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  Page 1 of 39 Porto-systemic shunts: classification, clinical andradiological implications. Poster No.: C-1699 Congress: ECR 2012 Type: Educational Exhibit Authors: F. M. DANZA 1 , A. M. De Gaetano 2 , A. Cipriani 3 , E. Antichi 4 , M.Falcione 3 , L. Bonomo 3 ; 1 ROME/IT, 2 Roma (RM)/IT, 3 Rome/IT, 4 Roma/IT Keywords: Congenital, Shunts, Decision analysis, Comparative studies,Ultrasound-Colour Doppler, MR, CT-Angiography, Portal system / Hepatic veins, Abdomen DOI: 10.1594/ecr2012/C-1699Any information contained in this pdf file is automatically generated from digital materialsubmitted to EPOS by third parties in the form of scientific presentations. Referencesto any names, marks, products, or services of third parties or hypertext links to third-party sites or information are provided solely as a convenience to you and do not inany way constitute or imply ECR's endorsement, sponsorship or recommendation of thethird party, information, product or service. ECR is not responsible for the content ofthese pages and does not make any representations regarding the content or accuracyof material in this file.As per copyright regulations, any unauthorised use of the material or parts thereof aswell as commercial reproduction or multiple distribution by any traditional or electronicallybased reproduction/publication method ist strictly prohibited.You agree to defend, indemnify, and hold ECR harmless from and against any and allclaims, damages, costs, and expenses, including attorneys' fees, arising from or relatedto your use of these pages.Please note: Links to movies, ppt slideshows and any other multimedia files are notavailable in the pdf version of presentations.www.myESR.org  Page 2 of 39 Learning objectives To illustrate the classification of porto-systemic shunts (PSS), the role of imaging indiagnosis of vascular anomalies and eventually associated liver focal lesions, suchas benign neoplasms or hepatocellular carcinoma (HCC). This in order to recognizemalformations, correlate nodular liver lesions associated to perfusion anomalies andobtain a prognostic stratification of patients.Furthermore, to define the contribution of radiological assessment in definition oftherapeutic strategies on the basis of residual portal circulation.In this poster we will analyse the value of contrast-enhanced (CE) MDCT and MRIprimarily in the definition of PSS and characterization of liver focal lesions respectively.Our aim is to make radiologists aware of the importance of correct identification,classification of PSS and interpretation of related diseases, in order to refer patients toan appropriate treatment. Background In PSS, porto-mesenteric blood drains into systemic circulation partially or completelybypassing the liver. These anomalies could be acquired or congenital. Acquired shunts  are the most common, their major causes being portal hypertension ortrauma. In the first case, increased pressure of portal blood causes normally existing butinsignificant porto-systemic anastomoses to enlarge. More than 20 such pathways havebeen described, from gastro-esophageal, para--esophageal, para-umbilical and spleno-renal to inferior mesenteric district. Congenital shunts  are a rare consequence of abnormal involution of vitelline veinsand their primitive anastomoses. The development of portal venous system is extremelycomplex and occurs between 4th and 10th week of embryonic life. Initially, right andleft vitelline veins emerge from yolk sac, cross septum transversum, and directly draininto sinus venosus (the primitive heart). Three cross communicating vessels developbetween the two vitelline veins: the subhepatic (cranio-ventral duodenal), intermediate(dorsal duodenal) and caudal (ventral duodenal), respectively. They anastomose eachother forming the figure of an 8 around developing duodenum. Selective involution ofthese vessels leads to the final configuration of portal vein (PV) that remains posterior toduodenum (Fig. 1a, b, c, d). It is clearly understandable how several abnormalities in theanatomy of portal system might arise due to errors in the development process described.  Page 3 of 39 Abnormal patterns of involution and persistence can result in pre-duodenal, pre-biliary orduplicated PV, as well as excessive involution may hesitate in PV absence [1].Associated anomalies can involve posterior venous system leading to azygoscontinuation of inferior vena cava (IVC). Fig. 1 References:   Langman J, Sadler TW in Langman's Medical Embryology. Williams andWilkins, 1990.Congenital PSS are classified into intrahepatic or extrahepatic. In the first, connectionsare created between branches of PV, after its division, and IVC or hepatic veins (HV).In the second, anastomoses are established outside the liver between porto-mesentericvasculature, before PV division, and a systemic vein. Both categories can be furtherdivided into various subtypes. Intrahepatic shunts  are classified by Park et al. [2] into:ã type 1 , a single large vessel connecting right PV to IVC  Page 4 of 39 ã type 2 , one or more communications between peripheral branches of PVand HV, within one hepatic segmentã type 3 , an aneurysmal communication between peripheral PV and HVã type 4 , multiple communications between PV and HV, distributed in bothlobesFirst two varieties are the most common [3]. Although rare, persistent patent ductusvenosus (DV) could be considered another type of intrahepatic PSS. In the fetus, DVarises from posterior aspect of left PV branch, opposed to the opening of umbilical vein,and drains into HV. Its spontaneous closure usually begins immediately after birth andbecomes definitive during first week of life in most full-term neonates. Yet it may takemuch longer to close in preterms or in presence of congenital heart defects [3], as wellas it may remain patent, leading to development of PSS. Extrahepatic shunts  are characterized by porto-mesenteric vasculature bypassing theliver through a congenital conduit. Most common drainage vessel is the IVC (porto-cavalshunt), followed by renal, iliac, azygos vein and right atrium [4]. Extrahepatic shunts areclassified by Morgan and Superina [5], according to Abernethy's description [6], into twotypes (Fig. 2).ãIn type 1 , there is a complete portal blood diversion into systemic circula-tion (end-to-side shunt), with absence of intrahepatic portal branches. Theyare further classified into two subtypes in which splenic (SV) and superiormesenteric vein (SMV) separately drain into systemic outflow (type 1a), or join together forming a common trunk (type 1b). Pathogenesis has beenattributed to excessive involution of primitive periduodenal vitelline venousloop or total failure of vitelline veins to establish critical anastomoses withhepatic sinusoids or umbilical veins [7, 8]. Resulting shunt may be due topersistence of right vitelline (draining into retrohepatic IVC) or left vitellinevein (right atrium or IVC above HV confluence) [3].ãIn type 2 , intrahepatic PV is intact, but part of portal flow is diverted intoa systemic vein through a side-to-side communication. Persistence ofanastomotic channels between vitelline and subcardinal veins has beenproposed as a cause [9]. Other authors suggest some type 2 shuntsprobably arise from persistence of right vitelline vein [10].
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