Budd-Chiari Syndrome: Hepatic Venous Outflow Tract Obstruction

2021 ◽  
pp. 79-92
Author(s):  
Virginia Hernández-Gea ◽  
Anna Baiges ◽  
Fanny Turon ◽  
Juan Carlos Garcia-Pagan
PEDIATRICS ◽  
1979 ◽  
Vol 63 (5) ◽  
pp. 808-812
Author(s):  
Arvind Taneja ◽  
S. K. Mitra ◽  
P. D. Moghe ◽  
P. N. Rao ◽  
N. Samanta ◽  
...  

Budd-Chiari syndrome is an uncommon disease caused by an obstruction to hepatic venous outflow either at the level of the hepatic veins or in the hepatic part of the inferior vena cava. Clinically, it presents with ascites, abdominal pain, hepatomegaly, edema, and occasionally jaundice. The syndrome was first recognised by Lamboran1 in 1842 and later described by Budd2 in 1846 and Chiari3 in 1899. The syndrome is caused by obstruction to the hepatic veins. In the Fig 1. Photograph showing massive ascites and dilated superficial abdominal veins. majority of cases, the obstruction is ascribed to obliterative thrombophlebitis of unknown cause.4


1970 ◽  
Vol 3 (2) ◽  
pp. 80-82
Author(s):  
Md. Mukhlesur Rahman ◽  
KMHS Sirajul Haque ◽  
Md. Mahmudur Rahman Siddiqui ◽  
Tanjima Parvin ◽  
Md. Khurshed Ahmed

'Budd Chiari syndrome (BCS)' is an uncommon condition induced by thrombotic or nonthrombotic obstruction to hepatic venous outflow. This disease can be potentially life-threatening but prognosis is more favorable in patient with IVC webs but is extremely poor in malignant and haematological cases. A cooperative collaboration of hepatologist and cardiologist can make the situation easy for diagnosis, even in treatment of some cases. (University Heart Journal 2007; 3 : 80-82)


2016 ◽  
Vol 141 (1) ◽  
pp. 98-103 ◽  
Author(s):  
Raul S. Gonzalez ◽  
Michael A. Gilger ◽  
Won Jae Huh ◽  
Mary Kay Washington

Context.—Cardiac hepatopathy and Budd-Chiari syndrome are 2 forms of hepatic venous outflow obstruction with different pathophysiology but overlapping histologic findings, including sinusoidal dilation and centrilobular necrosis. Objective.—To determine whether a constellation of morphologic findings could help distinguish between the 2 and could suggest the diagnoses in previously undiagnosed patients. Design.—We identified 26 specimens with a diagnosis of cardiac hepatopathy and 23 with a diagnosis of Budd-Chiari syndrome. Slides stained with hematoxylin and eosin and with trichrome were evaluated for several distinctive histologic findings. Results.—Features common to both forms of hepatic outflow obstruction included sinusoidal dilation and portal tract changes of fibrosis, chronic inflammation, and bile ductular reaction. Histologic findings significantly more common in cardiac hepatopathy included pericellular/sinusoidal fibrosis and fibrosis around the central vein. Only centrilobular hepatocyte dropout/necrosis was significantly more common in Budd-Chiari, regardless of duration. Conclusions.—The finding of pericellular/sinusoidal fibrosis in cardiac hepatopathy compared with Budd-Chiari is not unexpected, given the chronic nature of most cardiac hepatopathy. Portal tract changes are common in both forms of hepatic outflow obstruction and should not deter one from making the diagnosis of hepatic outflow obstruction. Fibrosis along sinusoids and around the central vein may be suggestive of cardiac hepatopathy in biopsies from patients without a prior diagnosis.


2021 ◽  
pp. 470-474
Author(s):  
Jeremy Polman ◽  
Sainandan Reddy ◽  
Aaron C. Williams ◽  
Aaron DeWitt

Budd-Chiari syndrome (BCS) is an uncommon illness that is characterized by obstruction of hepatic venous outflow. Patients typically present with nausea, vomiting, and abdominal pain, which can further progress into signs associated with liver failure, including jaundice, encephalopathy, and coagulopathy. The most common causes of BCS include pathologies that induce portal vein thrombosis, such as myeloproliferative disorders, malignancy, and acquired hypercoagulable states. In this case report, a patient who presented with abdominal pain and distention is diagnosed with BCS caused by an unusual etiology. He was found to have significant eosinophilia, prompting additional evaluation for parasitic infections. Using stool diagnostics/studies, he was found to have <i>Dientamoeba fragilis</i> trophozoites. The patient was treated with enoxaparin, warfarin, and metronidazole with a resolution of his symptoms. This case outlines a novel cause of BCS as well as the proposed mechanism of <i>Dientamoeba fragilis</i> induction of BCS.


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