Biomaterial-based extracellular vesicle delivery systems for wound healing: From fabrication to applications.

Adrenaline is the first-line treatment for anaphylactic shock owing to its potent α- and β-adrenergic properties and inhibitory effects on the release of mediators[]; it is also used to treat cases complicated by myocardial ischemia, such as Kounis syndrome,. However, its adrenergic effects may exacerbate myocardial ischemia and induce fatal arrhythmias,. Moreover, adrenaline induces hypokalemia through β2-adrenergic effects[]. When adrenaline-induced hypokalemia occurs in patients with anaphylaxis with ischemic and hypersensitive myocardium, it causes QT prolongation and, ultimately, torsades de pointes, ventricular tachycardia, and ventricular fibrillation,. While the physiological mechanism of adrenaline-induced hypokalemia is well established[], its clinical significance during the management of refractory anaphylaxis is insufficiently emphasized in previous case reports and current anaphylactic guidelines,–. We report this case to highlight the critical risk of severe hypokalemia and subsequent QT prolongation when high-dose adrenaline is warranted. A case of severe adrenaline-induced hypokalemia in a patient with anaphylactic shock and myocardial ischemia is reported.