Aneurysms

Introduction

An abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta more than 1.5 times the expected diameter. It involves all three layers of the vessel wall. For the infrarenal aorta in most adults, this is 3 cm, which is the trigger for annual follow-up once an AAA has been identified. AAAs are estimated to expand at 4 to 5 mm per year. Elective surgical repair is offered for AAAs discovered to be 5.5 cm or larger to prevent death from rupture. They may unfortunately rupture without evidence of growth during the previous year, and rupture of an individual aneurysm is therefore unpredictable.

The distal aorta is subject to the greatest changes in arterial pressure and therefore biomechanical stress. Hence the majority of AAAs are found below the renal arteries (90% to 95%). The remainder may involve the proximal renal arteries or even visceral branches of the aorta. They can also descend into the iliac vessels.

Most aneurysms are asymptomatic until a complication arises. These complications can be rupture, symptomatic expansion, thrombosis or embolism. The majority of ruptures are initially into the retroperitoneal space, where they may be temporarily contained. Intraperitoneal rupture can be primary or may follow a retroperitoneal event, and it has a higher mortality rate. Rarely, an AAA will be complicated by chronic rupture, formation of a false or inflammatory aneurysm, an arteriovenous or aortoenteric fistula, atheroembolism, small bowel obstruction or ureteric obstruction.

Epidemiology

Some 5% to 10% of men 65 to 79 years of age have an AAA, and the prevalence in men increases by 6% per decade. AAAs are more common in men, with a three- to four-fold higher prevalence than in women. The risk of aneurysmal rupture has been shown to be proportional to aneurysmal size, with aneurysms measuring less than 5.4 cm in diameter having an annual rupture rate of approximately 1% to 2%, whereas those greater than 7.0 cm have an annual rupture rate of 32.5%.

Risk factors for AAA are age over 55 years, male gender, smoking, positive first-degree relative family history, chronic obstructive pulmonary disease, Marfan syndrome and Ehlers-Danlos syndrome.

Aetiology/pathophysiology

Traditionally arterial aneurysms were considered to be a consequence of atherosclerotic disease, and intimal atherosclerosis does accompany AAA. Current thinking is evolving and recent data suggests a causative role for matrix metalloproteinases.

This overall pathophysiology is multifactorial, as follows:

• There is proteolytic degradation of the aortic wall connective tissue. Matrix metalloproteinases along with other proteases derived from macrophages/aortic smooth muscle cells are secreted into the extracellular matrix. This enhanced enzyme activity may lead to the breakdown of the structural matrix proteins, such as collagen and elastin. There is an autoimmune process, as IgG complexes have been located in the dilated aorta wall.

• Biomechanical wall stress is a component and the elastin-collagen ratio falls in the distal aorta. Diminished elastin is associated with aortic dilatation, and the collagen degradation predisposes to rupture.

Prevention/screening

Screening may reduce the risk in high-risk groups, and current regimens suggest one-time ultrasound (US) screening for all men above 65 years of age and for those 55 years of age with a positive family history. Surveillance imaging at 12-monthly intervals is recommended for AAA 3.5 to 4.4 cm in diameter. For those AAAs 4.5 to 5.4 cm, 6-monthly surveillance imaging is indicated. With regard to women in high-risk groups, one-time US is suggested for those above 65 years of age, although routine screening currently has insufficient evidence to support it.

Clinical features