Definition An AAA (abdominal aortic aneurysm) is defined as an enlargement of at least 3 cm of the abdominal aorta. Most abdominal aortic aneurysms begin below the renal arteries and end above the iliac arteries. The exact cause of (AAA) is unknown. However, it is believed to be due to a degenerative process of the abdominal aorta caused by atherosclerosis. Atherosclerosis represents a response to injury to the vascular wall caused by inflammation, genetically regulated defects in collagen and fibrillin, increased protease activity within the arterial wall, and mechanical factors (Stoelting p. 143). Pathophysiology The abdominal aorta is made up of three distinct tissue layers including: intima, media and adventitia. In a normal aorta, there is a reduction in the medial layers of elastin from the thoracic area to the abdominal portion. Aneurysms are due to the dilation of all layers of the vascular wall. AAAs generally enlarge on average 0.2 to 0.8 mm/year and eventually rupture (Gupta and Narani). Genetics, inflammation, immune responses, wall stress, and proteolytic degradation all contribute to the formation of AAAs. Proteolytic degradation of extracellular matrix proteins and elastin is the primary event in the development of an abdominal aortic aneurysm. Collagen and elastin content is reduced from the proximal to the distal aorta. Fragmentation and degeneration are harmful to the aneurysm walls, because elastin is the main load-bearing element of the aorta. These changes, together with changes in the protein matrix of aneurysms, may contribute to the propensity for aneurysm formation in the infrarenal aorta. Oxidative stress, lymphocytic and moncytic infiltration with immunoglobulin deposition in the paper medium treat aortic dissection. Verapamil and diltazem are used, due to their vasodilatory and negative inotropic effects (Coughlin). In all cases, a dopamine infusion may be used to improve renal perfusion. Heparin is given before cross-clamping of the aorta to reduce the risk of clotting disorders. Mannitol can be administered before cross clamping to prevent renal failure during resection of an AAA. Furosemide can be used after cross-clamp release to improve urinary output (LaMuralgia, Musch). The secret to effective management of these cases is preparation. Early involvement in anesthesia management and a thorough understanding of AAA pathophysiology (including rupture and dissection) and surgical and anesthetic implications for treatment will improve morbidity and mortality outcomes in this patient population.