The incidence of abdominal aortic aneurysm (AAA) tripled in the United States between 1970 and 2000, accounting for more than 15,000 deaths per year in 2000. A ruptured AAA is the tenth leading cause of death among those over fifty-five. The incidence of AAA in men over the age of eighty is 6.0 percent, and in women over the age of ninety it is 4.5 percent.
An aneurysm is a dilatation of the arterial vessel to between one-and-a-half and two times its normal diameter. These abnormal vessels can be subsequently divided into two broad categories: true and false aneurysms. A true aneurysm is one that involves a weakness of all three layers of the vessel wall (the intima, media, and adventitia). These are likely to be congenital malformations (e.g., Marfan’s syndrome or some other connective tissue abnormality) or, more commonly, an acquired weakness (e.g., atherosclerosis) of the blood vessel. Conversely, a false aneurysm is one that involves only part of the arterial wall. Examples of these are usually seen following a traumatic injury to the vessel, at sites of previous vascular surgery, anastomosis (surgical opening between blood vessels), and arterial puncture sites for diagnostic catheterization.
Aneurysms, like atherosclerosis, can occur anywhere in the arterial tree, but they most commonly involve the aorta. The aorta is the large artery that conducts the oxygenated blood from the heart to the rest of the body. The normal diameter of the abdominal aorta is between 1.8 and 2.5 centimeters (cm). When the aorta becomes larger, 3.5 or 4 cm, it is deemed aneurysmal.
The principle factor for acquired aneurysm formation appears to be atherosclerosis. It is not clear what causes the arterial wall to become weakened in some people, while others develop occlusive disease. There has been some suggestion that people who develop aneurysms may have a less elastic media (the middle layer of the artery), and subsequently weaker blood vessel walls. The risk factors for aneurysm development are the same as for large-vessel atherosclerosis (see above). Additionally, sites of aneurysm formation mirror sites of aortic occlusive disease—below the level of the kidneys and major branch sites.
Complication of aneurysms include the following:
- • Pain. Most AAAs are asymptomatic. A patient with an inflammatory aneurysm may have complaints of chronic back or flank pain, while a ruptured AAA usually presents as a sudden onset of severe, deep, abdominal, flank, or back pain.
- • Thrombosis/embolization. The dilated portion of the vessel displays turbulent blood flow patterns that predispose these areas to blood-clot formation. Portions of the blood clot may break off and migrate (embolize) and occlude an artery downstream, or the blood clot may block off the entire lumen of the aorta, producing an acute arterial occlusion.
- • Compression. As the aneurysm enlarges, it may encroach on other structures, such as the esophagus or ureters from the kidneys.
- • Fistual Formation. An aneurysm can also erode into other structures and form an abnormal connection. An example is an aortoenteric fistula, in which the aorta erodes into the duodenum or some other portion of the small bowel. These patients present with catastrophic upper gastro-intestinal tract bleeding.
- • Rupture. The most worrisome and devastating complication (see below).
Eighty percent of all aneurysms grow in diameter as time progresses. On average, an AAA grows about 0.2 cm in diameter per year. As the aneurysm gets larger, more tension is placed on the vessel wall and there is a greater risk of rupture. Other risk factors for rupture are: greater than 0.5 cm increase in diameter per year; an inflammatory AAA (a special type of aneurysm that involves an aggressive inflammatory process of the retro-peritoneum), elevated diastolic blood pressure, chronic obstructive pulmonary disease, and larger initial size. Aneurysms smaller than 4 cm rarely rupture. Risk of rupture for aneurysms measuring 5 to 6 cm in diameter is 10 to 12 percent per year, giving cumulative risk of 60 percent over five years. An 8 cm aneurysm has a risk of rupture of nearly 80 percent over two years.
Fifty to ninety percent of patients with a ruptured AAA do not survive the trip to the hospital. Of those that do make it to the hospital in time for an urgent procedure, only 50 percent survive to be discharged. The most common complications following repair of a ruptured AAA are cardiac complications, respiratory failure, and renal failure.
