[Primary antiphospolipid syndrome causing thrombosis of hepatic vein].
Explore the source record for details and available documents.
Adult↗
SEARCH · PubMed Health
Results for “HEPATIC VEIN THROMBOSIS”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Thrombosis of hepatic veins accompanying carbon tetrachloride induced cirrhosis.
Explore the source record for details and available documents.
Animals↗
[A case of Budd-Chiari syndrome due to diffuse thrombosis of hepatic veins without involvement of inferior vena cava].
Explore the source record for details and available documents.
Budd-Chiari Syndrome↗
On the mechanisms responsible for selection of hepatic veins as target for thrombosis following injection of endotoxin in hyperlipemic rats.
The feeding of a butter-rich diet, to sensitize rats for studying the phenomenon of hepatic vein thrombosis, is shown to produce severe liver steatosis leading to a sinusoidal barrage and portal hypertension. The portal pressure in these animals was 210 +/- 4 mm of saline, as compared to 113 +/- 3 mm in the normal rat. Blood circulation studies using carbon suspensions revealed production of a vascular stasis in the hepatic veins after 60 to 90 minutes, when endotoxin (Salmonella typhosa, 0.3 mg/kg) is introduced into the blood circulation to initiate hepatic vein thrombosis. Similar results were observed after 15 minutes with ellagic acid (1 mg/kg/min). The stasis was found in connection with an additional intrahepatic resistance to blood flow as evidenced by a rise in portal pressure and by a reduction in liver perfusion in relation with development of systemic hypotension. In contrast with this, endotoxin initiated only slight and transient changes in the normal rat. Thrombosis immediately followed production of stasis in the hepatic vein, whether the phenomenon was initiated by endotoxin or ellagic acid. Furthermore, inhibition of the vascular stasis of alpha-adrenergic blockade (phenoxybenzamine, 3 mg/kg) was accompanied by prevention of hepatic vein thrombosis. It is concluded that stasis in the hepatic veins resulting from a mechanical obstruction of the circulation by steatosis and by an additional reduction in blood flow initiated by endotoxin, is responsible for selection of hepatic veins as targets for thrombosis following injection of endotoxin in hyperlipemic rats.
Animals↗
The use of transjugular intrahepatic portosystemic shunt and surgical portocaval H-shunt for the treatment of colorectal variceal bleeding.
Surgical portocaval H-shunt was performed after the thrombosis of a transjugular intrahepatic portosystemic shunt inserted for colorectal variceal bleeding. The surgical procedure successfully controlled the variceal bleeding. However, the patient developed postoperative liver failure and hepatic encephalopathy due to complete portal vein thrombosis and the absence of prograde portal flow. This case illustrates the potential risks of the serial use of transjugular intrahepatic portosystemic shunt and surgical portocaval shunt leading to complete portal vein thrombosis, hepatic encephalopathy and acute liver failure.
Aged↗
[Diagnostic imaging of Budd-Chiari syndrome in adults and children].
Budd-Chiari syndrome is caused by the obstruction of the hepatic veins or of the inferior vena cava. It is characterized by the classic symptomatological triad: ascites, hepatomegaly, and abdominal pain. In 2/3 cases its etiology remains unknown. Budd-Chiari syndrome may be associated with polycythemia vera, neoplasms, chronic leukemia, congenital abnormalities, hypercoagulation conditions, pregnancy, oral contraceptives, and constrictive pericarditis. Even though its clinical diagnosis is difficult, radiology plays a decisive role with US, CT, MR imaging and, above all, angiography; the latter, together with liver biopsy, generally provides with an unquestionable diagnosis. Through the definition of stage of the disease, of level (intrahepatic, venous, caval, cardiac), of type (intrinsic or extrinsic), and degree of both obstruction and consequent development of collateral channels, radiology determines which patients should undergo a medical or a surgical treatment. In some case, percutaneous angioplasty can be performed. Four cases of Budd-Chiari syndrome, including two children, were investigated with US, CT, angiography, and liver biopsy; MR imaging was also employed in one case. The underlying cause was identified in 3 patients: constrictive pericarditis of probable congenital origin and web occlusion of the inferior vena cava near the right atrium in the 2 children; hepatic vein thrombosis due to essential thrombocythemia in the third case. In the fourth patient, thrombosis of the inferior vena cava and hepatic veins was unexplained. The diagnosis was established by means of liver biopsy and phlebography of the hepatic veins. Good diagnostic information was also supplied by non-invasive techniques, such as US, CT, and MR imaging.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Treatment of advanced Budd-Chiari syndrome by liver transplantation].
