Toxicology monographs / Antidotes
Antidotes
Read from the antidote's side: what each one is given for, and where its full monograph lives. Almost every antidote in existence is an answer to one of four things going wrong — a saturated elimination pathway, a minor metabolic route becoming the major one, protein binding coming undone, or a protective cofactor running out.
40 antidotes · 40 with a full monograph · dosing lives on drugs.resusdoc.uk, not here
Acetylcysteine (NAC)
Monograph on drugs.resusdoc.uk- Death cap and the amatoxin mushrooms — hepatoprotectant and antioxidant adjunct; not a specific amatoxin antidote — the specific agent, silibinin, is discussed in the text
- Paracetamol — restores the glutathione that NAPQI consumes
Activated charcoal
Monograph on drugs.resusdoc.uk- Anticoagulants — genuinely quantified for apixaban — halves AUC at 2 hours and shortens the half-life
- Antihistamines — considered early after ingestion — the chlorphenamine label names it explicitly
- Baclofen — considered early after oral ingestion, on general principles
- Caffeine — adsorbs caffeine well and, in repeated doses, interrupts enterohepatic recirculation — the same logic as for theophylline
- Carbamazepine — interrupts the delayed, relapsing absorption its own antimuscarinic effect creates — EXTRIP continues it even during dialysis
- Gabapentinoids — considered early, on general principles rather than on any gabapentinoid-specific evidence
- Isopropanol — poorly adsorbs alcohols and is generally not useful — named here to say so explicitly
- Lamotrigine — for a recent significant ingestion, on the label's recommendation
- Nicotine — adsorbs nicotine; considered after a significant ingestion, weighed against the early vomiting the poison itself causes
- Thallium — single or multiple dose, supported by in vitro binding and some animal data, and a reasonable adjunct where Prussian blue is not immediately available
- The anticholinergic toxidrome — considered late here, because the syndrome itself stops the gut
- Theophylline — the one truly disease-modifying intervention short of dialysis — interrupts enterohepatic and enterocapillary recirculation
- Venlafaxine and the SNRIs — the one intervention with overdose-specific evidence here — it lowers the probability of seizure, which is the dose-dependent danger of this drug
- Z-drugs (zopiclone and zolpidem) — for a recent significant ingestion, on both labels' recommendation
Andexanet alfa
Monograph on drugs.resusdoc.uk- Anticoagulants — a decoy factor Xa that soaks up the inhibitor
Anticholinergic antiparkinsonian agents
Monograph on drugs.resusdoc.uk- Antipsychotics — haloperidol's label recommends parenteral administration for severe extrapyramidal reactions
Atropine
Monograph on drugs.resusdoc.uk- Beta-blockers — first move for bradycardia, and usually insufficient alone
- Carbamate insecticides — the same muscarinic antagonism as in organophosphate poisoning, and here it is the whole of the specific treatment
- Clonidine and central α₂ agonists — for symptomatic bradycardia
- Foxglove and the cardiac-glycoside plants — opposes the vagotonic bradycardia and AV block, the same nodal effect seen with pharmaceutical digoxin
- Nicotine — for the muscarinic overflow of the stimulatory phase — bronchorrhoea, bradycardia, secretions — not for the nicotinic block itself
- Organophosphate insecticides — competes with accumulated acetylcholine at muscarinic receptors — it treats the secretions and the bradycardia and does not touch the neuromuscular junction
Benzodiazepines
Monograph on drugs.resusdoc.uk- Amphetamines and MDMA — the upstream intervention — they reduce agitation, muscle activity and therefore heat production all at once
- Antihistamines — for the convulsions, which both first-generation labels name
- Baclofen — for the seizures of overdose, and as a GABA-ergic holding measure in intrathecal withdrawal
- Cocaine — the closest thing to a mechanism-directed treatment: they oppose the central sympathetic drive that produces almost everything else
- Hemlock — poison hemlock and water hemlock — enhances GABA-A signalling, the receptor cicutoxin antagonises — first-line for the status epilepticus of water hemlock, though it is symptomatic control, not a specific antidote
- The anticholinergic toxidrome — the default for the agitation, and measurably worse than physostigmine at reversing the delirium in the one comparative study
- Tramadol — for the seizures, which the label directs be controlled with intravenous diazepam
Calcium salts
Monograph on drugs.resusdoc.uk- Calcium-channel blockers — raises the extracellular gradient to force current through the channels still open
- Hydrofluoric acid — supplies the ion the fluoride is precipitating — topically to bind it in the tissue, and intravenously to replace what has already been lost
Cyproheptadine
Monograph on drugs.resusdoc.uk- Amphetamines and MDMA — for the serotonergic component of MDMA toxicity, with the same weak evidence base described on the SSRI page
