B48-18 Serotonin Syndrome Complicated by Torsades De Pointes in a Patient Using Kratom for Chronic Pain

Abstract Introduction Mitragyna speciosa (kratom) is a herbal supplement gaining popularity in the U.S., touted as a natural treatment for chronic pain, depression, and opioid withdrawal, and sought for its euphoric effects—along with its addictive potential. Kratom has dose-dependent agonism at opioid, adrenergic, dopaminergic, and serotonin receptors and inhibits cytochrome P450 enzymes, creating numerous interaction risks. In many states it remains largely unregulated and easy to access. Given its pharmacokinetic profile, patients on chronic medications or with polysubstance use increasingly present to emergency departments with varied toxicities after starting kratom. We present a case of a 45-year-old female who presented with serotonin syndrome complicated by polymorphic ventricular tachycardia (PVT) and torsades de pointes (TdP) after beginning kratom for chronic pain. Case Presentation A 45-year-old female with a history of polysubstance abuse, anxiety, depression, hypothyroidism, prior gastric bypass, and chronic pain syndrome who presented with acute myoclonus, abdominal pain, and diarrhea. Examination revealed tachycardia, hyperthermia, diaphoresis, agitation, and altered mental status with visual hallucinations. Collateral revealed recent self-initiation of 5-10 kratom capsules (unknown sourcing or strength) daily for additional pain control. She was admitted to telemetry when a rapid response was activated for sustained PVT progressing to TdP which was treated with intravenous magnesium and calcium prior to transfer to the medical intensive care unit (MICU). Cyproheptadine was given for serotonin syndrome. Electrocardiogram (ECG) showed a QTc of 725 ms (Framingham). Medication reconciliation revealed multiple QT-prolonging drugs that the patient had taken for years with known minor QT prolongation. Psychiatry was consulted to reduce QTc prolonging agents in her medication regimen. The patient had another TdP episode requiring defibrillation and intubation. EP advised continued monitoring and isoproterenol or lidocaine drip if PVT recurred. Serial ECGs showed down trending QTc. Ultimately the patient’s symptoms improved, and she elected for subcutaneous internal cardiac defibrillator placement. Discussion Kratom contains numerous alkaloids, the most physiologically active being mitragynine and 7-hydroxymitragynine. These bioactive molecules can have clinically significant, potentially detrimental effects given potential interactions between various recreational substances and chronic medications. Mitragynine inhibits cardiac delayed rectifier potassium channels resulting in QT prolongation that may predispose patients to PVT and TdP. In our patient, kratom likely increased serotonergic activity and QT prolongment, creating a potentially devastating clinical picture she narrowly evaded. Kratom products require further regulation and research to prevent fatal drug interactions and define scenarios where its diverse receptor agonism may provide therapeutic benefit. This abstract is funded by: NONE