Department of Neurosurgery, Daegu-Gyeongbuk Cardiocerebrovascular Center, Kyungpook National University, Daegu, Republic of Korea.
Acta Neurochir (Wien). 2010 May;152(5):771-81. doi: 10.1007/s00701-009-0593-x. Epub 2010 Jan 23.
The present study investigated the incidence of acute rebleeding after successful coil embolization of a ruptured cerebral aneurysm, including clinical outcomes, and possible mechanisms of the events other than coil compaction and/or incomplete embolization.
This study included 591 consecutive patients who presented with aneurysmal subarachnoid hemorrhage, were treated with coil embolization, and whose post-procedural angiography revealed successful embolization. Data were collected retrospectively from six patients who showed acute rebleeding despite that angiographically successful coil embolization was achieved. All clinical, radiological data and intraoperative videos were reviewed to identify causative factors which could have contributed to the occurrence of rebleeding.
Incidence of acute rebleeding after successful coil embolization of ruptured cerebral aneurysm was 1.0% (6/591). In all of these six patients, complete angiographic occlusion was achieved except in one case where a small residual neck was intentionally left to avoid compromise of the parent artery. Four of the six patients showed poor clinical courses, either died or recovered with severe disability. Whenever possible, we performed an immediate craniotomy for exploration and additional clipping. Based on intraoperative findings, we hypothesized that uneven distribution of the coil masses and spontaneous resolution of thrombus among the strands of coil (inter-coil-loop thrombolysis) could be possible mechanisms of rebleeding.
Acute rebleeding is extremely rare, but is possible as a complication of coil embolization of a ruptured cerebral aneurysm even when a case is angiographically successful. The higher degree of morbidity and mortality is a major concern. Therefore, further investigation to discover risk factors and causative mechanisms for such a complication is sorely needed.
本研究调查了破裂脑动脉瘤成功线圈栓塞后急性再出血的发生率，包括临床结果，以及除线圈压实和/或不完全栓塞以外的事件的可能机制。
本研究纳入了 591 例因蛛网膜下腔出血就诊、接受线圈栓塞治疗且术后血管造影显示栓塞成功的连续患者。从 6 例尽管血管造影成功栓塞但仍出现急性再出血的患者中回顾性收集数据。回顾所有临床、影像学资料和术中录像，以确定可能导致再出血的原因。
破裂脑动脉瘤成功线圈栓塞后急性再出血的发生率为 1.0%（6/591）。在这 6 例患者中，除 1 例为避免母动脉狭窄而故意留下小残余颈部外，所有患者均实现完全血管造影闭塞。这 6 例患者中有 4 例临床预后较差，死亡或恢复后严重残疾。只要可能，我们立即进行开颅探查和额外夹闭。根据术中发现，我们假设线圈团块的不均匀分布和线圈之间血栓的自发溶解（线圈间环血栓溶解）可能是再出血的机制。
急性再出血极为罕见，但即使血管造影成功，破裂脑动脉瘤的线圈栓塞也可能发生这种并发症。更高的发病率和死亡率是一个主要关注点。因此，迫切需要进一步研究以发现这种并发症的危险因素和病因机制。
