Poisoning Overview & Toxidromes — Viva

Q1: The first 5 minutes (3 min)

An unconscious 30-year-old is brought in by ambulance. Outline your immediate structured approach to the poisoned patient. What empirical treatments do you give to any coma of unknown cause, in what order, and why?

Expected: Resuscitate and assess together. Apply ABCDE and treat threats to airway protection, ventilation and circulation while identifying the exposure. Airway intervention follows physiology and risk, not an automatic GCS cutoff. NICO's conservative strategy applied only to selected closely monitored adults and excluded immediate intubation indications, suspected cardiotropic poisoning, isolated reversible opioid or benzodiazepine poisoning, and known pregnancy.^[2][51]

Q2: The toxidromes (4 min)

Take me through Hoffman’s well-defined toxidromes, the additional GABAergic pattern, and serotonin toxicity — for each, give the receptor, the cardinal clinical signs, two example toxins, and the antidote. Why does the anticholinergic patient have dry skin and the cholinergic patient wet skin?

Expected:

• Sympathomimetic — alpha + beta adrenergic agonism; mydriasis, hyperthermia, tachycardia, hypertension, diaphoresis, agitation; cocaine, MDMA; supportive + benzodiazepine.^[1]
• Anticholinergic — muscarinic blockade; 'dry as a bone, red as a beet, hot as a hare, blind as a bat (mydriasis), mad as a hatter (delirium)', urinary retention, ileus; atropine, antihistamines, TCA, Jimson weed; supportive care and benzodiazepines for agitation (do not name physostigmine as routine).^[1]
• Cholinergic (DUMBELSS) — muscarinic + nicotinic agonism (AChE inhibition); miosis, bronchorrhoea, bronchospasm, salivation, lacrimation, sweating, GI hypermotility, bradycardia, fasciculations; organophosphates, nerve agents; atropine titrated to drying of secretions. Oxime benefit is uncertain; the WHO 30 mg/kg then 8 mg/kg/h pralidoxime regimen is not supported.^[1][30]
• Opioid — mu-receptor agonism; pinpoint pupils, respiratory depression, coma, hypothermia, hyporeflexia; heroin, morphine, fentanyl; naloxone titrated to ventilation.^[1][36]
• GABAergic / sedative-hypnotic — GABA-A agonism; sedation, ataxia, often near-normal pupils; benzodiazepines, ethanol, barbiturates; supportive; flumazenil is not empiric (more AEs than placebo).^[1][38]
• Serotonin toxicity (Dunkley/Isbister, not Hoffman’s sixth toxidrome) — clonus, hyperreflexia, tremor, diaphoresis, agitation; SSRIs, MAOIs, tramadol, linezolid; stop agent, benzodiazepines, cooling; cyproheptadine used but dosing is not uniform.^[8][46][20]

The skin distinction: muscarinic blockade (anticholinergic) abolishes sympathetic-driven sweating AND cholinergic sympathetic fibres to sweat glands → anhidrosis (dry); excess acetylcholine (cholinergic) stimulates the same sweat glands → hyperhidrosis (wet).^[1]

Q3: Decontamination and elimination (3 min)

When do you use activated charcoal, multi-dose charcoal, and whole-bowel irrigation? What are the contraindications to charcoal? Which poisons are dialysable, and what is the mnemonic? When is urine alkalinisation indicated?

Expected:

• Single-dose charcoal — selective, not routine. The 2026 recommended initial dose is 50 g in adults or 1 g/kg in children, capped at 50 g. Selection and timing depend on poison, formulation, expected toxicity and aspiration risk; selected later presentations may benefit. Do not give it to a non-intubated patient with absent airway protective reflexes.^[49]
• Additional-dose versus multiple-dose charcoal — an additional dose completes gastrointestinal decontamination; multiple doses enhance elimination in selected poisonings. The latter include carbamazepine, cardiac glycosides, colchicine, dapsone, phenobarbital, phenytoin, thallium and theophylline. The 2026 regimen begins with the single dose, then repeats that dose every 4 hours or half that dose every 2 hours, after individualised assessment.^[49]
• Whole-bowel irrigation — consider for toxic SR/enteric-coated ingestions presenting later than 2 h; substantial iron, lithium or potassium; and body-packers. Do not invent a 1 to 2 L/h PEG rate here.^[5]
• Ipecac is abandoned (Hojer 2013): routine use at the scene or ED should definitely be avoided.^[6]
• ECTR — not SLIME-with-iron. Iron is WBI, not EXTRIP HD. Salicylate: AMS (1D); concentration over 7.2 mmol/L (100 mg/dL) 1D and over 6.5 (90) 2D; IHD preferred.^[33] Lithium: impaired kidney AND Li over 4.0, OR reduced consciousness/seizures/life-threatening dysrhythmias at any level (1D); suggest over 5.0 or time-to-under-1.0 longer than 36 h (2D).^[32] Methanol: coma/seizures/new vision/pH 7.15 or lower/AG over 24; concentration cut-offs depend on fomepizole (over 21.8 mmol/L), ethanol (over 18.7) or no ADH blocker (over 15.6).^[34] Metformin: lactate over 20, pH 7.0 or lower, shock (1D).^[43] Ethylene glycol: suggest ECTR if fomepizole and EG over 50 mmol/L or OG over 50; recommend if coma, seizures or AKI.^[44]
• Urine alkalinisation — IV bicarbonate to urine pH 7.5 or higher; first-line for moderately severe salicylate not meeting HD criteria.^[39][55]

Q4: The high-risk pitfalls and antidotes (4 min)

Name four classic management pitfalls in poisoning and how each is avoided. Then give me the antidote and dose for: paracetamol, TCA, beta-blocker, calcium-channel blocker, digoxin, toxic alcohol, cyanide, methaemoglobinaemia, lead encephalopathy, and local-anaesthetic systemic toxicity.

