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Gastrointestinal Imaging |
1 From the Departments of Radiology and INSERM Unité 773 CRB3 (V.V., A.H.), Hepatology and INSERM Unité 773 CRB3 (B.C., A.P., D.C.V.), and Anatomic Radiology (D.C.), Assistance Publique des Hôpitaux de Paris (APHP), Hôpital Beaujon, 100 bld Général Leclerc, 92110 Clichy, France; and Department of Hepatogastroenterology, Fédération Digestive, CHU Purpan, Toulouse, France (C.B.). Received July 2, 2005; revision requested September 2; revision received September 12; accepted October 14; final version accepted January 9, 2006. Address correspondence to V.V. (e-mail: valerie.vilgrain{at}bjn.ap-hop-paris.fr).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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Materials and Methods: This study was institutional review board approved. Informed patient consent was not required. The computed tomographic (CT) results for 22 patients (14 male, eight female; mean age, 54 years) with cavernous transformation of the portal vein and no evidence of chronic liver disease at liver biopsy were retrospectively reviewed and compared with the CT results for 36 control subjects. Various morphologic changes in the hepatic lobes were qualitatively and quantitatively assessed by using the Student t test for unpaired data.
Results: Qualitative analysis revealed the atrophy-hypertrophy complex in most (n = 20, 91%) of the patients with cavernous transformation and in no control subjects. Atrophy of the left lateral segment and right liver lobe was seen in 16 (73%) and seven (32%) patients, respectively. Hypertrophy of the caudate lobe and liver segment IV was identified in 19 (86%) and 11 (50%) patients, respectively. All mean caudate lobe volume index values and mean caudate lobe–to–right lobe ratio values were significantly greater (P < .05) in the cavernous transformation group than in the control group. The mean segment IV diameter was significantly greater (41.6 vs 28.1 mm, P < .001) in the patients with cavernous transformation. Hepatic nodules and hepatic contour nodularity were not seen in the patients with cavernous transformation.
Conclusion: The atrophy-hypertrophy complex is frequently observed in patients with cavernous transformation of the portal vein. Some findings, such as hypertrophy of the caudate lobe, mimic chronic liver disease or signs of portal hypertension, but left lateral segment atrophy and a normal or enlarged segment IV are distinctive findings of cavernous transformation.
© RSNA, 2006
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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However, investigators in a recent multisection multiphasic CT study compared pre– and post–portal vein embolization contrast material–enhanced CT findings and found peripheral atrophy in conjunction with increased late arterial enhancement in the same region (5). Although that study was substantially different from our current investigation in that interventional embolization was conducted for liver surgery, the results are very important: The authors concluded that the collateral central portal vein flow preserves the central morphology and that the arterial flow to the liver periphery does not provide adequate nutrients (5). The purpose of our study was to retrospectively evaluate the morphologic changes in the liver associated with CTPV.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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We identified 98 patients. Of these patients, 67 underwent CT and 39 underwent liver biopsy. Twenty-two patients (14 male, eight female; age range, 17–74 years; mean age, 54 years) who underwent both CT and liver biopsy with no evidence of extensive fibrosis, Budd-Chiari syndrome, or hepatoportal sclerosis or cirrhosis formed the CTPV group. Causes of CTPV were myeloproliferative syndrome in 11 patients; antiphospholipid syndrome in three; protein S deficiency in three; undetermined in two; and antithrombin 3 deficiency, prothrombin gene mutation, and Bacteroides-related sepsis in one patient each.
The initial diagnosis of CTPV was made at US (16 patients) and/or CT (eight patients). Sixteen patients were referred for imaging because of signs of portal hypertension (splenomegaly in six and gastrointestinal bleeding in 10 patients), and CTPV was fortuitously discovered in five other patients. One patient received a diagnosis at the time of acute portal vein obstruction (with abdominal pain as the first symptom). No patient had hepatitis B or C infection.
The mean interval between the diagnosis of CTPV and the CT examination was 35 months (range, 0–252 months). CT was always performed at the time of or after the diagnosis of CTPV. No patient underwent CT before CTPV was diagnosed. One patient underwent a first CT examination at the time of acute portal vein thrombosis and another CT examination 16 months later. Patients in the CTPV group had been referred for CT for evaluation of the severity of portal hypertension. Twelve (54%) patients had a history of gastrointestinal bleeding. Six had biliary symptoms, including acute cholecystitis, jaundice, and cholangitis. Upper gastrointestinal endoscopy was performed in 20 patients and revealed varices in 18 (90%) of them.
