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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_585_Библиотеки_им_академика_М_И_Перельмана.pdf
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3 Imaging ofCommon Biliary Tract Diseases
63
c
e
d
f
Fig. 3.43 CT and MRI ndings of acute suppurative cholangitis with
hepatic abscess. (a) Plain CT scan shows dilatation of the bile duct in
the right lobe of the liver with high-density stone shadow, and circular
low-density shadow is seen in the distal stone liver parenchyma. (b–d)
CT enhanced scan shows honeycomb enhancement in each phase. (e, f)
Plain MRI scan shows bile duct dilatation in the right lobe of the liver,
and multiple short T2 and isot1 nodular stone shadows are observed.
(g–j) The bile duct wall is thickened by contrastive scanning, and the
distal liver parenchyma presents multiple circular enhancement shadows in the form of honeycomb.
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X. Quan et al.
Fig. 3.43 (continued)
Imaging ndings of biliary obstruction combined with
clinical manifestations and diagnosis can be established.
After the diagnosis of acute cholangitis, it is necessary to
identify the possible causes: calculi, neoplastic, or benign
stenosis.
3.4.3.1 CT Findings
CT is highly reliable for the detection of PSC.PSC is characterized by stenosis and dilation of the intrahepatic bile
ducts (shown as isolated, scattered, and localized dilatation
of the peripheral bile ducts at the distal end of the stenosis,
and occasionally diverticular dilatation). However, it is difcult for CT to show the stenotic portion of the bile duct.
3.4.3 Primary Sclerosing Cholangitis
Enhanced CT images at the arterial and portal venous phases
show segmental dilatation of the biliary tree on one or more
Primary Sclerosing Cholangitis (PSC) is a chronic cholestatic liver disease characterized by chronic inammation and
brosis of the intrahepatic and extrahepatic bile ducts, also
known as brotic cholangitis or occlusive cholangitis. The
main symptoms and signs are progressive exacerbation with
obstructive jaundice, yellowish staining of the skin and
sclera, and hepatomegaly.
slices. It is characterized by discontinuous, scattered, and
peripherally dilated ducts with fewer branches, which has
been described as the “pruned tree” sign; alternating narrowing and dilatation of the bile ducts with a “beaded” appearance suggests that intrahepatic bile duct dilatation is alternate,
which implies intrahepatic multiple biliary stenoses
(Halefoglu 2007). PSC can also involve the extrahepatic bile
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3 Imaging ofCommon Biliary Tract Diseases
65
duct, showing strictures and dilatation of the extrahepatic
bile ducts; however, it shows a mild degree, with the bile
duct wall less than 5mm thick, and the internal diameter of
the common bile duct less than 4mm. When the gallbladder
is involved, the gallbladder wall becomes thickened and the
gallbladder often shows atrophy.
Another type of primary sclerosing cholangitis involving
the intrahepatic bile ducts is characterized by small bile
ducts dilatation in a diffuse or segmental distribution in the
peripheral area; however, these small bile ducts are not
directly connected with the larger bile duct in the hilar area.
Fifty-four percent of the patients with cholangitis cirrhosis
have large intrahepatic hyperplastic nodules (the diameter of
such nodules is 3cm). Such nodules usually appear near the
hilar area, so this is termed as focal nodular hyperplasia,
typically associated with wedge-shaped atrophy of the
hepatic lobe and hypertrophy of the caudate lobe. Also, onefourth of primary sclerosing cholangitis is complicated with
diffuse micronodular cirrhosis of the liver.
3.4.3.2 MRI Findings
T2WI and MRCP can show segmental and discontinuous
dilatation, and multiple stenoses involving the intrahepatic
and extrahepatic bile ducts, with thickening of the bile duct
wall in the stenotic segment, associated with mild-tomoderate dilatation, and a reduction in bile duct branches
(Dave etal. 2010) (Fig. 3.44). When it is associated with
cirrhosis, giant nodular hyperplasia in the perihepatic area
can be observed. These lesions appear isointense or hyperintense on T1W1, and slightly hyperintense or isointense on
T2W1, or hypointense on T2W1. Enhanced scanning shows
unclear boundary of proliferative nodules in the hepatic
artery phase, and isointense in the portal venous phase. PSC
patients can also present with abnormal enhancement areas,
which may be related to secondary inammation of liver
parenchyma.
