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Results for “HEPATIC VEIN THROMBOSIS”

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At least 253 records · Page 14Linked to original sources
PubMed1990

Hepatic encephalopathy induced by small bowel obstruction in a noncirrhotic child with portal vein thrombosis.

A case of hepatic encephalopathy in a noncirrhotic child, who has undergone a previous mesocaval shunt for extrahepatic portal vein thrombosis, is presented. Hepatic encephalopathy developed 5 years after the operation and is believed to have been precipitated by the presence of small bowel obstruction. Exploratory laparotomy and lysis of an adhesion relieved the obstruction and led to the resolution of the encephalopathy.

Adolescent↗
PubMed1994

Orthotopic liver transplantation for acute hepatic failure in children.

Thirty children received 35 liver transplants for fulminant or late-onset liver failure between March 1988 and May 1993. Aetiology included non-A non-B hepatitis in 12, Wilson's disease in 8, drug-induced hepatic failure in 6, hepatitis B in 1, hepatitis A in 1, tyrosinaemia in 1 and congenital haemochromatosis in 1. Three patients were retransplanted, one each for hepatic artery thrombosis, non-A non-B graft reinfection, and chronic rejection. Two of these three patients received a third transplant for chronic rejection and hepatic artery thrombosis. One patient in the retransplant group survived. Overall, graft and patient survival at a mean follow-up of 17 months were 49% and 57%, respectively. Mortality was related to vascular complications in three patients (hepatic venous obstruction, portal vein thrombosis and hepatic artery thrombosis). Two patients died of primary sepsis (cerebral aspergillosis and cytomegalovirus (CMV) pneumonitis in association with graft-versus-host disease). Systemic sepsis and multiorgan failure was documented as a cause of death in four children and sepsis in association with chronic rejection in a further three patients. One child died of respiratory failure 4 weeks after transplantation. Mortality in eight children less than 2 years was 75% and this was significantly greater than for older children (P < 0.003, Mantel Cox). Earlier referral, even in the absence of a definitive diagnosis and particularly in children under 2 years is advisable and may improve survival.

Adolescent↗
PubMed1993

Portal hypertension as presenting feature of a myeloproliferative disorder. Diagnosis and therapeutic dilemmas.

In some patients presenting with complications of portal hypertension, thrombosis of hepatic or portal veins is identified as the cause. Hepatic or portal vein thrombosis may be secondary to recognized etiologies like infection or malignancy. When no etiology for the thrombosis is found, it is likely that a 'latent' myeloproliferative disorder (MPD) is the underlying abnormality. We present seven patients referred to us between 1988 and 1993 with complications of portal hypertension due to hepatic or portal vein thrombosis, in whom a 'latent', and in one patient overt, MPD was identified as the underlying disorder. Problems relating to the diagnosis of (latent) MPD in this subset of patients are discussed. The importance of in vitro 'endogenous' erythroid colony formation indicating the presence of MPD is emphasized. Also, a therapeutic strategy, with special emphasis on anticoagulation therapy, is suggested.

Adult↗
PubMedDate not supplied

CT features of abdominal manifestations of primary antiphospholipid syndrome.

PURPOSE: The purpose of this work was to evaluate the CT features of the abdominal manifestations of primary antiphospholipid syndrome (PAPS). METHOD: Of the 32 patients who were confirmed to have PAPS among 751 patients with elevated antiphospholipid antibodies during a 2 year period, we retrospectively reviewed the 14 patients who underwent abdominal CT. The clinical indications for abdominal CT included abdominal pain, abdominal distension, or lower leg swelling. CT findings were analyzed with regard to the abdominal vascular system and abdominal organ involvement patterns as well as ancillary findings. RESULTS: Of the 14 patients with PAPS, 10 had involvement of the venous system (72%), 2 of the arterial system (14%), and 2 of both systems (14%). Of the 12 patients who had venous system involvement, 4 had thrombosis in the inferior vena cava (IVC), 2 in both the IVC and the hepatic vein, 1 in the IVC and splenic and portal veins, 1 in the IVC and hepatic and adrenal veins, 1 in the hepatic, portal, and renal veins, and 3 in the portal and superior mesenteric veins. Budd-Chiari syndrome developed in five of the nine patients who had thrombosis of the IVC or hepatic vein. Arterial thrombosis was noted in four patients, hepatic artery in two, aorta in one, renal artery in one, pancreatic arcade in one, and splenic artery in one, with infarct of multiple organs including the liver, jejunum, colon, kidney, and adrenal gland. Seven of the 14 patients (50%) manifested thrombosis or infarct of multiple extra-abdominal organs. CONCLUSION: PAPS should be included in the differential diagnosis when CT demonstrates infarcts in multiple organs or patients have recurrent episodes of venous or arterial thrombosis.

