An Unusual Cause of Right-Sided Pleural Effusion

An Unusual Cause of Right-Sided Pleural Effusion

CLINICAL CHALLENGES AND IMAGES IN GI Grace Elta and Robert J. Fontana, Section Editors An Unusual Cause of Right-Sided Pleural Effusion Q3 Michael R...

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CLINICAL CHALLENGES AND IMAGES IN GI Grace Elta and Robert J. Fontana, Section Editors

An Unusual Cause of Right-Sided Pleural Effusion Q3

Michael Rasper, Jochen Gaa, and Ernst J. Rummeny Department of Radiology, Klinikum rechts der Isar, München, Germany

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Question: A 78-yearold man with an unremarkable past medical history presented in the emergency department with mild dyspnea, recurrent episodes of fever, diffuse abdominal pain, and a 10-kg weight loss within the last 6 months. After admission, abdominal ultrasonography revealed a large, cystic lesion in the right liver lobe. A rightsided pleural effusion was seen on chest radiography (not shown). Routine laboratory findings were normal except for elevated C-reactive protein (3.6 mg/dL; normal, <1.0 mg/dL) and slightly elevated gammaglutamyltransferase (68 IU/L; normal, <55 IU/L). Computed tomography showed rightsided pleural effusion (Figure A, arrow) and a large, irregularly shaped cystic lesion with peripheral calcifications in the right liver lobe (Figure B, arrow). On F-18 fluorodeoxyglucose positron emission tomography (PET)/computed tomography (CT), the liver lesion appeared with an increased peripheral activity (Figure C, arrows) and a large hypometabolic region centrally. The hypermetabolic area extended cranially where it reached the diaphragm (Figure D, arrows). What is the diagnosis? Look on page 000 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

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Acknowledgments The authors acknowledge Dr Christoph Spinner, who managed patient care and the Department of Nuclear Medicine, Klinikum rechts der Isar München (Head: Professor M. Schwaiger) for PET/CT data.

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Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2014.02.046

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Answer to the Clinical Challenges and Images in GI Question: Image 1 (page ): Echinococcosis With Hepatic Hydatide Cyst and Pleural Involvement This is a case of alveolar echinococcosis with hepatic hydatide cyst and pleural involvement. Peripheral metabolic activity of the hepatic cyst with extension to the diaphragm on 18-FDG PET/CT and detection of Echinococcus multilocularis DNA in the pleural aspirate were highly suggestive of cestode penetration through the diaphragm. Serum enzyme immunoassay was positive for Echinococcus antibodies. Because complete operative resection was not feasible in this patient, long-term therapy with oral albendazole was initiated. Five weeks later, he presented in an improved general condition. Ultrasonography showed stable hepatic disease. The gamma-glutamyltransferase remained slightly elevated. Alveolar echinococcosis is a zoonosis caused by the cestode E multilocularis. It is less common than cystic echinococcis (E granulosus), the other medically relevant form of hydatide disease. E multilocularis is endemic in North America, Asia, and parts of Europe.1 Transmission to humans usually happens through oral ingestion of E multilocularis eggs. People at risk are trappers, hunters, and others who contact the stool of wild foxes. The liver is the primary site of disease manifestation, but infiltration and metastatic spread to other organ systems are commonly seen in the course of alveolar hydatide disease. Patients often remain asymptomatic for years or even decades because of the slow growth of cestode formations. Abdominal pain, cholestasis, and fever are typical symptoms of later disease stages. Cyst rupture (traumatic/ iatrogenic) is followed by anaphylactic reactions or even anaphylactic shock. Associated with high morbidity and mortality, alveolar echinococcosis demands timely diagnosis and adequate treatment. Radiologic workup consists of abdominal sonography, CT, and/or MRI for evaluation of disease extension.2 Serologic testing for E multilocularis antigens and detection of specific nucleic acids via polymerase chain reaction (aspiration/biopsy material) verify the imaging results. F-18 fluorodeoxyglucose PET/CT can be helpful to evaluate parasite viability under medical treatment as indicated by peripheral metabolic activity of the cyst.3 Surgical removal of all parasite manifestations accompanied by oral benzimidazoles (eg, albendazole or mebendazole) is the only curative approach. Long-term benzimidazole therapy is the treatment of choice for disease containment in inoperable patients. Acute complications of pleural echinococcus invasion like symptomatic pleural effusions or pneumothorax require immediate treatment with chest tube. Prolonged airleak after pulmonary hydatide cyst resection or persistent pleural effusion may be treated with pleurodesis.

References 1. 2. 3.

Nunnari G, Pinzone MR, Gruttadauria S, et al. Hepatic echinococcosis: clinical and therapeutic aspects. World J Gastroenterol 2012;18:1448–1458. Brunetti E, Kern P, Vuitton DA, et al. Expert consensus for the diagnosis and treatment of cystic and alveolar echinococcosis in humans. Acta Trop 2010;114:1–16. Stumpe KD, Renner-Schneiter EC, Kuenzle AK, et al. F-18-fluorodeoxyglucose (FDG) positron-emission tomography of Echinococcus multilocularis liver lesions: prospective evaluation of its value for diagnosis and follow-up during benzimidazole therapy. Infection 2007;35:11–18.

For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).

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