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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
53
trophy of the mucosal epithelium in the gallbladder wall of
unknown etiology; GA is also known as intramural diverticula, intramural polyps, adenomas, adenomyoma, cystadenoma, proliferative nodular cholecystitis, and cystic
cholecystitis. GA occurs predominantly in middle-aged
females. This condition is typically asymptomatic; however,
when symptomatic, it manifests in a similar manner to cholecystitis or cholelithiasis.
Rokitansky-Aschoff sinuses (RAS) are the characteristic
imaging features of this condition (Hwang etal. 1998; Yang
etal. 2018).
3.3.7.1 CT Features
Adenomyomatosis is described as two morphological
types: diffuse and localized. The main sonographic nding
in the diffuse type is diffuse gallbladder wall thickening,
which measures 0.5 to 2.5cm in thickness. The inner and
outermost surface of the gallbladder lumen (serosal surface) is smooth, with a clear boundary, and hypodense in
the center of the gallbladder. Localized adenomyomatosis
is characterized by focal thickening, typically involving the
fundal region. The boundary between the lesion and the
normal gallbladder wall is clear, and the appearance after
enhancement is similar to that of the diffuse type (Figs.3.30
and 3.31).
3.3.7.2 MRI Features
Similar to CT, MRI can show localized or diffuse thickening
of the gallbladder wall. On the T2W1 sequence, a roundshaped hyperintense shadow of 2–7mm can be seen within
the mass of the gallbladder wall, or on the thickened gallbladder wall, which is the typical appearance of RAS, and is
the key sign for the diagnosis of this disease (Bang et al.
2014). The dynamic contrast-enhanced scan shows non-
enhanced low or no signal foci in a thickened gallbladder
wall (Fig.3.32).
3.3.8 Gallbladder Polyps andGallbladder
Adenoma
3.3.8.1 CT Features
Fig. 3.28 Thickening of the gallbladder wall, with hypointense
separation
Thin-sliced scanning and adjusting of the window width
and position, can sometimes reveal a slightly hyperdense
Fig. 3.29 A “hamburger” sign. (a) The gallbladder wall is smooth and contrast-enhanced scanning shows continuous enhancement with partial or
local interruption; (b) The enhancement of serosal and mucosal surfaces is more obvious, but that of the muscle layer is relatively weak
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X. Quan et al.
c
Fig. 3.30 Gallbladder adenomyomatosis. (a) The fundus of the gall-
bladder is thickened and bulges outward with a mucous membrane protruding inward. (b) The fundus of the gallbladder is thickened and
nodular bulge projecting into the lumen of the gallbladder.
bulges outward with a mucous membrane protruding inward. (c)
Epithelial hyperplasia or atrophy of the gallbladder; the form of
Rokitansky-Aschoff sinuses
3.3.9 Gallbladder Torsion
There is no inltration or thickening of the gallbladder
wall, unlike seen in nodular gallbladder carcinoma. The
enhancement was not obvious in the arterial phase, but
there was enhancement in the portal venous and delayed
phases (Fig. 3.33). The location of the lling defect in
relation to the gallbladder remains the same after a change
in patient position, and this can help in differentiating
gallbladder polyps from gallstones. At CT imaging, gall-
When gallbladder undergoes rotation more than 180°, hemorrhagic infarction of the gallbladder occurs. Clinical symptoms include persistent right upper quadrant pain, which
usually lasts longer than 8 hours without remission after
spasmolytic therapy (David et al. 2019). Two anatomical
variants of the gallbladder have the potential to undergo
torsion.
bladder polyps, and gallbladder adenomas appear basically the same. Gallbladder polyps can be multiple, and
range in size from 5mm to 6mm. Gallbladder adenomas
have a cauliower-like or mulberry-like contour, generally more than 7mm in size. The differentiation between
gallbladder adenomas (Fig. 3.34) and early-stage gall-
3.3.9.1 Type I
Free-oating gallbladder is characterized by gallbladder
rotation on its mesentery along the axis of the cystic duct and
cystic artery. The incidence of this condition is higher in
children.
bladder cancer is difcult. It is generally considered that
gallbladder adenomas greater than 10mm and associated
with localized gallbladder wall thickening have malignant
potential.
