Abnormal Intraluminal Bile Duct Findings

Cancer

In characteristic sonomorphology, periampullary and true papillary carcinomas result not only in biliary but also pancreatic obstruction, with the “double duct dilatation” of both duct systems (Fig. 3.14, Fig. 3.26). In cases of painless jaundice, this sonographic picture raises the hope of possible curative surgery.

Fig. 3.26 Periampullary cancer (y) obstructing the CBD (1) and pancreatic duct (x); inferior vena cava (6), splenic vein (8).

Uncommon Causes

Numerous other intraluminal foreign bodies of the bile duct causing different degrees of biliary obstruction (including endoscopic data):

● Metal fragments after gunshot injuries (Fig. 3.24a)

● Nonabsorbable clips after surgery (Fig. 3.24b, Fig. 3.29a)

●Sutures and parts of T-tube drains

●Food particles (after extensive endoscopic papillotomy or after choledochoduodenostomy)

●Parasites (Echinococcus, Ascaris, Opisthorchis sinensis, and others) (Fig. 3.29b–d)

The sonographic morphology of these biliary obstructions, other than those due to Echinococcus, is nonspecific.

c Lumen (x) of a self-expanding hepatoduodenal stent with satisfactory drainage.

Fig. 3.29

a Clip (x), with posterior shadowing (y), close to the CBD after laparoscopic cholecystectomy; portal vein (2); hepatic artery (3); CBD (1) with residual inflammation of the wall (after endoscopic papillotomy).

In today’s age of imaging modalities, the term cholestasis—meaning “stoppage of the bile flow”—is equated with mechanical obstruction of the bile flow. Thus, the differentiation of this term with respect to parenchymal cholestasis ( 3.3) in acute hepatitis ( 3.3a), hepatic congestion ( 3.3b), portal vein thrombosis

cirrhosis ( 3.3f–h) has become an issue of minor importance. This is understandable because the extent and duration of the ductal distension, and the type and anatomical location of the obstruction with its possible impact on bile flow dynamics, can be visualized so easily by means of ultrasonography.

As in all other fluid-filled tubular systems, any pressure increase in the bile-filled vessels

will increase their diameter, pressure in the adjacent tissue permitting, and thus result in distension. Therefore, the leading differential diagnostic sign in the sonographic morphology of cholestasis is distension of the intrahepatic and/or extrahepatic bile ducts, with or without clinical symptoms and rarely without concomitant rise in the blood level of bilirubin and/or the other enzymes characteristic of cholestasis.

Biliary Tree

Thickening of the Bile Duct Wall

Bile Duct Rarefaction

Bile Duct Dilatation and Intraductal Pressure

Abnormal Intraluminal Bile Duct Findings

Differential Diagnosis of Sonographic

Cholestasis

The Seven Most Important Questions

Relationship with the Biliary Tree Pressure Increase

Bile Duct Diameter Level of Flow Obstruction Possible Malignancy Duration of Obstruction

Thickness of Bile Duct Wall

1. Are the vascular structures in question truly part of the biliary tree? The first step in the differential diagnosis of vascular distension within the liver parenchyma or at the porta hepatis is to ascertain whether the vessels are truly part of the biliary tree. Intrahepatic arteries or the arteries and veins of the porta hepatis are typical examples of such misdiagnosed structures ( 3.3f,i,j). Even without the capabilities of color-coded Doppler scanning of the flow, precise knowledge of the anatomy with its numerous variants is essential for this first step in the differential diagnosis.

2. Are there signs of a (segmental or general) pressure increase in the biliary tree? The second aspect to be addressed when considering dilatation of the biliary tree is to resolve the issue of a pressure-independent increase in the diameter (“ectasia”) ( 3.4 d) or true dilatation by increased tubular pressure ( 3.4- e–h)—either within individual segments (“levels”) ( 3.4i–k,n,v) or the entire biliary tree ( 3.4 l–u, w–z). Congenital malformations such as choledochal cysts or Caroli disease and the age-dependent increase in the ductal diameter, particularly that of the prepancreatic CBD, are not pressure-dependent ( 3.4 d). The prevailing concept that the diameter of the common duct increases after cholecystectomy does not hold true.

3. What is the diameter of the bile ducts—ob- served and measured? The third question deals with the determination of the bile duct diameter. Values measured in millimeters at ill-

defined locations are diagnostically inferior to the morphological appearance of the biliary tree, since the latter allows much better conclusions to be drawn regarding the actual cause of the increased pressure within the bile ducts ( 3.4 d–h). Vessels distended owing to increased pressure are more or less dilated along their entire prestenotic course; it should be noted that in case of extrahepatic obstruction the hepatic duct confluence is easily differentiated from its surroundings. Only ectatic segments of the bile tree (preferably in the prepancreatic region of the CBD) with slender segments upstream ( 3.4 d) do not exhibit any intraductal pressure increase, i. e., no cholestasis.

