usg evalution of biliary tree and bile duct anatonical variation and pathology

1. Guide:Dr Naima ma’am
Presentation by Dr Mukesh Bijarniya

2. Branching order : Applies to the level of division of the
bile ducts starting from the common hepatic duct
 First-order branches are the right and let hepatic
ducts
 Second-order branches are their respective
divisions
 Normal Bile Ducts: Right and left hepatic ducts are
normally seen lying anterior to the portal veins.
 Common hepatic/common bile ducts of normal
caliber in sagittal view lying in the typical position
anterior to the portal vein and hepatic artery

3. ( C )Mid and distal common bile duct in longitudinal view. Note the pancreas (*), the
cranial margin of which demarcates the transition between the suprapancreatic and
intrapancreatic segments. ( D) Distal common bile duct and the ampulla of Vater
(short arrow) are shown running posterior to the pancreatic head and inserting into
the duodenum

4. Biliary branching pattern
Common Variants of Bile
Duct Branching. Right
posterior duct (RPD) is in
red. (A) RPD joins the right
anterior duct in 56% to 58%
of the population. (B)
Trifurcation pattern, 8%. (C)
RPD joins the left hepatic
duct, 13%. (D) RPD joins the
common hepatic or
common bile duct directly,
5%

5.  Normal caliber of the CHD/CBD in patients
without history of biliary disease is up to 6 mm.
 A ductal diameter of 7 mm or greater should
prompt further investigation
common bile duct is commonly divided into three
segments: (A) suprapancreatic
(B) retropancreatic
(C) interstitial/ampullary
components.
 It extends caudally within the hepatoduodenal
ligament, lying anterior to the portal vein and to
the right of the hepatic artery.

6.  Choledochal cysts represent a heterogeneous
group of congenital diseases that may
manifest as focal or difuse cystic dilation of
the biliary tree.
 Female-to-male ratio is 3:1 to 4:1.
 Although most patients present early in life,
about 20% of choledochal cysts are
encountered in adulthood

7.  Type I cyst :a fusiform dilation of the CBD, are
the most common (80%)
 Type II cysts :are true diverticula of the bile
ducts and are very rare.
 Type III cysts :the “choledochoceles,” are
confined to the intraduodenal portion of the CBD
 Type IVa cysts :are multiple intrahepatic and
extrahepatic biliary dilations
 Type IVb cysts :are confined to the extrahepatic
biliary tree.
 Type V cysts :is not a true choledochal cyst and
is known as Caroli disease, intrahepatic dilation
of biliary duct

8. Todani Classification for
Choledochal Cysts.

9. Type I. Fusiform dilation of the
common bile duct (CBD) is seen, but
no obstructive lesion is noted. This
is the most common type of
choledochal cyst.
Type II. A large diverticulum
(arrow) is shown in arising from
the common hepatic duct at the
portal hepatis and containing
mobile debris

10. Type III. Fusiform dilation of
the distal CBD (arrow) is
demonstrated protruding into
the duodenum
Type IV. Transverse view of the
left lobe of the liver depicts
marked enlargement of the left
hepatic duct with dilated
branches.

11.  A rare congenital disease of the intrahepatic
biliary tree that results from malformation of the
ductal plates.
 Caroli disease has been associated with cystic
renal disease, most often renal tubular ectasia
(medullary sponge kidneys).
 More than 80% of patients present before the age
of 30 years.
 Caroli disease leads to saccular dilation or, less
often, fusiform dilation of the intrahepatic biliary
tree, resulting in biliary stasis, stone formation,
and bouts of cholangitis and sepsis

12.  Most often affects the biliary tree diffusely,
but it may be focal.
The dilated ducts contain stones and sludge.
 If associated with congenital hepatic fibrosis,
findings of altered hepatic architecture and
portal hypertension are also present.
 Cholangiocarcinoma develops in 7% of patients
with Caroli disease.
of 2249

13. Oblique image through the
right lobe of the liver
demonstrates dilated ducts
with sacculations typical of
Caroli disease. the incomplete
bridging echogenic septa (short
arrows).
Transverse imaging through
the left lobe shows a
nonshadowing stone (arrow) in
the dilated duct

