EDUCATION EXHIBIT 141

Congenital and
Acquired Anomalies
of the Portal Venous
System1
Carmen Gallego, MD ● Maria Velasco, MD ● Pilar Marcuello, MD
ONLINE-ONLY
CME Daniel Tejedor, MD ● Lourdes De Campo, MD ● Alfonsa Friera, MD
See www.rsna
.org/education
/rg_cme.html. Knowledge of the normal anatomy, most frequent variants, and con-
genital and acquired anomalies of the portal venous system is of great
importance for liver surgery and interventional procedures such as cre-
LEARNING
OBJECTIVES ation of transjugular intrahepatic portosystemic shunts. Radiologic
After reading this
studies of the portal venous system include color Doppler ultrasonog-
article and taking raphy (US), computed tomography (CT), magnetic resonance imag-
the test, the reader
will be able to: ing, and arterial or direct portography. Among the most common
䡲 Recognize the nor- branching variants of the portal vein are trifurcation, right anterior por-
mal anatomy, normal
variants, and con- tal branch arising from the left portal vein, and right posterior portal
genital anomalies of branch arising from the main portal vein. Agenesis of the right or left
the portal venous
system.
portal vein is the most frequently reported congenital anomaly. Venous
䡲 Describe the imag- collateral vessels due to portal hypertension and cavernous transforma-
ing appearances of tion of the portal vein are best evaluated with cross-sectional imaging.
portosystemic collat-
eral vessels, intrahe- Intrahepatic portosystemic, arterioportal, and arteriosystemic fistulas
patic arteriovenous and associated perfusion anomalies have characteristic features at dual-
and venovenous
shunts, and aneu- phase helical CT. Color Doppler US is the single most useful tool for
rysms of the portal demonstration of aneurysms of the portal venous system and bland or
venous system.
neoplastic portal vein thrombosis. CT is also the best means of evaluat-
䡲 Identify perfusion
anomalies associated ing gas in the portal venous system, which is no longer an ominous sign
with changes in por- and must be differentiated from aerobilia.
tal vein hemodynam- ©
ics. RSNA, 2002

Abbreviations: HAP ⫽ hepatic arterial phase, PVP ⫽ portal venous phase

Index terms: Aneurysm, portal vein, 957.73 ● Portal vein, abnormalities, 957.13 ● Portal vein, anatomy, 957.92 ● Portal vein, flow dynamics, 957.711,
957.752 ● Portal vein, gas, 957.779 ● Portal vein, thrombosis, 957.751 ● Shunts, arterioportal, 957.759 ● Shunts, portosystemic, 957.759

RadioGraphics 2002; 22:141–159

1From the Department of Radiology, Hospital Universitario de la Princesa, Madrid, Spain. Presented as an education exhibit at the 2000 RSNA scien-
tific assembly. Received March 16, 2001; revision requested May 16 and received June 25; accepted July 2. Address correspondence to C.G., De-
partment of Radiology, Hospital Universitario 12 de Octubre, Avenida de Andalucia Km 5400, 28041 Madrid, Spain (e-mail: mamengallego@terra.es).
©
RSNA, 2002
142 January-February 2002
Introduction
The portal venous system comprises all of the
veins draining the abdominal part of the digestive
tract, including the lower esophagus but exclud-
ing the lower anal canal. The portal vein conveys
blood from viscera and ramifies like an artery at
the liver, ending at the sinusoids. Tributaries of
the portal vein, which make up the portal venous
system, are the splenic, superior mesenteric, left
gastric, right gastric, paraumbilical, and cystic
veins. Radiologic evaluation of anomalies of the
portal venous system is usually performed with
color Doppler ultrasonography (US), helical
computed tomography (CT), and magnetic reso-
nance (MR) imaging. Arterial portography, direct
portography, and splenoportography may also be
used, but these are invasive techniques that are
being supplanted by MR venography.
Helical CT is a useful tool for assessing abnor-
malities of the portal venous system. Biphasic dy-
namic contrast material– enhanced helical CT of
the liver can accurately demonstrate both macro-
scopic and perfusion disorders of the portal ve-
nous system. Most perfusion alterations are seen
during the hepatic arterial phase (HAP), with
normal attenuation in the portal venous phase
(PVP). For the past 3 years, we have been evalu-
ating the helical CT manifestations of congenital
and acquired anomalies of the portal venous sys-
tem. Our protocol for biphasic helical CT of the
abdomen is as follows: We inject a total of 150
mL of iodinated contrast material at a rate of
3–3.5 mL/sec. HAP images are acquired 20 –25
seconds after the start of the injection, and PVP
images are acquired 25–30 seconds later. Color
Doppler US, MR imaging, and MR angiography
are also performed in some cases.
Congenital anomalies of the portal venous sys-
tem comprise total or partial agenesis of the portal
RG f Volume 22 ● Number 1
vein, abnormal branching of the portal vein, ve-
nous malposition (in situs inversus totalis or in
midgut malrotation), arteriovenous malforma-
tions, and persistence of fetal valves. The etiology
of aneurysms of the portal venous system and
some intrahepatic portosystemic shunts is still
controversial. Acquired anomalies of the portal
venous system comprise portosystemic and porto-
portal collateral vessels; occlusion of the portal
vein; intrahepatic arterioportal or arteriosystemic
shunts; arteriovenous fistulas; and gas, thrombo-
sis, or stents in the portal venous system.
In this article, we present an overview of nor-
mal variants and congenital and acquired anoma-
lies of the portal venous system. Specific topics
discussed are branching variants of the portal
vein, congenital anomalies of the portal vein, por-
tosystemic collateral vessels, cavernous transfor-
mation of the portal vein, intrahepatic vascular
shunts, aneurysms of the portal venous system,
thrombosis of the portal venous system, and gas
in the portal venous system.
Branching Var-
iants of the Portal Vein
The portal vein results from the confluence of the
superior mesenteric and splenic veins posterior to
the neck of the pancreas. In its most common
branching pattern, it divides at the porta hepatis
into right and left portal veins. As it courses crani-
ally, the right portal vein first gives off branches to
the caudate lobe and then divides into anterior
and posterior branches, which subdivide into su-
perior and inferior segmental branches to supply
the right lobe of the liver. The left portal vein first
has a horizontal course to the left and then turns
medially toward the ligamentum teres (umbilical
portion), supplying the lateral segments (seg-
ments II and III) of the left lobe. It describes a
wide and anteriorly concave curve and ends in the
superior and inferior segmental branches of seg-
ment IV (Fig 1).
RG f Volume 22 ● Number 1 Gallego et al 143

