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Table 3.1 Gallbladder changes in nonbiliary disorders

 

 

 

Right-sided heart failure

Cirrhosis of the liver

Severe malabsorption

Acute hepatitis

Size

Normal or enlarged

More likely small

Normal or enlarged

More likely small

Shape

Normal or little fluid

Normal or little fluid

Smooth or rippled

Ovoid, little fluid

Wall

Smooth hypoechoic wall thick-

Smooth hypoechoic wall thick-

Wall thickening of mixed

Smooth hypoor hyperechoic

 

ening

ening, possibly varicose veins

echogenicity

wall thickening

Surroundings

Signs of cardiac congestion

Ascites

Edema of the intestinal wall

Lymph nodes

Symptomatic (Pathological)

Most fasting gallbladders with low or no fluid levels result from cystic duct obstruction (Fig. 3.43).

Inflammatory atrophy of the gallbladder with its lack of fluid is usually caused by chronic cholecystitis, where the shape of the gallbladder is irregular and its wall thickened and inhomogeneous (hyperechoic) (Fig. 3.45, Fig. 3.46). During acute exacerbation, hypo-

echoic areas in the wall may also be visualized. A typical finding would be several, sometimes even encrusted, intraluminal gallstones. In the end the atrophic gallbladder can only be identified by the encrusted calculi within the scar tissue.

This contracted gallbladder with its gallstones is characterized by a crescent-shaped band of echoes without demonstration of the

posterior wall. Sometimes even the anterior wall with its scar contraction may hardly be delimited from the gallstone echoes (Fig. 3.46). In these patients, differentiation of a possible concurrent gallbladder carcinoma can be problematic.

Fig. 3.45 Inflammatory atrophic gallbladder. Atrophied

b Completely folded-over gallbladder wall; the underly-

Fig. 3.46 The contracted gallbladder with low levels of

gallbladder (GB) void of any fluid.

ing gallstone obstructing the cystic duct is not depicted

liquid and filled with gallstones is characterized by a

a Calculous atrophied gallbladder. The atrophied gall-

in this image.

crescent-shaped band of echoes at the base and a blurry

bladder is visualized as a crescent-shaped band of echoes

 

ventral wall. The demonstration of the posterior wall

in the hepatic fossa with ill-defined contour of the anterior

 

often is impossible due to the gallstone echoes.

wall. Usually, the posterior wall cannot be demonstrated

 

 

due to posterior shadowing (S) of the gallstones.

 

 

■ Wall Changes

General Hypoechogenicity

Gallbladder

 

 

 

Changes in Size

 

 

Acute Cholecystitis

 

 

 

 

 

Wall Changes

 

 

Special Cases

 

 

 

 

 

 

 

 

 

 

General Hypoechogenicity

 

 

Wall Thickening in Hepatic/

 

 

 

 

 

 

 

 

 

General Hyperechogenicity

 

 

Pancreatic Disorders and Trauma

 

 

 

 

Focal Hypoechogenicity/Hyperechogenicity

 

 

 

 

 

 

 

General Tumor

 

 

 

 

 

 

 

Focal Tumor

 

 

 

 

 

 

 

Intraluminal Changes

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Nonvisualized Gallbladder

 

 

 

 

 

 

 

 

 

 

3

Wall Changes

151

3

Biliary Tree and Gallbladder

Acute Cholecystitis

Acute and chronic cholecystitis is characterized by uneven thickening of the gallbladder wall with irregular echo pattern. The typical finding in acute cholecystitis is the tensely distended afunctional/dysfunctional gallbladder with its hypoechoic wall that is tender on palpation (positive Murphy’s sign). Another sign is the ill-defined intraluminal and extraluminal contour of the wall, accompanied by hypoechoic inflammation of the surrounding tissue (pericholecystitis). Ultrasound morphology of the gallbladder wall spans the spectrum from diffuse hypoechoic thickening with poorly delim-

ited contour of the wall ( 3.6a,b) through hypoechoic necrosis all the way to complete destruction of the wall ( 3.6c; see Table 3.2).9 Intraluminal hyperechoic or inhomogeneously echogenic material can point the way to the diagnosis of cholecystic empyema.

Advanced and severe courses of acute cholecystitis may result in necrosis of the mucosa and filiform detachment of the tunica mucosa ( 3.6e). Usually, these cases present with hyperechoic inhomogeneous necrotic debris within the gallbladder. A pericholecystic film is typical of localized perforation ( 3.6 d,e).

Lacelike structures with hypoechoic necrotic areas are infrequent findings.

Imminent perforation may be preceded by ascites, ulcers of the gallbladder wall, or pericholecystic infiltrates/abscesses ( 3.6f). Hypervascularization of the gallbladder wall in color-flow duplex scanning of cholecystitis is by no means mandatory. The histological grading of edematous, phlegmonous, and gangrenous cholecystitis cannot be differentiated very well by ultrasound.

