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At least 37 records · Page 2Linked to original sources
PubMed1975

Hepatic vein thrombosis in Buffalo strain female rats ingesting dimethylnitrosamine.

Buffalo strain male and female rats 12 weeks of age ingested 0.0114% dimethylnitrosamine in a semisynthetic diet for 12 weeks. Hepatic vein thrombosis developed along with focal fibrosis of the liver in female rats. Male rats had focal hepatic fibrosis, but not thrombosis of hepatic veins. A high incidence of hepatic vein thrombosis has been observed previously in Buffalo strain rats given carbon tetrachloride and methylcholanthrene simultaneously.

Animals↗
PubMed1978

Inferior vena cava and hepatic vein thrombosis as a rare complication of ventriculoatrial shunt. Case report.

A case is reported of hepatic vein thrombosis (Budd-Chiari syndrome) complicating ventriculoatrial shunt for tumoral hydrocephalus. The diagnosis of hepatic vein thrombosis requires specific radiographic investigations that are unlikely to be undertaken unless the condition is specifically suspected. An awareness of this rare and frequently fatal complication is essential for proper diagnosis and treatment.

Budd-Chiari Syndrome↗
PubMed2005

Complications of percutaneous radiofrequency ablation for hepato-cellular carcinoma: imaging spectrum and management.

Percutaneous radiofrequency (RF) ablation is feasible for the treatment of unresectable hepatocellular carcinoma, and experience at the authors' institution during 5 years indicates that percutaneous RF ablation can be performed safely in most cases. However, early or late complications related to mechanical or thermal damage may be observed at follow-up examination. Complications may be classified in three groups: vascular (eg, portal vein thrombosis, hepatic vein thrombosis with partial hepatic congestion, hepatic infarction, and subcapsular hematoma), biliary (eg, bile duct stenosis and biloma, abscess, and hemobilia), and extrahepatic (eg, injury to the gastrointestinal tract, injury to the gallbladder, pneumothorax and hemothorax, and tumor seeding). Most complications can be managed with conservative treatment, percutaneous or endoscopic drainage, or surgical repair. Because an early and accurate diagnosis is necessary for proper management, radiologists should be familiar with the imaging features of each type of complication.

Aged↗
PubMed2002

Segmental hyperattenuation in the liver as a result of right hepatic vein thrombosis: an unusual complication of central venous catheterization.

Liver perfusion disorder secondary to hepatic vein occlusion is not often reported. This abnormality might be caused by invasion of the hepatic veins by tumour or compression by a large right adrenal mass. We present an unusual cause of hepatic perfusion disturbance due to right hepatic vein thrombosis resulting from inadvertent hepatic venous catheterization. On contrast-enhanced CT, the tip of a central venous catheter extended into the right hepatic vein, which was thrombosed. A sharply marginated wedge-shaped hyperdense region was demonstrated in the right lobe of the liver, thought to represent a compensatory increase in arterial flow to the affected territory.

Adolescent↗
PubMed2006

Portal and hepatic vein thrombosis in liver abscess: CT findings.

OBJECTIVE: Our aim is to describe imaging findings of portal and hepatic vein thrombosis in pyogenic liver abscess on contrast-enhanced MDCT and to determine the incidence and evolving patterns on follow-up imaging. METHODS: Over a 5-year period, 67 patients with liver abscess underwent single-phase (n=30) or triphasic (n=37) contrast-enhanced CT. Images were reviewed for the presence of portal vein (PV) or hepatic vein (HV) thrombosis, regional parenchymal attenuation, and changes on follow-up CT. RESULTS: Venous thrombosis was seen in 28/67 patients (42%), involving PV in 16/67 (24%) and HV vein in 15/67 (22%); 3/67 (4%) had both PV and HV thrombosis. Thrombosis was seen as non-enhancing linear structures without expanding the lumen in all cases. Regional parenchymal attenuation during the portal-phase was hyperattenuating (10/16, 63%) or isoattenuating (6/16, 38%) in PV thrombosis, and mostly hypoattenuating (13/15, 87%) in HV thrombosis (P<.001). Of 27 patients with follow-up contrast-enhanced CT, venous thrombosis resolved in 10/27 (37%) within 6 months and persisted in 17/27 (63%) for 3-38 months, including 13 PV thrombosis and 4 HV thrombosis. Interval parenchymal atrophy was seen only in four all with persistent PV thrombosis. CONCLUSIONS: Both PV and HV thrombosis frequently occurs in liver abscess and is seen as non-enhancing linear structures without expanding the lumen on contrast-enhanced CT. Regional attenuation changes in hepatic vein thrombosis were often hypoattenuating whereas none with portal vein thrombosis showed hypoattenuation.

