JOP. J Pancreas (Online) 2015 Jan 31; 16(1):20-24

REVIEW ARTICLE

Venous Complications of : A Review Yashant Aswani, Priya Hira Department of Radiology, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra INDIA

ABSTRACT Pancreatitis is notorious to cause vascular complications. While arterial complications include formation with a propensity to bleed, unusual venous complications associated with pancreatitis have, however, been described. In this article, we review multitudinous venous complications in thevenous setting complications of pancreatitis can andbe quite propose myriad. a system Venous to involvementclassify pancreatitis in pancreatitis associated often venous presents complications. with . From time to time case reports and series of

INTRODUCTION THROMBOTIC COMPLICATIONS IN PANCREATITIS is the most common complication of pancreatitis mediators and digestive enzymes. Consequently, pancreatitis associated complicationsPancreatitis is can a systemicbe myriad disease with vascular owing tocomplications release of inflammatorybeing a well known but infrequent phenomenon. These vascular complications affecting venous system. A surge in procoagulant inflammatory mediators, are seen in 25% patients suffering from pancreatitis and entail chronicstasis, vesselpancreatitis spasm, (CP) mass includes effects intimal from injury the surroundingdue to repeated inflamed acute pancreas causes thrombosis in [2] whereas etiology in of peripancreatic . Venous complications are less commonly significant morbidity and mortality [1]. There is predominant affliction tiesinflammation, with pancreas chronic results in splenic with involvement fibrosis, compressive in majority effectsof the of a pseudocyst or an enlarged inflamed pancreas [3]. Close anatomic complicationsreported and associated are often with confined pancreatitis to thrombosis have, however, of the been vein. described. Isolated 22% (Agrawal et al.) and 5.6% (Bernades et al.), respectively. Attempts to Thiscase article reports focuses and serieson multitudinous of unusual venous but significantly complications morbid in the venoussetting healingcases [4]. cause Prevalence collateral of formation splenic vein responsible and portal for vein left-sided thrombosis in CP is in the former while cavernous transformation of portal vein, portal clinicoradiologic grounds into 3 categories: thrombotic or hemorrhagic biliopathy and gall bladder wall varices in the latter. complicationsof pancreatitis and and complications classifies the arising potential due to venousimpaired complications venous drainage on (table 1). Chronic Thrombosis of Splenic Vein and Formation of Table 1. Collaterals clinicoradiologic basis A chronic obstruction to venous return from splenic vein (SV) can give Classification of venous complications of pancreatitis on 1 THROMBOTIC COMPLICATIONS rise to a compartmentalised form of portal hypertension called left- a) Chronic thrombosis sided or Sinistral portal hypertension Cavernous transformation of portal vein, portal biliopathy, Sinistral Portal Hypertension (SPH) [5]. Etiology of SPH is gall bladder wall varices multifactorial and in cases of pancreatitis includes SV thrombosis [6] or SV compression from mass-forming or a pseudocyst b) Acute thrombosis [5, 6]. CP associated SV thrombosis is the most common cause of SPH SplenicTransient infarction, hepatic attenuationspontaneous difference splenic rupture, subcapsular [6]. It may, however, be difficult to demonstrate the clot or SV itself in hematoma CP. Hence, the diagnosis involves detection of collaterals [7] which Bowel wall infarction include the short and posterior gastric and the gastroepiploic collaterals Hepatic parenchymal infarction and ransient hepatic [8]. While the former drain via sincecoronary primary vein intopathology the portal is not vein hepatic (PV) difference in[8], origin. the latter Imaging join features the superior include mesenteric signs of vein pancreatic (SMV) pathology, [8]. Flow t 2 HEMORRHAGIC COMPLICATIONS ,direction is still hepatopetal splenic [7] hilar and gastric and or attenuation 3 IMPAIRED VENOUS DRAINAGE gastroesophageal late-phase celiac angiography may depict an occluded splenic collaterals vein.These with normal portal vein and normal Received October 26th, 2014 – Accepted November 28th, 2014 morphology [5, 6]. A bleed. Upper gastrointestinal Key words Esophageal and ; Hypertension, Portal; hemorrhage in SPH, however, is gastrica rarity and [5] or gastroesophageal [9] Mesenteric ; Pancreatitis; Portal Vein; Splenic Vein collaterals may manifest as variceal In the series described by Abbreviations CP: Chronic Pancreatitis Agrawal et al. only 15% of patients with CPconstitutes upto 1% of life S Splenic vein threatening upper gastrointestinal bleed [6]. PV Portal vein associated SV thrombosis SPHV Sinistral portal hypertension Morepresented selective with hematemesisand compartmentalized [10]. forms of portal hypertension SMV Superior mesenteric vein following CP associated SV thrombosis have also been described. CTPV Cavernous transformation of the portal vein Burbige et al. reported a case of chronic pancreatitis with per rectal TIPS Transjugular Intrahepatic Portosystemic Shunts PH Portal hypertension PB Portal biliopathy Therebleeding. is no correlation demonstratedbetween the incidence colonic varices of SPH at and splenic the severity flexure GWV Gallbladder wall varices and angiography revealed an occluded SV and hence the collaterals [11]. THAD Transient Hepatic Attenuation Difference of pancreatitis [6]; SPH may be a consequence of a mild or subclinical EUS Endoscopic ultrasonography episode of pancreatitis [6]. Correspondence Yashant Aswani Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra WhileIt is important variceal clipping to exclude or Transjugular other causes Intrahepatic of portal hypertension Portosystemic and Shunts liver India (TIPS)pathologies is the [5, procedure 6] since managementof choice for refractoryfor SPH is bleedcompletely from collateralsdifferent [6]. in Phone +91-9029042971 E-mail [email protected] a compressing pseudocyst or CP associated adhesions, is the management liver [6], splenectomy with correction of primary pathology i.e.,

