Arterial Aneurysms

Ameurysms of the Abdominal Aorta


Essentials of Diagnosis

  • Most aortic aneurysms are asymptomatic, detected during a routine physical examination or a diagnostic study.
  • Severe back or abdominal pain, a pulsatile mass, and hypotension indicate rupture.
  • Concomitant atherosclerotic occlusive disease of lower extremities is present in 25%.

General Considerations

Over 90% of abdominal aneurysms originate below the renal arteries, and many extend into the common iliac arteries. The infrarenal aorta is normally 2 cm in diameter; an aneurysm is defined as an aortic diameter exceeding 3 cm. An aortic aneurysm is present in 5-8% of men over the age of 65 years. The reported incidence has tripled over the past 30 years. Routine ultrasound screening of high-risk groups is associated with a reduction in aneurysm-related deaths of 53%. Half of all newly detected aneurysms are under 5 cm in diameter, and nearly two-thirds of these will increase sufficiently in size to require repair. ß-Blockers and, more recently, oral roxithromycin (300 mg daily for 30 days) have been shown to decrease the expansion rate of small aneurysms. Patients with chronic obstructive pulmonary disease appear more likely to rupture smaller aneurysms.

Clinical Findings

A. Symptoms and Signs
1. Asymptomatic aneurysms
An aneurysm may be suspected on routine physical examination by detection of a prominent aortic pulsation. More often, asymptomatic aneurysms are discovered as incidental findings on abdominal ultrasound or CT scan. Peripheral pulses are often normal, but coexisting renal or lower extremity arterial occlusive disease is present in 25%. Popliteal artery aneurysms are present in 15% of patients with aneurysms of the abdominal aorta, and, conversely, more than one-third of patients with popliteal aneurysms have abdominal aortic aneurysms.

2. Symptomatic aneurysms
Midabdominal or lower back pain (or both) in the presence of a prominent aortic pulsation may indicate rapid aneurysmal growth, rupture, or an inflammatory aortic aneurysm. Inflammatory aneurysms account for fewer than 5% of aortic aneurysms and are characterized by extensive periaortic and retroperitoneal inflammation of unknown cause. These patients may have low-grade fever, elevated sedimentation rate, and a history of recent upper respiratory tract infection; they are often active smokers. Infected aortic aneurysms (either caused by septic emboli to a normal aorta or bacterial colonization of an existing aneurysm) are rare but should be suspected in patients with saccular aneurysms or aneurysms in conjunction with fever of unknown origin, particularly if blood cultures are positive for Salmonella. Peripheral emboli can also be a symptom of aneurysmal disease.

3. Ruptured aneurysms
Patients with ruptured aortic aneurysms present with severe back, abdominal, or flank pain and hypotension. Posterior rupture confined to the retroperitoneum carries a better prognosis than anterior rupture into the peritoneal cavity. As many as 90% of patients die either before they reach the hospital or in the immediate perioperative period. The only chance for survival is emergent surgical repair.

B. Laboratory Findings
Electrocardiogram, serum creatinine, hematocrit and hemoglobin, and type and crossmatch should be obtained routinely in all patients.

C. Imaging
Abdominal ultrasonography is the screening study of choice and is valuable also for following aneurysm growth in patients with small (> 5 cm) aneurysms. Aneurysms typically grow by about 10% of their diameter per year; annual ultrasound examinations are recommended for aneurysms greater than 3.5 cm. In about three-fourths of patients, size can be estimated by measurement of curvilinear calcifications in the aneurysm wall on an abdominal radiograph, but this is much less accurate than ultrasonography.

Contrast-enhanced CT scanning not only precisely sizes the aneurysm but also defines its relationship to the renal arteries. MRI is as sensitive and specific as CT and is useful if renal insufficiency precludes contrast-enhanced CT. Aortography is indicated prior to elective aneurysm repair when arterial occlusive disease of the visceral or lower extremity arteries is suspected or when endograft repair is being considered.

A. Standard Therapy

Unless contraindicated, all patients should receive perioperative ß-blockade to reduce cardiac complications. Surgical excision and synthetic graft replacement are the treatment of choice for most aneurysms of the infrarenal abdominal aorta greater than 5 cm. The maximum diameter of the aneurysm correlates best with the risk of rupture. Yearly rupture risk is 2% for 4- to 5.5-cm aneurysms, 7% for 6- to 6.9-cm aneurysms, and 25% for 7-cm aneurysms. Recommendation of an elective repair must be balanced with the risk of rupture. In asymptomatic good-risk patients, surgery is advised when the aneurysm exceeds 5 cm, whereas poor-risk patients may not be considered for repair until the aneurysm exceeds 6 cm. Urgent repair is indicated for symptomatic patients irrespective of aneurysm size.

Preoperative evaluation must include a detailed assessment of cardiac risk and examination of the carotid arteries since acute myocardial infarction, arrhythmia, and stroke remain among the most frequent perioperative complications. In patients with asymptomatic aneurysms and a history of angina or of carotid stenosis greater than 80%, coronary angioplasty, coronary bypass grafting, or carotid endarterectomy may be indicated before repair of the aneurysm.

