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Clinical Observations |
1 Department of Radiology, Soonchunhyang University Hospital, 657 Hannam-Dong,
Youngsan-Ku, Seoul, South Korea 140-743.
2 Medical Imaging, Toronto General Hospital, University Health Network, Toronto,
ON, Canada.
3 Department of Diagnostic Radiology, College of Medicine, Ewha Womans
University, Seoul, South Korea.
4 Department of Diagnostic Radiology, Kangnam St. Mary's Hospital College of
Medicine, The Catholic University of Korea, Seoul, South Korea.
5 Department of Diagnostic Radiology, Asan Medical Center, Seoul, South
Korea.
6 Department of Radiology, Cornell University Weill Medical College, New York,
NY.
Received March 19, 2005;
accepted after revision June 13, 2005.
Address correspondence to J. H. Kim
(junghkim{at}hosp.sch.ac.kr).
Abstract
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CONCLUSION. CT findings of cholangiocarcinoma associated with recurrent pyogenic cholangitis are important in order to improve early diagnosis and proper treatment. Cholangiocarcinoma associated with recurrent pyogenic cholangitis is predominantly located in the atrophic hepatic lobes and in the hepatic lobes of biliary calculi and is associated with the narrowing or obliteration of the portal vein.
Keywords: biliary system • cancer • cholangiocarcinoma • CT • liver disease • pyogenic cholangitis
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In general, recurrent pyogenic cholangitis is a well-known risk factor for cholangiocarcinoma. The pathogenesis is incompletely understood. Some investigators report that chronic bacterial infection, bile stasis, and mechanical irritation from biliary calculi can lead to the development of mucosal adenomatous hyperplia and chronic proliferative cholangitis, which can undergo a progressive change to atypical epithelial hyperplasia and, ultimately, to cholangiocarcinoma [5-7].
There are many clinical reports about recurrent pyogenic cholangitis associated with cholangiocarcinoma. The incidence of cholangiocarcinoma associated with recurrent pyogenic cholangitis is reported to be 1.5-11% of patients with recurrent pyogenic cholangitis [5, 6, 8-21]. Cholangiocarcinoma associated with recurrent pyogenic cholangitis has a poor prognosis as a consequence of delayed diagnosis, a low diagnosis rate, and few curative resections [11-14]. It is difficult to accurately diagnosis cholangiocarcinoma associated with recurrent pyogenic cholangitis before treatment. The CT features of recurrent pyogenic cholangitis include bile duct dilation, bile duct stricture, biliary calculi, hepatic atrophy, portal vein obliteration, hepatic abscess, and biloma. These findings may lead to delayed diagnosis of cholangiocarcinoma associated with recurrent pyogenic cholangitis because they may obscure the underlying cholangiocarcinoma [3, 4].
Although there are some reports of CT findings for cholangiocarcinoma associated with recurrent pyogenic cholangitis in a small number of patients [22], to our knowledge there has not been a report of a large series addressing the use of CT when these two pathologies are coincident. Thus, this study assesses the CT features of cholangiocarcinoma associated with recurrent pyogenic cholangitis in 82 patients.
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Cholangiocarcinoma is classified into three types on the basis of anatomic location. Peripheral cholangiocarcinoma is defined as carcinoma arising from second-order or more distal branches of the intrahepatic ducts. Hilar cholangiocarcinoma is defined as carcinoma arising from one of the hepatic ducts or the bifurcation of the common hepatic duct. Extrahepatic cholangiocarcinoma is defined as carcinoma arising from an extrahepatic bile duct distal to the hilum.
There were 66 patients with peripheral cholangiocarcinoma, nine patients with hilar cholangiocarcinoma, and seven patients with extrahepatic cholangiocarcinoma. All 82 patients had acute cholangitis with abdominal pain, fever, or jaundice at the time of admission. All patients had been symptomatic from 4 to 30 years (mean, 9.5 years) and had had recurrent attacks of the disease on more than three occasions. Leukocytosis and hyperbilirubinemia were also present in 63 and 42 patients, respectively. Thirty-five of the 82 patients had a history of Opisthorchis sinensis infestation and five of the 82 patients had a history of Escherichia coli in bile cultures. Thirty-six patients had previously undergone cholecystectomy because of gallbladder stone.
