SummaryWith the increased use of intravascular catheters and devices, they have become the major non-malignant cause of superior vein cava (SVC) syndrome. We report a patient with liver cirrhosis who had received a peritoneovenous drainage catheter for refractory ascites, and then developed SVC syndrome because of concomitant occlusions of both the SVC and the drainage catheter. The patient regained patency of both the occluded vessel and the drainage catheter through percutaneous transluminal venoplasty, and there was dramatic improvement of clinical symptoms and good performance of the drainage catheter. Percutaneous intervention may be a feasible and effective therapy for SVC syndrome and intra-catheter thrombosis-related dysfunction. (Int Heart J 2017; 58: 447-450) Key words: Superior vein cava syndrome, Percutaneous intervention, Angioplasty, Indwelling catheters S uperior vena cava (SVC) syndrome is characterized by stenosis or occlusion of the SVC leading to venous congestion of the venous drainage territory affecting the head, neck, upper extremities, and upper chest. The most common cause of SVC syndrome is external compression by malignancies. However, with their increased use, intravascular catheters and devices have become the major non-malignant cause of SVC syndrome.1) Herein, we report a patient with liver cirrhosis who had received a peritoneovenous drainage catheter for refractory ascites, and developed SVC syndrome because of concomitant occlusions of both the SVC and the drainage catheter. The patient regained patency of both the occluded vessel and the drainage catheter by means of percutaneous transluminal venoplasty, and showed a dramatic improvement in clinical symptoms with good performance of the drainage catheter thereafter.
Case ReportA 50-year-old male, with known alcoholic liver cirrhosis, stage C in the Child-Pugh classification, who had undergone implantation of a peritoneovenous shunt (Denver shunt) for refractory ascites 4 years before this event, was referred to our cardiovascular department due to progressive swelling of the face and bilateral upper arms, dyspnea on exertion, and increasing waist circumference for 4 months. The Child-Pugh stage had deteriorated from his usual stage B to stage C (11 points: albumin: 2.1 g/dL, total bilirubin: 0.5 mg/dL, prothrombin time prolongation: 6.1 seconds, ascites: severe, no hepatic encephalopathy). A high level of D-dimer (1740 μg/L, normal cut-off value: 550 μg/L) was found and contrast-enhanced chest computed tomography revealed that a huge thrombus had caused complete obstruction of the SVC, which also involved the tip of the Denver catheter. The result was malfunction of the peritoneovenous shunt and blood drainage of the upper venous system through the azygous and collateral veins ( Figures 1A and 1B). With the diagnosis of SVC syndrome, intravenous heparin and oral Coumadin were initiated. Biochemical analyses of coagulation/fibrinolytic factors (protein C, protein S, antithrombin III, fibrinogen, factor V Leiden, factor VIII, ...