JOP. Journal of the Pancreas–http://www.serena.unina.it/index.php/jop–Vol. 16 No. 1 – Jan 2015. [ISSN 1590-8577] 20 JOP. J Pancreas (Online) 2015 Jan 31; 16(1):20-24

Gallbladder Wall Varices decompression of splenic hilar venous collaterals on interruption of of choice in symptomatic SPH [5, 6, 8]. The rationale for splenectomy is Another set of collaterals in PV thrombosis includes gallbladder wall et al. described a successful laparoscopicarterial supply splenectomy [8]. Presence following of numerous splenic hilar arterycollaterals embolization favour an openin a thrombosis (Chawla et al.). These are portosystemic shunts between surgical approach. [8]. However, Patrono cysticvarices vein (GWV) branch (Figure of the 3) PV which either are to seensystemic in 30 anterior % of patients abdominal with wall PV candidates, splenic embolization has been described as a viable symptomatic case of CP associatedof procedure SV thrombosis. is partial For embolization poor surgical of the GWV appear as anechoic serpentine channels that show a continuous the artery. Management in asymptomatic SPH is controversial with some veins or to the patent PV branches within the liver [14]. On sonography, option [12] wherein the end point et al. advocated low velocity signal typical of portal venous system [14]. Their presence authors advising prophylactic splenectomy [6]. Agrawal risedoes to not hemobilia correlate or with intraabdominal the site and hemorrhage.extent of PV Therethrombosis is, however, [14]. The no splenectomy even in asymptomatic patients with CP associated SPH [6, varices may reduce the distensibility of gall bladder [21] or can give 10]. The authors stated that performing splenectomy did not increaseet al. morbidity or mortality [10]. The current evidence however, favors a studied 53 patients of CP associated SPH and advised against routine alteration in emptying of gall bladder or lithogenicity of bile [21]. Clinical conservative approach in asymptomatic individuals [6]. Heider during biliary track surgeries for risk of hemorrhage. implication of GWV include variceal bleed (seen in 1%) [22] and caution Cavernoussplenectomy in theseTransformation patients [13]. of Portal Vein, Portal Transient Hepatic Attenuation Difference Biliopathy and Gall Bladder Wall Varices: Sequelae to Transient epatic ttenuation ifference (THAD) occurs due regional Chronic h This leadsa to non-dilutiond of iodinated hepaticto artery blooddiminution in that in PVparticular flow [23]; region the diminution and forms can the be basisabsolute of Cavernous Transformation of Portal Vein increasedor relative. attenuation (difference maintained via cavernous transformation of the portal vein (CTPV) in attenuation) in these areas When the thrombus occludes the main PV, the hepatopetal flow is [24]. The compensatory increase in hepatic artery flow that compression occurs in PV thrombosis accentuates this phenomenon [24]. of(Figure the PV 1)[14]. Besides a lumen occluding thrombus, a pseudocyst or Morphologically THAD has been classified into Lobar multisegmental, themass-forming paracholedochal chronic veins pancreatitis of Petren, may that also run cause parallel extrinsic to biliary duct wall Sectorial, Polymorphous and Diffuse [23]. and the epicholedochaland consequently veins CTPV of [4]. Saint, CTPV that comprises are located of two on sets the of surface veins: THAD is seen on arterial phase of CT as an area of increased attenuation that returns to normal or near normal on portal venous phase [25]. Similar findings on MRI have been called Transient Hepatic Intensity sufferingof bile ducts from [15]. PV thrombosis.It takes approximately In spite of numerous 3 weeks’ collateraltime for cavernouspathways, Difference (THID) [26]. THAD