Figure 1. Normal branching pattern of the portal vein. Coronal (left) and axial (right) diagrams show that
the main portal vein (1) divides into the right (2) and left portal veins. The left portal vein first courses horizon-
tally (horizontal portion [3]), then turns anteriorly (umbilical portion [4]) toward the ligamentum teres (6).
The Cantlie line corresponds to the median fissure and extends from the gallbladder (7) to the inferior vena
cava. It is located to the right of the umbilical ligament and divides the liver into right and left lobes. 5 ⫽
branch to segment IV.

Figure 2. Most common anatomy of the portal venous system. (a) Contrast-enhanced CT scan shows the horizon-
tal portion of the left portal vein (arrow), which is large. (b) Contrast-enhanced CT scan shows the umbilical portion
of the left portal vein (arrowhead), which extends in a wide, concave, anterior curve toward the umbilical ligament.
(c) Contrast-enhanced CT scan shows the gallbladder, which is located to the right of the ligamentum teres (arrow).

The landmarks that we use to describe the nor-
mal anatomy of the portal venous system at the
liver are the main and right portal vein, the lateral
segment and umbilical portion of the left portal
vein, the ligamentum teres, the inferior vena cava,
and the fossa for the gallbladder. The Cantlie line
is defined as a line passing through the gallblad-
der toward the inferior vena cava and corresponds
to the median fissure. It serves as a boundary be-
tween the right and left lobes (Figs 1, 2).
144 January-February 2002 RG f Volume 22 ● Number 1

Figure 3. Four most common branching

patterns of the intrahepatic portal vein. A,
Coronal diagram shows the normal
branching pattern. B, Coronal diagram
shows trifurcation of the main portal vein.
The right portal vein is not present, and
the main portal vein divides into the right
anterior, right posterior, and left portal
veins at the same level. C, Coronal dia-
gram shows the right anterior branch aris-
ing from the left portal vein. The main por-
tal vein divides into the right posterior and
left portal veins, and the right anterior por-
tal vein arises from the left portal vein. D,
Coronal diagram shows the right posterior
branch arising from the main portal vein.
The first branch to split off is the right pos-
terior branch. The main portal vein then
continues to the right for a variable dis-
tance and bifurcates into the right anterior
and left portal veins.

Variants in the normal branching pattern of the

intrahepatic portal vein (Fig 3) have been re-
ported since 1957 and occur in approximately
20% of the population (1–3). The most common
patterns include trifurcation of the main portal
vein (Fig 4) (7.8%–10.8%), right posterior seg-
mental branch arising from the main portal vein
(4.7%–5.8%), and right anterior segmental
branch arising from the left portal vein (2.9%–
4.3%) (2– 4). A spectrum of branching variants of
the portal vein associated with malposition of the
gallbladder has been described in recent years
(5,6). Findings comprise an abnormal course of
the horizontal portion of the left portal vein and
an abnormal umbilical portion that is located
above the gallbladder fossa. The gallbladder is
deviated to the left and may lie to the left of or Figure 4. Portal vein trifurcation.
astride the ligamentum teres. The Cantlie line Contrast-enhanced CT scan shows tri-
furcation of the main portal vein.
does not serve as a boundary between the right
and left lobes in these cases (Figs 5, 6). The
theory proposed to explain these findings is ab- (5,6), it has yet to be established whether all
normal regression of the left umbilical vein with anomalous umbilical portions originate from a
persistence of the right umbilical vein. The persis- right umbilical vein.
tent right umbilical vein would form a right um- Knowledge of these variants is important be-
bilical portion of the left portal vein. Since a cause ligation of the left portal vein during liver
whole spectrum of this variant has been reported resection or split liver transplantation in some of
these cases may lead to necrosis of more than
80% of the liver (5,6).
RG f Volume 22 ● Number 1 Gallego et al 145

Figure 5. Portal vein anomaly associated with malposition of the gallbladder. Coronal (left) and axial (right)
diagrams show that the first branch to split off is the right posterior portal vein. The main portal vein (1) then
courses superiorly, giving off the right anterior portal vein and a small, ascending umbilical portion of the left
portal vein (4). The gallbladder (7) is located astride the umbilical ligament and does not serve as a boundary
between the right and left lobes. 2 ⫽ right portal vein, 3 ⫽ horizontal portion of the left portal vein, 5 ⫽ branch
to segment IV, 6 ⫽ ligamentum teres.

