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组织型纤溶酶原激活剂诱导的脑梗死:病例报告。

Tissue Plasminogen Activator-Induced Angioedema Involving a Posterior Cerebral Artery Infarct: A Case Presentation.

机构信息

Department of Medicine, Arnot Ogden Medical Center, Elmira, NY, USA.

出版信息

Am J Case Rep. 2021 Jan 14;22:e927137. doi: 10.12659/AJCR.927137.

DOI:10.12659/AJCR.927137
PMID:33441533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7811978/
Abstract

BACKGROUND Angioedema is characterized by localized swelling of subcutaneous or submucosal tissue resulting from fluid extravasation due to the loss of vascular integrity. It most commonly occurs with exposure to allergens and certain medications, namely nonsteroidal anti-inflammatory agents and angiotensin-converting enzyme inhibitors. There have been few incidences of angioedema following the administration of tissue plasminogen activator. CASE REPORT We describe an 84-year-old woman with a history of hypertension managed with lisinopril who presented with an acute onset of right-sided hemiparesis, slurred speech, and right-sided hemianopsia. Urgent computed tomography of the head revealed subacute infarct of the left pons without hemorrhage. Intravenous alteplase was administered and within 30 min our patient developed severe orolingual edema requiring emergent intubation. Subsequent imaging revealed acute to subacute infarct of the left occipital lobe in the posterior cerebral artery region, consistent with her initial presenting symptoms. CONCLUSIONS Angioedema induced by tissue plasminogen activator occurs in approximately 1-5% of patients receiving thrombolysis for ischemic stroke and can be life-threatening. The risk is increased in patients taking angiotensin-converting enzyme inhibitors, in patients with ischemic strokes of the middle cerebral artery, and in the presence of C1 esterase inhibitor deficiency. This phenomenon is usually self-limited and treatment is supportive, although evidence supports the use of antihistamines, steroids, epinephrine, and complement inhibitors. Due to the severity of angioedema and the potential progression to airway compromise, it is crucial to closely monitor patients receiving tissue plasminogen activator.

摘要

背景

血管性水肿的特征是由于血管完整性丧失导致液体渗出而引起的皮下或粘膜下组织局部肿胀。它最常发生于接触过敏原和某些药物,即非甾体抗炎药和血管紧张素转换酶抑制剂。使用组织型纤溶酶原激活剂后发生血管性水肿的情况很少见。

病例报告

我们描述了一位 84 岁的女性,患有高血压,用赖诺普利治疗,她因右侧偏瘫、言语不清和右侧偏盲急性发作就诊。头部紧急 CT 显示左侧脑桥亚急性梗死,无出血。给予静脉注射阿替普酶,30 分钟内患者出现严重的口周水肿,需要紧急插管。随后的影像学检查显示左侧枕叶后循环大脑后动脉区域的急性至亚急性梗死,与她最初的症状一致。

结论

接受溶栓治疗缺血性卒中的患者中约有 1-5%会发生组织型纤溶酶原激活剂诱导的血管性水肿,可能危及生命。服用血管紧张素转换酶抑制剂、大脑中动脉缺血性卒中以及 C1 酯酶抑制剂缺乏的患者风险增加。这种现象通常是自限性的,治疗是支持性的,尽管有证据支持使用抗组胺药、类固醇、肾上腺素和补体抑制剂。由于血管性水肿的严重程度以及向气道阻塞进展的潜在风险,密切监测接受组织型纤溶酶原激活剂治疗的患者至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/160151191113/amjcaserep-22-e927137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/ee34c0208dbf/amjcaserep-22-e927137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/dc1fbc525aaf/amjcaserep-22-e927137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/160151191113/amjcaserep-22-e927137-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/ee34c0208dbf/amjcaserep-22-e927137-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/dc1fbc525aaf/amjcaserep-22-e927137-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e9/7811978/160151191113/amjcaserep-22-e927137-g003.jpg

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Angioedema in Stroke Patients With Thrombolysis.溶栓治疗的脑卒中患者的血管性水肿。
Stroke. 2019 Jul;50(7):1682-1687. doi: 10.1161/STROKEAHA.119.025260. Epub 2019 Jun 11.
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Angioedema after thrombolysis with tissue plasminogen activator: an airway emergency.
组织型纤溶酶原激活剂溶栓后发生的血管性水肿:气道急症
Oxf Med Case Reports. 2019 Jan 24;2019(1):omy112. doi: 10.1093/omcr/omy112. eCollection 2019 Jan.
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Institutional Incidence of Severe tPA-Induced Angioedema in Ischemic Cerebral Vascular Accidents.缺血性脑血管意外中严重组织型纤溶酶原激活剂诱导的血管性水肿的机构发病率。
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Impact of Bradykinin Generation During Thrombolysis in Ischemic Stroke.缺血性脑卒中溶栓过程中缓激肽生成的影响
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A missense mutation in the plasminogen gene, within the plasminogen kringle 3 domain, in hereditary angioedema with normal C1 inhibitor.在遗传性血管性水肿伴正常C1抑制剂患者中,纤溶酶原kringle 3结构域内的纤溶酶原基因发生错义突变。
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