eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Anticholinergic

John J Bruns, Jr, MD, Clinical Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine

Updated: Mar 26, 2008

Introduction

Background

Anticholinergic syndrome (ACS) is produced by the inhibition of cholinergic neurotransmission at muscarinic receptor sites.

For a related CME activity, see CME - New Risk Score Predicts Risk for Anticholinergic Adverse Effects. 

Pathophysiology

Substances with anticholinergic properties competitively antagonize acetylcholine muscarinic receptors; this predominantly occurs at peripheral (eg, heart, salivary glands, sweat glands, GI tract, GU tract) postganglionic parasympathetic muscarinic receptors. Anticholinergic substances minimally compete with acetylcholine at other sites (eg, autonomic ganglia).

Central nervous system (CNS) manifestations result from central cortical and subcortical muscarinic receptor antagonism. The degree of CNS manifestation is related to the drug's ability to cross the blood-brain barrier.

Frequency

United States

Anticholinergic syndrome may be caused by intentional overdose, inadvertent ingestion, medical noncompliance, and geriatric polypharmacy. Systemic effects also have resulted from topical eye drops. Anticholinergic syndrome commonly follows the ingestion of a wide variety of prescription and over-the-counter medications.

Intentional abuse with hallucinogenic plants (eg, Datura stramonium [jimson weed]) and mushrooms (eg, Amanita muscaria) can cause anticholinergic syndrome due to the presence of anticholinergic tropane alkaloids. Scopolamine has been used in beverages as "knockout drops," and several cases of anticholinergic syndrome have been reported following Chinese herbal tea consumption.

According to the American Association of Poison Control Centers, almost 2.4 million cases of human poison exposure were reported to 65 US poison control centers in 2003.¹

In 2003, the Toxic Exposure Surveillance System reported 3094 symptomatic anticholinergic drug presentations with unintentional ingestions in 52%, intentional ingestions in 38%, and adverse reactions occurring in 7% of cases; moderate morbidity (requiring specific treatment) was reported in 20%, major morbidity (life-threatening) in 3.7%, and death in 5 cases (case-fatality proportion = 0.16%).¹

In 2003, the Toxic Exposure Surveillance System reported 70,251 symptomatic antihistamine presentations with 28,092 specific to diphenhydramine. A total of 64 deaths were attributed to antihistamine toxicity of which 38 were specifically diphenhydramine related for case-fatality proportions of 0.09% and 0.14%, respectively.¹

Patients with severe central manifestations (eg, hallucinations, psychoses, seizures, coma) have the highest morbidity rates.

Clinical

History

• For all patients with suspected poisoning, determine the precise substance(s) ingested, time of ingestion, quantity ingested, rationale for ingestion, and co-ingestants.
• Ascertain patient compliance, medical history, prescription medications, and nonprescription medications (including natural or herbal products).
• Many medications have anticholinergic properties, which can result in additive toxicity.
• Always inquire about use of dermally applied drugs (ie, scopolamine transdermal delivery system).

Physical

• Anticholinergic syndrome results from the inhibition of muscarinic cholinergic neurotransmission.
• Clinical manifestations are caused by CNS effects, peripheral nervous system effects, or both.
• Remember common signs and symptoms with the mnemonic, "red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare." The mnemonic refers to the symptoms of flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status (AMS), and fever, respectively.
• Additional manifestations include sinus tachycardia, decreased bowel sounds, functional ileus, urinary retention, hypertension, tremulousness, and myoclonic jerking.
• Patients with central anticholinergic syndrome may present with ataxia, disorientation, short-term memory loss, confusion, hallucinations (visual, auditory), psychosis, agitated delirium, seizures (rare), coma, respiratory failure, and cardiovascular collapse.

