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End-Stage Primary Sclerosing Cholangitis: CT Findings of Hepatic Morphology in 36 Patients¹

¹ From the Department of Radiology, University of Pittsburgh Medical Center, Pa. Received June 1, 1998; revision requested August 4; revision received August 18; accepted October 20. Address reprint requests to G.D.D., Department of Radiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78284-7800.

	Abstract

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
PURPOSE: To determine if there is a significant difference in the hepatic morphology depicted on computed tomographic (CT) scans in patients with end-stage cirrhosis caused by primary sclerosing cholangitis versus that in patients with end-stage cirrhosis caused by other factors.

MATERIALS AND METHODS: The frequency of five morphologic findings of the liver parenchyma and two intrahepatic biliary findings identified on CT scans in 36 patients with end-stage cirrhosis caused by primary sclerosing cholangitis were compared with the frequency of the same findings in 472 patients with end-stage cirrhosis caused by other factors. The morphologic findings were lobulation of the liver contour, atrophy of the lateral or posterior hepatic segments, hypertrophy of the caudate lobe, and pseudotumor of the caudate lobe. Lobulation, atrophy, and hypertrophy were subclassified as mild-moderate or severe. The biliary findings were ductal dilatation and calculi.

RESULTS: Each of the 11 findings occurred more frequently (P < .05) in patients with primary sclerosing cholangitis than in the other 472 patients. Six findings occurred more frequently (P < .05) in patients with primary sclerosing cholangitis than in patients with cirrhosis caused by any other single agent.

CONCLUSION: There is a significant difference in the hepatic morphology observed in patients with primary sclerosing cholangitis–induced end-stage cirrhosis versus that in patients with end-stage cirrhosis of other causes.

Index terms: Cholangitis, 76.288 • Liver, cirrhosis, 76.794 • Liver, CT, 76.12112

	Introduction

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
There have been numerous publications (1–3) in the medical literature on the computed tomographic (CT) appearance of primary sclerosing cholangitis; however, nearly all have focused solely on the appearance of the bile ducts. In our clinical practice and in an ongoing imaging-pathology correlation study (authors' data) of numerous patients with end-stage cirrhosis, we have identified several morphologic changes of the liver that occur more frequently in patients with end-stage cirrhosis caused by primary sclerosing cholangitis than in patients with cirrhosis caused by other factors. In this study, we present the spectrum of these findings as depicted by CT and analyze their frequency in 36 patients with end-stage cirrhosis caused by primary sclerosing cholangitis versus that identified in 472 patients with end-stage cirrhosis caused by other factors.

	MATERIALS AND METHODS

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
From August 1990 to October 1993, we performed a prospective correlation of pretransplantation hepatic CT scans with examinations of fresh explanted livers from approximately 700 hepatic transplant recipients. From this database, we selected at random approximately 500 patients with cirrhosis to serve as the cohort for a study of the imaging aberrations that occur in different types of cirrhosis. On the basis of the availability of film hard copies for rereview, this cohort ultimately consisted of 508 patients (311 male patients, 197 female patients; age range, 15–76 years; mean, 50 years). The causes of cirrhosis in these patients are listed in Table 1. Thirty-six of these patients (30 male patients, six female patients; age range, 16–76 years; mean, 50 years) with a clinical and pathologic diagnosis of primary sclerosing cholangitis are the primary focus of this article. The remaining 472 patients served as a control group.

The CT scans were obtained with 9800 or Advantage scanners (GE Medical Systems, Milwaukee, Wis) by using 120 kVp, 200–300 mA, 5- or 10-mm collimation, and 5–10-mm scan intervals. CT scanning performed with the use of intravenously administered contrast material was started at the dome of the right hemidiaphragm 40 seconds after the initiation of a 2 mL/sec injection of 150 mL of either Conray-60 (iothalamate meglumine; Mallinckrodt, St Louis, Mo) or Isovue 300 (iopamidol; E. R. Squibb, New Brunswick, NJ).

Immediately following transplantation, the resected livers were sectioned in the transverse plane at approximately 1-cm intervals. The CT images were directly correlated with the freshly sectioned livers. The liver specimens were examined for abnormalities identified on the CT images, and the CT images were reviewed for abnormalities identified in the liver specimens. Specimens with focal and diffuse abnormalities were submitted for histologic evaluation. An investigator (G.D.D., R.L.B., J.H.O., or M.P.F.) present at the specimen cuttings documented all gross pathologic and imaging findings on standardized work sheets.

After the final pathology reports had been rendered, the CT scans from the 508 patients were reread and were correlated with the original pathology work sheets and final histologic diagnoses. At least two of the four authors were present at the readings. All recorded data represented a consensus, with differences in opinion resolved by majority rule (if a difference in opinion occurred between two readers, it was resolved by a third reader).

