Abdominal Aortic Aneurysm

Definition

An AAA (abdominal aortic aneurysm) is defined as enlargement of at least 3 cm of the abdominal aorta. The majority of abdominal aortic aneurysms begins below the renal arteries and ends above the iliac arteries. The exact cause of (AAAs) is unknown. However, it is thought to be due to a degenerative process of the abdominal aorta caused by atherosclerosis. Artherosclerosis represents a response to vessel wall injury 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 consists of three distinct tissue layers including: the intima, media, and adventicia. There is a reduction in medial elastin layers from the thoracic area to the abdominal portion in a normal aorta. Aneurysms are due to dilation in all layers of the vessel wall. AAAs generally enlarge an average of 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 the extracellular matrix proteins and elastins are 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 is detrimental in aneurysm walls, because elastin is the principle load-bearing element in the aorta. These changes along with changes in the protein matrix in aneurysms may contribute to the propensity for the formation of aneurysms in the infrarenal aorta. Oxidative stress, lyphocytic and moncytic infiltration with immunoglobulin deposition in the a...

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...treat aortic dissection. Verapamil and diltazem are used, because of their vasodilatory and negative inotropic effects (Coughlin). A dopamine infusion may be used throughout the case in order to enhance renal perfusion. Heparin is given prior to the cross-clamping of the aorta to reduce the risk of coagulation disorders. Mannitol can be given prior to the cross-clamp to prevent renal failure during resection of an AAA. Furosemide may be used after the cross-clamp is released to improve urinary output (LaMuralgia, Musch).

The secret to the successful management of these cases is preparation. Early involvement in anesthesia management and a thorough understanding of the pathophysiology of AAAs (including rupture and dissection), and the surgical and anesthetic implications for treatment will improve morbidity and mortality outcomes in this patient population.