Adrenaline-induced hypokalemia and critical QT prolongation in a patient with refractory anaphylactic shock complicated by myocardial ischemia: a case report
Chikako Wada, Motohiro Sekino, Ryosuke Shintani, Shohei Kaneko, Akihiro Yokoyama, Yusuke Kasai, Naoya Iwasaki, Hiroshi Araki, Rintaro Yano, Taiga Ichinomiya, Ushio Higashijima, Tetsuya HaraIntroduction:
Adrenaline is the first-line treatment for anaphylactic shock. However, adrenaline administration may exacerbate myocardial ischemia and induce fatal arrhythmias. It can also cause hypokalemia, thereby increasing the risk of life-threatening cardiac events.
Case presentation:
A 58-year-old man developed refractory anaphylactic shock accompanied by electrocardiographic evidence of myocardial ischemia during spinal fusion surgery. A total of 3.6 mg of intravenous adrenaline was required. At 135 minutes after onset, the serum potassium level decreased to a nadir of 2.1 mmol/L, resulting in critical QT prolongation. Timely adrenaline discontinuation and potassium supplementation resolved the hypokalemia, resulting in a favorable outcome.
Discussion:
Adrenaline is known to induce hypokalemia through a rapid and severe intracellular potassium shift via β2-adrenergic stimulation; however, this effect may be underestimated. The synergistic interaction of myocardial ischemia during anaphylactic shock, the direct adverse effects of adrenaline on the myocardium, and adrenaline-induced hypokalemia significantly increases the risk of fatal arrhythmias.
Conclusion:
When using multiple and/or continuous doses of adrenaline, clinicians should consider proactive monitoring of potassium levels and potassium supplementation, thereby preventing life-threatening arrhythmias.