Persistent chronic peri-aortitis (‘inflammatory aneurysm’) after abdominal aortic aneurysm repair: systematic review of the literature

Bommel, Efh van; Veer, SJ van der; Hendriksz, Tadek R; Bleumink, GS

doi:10.1177/1358863x08091147

Cited by 41 publications

(28 citation statements)

References 64 publications

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“…There is some concern since adventitial infl ammation is unaff ected by the procedure. Progress [74] and even de-novo-evolution of retroperitoneal infl ammation were observed after stent-graft insertion [68]. Additionally, open surgery allows repair of ureteral obstruction which inevitably persists after endovascular stenting.…”

Section: Infl Ammatory Abdominal Aneurysm (Iaa)mentioning

confidence: 99%

Inflammatory diseases of the aorta

Caspary

2016

Vasa

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Summary:Infl ammatory aortic diseases may occur with and without dilatation and are complicated by obstruction, rupture and dissection. Infections originate from periaortic foci or septicaemia and tend to result in the rapid development of aneurysms. Large vessel vasculitis due to Takayasu arteritis in younger and giant cell arteritis (GCA) in older patients is located in all layers of the aortic wall and prevails in the thoracic section. GCA patients are prone to developing aortic complications in the late course of disease. In Behçet's disease, aneurysms may have an unusual morphology and localisation. The diagnosis of aortitis is usually obtained by vascular imaging, but partly made only by biopsy on occasion of an operation, especially in case of isolated aortitis of the ascending aorta which mostly remains inapparent until dissection or large aneurysms have developed. Periaortitis typically occurs in the abdominal aorta and may lead to infl ammatory aortic aneurysm (IAA). It is looked upon as a special form of vasculitis, with an overlap to primary retroperitoneal fi brosis (RF). An identical pathology is discussed for the three diseases. On the other hand, about 50 % of isolated aortitides and periaortitides as well as retroperitoneal fi broses can be classed among IgG4-related diseases. Periaortitis also is observed after treatment of aortic aneurysms by stent-graft implantation. Special attention should be paid to ureteral obstruction along with RF or IAA. Once infection is ruled out, immunosuppression is applied to all forms of infl ammatory aortic diseases, primarily with glucocorticoids. However, after successful surgery for isolated thoracic aortitis or infl ammatory aortic aneurysm immunosuppression may be dispensable and it is not required if periaortic tissue enlargement persists in chronic inactive disease. For some patients with periaortitis and RF, tamoxifen may be a valuable alternative.

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Section: Infl Ammatory Abdominal Aneurysm (Iaa)mentioning

confidence: 99%

Inflammatory diseases of the aorta

Caspary

2016

Vasa

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“…18,19) ESR could reflect the condition of GCA, 20) and we should suspect recurrence of inflammation if it is elevated again. At the same time, we should also be careful of exacerbation of aortic complications.…”

Section: Discussionmentioning

confidence: 99%

A Case of Ascending Aortic Dissection and Rupture Caused by Giant Cell Arteritis

et al. 2014

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SummaryGiant cell arteritis (GCA) is an autoimmune disease characterized by granulomatous inflammation in the wall of medium-sized and large-sized arteries, and it usually occurs in patients over 50 years of age.1) Symptoms are nonspecific, and include fatigue, fever, and headache.2) It is occasionally combined with aortic complications, and ruptures resulting in death. These complications occur as late events, usually several years after diagnosis and often after other symptoms have subsided.3) Physicians should therefore be alert for complications of the large arteries in GCA. Here we present a case of GCA combined with ascending aortic dissection and rupture 3 weeks after diagnosis. (Int Heart J 2014; 55: 555-559) Key words: Gallium scintigraphy, Steroid therapy, Surgical therapy Case ReportA 76-year-old woman was admitted to our hospital because of headache, disturbance of her field of view, jaw claudication, and high fever. Approximately 6 months earlier, she had new-onset headache, abnormality of view, and jaw claudication. One month before admission, her body temperature rose to 39°C. The patient saw a primary care physician a week before admission. Physical examination revealed a Levine grade 3 systolic murmur at the apex, and echocardiographic examination showed a thickened mitral valve and moderate mitral regurgitation. The physician suspected infectious endocarditis and referred the patient to our hospital for further examination.With regard to past history, the patient was receiving antihypertensive drugs. There was nothing of note in her family history, and she had never smoked and had never been abroad. Her body weight had fallen by 15 kg in the previous 6 months due to loss of appetite. Vital signs were stable except for an increase in body temperature (38°C). Systolic blood pressure was 120 mmHg and diastolic blood pressure was 70 mmHg, and there were no crosswise differences. Pulse rate was 90 beats per minute. The bulbar conjunctiva showed neither petechial hemorrhages nor anemia. There was no pain at her temporal lesion and no cervical lymphadenopathy. A pan-systolic murmur was heard at the apex (Levine grade 3), and respiratory sound was clear. There was no edema, petechia, or nodules on her limbs. On the day of admission, an electrocardiogram revealed sinus rhythm (90 beats per min) and no ST-T abnormality. Chest X-rays revealed slightly extended mediastinum. Laboratory data suggested the presence of severe inflammation (Table I).On transthoracic echocardiography, we found thickening of the anterior mitral leaflet and moderate mitral regurgitation. Transesophageal echocardiography showed no evidence of vegetation attached to the valves. We performed 2 sets of blood cultures, and they were sterile. In additional laboratory examinations, cytoplasmic antineutrophil antibody, perinuclear antineutrophil cytoplasmic antibody, and other specific antibodies were all negative, and complement was not decreased. Also, there was no elevation of IgG4. In order to investigate the focus of inflammation...

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“…Diagnosis involves clinical and radiological findings allied to blood inflammatory markers while treatment involves surgical intervention. However fibrosis and/or ureteral obstruction may recur (van Bommel et al, 2008). The incidence of acute renal failure following complex AAA repair is discussed in detail above.…”

Section: Complications Of Open Aaa Repairsmentioning

confidence: 99%