To the Editor:
At the end of 2020, the European Resuscitation Council published its draft guidelines on cardiac arrest management. 1 Cardiac arrest in special circumstances can be challenging for clinicians who are not accustomed to dealing with these uncommon clinical situations. We present a case of cardiac arrest as a result of aconite poisoning.
A 67-y-old male with no known allergies and no relevant medical history was walking in the forest. Two hours later, once at home, he experienced rapid onset of diarrhea and vomiting, perioral numbness, diaphoresis, and progressive decrease in level of consciousness. When first responders arrived, he reported accidental ingestion of a plant he found in the forest. Given this information, the initial differential diagnosis included an allergic reaction or plant-based intoxication. He was transferred by ambulance to the closest hospital and was administered methylprednisolone 125 mg, metoclopramide 10 mg, dexchlorpheniramine 5 mg, and 1250 mL crystalloids. Once at the emergency department, he continued to experience nausea, vomiting, diarrhea, and decreased responsiveness to stimuli. Examination revealed sinus tachycardia of 175 beats·min-1, hypotension (90/60 mm Hg), reduced consciousness, and bilateral mydriasis. Given his neurologic clinical status impairment, his airway was secured by tracheal intubation. A standard preoxygenation was performed during 2 min with facial mask and 0.15 mg of fentanyl; 20 mg of etomidate and 100 mg of succinylcholine were administered in bolus intravenously in a rapid sequence intubation. Anesthesia maintenance was obtained with midazolam and fentanyl perfusion. While awaiting transfer, the patient experienced cardiac arrest. Advanced cardiopulmonary resuscitation maneuvers were initiated, and the first rhythm detected by electrocardiography monitoring was ventricular tachycardia that quickly progressed to ventricular fibrillation and then torsades de pointes. A total of 3 defibrillations (200 J), 3 g of magnesium sulfate, and 300 mg of amiodarone were administered, with recovery of spontaneous circulation after 12 min of resuscitation. The patient was admitted to an intensive care unit with the initial diagnosis of plant intoxication and was transferred by helicopter under mechanical ventilation.
On arrival, noradrenaline infusion was required to maintain hemodynamic stability, and constant changes in electrical rhythm and QRS morphology were observed (alternating left bundle branch block, bigeminy, frequent ventricular extrasystoles, sinus rhythm, atrial fibrillation, and nodal rhythm). Lidocaine was administered, 100 mg intravenously in bolus, and 1.5 μg·kg·min-1. Transthoracic echocardiography was performed with no relevant findings. Therapeutic hypothermia was not pursued owing to the arrhythmogenic risk involved. Potassium and magnesium levels were checked regularly and remained within normal range.
After 3 h of treatment in the intensive care unit, electrocardiography showed short periods of sinus bradycardia alternating with atrial fibrillation. Within the first 24 h, the patient was successfully extubated with no neurologic damage observed (cerebral performance category 1). Seventy-two hours after cardiac arrest, he was discharged to a regional hospital.
Plant intoxication is a rare condition but can often be catastrophic. Aconitum napellus is a plant commonly found in the moderate altitude of European mountains. It contains several alkaloids with potent cardiac and neurologic toxicity. Aconite intoxication is a life-threatening situation owing to its manifestations in overexcitable tissues. Aconitine is an alkaloid (representing 30% of the alkaloids in this plant) with a high affinity for voltage-dependent sodium channels. The toxin causes these sodium channels to remain in an active state of continuous depolarization, giving rise to many severe clinical effects. 2 A lethal dose is estimated to be between 1 and 2 mg of aconitine for an 80-kg individual. In the case we report, the patient believed that the plant ingested was Molopospermum peloponnesiacum rather than Aconitum napellus, a very dangerous confusion.
Clinical manifestations are variable and depend on the toxicity of the alkaloids. The earliest symptoms are usually numbness and burning in the perioral area. Neurologic complications are also frequent and can include diaphoresis, obnubilation, blurred vision, color distortion, weakness, tingling, incoordination of extremities, and muscular paralysis that can result in respiratory arrest. Gastrointestinal symptoms include vomiting, diarrhea, and nausea. At a cardiovascular level, ventricular disturbances can quickly progress to cardiac arrest. 3 No antidote for aconitine poisoning has been discovered. 4 Treatment consists of supportive care and treatment of complications. Some drugs (amiodarone, flecainide, procainamide, mexiletine, lidocaine, magnesium sulfate) and electrical cardioversion have been tested with varying results. 5 Amiodarone and flecainide are the recommended first-line treatment. 6 The half-life of aconitine is about 3 h; therefore, resuscitation using extracorporeal life support to restore and maintain hemodynamics is recommended if necessary. A small number of cases successfully using extracorporeal life support have been described. 7
Aconitium napellus intoxication is a rare condition that can lead to catastrophic outcomes, including cardiac arrest. Early recognition of rare clinical conditions can be life-saving. Training clinicians in the resuscitation of patients in cardiac arrest in special circumstances and implementing educational information in mountain areas regarding potential dangers for mountaineers are strategies that should be promoted.