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Abdominal Aortic Aneurysms (AAA)
Abdominal aortic diameter ≥ 3 cm constitutes an abdominal aortic aneurysm; the most common cause is atherosclerosis. Most aneurysms grow slowly without causing symptoms, but some patients develop steady, deep pain in the lumbosacral region. Risk of rupture is proportional to the size of the aneurysm. Diagnosis is made by ultrasonography or CT. Treatment is surgery or endovascular stent grafting.
Abdominal aortic aneurysms (AAAs) account for three fourths of aortic aneurysms and affect 0.5 to 3.2% of the population. Prevalence is 3 times greater in men. AAAs typically begin below the renal arteries but may include renal arterial ostia; about 50% involve the iliac arteries. Generally, aortic diameter ≥ 3 cm constitutes an AAA. Most AAAs are fusiform; some are saccular. Many are lined with laminated thrombi. AAAs involve all layers of the aorta and do not involve dissection; however, a thoracic aortic dissection may extend to the distal abdominal aorta.
The most common cause is weakening of the arterial wall, usually caused by atherosclerosis.
Other causes include trauma, vasculitis, cystic medial necrosis, and postsurgical anastomotic disruption. Uncommonly, syphilis and localized bacterial or fungal infection, typically due to sepsis or infective endocarditis, weaken the arterial wall and cause infected (mycotic) aneurysms.
Smoking is the strongest risk factor. Other risk factors include hypertension, older age (peak incidence at age 70 to 80), family history (in 15 to 25%), race (more common in whites than in blacks), and male sex.
Most AAAs are asymptomatic; symptoms and signs, when they do occur, may not be specific. As AAAs expand, they may cause pain, which is steady, deep, boring, visceral, and felt most prominently in the lumbosacral region. Patients may be aware of an abnormally prominent abdominal pulsation. Rapidly enlarging aneurysms that are about to rupture are frequently tender, but most aneurysms grow slowly without symptoms.
The aneurysm may or may not be palpable as a pulsatile mass, depending on its size and patient habitus. The probability that a patient with a pulsatile palpable mass has an aneurysm > 3 cm is about 40% (positive predictive value). A systolic bruit may be audible over the aneurysm.
If an AAA ruptures, patients who do not die immediately typically present with abdominal or back pain, hypotension, and tachycardia. They may have a history of recent upper abdominal trauma, often minimal, or isometric straining (eg, lifting a heavy object).
Patients with an occult AAA sometimes present with symptoms of complications (eg, extremity pain due to embolization of mural thrombi) or of the cause (eg, fever, malaise, or weight loss due to infection or vasculitis). Uncommonly, large AAAs cause disseminated intravascular coagulation, perhaps because large areas of abnormal endothelial surface trigger rapid thrombosis and consumption of coagulation factors.
Most AAAs are diagnosed incidentally when they are detected during physical examination or when abdominal ultrasonography, CT, or MRI is done for other reasons. An AAA should be considered in elderly patients who present with acute abdominal or back pain whether a palpable pulsatile mass is present or not.
When symptoms or physical examination findings suggest AAA, abdominal ultrasonography or CT is usually the test of choice. Symptomatic patients should have immediate testing to make the diagnosis before catastrophic rupture. For hemodynamically unstable patients with presumed rupture, ultrasonography provides bedside results more rapidly, but intestinal gas and distention may limit its accuracy. Laboratory tests, including CBC, electrolytes, BUN, creatinine, PT, PTT, and blood type and cross-match, are done in preparation for possible surgery.
If rupture is not suspected, CT angiography (CTA) or magnetic resonance angiography (MRA) can more precisely characterize aneurysm size and anatomy. If thrombi line the aneurysm wall, CTA may underestimate true size; noncontrast CT may provide a more accurate estimate. Aortography is essential if renal artery or aortoiliac disease is suspected or if correction with endovascular stent grafts (endografts) is being considered.
Plain abdominal x-rays are neither sensitive nor specific; however, if obtained for other purposes, aortic calcification may outline the aneurysm wall. If a mycotic aneurysm is suspected, bacterial and fungal blood cultures should be done.
