Jimson Weed Poisoning Case Report

Jimson Weed (Datura stramonium) Overview

• Jimson weed is a wild herb found throughout the United States, commonly encountered by adolescents and young adults due to its hallucinogenic properties.

• Its ingestion results in an anticholinergic intoxication toxidrome.

• The plant typically matures between May and September, making it widely accessible.

• Other Names: Jimson weed is also known by historical and colloquial names such as Jamestown weed (originating from a recorded intoxication in Jamestown, Virginia, in 1676), thorn apple, angel's trumpet, stinkweed, and green dragon.

• Historical Context: For centuries, it has been utilized in traditional medicine for its anticholinergic effects to treat asthma, diarrhea, intestinal cramps, and nocturia. Its hallucinogenic properties are even alluded to in Homer's epic tale, The Odyssey.

Botanical Characteristics and Toxic Components

• Family: It belongs to the nightshade family.

• Physical Description:

  • Can grow up to 5 feet in height.

  • Features large, jagged leaves.

  • Produces trumpet-shaped flowers that can be either white or purple.

  • At maturity, it bears green, spiny fruit, each containing four compartments capable of holding as many as 100 seeds.

• Toxicity: All parts of the jimson weed plant are poisonous.

  • The leaves and seeds contain the highest concentration of toxic anticholinergic alkaloids.

• Key Toxic Alkaloids:

  • Atropine

  • Hyoscyamine

  • Scopolamine

• Lethality Data:

  • Approximately 100 seeds contain about 6mg of atropine.

  • An atropine dose exceeding 10 mg is considered potentially lethal.

Mechanism of Action (Anticholinergic Effects)

• The clinical manifestations of jimson weed poisoning are directly attributed to the anticholinergic properties of its constituent alkaloids: atropine, hyoscyamine, and scopolamine.

• These compounds block the action of acetylcholine at muscarinic receptors, leading to the characteristic anticholinergic toxidrome.

Clinical Presentation and Symptoms

• Symptoms typically manifest rapidly, usually within 30 to 60 minutes following ingestion.

• Initial Symptoms:

  • Hallucinations (visual and/or auditory)

  • Restlessness and agitation

  • Shaking

  • Dry mucous membranes and profound thirst

  • Mydriasis (dilated pupils) leading to blurred vision

  • Difficulty speaking and swallowing (dysphagia, dysarthria)

• Subsequent Effects (may develop as intoxication progresses):

  • Tachycardia (elevated heart rate, often exceeding 100 beats/minute )

  • Urinary retention

  • Ileus (decreased or absent bowel sounds due to severely decreased gastrointestinal motility)

• Rare, Severe Late Symptoms:

  • Hyperthermia ( dangerously high body temperature)

  • Respiratory arrest

  • Seizures

• Symptom Duration: The slowing of gastrointestinal motility can delay the elimination of toxins, causing symptoms to persist for an extended period, often 24 to 48 hours.

• Classic Anticholinergic Toxidrome Mnemonic: The mnemonic "Blind as a bat, dry as a bone, red as a beet, mad as a hatter, and hot as a hare" accurately describes the constellation of symptoms:

  • Blind as a bat: Refers to mydriasis and blurred vision.

  • Dry as a bone: Indicates dry mucous membranes and skin.

  • Red as a beet: Suggests flushed skin.

  • Mad as a hatter: Describes central nervous system effects like hallucinations, agitation, and confusion.

  • Hot as a hare: Points to hyperthermia.

Epidemiology

• Jimson weed poisoning is predominantly observed among adolescents and young adults who intentionally seek the plant's hallucinogenic effects.

• In 1998, the American Association of Poison Control Centers reported 152 cases nationally, though the actual incidence is believed to be significantly higher due to probable underreporting.

• Lethal outcomes are uncommon but are most frequently documented in individuals engaged in polysubstance abuse, such as ingesting jimson weed concurrently with alcohol, marijuana, or cocaine.

Case Report: 15-Year-Old Boy

• Presentation: A mother brought her 15-year-old son to the Emergency Department (ED) due to bizarre behavior, including hallucinating. This occurred after a neighbor informed her of other local youths experiencing similar symptoms after ingesting wild flowers.

