Forensic Medicine

Antidotes for Common Poisons: A Poison-to-Antidote Master Table for NEET PG

Reflex · 12 Nov 2026 · 12 min read

Last updated: 12 Nov 2026

Glass vial with blue stopper and clear liquid beside a syringe, illustrating antidotes for common poisons
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Antidotes are easiest to learn as pairs: one poison, one antidote, one mechanism and one trap. This post puts the common pairs into grouped tables so you can revise them in one sitting, then explains the few regimens that need more than a table cell.

Doses below are typical adult regimens from standard references, and sources differ slightly on some of them. Where they do, the post says so instead of picking one silently.

Key Takeaways
  • Organophosphate poisoning: atropine first (titrate to clear bronchorrhoea and bronchospasm), then pralidoxime.
  • Paracetamol: N-acetylcysteine, best started within 8 hours, loading then 4-hour and 16-hour infusions.
  • Opioids: naloxone. Benzodiazepines: flumazenil, which is contraindicated in seizure disorder and mixed overdose.
  • Methanol and ethylene glycol: fomepizole (or ethanol) to block alcohol dehydrogenase, with haemodialysis as definitive treatment.
  • Cyanide: hydroxocobalamin preferred. Iron: deferoxamine. Thallium: Prussian blue. Digoxin: digoxin-specific Fab.
  • Metals: dimercaprol, CaNa2 EDTA, succimer or penicillamine depending on the metal. In severe lead poisoning, dimercaprol goes before EDTA.
  • Indian snakebite: polyvalent anti-snake venom, plus a neostigmine trial for neurotoxic bites.

Once you have read the pairs below, test yourself with toxicology practice questions.

How to Use This Master Table of Antidotes

Read each table row as four questions: what blocks, binds or replaces the toxin, what is the typical dose, and what makes this antidote dangerous. The "caution" column is where most of the reasoning lives, so do not skip it.

Antidotes work in a few ways. Some compete at the receptor (naloxone, flumazenil), some block a toxic metabolite pathway (fomepizole, N-acetylcysteine), some bind the poison directly (chelators, Prussian blue, antibodies), and some restore a depleted substrate (pyridoxine, vitamin K). A useful revision habit is to group antidotes by mechanism rather than memorise a flat list.

An antidote never replaces supportive care. Airway, breathing, circulation and decontamination come first in most poisonings.

Antidotes for Pesticide and Cholinergic Poisoning

Organophosphate and carbamate poisoning is the classic antidote topic because it needs two drugs with different jobs. Atropine treats the muscarinic effects, and pralidoxime reactivates acetylcholinesterase that the organophosphate has inhibited (Merck Manual: Organophosphate and Carbamate Poisoning).

PoisonAntidoteMechanismTypical adult regimenKey caution
OrganophosphateAtropine, then pralidoximeAtropine blocks muscarinic receptors; pralidoxime reactivates inhibited acetylcholinesteraseAtropine 2 to 3 mg IV, doubled every 3 to 5 minutes until effect. Pralidoxime 1 to 2 g IV over 15 to 30 minutes, then 8 mg/kg/hTitrate atropine to clear bronchospasm and bronchorrhoea, not to pupil size or heart rate
CarbamateAtropine; pralidoxime only when the agent is unknownAs aboveAs aboveEffects usually clear within about 48 hours
Anticholinergic toxicityPhysostigmineInhibits acetylcholinesterase, raising acetylcholine1 to 2 mg IV over 5 minutesUse is controversial; involve a toxicologist

Atropine and pralidoxime in organophosphate poisoning

A 1 mg test dose that eases muscarinic signs supports the diagnosis, and the dose is then doubled every 3 to 5 minutes, sometimes reaching very large cumulative totals. Pralidoxime follows atropine, not the other way round. Benzodiazepines treat the seizures.

