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Indianer

Mechanism and Side effects of Aconite poisoning

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Hey guys. I hope this is the right place for it, a more academic question that demands experts to answer. The poison from Aconitum napellus (Monkshood/Wolfsbane) has found it´s way into my notes form a pharmacology training. However, details are hard to come by, and for a Biologist rather than a Medic hard to verify. To study the clinical picture of the poisoning I gained access to the publications in the bottom of this post.

A few questions remain for me that I hoped you might help with.

Aconite prolongs the opening phase of Na+-channels, although I don´t know about subtype sicificity. This would be why Class 1 antiarrhythmics seem to be most potent here, although still fickle. In limbs and skeletal muscle this leads to paresthesia and generalized weakness. Gastrointestinal features include nausea, abdominal pain, and diarrhea. In the referred-to papers, after onset of symptoms it took usually an hour, in a case much less for the patient to faint/ collapse. It wasn´t always obvious if "collapsed" was to be understood as "loss of consciousness". Postmortem examination in a case of accidental ingestion, likely of monkshood leaves, revealed this: "Internal examination showed severe congestion of all organs. Histologic examination revealed bilateral massive intrapulmonary hemorrhage and edema." (Pullela et al.).

I´d like to make the following assumption. An extract of neatly minced, uncooked (not thermostable) aconite root in about a mustard glass of red wine, possibly cut with vinegar (for solubility) is injected into the rectum. This is without question far beyond a lethal dose. That way the toxin would circumvent the liver passage. Questions:

  1. Is the paresthetic effect preceeded by cramps/ painful spasms, and if so, how long would they persist?
  2. Whilst the skeletal muscles are long paralysed the heart refuses to cease function, instead goes into tachycardia an then tachycard fibrillation. I assume this is due to the fact that cardiomyocytes can not be tetanized. Why?
    1. Possible answer: Due to them having sodium channels different from those in motoneurons. Cardiac Na+-channels, I guess, take longer to reopen their inactivation gate. In that case, cardiomyocytes have a brief time frame to repolarise in spite of the toxin, causing them not to cease function immediately but fibrillate instead. Skeletal muscles don´t. Is that it?
  3. Could the treatment avoid gastrointestinal side effects, esp. the nausea and emesis?
  4. What causes the collapse? My guess would be hypotension, but I am not sure the poison does not exert some effect on the CNS. So far I was under the impression that it could not negotiate the blood-brain barrier, but I might be wrong..
  5. I am not a medic. What does "congestion of all organs" mean, and why did it occur? Sounds painful, btw.

 

Thanks for any insight!

Best, Indi

........................................................

  • Lin C-C, Chan TY., Deng J-F (2004) Clinical features and management of herb-induced aconitine poisoning. Ann Emerg Med 43:574–579. doi: 10.1016/j.annemergmed.2003.10.046
  • Pullela R, Young L, Gallagher B, et al (2008) A Case of Fatal Aconitine Poisoning by Monkshood Ingestion. J Forensic Sci 53:491–494. doi: 10.1111/j.1556-4029.2007.00647.x
  • Strzelecki A, Pichon N, Gaulier JM, et al (2010) Acute Toxic Herbal Intake in a Suicide Attempt and Fatal Refractory Ventricular Arrhythmia. Basic Clin Pharmacol Toxicol 107:698–699. doi: 10.1111/j.1742-7843.2010.00566.x

For German Speakers:

  • Stetzenbach M, Schnorbus B, Sagoschen I, et al (2017) Reanimationspflichtige akute Eisenhutintoxikation in suizidaler Absicht. AINS - Anästhesiologie · Intensivmed · Notfallmedizin · Schmerztherapie 52:641–644. doi: 10.1055/s-0043-106283

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