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Gastrointestinal Imaging |
1 From the Department of Diagnostic Radiology and the Research Institute of Radiological Science, Yonsei University College of Medicine, YongDong Severance Hospital, 146-92 Dokok-Dong, Kangnam-Ku, Seoul 135-270, South Korea. Received July 14, 1999; revision requested August 25; revision received February 11, 2000; accepted March 30. Address correspondence to J.S.Y. (e-mail: yjsrad97@yumc.yonsei.ac.kr).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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MATERIALS AND METHODS: MR images in 25 patients with 38 small nontumorous arterioportal shunts verified with surgery or follow-up imaging were included in this study. The causes of arterioportal shunts were iatrogenic causes in 11 patients and/or cirrhotic changes in the remaining patients. Nonenhanced T1- and T2-weighted images and multiphase contrast material–enhanced dynamic images were retrospectively reviewed and compared with conventional hepatic arteriograms to determine the MR characteristics related to the focal hemodynamic changes.
RESULTS: On arterial-dominant–phase dynamic MR images, 29 (76%) of the 38 arteriographically suggested nontumorous arterioportal shunts displayed abnormal findings distinguished against the surrounding hepatic parenchyma, including wedge-shaped (n = 14), nodular (n = 9), or irregularly outlined (n = 6) areas of focal contrast enhancement. The signal intensity on nonenhanced T1- and T2-weighted images of the corresponding areas appeared unremarkable except for three wedge-shaped high-signal-intensity areas (three [8%] of 38) on T2-weighted images accompanied by prolonged contrast enhancement. Most (24 [83%] of 29) areas of abnormal signal intensity were located at the periphery of the liver parenchyma.
CONCLUSION: A small nontumorous arterioportal shunt should be considered one of the causes of focal parenchymal hyperperfusion abnormalities on contrast-enhanced dynamic MR images of the liver in the absence of abnormal signal intensity on static MR images.
Index terms: Liver, angiography, 761.1242 • Liver, cirrhosis, 761.794 • Liver, MR, 761.121412, 761.12143 • Shunts, arterioportal, 952.453, 957.453
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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As the use of dynamic MR imaging of the liver has become widespread, findings related to such shunts have inevitably shown up on MR images, and they can also be confused as a hypervascular tumor itself or a tumor-related condition. To our knowledge, the findings of small nontumorous arterioportal shunts revealed on state-of-the-art dynamic MR imaging studies have not yet been considered.
The purpose of this study was to determine retrospectively the MR imaging findings on contrast-enhanced dynamic MR images and on static T1- or T2-weighted images that were related to small nontumorous arterioportal shunts, as these shunts could be a pseudolesion mimicking a hypervascular tumor itself or a tumor-related shunt.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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Patients with hepatic arteriograms suggestive of nontumorous arterioportal shunts who were also examined with contrast-enhanced dynamic MR imaging (n = 28) were selected for this study. To accurately analyze the MR imaging findings directly related to the focal hemodynamic changes from a nontumorous arterioportal shunt, we excluded the images of three patients who had more than 3 months between arteriography and MR imaging, which is a long enough period for substantial changes including development of new tumors or aggravation of cirrhosis. Therefore, the images of 25 patients (19 men, six women; age range, 34–84 years; mean, 55 years) with one or more nontumorous arterioportal shunts were finally included in this study.
The possibilities of a hypervascular tumor itself or a tumor-related shunt were excluded by means of intraoperative ultrasonography (US) (n = 2) or follow-up (6–26 months; mean, 16 months) imaging including iodized oil–enhanced CT (n = 23), subsequently repeated hepatic arteriography (n = 8), or follow-up MR imaging (n = 4), as well as serial US in all patients. Lesions were defined as nontumorous arterioportal shunts if 3–4-week and further follow-up CT showed no focal and nodular iodized oil uptake after hepatic arteriography and complete washout of iodized oil in areas corresponding to the shunt, without any evidence of newly developing tumorous lesions on other images. In the 25 patients, the total number of shunts was 38 at hepatic arteriography, and the portal venous branches resulting from the shunts on the anteroposterior view were shorter than 1 cm in 12 shunts, 1–3 cm in 21 shunts, and longer than 3 cm in five shunts. The maximum interval between arteriography that depicted the shunt and MR imaging was 45 days (mean, 19 days).
