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Aneurysm of the intrahepatic branch of the portal vein
(;ASTKOENI‘E:KOL.O(;E’
Aneurysm of the Intrahepatic the Portal Vein
Branch
1984:86:169-73
of
Report of Two Cases KUNIHIKO OHNISHI, TAKATSUNE NAKAYAMA, MASAYUKI SAITO, FUMIO NOMURA, HIROFUMI JUNICHI TAMARU, ISAMU IWASAKI, and KUNIO First Departments
of Medicine
and Pathology. Chiba I!niversit\;
Two patients in rvhom real-time ultrasonography and percutaneous transhepatic portography or the venous phase of the arteriogram of the superior mesenteric artery demonstrated a localized saccular dilation of a peripheral branch of the portal vein are described. One patient subsequently died. and autopsy confirmed the diagnosis. A hypoechoic lesion continuous with a branch of the portal vein seems to be the characteristic sonographic picture. Radiologic e\~idence for portal vein aneurysm was obtained in only z of 300 patients with portal hypertension in whom percutaneous transhepatic portograph!, was performed. and in 2 of 3000 patients who visited our unit and in whom ultrasonography for the liver leas performed. Thus, aneurysm of the intrahepatic portal vein does occur, but very rarely. Barzilai and Kleckner (1) were apparently the first to report an aneurysm of the portal vein. They described a patient who developed postnecrotic cirrhosis. thrombosis of the right portal vein, and an aneurysm proximal to the thrombus with subsequent rupture into the biliary system. Ten other cases have since beon reported, but nine of these aneurysms were extrahepatic (Z-8). In only 1 case was ultrasound e\raluation made (8). The following 2 cases seem to be the first documentation of intrahepatic portal vein aneurysm discovered by ultrasound examination.
liwxived blay 26, 1983. Accepted August 6. 1983. Address requests for reprints to: Kunihiko Ohnishi. M.D., First Department of Medic.ine. Chiba liniversity School of Medicine. I8-l Inohan;r. Chiba Cit\l. Chiba. Japan. This Lvork \vas supported h! a Japan Ministry of Health and Welfare Gr,lnt. ’ 198-1ti\, the American (;astror?nterological Association OOlfi-5f)R,i
81’53.00
KOEN, OKUDA
School of Medicine.
Chib,i.
Case Reports Case
1
A 47-yr-old man was referred to us for the evaluation of a suspected mass in the liver on December 13,1982. He had been drinking heavily, an equivalent of -100 ml of ethanol per day in the form of Japanese sake. for the last 28 yr. Eight years before admission. he was told of his abnormal liver function tests and glucosuria, but he did not seek medical treatment. In November I 981, he developed easy fat&ability and heat sensation of the skin, and his physician found a lesion in the liver b!; ultrasound. On admission, he had spider angiomata, palmar erythema, and gynecomastia. but there WBS no jaundice. flapping tremor, ascites. or edema. The li\Ter was felt three finger breadths below the right costal margin. and the spleen was not palpable. Laboratory study disc.losed the following data: serum aspartate transaminase [AST). 81 IIJiL; alanine transaminase (ALT), 119 W/L: albumin. 1.2 g!til: r-globulin. 1.8 g/dl: total bilirubin. 0.8 rng~dl:
170
Figure
OHNISHI ET AL.
in the right subcostal scan in case 1 demonstrating a hypoechoic lesion in the anteroinferior segment of the right lobe of the liver.
GASTROENTEROLOGY
Vol. 86. No. 1
1. Ultrasonogram
Percutaneous transhepatic portography disclosed a saccular dilation of one of the peripheral branches of the portal vein in the early phase (Figure 4A), and a round stain with a filling defect in the center (Figure 4B). The portal vein pressure was measured to be 224 mmHpO. Hepatic vein catheterization showed a wedged hepatic vein pressure of 198 mmHZO, and free hepatic vein pressure of 25 mmH,O. Hepatic venography demonstrated irregularity of the peripheral branches of the right hepatic vein. The hypoechoic lesion surrounded by high-level echoes in the liver has since been followed, but it has not changed in size for at least 7 mo, until the time this article was prepared.
