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Abdominal Aortic Aneurysm (AAA) - the silent killer

AAAs are the 9th and 14th leading causes of death in men over 65 years in Canada and the United States respectively leading to an increasing public health burden in developed countries. Persons with AAAs rarely presents with symptoms until rupture and when they do the mortality rate is 60-80%.

Death resulting from a ruptured AAA accounts for approximately 1% of all deaths in the Western world.

An aneurysm is defined as a focal dilatation of a blood vessel 1.5 to 2 times the diameter of the native vessel.

There are different forms of aneurysms including:
·        Saccular–a localised dilatation of the wall of the vessel forming a sac.
·         Fusiform – an outpouching of the entire circumference of the vessel.
·        Pseudoaneurysm or false – occur when the outpouching wall is not made up of the actual vascular wall such as a haematoma. This normally occurs after penetrating trauma or at an anastomotic site.
Figure 1: Diagram showing the different types of aneurysms

Epidemiology of AAA

The prevalence of AAA is estimated at 2-5% in men over 60 years. The incidence is approximately 30-60% per 1000 population and there is strong evidence that the prevalence has increased over the past few decades. It is found in 1 in 5 patients with Peripheral Arterial Disease (PAD).

AAAs are more common in men than women with a ratio of 4:1 and it is commonly diagnosed in the 6th or 7th decade of life.

The normal diameter of the infrarenal aorta is about 2cm. 80% of aneurysm occur infrarenally with 70% involving the iliac arteries and 20% associated with the peripheries.

Pathophysiology of Aneurysm formation

Large and medium arteries consist of three distinct layers – intima, media and adventitia.
Intima - the innermost layer. This consists of a layer of flat endothelial cells supported on a thin underlying matrix of collagen and elastic fibres.

Media – middle layer. This layer consists of varying amounts of collagen, smooth muscles and elastic fibres. The innermost portion of the media gets its nutrients from circulating blood while the outer portion is nourished by the vasa vasorum. The vasa vasorum are small vessels that penetrate the outer walls of the media and it’s these vessels that are affected by the atherosclerotic process decreasing the strength of the wall.

Adventitia – outermost layer which contains a high elastic and collagen content.
The intima and the media are separated by an internal elastic membrane and an external elastic membrane separates the media from the adventitia.
[Image: artery.jpg]
 Figure 2: Different components of a blood vessel
Aneurysms form as a result of degeneration and weakening of the compartments of the arterial wall. Rupture will occur if the intraluminal pressure exceeds the tensile strength of the wall. Although the pathogenesis is complex, atherosclerosis is an important factor in the formation of aneurysms.

It is thought that the mechanisms in aneurysm formation is multifactorial -
1. Atherosclerotic damage to elastin and collagen – atherosclerosis is thought to increase the pressure load and reduce the ability of the vessel to bear load thus forming an aneurysm. Weakening of the arterial walls is due the changes in the blood vessels caused by atherosclerosis degeneration. The focal accumulation of lipids and fibrous and calcium deposits in the intima and media leads to the destruction of elastin and probably secondary failure of collagen.
It is suggested that atherosclerotic plaques may weaken the aortic wall either directly or through reduction in the amount of nutrient reaching the media via diffusion from the lumen. The vasa vasorum can also become obliterated which may result in necrosis of the media and additional weakening of the vessel.
Additionally, inflammatory mediators produced in response to the atherosclerotic process can weaken and destroy the media.
2. Genetic abnormality in collagen – there is no single genetic defect however there is a familial clustering of HLA subtype suggesting a genetic role.
3. Biomechanical wall stress – elastin levels and the elastin-collagen ratio decrease progressively distal down the aorta. Reduced elastin is related with dilatation and collagen degradation predisposes to rupture. 
4. Increased proteolytic enzyme activity – degradation of the smooth muscle cells in the media and macrophages increase the production of matrix metalloproteinases (MMPs) in the extracellular matrix. The leads to stimulation of the proteolytic enzymes in the aortic wall and destruction of the matrix proteins. there are increased expressions of collegenases MMP-1 and -13 and elastases MMP-2,-9 and -12 in AAAs.

