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

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Venous Complications of Pancreatitis: a Review Yashant Aswani, Priya Hira Department of Radiology, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra INDIA JOP. J Pancreas (Online) 2015 Jan 31; 16(1):20-24 REVIEW ARTICLE Venous Complications of Pancreatitis: 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 pseudoaneurysm 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 thrombosis. From time to time case reports and series of INTRODUCTION THROMBOTIC COMPLICATIONS IN PANCREATITIS Venous thrombosis is the most common complication of pancreatitis mediators and digestive enzymes. Consequently, pancreatitis associated complicationsPancreatitis is cana systemic be myriad disease with vascularowing to complications release of inflammatory being 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 acute pancreatitis [2] whereas etiology in of peripancreatic arteries. Venous complications are less commonly significant morbidity and mortality [1]. There is predominant affliction tiesinflammation, with pancreas chronic results inflammation in splenic veinwith involvement fibrosis, compressive in majority effectsof the of a pseudocyst or an enlarged inflamed pancreas [3]. Close anatomic complicationsreported and associatedare often withconfined 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 articlereports 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 hypertension 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 chronic pancreatitis 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 featuresthe superior include mesenteric signs of veinpancreatic (SMV) pathology,[8]. Flow t 2 HEMORRHAGIC COMPLICATIONS splenomegaly,direction is still hepatopetalsplenic [7]hilar and gastric and or attenuation 3 IMPAIRED VENOUS DRAINAGE gastroesophageal late-phase celiac angiography may depict an occluded splenic collateralsvein.These with normal portal vein and normal liver Received October 26th, 2014 – Accepted November 28th, 2014 morphology [5, 6]. A bleed. Upper gastrointestinal Key words Esophageal and Gastric Varices; Hypertension, Portal; hemorrhage in SPH, however, is gastrica rarity and[5] or gastroesophageal [9] Mesenteric Veins; 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 noColonoscopy correlation demonstratedbetween the incidencecolonic 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 cirrhosis [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 seen systemic in 30 anterior % of patients abdominal with wall PV candidates, splenic artery embolization has been described as a viable symptomatic case of CP associatedof procedureSV 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 Portal Vein Thrombosis 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
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