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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
33
Fig. 3.2 Type I congenital choledochal cysts. (a) T2WI combined with
MRCP shows that the course of the intrahepatic bile duct is normal,
with no obvious dilatation. Fusiform dilatation is observed on the upper
the gallbladder. Type I is further subclassied into three
types:
pancreatic part of the common bile duct, revealing a lling defect. (b)
The lower end of the common bile duct is bifurcated, and the cystic duct
is elongated and tortuous.
• Type IVA Cysts involving both the intra- and extrahe-
patic portions of the bile ducts
• Type IVB Multiple segmental dilatations limited to the
• Type IA Characterized by cystic dilatation of the extrahe-
extrahepatic ducts
patic bile duct
• Type IB Characterized by focal-segmental dilatation of
distal bile duct
• Type IC Characterized by fusiform dilatation of the
extrahepatic bile duct
Type V
Characterized by multiple or single cystic dilatation of the
intrahepatic biliary tree, also known as Caroli Disease, now
considered as an independent disease (Caroli 1973). Caroli
Disease, rst described by the French gastroenterologist
Type II
Rare, true diverticula of the common bile duct, accounting
for 2% of reported cases. Congenital biliary diverticula
may appear in the gallbladder and duodenal papilla. True
diverticula are usually large and can appear anywhere in
Jacques Caroli is a rare disorder characterized by segmental
nonobstructive saccular dilatation of the intrahepatic bile
ducts (Longmire Jr etal. 1971). Two forms of Caroli’s disease have been described (Desmet 1992; Yonem and
Bayraktar 2007; Chae etal. 2006):
the gallbladder. They involve all layers of the capsule
wall.
• Type I (simple/isolated type): Pure segmental cystic dilatation of the intrahepatic interlobular ducts, without cir-
Type III
Rare, characterized by a cystic dilatation of the intramural
portion of the common bile duct and accounting for 1.4% to
5%.
rhosis and portal hypertension (Fig.3.3).
• Type II (Caroli’s syndrome): Both the central intrahepatic
bile ducts and the ductal plates of the smaller peripheral
bile ducts are affected; less common, without or only with
mild dilatation of the proximal end of the bile duct,
Type IV
Multiple cysts, next most common, accounting for 19%. It is
divided into two subtypes:
accompanied by liver brosis, without calculus or cholangitis, probably with hepatic cirrhosis or portal
hypertension.
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Fig. 3.3 Type V congenital choledochal cysts. (a, b) T-tube cholangio-
gram, multiple heterogeneous intrahepatic cystic dilatation, and communication with the intrahepatic bile duct; (c) Multiple non-enhanced
intrahepatic cysts were found by CT enhanced scan, and these cysts are
distributed along the main branch of the bile duct; (d, e) T2WI MRI
shows multiple intrahepatic saccular hypointense signals on the T2WI
image, which were communicated with the intrahepatic bile ducts
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3 Imaging ofCommon Biliary Tract Diseases
35
3.2.2.2 Radiographic Features
CT Features
Radiographic features of choledochal cysts type I include
low-density cystic lesions in the hepatic hilum or pancreatic head region, thin and homogeneous cystic walls, no
dilatation or intrahepatic bile duct, lack of enhancement
in enhanced scan. The CT manifestations of Caroli’s disease are multiple, heterogeneous, and non-intensied
cysts, and may be combined with calculi. The cysts are
distributed along the main branches of the hepatic duct.
Some of the cysts are connected to the bile duct, showing
a
staged or beaded shape, and fusiform expansion which
conuences to the hepatic hilum. Contrast-enhanced CT
scans can detect enhancing dots within the dilated intrahepatic bile duct, presenting a “central-dot” sign. This is
equivalent to dilated bile duct with accompanying portal
vein branches. “Central dot” sign of CT has a signicance
in the diagnosis of Caroli disease (Fig.3.4) (Yamaguchi
1980).
Radiographic features of Caroli’s disease extend from
segmental dilatation of the bile duct to diffuse dilatation of
the bile duct, from saccular dilatation to fusiform dilatation,
from simple intrahepatic biliary involvement to both intra-
b
Fig. 3.4 CT manifestations of Caroli’s disease. (a) Dilatation of intrahepatic bile duct and hepatic duct; (b, c, d) The enhanced scan of the dilated
bile duct showed a bead-like pattern, and the small branches of the portal vein were strengthened, showing a “central dot sign”
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X. Quan et al.
and extrahepatic involvement, from benign complications
(calculus) to malignant complications.