Budd-Chiari syndrome (BCS) with hepatic vein occlusion is a rare disorder that can effectively be treated in advanced stages with orthotopic liver transplantation. We report on 16 patients who received 18 liver grafts and were followed up for at least 2 years. In 7 patients a hematological disorder was confirmed by bone marrow biopsy. One patient died after 4 months due to cytomegalovirus pneumonia; another patient died after 2 years due to progressive liver failure after portal vein thrombosis. The actuarial 5-year survival rate is 87.5% compared to 85.3% in all other 710 orthotopic liver transplantations performed from September 1988 to December 1995 at our institution. Anticoagulation consisted of intravenous heparin and overlapping continuation with dicoumarin. Three patients received hydroxyurea for thrombocytosis, one patient for 1 week only early after the transplantation. Two postoperative abdominal hemorrhages required laparotomy. Two patients had to be retransplanted, one for thrombosis of the hepatic artery and portal vein after discontinuation of dicoumarin due to GI bleeding and one for hepatic vein thrombosis after insufficient dicoumarin intake. Terminal BCS represents a good indication for orthotopic liver transplantation; however, life-long, closely monitored anticoagulation is essential.
Adolescent↗
Fistula between duodenum and portal vein caused by peptic ulcer disease and complicated by hemorrhage and portal vein thrombosis.
We document a patient with a penetrating peptic ulcer of the first part of the duodenum, that extended into the main portal vein forming a fistula. This is the first reported case of a duodenoportal fistula secondary to peptic ulcer disease. The fistula was complicated by massive gastrointestinal hemorrhage, extra- and intrahepatic portal vein thrombosis, hepatic parenchymal infarction, and intrahepatic portal vein foreign body granulomas containing vegetable matter.
Aged↗
Hepatic chemoembolization: safety with portal vein thrombosis.
PURPOSE: Nine patients with unresectable hepatic malignancy and portal vein thrombosis underwent hepatic chemoembolization. PATIENTS AND METHODS: Six patients had primary malignancies (hepatocellular carcinoma in five, hepatoblastoma in one), and three had metastatic tumor (adenocarcinoma of the colon in two, glucagonoma in one). Chemoembolization was performed with 10 mg/mL of cross-linked collagen, 10 mg/mL of mitomycin, 3 mg/mL of doxorubicin, and 3 mg/mL of cisplatin. Each patient was treated until flow in the hepatic artery ceased completely. RESULTS: All treatments were technically successful. Eight patients responded to treatment, including two long-term survivors (> 2 years). One patient died 31 days after treatment of progressive hepatic malignancy and atherosclerotic disease. No patient developed hepatic infarction or insufficiency as a result of treatment. Follow-up ranged from 1 to 26 months (mean, 13 months). CONCLUSION: Portal vein thrombosis should not be considered an absolute contraindication to hepatic chemoembolization. Hepatic chemoembolization can be performed safely in the presence of adequate collateral circulation.
Adult↗
In situ splitting of the cadaveric liver for two adult recipients.
BACKGROUND: Split-liver transplantation offers a unique opportunity to expand the existing donor pool. However, it has previously been stated that due to inadequate liver volume the advantages of split-liver transplantation would be lost when attempting to split the liver for two adult recipients. In this study, we sought to determine the safety, efficacy, and applicability of split-liver transplantation in select adult liver transplant recipients. METHODS: Liver allografts for eight adult recipients were procured by in situ splitting of four adult cadaveric livers. The donor ages were 17, 19, 22, and 25 years and weights were 72, 77, 78, and 87 kg, respectively. In situ splitting resulted in three right trisegmental grafts, one right lobe graft, one left lobe graft, and three left lateral segmental grafts. The median recipient age was 49 years (range 38-61 years), whereas the median recipient weight was 84 kg (range 78-98 kg) for the right-sided grafts and 52 kg (range 51-53 kg) for recipients of the left-sided grafts. The median graft-to-recipient body weight ratio for right trisegmental, right lobe, left lobe, and left lateral segmental grafts was 1.31%, 1.26%, 1.35%, and 0.70%, respectively. RESULTS: Overall patient and graft survival in this series is 100%. All prothrombin times were normalized within 4 days of transplantation. No evidence of ascites or prolonged hyperbilirubinemia was encountered in any right- or left-sided graft recipient. The incidence of hepatic artery, portal vein, and hepatic vein thrombosis is 0%, 0%, and 0%, respectively. Hepatic arterial anastomotic bleeding and a cut surface bile leak each occurred in one patient. Median United Network for Organ Sharing (UNOS) waiting time was 242 days (range 4-454 days) for the patients to which the donor liver was allocated. In contrast, the median waiting time for the four patients receiving the extra split-liver graft was reduced significantly to 37 days (range 21-101 days) (P<0.02). CONCLUSIONS: This study demonstrates that split-liver transplantation can expand the cadaveric donor liver pool available for select adult liver transplant recipients. When both the donor organ and the transplant recipient are chosen carefully, split-liver transplantation can be safely performed without a delay in allograft function, increase in technical complications, or compromise in graft or patient survival.