Figure 6. Portal vein anomaly associated with malposition of the gallbladder. (a) Contrast-enhanced CT scan
shows a small, ascending umbilical portion of the left portal vein (arrowhead). (b) Contrast-enhanced CT scan shows
the umbilical ligament (arrow). The horizontal portion of the left portal vein is not seen. (c) Contrast-enhanced CT
scan shows a neoplastic gallbladder (arrows), which is below the umbilical ligament. The Cantlie line is deviated to
the left.

Congenital Anom- Congenital agenesis of the major branches of

alies of the Portal Vein
Congenital anomalies of the main portal vein in-
clude prepancreatic portal vein, which is fre-
quently associated with situs inversus and other
congenital malformations (7); double portal vein;
congenital agenesis of the portal vein (8); and
congenital agenesis of the major branches of the
portal vein. Knowledge of these variants is impor-
tant for surgical planning and for creation of trans-
jugular intrahepatic portosystemic shunts.
the portal vein is the most frequently reported
congenital anomaly and should be differentiated
from acquired atrophy of the hepatic lobes (9 –
14). Congenital agenesis is thought to be second-
ary to failure of the right and left portal veins to
develop (10) or thrombosis of the affected lobe or
segment during embryologic growth (14). In con-
genital agenesis of the right hepatic lobe, the right
146 January-February 2002 RG f Volume 22 ● Number 1

Figure 7. Atrophy of the right hepatic lobe in a patient with choledocholithiasis. (a) Contrast-enhanced CT
scan shows a posteriorly located gallbladder. Agenesis can be ruled out because of the presence of intrahepatic
dilated branches of the right hepatic duct (arrow) and a severely atrophied right portal vein (arrowhead).
(b) Contrast-enhanced CT scan shows marked hypertrophy of the left hepatic lobe and caudate lobe in associa-
tion with posterolateral interposition of the hepatic flexure and upward deviation of the right kidney. Arrow ⫽
choledocholith.

portal vein, right hepatic duct, and right hepatic
vein are not identified (9,10). A retrohepatic gall-
bladder, posterolateral interposition of the right
colic flexure, and superior migration of the right
kidney are shared features of both congenital
agenesis and severe atrophy of the right lobe (Fig
7). Agenesis of the left hepatic lobe is indicated by
absence of hepatic parenchyma to the left of the
gallbladder fossa and absence of a recognizable
ligamentum teres and left portal vein (11). The
presence of a rudimentary left portal vein favors
the diagnosis of atrophy of the left lobe (Fig 8).
Common features of both agenesis and atrophy of
the left lobe are a superior location of the gall-
bladder just beneath the diaphragm, an abnormal
U-shaped configuration of the stomach, and an
abnormally high duodenal bulb on images from
an upper gastrointestinal series (12,13).
Contrast-enhanced thin-section helical CT is
probably the best modality for demonstrating
portosystemic collateral vessels in patients with
chronic liver disease (15,16). MR imaging may be
as accurate but is more expensive and less acces-
sible; in addition, some of the rarest pathways (eg,
pleuropericardial or thoracic wall varices) can be
missed. Familiarity with the most common flow
artifacts is mandatory for correct interpretation of
MR angiograms of the portal venous system
(17,18).
More than 20 pathways have been described,
with the most common being gastroesophageal,
paraumbilical, splenorenal, and inferior mesen-
teric collateral vessels. Pleuropericardial-perito-
neal, pancreaticoduodenal, splenoazygos, and
mesocaval collateral vessels are unusual pathways
for decompression of the portal vein.

Portosystemic Collateral Vessels Coronary, Esophageal, Paraesoph-

The most common cause of portosystemic collat-
eral vessels is portal hypertension. Other causes of
portosystemic collateral vessels are splenic or
splenomesenteric venous stenosis and obstruction
due to neoplasms, pancreatitis, or surgery.
ageal, and Gastric Collateral Vessels
Coronary collateral veins at the lesser omentum
are the most frequently depicted varices at cross-
sectional imaging (in approximately 80% of pa-
tients with portal hypertension) (15). They are
usually accompanied by esophageal and para-
esophageal varices and less commonly by retroga-
stric varices.
RG f Volume 22 ● Number 1 Gallego et al 147

Figure 8. Atrophy of the left hepatic lobe. (a) Contrast-enhanced CT scan ob-
tained during the PVP shows a rudimentary left portal vein (arrow) at the medial
surface of the liver. There is severe atrophy of the left hepatic lobe (arrowhead).
(b) Contrast-enhanced CT scan obtained at the level of the porta hepatis shows
absence of the left lobe and left portal vein.

Figure 9. Esophageal varices.

Contrast-enhanced CT scan shows Figure 10. Paraesophageal varices.
esophageal varices (arrow), which Contrast-enhanced CT scan shows
are difficult to see because they are paraesophageal varices, which simulate
embedded in the esophageal wall. a huge posterior mediastinal mass.

