Abdom Imaging 20:114-117 (1995)

Abdominal Ima g

�9 Springer-Verlag New York Inc. 1995

Intrahepatic bile duct dilatation secondary to hepatocellular carcinoma: CT features in 10 patients

P. Soyer, 1'* A. Sibert, 2 J. P. Laissy 2 1Department of Radiology, The Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21287-2180, USA 2Department of Radiology, H6pital Bichat, F-75877 Paris cedex, France

Received: 2 September 1993/Accepted: 17 October 1993

Abstract Background." To determine the computed tomographic (CT) features o f bile duct obstruction secondary to he- patocellular carcinoma (HCC). Methods: CT examinations of 10 patients (mean age, 58 years) with bile duct obstruction secondary to HCC were retrospectively reviewed. Resul t s : All tumors were intrahepatic. Eight tumors were wel l -del ineated and two were ill-defined. The largest diameters o f tumor ranged f rom 1 . 5 - 6 . 0 cm (mean, 3.6 cm). All tumors were hypodense before contrast and did not contain calcification. After con- trast, four tumors became hypodense , three were is- odense, and three were hyperdense to the liver. No tumor demonst ra ted encapsulat ion. Diffuse intrahe- patic bile duct dilatation was observed in seven pa- tients. One patient had extrahepat ic bile duct dilata- tion. Loca l ized bile duct dilatation was observed in three patients, in the hemi- l iver which conta ined the tumor. No tumor invaded the portal vein. Conclusion: Although rare, HCC should be included in the differential diagnosis o f bile duct obstruction. This diagnosis should be suggested in patients with bile duct obstruction when CT shows an associated intra- or ex- trahepatic mass. Our results suggest that HCC respon- sible for bile duct obstruction is remarkable for the ab- sence o f encapsulation.

Key words: Liver, CT s tudy- -Hepa toce l lu la r carci- n o m a - B i l e ducts obstruction.

* Present address: Department of Radiology, H6pital Foch, 40 rue Worth, BP 36, F-92151 Suresnes cedex, France.

Correspondence to: P. Soyer

Jaundice in association with hepatocellular carcinoma (HCC) is found in up to 40% of cases [1]. This com- plication is most ly attributable to underlying cirrhosis, or extensive tumor infiltration [2]. Intrahepatic bile duct dilatation secondary to hepatocellular carcinoma is a rare cause of jaundice, with an incidence o f 2 - 3 . 6 % [3, 4] and, thus far, only a small number of reports of HCC presenting with intrahepatic bile duct dilatation have been published [1, 2, 4 - 7 ] .

Cholangiographic findings obtained either by per- cutaneous or retrograde opacification have been previ- ously reported in radiologic literature [1, 4]. However, to our knowledge, computed tomographic (CT) features of bile duct obstruction due to HCC have never been published.

We report herein the results of CT examinations in 10 patients with bile duct obstruction due to a patho- logically documented HCC studied during a 3-year pe- riod.

Materials and Methods

Pat ient Populat ion

The study group included 10 non-Asian patients, nine men and one woman, aged 36-79 years (mean, 58 years). Signs and symptoms at presentation included epigastric pain (N = 6), jaundice (N = 7), fatigue (N = 5), and weight loss (N = 4). Eight patients had an underlying Laennec's cirrhosis with portal hypertension, and the other two patients had no history of hepatic disease. No patient had an acquired immunodeficiency syndrome nor was known to be in- fected with HIV virus. Hepatitis B virus surface antigen, as well as hepatitis C antibody, were negative in all patients. Laboratory in- vestigations showed abnormal liver function tests in all patients. The mean serum bilirubin level was 31 mol/L (range 21-80, normal 3- 20). The mean aspartamate transaminase level was 34 IU/L (range 30-75, normal 0-15) and the mean alkaline phosphatase was 147 IU/L (range 100-201, normal 20-75). Serum a-fetoprotein was

P. Soycr et al.: Bile duct obstruction secondary to HCC 115

>1000 ng/ml in seven patients. All patients included in this study were explored at the initial stage of their disease. No patient had previously undergone chemoembolization nor hepatic surgery for the treatment of their HCC.