It stands to reason that in cases of intraductal pressure increases the possibility of ductal dilatation depends on the pressure of the surrounding tissue: for instance, if the intrapancreatic course of the CBD becomes visible this is (almost) proof of a significant pressure increase in the prepapillary segment which must more than negate the compression exerted by the head of the pancreas. Cirrhosis of the liver will not result in dilatation of the intrahepatic biliary tree even if the pressure increases significantly.

4.At what level of the biliary tree is the obstruction located?

5.Is the obstruction malignant or benign? The fourth question concerning the “level” and the fifth question dealing with the nature (malignant or benign) of the biliary obstruction are

discussed in detail elsewhere in this chapter, in the section on “Bile Duct Dilatation and Intraductal Pressure.”

6. How long has the biliary tree been obstructed/dilated (acute—hours/days, or chron- ic—weeks/months)? The sixth issue focuses on the duration of the cholestasis and has to be resolved in the context of the patient’s history and laboratory work-up. Lacking any muscle layers, the walls of the bile ducts are quite thin, and therefore any pressure increase will result in immediate expansion of their diameter. In acute obstruction from calculi, e. g., impacted in the papilla of Vater, bile duct dilatation is the first detectable symptom ( 3.4h) and can be demonstrated several hours before any rise in the cholestatic enzymes.

Compensated chronic (weeks or months) obstruction in the intrahepatic or extrahepatic segments of the biliary tree ( 3.4f,h,j,l,u–z) can lead to bizarre bile duct dilatation ( 3.4x) and tortuosity.

7. Is there localized or diffuse thickening of the bile duct walls? The seventh aspect to be considered in the differential diagnosis of cholestasis concerns the thickness of the bile duct walls. If the obstructed bile flow is accompanied by cholangitis, quite often thickening and layering can be demonstrated in the bile duct walls, in particular after successful relief by interventional endoscopy. Irregular wall thickening, with juxtaposed segmental narrowing and dilatation of the bile ducts, is characteristic of PSC (Fig. 3.6).

3.3 Parenchymatous Cholestasis

Viral hepatitis, congested liver, portal vein thrombosis

a Gallbladder, with a lot of sludge but little fluid and ill-defined wall (7), in acute hepatitis A. 2 = branch of the portal vein; 5 = liver.

Abscess, metastases

d Cholangitis with intrahepatic (5) abscess

(a). 2 = branch of the portal vein; 6 = hepatic vein.

Cirrhosis

g Portal hypertension with convoluted varicosities (x) in the wall and lumen of the gallbladder (7).

Differential diagnosis of fluid-filled structures

i Portal vein (2); variant course of the hepatic artery (3). 6 = inferior vena cava.

Bile duct dilatation: shape, location, degree, origin. Pancreas (4), liver (5), inferior vena cava (6), gallbladder (7)

Bile duct dilatation: shape, location, degree, origin. Pancreas (4), liver (5), inferior vena cava (6), gallbladder (7)

a Dilated CBD (1) with distended cystic duct (x).

d Cholangiectasia with slender CBD (1) upstream and prepancreatic distension. 2 = portal vein; 3 = hepatic artery.

p Dilated CBD (1) due to fragmentation (x) of an intraductal calculus by ESWL. 2 = portal vein.

s Lymphadenophathy (x) probably inflammatory in autoimmune hepatitis. 2 = portal vein.

v Moderate “double-barreled shotgun” sign with dilatation of the intrahepatic bile ducts (1). 2 = branches of the portal vein.

y Maximum dilatation of the intrahepatic biliary tree (1) with almost lacunar transformation.

q Dilated CBD (1) due to nonfunctional stent; “anterior” (x) and “posterior” (y) wall of the stent. 2 = portal vein; 3 = hepatic artery.

t Dilatation of the intrahepatic biliary ducts (1) in a large CCC (x).

w Dilated intrahepatic CBD (1). 12 = superior mesenteric artery; x = gastroduodenal artery.

z Maximum (long-term chronic) dilatation of the CBD (1). 2 = portal vein; 3 = hepatic artery.

r Well-differentiated cholangiocarcinoma (initially biliary papillomatosis) with pronounced dilatation of the CBD (→ ←). 2 = portal vein; 3 = hepatic artery; x = biliary stent.

u Slightly dilated CBD (1). 2 = portal vein; 3 = hepatic artery.

x Significant (chronic) dilatation of the intrahepatic bile ducts (1).