Takayuki Yoshida1, Chisato Sumi2, Takeo Uba3, Haruka Miyata4, Takeshi Umegaki3, Takahiko Kamibayashi3. 1. Department of Anesthesiology, Kansai Medical University Hospital, 2-3-1 Shin-machi, Hirakata-city, Osaka, 573-1191, Japan. ytaka@mac.com. 2. Department of Anesthesiology, Chibune General Hospital, 3-2-39 Fuku-machi, Nishiyodogawa-ku, Osaka-city, Osaka, 555-0034, Japan. 3. Department of Anesthesiology, Kansai Medical University Hospital, 2-3-1 Shin-machi, Hirakata-city, Osaka, 573-1191, Japan. 4. Department of Anesthesiology, Baba Memorial Hospital, 4-244 Hamadera-funaocho-higashi, Nishi-ku, Sakai-city, Osaka, 592-8555, Japan.
Abstract
BACKGROUND: Profound bradycardia caused by sugammadex has been reported, although its mechanism is unclear. Herein, we suggest a possible culprit for this phenomenon. CASE PRESENTATION: A 50-year-old woman without comorbidity except mild obesity underwent a transabdominal hysterectomy and right salpingo-oophorectomy. After surgery, sugammadex 200 mg was intravenously administered. Approximately 4 min later, her heart rate decreased to 36 bpm accompanied by hypotension (41/20 mmHg) and ST depression in limb lead electrocardiogram (ECG). Atropine 0.5 mg was injected intravenously without improving the hemodynamics. Intravenous adrenaline 0.5 mg was added despite the lack of signs suggesting allergic reactions. Her heart rate and blood pressure quickly recovered and remained stable thereafter, although 12-lead ECG taken 1 h later still showed ST depression. CONCLUSIONS: In this case, the significant bradycardia appeared attributable to coronary vasospasm (Kounis syndrome) induced by sugammadex, considering the ECG findings and high incidence of anaphylaxis due to sugammadex.
BACKGROUND: Profound bradycardia caused by sugammadex has been reported, although its mechanism is unclear. Herein, we suggest a possible culprit for this phenomenon. CASE PRESENTATION: A 50-year-old woman without comorbidity except mild obesity underwent a transabdominal hysterectomy and right salpingo-oophorectomy. After surgery, sugammadex 200 mg was intravenously administered. Approximately 4 min later, her heart rate decreased to 36 bpm accompanied by hypotension (41/20 mmHg) and ST depression in limb lead electrocardiogram (ECG). Atropine 0.5 mg was injected intravenously without improving the hemodynamics. Intravenous adrenaline 0.5 mg was added despite the lack of signs suggesting allergic reactions. Her heart rate and blood pressure quickly recovered and remained stable thereafter, although 12-lead ECG taken 1 h later still showed ST depression. CONCLUSIONS: In this case, the significant bradycardia appeared attributable to coronary vasospasm (Kounis syndrome) induced by sugammadex, considering the ECG findings and high incidence of anaphylaxis due to sugammadex.
Authors: Ákos I Fábián; Edömér Tassonyi; Vera Csernoch; Marianna Fedor; Tamás Sohajda; Lajos Szente; Béla Fülesdi Journal: BMC Anesthesiol Date: 2021-08-17 Impact factor: 2.217
Authors: Nicholas G Kounis; Ioanna Koniari; George D Soufras; Grigorios Tsigkas; Panagiotis Plotas; Periklis Davlouros; George Hahalis Journal: JA Clin Rep Date: 2020-05-07