Case
Figure 2. Ultrasonogram in the right subcostal scan in case 1. Slight slanting of the transducer medially changes the hypoechoic lesion in Figure 1 to an echodense one (arrow) that seems to be continuous with the anteroinferior branch of the right portal vein.
2
A 56-yr-old man was admitted for evaluation of a masslike lesion found in the liver. He had had pulmonary tuberculosis, and had had resection of the right upper and middle lobes with many blood transfusions 23 yr earlier. Four years before this admission, his liver function tests were found to be abnormal, and he was followed by his physician. In July 1979, he developed ascites and was subsequently hospitalized with a diagnosis of cirrhosis. The ascites was controlled for some time, but he again developed ascites and a lesion was found in the liver by ultrasound on October 1, 1980. On admission, there were spider angiomata, palmar
F‘igure 3. Dynamic computed tomography in case 1, after bolus injection of contrast medium, opacified a low-density area during the venous chase Carrowl.
)anuary
Figure
ANL’E:I!KYSP\l OF THE
1984
IN’I’RAH~P:\Tl(:
POKTAI,
VEIN
171
4. Percutaneous transhepatic portography in case 1. A. Portogram demonstrating a saccular dilation (orrow) of one of the peripheral branches of the right portal vein in an early phase. H. Portogram of a late phase showing a round stain with a central
tilling defect (~W~OMJ)
erythema, ascites, and edema of the lower extremities. The liver and spleen were not palpable. Laboratory examination disclosed the following data: serum AST, 182 IUiL; 1.8 mgidl; prothrombin ALT, 143 IUIL; total bilirubin, time, 16.7 s with a control value of 12.0 s, and indocyanine green test, 490/o retention at 15 min. Serum HBsAg was negative. Endoscopy of the esophagus and stomach revealed large varices along the entire length of the esophagus. Ultrasound examination of the liver demonstrated, in the right intercostal section, an ovoid hypoechoic lesion in the posterosuperior segment of the right lobe. It seemed to be contiguous with one of the portal branches. The surface of the liver was irregular and there was massive ascites. Plain CT demonstrated a low-density area in the superior portion of the right lobe of the liver and ascites. Angiography of the proper hepatic artery demonstrated a corkscrew pattern of their branches, a typical pattern of cirrhosis. Superior mesenteric arteriogram revealed a saccular dilation (1.5 x 2 cm] of the posterosuperior branch of the right portal vein in the venous phase (Figure 5). All these findings were compatible with an aneurysm of the intrahepatic branch of the portal vein and liver cirrhosis with esophageal varices. One month after admission, ascites was controlled by low-salt diet and diuretics, and the patient was discharged. On February 1, 1981, he devel-
oped hepatic encephalopathy, massive ascites, and jaundice, and was readmitted. Despite intensive treatment, he died from hepatic failure on September 18, 1981. On autopsy. a localized dilation of an intrahepatic: branch of the right portal vein branch was seen in a liver with macronodular cirrhosis (Figure 6). The wall of the aneurysm was very thin, with markedly reduced tunica intima and media compared with the wall of the left portal vein branch of comparable size.
Discussion Ten literature the
junction
of the were
11 portal
located
of the
vein
outside
superior
aneurysms the
mesenteric
liver,
in past mostly
and
at
splenic
veins, or in the major (the first right or left) branch of the portal vein. There seems to bc no clear definition of portal vein aneurysm. The size of the portal vein varies somewhat with the individual. Douglass et al. (10) studied 92 dissections and found the diameter of the portal vein to be 0.64-1.2 cm, with an average of 0.89 cm in patients without cirrhosis or portal hypertension. Purcell et al. (11) made similar measurements and found the averagc diameter to be 1.09
172
OHNISHI
ET AL.