Do not treat pralidoxime as a sure thing. Rapid IV infusion can cause respiratory or cardiac arrest, it does not help once the enzyme has aged, and it penetrates the blood-brain barrier poorly. Systematic reviews of oxime therapy have shown no benefit or even possible harm (Chacko and Peter, Indian J Crit Care Med 2019). Dose schedules also vary: another reference gives 2 g over 20 minutes then 0.5 g/h.

A simple memory aid (our own, not a standard mnemonic): atropine dries the patient, pralidoxime frees the enzyme. If a stem asks what to titrate atropine against, the answer is secretions and bronchospasm, not the pupil.

For the receptor pharmacology behind this, see our notes on cholinergic drugs and organophosphate poisoning.

Specific Antidotes for Common Drug Overdoses

Drug overdose pairs are short to learn but each carries a contraindication. Learn the antidote and the one situation where giving it is harmful.

PoisonAntidoteMechanismTypical adult regimenKey caution
ParacetamolN-acetylcysteineSupplies cysteine for glutathione, which neutralises the toxic metabolite NAPQIIV 150 mg/kg loading, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hoursBest started within 8 hours, but still given later
OpioidsNaloxoneCompetitive antagonist at mu, delta and kappa receptors0.4 to 2 mg IV every 2 to 3 minutesShort half-life, so repeat doses; can precipitate withdrawal
BenzodiazepinesFlumazenilCompetitive antagonist at the benzodiazepine site of GABA-A0.1 to 0.2 mg IV every minute, maximum 2 mgContraindicated in seizure disorder, mixed overdose, benzodiazepine tolerance and prolonged QRS
IsoniazidPyridoxineReplenishes vitamin B6 and supports GABA productionGram for gram with the amount ingested; if the amount is unknown, a large empirical IV dose (references differ on the figure)Treats the seizures
Beta-blockersGlucagonRaises cAMP independent of beta receptors5 to 10 mg IV loadingSecond-line; causes nausea and vomiting
Local anaesthetic toxicity20% IV lipid emulsion"Lipid sink"1.5 mL/kg bolus, then 0.25 mL/kg/min for 30 to 60 minutesEvidence is mostly animal and case reports

N-acetylcysteine for paracetamol poisoning

N-acetylcysteine is the drug in this section with the most timing detail to learn. It works best when started within 8 hours of ingestion, and one review advises starting ideally between 4 and 8 hours and not later than 14 hours. Another reference still recommends treatment beyond 24 hours in a patient with significant toxicity (Merck Manual: Acetaminophen Poisoning).

The treatment nomogram line is 150 mcg/mL at 4 hours: a level at or below this line in a patient with no symptoms makes hepatotoxicity very unlikely. It applies only to a single acute ingestion with a known time. The loading infusion runs over 15 minutes in the Merck protocol and over 60 minutes in some other references, so learn the three-bag pattern (150, 50, 100 mg/kg) rather than a single loading time.

Naloxone and flumazenil: two competitive antagonists

Both reverse their target drug quickly, and both can cause harm by doing so. Naloxone can precipitate withdrawal, and if there is no response after 10 mg, reconsider the diagnosis. A lower starting dose of 0.04 mg is used when dependence is suspected (Chacko and Peter, 2019).

Flumazenil can provoke seizures when benzodiazepines are masking a tricyclic antidepressant overdose, and in dependent patients it can cause withdrawal (Merck Manual: Symptoms and Treatment of Specific Poisons). Resedation is possible as it wears off.

Antidotes for Toxic Alcohols and Cyanide

Methanol, ethylene glycol and cyanide share one theme: the parent compound is not the main danger, so the antidote either blocks conversion or mops up the poison. Early treatment matters in all three.