• Mother's Observations: Upon entering her son's room, she found him shaking, mumbling incoherently, and attempting to pick at nonexistent objects. She also discovered several white flowers in his room, which she brought to the ED.

• ED Examination Findings:

  • Behavior: Restless, incessantly pacing, and shaking.

  • Mental Status: Awake and alert, oriented to his name but disoriented to place and time, indicating confusion.

  • Vital Signs:

    • Oral Temperature: 99.3F(37.4C)

    • Blood Pressure: 117/72

    • Heart Rate: 103 beats/minute (tachycardia)

    • Respiratory Rate: 24 breathes/minute

  • Physical Examination:

    • Pupils: Dilated to 8mm, symmetric, and minimally reactive to light (mydriasis).

    • Mucous Membranes: Dry.

    • Bowel Sounds: Decreased.

    • Extremities: Warm to the touch, but not hyperthermic.

    • Neurologic Exam: Confused and mumbling, intact cranial nerves, normal motor strength, and reflexes. During the exam, he was observed reaching into the air as if trying to grasp nonexistent objects, confirming visual hallucinations.

• Diagnostic Workup:

  • Normal Results: Emergent fingerstick blood glucose, complete blood count (CBC), chemistry panel, and urinalysis were all within normal limits.

  • Negative Toxicology Screen: Screens for alcohol, benzodiazepines, amphetamines, marijuana, tricyclic antidepressant agents, opiate agents, and phencyclidine were negative.

  • Electrocardiogram (ECG): Showed sinus tachycardia but no other abnormalities.

  • Cranial Computed Tomography (CT) Scans: Administered without contrast medium, revealed normal cranial structures.

• Diagnosis: Based on the classic clinical presentation and a history of ingesting a wild plant, the ED physician suspected jimson weed intoxication. This was visually confirmed by comparing the plant specimen brought by the mother with an image of jimson weed from the Internet.

• Patient History (Initial vs. Subsequent): Initially, the patient denied drug use, claiming friends gave him a blended drink containing strawberries, a wild plant, and a small amount of alcohol. During a subsequent interview (after mental status improved), he admitted that he and his friends had deliberately consumed jimson weed for the first time, having heard of its hallucinogenic effects.

• Initial Treatment in ED: The patient received several doses of intravenous lorazepam to manage agitation.

• Hospital Course: He was admitted for observation and monitoring. His condition remained stable, and his mental status progressively improved. He was discharged from the hospital after 36 hours of observation.

Diagnosis of Jimson Weed Poisoning

• Diagnosis primarily relies on a high index of suspicion based on clinical evaluation and recognition of the anticholinergic toxidrome.

• Key Diagnostic Clues:

  • Presenting Complaint: Often starts with altered mental status.

  • Hallucinations: Patients commonly experience visual and/or auditory hallucinations.

  • Physical Examination Findings: Tachycardia, elevated blood pressure, mydriasis (dilated pupils), blurred vision, decreased bowel sounds, and dry mucous membranes are hallmark signs.

  • Hyperpyrexia: Occurs in approximately 20% of cases.

• Laboratory and Imaging Studies:

  • Toxicology Screen: Useful to rule out co-ingestion of other substances (polysubstance abuse), but typically does not detect pure anticholinergic poisons directly.

  • Other Lab Tests: Generally not helpful in specifically identifying jimson weed as the cause of symptoms.

  • Imaging: Typically normal unless there are complications or other underlying conditions.

• Confirmation is often clinical, supported by history and sometimes by identifying the plant specimen.

Management and Treatment

Effective management of jimson weed poisoning involves a stepwise approach:

1. Primary Survey (ABCs):

   • Immediate assessment of the patient's Airway, Breathing, and Circulation.

   • Although rare, some patients may present with severe complications like seizures or coma, potentially compromising the airway.

   • If airway compromise is suspected, prompt intubation and mechanical ventilation are indicated.

2. Elimination of the Poison:

   • Activated Charcoal: An agent that binds to toxins, thereby decreasing their overall absorption from the gastrointestinal tract.

     • Dose: The usual oral dose for adults is 1g/kg

   • Gastric Lavage: Considered for removal of ingested plant material if the patient seeks medical attention within several hours post-ingestion or if the patient has been intubated (to protect the airway).

