Abdominal aortic aneurysm (AAA) repair is performed because the mortality rates are as high as 78% following rupture. Open and endovascular surgery are the two approaches utilized for AAA repair. Open repair is accomplished by either accessing the aorta through a transabdominal or retroperitoneal approach. The aorta is then cross-clamped, the aneurysm sac is next opened and graft in, then sewn within the aorta to exclude the aneurysmal portion. Finally, the aneurysm sac is closed over the graft. In contrast, an endovascular aortic repair is typically performed by accessing the femoral artery through either cut-down or percutaneous means. The endograft is then delivered over a wire in a retrograde fashion to the affected aortic segment and deployed with the use of fluoroscopic imaging. Main repair indications include a large aneurysm diameter (5 cm in females, 5.5 cm in males), rapid expansion, symptomatic aneurysm, and frank rupture.
Smoking duration is the strongest risk factor in AAA development. Elevated risk of development also is seen with increasing age (males older than 50, females older than 60), male sex, white race and positive family history. Additional associations are found with vasculitides, infectious aortitis, a low-density lipoprotein receptor-related protein 1 (LRP1) variant, and rarely, Marfan syndrome. Factors specifically linked with high rupture risk include AAA greater than 6 cm, female gender, current smoking, uncontrolled hypertension, severe chronic obstructive pulmonary disease, AAA growth greater than 0.5 cm per year, and multiple family members with AAA.
Since the early 2000s, AAA prevalence, rupture rates, and mortality have declined when compared to data from the 1990s. Prevalence was previously reported to be between 4% to 9% in men whereas more recent studies report prevalence below 2%. Large reductions in smoking, which is associated with 75% of AAA; established screening guidelines, leading to approximately 40% mortality reduction; and increased number of elective endovascular aneurysm repairs have contributed to this trend.
AAA by definition is a concurrent dilatation of all three vessel wall layers: tunica intima, media, and adventitia, which result in a transaortic cross-sectional diameter of at least 3 cm. Although cigarette smoking provides the strongest link to AAA development, the exact mechanism by which it does so is not explicitly defined. The response of endothelial cells, vascular smooth muscle cells, and macrophages to cigarette smoke as well as genomic studies demonstrating a genetic predisposition to AAA development are active areas of investigation.
Resected segments of the aneurysmal aorta usually reveal varying degrees of neovascularity and a chronic inflammatory infiltrate. There is evidence of degeneration of the aortic walls.
Abdominal palpation and examination of the femoral and popliteal pulses are recommended for AAA evaluation, although up to 25% of AAAs larger than 5 cm are missed with focused physicals. Patients may report an exaggerated pulse or pulsating mass in the abdomen. Additional presentations include signs of embolic phenomena, originating from the aneurysm wall thrombus such as in blue toe syndrome, as well as signs of deep venous thrombosis from iliocaval compression by an aneurysm. Rare symptoms include chronic back pain from vertebral involvement, early satiety and nausea from gastric outlet obstruction, and urinary retention from ureter obstruction. Frank rupture elicits the classic triad of severe back or abdominal pain, hypotension and pulsatile abdominal mass in 50% of cases.
For screening, a one-time abdominal ultrasound is recommended for anyone 65 or older who have smoked or have a family history of AAAs. Screening for males with positive family history can begin as early as 55 years old. Yearly ultrasound surveillance is recommended for AAAs between 3.5 cm to 4.4 cm and repeat ultrasound is recommended every 6 months for AAAs between 4.5 cm to 5.4 cm. A high-quality CT angiography with computerized reconstruction is recommended for patients requiring aneurysm repair.
Endovascular and open surgery are currently the only two evidence-based treatment options for AAA repair. Endovascular aneurysm repair (EVAR) is the preferred approach for elective or emergent repair but requires favorable patient anatomy including a 1.0 cm to 1.5 cm aneurysm neck, a neck diameter less than 3.2 cm, aortic angulation less than 60 degrees, and access vessels amenable to endograft delivery. Open surgical repair (OSR) is typically reserved for the emergent repair of ruptured AAAs, aneurysms within 1 cm of or involving the renal arteries, and for patients with anatomy unfavorable to endovascular repair. Fenestrated and branched grafts are alternative endovascular approaches for aneurysms with renal artery involvement.
For elective AAA repair, the mortality is very low. However, for those who present with a rupture, the mortality can exceed 50%. Even those who survive surgery develop wound problems, bowel ischemia, heart failure, leg necrosis and multiorgan failure.
Once a diagnosis of an abdominal aneurysm is made, the vascular surgeon should be consulted.
Endoleaks are a complication in approximately 25% of EVARs that must be monitored with either postoperative triple-phase CTA scans or color duplex ultrasound. This surveillance is required as endoleaks allow blood to fill the aneurysm sac around the endograft and may contribute to the continued risk of sac rupture. Type II endoleaks are the most common and occur when aortic side branches such as lumbar, inferior mesenteric, or middle sacral arteries provide retrograde filling to the lower pressure aneurysm sac. These are often thought to be benign but are treated most commonly with translumbar or transarterial embolization when intervention is deemed necessary. Other endoleaks include Type I, sac filling around graft ends; Type III, sac filling at misaligned graft components; Type IV, sac filling through porous graft material; and Type V, sac filling through endotension).
Another devastating but rare complication following EVAR is graft infection. Its incidence has been reported to be between 0.2% to 5% of endovascular aortic repairs with increased occurrence after emergent repairs and in patients with infection complicating the index operation. Patients often present with nonspecific symptoms which can delay diagnoses such as back pain, abdominal pain, fever or chills. Additional findings include aortic fistula, endoleak, or aneurysm rupture. Endograft infections are often polymicrobial or caused by gram-positive organisms. Surgical management is the mainstay of endograft infection with graft excision, tissue debridement, and aortic conduit reconstruction being the overarching approach. This was traditionally accomplished with graft excision, over-sewing the aorta and performing an extraanatomical bypass to ensure distal perfusion. In-line reconstructions with venous conduits, cryo allografts, or antibiotic-impregnated prosthetic grafts are more widely utilized approaches. As persistent sepsis or recurrent infection remains a possibility following these procedures, patients should be placed on long-term antibiotic therapy.