GASTROENTEROLOGY
i:
Figure
5. Portogram obtained after superior mesenteric arteriography in case 2. An enlarged saccular dilation of the posterosuperior branch of the right portal vein is apparent.
cm. According to Reynolds (l2), the ter of the portal vein is 1.2cm, and it in cirrhosis. In the ultrasonographic Doust and Pearce of the portal vein
Figure
average diamebecomes greater study made by (13), the maxi-
6. Gross liver section in case 2, demonstrating rysm (arrow) and macronodular cirrhosis.
an aneu-
Vol.
86. No.
1
mum anteroposterior diameter never exceeded 1.5 cm in normal individuals and 1.9 cm in cirrhotics. The size of the intrahepatic portal branches is also variable. We measured ultrasonically the diameter of the right first branch of the portal vein at the bifurcation in 34 normal subjects and 49 cirrhotics, and found the average to be 0.66 + 0.11cm (SD] and 0.85 -+ 0.23 cm, respectively, among Japanese adults (14). Dilation much beyond this dimension may properly be classified as aneurysmal, especially if the vein outline assumes a fusiform or saccular configuration. Aneurysms of the portal vein are thought to have two etiologies: (a) congenital and (b) acquired secondary to portal hypertension. Most of the reported cases were incidental discoveries at the time of investigation for bleeding varices and cirrhosis, and some authors (1,~) believe that portal vein aneurysm is due to portal hypertension. Liebowitz and Rousselot (5), however, reported 1 case of agnogenic myeloid metaplasia and portal vein aneurysm with no evidence of portal hypertension; in this patient, the intrasplenic pulp pressure was normal without collateral circulation, and they assumed a congenital etiology. Thomas (4) shared a similar view for his 2 cases of portal vein aneurysm because there was no gross intra- and extrahepatic obstruction, the liver did not appear to be cirrhotic, and the aneurysm was saccular and thin walled. Some kind of congenital or developmental abnormality has also been suspected in other reports (3,6). In our cases, both congenital and acquired (portal hypertension) factors could have been involved. In case 1, the portal vein pressure was onlv 224 mmH,O. In case 2, the aneurysm of the right portal vein had an abnormally thin wall. Thus aneurysmal dilation may occur as portal hypertension develops in a person with hereditary weakness or developmental anomaly of the portal vein that occurred during its embryonic evolution from the vitelline vein. To detect a portal vein aneurysm in the liver as a masslike lesion is not difficult with real-time linear scan ultrasound. Diagnosis is almost certain if the vascular nature of the lesion is demonstrated. An uncomplicated portal vein aneurysm in the liver is characterized by an anechoic masslike lesion. Some portion of the aneurysm may be echogenic, due to a mural thrombus in it. In case 1, this might have been true. Three of the reported cases had a thrombus (1,2,4). The possibility that the echogenic material was a hepatocellular carcinoma invading the portal vein can be excluded by the negative aspiration cytology carried out under ultrasound guidance, and the unchanging size of the lesion for at least 7 mo of observation. In our unit, >3000 patients, including those with a normal or unremarkable hepatobiliary system, have so far been studied by real-time ultra-
January
ANEURYSM
1984
sound, and 300 patients with portal hypertension have been investigated by percutaneous transhepatic portography with complete opacification of the intrahepatic portal branches. Thus, the crude incidence of portal vein aneurysm among patients with portal hypertension was 2 of 300, and among the patients who came to the hospital with complaints related to the hepatobiliary system, the incidence was 2 of 3000.
6.
7. 8. 9. 10.
