AJR 2001; 176:891-897
© American Roentgen Ray Society
Periportal Contrast Enhancement and Abnormal Signal Intensity on State-of-the-Art MR Images
John N. Ly1 and
Frank H. Miller
1
Both authors: Department of Radiology, Northwestern Memorial Hospital,
Northwestern University Medical School, 676 N. St. Clair, Ste. 800, Chicago,
IL 60611.
Received June 21, 2000;
accepted after revision August 21, 2000.
Address correspondence to F. H. Miller.
Introduction
Periportal contrast enhancement and abnormal signal intensity on MR imaging
are nonspecific but important signs of pathologic insult to the portal tracts.
These findings should be actively sought in patients who undergo abdominal MR
examinations because these findings may be the only abnormalities identified.
The significance of these findings depends on the underlying pathologic
process affecting the portal tracts of the liver. Periportal contrast
enhancement and abnormal signal intensity can be invaluable in the detection
of bile duct, pancreatic, and gallbladder diseases and in depiction of
periportal lymphedema resulting from benign and malignant causes. These
findings may also be useful signs of diffuse hepatic injury due to viral and
bacterial infections and malignant cell infiltration involving the portal
tracts.
This pictorial essay illustrates the spectrum of causes of periportal
enhancement and abnormal signal intensity using state-of-the-art MR imaging.
We used predominantly half-Fourier acquisition single-shot turbo spin-echo
(HASTE) T2-weighted images and gadolinium-enhanced fast low-angle shot (FLASH)
T1-weighted sequences obtained with fat saturation.
Periportal Anatomy and MR Findings
A loose layer of connective tissue, known as the capsula fibrosa
perivascularis or the Glisson's capsule, surrounds branches of the portal
vein, hepatic artery, and bile duct. This network of connective tissue extends
from the porta hepatis to the intrahepatic portal triads. Hepatic lymphatics
are also located within the portal tracts but are not visualized routinely on
cross-sectional imaging
[1].
Periportal abnormal signal intensity is defined as a periportal ring or
tramline surrounding the intrahepatic portal veins. It is typically
hyperintense on T2-weighted images and hypointense on T1-weighted images
relative to the adjacent hepatic parenchyma. This abnormal signal intensity is
best appreciated on T2-weighted images. It is possible to differentiate
periportal abnormal signal intensity from dilated bile ducts. Dilated bile
ducts have an abnormal hyperintense signal along one side of the intrahepatic
portal veins (Fig.
1A,1B).
In contrast, periportal abnormal signal intensity surrounds the portal vein
and bile ducts [2] (Fig.
2A,2B).
Histologic studies of the liver in patients with periportal abnormal signal
intensity have shown these findings to be the result of edema, dilatation of
lymphatics, bile duct proliferation, or inflammatory or malignant cell
infiltration in the portal tracts
[2].

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Fig. 1A. 47-year-old woman with abdominal pain. Axial half-Fourier
acquisition single-shot turbo spin-echo (HASTE) T2-weighted MR image (TR/TE,
1475/64; flip angle, 180°) shows bile duct (solid arrow) anterior
to portal vein (open arrow).
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Fig. 1B. 47-year-old woman with abdominal pain. Axial
gadolinium-enhanced fastspoiled gradient-echo T1-weighted MR image (160/2.3;
flip angle, 70°) obtained with fat saturation shows bile duct (solid
arrow) anterior to portal vein (open arrow).
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Fig. 2A. Periportal lymphedema in 49-year-old man who had undergone
Whipple's procedure for pancreatic carcinoma. Axial half-Fourier acquisition
single-shot turbo spin-echo (HASTE) T2-weighted MR image (TR/TE, 1300/90; flip
angle, 120°) obtained with fat saturation shows periportal hyperintensity
(solid arrows). Note portal vein (open arrow).
