Botanical Name

Cestrum nocturnum Linn. [1]

Solanaceae

Cestrum nocurnum Linn . is a member of the Solanaceae family. It is an evergreen bush that can reach up to 2 m high. The leaves are ovate-lanceolate in shape measuring 8 - 16 cm long and 2.5 - 6 cm wide, dark green above and glabrous beneath. The flowers are greenish in colour and intensely fragrant especially at night. The fruit is a globose berry measuing 1 cm in diameter, deep red-purple in colour [1].

It is native of Mexico but now widely distributed as ornamentals because of the fragrant flowers.[1], [2]

In the tropical belt of Western Africa and Eastern America including the Caribbean Islands the plant is used both as medicine and also in religious ceremonies. As medicine it is used in the treatment of epilepsy, hysteria, nervousness and spasm. [4]

Leaves, berries [1] [2]

The leaves of Cestrum nocturnum contains atropine-like anticholinergic alkaloids. [1] The unripe berries contain solanine while the ripe berries has the anticholinergic glycoside toxins in them. [2]

While poisoning from this plant can pose serious effects on humans especially children, reported cases of poisoning is rather rare. To avoid incidences of poisoning especially in children, this plant should only be placed in areas where human movements are limited.

Clinical features of poisoning by this plant are due to two forms of toxic agents viz. anticholinergic alkaloid intoxication and glycoalkaloid poisoning from solanine.

Anticholinergic alkaloid intoxication

Acute symptoms include dry mouth, dysphagia, dystonia, tachycardia and urine retention. This would be followed by hyperthermia with flushed and dry skin. Neurological symptoms do occur a little later and include blurred vision, excitement and delirium, headache and confusion. This could be followed by somnolence, disorientation, hallucination and mumbling speech. It could end in seizure coma and death due to respiratory failure. Symptoms would appear within 2 hours of ingestion.[1], [5], [7]

Solanine poisoning

Solanine is a glycoalkaloid which could cause both gastrointestinal and neurological symptoms. Gastorintestinal symptoms includes burning of the throat, nausea, vomiting diarrhoea and colic. Neurological symptoms includes headache, dizziness, hallucinations, loss of sensation, paralysis. In severe cases the victim would progress from hallucination, loss of sensation, paralysis, fever, hypothermia and death. The symptoms can occur as early ad 30 minutes after ingestion but normally take between 8 – 12 hours to develop. [5], [7]

Management of Anticholinergic Alkaloid Poisoning

Management would include intravenous rehydration with electrolyte correction and anti-emetics if vomiting is present. In severe cases of intoxication one can use the available antidote, physostigmine. [1]

1. Advance life support with continuous cardiac monitoring and intravenous access should be established as necessary.
2. Activated charcoal should be considered but should not be repeated as there is the possibility of paralytic ileus developing subsequent to intoxication which can cause impaction or aspiration.
3. Patients with mild psychomotor hyperactivity should be observed and provided with nonspecific sedation like benzodiazepines when necessary.
4. Physostigmine is a specific antidote for anticholinergic intoxication. It is given in a dose of 1 – 2 mg as slow IV infusion over 2 – 5 minutes for adults. In children the does is 0.02 mg/kg, up to 0.5 mg. Doses can be repeated after 10 – 20 minutes if the anticholinergic effects persist or recur. Response is usually quick and remarkable, but recurrent toxicity is relatively common. The risk of cholinergic excess in overzealous treatment would be noticed should the patient developed bradycardia, bronchorrhea dan bronchospasm and seizures. This can be reversed by atropine. [3]

Management of Solanine Poisoning

There is no known definitive treatment for solanine poisoning. It is entirely supportive. Dehydration and electrolyte imbalance is the main feature in solanine poisoning thus, treatment would involve standard measures to correct the fluid and electrolyte imbalance. The seriously ill patients not responding to fluid replacement therapy should be given vasopressors if necessary and put on cardiac monitoring. Recovery is usually complete, but coma dna death have been reported in cases of severe poisoning. [6], [7]

References

1. Nelson L., Shih RD., Balick MJ., Handboook of Poisonous and Injurious Plants Springer Berlin 2007 pg. 118 – 119
2. Scott S., Thomas C., Poisonous Plants of Paradise: First Aid and Medical Treatment of Injuries from Hawaii’s Plants University of Hawaii Press Honolulu 2000 pg. 41
3. Linden CH., Rippe JM., Irwin RS Manual of Overdoses and Poisonings Lippincott, Williams & Wilkins Philadelphia 2006 pg. 30 – 33
4. Moran DQ Guide to Afro-Cuban Herbalism Author House Bloomington 2009 pg. 296
5. Brandenberger H., Maaes RAA.,  Analytical Toxicology: For Clinical, Forensic and Pharmaceutical Chemists Walter de Gruyter & Co. Berlin 1997 pg. 639
6. Barceloux DG., Medical Toxicology of Natural Substances: Food, Fungi, Medicinal Herbs John Wiley and Sons New York 2012
7. Metcafe DD., Sampson HA., Simon RA., Food Allergy: Adverse Reactions to Food and Food Additives Blackwell Science Malden 2003 pg. 404 - 405