Expected pitfalls:

1. Giving flumazenil empirically — more adverse events than placebo (RR 2.85); avoid in mixed/unknown overdose.^[38]
2. Delaying dextrose for thiamine in hypoglycaemia — treat glucose now; thiamine is adjunct, not a gate.^[67][12]
3. Reaching for an antiarrhythmic instead of sodium bicarbonate in TCA wide-complex tachycardia — sodium-channel-blocking class Ia/Ic agents share the toxin's mechanism; hypertonic sodium bicarbonate is the supported therapy, while lidocaine and phenytoin rest on animal studies and case reports only. Use sodium bicarbonate 1 to 2 mmol/kg.^[31][50]
4. Treating bupropion QRS widening as TCA sodium-channel block — gap-junction toxicity often does not respond to bicarbonate.^[22]
5. Forgetting paracetamol level in every overdose — covert co-ingestion; always check.^[57]
6. Teaching WHO pralidoxime 30 mg/kg then 8 mg/kg/h as required — oxime evidence is insufficient.^[30]

Antidotes (only doses that are sourced here):

• Paracetamol → N-acetylcysteine 150 mg/kg over 1 h then 50 mg/kg over 4 h then 100 mg/kg over 16 h (300 mg/kg over 21 h).^[53][57]
• TCA → IV sodium bicarbonate 1 to 2 mmol/kg, target pH about 7.45 to 7.55.^[31]
• Calcium-channel blocker / beta-blocker shock → HIET commonly 1 U/kg then 0.5 to 1 U/kg/h; name glucagon without inventing milligrams.^[41]
• Local-anaesthetic systemic toxicity → 20% lipid emulsion 1.5 mL/kg bolus then 15 mL/kg/h; recommended in bupivacaine arrest, not first-line for amitriptyline/CCB/bupropion.^[7][42]
• Digoxin → digoxin-specific Fab: for acute ingestion of an unknown amount with toxicity and no serum concentration, the DigiFab label gives 20 vials (children under 20 kg start with 10).^[68] Cyanide → hydroxocobalamin 5 g IV over 15 minutes; a second 5 g may be given for severe poisoning or poor response (total 10 g).^[69] Methaemoglobinaemia → methylene blue 1 mg/kg IV over 5 to 30 minutes; repeat up to 1 mg/kg after one hour if the level stays above 30 percent or symptoms persist.^[70] Lead encephalopathy → urgent parenteral chelation per WHO: dimercaprol 2.5 to 3 mg/kg deep IM on the schedule taper, with sodium calcium edetate up to 40 mg/kg twice daily for up to 5 days — never sodium edetate, which can cause fatal hypocalcaemia.^[71] Also name naloxone titrated to ventilation^[36][45], atropine titrated to drying of secretions in cholinergic poisoning^[29], and cyproheptadine with non-uniform dosing in serotonin toxicity^[20].

Q5: Pitfalls, prognosis and special populations (2 min)

Why is the prognosis for a poisoned patient not just about the agent? Name three validated poor-prognosis markers. How does your approach change in (i) the pregnant patient, (ii) the child, (iii) the elderly polypharmacy patient?

Expected: Prognosis depends on agent toxicity, dose, time to presentation, co-ingestants, age and comorbidity, and availability of antidote/dialysis.^[2] Aluminium phosphide in India: pooled mortality 54 percent (95 percent CI 48 to 61 percent), no definite antidote.^[19] Organophosphorus self-poisoning: case fatality generally more than 15 percent.^[29] Child — avoid ipecac^[6]; WBI is a consideration for iron/lithium/SR, not a numbered PEG rate^[5]. Elderly — the structured risk assessment weighs comorbidity and the treatments that may be required, including a lower threshold for ECTR when EXTRIP indications are met.^[2]

Pregnancy: begin with the poisoning, not the drug: in ethylene glycol poisoning, treat the pregnant patient as for the non-pregnant patient and do not withhold treatment on account of pregnancy. When an antidote is indicated, fomepizole is preferred at all stages of pregnancy because ethanol can cause harmful fetal effects, but ethanol should not be withheld where fomepizole is unavailable or not considered appropriate. Present fomepizole as preferred when indicated, not proven safe: pregnancy data are very limited, animal reproduction studies have not been conducted, fetal harm is unknown and the US label restricts use to pregnant women only if clearly needed. The answer is an individual risk–benefit decision with extended maternal and fetal monitoring and specialist discussion, not a general safety claim for all poisoned pregnancies.^[59][52]

References39ShowHide

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