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Fig. 2B. Periportal lymphedema in 49-year-old man who had undergone
Whipple's procedure for pancreatic carcinoma. Coronal gadolinium-enhanced
fast-spoiled gradient-echo T1-weighted MR image (127/1.9; flip angle, 65°)
obtained with fat saturation reveals nonehancing periportal low signal
intensity (open arrows), consistent with lymphedema. Note portal vein
(solid arrow).
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Periportal contrast enhancement is defined as a periportal ring or tramline
of enhancement surrounding the intrahepatic portal veins (Fig.
3A,3B,3C,3D).
It may be related to early or late diffusion of contrast material in
periportal areas that were initially hyperintense on T2-weighted images. Early
or late diffusion may result from endothelial insult
[3].

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Fig. 3A. 49-year-old woman with breast carcinoma and obstructive
jaundice treated by bile duct stenting. Pathologic diagnosis was metastatic
adenocarcinoma. Axial short tau inversion recovery MR image (TR/TE, 5000/77;
flip angle, 70°; inversion time, 150 msec) shows abnormal hyperintensity
along main portal vein and intrahepatic right portal vein
(arrows).
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Fig. 3B. 49-year-old woman with breast carcinoma and obstructive
jaundice treated by bile duct stenting. Pathologic diagnosis was metastatic
adenocarcinoma. Axial unenhanced fast low-angle shot (FLASH) T1-weighted MR
image (155/2.2; flip angle, 70°) obtained with fat saturation shows
low-signal-intensity soft tissue in porta hepatis (arrows).
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Fig. 3C. 49-year-old woman with breast carcinoma and obstructive
jaundice treated by bile duct stenting. Pathologic diagnosis was metastatic
adenocarcinoma. Axial portal venous phase gadolinium-enhanced FLASH MR image
obtained with fat saturation reveals enhancement in porta hepatis and along
right intrahepatic portal vein and dilated intrahepatic bile ducts
(arrows).
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Fig. 3D. 49-year-old woman with breast carcinoma and obstructive
jaundice treated by bile duct stenting. Pathologic diagnosis was metastatic
adenocarcinoma. Coronal delayed phase (10 min) gadolinium-enhanced FLASH MR
image (165/2.3; flip angle, 70°) obtained with fat saturation reveals
tramline of enhancement in porta hepatis and along intrahepatic portal veins
and dilated intrahepatic bile ducts (small arrows). Note common bile
duct (large arrow) and duodenum (d). Periportal enhancement was only
finding that suggested metastatic breast carcinoma, which was confirmed at
surgical biopsy.
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The pathogenesis of periportal enhancement and abnormal signal intensity
appears to be variable and may include the following: periportal tracking of
blood resulting from trauma, impaired lymphatic drainage caused by
lymphadenopathy or surgical interruption, periportal infection or
inflammation, malignant tumor infiltration, periportal fibrosis, periportal
bile duct proliferation [1],
and portal vein thrombosis.
Periportal Tracking of Blood
In the setting of trauma, neither periportal low attenuation on CT scans
nor abnormal hyperintense T2 signal intensity on MR images has been shown to
be related to obstructive lymphedema but, rather, to tracking of blood. The
mechanism proposed by Macrander et al.
[4] is the disruption of small
trigonal vessels and adjacent hepatic parenchyma, resulting in blood tracking
along the low-resistance connective tissue sheath that surrounds the portal
tracts.
Periportal Lymphedema
Periportal low attenuation on CT scans was first described in patients with
lymphedema due to hepatic transplantation, attributed to surgical interruption
of lymphatics, bile leakage, or transplant rejection
[2]. On MR imaging, periportal
lymphedema is seen as bright signal intensity on T2-weighted images and as a
lack of enhancement after IV gadolinium administration. Other causes include
bile duct obstruction, biliary tract surgery (Fig.
2A,2B),
compression of lymphatics by lymphadenopathy, congestive heart failure,
cirrhosis (Fig.