References Barzilai R. Kleckner MS. Hemocholecyst following ruptured aneurysm of portal vein. Arch Surg 1950;72:725-7. Leonsins AJ, Siew S. Fusiform aneurysmal dilatation of the portal vein. Postgrad Med J 1960;36:570-4. Hermann RE. Shafer WH. Aneurysm of the portal vein and portal hypertension. Ann Surg 1965;162:1101-4. Thomas TV. Aneurysm of the portal vein: report of two cases. One resulting in thrombosis and spontaneous rupture. Surgery 1967:61:550-5. Liebowitz HR. Rousselot LM. Saccular aneurysm of portal
11.
12. 13. 14.
OF THE INTRAHEPATIC:
PORTAL
VEIN
173
vein with agnogenic myeloid metaplasia. NY State J Med 1967;67:1443-7. Wenz W, Beckenbach H. Daum K. Dlcr kindliche I’fortader bei Erkrankungen der Oberbauchorgane Eur 1 Pediatr 1971; 9:354-62. Duhmke \‘E. Aneurysma der vena portac:. ROFO 197.1,; 125:474-5. Vine HS, Sequeira JC. Widrich 12’(:. Sachs HA. Portal vein aneurysm. AJR 1979;132:557-60. n‘akayama T. Hiyama Y. Ohnishi K. et al. Artfxrioportal shunts on dynamic: computed tomography. AJR 198:3;140:953-7. Douglass BE, Baggenstoss AA, Hollongshead WH. The anatomy of the portal vein and its tributaries. Surg Gynecol Obstet 1950;91:562-76. Purcell HK. Connor JJ, Alexander LVF. S(:ully NM. Observetion on the extra-hepatic major radic Ies of the portal systems. Arch Surg 1951;62:670&7. Reynolds RB. Portal hypertension 111:Schiff I., ed Diseases of the liver. Philadelphia: Lippincott. 1975:3:30-67. Doust B. Pearce J, Gray-scale ultrCw)nic. properties of the normal and inflamed pancreas. Kadiolngy 1976;120:653-7. Hatano H. Nakajima Y. Ohnishi K. Okuda K. Clinical significame of the measurement ot the portal vein diameter on ultrasonograms in various liver diseases. Jpn J Mttd Illtrason. Proceedings of the 41st meeting. 1982:Ci7-8.
Aneurysm of the Intrahepatic the Portal Vein
Branch
1984:86:169-73
of
Report of Two Cases KUNIHIKO OHNISHI, TAKATSUNE NAKAYAMA, MASAYUKI SAITO, FUMIO NOMURA, HIROFUMI JUNICHI TAMARU, ISAMU IWASAKI, and KUNIO First Departments
of Medicine
and Pathology. Chiba I!niversit\;
Two patients in rvhom real-time ultrasonography and percutaneous transhepatic portography or the venous phase of the arteriogram of the superior mesenteric artery demonstrated a localized saccular dilation of a peripheral branch of the portal vein are described. One patient subsequently died. and autopsy confirmed the diagnosis. A hypoechoic lesion continuous with a branch of the portal vein seems to be the characteristic sonographic picture. Radiologic e\~idence for portal vein aneurysm was obtained in only z of 300 patients with portal hypertension in whom percutaneous transhepatic portograph!, was performed. and in 2 of 3000 patients who visited our unit and in whom ultrasonography for the liver leas performed. Thus, aneurysm of the intrahepatic portal vein does occur, but very rarely. Barzilai and Kleckner (1) were apparently the first to report an aneurysm of the portal vein. They described a patient who developed postnecrotic cirrhosis. thrombosis of the right portal vein, and an aneurysm proximal to the thrombus with subsequent rupture into the biliary system. Ten other cases have since beon reported, but nine of these aneurysms were extrahepatic (Z-8). In only 1 case was ultrasound e\raluation made (8). The following 2 cases seem to be the first documentation of intrahepatic portal vein aneurysm discovered by ultrasound examination.
liwxived blay 26, 1983. Accepted August 6. 1983. Address requests for reprints to: Kunihiko Ohnishi. M.D., First Department of Medic.ine. Chiba liniversity School of Medicine. I8-l Inohan;r. Chiba Cit\l. Chiba. Japan. This Lvork \vas supported h! a Japan Ministry of Health and Welfare Gr,lnt. ’ 198-1ti\, the American (;astror?nterological Association OOlfi-5f)R,i
81’53.00
KOEN, OKUDA
School of Medicine.
