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Anticholinergic plant poisoning final
- 1. ANTICHOLINERGIC PLANT POISONING Dr. Jareama Patrick May 12th 2020 EM Medicine
- 2. Objectives • Introduction • Toxidromes • Common Anticholinergics • Anticholinergic plants and toxicities • Plant species • Pathophysiology • ED Management of anticholinergic plant poisons • Summary
- 3. Introduction: Toxic Plants • One of the most frequent poisonings reported to poison control centers (1) • 15,000 people a year poisoned by plants • Account for 5-10% of calls to poison control centeres • 69% of those involved children > 6 yrs (1) • Incidence is increasing • Toxicity can also occur when plants have been treated with herbicides, insecticides or fertilizers (2) 2. CDC Drug Surveillance Report https://www.cdc.gov/drugoverdose/pdf/pubs/2017-cdc-drug-surveillance-report.pdf 1. Aktar MW, Sengupta D, Chowdhury A. Impact of pesticides use in agriculture: their benefits and hazards. Interdiscip Toxicol. 2009;2(1):1‐12. doi:10.2478/v10102-009-0001-7
- 4. Introduction: Toxic Plants • Almost any plant can cause nausea, vomiting and intestinal cramping • Not all parts of a plant are always toxic and the toxic principle may be present only during certain times of the year
- 5. Introduction: General ED Management Approach • DECONTAMINATION • Resuscitation (ABCDE) • Supportive Care • Antidote* • Treat plant ingestion as potentially toxic until proven otherwise • Attempt to ID the plant • Time of ingestion and dose ingested is essential • Call poison control center • Appropriate disposition +/- social intervention
- 6. Toxidrome • A constellation of signs and symptoms that characterize a particular toxin or a category of toxins (3) • Helps in “unknown” situations to narrow down possible toxins • Vital signs and toxicology assessment is essential to identify possible toxidromes 3. Medical Dictionary: <a href="https://medical-dictionary.thefreedictionary.com/toxidrome">toxidrome</a>
- 8. Anticholinergic Toxidrome • Results from competitive antagonism of acetylcholine at central and peripheral muscarinic receptors Central inhibition: -Agitation -Delirium -Confusion -Carphologia -Hallucinations -Seizures -Coma Peripheral inhibition: - Hot, dry skin - Flushed appearance - Mydriasis - Tachycardia - Decreased bowel sounds - Urinary retention - Photophobia Boroughf WJ. Anticholinergic Syndrome. In Critical Care Toxicology 2nd Edition. Springer 2017
- 10. Anticholinergic Plants • Tropane Alkaloids Amines • Anticholinergic tropane alkaloids • Contain the compounds atropine, scopolamine, and hyoscyamine • Daily uses: • Recreational (hallucinogens) • Chinese herbal medicine ( asthma, bronchitis, flu like symptoms) • Analgesics in child’s birth • Natural antidote for cholinergic toxicity • Alcoholic beverages • Jimson Weed, angel’s trumpet, thorn apple (Datura species) • Mandrake root (Mandragora officinarum ) • Deadly Night Shade (Atropa belladonna)
- 12. Cholinergic syndrome in Tropane Alkaloids?????? WHOAATTTT!!!!
- 13. Anticholinergic Plant Toxicity: Epidemiology • 528 single exposures to anticholinergic plants were reported in 2017 in the USA (1) • 107 of those were treated in health care facilities. • Major outcomes occurred in four cases, but no deaths were documented • 82% of the cases occurred in males • 72% of cases occurred in those aged 13-19 years • Worldwide incidence is unknown • Most common reports involve the Datura species 1. 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report.