Some AAAs enlarge at a steady rate (2 to 3 mm/yr), some enlarge exponentially, and, for unknown reasons, about 20% remain the same size indefinitely. The need for treatment is related to size, which is linked to risk of rupture (see Table: Abdominal Aortic Aneurysm Size and Rupture Risk*).
Ruptured AAAs require immediate open surgery or endovascular stent grafting. Without treatment, mortality rate approaches 100%. With open surgical treatment, mortality rate is about 50%; mortality with endovascular stent grafting is generally lower (20 to 30%). The mortality remains high because many patients have coexisting coronary, cerebrovascular, and peripheral atherosclerosis. Patients who present in hemorrhagic shock require fluid resuscitation (see page Intravenous Fluid Resuscitation : Fluids) and blood transfusions, but mean arterial pressure should not be elevated to > 70 to 80 mm Hg because bleeding may increase. Preoperative control of hypertension is important.
Elective surgical repair is recommended for aneurysms > 5 to 5.5 cm (when risk of rupture increases to > 5 to 10%/yr), unless coexisting medical conditions contraindicate surgery. Additional indications for elective surgery include increase in aneurysm size by > 0.5 cm within 6 mo regardless of size, chronic abdominal pain, thromboembolic complications, and an iliac or femoral artery aneurysm that causes lower-limb ischemia. Before elective repair, clinical recognition of coronary artery disease (CAD) is essential (see Table: Tests for Assessing Cardiac Anatomy and Function) because many patients with an AAA have generalized atherosclerosis and surgical repair poses a major risk of cardiovascular events. Aggressive medical treatment and risk factor control are essential, and revascularization should be considered only in patients with unstable CAD. Routine preoperative coronary angioplasty or bypass surgery has not been shown to be necessary in most patients who can be prepared with good medical management before aneurysm repair.
Surgical repair consists of replacing the aneurysmal portion of the abdominal aorta with a synthetic graft. If the iliac arteries are involved, the graft must be extended to include them. If the aneurysm extends above the renal arteries, the renal arteries must be reimplanted into the graft, or bypass grafts must be created.
Placement of an endovascular stent graft within the aneurysmal lumen via the femoral artery is a less invasive alternative and is indicated when risk of perioperative complications is high. This procedure excludes the aneurysm from systemic blood flow and reduces risk of rupture. The aneurysm eventually thromboses, and 50% of aneurysms decrease in diameter. Short-term results are good, but long-term results are unknown. Complications include angulation, kinking, thrombosis, migration of the stent-graft, and endoleak (persistent flow of blood into the aneurysm sac after endovascular stent graft placement). Thus, follow-ups must be more frequent after endovascular stent graft placement than after a traditional repair. If no complications occur, imaging tests are recommended at 1 mo, 6 mo, 12 mo, and every year thereafter. Complex anatomy (eg, short aneurysm neck below renal arteries, severe arterial tortuosity) makes endovascular stent grafting difficult in 30 to 40% of patients.
Repair of aneurysms < 5 cm does not appear to increase survival. These aneurysms should be monitored with ultrasonography every 6 to 12 mo for expansion that warrants treatment. Control of atherosclerotic risk factors, especially smoking cessation and use of antihypertensives as appropriate, is important. If a small or moderate-sized aneurysm becomes > 5.5 cm and if risk of perioperative complications is lower than estimated risk of rupture, AAA repair is indicated; risk of rupture vs that of perioperative complications should be discussed frankly with the patient.
Treatment of a mycotic aneurysm consists of vigorous antimicrobial therapy directed at the pathogen, followed by excision of the aneurysm. Early diagnosis and treatment improve outcome.
Abdominal aortic diameter ≥ 3 cm constitutes an AAA.
AAAs typically enlarge at a steady rate, but some enlarge exponentially; about 20% remain the same size indefinitely.
Risk of rupture is proportional to the size of the aneurysm.
Diagnose using ultrasonography or CT; for unruptured aneurysms, CT angiography or magnetic resonance angiography can more precisely characterize aneurysm size and anatomy.
Ruptured AAAs require immediate open surgery or endovascular stent grafting.
Elective surgical repair is recommended for aneurysms > 5 to 5.5 cm, and those that are rapidly enlarging or causing ischemic or embolic complications.
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