Intrahepatic hepatic vein stenosis after living-related liver transplantation treated by insertion of an expandable metallic stent.
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Although the incidence of stenosis and obstruction of the hepatic venous anastomosis after right hepatic living-related liver transplantation (LRLT) has been found to be higher than after orthotopic liver transplantation (OLT), to the best of our knowledge, intrahepatic stenosis of the venous trunk in the early period after right hepatic LRLT has never been reported in the literature. A 53-year-old man who underwent right hepatic LRLT, postoperatively, developed liver dysfunction and an increasing amount of ascites, and a Doppler sonogram showed a flat waveform and low-flow velocity in the hepatic vein. Based on these findings an outflow block was suspected, and a hepatic venogram and manometry revealed intrahepatic stenosis of a tortuous hepatic venous trunk and a pressure gradient of 14 mmHg at the site of the stenosis. We inserted an expandable metallic stent (EMS) at the site of intrahepatic venous stenosis, and its insertion was followed by a decrease in pressure gradient. Liver function recovered, and the volume of ascitic fluid decreased after placement of the EMS. The results of an analysis of the venogram and CT volumetric data suggested that the pathogenesis of the stenosis was twisting of the venous trunk during hypertrophy of the liver parenchyma. (+info)
Inherited prothrombotic defects in Budd-Chiari syndrome and portal vein thrombosis: a study from North India.
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We studied 57 patients with Budd-Chiari syndrome (BCS) and 48 with portal vein thrombosis (PVT) for underlying inherited prothrombotic defects such as protein C, protein S, and antithrombin III deficiencies. Genetic mutations for factor V Leiden, prothrombin gene 20210A, and methyltetrahydrofolate reductase (MTHFR) C677T were studied in 29 patients in each group. Inherited prothrombotic defects were detected in 16 (28%) of 57 patients with BCS and 7 (15%) of 48 patients with PVT. Factor V Leiden mutation was the most common prothrombotic defect in BCS (5/29 [17%]) followed by protein C deficiency (7/57 [12%]) and protein S deficiency (4/57 [7%]), whereas in PVT, protein C deficiency was the most common inherited prothrombotic defect (4/48 [8%]) followed by protein S deficiency (2/48 [4%]). The factor V Leiden mutation was detected in only 1 (3%) of 29 cases of PVT. The heterozygous MTHFR C677T mutation was detected in 7 (24%) of 29 patients with BCS and 6 (21%) of 29 patients with PVT. Antithrombin III deficiency, homozygous MTHFR C677T mutation, and prothrombin G20210A mutation were not detected in any patients. (+info)
Orthotopic liver transplantation for patients with hepatocellular carcinoma complicated by portal vein tumor thrombi.
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BACKGROUND: Orthotopic liver transplantation (OLT) has been the valuable treatment of choice for patients with hepatocellular carcinoma (HCC). As the number of patients with portal vein tumor thrombi (PVTT) increases, most transplant centers become suspicious of the exact effect of the operation which has been accepted as a radical method. This study was designed to evaluate the clinical effects of OLT for patients with HCC associated with PVTT. METHODS: The follow-up of 24 patients with HCC complicated by PVTT who had received OLT (transplant group) from January 1999 to March 2003 was compared to that of 27 patients undergoing routine hepatic resection (resection group) and 59 patients without surgical treatment (non-surgical group). RESULTS: The perioperative mortality was zero for the transplant group. The 6-month, 1-year, and 2-year overall survival rates were 66.7%, 29.5% and 23.6% for the transplant group, 33.3%, 22.2% and 14.8% for the resection group (P=0.0335), and 42.1%, 24.4% and 4.1% for the non-surgical group, respectively (P=0.0316). The tumor free survival rates of recipients at 6-month, 1-year, and 2-year were 51.5%, 23.2% and zero, respectively. During the period of follow-up, the overall post-transplant intrahepatic recurrence or extrahepatic metastasis rate was 66.7% for the transplant group. CONCLUSION: OLT is an effective but palliative treatment modality for patients with HCC associated with PVTT followed by a prolonged survival but a poor tumor free survival rate. (+info)
Surgical treatment of 1360 cases of Budd-Chiari syndrome: 20-year experience.
