eMedicine Specialties > Radiology > Vascular/Interventional
Abdominal Aortic Aneurysm, Diagnosis
Updated: Oct 2, 2008
Introduction
Background
Approximately 40,000 patients undergo aneurysmorrhaphy each year. In the United States, 15,000 deaths per year are attributed to abdominal aortic aneurysms (AAAs).
Since 1951, when Dubost first performed repair of an AAA with a homograft, surgery has been the mainstay of treatment. Many refinements in technique have occurred during the interval, but none as significant as the stent-graft. In 1991, Parodi et al described a novel, less invasive technique for repairing AAAs by placing a graft from within the vessel. This technique was labor intensive and involved the customized construction of the graft for each patient by sewing the graft material to self-expanding metal skeleton. Today, designs are approved by the US Food and Drug Administration, and numerous devices are being used in clinical investigations.1,2,3,4,5
CT demonstrates an abdominal aortic aneurysm. The aneurysm was noted during workup for back pain, and CT was ordered after the abdominal aortic aneurysm was identified on radiographs. No evidence of rupture is seen (same patient as in Image 2 in Multimedia).
Arteriogram demonstrates an infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation of an endovascular repair of the aneurysm (same patient as in Image 2 in Multimedia).
Ultrasonogram of a patient with an abdominal aortic aneurysm. This aneurysm was best visualized on a transverse or axial image. This patient underwent a conventional abdominal aortic aneurysm repair.
Related eMedicine topics:
Aneurysm, Abdominal (Emergency Medicine)
Abdominal Aortic Aneurysm, Rupture
Abdominal Aortic Aneurysm (Vascular Surgery)
Pathophysiology
Classically, abdominal aortic aneurysms (AAAs) have been attributed to a weakening of the arterial wall as a result of atherosclerotic vascular disease caused by the atheromatous lesions seen on pathologic examination. Recent evidence supports a multifactorial process in which atherosclerosis is involved. Other etiologic cofactors under investigation include changes in the matrix of the aortic wall with age, proteolysis, metalloproteinase changes, inflammation, infectious agents (eg, syphilis, mycotic infections), and a genetic predisposition (eg, Marfan syndrome, Ehlers-Danlos syndrome).5,6,7
True aneurysms involve dilation of all 3 layers of the vessel wall, whereas false aneurysms are caused by the disruption of 1 or more layers of the vessel wall. Elastin and collagen are the primary structural elements of the aortic wall. Experimental findings have shown that the relative content of elastin and collagen are lowest in the infrarenal aorta and that, with the destruction of collagen and elastin, dilatation of the aorta ensues. Increased concentrations of several proteases capable of degrading collagen and/or elastin have been found in the walls of AAAs and in aortic occlusive disease; both are manifestations of atherosclerosis.
An immunologic component to atherosclerotic vascular disease has been recognized and is characterized by infiltration of the aortic wall by macrophages, T lymphocytes, and B lymphocytes; these are known to activate proteolytic activity. The nature of this response has led researchers to investigate autoimmunity in the pathogenesis of AAA. Reports describe Chlamydia pneumoniae antigens, in contrast to active infection, in the walls of AAA. After the infectious agent is cleared, an antigenic stimulus remains, stimulating proteolytic activity with weakening of the vessel wall and aneurysm formation.
Inflammatory aneurysms, once believed to be distinct entities, are currently considered one extreme in the spectrum of atherosclerotic aneurysms; these account for 3-10% of all AAAs. Clinical and imaging characteristics differentiate inflammatory from noninflammatory aneurysms.8
The familial pattern of AAA has long been recognized with a 15-19% incidence among first-degree relatives. This observation suggests that one or more genes are related to AAA and atherosclerosis. The identification of these genes may enable the early detection and prevention of AAA in high-risk patients.9
Frequency
United States
Abdominal aortic aneurysms (AAAs) are usually asymptomatic and detected on routine physical examination or during an unrelated radiologic examination. Therefore, the condition is likely underdiagnosed. In most studies, prevalence increases in those older than 60 years. In the United States, the reported incidence is 5-7% with a mean patient age of 70-75 years.
International
In Europe and Asia, the reported incidence of abdominal aortic aneurysms (AAAs) is 5-7%, with a mean patient age of 70-75 years.
Mortality/Morbidity
In the United States 15,000 deaths per year are attributed to abdominal aortic aneurysms (AAAs).
- When AAAs are repaired electively, the overall mortality rate is 0.9-5%.
