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1
Department of Radiology, Kyoto Prefectural University of Medicine, 465 Kajii,
Kawaramachi-Hirokoji, Kamigyo, Kyoto, 602-8566, Japan.
2
Department of Radiology, Akashi Municipal Hospital, 1-33, Takashyo, Akashi,
Hyogo, 673-8501, Japan.
3
Department of Radiology, Kyoto First Red Cross Hospital, 5-749, Motomachi,
Higashiyama, Kyoto, 605-0981, Japan.
Received October 9, 2000;
accepted after revision January 24, 2001.
Address correspondence to T. Yamagami.
Abstract
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SUBJECTS AND METHODS. In 34 patients who underwent CT during arterial portography to detect liver tumors, CT hepatic arteriography was performed before and after prostaglandin E1 injection via the superior mesenteric artery. Between each study, an interval of 10 minutes was set. On CT hepatic arteriogram obtained 15 to 20 sec after prostaglandin E1 injection, we distinguished changes in the size and shape of pseudolesions in the liver around the gallbladder as well as those of 42 tumorous lesions. In addition, we measured the change in CT attenuation of pseudolesions.
RESULTS. The size of the enhanced area of pseudolesions visible on CT hepatic arteriography decreased in 69% (25/36) of the pseudolesions after intraarterial prostaglandin E1 injection, with the mean diameter diminishing from 14.1 mm to 8.8 mm. Notably, in 11 pseudolesions, the enhanced area disappeared. In 86% (31/36), the CT attenuation decreased with the mean attenuation, diminishing from 211.3 H to 163.8 H. However, the size and shape of the enhanced area of tumorous lesions did not change.
CONCLUSION. The hemodynamic features of pseudolesions on angiographically assisted helical CT scans caused by cholecystic venous inflow are easily influenced by increased portal venous flow. Consequently, pseudolesions around the gallbladder usually can be distinguished from tumorous lesions by adding prostaglandin E1 injection via the superior mesenteric artery during CT hepatic arteriography.
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Nontumorous defects of portal perfusion in the liver adjacent to the gallbladder are among the most common pseudolesions seen on CT during arterial portography [5,6,7,8], the majority of which have been reported to be enhanced on CT hepatic arteriography [6,7,8]. Also, on dynamic CT or MR imaging studies, these pseudolesions occasionally show early enhancement [11,12,13]. Most of these pseudolesions can be differentiated comparatively easily from tumorous lesions not only by their location but also by their shape, which is typically described as wedge-shaped or serpiginous [5,6,7,8,9,10]. In some patients, however, they are round and difficult to differentiate from tumors [6, 8].
Such pseudolesions are believed to be caused by direct inflow of the cholecystic vein to the adjacent liver parenchyma [11, 14]. Previous surgical anatomical work described the veins of the biliary system as entering directly into the liver parenchyma and the peripheral portal branches as communicating with peripheral venous branches of the biliary system [15, 16]. This description led us to theorize that increased portal blood flow [17] and pressure [18] after injection of vasodilators, such as prostaglandin E1, via the superior mesenteric artery would influence the blood perfusion in the liver parenchyma in the area in which cholecystic veins enter directly. We conducted this prospective study to clarify the hemodynamic changes in the pseudolesions adjacent to the gallbladder that are shown after the increase in portal blood flow and to determine whether these pseudolesions could be distinguished from tumorous lesions on CT hepatic arteriograms by adding intraarterial infusion of prostaglandin E1 via the mesenteric artery.
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We enrolled patients who satisfied the following study admission criteria: no stenosis or obstruction of the portal vein or hepatic vein; fewer than five nondiffuse tumorous lesions; no stenosis of the superior mesenteric or celiac artery; no clinical findings of severe cirrhosis—type C of the Child-Pugh classification; no developed hepatofugal portosystemic venous collaterals or severely atrophic liver visible on diagnostic imaging; one hepatic artery supplying all hepatic segments; and no pathologic circulation in the liver, such as large arterioportal venous shunting. All patients underwent CT during arterial portography and CT hepatic arteriography to establish an angiographically derived diagnosis before surgical laparotomy or treatment using interventional techniques such as transcatheter arterial chemoembolization. The underlying diseases were hepatocellular carcinoma (n = 32 patients) and metastatic liver tumors from the breast (n = 1) and colon (n = 1). Informed consent from each patient and approval by the institutional ethics committee were obtained before the start of the study.
Imaging Methods
While each patient was in the angiography room, we inserted two 4- or
5-French angiographic catheters from the right inguinal region using the
Seldinger technique. The patient was transferred to the CT room after a test
injection of contrast medium confirmed that one catheter tip was located in
the superior mesenteric artery distal to the bifurcation of the inferior
pancreaticoduodenal artery and the other catheter tip in the common hepatic
artery. CT during arterial portography, CT hepatic arteriography, and CT
hepatic arteriography with prostaglandin E1 injection were done
sequentially in that order, with an interval of approximately 10 min set
between each of the three studies. CT during arterial portography imaging was
started 25-30 sec after the injection of 50-60 mL of 150 mgI/mL iopamidol
(Iopamiron; Schering, Berlin, Germany) at a rate of 2 mL/sec via the catheter
with its tip in the superior mesenteric artery. Vasodilators such as
prostaglandin were not used during CT during arterial portography.
