Abdominal aortic aneurysm repair: Matching patients with approaches

Abdominal aortic aneurysm (AAA) is a common condition that primarily affects older patients and can have fatal consequences. Rupture of an AAA has an overall mortality rate of 80%; in patients who reach the hospital alive, the mortality is close to 50%.1

AAA is present in approximately 2% of the population and responsible for more than 13,750 deaths annually. Moreover, AAA is an underlying or contributing cause of death in more than 19,000 patients and a factor in more than 63,000 hospital discharges per year in the United States.2 The prevalence of AAA increases by 6% per decade after 65 years of age.3 The abdominal aorta is the most common site of an arterial aneurysm. Most AAAs are asymptomatic and found incidentally on imaging for other complaints. Management of AAAs requires an understanding of the natural process of the disease, history, and treatment options.

DISCUSSION

Definition An aneurysm is a focal dilation of a blood vessel as compared to the original or adjacent artery. An AAA is defined as an aortic diameter that is at least 1.5 times the diameter of the aorta at the renal arteries. In adults, the average diameter of the infrarenal abdominal aorta is approximately 2.0 cm (range 1.66-2.39 cm).4 An infrarenal aorta with a diameter greater than 3.0 cm is considered to be aneurysmal (see Figure 1). Aneurysms can be classified as fusiform (exhibiting circumferential expansion) or saccular (demonstrating outpouching of a segment). (CT scans of a normal aorta and an aneurysmal aorta are shown in Figures 2 and 3.)

Etiology The mechanism for the development of AAA is not fully understood. Several studies have assessed aortic histology, protein abundance, and gene expressions. These studies have found a loss of extracellular matrix with an accumulation of proteolytic enzymes and cytokines that weaken the aortic wall through breakdown of smooth muscle cells and structural proteins.5,6 Smoking invokes an intra-aortic inflammatory response that affects the immune-mediated pathways, leading to expansion of the aorta.6

Risk factors The main risk factors for AAA are smoking, increasing age, male gender, and a family history of aneurysms. A study by Wilmink and colleagues found that smokers are seven times more likely to have an AAA and ex-smokers are three times more likely than age-matched controls to have an AAA.7 More than 90% of patients with an AAA have been smokers.3 The longer a patient has smoked, the higher the risk of AAA.7 The risk of an AAA steadily increases with age; AAAs are rarely found in persons younger than 60 years. Men are four to five times more likely to have an AAA than women.8 A family history of AAA has been reported in up to 5% of AAA patients.9 AAAs are more common in patients who have atherosclerosis; these patients are also at increased risk of other cardiovascular disorders.

Screening The United States Preventive Services Task Force recommends screening the following individuals:10

• Men aged 65 to 75 years who have ever smoked • Women 60 to 85 years old with cardiac risk factors

• Men and women older than 50 years with a family history of AAA

There is no recommendation for or against screening males aged 65 to 75 years who have never smoked.

The standard tool for screening is an ultrasound examination, which has a sensitivity close to 100% and a specificity close to 96%.10 Screening needs to be done with the patient in a fasting state. When an AAA is found, the recommended surveillance is based on the aortic diameter11 (see Table 1).

Indications for repair The decision to operate on an AAA should be made when the risk for rupture is greater than the risk associated with repair. In general, the American Heart Association recommends that patients with infrarenal or juxtarenal AAAs measuring 5.5 cm or larger should undergo repair to eliminate the risk of rupture.12 Since women have smaller-diameter aortas than men, one might think that a 4-cm AAA in a woman with a 1.5-cm aorta at the renal artery would pose a greater risk than a 4-cm AAA in a man with a 2.5-cm aorta at the renal artery. But this has not been found to be true. Repair is based on the 5.5-cm size in both men and women.13 The relative risks of rupture are dependent on aneurysmal size14 (see Table 2). The following are independent risk factors for rupture of an AAA: chronic obstructive pulmonary disease, hypertension, female gender, smoking, and symptoms of abdominal pain or back pain. Nonindependent risk factors for rupture are first-degree relative with an AAA, saccular aneurysm, and 0.6-cm expansion in diameter in 1 year.15 The clinical triad of abdominal and/or back pain, a pulsatile mass, and hypotension requires immediate surgical evaluation because its presence signals a probable rupture.15

Preoperative evaluation A thorough history and physical examination must be performed on all AAA patients who are undergoing elective repair. The focus of the evaluation should be on cardiac and pulmonary function. The association of carotid disease with AAAs is high, so obtaining a carotid ultrasound should be considered. Patients undergoing endovascular aneurysm repair (EVAR) require assessment of their renal function because of the nephrotoxicity of the IV contrast load administered in EVAR.

