Visceral artery aneurysms: Incidence, management, and outcome analysis in a tertiary care center over one decade

Abstract

ObjectivesTo evaluate the incidence, management, and outcome of visceral artery aneurysms (VAA) over one decade.Methods233 patients with 253 VAA were analyzed according to location, diameter, aneurysm type, aetiology, rupture, management, and outcome.ResultsVAA were localized at the splenic artery, coeliac trunk, renal artery, hepatic artery, superior mesenteric artery, and other locations. The aetiology was degenerative, iatrogenic after medical procedures, connective tissue disease, and others. The rate of rupture was much higher in pseudoaneurysms than true aneurysms (76.3 % vs.3.1 %). Fifty-nine VAA were treated by intervention (n = 45) or surgery (n = 14). Interventions included embolization with coils or glue, covered stents, or combinations of these. Thirty-five cases with ruptured VAA were treated on an emergency basis. There was no difference in size between ruptured and non-ruptured VAA. After interventional treatment, the 30-day mortality was 6.7 % in ruptured VAA compared to no mortality in non-ruptured cases. Follow-up included CT and/or MRI after a mean period of 18.0 ± 26.8 months. The current status of the patient was obtained by a structured telephone survey.ConclusionsPseudoaneurysms of visceral arteries have a high risk for rupture. Aneurysm size seems to be no reliable predictor for rupture. Interventional treatment is safe and effective for management of VAA.Key Points• Diagnosis of visceral artery aneurysms is increasing due to CT and MRI.• Diameter of visceral arterial aneurysms is no reliable predictor for rupture.• False aneurysms/pseudoaneurysms and symptomatic cases need emergency treatment.• Interventional treatment is safe and effective.

Visceral Artery Aneurysms and Pseudoaneurysms: Retrospective Analysis of Interventional Endovascular Therapy of 43 Aneurysms

“…2 million people. The etiology of the majority of aneurysms in the treated group and in comparison to other studies is vascular wall degeneration caused by atherosclerotic changes followed by pseudoaneurysm due to iatrogenic and inflammatory complications [4]. The number of iatrogenic changes, particularly the formation of pseudoaneurysms in the hepatic artery, has increased due to the growing number of percutaneous liver interventions, such as drain placement, biopsies, and PTCD (percutaneous transhepatic cholangiodrainage), and hepatobiliary surgery [5].…”

Endovascular Therapy for Splenic Artery Aneurysm: A Case Report

“…Unlike the usual atherosclerotic or degenerative aneurysmal disease, SAA are found much more frequently in women than men in an approximate ratio of 4 to 1. Usually SAAs are saccular and less than 2 cm in diameter and located in mid or distal splenic artery (7). The most common clinical risk factors are female gender, multiple pregnancy, and portal hypertension, and less common conditions including systemic lupus erythematosus, polyarteritis nodosa, and anomalous origin of splenic artery (7,8).…”

“…Usually SAAs are saccular and less than 2 cm in diameter and located in mid or distal splenic artery (7). The most common clinical risk factors are female gender, multiple pregnancy, and portal hypertension, and less common conditions including systemic lupus erythematosus, polyarteritis nodosa, and anomalous origin of splenic artery (7,8). Currently, most SAAs are found incidentally during abdominal imaging performed for other unrelated symptoms.…”

“…Aneurysms in pregnant females or those who are at a child bearing age, also, absolutely necessitates treatment. Less strict indications include aneurysms that are mentioned to be enlarged or those bigger than 2 cm in diameter, but these size criteria are not exclusive criteria (7,9). A celiac trunk with normal branching into splenic, hepatic and left gastric artery are reported in about 85% of people.…”

“…A replaced splenic artery from SMA is very unusual and is expected to happen in less than 1% of individuals (14). Splenic artery aneurysm is more frequently found in patients with cirrhosis and portal hypertension disorders, the underlying etiologies include atherosclerosis, pregnancy, hypertension, arteritis, and trauma (7,14).…”