Key result
High-dose intravenous MgSO4 effectively terminated recurrent pulseless ventricular tachycardia, and hemoperfusion reduced toxic aconite alkaloid levels in a patient with chronic kidney disease.
Why the study?
Ventricular tachyarrhythmias are the most common cause of death in aconite poisoning, and antiarrhythmic drugs and cardioversion are ineffective.
Does high-dose intravenous MgSO4 and hemoperfusion improve fatal tachyarrhythmias in a patient with aconite poisoning and chronic kidney disease?
Case Report (n=1)
No
Does high-dose intravenous MgSO4 and hemoperfusion improve fatal tachyarrhythmias in a patient with aconite poisoning and chronic kidney disease?
High-dose intravenous MgSO4 and hemoperfusion can be life-saving for aconite-induced fatal tachyarrhythmias, especially in patients with chronic kidney disease.
Aconite ingestion risks refractory VT unresponsive to standard therapy; single case leaves optimal management open.
Aconite contains four highly toxic diester-diterpene alkaloids, including aconitine, mesaconitine, hypaconitine, and jesaconitine, in all plant parts. Aconite has been used as for suicide, murder, and as an arrow poison since ancient Greek and Roman times. Ventricular tachyarrhythmias are the most common cause of death in aconite poisoning, and antiarrhythmic drugs and cardioversion are ineffective. A 61-year-old woman ingested the crushed raw roots of a single aconite plant. An ambulance brought her to the Tottori University Hospital 30 min after ingestion. She had a history of chronic stage 5 kidney disease but was not on dialysis. Her heart rate (HR) was 120 bpm upon arrival. The patient developed sustained supraventricular tachycardia (SVT) at an HR of 165 bpm with frequent premature ventricular contractions (PVCs) 15 min after arrival. She then developed sustained monomorphic ventricular tachycardia (VT) at an HR of 200 bpm 20 min after arrival, which progressed to pulseless polymorphic VT. Cardioversion was unsuccessful. External cardiac massage restored spontaneous circulation; however, her underlying rhythm remained sustained SVT with frequent PVCs. These arrhythmias repeatedly led to circulatory arrest. She was administered six intravenous boluses of 2 g of MgSO4 in the emergency department, which prevented her from going into sustained pulseless VT. Hemoperfusion (HP) with activated charcoal was performed 1.5 h after arrival. The aconitine, mesaconitine, and hypaconitine plasma concentrations were high at 8.9, 23.5, and 5.5 ng/mL, respectively, before the start of HP but decreased to 1.7, 4.0, and 2.7 ng/mL, respectively, after 7 h of HP. She returned to sinus rhythm on the second day of hospitalization; however, the patient required maintenance hemodialysis. We concluded that high-dose IV MgSO4 is an effective treatment for fatal tachyarrhythmias due to aconite poisoning, and that in cases of renal failure, HP may be required to remove aconite toxins from the body.
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Oshima et al. (2024) conducted a case report in Aconite poisoning with chronic kidney disease (n=1). High-dose intravenous MgSO4 and hemoperfusion was evaluated on Termination of pulseless ventricular tachycardia and reduction of aconite toxins. High-dose intravenous MgSO4 effectively terminated recurrent pulseless ventricular tachycardia, and hemoperfusion reduced toxic aconite alkaloid levels in a patient with chronic kidney disease.
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