14. Choledocholithiasisa
Hemobiliaa
Congenital biliary diseases:
Caroli disease
Choledochal cysts
Cholangitis
Infectious
Acute pyogenic cholangitis
Biliary parasitesa
Recurrent pyogenic cholangitis
HIV cholangiopathy
Sclerosing cholangitis
Causes of Biliary Obstruction : BENIGN MISCELLANEOUS

15. Cholangiocarcinoma
Gallbladder carcinoma
Locally invasive tumors
(esp. pancreatic
adenocarcinoma)
Ampullary tumors
Metastasis
Mirizzi syndromea
Pancreatitis
Adenopathy
NEOPLASMS
EXTRINSIC COMPRESSION

16. Pancreatic adenocarcinoma.
Short transition zone with
shouldering, large duct caliber,
along with an obstructive mass
are typical Findings in
malignant obstruction
Pancreatitis. Elongated tapering
of the duct suggests a benign
cause. Note mild sympathetic
gallbladder wall thickening
caused by adjacent
inflammation.

17.  A clinical syndrome of
jaundice with pain and fever
resulting from obstruction of
the CHD caused by a stone
impacted in the cystic duct.
 The impacted stone may
erode into the CHD, resulting
in a cholecystocholedochal
Fistula and biliary obstruction
 On sonography biliary
obstruction with dilation of
the biliary ducts to the CHD
level is seen with acute or
chronic cholecystitis

18. Sagittal sonogram shows a dilated
common bile duct obstructed by a
large stone impacted in the distal
cystic duct. This appearance may be
mistaken for a common bile duct
stone. There is thickening of the wall
of the cystic duct (arrow).

19.  Primary choledocholithiasis : Denotes
de novo formation of stones, often made of calcium
bilirubinate (pigment stones) within the ducts.
 The etiologic factors are often related to diseases
causing strictures or dilation of the bile ducts,
leading to stasis, as follows:
• Sclerosing cholangitis
• Caroli disease
• Parasitic infections of the liver (e.g., Clonorchis,
Fasciola, Ascaris) 20
• Chronic hemolytic diseases, such as sickle cell
disease
• Prior biliary surgery, such as biliary-enteric
anastomoses

20.  Secondary choledocholithiasis :
Migration of stones from the gallbladder into
the CBD constitutes
 Secondary choledocholithiasis is quite
common

21.  Most stones are highly echogenic with
posterior acoustic shadowing, although
small (<5 mm)or soft pigment stones
(especially in the patient with recurrent
pyogenic cholangitis) may not show
shadowing.
 When the affected ducts are filled with
stones, the individual stones may not be
appreciated; instead, a bright, echogenic
linear structure with posterior shadowing is
seen.

22. Intrahepatic stones. Small
stones (arrow) are seen in the
right lobe causing acoustic
shadowing. Note the dilated
duct proximal to the larger
stone.
Multiple stone clusters
(arrowheads) in the left lobe
appearing as echogenic linear
structures with shadowing

23.  The majority of stones in the CBD are in the distal duct
close to or at the ampulla of Vater.
 Difficult area to visualize because it may be hidden by
bowel gas
 Maneuvers to improve assessment include the following:
• Changes in patient position. The CBD may be examined in
supine, letf lateral decubitus, and standing positions. The
change in the relative position of adjacent organs and bowel
gas may allow improved visualization of the distal duct.
• Choice of sonographic window. The subcostal view is most
useful for the assessment of the porta hepatis and proximal
CBD. An epigastric view is best for the distal CBD.
• Use of compression sonography. Physically compressing
the epigastrium may collapse the superficial bowel and
displace the bowel gas that is blocking the view.

24. Small CBD stone (arrow) may not
show shadowing
Distal CBD stone (arrow) with
posterior acoustic shadowing
Diagnosis of choledocholithiasis include blood clot (hemobilia),
papillary tumors, and occasionally biliary sludge; none of these will
shadow. Surgical clips in the porta hepatis, mostly from previous
cholecystectomy, appear as linear echogenic foci with shadowing. The
short length, the relatively high degree of echogenicity, the lack of
ductal dilation, and the absence of the gallbladder should allow
diferentiation of surgical clips from stones.

