Altered Hemodynamics in the Budd-Chiari Syndrome Demonstrated by Selective Hepatic and Selective Splenic Angiography

Pollard, James J.; Nebesar, Robert A.

doi:10.1148/89.2.236

Cited by 45 publications

(10 citation statements)

References 5 publications

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“…5,8 This effect may result from a lower PV pressure that allows an increased pressure gradient between terminal arterioles and PVs, thereby improving retrograde sinusoidal and PV flow. 9,10 The present study demonstrates, for the first time, the histological appearance of vascular channels that likely conduct retrograde blood flow in the liver.…”

Section: Discussionmentioning

confidence: 55%

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

1998

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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.

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Section: Discussionmentioning

confidence: 55%

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

1998

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“…The direct evidence in selective celiac injection consists of visualization of the portal vein directly from the hepatic arteries, instead of as a late sequence of the flow of dye through the splenic vein into the portal system. In selective hepatic artery injection this direct flow is even better demonstrated, the dye not being dissipated within the liver [3].…”

Section: Discussionmentioning

confidence: 99%

“…Pollard and Nebesar [3] were the first who stressed the importance of hepatic artery to portal vein shunting as suggestive to the diagnosis of the Budd-Chiari syndrome. Recently, Deutsch et al [1] emphasized the diag nostic importance of cavography and selective hepatic venography and demonstrated the different collateral channels present in cases of primary occlusion of the hepatic veins.…”

Section: Discussionmentioning

confidence: 99%

“…selective hepatic venography and selective celiac or hepatic arteriography [1], Pollard and N ebesar [3] reported two autopsy-proven cases of complete occlusion of the hepatic veins in which special hemodynamic features of this syndrome were dem onstrated angiographically. Yet on the whole, celiac and hepatic arterio graphy has received scant attention in this syndrome.…”

mentioning

confidence: 99%

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Diversion of the Hepatic Arterial Flow into the Portal Vein in the Budd-Chiari Syndrome

Deutsch¹,

Adar²,

Bogokowsky³

et al. 1974

J Vasc Res

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“…Blood entering the liver from hepatic artery have to find an alternative pathway to leave liver. Histological study of biopsies and post-mortem tissue conducted by Leopold, Parry and Storring [64] provide evidence extravasation of RBCs occurred into the space of Disse. It was postulated that impairment of nutrition of sinusoidal cells that followed sinusoidal hypertension results to increase in gaps between endothelial cells that allowed egression of RBC into space of Disse where it intermingle with the cells of liver plates resulting in atrophy from compression.…”

Section: Change In Hepatic Microcirculation In Sinusoidal Hypertensionmentioning

confidence: 98%

Sinusoidal Hypertension: A Cause of Liver Cirrhosis in Developing Countries

Sm¹

2017

Austin J Gastroenterol

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Three primary diseases of the liver that cause hepatic venous outflow obstruction (HVOO) are recognized: sinusoidal obstruction syndrome (SOS), Budd-Chiari syndrome (BCS) and hepatic vena cava syndrome (HVCS). Liver cirrhosis develops in these diseases. This paper discusses the pathogenesis of cirrhosis in HVOO.HVOO results in sinusoidal hypertension. Because of the unique nature of hepatic sinusoid, sinusoidal hypertension is followed by rapid passage of fluid and macromolecules from sinusoid into the space of the Disse and reflex reduction of hepatic arterial flow. As the space between the endothelial cells widens egression of RBCs follows. Hemorrhage and ischemia result in atrophy and apoptosis of hepatocytes in the congested region around the terminal hepatic vein. Extinction of hepatocytes is followed by fibrosis which ultimately leads to development of venocentric cirrhosis. Sinusoidal hypertension also causes reversal of blood flow in portal vein. In BCS and HVCS thrombosis/ thrombophlebitis develops in portal vein and its branches. Atrophy and extinction of hepatocytes supplied by the obstructed portal vein branches lead to development of veno-portal type of cirrhosis in some.HVCS is endemic in some Asian and African countries. It is a disease related to poor hygienic living condition and caused by bacterial infection. HVOO may develop at anytime in the course disease precipitated by bacterial infection. It is followed by rapid development of ascites and cirrhosis. HVCS induced cirrhosis is characterized by distinctive clinical, histological and ultrasonographic/color Doppler features. HVCS may be a common cause of cirrhosis in developing countries.

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Altered Hemodynamics in the Budd-Chiari Syndrome Demonstrated by Selective Hepatic and Selective Splenic Angiography

Cited by 45 publications

References 5 publications

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

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

Diversion of the Hepatic Arterial Flow into the Portal Vein in the Budd-Chiari Syndrome

Sinusoidal Hypertension: A Cause of Liver Cirrhosis in Developing Countries

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