British Journal of Radiology (2008) 81, e13-e16
© 2008 British Institute of Radiology
doi: 10.1259/bjr/77979574
Spontaneous pancreatic pseudocyst-portal vein fistula presenting with pancreatic ascites: strength of MR cholangiopancreatography
S E Yoon, MD1,
Y-H Lee, MD1,
K-H Yoon, MD1,
C S Choi, MD2,
H-C Kim, MD2 and
K M Chae, MD3
Departments of 1 Radiology, 2 Internal Medicine and 3 Surgery, Wonkwang University School of Medicine, 344-2 Sinyongdong, Iksan, Jeonbuk 570-711, Korea
Correspondence: Seong Eon Yoon, Department of Radiology, Wonkwang University School of Medicine, 344-2 Sinyong-dong, Iksan, Jeonbuk, 570-711, Korea. E-mail: radiology{at}paran.com
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Abstract
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Pancreatic pseudocyst-portal vein fistulae are a very rare complication of acute or chronic pancreatitis. Another late complication of chronic pancreatitis is pancreatic ascites. We report the case of a 43-year-old man with a spontaneous pseudocyst-portal vein fistula presenting with pancreatic ascites diagnosed by various imaging modalities, in order to emphasize the strength and efficacy of magnetic resonance cholangiopancreatography.
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Introduction
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Pancreatic ascites is a rare condition resulting from pancreatic juice leak into the free peritoneal cavity secondary to the rupture of a pseudocyst or a pancreatic duct [1, 2]. The diagnostic criteria for pancreatic ascites have established that ascitic fluid has a high amylase content (>1000 IU l–1) and a high protein content (>3 g dl–1); in the absence of hypoalbuminaemia, the albumin level will be normal (>3 g dl–1) [1, 2]. Pseudocyst-portal vein fistula is a very rare condition, with only a few reports having been published in the English language literature [3–15]. Symptoms and signs of a pseudocyst-portal vein fistula vary from no symptoms to life-threatening sepsis or disseminated fat necrosis [3–15]. Herein, we report the case of a patient with a spontaneous pseudocyst-portal vein fistula presenting with massive pancreatic ascites; we also describe the imaging findings identified on CT, endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP).
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Case report
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A 43-year-old man was admitted to our hospital with a 1-month history of anorexia, mild abdominal pain and grossly distended abdomen. He had a past history of alcoholic pancreatitis and diabetes mellitus. Physical examination showed marked abdominal distension with mild tenderness. Laboratory blood test results were as follows (normal ranges are in parentheses): amylase 986 IU l–1 (0–200 IU l–1); lipase 2517 IU l–1 (13–60 IU l–1); aspartate aminotransferase (AST) 28 IU l–1 (5–35 IU l–1); alanine aminotransferase (ALT) 25 IU l–1 (5–40 IU l–1); and albumin 3.4 g dl–1 (3–5 g dl–1). Pancreatic ascites was confirmed by paracentesis results as follows: amylase 3819 IU l–1 (<1 IU l–1); lipase 17 300 IU l–1 (<1 IU l–1); and protein 3 g dl–1 (<2 g dl–1).
Contrast-enhanced CT scanning showed massive ascites, pancreatic duct dilatation with mild parenchymal atrophy, and biliary tree dilatation caused by distal common bile duct stricture sequelae to recurrent acute pancreatitis secondary to alcohol abuse. CT also confirmed a pseudocyst with internal debris in the pancreas head (Figure 1a
), no contrast enhancement of the portal vein (Figure 1b) and cavernous transformation around the portal vein. During ERCP, the portal vein was visualized using contrast material opacification, showing that it was connected to the pseudocyst (Figure 2). It was confirmed that the pancreatic pseudocyst had ruptured into the portal vein, i.e. a pseudocyst-portal vein fistula had formed. However, we could not explain the cause of the massive pancreatic ascites mentioned above, as ERCP did not identify any pancreatic juice leak through the pancreatic duct or pseudocyst into the peritoneal cavity. Interestingly, MRCP clearly demonstrated that pancreatic juice leak followed through the pancreatic pseudocyst-portal vein fistula, liver dome and into the peritoneal cavity (Figure 3a).
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Figure 1. (a) Contrast-enhanced CT scan shows massive ascites (asterisks) and a pancreatic duct dilatation (arrowhead) with mild parenchymal atrophy. Note the presence of a pseudocyst with internal debris in the pancreas head (arrows). (b) Contrast-enhanced CT scan shows low-attenuated fluid with no contrast enhancement of the portal vein (arrow), and cavernous transformation around the portal vein (arrowheads). Note an intrahepatic bile duct dilatation (open arrowhead) and massive ascites (asterisks).
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Figure 2. ERCP shows faint opacification of a pseudocyst(arrows) and the portal vein (arrowheads). However, ERCP did not show any pancreatic juice leak into the peritoneal cavity, which can be responsible for massive pancreatic ascites. b, common bile duct.
