[Clinical usefulness of infusion hepatic angiography for the diagnosis of space occupying lesions of the liver (author's transl)].
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Biomedical subjects
Publications and source records attributed to O Matsui.
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The purpose of this study was to determine the relationship between segmental hyperintensity of the liver on T1-weighted images and segmental cholestasis in patients with obstructive jaundice. T1-weighted and T2-weighted MR images were obtained of 73 patients with obstructive jaundice caused by various diseases. Fat-suppressed T1-weighted images were also obtained of 10 patients. Eleven patients with segmental intrahepatic bile duct dilatation (cholestasis) showed segmental hyperintensity on T1-weighted images and/or fat-suppressed T1-weighted images and no signal intensity difference on T2-weighted images. Sixty-two patients with widespread intrahepatic bile duct dilatation showed no intensity difference on T1-weighted and T2-weighted images (P < .01). Segmental hyperintensity on T1-weighted images was correlated with intrahepatic cholestasis.
We reported a case of the biliary cystadenoma of the liver. The cystic mass had lobulation and septation and showed marked hyperintensity on T1-weighted images and hypointensity on T2-weighted images; MR findings were very unusual for cystadenoma. The content of the cystic mass was jelly-like, thick mucinous fluid without intracystic hemorrhage. We concluded that these unusual signal intensities of the cyst were due to hyperproteinous mucinous fluid.
Gross hemorrhage is the most serious complication of anticoagulant therapy. We report the discovery and treatment of a large pseudoaneurysm of the superior gluteal artery in one patient who had been receiving oral anticoagulant therapy. We diagnosed the pseudoaneurysm by contrast-enhanced computed tomography, and embolized the artery with stainless steel coils. The exact cause of the pseudoaneurysm remains unclear, however, minor trauma appears most likely.
To improve safety and efficacy of the transjugular intrahepatic portosystemic shunt (TIPS) procedure, we introduced a new, thin-needle (21-gauge long PTC needle) puncture technique using biplane fluoroscopy and targeting of a guidewire tip in the right hepatic artery. After puncture of the right portal vein, a 0.016-inch guidewire was inserted into the portal vein, followed by a 4 Fr dilator. The 4 Fr dilator allowed introduction of a 0.035-inch working guidewire. We successfully performed TIPS in seven patients with postnecrotic cirrhosis using this technique and encountered no technical difficulties or complications.
BACKGROUND: Most hepatocellular carcinomas (HCCs) are hypervascular and arise in the liver with chronicity. Spiral volumetric CT (SVCT) is a new rapid-scan technique that offers whole-liver scanning during the arterial-dominant phase. The main aim of the present study is to evaluate the detectability of hypervascular HCC with SVCT as compared with ultrasonography (US) and magnetic resonance (MR) imaging. METHODS: Forty-three hypervascular HCCs in 512 patients with chronic liver disease were examined with US, precontrast SVCT, postcontrast SVCT during the arterial-dominant phase (CT-ADP) and during the equivalent-phase (CT-EP) noncontrast MR imaging and angiography including SVCT during arteriography and arterial portography. Angiographic and follow-up findings were used as the gold standard if the lesion was not confirmed histologically. RESULTS: The sensitivity was 61% with precontrast CT, 84% with CT-ADP, 58% with CT-EP, 70% with US, 72% with MR, and 95% with the combination of these five modalities. Five HCCs (12%) were detected with only CT-ADP. The vascularity of HCC was correctly evaluated as hypervascular in 38 nodules (88%) with the combination of precontrast CT and CT-ADP. CONCLUSIONS: We suggest that the combination of precontrast SVCT and CT-ADP is an essential modality to screen for HCC in patients with chronic liver disease. CT-EP did not contribute to the detection of hypervascular HCC.
We report a cirrhotic patient with complete occlusion of the portal vein with marked cavernous transformation due to chronic thrombosis in whom a transjugular intrahepatic portosystemic shunt (TIPS) was successfully created after direct minilaparotomy mesenteric vein catheterization, lysis and aspiration of the thrombus, and stenting in the portal vein. The methods used, we believe, provide a new technique for performing TIPS in chronically thrombosed portal veins in which previously no effective surgical therapeutic options were available.
The initial site of occlusion of the intrahepatic microvasculature in rats following hepatic artery embolization was studied by scanning electron microscopy of microvasculature casts. The rats were divided into four groups: embolization with gelatin powder (n = 3), polyvinyl alcohol (n = 3, 125-150 microns), gelatin sponge (n = 3, 212-250 microns), and ionized oil. Not only the hepatic arteries but also vessels in the peribiliary plexus were occluded. However, the size of the hepatic arteries and vessels of the peribiliary plexus occluded correlated with the size of the embolic material, except in the case of the gelatin powder which occluded vessels smaller than the particle size.
PURPOSE: The role of the portal system after hepatic artery embolization (HAE) was examined. METHODS: Using a Wistar strain rat model of liver cirrhosis, the route and occurrence of portoarterial (PA) shunts before and after HAE by scanning electron microscopic (SEM) and histologic methods were evaluated. HAE was performed with iodized oil and gelatin sponge particles. RESULTS: In the SEM study, PA shunts did not develop in normal rats regardless of whether they did (n = 10) or did not have HAE (n = 5). The cirrhotic rat model showed PA shunts in both HAE (n = 5) and non-HAE (n = 5) animals. PA shunts were established via the peribiliary plexus and direct arterioportal anastomosis. In the histologic study, the occurrence of PA shunts in liver cirrhosis was significantly increased by HAE (HAE = 6, non-HAE = 6, p < 0.01). CONCLUSION: The development of PA shunts, which help perfuse liver parenchyma, may explain why HAE can be safely performed in patients with liver cirrhosis.
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