BJR
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
British Journal of Radiology (2005) 78, 265-268
© 2005 British Institute of Radiology
doi: 10.1259/bjr/30325507
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Riddell, A
Right arrow Articles by Haider, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Riddell, A
Right arrow Articles by Haider, M

Case report

Pseudocyst rupture into the portal vein diagnosed with MRI

A Riddell, MB BS, FRCS, FRCR K Jhaveri, MD and M Haider, MD, FRCP(C)

Department of Medical Imaging, University Health Network, Princess Margaret Hospital, 610 University Avenue, Toronto, M5G 2M9, Canada


   Abstract
Top
 Abstract
Introduction
 Case report
 Discussion
 References
 
We report on the first documented case of rupture of a pancreatic pseudocyst into the portal vein diagnosed with MRI.


   Introduction
Top
 Abstract
 Introduction
Case report
 Discussion
 References
 
The development of a pseudocyst is a common complication of pancreatitis. Complications related to pseudocysts include rupture into adjacent viscera [1, 2], haemorrhage [3], disseminated fat necrosis [4, 5], arthritis [6], and vascular complications – pseudoaneurysm formation [7] and portal vein thrombosis [8, 9]. Pseudocyst rupture into either the portal or splenic vein is a rare complication. The diagnosis is usually made at endoscopic retrograde cholangiopancreatography (ERCP) or surgery. We report a case where this diagnosis was made with MRI and describe the MRI features. After an extensive literature search we believe this is the first documented case where the diagnosis was made using this technique.


   Case report
Top
 Abstract
 Introduction
 Case report
Discussion
 References
 
A 42-year-old female was transferred to our institution for management of the complications of chronic pancreatitis. She had no history of gallstones or alcohol abuse. At the time of transfer she was haemodynamically stable, afebrile with no signs of sepsis. An ultrasound on admission showed large volume ascites and a pseudocyst in the region of the neck of the pancreas. Analysis of the ascitic fluid showed a high amylase content 272 U l–1 (normal <1). A CT scan confirmed the presence of a 3 cm pseudocyst posterior to the neck of the pancreas. No contrast was present within the portal vein and there was cavernous transformation at the porta hepatis indicating this to be chronic (Figure 1Go). Sludge was present within the gallbladder, but no calculi.



View larger version (177K):
[in this window]
[in a new window]
  		Figure 1. This contrast enhanced CT shows low attenuation thrombus within the portal vein (black arrow) and small serpiginous contrast filled collaterals indicative of cavernous transformation.

 
The patient was discharged but re-admitted a month later. In the interim she had suffered a pulmonary embolism and was treated with warfarin sodium (Coumadin; Bristol-Myers Squibb Pharma Company, New York, NY). Her international normalized ratio (INR) was difficult to stabilize and anticoagulation was complicated by a retroperitoneal bleed. She was re-admitted for the insertion of an inferior vena cava (IVC) filter and for anticoagulation stabilization. On admission her INR was 1.1 and her activated partial thromboplastin time (aPPT) 45.5 s (range 28–40 s). CT was performed confirming a large retroperitoneal haematoma within the left psoas muscle. The pancreatic pseudocyst was still present and remained stable in size. An ultrasound confirmed lack of flow within the portal vein and also showed similar echogenic debris within the portal vein and pseudocyst (Figures 2a, bGo). MRI was performed during the same admission, which confirmed the presence of a large left psoas muscle haematoma. The signal intensity of the portal vein was that of fluid (low on T1 and high on T2 weighted images with no enhancement following gadolinium administration) rather than blood products, as would be expected in portal vein thrombosis. The T2 weighted breath-hold fast recovery sequence (Figure 3aGo) showed similar high signal intensity within the portal vein as seen in the intrahepatic bile ducts, rather than the signal void expected from a patent portal vein. The T1 weighted coronal images (Figure 3b, cGo) demonstrate homogeneous low signal within the pseudocyst and portal vein confirming the presence of fluid, rather than thrombus within these structures. The T2 weighted radial slab (Figure 4Go) showed similar signal intensity returned from the biliary tree, pseudocyst and portal vein. Direct communication between the portal vein and the pseudocyst was demonstrated on axial single shot fast spin echo (SSFSE) T2 images (Figure 5Go). No communication was seen between the pancreatic duct and the pseudocyst. The patient remains asymptomatic from the pancreatic-portal vein fistula and she has been treated conservatively but is under close clinical surveillance.