Hepatic cirrhosis from viral hepatitis (n = 20) or longstanding viral hepatitis (n = 5) was diagnosed histologically (n = 3) or was suggested by the patient’s clinical course and radiologic findings (n = 22). Regarding other causative factors of the nontumorous arterioportal shunts, percutaneous interventional procedures were performed before arteriography in four patients, including 16-gauge gun needle biopsy of the main tumors or liver parenchyma (n = 3) or intrahepatic needling for ethanol-injection therapy of a small hepatocellular carcinoma (n = 1). One patient underwent partial hepatectomy for resection of localized hepatocellular carcinoma. Another six patients had histories of hepatic arterial chemoembolization on more than one occasion prior to the discovery of a shunt.
During hepatic arteriography that revealed the findings of a nontumorous shunt, nodular hepatocellular carcinomas with definite tumor vessels remote from the shunt were found in 20 patients (80%) and were treated by means of partial hepatectomy (n = 2) or selective transcatheter arterial chemoembolization (n = 18). Besides two patients treated with partial hepatectomy immediately after hepatic arteriography, about 2–3 mL of iodized oil was additionally injected into the feeding vessels for the shunts (proper hepatic artery or first branch of the lobar arteries including the shunt vessels) for future follow-up iodized oil–enhanced CT in 23 patients.
MR Imaging
Hepatic MR imaging was performed with use of a 1.5-T MR imager (Magnetom Vision; Siemens, Erlangen, Germany). A four-element phased-array multicoil was used to improve the signal-to-noise ratio for the fast imaging sequences, and all images were obtained in the transverse plane with a single acquisition during each breath-holding period. Automated shimming was performed for each examination to maximize magnetic-field homogeneity. The imaging protocol consisted of the following pulse sequences: (a) T2-weighted turbo spin-echo sequence (repetition time msec/echo time msec, 3,540–4,350/138 [effective]; echo train length, 29; section thickness, 8–10 mm; intersection gap, 1.6–2.0 mm; number of signals acquired, one; time of acquisition, 18–21 seconds; number of sections, 15) with and without fat saturation with an additional chemical shift–selective saturation pulse before the excitation pulse; (b) T1-weighted multiplanar spoiled gradient-echo sequence (113–130/4.1; flip angle, 80°; section thickness, 8–10 mm; intersection gap, 1.6–2.0 mm; time of acquisition, 16–18 seconds; number of sections, 14–17) with and without fat saturation with an additional chemical saturation prepulse; and (c) T1-weighed fat-saturated four-phased dynamic imaging at 10 seconds, 35 seconds, 60 seconds, and 5 minutes after a bolus injection of 0.1 mmol of gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) per kilogram of body weight with use of the same imaging technique and parameters as for b. For dynamic imaging, the contrast agent was manually injected into the antecubital vein, and the speed of injection was intended to approximate a rate of 3–4 mL/sec and was followed by saline flushing.
Image Analysis
For detection and characterization of small nontumorous arterioportal shunts, the static T1- and T2-weighted MR images and dynamic contrast-enhanced images were retrospectively reviewed by two radiologists (K.W.K., M.G.J.), by consensus, who were blinded to the hepatic arteriographic findings. When an area of unusual signal intensity distinguishable from the signal intensity of surrounding liver parenchyma was observed, the lesion location was recorded and consensus interpretation as a pseudolesion from focal hemodynamic variation, tumor, or equivocal was made for differential diagnosis of the lesions according to the following criteria. Subcapsular wedge-shaped homogeneous enhancement on early-phase dynamic MR images with normal static imaging findings with or without early appearance of the portal venous branch prior to parenchymal enhancement was categorized as a pseudolesion. Nodular enhancement or irregularly outlined inhomogeneous enhancement was interpreted as a tumor nodule with or without peritumoral enhancement from the tumor-related arterioportal shunt. Subcapsular homogeneous wedge-shaped enhancement with abnormal static imaging findings or irregularly outlined homogeneous enhancement with normal static imaging findings was categorized as an equivocal lesion.