- 15. Pathophysiology • Manifests as classic anticholinergic poisoning • Symptoms onset: 30-60 mins • May last up to 48 hrs as tropane alkaloids result in delayed gastric emptying • Scopolamine • The primary compound responsible for the toxic effects • Acting as an antagonist at both peripheral and central muscarinic • Highest concentrations in roots and seeds • Atropine • Artifact of purification, produced by racemization of l-hyoscyamine. • Proportion of each alkaloid present varies among species, time of year, location, and part of plant. • As little as half teaspoon of Datura seed (0.1 mg of atropine/seed): CP Arrest
- 16. Datura Species Jimson WeedAngel’s Trumpet Thorn apple
- 17. Datura Species • Traditional Uses: • Flu like symptoms • Asthma • Arthritis • Antispasmodics • As additives to boost the effects of cannabis • MOA: • Blocks Ach at muscarinic receptor; block effects of parasympathetic system • High doses will block nicotinic receptors; autonomic dysfunction
- 18. Datura Species • Signs and Symptoms (9 Ds) • Dryness of mouth and throat • Difficulty in talking • Dysphagia • Dilation of cutaneous blood vessels • Dilation of pupils • Dry hot skin • Drunken skin • Delirium • Drowsiness • Fatal dose: • 100-125 seeds • Lethal dose: 60mg Adults, 4mg Children • Death usually occurs within 24 hours
- 19. Mandrake Root (Mandragora officinarum )
- 20. Mandrake Root (Mandragora officinarum ) • Uses: • Witchcraft • Gastric ulcers • Indigestion • Constipation • Asthma/ whooping cough • Hay fever • Convulsions • Rheumatism • Emetic • Sedative • Increase interest in sexual activity • MOA • Anticholinergic effects (leads to asphyxiation) • Hallucinogenic effects • Hypnotic effects • Other effects: • Severe diarrhea and vomiting leading to profund dehydration and death
- 22. Deadly Night Shade (Atropa belladonna)
- 23. Deadly Night Shade (Atropa belladonna) • Uses: • Sedative • Asthma and whooping cough • Viral Illness • Parkinson's disease • Inflammatory bowel disease • Ointments for joint pain • Neuralgia • Anxiety • Suppositories for hemorrhoids. • Approved by the FDA for homeopathic remedies*** • Without treatment: • 2-5 berries and 10-20 berries are lethal in children and adults respectively
- 24. Differential Diagnosis • CNS Disorders* • Reye’s syndrome • Head trauma • alcohol and sedative-hypnotic withdrawal • postictal state • Other intoxications* (sympathomimetic toxicity) • Neuroleptic malignant syndrome and acute psychotic disorders • Pharmacobezoar***
- 25. Management Approach to Anticholinergic Plant Toxicity
- 26. Question 1 • What is the antidote for anticholinergic plant poisoning and how does it work?
- 27. Question 2 • What physical exam findings are classic with anticholinergic syndrome?
- 28. Question 3 • What supportive management is usually required for patients with anticholinergic syndrome?
- 29. ED Management Approach • DECONTAMINATION • Resuscitation (ABCDE) • Supportive Care • Antidote • Treat plant ingestion as potentially toxic until proven otherwise • Attempt to ID the plant • Time of ingestion and dose ingested is essential • Call poison control center • Appropriate disposition +/- social intervention
- 30. Clinical Presentation • Symptoms • usually occur 30-60min after ingestion and includes a classical anticholinergic syndrome • Dryness of mouth • Dyphagia and dysarthria • Blurred vision and photophobia • Urinary retention • Altered mental status- from amnesia and confusion • Aggitation • Hallucinations • Seizures • Coma
- 31. Clinical Signs • Vital Signs: • Tachycardia • Hypertension • Hyperthermia • HEENT: • Mydriasis and cycloplegia • Dry mucus membranes • Skin: • Warm, dry, flushed • CNS: • AMS • Agitation • Delirium • Confusion • Hallucination • GI: • Decreased bowel sounds • Urinary retention
- 32. Investigations • No specific diagnostic tests exist • Toxicological analysis: only useful if co-ingestion is suspected (acetaminophen + salicylates most common) • ECG: marked tachyarrhythmias • Evaluation of complications: • CPK, U&Es and urinalysis: rhabdomyolysis, ARF
- 33. Treatment • Largely Supportive • ABC • Consider GI Decontamination • Gastric Lavage-controversial (increased risk of aspiration!) • 24-32 F tube in children • 36-42 F tube in adult • Activated Charcoal- may be useful • 1-2g/kg PO • Can be repeated after 4-6 hrs