   • Emesis (Syrup of Ipecac): May be induced to promote vomiting if the patient is awake and relatively alert.

     • Dose: The usual dose is 30mL for adults and 15mL for children.

3. Supportive Care and Continuing Observation:

   • Most cases of jimson weed poisoning are self-limiting and can be managed effectively with supportive care and close observation until symptoms resolve.

   • Monitoring: Continuous cardiac monitoring is crucial due to the risk of tachyarrhythmias caused by the inhibition of the vagal effect on the sinoatrial node.

   • Serial Assessments: Regular monitoring of vital signs and serial neurologic assessments are vital for detecting any life-threatening events and confirming symptom resolution.

   • Patients typically show improvement within 24 hours, with most requiring less than 48 hours of observation.

   • Intravenous fluid resuscitation is important to prevent complications such as hyperpyrexia and dehydration.

4. Treatment of Specific Complications:

   • Symptomatic Tachyarrhythmia:

     • Propranolol: May be used.

     • Dosage (Adults): 1mg intravenously over one minute, repeated every five minutes up to a maximum dose of 5mg

     • Dosage (Children): 0.01 to 0.1mg/kg with a maximum dose of 1mg

   • Hyperpyrexia: (seen in about 20% of cases)

     • Treated with external cooling measures such as sponging or cooling blankets.

     • Intravenous fluid resuscitation helps prevent this complication.

   • Convulsions/Seizures: Initially managed with benzodiazepine therapy.

   • Agitation: Benzodiazepine therapy is the primary treatment. Physical restraints may be necessary to prevent injury to the patient or hospital staff.

   • Hypertension: Usually transient and typically does not require pharmacologic intervention unless a hypertensive crisis is suspected.

5. Physostigmine (for Severe Anticholinergic Crisis):

   • Indication: Warranted only in severe cases presenting with symptoms of anticholinergic crisis, such as dysrhythmia, coma, seizures, clinically significant hypertension, or poorly controlled hyperpyrexia.

   • Mechanism: Physostigmine is an acetylcholinesterase inhibitor. It increases acetylcholine levels, thereby reversing both peripheral and central manifestations of anticholinergic excess.

   • Dosage:

     • Adults: Initial dose of 0.5 to 2mg administered slowly intravenously. The maximum adult dose should not exceed 4mg within a 30-minute period.

     • Children: Initial dose of 0.02mg/kg administered slowly intravenously.

   • Risks and Controversies:

     • Cholinergic Crisis: Overcorrection with physostigmine can lead to a cholinergic crisis, characterized by bradycardia, complete atrioventricular block, asystole, emesis, bronchorrhea, and seizures.

     • Management of Overcorrection: If cholinergic symptoms manifest due to suspected overcorrection, 0.5 mg of atropine may be given intravenously for every 1mg of physostigmine administered.

     • Routine Use: Routine use of physostigmine remains controversial because most cases resolve with supportive care alone. It is generally reserved for patients with clinically significant symptoms or complications. However, it can rapidly reverse central and peripheral nervous system dysfunction and aid in diagnosing anticholinergic excess; small, closely monitored doses have shown no adverse effects in some studies (e.g., 23 patients with jimson weed-induced hallucinations).

6. Avoidance of Certain Medications:

   • Clinicians must avoid drugs with anticholinergic properties (e.g., some antipsychotic and sedative drugs) as they can worsen the symptoms of jimson weed poisoning.

   • Agents such as haloperidol or chlorpromazine, while sometimes used for agitation, can exacerbate agitation and psychosis in this context and should therefore be avoided.

Prognosis and Outcome

• Jimson weed poisoning is generally self-limiting.

• Most patients experience a benign outcome with appropriate supportive care and observation.

• However, high levels of ingestion can lead to dangerous medical conditions including cardiac arrhythmia, hyperpyrexia, seizures, coma, and respiratory arrest, though these severe complications are rare.

Prevention

• Anticipatory Counseling: Crucial for teenagers and their parents, especially during the summer and early fall months when the jimson weed plant matures.

• This counseling aims to deter experimentation with the plant and prevent subsequent harm.