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PubMed1981

Oral contraceptives and hepatic vein thrombosis.

The purpose of this paper is to report on three cases of the Budd-Chiari syndrome in young women who were taking oral contraceptives. Two patients survived, with gradual resolution of hepatomegaly and ascites following discontinuance of the birth control pills. One death occurred soon after the patient's admission to the hospital. The pathophysiology of this phenomenon involves two major aspects. Oral contraceptives are known to cause a hypercoagulation state as well as a direct effect on the blood vessels. In this series the combination of hypercoagulation and progressive occlusion of the vessels in patients on oral contraceptives appeared to lead to the development of thrombosis of the liver vessels.

Adult↗
PubMed1997

[Hepatic vein thrombosis. Diagnostic and therapeutic difficulties].

Budd Chiari syndrome (liver vein thrombosis) may be a diagnostic and therapeutic problem. On the basis of four different cases we review the major diagnostic and therapeutic principles involved. Imaging techniques are necessary in order to establish the diagnosis. Ultrasound examination with Duplex doppler is usually sufficient, but MR angiography is also useful. Treatment options are thrombolysis, surgery or liver transplantation. What treatment is selected will depend on the clinical situation and the prognosis.

Adult↗
PubMed1997

Budd-Chiari syndrome: a common complication of Behçet's disease.

OBJECTIVE: The Budd-Chiari syndrome is characterized by venous outflow obstruction of the liver, usually occurring as a consequence of thrombosis of the hepatic veins. Vasculitis is a major component of Behçet's syndrome. The aim of this study was to determine the incidence of hepatic vein thrombosis in patients with Behçet's disease and to estimate the effect of this entity upon the clinical features and course of Behçet's syndrome. METHODS: During an 8-yr period from 1985 to 1994, from a total of 493 patients with Behçet's disease seen at Hacettepe University Hospital, the incidence and effect of hepatic vein thrombosis on the clinical course of Behçet's syndrome was investigated. The hepatic vein thrombosis in each case was documented by hepatic venography and confirmed by digital subtraction angiography, computed tomography, ultrasonography, and liver biopsy. Coagulation parameters including protein C, protein S, and anti-thrombin III levels were easured in each case. The survival of cases with Behçet's syndrome complicated by Budd-Chiari syndrome and the effect of the Budd-Chiari syndrome on the survival of individuals with Behçet's syndrome were determined using the Kaplan-Meier technique. RESULTS: Of the 493 cases of Behçet's syndrome, 53 (10.8%) were found to have one or more large vessel thrombosis. Of these 53 patients, 14 (26.4%) had hepatic vein thrombosis. Of these 14 patients, 8 had an additional inferior vena cava thrombosis and 4 had portal vein as well as total inferior vena cava thrombosis. Only two patients with isolated hepatic vein thrombosis were identified. These two patients and two additional patients with hepatic vein thrombosis plus thrombosis of the hepatic portion of the inferior vena cava are currently alive. Of the 10 patients with total inferior vena cava and hepatic vein thrombosis (4 also had portal vein thrombosis), all 10 died with a mean survival of 10.3 months. During the same time period, 37 patients obtained from a total of 1494 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction or inferior vena caval obstruction without Behçet's syndrome were found to have a Budd-Chiari syndrome. Of these 37 patients, 19 (51%) had an identifiable underlying disorder responsible for their hepatic vein thrombosis. CONCLUSION: Based upon this experience, it appears as if Budd-Chiari syndrome is a relatively frequent complication of Behçet's disease. When individuals with Behçet's syndrome have BCS, concurrent thrombosis of the portal vein and inferior vena cava are often found, if the patency of these vessels is assessed. The clinical course of patients with Behçet's syndrome complicated by Budd-Chiari syndrome is poor. The extent of the vascular thrombosis within the inferior vena cava rather than the presence of the hepatic vein thrombosis per se is the major determinant of survival.

Adolescent↗
PubMed2002

Inferior vena cava thrombosis at its hepatic portion (obliterative hepatocavopathy).

The Budd-Chiari syndrome was primarily described as hepatic vein thrombosis within the liver, but it now includes inferior vena cava (IVC) thrombosis and other conditions that cause hepatic vein outflow obstruction. This author and several others maintain that primary hepatic vein thrombosis and primary IVC thrombosis represent two different clinical disorders. Primary thrombosis of the IVC most commonly occurs in its hepatic portion, which seems to be predisposed to thrombosis and has been called membranous obstruction of IVC, because the thrombus organizes into a fibrous and frequently membranous occlusion of the IVC. The hepatic vein orifices are affected to varying degrees, resulting in congestive liver damage. The cause of IVC thrombosis may be a hypercoagulable state such as coagulation factor deficiency and myeloproliferative disorders, but is more often idiopathic. In Nepal, it is endemic with a suspected association with infections. To consider IVC thrombosis and the congestive liver damage as a disease entity, this author proposes the term obliterative hepatocavopathy, separate from hepatic vein thrombosis. Clinically obliterative hepatocavopathy is less severe in its acute phase compared with hepatic vein thrombosis, but it aggravates occlusion of hepatic vein orifices with recurrent thrombosis. Primary hepatic vein thrombosis and obliterative hepatocavopathy display different hemodynamics of the hepatic veins, IVC, and portal vein; dilatation of the subcutaneous veins in the body trunk is more pronounced in obliterative hepatocavopathy because the ascending lumbar vein becomes the major collateral route. Congestive liver cirrhosis develops after a long clinical course that may be complicated by hepatocellular carcinoma.