B. Endovascular Repair
Endovascular stent grafts, or “covered stents,” have evolved over the past decade for treatment of aortic aneurysms. Aortic stent grafts are configured to be uniiliac or bifurcated depending on the particular anatomy of the aneurysm. Uniiliac grafts are combined with endovascular occlusion of the contralateral common iliac artery and femoral-femoral bypass grafting. Both types of grafts are deployed via the common femoral arteries; in most cases, this involves bilateral inguinal incisions. The operation can be performed under epidural anesthesia, often in less than 2 hours and with minimal blood loss, which has made repair of aortic aneurysms feasible in high-risk patients previously deemed inoperable. Additional advantages include reduced incisional pain, fewer cardiopulmonary complications, and avoidance of postoperative ileus; most patients are discharged from the hospital on the second postoperative day. Endografts have been used successfully for repair of ruptured aneurysms, using balloon catheter control of the supraceliac aorta to facilitate intraoperative angiography and stent deployment.

Not all patients are candidates for standard endovascular repair. The proximal neck of the aneurysm must be adequate (at least 1.5 cm in length and less than 3 cm in width) to allow fixation and sufficient tissue apposition below the renal arteries. Iliac artery aneurysms, iliac stenoses, and iliac tortuosity or calcification all increase the complexity of stent deployment. The newest technology includes use of smaller introducer sheaths intended for eventual percutaneous deployment. Long-term durability of endovascular grafts needs to be established before comparison can be made with open repair for use in the good-risk patient with asymptomatic aortic aneurysm. Objective comparison with open surgical repair has been complicated by the multiplicity of continually evolving stent graft designs.

Complications after aneurysm resection include myocardial infarction, bleeding, respiratory insufficiency, ischemic colitis, limb ischemia, renal insufficiency, and stroke. Bowel infarction, liver dysfunction, acalculous cholecystitis, and renal failure are more common with emergent aneurysm repair or when repair of the aneurysm requires supraceliac or suprarenal cross-clamping. However, renal insufficiency can occur even when the clamp is infrarenal and there is no reported intraoperative hypotension, presumably because of renal artery vasoconstriction, atheroemboli, preoperative contrast administration for CT scan, and dehydration from fasting or bowel preparation. For this reason, mannitol (25-g intravenous bolus) is given as a diuretic and free-radical scavenger prior to cross-clamping, and dopamine (3 ug/kg/min) or fenoldopam (0.05-0.1 ug/kg/min) is continued in the immediate postoperative period to increase renal perfusion and glomerular filtration rate. Rarely (0.1% of cases), lower extremity paralysis complicates repair of abdominal aortic aneurysm because of occlusion of the spinal artery from atheroemboli, shock, or aortic cross-clamping. Graft infection and graft-enteric fistulas are late complications, occurring more often after emergent aneurysm repair. One complication specific to endovascular repair is persistent filling of the aneurysm (endoleak). Endoleaks are classified as type 1 (leak around the top or bottom of the stent graft), type 2 (leak from a back-bleeding patent lumbar artery or inferior mesenteric artery), and type 3 (leak through the graft material). They are detected by contrast CT obtained routinely on postoperative days 2 and 30, and at 6-month or yearly intervals thereafter. Type 1 endoleaks are restented to allow adequate proximal or distal fixation. Type 2 endoleaks are not uncommon (20-30% of patients) in the immediate postoperative period but usually disappear by the 1-month CT scan. Persistent type 2 endoleaks occur in 5% of patients and are correlated with the use of warfarin and the presence of a patent inferior mesenteric artery preoperatively. They can be eliminated by endovascular coil embolization of the feeding arteries.

Renal failure from contrast nephropathy, intraoperative atheroemboli, or graft impingement on the main or accessory renal arteries is another possible complication of endovascular repair. Conversion to open repair because of aortic or iliac rupture, inability to gain access, error in positioning, inadequate fixation, or stent malfunction is rare (1-3%) if patients are properly screened preoperatively.

Mortality following elective open or endovascular repair is 1-5%. In general, a patient with an aortic aneurysm greater than 5 cm has a threefold greater chance of dying as a consequence of rupture of the aneurysm than of dying from surgical resection. Five-year survival after surgical repair is 60%-80%. Five to 10 percent of patients will develop another aortic aneurysm adjacent to the graft or in the thoracic aorta.

Brewster DC et al: Guidelines for the treatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery. J Vasc Surg 2003;37:1106.

Lederle FA et al: Rupture rate of large abdominal aortic aneurysms in patients refusing or unfit for elective repair. JAMA 2002;287:2968.

Lederle FA et al: Ultrasonographic screening for abdominal aortic aneurysms. Ann Intern Med 2003;139:516.

Parodi JC et al: Endovascular treatment of aneurysmal disease. Cardiol Clin 2002;20:579.

Vammen S et al: Randomized double-blind controlled trial of roxithromycin for prevention of abdominal aortic aneurysm expansion. Br J Surg 2001;88:1066.

Provided by ArmMed Media
Revision date: July 3, 2011
Last revised: by Dave R. Roger, M.D.