Jimson Weed is a common weed along roadsides, in cornfields and pastures, and in waste areas. Datura stramonium comes from the family Solanaceae, the potato or nightshade family. The plant is native to Asia, but is also found in the West Indies, Canada, and the United States. Of the more than 12 species, Datura stramonium is the most common type found in the eastern United States.(2) Many names have been given to this plant including: Jimson Weed, Locoweed, Angel's Trumpet, Thorn Apple, Devil's Trumpet, Mad Apple, Stink Weed, Sacred Datura, Green Dragon, and Devil's Trumpet.(2,4)

Although exposure is sometimes unintentional by gardeners or farmers, its toxic effects are seen most commonly in teens, who intentionally misuse it for its hallucinogenic and euphoric effects, while presenting with serious illness or death from its anticholinergic properties.

EPIDEMIOLOGY

The plant has been described throughout history as a toxin famous for its mind-altering properties. There are references to it in Homer's Odyssey, and Shakespeare's plays: Hamlet, Romeo and Juliet, and Anthony and Cleopatra.(2)

It is one of a group of plants known as "belladonnas," thought to be named from their use by Italian women to dilate their pupils, which was considered beautiful.(3) It was also known to be used for the medicinal treatment of colds and asthma, and for religious purposes.(5) Its most common name, Jimson Weed, is a contracted form of Jamestown Weed, after its use was described in 1676, in Jamestown, Virginia. This was the first record in the United States of physical symptoms following its ingestion by British troops sent to halt Bacon's Rebellion, as noted in Beverly's "History and Present-State of Virginia."(4)

Accidental exposure of adults has also been reported in the literature. An 82 year old male mistakenly ate the root of an Angel's Trumpet, Datura innoxia for a horseradish in his garden.(8) "Gardener's Mydriasis" was reported in a 54 year old male who complained of blurred vision after cutting Angel's Trumpet, Datura suaveolens, in his garden.(9) A 49 year old woman presented with delirium after making a tea to use as a mouthwash for treating gingivitis from a plant in her friend's garden.(14) "Cornpicker's Pupil" is another presentation of mydriasis after exposure during harvesting.(2)

Intentional misuse by teenagers who eat seeds, drink tea and/or smoke cigarettes made of Jimson Weed has been reported by many authors.(1,5,6,13) Although most use is sporadic, there is often clustering or increased use around press reports which increase interest in the drug but do not emphasize risks. Jimson Weed is used in over-the-counter asthma preparations: Asthmador, Barter's Powder, Kinsman's Asthmatic Powder, Green Mountain Asthmatic Compound, and Haywood's Powder, often abused by teens. The American Association of Poison Control Centers' Toxic Exposure Surveillance System reported 318 cases of Jimson Weed poisoning in 1993.(5)

PHARMACOLOGY

The toxins in Jimson Weed are tropane belladonna alkaloids which possess strong anticholinergic properties. They include: hyoscyamine (leaves, roots, seeds), hyoscine (roots); atropine (d,l-hyoscyamine) and scopolamine (l-hyoscine).(2,3,4,7) They act as competitive antagonists to acetylcholine at peripheral and central muscarinic receptors at a common binding site.(3,7) The peripheral receptors are on exocrine glands which affect sweating, salivation, and smooth and cardiac muscle. Poisoning results in widespread paralysis of parasympathetic innervated organs.(3,7,10) As tertiary amines they also have central nervous system absorption, inhibit CNS receptors and result in a central anticholinergic syndrome of acute psychosis or delirium.(7,10)

These toxins are easily absorbed from mucous membranes and the GI tract. The half-life of atropine is approximately 4 hours. Metabolism occurs in the liver by hydrolysis which eliminates approximately half the drug. The remainder is excreted unchanged in the urine.(2,3)

TOXICOLOGY

Datura stramonium is an annual plant. It grows 4 to 6 feet tall and has dark green, long stemmed, lobed leaves which exude a foul odor. Its flower whic blooms in late spring is usually white, sometimes lavender, solitary and tubular. A four lobed, thorny, green seed pod fruit ripens in early fall. Each lobe contains 50-100, 2-3 mm, kidney-shaped, black/brown seeds.(2,4)