Open versus endovascular repair AAAs can be repaired using either an open approach or an endovascular approach. Traditionally, open repair with graft placement has been utilized to treat AAAs and is the gold standard. Open repair is well-established and requires essentially no follow-up studies; most patients have no graft-related complications for the rest of their lives.

Endograft repair involving stent placement was first approved by the FDA in 1999. This procedure is a good option for those patients who are at a high surgical risk or who have limiting coexisting medical conditions. Patients undergoing EVAR must satisfy certain specific anatomic requirements involving axial length of the aneurysm neck, shape and angulation of the neck, diameter of the iliac arteries, and potential length and condition of distal iliac arteries used as distal sites of stent-graft fixation3 (see Figure 4). These parameters can be measured by using high-resolution CT angiography with 3D reconstruction (see Figure 5). If any of the above requirements for EVAR are not met, open AAA surgery must be considered.

EVAR can be performed under local anesthesia, but given the possibility of a failed procedure or of encountering a complication requiring an open procedure, EVAR is done under general anesthesia, as is open repair. On average, EVAR patients stay in the hospital for 2 to 3 days. Patients with open repairs stay approximately 5 to 10 days.

Open surgical aortoiliac grafts tend to require less longterm follow-up than endografts. Reintervention rates are about 20% for endovascular grafts versus 6% in open repair.3 Younger, healthier patients might benefit from open surgery because it has the potential for less follow-up and fewer reinterventions.

Complications The major risks in open AAA repair are perioperative cardiac events and renal or respiratory failure. The graft failure rate is approximately 0.3% in open procedures, with most grafts outliving the patient.16 There is always the risk of infection, the risks associated with general anesthesia, and the risk of unknown cardiac complications. During open AAA repairs, there is also the risk of paraplegia since blood supply to the lumbar arteries can be compromised. Other less common complications include distal embolization, iliac vein compression resulting in a deep venous thrombosis, and aortoenteric or aortocaval fistulae. Elective open surgical AAA repair is a complex procedure with a 30-day mortality of 5% and a complication rate of 15% to 20%. The mortality rate can be as high as 50% in medically unfit patients, with the result that some high-risk patients are denied surgical repair.

Endograft complications include migration of the stent, obstruction, and endovascular leaks (endoleaks). There are four types of endoleaks. A type I leak occurs at either the proximal or distal graft attachment site and results from an incompetent seal. These leaks are often found during the procedure and must be repaired immediately. Repair entails inflating a larger balloon at the neck to form a tighter seal or inserting a cuff at the neck of the stent. Type II endoleaks involve flow to and from the aneurysm sac caused by patent branch vessels, such as lumbar or mesenteric vessels. These leaks are the most common type and are most often found on a postprocedural CT scan. Often, there is spontaneous resolution of these leaks, which usually are followed closely on surveillance CT scans. Type II leaks need not be repaired unless the size of the aneurysmal sac increases. Type III and type IV leaks are less common. Type III leaks are due to graft defects, such as a hole or a tear. Repair requires an additional endograft to eliminate flow in the aneurysm. Type IV leaks are due to increased porosity of the graft fabric and nearly always heal spontaneously over time. The 30-day mortality rate for endovascular repair is 1.7%.12 Overall, there was no significant difference in allcause mortality in a 5-year comparison of open versus endovascular repair.17

Postoperative follow-up Typically, endovascular AAA repairs require follow-up appointments at 1 month, 6 months, and then annually for life. CT angiography of the abdomen and pelvis is done at each visit to check the graft. This is in contrast to open repair, after which there is one follow-up appointment approximately 2 weeks after discharge for a wound check; the patient is seen again only if there are problems.

Nonsurgical management of AAAs Patients with infrarenal AAAs measuring 4.0 to 5.4 cm in diameter should be monitored by ultrasound or CT scans every 6 to 12 months to detect possible expansion and the need for repair.

All patients with AAAs should be educated on the symptoms of rupture, such as new or unusual pain in the back, groin, testicles, legs, or buttocks. The patient should immediately seek emergency medical treatment if these occur. Patients who do not undergo repair should be considered for statin therapy because statins may decrease the risk of rupture and reduce aneurysm growth rates.1 ACE inhibitors and angiotensin receptor blockers have also been shown to reduce aneurysmal growth. JAAPA

James Ginter is a PA in the Vascular Center, St. Luke's Medical Center, Milwaukee, Wisconsin, and president of the Wisconsin Academy of Physician Assistants. Jessica Linzmeyer is a PA student at the University of Wisconsin—Madison. The authors have indicated no relationships to disclose relating to the content of this article.

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