PoisonAntidoteMechanismTypical adult regimenKey caution
MethanolFomepizole (preferred) or ethanolInhibits alcohol dehydrogenase, blocking formation of toxic metabolitesFomepizole 15 mg/kg IV, then 10 mg/kg every 12 hours. Ethanol 10% in 5% dextrose, 10 mL/kg over 1 hour, then 1 to 2 mL/kg/h, targeting 100 mg/dLGive early; haemodialysis is definitive
Ethylene glycolFomepizole or ethanolAs above15 mg/kg IV, then 10 mg/kg every 12 hoursHaemodialysis is definitive
CyanideHydroxocobalamin (preferred); sodium nitrite and sodium thiosulfate kitHydroxocobalamin binds cyanide to form cyanocobalamin; thiosulfate donates sulfur to form thiocyanateHydroxocobalamin typically 5 g IVGive 100% oxygen as well
MethaemoglobinaemiaMethylene blueConverted to leucomethylene blue, which reduces methaemoglobin1% solution, 1 to 2 mg/kg IV slowlyInject slowly
Carbon monoxide100% oxygenOxygen is the treatmentConsider hyperbaric oxygen if COHb is above about 25%Hyperbaric oxygen is a consideration, not a routine step

Fomepizole schedules differ between references, with a longer schedule that steps the dose up after four doses and continues until ethanol falls below 20 mg/dL (Chacko and Peter, 2019). The principle is the same: block the enzyme early and keep blocking it until the toxin is cleared.

The cyanide kit sequence

The older kit works in a fixed order. Amyl nitrite is inhaled first, then 3% sodium nitrite 10 mL IV (given slowly), then 25% sodium thiosulfate 25 to 50 mL. Thiosulfate is slow and penetrates cells poorly, so it is usually considered when hypoxia persists despite maximum hydroxocobalamin.

Chelating Antidotes for Heavy Metal and Iron Poisoning

Chelators bind the metal and let the kidney or gut clear it. The choice depends on the metal, so learn the metal-to-chelator mapping first and doses second (Merck Manual: Chelation Therapy for Heavy Metal Poisoning).

PoisonAntidoteTypical regimenKey caution
Lead (severe poisoning)Dimercaprol plus CaNa2 EDTADimercaprol 3 to 4 mg/kg IM every 4 hours on day 1, then tapering; CaNa2 EDTA 25 to 35 mg/kg IM or slow IV every 12 hours for 5 to 7 daysDimercaprol first, to avoid redistributing lead to the brain
Lead (occupational adult exposure, or children with blood lead above 45 mcg/dL)Succimer10 mg/kg orally every 8 hours for 5 days, then every 12 hours for 14 daysOral option
Arsenic and mercuryDimercaprol and succimer for both; penicillamine is also listed for arsenicPenicillamine 5 to 7.5 mg/kg orally four times daily, maximum 2 g/dayDimercaprol is used for arsenic when oral therapy is not possible
Copper (Wilson disease)Penicillamine; trientineTrientine 750 to 1250 mg/day in 2 to 4 doses, age 13 and overTrientine is approved for Wilson disease only
ThalliumPrussian blue60 mg/kg four times daily via nasogastric tubeAvoid penicillamine, which can redistribute thallium to the CNS
IronDeferoxamineIV infusion starting at 15 mg/kg/h, titrated to blood pressureHypotension: give IV fluids

Why dimercaprol goes before EDTA

In severe lead poisoning, dimercaprol should precede EDTA to avoid redistribution of lead to the brain (Chacko and Peter, 2019). Dimercaprol dosing differs between references, so the table gives the Merck schedule as a typical regimen.

Deferoxamine for iron overdose

Deferoxamine chelates free serum iron. IV therapy is reserved for severe poisoning, such as acidosis, shock, severe gastroenteritis or a serum iron above 500 mcg/dL (Merck Manual: Iron Poisoning).

The Prussian blue dose also differs: another review lists 20 g/day, so treat the figure above as one reference's regimen. Prussian blue works because it traps thallium in the gut, where about 99% is then excreted in faeces.

Antidotes for Anticoagulant, Digoxin and Other Reversals

These are reversal agents, so the useful skill is matching each agent to its drug. Match the drug to its reversal and note the one limitation.