MRI Features
Similar to CT features, MRCP can display the location,
extent, and degree of intrahepatic bile duct dilatation more
comprehensively (Fig. 3.5) (Pavone et al. 1996). The bile
duct with saccular dilatation shows a hypointense signal on
the T1WI images and a hyperintense signal on T2WI images
due to high water content. No enhancement appears on the
duct wall in the enhanced scan. MRI clearly shows punctate
ow-voids within the cyst, and this is called the “central dot”
sign. It is not difcult to show intrahepatic cysts or dilatation
of intrahepatic bile duct on MRI. Caroli’s disease can be
diagnosed when MRCP clearly shows that the cystic cavity
is connected to the bile duct. When it is combined with bile
duct stones, a short T2-weighted signal can be seen in the
cavity.
3.2.3 Bile Duct Hamartomas
Bile duct hamartomas (BDHs), also termed von Meyenburg
complexes, are rare congenital malformations of the bile
duct. BDHs are multiple hepatic lesions, scattered or diffused throughout the liver parenchyma and distributed along
d
c
Fig. 3.5 MRI manifestations of Caroli’s disease. (a) The coronary
T2WI demonstrates the intrahepatic diffuse distribution of cystic hyperintense signals; (b) The axial T2WI shows intrahepatic diffuse distribution of cystic hyperintense signals; (c) Enhanced scan shows no obvious
enhancement of intrahepatic diffuse cystic shadows; (d) MRCP shows
intrahepatic diffuse distribution of small cystic structures, and the cystic
cavity is connected with the bile duct
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3 Imaging ofCommon Biliary Tract Diseases
37
the biliary tree. They are rare and have a non-specic imaging appearance such that they may also be mistaken for
metastases or microabscesses.
3.2.3.1 CT Features
On plain CT scan, the lesion shows a low-density change in
uid, with either clear or blurred margin and no obvious biliary duct dilatation (Fig. 3.6). While contrast-enhanced CT
scan displays no obvious enhancement, with a clear boundary and no capsules.
3.2.3.2 MRI Features
MRI plain scan showed long T1 and long T2 changes
(Fig. 3.7). T1W1 showed that the signal of the lesion was
slightly lower than that of the liver parenchyma. T2W1 was
characterized by abundant bile in the cystic cavity, showing
an obvious hyperintense signal. Unlike simple hepatic cysts,
the shape of bile duct hamartomas can be varied, either as
triangle or as short rod-shaped. When the lesions are diffused, they occur sporadically. No obvious enhancement was
found on contrast enhancement scans. Some lesions demonstrated circular or nodular enhancement. MRCP showed
intrahepatic multiple cystic hyperintense signals, without
communication with intrahepatic bile ducts.
3.3 Common Gallbladder Diseases
3.3.1 Acute Cholecystitis
Acute cholecystitis is bacterial or chemical inammation of
the gallbladder. About 95% of patients with cholecystitis
c
d
Fig. 3.6 CT manifestations of bile duct hamartomas. (a) Plain CT scan revealed a clearly dened cystic lesion, (b, c, d) No enhancement at each
stage of the enhanced scan
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Fig. 3.7 MRI manifestations of Bile duct hamartomas. (a) Diffusion multiple long T1 signals on T1W images; (b) No enhancement was found
on enhanced scan; (c) MRCP showed multiple cystic hyperintense signals, without communication with bile ducts
have gallstones (calculus cholecystitis), and about 5% of
patients lack gallstones (acalculous cholecystitis). Most
acute calculous cholecystitis results from: obstruction of the
cystic duct by gallstones, or the junction between the gallbladder and cystic duct by gallstones, or local mucosal erosion, or severe edema caused by stones (Watanabe et al.
2007). Obstruction leads to dilatation of the gallbladder,
accompanied by mucosal edema, venous and lymphatic
obstruction, cell inltration and local ischemia. Perforation
at the ischemic gangrenous area may develop choleperitoneum, or it is sealed off by omentum, resulting in a pericholecystic abscess. Chronic cholecystitis (such as brosis of
the gallbladder wall, inltration of chronic inammatory
cells, formation of Rokitansky-Aschoff sinuses) also occurs
in about 67% of patients with acute cholecystitis (Hwang
etal. 2014).
3 Imaging ofCommon Biliary Tract Diseases
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3.3.1.1 Radiographic Features
CT Features
• Increased density of bile in the gallbladder (20HU).
Normal bile density ≤10 HU.
• Full gallbladder contour. Because the average gallbladder
length varies signicantly on the axial image, it is more
reasonable to measure the width of the gallbladder. The
gallbladder with a width greater than 3.5cm is considered
to be dilated.
• Gallbladder wall thickening. About 50%–70% of acute
cholecystitis is characterized by diffuse gallbladder wall
thickening, but there are also a few cases of focal thickening. The standard for the thickness of gallbladder wall is
3mm.
