Intraabdominal arterio-venous fistulae and their relation to portal hypertension.

BACKGROUND/AIMS: The aim of the study was to present, on the base of own experience, clinical importance of arterio-venous fistulae involving the vascular system of the abdomen. METHODOLOGY: Clinical material consists of 18 patients in whom abnormal arterio-venous leakage in the abdomen was disclosed by means of imaging diagnostic techniques and Doppler sonographic hemodynamic investigations. Three groups of patients were determined: 1. Patients in whom arterio-venous fistula was a primary cause of portal hypertension (N = 6), 2. Patients in whom the presence of arterio-venous fistulae aggravated portal hypertension due to other pathology (N = 7). 3. Patients in whom the arterio-venous fistulae did not directly affect portal flow (N = 5). As each case presented a different clinical problem, the therapeutic approach had to be individualized. In 12 patients perarterial embolization was performed, 13 patients were operated on, one patient was listed for liver transplantation. RESULTS: Perarterial embolization was fully effective only in 4 cases. In the remaining 8 cases its effect was transient, but in 4 cases of liver tumors it allowed us to proceed with chemoembolization and the others were subsequently treated surgically. In 12 surgically treated patients the operation proved to be curative. In 1 case of multiple arterio-venous fistulae related to diffuse angiomatosis, surgical procedure was unfeasible. One patient, awaiting liver transplantation, died of liver failure. CONCLUSIONS: 1. Arterio-venous fistulae (of various etiology) are rarely found in the abdominal cavity, but their presence means usually serious consequences depending on their morphology and localization. 2. Arterio-venous fistulae involving the portal system may result in severe portal hypertension. 3. Individually chosen method of treatment, aimed at the occlusion of arterio-venous fistula often proves to be curative. 4. Overlooking or ignoring the presence of intraabdominal arterio-venous fistulae leads to unsuccessful, if not harmful treatment.

Surgical and interventional radiological treatment of Budd-Chiari syndrome: report of nine cases.

BACKGROUND/AIMS: The authors present the methods and results of treatment of patients with Budd-Chiari syndrome. METHODOLOGY: From a group of 15 patients with Budd-Chiari syndrome, treated in our department from January 1996 to September 2001, nine patients (6 females and 3 males, aged from 23 to 45 years) were qualified for surgical or radiological treatment. In 3 of them the hepatic vein thrombosis resulted from untreated polycythemia. In the remaining 6 cases the etiology of thrombosis remained unknown. In four patients with dominating portal hypertension symptoms, a meso-caval H-type graft was created. Four patients with severe liver insufficiency were qualified for orthotopic liver transplantation; all of them were transplanted. In 1 patient a balloon dilatation of the right and middle hepatic veins orifices was performed during the diagnostic cavography. The follow-up period ranged from 4 months to 5 years. RESULTS: In 2 patients with Budd-Chiari syndrome of unknown etiology, the "H"-shunt remained patent, and the patients were free of ascites and splenomegaly. During the period of follow-up (more than 5 years) they remained free of symptoms and demonstrated acceptable liver function parameters. Doppler sonography revealed the partial recanalization of the venous system. In 2 polycythemic patients, the shunt thrombosed, which was the indication for orthotopic liver transplantation in one of them. The transplantation was performed, but was unsuccessful because of hepatic graft artery thrombosis. The retransplantation in this case was also unsuccessful. The remaining 3 patients transplanted for cryptogenic Budd-Chiari syndrome are alive and well, 4, 5 and 11 months after orthotopic liver transplantation. In the patient subjected to interventional radiological hepatic veins dilation, the vessels remain patent 26 months post-procedure. The patient is free from ascites. CONCLUSIONS: Shunt surgery and liver transplantation are the valuable methods of treatment in selected cases of Budd-Chiari syndrome. In patients with polycythemia, however, thrombotic complications may occur in spite of anticoagulant and chemotherapeutic treatment. Balloon dilatation may appear an alternative to surgical treatment, but it seems that its indications should be limited to a highly selected group of patients.

Thrombolytic treatment of portal thrombosis.

BACKGROUND/AIMS: The authors present their experience with thrombolytic treatment of "acute" portal thrombosis. METHODOLOGY: Since 1980, portal thrombosis has been diagnosed in 305 patients treated in our Department. Portal thrombosis, mostly chronic, was associated with liver cirrhosis, Budd-Chiari syndrome, inflammatory and malignant liver tumors, as well as hypercoagulation conditions. In half of the patients the etiology of portal thrombosis remained obscure. Herewith, the authors present a retrospective review of 33 cases of rapidly developing portal thrombosis. Abdominal pain, ascites and jaundice were the most frequent initial symptoms. Time interval from the first symptoms appearance to hospitalization ranged from 8 to 60 days. The acute form of portal thrombosis was confirmed by Doppler sonography, spiral computed tomography and angiography. Sixteen female patients were regularly using oral contraceptives, in 8--portal thrombosis coexisted with the Budd-Chiari syndrome, in another 8--with polycythemia or myeloproliferative disorders and in 1 was observed during acute liver failure following paracetamol ingestion. RESULTS: Conservative treatment was unsuccessful in the first 5 cases: all of them died from esophageal variceal bleeding and liver failure. The next 28 patients received fibrinolytic treatment with streptokinase (3 cases) or recombinated tissue plasminogen activator. The results of therapy were evaluated on the basis of clinical picture and Doppler sonography monitoring. Rapid improvement of general condition, with Doppler sonography signs of the portal vein recanalization was noted in 10 patients, in all of whom the history of the disease did not exceed 14 days. In 13 patients with the longer history, partial portal vein occlusion persisted, but restored hepatopetal flow was sufficient to assure normal liver function. In the remaining 5 patients, with the history of the disease lasting longer than 30-40 days, the treatment failed and no clinical or Doppler sonography evidence of restoring of the portal flow were demonstrated. Four patients died: 2 from portal rethrombosis, 1 from liver failure and 1 from cerebral stroke (12, 16 months, 3 months and 4 years after therapy, respectively). Twenty-four patients are alive, the time of follow-up ranging from 9 months to 6 years. In 8 cases, five years after portal system recanalization the first symptoms of portal hypertension occurred. CONCLUSIONS: Thrombolytic treatment of acute portal thrombosis, if administered promptly, appears to be the only way to improve, or even restore, the portal system patency.