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Emergency And Acute Medicine - Anticholinergic Poisoning


Core Overview: Anticholinergic poisoning is caused by central and peripheral cholinergic blockade. Depending on the agent, antagonism may occur at muscarinic receptors (most common), nicotinic receptors, or both. Symptoms typically begin 15–30 minutes after ingestion, with effects lasting about 2–24 hours.


Common Causes: Many medications have anticholinergic properties that are usually mild at therapeutic doses but can become life-threatening in overdose. Frequent culprits include antihistamines, belladonna alkaloids and related compounds, antiparkinsonian agents, cyclic antidepressants, antipsychotics (neuroleptics), mydriatic eye drops, skeletal muscle relaxants (e.g., orphenadrine, cyclobenzaprine), antispasmodics, and certain mushrooms/plants (Amanita muscaria, Amanita pantherina, deadly nightshade, mandrake, henbane). Jimson weed may be smoked or ingested.


How It Presents: Clarify timing, dose, and exposure route. The classic toxidrome is often remembered as: “mad as a hatter” (delirium/AMS), “hot as a hare” (hyperthermia), “red as a beet” (flushed skin), “dry as a bone” (dry skin/mucosa), and “blind as a bat” (mydriasis with blurry vision). Findings may include hyperthermia and altered mental status; fixed mydriasis with loss of accommodation; sinus tachycardia, occasional dysrhythmias (typically only in massive ingestions), hypo/HTN, and rarely cardiogenic pulmonary edema; tachypnea or respiratory failure; decreased/absent bowel sounds, dysphagia, decreased GI motility, and reduced salivation; urinary retention; decreased sweating with dry, flushed skin; hallucinations, coma, or seizures.


Essential Evaluation: Diagnosis is clinical, based on toxidrome and a reliable exposure history when possible.


Recommended Tests: Obtain a urine toxicology screen if helpful for context; electrolytes, BUN/creatinine, glucose; CBC; CPK if rhabdomyolysis is a concern; urinalysis; and acetaminophen/salicylate levels to detect occult coingestions (e.g., combination nighttime products). ECG commonly shows sinus tachycardia; may reveal QRS prolongation, AV block, bundle branch block patterns, or dysrhythmias.


Key Differentials: Sympathomimetic intoxication, withdrawal syndromes, acute psychiatric conditions, sepsis, and thyroid disease.


Prehospital Actions: Bring all pills, bottles, and packaging to support accurate identification in the ED.


Immediate Stabilization: Prioritize ABCs—airway control can be critical. Provide supplemental oxygen, establish IV access, initiate cardiac monitoring and pulse oximetry, and consider naloxone, thiamine, and dextrose (D50 or bedside glucose-guided) when altered mental status is present.


Emergency Department Care: Management is largely supportive: IV rehydration with 0.9% NS and aggressive external cooling for hyperthermia. Use benzodiazepines to control agitation and seizures; avoid phenothiazines because they can worsen anticholinergic effects. Treat seizures with benzodiazepines and barbiturates if needed. Manage dysrhythmias with standard agents, but avoid class Ia antiarrhythmics due to quinidine-like effects seen with many anticholinergic drugs; sodium bicarbonate boluses may reverse these sodium-channel blockade effects. For decontamination, give activated charcoal for oral ingestions within about 1 hour when appropriate, and use ocular irrigation for eyedrop exposure.


Antidote Considerations: Physostigmine (Antilirium) is a reversible acetylcholinesterase inhibitor that crosses the blood–brain barrier and can temporarily reverse both central and peripheral effects. Consider it when peripheral anticholinergic signs are present plus severe features such as uncontrolled agitation or seizures not responding to conventional therapy. Use with caution if QRS is prolonged due to risks of dysrhythmias (including asystole), seizures, and cholinergic crises—continuous monitoring is required. Avoid physostigmine in cyclic antidepressant overdose and use caution/avoid in cardiovascular disease, asthma/bronchospasm, intestinal obstruction, heart block, peripheral vascular disease, or bladder obstruction.


Medication Options: Activated charcoal 1 g/kg PO; dextrose 50–100 mL D50 (peds: D25 2 mL/kg over 1 minute) IV and repeat if needed; diazepam 5–10 mg IV (peds 0.2–0.5 mg/kg) q10–15 min; lorazepam 2–4 mg IV (peds 0.03–0.05 mg/kg) q10–15 min; dopamine 2–20 μg/kg/min IV titrated for hypotension; phenobarbital 10–20 mg/kg IV loading dose (monitor respiration); thiamine 100 mg IV/IM (peds 50 mg). For physostigmine, 0.5–2.0 mg IV over 5 min (peds 0.02 mg/kg), repeat in 30–60 min if needed. First-line for agitation/seizures is lorazepam or diazepam; second-line is physostigmine with caution and toxicology input when available.


Disposition Guidance: ICU admission is appropriate for moderate-to-severe toxicity (temperature control, agitation control, seizure/dysrhythmia monitoring) and for any patient receiving physostigmine. Discharge may be reasonable for mild, improving symptoms after 6–8 hours of ED observation.


Referral And Follow-Up: Arrange substance use referral for recreational misuse, poison-prevention counseling for accidental exposures, and psychiatric evaluation for intentional ingestion. Ensure appropriate psychiatric follow-up for intentional overdoses.


Clinical Tips And Common Traps: Treat hyperthermia aggressively—antipyretics do not work for toxic hyperthermia. If physostigmine is considered, use it carefully with continuous monitoring and toxicology consultation when possible.


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