Expansion
Each major poison has a specific antidote acting by a defined mechanism
Mnemonic
Pair each poison with its antidote:
| Poison | Antidote |
|---|---|
| Paracetamol | N-acetylcysteine |
| Opioids | Naloxone |
| Benzodiazepines | Flumazenil, rarely used, risks seizures |
| Warfarin | Vitamin K, prothrombin complex concentrate |
| Heparin | Protamine |
| Digoxin | Digoxin-specific antibody fragments |
| Beta blockers | Glucagon, high dose insulin |
| Organophosphates | Atropine and pralidoxime |
| Iron | Desferrioxamine |
| Cyanide | Hydroxocobalamin, sodium thiosulphate |
| Methanol, ethylene glycol | Fomepizole or ethanol |
| Methaemoglobinaemia | Methylene blue |
| Lead | DMSA, EDTA |
| Malignant hyperthermia | Dantrolene |
“Toxbase before treatment”: for anything unfamiliar, the UK poisons database is the reference, and supportive care with airway, breathing and circulation outranks any antidote.
Expansion
| Poison | Antidote | Mechanism |
|---|---|---|
| Paracetamol | N-acetylcysteine | Replenishes glutathione |
| Opioids | Naloxone | Competitive antagonist; short half-life so repeat or infuse |
| Benzodiazepines | Flumazenil | Competitive antagonist; seizure risk, rarely used |
| Warfarin | Vitamin K, prothrombin complex concentrate | Restores carboxylation |
| Heparin | Protamine | Binds heparin |
| Dabigatran | Idarucizumab | Monoclonal antibody |
| Digoxin | Digoxin-specific antibody fragments | Binds digoxin |
| Iron | Desferrioxamine | Chelation |
| Lead | Dimercaprol, EDTA, penicillamine | Chelation |
| Organophosphates | Atropine plus pralidoxime | Blocks muscarinic effects; reactivates cholinesterase |
| Cyanide | Hydroxocobalamin, sodium thiosulphate | Binds cyanide |
| Methanol, ethylene glycol | Fomepizole or ethanol | Blocks alcohol dehydrogenase |
| Beta blockers | Glucagon, high dose insulin | Bypasses beta receptor |
| Local anaesthetic | Intravenous lipid emulsion | Lipid sink |
| Methaemoglobinaemia | Methylene blue | Reduces methaemoglobin |
The recurring principle is that antidotes either compete at the receptor, bind the poison, restore a depleted substrate, or bypass the blocked pathway.