Adolescent↗
Thrombocytosis and recurrent hepatic outflow obstruction (Budd-Chiari syndrome) after successful thrombolysis: case report and literature review.
Approximately two thirds of cases of hepatic flow obstruction are due to myeloproliferative disorders. Restoration of hepatic blood flow is the essential goal of treatment. Thrombolytic therapy seems to achieve good results at least in selected cases. A 32-year-old woman is presented, with an intermittent increase in platelet count (526-725 x 10(9)/L), two previous spontaneous abortions and acute symptomatic occlusion of hepatic veins, and in whom a diagnosis of essential thrombocythemia was initially carried out in agreement with the polycythemia vera study group criteria. She received recombinant tissue plasminogen activator followed by heparin with restoration of normal hepatic outflow. Asymptomatic re-occlusion of the hepatic veins was observed 1 year later, despite adequate continuous warfarin treatment. Angiography showed marked narrowing of the intrahepatic cava vein due to extrinsic compression by an enlarged liver, not due to a new thrombosis so that no specific intervention could be performed. In the presence of a dearly documented hepatic vein thrombosis, thrombolytic therapy should be considered. The patient was given low-molecular-weight heparin with a dramatic reduction in previously elevated fibrinogen level and a good control of the hepatic function.
Adult↗
Liver nodules resembling focal nodular hyperplasia after hepatic venous thrombosis.
We report the case of focal nodular hyperplasia-like nodular hepatic lesions, that developed in the liver of a 35-year-old Caucasian female who required orthotopic liver transplantation for Budd-Chiari syndrome. The rapid development of focal nodular hyperplasia-like lesions in a severe hepatic vascular disorder and in the absence of cirrhosis may represent an additional argument in favor of the vascular origin of focal nodular hyperplasia. The pathogenesis of the nodules is not clear, but pathological arterialization of the liver in hepatic vein thrombosis may be a candidate mechanism.
Adult↗
[Acute hepatic-vein occlusive disease, associated with portal vein thrombosis, splenic rupture and hepatic failure].
Explore the source record for details and available documents.
Budd-Chiari Syndrome↗
Budd-Chiari syndrome and thrombosis of other abdominal vessels in the chronic myeloproliferative diseases.
Of 501 patients with chronic myeloproliferative diseases (c-MPD) 18 developed thrombosis of major abdominal vessels including 6 with hepatic vein thrombosis (Budd-Chiari syndrome). The complication was seen in 14 of 140 (10%) patients with polycythemia vera (PV), 3 of 23 (13%) patients with essential thrombocythemia (ET), 1 of 106 (1%) patients with idiopathic myelofibrosis (IMF), and none of 232 patients with chronic myelogenous leukemia (CML). Leading symptoms and signs were abdominal pain, progressive splenomegaly, widening abdominal girth, ascites, venous collaterals, and nausea and vomiting. The diagnostic modalities with highest specificity were angiography and explorative laparotomy. A causal relationship between the thrombotic event and hematocrit, thrombocyte count, or hemostatic abnormalities at the time of diagnosis could not be established. Detailed laboratory tests of platelet function and coagulation and fibrinolytic parameters of 5 surviving patients did not show any specific defect. Despite medical and surgical intervention, 39% of the patients died within 2 months after diagnosis of the thrombosis. The majority of the survivors developed further complications like liver cirrhosis with portal hypertension and esophageal varices or the short bowel syndrome after extensive bowel resection for mesenterial infarction.
Blood Coagulation Tests↗
Surgical complications and outcome of paediatric liver transplantation: the Singapore experience.