Each of the 508 CT studies was evaluated for the presence of multiple focal and diffuse morphologic abnormalities of the liver. On the basis of our prior clinical observations and trends that we observed during the course of the study, we chose to analyze the frequency of several specific findings in patients with cirrhosis caused by primary sclerosing cholangitis versus findings in those with cirrhosis caused by other factors. The findings were a lobular liver contour, atrophy of the lateral or posterior segments, hypertrophy of the caudate lobe, and a low-attenuation rindlike appearance of the right lobe in the presence of caudate hypertrophy that manifested as a pseudotumor.

The liver contour was characterized as lobular if it was deformed by more than one nodule greater than 3 cm in diameter. The severity of the lobulation was classified subjectively as mild-moderate (mild to moderate) (Fig 1) or severe (Fig 2). Atrophy or hypertrophy was localized according to hepatic segment and classified subjectively as mild-moderate or severe (Figs 3, 4). The presence of a low-attenuation rindlike appearance of the right lobe in the presence of a higher-attenuation and enlarged caudate lobe (pseudotumor) was assessed independently on CT scans obtained both before and after the administration of contrast material (Figs 5, 6).

View larger version (129K): [in this window] [in a new window]   Figure 1. CT image obtained in a 48-year-old man with primary sclerosing cholangitis shows moderate lobulation (arrows) of the hepatic contour.

View larger version (128K): [in this window] [in a new window]   Figure 2. CT image obtained in a 46-year-old man with primary sclerosing cholangitis shows severe lobulation (arrows) of the hepatic contour.

View larger version (129K): [in this window] [in a new window]   Figure 3. CT image obtained in a 76-year-old man with primary sclerosing cholangitis shows complete atrophy of the lateral segment of the left hepatic lobe just medial to a patent paraumbilical vein (arrow) and compensatory hypertrophy of the caudate lobe (arrowheads).

View larger version (133K): [in this window] [in a new window]   Figure 4. CT image obtained in a 56-year-old man with primary sclerosing cholangitis shows severe atrophy of the posterior segment (arrows) of the right hepatic lobe.

View larger version (116K): [in this window] [in a new window]   Figure 5a. Pseudotumor of the caudate lobe and biliary calculi in a 57-year-old man with primary sclerosing cholangitis. (a) CT image obtained without the use of intravenous contrast material shows moderate hypertrophy of the caudate lobe (straight arrows) and decreased attenuation of the surrounding right lobe (arrowheads). The difference in attenuation accentuates the caudate lobe, thus manifesting as a pseudotumor. There are also high-attenuation biliary calculi (curved arrows) present. (b) Photograph of a hepatectomy specimen cut in the same plane as that in which the CT image was obtained shows a difference in the appearance of the caudate and right lobal parenchyma. The redder caudate lobe (straight arrows) contains more hepatocytes and less fibrosis than the whiter right hepatic lobe (arrowheads). Biliary calculi (curved arrows) are visible within the bile ducts.

View larger version (79K): [in this window] [in a new window]   Figure 5b. Pseudotumor of the caudate lobe and biliary calculi in a 57-year-old man with primary sclerosing cholangitis. (a) CT image obtained without the use of intravenous contrast material shows moderate hypertrophy of the caudate lobe (straight arrows) and decreased attenuation of the surrounding right lobe (arrowheads). The difference in attenuation accentuates the caudate lobe, thus manifesting as a pseudotumor. There are also high-attenuation biliary calculi (curved arrows) present. (b) Photograph of a hepatectomy specimen cut in the same plane as that in which the CT image was obtained shows a difference in the appearance of the caudate and right lobal parenchyma. The redder caudate lobe (straight arrows) contains more hepatocytes and less fibrosis than the whiter right hepatic lobe (arrowheads). Biliary calculi (curved arrows) are visible within the bile ducts.

View larger version (133K): [in this window] [in a new window]   Figure 6a. Pseudotumor of the caudate lobe in a 55-year-old man with primary sclerosing cholangitis. (a) CT image obtained without the use of intravenous contrast material shows marked hypertrophy of the caudate lobe (arrows), which in combination with an adjacent lower-attenuation right hepatic lobe manifests as a pseudotumor. (b) CT scan obtained after the intravenous injection of iodinated contrast material shows loss of the attenuation difference between the caudate and right lobes.