by itself is not pathological but indicates portaltransformation hypertension to occur[16]. (PH) still CTPVoccurs. is Patients found inbecome 70 -100% symptomatic of patients on an associated pathology. account of features of portal hypertension i.e., bleeding from collaterals and splenomegaly than due to biliary obstruction caused by enlarged portal,Pancreatitis-associated splenic or superior THAD mesenteric may arise veinsbecause (sectorial of inflammation or diffuse induced type). Aincrease sectorial in type arterial occurs inflow in the (polymorphous setting of thrombosis type) [27] of or portal thrombosis vein and in collaterals [16]. Variceal haemorrhage at presentation however, does not When the thrombus is present in the main PV trunk, collaterals in the influenceUltrasonography overall survivalis the [17].initial investigation that reveals numerous peri-hilartypically hasregion a wedge maintain shaped perfusion or atleast of the central one straight portion. border The periphery [23, 27]. anechoic vascular channels at porta. Gold standard for diagnosis of however, continues to receive undiluted contrast carried by hepatic CTPV is conventional angiography. However, MR angiography is as artery branches with consequent high attenuation of the periphery. Such accurate as conventional angiography. A prophylactic surgery in this case is debatable with some surgeons intervening only on development variceal hemorrhage. Endoscopic management in the form of band a THAD pattern that is called occurs central-peripheral due to thrombosis subtype of SV, of diffuseSMV or THAD partial (Figure thrombosis 4) [27]. ligation or sclerotherapy are preferred procedures. Portosystemic thrombosis with CTPV limits the success of TIPS since accessibility of PV mesentericor compression venous of PV blood involves contributing an entire posterolateral lobe [24]. Such column an observation of blood is created in those who fail to benefit from endoscopic measures. [17] PV inis basedthe PV on and the splenicfact that venous portal bloodblood occupyingflow is streamlined an anteromedial with superior place via transjugular route becomes difficult in chronically thrombosed vein produces left lobar THAD, while pathology of SMV or posterolateral PV [18]. Moreover, passage of wire through one of the collaterals across the [28]. Hence, obstruction of splenic vein or anteromedial portion of PV aoccluded case of segmentCP associated is either CTPV difficult where or TIPSimpossible. was performed Hence, PV employing thrombosis a with CTPV, a contraindication to TIPS [18]. Jourabchi however, described exhibits right lobar THAD [24]. Since this ultimately affects portal venous Splenicinflow, typically Complications there is presence Due of toone Splenic straight border. Vein Thrombosis combined transjugular and transhepatic approach [18]. Portal Biliopathy Pancreatitis associated splenic complications manifest as infarction, Collaterals in CTPV can mechanically obstruct the biliary track giving

spontaneous rupture of spleen (SSR) or subcapsular hematoma [29]. rise to Portal Biliopathy (PB) (Figure 2)[19]. Occurrence of PB in CP is a rare phenomenon [19, 20]. These vessels may cause ischemia induced occurfibrosis in of a thefew. track. However, Majority symptoms do not related manifest to anyportal symptoms hypertension of biliary are obstruction [16]; chronic , biliary pain and calculus et may al. described endoscopic ultrasonography (EUS) features of PB in a female more frequent than symptoms of chronic cholestasis [21]. Rana prominent common with anechoic serpentine veno-venous collateralssuffering fromaround acute the biliary severe tree. pancreatitis ERCP however, [20]. is EUS the key features investigation; include