Liver biopsy was performed when blood test results could not exclude an underlying chronic disease. Liver biopsy revealed a normal liver in 16 patients and mild portal vein fibrosis without septa in six. The mean delay between CT and liver biopsy was 4 months (range, 0–132 months). Liver biopsy was performed after CTPV was diagnosed and before or at the time of CT. In 15 of the 22 patients, the interval between CT and liver biopsy was less than 3 years.
Control Group
The control group consisted of 36 consecutive patients (19 men, 17 women; age range, 23–79 years; mean age, 50 years) who underwent abdominal CT for indications other than liver disease. Patients were excluded if liver neoplasms other than cysts were present. The control subjects were recruited during a 2-month period—January through February of 2005.
CT Technique
Our study was retrospective, and the CT examinations were performed by using different scanners (CT Twin Flash, Marconi Medical Systems, Haifa, Israel; CT LightSpeed, GE Healthcare, Milwaukee, Wis) and varying helical CT techniques. In general, nonenhanced examinations were performed with 5–10-mm collimation. During the study period, our standard dynamic CT protocol involved the use of a total of 120–150 mL of nonionic intravenous contrast material (350 mg of iodine per milliliter) administered by using a power injector at 3 mL/sec. In all patients, portal venous phase CT images were acquired 60–80 seconds after contrast material injection with a collimation of 5 mm, a pitch of 1.0–1.4, and reconstruction intervals of 5 mm. In six patients in the CTPV group, hepatic arterial phase data also were acquired.
Image Analysis
The CT images obtained in the control and CTPV group patients were intermingled, randomized, and then presented to reviewers. Two radiologists with 5 (A.H.) and 18 (V.V.) years experience in hepatic imaging independently and without knowledge of patient status analyzed the CT data by using film hard-copy images.
Qualitative Analysis
The reviewers evaluated the images qualitatively for the presence of morphologic changes in the liver (atrophy or hypertrophy of liver segments according to Couinaud classification system), features suggesting chronic liver disease or portal hypertension (liver surface nodularity, ascites, varices, or collateral vessels), bile duct dilatation, portal vein thrombosis, and CTPV. Splenic and mesenteric veins also were evaluated.
Quantitative Analysis
The following quantitative measurements were obtained: three axis measurements of the caudate lobe and the caudate lobe–to–right lobe ratio (CL/RL), the transverse diameter of liver segment IV, and the longitudinal axis of the spleen. The portal venous phase CT images obtained after contrast material administration were chosen for these measurements.
The caudate lobe was measured by using the methods described by Harbin et al (6), Awaya et al (7), and Okazaki et al (8). The CT image obtained at the highest level before either branching of the main portal vein or cavernous transformation at the hilum of the liver was chosen. The anteroposterior width of the caudate lobe to the left of the inferior vena cava and the craniocaudal extent of the caudate lobe were measured. Furthermore, the CL/RL, modified CL/RL, and caudate volume index were calculated according to the methods of Harbin et al (6), Awaya et al (7), and Okazaki et al (8), respectively.
Measurement of CL/RL
A line (line 1) was drawn parallel to the midsagittal plane through the right lateral wall of either the main portal vein or the CTPV. A second line (line 2) was drawn through the most medial margin of the caudate lobe parallel to line 1. A third line (line 3) was drawn perpendicular to lines 1 and 2, midway between the main portal vein and the inferior vena cava. The distances along line 3 between lines 1 and 2 (caudate lobe) and between line 1 and the right lateral margin (right lobe) were measured and expressed as the CL/RL (6).
Modified CL/RL
All lines were constructed as before (to measure CL/RL), with the exception that line 1 was drawn through the right lateral wall of the bifurcation of the right portal vein rather than the bifurcation of the main portal vein. In this case, the distances along line 3 were measured and expressed as the modified CL/RL (7).