View larger version (120K): [in this window] [in a new window]   Figure 6b. Pseudotumor of the caudate lobe in a 55-year-old man with primary sclerosing cholangitis. (a) CT image obtained without the use of intravenous contrast material shows marked hypertrophy of the caudate lobe (arrows), which in combination with an adjacent lower-attenuation right hepatic lobe manifests as a pseudotumor. (b) CT scan obtained after the intravenous injection of iodinated contrast material shows loss of the attenuation difference between the caudate and right lobes.

View larger version (125K): [in this window] [in a new window]   Figure 7. CT image obtained after the intravenous injection of iodinated contrast material in a 54-year-old woman with primary sclerosing cholangitis shows the spectrum of the severe liver changes that can occur in patients with this disease. They include severe caudate hypertrophy (solid straight arrows), marked atrophy of the lateral segment (upper arrowheads) and right lobe (lower arrowheads), biliary dilatation (curved arrows), and biliary calculi (open straight arrows).

	RESULTS

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
The frequency and statistical significance of the observations in patients with primary sclerosing cholangitis versus those in the other 472 patients, as well as those in the subgroup of patients without primary sclerosing cholangitis but with the same cause of cirrhosis and the highest frequency of the observed findings, are listed in Table 2. Each of the 11 observed findings occurred more frequently (P < .05) in patients with primary sclerosing cholangitis than in the other 472 patients. Six of the observed findings (mild-moderate lobulation, mild-moderate lateral segment atrophy, mild-moderate and severe caudate hypertrophy, caudate pseudotumor, and dilated ducts) occurred more frequently (P < .05) in patients with primary sclerosing cholangitis than they did in patients with cirrhosis caused by any other single agent. One of these, the low-attenuation rindlike appearance of the right lobe in the presence of hypertrophy of the caudate lobe (pseudotumor), was seen only on nonenhanced CT scans and only in patients with primary sclerosing cholangitis.

	DISCUSSION

TOP Abstract Introduction MATERIALS AND METHODS RESULTS DISCUSSION References

 
Primary sclerosing cholangitis is a chronic idiopathic inflammatory process of the bile ducts that occurs in association with inflammatory bowel disease. The process causes multifocal strictures of the biliary tree (5–7). On CT scans, this process is depicted as scattered, dilated intrahepatic ducts with no apparent connection to the main bile ducts (1–3). The multicentric nature and chronic obstruction of the bile ducts leads to cirrhosis in many patients.

To date, the imaging appearance of the nonbiliary hepatic morphology in patients with primary sclerosing cholangitis–induced cirrhosis has been described by using the typical findings of cirrhosis. These findings have included a nodular hepatic margin caused by variably sized regenerative nodules, bands or regions of confluent fibrosis, atrophy of the right hepatic lobe, and hypertrophy of the caudate lobe (8–11). Although there is considerable overlap in the morphologic changes of the liver that occur in patients with cirrhosis caused by different factors, some causes, such as Budd-Chiari syndrome, have unique morphologic changes (12). In a review of the literature, we could not find an imaging report of any unique morphologic changes of the liver associated with primary sclerosing cholangitis.

Our results show that the hepatic morphology in patients with primary sclerosing cholangitis–induced end-stage cirrhosis is significantly different from that seen in patients with end-stage cirrhosis caused by other factors (Table 2). Overall, the liver in patients with primary sclerosing cholangitis–induced end-stage cirrhosis is markedly deformed. The contour is grossly lobulated. Instead of the lateral segment hypertrophying as it does in most other forms of cirrhosis, it and the posterior segment atrophy. The caudate lobe hypertrophies in nearly every patient (98%), whereas in other forms of cirrhosis, caudate hypertrophy is much less common (36%). The net effect is the creation of a clearly abnormal rounded, lobulated organ (Figs 1 –7).

In addition, many of the livers exhibit a low-attenuation rindlike appearance of the right lobe surrounding the hypertrophied caudate lobe. This rind accentuates the hypertrophied (and higher-attenuation) caudate lobe, thus creating the effect of a pseudotumor (Figs 5 –7). Our findings regarding the intrahepatic biliary tree are similar to those previously reported (5–7), namely, a substantial number of patients had scattered, dilated intrahepatic bile ducts with no apparent connection to the main bile ducts (Figs 1, 3, 6, 7), and a substantial number had intrahepatic biliary calculi (Fig 5).

All of the changes that we identified in patients with primary sclerosing cholangitis are most likely the result of the chronic, multifocal obstruction of intrahepatic bile ducts that occurs in primary sclerosing cholangitis. The parenchymal atrophy occurs proximal to chronically obstructed bile ducts and is a sequela of parenchymal necrosis and fibrosis (13). The regional parenchymal hypertrophy occurs in response to the diminished hepatic function that accompanies the parenchymal atrophy (13,14). The hypertrophy likely occurs in areas with absent or less severe biliary obstruction.