• The liver parenchyma surrounding the gallbladder appears
as a low-density ring or nodular low-density foci, which is
caused by inammatory edema surrounding the gallbladder. Suppurative cholecystitis and gangrenous cholecystitis can spread to the surrounding liver parenchyma,
forming an intrahepatic abscess.
• The gallbladder wall shows obvious homogeneous
enhancement after contrast agent injection. In about 90%
of cases, a transient zone of enhancement in the arterial
phase appears in the liver parenchyma surrounding the
gallbladder fossa.
• Acute calculous cholecystitis often shows rounded and
sediment-like stones in the gallbladder neck and cystic
duct (Figs.3.8 and 3.9).
MRI Features
MRI features are similar to those of CT (Fig.3.10). Gd-DTPA
enhanced lipid suppression T1W1 is used to demonstrate
inammatory thickening of the gallbladder wall. Turbidity
and exudation of adipose tissue in the gallbladder fossa are
very sensitive. The gallbladder usually shows relatively uniform wall thickening and the signal intensity in the gallbladder wall is increased on T2W1. The inner portion of the
gallbladder wall is smooth, and the serosal surface is incomplete or unclear due to inammatory reaction and adhesion.
Enhanced scan shows gradual enhancement at cystic walls,
with signicant enhancement of the inner mucosa and serous
layers due to hyperemia, but not an obvious enhancement of
the middle edematous layer. Sometimes transient inammatory hyperemia (transient enhancement) occurs in the hepatobiliary junction in the arterial phase, which is helpful to
prompt diagnosis.
In summary, the coexistence of gallbladder distension and
gallbladder wall thickening, or gallbladder wall thickening
combined with rough intimal surface or vague serous surface
is suggestive evidence of acute cholecystitis. It is worth
pointing out that:
• CT and MRI features of a small number of acute chole-
cystitis may not be obvious, or appear close to normal,
suggesting that acute cholecystitis should be interpreted
combined with comprehensive clinical analysis.
• Acute acalculous cholecystitis accounts for only 2–12%
of acute cholecystitis (Hashimoto etal. 2016), but most
cases show atypical imaging features, mostly combined
with severe underlying diseases, so the symptoms are
concealed and there are many complications.
• The degree of gallbladder wall thickening does not cor-
relate with the severity of acute cholecystitis.
• In addition to gallbladder diseases, other risk factors caus-
ing gallbladder enlargement should also be excluded.
Acute pancreatitis, post-traumatic disease, the use of
drugs to inhibit gallbladder contraction, long-term fast-
ing, pregnancy, and acute hepatitis can also cause gall-
bladder distension.
• Though 98% of cases with gallbladder wall thickening
are pathological, some diseases such as heart failure,
renal failure, multiple myeloma, severe hypoproteinemia,
and total parenteral nutrition can also result in relative
thickened gallbladder wall.
Fig. 3.8 Acute cholecystitis with inammatory edema. Round-like
high-density calculi are visible in the gallbladder and change in inammatory exudate can be observed around the gallbladder
3.3.1.2 Special Types ofAcute Cholecystitis
andTheir Complications
Special types of cholecystitis include gangrenous cholecystitis, emphysematous cholecystitis, pediatric cholecystitis, and
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Fig. 3.9 Calculus impacted in the gallbladder neck with acute suppurative cholecystitis. (a) The gallbladder is slightly dilated, and the bile
density does not change signicantly; (b) A high-density calculus
shadow is seen in the gallbladder neck; (c) Contrast-enhanced scanning
shows that the gallbladder wall is thickened and strengthened
Fig. 3.10 Acute cholecystitis with cholecystolithiasis. (a) Calculi with round-like short T2 signal calculi were seen in the gallbladder on T2WI;
(b) Obvious thickened and edematous gallbladder wall
3 Imaging ofCommon Biliary Tract Diseases
41
pregnancy cholecystitis. In approximately 4% of acute cholecystitis, complications occur, including gallbladder empyema, perforation, and gallbladder hemorrhage.
Gangrenous Cholecystitis
Gangrenous cholecystitis (GC) is characterized by intramural hemorrhage, necrosis and abscess formation, necrotic
gallbladder mucosa or mucosal ulceration; and massive
purulent necrotic debris and cellulose exudation in the gallbladder cavity (Ganapathi etal. 2015). Any of the following
signs can suggest the presence of GC:
• Dense and uneven bile, exfoliated mucosal fragments in
the gallbladder.
• Irregular or absent gallbladder wall, asymmetrical wall
thickness, low-density necrotic foci, or long T1 and long
T2 irregular necrosis areas.
• Intramural hemorrhage in gallbladder wall or lumen,
irregular and discontinuous enhancement of the gallbladder wall.
