Chronic ACE-Inhibitor Induced Angioedema Requiring Emergent Nasotracheal Intubation: A Case Report

Jasminder K Malhi
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Abstract

ACE-inhibitor induced angioedema is a rare, potentially life-threatening phenomenon with unpredictable symptoms. With advanced angioedema, orotracheal intubation may not be possible necessitating nasotracheal intubation or cricothyroidotomy. This case describes a 76-year-old male with a history of hypertension controlled with lisinopril-hydrochlorothiazide who developed sudden-onset angioedema. Additionally, this case was complicated by the patient’s anticoagulation after recent abdominal aortic aneurysm repair. The patient’s acute respiratory distress was managed with nasotracheal intubation because of severe edema of the oral cavity including at the base of the tongue without improvement with epinephrine, a corticosteroid, or an antihistamine. He was extubated the following day, but mild edema of the oral cavity and left side of face persisted at discharge 4 days after presentation. When presenting to the emergency room with angioedema mediated via ACE-inhibitor use, time is of the essence to avoid cardiopulmonary arrest secondary to hypoxemia. Rapid identification and management of this condition is key to improve outcomes. After acute management, patients should be advised to avoid all ACE-inhibitors in the future.
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慢性ace抑制剂诱导血管性水肿需要紧急鼻气管插管:1例报告
ACE抑制剂诱导的血管性水肿是一种罕见的、可能危及生命的现象,症状不可预测。对于晚期血管性水肿,经口气管插管可能不可能,需要鼻气管插管或环甲状腺切开术。该病例描述了一名76岁男性,有用赖诺普利氢氯噻嗪控制的高血压病史,他突然出现血管性水肿。此外,该病例因患者近期腹主动脉瘤修复后的抗凝治疗而变得复杂。患者的急性呼吸窘迫是通过鼻气管插管治疗的,因为口腔(包括舌根)严重水肿,肾上腺素、皮质类固醇或抗组胺药没有改善。第二天拔管,但出院后4天,口腔和左侧面部轻度水肿持续存在。当出现通过使用ACE抑制剂介导的血管性水肿到急诊室时,时间至关重要,以避免低氧血症继发的心肺骤停。快速识别和管理这种情况是改善结果的关键。急性治疗后,应建议患者今后避免使用所有ACE抑制剂。
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