- SSRIs and serotonin toxicity — 5-HT2A antagonism — the receptor Dunkley's criteria were built around, though the evidence for the drug is observational
Desferrioxamine
Monograph on drugs.resusdoc.uk- Iron — a chelator that binds free iron and is excreted as ferrioxamine, restoring the margin transferrin has lost
Digoxin-specific antibody fragments (Fab)
Monograph on drugs.resusdoc.uk- Digoxin — binds digoxin in plasma and drags it out of tissue down the resulting gradient
- Foxglove and the cardiac-glycoside plants — cross-reacts with plant cardiac glycosides and binds them in plasma; the label carries a separate dosing scheme for non-pharmaceutical glycoside poisoning
Dimercaprol
Monograph on drugs.resusdoc.uk- Arsenic — the original antidote, developed in wartime Britain against an arsenical warfare agent — a dithiol offering arsenite a pair of thiols in preference to the patient's own
- Lead — the oldest of the dithiols, retained for severe poisoning and historically paired with edetate
- Mercury — the original dithiol, with a lower therapeutic index than its water-soluble successors
DMPS (unithiol)
Monograph on drugs.resusdoc.ukEthanol
Monograph on drugs.resusdoc.uk- Ethylene glycol — competitive alternative substrate for alcohol dehydrogenase
- Methanol — competitive alternative substrate for alcohol dehydrogenase
Flumazenil
Monograph on drugs.resusdoc.uk- Benzodiazepines — competitive antagonist at the benzodiazepine site — and rarely the right answer
- Z-drugs (zopiclone and zolpidem) — reverses them — they act at the benzodiazepine site — but the labels themselves restrict it: not in mixed overdose, short half-life, and it can precipitate convulsions
Folinic acid
Monograph on drugs.resusdoc.uk- Methanol — accelerates the folate-dependent step that disposes of formate
- Methotrexate — a pre-reduced folate that bypasses the enzyme methotrexate blocks, rescuing normal dividing cells — the specific antidote, given early and dosed against the methotrexate
Fomepizole
Monograph on drugs.resusdoc.uk- Ethylene glycol — blocks alcohol dehydrogenase — the first step of the pathway
- Methanol — blocks alcohol dehydrogenase before any formate is made
Glucagon
Monograph on drugs.resusdoc.uk- Beta-blockers — raises myocyte cyclic AMP through a receptor the blockade does not occupy — on animal evidence only
- Calcium-channel blockers — cyclic AMP by an unblocked route — animal evidence only
- Insulin — an adjunct that mobilises hepatic glycogen — useful as a first move but transient, and useless once glycogen stores are exhausted; glucose is the real treatment
High-dose insulin (euglycaemic therapy)
Monograph on drugs.resusdoc.uk- Beta-blockers — inotropy plus a metabolic rescue for a myocardium that has lost its fuel supply
- Calcium-channel blockers — replaces the insulin the poison stopped the pancreas from releasing
Hydroxocobalamin
Monograph on drugs.resusdoc.uk- Cyanide — each molecule binds one cyanide ion at its cobalt, forming cyanocobalamin, which is excreted in the urine
- Nitrous oxide — replaces the cobalamin the gas has oxidised — the mechanistic fit is exact, the dosing and duration are not established
Idarucizumab
Monograph on drugs.resusdoc.uk- Anticoagulants — binds dabigatran itself — the only true molecular antidote in this group
Intravenous lipid emulsion
Monograph on drugs.resusdoc.uk- Calcium-channel blockers — for refractory shock and periarrest, on very low quality evidence
- Lamotrigine — named on the UK label for cardiotoxicity that responds insufficiently to bicarbonate; case reports describe QRS recovery after it
- Local anaesthetic systemic toxicity (LAST) — the specific antidote — a purpose-designed rescue for local anaesthetic cardiotoxicity, given early for seizures or cardiovascular collapse
- Sodium-channel blockade — rescue in refractory collapse, on case-report evidence
- Tricyclic antidepressants — rescue only, in refractory cardiovascular collapse
- Venlafaxine and the SNRIs — a rescue measure for the cardiovascular collapse of a massive ingestion, on general lipophilic-poison grounds rather than venlafaxine-specific evidence
L-carnitine (levocarnitine)
Monograph on drugs.resusdoc.uk- Valproate — replaces the cofactor valproate depletes — for hyperammonaemic encephalopathy and hepatotoxicity, not for the sedation
Magnesium sulphate
Monograph on drugs.resusdoc.uk- Antipsychotics — for torsade de pointes, the consequence of the QT prolongation all three labels describe
- Hydrofluoric acid — replaces the second cation fluoride precipitates, and treats the arrhythmia the electrolyte disturbance produces
Methylthioninium chloride
Monograph on drugs.resusdoc.uk- Methaemoglobin inducers — at low concentration it speeds the conversion of methaemoglobin back to haemoglobin — and at high dose it produces methaemoglobinaemia itself
Naloxone
