124 Section 2: Diagnostic and therapeutic approaches for the biliary tree and gallbladder
Figure 6.3 Cholangiogram in a patient with primary sclerosing cholangitis demonstrates multiple long strictures (arrows)of the right hepatic ducts with areas of focal dilatation between the strictures.
The primary differential diagnosis of PSC is diffuse scleros-ing carcinoma of the bile ducts, which represents less than 10% of bile duct carcinomas . Diffuse metastatic disease to the liver can cause multiple strictures of the intrahepatic ducts without biliary dilatation.
Primary biliary cirrhosis can mimic PSC and is seen in middle-aged women. Recurrent biliary infections related to gallstones or surgical stricture produce similar ﬁndings. Sclerosing cholangitis can also be iatrogenic, occurring after infusion of chemotherapeutic agents through the hepatic artery .
Cystic biliary disease
The etiology of cystic biliary disease is unclear (see Chapter 17). The disorder may be related to anomalous drainage of the pancreatic and biliary ducts and loss of the distal sphinc-ter mechanism . The most commonly used classiﬁ cation system for biliary cystic disease is the Todanimodiﬁ cation of the Alonso–Lej classiﬁcation. This system describes ﬁve types of cysts . Type I is the most common (80 to 90%) and is a single cystic dilatation of the common hepatic duct, common bile duct, or both. Type II is a diverticulum of the common bile duct and accounts for 3%. Type III is a cystic di-latation of the common bile duct in the wall of the duode-num, accounting for 5%. Type IV is made up ofmultiple cysts
involving the extrahepatic and/or intrahepatic ducts and
Figure 6.4 Multifaceted gallstones (arrows) appear as ﬁlling defects throughout the gallbladder and bile ducts.
accounts for 10% of cases. Type V is the variant known as Caroli’s disease. Type V is commonly associated with con-genital ﬁbrosis and cysts outside of the liver.
Complications include biliary obstruction, hepatic abscess, cholangitis, and bile duct cancer. The risk of bile duct cancer is increased 20 fold in this patient group. It is unusual for gall-stones to befound in association with biliary cystic disease.
Stones in the bile ducts either form there primarily or migrate there from the gallbladder. Primary bile duct stones are com-posed mainly of calcium bilirubinate. Bile stasis, dietary fac-tors, and bacterial or parasitic infection contribute to their formation, although their precise pathogenesis is unknown .
Single or multiple ﬁlling defects in the biliary tree charac-terize the presence of gallstones (Figs 6.4 and 6.5). Because contrast may obscure gallstones in the biliary tree, the con-trast should be diluted with normal saline for optimal visual-ization. Air bubbles or blood clots can obscure or mimic gallstones. Changing patient positioning while observing
the ﬁlling defects under ﬂuoroscopy helps to differentiate air
Chapter 6: Percutaneous biliary imaging and intervention 125
bubbles from stones. The air bubbles seek ananterior location and coalesce with one another.
Blood clots are more difﬁcult to differentiate from stones. Blood often enters the biliary tree during the puncture by the PTC needle. The suspected presence of blood clots requires repeating the cholangiogram in several days. The lytic prop-erties of bile and the passing of clots through the drainage catheter will have cleared blood clots from the biliary tree during that time.
Gallstones sometimes become impacted within the bile ducts. In this form, they can be mistaken for a polypoid tumor . Manipulation with a stone extraction basket or balloon may help differentiate between the two entities.
Mirizzi’s syndrome occurs when a gallstone lodges in the cystic duct or gallbladder neck and causes extrinsic compres-sion of the common bile duct. The compression usually occurs at the lateral aspect of the common bile duct . The patient develops jaundice because of common bile duct obstruction.
Figure 6.5 Multifaceted gallstones appear as ﬁlling defects above a benign anastomotic stricture (arrow) which developed in a patient who underwent biliary-enteric bypass for a laparoscopic cholecystectomy
bile duct injury.
Benign biliary strictures
More than 90% of benign biliary strictures are the result of surgical trauma, most commonly cholecystectomy (see Chapter 10) . Surgical strictures may be caused by duct li-gation or clipping, as is seen with emergency maneuvers to control massive bleeding. They can also result from thermal injury or injury to the small arteries that run within the com-mon bile duct wall . Transection of the duct interrupts the delicate arterial blood supply to the ducts. This may be the reason for ischemia and stenosis sometimes seen with bili-ary–enteric bypass operations (Fig. 6.6). Torsion of the bile duct may also occur following choledochojejunostomy
Figure 6.6 A benign focal anastomotic stricture (arrow) is present in a patient who underwent biliary–enteric bypass for pancreatic cancer.
126 Section 2: Diagnostic and therapeutic approaches for the biliary tree and gallbladder
Figure 6.7 (A)Postoperative cholangiogram following biliary–enteric anastomosis ina patient who underwent hepatic trisegmentectomy for metastatic colon cancer. Torsion has occurred at the anastomosis causing
obstruction (arrow) of the bileduct.(B)The biliary-enteric anastomosis
(arrow) is widely patent following revision of the anastomosis. (B)
Benign biliary strictures are a common problem following Malignant biliary strictures
orthotopic liver transplantation and occur in 3 to 22% of the patients (see Chapter). The etiology of anastomotic stric-tures in this group is not well understood. Postoperative ﬁbrosis and possibly ischemia are felt to be the causes. Pro-longed cold ischemic time, hepatic artery thrombosis, surgi-cal interruption of the peribiliary arterial plexus, and chronic rejection are potential causes of nonanastomotic biliary stric-tures in the transplanted liver  (Figs 6.8 and 6.9).
