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At least 361 records · Page 20Linked to original sources
PubMed1994

Transjugular intrahepatic portosystemic stent-shunt (TIPSS): long-term follow-up.

We assessed the long-term efficacy of transjugular intrahepatic portasystemic stent-shunt (TIPSS) in 64 patients. Insertion was successful in 56 patients (87.5%). The reasons for its use were: variceal bleeding (49); ascites (6); portal hypertensive gastropathy (6); hypersplenism (2); and embolization of a spontaneous shunt (1). Fourteen patients were Childs A, 20 Childs B and 28 Childs C cirrhotics. Two patients were non-cirrhotic; one with amyloidosis and one with non-cirrhotic portal fibrosis. Patients were followed clinically and radiologically (Doppler ultrasonography and routine portography at 6 months). During 33 patient-years of follow-up, 22 died, 12 during index admission (two were procedure-related) and nine were transplanted. Twenty-five patients are alive, with a mean survival of 7.1 (SD 7) months. Variceal rebleeding occurred in 10 patients (22.7%), one of whom died, and was always associated with shunt insufficiency (shunt thrombosis 2, hepatic vein stenosis (HVS) 1, intimal hyperplasia (IH) 4, dislocated stent 1, inadequate stent 2). Clinical encephalopathy was induced in seven patients (17.1%) following TIPSS. All responded to medical therapy, but two required reduction in shunt size. Ascites improved after TIPSS in 36 patients (87.8%), but reaccumulated in seven (17.5%), associated with shunt dysfunction in five (SBP 2, IH 3, HVS 2). Fatal sepsis occurred in two patients, and 14 other episodes of infection required antibiotics. TIPSS is a useful treatment for variceal bleeding, resistant ascites and portal hypertensive gastropathy. Shunt dysfunction and sepsis occur frequently, and regular surveillance is necessary.

Female↗
PubMed1994

[Leiomyosarcoma of the inferior vena cava. Presentation of 1 case of autopsy and review of the literature].

This is a clinico-pathological report of a 30 years old male patient that presented with acute epigastric pain. Ultrasound examination showed a retroperitoneal tumor, thrombosis of the inferior vena cava and ascites. CAT scan disclosed thrombosis of hepatic vein and inferior vena cava with right atrium involvement. Necropsy showed a leiomyosarcoma of the inferior vena cava. There are seldom reports of this tumor in the last 5 years and an early diagnosis allows therapeutic interventions associating surgery, radiotherapy and chemotherapy.

Adult↗
PubMed2006

Noncirrhotic portal vein thrombosis exhibits neuropsychological and MR changes consistent with minimal hepatic encephalopathy.

Hepatic encephalopathy can arise from portal-systemic shunting in the absence of intrinsic liver disease. However, there are few descriptions of this form of encephalopathy. Portal vein thrombosis is an infrequent disease that causes portal-systemic shunting. Episodic hepatic encephalopathy has been described in patients with portal vein thrombosis, but it is not known if these patients develop minimal hepatic encephalopathy. We designed a study to investigate the neurological consequences of portal vein thrombosis in patients without cirrhosis and no clinical signs of encephalopathy. For this purpose, 10 patients underwent neuropsychological tests, an oral glutamine challenge test, and brain magnetic resonance (MR) imaging. The results were compared with those obtained in 10 healthy controls. Patients with portal vein thrombosis exhibited abnormalities in the results of neuropsychological tests, oral glutamine challenge test, and MR similar to those described in hepatic encephalopathy associated with cirrhosis. MR spectroscopy revealed a decrease in myo-inositol and an increase in glutamine. The increase in glutamine correlated with an increase in ammonia following the oral glutamine challenge test, signs of increased brain water (decrease in magnetization transfer ratio), and impairment of attention tests. In conclusion, patients with noncirrhotic portal vein thrombosis develop subclinical neurological abnormalities compatible with minimal hepatic encephalopathy. These disturbances, which include signs of increase in brain water and a compensatory osmotic response (decrease in brain myo-inositol), appear to be secondary to brain exposure to ammonia induced by portal-systemic shunting.

Administration, Oral↗
PubMed1980

[Acute post-gravidic Budd-Chiari syndrome. One case (author's transl)].

The sixth case of post-gravidic Budd-Chiari syndrome is reported. In the acute stage of the disease heparin seems to have given immediate favourable results, and the value of long-term heparin treatment is discussed. Post-mortem findings seven years after the acute episode confirmed the evolution towards a certain type of cirrhosis characterized by macroscopically and histologically heterogenous lesions and by persistent liver congestion. Portal hypertension was associated with arterialization of the portal vein and considerable dilatation of the right diaphragmatic veins. The venous drainage of the liver had undergone complex alterations: the supra-hepatic veins were affected with fairly recent incomplete ostial thrombosis, many intra-hepatic veins were reduced to a vestigial reticulum and others were the seat of recent or old re-canalized thrombosis. Cancerous transformation was found to be present in the larger hepatic nodules.

Acute Disease↗
PubMed2006

Gastric adenocarcinoma in a horse with portal vein metastasis and thrombosis: a novel cause of hepatic encephalopathy.

