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1 All authors: Department of Radiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-chyo, Kawaramachi-Hirokoji, Kamigyo, Kyoto 602-8566, Japan.
Received January 10, 2003;
accepted after revision April 30, 2003.
Address correspondence to T. Yamagami
(yamagami{at}koto.kpu-m.ac.jp).
Abstract
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SUBJECTS AND METHODS. Nine patients with portal hypertension underwent splenic arteriography and CT arterial portography during infusion of contrast material via the splenic artery. Images were obtained with the balloon catheter both inflated and deflated in the gastrorenal shunt, and results were compared.
RESULTS. During the portal phase of splenic arteriography, the intrahepatic portal vein was more clearly seen when the balloon occluded the gastrorenal shunt. Mean CT attenuation values of branches of the intrahepatic portal vein on CT arterial portograms acquired when the balloon catheter was inflated were higher than values acquired when the balloon was deflated; however, results for the inferior vena cava were the opposite. Differences in CT attenuation values were statistically significant for the right branch of the portal vein, main portal vein, right lobe of the liver parenchyma, and inferior vena cava.
CONCLUSION. Closure of large gastrorenal shunts (hepatofugal portasystemic shunts) causes the portal blood flow to switch from hepatofugal to hepatopetal, which increases the effective intrahepatic portal blood flow.
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In all patients, endoscopy revealed active bleeding (spurting or oozing) or signs of recent bleeding or growing gastric varices or both. Before BRTO was performed, the patients underwent CT arterial portography via the splenic artery with and without balloon occlusion of the gastrorenal shunt to simulate a change in hemodynamics of the portal vein in the liver.
BRTO Technique
We performed BRTO according to the method described by Kanagawa et al.
[6], details of which have been
described elsewhere
[6–8].
In brief, this technique consists of applying a local anesthetic and inserting
an 8-French catheter sheath-introducer (Catheter Introducer, Medikit, Tokyo,
Japan) into the patient's right femoral vein. A 6.5-French balloon catheter
with a 22-mm-diameter balloon (Artec Balloon catheter, Create Medics,
Yokohama, Japan) is advanced to the left renal vein through the
sheath-introducer, and the tip is wedged into the end of the gastrorenal
shunt. The balloon is then inflated with carbon dioxide to occlude the
vessel.
Using retrograde venography, we identified gastric varices and the inflowing and outflowing vessels and then determined the approximate dose of ethanolamine oleate necessary for obliteration. Contrast material was first cleared by deflating the balloon, and then the balloon was reinflated to occlude vessel flow. We administered 25–45 mL (mean, 37 mL) of a mixture of ethanolamine oleate iopamidol (5% solution) to fill the gastric varices that we had identified on retrograde venography and allowed the solution to remain in the vessel for 30 min, after which as much of the solution as possible was removed. During these procedures, 4,000 U of human haptoglobin was administered IV to prevent hemolysis-induced renal failure. We embolized the left inferior phrenic vein in two patients whose retrograde venographs showed that the vein had become another drainage vein for the gastric varices. Embolization was accomplished using microcoils via a microcatheter coaxially advanced from the balloon catheter inserted into the left renal vein in preparation for the BRTO. Splenic arteriography with and without single-detector helical CT was then performed in all patients to confirm the existence of a gastrorenal shunt and to evaluate the hemodynamics of the portal venous system.
Imaging Methods
With a 6.5-French balloon catheter already in place, we used the Seldinger
technique to insert a 5-French angiographic catheter from the right inguinal
region in the angiography room. After a test injection of contrast medium
confirmed that the tip of the second catheter was in the splenic artery, the
patient was transferred to the CT room. CT arterial portography was performed
while the balloon of the catheter in the gastrorenal shunt was inflated and
was repeated while the balloon was deflated, with an interval of approximately
10 min between each study.
