Abstracts

Postanesthetic Rufinamide Syndrome

Abstract number : 1.211
Submission category : 4. Clinical Epilepsy / 4C. Clinical Treatments
Year : 2023
Submission ID : 51
Source : www.aesnet.org
Presentation date : 12/2/2023 12:00:00 AM
Published date :

Authors :
Presenting Author: Allison Vassar, RN, BSN, CNRN – University of Minnesota

angela Birnbaum, PhD – Professor, College of Pharmacy, University of Minnesota; ilo leppik, MD – Professor, Neurology and Pharmacy, University of Minnesota; Rory Remmel, Phd – Professor, College of Pharmacy, University of Minnesota; Yuhan Long, BSChE, BS – PhD Graduate Student, Experimental and Clinical Pharmacology, University of Minnesota; Sima Patel, MD – Associate professor of Neurology, Neurology, University of Minnesota

Rationale: We began to notice some of rufinamide is extensively metabolized in the liver catalyzed mainly by carboxylesterases 1 and 2 with CES1, non-cytochrome P450 (CYP450) enzymes, with an elimination half-life of 8-12 hours. As metabolism is through non-P450 routes there are few drug interactions expected. It came to our attention that some patients receiving rufinamide developed adverse events (AEs) after undergoing procedures requiring general anesthesia. The objective of this study was to identify patients who were receiving rufinamide and experienced adverse events after a surgical procedure to characterize the relationship with drug blood concentrations.



Methods: The EPIC data base of the Fairview U of MN system was reviewed to identify persons prescribed rufinamide and who had surgery requiring general anesthesia over a three year period. Demographic data, occurrence of AEs, and rufinamide doses and blood concentrations were extracted.



Results: A total of 166 persons prescribed rufinamide were identified 82 males and 82 females, ages 4 to 68 years. Of these, 28 had undergone a procedure requiring general anesthesia. Their ages ranged from 4 years to 62 years, 16 were females 12 males, and more than half had a diagnosis of Lennox-Gastaut syndrome. Overall, 14 (50%) who received general anesthesia had significant AEs within three days of the procedure associated with marked increases in rufinamide concentrations from earlier measurements.  Seven patients had concentrations greater than 40 ug/ml with the highest being an increase to 67.1 ug/ml from an earlier concentration of 9.6 ug/ml. The mean pre-anesthesia rufinamide level was 16.79 ug/ml (SD 4.6); post-surgery mean 39.72 (SD 9.18). The increase was 136.5% (p = 1.63x10-5). The most common AEs were vomiting, nausea, anorexia and weight loss. There was no difference in sex or age between those with no AEs and those with AEs.

 



Conclusions: Many persons receiving rufinamide who underwent a surgical procedure developed AEs associated with anesthesia that was correlated with an increase in rufinamide concentrations. It is important to obtain baseline levels (personal therapeutic levels) when a person has attained the therapeutic goal so that causes of subsequent problems such as AEs or breakthrough seizures can be elucidated.



Funding: None

Clinical Epilepsy