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Anticholinergic Toxicity

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

Practice Essentials

Anticholinergic syndrome (ACS) is produced by the inhibition of cholinergic neurotransmission at muscarinic receptor sites. It commonly follows the ingestion of a wide variety of prescription and over-the-counter medications.[1, 2, 3] This syndrome may be caused by intentional overdose, inadvertent ingestion, medical noncompliance, or geriatric polypharmacy; systemic effects also have resulted from topical eye drops.

Signs and symptoms

Clinical manifestations are caused by CNS effects, peripheral nervous system effects, or both. Common manifestations are as follows:

  • Flushing
  • Dry skin and mucous membranes
  • Mydriasis with loss of accommodation
  • Altered mental status (AMS)
  • Fever

Additional manifestations include the following:

  • Sinus tachycardia
  • Decreased bowel sounds
  • Functional ileus
  • Urinary retention
  • Hypertension
  • Tremulousness
  • Myoclonic jerking

See Clinical Presentation for more detail.

Diagnosis

No specific diagnostic studies exist for anticholinergic overdoses. Laboratory studies that may be helpful include the following:

  • Acetaminophen and salicylate screening - in all intentional poisonings
  • Blood and urine cultures – in febrile patients
  • Serum chemistry and electrolyte analysis
  • Electrolyte and arterial blood gas (ABG) analysis
  • Urine pregnancy test - in all women of childbearing age

Additional studies that may be useful are as follows:

  • CT of the head and MRI imaging - for patients in whom AMS is insufficiently explained by the ingested agent or who are unresponsive to appropriate intervention
  • ECG - for all patients with suspected toxic ingestions
  • Lumbar puncture - for all patients with fever and AMS

See Workup for more detail.

Management

Patients presenting with anticholinergic toxicity should be transported to the nearest emergency facility with advanced life support (ALS) capabilities. Avoid administering ipecac syrup and activated charcoal unless prolonged transport time is anticipated.

After stabilizing the patient in the ED, it is usually necessary to remove the toxin from the GI tract. This can be accomplished in the vast majority of patients with single-dose activated charcoal by mouth or nasogastric tube. Gastric lavage (followed by activated charcoal administration) is acceptable for patients presenting obtunded and within 1 hour of ingestion.

The antidote for anticholinergic toxicity is physostigmine salicylate. Most patients can be safely treated without it, but it is recommended when tachydysrhythmia with subsequent hemodynamic compromise, intractable seizure, severe agitation or psychosis, or some combination thereof is present. Physostigmine is contraindicated in patients with cardiac conduction disturbancese agitation or psychosis, or some combination thereof is present. Physostigmine is contraindicated in patients with cardiac conduction disturbances on ECG.

See Treatment and Medication for more detail.

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Background

Anticholinergic syndrome (ACS) is produced by the inhibition of cholinergic neurotransmission at muscarinic receptor sites. It commonly follows the ingestion of a wide variety of prescription and over-the-counter medications.[1, 2, 3] This syndrome may be caused by intentional overdose, inadvertent ingestion, medical noncompliance, or geriatric polypharmacy; systemic effects also have resulted from topical eye drops.

Clinical manifestations are caused by central nervous system effects, peripheral nervous system effects, or both (see Presentation). Treatment usually includes gastric decontamination.The antidote for anticholinergic toxicity is physostigmine salicylate. Most patients can be safely treated without it, but it is recommended when tachydysrhythmia with subsequent hemodynamic compromise, intractable seizure, severe agitation or psychosis, or some combination thereof is present. Physostigmine is contraindicated in patients with cardiac conduction disturbances. (See Treatment and Medication.)

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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.

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Frequency

United States

Anticholinergic syndrome may be caused by intentional overdose, inadvertent ingestion, medical noncompliance, or 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.[1, 2, 3]

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.

In 2013, the American Association of Poison Control Centers (AAPC) National Poison Data System Annual Report documented 8729 single exposures to anticholinergic drugs. Unintentional ingestions accounted for 8208 presentations, intentional ingestions accounted for 332 presentations, and adverse reactions occurred in 151. Moderate morbidity (requiring specific treatment) was reported in 219 cases, major morbidity (life-threatening) in 16, and 1 death was reported.[4] Patients with severe central manifestations (eg, hallucinations, psychoses, seizures, coma) have the highest morbidity rates.

Antihistamines also have cholinergic properties. In 2013, the AAPCC documented 98,004 symptomatic antihistamine presentations, with 41,430 specific to diphenhydramine. A total of 11 deaths were attributed to antihistamine toxicity of which 10 were specifically diphenhydramine related.[4]

 

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

References
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