Abdominal Aortic Aneurysm

November 13, 2008 at 8:31 am

Abdominal aortic aneurysms (AAAs) represent a degenerative process of the abdominal aorta that is often attributed to atherosclerosis; however, the exact cause is not known. A familiar clustering of AAAs has been noted in 15-25% of patients undergoing repair of the problem. Degenerative aneurysms account for more than 90% of all infrarenal AAAs. 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.

History of the Procedure

Vesalius described the first AAA in the 16th century. Before the development of a surgical intervention for the process, attempts at medical management failed. The initial attempts at control used ligation of the aorta, with the expected consequences. In 1923, Matas performed the first successful aortic ligation on a patient. Attempts were made to induce thrombosis by inserting intraluminal wires. In 1948, Rea wrapped reactive cellophane around the aneurysm in order to induce fibrosis and limit expansion. This technique was used on Albert Einstein in 1949, and he survived 6 years before succumbing to rupture. In 1951, Charles Dubost performed the first AAA repair using a homograft.

Prior to this, aortic aneurysms were treated using a variety of methods, including ligation, intraluminal wiring, and cellophane wrapping. Unfortunately, early homografts became aneurysmal because of preservation techniques. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (ie, nylon). Later, these grafts were replaced by Dacron and Gore-Tex (ie, polytetrafluoroethylene [PTFE]) fabrics. The final advance was abandonment of silk sutures, which degenerated, in favor of braided Dacron, polyethylene, and PTFE (ie, Gore-Tex) sutures, all of which retain tensile strength.

Postoperative surgical mortality rates initially remained high (>25%) because the aneurysm sac generally was excised. Nearly simultaneously in 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy . This advancement dramatically reduced mortality. Today, operative mortality rates range from 1.8-5%.In the late 1980s, Parodi et al described endovascular repair using a large Palmaz stent and unilateral aortofemoral and femorofemoral crossover Dacron grafts.1 Currently, many devices are used for the endovascular treatment of AAA

Problem

Aneurysms are defined as a focal dilatation with at least a 50% increase over normal arterial diameter. Thus, an enlargement of at least 3 cm of the abdominal aorta fits the definition. In large ultrasound screening studies, increasing age; male sex; African American race; and increased height, weight, body mass index, and body surface area all were associated with increased infrarenal aortic diameter.

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.

Frequency

AAAs are uncommon in African Americans, Asians, and persons of Hispanic heritage.

United States

In autopsy studies, the frequency rate of AAA ranges from 0.5-3.2%. In a large US Veterans Administration screening study, the prevalence rate was 1.4%.2 The frequency of rupture is 4.4 cases per 100,000 persons.

AAA is 5 times more common in men than in women and is 3.5 times more common in white males than in African American males. The likelihood of development varies from 3-117 cases per 100,000 person-years. In men, the process appears to begin at approximately age 50 years and reaches peak incidence at approximately age 80 years. In women, the onset is delayed and appears to begin at approximately age 60 years. The reported incidence of rupture varies from 1-21 cases per 100,000 person-years.

International

The frequency rate of asymptomatic AAA is 8.2% in the United Kingdom, 8.8% in Italy, 4.2% in Denmark, and 8.5% in Sweden (in males only). The frequency rate of AAA in females is much lower, 0.6-1.4%. The frequency of rupture is 6.9 cases per 100,000 persons in Sweden, 4.8 cases per 100,000 persons in Finland, and 13 cases per 100,000 persons in the United Kingdom.

Risk factors

The peak incidence of AAA occurs in people aged 70 years. The male-to-female incidence ratio in people younger than 80 years is 2:1. When older than 80 years, the ratio changes to 1:1.

A family history of AAA is a risk factor for AAA. Approximately 25% of cases are in persons with first-degree relatives with AAA. Other risk factors include previous aneurysm repair or peripheral aneurysm (popliteal or femoral), smoking, coronary artery disease, and hypertension (1-15%).

Etiology

AAA is thought to be a degenerative process of the aorta, the cause of which remains unclear. It is often attributed to atherosclerosis because these changes are observed in the aneurysm at the time of surgery. Atherosclerosis fails to explain the development of occlusion, which is observed in the disease process.

AAA appears to have a familial prevalence rate of 15-25%. Studies by Majumder and associates suggest the genetic predisposition is isolated to a single dominant gene with low penetrance that increases with age. Tilson et al described the potential for an autoimmune basis for the development of AAA involving the DRB1 major histocompatibility locus. This locus has been identified as a basis for inflammatory AAA.The other causes of AAA include infection, cystic medial necrosis, arteritis, trauma, inherited connective-tissue (structural collagen) disorders, and anastomotic disruption producing pseudoaneurysms.