The diagnosis of HCC was histologically confirmed in nine pa- tients either after ultrasonographically guided percntaneous biopsy of the tumor, using a 18-gauge biopsy needle system (ASAP, Medi-tech/ Boston Scientific, Watertown, MA, USA; or Sure-Cut, Nycomed-In- genor, Denmark) in six patients or after surgical resection of the tumor in the remaining three patients. In one patient, the diagnosis was con- firmed by the elevation of the serum a-fetoprotein. Bile duct dilatation was confirmed, either via percutaneous transhepafic cholangiography in four patients or via endoscopic retrograde cholangiography in six patients.

After the diagnosis of HCC with bile duct dilatation, three pa- tients had a surgical resection of their tumor, six patients were pal- liated with a prosthesis placed percutaneously in the biliary tract, and one patient had his tumor treated by percutaneous ethanol in- jection. Among the six patients who had a prosthesis, two had a balloon expandable metallic stent (Strecker; Medi-tech/Boston Sci- entific), three were treated by a self-expandable stainless prosthesis (Gianturco; Cook, Bloomington, IN, USA) and one by a plastic stent (Roche; Cook).

Imaging Technique

The CT examinations were performed on a CT Pace Plus (General Electric, Medical System, Milwaukee, WI, USA) in five patients, CE 10.000 (General Electric-CGR, Paris, France) in three patients, Somatom DRH (Siemens, Eflangen, Germany) in one patient, or Somatom Plus in one patient. CT scans were performed with 4- to 10-mm collimation at 4- to 10-ram intervals, respectively. Ionic in- travenous contrast material, ioxitalamate (Telebrix 38, Guerbet, Aul- nay-sous-Bois, France) or diatrizoate sodium meglumine (Urografin, Schering, Berlin, Germany) was administered into an antecubital vein, either manually or using an automatic injector. Seven patients received a bolus of 120 ml of contrast material and three patients had a biphasic injection (initially 50 ml at 2 ml/s and subsequently 130 ml at 1 ml/s). Precontrast CT images were obtained in all pa- tients.

Image Analysis

CT examinations were retrospectively analyzed in consensus by two readers, blinded to the results of other examinations. Intrahepatic bile duct dilatation was considered to exist in the presence of focal areas of low attenuation which were localized adjacent to the portal branches but did not surround them, on both unenhanced and en- hanced CT scans. Intrahepatic segmental location of bile duct dilata- tion was recorded and correlated with the segmental location of the tumor.

Morphologic features such as tumor location, size (when a lesion was not round, the largest diameter was measured), shape and con- tours, invasion of neighboring structures, enlarged lymph nodes, and pancreatic duct dilatation (pancreatic duct and pancreatic duct diam- eter >3 mrn were noted [8]. Calcifications were searched for and, when present, their size, location, and morphologic patterns were re- corded.

Special attention was given to dynamic CT features such as tumor enhancement, periarterial abnormalities, and venous stenosis or oc- clusion. Because of the retrospective nature of the study, tumor density was not obtainable for all tumors. Therefore, the density of the tumor was qualitatively assessed in relation to normal liver and was classified as hypodense, isodense, or hyperdense. Presence of lymph nodes were

searched for. Stenosis or occlusion of the portal vein was diagnosed based on CT signs.

Results

An intrahepatic tumor was observed in ten patients. A diffuse and ill-defined tumor was observed in two pa- tients (Figs. 1 and 2). A well-delineated tumor was seen in eight patients (Fig. 3A). The tumor was located in the right hemil iver in six patients, in the left hemiliver in three patients, in both hemilivers in one patient. The largest diameter of the tumor ranged from 1 .5 -6 .0 cm, with a mean value of 3.6 cm. All tumors were hypo- dense before intravenous administrat ion of contrast. Af- ter intravenous administrat ion of contrast, enhancement of the tumor was observed in all patients; four tumors became hypodense, three were isodense, and three were hyperdense to the liver. No tumor demonstrated periph- eral r im suggesting encapsulation. Before contrast, no calcification was depicted within the tumors.

Extrahepatic bile duct dilatation was seen in one pa- tient who had associated intrahepatic bile duct dilata- tion. A diffuse intrahepatic bile duct dilatation, involv- ing all the hepatic segments, was observed in seven pa- tients. Localized bile duct dilatation was observed in three patients, in the hemi-l iver which contained the tu- mor. Associated ascites or pancreatic duct dilatation was absent in all patients. One patient had non compressive metastatic lymph node at the porta hepatis (Fig. 3B). No patient had involvement of the portal vein by their tu- mor, and this was confirmed by arterial portography in seven patients.