4A,4B),
portal hypertension, and Budd-Chiari syndrome
[5].

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Fig. 4A. Periportal lymphedema in 49-year-old woman who had cirrhosis
and portal hypertension. Axial half-Fourier acquisition single-shot turbo
spin-echo (HASTE) T2-weighted MR image (TR/TE, 1300/90; flip angle, 120°)
shows abnormal hyperintensity surrounding intrahepatic portal veins (solid
straight arrows). Note fat in porta hepatis is not as hyperintense as
lymphedema (curved arrow). Note portal vein (open
arrow).
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Fig. 4B. Periportal lymphedema in 49-year-old woman who had cirrhosis
and portal hypertension. Axial gadolinium-enhanced fast low-angle shot (FLASH)
T1-weighted MR image (127/1.9; flip angle, 65°) obtained with fat
saturation reveals lack of enhancement on either side of intrahepatic portal
veins (solid straight arrows), consistent with lymphedema. Note fat
in porta hepatis (curved arrow), portal vein (open arrow),
and hypointense Gamna-Gandy bodies within spleen.
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Peribiliary Cysts
Peribiliary cysts are cystic dilatation of peribiliary glands around large
portal tracts and are associated with cirrhosis. These cystswhich are
low signal intensity on T1-weighted images, high signal intensity on
T2-weighted images, and lack enhancement after IV gadolinium administration
(Fig.
5A,5B)vary
from tiny cystic lesions to a large solitary cyst. Recognition of these cysts
may help to avoid the misdiagnosis of dilated bile ducts, periportal
lymphedema, or malignancy
[6].

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Fig. 5A. Peribiliary cysts in 68-year-old man who had cirrhosis. Axial
half-Fourier acquisition single-shot turbo spin-echo (HASTE) T2-weighted MR
image (TR/TE, 1200/60; flip angle, 150°) shows nodular hyperintensity in
porta hepatis (arrows).
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Fig. 5B. Peribiliary cysts in 68-year-old man who had cirrhosis. Axial
equilibrium phase (4 min) gadolinium-enhanced fast low-angle shot (FLASH)
T1-weighted MR image (156/2.3; flip angle, 70°) obtained with fat
saturation reveals no enhancement in porta hepatis (arrows). Imaging
findings are consistent with peribiliary cysts. This finding should not to be
confused with edema, dilated bile ducts, or tumor.
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Periportal Infection or Inflammation
Common causes of periportal infection include pyogenic and viral
cholangitis (Fig.
6A,6B),
AIDS-related cholangitis [7]
(Fig.
7A,7B),
and chronic pyogenic cholangitis (Oriental cholangiohepatitis). All these
entities result in periportal abnormal hyperintensity on T2-weighted sequences
and in enhancement after IV gadolinium administration. The absence of
periportal abnormalities does not exclude these diagnoses.

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Fig. 6A. 49-year-old man who had painless jaundice caused by
pancreatic head carcinoma with chronic cholangitis. Coronal half-Fourier
acquisition single-shot turbo spin-echo (HASTE) T2-weighted MR image (TR/TE,
1700/64; flip angle, 110°) shows hyperintensity within porta hepatis and
surrounding common bile duct (thick straight arrows). Note common
bile duct (thin straight arrow), portal vein (curved arrow),
and duodenum (arrowhead).
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Fig. 6B. 49-year-old man who had painless jaundice caused by
pancreatic head carcinoma with chronic cholangitis. Coronal delayed phase (6
min) gadolinium-enhanced fast low-angle shot (FLASH) T1-weighted MR image
(115/1.9; flip angle, 65°) obtained with fat saturation reveals periportal
enhancement in porta hepatis and surrounding common bile duct (thick black
arrows). Note common bile duct (thin black arrow), portal vein
(curved arrow), and duodenum (white arrow). Periportal
enhancement was thought to be caused by tumor extension. However, chronic
cholangitis was revealed at surgery, revealing nonspecificity of periportal
enhancement.