Budd-Chiari Syndrome↗
PubMed2006

Contrast-enhanced versus conventional and color Doppler sonography for the detection of thrombosis of the portal and hepatic venous systems.

OBJECTIVE: We conducted a prospective study to compare sonography, color Doppler sonography, and contrast-enhanced sonography for the detection and characterization of portal and hepatic vein thrombosis complicating hepatic malignancies. SUBJECTS AND METHODS: Three hundred sixteen patients with biopsy-proved hepatic tumors were studied at baseline and 3 months later with sonography, color Doppler sonography, and contrast-enhanced sonography. Thrombosis was defined as the presence of intraluminal echogenic material at sonography, absence of intraluminal color signals at color Doppler sonography, and presence of nonenhancing intraluminal area at contrast-enhanced sonography. Thrombi were considered malignant if they displayed continuity with tumor tissue at sonography, intrathrombus color signals at color Doppler sonography, and enhancing signals at contrast-enhanced sonography, both having arterial waveforms at Doppler spectral examination. Definitive diagnoses were obtained by sonographically guided biopsy except for thrombi displaying at conventional sonography unequivocal continuity with tumor tissue. RESULTS: Thrombosis was detected in 79 (25.0%) of 316 patients at baseline and in 83 (26.3%) of 316 patients after 3 months. Eighty-one (97.6%) of the 83 thrombi were malignant. Definitive diagnosis was performed by imaging in 60 (72.3%) of the 83 cases and by biopsy in 23 cases (27.7%). For thrombus detection, contrast-enhanced sonography displayed significantly higher sensitivity than color Doppler sonography (p = 0.004) and borderline superiority over sonography (p = 0.058). For thrombus characterization, contrast-enhanced sonography was significantly more sensitive than color Doppler sonography (p < 0.0005) and conventional sonography (p = 0.02). CONCLUSION: Contrast-enhanced sonography is superior to sonography and color Doppler sonography for the detection and characterization of portal and hepatic vein thrombosis complicating hepatic malignancies.

Adult↗
PubMed2001

Interventional radiologic procedures in liver transplantation.

Postoperative biliary and vascular complications contribute significantly to morbidity and mortality in liver transplantation. Interventional radiologists are an integral part of the multidisciplinary team necessary for optimizing the management of these complications. During a 15-year period, 39 cadaveric and 25 living related liver transplantations were performed at the Chang Gung Memorial hospital, Taiwan. Of 64 liver transplant recipients, 9 (3 adult and 6 pediatric) underwent 13 interventional radiological procedures for the treatment of biliary sludge-casts (n = 2), bile duct occlusion or stenosis (n = 2), hepatic veins thrombosis (n = 1), hepatic veins stenosis (n = 1), portal vein stenosis with splenorenal shunting (n = 1), biloma (n = 1), and infected fluid collection or ascites (n = 4). Antegrade or retrograde interventional approach was used to successfully treat all biliary complications, and all percutaneous drainage procedures were effective in the control of intra-abdominal fluid collections. Portal vein stenosis was treated by balloon dilatation, and the associated splenorenal shunt was closed by metallic coil embolization via transhepatic catheterization of the portal vein. Hepatic vein stenosis was effectively treated by balloon dilatation and expandable metallic stent deployment via transfemoral and jugular venous approaches, respectively. Hepatic vein thrombosis was only partially lysed by transvenous streptokinase administration, and surgical thrombectomy was needed to achieve complete recanalization. The total success rate of the interventional procedures was 92 % with no procedure-related complications. The overall survival rate in this series is 89 %, and all patients who underwent living related liver transplantation maintain to date a 100 % survival rate. We can conclude that interventional radiological procedures are very useful for managing biliary and vascular complications after liver transplantation. These techniques provide a cure in most situations, thus obviating the need for further surgical intervention or re-transplantation.

Adolescent↗
PubMed1998

Does hepatic vein outflow obstruction contribute to the pathogenesis of hepatocellular carcinoma?

