EDAITUTOR
ED Briefs · Toxicology v1.0 Educational use only

Acute Poisoning
Management

Physiology first. Antidote second. Toxicologist always. — a structured approach to the undifferentiated poisoned patient, known agent or not.

RRSIDEADResuscitateRisk assessSupportive care
Poisons Information Australia — 13 11 26

24 hours, 7 days. Involve the Poisons Information Centre early — earlier advice, better outcomes. Repeated near Disposition below.

🔴 Treat the patient, not the toxin

Identifying the agent must never delay stabilising airway, breathing, circulation and CNS. Deterioration can be sudden — reassess continuously, get senior help early, and involve the Poisons Information Centre. Poisoning is a great mimic — and is mimicked; consider and exclude trauma and medical causes in every undifferentiated patient.

First principles — and a rapid assessment flow

Guiding principles

  • Do not delay life-saving treatment to identify the poison — treat the patient, not the toxin.
  • Reassess continuously — deterioration can be sudden and delayed.
  • Get senior help early and mobilise resources before the patient decompensates.
  • Involve the Poisons Information Centre early (13 11 26) — TOXBASE / specialist toxicology advice.
  • Consider trauma and medical mimics alongside poisoning in every undifferentiated presentation.

Rapid assessment flow

Unwell / unclear patient — consider poisoning + trauma + medical mimics
ABCDE + glucose + temperature
ECG + VBG/ABG + paracetamol level
Identify toxidrome(s)
Risk assessment — the five questions
Targeted treatment
Disposition — observe / ICU / discharge / psychiatry
⚪ the spineRRSIDEAD — Resuscitation · Risk assessment · Supportive care & monitoring · Investigations · Decontamination · Enhanced elimination · Antidotes · Disposition. A physiology-first structure for the poisoned patient.
Toxicology ABCDE — stabilise the patient first

AAirway

  • Protect the airway; loss of reflexes, vomiting, secretions, burns or GCS ≤8 → early intubation.
  • Left-lateral / recovery position if not intubating; RSI when indicated.
  • Do not test the gag reflex — may provoke vomiting / aspiration.
  • Seek thermal / caustic airway injury.
GCS ≤8 → secure airway

BBreathing

  • RR, SpO₂, ETCO₂, chest expansion; watch for respiratory depression, bronchorrhoea, pulmonary oedema.
  • Pulse oximetry is unreliable in CO poisoning and methaemoglobinaemia — use co-oximetry / ABG.
  • Serial ABG + ETCO₂ if neuromuscular or respiratory failure suspected.
SpO₂ can lie — co-oximetry

CCirculation

  • ECG, BP, HR, cap refill; shock is often mixed.
  • Treat ECG changes immediately (see ⚡ ECG) before antiarrhythmics.
  • Fluids, vasopressors / inotropes; HIET (high-dose insulin euglycaemia) for severe β-blocker / CCB toxicity.
  • Lipid rescue, pacing or ECMO in selected cases.
ECG changes first

DDisability

  • GCS, pupils, BGL; agitation, delirium, seizures, coma.
  • Benzodiazepines first-line for tox seizures — phenytoin is contraindicated (sodium-channel blockade).
  • Consider serotonin toxicity, NMS, anticholinergic and opioid toxicity. CT head if reduced GCS / focal signs.
  • Do not use GCS for prognosis — most tox comas recover fully.
no phenytoin

EExposure

  • Remove contaminated clothing; look for rashes, needle marks, burns, transdermal patches.
  • Measure temperature (invasive monitoring if needed) — treat hyper/hypothermia.
  • Consider body packers / stuffers.
find the patch

Reassess

Reassess frequently — deterioration can be sudden. Re-examine after every intervention; the poisoned patient is a moving target.

🔴 reassessDeterioration can be sudden. Repeat the primary survey and vital signs continuously — many poisons have delayed or biphasic effects.
Risk assessment — five critical questions that predict the clinical course
Question 1

Who?

Age, weight, pregnancy, comorbidities (renal / hepatic / cardiac / psychiatric), regular medications and interactions.

Question 2

What?

Drug / chemical / plant / animal; formulation (IR / SR / ER / patch); single vs combination; street drug or unknown — adulterants mean the named drug may not be the active chemical.

Question 3

When?

Time of exposure; single vs repeated; delayed presentation.

Question 4

How much?

Estimated dose; maximum possible dose; witnessed ingestion; tablet / packet counts (gather empty packets + collateral).

Question 5

What happens next?

Predict peak toxicity; redistribution / delayed absorption; protein binding & half-life; risk of delayed cardiovascular collapse (SR preps, bezoar, enterohepatic recirculation).

Structured risk assessment predicts the course and guides observation, investigation and disposition — it is the pivot between resuscitation and a management plan.

Common toxidromes — pattern recognition
ToxidromeKey featuresThink of
Opioid↓GCS, respiratory depression, miosisheroin, codeine, fentanyl, methadone, oxycodone
CholinergicDUMBELLS — Diarrhoea, Urination, Miosis, Bronchorrhoea / Bronchospasm, Bradycardia, Emesis, Lacrimation, Salivation, Sweatingorganophosphates, carbamates, muscarinic agonists
Anticholinergichot, dry, red, mad, blind; tachycardia, mydriasis, urinary retention, ileusantihistamines, TCAs, antipsychotics, atropine, scopolamine
Sympathomimeticagitation, mydriasis, diaphoresis, tachycardia, hypertension, hyperthermiacocaine, amphetamines, MDMA, SNRIs, TCAs
Serotoninaltered mental status, autonomic instability, neuromuscular hyperactivity (clonus, hyperreflexia), hyperthermiaSSRIs, SNRIs, MAOIs, linezolid, tramadol, MDMA
Sedative-hypnotic↓GCS, ataxia, nystagmus, respiratory depression (severe)benzodiazepines, alcohol, barbiturates, Z-drugs
⚪ mnemonicDUMBELLS = the classic cholinergic features. Distinguish sweaty, agitated sympathomimetic / serotonin pictures from the hot, dry anticholinergic patient — the skin tells you a lot.
Key investigations — what question does each test answer?
TestThe question it answers
ECGWhat electrical toxin is present? (QRS, QTc, arrhythmia)
VBG / ABGWhat metabolic process is occurring? (acidosis, alkalosis, lactate)
BGLIs hypoglycaemia present?
Paracetamol levelIs there occult hepatotoxicity? Measure in all deliberate self-harm; consider in all unknown poisoning.
U&Es, LFTs, CrOrgan dysfunction / severity?
LactateTissue hypoxia or mitochondrial poisoning?
CKMuscle injury / rhabdomyolysis?
TroponinIs this cardiotoxic?
FBC, coagsInfection, bleeding risk, DIC?
Targeted drug levelsWill it change management?
Other (as guided)Methanol, ethanol, salicylate, COHb, MetHb, cyanide; serum + osmolar gap for toxic alcohols — repeat to track the anion-gap rise.
⚪ baseline panelA reasonable screen for the undifferentiated poisoned patient: ECG, VBG (lactate / electrolytes / glucose), FBC, renal, LFT, Mg, CK, INR — plus a paracetamol level in deliberate self-harm.
⚡ ECG — the electrical vital sign — repeat frequently; dynamic changes are common
ECG findingThinkFirst response
Wide QRS (>120 ms) Na-channel blockade — TCA, cocaine, diphenhydramine, class Ia/Ic. May be preceded by dominant R in aVR / dominant S in aVL. Sodium bicarbonate 8.4% — 100 mL IV bolus if QRS >160 ms / arrest / VT; 50 mL if QRS 120–160 ms. (Paeds 1–2 mL/kg 8.4% central, or 2–4 mL/kg 4.2% peripheral.)
Long QT antipsychotics, SSRIs, TCAs, methadone, antiemetics, antihistamines Magnesium sulfate — adult 2 g IV over 10–15 min (paeds 25–50 mg/kg, max 2 g); correct K⁺ / Ca²⁺. Use the QT nomogram vs HR — not automated QTc.
Bradycardia / AV block β-blocker, CCB, digoxin, clonidine atropine, calcium, HIET, agent-specific antidote
VT / VF tricyclics, cocaine, QT-prolongers treat the arrhythmia, support circulation, correct electrolytes
Brugada pattern coved ST elevation V1–3 — TCA, cocaine, lithium, class Ia/Ic sodium bicarbonate; avoid Na-channel-blocking drugs
ST changes ST elevation → cocaine; ST sagging + short QT → digoxin cocaine: manage as ACS + benzodiazepines / nitrates. Digoxin: atropine (± digoxin-specific Fab)
🔴 repeatRepeat the ECG frequently — dynamic changes are common, and a widening QRS is an early warning of sodium-channel toxicity. Doses shown are an educational reference — confirm against local protocols and Poisons Information Centre advice.
Decontamination — external and gastrointestinal

External

  • Remove contaminated clothing; wash skin with soap and water.
  • Irrigate eyes 15–20 minutes; check corneal pH.
  • Inhalation — remove from source, give O₂, decontaminate.
  • Protect staff — appropriate PPE (especially organophosphates).

Gastrointestinal

  • Single-dose activated charcoal (1 g/kg) — only within ~1 hour, and only if the airway is protected / intubated.
  • Multi-dose charcoal for selected agents.
  • Whole-bowel irrigation for iron, lithium, SR preps, body packers.
  • Gastric lavage rarely indicated (discuss with Poisons Info); endoscopy / FB removal as indicated.
🔴 contraindicationsDo not give activated charcoal with reduced GCS / unprotected airway, caustics or corrosives, hydrocarbons (aspiration risk), or GI obstruction / perforation. Charcoal does NOT bind: iron, lithium, toxic alcohols (methanol / ethylene glycol), hydrocarbons, strong acids / alkalis, cyanide, potassium, lead.
Antidotes — grouped by physiology, not alphabet

Respiratory

  • Naloxone — opioids
  • Hydroxocobalamin — cyanide
  • Methylene blue — methaemoglobinaemia

Cardiovascular

  • Calcium — calcium-channel blockers
  • HIET — β-blocker / CCB
  • Sodium bicarbonate — Na-channel blockers
  • Lipid emulsion — lipophilic drug toxicity

Neurological

  • Benzodiazepines — seizures
  • Cyproheptadine — serotonin syndrome
  • Physostigmine — selected antimuscarinic delirium
  • Dantrolene / bromocriptine — NMS / malignant hyperthermia

Metabolic

  • N-acetylcysteine — paracetamol
  • Fomepizole — methanol / ethylene glycol
  • Pyridoxine — isoniazid (INH) toxicity

Chelators

  • Desferrioxamine — iron
  • Dimercaprol / succimer — arsenic, mercury, lead
  • EDTA / DMSA — lead

Other

  • Digoxin-specific Fab — digoxin
  • Idarucizumab — dabigatran
  • Protamine — heparin
⚪ physiology firstMost poisoned patients recover with excellent supportive care. Antidotes are the exception, not the rule — confirm indication, dose and timing with the Poisons Information Centre / clinical toxicologist.
Enhanced elimination — removing what is already absorbed

Urinary alkalinisation

salicylates, phenobarbital, TCAs

Haemodialysis

lithium, methanol, ethylene glycol, salicylates, valproate, theophylline

Haemoperfusion

carbamazepine, theophylline

Continuous RRT

critically ill / renal failure

MARS / plasma exchange

selected liver failure / highly protein-bound toxins

IV lipid emulsion

lipophilic drug toxicity

ECMO

refractory cardiogenic / respiratory shock

Modality choice depends on the toxin's dialysability (size, protein binding, volume of distribution) — discuss with toxicology and the renal / retrieval team.

Disposition — where does this patient go next?

DischargeHome

  • Asymptomatic / back to baseline cognition
  • Normal biochemistry, no anticipated deterioration
  • Observation period appropriate to the toxidrome / poison (TOXBASE-guided)
  • Capacity confirmed
  • Mental-health assessment completed for self-harm (per local legislation)

ObserveED / short stay

  • Potential delayed toxicity
  • Need for repeat ECG / labs
  • Uncertain time or dose

EscalateHDU / ICU

  • Abnormal observations or investigations
  • Arrhythmias, shock, seizures
  • Need for antidotes / HIET / ventilation
  • Risk of rapid deterioration
specialist referralPoisons Information Centre — 13 11 26 · clinical toxicologist · psychiatry · ICU / retrieval / dialysis team. Keep the mental-health pathway generic to your local legislation.
⚠ High-risk features — consider ICU early

Consider ICU / retrieval early if

  • Intentional self-harm; large or unknown dose; SR ingestion
  • Co-ingestants (including alcohol)
  • Abnormal ECG — QRS >100 ms, QTc >450/470 ms, arrhythmia
  • Persistent hypotension; serious arrhythmias
  • Seizures / status epilepticus
  • Severe acidosis (pH <7.1); hyperthermia (>40 °C)
  • Need for antidote / HIET; delayed presentation

Paediatric — "one pill / one sip can kill"

  • Sulfonylureas
  • Tricyclic antidepressants
  • Calcium-channel blockers / propranolol
  • Chloroquine / hydroxychloroquine
  • Opioids (e.g. methadone)
  • Organophosphates
  • Camphor / eucalyptus oil
  • GHB · theophylline · toxic alcohols · paraquat · lamotrigine
🔴 paediatric ruleIn small children, a single tablet or a mouthful of these agents can be lethal — transport and assess all suspected exposures, even when the child looks well.
Medical mimics

Poisoning is a great mimic — and is mimicked. Consider / exclude a non-tox cause in every undifferentiated patient.

Stroke / ICHSepsisHypoglycaemiaElectrolytes (Na⁺/Ca²⁺/Mg²⁺)HypoxiaCNS infectionTraumaPsychiatric illness
🟢 RCEM/NPIS 2025 · LITFL
Key pearls
  • Poisoning is a great mimicker — think broadly
  • Treat the physiology, not the lab result
  • ECG and VBG should be repeated
  • Deterioration can be sudden — reassess
  • Poisons Centre early → better outcomes
  • Mental-health assessment is essential in self-harm
🟢 EMCrit IBCC · EM Cases
Golden rules
  • Physiology first — stabilise A/B/C/CNS before chasing the agent
  • Antidote second — supportive care wins most cases
  • Toxicologist always — 13 11 26, early
  • The ECG is an electrical vital sign — repeat it
  • A paracetamol level in every deliberate self-harm
  • Predict the delayed / biphasic course before you disposition
🟢 RCEM/NPIS 2025 · QAS CPG

ED AI Tutor — ED Briefs Series · Toxicology · v1.0 · For clinician education only. Not a substitute for clinical judgement, local guidelines, Poisons Information Centre advice or senior oversight. The acutely poisoned patient must always be managed by physiology first, with continuous reassessment.