Causes

Agents with anticholinergic properties are as follows:

• Anticholinergics
  • Atropine, scopolamine
  • Glycopyrrolate
  • Benztropine, trihexyphenidyl
• Antihistamines
  • Chlorpheniramine
  • Cyproheptadine
  • Doxylamine
  • Hydroxyzine
  • Dimenhydrinate
  • Diphenhydramine
  • Meclizine
  • Promethazine
• Antipsychotics
  • Chlorpromazine
  • Clozapine
  • Mesoridazine
  • Olanzapine
  • Quetiapine
  • Thioridazine
• Antispasmodics
  • Clidinium
  • Dicyclomine
  • Hyoscyamine
  • Oxybutynin
  • Propantheline
• Cyclic antidepressants
  • Amitriptyline
  • Amoxapine
  • Clomipramine
  • Desipramine
  • Doxepin
  • Imipramine
  • Nortriptyline
  • Protriptyline
• Mydriatics
  • Cyclopentolate
  • Homatropine
  • Tropicamide
• Plants
  • Amanita muscaria (fly agaric)
  • Amanita pantherina (panther mushroom)
  • Arctium lappa (burdock root)
  • Atropa belladonna (deadly nightshade)
  • Cestrum nocturnum (night blooming jessamine)
  • Datura suaveolens (angel's trumpet)
  • Datura stramonium (jimson weed)
  • Hyoscyamus niger (black henbane)
  • Lantana camara (red sage)
  • Solanum carolinensis (wild tomato)
  • Solanum dulcamara (bittersweet)
  • Solanum pseudocapsicum (Jerusalem cherry)
  • Solanum tuberosum (potato)
  • Miscellaneous, including carbamazepine, cyclobenzaprine, and orphenadrine

Differential Diagnoses

Workup

Laboratory Studies

• No specific diagnostic studies exist for anticholinergic overdoses.
• Serum drug concentrations are not helpful and results rarely are available to aid in initial management. However, perform screening for acetaminophen and salicylate in all intentional poisonings because combination medication preparations and multiple ingestions often occur.
• Consider blood and urine cultures in febrile patients.
• Serum chemistry and electrolyte analysis may provide clues to the intoxicating agents and co-ingestants. Obtain a creatine kinase (CK) in patients with psychomotor agitation to rule out associated rhabdomyolysis.
• Perform electrolyte and arterial blood gas (ABG) analysis when bicarbonate therapy has been instituted for agents that also produce type 1A cardiac conduction disturbances; blood pH should be 7.45-7.55.
• Perform a urine pregnancy test on all women of childbearing age.

Imaging Studies

• Consider CT scan of the head and MRI imaging in patients with altered mental status that is insufficiently explained by the ingested agent or in patients that are unresponsive to appropriate intervention.

Other Tests

• Immediately perform electrocardiogram (ECG) analysis on all patients with suspected toxic ingestions.

Procedures

• Consider lumbar puncture (LP) in all patients with fever and altered mental status.

Treatment

Prehospital Care

• Rapidly transport the patient to the nearest emergency facility with advanced life support (ALS) capabilities. Focus primary assessment on circulatory, respiratory, and neurologic systems.
• Obtain IV access and frequently monitor vital signs. Administer naloxone and thiamine and assess for hypoglycemia in patients with altered mental status.
• Manage seizures with benzodiazepines.
• Physostigmine is not recommended in the prehospital setting.
• Avoid ipecac syrup and defer administration of activated charcoal unless a prolonged transport time is anticipated.

Emergency Department Care

Initial assessment and stabilization are required. Upon ED arrival, ensure an adequate airway and check that breathing is present and maintained. Provide oxygen and intubate if significant CNS or respiratory depression exists. Assess circulation and initiate cardiac and pulse oximetry monitoring. Examine the patient's body for transdermal drug delivery patches (eg, scopolamine) and remove, if found. Obtain an ECG soon after ED arrival. Sinus tachycardia is common and does not require treatment in the stable patient. Administer sodium bicarbonate to patients with QRS prolongation (>100 milliseconds) or the presence of terminal right axis (R wave in aVR > 3 mm) on the ECG. Collect blood for laboratory analysis and quick glucose measurement while obtaining IV access. Closely examine patients for signs of trauma. Agitated patients may respond to reassurance. If chemical restraint is required, physostigmine or benzodiazepines may be used.