Esophageal varices are of major clinical impor-
tance because they are a frequent source of gas-
trointestinal bleeding (15,16). They are embed-
ded in the wall of the esophagus and are some-
times difficult to see at cross-sectional imaging
(Fig 9) because of the lack of adipose tissue sur-
rounding them. Endoscopy is more sensitive than
CT to the presence of esophageal varices.
Paraesophageal collateral vessels (Fig 10) are
located outside the walls of the esophagus and
thus cannot be seen with endoscopy (15). They
are so bulky that they may simulate a posterior
mediastinal mass at chest radiography. Contrast-
enhanced CT is more sensitive to paraesophageal
varices than to esophageal varices.
148 January-February 2002 RG f Volume 22 ● Number 1

Figure 11. Paraumbilical vessels in a

patient with portal hypertension. Con-
trast-enhanced CT scan shows three
paraumbilical vessels (arrows). Aneu-
rysmal dilatation of one such vessel (ar-
rowhead) is also seen.

Gastric varices are located at the posterosupe- Splenorenal Collateral Vessels

rior aspect of the gastric fundus and may simulate
a gastric neoplasm on nonenhanced CT scans.
Most gastric varices drain into the esophageal or
paraesophageal veins, but occasionally they drain
into the left renal vein (15,16). When a gastrore-
nal shunt develops, the chances of hepatic en-
cephalopathy increase.
Paraumbilical Collateral Vessels
Paraumbilical collateral vessels are next in fre-
quency; their extent was usually underestimated
with conventional angiography alone until the
advent of cross-sectional imaging (15,18). Nu-
merous paraumbilical vessels can arise from the
left portal vein in patients with cirrhosis. Patent
paraumbilical vessels are a good predictor of por-
tal hypertension (Fig 11). They are an acceptable
means of decompression of the portal venous sys-
tem because they are not associated with gastroin-
testinal bleeding (15). The most common pattern
of drainage of paraumbilical veins is through the
epigastric veins into the external iliac veins (19).
Paraumbilical veins can also connect with subcu-
taneous vessels of the anterior abdominal wall,
creating the caput medusae: a varicose dilatation
of subcutaneous veins around the umbilicus
(15,16).
Collateral vessels from the splenic hilum to the
left renal vein are fairly common. They are desir-
able spontaneous shunts in portal hypertension
because they are not associated with gastrointesti-
nal bleeding (16). However, enlarged shunts are
significantly associated with hepatic encephalopa-
thy. A common feature depicted at cross-sec-
tional imaging is an enlarged left renal vein and
dilatation of the inferior vena cava at the level of
the left renal vein in the presence of a splenorenal
shunt.
Mesenteric Collateral Vessels
Inferior mesenteric collateral vessels are less fre-
quent than the collateral vessels mentioned earlier
but are of great importance because of their asso-
ciation with rectal bleeding. The portal venous
system (superior hemorrhoidal vein) and the sys-
temic venous circulation (middle and inferior
hemorrhoidal veins) connect via the hemor-
rhoidal plexus (15). If one is not aware of a pa-
tient’s portal hypertension, mesenteric collateral
vessels can be mistaken for a rectal mass protrud-
ing into the rectal lumen on nonenhanced CT
scans (16) (Fig 12).
Mesocaval shunts are portosystemic collateral
vessels between the inferior mesenteric vein and
inferior vena cava that are established through
lumbar and retroperitoneal veins (15–18). These
RG f Volume 22 ● Number 1 Gallego et al 149

Figure 12. Inferior hemor-

rhoidal varices. Contrast-en-
hanced CT scan obtained during
the PVP shows a lobulated mass
protruding into the rectal lumen.

Figure 13. Pleuropericardial-peritoneal collateral vessel. (a) Contrast-enhanced CT scan

shows an enhancing serpentine venous structure (arrowhead) that courses toward the ante-
rior thoracic wall. (b) Contrast-enhanced CT scan shows that the venous structure (arrow-
head) arises from the left portal vein.

collateral vessels are not associated with an in-
creased risk of rectal bleeding.
Mesentericorenal collateral vessels between the
superior mesenteric vein and the right and left
renal veins are the least frequent mesenteric
shunts (15).
Other Collateral Pathways
Rare collateral pathways have been reported, in-
cluding pleuropericardial-peritoneal (Fig 13),
splenoazygos, intrahepatic, and from the coronary
or splenic veins to the inferior pulmonary vein or
to diaphragmatic veins.
Portoportal and portosystemic collateral ves-
sels also develop if there is occlusion of the
splenic vein. If obstruction occurs near the splenic
hilum, collateral vessels develop at the gastric fun-
dus and the greater and lesser omentum, resulting
in gastric fundal varices and an enlarged vein of
Barkow (omental vein). When splenic vein occlu-
sion is near the splenomesenteric confluence, me-
socaval (via the inferior mesenteric vein), hemor-
rhoidal, splenorenal, or splenoretroperitoneal col-
lateral vessels are the usual portosystemic path-
ways of decompression (18,19).
In occlusion of the superior mesenteric vein,
mesenteric varices and mesentericorenal collateral
vessels develop (16,19).
Cavernous Transfor-
mation of the Portal Vein
Cavernous transformation of the portal vein con-
sists of formation of venous channels within and
around a previously stenosed or occluded portal
vein that act as portoportal collateral vessels. Two
other etiopathogenic theories have been proposed but
have not been demonstrated to date: (a) congenital
150 January-February 2002 RG f Volume 22 ● Number 1

