Back to 2016 Annual Meeting
Delayed Migration of a Thrombosed Aortic Endograft within a Thrombosed Aneurysm Sac Resulting in Continued Sac Expansion and Rupture
Edvard Skripochnik, MD, Nicos Labropolous, PhD, Shang A. Loh, MD.
Stony Brook University, Stony Brook, NY, USA.
Objective: Long-term surveillance of aortic endografts is critical in identifying late complications, such as endoleaks, stent migration, and stent thrombosis that can lead to serious consequences including rupture. We present the case of delayed migration of a thrombosed aortic endograft within a thrombosed aneurysm sac leading to sac expansion and rupture.
Case: The patient is a 68-year-old female with a past medical history significant for hypertension, known 4.5 cm thoracic aortic aneurysm, and severe emphysema on home oxygen who underwent an EVAR 6 years prior at an outside hospital. Repair was complicated intraoperatively by thrombosis of the contralateral limb and conversion to an aorto-uni graft with a femoral-femoral bypass. Three years later, she presented to our hospital with an ischemic left leg. A CTA was performed demonstrating complete thrombosis of the aortic endograft and aneurysm sac with an infected thrombosed bypass graft. A left axillary-femoral bypass was performed with excision of the infected femoral-femoral bypass. On follow up 17 months later, CT scan demonstrated aneurysm sac growth to 5.1 cm, sac and endograft thrombosis, no evidence of endoleaks, with stable endograft position. The patient elected for surveillance. Six months later a repeat CTA again demonstrated growth of the aneurysm sac to 5.6 cm. Aortic duplex at the time detected motion in the thrombus surrounding the endograft. An aortogram was then performed with no evidence of any endoleaks but with downward migration of the endograft by 5 mm. The patient again elected for observation. Another CTA 6 months later showed thrombosed sac growth to 6.1 cm and further downward migration of the thrombosed endograft with infrarenal aortic neck dilation to 3.6 cm. After extensive discussion with the patient regarding a high risk open repair given her severe emphysema, or a technically challenging endovascular rechanneling of her thrombosed endograft with proximal aortic extension and aortic anchors, the patient elected not to proceed with intervention. She presented 2 months later with a ruptured aneurysm. The patient’s family elected to make her comfort care.
Conclusion: Despite thrombosis of the aortic sac and endograft, persistent aortic pressure and neck dilation can contribute to endograft migration, sac expansion, and ultimately rupture. Continued surveillance is critical even with a thrombosed endograft.
Back to 2016 Annual Meeting