 [Image: 255939.jpeg]
 Figure 3: Diagram showing aneurysm formation infrarenally
In addition certain haemodynamic principles may assist in the formation of aneurysm such as the reflective pressure waves at the iliac bifurcation. When arterial flow reaches a bifurcation,as aortic flow into iliacs, some of the flow is reflected against the arterial wall just proximal to the bifurcation. When the ratio of the cross sectional area of the outflow arteries to the inflow artery is approx 1.0, the reflective wave pressure is minimum. With increasing age, this ratio decreases and the pressure of the reflective wave increases. This can result in dilatation of the vessel at this point.
Aetiology of AAA

1.       Atherosclerotic degeneration
2.       Congenital – Tuner Syndrome, Menke Syndrome, idiopathic
3.       Infection – Salmonella, Streptococcus, Staphylococcus, Syphilis
4.       Arteritis
5.       Mechanical – trauma, anastomotic
6.       Inflammatory
7.       Connective tissue abnormalities – Marfan’s Syndrome, Ehlers-Danlos Syndrome
Risk factors

It was found that the risk factors for the development of AAA and atherosclerosis are overlapping. The table shows the risk factors of aneurysm formation.

Table 1: Risk factors of Aneurysm Formation
Clinical Presentation

Most AAAs are silent until they rupture. An AAA can present in any one of the following ways:
1. Asymptomatic – 30% of AAAs are found incidentally in patients during routine physical examinations for other presenting complaints. During investigations such as abdominal X-rays, abdominal or Kidneys, Ureters and Bladder (KUB) ultrasounds or abdominal CT scans, AAAs are found. All patients with an incidental finding of an AAA should be referred to the vascular team for further investigations.
2.  Symptomatic – 20% of persons with AAAs present with pain in central abdomen, lumbar back, loin or groin areas. This pain is due to the stretching of the retroperitoneal fascia. AAAs can also cause a pulsatile beating in the abdomen, with a double impulse on respiration.
Thrombus formation within the sac can be a source of emboli to the lower limbs leading to reduced peripheral pulses and thrash feet.
3.  Rupture – a ruptured AAA can present with severe abdominal pain, pulsatile abdominal mass and even shock from hypotension. An AAA can rupture into the retroperitoneum, the peritoneal cavity or surrounding structures. Rupture most commonly occurs in the inferior vena cava leading to an aortocaval fistula.

Investigations and Diagnostic Studies

Based on clinical examinations and whether or not there are any presenting symptoms of the patient, the aim of the investigations is to confirm the diagnosis of an AAA. A number of radiological investigations can be performed with the gold standard being a dynamic contrast enhanced CT scan.

1. Radiographs - approximately two thirds of AAAs are calcified and can be exhibited on plain abdominal radiographs. An egg shell appearance representing the outline of the AAA circumference would be seen.

 [Image: GW422H500]
Figure 4: Abdominal X-ray showing the calcified edges of an AAA

2.  Ultrasound – the best method to calculate the size of the AAA and to confirm the diagnosis would be with an abdominal ultrasound scan. Ultrasounds can also be used for follow up of patients with asymptomatic AAAs.
3.  Dynamic contrast enhanced CT scans - this is the investigation of choice. Abdominal CT scans will provide information on the size and the extent of the aneurysm. In addition information about the actual location of the aneurysm is determined with a CT scan, whether there is renal or iliac involvement and other surrounding structures as well as other possible intra-abdominal pathology.
 [Image: CT-scan-image-showing-abdominal-aortic-aneurysm-AAA.jpg]
 Figure 5: Image of a Contrast Enhanced Abdominal CT Scan showing AAA
4. Aortography - can be used to help determine if there are other occlusive diseases if there is lower limb involvement.
In addition to radiological investigations, routine haematological investigations can be performed for supportive purposes. They can also be used to establish baseline data and in cases for preparation of emergency surgeries.

An AAA that persists over a number of years will cause turbulence of the blood flow stimulating platelets and the coagulation system. Thus with an AAA the haematological studies should highlight increased fibrinogen and a reduced platelet count.
Management of AAA

In considering the management of an AAA, the size of the aneurysm plays a major factor. In a number of trials that have performed is was found that surveillance of AAA of 4.0 cm to was safe in compliant patients and that early surgery did not result in any long term survival advantage.

