Differential: (causes of AAA)
1. Degenerative (these constitute the vast majority; 90% are seen in association with atherosclerosis)
3. Chronic dissection
6. Connective tissue disease
Abdominal aortic aneurysms may be defined by a measurement of greater than 3 cm diameter below the renal arteries. The vast majority are degenerative. Although atherosclerosis is commonly seen in association with degenerative AAA, deficiencies in elastin and collagen are thought to cause the disorder. There is a 4:1 male prevalence. Most patients are Caucasian and over 60 years old. Smoking, HTN and family history are risk factors for the disease.
The rate of expansion of aortic aneurysms is unpredictable. Wall tension increases with increasing diameter and increasing pressure as given by the law of LaPlace, T = PxR. The risk of rupture is significant for aneurysms over 5cm in diameter. Rupture usually results in massive retroperitoneal hemorrhage and carries a high mortality. Other potential complications include thrombosis, distal embolization, and the formation of aortocaval or aortoenteric fistulae.
Ultrasound is an excellent imaging modality for the detection, measurement and surveillance of abdominal aortic aneurysms. However, if surgery is contemplated, CT, MRA, and/or catheter angiography are required. Preoperative imaging should establish:
1. The proximal and distal extent of the AAA, including involvement of the renal or iliac arteries.
2. The number and location of renal arteries; the presence of renal artery stenosis
3. The presence of obstructive disease in the iliac or femoral arteries.
4. Patency of the mesenteric arteries
5. Renal anomalies, e.g., horseshoe kidney
6. The presence of an inflammatory or ruptured aneurysm
7. Renal vein or IVC anomalies
Endovascular repair of an abdominal aortic aneurysm carries less morbidity and allows a more rapid recovery than the traditional open repair. The procedure involves bilateral femoral artery cut downs and arteriotomies. The endograft itself consists of expandable metallic cages covered by fabric graft material. The endograft is positioned and expanded under fluoroscopic guidance. Hooks at the ends of the graft anchor it to the aneurysm neck and, in the case of a bifurcated graft, to the iliac arteries. As a result, the lumen of the aneurysm is excluded from flow and thromboses.
Complications include improper positioning of the graft (e.g., covering the ostia of the renal arteries), migration, thrombosis, infection, and leakage. The term "endoleak" refers to persistent blood flow within the lumen of the aneurysm, outside the graft. Graft-related, or type I, endoleaks may be the result of an incomplete seal between the graft and the vessel wall, or by tears or oozing through the fabric of the graft. Non graft-related, or type II endoleaks are the result of back filling of the aneurysm lumen though collateral vessels - commonly lumbar, inferior mesenteric, and median sacral arteries.
Most endoleaks are self-limited. Persistent graft related leakage may be treated by placement of a stent. Non graft-related leakage sometimes requires embolization of the feeding vessel.