Hepatocellular carcinoma (HCC) is one of the more common malignant diseases in the world. Here we have investigated role of hepatic venous outflow obstruction in the development of HCC. During a 10-year period from November 1986 to December 1996, 1,748 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction, or inferior vena cava obstruction without Behçet's disease (BD) and 512 patients with Behçet's disease were examined at Hacettepe University Hospital. The presence of and the effect of hepatic venous obstruction on the subsequent development of HCC was assessed. In each case, hepatic vein thrombosis was assessed by hepatic venography and by digital subtraction angiography (DSA), computed tomography (CT), ultrasonography (US), and liver biopsy. Coagulation factors, including protein C, protein S, anti-thrombin III, and routine laboratory studies assessing the coagulability of blood were also investigated. The role of hepatic venous outflow obstruction on the subsequent development of HCC was determined by periodic laboratory investigations that included alpha-fetoprotein (AFP), ultrasonography, and when indicated liver biopsy. During the same time period all patients diagnosed as having HCC were investigated to identify all potential etiologic factors responsible for the HCC. Fifty-five (10.7%) of the 512 patients with BD were found to have one or more large vein thromboses. Sixteen of these 55 (29%) patients had hepatic vein thrombosis. During the follow-up period HCC developed in 2 of these 16 patients (12.5%), 34 and 21 months after a diagnosis of hepatic vein thrombosis was established. Forty patients from a total of 1,748 patients with clinical evidence of portal hypertension and cirrhosis, but without BD, were found to have evidence of hepatic vein thrombosis. Twenty-one of these 40 patients had an identifiable underlying disorder responsible for their hepatic vein thrombosis. Despite a full clinical and laboratory investigation in the other 19 patients, the etiologic factor responsible for the hepatic vein thrombosis remained obscure. Only one of these 19 patients, who also had portal vein thrombosis, developed HCC during a 9-year follow-up. Thus, a total of three of the 56 (5.36%) of cases of hepatic vein thrombosis developed an HCC. All of the hepatic tumors were of the multicentric, nodular, rapidly growing type. Despite the presence of hepatic vein thrombosis, there was no clear-cut histologic evidence for cirrhosis. Our experience suggests that hepatic vein thrombosis may be a contributing factor responsible for HCC development. Moreover, we advise that individuals with hepatic vein thrombosis should be assessed periodically for the development of HCC.

Adult↗
PubMed1988

The successful management of portal vein thrombosis after hepatic transplantation with a splenorenal shunt.

Portal vein thrombosis is an infrequent complication after hepatic transplantation, but is quite dramatic when it occurs. It is usually managed by retransplantation with a significant mortality rate. We present a patient in whom portal vein thrombosis after hepatic transplantation was ultimately managed by a splenorenal shunt. The portal vein thrombosis was manifested by bleeding esophageal varices and, yet, normal hepatic function obviated the need for a new graft (one was not readily available). To the best of our knowledge, this is the first presentation of a patient with a transplant of the liver with acute portal vein occlusion and maintained hepatic function who has been successfully managed by a portosystemic shunt.

Child↗
PubMed2001

Membranous obstruction of the inferior vena cava (obliterative hepatocavopathy, Okuda).

Confusion prevails throughout the world regarding the definition and classification of the Budd-Chiari syndrome. The original patients (Budd and Chiari) described had hepatic vein thrombosis, but this syndrome now encompasses various hepatic venous outflow blocks, of which membranous obstruction of the inferior vena cava (IVC) is the most common. This author has been suggesting that the classical Budd-Chiari syndrome or hepatic vein thrombosis and membranous obstruction of IVC or primary thrombosis of IVC at its hepatic portion are epidemiologically, pathologically and clinically different, and that they should be treated as two clinical entities that are not to be mixed. The two diseases have a different onset, different clinical manifestations and a different natural history. Whereas hepatic vein thrombosis is a severe disease with an acute onset, IVC thrombosis presents mildly at onset, but it recurs and eventually turns into a fibrous occlusion of IVC of varying thickness or stenosis of a various degree. The fibrous IVC occlusion is found as a mysterious thin membrane, but is more often much thicker than a membrane, and therefore 'membrane' is a misnomer. Although the genesis is not established, formation of a thin membrane may be an outcome of recurrent thrombosis. The past congenital vascular malformation theory no longer holds, because the disease occurs mostly in adulthood, and transformation of thrombosis into a membrane has now been well documented pathologically as well as clinically. This author suggests that a term 'obliterative hepatocavopathy' replace membranous obstruction of IVC, the term 'Budd-Chiari syndrome' be abandoned, and that primary hepatic venous outflow block be divided into primary hepatic vein thrombosis and primary IVC thrombosis (obliterative hepatocavopathy).

Constriction, Pathologic↗
PubMed2002

Surgical complications and outcome of pediatric liver transplantation in Hong Kong.