Adolescent↗
PubMed2000

Retinal vein thrombosis associated with chronic hepatitis C: a case series and review of the literature.

The role of procoagulant autoantibodies in hepatitis C virus (HCV) infection is unclear. Three individuals with HCV infection and a unique genetic hypercoagulable state developed retinal vein thrombosis (RVT) in association with interferon-alpha (IFN-alpha) therapy. It is probable that a combination of active HCV infection in a genetically susceptible individual receiving IFN-alpha accounted for the observed RVT.

Adult↗
PubMed2006

Experimental hepatic radiofrequency ablation using wet electrodes: electrode-to-vessel distance is a significant predictor for delayed portal vein thrombosis.

The aim of this study was to examine possible explanatory variables associated with acute and delayed portal vein thrombosis after hepatic radiofrequency (RF) ablation using wet electrodes. Coagulations were created within 1.5 cm of the right portal vein (RPV) branch in 12 pigs with (n = 6) or without (n = 6) Pringle manoeuvre. Sham operations with Pringle manoeuvre were performed in four animals. Rotational portal venography was performed prior to ablation, 10 min after ablation and 4 days after ablation. Vessel diameters and vessel patency was determined from the portal venograms. Distance between the ablation electrode and RPV was measured from 3-dimensional reconstructions of the portal venograms. The portal veins were examined by microscopy. Delayed portal vein thrombosis was found in two of six animals in the Pringle group and three of six animals in the control group 4 days after ablation (P = 1.0, Fisher's exact test). All five occurrences of delayed portal vein thrombosis were found in the six animals with a distance between the ablation electrode and RPV of 5 mm or less (P = 0.030), indicating that the electrode-to-vessel distance may be an independent explanatory factor for delayed portal vein thrombosis after RF ablation with wet electrodes.

Animals↗
PubMed1998

[Thrombosis of the hepatic artery and portal vein secondary to invasive aspergillosis following liver transplantation].

Thrombosis of the main hepatic vessels is a severe, frequent complication in patients requiring liver transplantation. It is usually a cause of emergency retransplantation. Two cases of hepatic vascular thrombosis secondary to disseminated aspergillosis are presented. Both patients demonstrated a septic state and required a second transplantation despite which they died within a few days. Necropsy showed disseminated aspergillosis with invasion of the portal venous system and the hepatic artery. The risk factors associated with this infection and the possible pathogenic mechanisms are discussed.

Abscess↗
PubMed1998

Pathology of the liver in Budd-Chiari syndrome: portal vein thrombosis and the histogenesis of veno-centric cirrhosis, veno-portal cirrhosis, and large regenerative nodules.

Hepatic vein (HV) thrombosis causes ascites, hepatomegaly, and severe congestion of the liver (Budd-Chiari syndrome [BCS]). Severe hepatic fibrosis develops in this syndrome with a variety of histological patterns. Some livers have a pattern of cirrhosis in which there is fibrous bridging between HVs and portal tracts (veno-portal cirrhosis). Other livers have a pattern of "reversed-lobulation cirrhosis" (veno-centric cirrhosis), in which fibrous bridging between HVs and portal tracts is minimal. The prevalence and pathogenesis of these forms of cirrhosis and the effect of portal vein (PV) thrombosis in this disease have not been studied. We examined 15 resected livers from patients with BCS to determine the distribution of vascular obstruction and the character of the parenchymal response. Six livers had veno-portal cirrhosis, and all of these had severe PV obliteration caused by thrombosis. Three livers had veno-centric cirrhosis and had normal medium and large PVs. The remaining six livers had mixed veno-centric/veno-portal cirrhosis and had moderate PV obliteration. The nodules in veno-centric cirrhosis had evidence of an unusual circulation with small arteries supplying a midzonal venous plexus that appeared to drain retrogradely into patent small PVs. Nine livers had large regenerative nodules histologically similar to focal nodular hyperplasia. PV thrombosis is a frequent occurrence in BCS. The correlation between PV thrombosis and the pattern of cirrhosis suggests a role for PV obliteration in the genesis of veno-portal bridging fibrosis in this disease and possibly in other diseases leading to cirrhosis.

Adult↗
PubMed1994

Hepatic artery interruption followed by portal vein thrombosis in an adult liver transplant.

Vascular complications following liver transplantation result in significant morbidity and mortality. We report a 28-year-old man who, because of a mycotic false aneurysm, underwent ligation of the hepatic artery 4.5 weeks post-transplantation and who, 4.5 months later, suffered a portal-mesenteric vein thrombosis. Adverse hepatic sequelae did not follow these events, demonstrating the capacity of the collateral circulation to perfuse the transplanted liver.

Adult↗