脑动脉瘤线圈栓塞术中不良事件的处理:临床病例系列回顾。

A. Gordhan
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摘要

脑动脉瘤腔内线圈栓塞术的总并发症发生率为5%。这是一个说明性的病例系列,描述了在线圈栓塞期间的管理方面和不良事件的可能诱因,以及相关的影像学和临床结果。脑动脉瘤腔内线圈栓塞术中主要的术中颅内不良事件可分为三类。血栓栓塞、动脉瘤或母血管穿孔/破裂及栓塞相关。在每个类别中讨论具有抢救干预和结果的临床病例。1)血栓栓塞(病例1和2):这是最常见的并发症,也是发病率和死亡率的原因。由于持续和或充分的全身抗凝治疗失败,可能发生血栓栓塞。预防局部血小板和凝血级联激活在血栓形成装置引入线圈栓塞的背景下,是防止部分或完全的父母,分支或远端血管闭塞至关重要。血栓的栓塞性传播可能是由原生血管疾病引起的,也可能是由于在线圈输送和展开过程中机械装置的操作,以及使用辅助工具(如球囊辅助)造成的。经常监测ACT(活化凝血时间)值,以确认两倍的基线值的系统性抗凝肝素是主要的预防方法。术中应用短效和长效糖蛋白IIBIIIA抑制剂溶栓血小板,局部或全身均有效。提高脑灌注压可能增加侧支血流,从而降低缺血性后遗症的风险。在确定腔内血栓后,动脉或外周静脉给予GPIIBIIIA抑制剂可以防止进展为完全血管闭塞。通常在血管线圈/母血管界面处观察到最小的血栓形成。Eptifibatide的半衰期较短(2-4小时),在可能需要进行脑室造口术的破裂动脉瘤中比Abciximab更有优势。在适当的药理学诱导血压升高后服用液体丸,可以增强侧枝血管。血管痉挛可能导致血管口径改变或血流受限。这可以通过局部动脉内钙通道阻滞剂治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Management of Intraprocedural Adverse Events during coil embolization of cerebral aneurysms: A Clinical Case Series Review.
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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