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BACKGROUND: Budd-Chiari syndrome (BCS) is a disease caused by blood flow obstruction of the main hepatic veins (MHVs) and/or the outlet of the inferior vena cava (IVC), characterized by retrohepatic portal hypertension (PHT) and/or IVC hypertension. In the past decade, over 3000 cases of BCS have been reported in China. This study was to sum up our 20-year experience in surgical treatment of BCS and to investigate its pathological classification and principles of surgery. METHODS: The data from 1360 BCS patients were analyzed retrospectively. RESULTS: Four types (6 subtypes) were classified according to IVC angiography and hepatovenography: type Ia (594 patients), type Ib (123), type II (292), type IIIa (237), type IIIb (112), and type IV (2). Surgical procedures included: improved splenopneumopexy (265 cases), finger or balloon membranotomy (407), radical resection of membrane and thrombus (275), IVC bypass (88: cavocaval transflow 71 cases, and cavoatrial transflow 17 cases), mesocaval C-shape shunt (192), splenocaval shunt (32), splenoatrial shunt (23), splenojugular shunt (57), mesoatrial shunt (8), and combined methods (6), including plenal-cavoatrial shunt (4), and mesocavoatrial shunt (2), splenorenal shunt (4), mesojugular shunt (2), and other methods (1). The perioperative death rate and the complication rate after operation was 3.09% (42/1360) and 14.8% (201/1360) respectively. 885 cases were followed up from 9 months to 15 years (average 6.8+/-1.2 years. The 791 (89.4%) of 885 patients were successfully treated, 61 patients (6.89%) had a recurrence, and 33 died. CONCLUSION: Surgical treatment of BCS is dependent on a correct diagnosis and classification of the disease. (+info)
Radiofrequency ablation combined with percutaneous ethanol injection in the treatment of hepatocellular carcinoma and portal vein neoplastic thrombosis.
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In the last ten years new techniques, such as percutaneous ethanol injection (PEI) and radiofrequency ablation (RFA), have been developed for the treatment of hepatocellular carcinoma (HCC). Portal vein involvement is a complication of HCC and the role of surgical resection for HCC with tumor thrombi in the portal veins is controversial. Here we present the case of a 58-year-old man, with Child's class A cirrhosis and a focal lesion of HCC with thrombosis of the segmental portal branch extending into the right portal vein. We treated the nodule with RFA and the portal tumor thrombosis with ethanol injection. Twenty-two months after the combined treatment, an enhanced spiral CT scan showed complete necrosis of the nodule and color/power Doppler ultrasound demonstrated the complete patency of the right portal vein. (+info)
Course before and after treatment of a patient with Budd-Chiari syndrome monitored by iodine-123-iodoamphetamine scintigraphy per os and per rectum.
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A 55-yr-old woman with Budd-Chiari syndrome was treated by percutaneous transluminal angioplasty with a balloon catheter. Before and after treatment, portal scintigraphy was performed by the administration of [123I]iodoamphetamine per os and per rectum. An enteric capsule was used for the oral administration. Before treatment, the portal shunt index via the superior mesenteric vein was 40.5%; two weeks after treatment, it was 50.2%; and five months after treatment, it was 41.2%. Before treatment, the portal shunt index via the inferior mesenteric vein was 86.0%; two weeks after treatment, it was 87.6%; and five months after treatment, it was 21.8%. The treatment improved the portal circulation through the inferior mesenteric vein only, with little effect on the portal circulation through the superior mesenteric vein. (+info)
A 43 year-old woman presented with fever, abdominal pain, epato-splenomegaly, ascites, cholestasis, anemia, thrombocytopenia and previous diagnosis of sclerosing cholangitis based on liver biopsy and endoscopic retrograde cholangiopancreatography(ERCP). The bone marrow biopsy and the revision of liver biopsy using antitryptase stain diagnosed systemic mastocytosis. Because of the aggressive course of the disease the patient was treated with an acute myeloid leukaemia chemotherapy regimen without success. (+info)
Treatment of Budd-Chiari syndrome in a liver transplant unit, the role of transjugular intrahepatic porto-systemic shunt and liver transplantation.
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BACKGROUND: Budd-Chiari syndrome is an uncommon cause of liver failure usually associated with an underlying hypercoagulable state. AIM: To evaluate current trends in management of Budd-Chiari syndrome at our institution. METHODS: Twenty-two patients with Budd-Chiari syndrome underwent transjugular intrahepatic porto-systemic shunt, liver transplantation, or both in between 1992 and 2001. We analysed underlying diagnosis, medical therapy, complications, follow-up and overall outcomes. RESULTS: Five patients (17%) presented with fulminant liver failure and 17 patients (83%) with new-onset ascites or chronic liver disease. Seventeen patients (74%) underwent transjugular intrahepatic porto-systemic shunt: improvement or stabilization occurred initially in 14 (82%), whereas the other three patients died within a month. At a mean 3 years follow-up eight patients (47%) continued to do well clinically and four have died (23.5%); seven have required transjugular intrahepatic porto-systemic shunt revisions (mean 2.3 interventions), five have experienced transjugular intrahepatic porto-systemic shunt occlusion managed with new transjugular intrahepatic porto-systemic shunt placement and five patients underwent subsequent transplantation. Of the 10 patients who underwent liver transplantation, patient and graft survival are 80% at a mean 5.7 years of follow-up. No patient developed post-transplant Budd-Chiari syndrome. CONCLUSIONS: Transjugular intrahepatic porto-systemic shunt is usually feasible in patients with Budd-Chiari syndrome, and is best suited as a bridge to more timely liver transplantation. Long-term success of transjugular intrahepatic porto-systemic shunt is limited and usually requires revision, placement of a new shunt or liver transplantation. Liver transplantation with chronic anticoagulation offers excellent short- and medium-term patient and graft survival. In our series, there was no recurrence of Budd-Chiari syndrome after liver transplantation. (+info)