•Severe arteriosclerosis a major factor.

•20% familial incidence indicates a genetic defect in connective tissue component. Mutation of gene encoding type III procollagen implicated.

•Syphilis and other bacterial infections.

•Cystic medial necrosis.

•Trauma.

•Arteriosclerosis causes gradual destruction of the media with focal weakening of the wall.

•The intraluminal pressure is proportional to the radius (LaPlace^s Law). An incremental increase in pressure causes an increased pressure on the inner surface of the evolving aneurysm with an incremental increase in the radius, establishing a vicious cycle.

•Familial cases indicate the importance of genetic defects in connective tissues making the aorta susceptible to the formation of aneurysms due to arteriosclerosis.

•More common in men.

•Other complications of arteriosclerosis exist in majority of cases: ischemic heart disease, cerebrovascular disease, ischemic bowel disease, peripheral vascular disease.

•75 % occur in the abdominal aorta, and are easier to repair than thoracic or thoracicoabdominal lesions

•Asymptomatic until discovered on routine physical or imaging examinations, or as a cause of back pain.

•Patients may complain of pain and an associated leaking sensation, a sign of imminent rupture.

•Virtual inevitable rupture with increasing distension of an aneurysm (LaPlace^s Law) calls for careful monitoring in cases being followed conservatively.

•Fusiform dilatation of a severely arteriosclerotic aorta with sharp superior and inferior margins.

•Typically involves the abdominal aorta from just below the ostia of the renal arteries to the bifurcation of the aorta.

•Larger aneurysms, >7-8 cm in transverse diameter, contain a thick old laminated thrombus reducing the patent aneurysmal lumen to a diameter close to that of the lumen in the adjoining intact aorta.

•Aneurysmal thrombus does not organize due to the paucity of functioning vasa vasorum in the fibrotic thinned out aneurysmal wall.

•Wall of aneurysm made up of a barely identifiable media, which is replaced by a fibrotic arteriosclerotic lesion with focal aggregates of mononuclear cells.

•Adventitia is fibrotic with chronic inflammation and merges with media.

• Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 500-501.

• Harrison^s Principles of Internal Medicine, 13th Edition. New York, McGraw-Hill, 1994, pp. 1131-1133.

• Current literature from PubMed at National Library of Medicine