Abstract
Introduction. Datura species, especially Datura stramonium (e.g., jimsonweed), are the focus of scores of case reports that chronicle the toxidrome of anticholinergic toxicity. Mechanisms of toxicity. Toxicity occurs because of the presence of up to 28 belladonna alkaloids, predominated by atropine and scopolamine. There are significant interspecies differences in the ratio of the belladonna alkaloids, atropine to scopolamine, and the presence of at least 26 other related alkaloids will vary, even between and among specimens of the same species. The differences may account for unexpected dose–response effects that are observed in some patients and even different profiles of toxicity. All parts of the Datura species contain belladonna alkaloids; in decreasing order, the belladonna alkaloid content is generally the greatest in the petioles (flowers), stem, fruit (seeds), leaves, and roots. Features. The most prominent symptoms are due to the blockade of peripheral muscarinic receptors that innervate exocrine glands, smooth muscle, and cardiac tissue. Therefore, the primary toxic manifestations include mydriasis, which is due to the blockade of papillary sphincter muscle and iris muscle; dry mouth, secondary to parasympathetic blockade of salivary secretion; tachycardia, caused by competition at muscarinic receptors in postganglionic parasympathetic neurons and blockade of receptors in the SA node; and fever and erythema, because of vasodilation and inhibition of sweating. Direct ocular exposure. Well known to produce mydriasis after ingestion, Datura is also notorious for producing maladies such as “gardeners eye” and “cornpickers eye,” which is a testament to the high concentrations of belladonna alkaloids in the entire plant. When the sap or dried plant material from a member of the Datura species enters the eye directly, the papillary sphincter and ciliary muscles are affected resulting in mydriasis and cycloplegia. Pupil dilation is sudden in onset and often profound. In a dose–response fashion, the mydriasis and its persistence will be dependent on the alkaloidal content and quantity of the sap. The mydriasis can be bilateral, but most commonly it is unilateral, which is frightening to the victim and to the clinician and suggestive of significant cerebral pathology. Management. As with any toxic exposure, the foundation of patient management is supportive care and patient reassurance. Because of the central nervous system effects of the belladonna alkaloids, the patient may be agitated, combative, confused, and disoriented. Initial intervention focuses on addressing those issues that protect the patient and their caregivers. In severe cases, physostigmine, a cholinesterase inhibitor, should be used to reverse anticholinergic toxicity. Physostigmine should be given intravenously to an adult in a dose of 0.5–2.0 mg at a rate of no more than 1 mg/min; a second dose may be administered if necessary. Children should receive 0.02 mg/kg intravenously and the rate should not exceed 0.5 mg/min. Extracorporeal elimination and forced diuresis of the belladonna alkaloids are not viable options. Conclusions. Members of the Datura species contain abundant amounts of belladonna alkaloids that can produce both local and systemic anticholinergic toxicity. Fatalities because of Datura species exposure are rare, but adverse effects are very common. Treatment is supportive with the use of physostigmine in more severe cases of poisoning.
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