Abdominal Aortic Aneurysm (AAA)

Teaching topics from the New England Journal of Medicine - Vol. 358, No. 5, January 31, 2008

Abdominal Aortic Aneurysm
Abdominal aortic aneurysm is frequently asymptomatic and often detected incidentally on abdominal imaging (computed tomography, ultrasonography, or magnetic resonance imaging). Although some aneurysms may become symptomatic (manifesting with abdominal or back pain), the first clinical manifestation in many cases is rupture. The risk of rupture is low for aneurysms 5.5 cm or less in diameter, but above this threshold the risk increases markedly. In patients without symptoms, interventional management is generally recommended when the aneurysm exceeds 5.5 cm in diameter, becomes tender, or grows more than 1 centimeter in diameter per year.

Surgical versus Endovascular Repair
Open surgical repair has been the established treatment option for abdominal aortic aneurysm. This form of therapy is associated with a greater use of intensive or critical care, a longer hospital stay, and more postoperative pain than endovascular repair. Open repair requires general anesthesia. Endovascular repair, which may involve either general or local anesthesia, is associated with a lower early mortality but with a higher risk of subsequent need for reintervention and a less certain long-term outcome as compared to open repair. Endovascular repair is feasible only in patients who satisfy certain specific anatomical requirements regarding the aorta, the aneurysm, and the iliac arteries — which are usually assessed by means of CT.


Morning Report Questions

Q: What is a major risk factor for abdominal aortic aneurysm?
A: A major risk factor for the development of abdominal aortic aneurysm is smoking, and more than 90% of patients with such aneurysms have a history of smoking.

Q: What are two genetic disorders that increase the risk for developing abdominal aortic aneurysms?
A: Two rare monogenic disorders associated with an increased risk of abdominal aortic aneurysm are Marfan's syndrome (caused by a fibrillin-1 defect) and Ehlers–Danlos syndrome type IV (caused by a defect in the gene for type III collagen [COL3A1] in the majority of cases).
See OMIM: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=130050