History and exam

Key diagnostic factors

uncommon

palpable pulsatile abdominal mass

Aneurysm palpation on clinical examination has been shown to be sensitive only in thin patients and those with AAA >5 cm (sensitivity and specificity of 68% and 75%, respectively).[1][78] Detection rates are affected by aortic diameter, clinician experience, and body habitus of the patient.[3] The sensitivity of abdominal palpation for detecting AAA decreases in patients with an abdominal girth more than 100 cm.[78]​​​

Other diagnostic factors

uncommon

abdominal, back, or groin pain

The classic triad of abdominal and/or back pain, hypotension, and a pulsatile abdominal mass is present in about 50% of patients with a ruptured AAA.[3]​ However, the majority of patients are asymptomatic and their aneurysm is detected incidentally.[80]

hypotension

Patients with ruptured aneurysm present with cardiovascular collapse.[79]

Risk factors

strong

cigarette smoking

This is the risk factor most strongly associated with AAA.​​[13][15][22][23][24][25]​​​​

Active cigarette smoking is independently associated with histologic high-grade tissue inflammation.[43]

The duration of smoking is significantly associated with an increased risk in a linear dose-response relationship.[24]​ Each year of smoking increases the relative risk by 4%.[23]

hereditary/family history

Studies support a familial aggregation of and genetic predisposition to AAA.​[13][25]​​​[44]​​[45][46][47][48][49][50][51]​​​​

In a large population-based study, a positive first-degree family history for AAA was more common among cases than among controls (8.4% vs. 4.6%, P=0.0001).[52] The risk of AAA associated with family history was approximately doubled compared with no family history (odds ratio [OR] 1.9, 95% CI 1.6 to 2.2).

A Swedish twin registry study found that the twin of a monozygotic twin with AAA had a risk of AAA approximately 70 times greater than that of the twin of a monozygotic twin without AAA.[40]

increased age

Prevalence increases with age.[1][5]​​[15]​​

Most frequently diagnosed in men >55 years of age, and rupture rarely occurs before 65 years of age.[3]

AAA is typically discovered approximately 10 years later in women.[13][53]

male sex (prevalence)

AAAs are 4 to 6 times more prevalent in men than women.​[13][15][25]

female sex (rupture)

Risk of rupture is greater in women than in men.​[54][55]​​​​​

congenital/connective tissue disorders

Aortic degeneration is accelerated in patients with Marfan syndrome, and during pregnancy.[56][57][58]

Marfan syndrome specifically is associated with cystic medial necrosis of the aorta secondary to an autosomal dominant anomaly in fibrillin type 1, a structural protein that directs and orients elastin in the developing aorta.[56][57]​ As a result, the mature aorta demonstrates abnormal elastic properties, progressive stiffening, and dilation.[58]

weak

hyperlipidemia

Lipoproteins are elevated in patients with AAA independent of cardiovascular risk factors and extent of atherosclerosis.[59]​ Patients with AAA have a high incidence of genetically determined dyslipidemia.​[60]

AAA patients have significantly lower levels of apolipoprotein AI and HDL cholesterol than matched controls with aorto-iliac occlusive disease.​[59]

High serum total cholesterol is a relatively weak risk factor for AAA, whereas high HDL cholesterol was strongly associated with a low risk of AAA.[15]​ Statin therapy may reduce AAA growth rates and mortality.​[61][62][63]​​​​ ​

COPD

This is attributed to tobacco-induced elastin degradation.​[13]

Studies suggest that the association between reduced respiratory function and AAA may be due to the activation of inflammation and hemostasis in response to injury.[64]

atherosclerosis (i.e., coronary artery disease [CAD], peripheral arterial occlusive disease)

CAD is an independent risk factor.[1][22]

hypertension

Hypertension is a weak independent risk factor.​​[13][15][65]​​​​

There is a relation between systolic blood pressure and AAA in women, and an association with ever-use antihypertensive medication and AAA risk for both sexes.[15]​​

central obesity

One study of >12,000 men demonstrated an independent association between central obesity and AAA.[66]

nondiabetic

Research suggests that diabetes protects against the growth and enlargement of AAA.[26][27][28]​ However, the protective mechanism is yet to be determined.[27][28]​ Operative and long-term survival was lower among AAA repair patients with diabetes than those without, suggesting an increased cardiovascular burden.[26]

fluoroquinolone antibiotic use

Studies suggest an association between use of fluoroquinolone antibiotics and a small increase in risk of AAA.[67][68][69] However, having a small AAA is not a contraindication to using fluoroquinolone antibiotics.[3]​​

aneurysms elsewhere in the body

Co-prevalence of aneurysms is common; one in six patients with a primary aneurysm also has another aneurysm elsewhere. Screening for AAA in patients with intracranial aneurysms may be clinically indicated and cost-effective.[70]

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