- If repair is delayed until rupture, mortality rates as high as 75% are reported.10,11
- In aneurysms 4-5 cm in diameter, the risk of rupture is almost 25%, with an associated mortality rate as high as 75%.
Race
- Worldwide, abdominal aortic aneurysms (AAAs) are more common in white males than in others. In the United States, AAA is far more common in white males than in black males. This difference may be partially caused by increased detection in white males, resulting from better access to medical care.
- The prevalence in white and black females is almost identical.
- Etiologic explanations for these race-related differences include different genetic susceptibility, as well as exposure to environmental risk factors. Note that, in the United States, other clinical manifestations of atherosclerosis do not have this racial predilection.
Sex
Depending on the published series, the male-to-female ratio is 1.6-4.5:1.12
- Inflammatory aneurysms represent 3-10% of atherosclerotic abdominal aortic aneurysms (AAAs) and have a male-to-female ratio of 6-30:1.
- The reasons for male preponderance of AAA are not clear; however, hormonal factors, genetic susceptibility, and exposure to environmental factors are believed to play a role.
Age
- Abdominal aortic aneurysms (AAAs) occur in 5-7% of the population older than 60 years.
- AAAs are seen most often in patients aged 60-80 years.
- The mean age of patients with inflammatory aneurysms is 62-65 years; these patients are 5-10 years younger than those with noninflammatory AAA.
Anatomy
An aneurysm is defined as a localized dilation of an artery by at least 50% as compared with the expected normal diameter of the vessel. The term ectasia is used when the dilatation is less than 50%. If the arteries are diffusely enlarged by 50% or more, the condition is called arteriomegaly.13,14
The Society for Vascular Surgery and the International Society for Cardiovascular Surgery have suggested the classification of aneurysms by their site, origin, histologic features, and clinicopathologic manifestations. The anatomic site and morphology of an aneurysm can be preoperatively determined by radiologic means.15,16,17
The site of an aneurysm is related to its natural history, clinical presentation, and means of treatment. The site of abdominal aneurysms should be characterized as suprarenal, juxtarenal or pararenal, or infrarenal. Approximately 90-95% of abdominal aortic aneurysms (AAAs) involve the infrarenal abdominal aorta. Rarely do they extend above the renal arteries; however, extension into the common iliac arteries is fairly common.
Presentation
Abdominal aortic aneurysms (AAAs) occur in 5-7% of the population older than 60 years. Although most patients with AAA are asymptomatic, they can present with symptoms of mass effect, compression of abdominal organs, or visceral or peripheral emboli originating from the wall of the aneurysm. Rarely, patients present with back pain, which can represent rupture of the aneurysm, a surgical emergency. Patients older than 60 years who smoke and who are known to have atherosclerosis, hypertension, and/or chronic obstructive pulmonary disease are at increased risk for AAA. Routine screening of these patients is warranted.
Once an aneurysm is identified, it should be repaired or followed up with imaging, depending on the clinical scenario and the size of the aneurysm at the time of diagnosis. Most aneurysms (80%) demonstrate progressive enlargement. The diameter of an aneurysm is directly related to its risk of rupture. For aneurysms smaller than 4 cm in diameter, the risk of rupture is less than 10%. Once an aneurysm is 4-5 cm in diameter, the risk of rupture increases to almost 25%, with an associated mortality rate as high as 75%. The accepted surgical mortality rate remains less than 5% with the elective repair of these 4- to 5-cm aneurysms.
The morphologic features, including the maximum diameter in both the anteroposterior and lateral dimensions and the length of the aneurysm, should be reported. The shape of the aneurysm (fusiform or saccular) and its relationship to branch vessels should be described. Arterial wall complications such as the expansion over time, compression or erosion into adjacent structures, rupture, dissection, and thrombotic occlusion should be documented as well.
With the advent of the endoluminal repair of aneurysms, several additional morphologic characteristics should be recorded. These determine if endovascular repair is possible, and if so, what type of device can be used. These features include the following: (1) greatest mural diameter, (2) extent of aneurysm (eg, length of proximal and distal neck, extension into iliac arteries), (3) tortuosity of the aorta, (4) anatomy of the iliac arteries (eg, iliac artery occlusive disease, tortuosity, caliber, patency of internal iliac arteries and relation of aneurysm to them, presence of concomitant iliac artery aneurysms), (5) presence and degree of intraluminal thrombus, (6) presence and degree of calcification in the neck and iliac arteries, and (7) anatomy of the femoral arteries (eg, caliber, degree of calcification or occlusive disease).