CT arterial portography imaging was started 25–30 sec after the injection of 50–60 mL of 150 mgI/mL of iopamidol (Iopamiron, Schering, Berlin, Germany) at a rate of 2 mL/sec via the 5-French catheter, with its tip in the splenic artery. Each CT arterial portogram with and without balloon occlusion of the gastrorenal shunt was acquired with the same amount of iopamidol administered at the same rate in every patient. Images were obtained on helical CT unit (X-Vigor Laudator, Toshiba Medical System, Tokyo, Japan) during a single breath-hold with the entire liver imaged using the parameters of 120 kV; 190 mA; beam width, 7 mm; and table feed speed, 7 mm/sec. Image reconstruction was performed with a width of 7 mm and a matrix of 512 x 512.
We returned the patient to the angiography room where digital subtraction angiography was performed via the 5-French catheter with its tip in the splenic artery without balloon occlusion of the gastrorenal shunt; this procedure was followed by splenic arteriography with balloon occlusion. We used the same amount of contrast material delivered at the same rate of administration in every patient—20–25 mL of 370 mgI/mL of iopamidol injected at 4–5 mL/sec.
Investigated Parameters
Three radiologists experienced in abdominal diagnostic imaging analyzed the
images, with final judgments made by consensus. The reviewers were aware that
both portal phase splenic arteriography and CT arterial portography were
performed with and without balloon occlusion. In reviewing the portal phase
splenic arteriograms, the reviewers compared the visualization of the main
portal vein and right and left branches of the portal vein shown on these
images with those obtained with and without balloon occlusion of the
gastrorenal shunt.
Using the CT arterial portograms obtained while the balloon was inflated, we investigated the CT attenuation of the enhancement of the left and right branches of the portal vein, main portal vein, splenic vein, and inferior vena cava at the upper level of the cephalic site of the renal vein. Then, we retrospectively analyzed such changes after balloon deflation. We also examined changes in CT attenuation on CT arterial portography in the right and left lobes of liver parenchyma.
To quantify the CT attenuation of vessels and liver parenchyma, we measured the attenuation on CT arterial portograms using between one and five (mean, 4.1) 3- to 10-mm-diameter region-of-interest cursors. We placed the cursors over each vessel and calculated the average measurements of these regions of interest in each patient. We measured CT attenuation of the right or left lobe of the liver parenchyma by placing three to 10 (mean, 6.4) circular 10-mm region-of-interest cursors over the hepatic parenchyma, and the average measurements of these regions of interest were calculated in each patient, taking care to avoid measuring the regions of the hepatic arteries, veins, or portal branches. Attenuation of vessels and liver parenchyma on CT arterial portography after balloon catheter deflation was measured using the same regions of interest and locations used to measure attentuation when the balloon was inflated. Statistically, changes in the CT attenuation of vessels and liver parenchyma were analyzed using a paired Student's t test.
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In all patients, CT attenuation of the left and right branches of the portal vein and main portal vein on CT arterial portography with balloon occlusion decreased after deflation of the balloon, with the overall decrease varying from 9.7 to 180.7 H (mean, 54.7 H) in the left branch of the portal vein, from 14.8 to 139.2 H (mean, 52.2 H) in the right branch of the portal vein, and from 4.4 to 214.4 H (mean, 75.7 H) in the main portal vein. In eight (88.9%) of nine patients, CT attenuation of the splenic vein decreased; the overall decrease varied from – 0.5 to 326.4 H (mean, 65.5 H). In contrast, CT attenuation of the inferior vena cava in all patients increased; the overall increase varied from 7.6 to 152.2 H (mean, 49.0 H). CT attenuation of liver parenchyma decreased in 100% of patients (9/9) in the right lobe (range, 2.7–25.8 H; mean, 10.9 H) and in 88.9% (8/9) in the left lobe (range, from –9.6 to 9.1 H; mean, 3.1 H) (Figs. 1C and 1D).