Chib,i.
Case Reports Case
1
A 47-yr-old man was referred to us for the evaluation of a suspected mass in the liver on December 13,1982. He had been drinking heavily, an equivalent of -100 ml of ethanol per day in the form of Japanese sake. for the last 28 yr. Eight years before admission. he was told of his abnormal liver function tests and glucosuria, but he did not seek medical treatment. In November I 981, he developed easy fat&ability and heat sensation of the skin, and his physician found a lesion in the liver b!; ultrasound. On admission, he had spider angiomata, palmar erythema, and gynecomastia. but there WBS no jaundice. flapping tremor, ascites. or edema. The li\Ter was felt three finger breadths below the right costal margin. and the spleen was not palpable. Laboratory study disc.losed the following data: serum aspartate transaminase [AST). 81 IIJiL; alanine transaminase (ALT), 119 W/L: albumin. 1.2 g!til: r-globulin. 1.8 g/dl: total bilirubin. 0.8 rng~dl:
170
Figure
OHNISHI ET AL.
in the right subcostal scan in case 1 demonstrating a hypoechoic lesion in the anteroinferior segment of the right lobe of the liver.
GASTROENTEROLOGY
Vol. 86. No. 1
1. Ultrasonogram
Percutaneous transhepatic portography disclosed a saccular dilation of one of the peripheral branches of the portal vein in the early phase (Figure 4A), and a round stain with a filling defect in the center (Figure 4B). The portal vein pressure was measured to be 224 mmHpO. Hepatic vein catheterization showed a wedged hepatic vein pressure of 198 mmHZO, and free hepatic vein pressure of 25 mmH,O. Hepatic venography demonstrated irregularity of the peripheral branches of the right hepatic vein. The hypoechoic lesion surrounded by high-level echoes in the liver has since been followed, but it has not changed in size for at least 7 mo, until the time this article was prepared.
Case
Figure 2. Ultrasonogram in the right subcostal scan in case 1. Slight slanting of the transducer medially changes the hypoechoic lesion in Figure 1 to an echodense one (arrow) that seems to be continuous with the anteroinferior branch of the right portal vein.
2
A 56-yr-old man was admitted for evaluation of a masslike lesion found in the liver. He had had pulmonary tuberculosis, and had had resection of the right upper and middle lobes with many blood transfusions 23 yr earlier. Four years before this admission, his liver function tests were found to be abnormal, and he was followed by his physician. In July 1979, he developed ascites and was subsequently hospitalized with a diagnosis of cirrhosis. The ascites was controlled for some time, but he again developed ascites and a lesion was found in the liver by ultrasound on October 1, 1980. On admission, there were spider angiomata, palmar
F‘igure 3. Dynamic computed tomography in case 1, after bolus injection of contrast medium, opacified a low-density area during the venous chase Carrowl.