Preferred Examination
Because of portability, lack of ionizing radiation, cost, and availability, ultrasonography (US) should be the initial imaging modality when an asymptomatic, pulsatile abdominal mass is palpated.
If the aneurysm is approaching 5 cm or more or if rapid enlargement is seen on serial US images, a CT or CT angiogram (CTA) should be ordered to better delineate the extent of disease prior to conventional surgery or treatment with the insertion of an endovascular graft. In patients whose renal function does not permit the administration of iodinated contrast material, MRI and magnetic resonance angiography (MRA) provide good alternatives.
Angiographic examination may be requested because of a clinical concern that concomitant renal artery stenosis or peripheral vascular disease may require surgical intervention during repair of abdominal aortic aneurysms (AAAs). At some institutions, CTA and MRA have replaced routine diagnostic angiography in the preoperative evaluation of AAA.
In urgent situations in which the clinical diagnosis is fairly certain or rupture is imminent or suspected and in which the patient's condition is stable, CT and/or CTA may be the initial and only examination required.
Imaging of the aorta does not end with the repair of the aneurysm. After repair with either a traditional open surgical procedure or an endovascular procedure, follow-up imaging is necessary. In the case of conventional surgical repair, follow-up imaging is performed yearly, usually with US. For endovascular grafts, the follow-up is more stringent, with immediate postprocedural CT as well as 6-month and then yearly CT follow-up.
When the evaluation for AAA is performed with CT or MRI, note the extent of the aneurysm, any involvement of major branch vessels, and the existence of a retroaortic or circumaortic left renal vein. Note if the aneurysm has significant wall thickening, a typical characteristic of an inflammatory aneurysm, because the surgical approach for this condition differs from that needed for the more common, predominantly atherosclerotic aneurysm.
Limitations of Techniques
With conventional radiography in the anteroposterior or lateral projection, calcification of both opposing abdominal aortic walls must be present to outline abdominal aortic aneurysms (AAAs). However, this finding is present in less than 50% of cases. A tortuous, calcified aorta may mimic an AAA unless both walls can be seen clearly. The lack of overlying bony structures in the lateral projection may allow clearer definition of the aneurysm.
US is considered the screening examination of choice; however, it may not adequately depict the entire abdominal aorta if a large amount of bowel gas is present or if the patient is obese.
With or without contrast enhancement, CT is an excellent screening examination for AAA. CT depicts the absolute size of the aneurysm. However, the extent of mural thrombus and the presence of dissection cannot be evaluated without the administration of contrast material.
MRI with contrast enhancement provides an alternative to CT in patients with renal insufficiency. MRI has several absolute contraindications, including cardiac pacemakers and intracranial aneurysm clips. Claustrophobia and a patient's inability to remain motionless are likely to yield a nondiagnostic study. MRI is not as available as CT and US.
Angiography is also a safe procedure. However, because it is an invasive procedure, a small but definite risk to the patient exists. The true size of the aneurysm may not be discernible because of a mural thrombus; therefore, underestimation of the true extent of the aneurysm is possible. The role of angiography is in planning surgical or endovascular repair.
Patient Education: For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education article Aortic Aneurysm.
Differential Diagnoses
Abdominal Aortic Aneurysm, Rupture
Aorta, Dissection
Aorta, Trauma
Other Problems to Be Considered
Inflammatory aneurysm
Mycotic aneurysm
Penetrating ulcer
More on Abdominal Aortic Aneurysm, Diagnosis |
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| Imaging: Abdominal Aortic Aneurysm, Diagnosis |
| Follow-up: Abdominal Aortic Aneurysm, Diagnosis |
| Multimedia: Abdominal Aortic Aneurysm, Diagnosis |
| References |
| Further Reading |
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References
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Tan JW, Yeo KK, Laird JR. Food and Drug Administration-approved endovascular repair devices for abdominal aortic aneurysms: a review. J Vasc Interv Radiol. Jun 2008;19(6 Suppl):S9-S17. [Medline].
Lovegrove RE, Javid M, Magee TR, Galland RB. A meta-analysis of 21,178 patients undergoing open or endovascular repair of abdominal aortic aneurysm. Br J Surg. Jun 2008;95(6):677-84. [Medline].
