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• W4385962672 abstract "HomeRadioGraphicsVol. 43, No. 9 PreviousNext Cases from the Cooky JarFree AccessMass-forming Portal Cavernoma CholangiopathyMoozhan Nikpanah, Anne Sailer, Pegah Khoshpouri, Ananya Panda Moozhan Nikpanah, Anne Sailer, Pegah Khoshpouri, Ananya Panda Author AffiliationsFrom the Department of Radiology, University of Alabama at Birmingham, Birmingham, Ala (M.N.); Section of Interventional Radiology, Department of Radiology and Biomedical Imaging, Yale School of Medicine, New Haven, Conn (A.S.); Department of Radiology, University of Washington, Seattle, Wash (P.K.); and Department of Diagnostic and Interventional Radiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India 342005 (A.P.).Address correspondence to A.P. (email: [email protected]).Moozhan NikpanahAnne SailerPegah KhoshpouriAnanya Panda Published Online:Aug 17 2023https://doi.org/10.1148/rg.230074MoreSectionsPDF ToolsAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In Portal cavernoma cholangiopathy (PCC) refers to changes in the biliary tract resulting from extrinsic vascular compression and ischemic injury in patients with chronic extrahepatic portal vein obstruction (EHPVO) (1) (Fig 1). While most patients with PCC may remain asymptomatic, patients with a long-standing history of EHPVO can develop mild cholestatic jaundice, recurrent cholangitis, and choledocholithiasis (1). Rarely, PCC may present as diffuse masslike thickening of the common bile duct (CBD) due to fibrous tissue deposition, which may be mistaken for cholangiocarcinoma, CBD lymphoma, and immunoglobulin G4–related sclerosing cholangiopathy (4). Awareness of mass-forming PCC avoids unnecessary invasive procedures. Multiphasic cross-sectional imaging (CT, MRI with MR cholangiopancreatography) can help distinguish mass-forming PCC from other mimics and delineate the extent of portal cavernoma formation (Fig 2). At MRI, lack of diffusion restriction within the peribiliary mass and smooth and long-segment extrinsic narrowing of the CBD suggest a benign cause (2). Lack of fluorine-18 fluorodeoxyglucose uptake at PET/CT can also be useful in excluding malignancy (4).Figure 1. PCC is primarily caused by EHPVO, leading to the formation of multiple porto-portal collaterals (1). These collaterals extrinsically compress the bile ducts, causing indentations and an angulated appearance of the biliary tract, with mild upstream biliary dilatation giving an appearance of pseudosclerosing cholangiopathy. The common bile duct (CBD) is surrounded by two main venous channels: the paracholedochal plexus of Petren and the epicholedochal plexus of Saint. The paracholedochal plexus, consisting of larger veins, lies outside and parallel to the CBD and causes indentations on the CBD when enlarged. The epicholedochal plexus, which comprises smaller veins located within the wall of the CBD, causes thickening of the bile duct wall when enlarged (2,3). Both plexuses drain into 3-o'clock and 9-o'clock marginal veins, which then enter into branches of the portal vein (4). After thrombosis of the portal vein, porto-portal collateral circulation develops to compensate for portal vein obstruction, resulting in cavernous transformation of the portal vein (5). These porto-portal collaterals encompass the paracholedochal and epicholedochal venous plexuses, as well as the pericholecystic veins, exerting extrinsic compression on both the intrahepatic and extrahepatic bile ducts, leading to PCC (3,5). Concomitant inflammatory and ischemic alterations cause peribiliary fibrosis (6). The ischemic changes result from inadequate portal perfusion to the biliary ducts and thrombosis of small venules supplying the bile ducts, leading to strictures and fibrosis (6). In extreme cases, mass-forming PCC can develop as a fibrous tumorlike thickening due to connective tissue deposition around the bile ducts. Mass-forming PCC is T2-weighted hypointense or mildly hyperintense, similar to CBD lymphoma, immunoglobulin G4 cholangiopathy, and cholangiocarcinoma (4). The absence of diffusion restriction, progressive delayed enhancement due to both peribiliary fibrosis and serpentine venous collaterals, and extrinsic indentation of the suprapancreatic CBD, along with portal