scholarly journals Acute Budd–Chiari syndrome caused by inferior vena cava compression from a congenital diaphragmatic hernia

2020 ◽  
Vol 102 (8) ◽  
pp. e202-e204
Author(s):  
KM Wcislo ◽  
CE Hall ◽  
N Abbassi-Ghadi

Acute Budd–Chiari syndrome is a rare condition characterised by obstruction of hepatic venous outflow. We describe the case of a 52-year-old man, with a congenital Morgagni diaphragmatic hernia, who presented with acute onset abdominal pain, shortness of breath, lactic acidosis, hyperbilirubinaemia and transaminasaemia. Computed tomography revealed strangulation of the diaphragmatic hernia and extrinsic compression of the inferior vena cava from the herniated viscera. Emergency surgery was carried out to repair the hernia with a biosynthetic mesh, with complete resolution of the Budd–Chiari syndrome.

Author(s):  
Richa Subhash Udhwani ◽  
Michelle Nalini Fonseca ◽  
Deepali Swapnil Kapote

Presenting an unusual case of 27 years old female who presented at 18 weeks of pregnancy with second trimester bleeding per vaginum. Patient had history of recurrent abortions on examination was found to have hypertension and thrombocytopenia. Usg done revealed severe oligohydramnios. Patient was managed conservatively but aborted spontaneously at 22 weeks of gestation. Post-abortionl on day 2 patient developed abdominal distension and liver function tests were found to be deranged. USG and CT abdomen and pelvis was done, which revealed Budd chiari syndrome due to inferior vena cava (IVC) web. This extremely rare condition is characterized by obstruction of inferior vena cava by membrane or fibrous band. This condition is diagnosed by radiological techniques which in our patient revealed classical findings of caudate lobe hypertrophy, non-visualization of hepatic veins, moderate hepatomegaly and spleenomegaly and multiple collaterals. Esophagogastroduodenoscopy done which revealed large varieces for which endoscopic variceal ligation was done. IVCgram and IVC plasty was done by interventional radiology department 6 weeks after abortion. The aim of this case report is to highlight an extremely rare cause of Budd Chiari syndrome and IVC web in patient with recurrent abortion with spleenomegly leading to thrombocytopenia. It is important to rule out other differential diagnosis in these patients like APLA, ITP.


Surgery ◽  
1998 ◽  
Vol 124 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Takeo Yonekura ◽  
Akio Kubota ◽  
Masanori Hoki ◽  
Satosi Asano ◽  
Tuyoshi Nakayama ◽  
...  

2013 ◽  
Vol 7 (06) ◽  
pp. 489-493 ◽  
Author(s):  
Sami Akbulut ◽  
Mehmet Yilmaz ◽  
Aysegul Kahraman ◽  
Sezai Yilmaz

Budd-Chiari syndrome is an uncommon disorder characterized by the thrombotic or non-thrombotic obstruction of hepatic venous outflow anywhere along the venous course from the hepatic venules to the junction of the inferior vena cava and the right atrium. The etiology of Budd-Chiari syndrome is classified as primary, attributable to intrinsic intraluminal thrombosis or the development of venous webs; or secondary, caused by intraluminal invasion by a parasite or malignant tumor or extraluminal compression by an abscess, solid tumor, or cyst, such as a hydatid cyst. In this study, we present a case of a giant hydatid cyst manifesting Budd-Chiari syndrome symptoms and signs by compressing the inferior vena cava and hepatic veins. In brief, the case demonstrates that hydatid disease should be considered in the differential diagnosis of Budd-Chiari Syndrome in areas such as Turkey, where hydatid disease is endemic.


MedPharmRes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 22-26
Author(s):  
Uyen Vo ◽  
Duc Quach ◽  
Luan Dang ◽  
Thao Luu ◽  
Luan Nguyen

Budd–Chiari syndrome (BCS), a rare and life-threatening disorder due to hepatic venous outflow obstruction, is occasionally associated with hypoproteinemia. We herein report the first case of BCS with segmental obstruction of the intrahepatic portion of inferior vena cava (IVC) and hepatic veins (HVs) successfully treated by endovascular stenting in Vietnam. A 32-year-old female patient presented with a 2-month history of massive ascites and leg swelling. She refused history of oral contraceptives use. Hepatosplenomegaly without tenderness was noted. Laboratory data showed polycythemia, mild hypoalbuminemia and hypoproteinemia, slightly high total bilirubin and normal transaminase level. The serum ascites albumin gradient was 1.9 g/dL and ascitic protein level was 1.1 g/dL. The other data were normal. BCS was suspected because of the discrepancy between mild liver failure and massive ascites; and the presence of hepatosplenomegaly and polycythemia. On abdominal magnetic resonance imaging, the segmental obstruction of three HVs and IVC was 2-3 cm long without thrombus. Cavogram revealed the severe segmental stenosis of intrahepatic portion of IVC with no visualized HV and extensive collateral veins. A Protégé stent was deployed to IVC. Leg swelling and ascites were completely resolved within 3 days after stenting. During 1-year follow-up, edema was not recurred and repeated laboratory results were all normal.


2021 ◽  
pp. 153857442110020
Author(s):  
Reza Talaie ◽  
Hamed Jalaeian ◽  
Nassir Rostambeigi ◽  
Anthony Spano ◽  
Jafar Golzarian

Budd-Chiari syndrome (BCS) results from the occlusion or flow reduction in the hepatic veins or inferior vena cava and can be treated with transjugular intrahepatic portosystemic shunt when hepatic vein recanalization fails.1-3 Hypercoagulable patients with primary BCS are predisposed to development of new areas of thrombosis within the TIPS shunt or IVC. This case details a patient with BCS, pre-existing TIPS extending to the right atrium, and chronic retrohepatic IVC thrombosis who underwent sharp recanalization of the IVC with stenting into the TIPS stent bridging the patient until his subsequent hepatic transplantation.


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


1973 ◽  
Vol 18 (4) ◽  
pp. 337-346 ◽  
Author(s):  
Federico R. Justiniani ◽  
Gilbert H. Cohen ◽  
Sheldon A. Roen ◽  
Ignacio Arribas ◽  
Daniel S. Kushner

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