Pleural effusions arise by two mechanisms in association with amebic liver abscess. The first occurs when an amebic abscess produces diaphragmatic irritation and a sympathetic pleural effusion in a manner analogous to that seen with pyogenic liver abscesses (3,4) (see Chapter 18). Amebic liver abscesses also produce pleural effusions when the abscess ruptures through the diaphragm into the pleural space (3,4). In this situation, the pleural fluid is described as “chocolate sauce” or “anchovy paste” (1). Such pleural fluid does not contain purulent material but is rather a mixture of blood, cytolyzed liver tissue, and small solid particles of liver parenchyma that have resisted dissolution.

The sympathetic effusion seen with amebic liver abscess is more common than rupture of an abscess through the diaphragm into the pleural space (2,3,5). Approximately 20% to 35% of patients with an amebic liver abscess will have a sympathetic pleural effusion (2). Patients with the sympathetic effusion frequently experience pleuritic chest pain referred to the tip of the scapula or the shoulder. Most patients have a tender enlarged liver (6). Eosinophilia is not associated with extraintestinal amebiasis. The level of alkaline phosphatase is elevated in more than 75% of patients, whereas the levels of transaminases are elevated in 50% (1). The chest radiograph reveals a pleural effusion of small-to-moderate size, often with a concomitant elevation of the hemidiaphragm and plate-like atelectasis at the base (2,3,4). The pleural fluid in this situation has not been well characterized, but is an exudate (2,5).

The diagnosis of amebiasis should be considered in all patients with right-sided pleural effusions for which no other explanation is obvious. Ultrasonic studies and computed tomography (CT) scan can demonstrate the hepatic abscess but cannot differentiate the pyogenic from amebic abscesses (7). The diagnosis is aided by the use of serologic tests. The sensitivity of antibody tests for E. histolytica is 95% for patients with extraintestinal amebiasis (8). Serology is limited as a diagnostic tool in highly endemic areas, as individuals will remain seropositive for years after an infection has cleared and seropositivity rates of greater than 25% may exist in some areas (8). Polymerase chain reaction (PCR) techniques are being more frequently used for the diagnosis of amebiasis but there is yet no standardized commercially available test (8).

The transdiaphragmatic rupture of an amebic liver abscess is usually signaled by an abrupt exacerbation of pain in the right upper quadrant and may be accompanied by a tearing sensation (3). These symptoms are followed by the development of rapidly progressive respiratory distress and sepsis, occasionally with shock (3). The pleural effusion is frequently massive, with opacification of the entire hemithorax and shift of the mediastinum to the contralateral side (3). The rupture is into the right pleural space in more than 90% of patients. The symptoms are sometimes subacute or chronic in nature (9). The diagnosis of amebic abscess with transdiaphragmatic rupture is suggested by the discovery of anchovy paste or chocolate sauce pleural fluid on diagnostic thoracentesis. Amebas can be demonstrated in the pleural fluid in fewer than 10% of patients. Concomitant rupture into the airways occurs in approximately 30% of patients (3), and this complication is usually manifested by the expectoration of chocolate sauce sputum that may be confused with hemoptysis by the patient and the physician.

The diagnosis is established by the characteristic appearance of the pleural fluid and can be confirmed by serologic tests for amebiasis. Ultrasound or CT scanning of the abdomen can delineate the extent of the intrahepatic disease and the presence or absence of a subphrenic abscess. Patients with transdiaphragmatic rupture should be treated with the same drugs as patients with sympathetic pleural effusions due to amebic hepatic abscess. Patients with transdiaphragmatic rupture should also undergo percutaneous drainage of both the liver abscess and the collection of material in the pleural space. The drainage can be accomplished with small tubes (12 to 14 F) (10). The combination of the drugs and the percutaneous drainage tubes results in clinical cure in almost all patients (10).

Approximately one third of patients with transhepatic rupture also have a bacterial infection of their pleural space (4,9). Such patients should be treated with the appropriate antibiotics. In addition, an open-drainage procedure or decortication is frequently necessary, indications for which are outlined in Chapter 12. In patients who undergo decortication, the visceral pleura is found to be covered with a thick membrane (9), but this membrane can easily be stripped off the visceral pleura (9). Even when no bacterial superinfection is present, decortication should be performed if the lung has not fully expanded in 10 days (9). The prognosis with transdiaphragmatic rupture is excellent if the patient is not too debilitated initially or if the diagnosis is not delayed (3,4,9).

Pleural involvement with hydatid disease can occur in one of four situations (12,13): (a) a hepatic hydatid cyst or, on rare occasions, a splenic cyst may rupture through the diaphragm into the pleural space; (b) a pulmonary hydatid cyst may rupture into the pleural space; (c) on rare occasions, the pleura may be primarily involved by the slowly enlarging cyst (12); or (d) a pulmonary or hepatic hydatid cyst may be accompanied by a pleural effusion (14,15,16). The incidence of pulmonary and hepatic cyst rupture into the pleural space is equivalent (12). Fewer than 5% of hepatic (12,13) or pulmonary hydatid cysts (16) are complicated by intrapleural rupture. Approximately 5% of patients with a hepatic or a pulmonary hydatid cyst have a pleural effusion (14). The pleural fluid has been described as an exudate (16) which can be eosinophilic (17).