View larger version (48K):
[in this window]
[in a new window]
  		Figure 2. (a) Lack of flow within the portal vein is confirmed on ultrasound, with no flow on the spectral Doppler trace. Colour Doppler signal is seen in the portal collaterals. (b) This grey scale image shows echogenic material within the portal vein (black arrow), which is similar in appearance to that seen in the pseudocyst (white arrow). Sludge is seen layering in the gallbladder.

 


View larger version (100K):
[in this window]
[in a new window]
  		Figure 3. (a) Axial breath hold fast recovery (BHFR) T2 weighted image shows high signal fluid within the left portal vein (white arrow) and also within biliary radicals (white arrow heads). On this sequence flowing blood within a normal portal vein would be of low signal intensity, and thrombus of heterogeneous intermediate signal intensity. The pseudocyst, which is caudal to this image, had the same signal intensity as the portal vein. The patient also has ascites, predominantly surrounding the anterolateral margin of the liver. (b, c) Coronal T1 weighted images show homogeneous low signal intensity within (b) the portal vein (white arrow) and (c) anterior pseudocyst (white arrow), consistent with fluid rather than thrombus.

 


View larger version (131K):
[in this window]
[in a new window]
  		Figure 4. This T2 weighted radial slab image shows high signal fluid within the common bile duct and biliary tree (black arrowheads), the pseudocyst (open black arrow) and the portal vein (black arrow). Signal would not normally be returned from flowing blood within the portal vein.

 


View larger version (43K):
[in this window]
[in a new window]
  		Figure 5. A series of three axial single shot fast spin echo (SSFSE) T2 weighted images show a tract passing from (a) the posterior aspect of the pseudocyst to (c) the main portal vein.

 

   Discussion
Top
 Abstract
 Introduction
 Case report
 Discussion
References
 
The mechanism of the fistula formation is controversial, but it has been hypothesized that it occurs soon after thrombosis of the portal vein, when the portal system is cut off from the systemic circulation. The pancreatic enzymes then cause erosion of the wall of the vein and breakdown the fresh thrombus, substituting the vein contents with material from the pseudocyst [10].

There have been 11 cases of a fistulous communication between a pancreatic pseudocyst and either the portal or splenic vein reported to date. All these patients had a history of chronic pancreatitis secondary to alcohol abuse [4, 6, 9–17]. The majority of patients presented with abdominal pain, some with acute-on-chronic pancreatitis. Several showed signs of disseminated fat necrosis and arthritis [6, 11, 13, 15]. In the cases described to date, the diagnosis has been made by invasive imaging techniques such as ERCP (five cases) or surgically (three cases). Two cases were diagnosed by percutaneous splenoportography [16].

In our case the diagnosis was made with MRI, which confirmed the presence of the fistulous tract and the presence of static fluid within the portal venous system giving supportive evidence of the pseudocyst-portal vein communication. This provided a definitive diagnosis in a non-invasive manner. Although ERCP does provide a dynamic view of the ductal and portal systems it is invasive, with a 6.7% risk of inducing pancreatitis [18]. Also, if there is no communication between the main pancreatic duct and the pseudocyst, the pseudocyst-portal fistula will not be demonstrated at ERCP. The treatment depends on the patient's clinical symptoms. Asymptomatic patients, such as in our case, have been treated conservatively. Patients with signs of sepsis or disseminated fat necrosis are usually treated surgically by a pancreaticoenterostomy. We feel this case report illustrates the great strength of MRI, with its ability to characterize different soft tissue elements and highlights its use in the diagnosis of this rare complication of pancreatitis. Thus obviating the need for an invasive means of diagnosis.


   Footnotes
 
Current address for Dr Angela Riddell, Department of Radiology, The Royal Marsden Trust, Downs Road, Sutton, Surrey SM2 5PT, UK. Back

Received for publication March 12, 2004. Revision received October 19, 2004. Accepted for publication November 25, 2004.


