Article
Effect of intracranial aneurysm repair treatment modality on the risk of delayed cerebral ischemia after aneurysmal subarachnoid haemorrhage
Einfluss der Behandlungsmodalität intrakranieller Aneurysmen auf das Risiko von verzögerter zerebraler Ischämie nach aneurysmatischer Subarachnoidalblutung
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Authors
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Amr Abdulazim
- Universitätsklinikum Mannheim, Klinik für Neurochirurgie, Mannheim, Deutschland
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Katharina Hackenberg
- Universitätsklinikum Mannheim, Klinik für Neurochirurgie, Mannheim, Deutschland
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R. Loch Macdonald
- University of Toronto, Division of Neurosurgery, Toronto, Canada; University of California San Francisco, Department of Neurosurgery, Fresno, CA, United States
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Daniel Hänggi
- Universitätsklinikum Mannheim, Klinik für Neurochirurgie, Mannheim, Deutschland
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Nima Etminan
- Universitätsklinikum Mannheim, Klinik für Neurochirurgie, Mannheim, Deutschland
| Published: | June 26, 2020 |
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Outline
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Objective: In the management of patients with aneurysmal subarachnoid haemorrhage, surgical intracranial aneurysm (IA) repair has been previously reported as a detrimental determinant for the risk of delayed cerebral ischemia (DCI). To further elucidate this, we compared data of a prospective-randomized Phase III trial (NEWTON-II) with our institutional aSAH cohort with respect to the incidence of DCI and functional Outcome in relation to treatment modality for IA.
Methods: The NEWTON-II study cohort included 285 aSAH patients with WFNS grades II-IV. This cohort was compared to an aSAH cohort including 81 aSAH patients with WFNS grades II-IV that were treated at our institution between January 2016 and July 2018. Exploratory statistics and logistic regression analyses were performed to investigate whether IA modality is associated with the risk of DCI after aSAH.
Results: The two cohorts were comparable with respect to age, sex, and WFNS grade distribution though the proportion of Fisher grade III/IV SAH was higher in the NEWTON-II study cohort (94.0% vs. 86.4%, p=0.02) (Table 1 [Tab. 1]). However, the proportion of clipping procedures for IA repair was significantly higher in our institutional aSAH cohort (59.3% vs. 35.4%, OR: 2.65 [1.60-4.39]) and consecutively higher rates of clinical DCI (49.4% vs. 26.7%, OR: 2.68 [1.61-4.62]). However, after adjustment for treatment modality, there was no association of aneurysm repair modality and the risk of DCI as the odds ratio did not differ decisively (aOR: 2.74 [1.63-4.62]). Treatment modality was also not a determinant for DCI risk according to individual WFNS groups in the logistic regression model. Comparing only patients who received clipping in both cohorts still showed a significantly higher odds for DCI in our institutional cohort (50% vs. 31.2% OR: 3.21 [1.72-5.98]). The DCI associated infarction rate was comparable, however functional outcome at 3 months was significantly better in our institutional cohort (OR: 2.89 [1.65-5.09]) (Table 2 [Tab. 2]).
Conclusion: Our data refutes the previous notion that surgical IA repair is an additional risk factor for DCI and indicate that factors other WFNS grade, Fisher or IA repair modality determine the risk of DCI and the proportion of overall functional outcome.