Discussion

Intrahepatic bile duct dilatation secondary to HCC is a rare condit ion which can be diagnosed on CT [4]. This diagnosis can be suggested when intrahepatic bile duct dilatation is associated with a well-delineated intrahe- patic mass. However, as it was the case in two of our patients, our retrospective study demonstrates that this diagnosis may also be suggested even in the absence of a well delineated intrahepatic mass. Because differential diagnosis includes cholangiocarcinoma, percutaneous biopsy of the tumor remains useful if its result has im- pact on the pat ient ' s management . Prognosis in patients with intrahepatic bile duct dilatation is extremely poor [7]. This is due to the infiltration of the tumor through the liver resulting in a poor resectable rate. Therefore, the role of CT is to avoid unnecessary surgery in those inoperable patients and to plan the most appropriate ap- proach for biliary endoprosthesis placement.

The CT features of HCC in our series were unre- markable except for the absence of peri tumoral capsule.

116 P. Soyer et al.: Bile duct obstruction secondary to HCC

Fig. 1. A 42-year-old man with HCC. CT scan obtained after intra- venous administration of iodinated contrast shows intrahepatic bile duct dilatation in the right hemi-liver (arrow) with an ill-defined slightly hyperdense area (arrowheads).

Fig. 2. A 67-year-old man with HCC. CT scan obtained after intra- venous administration of iodinated contrast shows an ill-defined and heterogeneous hepatic mass (arrowheads) in the right hemi-liver. At this level, only a mild and localized intrahepatic bile duct dilatation is seen (arrow).

Fig. 3. A 64-year-old man with HCC. ACT scan obtained after intra- venous administration of iodinated contrast shows intrahepatic bile duct dilatation in the right hemi-liver (arrowheads) with a well-de- fined slightly hypointcnse intrahepatic mass (arrow) at the porta he- paris. B Another level shows a lymph node at the porta hepatis (ar- rowhead).

Encapsula t ion is a gross pattern which can be present in up to 78% of HCCs [10]. In our series this feature was absent in all 10 patients. The results of this retro- spect ive study suggest that lack o f encapsulat ion might favor ize bi le duct involvement .

A high f requency of tumor invasion of the portal sys tem has been repor ted in HCC with bi le duct dila- tation. In the series of Kubota et al. [4], 12 of 13 patients (92%) had portal vein involvement . In tile series by Ko- j i ro et al. [7], 21 of 24 patients (88%) had a tumor thrombus in the portal vein. This contrasts with our se- t ies, in which none o f our pat ients had tumor involve- ment of the portal vein.

Poss ible mechanisms o f bi le duct di latat ion in HCC are ( l ) extensive tumor infil tration o f the liver; (2) tumor invasion o f the ductal system; (3) lymph node com- press ion of extrahepat ic ducts; and (4) hemobi l i a with b lood clot format ion [4, 9].

To our knowledge , only four patients with fibrola- mel lar HCC respons ib le for obstruct ive j aundice have been repor ted in the l i terature [9, 11, 12]. In our current series, such a rare dist inct his tologic subtype of the usual HCC has not been found. It has been repor ted by Soyer et al. [12] that bi le duct di latat ion in f ibrolamellar HCC can be due to compress ion by metastat ic lymph nodes at the por ta hepatis. In our current series, nine of 10 patients had no lymph nodes at the porta hepatis, as depic ted on CT images, and the remain ing patient had lymph nodes at the porta hepat is that did not compress the main bi le duct. Therefore, it may be suggested that this mechan i sm was not a cause of bi le duct di latat ion in our patients.

In conclusion, this re t rospect ive s tudy highl ights that, a lbei t rare, HCC should be included in the differ- ential d iagnosis of bi le duct obstruction. This diagnosis should be sugges ted in patients with bi le duct obstruc- t ion when CT shows an associa ted wel l -de l inea ted or i l l -def ined intrahepat ic mass. Our results based on a l im- ited series o f pat ients suggest that HCC responsible for bi le duct obstruct ion might be remarkable for the ab- sence o f encapsulat ion.

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