25.  Blood within the biliary tree.
 Mostly caused by percutaneous biliary procedures or
liver biopsies, other causes: cholangitis or
cholecystitis , vascular malformations or aneurysms ,
abdominal trauma , and malignancies, especially
hepatocellular carcinoma and cholangiocarcinoma.
 Most often, the clot is echogenic or of mixed
echogenicity, and retractile, conforming to the shape
of the duct
 Hemobilia may appear tubular with a central
hypoechoic area. Acute hemorrhage will appear as
fluid with low-level internal echoes. Blood clots may
be mobile. Extension into the gallbladder is common.
clinical history is often essential to the diagnosis

26. Echogenic blood clot
(arrowhead) within a
dilated duct, after
insertion of biliary
drainage catheter
Echogenic clot in the
common hepatic duct
after liver biopsy.
Blood in gallbladder in different patients.
angled edge
typical of
blood clot.

27.  Air within the biliary tree that usually results
from previous biliary intervention, biliary-enteric
anastomoses, or CBD stents
 In the acute abdomen, pneumobilia may be
caused primarily by three entities:
1) Emphysematous cholecystitis
2) Choledochoduodenal fistula.
3) Cholecystenteric fistula.
 USG finding : Bright, echogenic linear structures
following the portal triads are seen, more often
in a nondependent position. Posterior “dirty”
shadowing, reverberation, and ring-down
artifacts are seen with large quantities of air.

28. Extensive air within the central
ducts manifests as linear
echogenic structures
paralleling the portal veins.
Note the dirty shadowing
(arrow) and ring-down artifact
Air in the gallbladder.Ring
down artifact present (arrow)

29.  Antecedent biliary obstruction is an essential
component of bacterial cholangitis, most
common cause CBD stones. Other causes: biliary
stricture, choledochal cysts, obstructive tumor.
 Clinical presentation: Charcot triad:- fever, RUQ
pain, jaundice
 Sonographic findings:
1) Dilation of the biliary tree
2) Choledocholithiasis and sludge
3) Bile duct wall thickening
4) Hepatic abscesses

30. Bile duct wall thickening
(arrow) in a dilated duct
Extensive periportal edema
manifest by echogenic
thickening of periportal
tissues (short arrows).

31.  Characterized by chronic biliary obstruction,
stasis, and stone formation, leading to recurrent
episodes of acute pyogenic cholangitis.
 Any segment of the liver may be affected, but the
lateral segment of the left lobe is most often
involved.
 The chronic stasis and inflammation eventually
lead to severe atrophy of the affected segment
 The typical appearance on sonography is dilated
ducts filled with sludge and stones

32. Segmental Recurrent Pyogenic Cholangitis. (A) Transverse sonogram and
(B) T1-weighted MRI scan depict severe atrophy of segment 3 around
dilated, stone-filled ducts (arrows).

33.  Human immunodeiciency virus (HIV) cholangiopathy is an
inflammatory process affecting the biliary tree in the
advanced stages of HIV infection
 Patients present with severe RUQ pain or epigastric pain, a
nonicteric cholestatic picture, and greatly elevated serum
alkaline phosphatase with a normal bilirubin level.
 USG finding:
• Bile duct wall thickening of the intrahepatic and
extrahepatic biliary tree.
• Focal strictures and dilations identical to those of
primary sclerosing cholangitis.
• Dilation of the CBD caused by an inflamed and stenosed
papilla of Vater (papillary stenosis). The inflamed papilla
itself may be seen as an echogenic nodule protruding into
the distal duct.
 Difuse gallbladder wall thickness

34. (A) Intrahepatic biliary tree. The thick rind of echogenic tissue
(arrowheads) surrounding the central portal triads and causing
irregular narrowing of the bile ducts. (B) Common bile duct (CBD)
is dilated, and its wall is minimally irregular. (C) Papillary stenosis.
The dilated CBD abruptly tapers in an echogenic, inflamed ampulla
(arrowhead). (D) Transverse view of ampulla (arrow), which is
enlarged and echogenic, viewed in the caudal aspect of pancreatic
head.

