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Sinus bradycardia : case report A 9-month old girl developed sinus bradycardia following concomitant administration of dexmedetomidine and tacrolimus. Additionally, fentanyl had contributed to the development of sinus bradycardia [not all routes and dosages stated]. At the age of 4 months, the girl was diagnosed with biliary atresia. At the age of 9 months, she underwent primary liver transplant from a deceased donor. During the transplant operative course, she developed hypotension managed with epinephrine and norepinephrine infusions. During the course, she was maintained on cisatracurium-besilate [Cisatracurium] infusion and sedative therapy with IV fentanyl 1 µg/kg/h infusion, followed by 2 µg/kg/h which was up-titrated to a maximum of 3 µg/kg/h. During the first 12h post-transplant, she had intermittent, fluid-responsive hypotension. During the post-transplant course, she was receiving immunosuppressive treatment with tacrolimus. Approximately 15h post-transplant, her muscle paralysis was weaned off and IV dexmedetomidine was added for sedation with ongoing fentanyl infusion. At 14:35 on post-operative day (POD) 1, she received an IV bolus of dexmedetomidine 0.08 mcg/kg followed by a continuous IV infusion at a rate of 1 mcg/kg/h. As, she continued to have intermittent agitation, she received an IV fentanyl bolus of 3 µg/kg/dose and an IV midazolam bolus. During this time, her vitals remained stable. However, at approximately 17:43 on POD 1, she developed sudden bradycardia with a HR of 30 beats-per-minute. She had a sinus pause lasting for 4 seconds that resolved spontaneously. After suctioning, bradycardia recurred with a sinus pause of 7 seconds as recorded by telemetry. Immediate after this, her bedside nurse initiated cardiopulmonary resuscitation (CPR). Within a minute of initiating CPR, her HR increased to 101–113 beats-per-minute and she became awake and agitated. Thereafter, dexmedetomidine was discontinued. She continued fentanyl infusion, and cisatracurium-besilate was restarted. Telemetry review showed sinus bradycardia. Extensive evaluation for the aetiology of bradycardia was performed. On the basis of unremarkable work up, sinus bradycardia was thought to be secondary to dexmedetomidine. Additionally, fentanyl had contributed to the development of sinus bradycardia. A pharmacokinetic interaction between dexmedetomidine and tacrolimus led to altered dexmedetomidine metabolism, which further led to bradycardia. After 12h, her vital signs returned to expected ranges with a mean HR of 105+/-14 beats-per-minute. The sinus bradycardia and sinus pause resolved. Banc-Husu AM, et al. Dexmedetomidine leading to profound bradycardia in a pediatric liver transplant recipient. Pediatric Transplantation : 28 Oct 2020. Available from: 803520062 URL: http://doi.org/10.1111/petr.13895

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Reactions 12 Dec 2020 No. 1834