   References
Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 

  1. Shah P, Pamakan R. Spontaneous rupture of a pseudocyst of the pancreas into the stomach. Am J Gastroenterol 1989;84:1466–7.
  2. Sbrocehi RD, Anderson MC. Erosion of adjacent organs by pancreatic pseudocysts. Am Surg 1984;50:191–6.
  3. Kelly SB, Gauhar T, Pollard R. Massive haemorrhage from a pancreatic pseudocyst. Am J Gastroenterol 1999;94:3638–41.[CrossRef][Medline]
  4. Zeller M, Hetz HH. Rupture of a pancreatic cyst into the portal vein. Report of a case and generalized fat necrosis. JAMA 1966;195:181–5.[Free Full Text]
  5. Sorensen EV. Subcutaneous fat necrosis. A review and two case reports. J Clin Gastroenterol 1988;10:71–5.[Medline]
  6. Hammar A, Sand J, Lumio J, Hirn M, Honkonen S, Tuominen L, et al. Pancreatic pseudocystportal vein fistula manifests as residivating oligoarthritis, subcutaneous, bursal and osseal necrosis: a case report and review of literature. Hepato-Gastroenterology 2002;49:273–8.[Medline]
  7. White AF, Baum S, Buranasiri. Aneurysms secondary to pancreatitis. AJR Am J Roentgenol 1976;127:393–6.[Abstract]
  8. Warshaw AL, Jin G, Ottinger LW. Recognition and clinical implications of mesenteric and portal vein obstruction in chronic pancreatitis. Arch Surg 1987;122:410–5.[Abstract/Free Full Text]
  9. McCormick PA, Chronos N, Burroughs AK, McIntyre N, McLaughline JE. Pancreatic pseudocyst causing portal vein thrombosis and pancreatico-pleural fistula. Gut 1990;31:561–3.[Abstract/Free Full Text]
  10. Procacci C, Mansueto GC, Graziani R, Bicego E, Pederzoli P, Mainardi P, et al. Spontaneous rupture of a pancreatic pseudocyst into the portal vein. Cardiovasc Interv Radiol 1995;18:399–402.[CrossRef][Medline]
  11. Skarsgard ED, Ellison E, Quenville N. Spontaneous rupture of a pancreatic pseudocyst into the portal vein. Can J Surg 1995;38:459–63.[Medline]
  12. Yamamoto T, Hayakawa K, Kawakami S, Nishimura K, Katsuma Y, Hayashi N, et al. Rupture of a pancreatic pseudocyst into the portal venous system. Abdom Imaging 1999;24:494–6.[CrossRef][Medline]
  13. Potts JR. Pancreatic-portal vein fistula with disseminated fat necrosis treated by pancreaticoduodenectomy. Southern Med J 1991;84:632–5.[Medline]
  14. Steenberg WV, Ponette E. Pancreaticoportal fistula: a rare complication of chronic pancreatitis. Gastrointest Radiol 1990;15:299–300.[CrossRef][Medline]
  15. Willis SM, Brewer T. Pancreatic duct-portal vein fistula. Gastroenterology 1989;97:1025–7.[Medline]
  16. Takayama T, Kato K, Sano H, Katada N, Takeichi M. Spontaneous rupture of a pancreatic pseudocyst into the portal venous system. AJR Am J Roentgenol 1986;147:935–6.[Free Full Text]
  17. Takayma T, Kato K, Katada N, Nishimura D, Shibata T, Kato K, et al. Radiological demonstration of spontaneous rupture of a pancreatic pseudocyst into the portal system. Am J Gastroenterol 1982;76:55–8.
  18. Freeman ML, DiSario JA, Nelson DB, Fennerty MB, Lee JG, Bjorkman DJ, et al. Risk factors for post-ERCP pancreatitis: a prospective, multicenter study. Gastrointest Endosc 2001;54:425–34.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 RadioGraphicsHome page
B. Kalb, J. M. Sarmiento, D. A Kooby, N. V. Adsay, and D. R. Martin
MR Imaging of Cystic Lesions of the Pancreas
RadioGraphics, October 1, 2009; 29(6): 1749 - 1765.
[Abstract] [Full Text] [PDF]

Home page
 Br. J. Radiol.Home page
S E Yoon, Y-H Lee, K-H Yoon, C S Choi, H-C Kim, and K M Chae
Spontaneous pancreatic pseudocyst-portal vein fistula presenting with pancreatic ascites: strength of MR cholangiopancreatography
Br. J. Radiol., January 1, 2008; 81(961): e13 - e16.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Riddell, A
Right arrow Articles by Haider, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Riddell, A
Right arrow Articles by Haider, M

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
BJR DMFR IMAGING  ALL BIR JOURNALS