35.  Primary sclerosing cholangitis is a chronic disease affecting the
entire biliary tree. The process involves a fibrosing inflammation
of the small and large bile ducts, leading to biliary strictures and
cholestasis and eventually biliary cirrhosis, portal hypertension,
and hepatic failure
 Other concomitant finindg inflammatory bowel disease, typically
ulcerative colitis.
 Sonographic findings include irregular, circumferential bile duct
wall thickening of varying degree, encroaching on and narrowing
the lumen. Focal strictures and dilations of the bile ducts. The
extrahepatic disease is more easily visible. A high degree of
suspicion and careful examination of the portal triads in all
hepatic segments is required to detect intrahepatic ductal
involvement. Irregularity of the thickened bile duct mucosa is a
key feature that should be sought.
 Patients with primary sclerosing cholangitis also have hepatic
findings of biliary cirrhosis, namely hepatomegaly, and enlarged
periportal lymph nodes.

36. Isoechoic inlammatory tissue
causing obliteration of right
and left hepatic ducts (short
arrows) with proximal
dilation.
Dilated intrahepatic ducts
“rat-tail” as they extend
centrally toward the hepatic
hilum. The hypoechoic
ductal/ periductal tissue
obstructing the central ducts
(arrowheads).

37. Saccular diverticula (arrow) of
the duct are occasionally
seen presumably due to
distal obstruction.
Intraductal stones (short arrows)
are seen, which often do not
shadow.

38. Common bile duct wall thickening of
moderate and severe degrees

47.  Previous cholecystectomy
 Physiologic contraction
 Fibrosed gallbladder duct—chronic
cholecystitis
 Air-filled gallbladder or emphysematous
cholecystitis
 Tumefactive sludge
 Agenesis of gallbladder
 Ectopic location

48.  Sonography is highly sensitive in the detection of stones
within the gallbladder. The varying size and number of
stones within the gallbladder lead to a variable appearance
on sonography
 USG finding: echogenic appearance with strong posterior
acoustic shadowing. Small stones (<5 mm) but will still
appear echogenic.
 Mobility is a key feature of stones, allowing diferentiation
from polyps
 WES COMPLEX: With stones the gallbladder wall is first
visualized in the near field, followed by the bright echo of
the stone, followed by the acoustic shadowing, called the
wallecho-shadow complex
 When air or calcification is present, the normal gallbladder
wall is not seen, and only the bright echo and the posterior
dirty shadowing are seen.

49. multiple dependent stones appearing
as echogenic foci with posterior
acoustic shadowing.
“Wall-echo-shadow complex” in a
gallbladder filled with stones.
Gallbladder wall (arrow) is thin.

50.  Biliary sludge, also known as biliary sand or
microlithiasis, is defined as a mixture of
particulate matter and bile that occurs when
solutes in bile precipitate
 The predisposing factors in development of
sludge are pregnancy, rapid weight loss,
prolonged fasting, critical illness, long-term total
parenteral nutrition, ceftriaxone or prolonged
octreotide therapy, and bone marrow
transplantation
 The complications of biliary sludge are stone
formation, biliary colic, acalculous cholecystitis,
and pancreatitis

51.  The sonographic appearance of sludge is that
of amorphous, low-level echoes within the
gallbladder in a dependent position, with no
acoustic shadowing. With a change in patient
position, sludge may slowly resettle in the
most dependent location.
 In fasting, critically ill patients, sludge may be
present in large quantities and completely fill
the gallbladder. Sludge that mimics polypoid
tumors is called tumefactive sludge.
 Sludge has the same echotexture as the
liver,called hepatization of the gallbladder,
this may be easily recognized by identifying
the normal gallbladder wall, and lack of
Doppler flow within the sludge.

52. Sagittal sonogram shows
gallbladder filled with tumor like
sludge
Transverse image shows a polypoid
appearance of sludge on the
dependent gallbladder wall, with an
embedded stone ( shadowing).

