DOI:10.2214/AJR.05.1649
AJR 2007; 188:W341-W347
© American Roentgen Ray Society
Biliary Abnormalities Associated with Portal Biliopathy: Evaluation on MR Cholangiography
Su Mi Shin1,
Suk Kim1,
Jun Woo Lee1,
Chang Won Kim1,
Tae Hong Lee1,
Suk Hong Lee1 and
Gwang Ha Kim2
1 Department of Diagnostic Radiology, College of Medicine, Pusan National
University Hospital, 10, Ami-Dong, Suh-Ku, Busan 602-739, Republic of
Korea.
2 Department of Internal Medicine, College of Medicine, Pusan National
University Hospital, Busan 602-739, Republic of Korea.
Received September 19, 2005;
accepted after revision January 19, 2006.
Address correspondence to S. Kim
(kimsuk{at}medigate.net).
WEB This is a Web exclusive article.
Abstract
OBJECTIVE. The purpose of our study was to evaluate the MRI features
of portal biliopathy.
CONCLUSION. MR cholangiography coupled with dynamic 3D gradient-echo
imaging could not only detect portal vein occlusion, cavernous transformation,
and gallbladder varices but is also suitable for delineating associated bile
duct abnormalities.
Keywords: biliary system • bile duct • cavernous transformation • extrahepatic portal vein occlusion • gallbladder • gallbladder varices • MR cholangiopancreatography • MRI
Introduction
It has now been well established that multiple thin hepatopetal
collateral veins form in response to extrahepatic portal vein obstruction.
These collateral veins, called portal cavernoma, arise somewhere in the
peripancreatic region along the occluded portal vein, enter the patent
intrahepatic portal branches, and hence provide an alternative route around a
thrombosed segment of the main portal vein in response to extrahepatic portal
vein obstruction [1,
2]. The portal cavernomis
composed of two venous systems including the paracholedochal veins, which run
parallel to the ductal wall, and the epicholedochal venous plexus, located on
the surface of the bile duct
[3,
4]
(Fig. 1). Portal biliopathy is
defined as biliary changes in patients with an extrahepatic portal vein
obstruction causing cavernous transformation. It has been reported in 70-100%
of patients with extrahepatic portal vein obstruction. Recently, studies have
suggested that the mechanisms of biliary abnormalities in extrahepatic portal
vein obstruction are either extrinsic compression by collaterals or ischemic
injury due to venous thrombosis
[3-9].
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Fig. 1 —Graphic shows collateral circulation in portal cavernoma. ECVP =
epicholedochal venous plexus, CV = cystic vein, PV = portal vein, GB =
gallbladder, PCVP = paracholedochal venous plexus, PSPDV = posterior superior
pancreaticoduodenal vein, CBD = common bile duct, LGV = left gastric vein, SMV
= superior mesenteric vein, SV = splenic vein.
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Portal biliopathy has been described in detail on endoscopic retrograde
cholangiography (ERC) but has received less attention in the radiology
literature
[5-9].
The purpose of this study was to describe the MRI features of portal
biliopathy.
Materials and Methods
Subjects
This was a retrospective, single-institution study approved by our
institutional review board. Because it was a retrospective study, informed
patient consent was not required. The patients were selected using several
criteria. First, we searched through our radiology databases to identify
patients (a total of 32 patients) with an MRI report containing the character
string, "cavernous," between April 2001 and June 2004.
Second, patients with abnormal findings of the biliary system on MRI were
selected. MRI findings considered as inclusion criteria included the
following: irregular contour, stricture, ductal dilatation, wall thickening,
and dynamic enhancement of the bile duct. The study population at this step
was composed of 23 (72%) of the original 32 patients. MRI was requested for
evaluation of hepatic masses or pancreatobiliary tumors (n = 11),
suspicion of recurrent pyogenic cholangitis (n = 4), suspicion of
bile duct abnormality on abdominal sonography or CT (n =7), and
suspicion of biliary symptoms associated with cystic duct remnants (n
=1).