Of these 82 patients, 53 underwent dual-phase CT and 29 underwent single-phase CT. There were 50 men and 32 women. Patient ages ranged from 30 to 72 years (mean, 56 years). The pathologic diagnoses were confirmed by surgical resection (n = 25), exploratory laparotomy (n = 7), percutaneous liver biopsy (n = 40), and percutaneous transhepatic choledochoscopy-guided biopsy (n = 10). Surgical procedures included right lobectomy (n = 5), left lobectomy (n = 14), and segmentectomy (n = 6). Serum for tumor markers, including carcinoembryonic antigen (CEA) and cancer antigen (CA) 19-9, were available for 53 patients. The normal value for CEA was less than 4 ng/mL; for CA19-9, it was less than 37 U/mL. CEA was elevated in 18 (34%) patients and CA19-9 was elevated in 29 (55%) patients. CEA values ranged from 6.51 to 83.1 ng/mL (mean, 41.5 ng/mL); CA 19-9 values ranged from 45 to 3,500 U/mL (mean, 655 U/mL).
Imaging
CT was performed with a 9800 Quick System (GE Healthcare), a HiLight
Advantage (GE Healthcare), or a Somatom Plus-S (Siemens Medical Solutions)
scanner. Each patient received 120 mL of contrast medium ([iopamidol] Iopamiro
300, Bracco; or [iopromide] Ultravist, Schering) by bolus injection in a
forearm vein at a rate of 3 mL/s. All patients ingested 1,000 mL of water
before scanning. Helical CT parameters included 8-mm collimation, table feed
of 10 mm, and reconstruction increments of 8 mm. Unenhanced CT scans were
obtained in all patients; and dual-phase CT scans, including hepatic arterial
and portal venous phases, were then obtained 35 and 70 seconds, respectively,
after initiation of the infusion. Single-phase CT scans were obtained 70
seconds after initiation of the infusion.
Analysis
CT findings were retrospectively analyzed independently by two
board-certified radiologists. We used a hard-copy system. When the reviewers'
interpretations differed, a third opinion was obtained. The radiologists'
experience with abdominal CT ranged from 5 to 15 years.
In cases of peripheral cholangiocarcinoma, the following imaging variables were analyzed: tumor size, number of lesions, contrast-enhancement patterns, intratumoral appearance, narrowing or obliteration of the portal vein, segmental atrophy, coincident biliary calculi, and other ancillary findings such as the presence of biloma or abscess.
In hilar cholangiocarcinoma and extrahepatic cholangiocarcinoma, imaging variables included the presence or absence of an ill-defined hypoattenuating mass in the hilum, enhancing intraductal mass, enhancing focally thickened biliary ductal wall, and narrowing or obliteration of the bile duct (Table 1). If a patient had multiple lesions, the largest mass was analyzed.
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In contrast-enhancement patterns, thick, lobulated contrast enhancement at the tumor periphery was diagnosed when the thickness was greater than 3 mm with a well-defined line at the margin of the mass. Ill-defined homogeneous enhancement was diagnosed when the margin of the mass could not be outlined. In intratumoral appearance, marked hypoattenuation was defined as a decreased attenuation similar to that of water but less than that of back muscle. Presence of a slightly hyperattenuated area was defined as slightly hyperattenuated area within the hypoattenuated mass. Septumlike linear structure was defined as a linear-enhanced line within the mass.
Narrowing of the portal vein was defined as a decreased diameter less than one third that of the main portal vein. Obliteration of the portal vein was defined as a vein being unapparent or unenhanced. Enhancing focally thickened biliary ductal wall was diagnosed when the thickness was greater than 5 mm.
For the variable CT findings in each patient, the interobserver agreement was evaluated using the kappa statistic. A kappa value less than 0.20 was considered poor; 0.21-0.4, fair; 0.41-0.60, moderate; 0.61-0.80, good; and 0.81-1.00 excellent. The incidence of cholangiocarcinoma was compared between atrophic lobe and nonatrophic lobes, between lobes with narrowing or obliteration of the portal vein and lobes with normal portal veins, and between lobes having biliary calculi and lobes without biliary calculi, using Fisher's exact test, after adjusting for the effect of clustering according to literature references [23, 24].
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Peripheral Cholangiocarcinoma
Sixty-six patients had peripheral cholangiocarcinoma. The size of the
masses as measured on CT was 20-85 mm (mean, 51.5 mm) in the largest
dimension. Five patients had multiple hepatic masses. The dominant mass was
located in the left lobe (n = 36), right lobe (n = 25), or
in both lobes (n = 5). Thin and lobulated contrast enhancement at the
tumor periphery was seen in 57 (86%) patients. The intratumoral appearance was
marked hypoattenuation in 63 (95%) patients and slight hyperattenuation in 50
(75%) patients (Fig. 1A,
1B,
1C).