Figure 14. Cavernous transformation of the portal vein. (a) Contrast-enhanced CT scan obtained during the
late HAP shows a beaded appearance (a mass of veins) at the porta hepatis. Because flow through the cavern-
ous portal vein is not sufficient to supply the liver, peripheral areas of increased uptake are seen (arrow), which
reflect peripheral increased arterial inflow. (b) Contrast-enhanced coronal MR angiogram obtained in a patient
with splenomegaly shows a cavernous portal vein and multiple collateral vessels. (Fig 14b courtesy of Carlos
Marı́n, MD, Hospital San Rafael, Madrid, Spain.)

agenesis of the portal vein leading to development
of periportal collateral vessels and (b) a hemangi-
oma of the portal vein (20). Conversely to what
was initially thought, cavernous transformation of
the portal vein can occur as soon as 6 –20 days
after the thrombotic event, even if partial recana-
lization of the thrombus develops (20). Dilated
biliary branches (cystic and pericholecystic veins)
and gastric branches (left and right gastric veins)
of the portal vein and the partially recanalized
thrombus compose the cavernous transformation
of the portal vein (20,21). The development of
these vessels supports the theory that cavernous
transformation of the portal vein is a portoportal
collateral pathway that substitutes for a throm-
bosed portal vein. The veins are usually insuffi-
cient to bypass the entire splenomesenteric in-
flow, and signs of portal hypertension frequently
coexist (20,22).
On contrast-enhanced CT scans, a characteris-
tic beaded appearance (mass of veins) at the porta
hepatis is the most frequent finding (Fig 14). In-
trahepatic extension of the cavernous transfor-
mation (20) and involvement of intrahepatic
branches with a normal-appearing main portal
vein have also been described (22). Inhomoge-
neous, peripheral, patchy areas of high attenua-
tion can be seen during the HAP. This pattern of
perfusion is frequently seen and occurs because
the central regions of the liver are better supplied
by the cavernous portal vein than are the periph-
eral regions; therefore, a peripheral increase in
arterial inflow develops (23,24).
At Doppler US, hepatopetal flow is observed,
but this flow lacks the characteristic respiratory
undulation of normal portal vein flow (20).
Prominent arterial inflow is also seen, reflecting
the diminished flow in the intrahepatic portal
veins.
Intrahepatic Vascular Shunts
Intrahepatic vascular connections between the
hepatic artery, the portal vein, and the hepatic
veins are rare. The most frequently reported ab-
normal communications are the small arteriopor-
tal shunts that occur in cirrhotic livers. Most
of them are so minute that they are below the
threshold of visualization with cross-sectional im-
aging. Large intrahepatic communications can
occur between the portal and hepatic veins (por-
tosystemic shunts), the hepatic artery and portal
vein (arterioportal shunts), and the hepatic artery
and hepatic veins (arteriosystemic shunts) (25).
Portosystemic Shunts
Direct communication between a portal vein and
a hepatic vein is uncommon. Several appearances
of intrahepatic portosystemic shunts have been
described (26). The most frequently reported in-
trahepatic portosystemic shunt occurs between
the right portal vein and the inferior vena cava. It
is considered a type of portosystemic collateral
vessel because it usually occurs in the clinical set-
ting of portal hypertension and is frequently asso-
ciated with hepatic encephalopathy (25–27). The
least common intrahepatic portosystemic shunt is
a communication between a portal vein branch
RG f Volume 22 ● Number 1 Gallego et al 151

Figure 15. Spontaneous intrahepatic portosystemic

shunt. (a) Longitudinal color Doppler US image shows
an abnormal communication between the left portal vein
(VPI) and the middle hepatic veins (VHM). (b) Trans-
verse duplex Doppler US image shows that the left portal
vein has an abnormal spectral pattern. The undulating,
triphasic waveform resembles that of the middle hepatic
vein. (c) Transverse duplex Doppler US image shows
that the right portal vein has a normal spectral pattern.
(d) Longitudinal duplex Doppler US image shows the
spectral pattern of the middle hepatic vein. (e) Oblique
coronal two-dimensional contrast-enhanced CT scan ob-
tained with multiplanar reconstruction shows the commu-
nication, which occurs through an aneurysmal dilatation
of a branch of the left portal vein.

