- antihistamines (e.g. diphenhydramine/Benadryl)
- antiemetics (e.g. dimenhydramine/Gravol)
- tricyclic antidepressants (e.g. amitriptyline, nortriptyline)
- scopolamine
- "contaminated" recreational drugs (e.g. heroin cut with scopolamine)
- atropine
- neuroleptics (e.g. quetiapine/Seroquel, clozapine, olanzapine/Zyprexa)
- antiparkinson medications (e.g. benztropine)
Anticholinergic drugs competitively inhibit binding of acetycholine to muscarinic cholinergic receptors found in smooth muscle (GI, bronchial, cardiac), secretory glands (salivary, sweat), ciliary body of eye, and the CNS.
Knowing this makes for remember this classic description of anticholinergic toxicity easy as pie:
"Red as a beet" - cutaneous vasodilation
"Dry as a bone" - dry skin
"Hot as a hare" - interference with sweat production interupts thermoregulation
"Blind as a bat" (nonreactive mydriasis) - pupillary dilation and ineffective accomodation = blurry vision
"Mad as a hatter" (delirium, hallucinations) - CNS symptoms of muscarinic blockade, which to the extreme, may result in seizure or coma
"Full as a flask" (urinary retention) - relaxation of detrusor muscle and constriction of urethral sphincter
The fundamental principles of management include:
- Call the Poison Control Centre.
- Stabilize the patient's ABCs.
- Supportive care and cardiorespiratory monitoring.
- Sodium bicarbonate in the setting of QT interval prolongation.
- Treatment of seizures and/or aggitation with benzodiazepines (e.g. lorazepam); do NOT use antipsychotic medications, as these may further prolong an already prolonged QT interval.
- Consideration of physostigmine, an antidote that is an acetylcholinesterase inhibitor that binds reversibly to inhibit acetylcholinesterase in both the peripheral and central nervous system. It's usage is controversial, and no studies have demonstrated its efficacy or safety to date.
- Consideration of activated charcoal depending on the timing of the ingestion, and the patient's level of consciousness.