In our series, the caudate lobe was the most frequent region of hypertrophy; caudate hypertrophy was present in 98% of the patients with primary sclerosing cholangitis. This implies that the bile ducts of the caudate lobe appear to be spared or less affected in some patients with primary sclerosing cholangitis. There is a potential explanation for this phenomenon. It has been reported (15) that the most severely affected segments of the biliary tree in primary sclerosing cholangitis are the main right and left bile ducts. The bile ducts of the caudate lobe drain into the main right and left ducts immediately before the confluence of the right and left ducts into the common hepatic duct (16). Thus, in patients with primary sclerosing cholangitis and caudate hypertrophy, the caudate ducts may drain freely into patent stumps of otherwise obstructed or severely diseased main right and left bile ducts.

The accentuated lobulation of the hepatic contour is the result of asymmetric atrophy and marked focal hypertrophy. The low-attenuation rindlike appearance of the right hepatic lobe in association with a hypertrophied and higher-attenuation caudate lobe is likely the result of different amounts of fibrosis and hepatic parenchyma in the two regions. The atrophic right lobe (parenchyma proximal to obstructed ducts) contains more fibrosis and is thus of lower attenuation than the hypertrophied caudate lobe. Biliary calculi develop in obstructed ducts as a consequence of biliary stasis and possible secondary infection (4).

Although most of the findings that we have identified occur more frequently in patients with primary sclerosing cholangitis–induced cirrhosis, some occur in patients with end-stage cirrhosis caused by other factors. The greatest frequency of overlap occurred in patients with either cryptogenic biliary cirrhosis or cryptogenic cirrhosis. The overlap in patients with cryptogenic biliary cirrhosis is easy to understand, as the cause of cirrhosis was biliary tract disease. The shared findings in patients with cryptogenic biliary cirrhosis included a lobular hepatic contour, intrahepatic biliary dilatation, and intrahepatic biliary calculi. The overlap in patients with cryptogenic cirrhosis is mostly insignificant; the only significant overlap was that of caudate hypertrophy. In these patients with caudate hypertrophy, the unknown cause of cirrhosis could have been biliary in origin or perhaps a missed case of Budd-Chiari syndrome.

It is interesting to note that there was no overlap in the hepatic morphology in patients with end-stage cirrhosis caused by primary sclerosing cholangitis and that in patients with end-stage cirrhosis caused by primary biliary cirrhosis. Although the main pathologic process in primary biliary cirrhosis is a global autoimmune destruction of the small and medium intrahepatic bile ducts, these patients do not develop biliary obstruction or any of the other unique morphologic findings detected in the livers of patients with primary sclerosing cholangitis.

There are a few limitations in our study. The random selection process that we used to obtain our patient cohort failed to include any patients with end-stage cirrhosis caused by Budd-Chiari syndrome (12) or Alagille syndrome (authors' data). Both of these syndromes are known to cause at least some of the findings that we identified in patients with primary sclerosing cholangitis. The absence of patients with these syndromes in our study prevents us from making any statements regarding this potential overlap. In addition, there was a fairly long time between obtaining the pretransplantation CT scans and transplantation in some patients. This interval could have introduced undetected discrepancies between the CT findings and the pathologic specimens. However, of the variables that we evaluated, all are typically caused by a chronic process and are unlikely to have changed much during the delay between imaging and transplantation.

In conclusion, we have identified a spectrum of morphologic changes of the liver that occur statistically more frequently in patients with primary sclerosing cholangitis–induced end-stage cirrhosis than in patients with end-stage cirrhosis caused by other factors. Although there is considerable overlap in the hepatic morphology in patients with end-stage cirrhosis of various causes, the identification of the combination of morphologic findings that we described and the known ductal abnormalities of primary sclerosing cholangitis allow one to strongly suggest primary sclerosing cholangitis as the cause of the cirrhosis. Furthermore, the pseudotumor of the caudate lobe in these patients should be recognized as such and not misinterpreted as neoplasm.

	Footnotes

 
Author contributions: Guarantors of integrity of entire study, G.D.D., R.L.B.; study concepts and design, G.D.D., R.L.B.; definition of intellectual content, G.D.D., R.L.B.; literature research, G.D.D.; data acquisition, J.H.O., M.P.F.; data analysis, G.D.D.; statistical analysis, G.D.D.; manuscript preparation and editing, G.D.D.; manuscript review, G.D.D., R.L.B., J.H.O., M.P.F.

	References

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This Article Abstract Figures Only Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dodd, G. D. Articles by Federle, M. P. Search for Related Content PubMed PubMed Citation Articles by Dodd, G. D., III Articles by Federle, M. P.