Toxicology Flashcards
anticholinergic toxicity - overview
*muscarinic receptors are present on the target organ cells of the parasympathetic nervous system & the sweat glands (sympathetic)
*ANTICHOLINERGICS antagonize muscarinic receptors (dampening parasympathetic fxns and reducing sweating)
anticholinergic toxicity - clinical presentation
*general: hyperthermia
*CV: tachycardia, flushing, dysrhythmias
*GI: decreased gut motility, constipation, vomiting, decreased saliva & tear production
*GU: urinary retention
*HEENT: blurry vision, mydriasis (DILATED pupils), narrow-angle glaucoma, potential vision loss
*skin: DRY skin (through inhibition of sweating)
*MSK: diminished muscle contraction
anticholinergic toxicity - mnemonic/memory aid for sx
red as a beet - flushed skin
dry as a bone - dry skin
blind as a bat - blurry vision / mydriasis
mad as a hatter - CNS toxic effects: confusion, dysarthria, agitation, anxiety, hallucinations, delirium, seizures, coma
hot as a hare - hyperthermia
full as a flask - urinary retention
anticholinergic toxicity - common causes
*jimson weed
*atropine / scopolamine
*antihistamines
*tricyclic antidepressants (amitriptyline, imipramine, doxepin)
*antipsychotics (chlorpromazine, haloperidol, olanzapine, quetiapine)
*antispasmodics (dicyclomine)
anticholinergic toxicity - management
SUPPORTIVE CARE is adequate for the majority of cases
1. ABCs - airway, breathing, circulation
2. GI decontamination with activated charcoal
3. consider sodium bicarbonate for prolonged QRS intervals & wide complex tachyarrhythmias
4. physostigmine (acetylcholinesterase inhibitor can be used in pts with moderate to severe delirium, but this is not the standard of care; watch for cholinergic sx
anticholinergic toxicity - disposition
- asymptomatic pts w/ recent ingestion - GI decontamination with activated charcoal; remain asymptomatic, discharge
- mild anticholinergic toxicity - activated charcoal & benzos if needed; if sx resolve within 6 hours, discharge; if not, admit & obs
- severe anticholinergic poisoning or tx with physostigmine - admit to ICU for closer obs
TCA (tricyclic antidepressant) overdose - pathophysiology
*in an overdose, TCAs ANTAGONIZE a lot of receptors:
-central & peripheral muscarinic Ach receptors
-peripheral alpha-1 adrenergic receptors
-histamine receptors
-CNS GABA receptors
-cardiac fast sodium channels
TCA overdose - clinical presentation
*mnemonic for TCA toxicity: Tri Cs: convulsions, coma, cardiac arrhythmias
*sx usually appear 30 min - 2 hrs post-ingestion, with toxicity lasting 24-48 hrs, and sx include:
1. altered mental status - specifically, sedation
2. anticholinergic toxicity: hyperthermia, flushing, dilated pupils (mydriasis)
3. cardiovascular toxicity - sinus tachycardia, with progression to hypotension & more cardiac conduction abnormalities
4. neurologic toxicity - changes in mental status, usually somnolence; delirium; seizures
TCA overdose - diagnosis/workup
*clinical evaluation (history & physical exam)
*classic EKG finding: prolonged QRS > 100 msec; perform serial EKGs
note - increasing length of the QRS > 100 is associated with higher risk of seizures and ventricular arrythmias
TCA overdose - management
- ABCs- airway, breathing, circulation (many pts require intubation; be cautious with arrythmias and hypotension; BP & arrhythmias should be addressed PRIOR to intubation)
-IV fluids for hypotension
-IV benzos for seizures - sodium bicarbonate is the standard of care and is absolutely indicated in those with QRS > 100 on EKG
utility of sodium bicarbonate in TCA overdose
*sodium bicarbonate administration is the standard of care in TCA overdose, particularly when QRS > 100 msec on EKG
*mechanism: sodium bicarb increases serum pH and increases extracellular sodium which restores the peach during phase 0 depolarization and makes TCA less available to bind to sodium channels
opioid toxidrome - clinical presentation
*classic triad: pinpoint pupils, respiratory depression (decreased respiratory rate and/or breath sounds), and altered mental status
*additional sx: bradycardia, constipation, track marks, hypotension
note - pinpoint pupils are the least reliable sign of opioid ingestion
opioid toxidrome - disposition & complications
*disposition: obs for about 2-4 hours
*complication: non-cardiogenic pulmonary edema (look at the capnography)
5 steps to management of a patient with an ingestion
- ABCs (airway, breathing, circulation) & NGT (naloxone, glucose, thiamine; “coma cocktail”)
- 5 vital signs - correction/support & monitoring (include capnography / end-tidal CO2)
- antidote (if the patient is “sick”)
- decrease absorption - activated charcoal,
- increase elimination
guidelines for activated charcoal in toxic ingestions
*activated charcoal decreases GI absorption of toxic ingestions
*should be given within 1-2 hours, generally
*don’t give for: metals (iron, magnesium, lithium, lead), caustic agents (acidic/alkaline), liquids, do NOT give down an NG tube, do NOT give if concerned of a bowel perforation
sympathomimetic toxidrome - management
*benzodiazepines (lorazepam, diazepam, etc)
*sodium bicarbonate (if the QRS complex is WIDE)