CT hepatic arteriography was started 7 sec after the injection of 20-25 mL of iopamidol (150 mgI/mL) at a rate of 1 mL/sec via the catheter with its tip in the common hepatic artery.
For the CT hepatic arteriography with prostaglandin E1 injection, each patient was injected with 20 µg of prostaglandin E1 diluted with 10 mL of physiological saline via the catheter in the superior mesenteric artery. Fifteen to 20 sec after the injection of prostaglandin E1, iopamidol (150 mgI/mL) was injected via the catheter in the common hepatic artery in the same amount and at the same rate used for CT hepatic arteriography. We began CT scanning 7 sec after the injection of iopamidol. Scans from CT during arterial portography, CT hepatic arteriography, and CT hepatic arteriography with prostaglandin E1 injection were obtained during a single breath-hold with the entire liver imaged using a helical CT system (X Vigor Laudator; Toshiba Medical Systems, Tokyo, Japan) with settings at 120 kV and 190 mA. The beam width was 7 mm, table feeding speed was 7 mm/sec, and image reconstruction was performed with a width of 7 mm and a 512 x 512 matrix.
Parameters Investigated
Image analysis was performed by three radiologists experienced in abdominal
diagnostic imaging who reached their interpretations through consensus.
First, within the nontumorous defects of portal perfusion seen in the liver parenchyma around the gallbladder on CT during arterial portography, the areas with enhancement on CT hepatic arteriography were determined. Then, changes in the size and shape of the enhancement of such pseudolesions on CT hepatic arteriography after intraarterial prostaglandin E1 injection via the superior mesenteric artery were retrospectively investigated. In addition, CT attenuation was measured in the region of interest corresponding to the enhanced area on CT hepatic arteriography. CT attenuation on CT hepatic arteriography after prostaglandin E1 injection was measured using the same region-of-interest size and location as with CT hepatic arteriography without prostaglandin E1 injection. Changes in the CT attenuation in the region of interest were analyzed using a paired t test.
At the same time, changes in size and shape on CT hepatic arteriography of 42 tumorous lesions after prostaglandin E1 injection were evaluated. All tumorous lesions were pathologically proven by surgical laparotomy or percutaneous needle biopsy (hepatocellular carcinoma, n = 39 lesions; metastatic liver tumor, n = 3).
In 28 patients subjected to laparotomy with intra-operative sonography, pseudolesions were differentiated from tumorous lesions according to the intraoperative findings. Follow-up studies for the six patients not undergoing laparotomy were performed with other modalities such as sonography, CT, and MR imaging serially over more than 12 months, with no change noted in the findings of the pseudolesions.
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The enhanced size of 25 (69%) of these 36 pseudolesions decreased on CT hepatic arteriography after intraarterial prostaglandin E1 injection via the superior mesenteric artery (Fig. 1A,1B,1C). The mean maximal diameter of the nontumorous lesions on the largest transverse section after intraarterial prostaglandin E1 injection was 8.8 mm (Table 1). Notably, in 11 regions (segment V, n = 6; segment IV, n = 4; segment I, n = 1), the enhanced area disappeared. In none of the pseudolesions did the enhanced areas on CT hepatic arteriography show any increase in size after intraarterial prostaglandin E1 injection.
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In 31 (86%) of 36 pseudolesions in the liver parenchyma adjacent to the gallbladder, CT attenuation on CT hepatic arteriography decreased after intraarterial prostaglandin E1 injection. The overall change in CT attenuation after prostaglandin E1 injection varied from -247 to +14 H (mean, -47.6 H). In 15 lesions, the amount of decrease in CT attenuation was more than 50 H, a figure nearly equal to this mean value (Fig. 2A,2B,2C). The mean CT attenuation value on CT hepatic arteriography of all nontumorous lesions significantly decreased from 211.3 H (range, 98-446 H) to 163.8 H (range, 96-335 H; p<0.0001, paired t test).
As for tumorous lesions, the maximal diameter of the enhancement on CT hepatic arteriography ranged from 8 to 48 mm with a mean of 22.3 mm, with all of these lesions round or oval. There was no change in the size or shape of the enhanced area on CT hepatic arteriography after prostaglandin E1 injection in any of the 42 tumorous lesions (Fig. 3A,3B,3C).
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The main cause of these nontumorous defects seen on CT during arterial portography has been clarified radiologically as nonportal venous direct inflow from the cholecystic vein [11, 14]. Enhancement of these decreased areas of portal perfusion on CT hepatic arteriography has been explained by the relatively early venous return into these pseudolesions from the cholecystic arterial system compared with that of the surrounding liver parenchyma [11]. The most common sites of liver parenchyma receiving cholecystic venous inflow have been reported to be segments V and IV, followed by segments I and VI [11]. These segments correspond to the regions in which pseudolesions were seen in our study. Among pseudolesions shown on angiographically assisted CT images around the gallbladder in segment IV, those noted at the dorsal part are well known to be also caused by nonportal venous inflow from the parabiliary venous system [9,10,11], which is the vessel network expanding in the hepatic hilum named by Couinaud [19]. This nonportal venous system originates from the pancreaticoduodenal and gastric regions, running along the common biliary duct, hepatic artery, and portal vein, and communicates with the cholecystic veins [10, 19].
