Aconite poisoning presenting as hypotension and bradycardia

Abstract

<jats:p> The principal toxic ingredients of aconite roots include aconitine, mesaconitine and hypaconitine, which are known cardiotoxins and neurotoxins. A 58-year-old man took a decoction of 11 g each of processed ‘chuanwu’ (the main root of Aconitum carmichaeli) and processed ‘caowu’ (the root of A. kusnezoffii) as treatment for his neck pain. One hour later, he experienced numbness of tongue and the four limbs, generalized weakness, nausea, vomiting, diarrhoea and dizziness. Three hours after ingestion, he was admitted to hospital. His blood pressure was 106/53 mmHg and heart rate 65 beats/min. Six hours after ingestion, he became hypotensive (systolic blood pressure &lt;100 mmHg) with bradycardia (heart rate &lt;60 beats/min). As treatments for the hypotension, he was given intravenous infusions of 0.9% saline (125 mL/hour) for 15 hours (7-21 hours after ingestion) and dopamine (3 μg/kg/min) for 36 hours (10-45 hours after ingestion). He was given atropine 0.6 mg intravenously 7 and 24 hours after ingestion. He was hypotensive for 31 hours (6-36 hours after ingestion), with a systolic blood pressure of 84-106 mmHg (mean 93.5) and a diastolic blood pressure of 40-59 mmHg (mean 51.8). He had bradycardia for 36 hours (6-41 hours after ingestion), with a heart rate of 45-68 beats/min (mean 56.5). On discharge (48 hours after ingestion), his blood pressure was 117/82 mmHg and heart rate 70 beats/min. In patients with aconite poisoning, prolonged hypotension and sinus bradycardia may occur and supportive therapy with close monitoring of blood pressure and cardiac rhythm are essential. </jats:p>

Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

“…Higher concentrations of aconitine suppress action potential transmission by continuous opening of the Na + channel, which reduces the release of acetylcholine at the axonal end terminus and the vagotonic effects at the myocardium [18,25]. The bradycardia and hypotensive manifestations can be explained by activation of the ventromedial nucleus of the hypothalamus associated with depression of the circulatory system and inhibition of L-type calcium channel currents that serve as a major driver of pacemaker monocytes [18,21,25,26,27]. These complex electrophysiological mechanisms generate self-excitatory abnormal microcircuits within the cardiac and nervous systems, which can trigger cardiovascular features such as arrhythmia, conduction blocks, bradycardia and asystole [18,25].…”

“…However, its success rate in re-establishing sinus rhythm after aconite poisoning is not satisfactory, probably because of the various cardiovascular toxicity of aconite, which can cause more than just arrhythmias [25]. For the bradycardia and hypotension in the present case, we administered an intravenous infusion of 0.9% saline and vasopressor agents, including atropine and dopamine [21]. Another putative mechanism of bradycardia and hypotension is hypermagnesemia, which generally occurs with renal insufficiency and excessive magnesium intake [20,28,29,30].…”

“…1). Based on these preliminary data, the possible differential diagnoses were age-related sick sinus syndrome, coronary artery disease compromising the arteries supplying the sinoatrial node, endocrine diseases associated with declining general cardiac activity, such as hypothyroidism or adrenal insufficiency, medication-related side effects, or long QT syndrome [20,21,22]. She was immediately administered an intravenous (IV) infusion of 0.9% of normal saline (80 ml/h), 2 ampules dopamine (200 mg/5 ml/ampule, with an IV drip at 10 ml/h, 5.3 μg/kg/min), atropine 0.5 ampule (1 mg/1 ml/ampule, as an IV bolus), and oxygen inhalation (10 l/min).…”

Successful Rescue of a Patient with Acute Aconitine Poisoning Complicated by Polycystic Renal Hemorrhage

“…Because of faulty processing, overdosing, and drinking herbal medicinal wine made with alkaline aconitine herbs, aconitine poisoning remains common in China and other parts of Asia 4 . Various toxic symptoms, such as paresthesia, anesthesia, and weakness, are observed within a few minutes of aconitine ingestion and are followed by gastrointestinal symptoms, such as nausea, vomiting, diarrhea, and cardiac problems, the most common of which is ventricular arrhythmia 5 . Although aconitine toxicity has been recognized for many years, information about treating the toxic effects remains poor 6 .…”

Aconitine mediates connexin43 and PKC phosphorylation status in cultured ventricular myocytes of neonatal rats

“…ingestion are matters of common occurrences; however, cases of suicide and homicide meet the same condition according to forensic identification (Elliott, 2002;Pullela et al, 2008;Chan., 2009). Aconitine suppresses the deactivation of voltage-gated sodium channels, which prevents complete repolarization of the excitable membrane of cardiac tissues (Liu et al, 2008;Wang et al, 2003;Moric, et al, 2003;Li et al, 2007), all which caused aconitine-induced arrhythmias.…”