Hepatic Vein Lesions Research Articles

Usefulness of central radiologic review in clinical trials of children with hepatoblastoma.

No previous research papers have reported a comparative survey of local radiologic diagnoses and central review in children with hepatoblastoma. To evaluate the utility of central review of children with hepatoblastoma enrolled in a clinical trial. The study included 91 children enrolled in a clinical trial conducted by the Japanese Study Group for Pediatric Liver Tumor. We compared the results of the initial pre-treatment extent of tumor (PRETEXT) disease staging performed at local sites with the results obtained on central review to determine the concurrence rates for tumor staging and additional criteria. The concurrence rate for PRETEXT staging was 70%. As the stage increased, the concurrence rate decreased. Using additional criteria, central review identified 143 lesions (157.1%), about 1.8 times higher than the number identified for the local site diagnoses. The additional criterion found most often on central review was "multifocal lesion" (n=19). The concurrence rate for lung metastases was high. However, our central review found many false-positive assertions of hepatic vein lesions, portal vein invasion and extrahepatic lesions among the local site diagnoses. In a clinical trial of hepatoblastoma, central review provided a more precise diagnosis than local site diagnoses with respect to severe PRETEXT stages III and IV cases and other cases including hepatic and portal vein invasion. The central review process appears to be effective and essential for improving the quality of clinical trials.

Endovascular treatment of Budd-Chiari syndrome with hepatic vein obstruction in China.

Abstract Purpose: To evaluate characteristics of obstructions of the hepatic veins (HVs) in Chinese patients, technical aspects of puncture of the HVs, short- and mid-term outcomes, and complications of endovascular treatment. Forty-eight HV patients with different degrees of symptoms and signs of portal hypertension were enrolled in our study. Endovascular treatments with balloon and stents were performed. Catheter-directed thrombolysis (CDT) was performed in patients with thrombosis in the HVs. For patients with lesions of both the HVs and the inferior vena cava (IVC), balloon expansions or stenting were performed at the IVC lesions also. Endovascular treatments were successful in 43 patients. The technically success rate was 89.6% (43/48). Fifteen patients underwent solely balloon expansions, 28 patients had balloon expansions and stentings, 5 patients underwent CDT, and 3 patients had implanted stents in the IVC lesions at the same time. The symptoms of portal hypertension were alleviated in 39 patients postoperatively. In the other 4 cases portal hypertension was mildly alleviated at discharge. Thirty-nine of the 43 patients were followed up for an average of 24±1.3 months (range, 6-62 months). Ascites were completely resolved in 32 cases, with a small amount of ascites in 4 patients and moderate to massive amounts in 3 patients. Hepatomegaly and splenomegaly completely disappeared in 30 patients and still could be touched in 6 patients. The HVs were patent in 29 patients. Restenosis and re-occlusion of the HVs appeared in 4 cases. All patients were successfully treated by endovascular treatments. Endovascular treatments for patients with obstruction of the HVs have a high technical success rate, fewer complications, and better short- and mid-term clinical outcome. The key to successful endovascular treatment is successful puncture of HVs. For patients who have occlusive lesions of HVs combined with occlusive IVC, recanalization of the lesions of the HVs could achieve good results.

Dilatation of preexisting venous collateral pathways as a possible treatment option in patients with Budd–Chiari Syndrom

Treatment of inferior vena cava (IVC) over-long segmental occlusion in Budd–Chiari syndrome (BCS) remains challenging. IVC segmental occlusion in BCS is often associated mainly with hepatic vein lesions in BCS, while the accessory hepatic vein (AHV) is typically patent and more intrahepatic collateral vessels are widely well-developed. Herein, we report our use of angioplasty for hepatic venous or the accessory hepatic vein for long segmental occlusion of the IVC in two BCS cases, rather than opening the IVC, in cases with a well-developed intrahepatic collateral. This method provides satisfactory outcome in short follow-up period of 8 and 5 months respectively, and is practical and feasible.

Western Trauma Association Critical Decisions in Trauma: Nonoperative Management of Adult Blunt Hepatic Trauma

Western Trauma Association Critical Decisions in Trauma: Nonoperative Management of Adult Blunt Hepatic Trauma

Primary Budd-Chiari syndrome: Outcome of endovascular management for suprahepatic venous obstruction

Primary Budd-Chiari syndrome (BCS) is a rare form of hepatic venous outflow obstruction at the suprahepatic inferior vena cava (IVC), the hepatic veins, or both. We assessed our 4-year experience in the management of BCS to evaluate the results of our methods of care. We conducted a retrospective review of a nonrandomized clinical trial conducted in three teaching hospitals. Among 28 primary BCS patients, 9 remained in medical treatment only, and 19 who failed to respond to medical treatment received additional endovascular (n = 17) or surgical therapy (n = 2). Nine underwent IVC balloon angioplasty alone, 6 had angioplasty plus stents, and 2 had transjugular intrahepatic portosystemic shunts (TIPS) for hepatic vein lesions. One patient had a mesoatrial bypass; another had liver transplantation. Immediate response to the therapy was assessed with angiography and ultrasonography based on anatomic and/or hemodynamic correction or reduction of the lesion. Subsequent assessment of portal hypertension status was made with periodic clinical and laboratory evaluation (eg, ultrasonography, liver biopsy). Twenty-six patients had had IVC stenosis or occlusion by focal or segmental lesion. Two patients had hepatic vein outlet obstruction. There was no evidence of coagulopathy as the pathogenesis; all were related to membranous obstruction of the vena cava. Excellent immediate response to the endovascular therapy and subsequent relief of portal hypertension were achieved in 14 patients. Four patients had restenosis or progression of the residual lesion within 2 years; three responded to repeated stenting. Primary patency was 76.5%, and primary assisted patency was 94.1%. Two patients with TIPS and two with surgical therapy maintained excellent results. The medical treatment remained effective only in a limited group of 6 (21.4%) of the 28 patients. In BCS, both endovascular and surgical interventions provide excellent results and potentially halt liver parenchymal deterioration caused by portal hypertension. Liver transplantation remains the ultimate solution for advanced liver failure.