- 34. Supportive Care • Agitation/Hallucination: • Reassurance • Benzodiazepines • Diazepam 5-10mg IV in adults, 0.2-0.5 mg/kg IV in children • Lorazepam 1-2 mg IV in adults, 0.05 mg IV in children • Mechanical restrains • Caution as use may precipitate rhabdomyolysis • HALOPERIDOL IS CONTRAINDICATED • Seizures • Diazepam • Phenobarbitone
- 35. • Urinary retention: • Foley Catheter • Maintain urine output at 1-2 ml/kg/hr
- 36. Antidote • PHYSOSTIGMINE • Indications: • Patient unresponsive to supportive treatment • Tachyarrhythmias with hemodynamic compromise • Intractable seizures unresponsive to benzodiazepines • Severe agitation or psychosis • Dose: • Adults: 0.5-1mg IV slow push over 5 minutes, repeat every 10 minutes until desired clinical effects • Paediatrics: 0.02mg/kg (maximum 0.5mg)
- 37. Contraindication to Physostigmine use • TCA Overdose/toxicity • Widened QRS complex (> 100ms) • Bradydysrhythmias, intraventricular and AV blocks • Bronchospasm • Its use should be cautioned as it can precipitate a cholinergic crisis
- 38. Disposition 1. Patients with mild symptoms of anticholinergic toxicity that resolve after 6 hours of ED observation may be medically cleared. 2. Patients with more than mild symptoms, as well as those who have received physostigmine, require hospital observation until symptoms resolve or approximately 12 hours after the last dose of physostigmine.
- 39. Summary • Anticholinergic properties are present in over 600 compounds, including prescription drugs, over-the-counter medications, and plants • Many of these substances possess anticholinergic activity as either a direct therapeutic effect or as an adverse effect in addition to their primary or predominant pharmacologic effect. • Plant poisonings can present as an anticholinergic toxidrome. • Management options are based on clinical signs and symptoms and administering the appropriate antidote.
- 40. References 1.Nguyen TK, Jamali A, Lanoue A, Gontier E, Dauwe R. Unravelling the architecture and dynamics of tropane alkaloid biosynthesis pathways using metabolite correlation networks. Phytochemistry. 2015 Aug. 116:94-103. 2.Glatstein M, Alabdulrazzaq F, Scolnik D. Belladonna Alkaloid Intoxication: The 10-Year Experience of a Large Tertiary Care Pediatric Hospital. Am J Ther. 2016 Jan-Feb. 23 (1):e74-7. 3.Blackford MG, Fitzgibbon JJ, Reed MD. Assessment of serum creatine kinase among adolescent patients following jimsonweed (Datura stramonium) and moonflower (Datura inoxia) ingestions: a review of 11 cases. Clin Toxicol (Phila). 2010 Jun. 48(5):431-4. 4. Tintinalli's Emergency Medicine A Comprehensive Study Guide (Tintinalli) 9 ed (2021).pdf 5.Berdai MA, Labib S, Chetouani K, Harandou M. Atropa belladonna intoxication: a case report. Pan Afr Med J. 2012. 11:72. 6.Kwakye GF, Jiménez J, Jiménez JA, Aschner M. Atropa belladonna neurotoxicity: Implications to neurological disorders. Food Chem Toxicol. 2018 Apr 10.
- 41. THE END Beauty lies in the eyes of the beholder
Editor's Notes
- Antidote*-Atropine is the antidote for cholinergic syndromes produced from nerve agents or organophosphate insecticides. Administration of high dose atropine to someone without cholinesterase poisoning can result in anticholinergic toxicity. This occurred in Israel during the first Gulf War in 1991, when frightened civilians dosed themselves with atropine fearing an incoming Scud missile chemical weapon attack
- Anticholinergic is a misnomer as it’s really a antimuscarinic toxidrome as it does not competitively antagonizes Ach at the nicotinic receptors Carphologia picking at imaginary objects
- Atropine is the prototypical anticholinergic (anti-muscarinic) drug
- Adulteration of commonly abused drugs (e.g., heroin, cocaine) with scopolamine or atropine has been observed.
- Although most tropane alkaloids cause an anticholinergic syndrome, a case report indicates that the tropane alkaloid–containing medicinal herb Erycibe henri Prain ("Ting Kung Teng") contains a tropane alkaloid that may cause a cholinergic syndrome, as well as renal, hepatic, and erythrocyte toxicity. [13] This is considered atypical for the tropane alkaloids, which are predominantly strongly anticholinergic Journal of Clinical Toxicology
- 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report.
