Mechanism of failure in the treatment of type II endoleak with percutaneous coil embolization

Purpose:Type II endoleak after endovascular abdominal aortic aneurysm repair is a failure of aneurysm sac exclusion with unknown long-term consequences. Elevated aneurysm sac pressures documented in these patients have led us to aggressively treat type II endoleaks with percutaneous transluminal coil embolization (PTCE). The purpose of this study was to evaluate the results and the mechanisms of failure of PTCE for type II endoleak. Methods: One hundred ninety-one patients underwent endograft repair of infrarenal aortic aneurysms. Twenty-three of 28 patients with persistent primary (>3 months) or secondary (new-onset) endoleak underwent angiography; 14 of these patients had type II endoleaks. We reviewed our endovascular registry data, hospital charts, and radiologic studies of patients with type It endoleaks and analyzed the results in those treated with PTCE of the inflow vessel. Results: All 14 patients with type II endoleaks were men, with a mean age of 76.7 years and a mean preoperative maximal aneurysm diameter of 5.7 +/- 1.0 cm. The type II endoleak was primary in 12 patients (86%) and secondary in two patients (14%) and iliolumbar in 11 patients (78%) and mesenteric in three patients (21%). Although a dominant affluent collateral channel (inosculation) was apparent in eight patients (57%), six patients (43%) showed a network of collateral vessels (retiform anastomosis). In six patients (43%), angiography revealed a second or "outflow" vessel indicative of a complex endoleak. In four patients with retiform iliolumbar type II endoleaks, PTCE was not attempted because of the retiform nature of the endoleak. The remaining 10 patients underwent PTCE, with coil deployment in all 10 and apparent initial technical success in nine patients. Follow-up computed tomographic scans revealed persistent endoleaks in six patients (60%). Mechanisms of failure included persistent flow through the coils in the treated vessel in two patients, development of a retiform anastomosis around the coiled vessel in three patients, and development of a new mesenteric endoleak after successful occlusion of an iliolumbar endoleak in one patient. Two patients underwent repeat PTCE with successful aneurysm sac exclusion in one. Internal iliac artery injury complicated one of the 12 PTCEs, and the resulting pseudoaneurysm was successfully treated with PTCE. Angiographic visualization of an outflow vessel (complex endoleak) was associated with PTCE failure (P = .008). Conclusion: PTCE of type II endoleaks has a high failure rate because of multiple anatomic mechanisms.