Recognition and management of Budd-Chiari syndrome: Report of one hundred cases

Wang, Zhonggao; Zhu, Yu; Wang, Shihua; Pu, Lanping; Du, Yonghua; Hai, Zhang; Chi, Yuan; Chen, Zhong; Wei, Manlin; Pu, Lee Li-Qun; Du, Wei; Liu, Ming; Liu, Xiaoming; Johnson, George

doi:10.1016/0741-5214(89)90348-0

Cited by 84 publications

(28 citation statements)

References 8 publications

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“…In our series, IVC involvement in the majority of cases was due to IVC thrombosis. Previously, MOVC and IVC thrombosis were considered to be idiopathic in origin by most Indian and Asian workers [5,6,11,[13][14][15]17,35,49,50,53,54] ; but this view has been challenged recently in a few reports [22,29,30,42,[55][56][57][58] . In cases of IVC thrombosis in our study, the etiology was identified in 50%.…”

Section: Discussionmentioning

confidence: 99%

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Amarapurkar¹,

Punamiya²,

Patel³

2008

WJG

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AIM:To evaluate patterns of obstruction, etiological spectrum and non-surgical treatment in patients with Budd-Chiari syndrome in India. METHODS:Forty-nine consecutive cases of BuddChiari syndrome (BCS) were prospectively evaluated. All patients with refractory ascites or deteriorating liver function were, depending on morphology of inferior vena cava (IVC) and/or hepatic vein (HV) obstruction, triaged for radiological intervention, in addition to anticoagulation therapy. Asymptomatic patients, patients with diuretic-responsive ascites and stable liver function, and patients unwilling for surgical intervention were treated symptomatically with anticoagulation. RESULTS:Mean duration of symptoms was 41.5 ± 11.2 (range = 1-240) mo. HV thrombosis (HVT) was present in 29 (59.1%), IVC thrombosis in eight (16.3%), membranous obstruction of IVC in two (4%) and both IVC-HV thrombosis in 10 (20.4%) cases. Of 35 cases tested for hypercoagulability, 27 (77.1%) were positive for one or more hypercoagulable states. Radiological intervention was technically successful in 37/38 (97.3%): IVC stenting in seven (18.9%), IVC balloon angioplasty in two (5.4%), combined IVC-HV stenting in two (5.4%), HV stenting in 11 (29.7%), transjugular intrahepatic portosystemic shunt (TIPS) in 13 (35.1%) and combined TIPS-IVC stenting in two (5.4%). Complications encountered in follow-up: death in five, re-stenosis of the stent in five (17.1%), hepatic encephalopathy in two and hepatocellular carcinoma in one patient. Of nine patients treated medically, two showed complete resolution of HVT. CONCLUSION:In our series, HVT was the predominant cause of BCS. In the last five years with the availability of sophisticated tests for hypercoagulability, etiologies were defined in 85.7% of cases. Non-surgical management was successful in most cases.

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Section: Discussionmentioning

confidence: 99%

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Amarapurkar¹,

Punamiya²,

Patel³

2008

WJG

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“…[6][7][8][9][10][11][12] Surgery though successful, carries higher risk of complications in patients who already had impaired liver function. [3][4][5] Mortality in surgical group is higher-33-40% (Kimura et al & Iwaragi et al).…”

Section: Discussionmentioning

confidence: 99%

Inferior vena cava obstruction: long-term results of endovascular management

Srinivas

Dattatreya

Srinivasa

et al. 2012

Indian Heart Journal

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Background: Hepatic venous outflow obstruction (HVOO) can have acute or chronic presentation.In the chronic variety of inferior vena cava (IVC) obstruction, endovascular management with balloon angioplasty and stent implantation has emerged as a feasible, safe alternative to surgery which has high incidence of mortality and morbidity. Aims and objectives:To study the feasibility and long-term follow-up of endovascular management of chronic IVC obstruction. Methods:We studied 12 cases of HVOO who underwent endovascular management (balloon dilatation ± stenting). In most of the cases, the cause of obstruction was not obvious, but one case had metastatic hepatic nodules compressing on IVC. Diagnosis was established by clinical examination, venous Doppler and was confirmed by venography and/or computed tomography (CT) angiography. Cases underwent balloon dilatation and/or stenting.Results: Out of 12 cases, six had membranous obstruction (four complete and two incomplete), five cases had segmental stenosis and one case had tumour compression. The lesion was crossed with either guide wire or Brockenbrough needle with Mullins sheath assembly and balloon dilatation was done with Inoue or Mansfield balloon. Seven cases underwent balloon dilatation alone while five cases underwent stenting. There was procedural success in all cases with reduction of gradient by 84%, disappearance of collaterals and clinical improvement. During the follow-up of 13 years, one case had restenosis, which was managed by stenting.Conclusion: Endovascular management of IVC obstruction is safe with good long-term patency rates.

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“…Obstruction of the hepatic portion of the inferior vena cava (IVCO) is a form of BCS commonly seen in Asia [1][2][3][4][5][6][7][8][9] and Africa [10][11][12] but rarely reported from western countries [13,14]. It is a primary disease of the hepatic portion of the IVC caused by bacterial infection.…”

Section: Introductionmentioning

confidence: 99%

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Shrestha¹

2009

Hepatol Int

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Purpose Hepatic vena cava disease (HVD), a form of Budd-Chiari syndrome, is caused by the obstruction of hepatic portion of the inferior vena cava. It is a chronic disease characterized by the development of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). As HVD occurred in areas with high incidence of hepatitis B virus (HBV) infection and some patients tested HBsAg positive, it was thought to be the cause of LC and HCC. To assess the pathogenesis of LC or HCC in HVD, a long-term follow-up study was done. Method Fifty-six patients with HVD diagnosed by ultrasound (US) and confirmed by cavography in 31 and liver biopsy in 34 were followed up for an average of 14.8 ± 9 years. The occurrence of LC was diagnosed by US and/or liver biopsy and that of HCC by US, elevated level of a-fetoprotein, and liver biopsy or fine-needle aspiration cytology, or computed tomographic scan. Other risk factors for LC/HCC such as alcohol use and HBV and hepatitis C virus (HCV) infections were assayed. Results Forty-four (78.5%) and 6 (10.7%) patients developed cirrhosis and HCC, respectively. LC/HCC occurred more frequently among those who had severe or frequent acute exacerbations (P = 0.017), but it was not related to alcohol use or HBV and HCV infections. Conclusion HVD is independent risk factors for LC and HCC. Severe and/or recurrent loss of hepatocytes caused by hepatic venous outflow obstruction and/or thrombotic obstruction of small radicals of hepatic and portal veins that occurred during acute exacerbations was considered important in the pathogenesis of LC and HCC in HVD.

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Recognition and management of Budd-Chiari syndrome: Report of one hundred cases

Cited by 84 publications

References 8 publications

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Inferior vena cava obstruction: long-term results of endovascular management

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

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