• Absence of mural enhancement.
• Localized effusion in different forms around the
gallbladder.
Emphysematous Cholecystitis
Emphysematous cholecystitis, a variant of acute cholecystitis develops in 1% of acute cholecystitis (Fig.3.11) but pres-
ents signicantly higher morbidity and mortality (Kowalski
etal. 2020). Emphysematous cholecystitis involves an acute
infection of the gallbladder wall or lumen infected by gasproducing organisms. It is more common in patients who
have diabetes, with men accounting for 75% of cases, and
occurs at an average of 60years. It has a sudden onset and
rapid progress to systemic poisoning. Gas-forming organisms include Clostridium perfringens, Escherichia coli, and
Klebsiella. The gas can be distributed intraluminally or intra-
Fig. 3.11 Gas on the gallbladder wall in a patient with emphysematous
cholecystitis
murally and occasionally diffused into the intra- and extrahepatic bile ducts. In severe cases, transmural perforation and
pericholecystic abscess are very common. CT can easily display gas bubbles or linear gas in the gallbladder wall or
lumen, which is conducive to diagnosis. MRI can also identify low signal gas shadows, and it is generally considered
that gas appears 12–24h after symptom onset.
Pediatric Cholecystitis
Pediatric cholecystitis is common in children with obesity,
hemolytic disease, and chronic liver disease. Imaging features of pediatric cholecystitis are similar to those seen in
adults. However, pediatric cholecystitis rarely progresses to
suppurative cholecystitis or gangrenous cholecystitis.
Pregnancy Cholecystitis
Pregnancy cholecystitis usually occurs during the last trimester of pregnancy. The pathogenesis may be associated
with compression of the biliary duct at porta hepatis in the
last trimester of pregnancy, which causes gallbladder excretion disorders. The imaging features are similar to those of
acute cholecystitis.
Gallbladder Empyema
Gallbladder empyema involves a progression of acute cholecystitis with bile stasis and cystic duct obstruction. The bile
has superinfection with bacteria that result in suppuration in
the inamed gallbladder, which lls with pus, debris, and
exudative material. Without thorough and prompt treatment,
acute cholecystitis may progress to gallbladder empyema. It
is common in diabetic patients and substantially equivalent
to an abdominal abscess. CT shows increased bile density
(30 HU); thick pus presents as a moving deposit in the gallbladder lumen.
Gallbladder Perforation
Gallbladder perforation is the most severe complication of
acute cholecystitis with a mortality rate reaching as high as
15%–20%. It occurs in about 10% of acute cholecystitis.
Most gallbladder perforation is caused by direct corrosion of
the gallbladder wall or high pressure within the gallbladder,
resulting in obstruction of the gallbladder venous reux, or
accumulation of a bacterial toxin. Due to relatively inadequate blood supply at the bottom of the gallbladder, perforation occurs at this site frequently. Perforation should be
suspected clinically in those patients who suddenly become
toxic and whose clinical condition deteriorated rapidly.
When perforated, bile leakage ensues. If leakage becomes
encapsulated and walled off, it may lead to pericholecystic
effusion or biloma in other parts of the peritoneal cavity.
Otherwise, diffuse biliary peritonitis may occur. The majority of cases will rapidly evolve into liver abscesses due to
infectious bile encapsulated inside the biloma.
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Fig. 3.12 Gallbladder perforation. (a) Thickened gallbladder wall, focal wall defect, and low attenuation surrounding the gallbladder; (b)
Contrast-enhanced CT reveals enhancement of gallbladder wall, and no enhancement at the site of the defect; (c) Exudation surrounding the defect
CT and MRI Features The imaging ndings of gallbladder perforation (Fig.3.12) and gangrenous cholecystitis are
similar. Their similarities mainly present in the following
aspects:
If bile enters the abdominal cavity, biliary peritonitis occurs,
which is characterized by a large concentration of uid in the
abdominal cavity. If bile enters hepatic parenchyma, a secondary
hepatic cyst occurs due to bile erosion, which is characterized by
lobular low-density shadowing of the hepatic parenchyma with
• Reduced uid in the gallbladder and reduced gallbladder
wall tension.
• Blurring, thickening, and discontinuity of gallbladder
circular enhancement. If the gallbladder perforation is conned
to the gallbladder bed and adheres to the surrounding tissues, it
can form an abscess around the gallbladder.
wall.
• The gallbladder is encapsulated by omentum and surrounding tissues leading to the buildup of pericholecystic
effusion or to form a vague inammatory mass.
Hemorrhagic Cholecystitis
Hemorrhage within the gallbladder lumen can form blood
clots, forming loose solid-like shadows in the gallbladder.