A 17-year-old Quarter horse mare was referred to Cornell University for postmortem examination after 72 hours of encephalopathy that consisted of depression, mania, and blindness. A plasma sample and cerebral spinal fluid demonstrated hyperammonemia. Gross necropsy examination findings included the following: mild icterus, a transmural mass in the glandular portion of the gastric fundus, multiple masses throughout the liver, and a large tumor thrombus in the portal vein. Microscopically, the gastric mass, hepatic masses, and portal vein thrombus were composed of similar neoplastic epithelial cells that formed variably sized acini and branching cords separated by a dense desmoplastic stroma. Throughout the cerebral frontal cortex were numerous Alzheimer type II astrocytes. Hepatic encephalopathy was caused by gastric adenocarcinoma, with metastasis to the liver and the portal vein. The clinical and pathologic lesions from this unique case, as well as hyperammonemia and portal vein thrombosis in the pathogenesis of hepatic encephalopathy, are discussed.

Adenocarcinoma↗
PubMed2003

[Postoperative management and complications in living-related liver transplantation].

Living-related liver transplantation is widely accepted as a treatment for patients with end-stage liver disease, with survival rates of up to 80%. Liver transplant recipients are at risk for the same postoperative complications as any patient undergoing a major intraabdominal operation, in addition to several complications specific to this procedure. Maintenance immunosuppression relies principally on administration of tacrolimus and methylprednisolone. Nevertheless, approximately 36% of liver transplant recipients suffer acute rejection in the early posttransplant period and require bolus steroid therapy as a rescue agent. Vascular complications, including hepatic arterial thrombosis and portal vein thrombosis, are additional major problems. When they occur in the immediate postoperative period, they can produce fulminant hepatic necrosis requiring retransplantation, so intensive anticoagulation therapy is needed as prophylaxis against these vascular complications. If thrombosis of the hepatic artery or portal vein is diagnosed early in the postoperative course, emergency thrombectomy with reanastomosis should be attempted. Outflow obstruction by hepatic vein stenosis sometimes causes liver dysfunction, pleural effusion, and hepatosplenomegaly. Percutaneous transhepatic or transjugular approached hepatic vein dilatation is very useful in case of hepatic vein stenosis. Recipients are generally immunocompromised secondary to immunosuppressive therapy and their poor clinical condition and are at high risk for postoperative infection. Infection is a major cause of morbidity and the most common cause of death in liver transplant recipients. Antibiotic, antifungal, and antiviral agents are used empirically, and serologic examinations and bacterial investigations of blood, sputum, stool, urine, and discharge from drains should be performed as well as antibiotic sensitivity tests when necessary. Other complications related to the operation are intraabdominal bleeding, bile leakage, biliary anastomotic stenosis, and intestinal perforation. The postoperative course of liver transplant recipients with these complications depends on making an accurate diagnosis promptly and initiating appropriate management. Postoperative complications of living-related liver transplantation are protean, so it is very important to communicate with professionals in each specialized field to ensure optimal treatment.

Humans↗
PubMed1989

Thrombosis of portal vein in absence of hepatic disease.

Of 602 patients referred for portal hypertension during a 20 year period, 18 children (mean age of 5.0 years) and 29 adults (mean age of 26.5 years) had thrombosis in the portal bed with a healthy liver (7.8 per cent incidence). In 29 of the 47 patients we studied, the causative factor remained obscure. Variceal hemorrhage occurred in all and was the indication for our observation and treatment. In 11 adult patients (mean age of 22.1 years), surgical treatment was not performed because of reluctance of the patient or because of technical reasons: nine of the patients rebled and one patient died because of massive bleeding. Direct procedures on esophageal varices had a high rate of rebleeding (seven of 11 patients) independent of the age of the patient when the operation was performed. In 13 patients, shunting offered a good chance of long term protection: three of the 13 rebled at a mean follow-up study of 5.7 years. No recurrence of bleeding was observed in 15 patients when variceal eradication had been obtained after chronic endoscopic sclerotherapy at one to eight years of follow-up study (mean of 3.9 years). The data from this study indicate that sclerotherapy should be the first choice of treatment to control recurrent bleeding in extrahepatic portal hypertension caused by thrombotic obstruction, particularly in the young patient.

Adolescent↗
PubMedDate not supplied

Neoplasms containing normal hepatic vessels: imaging features.

BACKGROUND: We investigated the incidence and imaging features of hepatic neoplasms containing normal hepatic vessels. METHODS: Among 3183 patients with various hepatic neoplasms, we found nine patients with normal hepatic vessels traversing hepatic neoplasms. The presence of mass effect on the vessel traversing hepatic neoplasms was evaluated. Other suggestive findings of neoplasms such as altered hepatic contour, portal vein thrombosis, mass effect on extratumoral vessel, and bile duct dilatation were analyzed. RESULTS: Thirteen hepatic vessels (nine hepatic veins and four portal veins) extended through hepatic neoplasms in nine patients. Undisturbed hepatic vessels within the neoplasms were found in five patients with either primary or metastatic hepatic neoplasm. In one patient with undisturbed hepatic vessels within the neoplasm, there were no associated abnormal findings such as biliary dilatation, change of hepatic contour, or any changes involving the vessels external to neoplasms. CONCLUSION: Although rare, various primary and secondary hepatic neoplasms can have normal hepatic vessels passing through them without mass effect. However, correct diagnosis in most neoplasms would be possible with careful examination of associated findings.

Adolescent↗