Plant Toxicity

OVERVIEW

  • severe toxicity from plants is rare in humans
  • risk assessment is often difficult
    — plant identification may be difficult
    — toxin quantification may be impossible (e.g. variation with species, plant part, stage of life cycle, season and location)

EXPOSURE

  • usually affects young children or when toxic plants are mistaken as an edible variety (e.g. immigrants)
  • also: recreational use, alternative medicines and self harm
  • may include any part of the plant (e.g. root, leaves, berries, seeds), either raw, cooked or as a drink (e.g. ‘tea’)
  • as well as ingestion, cutaneous and ocular exposure may also be symptomatic

ASSESSMENT

Aconite, e.g. Acontium spp and Delphinum spp, may be in Asian herbal medicines

  • sodium channel activator
  • GI symptoms: N&V, abdominal cramps, diarrhoea
  • tachycardia, dysrhythmia, shock
  • CNS effects: paresthesiae, paralysis, coma, seizures
  • MODS, lactic acidosis

Belladona alkaloids, e.g. Datura spp (jimsonweed, Angel’s trumpet), Atropa belladona, Hyoscyamus niger (henbane)

  • anticholinergic syndrome

Calcium oxalate crystals, e.g. Dieffenbachia spp and Philodendron spp

  • contact leads to severe mechanical irritation of mucous membranes

Cardiac glycosides, e.g. Digitalis purpurea (foxglove), Nerium spp (pink oleander), Thevetia spp (yellow oleander)

  • mimics digoxin toxicity: GI symptoms, cardiotoxicity (AV blockade, increased automaticity and dysrhythmias)

Colchicine, e.g. Colchicum autumnale (autmun crocus), Gloriosa superba (glory lily)

  • GI symptoms, bone marrow failure, MODS (see Colchicine toxicity)

Coniine, e.g. Conium maculatum (poison hemlock)

  • alkaloid similar to nicotine
  • GI symptoms, dysrhythmia, ascending paralysis, rhabdomyolysis and renal failure

Cyanogenic glycosides such as amydalin, e.g. Prunus spp. seed kernels (apricot, almond, plum, pear, cherry)

  • hydrolysed to form cyanide
  • coma, lactic acidosis, MODS, shock

Hypoglycin, e.g. Blighia sapia (ackee)

  • hypoglycaemia, acidemia, vomiting, coma, seizures

Nicotine, e.g. Nicotiana spp (tobacco)

  • ingestion, inhalation or transdermal exposure is possible
  • nicotinic syndrome: GI symptoms, sweating, tachycardia, hypotension, tremor, seizures

Psychotropic alkaloids, e.g. Ipomea spp (morning glory) and Lophophora wiliamsoni (peyote cactus)

  • e.g. direct serotonin agonists like lysergic acid (LSD) and mescaline
  • psychosis including visual hallucinations

Ricin, e.g. Ricinus communis (castor beans), and Abrin, e.g. Abrus precatorius (jequirity beans)

  • similar antimitotic effects to colchicine: GI symptoms, bone marrow failure, MODS

Taxine, e.g. Taxus spp (yew)

  • sodium and calcium channel inhibition
  • GI symptoms, bradycardia, dysrhythmias, altered mental state

INVESTIGATIONS

  • guided by clinical assessment
  • digoxin levels do not reliably correlate with severity of toxicty from plant cardiac glycosides
  • consider: FBC, UEC, CMP, LFTs, coags, CK, glucose, ECG, blood gas and lactate

MANAGEMENT

Resuscitation

  • rarely necessary
  • life-threats include:
    — cardiotoxicity and shock (e.g. aconitine, cardiac glycosides, cyanogenic alkaloids, taxine)
    — seizures or coma (e.g. nicotine, coniine,
    — MODS (e.g. colchicine, ricin)
    — hypoglycemia (e.g. hypoglycin toxicity)
    — anaphylaxis

Supportive care and monitoring, may include:

  • neurological observations for seizures, coma and paralysis
  • delirium management
  • glucose monitoring
  • cardiac monitoring
  • rehydration and antiemetics
  • treatment of contact or allergic dermatitis

Decontamination

  • activated charcoal 50g (1g/kg in children) if potential for severe toxicity — ensure airway protection if risk of seizures or coma
  • irrigate exposed eyes, mucous membranes and skin

Antidotes

  • anticholinergic syndrome — physostigmine
  • cyanogenic glycosides — hydroxocobalamin and sodium thiosulfate (see cyanide poisoning)
  • cardiac glycosides — digoxin immune Fab
  • colchicine — antidote has been developed in France but is not commercially available

Disposition

  • discharge home if risk assessment does not predict severe toxicity and:
    — asymptomatic, or
    — mild GI symptoms only
  • observe in hospital:
    — significant symptoms
    — risk assessment predicts potential for severe toxicity
  • admit to HDU/ ICU:
    — severe toxicity

CCC Toxicology Series

  • Eddleston M, Persson H. Acute plant poisoning and antitoxin antibodies. J Toxicol Clin Toxicol. 2003;41(3):309-15. PMC1950598.
  • Froberg B, Ibrahim D, Furbee RB. Plant poisoning. Emerg Med Clin North Am. 2007 May;25(2):375-433; abstract ix. PMID: 17482026.
  • Schep LJ, Slaughter RJ, Beasley DM. Nicotinic plant poisoning. Clin Toxicol (Phila). 2009 Sep;47(8):771-81. PMID: 19778187.
CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the  Clinician Educator Incubator programme, and a CICM First Part Examiner.

He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the FOAM movement (Free Open-Access Medical education) has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.

His one great achievement is being the father of three amazing children.

On Bluesky, he is @precordialthump.bsky.social and on the site that Elon has screwed up, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.