3.4.4 Secondary Sclerotic Cholangitis
Inammation and brosis of intrahepatic and extrahepatic
bile ducts have various causes, including ascending bacterial
infection of the biliary tract that occurs with some degree of
obstruction in the distal bile ducts caused by stones and
tumors, ischemic cholangitis (biliary ischemia such as sclerosing cholangitis caused by hepatic artery thrombosis),
hepatic arterial infusion chemotherapy-induced sclerosing
cholangitis, and bile duct injury (including iatrogenic bile
duct injuries). These instigators of Secondary Sclerotic
Cholangitis (SSC) can also affect the tissues surrounding the
bile duct, including adjacent liver tissues. The biliary changes
they bring in are similar to those seen in Primary Sclerotic
Cholangitis (PSC); however, this condition is secondary to
another underlying disease, thus it is called secondary sclerotic cholangitis. The clinical features suggesting SSC
include the presence of sclerosing cholangitis syndrome,
such as recurrent attacks of fever, right upper abdominal
pain, and jaundice caused by inammation and brosis of
the bile ducts, based on another underlying disorder.
Some diseases that can promote the development of SSC,
such as AIDS and bile duct injury (including iatrogenic bile
duct injuries) often present obvious history, physical signs,
and laboratory ndings. They are often treated under radiographic monitoring. In the absence of secondary cholangitis,
there are no radiographic signs of bile duct abnormalities.
However, when patients exhibit clinical symptoms of SSC
Fig. 3.44 Primary sclerosing cholangitis. (a) T2WI shows segmental, discontinuous dilatation, and multiple strictures of the intrahepatic and
external bile ducts. (b) MRCP shows thickening of the bile duct wall and reduction of bile duct branches in the stricture segment
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X. Quan et al.
such as jaundice, repeated fever, and upper quadrant abdominal pain; and radiographic examination reveals signs of SSC
(similar to PSC), the diagnosis of SSC can be conrmed. If
patients present with abnormal manifestations of the bile
duct other than SSC, it can only be diagnosed as a biliary
disease secondary to the primary disease (non-SSC), such as
the absence of liver or gallbladder invasion in AIDS patients;
AIDS-associated SSC can be diagnosed if subsequent recurrent fever, jaundice and right upper quadrant pain occur and
radiographic examination (direct cholangiography or MRCP)
reveal multiple intrahepatic and extrahepatic biliary tract
limitations, segmental stenosis, mild or moderate dilatation
or non-dilation of proximal bile duct with stenosis; if CT and
MRI detected PSC-like imaging changes (intrahepatic and
extrahepatic biliary dilatation, especially leaping dilatation,
as well as changes in density and signal intensity before and
after enhancement in the portal area and adjacent hepatic
parenchyma), AIDS-associated SSC can also be diagnosed.
If radiographic examination only shows distal choledochal
stenosis and papillary hyperplasia, it can only be diagnosed
as AIDS-related cholangitis (non-SSC).
Since such conditions as ischemic cholangitis and cholangitis caused by perfusion chemotherapy of primary or metastatic carcinoma of the liver through the hepatic artery belong
to sclerosing cholangitis, diagnosis of SSC can be conrmed
when (Fig.3.45):
• Radiographic examination of these diseases showed sin-
gle or multiple intrahepatic and extrahepatic bile duct ste-
nosis associated with mild and slight dilatation or
non-dilatation above the stenosed portion.
• CT and MRI detected changes in density and signal inten-
sity in the portal area and adjacent hepatic parenchyma.