All parts of the plant are toxic. They are ingested, smoked and absorbed topically especially through mucous membranes. The exact concentration of specific alkaloids varies with species, cultivation, environment, temperature, moisture, and storage. The range of toxicity is highly variable and unpredictable; toxicity may vary from leaf to leaf, plant to plant and season to season. This contributes to the danger of misuse of the plant since the dose cannot be predicted.(5,7) The highest concentration occurs in the seeds: approximately 0.1 mg of atropine per seed or 3-6 mg/50-100 seeds.(4) An estimated lethal dose in an adult is >10 mg atropine or >2-4 mg scopolamine.(5)

CLINICAL EFFECTS

The mnemonic for clinical effects of typical atropine poisoning is: "blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone." Symptoms include mydriasis; cycloplegia; flushed, warm, dry skin; dry mouth; ileus; urinary retention; tachycardia; hyper or hypotension; delirium with hallucinations; jerky, myoclonic movements; choreoathetosis; hyperthermia; coma; respiratory arrest; rare seizures; and central stimulation followed by depression.(5,7) Hallucinations are reported in as many as 83% of cases; typically they are simple visual images in natural colors, but infrequently also tactile hallucinations of crawling insects.(2)

The onset of symptoms occurs within 30 to 60 minutes after smoking leaves or drinking tea; and 1-4 hours after ingestion of plant material or seeds.(4) Initial symptoms include dry mouth then pupil dilatation.(2) The duration of symptoms is often 24-48 hours because of delayed gastrointestinal motility; symptoms have been reported to last up to 1-2 weeks.(4,5) Although poisoning may lead to fatal medullary paralysis, arrhythmias and cardiovascular collapse,(8) Jimson Weed-related deaths mainly are as a result of impaired judgment and coordination resulting in risk-taking activities associated with accidental death.(1,2)

The differential diagnosis of Jimson Weed poisoning includes any other medicines with anticholinergic properties such as: antihistamines, antispasmodic GI preparations, over-the-counter sleep aids, cold preparations, muscle relaxants, antipsychotics, other plants, mushrooms, scopolamine, or cyclic antidepressants.(7)

LABORATORY EVALUATION

Laboratory evaluation is usually considered unnecessary since treatment is based on clinical evaluation.(7) The toxicology screen is not considered helpful for management, although some anticholinergics such as atropine and hyoscyamine may be detected in urine. Elevated aspartate aminotransferase, LDH, bilirubin and prothrombin time have been reported, possibly secondary to muscle breakdown from seizures, increased tone and hyperthermia. EEG changes include prominent lambda activity, increased slow wave activity and a bizarre high voltage pattern.(2,10)

Thin-layer chromatography and gas chromatography/mass spectrometry may confirm the presence of atropine and scopolamine in samples of the plant.(8) Other tests to identify Jimson Weed have been described where juice from seeds or urine from a patient may be instilled into a rabbit's eye to test for dilatation of the pupils. Another test uses mashed seeds mixed with water; when tested with long-wave UV light, the glycoside scopolin which accompanies the alkaloids fluoresces light blue.(10)

MANAGEMENT

Management of Jimson Weed poisoning is generally conservative beginning with the usual ABC's of resuscitation. If the patient presents with stupor or coma, treatment may include dextrose, thiamine, naloxone, etc. Otherwise the main component of management is support and observation. The patient should be placed in a nonstimulating environment and monitored with frequent vital signs. A cooling blanket can be used for hyperthermia. The patient may require bladder catheterization for urinary retention.

Decontamination should be considered even hours after ingestion secondary to the anticholinergic properties which may delay the gastric emptying and absorption of the vegetable matter.(2) Lavage has been proposed up to 48 hours after ingestion secondary to delayed gastric emptying.(8) Activated charcoal is an effective alternative to lavage in preventing further drug absorption and should be given with a cathartic if no ileus is present.(4,7) Multidose activated charcoal and hemodialysis are not considered effective, although Haddad has speculated that multidose activated charcoal may decrease continued, delayed absorption secondary to the decreased GI motility.(7,10) Hemodialysis and forced diuresis do not enhance th elimination of atropine.(1)