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Fig. 7A. 39-year-old woman with AIDS who had right upper quadrant
pain. Bile ducts were not dilated, but abnormal signal intensity and
enhancement in periportal region were only findings to suggest AIDS-related
cholangitis. Diagnosis was confirmed by presence of cytomegalovirus inclusion
bodies found on brushing specimens at endoscopic retrograde cholangiography.
Coronal half-Fourier acquisition single-shot turbo spin-echo (HASTE)
T2-weighted MR image (TR/TE, 1400/60; flip angle, 150°) shows abnormal
hyperintensity in porta hepatis and surrounding common bile duct (thick
black arrows). Note common bile duct (thin black arrow),
pancreatic duct (curved arrow), and duodenum (white
arrow).
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Fig. 7B. 39-year-old woman with AIDS who had right upper quadrant
pain. Bile ducts were not dilated, but abnormal signal intensity and
enhancement in periportal region were only findings to suggest AIDS-related
cholangitis. Diagnosis was confirmed by presence of cytomegalovirus inclusion
bodies found on brushing specimens at endoscopic retrograde cholangiography.
Axial arterial phase gadolinium-enhanced fast low-angle shot (FLASH)
T1-weighted MR image (165/2.3; flip angle, 70°) obtained with fat
saturation reveals enhancement in periportal distribution (arrows),
suggestive of periportal infection or inflammation.
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Primary sclerosing cholangitis is an autoimmune inflammatory disease of the
bile ducts. Complications include biliary obstruction caused by intra- or
extrahepatic strictures, periportal inflammation and fibrosis, cirrhosis, or
cholangiocarcinoma. Periportal abnormalities may be associated with
inflammation due to sclerosing cholangitis and with tumor infiltration due to
cholangiocarcinoma [8] (Fig.
8A,8B).

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Fig. 8A. Primary sclerosing cholangitis in 48-year-old man who had
unsuspected cholangiocarcinoma. Coronal half-Fourier acquisition single-shot
turbo spin-echo (HASTE) T2-weighted MR image (TR/TE, 1700/64; flip angle,
110°) shows hyperintensity in porta hepatis with extension into
intrahepatic portal tracts (short solid arrows). Note beaded
appearance of intrahepatic bile ducts (long arrows) and portal vein
(open arrow).
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Fig. 8B. Primary sclerosing cholangitis in 48-year-old man who had
unsuspected cholangiocarcinoma. Coronal delayed phase (10 min)
gadolinium-enhanced fast low-angle shot (FLASH) T1-weighted MR image (160/2.3;
flip angle, 70°) obtained with fat saturation reveals marked tramline
enhancement (arrows) surrounding dilated intrahepatic ducts. Marked
asymmetric enhancement is highly suggestive of cholangiocarcinoma, which was
proven by brushing specimens obtained during endoscopic retrograde
cholangiography.
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Periportal Malignant Cell Infiltration
Malignancy has been associated with periportal abnormal signal intensity.
The mechanism involved may be the compression and obstruction of the hepatic
lymphatics by enlarged lymph nodes in the porta hepatis or along the
hepatoduodenal ligament [3].
Concomitant contrast enhancement should suggest cellular infiltration due to
cholangiocarcinoma (Figs.
8A,8B
and
9A,9B,9C,9D),
lymphoma (Fig.
10A,10B,10C),
leukemia, or metastasis (Fig.
3A,3B,3C,3D).

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Fig. 9A. Pathologically proven cholangiocarcinoma in 63-year-old woman
who had obstructive jaundice. Coronal half-Fourier acquisition single-shot
turbo spin-echo (HASTE) T2-weighted MR image (TR/TE, 1300/90; flip angle,
150°) obtained with fat saturation shows abnormal soft tissue with
heterogeneous mild hyperintense signal intensity relative to liver in porta
hepatis. This results in marked compression of common bile duct (short
arrows). Note dilated intrahepatic bile ducts (long arrows).