MR has the additional advantage of distinguishing bile although MRCP is equally accurate for diagnosing PB[21]. MRCP with duct varices from biliary duct calculi. Cholangiographic findings include Thesegmental strictures upstream are typically dilation, smooth caliber unlike irregularity, those of sclerosing stricture, cholangitis extrinsic impression due to collaterals (-the pseudocholangiocarcinoma sign) [21]. Figure 1: Sonogram shows replacement of main portal vein with and features of obstructive jaundice. In patients with a shuntable vein, a multiple serpiginous, anechoic channels (arrow) that on color Doppler [21]. Intervention is required in patients with a dominant biliary stricture is performed or else endotherapy is preferred [21]. interrogation revealed slow flow. JOP. Journal of the Pancreas–http://www.serena.unina.it/index.php/jop–Vol. 16 No. 1 – Jan 2015. [ISSN 1590-8577] 21 JOP. J Pancreas (Online) 2015 Jan 31; 16(1):20-24

bowel ensues if the inciting ischemic injury is severe. The gut mucosa may reveal[33]. On ulceration the other and hand, there gangrene may be [34] associated or perforation mesenteric [34, 35, panniculitis 36] of the

[32]. Bowelet infarctions al. secondary to pancreatitis associated thrombotic infarctionvenous states with have perforation been described treated for by subtotal [32, 36, 37] and colondiversion [34, ileostomy35]. Nottle followed [35] at areported later date a bycase ileosigmoid of pancreatitis . associated colonic Portal Vein-Pseudocyst Fistulisation

of mechanism of thrombosis (table 2): indirect, wherein procoagulant Venous thrombosis in pancreatitis can also be classified on the basis

Figure 2: CECT coronal reformation demonstrates dilated common bile inflammatory mediators increase or direct wherein duct (green arrows) surrounded by numerous collaterals in a setting of empties itself directly into venous lumen (vein-pseudocyt fistulisation). portal biliopathy. The latter has been described usually in the context of PV. Portal vein- etpseudocyst al. described a patientmay present with clinicallyresidivating as vagueoligoarthritis, abdominal subcutaneous, pain [38] or bursalwidespread and osseal necrosis necrosis [38, in 39,the 40]setting with of increased Pancreatic morbidity. pseudocyst-portal Hammar

vein fistula [41]. Pseudocyst-portal vein fistula is commonly seen in males particularly enzymeswith a history from of an alcohol-induced adjacent pseudocyst pancreatitis with [38]. initial The mechanism thrombus formation.of fistulisation involves erosion of the venous wall by the uninhibited

Later, there is lysis of the thrombus and filling in of the vein with pancreatic succus [42]. Since the pseudocyst is a high pressure Tablezone, devastating 2. bleeding is rare [38]. basis of mechanism of thrombus formation Classification of venous complications in pancreatitis on the 1 INDIRECT

Due to surge in inflammatory mediators, stasis, spasm of vessel, mass 2 DIRECTeffects of pseudocyst or inflamed pancreas, intimal injury, chronic inflammation with fibrosis pseudocyst Due to direct fistulisation between venous lumen and a pancreatic

Figure 3: Sonogram depicts dilated venous channels in the wall of gall bladder.

Involvement of the organ may occur via enzymatic between splenic and capsule or dissection though the splenic capsule

orfor both development [29]. Since of pancreatic such complications. tail lies in anatomic These complicationscontiguity with aresplenic more hilum, pronounced inflammation with around pancreatitis the pancreatic associated tail SV is thrombosisa prerequisite (Malka et al.)

SSR is an uncommon surgical[29]. emergency. Clinical features include

CECT arterial phase demonstrate a sectorial type of transient left hypochondriac pain, , guarding and rigidity [30, 31]. Figure 4a: and any patient of acute pancreatitis presenting with signs of shock hepatic attenuation difference with a straight border (solid arrow). Kehr’s sign may be positive [30]. High index of suspicion is necessary should be evaluated for SSR. Management depends on hemodynamic Also s collection in the body of pancreas. No active intervention is required if the patient is hemodynamically note thrombosis in a tributary of portal vein (arrow) with fluid stable;stability, these degree patients of can be kept under and severityclose clinical of splenic and sonographic injury [31]. monitoring. Conservative approach was employed by Mujtaba et al. in

