Epinephrine induced lactic acidosis during the management of anaphylactic shock: a case report.

IF 1.9 Q2 EMERGENCY MEDICINE
Hyo Suk Oh, Chi Ryang Chung, Chi-Min Park, Gee Young Suh, Ryoung-Eun Ko
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引用次数: 0

Abstract

In a case of contrast media-induced anaphylactic shock managed with epinephrine, a 57-year-old male developed lactic acidosis without cardiogenic shock or global hypoperfusion, highlighting epinephrine's potential to trigger lactic acidosis. Despite previous management of similar reactions with antihistamines and corticosteroids, this case required intensive care unit admission and emergency intervention, with lactate levels peaking alarmingly. The rapid resolution of acidosis following epinephrine discontinuation underscores the need for careful monitoring and the consideration of alternative vasopressor strategies in severe anaphylaxis, illustrating the complex relationship between epinephrine's metabolic effects and anaphylaxis-induced tissue hypoperfusion.

过敏性休克治疗过程中肾上腺素诱发的乳酸酸中毒:病例报告。
在一例使用肾上腺素处理的造影剂诱发过敏性休克病例中,一名57岁的男性出现了乳酸酸中毒,但没有心源性休克或全身灌注不足,这突显了肾上腺素引发乳酸酸中毒的可能性。尽管之前曾用抗组胺药和皮质类固醇治疗过类似反应,但由于乳酸水平达到惊人的峰值,该病例需要入住重症监护室并进行紧急干预。停用肾上腺素后酸中毒迅速缓解,这强调了对严重过敏性休克患者进行仔细监测和考虑替代性血管加压策略的必要性,说明了肾上腺素的代谢作用与过敏性休克诱发的组织灌注不足之间的复杂关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.80
自引率
10.50%
发文量
59
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