■ Bile Duct Rarefaction

Localized and Diffuse

PSC and Cirrhosis of the Liver

The more pronounced the acute rise in pressure (for instance, in status post cholecystectomy there is no possibility of pressure compensation by the gallbladder), the more pronounced the changes become in the intrahepatic biliary tree (Fig. 3.2b)—dilatation that can be demonstrated quite well (“double-barreled shotgun sign”) at the sonographically easily accessible segments II and III, since there the hepatic triads branch in a plane paralleling the probe (Fig. 3.3). However, this is true only if the tissue surrounding the bile ducts is elastic enough to allow this dilatation; in bile ducts passing through cirrhotic parenchyma, even high intraductal pressure may not result in dilatation.

Intrahepatic

Intrahepatic Gallstones

Heptocellular Carcinoma (HCC)/Cholangiocellular Carcinoma (CCC)

In most cases benign obstruction of the intrahepatic bile ducts is caused by intrahepatic biliary calculi (cholangiolithiasis and hepatolithiasis) (Fig. 3.15).

Focal liver lesions usually do not affect the intrahepatic bile ducts, or at most they displace them without any significant biliodynamic consequences. This is also true for (very) large benign and malignant focal lesions (e. g., voluminous hemangiomas, cysts, or metastases of colorectal cancer).

Fig. 3.15 Multiple intrahepatic biliary calculi (hepatoliths) (xx).

Even aggressive metastatic spread within the liver usually respects the structures of the biliary tree. HCC may be the one exception, since it is known to invade not only the blood vessels but the bile ducts as well; tumor thrombi in the venous (Fig. 3.16) and biliary vessels (see Figs. 3.20, 3.21, 3.22) are pathognomonic for HCC. As a possible cause of pressure-induced malignant dilatation of intrahepatic bile ducts, its incidence is well above that of the (quite rare) true CCC (Fig. 3.17); however, in undifferentiated tumors even pathological histomorphology and/or cytomorphology will sometimes be unable to diagnose precisely whether one is dealing with HCC or CCC.

Fig. 3.16 Small hepatocellular carcinoma (x) invading a hepatic vein (y).

Fig. 3.17 Cholangiocellular carcinoma (x) with localized intrahepatic biliary obstruction (1) (segment II).

Gallstones. The primary cause of benign biliodynamic obstructions in the porta hepatis and the prepancreatic CBD is biliary calculi ( 3.2), which may differ significantly in terms of shape, size, and number. Gallstones at the hepatic duct confluence and in the CBD will be easier to detect by ultrasound the bigger they are and the more they are encased by fluid. In addition, “young” calculi made up of pure cholesterol ( 3.2c) display a higher impedance than old pigmented gallstones of low reflectivity ( 3.2 d). Direct detection of intrahepatic and common duct biliary calculi may also depend on the quality of the ultrasound platform employed and, primarily, on the diligence and experience of the sonographer. Sonographic visualization of small and minute gallstones (“microlithiasis”) ( 3.2e,h) is particularly challenging, since their passage through the papilla of Vater appears to be the underlying cause in most cases of so-called idiopathic pancreatitis. When considered in the context of a typical history and clinical findings, ultrasound can detect the presence of such microliths only indirectly by demonstration of the dilated bile ducts. Even in endoscopic retrograde cholangiopancreatography (ERCP) studies there is

sometimes lingering doubt about the possible presence of microliths, which may be screened out by the contrast agent. In these cases it pays to insonate the gallbladder immediately after endoscopic retrograde cholangiographic (ERC) cystography: these minute calculi may now be seen in the boundary layer between the (heavier) contrast agent and the (lighter) bile, although they may have escaped detection in previous studies despite patient positioning ( 3.2h). When dealing with small CBD calculi, posterior shadowing may facilitate detection much better than actually looking for the biliary calculus itself ( 3.2b,e).

Intraductal gallstones without any clinical or biochemical findings are quite rare and should always be treated by interventional endoscopy (while silent calculi in the gallbladder may be left alone).

A special case of calculus-induced inflammatory bile duct obstruction is Mirizzi syndrome, which can be difficult to visualize on ultrasound (Fig. 3.18).

Hemobilia. In most cases hemobilia is iatrogenic; because of the highly thrombolytic ac-

tivity of bile, biliary obstruction is the exception rather than the norm ( 3.2j).

Cicatricial stenosis. Only rarely is stenosis of the hilar biliary tree and common duct due to scarring the sole cause of the obstruction— most often this will be compensated for a considerable time, and additional factors, such as (micro-)lithiasis, are required for full-blown cholestasis to develop.

Because of their propensity for scar contraction, bilioenteric anastomoses may, however, decompensate without any additional lithic obstruction. These strictures are too short to be amenable to direct sonographic visualization.

Vascular causes. Intramural venous malformations have been described as a vascular cause underlying common duct obstruction.

Lymph node enlargement. Differential diagnosis should always include mechanical cholestasis by lymph node enlargement, no matter what the etiology (Fig. 3.19).

Fig. 3.18 a and b Mirizzi syndrome with cholecystolithiasis in typical infundibular position (x), with hydrops and inflamed thickened wall (y) and biliary outlet obstruction

(1).

Malignant Tumors

Once again, when viewed in the direction of bile flow, malignant obstruction at the level of the hilar hepatic confluence or the prepancreatic common duct is due to CCC of the Klatskin type, and in the case of CBD involvement it is the invasive carcinoma of the gallbladder or HCC infiltrating the biliary tree (Figs. 3.20, 3.21, 3.22). Most of these masses are isoechoic with the adjacent hepatic parenchyma and their only evidence is obstruction of the biliary vessels resulting in bile duct dilatation.

Cholangiocellular carcinoma of the Klatskin type, obstructing just one of the two hepatic ducts, is characterized by the difference in echogenicity of the two hepatic lobes, which

Classification of Klatskin Tumors

Klatskin tumors is a collective term for bile duct adenocarcinomas located at the bifurcation of the hepatic duct. They were subdivided into three types by Bismuth and Corlett in 1975, modified to four types.6 Type I tumors involve the common hepatic duct, with no involvement of the right and left secondary ducts. Type II tumors involve

is due to the different amounts of fluid in the parenchyma.

the hepatic duct bifurcation, without involving the secondary intrahepatic ducts. Type III tumors involve the hepatic duct bifurcation, infiltrate the common hepatic duct, and also involve the right (IIIa) or left (IIIb) hepatic ducts. Type IV tumors involve second-order bile ducts. The different types are easily identified by ultrasound.