Lim Jaims, Shallwani Hussain, Vakharia Kunal, Siddiqui Adnan H
Department of Neurosurgery, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York.
Department of Neurosurgery, Gates Vascular Institute at Kaleida Health, Buffalo, New York.
Oper Neurosurg (Hagerstown). 2020 Jun 1;18(6):E184-E190. doi: 10.1093/ons/opz330.
Few studies describe the use of adenosine-induced cardiac systole for treatment of cerebrovascular pathologies. We describe a midbrain arteriovenous malformation (AVM) treated with transvenous embolization using adenosine-induced asystole to achieve transient systemic hypotension with the purpose of furthering discussion on the technique and operative considerations for adenosine use in endovascular AVM treatments.
A 29-yr-old man presented with sudden onset of severe bilateral headache, blurred vision, and numbness on the right side of his face and tongue. Noncontrast head computed tomography revealed fourth ventricle hemorrhage. Diagnostic cerebral angiography revealed a high-flow midbrain AVM with a posterior wall perforator from the basilar artery terminus and a draining vein into the straight sinus. Transarterial AVM embolization was successful. The patient was discharged with no residual neurological deficits but returned 1 wk later with slurred speech and left-sided dysmetria. Repeat angiography revealed partial AVM filling. Attempts at transarterial embolization were unsuccessful. Thus, transvenous AVM embolization with adenosine-induced cardiac asystole and systemic hypotension was performed. A total of 60 mg of adenosine was administered, followed by 2 additional doses of 60 and 40 mg; and complete cardiac asystole with a mean arterial pressure of 40 mmHg was maintained, resulting in successful embolization of the AVM. No residual filling was visualized on postembolization arterial angiography runs. The patient was neurologically stable and discharged on postoperative day 2.
With appropriate and safe dosing, adenosine-induced asystole and systemic hypotension may be a feasible, safe option to reduce flow and assist endovascular transvenous embolization of high-flow AVMs.
很少有研究描述使用腺苷诱导心脏停搏来治疗脑血管疾病。我们描述了一例中脑动静脉畸形(AVM),采用经静脉栓塞术,利用腺苷诱导心脏停搏以实现短暂的全身低血压,目的是进一步探讨在血管内AVM治疗中使用腺苷的技术及手术注意事项。
一名29岁男性,突发严重双侧头痛、视力模糊,右侧面部及舌部麻木。头颅非增强计算机断层扫描显示第四脑室出血。诊断性脑血管造影显示一个高流量中脑AVM,有来自基底动脉末端的后壁穿支动脉及一条引流静脉汇入直窦。经动脉AVM栓塞成功。患者出院时无残留神经功能缺损,但1周后因言语不清和左侧辨距不良再次入院。重复血管造影显示AVM部分充盈。经动脉栓塞尝试未成功。因此,进行了经静脉AVM栓塞术,采用腺苷诱导心脏停搏及全身低血压。共给予60mg腺苷,随后追加2剂,分别为60mg和40mg;维持完全性心脏停搏,平均动脉压为40mmHg,AVM栓塞成功。栓塞后动脉血管造影未见残留充盈。患者神经功能稳定,术后第2天出院。
通过适当且安全的给药,腺苷诱导的心脏停搏和全身低血压可能是一种可行、安全的选择,可减少血流并辅助高流量AVM的血管内静脉栓塞。