Primary Budd-Chiari syndrome: ultrasonic demonstration.

Makuuchi, M; Hasegawa, Hideo; Yamazaki, Susumu; Moriyama, Nobuo; Takayasu, Kenichi; Okazaki, Makoto

doi:10.1148/radiology.152.3.6087405

Cited by 57 publications

(15 citation statements)

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“…This has also been the experience of others using sonography [6][7][8]. Nonvisualization of hepatic veins with flow demonstrated on duplex Doppler tracing was seen in four of our cases and we believe this is suggestive of Budd-Chiari, especially in patients with hepatomegaly.…”

Section: Discussionsupporting

confidence: 82%

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Budd-Chiari syndrome: Imaging with pathologic correlation

et al. 1993

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We retrospectively evaluated 21 patients with Budd-Chiari syndrome who underwent liver transplant. The pathological findings were correlated with imaging studies that included computed tomography (CT) in all cases, sonography in 20, and magnetic resonance (MR) in 15. Pathological features of Budd-Chiari syndrome in subacute or chronic form, such as parenchymal fibrosis, hemorrhage, and congestion, were found in all resected livers. These occurred usually in conjunction with restricted hepatic veins due to thrombosis or fibrosis with partially recanalized lumen. The status of hepatic veins was correctly assessed and correlated with pathology in 13 of 20 patients who had sonograms, in 12 of 15 patients who had MR, and in nine of 18 patients with contrast-enhanced CT scans. Patency of the inferior vena cava was well seen by all three modalities; parenchymal abnormalities were best visible on CT (19 of 21), while ascites, caudate lobe enlargement and collateral vessels were best detected with MR or CT. We conclude that each imaging modality offers certain values and limitations in the assessment of vascular or parenchymal findings in Budd-Chiari syndrome.

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Section: Discussionsupporting

confidence: 82%

“…The recanalized hepatic veins do not function well enough to preserve liver viability. Direct visualization of thrombus in the hepatic veins [6,8], reversal of flow in the hepatic veins [6][7][8][9][10], and intrahepatic collaterals [6,7] were not seen retrospectively nor mentioned in the formal sonographic reports of our patients.…”

Section: Discussionmentioning

confidence: 87%

Budd-Chiari syndrome: Imaging with pathologic correlation

et al. 1993

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“…5 The sonographic findings of MOVC are well described and are as follows: (1) obstruction of the hepatic portion of the inferior vena cava, (2) obstruction of 1 or more hepatic veins, (3) reversed flow in the hepatic veins, (4) an enlarged inferior right hepatic vein, and (5) communicating vessels between the inferior right hepatic vein and the right or middle hepatic vein, or both. 6,7 Previous reports have described the color Doppler features of MOVC as absence of flow across the web, reversed flow in the hepatic veins, and flow in the intrahepatic intercommunicating veins. 5,[8][9][10] To our knowledge, no report has described retrograde flow across the web.…”

Section: Discussionmentioning

confidence: 99%

Valvular-Type Membranous Obstruction of the Inferior Vena Cava With Vertebral Collaterals

Vijayaraghavan¹,

Ramchandran

Cherian

2003

Journal of Ultrasound in Medicine

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“…Two patients intended for long-term follow-up who died within 2 years of the onset of the disease were also included. The diagnosis of HVD was based on clinical features and ultrasound (US) examination [23,24]. It was confirmed by inferior vena cavography [10] in 31, hepatography or transhepatic venography [25] in 5, and liver biopsy in 34 patients.…”

Section: Methodsmentioning

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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Primary Budd-Chiari syndrome: ultrasonic demonstration.

Cited by 57 publications

References 0 publications

Budd-Chiari syndrome: Imaging with pathologic correlation

Budd-Chiari syndrome: Imaging with pathologic correlation

Valvular-Type Membranous Obstruction of the Inferior Vena Cava With Vertebral Collaterals

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

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