Caudate Volume Index
The caudate volume index (8) was calculated as the product of the three diameters of the caudate lobe, with the transverse diameter chosen according to the method of Harbin et al (6). The transverse diameter of segment IV was adapted from the landmarks defined by Lafortune et al (9): For the gallbladder and the ascending portion of the left portal vein, oblique scans should be obtained, and these are easily acquired at US but not at CT (9). Therefore, to measure the segment IV transverse diameter, the middle hepatic vein—which is also the boundary between the right and left liver lobes—was used instead of the gallbladder. For practical purposes, segment IV was measured in terms of the distance between the left side of the middle hepatic vein and the ascending portion of the left portal vein at the point where the left portal branch gives rise to the branch supplying segment IV. The line of measurement paralleled the anterior surface of the liver. The craniocaudal extent of the spleen was measured and considered to be enlarged when it was more than 12 cm in diameter (10).
Statistical Analyses
The interobserver variability of each measurement was assessed by using coefficients of variation (standard deviation divided by mean, times 100). Differences in mean measurements of the spleen, caudate lobe (ie, CL/RL, modified CL/RL, and caudate volume index), and segment IV diameter between the CTPV and control groups were analyzed by using the Student t test for unpaired data. P < .05 was considered to indicate a significant difference. Sensitivity, specificity, accuracy, and positive predictive values for the diagnosis of CTPV-associated morphologic changes in the liver were calculated by using the CL/RL, modified CL/RL, and mean segment IV diameter.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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In the CTPV group, left lateral segment atrophy was seen in 16 (73%) patients and right liver lobe atrophy was seen in seven (32%) patients, including five with atrophy of both the left lateral segment and the right liver lobe. Qualitative assessment of findings in the CTPV group revealed a normal-sized segment IV in 11 (50%), segment IV hypertrophy in 11 (50%), and caudate lobe hypertrophy in 19 (86%) patients (Figs 1 and 2).
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All CTPV group patients had thrombosis of the main portal vein and the right and left portal branches, and extension of the thrombosis to the splenic and/or superior mesenteric vein was seen in 16 patients with CTPV. CTPV with intrahepatic extension was observed in 11 patients, and CTPV extended to the splenic and mesenteric veins in the remaining patients with CTPV. In the CTPV group, three patients had gallbladder varices and three other patients underwent cholecystectomy.
Quantitative Results
The mean coefficient of variation for the liver measurements was low: 7% ± 10 (standard deviation). Since there was little interobserver disagreement among the measurements, the CT measurements averaged for the two observers were used for further analyses.
Mean CL/RL values for the control and CTPV groups were 0.373 ± 0.174 and 0.634 ± 0.169, respectively (P < .04). Mean modified CL/RL values for the control and CTPV groups were 0.680 ± 0.330 and 0.969 ± 0.231, respectively (P = .01). Mean caudate volume indexes for the control and CTPV groups were 36.5 ± 20.7 and 113.60 ± 68.8, respectively (P < .001).
In the CTPV group, the patients with minimal fibrosis (n = 6) and the patients with a normal liver (n = 16) were examined separately, and quantitative results showed no significant difference between the two cohorts. Also, results for the CTPV group patients in whom the CT–liver biopsy interval was more than 3 years were not markedly different from those for the CTPV group patients with shorter CT–liver biopsy intervals.
With use of the previously published criteria of a CL/RL of greater than 0.65 (5), the sensitivity, specificity, accuracy, and positive predictive values for the diagnosis of CTPV-associated morphologic changes in the liver were 50%, 100%, 81%, and 100%, respectively. With use of a modified CL/RL greater than 1.00, the sensitivity, specificity, accuracy, and positive predictive values were 59%, 97%, 83%, and 93%, respectively (6).
The mean segment IV diameter was 28.1 mm ± 4.4 in the control group and 41.6 mm ± 7.2 in the CTPV group (P < .001). With use of a segment IV diameter limit of 35 mm, the sensitivity of segment IV hypertrophy for the diagnosis of CTPV was 86%; the specificity, 94%; the accuracy, 91%; and the positive predictive value, 90%, according to our current study results.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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Some of the imaging findings observed in the CTPV group resembled those of cirrhosis: morphologic changes in the liver in 20 (91%), splenomegaly or history of splenectomy in 20 (91%), varices and collateral veins in 15 (68%), and ascites in five (23%) patients. However, four findings were atypical of cirrhosis: (a) Surface nodularity was observed in only two patients with CTPV. This finding is reportedly seen in 88% of patients with cirrhosis (11). (b) Left lateral segment atrophy was observed in the majority of patients with CTPV, unlike in patients with cirrhosis, in whom this segment is usually enlarged (12). (c) All but one patient with CTPV had a normal or hypertrophied segment IV, whereas a decreased segment IV diameter is frequent in patients with cirrhosis (9). (d) Biliary dilatation is very uncommon in patients with cirrhosis.
