Abdominal Aortic Aneurysm

Epidemiology

The prevalence of AAA increases with advancing age and is found in 2% to 5% of men older than 50 years. Men are affected more often than women, although recent research suggests AAA may be more common in women than previously suspected, particularly among women who smoke. The patient often has concomitant atherosclerotic occlusive disease, including coronary, carotid, or peripheral vessels, which may influence the clinical presentations, complications, and management.

Several risk factors for the development of an AAA have been established, but risk factors are epidemiologic, not individual characteristics. Age is the most significant risk factor for the development of an AAA. An AAA can be found in 5% to 10% of all older men who are screened with ultrasonography with increasing prevalence in those who have concomitant coronary artery disease or peripheral vascular disease. A family history of an AAA is a powerful risk factor; those with an affected first-degree relative have a markedly increased risk of developing an AAA. Although awareness of high-risk groups can speed the recognition of AAA, the consideration of AAA should not be restricted to patients in these groups. Some evidence suggests that women may experience delays in diagnosis and worse operative mortality after ruptured AAA. Up to half of AAAs in the United States occur in women, nonsmokers, or those younger than 65 ( Table 72.1 ).

Pathophysiology

AAAs have traditionally been attributed to atherosclerosis, but patients with advanced atherosclerosis have occlusive disease, not aneurysms. Patients with AAA have biochemical abnormalities leading to the loss of elastin and collagen, which are the major structural components of the aortic wall. The propensity to form aneurysms may have a genetic basis, but the exact mode of inheritance is uncertain. The Society for Vascular Surgery has recommended labeling the typical degenerative AAA as “nonspecific,” rather than “atherosclerotic,” to reflect this uncertainty surrounding the etiology.

AAAs may also have specific etiologies, such as infection, trauma, connective tissue diseases, and arteritis. Such aneurysms are rare, however, compared with nonspecific degenerative aneurysms.

Natural History

AAAs progressively enlarge, ultimately resulting in rupture of the aneurysm and potentially fatal hemorrhage. Although other complications are possible, by far the most common and most clinically significant is rupture.

The most important factor determining the risk of rupture is the size of the aneurysm. The risk of rupture increases substantially with increased aneurysm size, and most ruptured AAAs have diameters greater than 5 cm. The growth rate of the AAA, in addition to other anatomic factors, may also be important in determining the risk of rupture. Although rupture of aneurysms smaller than 4 cm is rare, no aneurysm is completely “safe.” Any aneurysm can rupture and cause significant consequences.

AAA most commonly ruptures into the retroperitoneum, where hemorrhage may be temporarily limited by clotting and tamponade at the rupture site, but 10% to 30% involve free intraperitoneal rupture, which is often rapidly fatal. Occasionally, rupture occurs into the gastrointestinal tract or the inferior vena cava.

Complications can also arise from an intact AAA. The walls of an AAA are often lined with clot and atheromatous material, which can embolize and occlude distal vessels. Sequelae of occlusion and embolization may be the only diagnostic clues to AAA. Aortic thrombosis may occur rarely and patients can also have complications caused by impingement of the aneurysm on adjacent structures.

In approximately 5% of AAAs, a dense inflammatory and fibrotic reaction develops in the aneurysm wall and adjacent retroperitoneal tissue. In these “inflammatory” AAAs, periaortic fibrosis may incorporate and obstruct adjacent structures, such as the ureters or duodenum.

The principal concern in the patient with an AAA is the potential for rupture of the aneurysm, which can be prevented only by timely repair.

Unruptured Aneurysms

Because most AAAs do not cause symptoms until they expand or rupture, the prevalence of symptoms in patients with unruptured AAAs is difficult to determine. Patients may have symptoms that lead to the aneurysm’s discovery before rupture. These symptoms can include pain in the abdomen, back, or flank; an awareness of an abdominal mass or fullness; or a sensation of abdominal pulsations. Clinical suspicion of AAA, which includes both the patient’s history and physical examination findings, warrants further investigation with imaging.