Physostigmine is a naturally occurring alkaloid from a West African vine, Physostigma venenosum. It works by reversible inhibition of acetylcholinesterase, the enzyme that degrades acetylchoine. This increases the concentration of acetylcholine which causes the stimulation of muscarinic and nicotinic receptors. The tertiary amine structure allows penetration of the blood-brain barrier to allow exertion of a central cholinergic effect. Cholinergic stimulation of the brainstem reticular activating system causes nonspecific analeptic arousal effects. However physostigmine's use may precipitate seizures, cholinergic crisis, bradyarrhythmias and asystole. Relative contraindications include: history of cardiovascular disease, gangrene, asthma, glaucoma, and GI/GU obstruction.(2,7,10) Thus its use as a cholinergic agent in Jimson Weed poisoning is controversial and is generally reserved for life-threatening, intractable, anticholinergic effects including hypertension, seizures, unstable tachycardia, hyperthermia, or pronounced hallucinations unresponsive to other agents.(7,10) The dose is 0.5 mg every 5 minutes as needed in a child to a maximum total of 2 mg; 2 mg in an adult slow IV Push, or 0.02 mg/kg repeated every 20-30 minutes. Onset of action is within 3-8 minutes, duration is 30-60 minutes, and elimination half-life is 15-40 minutes. Atropine (0.5 mg/1 mg physostigmine given in the last dose) should be available for reversal of symptoms of cholinergic excess from the physostigmine: bradycardia, heart block, or excessive secretions.(2,10)

Shenoy described the use of physostigmine as a diagnostic tool with a hallucinating patient who became worse on haloperidol. He was given 2 mg of physostigmine as a challenge, and became lucid enough to give the history of the ingestion, then was treated with lorazepam.(12) Guharoy suggested its use in treating mild symptoms in three teens, who were discharged without problems in 24 hours.(6) Rodgers proposed conservative treatment after reviewing 29 cases over 7 years that received no physostigimine. He felt that charcoal, sedatives and monitoring were adequate and that the majority of ingestions pose little threat.(11)

Alternatives or adjuncts to using physostigmine to treat tachyarrhythmias, are alkalization of the blood to pH 7.5 and propranolol. The dosing of propranolol is for an adult:2 mg IV over 1 minute, repeating every 2-5 minutes to a maximum of 5 mg total. For children 0.01-0.1 mg/kg/dose over 10 minutes, maximum 1 mg/dose.10 For patients that require sedation for extreme agitation, benzodiazepines or hydroxyzine should be used instead of phenobarbitol, phenothiazines, or haloperidol secondary to their additive anticholinergic effects.(2) A patient should be admitted if physostgmine is needed or until CNS symptoms resolve.

PREVENTION

Defoliation programs are one way to decrease access to Jimson Weed. It is important to educate health care providers about the hazards and symptoms involved with contact with Datura stramonium. However information to the public should stress hazards and avoid explicit descriptions and locations of the plant which might encourage some to purposefully seek out Jimson Weed for its use as a recreational drug.

Amy M. Arnett, MD
Fellow, Pediatric Emergency Medicine
Boston Children's Hopsital

References (Lead Author Only)

(1) Coremans P: Clin Toxicol 1994;32(5):589-592.
(2) Ellenhorn MJ: Medical Toxicology, Elsevier Science, NY, 1988.
(3) Gilman AG: The Pharmacological Basis of Therapeutics, 8th ed., Pergamon Press, NY, 1990.
(4) Goldfrank LR: Toxicologic Emergencies, 5th ed., Appleton & Lange, Norwalk, CT, 1994.
(5) Goodman RA: MMWR 1995;44(3): 41-44.
(6) Guharoy SR: Vet Hum Toxicol 1991;33(6):588-589.
(7) Haddad LM Winchester: Clinical Management of Poisoning and Drug Overdose, W.B. Saunders Co., New York, 1990.
(8) Hanna JP: Clin Neuropharm 1992;15(2):109-113.
(9) Pereira CAL: Clin Toxicol 1994;32(3):329-331.
(10) Poisindex Toxicologic Management, Micromedex Corporation, Denver, Colorado, 1995.
(11) Rodgers GC: Vet Hum Toxicol 1993;35(1):32-33.
(12) Shenoy RS: Am J Psychiat 1994;151:9.
(13) Vanderhoff ST: Am Fam Physician 1992;46(2):526-530.
(14) Voltz R: Lancet 1992;339:752.

Clinical Toxicology Review is published monthly by the Massachusetts Poison Control System