Endovascular Treatment of Inflammatory Abdominal Aortic Aneurysms


Inflammatory abdominal aortic aneurysms (iAAAs) represent a small but challenging proportion of all AAAs. The evidence base for the management of iAAAs is sparse, particularly with respect to endovascular aneurysm repair (EVAR). iAAAs have historically been treated by a variety of open approaches with increased technical difficulty, but mortality is comparable to that of open repair of noninflammatory AAAs. Few data exist regarding iAAA repair in the endovascular era, but endovascular repair is attractive given the hostile nature of the retroperitoneum in this group of patients. Less certain following EVAR is the fate of the retroperitoneal fibrosis and any associated ureteric obstruction.

Clinical Features

Inflammatory AAAs account for 5% to 10% of all AAAs. They appear to occur predominantly in men and in an age group 5 to 10 years younger than those with noninflammatory AAA. The rupture rate is thought to be lower than that for other AAAs. Between 80% and 90% of patients with iAAAs are symptomatic at presentation, in contrast to atherosclerotic AAA, where the majority are asymptomatic until rupture. One series reported a fourfold increase in the presentation of iAAA as an incidental finding when compared with earlier experience, which might reflect the increased availability of computed tomography (CT) and the advent of AAA screening programs.

Periaortic adhesions most commonly involve the duodenum (97%–100%), inferior vena cava (IVC) (70%), left renal vein (50%), and ureter (44%). Entrapment of these adjacent structures can complicate iAAAs with duodenal obstruction, IVC obstruction, varicocele, hydrocele, or ureteric colic. All of these contribute to technical difficulties with open AAA repairs.

The principal imaging modality used for the diagnosis of an iAAA is CT ( Figure 1 ). With contrast enhancement, this imaging technique has a sensitivity rate of 83%, with specificity and accuracy rates of 100% and 94%, respectively. In the majority of cases, the periaortic fibrotic plaque is well defined and of soft tissue density. Thickening of the aneurysm wall is most prominent in the anterolateral wall, with relative sparing of the posterior wall.

FIGURE 1, A and B, Coronal and axial computed tomography appearance of infrarenal inflammatory abdominal aortic artery. There is extensive and circumferential perianeurysmal inflammatory tissue.

Magnetic resonance imaging (MRI) demonstrates a high sensitivity in detecting perianeurysmal inflammatory change, with the inflammatory cuff predominantly visible on T2-weighted and short T1 inversion recovery (STIR) sequences. The inflammatory cuff readily enhances with gadolinium, enabling detailed assessment of ureteric involvement. MRI enhanced with gadolinium may be a worthwhile alternative to contrast-enhanced CT, particularly in patients with preoperative kidney failure.

The introduction of screening programs for AAA has highlighted the importance of recognizing iAAAs by ultrasound examination. Ultrasound diagnosis relies on identifying a cuff of soft tissue adjacent to the calcified margin of the aneurysm. In addition, accurate measurement of perpendicular AAA diameter between the outer aspects of the anterior and posterior wall is needed to demonstrate progression of periaortic fibrosis. Measuring between the inner walls of the AAA lumen can fail to detect a number of iAAAs and is common practice in some screening programs.

The issue of immunosuppressive therapy in iAAA is contentious and, despite anecdotal evidence of symptomatic relief and regression of periaortic inflammation on postoperative imaging, no controlled trials exist evaluating its role.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here