For example, in the case of multiple hepatic metastases
after surgical resection of colon cancer, SSC symptoms are
observed after hepatic arterial infusion of 5-uorouracil for a
period of time or several months. Contrast-enhanced CT
reveals heterogeneous distribution of bile ducts with different degrees of (leaping) dilatation, with or without adjacent
portal areas, and excessive enhancement of liver parenchyma
(especially in the arterial phase). Direct cholangiography (or
MRCP) shows similar PSC manifestations, including multifocal segmental strictures involving both the intrahepatic and
the extrahepatic bile ducts, alternating strictures of bile duct
in the proximal portion, mild bile duct dilatation, and ductalwall irregularities, which can be diagnosed as ChemotherapyInduced Sclerosing Cholangitis (CISC), occasionally
triggered by hepatic arterial infusion chemotherapy with
uoropyrimidines.
3.4.5 Recurrent Pyogenic Cholangitis
Recurrent Pyogenic Cholangitis (RPC) is a hepatobiliary
disease caused by cholangitis (inammation of the bile duct,
especially suppurative cholangitis) and bile duct stones
(especially hepatolithiasis). RPC predominantly affects
women aged from 30 to 50 years, and the male-to-female
ratio is 1:19. Most patients have a history of recurrent episodes, with symptoms and signs similar to those of acute
cholangitis.
3.4.5.1 CT Findings
Non-contrast CT scanning is reasonably sensitive for the
detection of stones composed of calcium or other heavy metals (Fig.3.46). The CT values are in the range of 20 and 160
HU, with an average of 79 HU.The stones become obvious
when the CT value of the stone is greater or less than that of
the liver parenchyma, if the stone is surrounded by lowdensity bile within the dilated bile duct (Federle etal. 1982;
Chan et al. 1989; Itai et al. 1980); when the intrahepatic
ducts are completely lled by iso-dense calculi, missed diagnosis of stones is possible, and even the dilated bile duct
itself is difcult to identify. Contrast-enhanced CT scans can
show associated parenchymal changes of the liver and mild
dilatation and stenosis of intrahepatic bile ducts. The distribution of dilated bile duct is usually conned to one lobe or
to a few segments, especially in the left lateral lobe. For
example, the left lobe is often more severely invaded in diffuse invasion, and a few patients present bile duct dilatation
on the right. Bile ducts show morphological heterogeneity.
RPC can present involvement to the bile duct only if the central part of the liver is involved, and the peripheral bile duct
is invisible; it can also be manifested as a stricture of the
intrahepatic bile duct or severe obstruction of the bile duct.
The bile duct above the stenosed portion is cystic and the
capsule can be both calculous and a-calculous; or can present
as a more severe obstruction of the bile duct in the central
part of the liver, in which case the proximal bile duct and its
surroundings are homogeneously distended. Occasionally
the peripheral bile duct and its surrounding are prominently
brotic, resulting in signicant stenosis, and the position
where the central bile duct is connected suddenly becomes
thinner, tapered, and arrowhead. Extrahepatic bile duct dilatation is not unusual, but only sometimes accompanied by
stones. The stenosed portion of the intrahepatic bile duct is
normally shorter and cannot be shown by CT; if it can be
seen, it is less likely that the connection of the dilated bile
ducts above the stenosed portion and the stenosed portion
can be displayed in the same plane. Most show dilatation of
the stenosed portion and the upstream of the bile duct, dilata-
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3 Imaging ofCommon Biliary Tract Diseases
67
c
Fig. 3.45 Secondary sclerosing cholangitis after transcatheter arterial
chemoembolization for liver cancer. (a~b) Plain scanning on T1WI
and T2WI shows segmental dilatation of the bile duct in the right lobe
of the liver, live dilatation of the bile duct in the right lobe of the liver,
and patellar Long T1 and Long T2 signals were observed in the adjacent
d
liver parenchyma. (c) The adjacent liver parenchyma presents obvious
nonuniform enhancement during enhanced scanning arterial phase;
(d~e) The enhancement degree decreases in the portal vein stage and
the delayed stage. (f) The hepatobiliary specic period shows low signal change
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Fig. 3.45 (continued)
X. Quan et al.
Fig. 3.46 CT of RSC. (a) Plain scan shows atrophy of the left lateral lobe of liver, dilatation of the intrahepatic bile duct, and multiple stone
shadows. (b) Enhancement can be seen on part of the bile duct wall during contrast-enhanced scan
tion or non-dilatation downstream of the bile duct. Therefore,
planar reformation facilitates the display of the stenotic part
of the bile duct. Contrast-enhanced CT scans can show the
thickening of the tube. It is important to note that recurrent
attacks of RPC may result in atrophy in the invaded lobes or
ment was enhanced during the acute attack, and the enhancement was mostly heterogeneous, or occasionally
homogeneous, which might be related to factors such as
acute inammatory arterial congestion and micro-abscess
formation.