Special Cases

Emphysematous cholecystitis. The characteristic sign of emphysematous cholecystitis is intraluminal and intramural gas (from infection by gas-producing pathogens) ( 3.6 g,h).

Acalculous and xanthogranulomatous cholecystitis. Other special cases are acalculous ( 3.6i) and xanthogranulomatous ( 3.6j,k) cholecystitis. Acalculous cholecystitis is a typical disorder in the immune-compromised patient in the intensive care unit or after chemotherapy. It is characterized by a nonfunctional gallbladder that is tender on palpation, with edema of the wall and possible sludge. In large hydropic gallbladders, ultrasound may only demonstrate slight thickening of the wall despite the presence of phlegmon. Xanthogranu-

Table 3.2 Differentiating cholecystitis

 

Acute cholecystitis

Size

Large

Shape

Irregular

Echogenicity

Hypoechoic—layered

Lumen

Large, calculi

Wall

Thickened

lomatous cholecystitis, on the other hand, is characterized by pseudotumorous thickening of the wall with loss of the usual layering.

Chronic cholecystitis

Normal or atrophied

Round

Hyperechoic

Small or lacking

Thickened

This entity is almost impossible to differentiate from gallbladder carcinoma on the basis of sonographic morphology alone.

Wall Thickeningin Hepatic/PancreaticDisorders andTrauma

The differential diagnosis of cholecystic wall changes has to include not only calculous cholecystitis but also wall thickening secondary to acute hepatitis, decompensated cirrhosis of the liver, and acute episodes of (chronic) pancreatitis ( 3.6 m–p).

152

3.6 Acute Cholecystitis: Complications and Special Cases

a Acute cholecystitis in cholecystolithia-

b Acute phlegmonous cholecystitis: en-

c Necrotizing cholecystitis: complete sep-

d Perforated gallbladder with intrahepatic

sis: irregularly thickened gallbladder wall

larged gallbladder with painful palpation:

aration of the wall layering; fistula to the

bile leak (bilioma); phlegmonous gall-

with positive Murphy’s sign.

ill-defined (hypoechoic) wall and small

abdomen wall (x).

bladder with sludge in the lumen, peri-

 

amount of sludge in the lumen; side-lobe

 

cholecystic bile leak with fluid (bile).

 

artifact.

 

 

3

Wall Changes

e Perforated gallbladder: phlegmonous gallbladder with filiform desquamation and extensive pericholecystic intraperitoneal fluid (bile).

f Empyema of the gallbladder with extensive cholecystitis and pericholecystic abscess.

g Emphysematous cholecystitis: extensive intramural gas collection in emphysematous cholecystitis.

h Emphysematous cholecystitis with mild gas formation: difficult study conditions may render the diagnosis more problematic (image courtesy of Dr. W.B. Stelzel, Frankfurt, Germany).

i Acalculous cholecystitis in an ICU patient with total parenteral nutrition: gallbladder tender on palpation, with or without sludge and wall edema.

j and k Xanthogranulomatous cholecystitis: rare special case with tumor-like thickening of the gallbladder wall and complete loss of normal wall layering (images courtesy of Dr. W.B. Stelzel, Frankfurt, Germany).

l Differentiation of the chronic cholecystitis: hyperechoic (callous) irregular wall thickening.

m Intensive complex thickening of the gallbladder wall without fluid in acute hepatitis and AIDS.

n Hypoechoic swelling of the wall (cursors) in decompensated toxic liver cirrhosis.

o Concurrent inflammatory wall thickening in an acute episode of chronic pancreatitis; perihepatic fluid film (arrows); surgery did not yield any gallstones.

p Traumatic wall thickening (with initial obstruction of the lumen) as part of a contusion; sparse vascularization in colorflow Doppler scanning.

153

3

Biliary Tree and Gallbladder

General Hyperechogenicity

Gallbladder

 

 

 

Changes in Size

 

Chronic Cholecystitis

 

 

 

 

 

Wall Changes

 

Porcelain Gallbladder

 

 

 

 

 

 

 

 

 

General Hypoechogenicity

 

 

 

 

 

 

 

 

 

 

 

 

General Hyperechogenicity

 

 

 

 

 

 

 

 

 

 

 

 

Focal Hypoechogenicity/Hyperechogenicity

 

 

 

 

 

 

General Tumor

 

 

 

 

 

 

Focal Tumor

 

 

 

 

 

 

Intraluminal Changes

 

 

 

 

 

 

 

 

 

 

 

 

Nonvisualized Gallbladder

 

 

 

 

 

 

 

 

Chronic Cholecystitis

Chronic cholecystitis is accompanied by hyperechoic thickening of the gallbladder wall, ranging from barely noticeable to pronounced callous thickening (3.6 l). After oral intake these gallbladders present as dysfunctional or even nonfunctional organs. In the early stages of chronic inflammation the luminal wall displays not only areas of scarred hyperechoic thickening but also acutely inflamed (hypoechoic) lesions of the mucosa. The terminal stage of chronic scarred cholecystitis is characterized by extensive callous (hyperechoic) thickening of the wall with complete loss of layering. The

differentiation between acute and chronic cholecystitis is listed in Table 3.2.