• Following initial stabilization, GI decontamination usually is necessary after anticholinergic poisoning by ingestion. Ipecac syrup is contraindicated because of the potential for AMS and seizures.
  • For the vast majority of patients, single dose activated charcoal (1 g/kg with or without a cathartic) by mouth or nasogastric tube is sufficient for GI decontamination. Gastric lavage (followed by activated charcoal administration) is acceptable for patients presenting obtunded and within one hour of ingestion. GI decontamination with activated charcoal is recommended, even when patients present many hours postingestion, because of delayed gut emptying of anticholinergic agents and slowed peristalsis. Repeated doses of activated charcoal are not necessary for most patients.
  • Most anticholinergic agents have large volumes of distribution and are highly protein-bound; therefore, hemodialysis and hemoperfusion are ineffective treatment methods.
• Following GI decontamination, patients often recover well with supportive care. Tachycardia often resolves with crystalloid infusions, control of agitation (eg, benzodiazepines), and fever control (eg, fluids, antipyretics, active cooling measures). Administer a trial dose of physostigmine over 2-5 minutes for patients with narrow QRS supraventricular tachydysrhythmias resulting in hemodynamic deterioration or ischemic pain. Ventricular arrhythmias can be treated with lidocaine.
  • Manage seizures with benzodiazepines, preferably diazepam or lorazepam. Use phenobarbital and other barbiturates for intractable seizures. Phenytoin has no proven role for toxin-induced seizures. Repeat ECG analysis immediately following seizure activity because acidosis can potentiate conduction aberrancies with certain agents.
  • Patients with hallucinations often respond to reassurance and do not require specific treatment unless associated with significant psychomotor agitation. Agitation may be treated with the specific antidote, physostigmine, or nonspecifically with benzodiazepines. Although its use is controversial, physostigmine administration is safe and effective for controlling agitated delirium if the ECG indicates the absence of prolonged PR and QRS intervals. Phenothiazines are contraindicated because of their anticholinergic properties. Perform bladder catheterization if signs or symptoms of urinary retention exist.
• The antidote for anticholinergic toxicity is physostigmine salicylate. Physostigmine is the only reversible acetylcholinesterase inhibitor capable of directly antagonizing the CNS manifestations of anticholinergic toxicity; it is an uncharged tertiary amine that efficiently crosses the blood brain barrier.
  • By inhibiting acetylcholinesterase, the enzyme responsible for the hydrolysis of acetylcholine, an increased concentration of acetylcholine augments stimulation at muscarinic and nicotinic receptors. Physostigmine can reverse the central effects of coma, seizures, severe dyskinesias, hallucinations, agitation, and respiratory depression. The most common indication for physostigmine is to control agitated delirium.
  • The most common adverse effects from physostigmine are peripheral cholinergic manifestations (eg, vomiting, diarrhea, abdominal cramps, diaphoresis). Physostigmine also may produce seizures, a complication frequently reported when administered to individuals with tricyclic antidepressant poisoning. Rarely, physostigmine may produce bradyasystole; this complication has been reported 3 times in literature, and each occurred when physostigmine was administered to patients with severe tricyclic antidepressant poisoning. To avoid bradyasystole in patients, do not administer physostigmine in the presence of prolonged PR or QRS intervals on the ECG.
  • Most patients can be treated safely without physostigmine, but it is recommended for use when at least one of the following aberrations are present: tachydysrhythmias with subsequent hemodynamic compromise, intractable seizures, or severe agitation or psychosis (in which the patient is considered a threat to self or others).
  • Although some recommend the use of benzodiazepines as first-line agents for the control of agitation associated with the anticholinergic syndrome, a recent study suggests that physostigmine is significantly more effective and no less safe for use in this setting.
  • Physostigmine is contraindicated in patients with cardiac conduction disturbances (prolonged PR and QRS intervals) on ECG analysis.

Consultations

• Consult with a regional poison center and/or toxicologist in all toxic exposures for assistance with decontamination and therapeutic intervention decisions, particularly regarding the use of physostigmine.
• Psychiatric consultation is mandatory in all intentional ingestions.
• In chronic intoxication or overmedication, contact the prescribing physician to prevent recurrence.

Medication

Medical therapy consists of anticonvulsants, antitachydysrhythmics, sodium bicarbonate, physostigmine, and sedatives.

GI decontaminant

Empirically used to minimize systemic absorption of the toxin.

Activated charcoal (Liqui-Char)

Most useful if administered within 4 h of ingestion. Repeat doses may be used, especially with ingestion of sustained release agents. Limited outcome studies exist, especially when administration is more than 1 h of ingestion.
Administration of charcoal by itself (in aqueous solution), as opposed to coadministration with a cathartic is becoming the current practice standard; this is because studies have not shown benefit from cathartics and, while most drugs and toxins are absorbed within 30-90 min, laxatives take hours to work. Also, dangerous fluid and electrolyte shifts have occurred when cathartics are used in small children.
When ingested dose is known, charcoal may be given at 10 times ingested dose of agent over 1 or 2 doses.

