Abstract
The overall complication rate for endovascular coil embolization of cerebral aneurysms is 5% percent. This is an illustrative case series that describes management aspects and probable precipitants of adverse events during coil embolization and related imaging and clinical outcomes. Major intraprocedural intracranial adverse events during endovascular coil embolization of cerebral aneurysms can be divided into three categories. Thromboembolic, aneurysm or parent vessel perforations/ruptures and embolysate related. Clinical case examples with rescue intervention and outcomes are discussed within each category. 1) Thromboembolic (Case 1 and 2): This is the most frequent complication and cause of morbidity and mortality. Thromboembolic may occur consequent to failure of sustained and or sufficient systemic anticoagulation. Prevention of localized platelet and clotting cascade activation in the context of thrombogenic device introduction for coil embolization is vital in preventing partial or complete parent, branch or distal vessel occlusion. Embolic propagation of thrombus may arise from native vessel disease and or consequent to mechanical device manipulation during coil delivery and deployment, as well as with the use of adjuncts such as balloon assist. Frequent monitoring of ACT (Activated Clotting Time) values for systemic anticoagulation with Heparin to confirm twice the baseline value is the primary preventative method. Intraprocedural pharmacologic platelet thrombus dissolution with short and long acting Glycoprotein IIBIIIA inhibitors are effective when administered locally or systemically. Raising cerebral perfusion pressure may augment collateral flow with consequent reduction in the risk of ischemic sequelae. Intra arterial or peripheral venous administration of GPIIBIIIA inhibitors upon identification of intraluminal thrombus may prevent progression to complete vascular occlusion. Minimal thrombus formation at the coil/parent vessel interface is often observed. Eptifibatide has a shorter half life (2-4 hours) and is advantageous over Abciximab in ruptured aneurysm that potentially require post procedural placement of a ventriculostomy. A fluid bolus followed by appropriate pharmacologic induction of increased blood pressure allows for augmentation of collateral vasculature. Vessel caliber change or limitation of flow may be consequent to vasospasm. This can be addressed by localized intra arterial calcium channel blocker administration.
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