Emergency case in focus
A male patient in his 60s, presented to the Emergency Department (ED) with symptoms of acute onset facial and upper limb numbness, dizziness, nausea and vomiting, as well as chest discomfort after consuming a herbal decoction. He was a chronic smoker with a past medical history of gout for which he was not on any regular prescription medication.
Upon arrival at the ED, he was conscious and alert but was also found to be diaphoretic, with a heart rate of 110 bpm, blood pressure of 62/34 mmHg and SpO2 was 98% on room air. His other eaminations were unremarkable. His electrocardiogram (ECG) reading showed sinus tachycardia with frequent premature ventricular complexes. A total of 2 of fluid boluses were immediately administered and vasopressor support with noradrenaline of up to 0.15 mcg/kg/min was initiated. He was also given intravenous amiodarone 150 mg bolus
followed by an infusion at 1 mg/min over 6 hours, and 0.5 mg/min over the next 18 hours.
His biochemistry investigations and toicology screens were unremarkable. Upon further history-taking, he revealed that the herbal decoction which he had consumed was based on a recipe that he found on social media. It consisted of Radix Aconiti Lateralis Praeparata (附子), Panax Ginseng (人参）, Rhizoma Atractylodis Macrocephalae (白术）, Radix Paeoniae Alba (白芍), Poria cocos mushroom (茯苓). This herbal decoction formulation is also commonly known as 附子汤.
He was transferred to the Medical High Dependency Unit where he remained haemodynamically stable and was gradually weaned off from his vasopressor support over the next 24 hours. An ECG test was repeated on day 2 of admission showed normal sinus rhythm. A transthoracic echocardiogram showed normal left ventricular systolic function with no signicant valvular pathology. He recovered fully and was discharged on day 3.
Aconitum, also known as aconite, monkshood and wolfsbane, is a genus of at least 350 species of herbaceous plants. Aconitine, an alkaloid and other types of alkaloids are found in all parts of the Aconitum plant and are most abundant in the roots. Traditionally, it has been used in the Indian Aryuvedic treatment and in the Traditional Chinese Medicine for the treatment of rheumatism, arthritis and pain. Specically, in Traditional Chinese Medicine, root tuber of Aconitum Carmichaelii (also known as Radix Aconiti Cocta, or 制附子) and root tuber of Aconitum Kusnezoffii (also known as Radxi Aconiti Kusnezoffii Cocta, 制草乌), and lateral root tuber of A. carmichaeli (also known as 附子) are often used. However, raw aconite roots are highly toixc cardiotoxins and neurotoxins. In faxct, they have been used in the past as arrow poisons. The estimated lethal dose of pure aconitine has been reported to be as low as 2mg and 1g of the wild plant(1).
Hence, aconite roots are only used after processing (by prolonged soaking or boiling) which leads to the hydrolysis of aconitine alkaloids and reduction of alkaloid content of up to 90% (2). Aconitum toicity usually results either from the accidental ingestion of wild plants, inadequate processing (commonly due to a shorter than required duration of boiling) or erroneous prescription (3,4). Inappropriate usage of Aconitum plants appears to be a common feature among previously reported cases of Aconitum toicity.
A locally published case report describes an accidental over-dosage of aconite caused by the incorrect transcription of an internet herbal recipe(5). In the case above, it may be possible that the patient had not boiled the herbal decoction for a suffcient amount of time.
Mechanism and features of Aconitum toxicity
Aconitine binds with high affnity to the open state of voltage-sensitive sodium channels in the excitable membranes (myocardium, nerve, muscle), resulting in persistent activation, continuing sodium influx and sustained depolarisation(6). Patients with aconite poisoning classically present with a combination of neurological, cardiovascular and gastrointestinal features. Short latency (as short as 10 minutes) between the ingestion of aconite and onset of symptoms has been described in literature(3,7). Likewise our patient developed symptoms of paraesthesia, chest discomfort, nausea and vomiting within 30 minutes of consumption of the herbal decoction.
Some of the cardiovascular features include hypotension, heart palpitations, chest pain, bradycardia, sinus tachycardia and ventricular arrhythmias. Aconitine can induce ventricular arrhythmia including ventricular ectopics, ventricular tachycardia, torsades de pointes and ventricular fibrillation. This is caused by myocardium automaticity triggered by the delayed after depolarisation and early after depolarisation(1).
Neurotoxicity of aconitine is precipitated by its action on voltage-sensitive sodium channels in axons which block the release of acetylcholine. Neurological features include sensory (paraesthesia and numbness of the face, perioral area and the four limbs), motor (muscle weakness) or both(1).
There is no specic antidote to aconite poisoning and supportive care is the mainstay of treatment. Mortality from aconite toxicity has been described to be 5.6%(8). Ventricular arrhythmias secondary to aconite toxicity are often refractory to cardioversion and anti-arrhythmic drugs. Anti-arrhythmics of choice described in previous case reports for the treatment of aconite induced ventricular arrhythmias include flecainide and amiodarone(1,9).
Adverse events may occur with herbal-based traditional remedies, such as the Radix Aconiti Lateralis Praeparata or other aconite-containing herbs. Healthcare professionals are encouraged to ask patients if they are taking any traditional herbal remedy, be vigilant for suspected adverse events associated with its use.
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