Combination of thrombolytic therapy and angioplastic stent insertion in a patient with Budd-Chiari syndrome

Abstract

A 31-year-old female who had well-established polycythemia vera one year before, presented with the sudden onset. She had severe ascites and hepatic encephalopathy 12 d prior to admission. Real-time ultrasonography revealed a supra hepatic thrombosis extending toward the inferior vena cava (lVC). Thrombolytic therapy with systemic streptokinase (250000 IU loading + 100000 IU/h infusion) was started. At the end of 72 h infusion, the patient's general condition improved. A color Doppler ultrasonography then showed complete and partial resolution of the thrombosis in the supra hepatic vein and IVC, respectively. Despite this good response, 12 d later, the symptoms recurred. Venography detected complete obstruction of the lVC. Percutaneous balloon angioplasty with stent insertion was performed successfully and the patient was discharged without any evidence of liver disease. A combination of systemic streptokinase and radiological intervention was effective in our patient.

Tratamiento endovascular del síndrome de Budd-Chiari, a propósito de un caso

“…El tratamiento médico con anticoagulación no es el adecuado y se debe complementar siempre con un procedimiento de nueva perfusión de los vasos ocluidos, ya sea quirúrgica o endovascular; la anticoagulación sola tiene una mortalidad del 80 % en un periodo de dos años. Los objetivos del tratamiento en el síndrome de Budd-Chiari son disminuir la congestión hepática y la ascitis, y evitar el deterioro hepático [23][24][25] .…”

Catheter-directed thrombolytic therapy combined with angioplasty for hepatic vein obstruction in Budd-Chiari syndrome complicated by thrombosis

“…Numerous factors, including malignancy, myeloproliferative disease, rheumatological disorders, hypercoagulability, infection and ulcerative colitis are potential etiological factors of thrombosis. However, the causes remain unidentified in 16–35% cases (1–3,16). Kuo et al (17) studied three cases of BCS complicated by hepatic vein thrombosis, in which the hepatic veins were recanalized without stenosis or occlusion following the removal of the thrombus by thrombolysis.…”

“…In western countries, BCS usually results from hypercoagulability (including myeloproliferative disorders, oral contraceptives and pregnancy)-induced thrombosis in one to three hepatic veins, or even in the IVC, which is characterized by an acute onset (1). It has been demonstrated that these patients may be treated with anticoagulation and thrombolytic (streptokinase) therapies to dissolve the thrombi in the hepatic veins (2,3). However, in eastern countries, membranous obstruction of the IVC and/or the hepatic veins is the most frequently occurring underlying cause of BCS (4), and this is most likely induced by organized thrombi or congenital factors.…”

“…It has been demonstrated that, for simple hepatic vein membranous or segmental occlusion in BCS without thrombosis, balloon dilatation or stenting treatment may result in a satisfactory therapeutic efficacy (9,10). Anticoagulant and systemic thrombolytic therapy may be conducted for hepatic vein thrombosis in BCS without membranous or segmental occlusion (2,3). In contrast with the previously mentioned lesions, membranous or segmental occlusion of the hepatic vein and hepatic vein thrombosis co-exist in patients with BCS in which the hepatic vein obstruction is complicated by thrombosis.…”