Monograph on drugs.resusdoc.uk- Clonidine and central α₂ agonists — named on the label as an adjunct for respiratory depression — and the reason it works is not settled
- Gabapentinoids — for the co-ingested opioid, which is usually the reason the patient is not breathing — it does nothing to the gabapentinoid
- Opioids — competitive µ-receptor antagonist — the only true reversal agent in Band A
- Tramadol — reverses the respiratory depression only — the label states it will not antagonise the monoamine reuptake or serotonin-releasing effects, and in animal experiments had no effect on convulsions
Noradrenaline
Monograph on drugs.resusdoc.uk- Calcium-channel blockers — vasoconstriction for the vasoplegic component
Octreotide
Monograph on drugs.resusdoc.uk- Sulfonylureas — suppresses the insulin the sulfonylurea keeps releasing — the mechanism-directed treatment for recurrent hypoglycaemia, not a substitute for glucose
Oxygen
Monograph on drugs.resusdoc.uk- Carbon dioxide and the simple asphyxiants — the only page in this band where oxygen is not a workaround but the actual correction — the deficiency is of oxygen itself
- Carbon monoxide — competitive displacement from haem — the antidote is the substrate
Penicillamine
Monograph on drugs.resusdoc.uk- Lead — the only one of the four with a UK marketing authorisation naming lead poisoning, and licensed in children only below a stated blood lead concentration
Phentolamine
Monograph on drugs.resusdoc.uk- Cocaine — alpha blockade, at the receptor cocaine's excess noradrenaline is acting on
Physostigmine
Monograph on drugs.resusdoc.uk- The anticholinergic toxidrome — raises acetylcholine at the blocked receptor and crosses into the brain — the contested one
Phytomenadione (vitamin K1)
Monograph on drugs.resusdoc.uk- Anticoagulants — replaces the vitamin the poison stopped recycling — for vitamin K antagonists only, and useless against every direct inhibitor
Pralidoxime
Monograph on drugs.resusdoc.uk- Organophosphate insecticides — reactivates acetylcholinesterase that has not yet aged — it reached its target in a randomised trial and mortality went the wrong way
Prothrombin complex concentrate
Monograph on drugs.resusdoc.uk- Anticoagulants — supplies the factors themselves, bypassing both the enzyme and the wait
Prussian blue
Monograph on drugs.resusdoc.uk- Thallium — an ion-exchange lattice given orally to trap thallium in the gut and interrupt its enterohepatic and enteroenteric recycling — described as the drug of choice on safety rather than on demonstrated efficacy
Pyridoxine (vitamin B6)
Monograph on drugs.resusdoc.uk- Isoniazid — replaces the cofactor isoniazid depletes, restoring GABA synthesis and terminating the seizures — in a quantity matched to the isoniazid ingested
Sodium bicarbonate
Monograph on drugs.resusdoc.uk- Antihistamines — for the sodium-channel blockade some of these drugs produce, aimed at the QRS rather than at the antihistamine
- Antipsychotics — if the QRS widens — quetiapine's label warns against physostigmine in exactly that situation
- Beta-blockers — for the propranolol-specific QRS prolongation, not for the beta-blockade
- Carbamazepine — for QRS widening from sodium-channel blockade, as in the tricyclics it structurally resembles
- Cocaine — for the QRS widening — cocaine is a sodium-channel blocker, and this treats the channel rather than the drug
- Iron — for the anion-gap acidosis, treating a consequence rather than the poison
- Lamotrigine — the first-line answer to QRS broadening, borrowed intact from the sodium-channel-blockade approach — though it fails more often here than with the tricyclics
- SSRIs and serotonin toxicity — for the QRS widening that citalopram in particular can produce
- Salicylate — ion trapping — keeps salicylate out of the brain and in the urine
- Sodium-channel blockade — sodium load plus alkalosis, aimed at the channel rather than at the drug
- The anticholinergic toxidrome — for the wide QRS that several anticholinergic drugs also produce — the reason physostigmine is withheld
- Tricyclic antidepressants — sodium load plus alkalosis — the only intervention aimed at the channel
- Yew (taxine alkaloids) — the sodium-channel-blockade manoeuvre for the widened QRS — a sodium load and a pH shift, not a specific antidote to taxine
Sodium calcium edetate
Monograph on drugs.resusdoc.uk- Lead — parenteral chelation, mobilising lead principally from bone by exchanging its central calcium ion for lead
Sodium nitrite and sodium thiosulfate
Monograph on drugs.resusdoc.uk- Cyanide — thiosulfate supplies the sulphane sulphur that rhodanese runs out of; nitrite creates methaemoglobin to compete for the ion
Succimer (DMSA)
Monograph on drugs.resusdoc.uk- Arsenic — the oral water-soluble analogue, with the same advantage over dimercaprol
- Lead — oral chelation acting principally in the kidney, with a better adverse-effect profile and no parenteral line
- Mercury — the oral dithiol analogue, with the same advantage over dimercaprol of not redistributing mercury to the brain