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IMAGE IN EUS
Year : 2013  |  Volume : 2  |  Issue : 4  |  Page : 228-229

Portal hypertensive biliopathy developing after acute severe pancreatitis


Department of Gastroenterology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission25-Oct-2012
Date of Acceptance10-Mar-2013
Date of Web Publication15-Nov-2013

Correspondence Address:
Surinder Singh Rana
Department of Gastroenterology, Post Graduate Institute of Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2303-9027.121244

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How to cite this article:
Rana SS, Bhasin DK, Rao C, Singh K. Portal hypertensive biliopathy developing after acute severe pancreatitis. Endosc Ultrasound 2013;2:228-9

How to cite this URL:
Rana SS, Bhasin DK, Rao C, Singh K. Portal hypertensive biliopathy developing after acute severe pancreatitis. Endosc Ultrasound [serial online] 2013 [cited 2020 Jul 2];2:228-9. Available from: http://www.eusjournal.com/text.asp?2013/2/4/228/121244

A 46-year-old female patient was presented with a severe epigastric pain and vomiting of 3 days duration. Her serum amylase was 630 (70-200) U/L and serum bilirubin was 0.5 (0.3-1.3) mg/dL. She had normal hemogram, renal function tests, calcium and lipid profile and intact parathormone levels. There were no gall stones on ultrasound of the abdomen. Contrast enhanced computerized tomography (CT) showed grade E acute pancreatitis (AP) with a CT severity index of 8. She was managed conservatively and improved. An endoscopic ultrasound (EUS) evaluation performed 1 month later revealed normal gall bladder and common bile duct and she was diagnosed as a case of idiopathic AP.

On follow-up, 9 months later, she was found to be having elevated serum alkaline phosphatase 356 (N: 42-128) U/L with normal aminotransferases. Ultrasound of the abdomen was revealed prominent central intrahepatic biliary radicles with thrombosed portal and splenic vein. EUS revealed a large number of intra-abdominal venous collaterals. These collaterals were prominent around the gastro-esophageal junction, porta and peri pancreatic location [Figure 1]. The common bile duct was found to be prominent (8 mm) with extensive venous collaterals compressing it from outside as well as intra choledochal collaterals were noted [Figure 2],[Figure 3] and [Figure 4]. The pancreatic body and tail were atrophied and main pancreatic duct was not dilated. A diagnosis portal hypertensive biliopathy (PHB) secondary to segmental portal hypertension was made. There was no jaundice and there are no esophagogastric varices. She has been advised regular follow-up and she is asymptomatic at 6 months follow-up.
Figure 1. Endoscopic ultrasound showing extensive peri pancreatic collaterals

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Figure 2. Endoscopic ultrasound showing prominent common bile duct with multiple anechoic channels around it

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Figure 3. Color Doppler showing multiple collaterals around the common bile duct

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Figure 4. Power Doppler showing multiple collaterals around the common bile duct. An intra-choledochal collateral is also noted (*)

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PHB is usually secondary to extra-hepatic portal vein obstruction, non-cirrhotic portal fibrosis or liver cirrhosis. It is due to the biliary obstruction or ischemia caused by the adjacent porto-portal collaterals formed secondary to long standing portal vein obstruction. [1] Left sided portal hypertension secondary to thrombosis of spleno-portal axis occurs in up to 15% of chronic pancreatitis (CP) and 22% of AP patients. [2],[3] Occurrence of PHB is rare with CP and has been rarely reported. [4] PHB has also been rarely reported to occur following AP and this may be because the vascular thrombosis in AP may resolve in at least one-third cases after recovery and also the portal hypertension is of shorter duration, probably giving no time for the formation of collaterals. [5],[6] Choledochal varices in these patients can be documented by using EUS or intraductal ultrasonography. [7]

 
  References Top

1.Dhiman RK, Behera A, Chawla YK, et al. Portal hypertensive biliopathy. Gut 2007; 56: 1001-8.  Back to cited text no. 1
[PUBMED]    
2.Bhasin DK, Rana SS, Chandail VS, et al. Clinical profile of calcific and noncalcific chronic pancreatitis in north India. J Clin Gastroenterol 2011; 45: 546-50.  Back to cited text no. 2
[PUBMED]    
3.Butler JR, Eckert GJ, Zyromski NJ, et al. Natural history of pancreatitis-induced splenic vein thrombosis: A systematic review and meta-analysis of its incidence and rate of gastrointestinal bleeding. HPB (Oxford) 2011; 13: 839-45.  Back to cited text no. 3
[PUBMED]    
4.Rana SS, Bhasin DK, Behera A. Rare cause of jaundice in chronic pancreatitis: Portal hypertensive biliopathy. Clin Gastroenterol Hepatol 2011; 9: e64-5.  Back to cited text no. 4
[PUBMED]    
5.Gonzelez HJ, Sahay SJ, Samadi B, et al. Splanchnic vein thrombosis in severe acute pancreatitis: A 2-year, single-institution experience. HPB (Oxford) 2011; 13: 860-4.  Back to cited text no. 5
[PUBMED]    
6.Palazzo L, Hochain P, Helmer C, et al. Biliary varices on endoscopic ultrasonography: Clinical presentation and outcome. Endoscopy 2000; 32: 520-4.  Back to cited text no. 6
[PUBMED]    
7.Rai T, Irisawa A, Takagi T, et al. Intraductal sonography of biliary varices associated with extrahepatic portal vein obstruction. J Clin Ultrasound 2007; 35: 527-30.  Back to cited text no. 7
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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