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Fig. 9B. Pathologically proven cholangiocarcinoma in 63-year-old woman
who had obstructive jaundice. Axial arterial phase gadolinium-enhanced fast
low-angle shot (FLASH) T1-weighted MR image (165/2.3; flip angle, 70°)
obtained with fat saturation reveals minimal enhancement of infiltrative soft
tissue (straight arrows) along dilated intrahepatic ducts (curved
arrow).
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Fig. 9C. Pathologically proven cholangiocarcinoma in 63-year-old woman
who had obstructive jaundice. Axial portal venous phase gadolinium-enhanced
FLASH MR image obtained with fat saturation reveals progressive enhancement of
infiltrative soft tissue (straight arrows) along dilated intrahepatic
ducts (curved arrow).
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Fig. 9D. Pathologically proven cholangiocarcinoma in 63-year-old woman
who had obstructive jaundice. Coronal delayed phase (10 min)
gadolinium-enhanced FLASH MR image obtained with fat saturation reveals marked
extensive enhancement of infiltrative soft tissue (short arrows)
along dilated bile ducts (long arrow). Imaging appearance is highly
suggestive of malignant cellular infiltration such as cholangiocarcinoma.
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Fig. 10A. 53-year-old man with Hodgkin's lymphoma that was treated with
autologous bone marrow transplantation. Axial half-Fourier acquisition
single-shot turbo spin-echo (HASTE) T2-weighted MR image (TR/TE, 1000/60; flip
angle, 150°) shows abnormal hyperintensity along intrahepatic right portal
vein and bile ducts (short arrows). Note bile duct (long
arrow).
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Fig. 10B. 53-year-old man with Hodgkin's lymphoma that was treated with
autologous bone marrow transplantation. Axial unenhanced fast low-angle shot
(FLASH) MR image (156/2.3; flip angle, 70°) obtained with fat saturation
reveals infiltrative low-signal-intensity soft tissue in porta hepatis
(arrows).
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Fig. 10C. 53-year-old man with Hodgkin's lymphoma that was treated with
autologous bone marrow transplantation. Axial delayed phase (10 min)
gadolinium-enhanced FLASH MR image obtained with fat saturation reveals
abnormal enhancement along intrahepatic portal vein and bile duct due to
lymphoma (short arrows). Note bile duct (long arrow).
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Portal Vein Thrombosis
Portal vein thrombus results from either bland (Figs.
11A,11B,11C,12A,12B,12C,13A,13B)
or tumor thrombus involving the portal vein. Periportal enhancement caused by
chronic thrombus is associated with enhancement of the collateral venous
vessels. The most common malignancy associated with tumor thrombus is hepatoma
(Fig.
14A,14B).

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Fig. 11A. 49-year-old woman with portal vein thrombosis and splenic
infarct. Axial half-Fourier acquisition single-shot turbo spin-echo (HASTE)
T2-weighted MR image (TR/TE, 1475/64; flip angle, 180°) shows abnormal
hyperintensity surrounding portal vein (small arrows). Note
thrombosed left portal vein (open arrow) and splenic infarct
(large arrows).
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Fig. 11B. 49-year-old woman with portal vein thrombosis and splenic
infarct. Axial portal venous phase gadolinium-enhanced fast low-angle shot
(FLASH) MR image (165/2.3; flip angle, 70°) obtained with fat saturation
shows filling defect within left portal vein (open arrow) and
periportal enhancement (small arrows). Periportal enhancement may
relate to enhancement of vaso vasorum of portal vein wall or flow around clot.
Note splenic infarct (large arrows).
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Fig. 11C. 49-year-old woman with portal vein thrombosis and splenic
infarct. Coronal gadolinium-enhanced FLASH MR image (165/2.3; flip angle,
70°) obtained with fat saturation shows filling defect within main portal
vein (open arrow) and periportal enhancement (solid black
arrows). Note bile duct (solid white arrow).