3.3.9.2 Type II
Though the gallbladder is located in the normal position
attached by the cystic mesentery, there is a long mesentery
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3 Imaging ofCommon Biliary Tract Diseases
55
Fig. 3.31 CT features of gallbladder adenomyomatosis. (a) Thickening
in the gallbladder wall, with a slightly hyperdense soft tissue mass in
the gallbladder lumen; (b) A ring-form thickening of the gallbladder
that is prone to torsion, especially in patients associated with
gallstones.
wall in arterial phase; (c, d) Delayed enhancement in portal venous
phase and delayed phase, which presents with an increased enhancement range and degree compared to the arterial phase
3.3.10 Milk ofCalcium Bile andGallbladder
Sludge
In the case of gallbladder torsion, the wall of the gallbladder becomes hemorrhagic, edematous and thickened, and the
gallbladder appears distended.
In gallbladder distension, the gallbladder enlarges, sags,
and leaves the gallbladder fossa. The short axis of the gallbladder is almost horizontal, and the tissue is twisted in the
neck of the gallbladder. The hematogenous contents of the
gallbladder show as slightly high-density shadows within the
gallbladder, and the MRCP and MRI axial images reveal a
beak-like blockage of the cystic duct (Chai et al. 2020).
Torsion can be classied as incomplete (<180°) or complete
(>180°) (Reilly etal. 2012).
3.3.10.1 Milk ofCalcium Bile
Milk of calcium bile, also called limy bile, is characterized
by the accumulation of calcium carbonate in the gallbladder. It is manifested by an increase in the density of the
bile, mainly involving an obstructed cystic duct and associated infection. Once the bile excretion is impaired, milk
of calcium bile forms as a consequence of increased bile
concentration and precipitation of calcium salts and cholesterol crystals. CT shows hyperdense contents (CT attenuation 60–80 HU) in the gallbladder lumen. The entire
gallbladder becomes lled with calcium bile rather than
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X. Quan et al.
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c
d
e
Fig. 3.32 MRI features of gallbladder adenomyomatosis. (a) Diffuse
thickening of the gallbladder wall on T2WI and multiple RAS formation on the inner wall. (b) Diffuse thickening of the gallbladder wall,
and the inner wall is ring-shaped; (c) By MRCP the gallbladder wall is
clearly displayed, the inner wall is uneven, and multiple small hyper-
intense saccules communicating with the lumen; (d) The gallbladder
wall was slightly enhanced in the arterial phase of enhanced scanning.
(e) During the equilibrium phase of enhanced scanning, the enhancement of gallbladder wall was delayed, and the gallbladder lumen
appeared contracted
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3 Imaging ofCommon Biliary Tract Diseases
57
a
Fig. 3.33 Gallbladder polyps. (a) CT scan shows heterogeneous den-
sity in the gallbladder lumen, and no clear high-density or low-density
lling defect is found. (b) Contrast-enhanced scan of the fundus of the
b
gallbladder shows a circular enhanced shadow, with pedicle structure
connected to the gallbladder wall
Fig. 3.34 Gallbladder adenoma. (a) Contrast-enhanced scan shows
signicant enhancement of nodular bulge projecting into the lumen of
the gallbladder at the body of the gallbladder (near the fundus) in the
diffuse calcication of the gallbladder wall. Calcium bile
tends to have a higher and homogenous density (Fig.3.35)
than gallbladder bleeding (15–20 HU higher than gallbladder bleeding).
arterial phase. (b) Delayed scan shows enhancement of the lesion, and
there is no thickening of the capsule wall adjacent to the nodules
non-acoustic shadowing gallstones can sometimes be confused. In comparison, gallbladder sludge has a slower rolling
speed, which requires several seconds to several minutes,
and its shape can be changed after rolling, while the condition of gallstones does not. Gallbladder sludge can eventu-
3.3.10.2 Gallbladder Sludge
Gallbladder sludge forms with the further agglomeration of
the calcium bile. Such sediment comprises calcium bilirubinate pigment and cholesterol crystals. Gallbladder sludge is
gravity-dependent and moves freely within the gallbladder
orientation. By ultrasound, it does not cast an acoustic
shadow and presents no internal structure or blood ow signals. However, the spherical rolling gallbladder sludge and
ally evolve into gallstones, or spontaneously disappear.
