Case Reports
Sunday, November 12, 2023
12:45 PM–02:15 PM
Abstract
Introduction:
With the advent of nanoparticle molecular delivery systems, it is crucial to acknowledge that novel, but clinically relevant drug interactions remain to be discovered. Thus, it is important to proactively evaluate theoretical drug-drug relationships to mitigate any associated adverse drug reactions in clinical scenarios.
Case:
A 49-year-old-man with autism was initiated on electroconvulsive therapy (ECT) for medication-refractory catatonia. Relevant past medical history included catatonia that was worsened by neuroleptics, complicated by benzodiazepine-induced respiratory failure, but repeatedly improved with amantadine. He was initially admitted on scheduled lorazepam 1 mg thrice daily. During ECT-1 (day-5), while intubated and sedated, he was receiving the following psychoactive medications: amantadine 200 mg twice daily, lorazepam 2.5 mg (total), and continuous dexmedetomidine. No sugammadex was administered. For all ECT sessions, he received rocuronium and methohexital at similar doses. Following ECT-2 (day-7), sugammadex was administered and he was later extubated with dexmedetomidine discontinuation. Psychiatry recommended continued lorazepam down-taper, which was discontinued the next day (day-8). Relative to ECT-1/-2, ECT-3 utilized twice the electric charge. Post ECT-3 (day-10), following sugammadex administration, he was soon found to be acutely dystonic. Exam revealed tachycardia, rigidity, and abnormal motor movements, which consisted of oculogyric crisis, cogwheeling, fingers contracting towards the palms, and perioral twitching. Intravenous diphenhydramine 25 mg given 6 hours later did not significantly improve symptoms. Electroencephalogram, though limited due to artifact from constant eye and head movements, was negative for epileptiform activity. Sugammadex was held, amantadine was further up-titrated, and the patient slowly improved.
Discussion:
In vitro, cyclodextrin molecules display high binding association constants with amantadine moieties, creating potential clinical implications. During ECT-3, absent sedation/benzodiazepines, he was predisposed for acute dystonia secondary to sudden dopaminergic withdrawal following sugammadex-related amantadine removal.
Conclusion:
Sugammadex-amantadine's likely physiochemical interaction in this case’s context warrants further research in both laboratory and clinical models.
Presenting Author
Philip K. King PharmD, BCPSSumma Health, Akron City Hospital
Authors
Caiden Lukan PharmD Candidate
Butler University College of Pharmacy and Health Sciences
Warren B. Gavin MD
Indiana University Health Adult Academic Health Center – Methodist Hospital
Aimee Patel MD
Indiana University School of Medicine
Jacob R. Peters PharmD, BCPP, BCPS
Indiana University Healht and Butler University College of Pharmacy and Health Sciences