J Neurol Surg A Cent Eur Neurosurg 2020; 81(02): 177-184
DOI: 10.1055/s-0039-1693108
Case Report
Georg Thieme Verlag KG Stuttgart · New York

Early Rupture of a Giant Basilar Artery Aneurysm after LEO Stenting: Case Report and Review of the Literature

1   Department of Neurosurgery, Kantonsspital Aarau (KSA), Tellstrasse, Aarau, Switzerland
,
Jenny Kienzler
1   Department of Neurosurgery, Kantonsspital Aarau (KSA), Tellstrasse, Aarau, Switzerland
,
Beda Muehleisen
2   Department of Pathology, Kantonsspital Aarau (KSA), Aarau, Switzerland
,
Michael Diepers
3   Division of Neuroradiology, Kantonsspital Aarau, Aarau, Switzerland
,
Javier Fandino
1   Department of Neurosurgery, Kantonsspital Aarau (KSA), Tellstrasse, Aarau, Switzerland
,
Luca Remonda
3   Division of Neuroradiology, Kantonsspital Aarau, Aarau, Switzerland
,
1   Department of Neurosurgery, Kantonsspital Aarau (KSA), Tellstrasse, Aarau, Switzerland
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Publikationsverlauf

17. Dezember 2018

02. April 2019

Publikationsdatum:
14. Januar 2020 (online)

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Abstract

Background Advances in the endovascular armamentarium, such as flow diversion and stenting devices, provide treatment options for posterior circulation intracranial aneurysms (IAs) with complex angioarchitecture. Delayed IA rupture following flow diversion is a rare but often fatal complication. Giant IAs likely pose a higher risk because of the extensive clot formation and its suspected detrimental effect on the aneurysmal wall. However, mechanisms that lead to delayed rupture are poorly understood, and few cases provide thorough documentation of macroscopic and histologic findings.

Clinical Presentation After our 60-year-old patient with a giant basilar aneurysm underwent treatment with a LEO stent, the postoperative clinical course remained uneventful until day 4 when he suffered an unexpected fatal subarachnoid hemorrhage (SAH). Autopsy demonstrated extensive hemorrhage, large intraluminal thrombus, and ruptured IA wall. The aneurysm, which ruptured linearly, was completely filled with a clot that seemed to have outgrown the thin aneurysm wall. Histologic specimens revealed thinning and degenerative changes of the aneurysm's wall, and sparse neutrophilic and histiocytic inflammatory infiltrate adjacent to the rupture site, a finding consistent with recently published cases of IA rupture.

Conclusions Our case report highlighting the clinical course and autopsy findings of a fatal SAH shortly after stenting this giant basilar artery aneurysm adds to the few previously reported fatal cases of IA rupture after endovascular treatment. Our macroscopic and histologic findings suggested that multimodal changes of inflammation, wall sheer tress (mechanical), and recanalization were involved.