Pathophysiology

A multidisciplinary research program supported by the US National Heart, Lung, and Blood Institute identified proteolytic degradation of aortic wall connective tissue, inflammation and immune responses, biomechanical wall stress, and molecular genetics as mechanisms important in the development of AAA.5

The aortic wall contains smooth muscle, elastin, and collagen arranged in concentric layers in order to withstand arterial pressure. The number of medial elastin layers from the proximal thoracic aorta to the infrarenal aorta is markedly reduced, with medial thinning and intimal thickening. A reduction in collagen and elastin content is noted from the proximal to the distal aorta. Elastin is the principal load-bearing element in the aorta. Elastin fragmentation and degeneration are observed in aneurysm walls. The decrease in content coupled with the histological changes of this matrix protein in aneurysms may explain the propensity for aneurysm formation in the infrarenal aorta.Immunoreactive proteins are found more conspicuously in the abdominal aorta, and this may contribute to the increased frequency of aneurysms in this location.

The aortic media appear to degrade in AAA by means of a proteolytic process. This implies an increase in the concentration of proteolytic enzymes relative to their inhibitors in the abdominal aorta as the individual ages. Reports have documented increased expression and activity of matrix metalloproteinases (MMPs) in persons with AAAs. MMPs and other proteases have been shown to be secreted into the extracellular matrix of AAAs by macrophages and aortic smooth muscle cells. MMPs and their inhibitors are present in normal aortic tissue and are responsible for vessel wall remodeling. In aneurysmal tissue, a tendency exists for increased MMP activity favoring the degradation of elastin and collagen. The mechanism that tips the balance in favor of degradation of elastin and collagen in the aortic wall of AAAs by MMPs and other proteases is presently unknown.

AAAs demonstrate a chronic adventitial and medial inflammatory infiltrate upon histological examination. Infiltration of AAAs with lymphocytes and macrophages may trigger protease activation via various cytokines (interleukin [IL]–1, IL-6, IL-8, and tumor necrosis factor-alpha). Further study has defined a matrix protein that is immunoreactive with immunoglobulin G in the aneurysm wall. This autoantigen appears to be a collagen-associated microfibril. Certain infectious agents have been associated with the development of this protein, including Chlamydia pneumoniae and Treponema pallidum; however, a direct cause-and-effect relationship has not been demonstrated.

AAAs arise as a result of a failure of the major structural proteins of the aorta (elastin and collagen). The inciting factors are not known, but a genetic predisposition clearly exists. Surgical specimens of AAA reveal inflammation, with infiltration by lymphocytes and macrophages; thinning of the media; and marked loss of elastin . Recent research has focused on the role of the metalloproteinases, a group of zinc-dependent enzymes responsible for tissue remodeling.

In general, AAAs gradually enlarge (0.2-0.8 mm/y) and eventually rupture. Hemodynamics play an important role. Areas of high stress have been found in AAAs and appear to correlate with the site of rupture. Computer-generated geometric factors have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications in determining which AAAs require surgical repair.

Additionally, molecular genetics has provided some insight into the development of AAAs. Through gene microarray analysis, various genes involved in extracellular matrix degradation, inflammation, and other processes observed in AAA formation have been shown to be up-regulated, while others that may serve to prevent this occurrence are down-regulated. The combination of proteolytic degradation of aortic wall connective tissue, inflammation and immune responses, biomechanical wall stress, and molecular genetics represents a dynamic process that leads to aneurysmal deterioration of aortic tissue.

Clinical

  • 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%).
  • Rupture: 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.
  • Peripheral emboli: Atheroemboli from small AAAs produce livedo reticularis of the feet or blue toe syndrome
  • Acute aortic occlusion: Occasionally, small AAAs thrombose, producing acute claudication.
  • Aortocaval fistulae: AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia.
  • Aortoduodenal fistulae: Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.

Physical examination

Bilateral upper extremity blood pressures are discernible in patients with AAAs. Hypertension may trigger a workup for renal artery stenosis. Unequal blood pressures (>30 mm Hg) indicate subclavian artery stenosis, and perioperative monitoring is important.

Cervical bruits may indicate carotid artery stenosis. Abdominal examination includes palpation of the aorta and an estimation of the size of the aneurysm. Bruits may indicate the presence of renal or visceral artery stenosis; a thrill is possible with aortocaval fistulae.

Regarding the peripheral pulses, palpate femoral popliteal and pedal pulses (dorsalis pedis or posterior tibial) to determine if an associated aneurysm (femoral/popliteal) or occlusive disease exists. Flank ecchymosis (Grey Turner sign) represents retroperitoneal hemorrhage.

With respect to rectal aspects of the physical examination, guaiac-positive stool is present with associated colon cancer.

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.

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.

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Entry filed under: Aortic aneurysm. Tags: .

Thoracic Aortic Aneurysm Vascular wall flow-induced forces in a progressively enlarged aneurysm model.


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