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服用血管紧张素转换酶抑制剂的患者在使用组织型纤溶酶原激活剂后发生的口咽血管性水肿

Orolingual Angioedema After Tissue Plasminogen Activator Administration in Patients Taking Angiotensin-Converting Enzyme Inhibitors.

作者信息

Burd Megan, McPheeters Chelsey, Scherrer Leigh Ann

机构信息

Department of Pharmacy, University of Louisville Hospital, Kentucky.

出版信息

Adv Emerg Nurs J. 2019 Jul/Sep;41(3):204-214. doi: 10.1097/TME.0000000000000250.

Abstract

Orolingual angioedema is a rare adverse effect (1%-5%) of tissue plasminogen activator (tPA) that can lead to significant morbidity in patients with acute ischemic stroke. It is thought that increased levels of bradykinin and histamine resulting from tPA administration can result in angioedema. Angiotensin-converting enzyme (ACE) inhibitors can also lead to increased levels of bradykinin and appear to be a risk factor for tPA-associated angioedema. A literature review was conducted to examine previous cases of orolingual angioedema associated with tPA administration in patients also taking ACE inhibitors to better understand the relationship between ACE inhibitors and tPA-induced angioedema. Over a 20-year period, 27 patients who experienced angioedema with tPA while on ACE inhibitor therapy were identified. In this patient population, the onset of angioedema symptoms appeared as soon as 15 min after the tPA bolus and as late as 2 hr after the tPA infusion. Most patients required a combination of supportive medications such as corticosteroids (81.5%), antihistamines (74%), and epinephrine (18.5%) for the management of angioedema. Severe presentations of orolingual angioedema resulted in intubation for airway protection (26%). Symptom resolution ranged from shortly after the administration of supportive medications to 72 hr after symptom onset. Orolingual angioedema after tPA administration has the potential to cause significant morbidity, indicating patients should be monitored closely for a few hours after administration for the development of airway compromise. ACE inhibitors should not be the preferred antihypertensive agents for patients who require blood pressure lowering prior to tPA administration.

摘要

口咽血管性水肿是组织型纤溶酶原激活剂(tPA)罕见的不良反应(1%-5%),可导致急性缺血性中风患者出现严重发病情况。据认为,tPA给药导致缓激肽和组胺水平升高可引发血管性水肿。血管紧张素转换酶(ACE)抑制剂也可导致缓激肽水平升高,似乎是tPA相关血管性水肿的一个危险因素。进行了一项文献综述,以研究在服用ACE抑制剂的患者中与tPA给药相关的口咽血管性水肿的既往病例,以便更好地了解ACE抑制剂与tPA诱导的血管性水肿之间的关系。在20年期间,确定了27例在接受ACE抑制剂治疗时使用tPA后出现血管性水肿的患者。在这个患者群体中,血管性水肿症状最早在tPA推注后15分钟出现,最晚在tPA输注后2小时出现。大多数患者需要联合使用皮质类固醇(81.5%)、抗组胺药(74%)和肾上腺素(18.5%)等支持性药物来治疗血管性水肿。口咽血管性水肿的严重表现导致为保护气道进行插管(26%)。症状缓解时间从给予支持性药物后不久到症状出现后72小时不等。tPA给药后发生的口咽血管性水肿有可能导致严重发病,这表明在给药后应密切监测患者数小时,以防出现气道受损情况。对于在tPA给药前需要降低血压的患者,ACE抑制剂不应作为首选的抗高血压药物。

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