Dosing

Adult

1g/kg PO/NG (50-75 g usual dose); may administer 0.5 g/kg PO/NG as repeat dose if desired
Cathartic: Not recommended

Pediatric

Administer as in adults (12.5-25 g usual dose); may administer 0.5 g/kg PO/NG as repeat dose if desired
<2 years: Cathartic administration not recommended

Interactions

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; decreased levels occur when administered with sherbet, milk, or ice cream

Contraindications

Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies; unprotected airway with absent gag reflex

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Protect airway before administration in patients with absent gag reflex or a depressed level of consciousness; when considering repeat dosing, monitor for active bowel sounds to minimize risk of charcoal ileus

Benzodiazepines and other sedatives

For patients with agitation or psychosis, verbal reassurance and a quiet dimly lit room may be effective. When pharmacological intervention is required, control of agitation may be achieved with the administration of physostigmine or benzodiazepines (DOC). Treat seizures initially with benzodiazepines.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Dosing

Adult

5-10 mg IV q10min; titrate to effect; significant doses may be required to control agitation

Pediatric

30 days to 5 years: 0.2-0.5 mg IV (slowly) q2-5min; titrate to effect
>5 years: 1 mg IV (slowly) q2-5min

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor for respiratory depression with high or repeated doses; caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.
By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Dosing

Adult

2 mg IV/IM; titrate to effect; some patients may require much larger doses

Pediatric

0.05 mg/kg IV/IM

Interactions

Effects are potentiated by phenothiazines, narcotics, barbiturates, MAOIs, and other antidepressants

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor for respiratory depression with high or repeated doses; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Phenobarbital (Luminal)

Used for patients refractory to diazepam or lorazepam.

Dosing

Adult

70-100 mg slow IV initial to control agitation; small increments may be given not to exceed 500 mg
10-20 mg/kg IV no faster than 100 mg/min to control seizures

Pediatric

50 mg IV initial (2-6 mg/kg); small increments may be given at 1-min intervals not to exceed 10-20 mg/kg; children will likely need intubation with larger doses

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and fatality; chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy); menstrual irregularities also may occur

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritic patients

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for respiratory depression with high or repeated doses; in prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema

Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

Dosing

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV given slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg followed by continuous infusion of 1 mcg/kg/min, titrating dose upward q5min until seizures controlled

Interactions

Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when using together

Contraindications

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and patients >60 y; monitor for respiratory depression with high or repeated doses; consider lower dosages in patients with organic brain syndrome, and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Cardiovascular agents

Used only when patient is diagnosed with tricyclic antidepressant overdose or when evidence of sodium channel blockade is present. Routine use is not recommended.

Sodium bicarbonate

Anecdotally, has been effective in treating antihistamine induced QRS prolongation (>100 ms) with a quinidinelike ECG pattern.

Dosing

Adult

1 mEq/kg IV push; may repeat once; if effective, (narrowing of QRS), begin sodium bicarbonate gtt, 3 amps (44 mEq/amp) in 1 L D₅ W; infuse at twice maintenance; not to exceed 50-100 mEq; monitor serum pH frequently and keep in a range of 7.50-7.55; discontinue drip when anticholinergic manifestations resolve and monitor for recurrence

Pediatric

Administer as in adults

Interactions

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; Increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Contraindications

Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause alkalosis (monitor serum pH; not to exceed 7.55), decreased plasma potassium, hypocalcemia and hypernatremia; caution in electrolyte imbalances such as patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because can cause tissue necrosis

Cholinergic agents

Reversible anticholinesterase inhibitor that increases the concentration of ACh at the sites of cholinergic neurotransmission. Readily crosses the blood-brain barrier to produce desired CNS effects.

Physostigmine (Antilirium)

Inhibits destruction of acetylcholine by acetylcholinesterase, which facilitates transmission of impulses across myoneural junction.
Clinical effects last 20-60 min. Repeat prn.

