1/31/2024 0 Comments Sindrome diogenes causas![]() Tests for thrombophilia were run after withdrawal of anticoagulation, with normal results. Postoperative follow-ups at 1, 3, and 12 months were favorable, without signs of portal hypertension syndrome (PHS) in clinical examinations, laboratory tests, or imaging exams. In (D), control phlebography demonstrating considerable improvement in outflow. ![]() Observe the reduced stenosis induced in the balloon. Observe the stenosis induced in the balloon. In (B), pre-dilation with an 8 mm balloon. In (A), phlebography demonstrating hepatic vein stasis, caused by stenosis of the suprahepatic vein outflow. Images from intraoperative phlebography of the suprahepatic vein followed by balloon angioplasty in the first intervention. The patient recovered satisfactorily during the postoperative period, with considerable reductions in waist circumference and collateral abdominal vessels, and was discharged from hospital 15 days after the procedure, on rivaroxaban, which it was intended she would take for 6 months. Flow was reestablished by angioplasty of the stenosis using high pressure balloons, initially an 8 mm balloon and then a 12 mm balloon, ( Figure 2). A 0.035 x 260 mm hydrophilic guidewire (Terumo Medical, Somerset, NJ, United States) was then used to cross the critical suprahepatic stenosis, via the right jugular vein. This confirmed > 80% stenosis of the outflow of the right and left HVs and phlebography demonstrated venous stasis in both these veins, in addition to critical stenosis of the outflow. Intravascular ultrasound (IUS) was then employed to achieve better visualization of the HV outflow into the IVC. Venography was conducted under local anesthesia and analgesia with conscious sedation, using a transjugular approach, but it was difficult to catheterize the suprahepatic vein. Non-opacification of the middle hepatic vein is also observed. Portal phase axial tomographic images during preoperative preparation for the first endovascular intervention (A) and before the second endovascular intervention (B) (2 years and 8 months later), demonstrating development of the stenoses in the outflows of the hepatic veins (long arrows) and the change in the proportion of perfusional disorder in the hepatic parenchyma (arrowheads). The patient was diagnosed with BCS, probably due to obstruction of the suprahepatic outflow and was referred to the interventional radiology service for venography and treatment, after upper digestive endoscopy with endoscopic sclerotherapy of esophageal varices. Visibility of the middle HV was poor, suggesting thrombosis ( Figure 1A). Computed tomography (CT) with contrast showed hepatomegaly with heterogenous highlighting (known as “nutmeg” liver), hypertrophic caudate lobe, and right and left hepatic veins with contrast retention. Ultrasonographic examination showed ascites and normal hepatopetal portal blood flow. Laboratory test results for hepatic enzymes, coagulation, and bilirubin were within normal limits and serum albumin was low. Clinical examination confirmed abdominal distension, with collateral abdominal veins, hepatomegaly, and ascites. She denied having any degree of Asian heredity. ![]() ![]() She had no history of traumas, prior thromboses, pregnancy, abdominal pains, jaundice, hematoma, or acholic stools. The patient was a previously healthy, white, 24-year-old female, born and resident in Feira de Santana, BA, Brazil, with a history of abdominal distension, prostration, and an episode of hematemesis 3 months before presentation. ![]() The Research Ethics Committee approved this study (decision number 4.749.464). We describe endovascular treatment of a case of BCS caused by membranous occlusive of the suprahepatic outflow, with clinical and hemodynamic repercussions, conducted via transjugular venography using balloon angioplasty. In China, and in many other oriental countries, the principal cause is venous occlusive disease caused by membranes in any hepatic venous segment up to the cavoatrial junction, and angioplasty with or without stent is the first-choice option for treatment. In the majority of occidental countries, the principal etiology of BCS is thrombotic and, because of this, the principal forms of treatment are thrombolysis and transhepatic portosystemic shunt (TIPS), as bridges to liver transplantation. The etiopathogenesis of BCS differs in oriental and occidental countries. 1 - 3 Global epidemiological data on BCS are scarce and it is estimated that incidence is around one case per million inhabitants per year, considering epidemiological studies conducted in Asia and Europe. It is caused by obstruction of venous outflow, generally at the level of the hepatic vein (HV) or the inferior vena cava (IVC). Primary Budd-Chiari syndrome (BCS) is an extremely rare hepatic vascular disease. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |