creation date: 2026-06-18 21:21
tags: Pathologies
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.
More information is available by calling poisoning control:
- National: 1-844-POISON-X
- Ontario: 1-844-764-7669
- Have the following prior to calling: patient age, weight, medical history, substance involved, amount and time of exposure, current vitals and symptoms, and any interventions performed
Clinical Syndrome
Anticholinergic
Mechanism of Toxicity
Blocks muscarinic receptors, preventing acetylcholine binding, leading to parasympathetic nervous system inhibition.
These receptors are found in the CNS, heart, and peripheral postganglionic cholinergic nerves in smooth muscles (intestinal and bronchial), secretory glands (salivary and sweat), and ciliary body of the eye.
Note, anticholinergic agents do not antagonize nicotinic acetylcholine receptors, and thus is technically better described as “antimuscarinic toxicity”
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 (acetaminophen and salicylate concentration)
Additionally, a number of routine studies are done, although not strictly necessary:
- CBC
- Extended electrolytes
- Creatinine
Management
Stabilization
Ensure ABCs
- Evaluate airway patency and consider early intubation as needed
- Supplemental oxygen as needed, monitor O2 sat
- Establish IV access
Trauma and temperature
Conduct a thorough examination of neurological status and exposure. Monitor temperature and cool if hyperthermic.
Decontamination
Activated Charcoal
Mechanism of action
- Absorbs toxins in the gastrointestinal tract
Indications
- Toxic ingestions within 1-2 hours that can be absorbed by AC
- Patient must have intact airway protection to prevent aspiration
Administration
- Adults: 50-100g as slurry
- Children 1-2g/kg
- Can be multiple doses or single dose
Contraindications
- Unprotected airway
- Altered mental status
- Caustic ingestions
- Bowel obstruction
- Ingestion of non-absorbable toxins (eg. alcohol, metals, lithium)
Gastric Lavage
Mechanism of action
- Directly removes toxins from stomach through orogastric tube via flush and suction
Indications
- Life-threatening ingestions within 1 hour
- No safer alternative
Administration
- Secure airway typically via intubation
- Large bore (36-40 Fr in adults) orogastric tube
- Flush with 50-100 mL tepid water or saline until clear return
Contraindications
- Caustic or hydrocarbon ingestion
- Unprotected airway
- Esophageal disease or varices
- Ingestion occurred >1 hour ago (relative CI)
Whole Bowel Irrigation
Mechanism of action
- Large volumes of PEG solution used to mechanically flush the GI tract
Indications
- Sustained-release medications
- Drug packets from body packers/stuffers
- Drugs not absorbed by charcoal
- Heavy metals like lead/metal fragments
Administration
- PEG solution given orally or via NG tube, given until rectal effluent is clear
- Adults: 1-2 L/hr
- Children: 25 mL/kg/hr
Contraindications
- Bowel obstruction, perforation, or ileus
- Hemodynamic instability
- Unprotected airway
- Significant GI bleeding
Antidotes
Antidotes may be available depending on the toxin. These pharmacologically reverse/neutralize the effects.
Common pairs:
- Opioids: naloxone
- Acetaminophen: N-acetylcysteine
- Toxic alcohols: fomepizole/ethanol
- Benzodiazepine: flumazenil
- Anticholinergics: physostigmine
Very few drugs have antidotes and in such case, poison control will advise on their use.
Enhanced Elimination (Dialysis)
Dialysis can remove toxins directly from the bloodstream. This is indicated for:
- Severe toxicity unresponsive to supportive care
- End-organ damage (eg. renal or liver failure)
- Live-threatening lab abnormalities
Specific toxins that calls for immediate dialysis are:
- Methanol
- Ethylene glycol
- Lithium
- Salicylates
Disposition
Patients can be discharged if:
- Asymptomatic after observation
- No risk of delayed toxicity
- Predictable toxicokinetics
- Psychiatric clearance if intentional ingestion
Admission is indicated for:
- Persistent symptoms needing treatment
- Anticipated delayed toxicity
- Need for antidotes/dialysis
- Psychiatric evaluation
ICU care is indicated for:
- Hemodynamic instability
- Respiratory insufficiency
- Severe altered mental status
- Antidote complications
- Severe acid-base/electrolyte imbalances