Third, the resulting list of patients was narrowed using the following
exclusion criterion: patients with a history of another cause of biliary
abnormality, such as hepatocellular carcinoma (HCC) or pancreatobiliary
tumors, which might cause dilatation of the biliary system.
We identified 12 patients who met these criteria. The final study group
consisted of these 12 patients (six men and six women) whose mean age was 53
years (age range, 24-74 years).
MRI Technique
MRI was performed using a superconductive 1.5-T scanner (Sonata, Siemens
Medical Solutions) and a phased-array multicoil. Initially, a halfFourier RARE
sequence in the axial plane was obtained. We applied two MR cholangiographic
techniques: multislice half-Fourier RARE and thick single-slice turbo
spin-echo (TSE) sequences. Thick-slice MR cholangiopancreatography (MRCP)
images were obtained in the coronal plane. The multislice half-Fourier RARE
images were obtained in the coronal, sagittal, and oblique planes. The imaging
parameters for multislice half-Fourier RARE sequences were TR/TE, 1,000/87;
flip angle, 150°; slab thickness, 3-4 mm with no gap; field of view, 310
x 310 mm; matrix, 256 x 218; and acquisition time, 18 seconds.
Dynamic 3D gradientecho (volumetric interpolated breath-hold [VIBE]
examination) images (3.8/1.67; flip angle, 10°; matrix, 256 x 115 or
256 x 134) were obtained before and after an IV bolus injection of 20 mL
of gado-pentetate dimeglumine (Magnevist, Schering) at a rate of 2 mL/s.
Arterial, portal, and delayed-phase images were obtained. Five of the 12
patients also underwent ERC or percutaneous transhepatic cholangiography
(PTC).
Clinical Features
An experienced gastroenterologist reviewed all available clinical records
including clinical symptoms—that is, jaundice, abdominal pain, fever,
and chills—and the laboratory findings—that is, bilirubin and
alkaline phosphatase levels.
Image Analysis
The MR scans on the PACS (Maroview, Maro-tech) were evaluated
retrospectively and jointly by two radiologists who were blinded to all
clinical information but who had knowledge of the diagnosis of portal
biliopathy. Disagreement was resolved by consensus. The two radiologists
analyzed the presence of extrahepatic portal vein obstruction, cavernous
transformation, portosystemic collaterals, bile duct abnormalities, and
transient zonal differentiation of the hepatic parenchyma.
Extrahepatic portal vein obstruction was defined as the blocked portal vein
replaced by portal cavernoma. Cavernous transformation was determined to be
present if abnormally dilated and tortuous collateral venous vessels were
noted in the periportal regions and in the porta hepatis. Portosystemic
collaterals were determined by the presence of splenomegaly, esophagogastric,
or splenorenal varices. Splenomegaly was defined as greater than 13 cm in
diameter at the splenic hilum level. The biliary ductal system was evaluated
regarding the presence of irregular contour, stricture, ductal dilatation,
wall thickening, and increased enhancement of the ductal wall on dynamic
scans. Extrahepatic ductal dilatation was defined as a diameter of the common
bile duct greater than 7 mm in patients with a gallbladder and greater than 10
mm in patients after cholecystectomy. Stricture was defined as a short or long
segment of ductal narrowing with proximal ductal dilatation on MRCP.
The MRCP findings were compared with ERC (n = 4) and PTC
(n = 3) in five patients in terms of the bile duct contour, level of
the stricture, and duct dilatation. On dynamic 3D gradient-echo images, the
presence of areas with perfusion defects in the liver parenchyma was
evaluated. The benign nature of this biliary change was based on the biopsy,
follow-up CT, or clinical features. The median follow-up period was 32 months
(range, 12-76 months).
Results
Clinical Features
Nine of the 12 study patients were asymptomatic. The remaining three
patients had biliary symptoms such as abdominal pain, fever, and chills
suggesting cholangitis.
