Clinical diagnosis
Case 275
【Progress】
He was admitted in our hospital for under extensive care and given antibiotics.
【Discussion】
The key difference between true abdominal aortic aneurysm and inflammatory aortic aneurysm is that inflammatory aortic aneurysms have fibrotic tissue at its outside while true aortic abdominal aneurysms do not. The origin of the fibrotic tissue covering aortic aneurysm is yet to be clarified. However, three possible mechanisms are considered. First is that pathogen either bacillus or virus reach and infect to aortic aneurysm, causing increase of forming granulation tissue. Recently, Chlamydia pneumonia is documented as one of the pathogens: in this situation, the use of Macrolide antibiotics can be effective (1). Second, small leak or hemorrhage from aortic aneurysm causes to form granulation tissue as a reparative process. Cease of anticoagulant or antiplatelet might be necessary. Third, immunological response to fragile and degenerative aortic wall, elastin derived peptide which becomes foreign body, induces to form granulation tissue. In this situation, steroid might be useful. But some clinicians consider steroid weakens aortic wall (1-3).
Inflammatory aortic aneurysm predominantly occurs in current smokers (1-3). In clinical symptoms of inflammatory aneurysm, triads are known; elevation systemic inflammatory markers like CRP, back pain and weight loss (1-3). Three triads do not always meet in clinical reality (1). In our case, elevation of inflammatory markers was found but not back pain and weight loss.
Abdominal CT is useful to detect inflammatory aortic aneurysm enlarging or shrinking soft tissue surrounding aortic aneurysm. It is crucial to differentiate inflammatory aneurysm from penetrating atherosclerotic ulcer.
Atheroma of aorta is formed as follows (4-7); low density lipoprotein (LDL) cholesterol enters intima of vascular wall and macrophages phagocyte LDL for processing and absorbing. However, repeated too much LDL for macrophages to dispose, accumulate LDL cholesterol in intima of aortic wall, namely formation of atheroma. As atheroma volume enlarge, it compresses not just intima but also intimal elastic plate and tunica media. When intima rupture occurs, atheroma can be embolic material to occlude peripheral arterial branches such as coronary artery. Intimal elastic fiber and tunica media can become thinning and finally rupture of internal elastic fiber and tunica media. As atheroma further grows, it becomes to compress external elastic fiber plate and adventitia, forming adventitia false aneurysm and finally leading transmural rupture (4-7). Minute leakage from penetrating atherosclerotic ulcer can cause to form connective tissue surrounding abdominal aneurysm, mimicking inflammatory aortic aneurysm. In our case, the following CT showed no enlargement of abdominal aneurysm, indicating inflammatory aortic aneurysm rather than penetrating atherosclerotic aneurysm with possible leakge.
【Summary】
We presented an eighty six-year-old male for fever and atrial fibrillation. CT depicted abdominal aortic aneurysm (AAA) with soft tissue attenuation surrounding AAA. Although the origin of granulation tissue surrounding AAA is yet to be clarified, three possible explanation was made: first, infection to AAA by pneumonia Chlamydia or other pathogen; second minute leakage from AAA: third, immunologic reaction to fragile aortic wall, elastin peptide recognized as foreign body. It is crucial to differentiate inflammatory aneurysm from penetrating aortic atheromatous ulcer. It is borne in mind that aortic atheromatous ulcer is formed by rupture of fibrous cap covering atheroma composed of LDL cholesterol and as atheroma grows, atheroma compress and penetrating internal elastic plate, tunica media, external elastic plate and finally adventitia, leading transmural rupture.
【References】
1.Tang T, et al. Inflammatory Abdominal Aortic Aneurysms. European Journal of Vascular and Endovascular Surgery. 2005; 29:353-362
2.Gans, RO, et al. The inflammatory abdominal aortic aneurysm. Prevalence, clinical features and diagnostic evaluation. Neth J Med. 1993; 43: 105-115
3.Rasmussen TE et al. Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis. Ann Surg, 1997; 225: 155-164
4.Hayashi H, et al. Penetrating Atherosclerotic Ulcer of the Aorta: Imaging Features and Disease Concept. Radiographics. 2000;20(4):995-1005.
5.Cooke J, et al. The Penetrating Aortic Ulcer: Pathologic Manifestations, Diagnosis, and Management. Mayo Clin Proc. 1988;63(7):718-25.
6.Braverman A. Penetrating Atherosclerotic Ulcers of the Aorta. Curr Opin Cardiol. 1994;9(5):591-7.
7.Coady M, Rizzo J, Elefteriades J. Pathologic Variants of Thoracic Aortic Dissections. Penetrating Atherosclerotic Ulcers and Intramural Hematomas. Cardiol Clin. 1999;17(4):637-57.
2022.8.23