Correspondence to: Andries Engelbrecht (firstname.lastname@example.org)
Exposure to potentially toxic plants usually occurs in one of two ways. The first is where small children ingest parts of household plants such as leaves or seeds. Most of these exposures are of minimal toxicity because of the small quantity of material ingested.1 More serious poisonings involve adults who deliberately consume raw plant material or tea made from a plant for mind-altering or medicinal effects.
Plant identification can be very difficult and a digital image
of the plant is useful.2 The image can be sent to a
poison centre, which should have access to a botanical
consultant. Most plant intoxications can be treated with
decontamination using activated charcoal within the first 2
hours of ingestion and with supportive measures (see Table 1).
Antidotes are only of potential value in the treatment of plants
containing cardiac glycosides and those that present with
cholinergic and anticholinergic toxidromes.
Table 1. Dosage of activated charcoal
50 - 100 g in 250 ml flat coke or tap water
1 g/kg or 25 - 50 g in 125 ml flat coke or tap water
The authors of this article identified and photographed common toxic weeds, trees and garden plants in and around Pretoria, Gauteng. These plants are common throughout most of South Africa and knowledge of these plants can be useful to staff working in emergency centres.
This plant is also known as Jimson weed, devil’s trumpet,
angel’s trumpet, devil’s weed, thorn apple, crazy tea,
stinkweed or malpitte. It is common throughout South Africa
and grows well in recently disturbed ground (Fig. 1). It is
frequently seen on roadsides and rubbish heaps.
Fig. 1. Datura stramoniun seed pod containing seeds also known as malpitte.
Poisonings occur when the leaves are accidentally
collected as wild spinach (marog).3
Severe poisonings also occur when the black seeds, which
contain up to 0.2 mg of atropine, are ingested or used to
brew a tea (Fig. 2). All parts of the plant are poisonous and
contain various amounts of atropine and scopolamine.
The onset of symptoms usually occurs within 30 - 60 minutes. It may last for days if intoxication is due to ingestion of seeds. The clinical picture includes hallucinations, mumbling speech and agitation. Patients may behave inappropriately and undressing is common. On physical examination, tachycardia, mydriasis, urinary retention, a flushed skin and fever may be present.
Management includes decontamination with activated charcoal (presentation within 2 hours) and placement of an intravenous line for rehydration. Patients can be calmed by administration of a benzodiazepine. Phenothiazines such as haloperidol may have a synergistic effect with the poison and should be avoided.
Physostigmine can be given in a dose of 0.5 - 2 mg in adults and 0.02 mg per kg in children in cases of severe intoxication where central and peripheral signs are present. Seizures, bradycardia, heart block and asystole have been reported with the use of physostigmine and it should be avoided in asthmatic and epileptic patients and in those with cardiac conduction abnormalities.
Also known as castor oil plant, kasterolieboom or Mokhura. This
large shrub is common in many parts of South Africa. It is used
in the production of castor oil. The spiny seeds grow near the
top of the plant (Fig. 3). All parts of the plant are poisonous.
The toxic ingredient is ricin.
Fig. 3. Spiny seeds of Ricinus communis.
Ricin is a strong cytotoxin that inhibits ribosomal protein synthesis. It reduces net absorption of fluids and electrolytes and stimulates peristalsis. The clinical picture includes a latent period of several hours followed by vomiting and bloody diarrhoea. Dehydration and electrolyte abnormalities can occur. It is also cardio-, hepato- and nephrotoxic. If chewed, 5 - 6 seeds may kill a child and 10 - 20 an adult.4
When the seeds are swallowed intact they tend to pass through the bowel without causing toxicity. However, absorption of ricin may theoretically occur in seeds that were perforated for use as jewellery. Decontamination with activated charcoal and/or whole-bowel irrigation should be considered. Aggressive fluid resuscitation with attention to electrolytes and hydration status is the mainstay of therapy in severe intoxications. Patients should be admitted for treatment and observation.
Also known as oleander or selonsroos. This is a common
garden shrub with attractive pink, white or yellow flowers
(Fig. 4). It is one of many plants that contain cardiac
glycosides. All parts of the plant are toxic. Ingestion of
several leaves is unlikely to cause significant symptoms.5
Serious exposures can be due to suicide attempts or the result
of misidentification of plants used for herbal products. The
clinical picture includes nausea, vomiting, visual
disturbances, bradycardia and heart block. In severe cases
ventricular fibrillation or asystole may occur. Serum digoxin
levels may be elevated but a low or negative result does not
rule out poisoning. Treatment includes decontamination, close
cardiac monitoring, supportive care and digoxin-specific Fab
fragments if it can be obtained.
Fig. 4. Nerium oleander.
Also known as syringa tree or seringboom. Syringa trees were
introduced to South Africa from Asia as ornamental plants, but
are now a major problem as invaders of natural vegetation. These
medium-to-large trees produce attractive clusters of yellow
berries that are poisonous (Figs 5 and 6). Human poisoning in
South Africa is common.3 The clinical picture is caused
by meliatoxins and may include vomiting, respiratory distress,
dilated pupils and seizures. Most cases of intoxication are mild
but fatalities have occurred.3 Decontamination, supportive
therapy and benzodiazepines to terminate seizures are indicated.
Fig. 5. Syringa tree seeds (Melia azedarach).
Dieffenbachia (spotted dumb cane), Philodendron (elephant ear), Monstera deliciosa (delicious monster) and Zantedechia (arum lily)
These lily-related, popular exotic ornamental plants are often
found indoors and often in pots (Fig. 7). They contain calcium
oxalate crystals, which are needle-shaped and cause irritation
and inflammation by penetration of the mucous membranes of the
mouth, throat and eyes. Most cases are confined to the
oropharynx due to rapid onset of burning and irritation. Rare
cases of airway compromise have been reported in the literature.6 Treatment
is aimed at pain relief and supportive measures. Children can be
allowed to eat water-based ice-cream to get symptomatic relief.
1. Froberg B, Ibrahim D, Furbee RB. Plant poisoning. Emerg Med Clin N Am 2007;25:375-433.
2. Dyer S. Plant exposures: wilderness medicine. Emerg Med Clin N Am 2004;22:299-313.
3. Watt JM, Breyer-Brandwijk MG. The Medicinal and Poisonous Plants of Southern and Eastern Africa, 2nd ed. London: Livingstone, 1962.
4. Wink M, Van Wyk B. Mind-altering and poisonous plants of the world. Portland:Timber Press, 2008.
5. Clark RF, et al. Digoxin specific Fab fragments in the treatment of oleander toxicity in a canine model. Ann Emerg Med 1991;20;1073.
6. Cumpston KL, et al. Acute airway compromise after brief exposure to Dieffenbachia plant. J Emerg Med 2003;25:391.
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