Therefore, timely detection and treatment are crucial.
Ultrasonography is the preferred imaging modality in discovering gallbladder sludge, while CT or cholecystography
is not sensitive to the detection of such sediment. Loose sediment within the gallbladder is easily detected on T2WI MRI,
but differentiation from sediment-like gallstones is hardly
possible (Shaffer 2001).
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Fig. 3.35 Milk of calcium bile, Plain CT scan showing a signicant
increase in the density of the entire gallbladder
3.3.11 Mirizzi’s Syndrome
In 1948, Mirizzi described a functional hepatic syndrome,
also known as common hepatic duct obstruction syndrome.
It is a rare complication of cholelithiasis and has been
explained as a condition in which gallstones become
impacted in the neck of the gallbladder or the cystic duct,
leading to compression of the common bile duct. The
impacted gallstones associated with the inammatory
responses cause obstruction of the bile duct. Mirizzi’s syndrome has four features:
• The cystic duct courses parallel to the common bile duct
or the common hepatic duct.
• Gallstones become impacted in the neck of the gallblad-
der or the infundibulum.
• The gallbladder appears signicantly distended.
• Obstruction of the common hepatic duct is associated
with extrahepatic and intrahepatic biliary dilatation.
X. Quan et al.
tered, the dilated common bile duct can easily be mistaken
for the cystic duct and inadvertently ligated and transected
during surgical maneuvers, which is a thorny problem in
biliary surgery.) Also, Mirizzi’s syndrome represents a highrisk factor for gallbladder cancer and should be taken
seriously.
3.3.11.1 CT Features
Bile duct dilation above the cystic duct. If the value of CT for
gallstones is positive, it can be seen that the cystic duct or the
gallbladder neck protrudes into the common bile duct or the
common hepatic duct, and the gallbladder wall is thickened,
associated with pericholecystic abscess. CT is highly specic, if gallstones in the cystic duct are found to be in the
common bile duct while the gallbladder is atrophied. The
negative value of gallstones only shows the precence of biliary obstruction and acute cholecystitis above the porta hepatis, and a distended gallbladder. If the effect of tumor
compression and hilar lymph nodes can be excluded, the
possibility of this disease is highly suspected.
3.3.11.2 MRI Features
Multiple gallstones appear as signal void-lling defects in
the gallbladder neck or cystic duct. On T2WI MRCP. The
common bile duct at the level of the gallbladder has an arcshaped lateral indentation and narrows. The indentation of
the gallstone is smooth edged, which is different from the
vast, narrow range, and irregular edge of gallbladder cancer.
The common hepatic duct above the stenosed plane is
dilated, and the diameter of the distal common bile duct is
normal (Byoung etal. 2000) (Fig.3.36).
The underlying mechanism of this disease is the presence
of recurrent episodes of chronic biliary inammation secondary to a pressure ulcer that is caused by impacted multiple and large gallstones in the infundibulum or in the neck of
the gallbladder. Impacted gallstones compress the gallbladder wall for a long time to form necrosis, eventually resulting
in the formation of a cholecystocholedochal stula.
The clinical signicance of Mirizzi syndrome is that the
cystic duct is pathologically atrophic and adhered to the
common bile duct. There is a high incidence of bile duct
injuries associated with standard laparoscopic cholecystectomy. (When Calot’s triangle and hepatoduodenal ligament
are severely adhered and anatomical variations are encoun-
Fig. 3.36 MRI features of Mirizzi’s syndrome, MRCP indicating a
large and short T2 signal in the neck of the gallbladder with calculous
shadow and stone compression of the hepatic duct
3 Imaging ofCommon Biliary Tract Diseases
59
3.3.12 Post-Cholecystectomy Syndrome
Post-Cholecystectomy Syndrome(PCS) comprises a heterogeneous group of gastrointestinal disorders, consisting of
right upper quadrant abdominal pain, obstructive jaundice,
abdominal distension, nausea, and vomiting. These symptoms recur or persist due to anatomical and physiological
disorders of the extrahepatic bile duct after cholecystectomy.
