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Aetiology

An aneurysm in an irreversible dilatation, generally fusiform in shape, and can occur at any level.

There is no fixed definition, certainly for abdominal aortic aneurysms (AAA), one definition being =50% dilatation of the normal aorta (defined from the literature, adjusted for age/gender/radiological modality). However the most pragmatic, and widely used definition is an aorta that is dilated at least 1.5 times that of the adjacent intact aorta (usually the intrarenal or suprarenal aorta). Any abdominal aortic diameter =3.0cm (normally 2.1cm in males, 1.8cm in females =55yrs) may also be considered an AAA.

Atherosclerosis is no longer considered the principal precipitating factor, and it is better to substitute the term "degenerative" to emphasise the multifactorial aetiology.

Hypotheses focus on metabolic, structural, and genetic derangements: Metabolic: Can develop from infection: bacterial endocarditis, sepsis, and syphilis. The diagnosis of syphilis is more likely the more proximal the lesion and it is rare below the diaphragm. Cystic medial degeneration, arteritis (particularly Takayasu's disease), and an autoimmune basis are also factors. Structural: Increase in arterial pressure wave as diameter reduces, compounded by reflected pressure waves from the extremities, impacts on a stiffened AAA (contains less elastin and more collagen than thoracic part). The aging process (changes in collagen and elastin) and atherosclerosis, which compromises repair (which is dependent on diffusion, as there are no vessels in the wall as present in the thoracic part), increases this pressure. This can weaken the wall leading to dilatation, and a vicious circle of increased wall tension and greater wall stress according to the Laplace' Law (wall tension is proportional to pressure x radius2).

Genetic: 20% of patient with thoracic aneurysms that require surgery have a relative with the condition and it is usually inherited as an autosomal dominant (low penetrance but increasing with age) with or without Marfan’s syndrome. Marfan’s syndrome is associated with thoracic aortic aneurysm, usually proximal and there may be involvement of the aortic valves. Ehrlos-Danlos' syndrome is another genetic connective tissue defect. Hypertension increases the risk of aortic aneurysm both above and below the diaphragm, again according to the Laplace Law. A previous aortic dissection with persistent false channel may produce aneurysmal dilatation.

Trauma can cause aortic aneurysm but it is uncommon below the diaphragm. Thoracic lesions can result from shearing forces in a RTA. Smoking is a major risk factor, possibly related to increased activity of leukocyte-derived pancreatic elastase II. 1. COPD is also a risk factor.

Ref: http://www.patient.co.uk/showdoc/40024885/

The natural history of an individual case is difficult to predict, and AAAs can have intervals of stability and slow and rapid expansion. The general recommendation is to consider elective aneurysmorrhaphy for aneurysms with a diameter of 5 cm or greater or for small aneurysms that have an average growth rate of more than 0.5 cm/y (Hollier, 1992). Approximately 20% of aneurysms expand faster than 0.4 mm/y; the rest do so at slower rates.

Size Criteria < 5.0 cm – Observe With Serial Ultrasounds 5.0 – 6.0 cm – Repair Depending upon Co- morbidities >6.0 cm – Repair Increase in Size of >5mm in 6 months Symptoms

Less Common Indications Saccular Aneurysm Retroperitoneal Fibrosis Causing Ureteric Obstruction Embolism or Thrombosis

Open vs Endovascular Repair Anatomical Requirements for Stent grafts Aortic Neck > 1.5cm in Length Aortic Neck Correct Shape - Cylindrical Aortic Neck Appropriate Diameter - <30mm An Area of Iliac Artery of Normal or Near Normal Diameter No Significant Iliac Stenosis