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As shown in Table 2, the mean attenuation value on CT arterial portography with balloon occlusion of the gastrorenal shunt was higher in the bilateral branches of the portal vein, main portal vein, and splenic vein in the vessels we evaluated and in the bilateral lobes of the liver parenchyma than the mean attenuation value of these vessels and lobes on CT arterial portography without balloon occlusion of the gastrorenal shunt; however, this attentuation value was lower in the inferior vena cava. Statistically significant differences in CT attenuation values after balloon deflation were decreased in the right branch of the portal vein, main portal vein, and right lobe of the liver parenchyma and increased in the inferior vena cava.
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On endoscopy performed 1–2 months after BRTO, gastric varices had disappeared in seven patients and the size of the varices had remarkably decreased in the other two patients. To date, no patient has experienced a rupture of gastric varices. Encephalopathy-related symptoms in the patient with portasystemic encephalopathy were relieved. In two patients, esophageal varices increased 6 and 8 months, respectively, after BRTO. No complication related to BRTO has occurred; no decline in liver function has been noted.
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The effectiveness of BRTO as a treatment for hepatic encephalopathy caused by a portasystemic shunt has been well documented [5, 9, 10, 15]. Ohmoto et al. [15] reported improvement after BRTO in a patient with liver cirrhosis in whom gastric varices were accompanied by portasystemic encephalopathy. Kato et al. [9] reported on six patients in whom clinical evidence of portasystemic encephalopathy disappeared after BRTO within 2 days after the treatment, and the patients remained free from encephalopathy during the following 6 months. Also, 1 month after BRTO, the patients' serum ammonia levels were significantly reduced compared with the levels before treatment. This reduction was sustained for up to 12 months. Another case report found that BRTO of a splenorenal shunt led to improvement in a patient with portasystemic encephalopathy [16]. With regard to improvement of liver function after BRTO, Akahane et al. [10] noted that in all nine patients who underwent BRTO, the 15-min retention rate of indocyanine green significantly improved from a mean of 31.8% (SD, ± 16.1%) to a mean of 21.8% (± 12.4%) within 3 weeks after the treatment. Fukuda et al. [5] found an improvement in the Child-Pugh scores for 50% of 43 patients with gastric varices or portasystemic encephalopathy or both 6 months after BRTO. These researchers also described the disappearance of symptoms in all patients with portasystemic encephalopathy (n = 11).
We performed portal phase splenic arteriography and CT arterial portography via the splenic artery under conditions similar to those induced by BRTO (i.e., during balloon occlusion of gastrorenal shunt) and found that hepatopetal portal venous flow was more clearly seen and that enhancement of the intrahepatic portal vein and liver parenchyma was stronger than on the imaging performed without balloon occlusion. However, enhancement of the inferior vena cava was more blurred in imaging performed with balloon occlusion. These phenomena led us to suggest that the reported improvement of portasystemic encephalopathy or liver function after BRTO is the result of the closure of the large hepatofugal portasystemic shunt (i.e., gastrorenal shunt) and the consequent switch of portal flow from hepatofugal to hepatopetal, which in turn increases effective intrahepatic portal blood flow. In another study evaluating the change in hemodynamics after BRTO, Akahane et al. [10] found that hepatopetal portal flow visualized on Doppler sonography increased from a mean of 5.4 (± 1.1) cm/sec to a mean of 7.85 (± 1.4) cm/sec.
In conclusion, our results strongly support the idea that BRTO is useful as a treatment for portasystemic encephalopathy or liver dysfunction, as well as a treatment for gastric varices resulting from portal hypertension, which has been the usual indication for the procedure. However, a limitation of our study is that it fails to clarify to whether the change in hemodynamics engendered by the treatment persists over a long-term follow-up period. To our knowledge, scant information on long-term observation of hemodynamics exists in the literature. Clinically or biochemically evident recrudescence of liver function 6–12 months after BRTO has been reported [5, 9, 10]. Before undertaking BRTO therapy, researchers may need to determine whether effective hemodynamics of the intrahepatic portal vein could be achieved in a particular patient by performing splenic arteriography and CT arterial portography as we described. However, our study shows that CT arterial portography with or without balloon occlusion is more sensitive than conventional portography with or without balloon occlusion.
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