Fibrous obliterative lesions of veins contribute to progressive fibrosis in chronic liver allograft rejection

Fibrosis in liver allografts undergoing chronic rejection (CR) is variable and poorly understood. The temporal and spatial relationships of venous, arterial, and biliary lesions were studied to clarify their potential contributions to graft fibrosis. The severity, prevalence, and morphology of intimal lesions of vessels were analyzed and compared with the fibrosis stage. Three groups were found; group 1 (n = 5) with no hepatic vein (HV) lesions, group 2 (n = 5) with HV lesions only, and group 3 with lesions of both HV and portal veins (PV). The earliest lesion to develop, in 71% of grafts, was concentric intimal thickening of small HV. This was significantly more severe and frequent in grafts from group 3. With increasing frequency and severity of small HV sclerosis, fibrosis developed in medium/large veins. The morphology of larger vessel lesions suggested organized thrombus. Centrilobular fibrosis was significantly more severe in group 3 and developed unpredictably and sometimes rapidly. Conversely, portal fibrosis scores were significantly higher in grafts with ductular proliferation and did not correlate with venous lesions. This suggests that in CR, veno-occlusive-like lesions develop commonly in terminal hepatic venules, probably caused by immune-mediated damage. In only a proportion, with increased frequency and severity of the lesions, stasis and thrombosis in portal and larger veins occur and could result in loss of hepatic and portal venous outflow, which leads to ischemia and fibrosis. The stage of fibrosis did not correlate with foam-cell arteriopathy. A second pathway of portal fibrosis occurs in patients with longstanding biliary proliferation. (Hepatology2000;32:1240-1247.)

Hepatic Radiation Injury in the Rat

The whole livers of rats were exposed intraoperatively to graded doses (0 to 75 Gy) of 137Cs gamma radiation. At various times (0 to 155 days) after liver irradiation, minimally invasive, nondestructive tests (rose bengal retention and plasma alkaline phosphatase, glutamic-oxaloacetic acid transaminase, glutamic-pyruvic transaminase) were performed on at least half the surviving animals in each dose group to assess developing liver injury. Liver histology was done on animals sacrificed 96 to 100 days after irradiation. Radiation damage to the stomach killed approximately 50% of the animals 30 to 60 days after exposure to doses of 25 Gy or higher. These deaths were significantly reduced when care was taken to shield the stomach during irradiation. Stomach injury did not, however, appreciably affect liver function as measured by rose bengal retention. Whole-liver irradiation to 15 Gy resulted in reduced liver size and minimal histological changes, but did not result in increased rose bengal retention or plasma alkaline phosphatase concentration. The next highest dose group studied (25 Gy) showed significant histological abnormalities and liver injury as measured by increased rose bengal retention and liver enzymes. The latent period for development of hepatic injury, as measured by increased rose bengal retention, was 35 to 42 days and was relatively invariant over the 25- to 75-Gy dose range. Hepatic vein lesions and cellular necrosis were the most prominent histological lesions observed in 25-Gy-irradiated liver.

Hepatic vein lesions in alcoholic liver disease: retrospective biopsy and necropsy study.

Obliteration of the terminal hepatic venules with perivenular fibrosis (phlebosclerosis) is a well recognised feature in alcoholic liver disease. Veno-occlusive lesions with intimal obliteration of hepatic veins and a lymphocytic phlebitis of hepatic veins may also be present. We looked for these lesions in 256 liver biopsies and 50 livers obtained at necropsy from patients with alcoholic liver disease. Phlebosclerosis was a universal finding in alcoholic hepatitis and cirrhosis and showed increasing severity with progressive liver injury. Veno-occlusive lesions, however, were found in only 25 of 256 (9.8%) of biopsies and 11 of 50 (22%) of livers obtained at necropsy, showing alcoholic hepatitis or cirrhosis: lymphocytic phlebitis was found in 10 of 256 (3.9%) and two of 50 (4%), respectively. Moreover, veno-occlusive lesions were generally mild. The prevalence of veno-occlusive lesions and lymphocytic phlebitis was considerably less than has been previously documented. Phlebosclerosis may have a different mechanism and be a more important contributory factor in progressive liver injury.

Quantitation and serial section observations of focal venocclusive lesions of hepatic veins in liver cirrhosis.

The pathogenesis and functional significance of the venocclusive (VO) lesions in small hepatic veins occurring in liver cirrhosis, remain controversial. The present study, using quantitative examination and serial sections has disclosed that these lesions are present in 71.7% of 106 autopsy livers with alcoholic, HBsAg-positive, biliary or cryptogenic cirrhosis. The lesions were usually focal: their number in a liver section (10 cm2) was below 15 in 86.7% of the livers having them. The incidence and morphology of the lesions appeared similar in cirrhotic livers with different aetiology. Serial sections disclosed that the affected veins disappeared within the fibrous stroma at one side and were directly connected with the patent larger hepatic veins at other side, indicating that these veins had lost their function as a draining vein of the hepatic parenchyma. In addition, there was frequent recanalization within the VO lesions, and the recanalized vessels frequently communicated with neighboring thin-walled veins in cirrhotic stroma, suggesting an intrahepatic vein to vein anastomosis. In conclusion, VO lesions, when focal, may themselves be responsible to a lesser degree for obstruction of hepatic venous outflow in liver cirrhosis.