Mirizzi syndrome. If the inflammatory changes induced by a stone impacted in the neck of the gallbladder spread beyond the border of the gallbladder on to the porta hepatis, leading to obstruction of the CBD, this may result in Mirizzi syndrome (Fig. 3.47).

Cholelithic gallbladder perforation. Spontaneous perforation of calculi into the gastrointestinal tract is a rare complication of chronic cholecystitis. Fecal studies have demonstrated

spontaneous passage of stones up to 5.7 cm in diameter. Most often the stones perforate from the gallbladder into the duodenum (52%); perforation into the stomach occurs rather infrequently (ca. 3%), while the remainder of the gastrointestinal tract is affected in 45% of cases. The ultrasound signs of a perforated stone are its atypical anatomical location, gas echoes (pneumobilia) (Fig. 3.49b) within the lumen of the gallbladder (may not be present in case of fistulas), demonstration of a fistula, and atrophic gallbladder with visualization of calculi (Fig. 3.48, Fig. 3.49).

Fig. 3.47 Mirizzi syndrome: calculus impacted in the neck of the gallbladder, with adjacent inflammation and dilatation of the CBD.

Fig. 3.48 Gallstone perforation from the gallbladder into the gastric antrum.

a Barrel-shaped gallstone impacted in a fistula (arrow) between gallbladder and gastric antrum.

b Successful disintegration of the calculus into multiple fragments after extracorporeal shock-wave lithotripsy.

Fig. 3.49 Cholecystoduodenal gallstone perforation.

a Barrel-shaped gallstone impacted in the duodenal bulb after perforation through the gallbladder wall.

b Successful shock-wave lithotripsy with spontaneous passage of the fragments, now with demonstration of a wide hyperechoic fistula (arrow) between the atrophied gallbladder and the duodenal bulb (fluid-filled gastric antrum).

154

Porcelain Gallbladder

Porcelain gallbladder is considered a precancerous condition because in 10–60% of all cases gallbladder carcinoma will develop. Porcelain gallbladder is characterized by intramural shell-like calcification that may affect the entire wall or (more commonly) just parts of it (e. g., the fundus) (Fig. 3.50a,b, Fig. 3.52). Depending on the thickness of the calcified layer, the gallbladder wall may be sonolucent. In cases of severe calcification, any ultrasound differentiation of possible malignancy may prove to be infeasible. In the diffuse type there is complete calcification of the gallbladder wall, which may not be penetrated by the ultrasound beam in severe cases. If porcelain gallbladder is suspected, a plain radiograph of the gallbladder should be obtained (Fig. 3.50b).

Fig. 3.50

a Classic diffuse porcelain gallbladder: visualization of a broad calcified intramural crescent.

b Plain film of the gallbladder: typical radiographic image of diffuse porcelain gallbladder.

Focal Hypoechogenicity/Hyperechogenicity

Gallbladder

Changes in Size

Focal Inflammation

Wall Changes

Gallbladder Varicosity

 

 

General Hypoechogenicity

 

 

General Hyperechogenicity

 

 

Focal Hypoechogenicity/Hyperechogenicity

 

 

General Tumor

 

 

Focal Tumor

 

 

Intraluminal Changes

 

 

Nonvisualized Gallbladder

 

Focal Inflammation

 

Based on the morphology of the outflow obstruction in gallbladder anomalies, the inflammatory changes of the gallbladder wall may be focal (e. g., inflammation of the fundus in Phrygian cap). The sonographic morphology of focal inflammatory lesions resembles that of the diffuse changes (Fig. 3.51). Just as in diffuse calcification, focal calcium deposits are classified as porcelain gallbladders (see above) (Fig. 3.52). Cholecystitis in focal porcelain gallbladder may be hard to differentiate.

Fig. 3.51 Focal cholecystitis (in Phrygian cap).

Fig. 3.52 Porcelain gallbladder with sonolucent wall: fine focal calcification of the fundus wall with translucent lumen of the gallbladder and identifiable cholecystolithiasis (with sludge) (image courtesy of Dr. W.B. Stelzel, Frankfurt, Germany).

3

Wall Changes

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