Neurosurgical review · 2025
Earlier onset of cerebral vasospasm in ruptured infectious intracranial aneurysms.
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Zohdy Youssef M, Lamanna Jason, Bsn Laurie Dimisko, Grossberg Jonathan A, Barrow Daniel L, Cawley C Michael, Saad Hassan, Akbik Feras, Pradilla Gustavo, Garzon-Muvdi Tomas, Sadan Ofer, Samuels Owen B, Alawieh Ali M, Howard Brian M
Аннотация
INTRODUCTION: Infectious intracranial aneurysms(IIAs) are a rare complication of systemic and intracranial infections. IIAs are often diagnosed upon rupture, often leading to subarachnoid hemorrhage(SAH) similar to non-infectious aneurysms(non-IIAs). Although vasospasm is a common complication of both SAH and meningitis, the incidence, timing, and management of vasospasm in IIA patients are yet to be studied.
METHODS: This is a retrospective study of patients presenting with SAH secondary to IIAs or non-IIAs between 2015 and 2023. Patients with SAH who died within 48 h were excluded. Patients' charts were reviewed for demographics, imaging findings, management, and the timing, severity, and management of vasospasm. Propensity-score-matching was used to compare patients with IIAs versus non-IIAs. Primary outcome included incidence of vasospasm. Secondary outcomes included time to vasospasm, and treatment response.
RESULTS: Twenty patients with ruptured IIAs were included in this study of which 30%(n = 6) developed vasospasm. Among patients with vasospasm, 83% had neurological deficits due to vasospasm. Vasospasm was managed using intrathecal nicardipine in 5 patients(83%), while 2 patients required intra-arterial vasodilators. Compared to propensity-score-matched non-IIAs, patients with IIAs had a comparable rate of vasospasm(30%vs39%,P = 0.448). However, patients with IIAs developed vasospasm significantly earlier with a mean time from rupture to vasospasm of 3.5 ± 1.05days compared to 5.27 ± 3.15days in non-IIAs(P = 0.002).
CONCLUSION: Patients with ruptured IIAs are at a similar risk of vasospasm compared to non-IIAs; however, they develop symptomatic and radiographic evidence of vasospasm earlier in the course of their disease. These findings argue for the need for routine and early screening for vasospasm in patients with ruptured IIAs.
METHODS: This is a retrospective study of patients presenting with SAH secondary to IIAs or non-IIAs between 2015 and 2023. Patients with SAH who died within 48 h were excluded. Patients' charts were reviewed for demographics, imaging findings, management, and the timing, severity, and management of vasospasm. Propensity-score-matching was used to compare patients with IIAs versus non-IIAs. Primary outcome included incidence of vasospasm. Secondary outcomes included time to vasospasm, and treatment response.
RESULTS: Twenty patients with ruptured IIAs were included in this study of which 30%(n = 6) developed vasospasm. Among patients with vasospasm, 83% had neurological deficits due to vasospasm. Vasospasm was managed using intrathecal nicardipine in 5 patients(83%), while 2 patients required intra-arterial vasodilators. Compared to propensity-score-matched non-IIAs, patients with IIAs had a comparable rate of vasospasm(30%vs39%,P = 0.448). However, patients with IIAs developed vasospasm significantly earlier with a mean time from rupture to vasospasm of 3.5 ± 1.05days compared to 5.27 ± 3.15days in non-IIAs(P = 0.002).
CONCLUSION: Patients with ruptured IIAs are at a similar risk of vasospasm compared to non-IIAs; however, they develop symptomatic and radiographic evidence of vasospasm earlier in the course of their disease. These findings argue for the need for routine and early screening for vasospasm in patients with ruptured IIAs.