Anticholinergic toxicity

Revision as of 20:14, 30 January 2012 by Jswartz (talk | contribs)

Background

  • Meds
    • Atropine
    • Antihistamines
    • Antidepressants (SSRIs, TCAs)
    • Antipsychotics
    • Muscle relaxants
  • Plants
    • Jimson weed (Devil's trumpet)
    • Amanita mushroom

Clinical Features

  • Dry as a bone: anhidrosis (esp axillae, mouth)
  • Hot as a hare: anhydrotic hyperthermia (may become severe w/ agitation)
  • Red as a beet: cutaneous vasodilation
  • Blind as a bat: nonreactive mydriasis (often delayed 12-24hr)
  • Mad as a hatter: delirium; attention deficit; hallucinations; dysarthria; lethargy
  • Full as a flask: urinary retention
  • Tachycardia (HR 120-160) and decreased/absent bowel sounds

DDX

  1. Sympathomimetic toxicity
    1. Red, dry skin and absent bowel sounds favors anticholinergic toxicity
  2. Encephalitis
  3. Head trauma
  4. ETOH/sedative withdrawal
  5. Neuroleptic Malignant Syndrome (NMS)
  6. Acute psychotic disorder

Treatment

  1. GI decon
    1. Activated charcoal may be effective even >1hr after ingestion (decreased GI motility)
  2. Sedation
    1. Decreases the risk of hyperthermia, rhabdo, traumatic injuries
    2. Benzos are agents of choice
  3. Cholinesterase inhibition
    1. Indicated for severe agitation or delirium (esp if unresponsive to benzos)
    2. Avoid when cardiac conduction abnormalities are present
    3. Physostigmine
      1. Dosing: 0.5-2mg IV over 5min
      2. Onset of action: 15-20min
      3. Side effects: bradycardia, dysrhythmias, cholinergic excess

Disposition

  • Consider d/c for pts w/ mild symptoms after 6hr obs if their symptoms resolve
  • Admit if physostigmine was given (half-life of physo is often shorter than the ingested drug)

See Also

Source

Tintinalli