Abdominal aortic aneurysm (AAA) is a relatively common, potentially life-threatening condition. It has a wide spectrum of presentations and should be considered in the differential diagnosis for a number of symptoms. AAA is usually the result of degeneration in the media of the arterial wall, resulting in a slow and continuous dilatation of the lumen of the vessel. In fewer than 5% of cases, AAA is caused by mycotic aneurysm of hematogenous origin. In these cases, local invasion of the intima and media gives rise to abscess formation and aneurysmal dilation of the vessel. Other causes include infection, cystic medial necrosis, arteritis, trauma, inherited connective-tissue disorders, and anastomotic disruption. The disease generally affects elderly white men. Smoking appears to be the risk factor most strongly associated with AAA.
The 3 layers comprising the normal aorta are the intima, media, and adventitia. Structural and elastic properties of major arteries are mostly imparted by the media, which is composed of smooth muscle cells surrounded by elastin, collagen, and proteoglycans. AAA develops following degeneration of the media due to atherosclerotic changes. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity.
Most AAAs occur in association with advanced atherosclerosis. Atherosclerosis may induce AAA formation by causing mechanical weakening of the aortic wall with loss of elastic recoil, along with degenerative ischemic changes, through obstruction of the vasa vasorum. Many patients with advanced atherosclerosis do not develop AAA, while some patients having no evidence of atherosclerosis do. The observed association between atherosclerosis and AAA is probably not causative; however, atherosclerosis may represent a nonspecific secondary response to vessel wall injury that is induced by multiple factors.
Most cases of AAA begin below the renal arteries and end above the iliac arteries. They generally are spindle shaped; however, size, shape, and extent vary considerably. Of AAA cases, 10-20% have focal outpouchings or blebs that are thought to contribute to the potential for rupture. The wall of the aneurysm becomes laminated with thrombus as the blebs enlarge. This can give the appearance of a relatively normal intraluminal diameter in spite of a large extraluminal size.
Ruptured AAA is the 13th-leading cause of death in the US, causing an estimated 15,000 deaths per year. The incidence of AAA is 2-4% in the adult population, and 11% of cases in that subset occur in males older than 65 years. Despite increased survival following diagnosis, incidence and crude mortality seem to be increasing.
In 1998, 50,000 surgical reconstructions for AAA were performed in the US, with substantial mortality differences between elective versus emergency operations. As elective aneurysm repair has a mortality rate drastically lower than that associated with rupture, the emphasis must be on early detection and repair free from complications.
Asymptomatic: Most patients present without an asymptomatic pulsatile abdominal mass. The aortic bifurcation is located just above the umbilicus. Occasionally, an overlying mass (pancreas or stomach) may be mistaken for an AAA. An abdominal bruit is nonspecific for a nonruptured aneurysm. Patients with popliteal artery aneurysms frequently have AAAs (25-50%).
Persons with AAAs that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, or flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.
Most persons with AAAs are asymptomatic. Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass. At times, AAAs may cause symptoms from local compression, including early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression. Back pain can be caused by erosion of the AAA into adjacent vertebrae. Other symptoms include abdominal pain, groin pain, embolic phenomenon to the toes, and fever. Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture. Uneven blood pressures or pulses when both extremities are checked is also a classic finding.
Most clinically significant aneurysms are palpable upon routine physical examination; however, the sensitivity of the technique is based on the experience of the examiner, the size of the aneurysm, and the size of the patient. In a recent study, 38% of AAA cases were detected based on physical examination findings, while 62% were detected incidentally based on radiologic studies obtained for other reasons.
Even patients who do not have symptoms from their AAAs require surgical intervention because the result of medical management in this population is a mortality rate of 100% over time due to rupture. In addition, these patients have a high likelihood of limb loss from peripheral embolization.
Monitor patients with AAAs smaller than 4 cm in diameter with ultrasound every 6 months, and offer surgical intervention if the aneurysm expands or causes symptoms. In patients with AAAs of 4-5 cm in diameter, elective repair may be of benefit if they are young, have a low operative risk, and have a good life expectancy. Additionally, AAAs in women have been shown to rupture at smaller diameters in comparison with men; therefore, a threshold of 4.5 cm for elective repair has been advocated in this patient population. Patients with AAAs of 5-6 cm in diameter may benefit from repair, especially if they have other contributing factors for rupture, including hypertension, continued smoking, or chronic obstructive pulmonary disease (COPD). For patients at higher risk, the threshold for repair may be a diameter of 6-7 cm, depending on their condition. At this size, the risk of rupture increases with age. These sizes apply to males of average height (170 cm).
In patients with small AAAs, one should attempt to reduce the expansion rate and rupture risk. Smoking cessation is of paramount importance. Aggressively control hypertension. Institute beta-blocker therapy to reduce blood pressure and stress on the artery wall. These can be administered safely unless the patient has contraindications to their use, such as COPD, allergy to the drug, bradycardia, or severe CHF.
Abdominal aortic aneurysms are typically repaired by an operative intervention. The procedure can be approached through the traditional open laparotomy approach or, now, by newer minimally invasive methodologies or by the placement of endovascular stents. Endovascular stent grafts for the treatment of AAA are a less invasive form of treatment. Patients are discharged 1-2 days following surgery. The graft is placed through 2 small incisions. In September 2000, 2 grafts were approved by the US Food and Drug Administration (FDA). Since then, several more devices have received FDA approval. Recently, the FDA has recommended careful follow- up because of persistent endoleaks and late ruptures.
Patients who complain of back, flank, groin, or abdominal pain but have stable vital signs and do not appear ill present diagnostic challenges. They may be sent home or kept for extended periods in the ED while waiting for diagnostic testing for suspected ureterolithiasis or other benign abdominal conditions. If AAA ruptures and shock ensues, morbidity and mortality increase dramatically. Physicians have been held liable for failure to diagnose AAA and obtain appropriate consultation in these situations. A high index of suspicion is necessary to avoid this medical-legal pitfall.
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