British Journal of Radiology (2004) 77, 966-968
© 2004 British Institute of Radiology
doi: 10.1259/bjr/68883992
Intrahepatic portosystemic venous shunt passing through the left inferior phrenic vein and draining into the left renal vein
T Hirota, MD,
T Yamagami, MD, PhD,
T Matsumoto, MD,
H Seo, MD,
O Tanaka, MD, PhD,
S Iida, MD, PhD,
T Kato, MD, PhD and
T Nishimura, MD, PhD
Department of Radiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo, Kyoto, 602-8566, Japan
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Abstract
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We report a case of an intrahepatic portosystemic venous shunt (IPSVS) passing through the left inferior phrenic vein and draining into the left renal vein and then to the inferior vena cava. We incidentally detected the IPSVS while performing a transcatheter arterial embolisation for the treatment of hepatocellular carcinoma. IPSVS with the left inferior phrenic vein as the draining vein is very rare. The complete pathway of this IPSVS could be clearly demonstrated by multidetector row CT during arterial portography.
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Introduction
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Intrahepatic portosystemic venous shunt (IPSVS) is rare, but as a result of the development of radiological techniques, such as CT and MRI with contrast materials and ultrasound with Doppler analysis, the number of reports of IPSVS has recently been increasing [1–12]. Previous reports have described a variety of morphological findings in IPSVS, but no IPSVS draining into the left renal vein through the left inferior phrenic vein has ever been described. IPSVS draining into the left renal vein through the left inferior phrenic vein was clearly demonstrated by 16-slice multidetector row CT during arterial portography in our patient, and this is the first report of such a case in the English literature.
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Case report
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A 68-year-old man with recurrent hepatocellular carcinoma (HCC) was admitted to our department. Liver biopsy performed 10 years earlier had revealed chronic liver disease. The segment (S) of the liver that was biopsied was unknown. Transcatheter arterial embolisation (TAE) and percutaneous ethanol injection therapy (PEIT) of S3, S4, S5, S6 and S7 had been repeatedly performed for HCC following diagnosis 1 year previously. There was no history of trauma, and there had been no episodes of hepatic encephalopathy. The laboratory data showed only slight abnormalities of liver function tests, and negativity for antibody of type B or C viral hepatitis.
Dynamic single-detector row CT revealed an enhancing mass in S2 of the liver, and recurrence of HCC was suspected. Arteriographic studies with and without CT were performed to further evaluate the mass in the liver. The lesion was detected as an area of decreased portal perfusion on 16-slice multidetector row CT during arterial portography (CTAP) (Aquillion; Toshiba, Tokyo, Japan) and it showed tumour vascularity on digital subtraction coeliac arteriography, confirming the mass to be HCC. In addition to the hepatic mass lesion, an anomalous vessel was detected as an incidental finding on the imaging studies.
Single-detector row CT showed abnormal dilated vessels penetrating the surface of S2 (Figure 1
). Digital subtraction arterial portography by superior mesenteric artery injection of contrast material demonstrated abnormal dilated vessels from the peripheral posterosuperior portal vein branch extending outside the liver (Figure 2). Based on this finding, the abnormal vessels were suspected of being an IPSVS, but the images did not clearly depict the whole pathway. Multidetector row CTAP (Figure 3) and three-dimensional (3D) images (Figure 4) demonstrated a dilated left posterosuperior portal vein branch in the periphery penetrating the liver surface posteriorly running beneath the inferior aspect of the diaphragm and draining into the left renal vein, and then into the inferior vena cava. These findings indicated that the dilated peripheral portal vein communicated with the left renal vein through the left inferior phrenic or suprarenal vein.
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Figure 1. Transaxial images of single-detector row CT with contrast materials showed an abnormal dilated vessel (solid arrow) extending from the peripheral posterosuperior portal vein to outside the liver, but they failed to show where the dilated vessel drained.
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Figure 2. Digital subtraction portography after superior mesenteric arteriography shows the left posterosuperior portal vein branch dilated in the periphery (solid arrow), and forming a loop caudally (open arrow), but it failed to show the portosystemic shunt itself.
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Figure 3. Transaxial images of multidetector row CT demonstrate the peripherally dilated left posterosuperior portal vein branch, (a) penetrating the liver surface posteriorly (solid arrow) and (a, b) draining into the left renal vein (open arrow).
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Figure 4. Anteroposterior view images reconstructed from multidetector row CT during arterial portography by maximum intensity projection techniques, demonstrating almost the entire pathway of the IPSVS. The draining vein passes through the left inferior phrenic vein (solid arrow).
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The single-detector row CT images were obtained in the craniocaudal direction with a 5 mm collimation and a 7 mm s–1 table speed while the patient held his breath for 30 s following a 90 s delay after the transvenous injection of 100 ml of 300 mgI ml–1 of contrast medium at a rate of 3 ml s–1. The multidetector row CTAP was obtained in the craniocaudal direction with 7 mm collimation and a 15 mm s–1 table speed during a 20 s breath-hold following a 35 s delay after a transcatheter superior mesenteric arterial injection of 70 ml of 150 mgI ml–1 contrast medium at 2 ml s–1. Contiguous transaxial images of 3 mm thick with no gaps were reconstructed from the volumetric data set, and 3D images reconstructed from these CTAP images were obtained using maximum intensity projection techniques on the workstation (Aquarius; Tera Recon Inc., Silicon Valley, USA).
Radiofrequency ablation was used to treat the recurrent HCC. The IPSVS has been monitored without treatment, and there have been no manifestations of hepatic encephalopathy.
