Management of an inflammatory abdominal aortic aneurysm caus
Now open: Certificate Course in Management of Covid-19 by Govt. Of Gujarat and PlexusMDKnow more...Now open: Certificate Course in Management of Covid-19 by Govt. Of Gujarat and PlexusMDKnow more...
A 53-year old male with no other past medical history of note presented to the emergency department (ED) with acute onset nausea and vomiting. This was preceded by a 2week history of non-specific malaise and generalized bilateral flank pain, worse on the right. He was an active smoker, with a 30-pack year history. He took no regular medications and had not undergone any previous surgical interventions. He denied any recent weight loss, night sweats, or swollen glands. Abdominal examination revealed right flank tenderness on both light and deep palpation with active bowel sounds and no palpable masses. Murphy’s sign was negative.

Blood tests demonstrated a severe AKI without significant neutrophilia but a mildly elevated C-reactive protein (Table 1). Given the flank tenderness and AKI, a non-contrast computed tomography of kidney, ureters, and bladder (CT-KUB) was performed to exclude a renal or urological pathology. This demonstrated a large infra-renal AAA with surrounding retroperitoneal stranding and bilateral hydronephrosis. He underwent an endovascular aortic aneurysm repair (EVAR) with bilateral iliac branched devices (IBD) during his initial presentation, and his on-table completion angiogram demonstrated good flow through the grafts with no endoleak.

Post-aortic stenting, a percutaneous US-guided biopsy of the para-aortic fibrosis was obtained for histopathological evaluation. Results reported non-specific fibrous tissue with chronic inflammation and no features of granulomatous inflammation or malignancy. He was subsequently discharged on Day 8 post-EVAR and on 30-day follow-up, a repeat CTA showed all grafts remained patent with no evidence of endoleak or evidence of aneurysmal enlargement. He subsequently had his ureteric stents removed, with continued normalization of renal function, and was referred to a rheumatology specialist for ongoing management of suspected systemic IgG-4 related disease.