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Figure 3. (a) MRCP clearly demonstrates pancreatic juice leak through the pancreatic pseudocyst-portal vein fistula (arrowheads), liver dome (arrow) and into the peritoneal cavity (asterisks). (b) Intraoperative pseudocystography via a catheter (arrow) shows the pseudocyst-portal vein fistula (arrowheads). Note a large amount of contrast material spilling into the duodenum (asterisk); this accounted for the inability to demonstrate pancreatic leak. b, common bile duct; ps, pancreatic pseudocyst.
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The pancreatic ascites was drained via an external drainage tube. The patient underwent surgery after total parenteral nutrition for 2 weeks. During surgery, pseudocystography confirmed the pseudocyst-portal vein fistula (Figure 3b
) but did not show any pancreatic juice leak through the liver dome, as depicted on MRCP. We thought that pseudocystography may have failed owing to poor spatial and contrast resolution, as well as to the pressure and volume of contrast material being insufficient to show any pancreatic juice leak through the liver dome. Therefore, our conclusion agreed with MRCP findings. The patient was taken for distal pancreaticoenterostomy for internal drainage of the pancreatic juice. The patient was discharged 2 weeks later without any other complications, such as recurrence of the pancreatic ascites.
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Discussion
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To the best of our knowledge, there have been 13 cases of pancreatic pseudocyst connecting with the portal vein in the English language literature [3–15]. The mechanism of fistula formation between a pseudocyst and the portal vein is still theoretical: activated pancreatic enzymes within a pseudocyst cause inflammation and erosion of the portal vein wall and induce portal vein thrombosis. The pancreatic juice leak then breaks down the fresh thrombus, substituting the portal vein contents with material from the pseudocyst [7, 9]. The majority of patients with pancreatic pseudocyst-portal vein fistulae have previously suffered from chronic pancreatitis secondary to alcohol abuse [3–12, 15]. Clinically, the majority of these patients presented with a symptomatic or mild abdominal pain; however, some have life-threatening complications such as gastrointestinal bleeding [9], sepsis [14], disseminated fat necrosis or intramedullary bone necrosis [3, 5, 7, 13]. Our patient presented with pancreatic ascites, which is a unique presentation to date.
According to previous reports [6, 12, 14, 15], contrast-enhanced CT demonstrated low-attenuation thrombus with no contrast enhancement of the portal vein; CT was also able to depict the location and extent of the pseudocysts. However, as CT may not visualize the pseudocyst-portal vein fistula tract itself, ERCP has been mandatory for diagnosing pseudocyst-portal vein fistulae [4, 11, 13]. ERCP can also show the site of a pancreatic juice leak responsible for pancreatic ascites [16]. However, ERCP is invasive and may not be able to demonstrate fistulae in all cases. Failure to detect a fistula may result from incomplete opacification of the pancreatic duct, resulting form a proximal stricture or a stone in the main pancreatic duct [16]. Furthermore, if a pseudocyst has no connection to the main pancreatic duct, the pseudocyst-portal vein fistula will not be shown on ERCP [15, 16]. In our case, ERCP confirmed the pseudocyst-portal vein fistula but could not demonstrate the site of the pancreatic juice leak, as ERCP images did not include the area of leakage. ERCP could have shown the leak if the dome of the liver had been evaluated.
Unlike ERCP, MRCP is non-invasive, has a larger field of view and there is no need for contrast material. MRCP has also been useful in evaluating pancreatic duct disruption and leakage from the duct with secretin [17–19]. Riddell et al [15] confirmed the presence of a fistulous tract of the pseudocyst-portal vein using MR images. They described T2 weighted high-signal fluid within the portal vein and pseudocyst, as in our case. In our study, MRCP clearly showed a connection between the pancreatic pseudocyst and the portal vein. In addition, MRCP showed a unique site of pancreatic juice leak through the pseudocyst-portal vein fistula and liver dome and into the peritoneal cavity, which may be out of the field of view in ERCP.
It is clinically important to evaluate the precise site of, and any relationship between, a pancreatic juice leak to a pseudocyst-portal vein fistula, as the therapeutic options (e.g. pancreatic duct stent) and surgical approach depend on the ERCP, CT and MR findings [2, 16]. In most cases, distal pancreatectomy with a drainage procedure may be appropriate; surgical intervention to repair leaking sites should not be necessary, as in our case [2].
We report the first case of a pancreatic pseudocyst-portal vein fistula presenting with massive pancreatic ascites. Early recognition of a pancreatic pseudocyst-portal vein fistula and precise recognition of the site of the pancreatic juice leak are important in order to avoid life-threatening complications and to plan appropriate therapeutic options. MRCP can demonstrate not only the fistulous tract of the pseudocyst-portal vein but also the site of pancreatic juice leak.
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Acknowledgments
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We thank Bonnie Hami, Department of Radiology, University Hospitals Health System, Cleveland, OH, for her editorial assistance in preparing the manuscript. This paper was supported by Wonkwang University in 2005.
Received for publication July 2, 2006.
Revision received October 4, 2006.
Accepted for publication October 26, 2006.
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Abstract
Introduction
