creation date: 2026-06-18 21:21
tags: Assessments
Toxidromes
Background
Toxidromes are a group of signs and symptoms that occur together, indicating a specific class of substance poisoning. This allows for rapid assessment and initiation of treatment without identifying the exact responsible agent.
Clinical Syndrome
Anticholinergic
Mechanism of Toxicity
Blocks muscarinic receptors leading to parasympathetic nervous system inhibition.
Clinical Presentation
- Hyperthermia (“hot as a hare”)
- Mydriasis (“blind as a bad”)
- Dry skin and mucous membranes (“dry as a bone”)
- Flushed skin from vasodilation (“red as a beet”)
- Agitation and hallucinations (“mad as a hatter”)
Note, dry and flushed skin is key to differentiating from sympathomimetic toxidrome.
Common Causes
- Tricyclic antidepressants
- Antihistamines
- Atropine
- Scopolamine
Sympathomimetic
Mechanism of Toxicity
Mimics the action of the sympathetic nervous system, triggering fight-or-flight response.
Clinical Presentation
- Tachycardia
- Hypertension
- Hyperthermia
- Diaphoresis
- Mydriasis
- Agitation, paranoia, delusions
Note, sweaty and pale skin is key to differentiating from anticholinergic toxidrome.
Common Causes
- Stimulants
- Cocaine
- Amphetamine
- Methamphetamine
- Pseudoephedrine, methylphenidate
- MDMA
- Synthetic cathinones
- High doses of caffeine
Sedative-Hypnotic
Mechanism of Toxicity
Enhances GABA neurotransmitter effects resulting in CNS depression.
Clinical Presentation
- Decreased level of consciousness (ranging from confusion to coma)
- Slurred speech
- Ataxia
- Respiratory depression
- Hypotension
- Hypothermia
- Normal or slightly constricted pupils and nystagmus
Common Causes
- Benzodiazepines
- Barbituates
- Sleep medications (eg. zolpidem, zopiclone)
- Alcohol
- Gamma-hydroxybutyrate
Opioid
Mechanism of Toxicity
Activation of opioid receptors results in sedative effect and significant respiratory depression.
Clinical Presentation
- Decreased level of consciousness (ranging from confusion to coma)
- Slurred speech
- Ataxia
- Respiratory depression with significant bradypnea
- Hypotension
- Hypothermia
- Pinpoint pupils
Note, pinpoint pupils and bradypnea is key to differentiating from sedative-hypnotic toxidrome. Additionally, a trial of naloxone can confirm.
Common Causes
- Opioids (prescriptions or illicit)
Cholinergic
Mechanism of Toxicity
Excess acetylcholine activates muscarinic and nicotinic receptors, stimulating the parasympathetic nervous system.
Clinical Presentation
Fluids and secretions from everywhere:
- Diaphoresis
- Bronchorrhea
- Lacrimation
- Salivation
- Urination
- Diarrhea
- Emesis
- Bradycardia
- Miosis
- Bronchospasm
- Seizures
- Excitation of skeletal muscles
Common Causes
- Organophosphate pesticides
- Carbamate insecticides
- Nerve agents
- Certain mushrooms
- Physostigmine, pyridostigmine
Cardiovascular Drug
Mechanism of Toxicity
Direct effect on cardiac conduction, myocardial contractility, and vascular tone. Has downstream effect on heart rhythm and blood pressure regulation.
Clinical Presentation
Common findings:
- Refractory bradycardia
- Hypotension
- AV blocks
- QRS prolongation
- Changes in mental status due to impaired cerebral perfusion
Drug-specific findings:
- Beta blockers: hypoglycemia, bronchospasm, seizures
- Calcium channel blockers: hyperglycemia, bowel ischemia
- Digoxin: visual disturbances, nausea, vomiting, hyperkalemia
Common Causes
- Beta-blockers
- Calcium channel blockers
- Cardiac glycosides (digoxin)
- Antiarrhythmics
Investigations
History & Physical
Critical components of a toxic exposure history includes:
- Substance identification
- Exact name and formulation
- Concentration of toxin
- Time of exposure
- Acute vs. chronic ingestion
- Quantity and formulation
- Number of pills, volume, or estimated amount
- Immediate vs. extended release
- Intent and co-ingestants
- Accidental vs. intentional ingestion
- Identify any co-ingestants (eg. alcohol)
Physical exam should note vitals:
- Temperature
- Heart rate
- Blood pressure
- Respiratory rate
Laboratory Studies
Every patient with toxicity should have the following investigations:
- Electrolytes and blood gases
- Osmolar gap components
- ECG
- Co-ingestants
Additionally, a number of routine studies are done, although not strictly necessary:
- CBC
- Extended electrolytes
- Creatinine