At the time of MRI, the liver function test results were as follows:
elevated alkaline phosphatase in seven (58%) of the patients and elevated
serum bilirubin in three (25%) of the patients. The level of bilirubin was
mildly elevated (1.5-2.2 mg/dL) in these patients.
Image Analysis
The imaging findings in all 12 patients with portal biliopathy are
summarized in Table 1.
Extrahepatic portal vein obstruction—In our study, the
causes of extrahepatic portal vein obstruction included unknown cause
(n =8) and recurrent pyogenic cholangitis (n =4).
Cavernous transformation—The cavernous transformation
depicted on the MR scans was in paracholedochal veins in 12 patients and in
epicholedochal veins in six patients (Fig.
2A,
2B,
2C,
2D,
2E). Gallbladder varices were
observed in five (100%) of the patients who had not undergone cholecystectomy.
The remaining seven patients had previously undergone cholecystectomy.
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Fig. 2A —45-year-old man with stricture and proximal ductal dilatation
(patient 2 in Table 1). Initial
CT scans show dotlike enhancing foci, suggesting epicholedochal veins within
thickened wall (arrow, B), paracholedochal veins
(arrowheads), and proximal ductal dilatation.
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Fig. 2B —45-year-old man with stricture and proximal ductal dilatation
(patient 2 in Table 1). Initial
CT scans show dotlike enhancing foci, suggesting epicholedochal veins within
thickened wall (arrow, B), paracholedochal veins
(arrowheads), and proximal ductal dilatation.
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Fig. 2D —45-year-old man with stricture and proximal ductal dilatation
(patient 2 in Table 1).
Endoscopic retrograde cholangiography image shows focal stricture of common
bile duct (arrow) without depiction of proximal bile duct.
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Fig. 2E —45-year-old man with stricture and proximal ductal dilatation
(patient 2 in Table 1). MRCP
image is able to depict entire biliary tree despite obstruction or stenosis.
Physician attempted to perform endoscopic placement of plastic stent but
failed. Follow-up MRCP (E) 26 months later shows there is also no
significant interval change of bile duct (arrows). These changes in
bile duct ("pseudocholangiocarcinoma sign") are caused by portal
biliopathy.
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In all patients, the paracholedochal veins and gallbladder varices appeared
as low signal intensity on T2-weighted images and as enhancing tortuous
collaterals on dynamic 3D gradient-echo images (Fig.
3A,
3B,
3C,
3D). The epicholedochal
collaterals appeared as dotlike enhancing structures in the bile duct
wall.
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Fig. 3A —74-year-old man with stricture and proximal ductal dilatation
(patient 8 in Table 1). Axial
T2-weighted image (A) and dynamic 3D gradient-echo image (B)
show focal and circumferential wall thickening with dotlike enhancing foci,
suggesting epicholedochal veins (thick arrows) in proximal common
hepatic duct (thin arrows). Paracholedochal veins
(arrowheads) and gallbladder varices (open arrows) appear as
low signal intensity on T2-weighted image (A) and as enhancing tortuous
collaterals on dynamic 3D gradient-echo image (B).
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Fig. 3B —74-year-old man with stricture and proximal ductal dilatation
(patient 8 in Table 1). Axial
T2-weighted image (A) and dynamic 3D gradient-echo image (B)
show focal and circumferential wall thickening with dotlike enhancing foci,
suggesting epicholedochal veins (thick arrows) in proximal common
hepatic duct (thin arrows). Paracholedochal veins
(arrowheads) and gallbladder varices (open arrows) appear as
low signal intensity on T2-weighted image (A) and as enhancing tortuous
collaterals on dynamic 3D gradient-echo image (B).
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Fig. 3C —74-year-old man with stricture and proximal ductal dilatation
(patient 8 in Table 1).
Stricture with proximal bile duct dilatation is shown on MR
cholangiopancreatography (MRCP) image (C) and endoscopic retrograde
cholangiography (ERC) image (D). ERC image (D) shows stricture
portion is not distended with pressure-guided injection of contrast material
in this patient. Biliary ductal wall thickening (arrows) indicates
delayed enhancement on dynamic 3D gradient-echo image (B).
