A large series of true pancreaticoduodenal artery aneurysms.

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INTRODUCTION: True pancreaticoduodenal artery aneurysms (PDAAs) are rare, and prior reports often fail to distinguish true aneurysms from pseudoaneuryms. We sought to characterize all patients who presented to our health system from 2004 to 2019 with true PDAAs, with a focus on risk factors, interventions, and patient outcomes.

METHODS: Patients were identified by querying a single health system picture archiving and communication system database for radiographic reports noting a PDAA. A retrospective chart review was performed on all identified patients. Patients with pseudoaneurysm, identified as those with a history of pancreatitis, abdominal malignancy, hepatopancreaticobiliary surgery, or abdominal trauma, were excluded. Continuous variables were compared using t-tests, and categorical variables were compared using Fisher's exact tests.

RESULTS: A total of 59 true PDAAs were identified. Forty aneurysms (68%) were intact (iPDAAs) and 19 (32%) were ruptured (rPDAAs) at presentation. The mean size of rPDAAs was 16.4 mm (median size, 14.0 mm; range, 10-42 mm), and the mean size of iPDAAs was 19.4 mm (median size, 17.5 mm; range, 8-88 mm); this difference was not statistically significant (P = .95). Significant celiac disease (occlusion or >70% stenosis) was noted in 39 aneurysms (66%). Those with rupture were less likely to have significant celiac disease (42% vs 78%; P = .017) and less likely to have aneurysmal wall calcifications (6% vs 53%; P = .002). Thirty-seven patients underwent intervention (63%), with eight (22%) undergoing concomitant hepatic revascularization (two stents and six bypasses) due to the presence of celiac disease. Eighteen patients with occluded celiac arteries underwent aneurysm intervention; of those, 11 were performed without hepatic revascularization (61.1%). Those with rPDAAs experienced an aneurysm-related mortality of 10.5%, whereas those with iPDAAs experienced a rate of 5.6%. One patient with celiac occlusion and PDA rupture who did not undergo hepatic artery bypass expired postoperatively from hepatic ischemia. rPDAAs showed a trend toward the increased need for aneurysm-related endovascular or open reintervention, but this was not statistically significant (47% vs 28%; P = .13).

CONCLUSIONS: These findings support previous reports that the rupture risk of PDAAs is independent of size, their development is often associated with significant celiac stenosis or occlusion, and rupture risk appears decreased in patients with concomitant celiac disease or aneurysm wall calcifications. Endovascular intervention is the preferred initial treatment for both iPDAAs and rPDAAs, but reintervention rates are high in both groups. The role for hepatic revascularization remains uncertain, but it does not appear to be mandatory in all patients with complete celiac occlusion who undergo PDAA interventions.





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Medicine and Health Sciences




Department of Medicine, Cardiology Division

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