Inaba et al. [7], in a review of 200 images obtained from CT during arterial portography and CT hepatic arteriography, found 100 pseudolesions around the gallbladder showing both nontumorous defects of portal perfusion on CT during arterial portography and enhancement on CT hepatic arteriography. In 92% of such pseudolesions, the extent of nontumorous enhancement on CT hepatic arteriography was greater than the decreased area of portal perfusion on CT during arterial portography. Yoshimitsu et al. [11] performed CT during selective cholecystic arteriography in 28 patients to clarify the anatomical variants of the cholecystic venous system. In their study, the peripheral branches of the portal vein were revealed after the blood flow of the cholecystic vein entered the regions of the pericholecystic liver parenchyma in 93% (26/28) of the patients. In our previous study [10], some enhancements of pseudolesions caused by inflow from the parabiliary venous system revealed on CT during selective pancreaticoduodenal or gastric arteriography in the venous phase were occasionally wider than the corresponding nontumorous defects of portal perfusion seen on CT during arterial portography. These reported phenomena [7, 10, 11] lead us to suggest the existence of areas supplied by both the portal venous and nonportal venous systems consisting of the cholecystic veins and the parabiliary venous system through their communicating anastomoses. Such areas may be especially likely to appear in the peripheral region of pseudolesions where terminal branches between the portal and nonportal venous systems communicate. Moreover, the blood flow running through these anastomoses is speculated to be bidirectional because of the minor pressure gap between the cholecystic vein, including the parabiliary venous system and peripheral portal branches.
If our contention is accepted, the fact that most (69%) of the 36 pseudolesions with enhancement on CT hepatic arteriography decreased in size or even disappeared after intraarterial prostaglandin E1 injection and that CT attenuation decreased in 86% of the pseudolesions after intraarterial prostaglandin E1 injection can be explained by the following: First, nonportal venous inflow from the gallbladder, pancreaticoduodenal, and pyloroduodenal regions, to which contrast medium is carried at the time of CT hepatic arteriography from the common hepatic artery, caused enhancement of the pseudolesion. Second, blood reflux from the portal venous system (in which contrast material is not taken up during CT hepatic arteriography into the pseudolesion) occurred through the anastomoses between peripheral branches of the portal and nonportal venous systems after increases in portal blood flow [17] and pressure [18] caused by the prostaglandin E1 injection via the superior mesenteric artery. Third, nonportal venous inflow, including contrast material from the nonportal venous system into the pseudolesion, decreased. Finally, the enhancement on CT hepatic arteriography of the pseudolesion, showed diminution in size or was attenuated. However, pseudolesions in which no changes in the size, shape, or CT attenuation of enhancement after prostaglandin E1 injection were visible might be located in regions in which anastomoses with portal branches are rare, with nonportal venous inflow running directly into the sinusoids.
In our study, however, neither the size nor shape of enhancement on CT hepatic arteriography of 42 tumorous lesions changed after intraarterial prostaglandin E1 injection. The pseudolesions seen on the liver around the gallbladder showing portal defects on CT during arterial portography and enhancement on CT hepatic arteriography occasionally mimic tumorous lesions, for example when they are round [6, 8]. In such cases, adding CT hepatic arteriography with intraarterial prostaglandin E1 injection can help to clearly differentiate pseudolesions from tumorous lesions by revealing changes in the enhancement features on CT hepatic arteriography.
The finding of pseudolesions adjacent to the gallbladder as seen on angiographically assisted CT images has been shown to be easily influenced by increases in portal blood flow. Some of these pseudolesions have been reported to be enhanced on dynamic CT or MR imaging studies [11,12,13]. Angiographically assisted CT has been found to be the most useful imaging modality available to precisely evaluate hemodynamic features in the liver without surgical laparotomy [4]. Hence, although the number of patients in our study was small, we believe that the information we gained can contribute to the correct interpretation of pseudolesions as shown on various noninvasive hepatobiliary images obtained using intrahepatic hemodynamic features, such as Doppler sonography, dynamic CT, and dynamic MR imaging.
Acknowledgments
We express our deep gratitude to Yuji Itai of the Department of Radiology,
Institute of Clinical Medicine, University of Tsukuba, for valuable advice
regarding this study.
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  T. Yamagami, T. Nakamura, S. Iida, T. Kato, O. Tanaka, and T. Nishimura Effects of Prostaglandin E1 Injection Through the Superior Mesenteric Artery on the Hemodynamics of Hepatocellular Carcinoma Am. J. Roentgenol., February 1, 2002; 178(2): 349 - 352. [Abstract] [Full Text] [PDF]
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