Approximately 10%–15% of patients who have previously
received cholecystectomy still present with different degrees
of gastrointestinal symptoms (Isherwood etal. 2019). If cholecystitis and gallstone symptoms persist after gallbladder
removal, or even become worse, the possibility of PCS
should be suspected. Related organic diseases can be found
in 90% of cases, such as long cystic duct remnants, a residual
biliary tract stone, and biliary stricture (Girometti etal. 2010)
(Figs.3.37, 3.38, and 3.39).
3.4 Diseases oftheBiliary Tract
3.4.1 Bile Duct Stones
Bile duct stones can be divided into intrahepatic and extrahepatic bile duct stones according to the anatomical location.
Intrahepatic bile duct stones (hepatolithiasis) are associated
with bile duct infection, cholestasis, and parasites, and most
of them are mixed with pigment bile with varying morphology; these stones are specically located proximal to the
conuence of the left and/or right hepatic ducts. Stones cause
repeating cycles of biliary obstruction and infection, which
eventually leads to strictures, dilatation of bile ducts, and
liver brosis.
3.4.1.1 Radiographic Features ofHepatolithiasis
CT Findings
The left and right hepatic ducts and their branches appear
as round and branched shadows, which are consistent with
the shape of hepatic ducts. The peripheral bile ducts are
dilated, the edges of the stones are smooth, and the density
is generally slightly higher than that of the liver parenchyma. Sediment-like stones can be low-density, so the differentiation from bile in the dilated bile duct is not easy
(Fang etal. 2015) (Fig.3.40). According to the location of
bile duct stones, they can be divided into the following
types:
• Diffuse type: Stones are accumulated upwardly from the
extrahepatic bile duct, and the scope can almost ll the
entire intrahepatic bile duct system.
• Scattered type: Stones are scattered in branches of the
intrahepatic bile duct, and it is more common in the conuence of the left and right hepatic ducts.
• Regional type: it usually occurs in the presence of obstruction or hepatic bile duct stricture. The branches of the
hepatic bile duct are lled with stones, and the bile ducts
and their branches are dilated.
Fig. 3.37 Long cystic duct stump after cholecystectomy, and the lower
end merges into the left lateral wall of the hepatic duct, accompanied by
multiple stones in the remaining end of the cystic duct
Enhanced scanning shows that the display of stones is
affected by the increased density of hepatic parenchyma, but
the dilated bile duct is more clearly displayed.
Hepatolithiasis can be associated with atrophy of the
adjacent hepatic lobe and compensatory hypertrophy of normal liver tissues, which leads to abnormal morphology of the
whole liver tissue.
MRI Findings
Intrahepatic stones appear as a slightly hyper-, iso-, or hypointensity signal on T1WI, and a hypo- or no intensity signal
on T2WI or MRCP, with tubular, circular, or irregular structures, and the bile duct above the level of obstruction is
dilated (Fig.3.41).
3.4.1.2 Radiographic Features ofExtrahepatic
Bile Duct Stones
• Extrahepatic bile duct stones are mostly located in the
middle and lower segments of the common bile duct:
Most of them come from gallstones or intrahepatic bile
duct stones, mainly manifested as recurrent biliary
obstruction and suppurative cholangitis, characterized by
multiple or single stone(s), with shape, size, and character
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Fig. 3.38 Post-cholecystectomy. (a, b) Cystic duct excess, and small gallbladder associated with stones
X. Quan et al.
Fig. 3.39 Long cystic duct remnant after cholecystectomy
similar to the coexisting gallstones and intrahepatic bile
duct stones.
• Primary bile duct stones: Pigmented stones are composed
mainly of high levels of bilirubin and calcium salts in different shapes with soft, fragile, and ne sand-like
characteristics.
Most patients with choledocholithiasis have a history of
acute and chronic biliary infection. Up to 90% of these
patients will have positive biliary cultures (Kimura et al.
