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

References and Links

• 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.