Diagnosis. A physical examination is relatively unreliable, unless the patient is thin and the aneurysm is quite large. Most commonly, the AAA is found incidentally on an abdominal ultrasound done for other reasons. Abdominal ultrasound is accurate in diagnosing and determining the size of AAA, is relatively quick and painless, and does not expose the patient to X-ray radiation. Additionally, it can be used for serial examination to monitor changes in size. Computerized tomography (CT scan) with intra-arterial contrast is still the ‘‘gold-standard,’’ however with diagnosis sensitivity of nearly 100 percent. A CT scan has an advantage over ultrasound in assessing an AAA rupture or leak. The disadvantages of a CT scan are that it is relatively time-consuming and requires exposure to contrast material and X-ray radiation.
Treatment. The goal of treatment is to prevent rupture and other complications, and to restore arterial continuity. Medical therapy has been largely unsuccessful in preventing progressive AAA dilatation. As such, surgery has been the mainstay of therapy. As with large-vessel atheromatous disease, the decision to treat an aneurysm must weigh the risks of surgery against the risk of complication of the disease process itself. The mortality and morbidity of an open, elective AAA repair is 4 to 10 percent, depending on size, characteristics, and comorbidities of the individual patient. Complications of surgery include myocardial infarction (in a nonrevascularized patient), renal failure, and colonic ischemia. These complications are greater in high-risk patients and elderly patients, again secondary to comorbidities.
For an abdominal aortic aneurysm less than 4 cm the risk of rupture is nearly zero. In general, the accepted sized of an AAA that necessitates surgery is 5 cm or greater. Various surgical and epidemiological studies have determined thus that the risk/benefit ratio favors operative treatment at this size. The traditional open repair of an AAA involves a large incision in the abdomen to gain direct access to the aorta. The aneurysmal segment is then replaced by a synthetic graft (usually Gortex or Dacron) to re-establish continuity to the ‘‘normal’’ artery above and below the weakened segment (in actuality, the artery above and below is rarely entirely normal; however, the goal is to achieve continuity to a normal caliber segment). More recently, a less invasive technique of endovascular stenting is being used.
An endovascular stenting procedure is usually done in concert with both a radiologist and a vascular surgeon. Instead of the large abdominal incision, a smaller incision is made in the groin to get access to the femoral artery (the main blood vessel in the leg). A catheter is then fed in a retrograde fashion into the abdominal aorta to deploy a synthetic graft/stent in the aneurysmal area. This procedure, in essence, achieves the same goal as the open procedure by excluding the weakened dilated arterial wall and establishing arterial continuity with two relatively normal segments. Most studies on patients who have undergone this procedure report a mortality rate of less than 1.2 percent for elective procedures.
Medical treatment for a rupture has a success rate of zero percent. The only hope of survival is operative treatment. However, as stated above, the thirty-day perioperative mortality rate is extraordinarily high (nearly 50 percent).
AAA repair in elderly patients. Like large vessel atheromatous disease of the aorta, older adults with an AAA have traditionally been deemed to be high-risk patients. As such, they have often gone untreated, and thus have a great risk of rupture. As previously discussed, the survival rate in this setting is dismal. It has now been shown that elective, direct AAA resection/repair carries equivalent mortality in octogenarians as in younger counterparts. With regards to the endovascular technique in suitable patients age seventy and older, the operative mortality rate is 1 percent. This outcome is far preferred to those found in the setting of a rupture repair.
Surgical decision-making for the octogenarian with a ruptured AAA is perhaps less clear. Johnston et al. have examined the preoperative, intraoperative, and postoperative risk factors associated with poor outcomes following ruptured AAA repair. In their analysis of 147 patients, they were unable to find a combination of preoperative risk factors or comorbidities that provided little or no chance of survival. Specifically, a ruptured AAA in a patient age seventy-five or older carries a survival rate of approximately 10 percent at six years post-repair. While this rate of death is still extraordinarily high (as compared to the elective group) it is still greater than zero. As such, the decision to treat the elderly with a ruptured AAA should be made on an individual basis, with the appropriate discussion held with the patient and his or her family.