2007), and Escherichia coli is the predominate cause. Due to
recurrent infection of the biliary tract, clinical disorders
including chronic inammation of the distal common bile
duct and the papilla of Vater, the proliferation of brous tissue, narrowing of the lumen, and Sphincter of Oddi dysfunction may cause cholestasis, providing a conducive milieu for
stone formation. Obstruction predisposes to calculus, and
calculus is conducive to the formation of an obstruction. This
procedure leads to growth or clusters of calculus. Due to the
mobility of stones, the obstruction that formed is mostly
incomplete unless the stone is impacted. The most typical
symptoms of extrahepatic bile duct stones are Charcot’s
triad, which consists of right-upper-quadrant pain, fever, and
jaundice.
3.4.1.3 Imaging Findings ofCholedocholithiasis
CT Findings
For obstruction caused by choledocholithiasis, the diameter
of the dilated common bile duct ranges from 8 to 10mm. The
intrahepatic duct is mildly dilated. The dilated intrahepatic
ducts on the axial imaging appear as a continuous circular
low-density ring with clear boundaries, decreasing from top
to bottom. The lower end of the common bile duct is the best
site for the occurrence of calculi. The CT density of calculi
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3 Imaging ofCommon Biliary Tract Diseases
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61
Fig. 3.40 Bile duct stones. (a) Bile duct dilatation and multiple stones in the hilar; (b) Multiple stones and gas accumulation in the intrahepatic
bile duct; (c) Calculi in the lower segment of the common bile duct
a
Fig. 3.41 Intrahepatic bile duct stones in T1WI and T2WI. (a) T1WI shows obvious dilatation of the bile ducts in the left liver, presenting a tortu-
ously tubular form. (b) Short T2 and short T1 nodular stone shadows can be seen in T2WI dilated bile ducts
b
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X. Quan et al.
c
Fig. 3.42 Coronal position of T2WI, T2WI, MRCP, and T1WI of
extrahepatic bile duct stones. (a, b) Multiple short T2 signal stone shadows are observed in the bile ducts in the hilar of coronal and transected
d
themselves depends on stone calcium level, and stones may
present as high density, a soft-tissue density, a mixed density,
or an iso−/hypodense calculi. Stones can ll the entire
lumen. The CT ndings include the target sign with the calculus seen as a central density surrounded by hypodense
bile, and the crescent sign.
MRI Findings
Though the composition of the common bile duct stones varies, most of them show a hypointense signal on heavy T2WI
or MRCP, representing a central hypointense intraductal
round, oval, or irregular lling defects surrounded by a
high- signal- intensity bile (target sign). When the stone is
impacted, a cup-shaped lling defect that opened with
upward arcs in the common bile duct obstruction can be
observed (Fig.3.42).
3.4.2 Suppurative Cholangitis/Acute Cholangitis
This clinical entity is characterized by intrahepatic and extrahepatic bile duct dilatation, cholestasis, and purulent bile in
T2WI; (c) MRCP shows multiple nodular lling defects in the hilar bile
duct and common bile duct. (d) Short T1 nodular stone shadows can be
seen in the dilated extrahepatic bile ducts
the bile ducts; often accompanied by incomplete biliary
obstruction caused by common bile duct stones, parasitic
infections, and internal stents. Main manifestations of this
condition include fever, chills, and right upper quadrant pain,
usually associated with jaundice and leukocytosis. Without
timely removal of its etiology or decrease in serum bilirubin
level; liver abscess, subphrenic abscess, and septic shock
may occur.
3.4.2.1 CT andMRI Findings
• Intrahepatic and extrahepatic bile duct dilatation (the
diameter of the common bile duct is greater than 20mm)
and bile duct wall thickening, often accompanied by gallbladder enlargement.
• Shadows of the stones can be observed in the extended
bile duct.
• CT shows increased density in bile and MRI shows
stricture of the lumen, thickening of the bile duct wall,
and enhancement of large-scale wall in early enhanced
scan.
• When pyogenic inammation of the bile duct affects the
liver, abscesses or parenchymal liver inammation may
occur (Fig.3.43).