Dosing

Adult

2 mg IV at a slow, controlled rate (no faster than 4 min)

Pediatric

0.02-0.06 mg IV at a slow, controlled rate, not to exceed 0.5 mg/min or 2 mg as a single dose

Interactions

Atropine antagonizes muscarinic effects; effects of neuromuscular agents are increased

Contraindications

Documented hypersensitivity; GI or GU obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor heart rate and rhythm during use.
IV injection contains benzyl alcohol; should not be used in neonates; caution in epilepsy, asthma, bradycardia, hyperthyroidism, cardiac arrhythmias, gangrene, peptic ulcer, diabetes, and patients receiving choline esters of depolarizing neuromuscular blockers; anticholinesterase insensitivity can develop for brief or prolonged periods

Follow-up

Further Inpatient Care

• Admission decisions are based on patient symptomatology. Asymptomatic patients without anticholinergic signs or symptoms can be discharged after a 4-6 hour observation period. Individuals with initial mild toxicity that resolve during initial observation also may be discharged.
• Admit and monitor symptomatic patients, usually in an ICU setting, until a symptom-free period of 4 hours without the aid of antidotes or supportive therapy is documented.

References

1. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline]. [Full Text].

2. Bryson P. Comprehensive Review in Toxicology. Hemisphere Publishing; 1989:3-11, 75-83, 566-7.

3. Burns MJ, Linden CH, Graudins A, et al. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. Apr 2000;35(4):374-81. [Medline].

4. Daunderer M. Physostigmine salicylate as an antidote. Int J Clin Pharmacol Ther Toxicol. Dec 1980;18(12):523-35. [Medline].

5. Ellenhorn MJ, Barceloux D. Medical toxicology. In: Elsevier Applied Science. Elsevier Science; 1988:16, 25-31, 83, 93, 106-9, 117, 407, 472, 474, 592, 666.

6. Goldfrank L, Flomenbaum N, Lewin N, et al. Anticholinergic poisoning. J Toxicol Clin Toxicol. Mar 1982;19(1):17-25. [Medline].

7. Haddad LM, Winchester JF, eds. Clinical Management of Poisoning and Drug Overdose. 2^nd ed. WB Saunders Co; 1990:861-7, 83, 231, 385.

8. Kaye S. Handbook of Emergency Toxicology: A Guide for the Identification, Diagnosis and Treatment of Poisoning. 5^th ed. Charles C Thomas Pub Ltd; 1988:31-44.

9. Lu F. Basic Toxicology: Fundamentals, Target Organs, and Risk Assessment. 3^rd ed. Taylor & Francis; 1996:52-4, 65, 279-84.

10. McFarland KA. Anticholinergic poisoning. In: Emergency Medicine. 1998.

11. Nice A, Leikin JB, Maturen A, et al. Toxidrome recognition to improve efficiency of emergency urine drug screens. Ann Emerg Med. Jul 1988;17(7):676-80. [Medline].

Keywords

anticholinergic toxicity, anticholinergic syndrome, ACS, anticholinergic drug ingestions, anticholinergic drug overdose, anticholinergic poisoning, antihistamines, antipsychotics, antispasmodics, cyclic antidepressants, mydriatics, atropine, scopolamine, glycopyrrolate, benztropine, trihexyphenidyl, chlorpheniramine, cyproheptadine, doxylamine, hydroxyzine, dimenhydrinate, diphenhydramine, meclizine, promethazine, chlorpromazine, clozapine, mesoridazine, olanzapine, quetiapine, thioridazine, clidinium, dicyclomine, hyoscyamine, oxybutynin, propantheline, amitriptyline, amoxapine, clomipramine, desipramine, doxepin, imipramine, nortriptyline, protriptyline, cyclopentolate, homatropine, tropicamide, Amanita muscaria, fly agaric, Amanita pantherina, panther mushroom, Arctium lappa, burdock root, Atropa belladonna, deadly nightshade, Cestrum nocturnum, night blooming jessamine, Datura suaveolens, angel's trumpet, Daturastramonium, jimson weed, Hyoscyamus niger, blackhenbane, Lantana camara, red sage, Solanum carolinensis, wild tomato, Solanum dulcamara, bittersweet, Solanum pseudocapsicum, Jerusalem cherry, Solanum tuberosum, potato, carbamazepine, cyclobenzaprine, orphenadrine

Contributor Information and Disclosures

Author

John J Bruns, Jr, MD, Clinical Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

David C Lee, MD, Research Director, Department of Emergency Medicine, Assistant Professor, North Shore University Hospital and New York University Medical School
David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center
Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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