[Best Evidence] Lederle FA, Kane RL, MacDonald R, Wilt TJ. Systematic review: repair of unruptured abdominal aortic aneurysm. Ann Intern Med. May 15 2007;146(10):735-41. [Medline].
Pearce WH, Shively VP. Abdominal aortic aneurysm as a complex multifactorial disease: interactions of polymorphisms of inflammatory genes, features of autoimmunity, and current status of MMPs. Ann N Y Acad Sci. Nov 2006;1085:117-32. [Medline].
Hirose H, Takagi M, Miyagawa N. Genetic risk factor for abdominal aortic aneurysm: HLA-DR2(15), a Japanese study. J Vasc Surg. Mar 1998;27(3):500-3. [Medline].
Golledge J, Muller J, Daugherty A, Norman P. Abdominal aortic aneurysm: pathogenesis and implications for management. Arterioscler Thromb Vasc Biol. Dec 2006;26(12):2605-13. [Medline].
Rasmussen TE, Hallett JW Jr. Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis. Ann Surg. Feb 1997;225(2):155-64. [Medline].
Salo JA, Soisalon-Soininen S, Bondestam S. Familial occurrence of abdominal aortic aneurysm. Ann Intern Med. Apr 20 1999;130(8):637-42. [Medline].
Craig SR, Wilson RG, Walker AJ. Abdominal aortic aneurysm: still missing the message. Br J Surg. Apr 1993;80(4):450-2. [Medline].
Alexander S, Bosch JL, Hendriks JM, Visser JJ, Van Sambeek MR. The 30-day mortality of ruptured abdominal aortic aneurysms: influence of gender, age, diameter and comorbidities. J Cardiovasc Surg (Torino). Oct 2008;49(5):633-7. [Medline].
Harthun NL. Current issues in the treatment of women with abdominal aortic aneurysm. Gend Med. Mar 2008;5(1):36-43. [Medline].
Blanchard JF. Epidemiology of abdominal aortic aneurysms. Epidemiol Rev. 1999;21(2):207-21. [Medline].
Rehm JP, Grange JJ, Baxter BT. The formation of aneurysms. Semin Vasc Surg. Sep 1998;11(3):193-202. [Medline].
Ahn SS, Rutherford RB, Johnston KW. Reporting standards for infrarenal endovascular abdominal aortic aneurysm repair. Ad Hoc Committee for Standardized Reporting Practices in Vascular Surgery of The Society for Vascular Surgery/International Society for Cardiovascular Surgery. J Vasc Surg. Feb 1997;25(2):405-10. [Medline].
Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery. J Vasc Surg. Jun 1992;15(6):1046-56. [Medline].
Johnston KW, Rutherford RB, Tilson MD. Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovasc. J Vasc Surg. Mar 1991;13(3):452-8. [Medline].
Grollman J, Bettmann MA, Boxt LM. Pulsatile abdominal mass. American College of Radiology. ACR Appropriateness Criteria. Radiology. Jun 2000;215 Suppl:55-9. [Medline].
Rentschler ME, Baxter BT. Medical therapy approach for treating abdominal aortic aneurysm. Vascular. Nov-Dec 2007;15(6):361-5. [Medline].
Rayt HS, Sutton AJ, London NJ, Sayers RD, Bown MJ. A Systematic Review and Meta-analysis of Endovascular Repair (EVAR) for Ruptured Abdominal Aortic Aneurysm. Eur J Vasc Endovasc Surg. Sep 16 2008;[Medline].
Muszbek N, Thompson MM, Soong CV, Hutton J, Brasseur P, van Sambeek MR. Systematic review of utilities in abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. Sep 2008;36(3):283-9. [Medline].
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Further Reading
Screening for abdominal aortic aneurysms: recommendation statement .
United States Preventive Services Task Force. 1996 (revised 2005). 16 pages. NGC:003960
Aortic aneurysm and dissection .
Finnish Medical Society Duodecim. 2004 Feb 26. Various pagings. [NGC Update Pending] NGC:004359
Acute chest pain - suspected aortic dissection .
American College of Radiology. 1995 (revised 2005). 5 pages. NGC:004621
Keywords
abdominal aortic aneurysm, inflammatory aortic aneurysm, aortic aneurysm, AAAs, triple-A, triple A, abdominal aneurysm, noninflammatory aneurysms, inflammatory aneurysms, abdominal aortic dissection, aneurysm, dissection






Overview: Abdominal Aortic Aneurysm, Diagnosis