McKnight Brain Institute, Department of Neurosurgery, University of Florida, Gainesville, Florida, USA.
Department of Neurocritical Care, University of Florida, Gainesville, Florida, USA.
World Neurosurg. 2020 Dec;144:209-212. doi: 10.1016/j.wneu.2020.09.089. Epub 2020 Sep 22.
Perimesencephalic nonaneurysmal subarachnoid hemorrhage (PNSH) is characterized by a typical pattern of localized pretruncal hemorrhage on head computed tomography. PNSH is usually associated with a benign clinical course and a lower incidence of complications. The etiology is unknown, but many explanations have been proposed, including venous injury or rupture followed by thrombosis of a ruptured microaneurysm.
A 48-year-old man on apixaban for multiple venous thromboembolisms presented with the worst headache of his life associated with blurry vision, nausea, and neck stiffness. Computed tomography demonstrated a perimesencephalic pattern of blood (Hunt and Hess grade 2, Fisher grade 3). Computed tomography angiography and 6-vessel digital subtraction angiography demonstrated no precipitating cause. Systemic tissue plasminogen activator (tPA) was administered on postbleed day 8 owing to obstructive shock from saddle pulmonary embolism and pulseless electrical activity. He was safely discharged to rehabilitation with moderate neurological deficits attributed to ischemic effects of his cardiac arrest.
Symptomatic saddle pulmonary embolism in the setting of intracranial hemorrhage creates conflicting risks of medical intervention. There are no case reports or evidence of the use of systemic thrombolysis in the setting of SAH. Owing to the benign natural history of PNSH, tPA may be a safe intervention. Neurointensivists and neurosurgeons should be aware that intravenous tPA was used safely for life-threatening pulmonary embolism in the setting of PNSH. Additionally, the use of tPA without resultant rebleeding in this case opposes the theory of the presence of a thrombosed ruptured microaneurysm.
脑桥旁非动脉瘤性蛛网膜下腔出血(PNSH)的特征是头部计算机断层扫描显示典型的局限性前颅窝出血模式。PNSH 通常与良性临床病程和较低的并发症发生率相关。其病因不明,但提出了许多解释,包括静脉损伤或破裂后破裂的微动脉瘤血栓形成。
一名 48 岁男性因多发静脉血栓栓塞症服用阿哌沙班,出现一生中最严重的头痛,伴有视力模糊、恶心和颈部僵硬。计算机断层扫描显示有脑桥旁出血模式(Hunt 和 Hess 分级 2 级,Fisher 分级 3 级)。计算机断层血管造影和 6 血管数字减影血管造影未发现促发原因。由于鞍状肺栓塞和无脉电活动引起的阻塞性休克,在出血后第 8 天给予全身组织型纤溶酶原激活剂(tPA)。他因心脏骤停的缺血影响而出现中度神经功能缺损,安全出院至康复科。
颅内出血合并症状性鞍状肺栓塞会产生相互冲突的治疗风险。在蛛网膜下腔出血的情况下,没有关于全身溶栓的病例报告或证据。鉴于 PNSH 的良性自然史,tPA 可能是一种安全的干预措施。神经重症监护医生和神经外科医生应该意识到,在 PNSH 情况下,静脉内 tPA 可安全用于危及生命的肺栓塞。此外,在这种情况下,tPA 的使用没有导致再出血,这与存在血栓形成的破裂微动脉瘤的理论相悖。