We identified caudate lobe hypertrophy in the CTPV group by comparing all of the measurements—CL/RL, modified CL/RL, and caudate volume index—in these patients with those in the control subjects. All mean values were different between the two groups. It is interesting that the values obtained in our control subjects were similar to the control subject values reported by Awaya et al (CL/RL, 0.373 and 0.433, respectively; modified CL/RL, 0.680 and 0.771, respectively) (7).
Furthermore, we found that the modified CL/RL had better sensitivity and accuracy than did the previously described CL/RL in the CTPV group. This finding is in agreement with that for the patients with cirrhosis in the Awaya et al study (7). Although caudate lobe volume indexes show differences between CTPV and control populations, CL/RL values are much more practical and can be obtained with only the measurements on one transverse view.
Caudate lobe hypertrophy occurs with many other conditions, such as cirrhosis (the most common), Budd-Chiari syndrome, end-stage primary sclerosing cholangitis, and congenital hepatic fibrosis (13–16). Among these conditions, Budd-Chiari syndrome is easy to differentiate from the morphologic changes associated with CTPV, because other imaging findings—such as absent or abnormal hepatic veins and hepatic vein collateral vessels—are associated and portal vein thrombosis is rare with this disease (14).
End-stage primary sclerosing cholangitis is more difficult to distinguish from CTPV-associated liver changes because both diseases may involve left lobe atrophy and biliary dilatation (4,15). However, some findings, such as marked liver deformity, caudate lobe pseudotumor, scattered ductal dilatation without connection to the main ducts, and intraductal calculi, are strongly suggestive of primary sclerosing cholangitis (15).
Congenital hepatic fibrosis also is difficult to differentiate from CTPV-associated liver changes, and CTPV has been reported in patients with this disease (16). However, various biliary and renal abnormalities have been observed with congenital hepatic fibrosis (17).
A normal (n = 3) or hypertrophied segment IV (n = 19) was a key finding in the patients with CTPV. It was surprising that the mean segment IV diameters were 28.1 and 41.6 mm, respectively, for the control and CTPV groups in our study and 43 and 28 mm, respectively, for the control and cirrhosis groups in the Lafortune et al study (9). The different measures in the control subjects might be explained by the imaging modality used: With US, the defined landmarks (left wall of gallbladder and ascending portion of left portal vein) are seen on oblique views, whereas in our study, the modified landmarks (middle hepatic vein and ascending portion of left portal vein) were analyzed on transverse CT views.
Thus, global analysis of the morphologic changes in the liver revealed that with CTPV, the central part of the liver (ie, segment IV and caudate lobe) becomes enlarged, whereas the peripheral part (ie, left lateral segment and/or right liver lobe) becomes smaller. Although these findings were striking in this study, the sensitivity of the CL/RL and the modified CL/RL were between 50% and 59%, with specificity of 97%–100%. The chosen measurements might not be optimal because the peripheral and central portions of the liver are not differentiated. New ratios such as the caudate lobe–left lateral segment ratio or the segment IV–left lateral segment ratio might be more accurate. However, the use of some of these ratios in patients with cirrhosis has been disappointing (18).
The configuration of the so-called atrophy-hypertrophy complex of the liver described in this study has been observed mainly with lobar or segmental impairment of bile flow or portal venous flow in rats (19). It is interesting that such a complex has also been observed in patients with a history of portal vein thrombosis and cavernous transformation, as seen in our study, and in patients who underwent portal vein embolization (5).
The reason why the right liver lobe and the left lateral segment become atrophic with CTPV cannot be elucidated on the basis of our current study findings. It can be speculated that their location far from the cavernous transformation leads to compromised portal venous flow. Impairment of the portal venous flow with arterial compensation is well demonstrated in patients with acute portal vein thrombosis: CT findings show increased enhancement of the periphery during the arterial dominant phase (20). It has been shown in rats that after ligation of one portal vein branch, the atrophy becomes progressive and may be profound (21). This atrophy is secondary to a reduction in cell volume and to hepatocyte cell death that is due mainly to apoptosis (21). The atrophy can also be explained by a reduction in hepatocyte volume, because hepatocytes constitute 80%–90% of the liver volume (21).