The purpose of this study was to analyse the early and late results of paediatric liver transplantation (LT), with particular reference to complications that required surgical intervention. The charts of all children who underwent LT between 1990 and 2002 were reviewed retrospectively. Results were analysed with a minimum follow up of 9 months. Thirty-five children have undergone 38 LTs; 22 received grafts from their parents, 16 received cadaveric organs and three children had retransplantation. The ages of the children ranged from 12 to 168 months. Biliary atresia was the most frequent indication for transplant (n=27). Twenty-seven children had complications that required surgical or radiological interventional procedures. Vascular complications included hepatic artery thrombosis (n=2), hepatic vein (HV) thrombosis (n=1), and the majority being portal vein thrombosis (n=6). Bile leaks were observed in eight children. Other complications included intestinal perforation (n=2), intra-abdominal abscesses (n=1), wound dehiscence (n=2), post-operative bleed (n=2), intestinal obstruction (n=2), ventral hernia (n=1), and multiple abdominal wound sinuses (n=1). Three children underwent retransplantation, two for hepatic artery thrombosis with multiple episodes of cholangitis and intrahepatic biliomas and the third was done for hepatic vein thrombosis. Patient and graft survival at 1 year is 81.5 and 74.2%, respectively. Paediatric LT is associated with significant morbidity, the main complications being vascular and biliary.
Adolescent↗
Recurrent spontaneous bacterial peritonitis in a patient with polycythemia vera.
Spontaneous bacterial peritonitis (SBP) is an infectious process that usually occurs in patients with cirrhosis. There are few reports of SBP in patients with other pathologies such as nephrotic syndrome, acute and chronic hepatitis, cardiac ascites, and ascites secondary to neoplastic disease. We report a patient with polycythemia vera in whom recurrent episodes of SBP occurred 8 months following a portacaval shunt operation for Budd-Chiari syndrome. Conceivably, the polycythemia vera (PV) complicated by hepatic vein thrombosis and portacaval shunt resulted in significant loss of hepatic reticuloendothelial system function and predisposed the patient to bacterial peritonitis.
Budd-Chiari Syndrome↗
Cavernous transformation of the portal vein: a common manifestation of Behçet's disease.
Behçet's disease (BD) is a chronic, multisystem inflammatory disorder of unknown etiology, which is characterized by recurrent aphthous ulcers of the mouth and genitalia, uveitis with hypopyon, and a diffuse vasculitis that involves the arterial and venous systems. From January 1968 to July 1993, 66 of 844 patients with BD seen at the Hacettepe University Hospital, Ankara, Turkey, experienced a vascular complication other than peripheral thrombophlebitis. The vascular complication in each case was identified based upon a combination of clinical data, digital subtraction angiography, CT, and ultrasonography findings. Six of these 66 (9.1%) had cavernous transformation of the portal vein. Five of these six had additional large vein involvement resulting in the Budd-Chiari syndrome with or without inferior vena caval obstruction. Based upon this experience, it can be concluded that portal vein thrombosis is not a rare complication of BD. When patients with BD are found to have or develop splenomegaly, portal vein thrombosis should be suspected and investigated. If hepatomegaly and ascites are detected, Budd-Chiari syndrome due to hepatic vein thrombosis should be suspected. Finally, if hepatosplenomegaly, ascites, and dependent edema of the lower body are present, thrombosis of the inferior vena cava should be suspected.
Behcet Syndrome↗
Outcome of portal-systemic shunt surgery for portal hypertension associated with intrahepatic obstruction in patients with agnogenic myeloid metaplasia.
Life-threatening portal hypertension (PHN) in patients with chronic myeloproliferative disorders may result from increased portal flow caused by marked splenomegaly or an increased resistance to portal flow from either a large vein thrombosis or an intrahepatic obstruction usually associated with agnogenic myeloid metaplasia (AMM). The former cause is correctable by splenectomy alone, whereas the latter requires portal-systemic shunt surgery. Few data exist regarding the outcome of portal-systemic shunt surgery in patients with AMM and intrahepatic obstruction. During the past 25 years, 13 patients with chronic myeloproliferative disorders underwent portal-systemic shunt surgery at our institution. The cause of PHN was intrahepatic obstruction in ten patients and hepatic vein thrombosis in three. Ten of the thirteen patients had AMM as initial diagnosis. Only one patient had intraoperative complications, and four patients had either sepsis or thrombosis during the postoperative period. Twelve patients survived the postoperative period and had a median postsurgical survival of 3 years (range, 0.25 to 19 years). The long-term complications of the operation were very few and included hepatic encephalopathy (one patient), portal vein thrombosis (one patient), and shunt occlusion (one patient). The procedure was successful in alleviating complications of PHN in all but one patient. Deterioration of hepatic function and subsequent hepatomegaly were unusual. Portal-systemic shunt surgery seems to be a useful option in patients with AMM and life-threatening PHN from intrahepatic obstruction.
Adult↗