Abstract
Aconitine, a potent plant alkaloid used in traditional Asian medicine, possesses significant toxicity risks. This case report presents a 42-year-old male with alcohol use disorder who developed life-threatening ventricular tachycardia after ingesting a homemade herbal liqueur. Initially thought to contain Cassia alata (candle bush), further investigation revealed that the tincture was instead prepared from Aconitum root (Wolfsbane) based on advice from an online social media video. He subsequently developed life-threatening ventricular tachycardia and cardiac arrest refractory to initial interventions. In the absence of extracorporeal membrane oxygenation (ECMO), flecainide, or procainamide, a multimodal approach involving multiple antiarrhythmics, including amiodarone, phenytoin, and stellate ganglion block, ultimately restored normal sinus rhythm. This case underscores the importance of early recognition and a flexible, multimodal treatment strategy in managing aconitine-induced arrhythmias, especially in resource-limited settings.
Keywords: Aconitine poisoning, ventricular tachycardia, herbal liqueur, stellate ganglion block
1. Introduction
Aconitine, a prominent component in various Aconitum species, possesses a diverse pharmacological profile encompassing analgesic, antiinflammatory, and cardiotonic properties. However, historical accounts highlight its recurrent misuse as a potent poison and accidental ingestion. Aconitine exerts its toxicity by persistently activating voltage-gated sodium channels, leading to continuous depolarization. This results in a characteristic progression of symptoms—from early neurologic signs like paresthesias and muscle weakness to gastrointestinal symptoms, and ultimately life-threatening ventricular arrhythmias.1 This case report presents a patient who developed severe cardiac complications following aconitine poisoning from a herbal liqueur. The following narrative aims to illuminate the clinical presentation, therapeutic challenges, and successful management strategies employed in this critical case, particularly focusing on a multimodal approach to treat refractory ventricular tachycardia (VT) in resource-limited settings where extracorporeal membrane oxygenation (ECMO) and preferred antiarrhythmics, such as flecainide and procainamide,2 are unavailable.
2. Case Presentation
A 42-year-old male with a history of alcohol use disorder presented to a tertiary care hospital in northern Thailand approximately 6 hours after ingesting a homemade herbal tincture. The concoction was initially believed to contain Cassia alata, a plant commonly used in traditional Thai medicine. Following instructions from an online video promoting its health benefits, the preparation involved soaking 100 g of the roots in 500 mL of 40% ethanol at room temperature for 24 hours before consumption.
Shortly after the ingestion, the patient experienced rapidly progressing symptoms, beginning with muscle weakness, numbness, and drowsiness. Three hours later, he developed sustained VT with palpable pulses (Fig 1), hypotension, and altered mental status. Urgent synchronized cardioversions were performed to achieve hemodynamic stability. Despite initial management with intravenous lidocaine and magnesium sulfate, the VT persisted. To maintain hemodynamic stability, infusions of lidocaine and norepinephrine were initiated before transfer to the cardiac care unit for close monitoring and further investigation and management by a cardiologist, as the cause of the ventricular arrhythmia was initially unclear.
Figure 1.
Electrocardiogram of the patient 3 hours after hospital arrival.
Initial blood tests revealed significant hypokalemia (serum potassium 2.5 mEq/L), which was corrected with intravenous potassium chloride in normal saline. Other laboratory findings were unremarkable. Bedside cardiac ultrasound showed no regional wall motion abnormalities, lowering the suspicion of myocardial infarction. Gastrointestinal decontamination, including activated charcoal and nasogastric lavage, was not performed because of the high risk of aspiration.
Six hours after admission, the patient experienced cardiac arrest with pulseless VT. Cardiopulmonary resuscitation and defibrillation attempts were performed adhering to the American Heart Association Advanced Cardiac Life Support 2020 guideline. Subsequently, the patient received a combination of antiarrhythmic medications, including intravenous lidocaine, amiodarone, and phenytoin. Additionally, a bilateral stellate ganglion block using 1% lidocaine was administered. At 54 minutes after the initiation of cardiopulmonary resuscitation, this combination of pharmacological and interventional strategies successfully terminated the refractory VT and restored normal sinus rhythm. The patient’s postresuscitation course was characterized by a period of unconsciousness, followed by successful extubation without complications. He was subsequently transferred to a private health care facility for ongoing management and discharged after 5 days. Further history revealed that the tincture was prepared using Aconitum root (Wolfsbane) (Fig 2), which had been harvested from the patient’s backyard. Retrospective toxicological analysis of the tincture via liquid chromatography identified aconitine and ethanol, definitively excluding Cassia alata and confirming aconitine toxicity. The patient achieved full recovery and was discharged following a 5-day hospitalization.
Figure 2.
Residue of the Wolfbane root in the homemade herbal liqueur.
