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Anticholinergic Toxicity - Causes, Symptoms, Diagnosis, and Management

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When cholinergic neurotransmission at receptor sites gets inhibited, it results in anticholinergic syndrome. Read the article to learn more.

Written by

Dr. Shikha

Medically reviewed by

Dr. Abhishek Juneja

Published At February 6, 2023
Reviewed AtJune 23, 2023

What Is Anticholinergic Toxicity?

Acetylcholine and muscarinic receptors in the brain and periphery compete with one another, leading to anticholinergic syndrome. This toxidrome is characterized by central inhibition, which results in hyperactive delirium that frequently includes bewilderment, restlessness, and picking at fictitious things. Although the signs and symptoms of peripheral inhibition can vary, they may include hot, dry skin, flushed skin, mydriasis (dilated pupils), tachycardia, reduced bowel noises, and urine retention.

Seizures, coma, and cardiovascular toxicity may not be mediated by muscarinic effects but rather by secondary to drug effects at other receptors, as many anticholinergic medicines are active at numerous receptors or ion channels. There is a spectrum of intensity ranging from mild symptoms to life-threatening conditions. Overdosing on many medications may obscure the anticholinergic toxidrome.

It can be challenging to control anticholinergic toxicity. Due to the symptoms or altered mental state, many patients are unable to give a history, and family members are not always there to provide additional information. Secondly, the toxicity of anticholinergic substances can initially and frequently be thought of as a cause of the patient's symptoms of other diseases. Any number of prescription and over-the-counter drugs may cause it to occur after consumption. Intentional overdose, accidental intake, medical noncompliance, geriatric polypharmacy, and systemic effects from topical eye drops have all been reported as causes of this condition.

What Are Anticholinergic Substances?

Drugs called anticholinergics stop the effects of acetylcholine, a neurotransmitter or chemical messenger. It moves signals among specific cells to influence how the body works. Several conditions can be treated with anticholinergics, including urination and bladder problems, COPD, and a few different poisonings. Additionally, they aid in preventing the uncontrollable muscle spasms linked to conditions like Parkinson's disease. They may also be administered prior to surgery to support the maintenance of bodily processes while a patient is under anesthesia.

What Are the Causes of Anticholinergic Toxicity?

There are many drugs that have anticholinergic effects. Medications that have an anticholinergic effect include antidepressants, antihistamines, antipsychotics, and muscle relaxants. Although the plant called Jimson weed is hardly encountered in real life, it can also result in anticholinergic toxicity.

What Are the Signs and Symptoms?

The clinical symptoms observed in the patients are:

  • Red as a beet: Cutaneous vasodilation.

  • Mad as a hatter: Delirium, attention deficit, hallucinations, dysarthria, and lethargy.

  • Blind as a bat: Non-reactive mydriasis (often delayed 12 to 24 hours).

  • Hot as a hare: Anhidrotic hyperthermia (may become severe with agitation).

  • Dry as a bone: Anhidrosis (especially the axillae and mouth).

  • Full as a flask: Urinary retention.

Sinus tachycardia is present. Hallucinations, irritability, restlessness, and disorientation are all symptoms of delirium. Myoclonus (involuntary muscle jerks), dysarthria (slurred speech), and high-pitched cries are all observed.

How to Diagnose Anticholinergic Toxicity?

Patients with anticholinergic toxicity must be identified by a comprehensive history and physical examination. In the past, patients may have intentionally consumed common anticholinergic substances like antihistamines or jimson weed, but this is not always the case. Patients who have attempted suicide might show up but be unable or reluctant to reveal what they ingested. A parent or caregiver may bring a young child in with suspected ingestion of an unknown substance.

Any suspected poisoned patient should be treated according to a standard procedure by the clinician. Evaluation of the patient's airway, respiratory, and circulatory state should be done just like with any potentially critically ill patient. It is important to take the temperature, heart rate, respiration rate, blood pressure, and oxygen saturation. In order to test for topical sources of toxicity, such as a hyoscine patch, the patient should be thoroughly exposed.

Additionally, the patient needs to be connected to an ongoing cardiac monitoring system and given access to an intravenous (IV) line. It is recommended to obtain diagnostics such as an electrocardiogram, urinalysis, finger-stick glucose, urine drug screen, salicylate and acetaminophen levels, and a pregnancy test for females. A metabolic panel, creatine kinase, and liver enzyme should all be ordered for further laboratory assessment if seizures or severe hyperthermia are present.

It is crucial to realize that anticholinergic poisoning is a clinical diagnosis, although it contrasts with sympathomimetic toxicity (both prescription and over-the-counter sympathomimetic medications or adrenergic drugs can cause poisoning). Lack of perspiration suggests anticholinergic toxicity.

What Are the Treatment and Management?

  • The most common form of treatment for anticholinergic toxicity is supportive care. Managing the agitation that can be extremely severe in individuals with anticholinergic toxicity is the most challenging task. The first-line treatment for agitation should be Benzodiazepines given intravenously. When benzodiazepines are ineffective in treating severe cases, physostigmine may be recommended.

  • If there is hypotension or there is a suspicion of rhabdomyolysis (muscle breakdown that causes the release of a harmful protein into the blood. Myoglobin is a protein that is released into the blood as a result of the breakdown of muscle tissue and can harm renal tissue); intravenous fluids should be given.

  • In the event of substantial hyperthermia (overheating or when body temperature is too high), cooling procedures should be started.

  • If the consumption took place less than an hour before the patient's presentation, activated charcoal should be taken into consideration.

  • Anticholinergics reduce gastrointestinal motility; hence it may be appropriate to provide medication outside of this window.

  • When wide-complex dysrhythmias (irregular or abnormal heartbeat) start to appear, intravenous sodium bicarbonate must be given.

  • Physostigmine is typically only used when anticholinergic toxicity manifests as both peripheral and central symptoms. Before administering Physostigmine, resuscitation tools, including Atropine, should be easily accessible. If symptoms return after about 30 minutes, another dose might be necessary. Physostigmine is typically only advised in cases of pure anticholinergic toxicity.

  • Severe diphenhydramine overdoses that have failed to respond to previous treatments have reportedly been successfully treated with intravenous fat emulsion.

Conclusion:

Employing an interprofessional team-based strategy can maximize the treatment and prevention of anticholinergic toxicity. Anticholinergic poisoning will exhibit symptoms very similar to a sympathomimetic reaction. The primary distinction is that patients with anticholinergic poisoning will also have anhidrosis and mydriasis that are non-responsive to light. Hospital and community pharmacists are great resources for informing patients and the public about pharmaceutical side effects, dosage, and the synergistic effects of using many anticholinergic drugs.

Dr. Abhishek Juneja
Dr. Abhishek Juneja

Neurology

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