PURPOSE: The aim of this study was to analyze the early and late results of pediatric liver transplantation, with particular reference to complications that required surgical or radiologic intervention. METHODS: The records and code sheets of children who underwent liver transplantation in the authors' institution between September 1993 and December 2001 were reviewed. RESULTS: Twenty-nine children (16 boys and 13 girls) underwent 31 liver transplantations (23 living donor, 8 cadaveric donor) during the study period. The ages of the children ranged from 4 months to 132 months (median, 16 months). Eighteen children had complications that required surgical or radiologic interventional procedures. Complications included, among others, hepatic vein thrombosis (n = 1, 3%), hepatic vein stenosis (n = 2, 7%), portal vein thrombosis (n = 2, 7%), biliary stricture (n = 3, 10%), bile leakage (n = 2, 7%), hepatic artery pseudoaneurysm (n = 1, 3%), jejuno-jejunostomy leakage (n = 1, 3%), graft hepatitis (n = 1, 3%), and posttransplant lymphoproliferative disorder (n = 2, 7%). In addition, 6 children (21%) suffered from intraabdominal bleeding from a variety of causes. After appropriate interventions, at a median follow-up of 38 months (range, 1 to 96 months), patient and graft survival rates were 79% and 74%, respectively. The retransplantation rate was only 7%. There was no incidence of hepatic artery thrombosis. All living donors remain alive and well. CONCLUSIONS: Complications are inevitable in pediatric liver transplantation. However, with timely recognition and active intervention, a good outcome can be achieved.

Child↗
PubMed2002

Obliterative hepatocavopathy-inferior vena cava thrombosis at its hepatic portion.

Budd-Chiari syndrome was formerly described as hepatic vein thrombosis within the liver, but it now includes inferior vena cava (IVC) thrombosis and other conditions that cause hepatic vein outflow obstruction. The author consider that primary hepatic vein thrombosis and primary IVC thrombosis represent two different clinical disorders.

Budd-Chiari Syndrome↗
PubMed1993

Liver transplantation in babies and children with extrahepatic biliary atresia.

Orthotopic liver transplantation (OLT) is a life-saving procedure for end-stage liver failure. We reviewed 39 children (24 girls, 15 boys) who received OLT for biliary atresia from 1987 to 1991. Twenty had unsuccessful portoenterostomy, 6 were referred too late for a drainage operation, and the remaining 13 achieved bile drainage but developed portal hypertension. At transplant 37 had decompensated liver disease with varices (28), ascites (24), encephalopathy (17), and gastrointestinal bleeding (12). The median weight and age at transplant were 8 kg and 12.6 months, respectively. The median waiting time was 65 days. Forty-eight grafts (30 reduced and 18 whole) were performed; graft loss was 33% and 27%, respectively. Of the 30 segmental grafts, 15 were reduced conserving the left lateral segment and hepatic vein (Brisbane technique)--13 were from the left lobe and 2 from the right lobe. The overall subject survival rate is 72%. Eleven deaths occurred: primary nonfunction (3), sepsis (3), perioperative bleed (3), and other causes (2). Early complications included: hepatic artery thrombosis (5), hepatic vein thrombosis (2), bowel perforation (3), biliary leak (3), and acute rejection (8). Later complications were chronic rejection (4) and biliary stricture requiring reconstruction (3). Follow-up at 12 months confirms good quality of life for both child and family with catch up growth and normal development. Technical advances in reduction hepatectomy have allowed us to treat small babies under 1 year with an urgent requirement for OLT, with comparable results to those obtained with whole grafts. In conclusion, in the future size and age need not be a contraindication to OLT in children with biliary atresia.

Biliary Atresia↗
PubMed2006

Management of Budd-Chiari syndrome.

KEY CONCEPTS: 1. Medical therapy alone is rarely sufficient for long-term management of patients with hepatic vein thrombosis. 2. Enthusiasm for intravascular stents (transjugular intrahepatic portosystemic shunt [TIPS] or vena caval stents) for the management of Budd-Chiari syndrome must be tempered by the limited interval of expected utility, the likelihood of stent occlusion/revisions, and the potential complications that stent migration would impose upon a subsequent liver transplant. 3. Both decompressive shunts and liver transplantation provide excellent long-term survival for patients with the Budd-Chiari syndrome. The determination of which surgical procedure is most appropriate is aided by assessment of the etiology of hepatic vein thrombosis, hepatic reserve, liver histology, and splanchnic venous anatomy. 4. Progressive hepatic damage may develop in patients with Budd-Chiari syndrome who have patent surgical shunts or TIPS. Lifelong follow-up and tracking of hepatic function are indicated. Some patients with shunts will require salvage with liver transplantation. 5. Long-term anticoagulation should be considered after transplantation, even in patients who do not have an identifiable coagulation disorder.

Budd-Chiari Syndrome↗