A large number of prescription and nonprescription drugs, as well as a variety of plants and mushrooms, can inhibit the effects of acetylcholine at muscarinic receptors. Some drugs used for other purposes (eg, antihistamines) also have anticholinergic effects, in addition to other potentially toxic actions. For example, antihista-mines such as diphenhydramine can cause seizures; tricyclic anti-depressants, which have anticholinergic, quinidine-like, and α-blocking effects, can cause severe cardiovascular toxicity.
The classic anticholinergic (technically, “antimuscarinic”) syn-drome is remembered as “red as a beet” (skin flushed), “hot as a hare” (hyperthermia), “dry as a bone” (dry mucous membranes, no sweating), “blind as a bat” (blurred vision, cycloplegia), and “mad as a hatter” (confusion, delirium). Patients usually have sinus tachy-cardia, and the pupils are usually dilated . Agitated delirium or coma may be present. Muscle twitching is common, but seizures are unusual unless the patient has ingested an antihis-tamine or a tricyclic antidepressant. Urinary retention is common, especially in older men.
Treatment for anticholinergic syndrome is largely supportive. Agitated patients may require sedation with a benzodiazepine or an antipsychotic agent (eg, haloperidol). The specific antidote for peripheral and central anticholinergic syndrome is physostigmine, which has a prompt and dramatic effect and is especially useful for patients who are very agitated. Physostigmine is given in small intravenous doses (0.5–1 mg) with careful monitoring, because it can cause bradycardia and seizures if given too rapidly. Physostigmine should not be given to a patient with suspected tricyclic antidepressant overdose because it can aggravate cardio-toxicity, resulting in heart block or asystole. Catheterization may be needed to prevent excessive distention of the bladder.