Introduction
Background
Abdominal aortic aneurysm (AAA) is a relatively common, potentially life-threatening condition. Most cases are asymptomatic and are often detected as an incidental finding using diagnostic imaging obtained for other reasons. There is a wide spectrum of clinical presentations and abdominal aortic aneurysm should be considered in the differential diagnosis for a number of symptoms.
Abdominal aortic aneurysm is usually the result of degeneration in the media of the arterial wall, resulting in a slow and continuous dilatation of the lumen of the vessel. In fewer than 5% of cases, abdominal aortic aneurysm is caused by mycotic aneurysm of hematogenous origin. In these cases, local invasion of the intima and media gives rise to abscess formation and aneurysmal dilation of the vessel. Gram-positive organisms most commonly cause mycotic aneurysm. As with aneurysm of the thoracic aorta, abdominal aortic aneurysm may be described as fusiform, which is circumferential, or saccular, which is more localized.
The lateral view clearly shows calcification of both walls. Abdominal aortic aneurysm can be diagnosed with certainty.
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Pathophysiology
After age 50, the normal diameter of the infrarenal aorta is 1.5 cm in women and 1.7 cm in men. An infrarenal aorta that is 3 cm in diameter or larger is considered an abdominal aortic aneurysm (AAA), even if asymptomatic. Approximately 90% of abdominal aortic aneurysms are infrarenal.
The 3 layers comprising the normal aorta are the intima, media, and adventitia. Structural and elastic properties of major arteries are mostly imparted by the media, which is composed of smooth muscle cells surrounded by elastin, collagen, and proteoglycans. Abdominal aortic aneurysm develops following degeneration of the media due to atherosclerotic changes. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity. While abdominal aortic aneurysm is known to primarily involve the media, the exact etiology is not known.
Most abdominal aortic aneurysms occur in association with advanced atherosclerosis. Atherosclerosis may induce abdominal aortic aneurysm formation by causing mechanical weakening of the aortic wall with loss of elastic recoil, along with degenerative ischemic changes, through obstruction of the vasa vasorum. Many patients with advanced atherosclerosis do not develop AAA, while some patients having no evidence of atherosclerosis do. The observed association between atherosclerosis and AAA is probably not causative; however, atherosclerosis may represent a nonspecific secondary response to vessel wall injury that is induced by multiple factors.
Frequency
United States
Ruptured AAA is the 13th-leading cause of death in the United States, causing an estimated 15,000 deaths per year. The incidence of AAA is 2-4% in the adult population, and 11% of cases in that subset occur in males older than 65 years. Despite increased survival following diagnosis, incidence and crude mortality seem to be increasing.
Mortality/Morbidity
In 1988, 40,000 surgical reconstructions for abdominal aortic aneurysm (AAA) were performed in the US, with substantial mortality differences between elective versus emergency operations. As elective aneurysm repair has a mortality rate drastically lower than that associated with rupture, the emphasis must be on early detection and repair free from complications.
Race
White males have the highest incidence of AAA.
Sex
Males are affected 7 times more often than females.
Age
AAA occurs most commonly in patients between age 65 and 75 years, and it is more frequent in men smokers.
Clinical
History
Abdominal aortic aneurysms (AAAs) are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time prior to rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis.
- Expanding AAA causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, and pain may be a less significant symptom to the patient.
- Patients with a ruptured AAA may present in frank shock as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension.
- At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital.
- Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease.
- A history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension often is elicited.
- Less frequent causes of AAA include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm.
- Patients who have a first-degree relative with AAA are at increased risk.
- It is important to note progressive symptoms (eg, abdominal or back pain, vomiting, syncope, claudication). These should alert the clinician to the possibility of expansion with imminent rupture.
Physical
- While abrupt onset of pain due to AAA may be quite dramatic, associated physical findings may be very subtle.
- Patients may have normal vital signs in the presence of a ruptured AAA due to retroperitoneal containment of hematoma.
- Presence of a pulsatile abdominal mass is virtually diagnostic but is found in less than half of cases. It is more commonly seen with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in 25% of patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery.
- Misdiagnosis is fairly common because the classic presentation of pain associated with hypotension, tachycardia, and a pulsatile abdominal mass is present in fewer than 30-50% of cases. The leading misdiagnosis is renal colic, as dissection of the renal artery may produce flank pain and hematuria.
- Presence of an abdominal bruit or lateral propagation of the aortic pulse wave offer subtle clues and may be more frequently found than the pulsatile mass.
- The clinician need not be afraid of properly palpating the abdomen because no evidence exists that aortic rupture can be precipitated by this maneuver.
Causes
- Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease.
- A history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension often is elicited. The US Preventive Services Task Force recommends ultrasonography screening in men aged 65-75 years who have ever smoked.1
- Less frequent causes of AAA include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm.
- Patients who have a first-degree relative with AAA are at increased risk.
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Further Reading
Keywords
abdominal aneurysm, abdominal aortic aneurysm, AAA, mycotic aneurysm, abscess formation, atherosclerosis, smoking, chronic obstructive pulmonary disease, COPD, hypertension, syncope, shock, cyanosis, sudden cardiovascular collapse, peripheral atherosclerotic vascular disease, Marfan syndrome, Ehlers-Danlos syndrome, collagen vascular diseases, mycotic aneurysm, claudication, pulsatile abdominal mass, abdominal bruit, aortic rupture