Postoperative benign strictures are usually short and have an abrupt change in caliber at the site of abnormality. There is ductal dilatation above the stricture. Intrahepatic abscesses may be present. A longer stricture should raise the suspicion of malignancy .
Nonsurgical causes of benign biliary obstruction include gallstone erosion into the main bile duct, pericholedochal abscess, blunt trauma, compression by pseudoaneurysm or
pseudocyst, and pancreatitis (Figs 6.10 and 6.11).
Distinguishing between malignant and benign strictures is difﬁcult. Although certain cholangiographic features de-scribed in this section may suggest the presence of a malig-nant stricture, these features are not speciﬁc. Clinical information and results of noninvasive radiologic tests, such as CT, MRI, and ultrasound, may help to conﬁrm a diagnosis of malignancy. CT, MRI, and ultrasound provide informa-tion about liver tissue surrounding the intrahepatic ducts and organs that surround the extrahepatic ducts. Results of these imaging modalities may be inconclusive, in which case a biliary biopsy may be helpful.
Cholangiocarcinoma is a slowly growing tumor that usu-ally presents in the sixth decade of life (see Chapter 20). Pa-tients present at a younger age if the tumor is found in association with other diseases that predispose to cholangio-carcinoma, suchas primary sclerosing cholangitis and chole-
Chapter 6: Percutaneous biliary imaging and intervention 127
Figure 6.8 Multiple focal ischemic strictures following orthotopic liver transplantation.
Figure 6.9 Ischemic stricture (arrowhead) involving a branch of the right hepatic duct following orthotopic liver transplantation for primary sclerosing cholangitis. There is gross dilatation of the bile ducts above the stricture and a large amount of debris within the ducts.
Figure 6.10 Obstruction of the common bile duct (arrow) secondary to chronic pancreatitis.
128 Section 2: Diagnostic and therapeutic approaches for the biliary tree and gallbladder
Figure 6.11 A pancreatic pseudocyst causes obstruction (arrow) of the common bile duct by extrinsic compression.
Cholangiocarcinoma presents as long or focal bile duct strictures. It spreads through local extension along the bile ducts or into the liver substance . The distal left or right main bile ducts and the common hepatic duct are the most common sites of involvement (Fig. 6.12). The tumor occurs at the junction of the left and right main hepatic ducts in 20.5 to 45.5%, the common bile duct in 33 to 40.5%, and the cystic duct in 6% . The differential diagnosis for intrahepatic ductal involvement of cholangiocarcinoma includes PSC and liver metastases (Fig. 6.13). Pancreatic carcinoma, ampulla-ry carcinoma, and chronic pancreatitis should be considered when the disease is conﬁned to the distal common bile duct.
Gallbladder carcinoma occurs more frequently in females and usually presents in the sixth and seventh decades of life (see Chapter 15). Choledocholithiasis is found in 80% of the patients . Direct extension of the tumor is common and sometimes causes jaundice by obstructing the common he-patic duct (Fig. 6.14). The other common form of tumor spread is lymphangitic.
Pancreatic carcinoma is the fourth leading cause of cancer death in the United States. It is the most common cause of malignant biliary obstruction in patients in their sixth de-cade of life or older. Pancreatic cancer causes compression and obstruction of the mid to distal common bile duct (Fig. 6.15). The contrast column passing through the tumor is typ-ically irregular, with a “rat tail” appearance. Narrowing is usually concentric. The site of obstruction may have a nipple-like appearance . The proximal bile ducts are usually dilated.
Most patients with ampullary carcinoma present in the
sixth and seventh decade of life. Ampullary carcinoma on
Figure 6.12 A cholangiocarcinoma causes a malignant stricture (arrows) of the common hepatic duct, left main hepatic duct, and the ﬁrst two divisions of the right hepatic duct.
cholangiography appears as an irregular ﬁlling defect located in the distal most portion of the common bile duct.
Metastatic disease from other organs causes biliary ob-struction when it involves the hepatic hilum, periportal lymph nodes, or peripancreatic lymph nodes (Figs 6.16, 6.17, and 6.18). Direct extension of tumor from adjacent organs, such as the stomach, may also cause biliary obstruction (Fig. 6.19). Tumor encasement can cause irregularity and dis-placement of the contrast column on cholangiography. Por-tal lymph nodes replaced by tumor may produce extrinsic compression of the contrast column.
Most bile leaks are iatrogenic and occur following cholecys-tectomy, partial liver resection, or orthotopic liver transplan-tation. Uncomplicated bile leaks, such as cystic duct leak and Duct of Lushka leak following cholecystectomy, usually respond to biliary decompression with an endoscopic stent
. More extensive bile duct injuries require surgical
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