segments of the liver, but compensatory hypertrophy in the
non-invaded or lighter parts, causing changes in the entire
liver morphology and proportion of the liver lobe, is commonly seen as severe atrophy of the invaded left hepatic lobe
and hypertrophy of the right lobe, including caudate lobe.
Contrast-enhanced imaging showed that that the hepatic seg-
MRI andMRCP Findings
MRI and MRCP show obvious intrahepatic bile duct dilata-
tion (Fig. 3.47). The dilatation is usually disproportionate;
patients often have bile duct dilatation without the presence
of strictures, and the proximal and distal parts can be dilated,
3 Imaging ofCommon Biliary Tract Diseases
69
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Fig. 3.47 MRI of RSC. (a) The intrahepatic bile duct is dilated, and the left outer lobe of the liver is more obvious, containing multiple short T2
stone shadows. (b) The tube wall is thickened, and the left outer lobe of the liver is atrophic
and those without stones can also present dilatation.
Extrahepatic bile duct strictures are often located at the conuence of left and right hepatic ducts and common hepatic
duct, with varying degrees, and the edge can be smooth or
rough. Intrahepatic bile duct dilatation is most commonly
segmental or lobar in distribution; the diffuse form is less
common. Intrahepatic bile duct dilatation is frequently
accompanied by stenosis or calculus. When the stenosis is
severe, the obstructed proximal bile duct may dilate as sacs.
Similar to CT ndings, peripheral bile ducts and their surrounding brosis are markedly narrowed, with the central
bile duct suddenly thinning and tapering to form an arrowshaped appearance. The stenosed portion of the intrahepatic
bile duct is usually short, with a ring stenosis or a centripetal
or eccentric stenosis smaller than 1cm. Stricture of the hilar
bile duct is more common and can be satisfactorily displayed
by MRCP. On T1WI, the enhanced bile duct wall can be
seen.
RPCs can have both intrahepatic and extrahepatic ducts.
Within the high signal intensity bile, T2WI and MRCP present low signal lling defects of varying quantity, size, and
shape. On T1WI, especially when the echo time (TE) is very
short, most of the stones show hyperintense or isointense signals compared with the liver signal; some stones present as a
typical “target sign,” representing a central hypointense lling defect surrounded by hyperintense bile.
Similar to CT, MRI can also show hepatic morphological
alterations caused by atrophy or hypertrophy of the hepatic
lobe and segment. The liver parenchyma of the atrophic
hepatic lobe or hepatic segment presents as iso-, slightly
hypo-, or slightly hyper-intense on T1WI, and iso- or hyperintense on T2WI.Hepatic lobar atrophy and liver enhancement can be observed after contrast medium administration.
After MRI enhancement, intrahepatic cholangiocarcinoma, inammatory pseudotumor, liver abscess, and biliary
tumor can be observed. Inammatory pseudotumor appears
as low signals on T1WI and high signals on T2WI.After
enhancement, the surrounding area is enhanced while the
central part is mostly not, or slightly enhanced.
3.4.6 Extrahepatic Cholangiocarcinoma
Cholangiocarcinoma can be classied into intrahepatic cholangiocarcinoma and extrahepatic cholangiocarcinoma.
Extrahepatic cholangiocarcinoma is a general term for
malignant tumors that occur in the extrahepatic bile duct
(including the left and right hepatic ducts to the lower end of
the common bile duct), excluding intrahepatic cholangiocarcinoma, cholangiocarcinoma, gallbladder carcinoma, and
cancer of the ampulla of Vater. It is a relatively rare form of
cancer that arises from the epithelial cells of the extrahepatic
bile ducts. The age of onset is most common between age 40
and 60years; the incidence rate of males is higher than that
of females.
