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Biliary Tree and Gallbladder

■ Thickening of the Bile Duct Wall

Localized and Diffuse

 

 

 

 

Thickening of the Bile Duct Wall

 

 

Benign Thickening of the Bile Duct Wall

Tree

 

 

 

 

Localized and Diffuse

 

 

Malignant Thickening of the Bile Duct Wall

 

 

 

 

 

 

 

 

Bile Duct Rarefaction

 

 

 

Biliary

 

 

 

 

 

Bile Duct Dilatation and Intraductal Pressure

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Abnormal Intraluminal Bile Duct Findings

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Differential Diagnosis of Sonographic

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Cholestasis

 

 

 

Benign Thickening of theBile Duct Wall

Transcutaneous ultrasonography can assess localized benign thickening of the bile duct wall in two disorders of the biliary system: intrahepatic and extrahepatic presentation of primary sclerosing cholangitis (PSC) (Fig. 3.6), and the solely extrahepatic manifestation of (severe) suppurative cholangitis (Fig. 3.7). Except for a few cases, in both instances the sonographic morphology cannot be considered as primary proof but rather “suggests” the suspected diagnosis, with a greater or lesser degree of probability, which then will have to be confirmed by other means (clinical findings,

blood chemistry, and endoscopic retrograde cholangiography).

The prolonged course of chronic inflammatory bowel disease (Crohn disease, ulcerative colitis) is often accompanied by the sonographic telltale signs of PSC, from segmental diffuse bile duct wall thickening all the way to complete obstruction of the lumen, alternating with dilated/ectatic bile duct segments; ducts may also appear simply to break off, and intraductal sludge is a frequent finding (Fig. 3.6a,b). It is not possible to rule out early cholangiocellular carcinoma (CCC), and even fine-needle aspiration cytology has its prob-

lems. PSC-like changes have been described for HIV infections with manifest AIDS symptoms.

Acute suppurative cholangitis may result in thickening of the common duct wall, which can be demonstrated for the extrahepatic segment. This thickening of the wall becomes particularly evident if endoscopic intervention (endoscopic papillotomy, EPT) has provided pressure relief by removing or bypassing the biliary obstruction: the dilated bile duct walls, originally thinned out by their distension, collapse and their inflamed and swollen true structure becomes exceptionally well visualized (Fig. 3.7a).

Fig. 3.6 Primary sclerosing cholangitis.

a Dilatation and wall thickening (calipers) of the intrahepatic bile duct (1) in segment III. Accompanying branch of the portal vein (2).

b Dilation and thickening of the wall of the intrahepatic branch of a bile duct (1) in segment III and II, rudimentary also (ventral) second intrahepatic branching of a portal vessel (2).

c Wall thickening (“sclerosis”) of the common duct (1); hepatic artery (3) crossing in between.

Fig. 3.7

a Suppurative cholangitis, subsiding after endoscopic papillotomy and extraction of calculi, with thickened wall (calipers) of the common duct (1); portal vein (2); hepatic artery (3) crossing in between.

b Wall thickening of the prepapillar intrahepatic CBD (cursors) after stent delivery – accentuated lumen (1); pancreas (P), left renal artery and collapsed caval vein (x), right renal artery (y).

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Malignant Thickeningof the BileDuctWall

Malignant bile duct wall thickening may be localized as in CCC or infiltrating as in hepatocellular carcinoma (HCC), and in both cases ultrasound detects these changes solely in terms of the resulting biliary obstruction with its subsequent prestenotic dilatation of the duct. Consequently, these entities are discussed

in the section on pressure-induced bile duct dilatation.

One rare special case is mucinous biliary papillomatosis with its fluent transition to well-differentiated cholangiocarcinoma (Fig. 3.8). The ultrasound findings show a nonexpansile solid mass originating in the surrounding bile duct wall, which it dilates to

sometimes bizarre shapes, but well defined and demarcated from the bile duct wall itself; complete biliary obstruction tends to occur late in the disease. It has a rather indolent course (over many years), and treatment is characterized by effective long-term interventional endoscopy (stenting, removal of the tumor masses).

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Thickening of the Bile Duct Wall

Fig. 3.8

a Obstruction of the common duct (1) in intraductal spread of cholangiocarcinoma (xx); portal vein (2); hepatic artery (3).

b Tumor invasion into the CBD.

d Biliary obstruction of the left liver lobe—increased (biliary) fluid content of the left lobe in contrast to the right lobe (therefore only under this condition is there exact differentiation of both liver lobes).

c Klatskin tumor (CCC) involving the hepatic duct bifurcation (arrows) and infiltrating the right (1) and left (2) hepatic duct. Middle: Corresponding ERC with tumor stenosis of the right (1) and left (2) hepatic duct. Right: After double stent implantation (x,y): diminished stasis of the hepatic ducts (1, 2).

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