A recent CT study (5) revealed that peripheral enhancement during the late arterial phase after portal vein embolization was associated with parenchymal atrophy. This finding clearly demonstrates that there is an increase in hepatic arterial flow, but the associated relative increase in oxygen delivery is insufficient to prevent atrophy in the peripheral portions.
Similarly, it can be speculated that the reason why segment IV and the caudate lobe become hypertrophic with CTPV is related to their location next to the cavernous transformation, which results in maintained portal inflow, as has been seen at US with portoportal collateral circulation to the intrahepatic portal veins that develop after portal vein thrombosis (22). Moreover, anatomic factors may explain the hypertrophy: First, frequently there are multiple (average, five) portal branches of the caudate lobe, and some of them may arise from the portal vein itself (23). Second, according to Couinaud (24), the caudate lobe and segment IV develop late during the embryologic process and form a specific pedicle that is independent of the portal vein. Occasionally, the right gastric vein, parabiliary venous system, or duodenopancreatic arcades drain directly into these two segments. The hypertrophy of these segments may be similar to that observed after portal hepatectomy or contralateral portal vein embolization or ligation. This regeneration is mainly favored by liver growth factors (eg, human growth factor, epidermal growth factor, transforming growth factor-
, and insulin), some of which come from the portal blood.
It has been shown experimentally that the compensatory hyperplasia that follows portal branch ligation can be divided into an early phase that occurs independently of the reduction in liver mass and a late phase that is controlled by this reduction (25). Since our patients were not examined prospectively, we could not confirm the chronologic atrophy-hypertrophy sequence.
Our study had several limitations. First, few patients in the CTPV group underwent both arterial phase and portal venous phase CT. Therefore, we could not show that the morphologic changes were associated with CT attenuation differences in our series, but the hemodynamic and morphologic changes after portal vein embolization support the hypothesis that these changes are secondary to decreased or increased portal blood flow (5). Second, owing to the cavernous transformation in the CTPV group, errors in measuring the caudate lobe could have occurred because of the branching of the main portal vein being a landmark for the choice of the section. In difficult cases, the biliary confluence was the landmark because CTPV and biliary confluence are closely related. A third bias may have stemmed from the selection of patients in the CTPV group, because only patients who had undergone liver biopsy were included. This factor may have influenced the interpretation of the actual incidence of the morphologic alterations observed and could have caused an increase in the prevalence of the atrophy-hypertrophy complex in our study. However, we believed it was more important to exclude patients with cirrhosis who had portal vein thrombosis and patients with other vascular disease such as hepatoportal sclerosis, a condition often associated with portal vein thrombosis.
Six patients in this series had mild portal vein fibrosis without septa. Such fibrosis is never by itself associated with morphologic changes in the liver; thus, the changes observed were due to the presence of CTPV. Furthermore, comparison of these patients' quantitative results with those of the patients with a normal liver at histologic analysis revealed no significant difference. Finally, because this study was retrospective, the range of time between CT and liver biopsy was long for some patients. Although this factor may affect results, the patients in the CTPV group with long CT-biopsy intervals were not different from the other patients with CTPV. Also, we were unable to find any patients who underwent baseline prethrombosis CT, but one patient (Fig 2) underwent CT both at the time of and after the diagnosis of acute portal vein thrombosis. Comparison of the results of the two examinations revealed substantial morphologic changes, indicating that the changes in morphology were related to CTPV.
In conclusion, results of this study show that morphologic changes in the liver are observed in patients who have CTPV and normal or almost normal liver histologic findings. These changes represent an atrophy-hypertrophy complex, with atrophy of the left lateral segment and/or the right liver lobe and hypertrophy of segment IV and the caudate lobe. Recognizing the morphologic changes in the liver in patients with portal vein thrombosis and cavernous transformation is clinically important.
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ADVANCES IN KNOWLEDGE |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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FOOTNOTES |
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Abbreviations: CL/RL = caudate lobe–to–right lobe ratio • CTPV = cavernous transformation of the portal vein
Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, V.V., B.C.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, V.V., B.C., A.H.; clinical studies, V.V., B.C., C.B., A.P., D.C.; statistical analysis, V.V.; and manuscript editing, V.V., B.C.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
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