53. “hepatization” of the gallbladder, with internal
echoes mimicking the normal liver parenchyma.

54.  It is caused by gallstones in more than 90% of
patients. Impaction of the stones in the cystic duct or
the gallbladder neck results in obstruction, with
luminal distention, ischemia, superinfection, and
eventually necrosis of the gallbladder
 Sonographic findings include the following
• Thickening of the gallbladder wall (>3 mm)
• Distention of the gallbladder lumen (diameter > 4
cm)
• Gallstones
• Impacted stone in cystic duct or gallbladder neck
• Pericholecystic fluid collections
• Positive sonographic Murphy sign
• Hyperemic gallbladder wall on Doppler interrogation

55.  Gallbladder wall thickening cause
Congestive heart failure
Renal failure End-stage
cirrhosis
Hypoalbuminemia
Primary ::Acute cholecystitis
Cholangitis
Chronic cholecystitis
Secondary:: Acute hepatitis
Perforated duodenal ulcer
Pancreatitis
Diverticulitis/colitis
Gallbladder
adenocarcinoma
Metastases
Adenomyomatosis
Mural varicosities
GENERALIZED
EDEMATOUS STATES
INFLAMMATORY CONDITIONS
NEOPLASTIC
CONDITIONS
MISCELLANEOUS

56. patient with
hypoalbumin
emia show
marked
thickening of
the
gallbladder
wall with a
small lumen
patient with cirrhosis
demonstrating GB wall
edema
Generalized Causes of Gallbladder Wall Edema.

57.  INFLAMMATORY CONDITIONS :
the gallbladder show marked circumferential
thickening of the gallbladder wall. The lumen
is not distended
Left lobe of the liver shows
periportal cufing

58. Perforation of a duodenal
ulcer. Shows
Asymmetrical, marked
thickening of the
gallbladder wall.
Case of Acute
pyelonephritis
shows
asymmetrical
thickening of GB
wall.

59. Image show a tense distended
gallbladder, wall thickening, fluid-
debris level, and a nonobstructive
stone with posterior acoustic
shadowing.
distended cystic duct reveals the
obstructive stone (arrow).

60. image shows a
prominent
cystic artery
and hyperemia
in the wall of
the
gallbladder as
well as the
adjacent liver.

61.  Murphy sign : Maximal tenderness over the
gallbladder when the probe is used to compress
the RUQ
 It is often better elicited with deep inspiration,
which displaces the gallbladder fundus below the
costal margin, allowing for direct compression.
Sonographic Murphy sign may be absent in older
patients, if analgesics were taken before the
study, or when prolonged infammation has lead to
gangrenous cholecystitis. Hyperemia in the
gallbladder wall and the adjacent liver and
prominent cystic artery are relatively specific
findings in acute cholecystitis
 Doppler ultrasound quite useful in equivocal
cases.
 Murphy sign also seen positive in Perforated
duodenal ulcer, acute hepatitis, pancreatitis,
colitis or diverticulitis, and even pyelonephritis.

62.  Early perforation and sequelae
The gallbladder is tense
with thickened walls and
sludge and a stone. There is
poor definition of its near
wall (arrow) with adjacent
heterogeneity of the hepatic
parenchyma
a localized fluid collection
between the wall of the
gallbladder and liver
parenchyma

63. shown as disruption of the
gallbladder wall (arrow)
with a subhepatic abscess
Perforation into the liver. There
is a large defect (arrow) in the
wall of the gallbladder with an
adjacent hepatic abscess
Clues to perforation are the deflation of the gallbladder,
with loss of its normal gourdlike shape, and a focal
pericholecystic fluid collection

64.  Due to ischemic necrosis of the gallbladder wall in
patients with severe acute cholecystitis
 Most common in patients with diabetes and
leukocytosis
 Acute surgical emergency (preferred treatment is open
cholecystectomy)
Imaging Findings:
 US: Heterogeneous and striated thickening of the
gallbladder wall, with intraluminal membranes and
pericholecystic fluid
 Sonographic Murphy sign is negative in two-thirds of
patients because of denervation of the gallbladder wall