Segmental atrophy was seen in 41 (62%) patients. Segmental atrophy of the liver was seen in the lateral segment of the left lobe (n = 21), posterior segment of the right lobe (n = 11), left lobe (n = 5), and anterior segment of the right lobe (n = 4). Among these 41 patients, 36 (88%) patients had a mass within the atrophic segment (Fig. 2A, 2B, 2C). The incidence of cholangiocarcinoma was greater in the atrophic lobe (88%; 36 of 41 atrophic lobes) than in the nonatrophic lobe (33%; 30 of 91 nonatrophic lobes) (p < 0.0001). All atrophic segments showed narrowing or obliteration of the portal vein. Radiographic changes of the portal vein, including luminal narrowing or obliteration, were seen in 60 (91%) patients. Narrowing or obliteration of the portal vein was seen in the right portal vein (n = 22) and the left portal vein (n = 38). Among these 60 patients, 50 (83%) had a mass within the lobe associated with narrowing or obliteration of the portal vein (Fig. 3A, 3B).
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Intrahepatic biliary calculi were seen in 39 (59%) patients. Intrahepatic biliary calculi was seen in the right intrahepatic bile ducts (n = 14), the left intrahepatic bile duct (n = 21), and both intrahepatic bile duct (n = 4). Among the 39 patients with intrahepatic biliary calculi, 26 (67%) had a mass within the same lobe. The incidence of cholangiocarcinoma was also greater in lobes having biliary calculi (67%; 26 of 39 lobes having biliary calculi) than in lobes without biliary calculi (43%; 40 of 93 lobes without biliary calculi) (p < 0.02). Biloma and abscess were seen in six and five patients, respectively. Three (50%) of six patients with biloma and two (40%) of five patients with abscess were correctly diagnosed.
Hilar and Extrahepatic Cholangiocarcinoma
Sixteen patients had hilar and extrahepatic cholangiocarcinoma. No patient
had multiple hepatic masses. Hilar cholangiocarcinoma presented as an
enhancing, focally thickened biliary duct in five (55%) patients, and as
narrowing or obliteration of the bile duct in all (100%) patients (Fig.
4A,
4B). Extrahepatic
cholangiocarcinoma presented as an enhancing, focally thickened biliary duct
in six (85%) patients, and narrowing or obliteration of the ductal lumen in
all (100%) patients. Segmental atrophy and narrowing or obliteration of the
portal vein was seen in three and five patients, respectively. Intrahepatic
biliary calculi were seen in four patients.
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Su et al. [6] report that cholangiocarcinoma associated with recurrent pyogenic cholangitis had a significantly worse survival rate than that of cholangiocarcinoma without recurrent pyogenic cholangitis. The 5-year survival rate was 42% in patients with cholangiocarcinoma without recurrent pyogenic cholangitis, which was significantly better than the 6% survival rate reported in those patients with cholangiocarcinoma associated with recurrent pyogenic cholangitis. These differences in survival rates may be attributed to delayed diagnosis, previous liver damage caused by long-standing cholangitis, the relatively fewer curative resections in cholangiocarcinoma associated with recurrent pyogenic cholangitis, and a lower diagnostic rate of radiologic studies.
The diagnostic rate of radiologic studies is reported to range from 0-42% [6, 10-14]. Various reasons are postulated for the lower diagnostic rate, including limitations of the imaging studies such as difficulty differentiating cholangiocarcinoma associated with recurrent pyogenic cholangitis from abscess or biloma, or occurrence of an infiltrative tumor, usually in a stricture segment [6, 13]. Because the radiologic findings for cholangiocarcinoma associated with recurrent pyogenic cholangitis are not well established, accurate preoperative diagnosis is usually difficult. In most patients, the diagnosis is made during surgery. Consequently, identifying established CT findings of cholangiocarcinoma associated with recurrent pyogenic cholangitis is important to improve early diagnosis and proper treatment.
In our study, cholangiocarcinoma associated with recurrent pyogenic cholangitis predominantly localizes in segments with atrophy and with narrowing or obliteration of the portal vein. Segmental atrophy was seen in 54% (44 of 82 patients), and narrowing or obliteration of the portal vein in 79% (65 of 82 patients). Segmental atrophy of the liver was predominantly located in the lateral segment of the left lobe (n = 21) and the posterior segment of the right lobe (n = 11), where intrahepatic ductal calculi usually occurred. This may be related to the more acute angulation of these ducts, resulting in less efficient drainage on this side of the biliary system. All atrophic segments showed narrowing or obliteration of the portal vein.
