hepatic venous outflow
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Budd-syndrome Chiari's is a rare condition is causes by obstruction to hepatic venous outflow. The female patient 25-year old who was admitted to Acharya Vinoba Bahave Rural Hospital on date 19/06/2019. 4 months ago, she noticed that her abdomen had become prominent. Her appetite became poor and she had vomiting bouts whenever she took food. A detailed clinical evaluation of the The syndrome of Budd-Chiari is based on a comprehensive history of of the patient, angiography is often used to assist in the diagnosis. The treatment also uses (MRI) and ultrasound technique. If the condition is detected early, treatment of Budd-Chiari syndrome is more effective. Large doses of corticosteroid, prednisone can also be recommended as heparin like anticoagulants can be efficient in the treatment of Budd-Chiari syndrome individuals. However, the condition typically has an acute onset and can become chronic later in life. The present case with right anticoagulant therapy, early diagnosis and successful treatment is reported.

Abstract Background Budd-Chiari syndrome (BCS) is a rare disease caused by hepatic venous outflow obstruction and results in hepatic failure due to sinusoidal congestion, decrease in the blood supply to the to the liver and increase the pressure in portal vein . Objectives The aim beyond this study is assessment of the maternal and foetal events in a group of women who became pregnant while having BCS. Patients and methods It is a prospective and retrospective study which was conducted on 32 patients with Budd- Chiari syndrome admitted to Ain Shams University Hospitals, Tropical Medicine department or attended the outpatient clinics during the period from May 2006 to March 2019 who became pregnant after diagnosis by BCS . Results Number of cases that underwent tips revision 3 cases and one case underwent liver transplantation after delivery and 2 cases had died during follow up.Using . of enoxaparin in 1st trimester in our cases as a significant protective factor against abortion. Conclusion BCS isn’t a contraindication to pregnancy in patients with a well-controlled disease. Fetal outcome remains relatively poor, which is at least partly due to the underlying prothrombotic disorders. so patients should be accurately informed about the risk of this pregnancies .

A young adult male was referred for a second opinion of deranged liver biochemistry. He initially presented two years prior with abdominal pain, lethargy and fevers due to a segment two pyogenic liver abscess. He received empirical antibiotic therapy to resolution. Computed tomography for abscess follow-up revealed an intrahepatic inferior vena cava thrombus. He was anti-coagulated with warfarin. He was lupus anticoagulant positive and had a highly positive beta-2 glycoprotein antibody on serial measurement and was diagnosed with anti-phospholipid syndrome. On current review, the patient had no clinical stigmata of chronic liver disease. There were dilated veins on the supraumbilical abdominal and chest walls. There was mild hepatomegaly but no splenomegaly. Laboratory investigations revealed mildly cholestatic liver function tests with hyperbilirubinaemia (40μmol/L) but no liver synthetic dysfunction. Serological screening did not reveal any cause of chronic liver disease. The patient underwent multiphase abdominal CT and formal hepatic venography. What is the diagnosis and describe the hepatic venous outflow?

Abstract Background In living donor liver transplantation (LDLT) for patients with Budd‒Chiari syndrome (BCS), there are several concerns about reconstruction of the inferior vena cava (IVC) and hepatic veins. Herein, we report the case of a patient with BCS who underwent LDLT with right posterior segment graft (RPSG) and patch plasty for reconstruction of the hepatic venous outflow, using the patient’s own superficial femoral vein (SFV). Case presentation A 19-year-old man, who was diagnosed with primary BCS, underwent LDLT. His main hepatic veins were totally obstructed, and membranous stenosis was seen in the IVC. The LDLT donor was his mother; however, liver volumetric analysis showed that only her RPSG was appropriate. In the recipient surgery, 16 cm of the left SFV was harvested and was cut longitudinally and opened. The right hepatic vein (RHV) of the RPSG was anastomosed to the sidewall of the SFV graft. After explantation of native diseased liver was completed, the stenotic and thickened wall of the IVC was widely resected, and a large anastomotic orifice was created. Patch cavoplasty was performed with the RHV‒SFV graft patch. After portal reperfusion started, hepatic venous outflow was satisfactory, and there was no venous graft congestion. Both his postoperative course and his long-term course after discharge were uneventful. Conclusions In LDLT for BCS patients, ingenuity is required for the reconstruction of venous outflow. The SFV patch can be safely harvested from liver transplant recipients and is suitable for venous reconstruction. In addition, RPSG is an alternative type of liver graft for LDLT if a conventional right- or left-lobe graft cannot be used.

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.