This pictorial essay focuses on the pathophysiology of enlargement and rupture of the atherosclerotic aortic aneurysm and on mechanisms involved in traumatic aortic transection related to deceleration injury.
The wall stress related to blood pressure in the nonaneurysmal aorta is relatively low and uniformly distributed, whereas within the aortic aneurysm, regions of high- and low-stress distribution are present [1]. Increased tension stress results in progressive vessel dilatation and weakening of the aortic media. According to Laplaces law, wall tension is proportional to the vessel radius for a given blood pressure. When an artery wall develops a weak spot and expands as a result, it might seem that the expansion would provide some relief, but in fact the opposite is true. The expansion subjects the weakened wall to even more tension. The weakened vessel continues to expand (Fig. 1). A localized weak spot in an artery might gain temporary tension relief by expanding toward a spherical shape because a spherical membrane has half the wall tension for a given radius. Unfortunately, in an expanding aneurysm, forming a near-spherical shape cannot give sufficient tension relief. Aortic aneurysm rupture is believed to occur when the mechanical stress on the wall exceeds the strength of the wall tissue (Fig. 2). Infected aortic aneurysm is a rare lesion, which may progress rapidly to aortic rupture or uncontrolled sepsis with high mortality rate.