Double trouble: tPA-induced angioedema

医学 血管性水肿 C1抑制剂 阿司匹林 缓激肽 内科学 皮肤病科 赖诺普利 胃肠病学 血管紧张素转换酶 外科 受体 血压
作者
Balaji Krishnaiah,Daniel P. McLaughlin,Jennifer Lee,David C. Good
出处
期刊:Postgraduate Medical Journal [BMJ]
卷期号:93 (1096): 103-104 被引量:4
标识
DOI:10.1136/postgradmedj-2016-134501
摘要

Angioedema results from the release of one or more mediators, most often histamine and bradykinin, in the deeper layers of the skin and mucous membranes. There is an increase in vascular permeability of the affected tissue that leads to asymmetric, non-dependent and non-pitting swelling. There are several types of angioedema, including hereditary angioedema (HAE) types I and II, HAE with normal C1 inhibitor (C1-INH or type III), non-allergic ACE inhibitor (ACEI)-induced angioedema (ACEI-AAE) and acquired angioedema due to C1-INH deficiency (C1-INH-AAE).1 The most well-documented cause of drug-induced angioedema is secondary to ACEI use, and attacks commonly affect the head and neck, particularly the mouth, tongue and larynx.1 The reported incidence of ACEI-AAE is 0.1%–2%; however, other medications are capable of causing similar symptoms. Angioedema of the tongue subsequent to intravenous tissue plasminogen activator (tPA) is rare with prevalence of 0.2%–5.1%.2 A 70-year-old, right-handed, Caucasian male with a history of hypertension and diabetes mellitus presented with witnessed left facial droop, left-sided hemiparesis, hemisensory loss and right gaze deviation <1 hour prior. His home medications included lisinopril 10 mg daily, metformin 500 mg twice daily and aspirin 325 mg daily. He has no known medication or food allergies and also has no family history of angioedema. The patient’s initial non-contrast CT scan was negative for acute intracranial abnormality. He received intravenous tPA. He initially showed improvement defined by no longer has gaze deviation and improvement in his weakness. He then proceeded to deteriorate with examination findings reverting to his initial status, but with increased swelling of tongue 30 min after tPA administration. The tongue oedema reportedly began on the left side and progressed to involve the entire tongue. Patient had difficulty speaking and swallowing secretions. As a result, anaesthesia was contacted for emergency intubation. Otolaryngology was consulted due to concern for lingual haematoma. A fibreoptic endoscope revealed left arytaenoid water bag oedema and the rest of the cavity was difficult to visualise due to the nasotracheal tube. So his tongue swelling was deemed secondary to angioedema. His angioedema resolved over the next 24 hours after intravenous Solu-Medrol and diphenhydramine.

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