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Fig. 3D —74-year-old man with stricture and proximal ductal dilatation
(patient 8 in Table 1).
Stricture with proximal bile duct dilatation is shown on MR
cholangiopancreatography (MRCP) image (C) and endoscopic retrograde
cholangiography (ERC) image (D). ERC image (D) shows stricture
portion is not distended with pressure-guided injection of contrast material
in this patient. Biliary ductal wall thickening (arrows) indicates
delayed enhancement on dynamic 3D gradient-echo image (B).
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Portosystemic collaterals—The spleen size in our study
patients was mostly in the normal range but was mildly enlarged by 13.7-15.0
cm in three (25%) of the patients. Portosystemic collaterals, including
esophagogastric (n = 2) and splenorenal (n = 1) varices,
were noted in three (25%) of the patients.
Bile ducts—Irregular contour of the duct, predominating in
the suprapancreatic common bile duct, was present in all 12 study patients
(Fig. 4A,
4B,
4C). Among these patients,
biliary stricture with proximal ductal dilatation (Figs.
2A,
2B,
2C,
2D,
2E and
3A,
3B,
3C,
3D) was present in six
patients, wall thickening of the duct in five patients, and delayed and
prolonged enhancement of the thickened wall in three patients.
Choledocholithiasis was noted in one patient and a gallbladder stone in one
patient.
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Fig. 4A —40-year-old man with irregular contour of bile duct (patient 7 in
Table 1). Sequential CT scans
from level of porta hepatis to level of suprapancreatic common bile duct show
irregularity of biliary ductal wall (arrows) due to cavernous
transformation (arrowheads).
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We classified these biliary abnormalities as the varicoid type in six (50%)
of the patients, fibrotic type in three (25%) of the patients, and mixed type
in the remaining three (25%) patients.
In the varicoid type of biliary abnormality, the irregular contour of the
bile duct was primarily caused by multiple smooth extrinsic compressions of
the dilated and tortuous paracholedochal vein along the common bile duct. This
was clearly depicted on both MR portography and MRCP (Fig.
4A,
4B,
4C).
In the fibrotic type of biliary abnormality, the MR scans showed localized
strictures with bile duct dilatation. The smooth localized strictures were
seen arising at the level of the thickened wall of the common bile duct on
MRCP; the thickened wall showed delayed increased enhancement on dynamic 3D
gradient-echo images (Fig. 3A,
3B,
3C,
3D).
In the mixed type of biliary abnormality, irregular contours with multiple
areas of narrowing and dilatation were also noted, but wall thickening at the
level of the narrowed portion did not show delayed increased enhancement in
this type.
Comparison of MRCP with direct cholangiography—The MRCP
findings were compared with the direct cholangiography findings in five
patients. There was no discrepancy in the general contour or level of
stricture and dilatation of the bile duct.
Varicoid type (Fig. 5A,
5B,
5C) showed smooth indentation
of the bile duct by its cavernous transformation. Mixed type (Fig.
6A,
6B,
6C,
6D,
6E,
6F) showed irregular contour
with multiple areas of narrowing and dilatation. In one patient, the narrowing
portion was obscured and distended on PTC and choledochoscopy with
pressure-guided injection of contrast material and water. However, in the
fibrotic type (Fig. 3A,
3B,
3C,
3D), the stricture portion was
not distended on ERC.
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Fig. 5A —59-year-old woman with varicoid type biliary abnormality (patient 4
in Table 1). T-tube
cholangiography image after cholecystectomy shows smooth indentation of bile
duct (arrows) by its cavernous transformation. Follow-up MRI for
evaluation of biliary symptoms associated with cystic duct remnants was
performed 1 month later (not shown).
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Fig. 5B —59-year-old woman with varicoid type biliary abnormality (patient 4
in Table 1). Coronal dynamic 3D
gradient-echo image (B) and MR cholangiopancreatography (C) show
cavernoma (arrowhead, B) and irregular contour of bile duct
(arrows).