Rypensa hemodynamically et al. stable patient of acute pancreatitis (with crohn’s associateddisease) who splenic developed complications SSR following may potentially SV thrombosis regress [31]. over Similarly, time. On the contrary, [30]suggested surgical intervention a wait and is watch warranted policy if since the pancreatitispatient has precipitousBowel Wall drop Infarction in or develops signs of [31]. A thrombosis in mesenteric venous system can also be a harbinger of an acute complication. Thrombotic occlusion of veins may result in bowel Figure 4b: CECT venous phase shows near complete resolution of transient hepatic attenuation difference with thrombosis in a tributary wall infarction [32, 33, 34]. Extent and severity of infarction along with of portal vein (arrow). other co-morbid conditions predict the final outcome. Ischemic insult, if mild, heals with of lumen [32] and may mimic a neoplastic process JOP. Journal of the Pancreas–http://www.serena.unina.it/index.php/jop–Vol. 16 No. 1 – Jan 2015. [ISSN 1590-8577] 22 JOP. J Pancreas (Online) 2015 Jan 31; 16(1):20-24

MRI may delineate the fistula as a T2 hyperintense tract joining the Conflict of Interest pseudocyst and the vein [38]. ERCP may help if the pancreatic duct communicates with the pseudocyst [15]. The role of ERCP may be limited if the pancreatic duct has strictures or calcifications clogging the duct Authors declare to have no conflict of interest. [38]. Percutaneous transhepatic portography may also be helpful [38]. References In a few cases, however, diagnosis was established on autopsy [38, 43, 1. 44]. Differentials for a low attenuation of portal vein include a portal vein-pseudocyst fistula, a bland thrombosis in hypercoagulable states or Mallick IH, Winslet MC. Vascular complications of pancreatitis. JOP mass effect by tumor or lymph nodes. The portal vein-pseudocyst fistula 2004;2. 5 (5): 328-37. [PMID: 15365199] may reveal complex fluid in the PV on ultrasonography. The other two be administered for portal vein thrombosis associated with acute conditions are similar except the extrinsic mass will be seen causing Park WS, Kim HI, Jeon BJ, Kim SH, Lee SO. Should anticoagulants narrowingPatients with of the mild PV [38]. symptoms can be managed conservatively while reserving pancreatitis? World J Gastroenterol 2012; 18(42): 6168-71. [PMID: 23155349]3. Sakorafas GH, Tsiotou AG. Splenic-vein thrombosis complicating aggressive surgical intervention for symptomatic ones. Definitive surgical methods include PV plasty [38]; diversion of pancreatic secretions chronic pancreatitis. Scand J Gastroenterol 1999; 34: 1171-7. [PMID: mayMiscellaneous be attempted at a later date when acute symptoms subside [38]. 10636062]4. 1) Infarction of liver is uncommon owing to dual blood supply by PV Izbicki JR, Yekebas EF, Strate T, Eisenberger CF, Hosch SB, Steffani K, and hepatic artery with PV constituting 80% of the share. Pancreatitis Knoefel WT. Extrahepatic portal hypertension in chronic pancreatitis: an old5. problem revisited. Ann Surg 2002; 236(1): 82-9. [PMID: 12131089] hypertension: clinical features and surgical treatment of chronic splenic be caused by marked diminution of blood supply to liver due to PV Wang L, Liu GJ, Chen YX, Dong HP, Wang LX. Sinistral portal associated hepatic infarction iset al. a rare entity [45, 46]; postulated to vein6. Kokabi occlusion. N, MedLee PrincE, Echevarria Pract 2012; C, 21(1):20-3. Loh C, Kee [PMID: S. Sinistral 22024761] portal occurredthrombosis due [45, to 46,both 47]. PV Walsh thrombosis [48] as well described as shunting a case of of blood pancreatitis across iatrogenicallyassociated hepatic created infarction portosystemic where shunt. severe reduction in hepatic inflow hypertension: presentation, radiological findings, and treatment options 7. 