cavernoma, differentiate mass-forming PCC from other entities.Figure 1.Download as PowerPointFigure 2. PCC in a 52-year-old man who presented with abdominal pain, mild cholestatic jaundice, and intermittent episodes of hematemesis. (A) Axial portal venous phase contrast-enhanced CT image shows an enhancing peribiliary mass (yellow arrow) encasing the hypertrophied common hepatic artery (red arrow). The hepatic arteries are hypertrophied due to hepatic artery buffer response. Perfusional changes in the liver, splenomegaly, and portosystemic collaterals are also present. Mass-forming PCC appears as a hypoenhancing mass in the arterial phase (not shown), with progressive and persistent enhancement in the portal venous and delayed phases. (B) Coronal portal venous phase contrast-enhanced CT image demonstrates the mildly enhancing peribiliary mass (yellow arrow) extending from the porta hepatis along the hepatoduodenal ligament, severely narrowing the suprapancreatic CBD (red arrow) with mild upstream central intrahepatic biliary radical dilatation (white arrow). Additional multiple peripancreatic and periportal venous collaterals (blue arrow) are present due to chronic portal vein and superior mesenteric vein occlusion. (C) Coronal T2-weighted fat-suppressed MR image demonstrates the mildly hyperintense peribiliary mass (yellow arrow) extending from the porta hepatis along the hepatoduodenal ligament and causing extrinsic compression and severe narrowing of the suprapancreatic CBD (red arrow). (D) Axial diffusion-weighted image (b value = 800 sec/mm2) demonstrates the absence of diffusion restriction within the mass-forming PCC (arrow). (E) Axial postcontrast T1-weighted delayed phase MR image shows enhancement of the mass-forming PCC (yellow arrow) and pericholedochal and pericholecystic collaterals (white arrow).Figure 2.Download as PowerPointDisclosures of conflicts of interest.—All authors have disclosed no relevant relationships.References1. Dhiman RK, Saraswat VA, Valla DC, et al. Portal cavernoma cholangiopathy: consensus statement of a working party of the Indian national association for study of the liver. J Clin Exp Hepatol 2014;4(suppl 1):S2–S14. Crossref, Medline, Google Scholar2. Hulshoff JB, Cuperus FJC, de Haas RJ. Mass-Forming Portal Biliopathy Presenting as Extreme Wall-Thickening of the Common Bile Duct. Diagnostics (Basel) 2020;10(9):623. Crossref, Medline, Google Scholar3. Walser EM, Runyan BR, Heckman MG, et al. Extrahepatic portal biliopathy: proposed etiology on the basis of anatomic and clinical features. Radiology 2011;258(1):146–153. Link, Google Scholar4. Gunasekaran V, Mohan SL, Chakkalakkoombil SV, Senthamizhselvan K. Mass-Like Extreme Wall Thickening of the Entire Common Bile Duct in a Case of Portal Cavernoma Cholangiopathy. Journal of Gastrointestinal and Abdominal Radiology 2021;5:63–69. Google Scholar5. Elsayes KM, Shaaban AM, Rothan SM, et al. A Comprehensive Approach to Hepatic Vascular Disease. RadioGraphics 2017;37(3):813–836. Link, Google Scholar6. Kalra N, Shankar S, Khandelwal N. Imaging of portal cavernoma cholangiopathy. J Clin Exp Hepatol 2014;4(suppl 1):S44–S52. Crossref, Medline, Google ScholarArticle HistoryReceived: Apr 2 2023Revision requested: Apr 5 2023Revision received: Apr 18 2023Accepted: Apr 26 2023Published online: Aug 17 2023 FiguresReferencesRelatedDetailsRecommended Articles Imaging Diagnosis of Intrahepatic and Perihilar Cholangiocarcinoma: Recent Advances and ChallengesRadiology2018Volume: 288Issue: 1pp. 7-13Multimodality Imaging after Liver Transplant: Top 10 Important ComplicationsRadioGraphics2022Volume: 42Issue: 3pp. 702-721Insight into Bile Duct Reaction to Obstruction from a Three-dimensional Perspective Using ex Vivo Phase-Contrast CTRadiology2021Volume: 299Issue: 3pp. 597-610Imaging Features of Premalignant Biliary Lesions and Predisposing Conditions with Pathologic CorrelationRadioGraphics2022Volume: 42Issue: 5pp. 1320-1337Imaging Features of Primary Sclerosing Cholangitis: From Diagnosis to Liver Transplant Follow-upRadioGraphics2019Volume: 39Issue: 7pp. 1938-1964See More RSNA Education Exhibits Diffuse Bile Ducts Abnormalities: A Case Base Review with Histopathologic CorrelationDigital Posters2022What Went Wrong? 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