Especially for interpretation of dynamic contrast-enhanced MR images, we regarded the arterial-dominant phase as a phase with contrast material enhancement of the hepatic artery and/or portal vein without enhancement of the hepatic veins. Finally, all MR images were directly compared to hepatic arteriograms to investigate the MR imaging features of the nontumorous arterioportal shunts with the aid of the arteriographic findings suggested by another radiologist (J.S.Y.) who performed hepatic arteriography.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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The 29 lesions could be localized as being roughly on segment 8 (n = 9), segment 7 (n = 3), segment 6 (n = 6), segment 5 (n = 5), segment 4 (n = 3), segment 3 (n = 2), or segment 2 (n = 1). Fourteen wedge-shaped, nine nodular, and six irregularly outlined areas of high signal intensity (0.7–4.5 cm in the longest dimension; mean, 1.9 cm) were found during the arterial-dominant phases (Figs 1–4). Ten (26%) peripheral subsegmental portal venous branches were also observed within or adjacent to the focal parenchymal enhancement (Fig 1). Among the 29 arterial enhancing lesions, the high signal intensity of 13 lesions (size range, 1.2–3.4 cm; mean, 2.2 cm) in 10 patients was maintained on the subsequent images obtained at 35 or 60 seconds after contrast material injection, with decreased lesion-to-liver contrast with marginal blurring. Another 16 lesions were no longer distinguished from the surrounding hepatic parenchyma during the late phases.
On the 5-minute delayed contrast-enhanced images, three wedge-shaped lesions (size range, 2.8–3.4 cm; mean, 3.2 cm) were still manifested as areas of high signal intensity in two patients, and they also readily corresponded to high-signal-intensity areas (three [8%] of 38) on T2-weighted images (Fig 2). The nonenhanced T1-weighted images were grossly normal without areas of increased or decreased signal intensity that corresponded to the location of the arteriographically demonstrated arterioportal shunts in all patients.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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Relying on several articles (5,11–13) on dynamic CT, we would expect that similar pseudolesions of temporarily increased parenchymal enhancement from these nontumorous shunts should be depicted on dynamic MR images. For the pseudolesions from focal perfusional variations, Ito et al (4,14) describe several mechanisms including decreased portal venous flow, siphoning effect of hypervascular tumor, aberrant right gastric venous drainage, aberrant cystic venous drainage, rapid drainage by subcapsular vein, percutaneous ethanol injection, percutaneous needle biopsy, and cirrhosis or unknown cause. In their article (4), however, seven (19%) of 36 lobar or segmental, eight (25%) of 32 subsegmental, and 23 (82%) of 28 subcapsular hyperperfusion abnormalities showed no additional cause except cirrhosis. We believe that small nontumorous arterioportal shunts originating from the cirrhotic change of the liver with or without previous chemoembolization could readily explain the cause of some hyperperfusion abnormalities in their cases.
Regarding the transient hepatic parenchymal enhancement in the early phases of dynamic MR imaging, normal findings on nonenhanced T1- and T2-weighted images may be helpful for the exclusion of tumor-related conditions for the larger subsegmentally wedge-shaped areas of homogeneously increased signal intensity. According to several articles (15,16), however, a number of small hepatocellular carcinomas are detected only on arterial-phase images as a transient focal enhancement without any distinguishable abnormalities on nonenhanced T1- and T2-weighted images, and some dysplastic nodules could be manifested as a nodular enhancement in a cirrhotic liver (17). Particularly in advanced cirrhosis, benign cirrhotic nodules, nodularity of the liver surface, and/or architectural distortion of the hepatic parenchyma can increase the chance of irregularly outlined inhomogeneous focal enhancement around the small shunt.
Furthermore, despite normal findings on static images, differentiation of the tumorous condition from nontumorous arterioportal shunt is not possible for the smaller, nodular or irregularly outlined, and/or inhomogeneously increased signal intensities on arterial-phase images. Moreover, typically a wedge-shaped lesion on an anteroposterior projection of a conventional arteriogram can also be manifested as a nodular lesion on the transverse MR image depending on its three-dimensional location. Like the results of this study, many areas of transiently increased signal intensity from the nontumorous shunts were suspected in the daily practice as being a hypervascular tumor itself or equivocal lesions due to their small size and atypical contours.