)anuary
Figure
ANL’E:I!KYSP\l OF THE
1984
IN’I’RAH~P:\Tl(:
POKTAI,
VEIN
171
4. Percutaneous transhepatic portography in case 1. A. Portogram demonstrating a saccular dilation (orrow) of one of the peripheral branches of the right portal vein in an early phase. H. Portogram of a late phase showing a round stain with a central
tilling defect (~W~OMJ)
erythema, ascites, and edema of the lower extremities. The liver and spleen were not palpable. Laboratory examination disclosed the following data: serum AST, 182 IUiL; 1.8 mgidl; prothrombin ALT, 143 IUIL; total bilirubin, time, 16.7 s with a control value of 12.0 s, and indocyanine green test, 490/o retention at 15 min. Serum HBsAg was negative. Endoscopy of the esophagus and stomach revealed large varices along the entire length of the esophagus. Ultrasound examination of the liver demonstrated, in the right intercostal section, an ovoid hypoechoic lesion in the posterosuperior segment of the right lobe. It seemed to be contiguous with one of the portal branches. The surface of the liver was irregular and there was massive ascites. Plain CT demonstrated a low-density area in the superior portion of the right lobe of the liver and ascites. Angiography of the proper hepatic artery demonstrated a corkscrew pattern of their branches, a typical pattern of cirrhosis. Superior mesenteric arteriogram revealed a saccular dilation (1.5 x 2 cm] of the posterosuperior branch of the right portal vein in the venous phase (Figure 5). All these findings were compatible with an aneurysm of the intrahepatic branch of the portal vein and liver cirrhosis with esophageal varices. One month after admission, ascites was controlled by low-salt diet and diuretics, and the patient was discharged. On February 1, 1981, he devel-
oped hepatic encephalopathy, massive ascites, and jaundice, and was readmitted. Despite intensive treatment, he died from hepatic failure on September 18, 1981. On autopsy. a localized dilation of an intrahepatic: branch of the right portal vein branch was seen in a liver with macronodular cirrhosis (Figure 6). The wall of the aneurysm was very thin, with markedly reduced tunica intima and media compared with the wall of the left portal vein branch of comparable size.
Discussion Ten literature the
junction
of the were
11 portal
located
of the
vein
outside
superior
aneurysms the
mesenteric
liver,
in past mostly
and
at
splenic
veins, or in the major (the first right or left) branch of the portal vein. There seems to bc no clear definition of portal vein aneurysm. The size of the portal vein varies somewhat with the individual. Douglass et al. (10) studied 92 dissections and found the diameter of the portal vein to be 0.64-1.2 cm, with an average of 0.89 cm in patients without cirrhosis or portal hypertension. Purcell et al. (11) made similar measurements and found the averagc diameter to be 1.09
172
OHNISHI
ET AL.
GASTROENTEROLOGY
i:
Figure
5. Portogram obtained after superior mesenteric arteriography in case 2. An enlarged saccular dilation of the posterosuperior branch of the right portal vein is apparent.
cm. According to Reynolds (l2), the ter of the portal vein is 1.2cm, and it in cirrhosis. In the ultrasonographic Doust and Pearce of the portal vein
Figure
average diamebecomes greater study made by (13), the maxi-
6. Gross liver section in case 2, demonstrating rysm (arrow) and macronodular cirrhosis.
an aneu-
Vol.
86. No.
1
mum anteroposterior diameter never exceeded 1.5 cm in normal individuals and 1.9 cm in cirrhotics. The size of the intrahepatic portal branches is also variable. We measured ultrasonically the diameter of the right first branch of the portal vein at the bifurcation in 34 normal subjects and 49 cirrhotics, and found the average to be 0.66 + 0.11cm (SD] and 0.85 -+ 0.23 cm, respectively, among Japanese adults (14). Dilation much beyond this dimension may properly be classified as aneurysmal, especially if the vein outline assumes a fusiform or saccular configuration. Aneurysms of the portal vein are thought to have two etiologies: (a) congenital and (b) acquired secondary to portal hypertension. Most of the reported cases were incidental discoveries at the time of investigation for bleeding varices and