2) While thrombosis of veins in peripancreatic region is a common event, - a case report. J Radiol Case Rep 2010; 4(10):14-20. [PMID: 22470692] et al. Rösch W, Lux G, Riemann JF, Hoh L. [Chronic pancreatitis and the neighboring organs]. Fortschr Med 1981; 99(29): 1118-21. [PMID: thrombosis in extrasplanchnic system is sparingly reported. Parikh subclavian and common iliac veins without involvement of splanchnic 7262798]8. described thrombosis of superior and inferior vena cava, axillary, Left-sided portal hypertension: Successful management by laparoscopic Patrono D, Benvenga R, Moro F, Rossato D, Romagnoli R, Salizzoni M. veins [49]. Similarly many authors have also described thrombosis of inferior vena cava [50, 51], pulmonary artery [52], inferior vena splenectomy following splenic artery embolization. Int J Surg Case Rep 2014;9. Köklü 5(10): S, Coban652-5. S,[PMID: Yüksel 25194596] O, Arhan M: Left-sided portal hypertension. cava and renal veins [53], inferior vena cava with pulmonary artery Dig Dis Sci 2007; 52: 1141–1149. described[54]. Of particular by Molacek interestet al is in Phlegmasia the setting cerulea of acute dolens, hemorrhagic- a form of 10. necrotisingdeep venous thrombosis with a proximal localization of the blockage, . Agarwal AK, Raj Kumar K, Agarwal S, Singh S. Significance of splenic pancreatitis [55]. The condition most frequently involves vein thrombosis in chronic pancreatitis. Am J Surg 2008; 196(2): 149-54. HEMORRHAGICileofemoral region and COMPLICATIONS is usually seen in terminal IN PANCREATITIS stages of malignancies [PMID:11. 18585674] [55]. Pancreatitis associated hemorrhagic complications may be both arterial Burbige EJ, Tarder G, Carson S, Eugene J, Frey CF. Colonic varices. A as well as venous. Rarely, the venous erosion by tryptic enzymes may not complication of pancreatitis with splenic vein thrombosis. Am J Dig Dis 1978;12. 23(8): 752-5. [PMID: 685944] gastric varices in patients with sinistral portal hypertension. Dig Dis Sci be contained (unlike pseudocyst- portal vein fistula). Instead, erosion Liu Q, Song Y, Xu X, Jin Z, Duan W, Zhou N. Management of bleeding of venous wall may result into a massive abdominal haemorrhage[56]. 2014;13. 59(7): 1625-9. [PMID: 24500452] Instances have been described for portal [56, 57] as well as SV [58]. On pancreatitis-induced splenic vein thrombosis. Ann Surg 2004; 239 (6): Heider TR, Azeem S, Galanko JA, Behrns KE. The natural history of diagnostic.ultrasonography, Management fluid with involves echoes placement can be demonstrated. of a stent graft However, across CT the is the modality of choice and needle aspiration of serosanguinous fluid is 876-80.14. [PMID: 15166967] IMPAIREDmural defect [56, VENOUS 57]. DRAINAGE IN PANCREATITIS Chawla Y, Dilawari JB, Katariya S. Gallbladder varices in portal vein thrombosis.15. Brown A, AJR Malden Am J Roentgenol E, Kugelmas 1994; M, Kortz162(3): E. 643-5.Diagnosis [PMID: of pancreatic 8109513] pseudocyst may lead to impaired venous drainage. Such a non-thrombotic, Pancreatitis associated partial thrombosis or extrinsic compression by a duct-portal vein fistula; a case report and review of the literature. J Radiol Case16. Rep 2014; 8(3): 31-8. [PMID: 24967026] and testicular veins. The diminution in drainage gave rise to engorgement gastric ulcers causing acute pancreatitis and portal biliopathy: what's the compressive effect of pseudocyst [59, 60] has been described for left renal of venous bed of testis (secondary ). Such an occurrence is Mensier A, Bounoua F, Beretvas G, Mosoi A, Dardenne S. Kissing 17. present with heaviness and vague pain in scrotum. Ultrasonography link? JOP 2013; 14(6): 646-8. [PMID: 24216552] showsextremely dilated, rare andtortuous has been venous reported channels only twice located [59, posterolateral60]. The patients to thrombosis:Janssen HL,aetiology Wijnhoud and A,determinants Haagsma EB, of van survival. Uum SH, Gut van 2001; Nieuwkerk 49 (5): the testis. A CECT demonstrates compression of the draining veins. CM, Adang RP, Chamuleau RA, van Hattum J, Extrahepatic portal vein

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