As pathologic proof of small arterioportal shunts is not possible in practical terms, exclusion of the possibility of tumor-related shunt has depended on serial follow-up imaging including iodized oil–enhanced CT, as in this study. Among the several mechanisms of arterioportal shunt related to hepatocellular carcinomas described by Okuda et al (6), the possibility of invasion of the portal venous branches by overt hepatocellular carcinoma resulting in a profound, proximal arterioportal shunt (10) could be excluded by the absence of mass lesions on various images. In our experience, transtumoral shunts related to the primary hepatocellular carcinomas were not accompanied by tumors that were too small to be seen on the various imaging studies (J.S.Y., unpublished data, 1999).
To the best of our knowledge, the incidence of arterioportal shunts related to dysplastic nodules or early well-differentiated hepatocellular carcinomas has not been clearly reported in the literature. Rapidly enhancing small cavernous hemangiomas often accompany the arterioportal shunt (18); however, these hemangiomas typically show high signal intensity easily detected on T2-weighted images. Retrograde or antegrade filling of the small portal venous branches by way of the peripherally embolized tumor nodules from liver-to-liver metastases of the adjacent overt hepatocellular carcinoma via the portal venous pathway is still problematic for the differential diagnosis of small nontumorous shunts. To rule out this condition, iodized oil infusion into the feeder vessels of the arterioportal shunt during transcatheter arterial chemoembolization for the primary tumors is still useful for the follow-up CT examination of patients with a high possibility of liver-to-liver metastases of hepatocellular carcinomas.
In an article by Yu et al (5), there was no focal abnormal signal intensity on conventional T1- and T2-weighted MR images that corresponded to the small nontumorous arterioportal shunts in 10 patients. Regarding the high-signal-intensity pseudolesion on arterial-dominant–phase dynamic MR images (4,14,19), no abnormalities were observed in the location corresponding to those of abnormalities on static T1-weighted images, as in our current study. On T2-weighted images, the signal intensity was unchanged in the majority of patients in the previous articles (4,14,19). In our current study, however, three arterioportal shunts in two patients depicted as wedge-shaped hyperperfusion abnormalities had slightly high signal intensity on T2-weighted images and showed prolonged enhancement on delayed contrast-enhanced images. According to the results of previous studies (4,20), high signal intensity on T2-weighted images and/or delayed contrast enhancement is associated with portal venous obstruction. If, for whatever reason, occlusion of the intrahepatic portal vein occurs, changes previously known as a Zahn infarct and now referred to as sinusoidal congestion and subsequent hepatocellular atrophy may result (21) and be presumed to be a cause of prolongation of T2 and delayed washout of contrast agent.
In this study, one patient with two wedge-shaped areas of abnormal perfusion had a history of partial hepatectomy, and the lesion was near the resection margin. We thought that the major traumatic event of hepatic resection could be associated with focal atrophic and fibrotic changes of the hepatic parenchyma near the resection margin accompanied by minor intrahepatic vascular insult. In this case, the small arterioportal shunts would not be the primary cause of abnormal signal intensity on the T2-weighted images and delayed contrast-enhanced T1-weighted images. For another patient with previous splenectomy, however, the cause of abnormal signal intensity on the static images was not clearly explained (Fig 2). An unusual condition of isolated nontumorous occlusion of the proximal segmental portal venous branch accompanied by a small arterioportal shunt on the distal subsegmental branch with or without any possible iatrogenic insult was only speculative.
In general, unlike a tumor-induced shunt, where the tumor or tumor thrombus completely blocks the portal flow and the peripheral blood flow is purely replaced by hepatic arterial flow, the area of nontumorous arterioportal shunt would be perfused by pulsed flow in the hepatic artery and would still be open to the steady hepatopetal flow of the portal vein. The amount of blood flow and perfusional pressure for the area of nontumorous arterioportal shunts would never decrease more than the usual condition; therefore, there can be less chance of secondary parenchymal changes as shown in the occlusion of the intrahepatic portal vein.
As our results indicate, not all shunts shown at arteriography cause abnormalities at MR imaging. The discrepancy between hepatic arteriography and MR imaging can be explained by several factors. First, the limited through-plane resolution of MR imaging and magnetic field inhomogeneity produced from the paired abdominal phased-array multicoils essential for enhancing the signal-to-noise ratio during fast MR imaging (22) may be a cause of low sensitivity, especially for the detection of smaller shunts. Small lesions located on the anterior or posterior portion near the surface coils could be overlooked by the high signal intensity of surrounding liver parenchyma.