3.4.6.1 CT Findings
Hilar cholangiocarcinoma has different CT imaging features
because of its different growth patterns. It is characterized by
intrahepatic bile duct dilatation, while gallbladder volume
and lumen of the extrahepatic bile duct are normal. MSCT
can indicate the obstruction site of cholangiocarcinoma and
the extent of tumor inltration of the liver parenchyma and
portal vein. On plain scan, it only shows an unclear hepatic
portal structure. The intrahepatic bile duct is clearly dilated,
or the left and right hepatic ducts are interrupted and cannot
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X. Quan et al.
converge. After enhancement, localized bile duct wall thickening and enhancement is demonstrated. Sometimes a dendritic or irregular mass above the liver parenchyma with an
unenhanced necrotic area can be seen in the center. Nodular
carcinoma manifests as left and right hepatic duct dilatation
or nodular soft tissue shadow in the common hepatic duct,
with slight or obvious strengthening after enhancement. The
middle and lower cholangiocarcinoma showed thickening of
the bile duct wall, lling defects and soft tissue shadows of
different sizes within, and the intrahepatic and extrahepatic
biliary duct above it were dilated. After enhancement, localized, eccentric, or concentric bile duct wall thickening or
growth into the lumen may result in intracavity lling defects
(Fig. 3.48). In addition, patient’s history of clonorchiasis
should be thoroughly investigated. On CT scan, Opisthorchis
a
spp. is demonstrated as high-density shadows, and thus it is
easy to identify (Kim 2003).
MRI Findings
The signal of well-differentiated adenocarcinoma on T1WI
is similar to that of liver parenchyma but is hyperintense relative to liver parenchyma on T2WI; scirrhous adenocarcinoma contains a mass of dense brous tissue with shorter T2
relaxation times, showing slightly hypointense relative to
liver parenchyma. Hilar cholangiocarcinoma: The left or
right lobe or intrahepatic bile ducts in the left or right lobe
were markedly dilated in a dendritic manner, and the extrahepatic bile ducts were not dilated. Irregular masses along
the left or right lobes could be seen in the hilar region, showing slightly hypointense on T1WI and hyperintense on
b
Fig. 3.48 CT ndings of extrahepatic cholangiocarcinoma. (a) Plain
CT scan shows different degrees of dilatation of the bile duct and
obstructed proximal bile duct; (b ~ d) Nonuniform thickening of the
bile duct wall at the obstruction end, and enhancement in each phase of
the enhanced scan
3 Imaging ofCommon Biliary Tract Diseases
71
T2WI, and the intrahepatic bile ducts and tumor portal could
be seen to be dilated due to tumor obstruction. After injection
of Gd-DTPA, the arterial and portal venous phases were
mildly or moderately enhanced, and the delayed phase moderately or signicantly enhanced. Coronal enhanced scan
was used to identify the spread of intraluminal tumor and the
difference between the surrounding blood vessels and the
bile duct. Middle and distal bile duct carcinomas: the intrahepatic bile duct and the bile duct proximal to the obstruction were obviously dilated, and the obstructive end was
obviously narrowed or suddenly truncated. The bile duct
wall can appear as irregular thickening, occasionally papillary nodules or masses, showing slightly hypointense on
T1WI and iso- or hyperintense on T2WI.After Gd-DTPA
injection, they showed mild or moderate enhancement in the
arterial and portal venous phases, and mild-to-moderate
enhancement in the delayed imaging (Fig.3.49).
Biliary obstruction is a very common disease in clinic,
and the prerequisite for its further treatment is to conrm the
location and cause of obstruction. In localization and quantitation of biliary obstruction, MRCP is of great value. It provides a good overall picture of the biliary system, which can
present the shape and degree of the dilated bile duct; MRCP
combined with MRI can signicantly improve the ability of
MRI to diagnose obstructive jaundice, so that the accuracy of
quantitation is similar to that of damaged PTC or ERCP,
which can be used to diagnose diseases such as bile duct
stones and cholangiocarcinoma. At the same time, MRCP
can display the presence or absence of stones and tumors in
the gallbladder, and the shape of pancreatic duct dilatation; it
can also provide more information for determining the cause
of obstruction.