65. Sloughed membranes (short arrow)
appear as linear intraluminal echoes.

66.  Gas within the gallbladder wall and/or lumen not due to direct
communication with the gastrointestinal tract
 Due to vascular compromise of the cystic artery (ischemic necrosis)
and acute gallbladder wall infection by gas-forming organisms
(Escherichia coli or Clostridium)
 Diabetes and male sex are predisposing factors
 Rapidly progressive course characterized by early gangrene,
perforation, and high mortality (15%)
Imaging Findings:
 Radiography: Gallbladder has curvilinear lucencies or air-fluid level.
 US: Positive Murphy sign in <1/3 of patients is due to ischemic necrosis
or sequelae of diabetes mellitus. Hyperechoic foci, often with
reverberation (ring-down artifact) correspond to foci of gas in the wall or
lumen. Differential considerations include pneumobilia, porcelain
gallbladder, and gallbladder filled with gallstones.
.

67. sonogram of the gallbladder with
a focus of intraluminal air
appearing as a bright echogenic
focus (arrow) with dirty
shadowing.
Gallbladder that is filled with air
(arrow). The gallbladder is not actually
visualized, and knowledge of the
location of the gallbladder fossa is
essential to avoid mistaking this for
bowel gas

68.  Most common in critically ill patients and
patients receiving total parenteral nutrition.
 Gradual increase in bile viscosity leads to
functional obstruction of the cystic duct.
 Mortality is about 30%, with percutaneous
drainage equivalent to surgical
management in terms of treatment outcome.
Imaging Findings:
 US: gallbladder distention, gallbladder wall
thickness of >3 mm, pericholecystic fluid in
the absence of ascites, biliary sludge
without stones
Thickened GB
wall and
distended GB

69.  Common inflammatory disease related to
multiple episodes of acute cholecystitis or biliary
colic
 >95% of cases are associated with gallstones
 May be associated with Helicobacter pylori
Imaging Findings:
 Gallstones and gallbladder wall thickening are
the major features. The gallbladder may be
contracted, and inflammatory changes are
usually absent.
 Differentiation from acute cholecystitis is made
by the absence of other signs, namely,
gallbladder distention, Murphy sign, and
hyperemia in the wall.
images show
diffuse gallbladder
wall thickening and
gallstones

70.  Rare destructive inflammatory process with accumulation of
lipid-laden macrophages, fibrous tissue, and inflammatory cells
 Caused by extravasation of bile into the gallbladder wall via the
Rokitansky-Aschoff sinuses or mucosal ulceration in the setting
of cholelithiasis or obstruction
 Most commonly seen in women aged 60–70 years
 Complications (seen in 30% of patients) include perforation,
abscess formation, fistulous tracts to the duodenum or skin,
and extension of the inflammatory process regionally to the
liver, colon, or soft tissues
Imaging Findings:
 US : thickened gallbladder wall with gallstones; may have
hypoechoic nodules; may be focal or diffuse
gallbladder wall
thickening with a central
area of
hypoechogenicity
(arrow) associated with
a large gallstone(*)

71.  Porcelain gallbladder is an uncommon sequela of
chronic cholecystitis.
 When the entire gallbladder wall is thickly
calcified, a hyperechoic semilunar line with dense
posterior acoustic shadowing is noted.
 Mild calcification appears as an echogenic line
with variable degrees of posterior acoustic
shadowing. The luminal contents may be visible.
Interrupted clumps of calcium appear as
echogenic foci with posterior shadowing
 Diferential diagnosis includes gallstones and
emphysematous cholecystitis. Because the
calcifications occur in the wall of the gallbladder,
the wall-echo-shadow complex is absent
Imaging Findings:
 US: echogenic gallbladder wall with possible
shadowing
US image shows
hyper-echoic foci in
the gallbladder wall
(arrow) with
associated
shadowing (*).