Second, regarding the method of image acquisition, while serial imaging of more than one acquisition per second is used at hepatic arteriography to enable the visualization of thin shunt vessels and subsequent parenchymal staining, MR imaging is use to search for transient parenchymal enhancement secondarily caused by contrast agent flowing from the artery to the portal vein. Therefore, the shunt may not be visualized at MR imaging if the contrast between the shunt area and the surrounding liver parenchyma is not sufficient in the time required for filling the central k space (3 seconds) during the process of signal acquisition (23).
Peterson et al (15) reported the usefulness of acquisition of multiple arterial-phase images at dynamic MR imaging to minimize the chance of missing tumoral enhancement. As those researchers mentioned, however, their gradient-echo sequence with sequential acquisition without breath holding had some potential limitations of image degradation and section misregistration by respiratory motion. The spoiled gradient-echo sequence used in the dynamic MR imaging protocol during our study was a fast multisection technique acquired during a breath-holding period, which permits isolation of distinct enhancement phases, direct monitoring of the flow of the contrast medium, higher image quality, and no risk of image misregistration (16,23). One limitation of our sequence is the skip periods of 7–9 seconds between the inevitable phases of rebreathing, which has the potential for missing a transient enhancement during the short intervals. Earls et al (24) demonstrated the timing examination technique with the use of an MR-compatible automatic contrast agent injector to overcome the individual circulation time and optimization of arterial-phase imaging. This method might offer a chance to acquire optimal arterial enhancement of the small nontumorous arterioportal shunts; however, the exact effect of this method has yet to be determined.
Third, the intraarterial pressure during selective hepatic arteriography may be higher than the physiologic arterial pressure during dynamic MR imaging with intravenous administration of contrast material. Despite the nonvisualization of small arterioportal shunts on dynamic MR images, the higher intraarterial pressure during selective arteriography may induce a larger amount of shunt flow to be detected on arteriographic images.
Finally, there should be a fundamental limitation in the correlation of the cross-sectional MR images and anteroposterior projections at conventional arteriography for a precise one-to-one match. Regarding the findings of the early appearance of subsegmental portal venous branches during the arterial phase, which were found in only 26% of all arterioportal shunts at retrospective review, MR imaging is inferior to hepatic arteriography because of its limited spatial plane in routine imaging and the difficulty of optimal timing of sectional imaging for the visualization of temporary changes as mentioned above. Even in the arterial-dominant phase, the normal hepatopetal flow of contrast-enhanced portal venous blood can be partially mixed with the shunt flow after intravenous injection of contrast material. Sectional MR imaging could not reveal the flow direction in the portal venous branch, and we could not readily differentiate the shunt vessel from the normal portal venous flow in many cases.
This study had several limitations. As already mentioned, pathologic proof of small arterioportal shunts is not possible in practical terms. Although the majority of arterioportal shunts were of a nontumorous condition verified by means of follow-up imaging, there was the possibility of an extremely slow–growing small tumor or small portal venous thrombosis that was not detected with various imaging techniques during the follow-up periods. However, there was no way to verify the hidden tumorous condition except with further meticulous follow-up imaging in these patients with a high risk of newly developing hepatocellular carcinoma. We did not analyze the arteriographic findings of nontumorous hyperperfusion abnormalities detected with dynamic MR imaging but just analyzed the MR imaging findings for the arterioportal shunts demonstrated during hepatic arteriography. As well, there is the possibility of missing a small arterioportal shunt that was manifested as an abnormality on MR images but not detected on hepatic arteriograms. The visibility of small arterioportal shunts, which depend on the resolution capabilities of the arteriographic equipment, may be different in each institution. The amount, administration rate, or injection pressure of contrast material, which was not monitored in this study, may affect the amount of arterial blood flow through the arterioportal shunt and the extent of abnormal perfusion. Also, we could not readily estimate the prevalence of nontumorous arterioportal shunts.
In conclusion, despite the limitations of this study, we have demonstrated that small nontumorous arterioportal shunts can be one of the causes of pseudolesions, which result in various forms of focal enhancement in the hepatic parenchyma during the early phases of dynamic MR imaging of the cirrhotic liver with or without iatrogenic parenchymal injury. In the majority of patients, contrast enhancement during the arterial-dominant phase was found in the periphery of the liver parenchyma, and there were no abnormal signal intensity changes on static T1- and T2-weighted MR images.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
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