E-024 Intra-arterial nimodipine injection for the treatment of cerebral vasospasm following aneurysm subarachnoid hemorrhageand the factors associated with delayed cerebral infarction. (23rd July 2017)

• Record Type: Journal Article
• Authors: Park, K; Kim, B; Park, D; Lee, N
• Is Part Of: Journal of neurointerventional surgery. Volume 9(2017)Supplement 1
• Page Start: A52
• Page End: A52
• Publication Date: 2017-07-23
• Subjects: Nervous system -- Surgery -- Periodicals; Cerebrovascular disease -- Surgery -- Periodicals; 617.48
• DOI: 10.1136/neurintsurg-2017-SNIS.96
• Languages: English
• ISSNs: 1759-8478

Abstract

Abstract : Objective: The purpose of this study was to evaluate the effectiveness of neuro-interventional treatment through intra-arterial nimodipine (IAN) injection for cerebral vasospasm occurring after aneurysmal subarachnoid hemorrhage (SAH), and to describe the factors associated with delayed cerebral infarction in aneurysmal SAH patients treated with IAN in a single institute during a recent 5 year period. Methods: We retrospectively reviewed the data of 73 patients who underwent aneurysm clipping or coiling for ruptured cerebral aneurysm and who received IAN following presenting with symptomatic vasospasm. The effectiveness of IAN was assessed by angiographical change of vessel diameter, and by any improvements in clinical symptoms. Various patient parameters and angiographic characteristics of vasospasm were recorded, and the predictors of delayed cerebral infarction were evaluated with a linear regression analysis. Results: Positive angiographic response was observed in 53 of 73 patients with a mean of 35% of diameter increase. For thirty-eight patients, clinical improvements indicated by increase Glasgow Coma Scale (GCS) scores over two points) were shown after IAN, and there was positive correlation between the change in GCS scores after IAN and the improvement of vessel diameter (p=0.034). Despite IAN treatment, delayed cerebral infarction developed in eleven patients. The vasospasm occurring in dominantly contralateral side to ruptured aneurysm (p=0.0213) and premorbid atherosclerosis in cerebral vessels (p=0.016) were significantly associated with delayed cerebral infarction. Conclusions: IAN seems to be reasonable treatment for symptomatic vasospasm after aneurysm subarachnoid hemorrhage. However, the treatment is not always prevent delayed cerebral infarction. The premorbid cerebral atherosclerosis and the pattern of vasospasm is likely to affect the treatment results of IAN. Disclosures: K. Park: None. B. Kim: None. D. Park: None. N. Lee: None.