Abstract Number ‐ 136: Aspirin Desensitization in Cerebral Aneurysms and Management for the Neurointerventionalist

Introduction Aspirin (ASA) is the pillar of cerebrovascular and systemic vascular disease management. ASA allergy/hypersensitivity presents a challenge to the NeuroInterventionalist due to difficulties achieving optimum medical management prior to and after neurointerventional treatment. Currently there is vast cardiovascular literature describing successful ASA desensitization protocols, however the same cannot be said for neurointervention.The purpose of our study was to describe our experience with ASA hypersensitivity management in cerebrovascular disease and review of the relevant literature in patients with aneurysms. We present two cases of patients with cerebrovascular aneurysms requiring neurointervention with a pipeline embolization device who were successfully desensitized to their ASA hypersensitivity prior to treatment and the different variables encountered/approach for each patient. Methods N/A Results 37 yo F with history of pre‐eclampsia while pregnant with twins presented with complaints of a severe headache 22 days after delivery and on MRA head and neck had unruptured bilateral paraclinoid para‐ophthalmic internal carotid artery aneurysms. She was placed on Brilinta instead of Plavix due to subtherapeutic PruTest. She underwent successful endovascular coil embolization of the unruptured RIGHT paraclinoid para‐ophthalmic internal carotid artery aneurysm. Post coil embolization she underwent desensitization in the ICU for ASA under the care of the ICU physician and the allergist; 1mg, 5mg, 10mg, 20mg, 45mg ‐ each given 30 min apart. The protocol was followed by ASA 81mg the next morning and had successful endovascular flow diversion with Pipeline Flex Embolization Device for LEFT paraclinoid para‐ophthalmic internal carotid artery aneurysm. 71 yo F with history of uncontrolled HTN. During her hypertensive work‐up was found to have an approximately 6 mm unruptured right internal carotid artery aneurysm on CTA. She was successfully desensitized to ASA and optimized with Aspirin and Brilinta. She underwent successful endovascular flow diversion with Microvention FRED X Flow Diverter of the unruptured medially directed right paraclinoid ophthalmic segment internal carotid artery aneurysm. Conclusions There are few reports of ASA desensitization in patients with cerebral aneurysms ‐ due to this there are few established set protocols. We describe our protocol for high risk patients and post‐op management of patients undergoing neurointerventional procedures.We report these 2 case reports to help add to the current literature of ASA desensitization utilization in patients with CNS aneurysms and may help create more standardized protocols

Abstract 1122‐000013: Spinal Dural Arterio‐Venous Fistula: A Masquerade as a Longitudinal Myelitis

Introduction: SDAVF are rare and frequently misdiagnosed due to their nonspecific symptomatology and delay of presentation on imaging. Spinal digital subtraction angiogram is the gold standard diagnostic test. Delayed diagnosis and treatment of SDAVF can lead to irreversible neurologic damage. Methods: None Results: Two female patients, 69 and 74 years old, each developed recurrent episodes of subacute worsening myelopathy and urinary retention. The subacute onset of symptoms and longitudinal appearance on cord imaging raised concern for inflammatory myelitis. Despite a negative CSF analysis, and the absence of serum inflammatory, metabolic and infectious markers, the working diagnosis was seronegative neuromyelitis optica spectrum disorder. In accordance, both patients were treated with plasma exchange and IV rituximab, initially displaying stabilization on imaging. However, further worsening and extension of the myelopathy alongside the presence of flow voids in one patient’s repeat MRI nine months post‐presentation raised the question of an alternate etiology. A spinal angiogram was ordered for the patient, revealing SDAVF. Subsequently, the patient underwent complete Onyx embolization of the right L2 feeder and surgical clipping of the right L1 feeder. This resulted in stabilization and improvement of symptoms. Although the second patient did not display flow voids in their MRI, they were ordered a spinal angiogram due to their similar clinical course, indeed confirming SDAVF. The patient underwent successful complete embolization of the L3 segmental artery on the right resulting in improvement of symptoms. Conclusions: Clinicians should have a high index of suspicion for SDAVF when a patient presents with a longitudinally extensive transverse myelitis negative for inflammatory markers and is unresponsive to treatment. While the appearance of flow voids on imaging is a helpful diagnostic feature, these may not be present in patients