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Fig. 5C —59-year-old woman with varicoid type biliary abnormality (patient 4
in Table 1). Coronal dynamic 3D
gradient-echo image (B) and MR cholangiopancreatography (C) show
cavernoma (arrowhead, B) and irregular contour of bile duct
(arrows).
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Fig. 6A —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Paracholedochal
venous plexus (arrowhead, A) appears as low signal intensity
on MR cholangiopancreatography (MRCP) image (A) and as enhancing
tortuous collaterals on dynamic 3D gradient-echo image (B). MRCP shows
multifocal strictures of intrahepatic and extrahepatic bile ducts with
upstream bile duct dilatation (arrows), which may be caused by portal
cavernoma (arrowhead, B) and fibrous scarring.
Three-dimensional gradient-echo images during delayed phase (not shown)
revealed no delayed prolonged enhancement of stricture segment.
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Fig. 6B —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Paracholedochal
venous plexus (arrowhead, A) appears as low signal intensity
on MR cholangiopancreatography (MRCP) image (A) and as enhancing
tortuous collaterals on dynamic 3D gradient-echo image (B). MRCP shows
multifocal strictures of intrahepatic and extrahepatic bile ducts with
upstream bile duct dilatation (arrows), which may be caused by portal
cavernoma (arrowhead, B) and fibrous scarring.
Three-dimensional gradient-echo images during delayed phase (not shown)
revealed no delayed prolonged enhancement of stricture segment.
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Fig. 6C —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Percutaneous
transhepatic cholangiography (PTC) images of mixed type biliary abnormality
show irregular contour with repetitive portions of narrowing and dilatation.
Narrowing portion (arrows) was obscured and distended on PTC with
pressure-guided injection of contrast material.
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Fig. 6D —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Percutaneous
transhepatic cholangiography (PTC) images of mixed type biliary abnormality
show irregular contour with repetitive portions of narrowing and dilatation.
Narrowing portion (arrows) was obscured and distended on PTC with
pressure-guided injection of contrast material.
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Fig. 6E —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Choledochoscopic
findings show common bile duct stricture before (E) and distension
after (F) pressure-guided injection of water similar to findings on
PTC.
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Fig. 6F —43-year-old man with mixed type biliary abnormality (patient 11 in
Table 1). Choledochoscopic
findings show common bile duct stricture before (E) and distension
after (F) pressure-guided injection of water similar to findings on
PTC.
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Transient zonal differentiation—None of our 12 patients
showed transient hepatic zonal attenuation differences.
Discussion
Portal biliopathy is recent terminology used to describe changes in the
bile duct due to cavernous transformation in patients with portal hypertension
[4]. Such changes in the bile
duct are more frequent in portal hypertension caused by extrahepatic portal
vein occlusion than in cirrhosis or other causes of portal hypertension.
In one study, the majority of the patients with portal biliopathy were
asymptomatic. Only 14% of the patients had biliary symptoms
[3]. In our study, mildly
elevated serum bilirubin levels (1.5-2.2 mg/dL) were observed in three (25%)
of 12 patients.
Direct cholangiographic findings in patients with extrahepatic portal vein
obstruction, including segmental upstream dilatation, caliber irregularity,
stricture, and extrinsic impression on the bile duct due to collaterals, have
been called "pseudocholangiocarcinoma sign" because they mimic a
cholangiocarcinoma spreading along the bile duct
[3-9].
The mechanisms of biliary abnormalities in extrahepatic portal vein
obstruction are either extrinsic compression by collaterals or peribiliary
fibrosis resulting from ischemic or inflammatory changes underlying portal
thrombosis [3,
7,
8]. Dhiman et al.
[10] observed partial or
complete regression of portal biliopathy in four patients and no regression in
one patient among five patients with extrahepatic portal vein obstruction who
underwent portosystemic shunt surgery. In cases of reversible biliary change
after shunt surgery, mechanical compression by collaterals is the mechanism
behind biliary abnormalities in extrahepatic portal vein obstruction. In cases
of persistent biliary abnormalities, ischemia or fibrous scarring of the bile
duct is considered the major cause of biliary abnormalities.