What influences the decision to select patients for surgery?
The decision to select patients for AAA repair is influenced by the following:
1. Aneurysm rupture risk – the diameter of an AAA is the best predictor of rupture risk.5 Rupture risk increases proportionally with increasing diameters from 5cm to 6cm. AAAs <5cm have a very low rupture risk and most vascular surgeons tend to use this size as the cut off for an indication for surgery.
 Table 2: Estimated annual rupture risks with increasing diameter

2. Expansion rate - the rate of growth of an aneurysm is an important determinant in the choice of surgery. A small AAA that expands 0.5cm or more over a six month period is considered high risk for rupture and will need elective surgery.
3.  Life expectancy and operative risk – age and other existing comorbid conditions must be considered when deciding on elective surgery. In general the 5-year survival rate following AAA repair is reduced compared to age and sex matched population data averaging 60% to 65% as compared with 75% to 80% anticpated. Higher 5-year survival rates are associated with younger ages, no comorbidities, a serum creatinine value <1.5, no or minimal angina and no significant COPD.
4.  Patient preference – active patient participation is required at all stages of the management process regardless of the diameter of the aneurysm.  Compliant patients tend to have better outcomes and they are willing to show up for follow up clinics, agree to smoking cessation and medication compliance. In addition the patient ultimately agrees for elective surgery and must be cognizant of the situation.


Selective screening can be costly to the average patient and sometimes it might be worth performing a cost benefit analysis. Abdominal ultrasounds is the most appropriate form of investigation to be used for screening purposes. Screening is recommended in:
·         Men aged 65 -75 years who have a history of smoking should be screened at least once. There is little benefit in repeat screening with negative results.
·         Family history of aneurysms
·         Known extremity aneurysms
·         Persons aged 55-80 years and have existing peripheral vascular disease
Figure 6: Flowchart showing Treatment Options
Medical Management

Medical therapy may be helpful in patients with small to medium sized aneurysms that have not been chosen for elective surgery. It is recommended that patients be put on beta blocker therapy as it not only controls HTN or angina but also have shown to reduce the rate of expansion of AAA.

It has also been shown that patients who were receiving antibiotic therapy have a reduced rate of mean annual expansion compared to those receiving placebo therapy.

Surgical Management
Open repair of AAA is carried out through a long midline incision. Control of the aorta is achieved by occluding the aorta and iliac vessels. Aortic clamping should be infrarenal to prevent renal ischaemia during the procedure and thus, it may not be possible to repair juxtarenal aneurysms. The aneurysm is repaired by placing a synthetic graft (such as Dacron) in the lumen of the aneurysm. This may either be a tube graft, which is anastamosed to the infrarenal aorta proximally and the supra-iliac aorta inferiorly, or a bifurcated graft which replaces aneurysmal common iliac arteries as well as the aorta.
Endovascular aneurysm repair (EVAR) has emerged as the definitive treatment for AAAs it offers fewer complications, reduced blood less, reduced intensive care and hospital stay and faster recovery. EVAR is less invasive compared to the conventional open repair. However there can be complications during an EVAR procedure which may require switching to an open repair.
EVAR has the advantage of small incisions, avoids a laparotomy and does not require aortic cross clamping. It is carried out under direct radiological guidance by passing the graft through small groin incisions and expanding it in the aneurysm.  One of the disadvantages of the technique is that the patients receive a relatively high dose of nephrotoxic contrast, which can cause postoperative renal dysfunction. In the medium term, blood can leak around the graft to fill the aneurysm sac (termed endoleak) requiring further operative intervention. These patients require frequent and prolonged clinical and radiological follow-up to monitor for endoleaks.
1. Aggarwal S. et al. (2011) Abdominal aortic aneurysm: A comprehensive review. ExpClin Cardiology 16(1):11-15 Available at http:///

2. Singh K. et al (2001) Prevalence of and risk factors for Abdominal Aortic Aneurysm in a population-based study. American Journal of Epidemiology Vol 154,3:236-244. Available at

3. Blanchard J. et al (2000) Risk factors for Abdominal Aortic Aneurysm: Results of a Case-Control study. American Journal of Epidemiology Vol 151,6:575-583. Available at

4. Fillinger MF et al. (2002) In vivo analysis of mechanical wall stress and abdominal aortic aneurysm rupture risk. Journal of Vascular Surgery Vol 36,3:589-597. Available at

5. Brewster DC et al. (2003) 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. Journal of Vascular Surgery 5:1106-1117. Available at http:///
6. Ouriel K et al. (1992) An evaluation of new methods of expressing aortic aneurysm size: Relationship to rupture. J Vasc Surg. 15:12–8. Available at

7. Silverberg E, Boring CC, Squires TS. (1990)Cancer statistics 1990. CA Cancer J Clin. 40:9–26. Available at

8. McPhee JT, Hill JS and Eslami MH. (2007)The impact of gender on presentation, therapy, and mortality of abdominal aortic aneurysm in the United States, 2001–2004. J Vasc Surg. 45:891–9. Available at
9. Singh K et al. (2001)Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: The Tromso Study. Am J Epidemiol. 154:236–44. Available at