and a hepatic vein through an aneurysm (Fig 15).
Multiple diffuse communications between pe-
ripheral portal and hepatic veins and a single
communication between a portal vein branch and
a hepatic vein in one hepatic segment are other
appearances of intrahepatic portosystemic shunts
(26).
Both congenital and acquired causes have been
postulated for intrahepatic portosystemic shunts,
but their origin is still controversial. Persistence of
an omphalomesenteric venous system with the
right horn of the sinus venosus and rupture of a
152 January-February 2002
Figure 16. Minute arterioportal fistula in a patient with liver cirrhosis. (a) Contrast-enhanced CT scan ob-
tained during the HAP shows a peripheral, wedge-shaped, transient area of high attenuation (arrow). A direct
communication between the hepatic artery and the portal vein is not seen. (b) Corresponding contrast-en-
hanced CT scan obtained during the PVP shows normal attenuation of the hepatic parenchyma. Two-year fol-
low-up revealed no changes in size or morphology.
congenital aneurysm of the portal vein into a he-
patic vein are congenital conditions that have
been proposed to explain intrahepatic portosys-
temic shunts. Acquired conditions that would
explain intrahepatic portosystemic shunts are de-
velopment of intrahepatic portosystemic collateral
vessels in cirrhotic patients and trauma (25,27).
Helical CT scans obtained during the PVP
show a communication between a portal vein
branch and the hepatic vein, as well as early and
asymmetric enhancement of the hepatic vein.
Color Doppler US is the single most useful
tool for diagnosis of intrahepatic portosystemic
shunts, but in most cases helical CT is performed
to confirm the diagnosis. Because resistance is
diminished in the portal vein, flow in the involved
branch can assume the wavy, triphasic flow pat-
tern of the hepatic veins (Fig 15).
Arterioportal Shunts
Arterioportal shunts may be congenital (vascular
malformations in Rendu-Osler disease) or ac-
quired (trauma, iatrogenic causes, cirrhosis) and
consist of a communication between the hepatic
artery and the portal venous system. They are
minute or large intrahepatic arterioportal shunts.
Minute arterioportal shunts in cirrhosis are
well documented and are not necessarily related
to hepatocarcinoma (Fig 16). They appear as
small, wedge-shaped, peripheral or subcapsular
areas of increased attenuation with early portal
venous filling on HAP CT scans or hepatic arte-
RG f Volume 22 ● Number 1
riograms (25) and demonstrate normal attenua-
tion during the PVP. Occasionally, small, nontu-
morous arterioportal shunts appear as a nodular,
irregularly outlined contour and inhomoge-
neously increased uptake during the HAP. In this
clinical setting, the arterioportal shunt may not be
distinguished from a small hepatocarcinoma, and
exclusion of a tumor-related arterioportal shunt
requires serial examinations (28).
Congenital arteriovenous malformations, liver
biopsy (Fig 17), trauma, or liver neoplasms (Fig
18) may lead to large arterioportal fistulas. Not
frequently, these fistulas themselves cause portal
hypertension and high-output heart failure
(29,30). In such cases, portal hypertension may
develop rapidly (in weeks to months) due to the
increased flow and pressure in the portal venous
system. Subsequently, hepatoportal sclerosis and
fibrosis of the portal radicles develop, which fur-
ther contribute to the portal hypertension (30).
Helical CT performed during the HAP shows
early and marked enhancement of the main portal
vein, segmental branches, or major tributaries
with an attenuation approaching that of the aorta
and early enhancement of the portal vein with
nonenhancement of the splenic and mesenteric
veins.
Two types of perfusion anomalies have been
reported in large arterioportal shunts (23,24,
31,32): (a) A nonspecific, homogeneous, regional
increase in arterial inflow has been reported in the
presence of diminished portal vein inflow (in
cases of neoplastic thrombosis and arterioportal
fistula). This anomaly is not related to the shunt
RG f Volume 22 ● Number 1 Gallego et al 153

Figure 17. Postbiopsy arterioportal fistula. (a) Contrast-enhanced CT scan obtained during the HAP shows
contrast material in the aorta (arrowhead) and the peripheral segmental branches of the right anterior portal
vein (black arrow). The main portal vein and lobar branches are not enhanced. A wedge-shaped, hyperattenu-
ating region of hepatic parenchyma (white arrows) surrounds the fistula. This finding is related to an increase in
arterial inflow in the area around the fistula. (b) Axial maximum intensity projection image obtained during the
HAP shows the same findings. The aorta, the hepatic artery (arrowhead), and the sublobar branches of the
right portal vein (arrow) are markedly enhanced.