The pathogenesis of cholangiocarcinoma associated with recurrent pyogenic cholangitis is incompletely understood. Some investigators report that chronic proliferative cholangitis in the presence of biliary calculi can undergo progressive changes to atypical epithelial hyperplasia, which may progress to cholangiocarcinoma [5-9]. In our study, the coincident rate of peripheral cholangiocarcinoma in hepatic atrophy was 88% (36 of 41 cases), and that of peripheral cholangiocarcinoma in portal vein narrowing or obliteration was 83% (50 of 60 cases). Kubo et al. report [11] that portography might be useful for diagnosing cholangiocarcinoma associated with recurrent pyogenic cholangitis. In their report, the portal vein in the hepatic lobe with cholangiocarcinoma could not be seen in any of the five patients with cholangiocarcinoma associated with recurrent pyogenic cholangitis. Therefore, they insist that portal vein obstruction indicates deterioration of the hepatic tissue and strongly suggests the existence of cholangiocarcinoma. Although we do not have a pathologic correlation, portal vein obliteration and subsequent parenchymal atrophy can be a result of involvement of the portal vein by the tumor instead of occurring before the development of the tumor. In any event, there is high frequency of coexistence of the two events—cholangiocarcinoma and portal vein or parenchymal change—and one should look for the tumor carefully in the hepatic segment or lobe with portal vein obliteration and parenchymal atrophy.
In our study, intrahepatic biliary calculi were seen in 52% (43 of 82) of patients. Twenty-six (32%) patients had a mass within the same lobe. Su et al. [6] report that tumor and biliary calculi were closely related in 26 (96%) of 27 patients with cholangiocarcinoma associated with recurrent pyogenic cholangitis. In previous reports, biliary calculi were present in approximately 75-80% of cases of recurrent pyogenic cholangitis; in the remaining cases, the biliary tree was recurrently infected in the absence of calculi [1-4].
Complications of hepatolithiasis include abscess and biloma. It is also often difficult to differentiate between these benign lesions and cholangiocarcinoma [11, 13]. Kubo et al. [11] report that 50% (five of 10) of their patients with cholangiocarcinoma associated with hepatolithiasis were initially diagnosed as having hepatolithiasis with liver abscess or cholangitis. These findings may lead to delayed diagnosis of cholangiocarcinoma associated with hepatolithiasis. In our study, 50% (three of six) patients with biloma and 40% (two of five) patients with abscess were correctly diagnosed. Because of the difficulty differentiating between these benign lesions and cholangiocarcinoma, further prospective study is required to establish the differences between these lesions.
Our study has some limitations. First, the study was performed retrospectively without a control group. We did not evaluate the sensitivity and specificity of the observed CT findings to establish the diagnosis of cholangiocarcinoma associated with recurrent pyogenic cholangitis. Second, surgical correlation of recurrent pyogenic cholangitis with cholangiocarcinoma was not available for all patients. A prospective study with pathologic correlation is required to elucidate the pathogenesis of cholangiocarcinoma from recurrent pyogenic cholangitis. Third, we used thick collimation by using helical CT; if we had used thinner collimation by using MDCT, we would have increased the number of good results.
Despite these limitations, our study suggests several unique CT findings of cholangiocarcinoma associated with recurrent pyogenic cholangitis. We analyzed the relationship of cholangiocarcinoma, hepatic atrophy, and portal vein obliteration. The interrelationship of hepatic atrophy, portal vein obliteration, and cholangiocarcinoma in patients with recurrent pyogenic cholangitis, as evaluated by CT, is unknown. This significant correlation of cholangiocarcinoma, hepatic atrophy, and portal vein obliteration should be recognized because doing so improves the early diagnosis and proper treatment of patients with recurrent pyogenic cholangitis.
In conclusion, cholangiocarcinoma associated with recurrent pyogenic cholangitis is predominantly located in atrophic hepatic segments or lobes and is associated with narrowing or obliteration of the portal vein. In peripheral cholangiocarcinoma, it is almost always a markedly hypoattenuating mass with thin, lobulated contrast enhancement at the tumor periphery. Hilar and extrahepatic cholangiocarcinoma are most often accompanied by narrowing or obliteration of the bile duct with enhancing focal thickening. Correlation with clinical and laboratory findings is warranted because benign inflammatory processes can mimic malignancy.
Acknowledgments
We thank Bonnie Hami, University Hospitals of Cleveland, Cleveland, Ohio,
for her editorial assistance in the preparation of this manuscript and Jeong
Kon Kim, Asan Medical Center, University of Ulsan College of Medicine, Seoul,
Korea, for his assistance with statistical analysis.
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