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一例血管紧张素受体阻滞剂治疗患者的创伤相关气道血管性水肿病例。

A Case of Trauma-Related Angioedema of the Airway in a Patient on an Angiotensin Receptor Blocker.

机构信息

Department of Internal Medicine, Piedmont Athens Regional Medical Center, Athens, GA, USA.

出版信息

Am J Case Rep. 2024 Feb 28;25:e943407. doi: 10.12659/AJCR.943407.

DOI:10.12659/AJCR.943407
PMID:38414232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10914075/
Abstract

BACKGROUND Angioedema is non-pitting edema that occurs in the deep layers of the skin and subcutaneous tissue due to vascular leakage of plasma resulting from 1 of 2 major pathophysiological processes: mast cell-mediated angioedema and bradykinin-mediated angioedema. While it is a well-recognized adverse reaction of angiotensin-converting enzyme inhibitors, the association of angioedema with angiotensin receptor blockers is relatively less studied. Direct local trauma, although rarely, has been suggested to induce angioedema under certain conditions. We present a unique case of direct, local, trauma-related angioedema in a patient on an angiotensin receptor blocker. CASE REPORT The patient, an 83-year-old woman on telmisartan for hypertension, hit her neck against the edge of a chair during a fall. Shortly thereafter, she developed progressive airway compromise due to airway angioedema, as noted on direct laryngoscopy. A contrast CT scan of the neck also noted edema of the periglottic and supraglottic regions. She required intravenous corticosteroid administration and intubation in the emergency room and was successfully extubated 3 days after admission. She had no prior history of angioedema or allergy. We hypothesize that increased levels of circulatory bradykinin in the setting of telmisartan, combined with a local release of bradykinin from trauma, was the main pathophysiologic cause of the angioedema. CONCLUSIONS This case report highlights the rare and often forgotten adverse reaction of angioedema with use of angiotensin receptor blockers and confirms the finding of local trauma as a possible trigger.

摘要

背景

血管性水肿是由于血浆从血管中漏出导致的深层皮肤和皮下组织的非凹陷性水肿,这是由两种主要病理生理过程之一引起的:肥大细胞介导的血管性水肿和缓激肽介导的血管性水肿。虽然血管紧张素转换酶抑制剂的不良反应广为人知,但血管紧张素受体阻滞剂与血管性水肿的关联相对较少研究。尽管很少见,但有研究提示,在某些情况下,直接局部创伤可能会引发血管性水肿。我们报告了一例在使用血管紧张素受体阻滞剂的患者中发生的直接、局部、与创伤相关的血管性水肿的独特病例。

病例报告

患者为一名 83 岁女性,因高血压服用替米沙坦,在跌倒时颈部撞到椅子边缘。此后不久,她因气道血管性水肿导致气道逐渐阻塞,直接喉镜检查发现。颈部对比 CT 扫描还发现会厌和声门上区域水肿。她在急诊室需要静脉注射皮质类固醇和插管,并在入院后 3 天成功拔管。她没有血管性水肿或过敏的既往病史。我们假设替米沙坦引起的循环中缓激肽水平升高,加上创伤引起的局部缓激肽释放,是血管性水肿的主要病理生理原因。

结论

本病例报告强调了血管紧张素受体阻滞剂使用时血管性水肿这一罕见且常被遗忘的不良反应,并证实了局部创伤可能是一个潜在的触发因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbd/10914075/76bba8ebca7c/amjcaserep-25-e943407-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbd/10914075/66fcfba65bd5/amjcaserep-25-e943407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbd/10914075/76bba8ebca7c/amjcaserep-25-e943407-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbd/10914075/66fcfba65bd5/amjcaserep-25-e943407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbd/10914075/76bba8ebca7c/amjcaserep-25-e943407-g002.jpg

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