cirrhosis, and some authors (1,~) believe that portal vein aneurysm is due to portal hypertension. Liebowitz and Rousselot (5), however, reported 1 case of agnogenic myeloid metaplasia and portal vein aneurysm with no evidence of portal hypertension; in this patient, the intrasplenic pulp pressure was normal without collateral circulation, and they assumed a congenital etiology. Thomas (4) shared a similar view for his 2 cases of portal vein aneurysm because there was no gross intra- and extrahepatic obstruction, the liver did not appear to be cirrhotic, and the aneurysm was saccular and thin walled. Some kind of congenital or developmental abnormality has also been suspected in other reports (3,6). In our cases, both congenital and acquired (portal hypertension) factors could have been involved. In case 1, the portal vein pressure was onlv 224 mmH,O. In case 2, the aneurysm of the right portal vein had an abnormally thin wall. Thus aneurysmal dilation may occur as portal hypertension develops in a person with hereditary weakness or developmental anomaly of the portal vein that occurred during its embryonic evolution from the vitelline vein. To detect a portal vein aneurysm in the liver as a masslike lesion is not difficult with real-time linear scan ultrasound. Diagnosis is almost certain if the vascular nature of the lesion is demonstrated. An uncomplicated portal vein aneurysm in the liver is characterized by an anechoic masslike lesion. Some portion of the aneurysm may be echogenic, due to a mural thrombus in it. In case 1, this might have been true. Three of the reported cases had a thrombus (1,2,4). The possibility that the echogenic material was a hepatocellular carcinoma invading the portal vein can be excluded by the negative aspiration cytology carried out under ultrasound guidance, and the unchanging size of the lesion for at least 7 mo of observation. In our unit, >3000 patients, including those with a normal or unremarkable hepatobiliary system, have so far been studied by real-time ultra-
January
ANEURYSM
1984
sound, and 300 patients with portal hypertension have been investigated by percutaneous transhepatic portography with complete opacification of the intrahepatic portal branches. Thus, the crude incidence of portal vein aneurysm among patients with portal hypertension was 2 of 300, and among the patients who came to the hospital with complaints related to the hepatobiliary system, the incidence was 2 of 3000.
6.
7. 8. 9. 10.
References Barzilai R. Kleckner MS. Hemocholecyst following ruptured aneurysm of portal vein. Arch Surg 1950;72:725-7. Leonsins AJ, Siew S. Fusiform aneurysmal dilatation of the portal vein. Postgrad Med J 1960;36:570-4. Hermann RE. Shafer WH. Aneurysm of the portal vein and portal hypertension. Ann Surg 1965;162:1101-4. Thomas TV. Aneurysm of the portal vein: report of two cases. One resulting in thrombosis and spontaneous rupture. Surgery 1967:61:550-5. Liebowitz HR. Rousselot LM. Saccular aneurysm of portal
11.
12. 13. 14.
OF THE INTRAHEPATIC:
PORTAL
VEIN
173
vein with agnogenic myeloid metaplasia. NY State J Med 1967;67:1443-7. Wenz W, Beckenbach H. Daum K. Dlcr kindliche I’fortader bei Erkrankungen der Oberbauchorgane Eur 1 Pediatr 1971; 9:354-62. Duhmke \‘E. Aneurysma der vena portac:. ROFO 197.1,; 125:474-5. Vine HS, Sequeira JC. Widrich 12’(:. Sachs HA. Portal vein aneurysm. AJR 1979;132:557-60. n‘akayama T. Hiyama Y. Ohnishi K. et al. Artfxrioportal shunts on dynamic: computed tomography. AJR 198:3;140:953-7. Douglass BE, Baggenstoss AA, Hollongshead WH. The anatomy of the portal vein and its tributaries. Surg Gynecol Obstet 1950;91:562-76. Purcell HK. Connor JJ, Alexander LVF. S(:ully NM. Observetion on the extra-hepatic major radic Ies of the portal systems. Arch Surg 1951;62:670&7. Reynolds RB. Portal hypertension 111:Schiff I., ed Diseases of the liver. Philadelphia: Lippincott. 1975:3:30-67. Doust B. Pearce J, Gray-scale ultrCw)nic. properties of the normal and inflamed pancreas. Kadiolngy 1976;120:653-7. Hatano H. Nakajima Y. Ohnishi K. Okuda K. Clinical significame of the measurement ot the portal vein diameter on ultrasonograms in various liver diseases. Jpn J Mttd Illtrason. Proceedings of the 41st meeting. 1982:Ci7-8.