PURPOSE: To present and analyze several cases that illustrate persistent sac pressurization following endovascular abdominal aortic aneurysm (AAA) repair. METHODS AND RESULTS: Four patients with successful endovascular AAA exclusion presented in follow-up with an expanding aneurysm. Two had initial sac diameter decrease, but by 18 and 24 months, respectively, the AAA had enlarged and become pulsatile. There was no endoleak evident, but the proximal attachment stents had mig rated distally in both cases. One patient developed endoleak with aneurysm expansion at 6 months; contained rupture occurred at 12 months. The last case had slowly evolving aneurysm expansion over 36 months but no endoleak. All endografts were removed and successfully replaced with conventional grafts. Intrasac thrombus was implicated as the means of pressure transmission that precipitated AAA expansion in these cases. CONCLUSIONS: Excluded AAAs can increase in size owing to persistent or recurrent pressurization (endotension) of the sac even when there is no evidence of endoleak. One proposed mechanism is pressure transmission via thrombus that lines the attachment site. Endotension may also represent an indiscernible, very low flow endoleak that allows blood to clot at the source of leakage.
PURPOSE: To present and analyze several cases that illustrate persistent sac pressurization following endovascular abdominal aortic aneurysm (AAA) repair. METHODS AND RESULTS: Four patients with successful endovascular AAA exclusion presented in follow-up with an expanding aneurysm. Two had initial sac diameter decrease, but by 18 and 24 months, respectively, the AAA had enlarged and become pulsatile. There was no endoleak evident, but the proximal attachment stents had mig rated distally in both cases. One patient developed endoleak with aneurysm expansion at 6 months; contained rupture occurred at 12 months. The last case had slowly evolving aneurysm expansion over 36 months but no endoleak. All endografts were removed and successfully replaced with conventional grafts. Intrasac thrombus was implicated as the means of pressure transmission that precipitated AAA expansion in these cases. CONCLUSIONS: Excluded AAAs can increase in size owing to persistent or recurrent pressurization (endotension) of the sac even when there is no evidence of endoleak. One proposed mechanism is pressure transmission via thrombus that lines the attachment site. Endotension may also represent an indiscernible, very low flow endoleak that allows blood to clot at the source of leakage.
Authors: Zvonimir Krajcer; Lawrence Rajan; Venkata Thota; Kathryn G Dougherty; Neil E Strickman; Ali Mortazavi; Benjamin Y C Cheong Journal: Tex Heart Inst J Date: 2011