In accordance with the Dhiman et al.
[10] description, we
classified these biliary abnormalities as varicoid, fibrotic, or mixed type on
the basis of the presence or absence of stricture and on the pathogenesis. In
the varicoid type, the irregular contour of the bile duct was primarily caused
by multiple smooth extrinsic compressions of the cavernoma. This was clearly
depicted on both MR portography and MRCP (Fig.
4A,
4B,
4C). In the fibrotic type, MR
scans show localized strictures with proximal duct dilatation. The strictures
were primarily caused by fibrous scarring related to chronic inflammation and
ischemic injury (Fig. 3A,
3B,
3C,
3D).
Gibson et al. [11] reported
the presentation and natural history of extrahepatic portal vein obstruction
in patients and noted that of 28 study patients, only five had jaundice.
Jaundice in a patient with portal biliopathy could be caused by the
development of a narrowing or stricture in the common bile duct or because of
choledocholithiasis. The majority of these patients are asymptomatic and do
not need any treatment. However, choledocholithiasis or symptomatic bile duct
stricture can be managed by endoscopic procedures such as sphincterectomy,
balloon dilatation, and stenting. The endoscopic procedure should be carefully
undertaken because of the large venous collaterals in the periampullary region
[4,
10-12].
In our study, no patients experienced symptoms suggesting progressive or
persistent biliary obstruction. In one case, the physician attempted to
perform endoscopic placement of the plastic stent but failed (Fig.
2A,
2B,
2C,
2D,
2E). Clinical and imaging
follow-up during 26 months showed no worsening of laboratory values or
symptoms. Therefore, we think that the biliary stenting procedure for portal
biliopathy is not frequently needed.
When blockage takes place at the level of the portal trunk, portal flow
remains adequate for the central zones of the liver but not for the peripheral
zones [13]. The arterial
response, based on activation of the peribiliary plexus, produces enhancement
of the peripheral hepatic parenchyma with relatively less enhancement of the
central perihilar area. But none of our 12 study patients showed these
transient zonal attenuation differences. Transient zonal attenuation
differences are considered to originate from the well-developed cavernous
transformation and the consequent decrease in arterial compensation in the
chronic stage of portal vein occlusion.
There are several limitations to our study. First, because this study was a
retrospective review, selection bias was unavoidable. Extrahepatic portal vein
obstruction with cavernous transformation was revealed in 101 patients on
contrast-enhanced CT scans during the study period, which was mostly caused by
HCC, metastasis, and liver cirrhosis. Usually, CT alone was sufficient to
diagnose these diseases, so liver MRI with MRCP was not performed in most of
our patients. Therefore, from the large series of patients with extrahepatic
portal vein obstruction, only 12 patients formed the basis of the study.
Second, the small number of patients involved also limited our study.
Therefore, our results cannot be taken to be representative of portal
biliopathy. Third, because this study was a retrospective review, MRCP and ERC
findings of all suspected portal biliopathy patients could not be compared,
even though the comparison is quite meaningful in diagnosis. However, we think
that MRCP with additional dynamic 3D gradient-echo imaging could provide all
the diagnostic components of portal biliopathy, such as extrahepatic portal
vein obstruction, cavernous transformation, and bile duct change. Finally,
pathologic proof was not available for all the cases; however, the benign
nature of the disease was characterized using clinically accepted and widely
used techniques.
In summary, MR cholangiography coupled with dynamic 3D gradient-echo
imaging offers the advantages of being noninvasive and providing all the
diagnostic components of portal biliopathy, including extrahepatic portal vein
obstruction, portal cavernoma, gallbladder varices, and bile duct
abnormalities, and delineating the extent and severity of bile duct
stricture.
Acknowledgments
We thank Bonnie Hami, department of radiology, University Hospitals of
Cleveland, for copyediting the manuscript.
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Abstract
Introduction