Figure 18. Neoplastic arterioportal fistula in a pa-

tient with multicentric hepatocellular carcinoma.
(a) Contrast-enhanced CT scan obtained during the
HAP shows tumor (*) invading the left portal vein (ar-
row) and a tumoral thrombus within the vein. (b) Con-
trast-enhanced CT scan obtained during the HAP
shows that an arterioportal fistula has developed due to
invasion by the tumor (*). There is increased uptake of
contrast material in the portal vein. Ill-defined areas of
increased attenuation are seen (arrowheads), which are
related to increased inflow in the peripheral portal vein
branches due to the shunt itself. (c) Axial maximum
intensity projection image shows equal and simulta-
neous enhancement of the aorta, hepatic artery, and
portal vein. The thrombus in the left portal vein is evi-
dent.
154 January-February 2002
Figure 19. Aneurysm of the portal venous system. (a) Contrast-enhanced CT scan obtained during the PVP
shows a giant aneurysm of the splenomesenteric venous confluence. (b) Axial maximum intensity projection
image obtained during the PVP shows the same findings.
itself and is seen in other clinical settings. It ap-
pears as an ipsilateral increase in the attenuation
of the hepatic parenchyma during the HAP.
(b) An increase in portal vein inflow due to the
shunt itself has also been reported. This anomaly
appears as a contralateral increase in the attenua-
tion of the hepatic parenchyma with prolonged
enhancement of the portal vein during the HAP
and PVP.
Reduction and loss of the geographic enhance-
ment of the splenic parenchyma during the HAP
has also been reported in association with large
arterioportal shunts. This finding has been attrib-
uted to diminished splenic artery inflow (31).
At color Doppler US, hepatic artery to portal
vein shunts manifest as pulsatility of the portal
vein flow.
Arteriosystemic Shunts
The rarest form of an intrahepatic shunt is a com-
munication between the hepatic artery (or other
systemic arteries) and the hepatic veins. Such
shunts have been reported in congenital arterio-
venous malformations of the liver like hereditary
hemorrhagic telangiectasia (Rendu-Osler dis-
ease), hepatocarcinoma, and large hemangiomas
(25,33). Contrast-enhanced CT performed dur-
ing the HAP shows increased asymmetric and
early enhancement of a hepatic vein. Significant
changes in the Doppler US waveform of the he-
patic vein are seen only in severe cases of congeni-
tal arteriovenous malformation (33).
Aneurysms of the
Portal Venous System
Most aneurysms of the venous system occur in
the popliteal, jugular, or saphenous veins, with
the rarest being those affecting the femoral, caval,
RG f Volume 22 ● Number 1
forearm, or portal veins (34). Aneurysms of the
portal vein were once thought to be extremely
rare but nowadays are well documented and not
unusual. They still represent only 3% of all aneu-
rysms of the venous system (35).
Although aneurysms of the portal venous sys-
tem may be present in patients with liver disease,
an overwhelming majority of patients do not have
portal hypertension or chronic liver disease.
Therefore, portal hypertension could be contribu-
tory but is not essential to the development of
portal venous system aneurysms (36). Both con-
genital and acquired causes have been proposed.
Reasons to favor a congenital origin are the in
utero diagnosis of a portal vein aneurysm (37),
evidence of portal venous system aneurysms in
patients with histologically proved normal livers
(34), and the frequent stability of the aneurysms
at follow-up (34 –36). Incomplete regression of
the distal right vitelline vein leading to a diverticu-
lum that would ultimately develop into an aneu-
rysm in the proximal superior mesenteric vein
could explain aneurysms in that location. An in-
herent weakness of the vessel wall is another
theory proposed to support a congenital origin.
Theories about an acquired origin are based on
the significant presence of aneurysms in patients
who have portal hypertension, have had necrotiz-
ing pancreatitis, or have undergone abdominal
trauma or surgery (35,36,38).
The most common locations are the sple-
nomesenteric venous confluence (Fig 19), main
portal vein, and intrahepatic portal vein branches
at bifurcation sites; the rarest locations are the
splenic, mesenteric, and umbilical veins (Fig 11)
(36). Since there are variations in the diameters of
both normal and cirrhotic portal veins, an aneu-
rysm of the portal venous system is considered to
be present if the vessel diameter is significantly
larger at that point than in the remainder of the
RG f Volume 22 ● Number 1
Figure 20. Portal vein aneurysm in a patient with unrelated disease. (a) Longitudinal US image shows an
aneurysm of the main portal vein, which was an incidental finding. (b) Follow-up transverse US image ob-
tained 4 years later shows partial thrombosis of the aneurysm. The patient remained asymptomatic.
vessel, especially if the morphology is saccular or
fusiform (36). Bilobulated (38) and synchronous
(39,40) portal vein aneurysms have also been re-
ported.
Most portal venous system aneurysms are
asymptomatic and do not demonstrate a signifi-
cant increase in size once discovered, although
some manifest with nonspecific abdominal pain
as a major symptom. Complications of portal ve-
nous system aneurysms are abdominal pain;
thrombosis (Fig 20); portal hypertension (due to
flow alterations or compression of the main portal
vein); rupture; thrombosis and distal embolism;
compression of the common bile duct causing
jaundice, cholestasis, and cholelithiasis; and com-
pression of the duodenum.
Color Doppler US is the single most useful
diagnostic tool, and further work-up may not be
necessary.
There is some controversy about treatment,
since some complications have been reported. If
the aneurysm is found incidentally, it is expected
not to grow and close surveillance is a common
management approach. Portacaval shunts in the
past and more recently prophylactic surgery or
aneurysmorrhaphy are the therapeutic options,
especially when aneurysms are growing or when
complications develop (34,38).
Thrombosis of the
Portal Venous System
Portal vein thrombosis occurs in various clinical
settings, with the most common being liver cir-
rhosis. Other processes that may cause portal ve-
Gallego et al 155
nous system thrombosis are infectious diseases
(eg, sepsis, cholangitis, pancreatitis), neoplasms,
hypercoagulable states, myeloproliferative disor-
ders, surgery, and embolism from a thrombus
located in the superior mesenteric or splenic vein
(41).
Color Doppler US is the single most useful
tool for detection of portal vein thrombosis; how-
ever, it is operator dependent, and some of the
manifestations associated with portal venous sys-
tem thrombosis (eg, varices, superior mesenteric
vein thrombosis) may be overlooked (42). It is
also useful for distinguishing between bland and
neoplastic thrombosis.
Nonenhanced CT may show focal high attenu-
ation in the portal, superior mesenteric, or splenic
vein and venous enlargement when thrombosis is
acute. Chronic venous thrombosis can manifest
as linear areas of calcification within the throm-
bus (16). Contrast-enhanced helical CT demon-
strates a filling defect partially or totally occluding
the vessel lumen. Rim enhancement of the vessel
wall may also be seen and is presumed to be due
to normal flow in the vasa vasorum. Indirect signs
of portal vein thrombosis are the presence of cav-
ernous transformation of the portal vein and the
presence of portosystemic collateral vessels and
arterioportal shunts. Care must be taken to avoid
confusion of the “pseudothrombus image” with a
true portal vein thrombus. The pseudothrombus
appearance occurs during the HAP in the main
portal vein lumen and is due to mixed flow from
156 January-February 2002 RG f Volume 22 ● Number 1

Figure 21. Pseudothrombus appearance. (a) Contrast-enhanced CT scan obtained during the HAP shows
an apparent partial thrombus of the portal vein. (b) Contrast-enhanced CT scan obtained during the PVP
shows a patent portal vein.

