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Anticholinergic Toxicity Treatment & Management

  • Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Asim Tarabar, MD  more...
Updated: Aug 09, 2015

Prehospital Care

Prehospital care includes the following:

  • 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 intravenous 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 in the emergency department (ED). Upon arrival, ensure that the airway is adequate and that breathing is present and maintained.[3] Provide oxygen and intubate if significant central nervous system (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 any if found.

Obtain an electrocardiogram (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 intravenous 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, gastrointestinal (GI) decontamination usually is necessary after anticholinergic poisoning by ingestion. Ipecac syrup is contraindicated because of the potential for altered mental status and seizures, which may result in aspiration.

For the vast majority of patients, a single dose of 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 1 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 and should not be used. Perform a repeat ECG 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 they also have significant psychomotor agitation. Agitation may be treated with the specific antidote, physostigmine, or nonspecifically with benzodiazepines. Although its use is controversial, physostigmine 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; three cases of this complication have been reported in literature, and all occurred in patients given physostigmine for severe tricyclic antidepressant poisoning. To avoid bradyasystole, do not administer physostigmine to patients whose ECG shows a prolonged PR or QRS interval.

Most patients can be treated safely without physostigmine, but it is recommended for use when at least one of the following aberrations is 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, one study suggests that physostigmine is significantly more effective and no less safe for use in this setting.[6]

Physostigmine is contraindicated in patients with cardiac conduction disturbances (prolonged PR and QRS intervals) on ECG analysis.



See the list below:

  • 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.
Contributor Information and Disclosures

Mityanand Ramnarine, MD, FACEP Assistant Professor of Emergency Medicine, Program Director, Emergency/Internal Medicine/Critical Care, Hofstra Northwell School of Medicine at Hofstra University; Attending Physician, Department of Emergency Medicine, Long Island Jewish Medical Center

Mityanand Ramnarine, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.


Danish A Ahmad, MD Resident Physician, Departments of Emergency Medicine and Internal Medicine, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

David C Lee, MD Research Director, Department of Emergency Medicine, Associate 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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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