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Fig. 12A. 55-year-old man with hepatitis C and left intrahepatic portal
vein thrombosis. Axial half-Fourier acquisition single-shot turbo spin-echo
(HASTE) T2-weighted MR image (TR/TE, 1600/64; flip angle, 180°) shows
abnormal hyperintensity along left portal vein (open arrows). Note
thrombosed left portal vein (solid arrow).
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Fig. 12B. 55-year-old man with hepatitis C and left intrahepatic portal
vein thrombosis. Axial two-dimensional time-of-flight MR image shows thrombus
within left portal vein (solid arrow). Note collateral vessels
develop as a result of portal vein thrombus (open arrows).
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Fig. 12C. 55-year-old man with hepatitis C and left intrahepatic portal
vein thrombosis. Axial portal venous phase gadolinium-enhanced fast low-angle
shot (FLASH) MR image (140/2.2; flip angle, 70°) obtained with fat
saturation shows filling defect within left portal vein (solid arrow)
and periportal enhancement of collateral vessels (open arrows). This
should not be confused with tumor, infection, or inflammation.
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Fig. 13A. 71-year-old man with main portal vein thrombosis and
cavernous transformation. Coronal half-Fourier acquisition single-shot turbo
spin-echo (HASTE) T2-weighted MR image (TR/TE, 1600/64; flip angle, 180°)
shows abnormal heterogeneous signal intensity within porta hepatis (short
thin arrows). Note common bile duct (short thick arrow),
pancreatic duct (long thin arrow), and small hepatic cyst (curved
arrow).
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Fig. 13B. 71-year-old man with main portal vein thrombosis and
cavernous transformation. Coronal equilibrium phase gadolinium-enhanced fast
low-angle shot (FLASH) MR image (136/1.9; flip angle, 70°) obtained with
fat saturation reveals nodular and serpiginous enhancement of collateral
vessels in porta hepatis (thin arrows) and along common bile duct
(thick arrow). Note duodenum (d) and hepatic cyst (curved
arrow).
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Fig. 14A. 51-year-old man with hepatoma and thrombosis of main portal
vein and branches as result of tumor thrombus. Coronal half-Fourier
acquisition single-shot turbo spin-echo (HASTE) T2-weighted MR image (TR/TE,
1600/60; flip angle, 180°) shows abnormal bright signal intensity in porta
hepatis in periportal distribution (short arrows). Cordlike portal
vein (open arrow) is filled with tumor thrombus. Heterogeneous
hyperintensity in liver is caused by infiltrative hepatoma (H). Note common
bile duct (long arrow).
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Fig. 14B. 51-year-old man with hepatoma and thrombosis of main portal
vein and branches as result of tumor thrombus. Coronal equilibrium phase
gadolinium-enhanced fast low-angle shot (FLASH) MR image (160/2.3; flip angle,
70°) obtained with fat saturation reveals linear enhancement (solid
arrows) on both sides of main portal vein containing mildly enhancing
tumor thrombus (open arrow). Note presence of heterogeneous
enhancement within right lobe of liver, consistent with hepatoma (H). Presence
of enhancing portal vein thrombus helped in identification of underlying
diffuse hepatoma.
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Conclusion
It is important that radiologists be familiar with the findings of
periportal contrast enhancement and abnormal signal intensity on abdominal MR
imaging because these findings may be the only sign of intraabdominal disease.
MR imaging is more sensitive to periportal findings than CT and sonography,
and MR imaging is especially helpful in patients with jaundice or biochemical
abnormalities of the liver. The MR findings illustrated in this pictorial
essay include a variety of neoplastic, inflammatory, and vascular causes as
well as periportal lymphedema and peribiliary cysts. Proper recognition of
these MR findings may help to identify the underlying pathologic process.
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