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Discussion
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The frequency of reports of cases of IPSVS has been increasing in parallel with improvements in radiological techniques [1–12] after Raskin et al first described the condition in 1964 [1]. Itai et al reviewed 1000 consecutive CT scans of the liver performed with contrast material to retrospectively examine them for IPSVS [2]. They found IPSVS in 37 patients and divided the lesions into two subtypes according to whether the communicating systemic vein was outside (external type) or inside (internal type) the liver. Before the report of Itai et al [1], Park et al [3] had classified published cases of the internal type of IPSVS into the following four types according their configuration: (1) a single large tube of constant diameter connecting the right portal vein to the inferior vena cava; (2) a localized peripheral shunt with single or multiple communication between the peripheral branches of the portal and hepatic vein in one hepatic segment; (3) a connection between peripheral portal and hepatic veins through an aneurysm; and (4) diffuse and multiple communications between peripheral portal and hepatic veins in both lobes.
There have been few reports of the external type of IPSVS in S2 in the English literature [2, 4, 5]. In these few reports, the inferior phrenic vein draining into the abdominal wall or pericardiacophrenic vein was suggested as the shunt vessel's route outside the liver. In our patient, multidetector row CT during arterial portography clearly demonstrated that the IPSVS originated in the left portal vein branch, passed through the inferior phrenic or suprarenal vein, and drained into the left renal vein, and then inferior vena cava. 3D reconstruction of these CTAP images was especially useful in determining the entire pathway of this rare anomalous shunt.
The cause of IPSVS is a matter of controversy, except in cases occurring after liver biopsy or injury. Some authors believe that it is congenital [1, 6–9], that is, that a persistent embryonic venous anastomosis, such as the ductus venosus [6] or a right vitelline vein [7], may be the cause. Others advocate an acquired cause, such as iatrogenic or traumatic episodes, rupture of a portal venous aneurysm into a hepatic vein, portal hypertension secondary to chronic hepatitis or cirrhosis [10–12], or a dilated portal vein communicating with the inferior phrenic or suprarenal vein [11]. Kudo et al advocated that most IPSVSs are acquired, pointing to a case in which IPSVS was newly developed after a 7 year period [9]. A dilated portal vein communicating with the inferior phrenic or suprarenal vein is presumed to have been the cause in our case, but an iatrogenic cause could not be ruled out, because the patient had undergone liver biopsy, TAE and PEIT.
Treatment options include dietary control, transcatheter embolisation and surgical correction [1, 3, 7], although no consensus has been achieved. Our patient was not treated for the IPSVS, because no clinical manifestations, such as hepatic encephalopathy, were present. However, when IPSVS presents with hepatic encephalopathy, correct diagnosis and appropriate treatment are important clinically.
Received for publication September 25, 2003.
Revision received January 5, 2004.
Accepted for publication April 20, 2004.
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References
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- Raskin NH, Price JB, Fishman RA. Portal systemic encephalopathy due to congenital intrahepatic shunts. New Engl J Med 1964;270:225–9.
- Itai Y, Kurosaki Y, Saida Y, Niitsu M, Kuramoto K. CT and MRI in detection of intrahepatic portosystemic shunts in patients with liver cirrhosis. J Comput Assist Tomogr 1994;18:768–73.[Medline]
- Park JH, Cha SH, Han JK, Han MC. Intrahepatic portosystemic venous shunt. AJR Am J Roentgenol 1990;155:527–8.[Free Full Text]
- Kanematsu M, Enya M, Kondo H, Yokoyama R, Hoshi H. Hepatodiaphragmatic portosystemic shunt in cirrhosis. Eur J Radiol 1998;28:276–9.[CrossRef][Medline]
- Minami M, Kawauchi N, Itai Y, Kokubo T, Sasaki Y. Transdiaphragmatic portosystemic shunt to the pericardiacophrenic vein. AJR Am J Roentgenol 1993;161:569–71.[Free Full Text]
- Ohnishi K, Hatano H, Nakayama T, Kohno K, Okuda K. An unusual portal-systemic shunt, most likely through a patent ductus venosus. A case report. Gastroenterology 1983;85:962–5.
- Wittich G, Jantsch H, Tscholakoff D. Congenital portosystemic shunt diagnosed by combined real-time and doppler sonography. J Ultrasound Med 1985;4:315–8.[Medline]
- Fernandez MS, Gutierrez C, Vila JJ, Lopez A, Ibanez V, Sanguesa C, et al. Congenital intrahepatic portocaval shunt associated with trimethylaminuria. Peditr Surg Int 1997;12:196–7.[CrossRef]
- Kudo M. Intrahepatic portosystemic venous shunt in liver cirrhosis: is it congenital or acquired? AJR Am J Roentgenol 1993;160:421–2.[Medline]
- Takayasu K, Moriyama N, Shima Y, Muramatsu Y, Goto H, Yamada T, et al. Spontaneous portal-hepatic venous shunt via an intrahepatic portal vein aneurysm. Gastroenterology 1984;86:945–8.[Medline]
- Kozuka S, Sassa R, Kakumu S. An enormous intrahepatic shunt between portal vein and hepatic one. Angiology 1975;26:365–71.
- Grattagliano A, Rapaccini GL, Camaldo G, Pompili M, Marino P, Mastromatteo AM, et al. Spontaneous intrahepatic portosystemic venous shunt in a patient with cirrhosis: diagnosis by combined color Doppler and pulsed Doppler ultrasonography. Liver 1997;17:307–10.[Medline]
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Abstract
Introduction