Adult↗
PubMed1987

Hepatic vein thrombosis in paroxysmal nocturnal hemoglobinuria. A spectrum from asymptomatic occlusion of hepatic venules to fatal Budd-Chiari syndrome.

In a series of 40 patients with Budd-Chiari syndrome, 5 (12%) were found to be afflicted with paroxysmal nocturnal hemoglobinuria. The clinico-pathological features in these 5 patients and in 26 well-documented previously reported cases could be ascribed to three groups of increasing severity: thrombosis limited to small-sized hepatic veins with no or transient ascites, partial thrombosis of large-sized hepatic veins with chronic ascites, and complete thrombosis of large-sized hepatic veins with a life-threatening course. These three groups did not differ with regard to sex, age, and duration and characteristics of paroxysmal nocturnal hemoglobinuria. In view of the relationship between prognosis and the extent of hepatic vein obstruction, we suggest that early therapy directed toward limiting the extension of thrombosis, or toward dissolving formed thrombi, should improve the prognosis of this severe complication of paroxysmal nocturnal hemoglobinuria.

Adult↗
PubMed1985

Primary myeloproliferative disorder and hepatic vein thrombosis. A prospective study of erythroid colony formation in vitro in 20 patients with Budd-Chiari syndrome.

We assessed the prevalence of overt and latent primary myeloproliferative disorders in hepatic vein thrombosis. Cultures of bone marrow or peripheral blood mononuclear cells were done in 20 patients with Budd-Chiari syndrome. Erythroid colony formation in the absence of erythropoietin, which is a reliable indicator for a primary myeloproliferative disorder, was seen in 16 patients in whom Budd-Chiari syndrome was due to hepatic vein thrombosis, including 13 women aged 18 to 45 years. Among these 16 patients, the conventional criteria for the diagnosis of a primary myeloproliferative disorder were met in only 2. Primary myeloproliferative disorder, often without peripheral blood changes, is a major cause of hepatic vein thrombosis in young women.

Adolescent↗
PubMedDate not supplied

Case report: hepatic vein thrombosis (acute Budd-Chiari syndrome) in acute leukemia.

A 29-year-old female with acute promyelocytic leukemia presented with severe liver dysfunction and disseminated intravascular coagulation. Her condition rapidly deteriorated and she expired before any antileukemic therapy could be administered. At autopsy, she was found to have massive thrombosis of hepatic veins and their tributaries. Microscopic picture of liver was consistent with acute Budd-Chiari Syndrome, presumably due to the coexisting acute promyelocytic leukemia.

Adult↗
PubMed2002

Portal or hepatic vein thrombosis as the first presentation of a myeloproliferative disorder in patients with normal peripheral blood counts.

Myeloproliferative disorders (MPD) are associated with an increased risk of thrombotic complications. We describe three patients with portal or hepatic vein thrombosis and normal peripheral blood counts who had MPD on bone marrow morphology and growth factor-independent megakaryocyte or erythroid colony growth in vitro. The peripheral blood counts have become abnormal subsequently in two patients. Patients presenting with unexplained portal or hepatic vein thrombosis should be investigated systematically for the presence of a MPD, which may not be apparent using conventional diagnostic criteria.

Adult↗
PubMed1989

Thrombotic cutaneous nodules and hepatic vein thrombosis in the anticardiolipin syndrome.

A patient with the anticardiolipin syndrome presented with hepatic vein thrombosis (Budd-Chiari syndrome) and non-ulcerating, thrombotic, cutaneous nodules. This cutaneous manifestation of the anticardiolipin syndrome has not been described before, though its histological appearances resemble those of previously reported cutaneous complications, such as chronic ulceration, livedo reticularis and distal cutaneous ischaemia. Recognition of the skin lesion could allow the prevention of major systemic complications.

Adult↗
PubMed1996

[Portal vein and hepatic vein thrombosis in occult myeloproliferative syndrome. Progression of thrombosis under heparin therapy].

In a 45-year-old woman presenting with subacute liver failure and portal hypertension the diagnostic workup revealed portal vein thrombosis and occlusion of small hepatic veins. An occult myeloproliferative syndrome was assumed. During full-dose heparin therapy the thrombotic process progressed to segmental venous small bowel infarctions, liver failure and death. In-vitro culture of mononuclear blood cells showed spontaneous growth of erythroid precursor cells. Necropsy demonstrated acute hemorrhagic necrosis of the liver, thrombotic material within the portal and mesenteric veins, thrombosis, dilatation, sclerosis, and partial obliteration of small portal vein branches, and obliterative fibrosis and thrombosis of small intrahepatic veins. The bone marrow and spleen findings support the diagnosis of a myeloproliferative disorder.

Fatal Outcome↗
PubMed1994

Tissue plasminogen activator for hepatic vein thrombosis in paroxysmal nocturnal haemoglobinuria.