Figure 22. Neoplastic thrombus in a patient with hepatocellular carcinoma. (a) Contrast-enhanced CT scan
obtained during the HAP shows partial uptake of contrast material by a neoplastic thrombus (arrow). (b) Con-
trast-enhanced CT scan obtained during the PVP shows continued enhancement of the neoplastic thrombus,
whereas a bland thrombus is hypoattenuating.

the enhanced splenic vein return and the nonen-
hanced superior mesenteric vein return. How-
ever, a homogeneously enhanced portal vein is
seen during the PVP (Fig 21).
Differentiation between a bland thrombus and
a tumoral thrombus in a patient with hepatocellu-
lar carcinoma is not always possible with helical
CT. Increased, streaky enhancement of the
thrombus during the HAP suggests the presence
of portal vein invasion and tumoral thrombosis
(Fig 22). Two types of perfusion anomalies have
been reported in portal vein thrombosis (23,24,
43): (a) A transient hepatic attenuation difference
during the late HAP has been reported. This
anomaly appears as an increase in the attenua-
tion of segments poorly perfused by the portal
vein and is due to an increase in arterial inflow.
(b) Diminished enhancement during the PVP due
to locally decreased portal vein perfusion has also
been reported.
Gas in the Portal Venous System
Traditionally, the presence of gas in the portal
venous system was interpreted as an ominous sign
in the clinical setting of mesenteric ischemia in
adults or necrotizing enterocolitis in infants. It
was a surgical emergency, with a mortality rate of
75%–90% (44 – 46). Nowadays, mortality rates
associated with portal venous system gas have
declined to 29%– 43% (44,46). This decline is
due not to improved therapy but rather to new
and better imaging techniques, which have al-
lowed recognition of an increasing number of
causes of gas in the portal venous system. The
accessibility to CT units has increased the sensi-
tivity for detection of portal venous system gas
RG f Volume 22 ● Number 1 Gallego et al 157

Figure 23. Portal vein gas. (a) Contrast-enhanced

CT scan obtained in a patient with mesenteric isch-
emia shows gas distributed in a branching pattern at
the periphery of the liver, especially in the left lobe.
(b) Contrast-enhanced CT scan obtained in the
same patient shows gas in the main portal vein (ar-
row). (c) Contrast-enhanced CT scan obtained in a
patient with pneumoperitoneum shows gas dissect-
ing through the walls of the portal vein.

seen in branches of the mesenteric veins or in the

from various causes with a favorable prognosis
(44 – 46). In most of these cases, surgery may not
be necessary.
Reported causes of portal venous system gas
are necrotizing pancreatitis, abdominal abscess,
intestinal obstruction, perforated gastric ulcer or
carcinoma, diverticulitis, inflammatory bowel dis-
ease, abdominal trauma, ingestion of a caustic
agent, enema administration, colonoscopy, gas-
trostomy tubes, and liver transplantation. In
5%–15% of cases, the cause remains unknown
(44,46).
Plain radiographs of the abdomen demonstrate
streaks of low opacity at the periphery of the liver.
Conventional imaging performed with the patient
in the supine position allows detection of small
quantities of air in the right upper quadrant (46).
However, conventional imaging is not sensitive to
the presence of gas in the mesenteric vessels.
On CT scans, air in the portal vein manifests
as ramifying streaks with air attenuation that can
reach the capsule at the periphery of the liver. Air
has a propensity to accumulate in the intrahepatic
radicles of the left portal vein due to its more ven-
tral location (Fig 23). Portomesenteric air can be
main venous trunks.
Intrahepatic portal vein gas should be differen-
tiated from aerobilia. The distribution of hepatic
gas in patients with aerobilia is central, around
the portal hilum, and does not extend to within 2
cm of the liver capsule (44,46). Gas in mesenteric
vein branches should be differentiated from pneu-
moperitoneum (Fig 23c). Pneumoperitoneum
does not have a linear, ramifying configuration
and can be present in the antimesenteric border
of the intestine.
The finding of portomesenteric venous gas on
CT scans is no longer a sign of a poor prognosis,
even in patients with mesenteric ischemia (46),
and should be evaluated within the clinical con-
text so that the correct therapeutic decision can
be made. Surgery is still mandatory in patients
suspected to have mesenteric ischemia, in cases of
diverticulitis or abscess when medical treatment is
not effective, and in cases of obstruction when
there are accompanying signs of mesenteric isch-
emia. Portal venous system gas due to iatrogenic
causes, blunt trauma or barotrauma, or unknown
causes can be managed medically with close sur-
veillance (46).
Conclusions
Knowledge of the normal venous anatomy,
normal variants, and congenital and acquired
anomalies of the portal venous system can help
158 January-February 2002
us correctly interpret radiologic findings in the
abdomen. Biphasic helical CT is a useful tool for
assessment of perfusion disorders of the liver as-
sociated with portal venous system anomalies.
Color Doppler US and MR imaging can aid in
diagnosis and evaluation of these conditions.
Such entities include portosystemic collateral ves-
sels; cavernous transformation of the portal vein;
intrahepatic vascular shunts; and aneurysms,
thrombosis, and gas in the portal venous system.
Acknowledgment: The authors acknowledge Carlos
Marı́n, MD, for his contribution to this article.
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