Open and Endovascular Treatment of Anastomotic Aneurysms after Aortoaortic, Aortoiliac, and Aortofemoral Bypass


Anastomotic aneurysms result from a disruption of the native artery–to–graft anastomosis. They are characterized by type (true or false), location (aortic, iliac, or femoral), and etiology (mycotic or nonmycotic). The majority are false aneurysms (pseudoaneurysms), with blood extravasation contained by periarterial tissue. True aneurysms can develop as the native artery itself dilates. Retroperitoneal anastomotic aneurysms often lead to life-threatening complications because of potential for rupture, and in the absence of major contraindications to intervention, they should be repaired. Several endovascular and open surgical options exist, but they are often complex and technically challenging.

Incidence

The overall incidence of aortic and iliac anastomotic aneurysm formation is likely underestimated by retrospective reviews because long-term graft surveillance is not the standard of care. These aneurysms are usually asymptomatic and, given their retroperitoneal location, are difficult to diagnose with physical examination. Studies using routine ultrasound surveillance to identify anastomotic abdominal aortic aneurysms estimate the incidence somewhere between 5% after 8 years and up to 27% after 15 years. Retrospective data on iliac anastomotic aneurysms estimate the incidence to be 6.3% at 15 years. Femoral anastomotic aneurysms after aortofemoral bypass are common, with an incidence in some reports as high as 24% at 15 years.

Pathophysiology

The development of a true or false anastomotic aneurysm is influenced by the indication for the initial arterial reconstruction. Patients treated for aneurysmal disease are more likely to develop true anastomotic aneurysms than patients treated for occlusive disease. In a study of 49 true anastomotic aneurysms, histologic evaluation of 28 resected arterial segments showed degeneration, with replacement of the media smooth muscle with acellular fibrous connective tissue, decrease or absence of elastic fibers, and hyaline degeneration of the adventitia.

Patients with the connective tissue disorders Ehlers–Danlos syndrome, α 1 -antitrypsin deficiency, and Marfan’s syndrome or with systemic vasculitis such as Beçhet’s or Takayasu’s arteritis are predisposed to develop true anastomotic aneurysms owing to abnormalities of the native arterial wall.

Technical factors contributing to the development of anastomotic aneurysms include creation of the anastomosis in residual aneurysmal tissue, use of an oversized graft in relation to native arteries, end-to-side anastomosis, use of a Dacron graft, and endarterectomy of the arterial wall.

Several etiologies have been proposed for the development of anastomotic false aneurysms. Historically, the use of braided or silk suture was thought to be the main factor in their development. As an antigenic material, these sutures elicited an inflammatory response that destroys the suture over time. Widespread use of monofilament suture has made such an event no longer an issue. Other suggested causes of pseudoaneurysm formation include suture failure from overmanipulation or knotting, aggressive arterial wall endarterectomy, mismatch in the compliance of the vessel and graft, graft dilation, and, most importantly, infection.

Occult infection as a nidus of anastomotic aneurysms, especially of the femoral arteries, is commonly underestimated. After repair of 45 femoral pseudoaneurysms with no clinical sign of infection, 60% of the resected prosthetic graft specimens cultured were found to be positive for Staphylococcus species. Others have found graft infection rates as high as 80% after repair. The incidence of infection is unknown because microbiology laboratories often do not subject vascular graft material to ultrasonication to separate bacteria from the interstices of the material before culture. This likely led to erroneous reports of negative culture results. A postoperative wound infection with complete healing has been shown to increase the relative risk of femoral pseudoaneurysm formation by ninefold at 5 years.

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