Paroxysmal nocturnal haemoglobinuria (PNH) is an acquired clonal disorder thought to arise in a multipotent haemopoietic stem cell. A distinct clinical feature is a tendency to thrombosis, with a particular predilection for the hepatic veins (Budd-Chiari syndrome). We report here on two patients with PNH who developed hepatic vein thrombosis (HVT) and who were treated with tissue plasminogen activator (t-PA). Both patients had a marked clinical and radiological improvement following the t-PA treatment and remain well over 2 years and 6 years after the treatment. This method of thrombolysis for HVT occurring in PNH has only been reported in two previous patients with limited follow-up. We suggest that this therapy is a useful first-line treatment for PNH patients who develop HVT.

Adult↗
PubMed1989

Hepatic vein thrombosis (Budd-Chiari syndrome) in the microgranular variant of acute promyelocytic leukemia.

The microgranular form of acute promyelocytic leukemia (APL) was described in the late 1970s and adopted by the French, American, and British classification system in the early 1980s. Morphologically, this form shows distinct differences from the classic form of APL, but clinically it shares many of the same traits. Among these is the predilection for coagulopathies, including disseminated intravascular coagulation (DIC). This DIC has been associated with one previously reported case of fatal hepatic vein thrombosis (Budd-Chiari syndrome), in association with an untreated case of APL. The authors present a case of the microgranular variant of acute promyelocytic leukemia (FAB-M3V), with autopsy and electron microscopic evidence in support. It is important to recognize this variant form of APL and its association with hepatic vein thrombosis, because any successful attempt at therapy must be instituted early in the course of the disease.

Adult↗
PubMed1981

Veno-occlusive disease and primary hepatic vein thrombosis in Israeli Arabs.

In a survey of nine major Israeli hospitals, 29 patients diagnosed between 1955 and 1975 as suffering from hepatic vein thrombosis were identified. Fifteen of the patients were Jews and 14 were Arabs. In contrast to the Jewish patients, all of whom were adults, the majority of the Arab patients were children below 10 years of age. Primary hepatic vein occlusion was 2.4 times more common among Arab than among Jewish patients. Of the 11 Arab patients with primary hepatic vein occlusion, three had histological changes typical of veno-occlusive disease; whereas in five others, thrombotic occlusion of large hepatic veins or of the vena cava was documented. Although no plant alkaloids could be directly implicated in any of the Arab patients, circumstantial evidence strongly supports such an etiology. All of our Arab patients originated from small agricultural communities where ancient methods of winnowing, which expose the home-ground wheat to a high risk of contamination by grains containing pyrrolizidine alkaloids, are still in use. This report confirms the world-wide distribution of veno-occlusive disease, and under-lines the need for a systematic search for possible sources of poisoning by pyrrolizidine alkaloids.

Adolescent↗
PubMedDate not supplied

[Paroxysmal nocturnal hemoglobinuria revealed by hepatic vein thrombosis (Budd-Chiari syndrome) during Infliximab therapy].

We report the case of a 41-Year-old man presenting with hepatic vein thrombosis (Budd-Chiari syndrome) during Infliximab therapy for ankylosing spondylitis. The systematic work-up revealed paroxysmal nocturnal hemoglobinuria. One Year later the patient was receiving anticoagulation therapy and was in good condition. The role of Infliximab in the development of thrombosis in this patient with rare underlying thrombophilia is discussed.

Adult↗
PubMed2000

Segmental hepatic vein thrombosis associated with heparin-induced thrombocytopenia II.

We report the case of a 55-year-old man who developed heparin-induced thrombocytopenia II after a vertebral fracture. Autopsy revealed segmental hepatic vein thrombosis of the right lobe with subacute congestion and an activation of hepatic stellate cells. This case shows that heparin-induced thrombocytopenia II is a possible cause of the Budd-Chiari syndrome.

Anticoagulants↗
PubMed1989

The Budd-Chiari syndrome caused by a zygomycete. A new pathogenesis of hepatic vein thrombosis.

The clinical history of a 60-year-old woman suffering from chronic lymphocytic leukemia with sudden deterioration and death is reported. The postmortem macroscopic and microscopic findings included pulmonary aspergillosis and pulmonary zygomycosis (mucormycosis). Hematogenous dissemination of the zygomycete causing cardiac zygomycosis, cerebral infarcts due to vascular occlusion by hyphae, and thrombosis of the major hepatic veins (Budd-Chiari syndrome) with submassive necrosis of the right liver lobe were also observed. To our knowledge, this is the second report dealing with occlusion of the hepatic veins caused by a fungus and the first study reporting the Budd-Chiari syndrome due to a mold of the subclass Zygomycetes.

Budd-Chiari Syndrome↗