An abdominal aortic aneurysm (AAA) is defined as a focal dilation of the aorta beyond a diameter of 3.0 cm. The causes of aneurysmal degeneration of the aorta are multifactorial, and likely involve a combination of risk factors that lead to a loss of vascular structural proteins and wall strength. Both age and gender are important predisposing factors, as demonstrated by the observation that the rate of AAA rises sharply after age 60, and men develop aortic aneurysms more frequently than women. The greatest acquired risk factor for both the onset and growth of an AAA is smoking. Poorly controlled hypertension also contributes to aneurysm formation and growth.

Most AAAs develop in the region between the renal arteries and the aortic bifurcation, and are accordingly termed infrarenal aortic aneurysms (Fig. 29.1). The reason that aneurysms form in this location is likely related to the changes in fluid dynamics and increased wall pressures that occur as the aorta bifurcates into the iliac arteries. Structural differences and a lower collagen to elastin ratio in the abdominal aortic wall as compared to thoracic aorta, may also play a role. As an aneurysm progresses, it can expand proximally above the level of the renal arteries, as well as distally to cause aneurismal dilatation of the iliac arteries.

Most patients with an AAA are asymptomatic, and the aneurysm is only detected as an incidental finding on imaging studies performed for other purposes. Occasionally, a pulsatile mass is detected on routine physical examination. AAA can also present with lower extremity ischemia due to distal embolization of atherosclerotic debris from the aneurysm sac. When symptoms of AAA do occur, patients may present with vague abdominal or back pain, presumably from compression of nearby structures by the enlarging aneurysm sac. The presence of severe back pain may be an ominous sign of impeding rupture. However, since AAAs are typically asymptomatic, individuals considered at high risk should be enrolled in screening programs that use abdominal ultrasounds to measure aortic diameter.

The natural history of AAAs is of a progressive increase in size and eventual rupture (Fig. 29.2). There are currently no treatments to reverse the course of an AAA, but growth of the aneurysm can be slowed with exercise, control of blood pressure, and smoking cessation. Once a patient has been diagnosed with an aneurysm, close surveillance is necessary to follow its diameter. Expansion rates vary between individuals, and the growth of an aneurysm typically accelerates as the diameter becomes increasingly wide. The risk for rupture rises markedly at aneurysm diameters greater than 5.5 cm. As a result, surgical repair is generally advised when aneurysm size approaches this size, or if an aneurysm is noted to be expanding rapidly on serial imaging.

Intervention prior to rupture is critical since—once rupture occurs—only about half of patients survive long enough to reach a medical facility. Free rupture of an AAA with intraperitoneal hemorrhage produces profound hemodynamic instability and is rapidly fatal. However, rupture of the posterior aortic wall may be initially contained within the retroperitoneum, allowing the opportunity for treatment. Rupture of an AAA is said to produce a triad of severe acute pain, a pulsatile abdominal mass, and hypotension, although this classic presentation is only seen in about half of patients.

Any patient seen in the emergency room with a suspicion of a ruptured AAA must be evaluated immediately. Physical examination should include assessment of the palpation of the abdomen in the region between the xiphoid and umbilicus, to identify a pulsatile mass. If the patient has a contained rupture, the associated retroperitoneal hematoma may track to the skin to produce a visible ecchymosis in the mid-back (Grey–Turner sign) or in the periumbilical region (Cullen’s sign). Despite the fact that patients with a ruptured AAA will be hypotensive, fluid restriction should be restricted, since any added intravascular volume may convert a contained rupture into a free rupture.

In a hemodynamically unstable patient, with a known history of an AAA, who presents with signs of rupture, imaging is not required to confirm the diagnosis. In this scenario, patients who are candidates for surgical repair should be taken straight to the operating room without any preceding imaging study. In patients with no history of an AAA, a rapid non-contrast CT scan should be obtained to confirm the presence of an aneurysm.

Abdominal aortic aneurysms can be repaired by an open surgical approach or via endovascular aneurysm repair (EVAR). In open surgery, the aneurismal portion of the aorta is replaced with a synthetic graft. The endovascular approach involves the use of an endograft, which is deployed within the aneurismal aorta from a remote site, typically the femoral artery. Fixation of the endovascular device is achieved against the normal (non-dilated) segment of the aortic wall proximally just below the renal arteries, and distally in each of the iliac arteries distally. The device creates a seal, excluding the aneurysm sac from blood flow, and thereby preventing expansion of the AAA.

The pros and cons of the open versus endovascular approach should be considered on a case-by-case basis.

However, not all patients are candidates for both types of repair. One consideration in selecting the approach is that open AAA repair must be performed under general anesthesia, while EVAR can be performed with local anesthesia and sedation. Contraindications to open repair of an AAA include extensive intra-abdominal adhesions, morbid obesity, and major cardiac or pulmonary comorbidities.

By contrast, contraindications for endovascular repair are largely centered on technical aspects of the aneurysm’s shape and location. In order to successfully exclude blood flow into the aneurysm sac, the endograft must provide an adequate seal where it contacts the arterial wall. A short neck between the AAA and the renal arteries is therefore a relative contraindication to endovascular repair. In addition, features such as sharp angulation of the aorta or iliac arteries can interfere with proper positioning and fixation of the device. Prior to AAA repair, CT or MR angiography is used to evaluate the anatomic features of the aneurysm that may affect the approach to repair. Finally, since endograft size and shape must be carefully customized for each patient’s specific anatomy, emergent repair of a ruptured AAA via the endovascular approach is only possible in centers where a wide selection of variously sized endografts is immediately available.Overall endovascular repair is associated with less mortality and morbidity but requires lifelong surveillance of the endograft with CT angiography. Because of the higher perioperative survival, endovascular repair is emerging as the preferable technique in patients undergoing elective repair who have suitable anatomy.