72. Common Polypoid Masses of the Gallbladder:
BENIGN :>
Cholesterol polyps (50%-60%)
Inflammatory polyps (5%-10%)
Adenoma (<5%)
Focal adenomyomatosis
MALIGNANT:>
Metastases (especially melanoma)
Gallbladder adenocarcinoma
Indications for Surgical Management:
 Symptomatic biliary colic
 Increased malignancy risk:
• Polyps ≥10 mm
• Primary sclerosing cholangitis
Imaging Follow-up:
 Polyps 7–10 mm require 12-month
interval follow-up US
No Follow-up Indicated:
 Polyps ≤6 mm

73.  Hyperplastic cholecystosis due to proliferation of surface
epithelium and cholesterol accumulation in intramural diverticula
(Rokitansky-Aschoff sinuses) that extend into the hypertrophic
muscularis propria of the gallbladder wall
 Prevalence: 2%–5% of cholecystectomy specimens
 Benign mimic of gallbladder carcinoma
 Three types: diffuse, segmental, fundal
 Focal adenomyomatosis is most common in the gallbladder
fundus, less often narrowing the midportion of the organ, called
hourglass gallbladder
Imaging Findings:
 US: thickened gallbladder wall with anechoic diverticula, with or
without acoustic shadows or reverberation artifact (comet-tail
artifact) at gray-scale US; twinkling artifact at color Doppler US

74. Fundal adenomyoma. Hourglass adenomyomatosis
Small focal area of thickening of the
anterior fundal wall (arrow) with a bright
echogenic focus with a distal comet-tail
artifact
Multiple bright foci (arrow)
with distal artifacts

75. Adenomyoma appears
hypoechoic and masslike
Caplike area with multiple tiny,
highly echogenic foci that
suggest multiple crystals in the
Rokitansky-Aschoff sinuses.

76. Masslike areas obliterating the
gallbladder lumen. Multiple cystic
spaces
Multiple echogenic foci suggest
crystals in the Rokitansky-Aschoff
sinuses.

77.  Approximately one-half of all polypoid
gallbladder lesions are cholesterol polyps.These
represent the focal form of gallbladder
cholesterolosis, a common nonneoplastic
condition of unknown origin
 Cholesterolosis results in accumulation of lipids
within macrophages. The difuse form, commonly
known as “strawberry gallbladder,”
 Cholesterol polyps usually are 2 to 10 mm
 The sonographic appearance of cholesterol
polyps is multiple ovoid, nonshadowing lesions
attached to the gallbladder wall

78. Small size (≤10 mm) and
multiple tumors are features
most suggestive of a benign
lesion.
images show two polypoid
nonshadowing,
nonmobile lesions larger than 10 mm
(arrows) in the gallbladder.

79.  Adenomas are true benign neoplasms of the
gallbladder, with a premalignant potential
much lower than for colonic adenomas.
 Adenomas are usually pedunculated, and
larger lesions may contain foci of malignant
transformation
 Adenomas tend to be homogeneously
hyperechoic but become more heterogeneous
as they increase in size
 Thickening of the gallbladder wall adjacent to
an adenoma should suggest malignancy

80. a polypoid lesion found incidentally in a
patient with mild acute cholecystitis. The
lesion was a tubulovillous adenoma on
resection.

81.  In a majority of cases, carcinoma is associated
with gallstones. Chronic gallstone disease and
resultant dysplasia have been cited as a causative
factor.
 Other risk factor chronic Salmonella typhi carrier
state
 Three patterns of disease:
• Mass arising in the gallbladder fossa,
obliterating the gallbladder and invading the
adjacent liver (most common pattern)
• Focal or difuse, irregular wall thickening
• Intraluminal polypoid mass

82. Sonographic Appearance :
 A mass replacing the normal gall bladder
fossa
 A clue to the diagnosis is the common
presence of an immobile stone that is
engrossed by the tumor , the “trapped stone.”
 On Doppler interrogation the mass may
demonstrate internal arterial and venous flow
 Diffuse, malignant thickening of the wall difers
from other causes in that the wall is irregular
with loss of the normal mural layers.

83. Extensive
asymmetrical,
heterogeneous wall
thickening in a
markedly enlarged
gallbladder with
abnormal low on
Doppler assessment.
Huge mass replacing the gallbladder
fossa and invading the liver