Clinical findings include hypotension or hypertension, tachycardia, hypoactive or absent bowel sounds, urinary retention, flushed skin, hyperthermia, dry skin and mucus membranes, mydriasis, confusion, agitation, disorientation, and auditory and visual hallucinations. Table 101-1 compares muscarinic and antimuscarinic effects.
Table 101-1 Muscarinic and Antimuscarinic Effects ||Download (.pdf)
Table 101-1 Muscarinic and Antimuscarinic Effects
Stimulation or Muscarinic Effect
Antagonism or Antimuscarinic Effect
Complex interactions, possible improvement in memory
Complex interactions, impairs memory, produces agitation, delirium, hallucinations, and fever
Constricts pupil (miosis), decreases intraocular pressure, increases tear production
Dilates pupil (mydriasis), loss of accommodation (blurred vision), increases intraocular pressure
Increases saliva production
Decreases saliva production, dry mucous membranes
Bronchospasm, increases bronchial secretions
Bradycardia, slows atrioventricular condition
Tachycardia, enhances atrioventricular conduction
Vasoconstriction (very modest)
Increases motility, increases gastric acid production, produces emesis
Decreases motility, decreases gastric acid production
Stimulates bladder contraction and expulsion of urine
Decreases bladder activity, promotes urinary retention
Increases sweat production
Decreases sweat production (dry skin), cutaneous vasodilation (flushed appearance)
The diagnosis is primarily clinical. In isolated anticholinergic toxicity, routine laboratory studies should be normal, and routine toxicology screening is often of little value. Nonetheless, electrolytes, glucose, creatine phosphokinase, and pulse oximetry should be obtained. The differential diagnosis includes viral encephalitis, Reye syndrome, head trauma, other intoxications, neuroleptic malignant syndrome, delirium tremens, acute psychiatric disorders, and sympathomimetic toxicity.
Treatment is primarily supportive. The goal is to prevent life-threatening complications, which include status epilepticus, hyperthermia, cardiovascular collapse, and rhabdomyolysis.
The patient should be placed on a cardiac monitor and intravenous or intraosseus access secured.
Activated charcoal may decrease drug absorption, even beyond 1 hour of ingestion.
Temperature monitoring is essential. Hyperthermia is treated conventionally.
Hypertension usually does not require intervention, but should be treated conventionally as necessary.
Standard antiarrhythmics are usually effective, but avoid class IA medications (eg, procainamide). Treat dysrhythmias, widened QRS complexes, and hypotension from sodium blocking agents (eg, cyclic antidepressants) with IV sodium bicarbonate 1 mEq/kg.
Treat agitation with benzodiazepines (lorazepam 2 to 4 milligrams IV or 0.1 milligram/kilogram). Phenothiazines should be avoided.
Treat seizures with benzodiazepines (lorazepam 2 milligrams IV).
Physostigmine treatment is controversial. It is indicated if conventional therapy fails to control seizures, agitation, unstable dysrhythmias, coma with respiratory depression, malignant hypertension, or hypotension. The initial dose is 0.5 to 2 milligrams IV (0.02 milligram/kilogram in children, maximum dose 0.5 milligram/dose), slowly administered over 5 min. When effective, a significant decrease in agitation may be apparent within 15 to 20 min. Physostigmine may worsen cyclic antidepressant toxicity and lead to bradycardia and asystole. It is contraindicated in patients with cardiovascular or peripheral vascular disease, bronchospasm, intestinal or bladder obstruction, cardiac conduction disturbances, and suspected concomitant sodium channel antagonist poisoning. The patient should be observed for cholinergic excess.
Patients with mild anticholinergic toxicity can be discharged after 6 hours ...