The pain associated with stable, intact aneurysms often has a gradual onset and a vague, dull quality. It is usually constant but may be described as throbbing or colicky. Acute or severe pain is an ominous symptom that suggests imminent or actual aortic rupture.

In most cases, an AAA is asymptomatic and is discovered incidentally on physical examination, on a radiologic study done for unrelated issues, or by ultrasonography as part of an aneurysm screening program. Symptoms may not develop until the aneurysm ruptures, and the finding of an AAA may or may not be related to the patient’s current visit. If determined not to be related, follow-up will be necessary even when found incidentally.

The most prominent physical finding is a pulsatile, expansile abdominal mass above the level of the aortic bifurcation. If the iliac arteries are also aneurysmal, the mass may extend below the umbilicus. The right border of an AAA may be palpable to the right of midline, whereas a normal or tortuous aorta is usually not. Most intact AAAs are nontender; tenderness suggests aneurysm expansion or rupture.

Symptomatic aneurysms are usually relatively large and are often palpable with a careful abdominal examination. However, an AAA may be challenging to palpate if the aneurysm is small or the patient is obese. Published reports indicate that 30% to 60% of unruptured aneurysms measuring 3.0 to 3.9 cm on ultrasonography can be detected by abdominal palpation; 50% to 70% of aneurysms measuring 4.0 to 4.9 cm and 75% to 85% of aneurysms 5 cm or larger can be palpated. These reports are based on the examination of patients with intact, asymptomatic aneurysms, with the examination specifically directed at sizing the aorta. The sensitivity is likely much lower when the abdomen is not palpated deeply, in hypotensive patients, or in those with significant abdominal guarding. There is virtually no risk of causing aneurysm rupture by abdominal palpation.

Physical examination may reveal findings consistent with an AAA even when the aorta is of normal size. A tortuous aorta may feel enlarged, and prominent aortic pulsations, especially in a thin patient, may simulate an aneurysm. Pulsations from a normal aorta may be transmitted to an adjacent abdominal mass.

An abdominal bruit is an uncommon finding in patients with AAAs. The presence of a bruit is also nonspecific, because bruits can originate from a stenotic renal, iliac, or mesenteric artery. A loud continuous bruit suggests the diagnosis of arteriovenous fistula, a rare complication of AAAs.

Perfusion distal to an AAA is usually well maintained, and most patients have normal femoral pulses. Diminished femoral pulses may result from iliofemoral occlusive disease or hypotension related to hemorrhagic shock in the patient bleeding from a ruptured aneurysm.

Thromboembolic complications can occur spontaneously or when atheromatous plaques are disrupted during invasive intravascular procedures. Large emboli can acutely occlude major vessels, such as the iliac, femoral, or popliteal artery, causing painful lower extremity ischemia with absent distal pulses. Rarely, the aneurysm itself can thrombose, rendering both lower extremities acutely ischemic. More commonly, microemboli consisting of cholesterol crystals or clot obstruct small distal vessels, such as the digital arteries of the toes and arterioles and capillaries of the skin. These patients can present with livedo reticularis; one or more cool, painful, cyanotic toes; and palpable pedal pulses. This constellation of findings, often called the blue toe syndrome, is highly suggestive of a proximal source of emboli. When an AAA is the source, the aneurysm is often too small to palpate and only recognized with radiologic investigation.

In rare instances, an intact AAA can cause symptoms by compressing adjacent structures, with symptoms arising from those structures involved. Large, long-standing aneurysms can cause vertebral body erosion and severe back pain. Compression of the duodenum between the superior mesenteric artery and an AAA can cause duodenal obstruction, vomiting, and weight loss. Obstruction of the ureters in the patient with an inflammatory aneurysm can cause symptoms suggestive of ureteral colic.

Ruptured Aneurysms