- The usual route of ingestion is as a tea, although ingesting seeds or other plant parts and smoking dried leaves also are common.
- Leaves are alternate with lobed or tooth margins Flowers are erect or spreading trupet shaped with colurs varying from white, yellow, pink, purple Fruit is a spiny capsule opening to release numerous small seeds
- Roots are bifurcated and resemble human figures one-flowered nodding peduncles spring from the neck bearing whitish-green or purple flowers, nearly 5 centimetres (2.0 in) broad, which produce globular, orange to red berries, resembling small tomatoes. All parts of the mandrake plant are poisonous Belonging to the nightshades family (Solanaceae)
- Perennial herbaceous plant in the nightshade family Solanaceae, which includes tomatoes, potatoes, and eggplant Known as “devil’s cherries” Extrem;y toxic in small portions
- ***No evidence of definitive results of same
- The difference between anticholinergic toxicity and sympathomimetic toxicity (e.g., cocaine toxicity, delirium tremens) can be subtle, because patients with either may develop tachycardia, mydriasis, and delirium. The presence of red dry skin and the absence of bowel sounds suggest anticholinergic poisoning *Other CNS disorders, such as viral encephalitis, may also affect cholinergic outflow and produce similar anticholinergic clinical signs not related to a toxic exposure ***BEZOARS are retained concretions of indigestible foreign material that accumulate and conglomerate in the gastrointestinal tract, most commonly in the stomach. A rare case of pharmacobezoar has been reported with diphenhydramine overdose; this should be a consideration if the toxidrome continues longer than expected
- Physostigmine is the antidote for anticholinergic syndrome. It inhibits acetylcholinesterase, the enzyme that degrades acetylcholine, thereby increasing the concentrations of acetylcholine and overcoming the competitive inhibition at nerve terminals.
- Physical exam findings suggesting anticholinergic poisoning include hyperthermia, dry mouth, tachycardia, mydriasis, flushed dry skin, absent bowel sounds, urinary retention, agitation, hallucinations, lethargy, mumbling speech, undressing behavior (generally due to hyperthermia) and repetitive picking behavior. Blurred vision and photophobia may be due to mydriasis and paralysis of accommodation. Seizures, paralysis, respiratory depression, and coma may occur in severe toxicity. Anticholinergic effects delay gastric emptying, resulting in a prolonged duration of action
- Treatment primarily consists of supportive care. Hypotension generally responds to isotonic fluid administration. Agitation, psychosis, or seizures are treated with benzodiazepines such as diazepam or lorazepam. Cooling via evaporative methods is generally sufficient if hyperthermia is present. Physostigmine can reverse the peripheral or central anticholinergic syndrome if clinically indicated. GI decontamination -Activated charcoal May be more effective due to the decreased GI motility Sedation Benzodiazepines Decreases the risk of hyperthermia, rhabdomyolysis, and traumatic injuries Wide-complex Tachyarrhythmias -Sodium bicarbonate Arrhythmia due to sodium channel blockade; avoid class IA antiarrhythmics (procainamide) Cholinesterase Inhibition- Physostigmine Use for cases of severe agitation or delirium; avoid when cardiac conduction abnormalities are present
- 1.Emesis by Ipecac -contraindicated 2.Gastric Lavage-controversial (increased risk of aspiration!) 24-32 F tube in children 36-42 F tube in adult 3. Activated Charcoal- useful 1-2g/kg po or via nasogastric/orogastric tube Can be repeated after 4-6 hrs
- Stuffed as a Pipe
- Hemodialysis and Hemoperfusion is not useful because of high lipid solubility of tropane alkaloids
- The major adverse effects of physostigmine—profound bradycardia and seizures—were historically touted as common, but evidence for this belief is lacking.42 Importantly, the risk of these adverse effects appears greater in patients without anticholinergic toxicity, so accurate diagnosis of anticholinergic toxicity is important before administering physostigmine In cases of uncertain anticholinergic poisoning, a diagnostic challenge with physostigmine is not recommended because of the small but increased risk of adverse effects in patients without anticholinergic toxicity
- Because the duration of action of physostigmine is generally shorter than the duration of action of many anticholinergic agents, the reversal effect may dissipate, resulting in recurrent toxicity.