British Journal of Radiology 74 (2001),654-656 © 2001 The British Institute of Radiology
CT findings of portal vein aneurysm caused by gastric adenocarcinoma invading the portal vein
D M Yang, MD
M H Yoon, MD
H S Kim, MD
W Jin, MD
H Y Hwang, MD
and
H S Kim, MD
Department of Radiology, Gachon Medical College Gil Medical Center, 1198, Guwol-Dong, Namdong-Gu, Inchon 405-760, South Korea
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Abstract
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The known causes of acquired origin portal vein aneurysm are portal hypertension, pancreatitis and trauma. We describe the CT findings of an additional cause of acquired origin portal vein aneurysm, namely gastric adenocarcinoma invading the portal venous system.
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Introduction
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Portal vein aneurysm is a rare vascular abnormality defined as a localized dilatation of the portal vein beyond normal limits [1, 2]. It usually occurs at the junction of the superior mesenteric and splenic veins, or at the hepatic hilus at the bifurcation of the right and left portal veins [1]. Histopathologically, portal vein aneurysm consists of a thin wall with markedly reduced tunica intima and media [3]. Two aetiologies, congenital and acquired, have been proposed as the cause of portal vein aneurysm [1–8]. Portal hypertension, pancreatitis and trauma are known causes of acquired portal vein aneurysm [1–5].
We describe the CT findings in a case of acquired origin portal vein aneurysm caused by gastric adenocarcinoma invading the portal vein, which to our knowledge has not been described before.
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Case report
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A 64-year-old man with gastric adenocarcinoma proven by endoscopic biopsy was admitted to hospital for surgery. Helical CT (Somatom Plus 4; Siemens, Erlangen, Germany) showed an encircling mural thickening of the gastric antrum with loss of the fat plane between the tumour and the pancreas (Figure 1a
). The portal vein was normal (Figure 1b). At laparotomy, a mass the size of an adult fist was found in the gastric antrum and there was invasion of the pancreas. Palliative gastrojejunostomy was performed.
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Figure 1. (a,b) Helical CT showing an encircling mass in the gastric antrum (arrow) with invasion of the pancreas head. The portal vein is normal.
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The patient was re-admitted 2 months later with jaundice. There were elevated levels of serumaspartate aminotransferase (93 U l-1), serum alanine aminotransferase (138 U l-1) and serum bilirubin (13 mg dl-1). On CT, the gastric mass was enlarged and now extended into the duodenum, pancreas head and hepatoduodenal ligament (Figure 2a). Multiple enlarged gastrohepatic, retroportal and posterior pancreatoduodenal lymph nodes were also observed, together with a marked dilatation of intrahepatic bile ducts owing to extrinsic compression by the adjacent enlarged lymph nodes. The main portal vein and superior mesenteric vein were invaded by the tumour (Figures 2a,b) and their lumens were narrowed. There was fusiform dilatation of the right portal vein, with a diameter of 3 cm, distal to the narrowed main portal vein (Figure 2c). The left portal vein was normal in diameter.
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Figure 2. (a) 2 months later, helical CT shows enlargement of the gastric mass (large arrow), with tumour invasion of the duodenum, pancreas head and superior mesenteric vein (small arrow). (b) The main portal vein is invaded by the tumour (small arrow) and the lumen of the main portal vein is narrowed. An enlarged retroportal lymph node is seen (large arrow). (c) Fusiform dilatation of the right portal vein is present.
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The patient underwent percutaneous biliary drainage. No specific treatment was given for the portal vein aneurysm. The patient's condition progressively deteriorated and he died 4 months after detection of the portal vein aneurysm.
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Discussion
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Although portal vein aneurysm is still rare, previously unrecognized portal vein aneurysm is now detected more frequently with the increasing use of cross-sectional imaging in the evaluation of abdominal complaints. However, the cause, clinical manifestation and management of portal vein aneurysm are still not clear [1].
Congenital portal vein aneurysm results from an inherent weakness of the vessel, which is supported by the fact that most patients with an aneurysm have no relevant history such as portal hypertension [6]. In addition, in utero diagnosis of a portal vein aneurysm has suggested a congenital origin [9].
Known acquired aetiologies of portal vein aneurysm are portal hypertension, pancreatitis and trauma [1–5]. A significant number of patients have underlying diseases such as hepatocellular disease and portal hypertension [1–4]. The release of pancreatic juice in pancreatitis could cause a weakening of the vessel wall withconcomitant development of portal vein aneurysm [4].
In our case, the portal vein aneurysm was acquired because the portal vein had been normal 2 months earlier. We suggest that post-stenotic dilatation of the portal vein, with or without an inherent weakness of the vessel wall owing to turbulence of blood flow, is a possible cause of the portal vein aneurysm in this case. Although four cases of portal venous thrombus associated with gastric adenocarcinoma have been reported, portal vein aneurysm associated with gastric adenocarcinoma invasion of the portal vein has not been described [10].
We were able to exclude portal hypertension as a cause of portal vein aneurysm in our patient as there was no evidence of portal hypertension, such as portosystemic collateral vessels, splenomegaly and ascites, in this case although direct portal pressure measurement was not performed. Acute thrombus in venous systems may produce aneurysmal dilatation [11]. In our case, however, the thrombus was not located in the lumen of the aneurysmal dilatation of the portal vein, but proximal to it.
Received for publication December 5, 2000.
Revision received March 21, 2001.
Accepted for publication April 4, 2001.
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References
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Abstract
Introduction
