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P-033 ethanol sclerotherapy of feeding artery and nidal aneurysms in ruptured cerebral arteriovenous malformations
  1. F Settecase,
  2. M Amans,
  3. A Nicholson,
  4. S Hetts,
  5. D Cooke,
  6. C Dowd,
  7. R Higashida,
  8. V Halbach
  1. Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA

Abstract

Background Embolic agents for embolization of cerebral arteriovenous malformations (AVMs) currently include n-BCA, Onyx, particles, and detachable coils. Ethanol sclerotherapy is seldom used in the treatment of cerebral AVMs due to safety concerns.1,2 In some circumstances, however, such as when limited reflux of an embolic agent is permissible, the use of ethanol may be preferable. In this retrospective case series, we report on patients with brain AVMs presenting with acute hemorrhage at our institution in whom ethanol was used to successfully treat a feeding artery aneurysms or intranidal aneurysms.

Methods A keyword search of our neurointerventional database identified 10 patients with cerebral AVM feeding artery aneurysms or intranidal aneurysms treated using ethanol sclerotherapy between 2005 and 2014. Neuroimaging, angiograms, operative reports and electronic medical records were reviewed.

Results 13 feeding artery or intranidal aneurysms were identified in 10 patients, of which 12 were treated with intraarterial ethanol sclerotherapy (Table 1). One of the 13 aneurysms was not treated due to risk of non-target embolization of calcarine artery branches.

Abstract P-033 Table 1

All patients presented with acute intracranial hemorrhage. Dehydrated ethanol 60–80% (70% ethanol was used in 7 of the 10 patients) was delivered slowly under roadmap-mask guidance directly into the artery supplying the aneurysm. Post-therapy angiography to assess for aneurysm occlusion was performed 10–20 min after ethanol injection. Volume of ethanol injected ranged from 2–22 cc (median 3.75 cc) (Table 1). Complete occlusion of the aneurysm was seen in 11/12 treated aneurysms (92%) (Figure 1). Follow-up was available in 9/10 patients (mean follow-up was 1.3 years). None required more than one treatment session and there were no recurrences. A complication was encountered in one patient, who developed hemiparesis and aphasia due to non-target embolization of posterolateral choroidal artery branches to normal brain. No deaths were attributed to ethanol sclerotherapy.

Conclusion In a subset of ruptured cerebral AVMs in which other embolic agents cannot be safely used, ethanol sclerotherapy of feeding artery or nidal aneurysms can be performed with a high degree of technical success and a low rate of permanent neurologic complication.

References

  1. Yakes WF, Krauth L, Ecklund J, et al. Ethanol endovascular management of brain arteriovenous malformations: initial results. Neurosurgery 1997;40(6):1145–52; discussion 52–4

  2. Wong GA, Armstrong DC, Robertson JM. Cardiovascular collapse during ethanol sclerotherapy in a pediatric patient. Paediatric Anaesthesia 2006;16(3):343–6

Disclosures F. Settecase: None. M. Amans: None. A. Nicholson: None. S. Hetts: None. D. Cooke: None. C. Dowd: None. R. Higashida: None. V. Halbach: None.

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