Fluid transfer as a mechanism leading to endotension.
Some abdominal aortic aneurysms bridged with a minimally invasively introduced stent graft prosthesis increase in size without any diagnosable evidence of endoleakage (endotension). There are three possible pathways proposed through which undetectable low rates of blood flow may cause an aneurysm sac to be refilled: through the thrombus at the prosthesis attachment sites, through the clotted collaterals and through the clotted stent graft wall. If the inflow is more rapid than any drainage through the wall of the aneurysm is re-pressurised. However, critical magnitudes for the permeability of the clotted graft and the geometry of the thrombus at the aneurysm, necessary to inhibit endotension, are not known. The aim of this study was to determine which boundary conditions prevent endotension. An analytical model based on Darcy's Law was used to estimate the pressure in the aneurysm sac due to fluid transfer. Experimentally determined time- and pressure-dependent permeability of red and intraluminal thrombus, and of clotted graft materials were input into the model. The computational analysis showed that endotension is unlikely to be caused by fluid transfer from the collaterals or via the prosthesis attachment sites, but rather due to flow through the stent graft wall. Based on this study it can be stated that grafts with a permeability below 2e-13 mm(2) should diminish the occurrence of endotension.
de Uhlenbrock
A Gebert
AG
Biomechanics Section, TUHH Hamburg University of Technology, Denickestrasse 15, D-21073 Hamburg, Germany. a.uhlenbrock@tuhh.de
Wintzer
C
C
Imig
H
H
Morlock
M M
MM
D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D001777:Blood Coagulation; D001794:Blood Pressure; D057867:Endoleak / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D057446:Hydrodynamics; D010539:Permeability; D015607:Stents; D058017:Vascular Grafting