A cerebral arteriovenous malformation (AVM) is a congenital vascular lesion of the brain composed of a complex tangle of arteries and veins, which are linked by one or more fistulae [1]. Arterial blood is shunted through the AVM directly to the venous system, precluding arterial blood from perfusing adjacent brain structures. The most common presentation of this disease is cerebral hemorrhage secondary to AVM rupture, with an associated mortality of 15% and a morbidity of 50% [1]. One modality to treat this pathology is endovascular embolization. Generally, endovascular embolization serves as an adjunct treatment to either surgery or radiosurgery, but is a curative treatment in approximately 15% of AVM cases [2]. The most common embolic agent used to occlude AVMs is a mixture of n-butyl 2-cyanoacrylate (NBCA) and Lipiodol®. NBCA is a rapidly polymerizing liquid adhesive that polymerizes with contact to blood. Lipiodol® is an ethiodized oil, which imparts radiopacity to the embolic mixture. Moreover, Lipiodol® has been reported to delay the polymerization of NBCA [3]. To further increase the polymerization time of NBCA, minute quantities of glacial acetic acid (GAA) may be added to the embolic mixture.

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