAL EFFUSIONS

Hepatic Hydrothorax

    Pleural effusions develop in approximately 6% of patients with hepatic cirrhosis. These effusions are usually unilateral and right-sided but may occur on the left (16%) or be bilateral (16%). They may vary in size from small to massive. Large effusions may cause significant dyspnea. Therapy is directed at reducing the ascites with diuretics and sodium restriction. Therapeutic thoracentesis will bring only temporary relief because the ascitic fluid rapidly reaccumulates in the pleural cavity. Chemical pleurodesis may be attempted, but insertion of a chest tube involves risk. Tube thoracostomy may drain both the pleural fluid and the ascites, resulting in severe hypovolemia. If pleurodesis is not successful, thoracoscopy or thoracotomy to repair the diaphragmatic defects may be required to control the patient’s symptoms.

Peritoneal Dialysis

    Pleural effusions are observed in approximately 2% of continuous ambulatory peritoneal dialysis (CAPD) patients. Large, symptomatic effusions can develop within hours of initiating peritoneal dialysis. The dialysate moves from the peritoneal to the pleural cavity across the diaphragm in a manner analogous to the movement of ascitic fluid in the patient with cirrhosis. If this problem is going to occur, it usually develops in the first month after dialysis is initiated. However, it may be a year or more before the effusion develops in some patients. Most effusions are right-sided but left-sided or bilateral effusions do occur. Patients with dialysis-related effusions generally complain of dyspnea, but approximately 25% of the effusions cause no symptoms and are discovered on routine radiographs. Therapy comprises stopping the dialysis and draining the peritoneal fluid. The patient should be switched to hemodialysis. If this is not feasible, chemical pleurodesis should be performed prior to reinstituting CAPD. Small-volume peritoneal dialysis in the semierect position may be attempted while pleurodesis is being performed. The diaphragmatic defect may have to be repaired surgically if pleurodesis is unsuccessful.

Urinothorax

    A urinothorax is a rare cause of a transudative effusion. The pleural effusion is due to the retroperitoneal leakage of urine that enters the pleural space via diaphragmatic lymphatics. It generally develops in association with obstructive uropathy but has been reported in patients with trauma, malignancy, kidney biopsy, and renal transplantation. Patients generally present with complaints related to the urinary tract obstruction. The pleural effusion is suspected because of dyspnea, or it may be asymptomatic and recognized on a routine chest radiograph. The pleural effusion is invariably ipsilateral to the urinary obstruction. Thoracentesis yields fluid that looks and smells like urine. The fluid has the characteristics of a transudate, but the pH may be high or low depending on urine pH; in fact, a urinothorax is the only cause of an acidic transudative effusion with a normal serum pH. The pleural fluid creatinine is always higher than the serum creatinine in a urinothorax. Relief of the urinary obstruction results in prompt resolution of the associated effusion.

Nephrotic Syndrome

    Pleural effusions are frequently present in patients with the nephrotic syndrome. In one study, radiographic evidence of effusions was found in 21% of 52 children with nephrosis. Hypoalbuminemia leads to a decrease in the plasma oncotic pressure, while salt retention produces hypervolemia and increased hydrostatic pressures, thereby favoring the development of transudative effusions. The effusions are bilateral and are frequently infrapulmonary. They are often associated with the presence of peripheral edema. Thoracentesis should be performed whenever an effusion is recognized in a patient with nephrotic syndrome, to confirm that the fluid is a transudate. If an exudate is found, thromboembolism is the most likely cause. These patients suffer from a hypercoagulable state, and venous thrombosis in the legs and at other sites is common. Treatment is directed at the underlying nephropathy. Therapeutic thoracentesis is indicated if there is severe dyspnea. Failure to medically control symptomatic effusions is an indication for chemical pleurodesis.

Exudative Effusions

Parapneumonic Pleural Effusions and Empyema

    Pleural effusions are present in 30–40% of patients with bacterial pneumonia, but the majority are “simple,” meaning they are small, free flowing effusions and fully resolve on antibiotic therapy alone. A minority, however, are complicated by persistent bacterial invasion into the pleural space and can evolve into empyema, defined by visible bacteria on pleural fluid Gram stains or the presence of frank pus on pleural aspiration. Complex pleural effusions and empyema are associated with a 20% mortality rate and with other chronic thoracic complications, including secondary lung abscess, bronchopleural fistulas, empyema necessitans (broncho-pleural-cutaneous fistula), and pleural fibrosis and lung entrapment. Since definitive pleural space drainage in addition to antibiotic therapy can prevent these complications, proper classification of pleural space infections is critical. Table 32.5 summarizes the pleural space anatomic and fluid characteristics that place patients at high risk for complications without definitive pleural drainage.

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