MRCP Features
The distal cholangiocarcinoma mainly manifests as segmental torsion and interruption of the bile duct, with a conical or
tail-like broken end, short lesion range, and irregular stenosis
of the bile duct lumen; hilar cholangiocarcinoma mainly
manifests as a vacant area of the bile duct in the hilar region,
with the left and right hepatic duct interrupted before conuence, and most of the intrahepatic bile ducts are moderately
or severely dilated in “soft rattan” form, rarely cystic, and the
extrahepatic bile ducts are in their normal shape. Overall,
MRCP can well display the degree and extent of biliary dilatation and shape of biliary obstruction in various types of
cholangiocarcinoma (Oliveria etal. 2017).
PTC can clearly show the location of obstruction, the
extent of bile duct involvement, and the shape of the upper
bile duct. For the isolation of intrahepatic bile duct caused
by upper bile duct obstruction, it is often necessary to use
multiple bile duct PTCs to assess the extent of inltration
of the bile duct tree. Endoscopic Retrograde
Cholangiopancreatography (ERCP) can only show the
whole biliary tract involvement in patients with incomplete biliary obstruction caused by hilar cholangiocarcinoma. If the biliary tract is completely obstructed, it can
only show the condition of the bile duct below the
obstructed site. Therefore, ERCP has limited value in the
diagnosis and resectability judgement of hilar cholangiocarcinoma. Because both PTC and ERCP are invasive
examinations, which may lead to bleeding and/or biliary
tract infection, they are not recommended as routine examinations; however, if necessary, they can be performed for
patients with unclear MRCP ndings or unsuitable for
MRCP.
3.4.7 Intrahepatic Cholangiocarcinoma
The incidence of Intrahepatic Cholangiocarcinoma (ICC)
accounts for between 5% and 30% of primary liver cancer
(Chan etal. 2018); it occurs from the secondary branch of
the intrahepatic bile duct to the distal bile duct. It is usually
classied as the bile duct cell type of primary liver cancer,
also known as Peripheral Cholangiocarcinoma (PCC).
Radiographic Findings
ICC is more common in masses,
without capsules. It often encloses adjacent blood vessels
and bile ducts and inltrates along lymphatic vessels.
Metastatic lymph nodes are common in hepatic hilum.
3.4.7.1 CT Findings (Fig.3.50)
Plain Scan Because the irregular low-density lesion in the
liver has no capsule, the boundary is often blurred. It invades
the bile duct, resulting in a dilated bile duct shadow (intratumoral bile duct sign) and is associated with bile duct
stones. The density of the lesion is heterogenous and there
are multiple small focal liquid density necrosis areas, while
large-scale necrosis is rare. Fiber traction can cause local
depression of the liver capsule around the lesion.
Enhanced Scan ICC mainly shows a slow wash-in and
wash-out pattern. It is generally believed that the degree of
enhancement in the early stage depends on the ratio of tumor
tissue to brous tissue content. However, the progressive and
delayed pattern of enhancement is caused by the slow rate of
contrast agent entering and exiting the brous stroma because
of large amount of brous tissue contained in the tumor. The
boundary of the lesion is clearer after enhancement. The half
of the liver where the lesion is located shows increased perfusion, usually with a wedge-shaped appearance. It can last
until the portal phase. Most cases in the portal phase are isodense, and a small portion of them are slightly hyperdense to
normal liver parenchyma, which might be explained by pressure on the portal vein and increase in hepatic arterial blood
ow compensation.
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d
f
e
Fig. 3.49 MRI ndings of extrahepatic cholangiocarcinoma. (a, b)
T1W and T2W show obvious dilation of intrahepatic bile duct. (c)
MRCP shows different degrees of dilation of intrahepatic bile duct with
obvious stenosis at the obstruction end; (d–f) Enhanced scan of each
phase shows irregular thickening of the bile duct wall at the obstruction,
and enhanced scan shows enhancement.