3. Discussion
This case illustrates severe aconitine poisoning resulting from the ingestion of a homemade herbal tincture containing Aconitum root (Wolfsbane). Aconitine is a C19 diterpenoid alkaloid known for its toxicity. It primarily disrupts normal neuronal function by persistently activating voltage-gated sodium channels, preventing repolarization and leading to continuous depolarization across various tissues. This mechanism causes the classic progression of poisoning symptoms: early neurologic features such as paresthesias and muscle weakness, followed by gastrointestinal disturbances, including nausea, vomiting, and diarrhea, and ultimately, cardiovascular manifestations, especially refractory ventricular arrhythmias.1 The clinical course of our patient closely resembled the classical clinical course.
There is no known antidote for aconitine poisoning; therefore, management is largely supportive. Refractory ventricular arrhythmias are common and often unresponsive to standard resuscitative measures. The multimodal approach involving multiple antiarrhythmic medications and stellate ganglion block3,4 was potentially life-saving, especially in the resource-limited setting where ECMO and more effective antiarrhythmics such as procainamide and flecainide are unavailable.2 However, the use of the approach also introduces significant clinical risk. Coadministration of lidocaine and amiodarone can potentially cause lidocaine toxicity, manifesting as seizures compared with lidocaine alone, through the strong CYP450 inhibition effect of amiodarone.5 Norepinephrine, used for circulatory support, can exacerbate ventricular arrhythmias by increasing myocardial oxygen demand and promoting catecholamine-induced automaticity.6,7 The usage of phenytoin also has potential cardiac toxicity from its solvent, propylene glycol, which is a cardiac depressant and can lead to bradycardia, hypotension, and asystole with rapid administration.8 Thus, the risks of pharmacologic synergy must be balanced with the urgency of the clinical situation.
Beyond clinical management, this case highlights the dangers of unregulated herbal preparations and the ease with which toxic plants can be misused or misrepresented, especially when influenced by misinformation on social media. The patient’s wife prepared the tincture based on unverified online advice, without knowledge of the plant’s toxic profile. This underscores the urgent need for public education about the risks associated with homemade herbal remedies and the importance of regulatory oversight of traditional and alternative medicines. Moreover, it reinforces the critical role of early toxicological screening and poison center consultation in emergency settings to guide appropriate diagnosis and management.
This case highlights the severe consequences of aconitine poisoning resulting from the misuse of a homemade herbal tincture prepared based on unverified online information. The patient's life-threatening ventricular arrhythmias were successfully managed using a multimodal approach consisting of multiple antiarrhythmics and stellate ganglion block after conventional therapies failed. This case emphasizes the importance of considering these options for refractory arrhythmias while carefully weighing their potential risks. Furthermore, it underscores the importance of improving public health awareness and implementing stricter regulatory measures to prevent poisoning associated with unverified or improperly prepared herbal products.
Funding and Support
By JACEP Open policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article as per ICMJE conflict of interest guidelines (see www.icmje.org). The authors have stated that no such relationships exist.
Footnotes
Supervising Editor: Lara Goldstein, MD, PhD
References
- 1.Chan T.Y. Aconite poisoning. Clin Toxicol (Phila) 2009;47(4):279–285. doi: 10.1080/15563650902904407. [DOI] [PubMed] [Google Scholar]
- 2.Fudim M., Boortz-Marx R., Ganesh A., et al. Stellate ganglion blockade for the treatment of refractory ventricular arrhythmias: a systematic review and meta-analysis. J Cardiovasc Electrophysiol. 2017;28(12):1460–1467. doi: 10.1111/jce.13324. [DOI] [PubMed] [Google Scholar]
- 3.Ganesh A., Qadri Y.J., Boortz-Marx R.L., et al. Stellate ganglion blockade: an intervention for the management of ventricular arrhythmias. Curr Hypertens Rep. 2020;23(12):100. doi: 10.1007/s11906-020-01111-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Coulson J.M., Caparrotta T.M., Thompson J.P. The management of ventricular dysrhythmia in aconite poisoning. Clin Toxicol (Phila) 2017;55(5):313–321. doi: 10.1080/15563650.2017.1291944. [DOI] [PubMed] [Google Scholar]
- 5.Mar P.L., Horbal P., Chung M.K., et al. Drug interactions affecting antiarrhythmic drug use. Circ Arrhythm Electrophysiol. 2022;15(5) doi: 10.1161/CIRCEP.121.007955. [DOI] [PubMed] [Google Scholar]
- 6.Wieruszewski E.D., Jones G.M., Samarin M.J., Kimmons L.A. Predictors of dysrhythmias with norepinephrine use in septic shock. J Crit Care. 2021;61:133–137. doi: 10.1016/j.jcrc.2020.10.023. [DOI] [PubMed] [Google Scholar]
- 7.Suita K., Fujita T., Hasegawa N., et al. Norepinephrine-induced adrenergic activation strikingly increased the atrial fibrillation duration through β1- and α1-adrenergic receptor-mediated signaling in mice. PLoS ONE. 2015;10(7) doi: 10.1371/journal.pone.0133664. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Iorga A., Horowitz B.Z. 2025. Phenytoin Toxicity.http://www.ncbi.nlm.nih.gov/books/NBK482444/ StatPearls. StatPearls Publishing; [PubMed] [Google Scholar]