Drug or poisonAntidoteMechanismKey point
WarfarinVitamin K1, plus FFP or prothrombin complex concentrate for rapid reversalDirectly antagonises warfarinIV vitamin K only if oral is not possible, because of anaphylactoid risk
HeparinProtamine sulfateForms an inactive complexGive slowly over 10 to 15 minutes; only partly neutralises LMWH
DigoxinDigoxin-specific FabAntibody fragments bind digoxinEach vial binds 0.5 mg; 10 vials for an unknown adult ingestion

Five more pairs are best learned as straight poison-to-antidote matches (Merck Manual: Common Specific Antidotes).

Poison or drugAntidote
Tricyclic antidepressantsSodium bicarbonate
SulfonylureasOctreotide
MethotrexateLeucovorin or glucarpidase
DabigatranIdarucizumab
Ionising radiationPotassium iodide

Digoxin Fab is not for asymptomatic patients, and digoxin levels read falsely high for at least 3 weeks after Fab therapy. That is a useful reasoning point if a stem shows a high level after treatment.

Snakebite: Anti-Snake Venom and the Neostigmine Trial

In India, the antidote for venomous snakebite is polyvalent anti-snake venom (ASV), and neurotoxic bites also get a neostigmine trial. The figures below come from one ICU series that cites the National Snakebite Management Protocol, so treat them as that series' regimen (Saini et al., IJCCM 2014).

ItemDetail
Initial ASV8 to 10 vials IV over 1 hour
Maximum ASV30 vials for haemotoxic bites; 20 vials for neurotoxic bites
Atropine then neostigmine regimenAtropine 0.6 mg (child 50 mcg/kg) first, then neostigmine 0.01 to 0.04 mg/kg every 1 to 3 hours, maximum 10 mg/24 hours IM or IV

Neostigmine likely does not work in presynaptic envenoming (krait, Russell's viper) but can work in postsynaptic envenoming (cobra). Antivenom has not been shown to reverse established presynaptic paralysis (Toxins 2023 review). Anaphylaxis can follow any amount of ASV, and routine premedication remains controversial (Lancet Reg Health SE Asia 2025).

The atropine given before neostigmine blocks the muscarinic side effects of neostigmine. Remember that sequence as "atropine first, then neostigmine".

Common Mistakes When Revising Antidotes

Most mistakes in this topic come from mixing near-neighbours. These are the ones to guard against.

  • Pupils as the atropine endpoint. The endpoint is clearing of bronchorrhoea and bronchospasm.
  • Flumazenil in any benzodiazepine overdose. It is unsafe in seizure disorder, mixed overdose and tolerance.
  • Giving EDTA before dimercaprol in severe lead poisoning.
  • Penicillamine for thallium. Prussian blue is the antidote, and penicillamine can move thallium into the CNS.
  • Calling pralidoxime curative. Its benefit in trials is mixed.
  • Forgetting that neostigmine depends on the venom type (postsynaptic versus presynaptic).

A good revision method is to cover the antidote column and recall it from the poison, then cover the caution column and recall it from the antidote. Repeat until the pairs come without prompting.

You can then check your recall with pharmacology toxicology and antidotes practice.

Conclusion

Antidotes become manageable once you sort them by mechanism: receptor antagonists, enzyme blockers, chelators, binders and reversal agents. For each pair, hold on to the one caution that changes management, such as the atropine endpoint, the flumazenil contraindications, dimercaprol before EDTA and the presynaptic limits of neostigmine. Practise the pairs with toxicology questions after each pass through the tables.

Practise this on Reflex

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FAQ

Frequently asked questions

The questions aspirants ask most about this topic.

Atropine is given first and doubled every 3 to 5 minutes, titrated to clear bronchospasm and bronchorrhoea rather than pupil size or heart rate. Pralidoxime follows to reactivate inhibited acetylcholinesterase, although trials of oximes show mixed benefit.

N-acetylcysteine. It supplies cysteine for glutathione, which neutralises the toxic metabolite NAPQI. It works best when started within 8 hours of ingestion, and a typical IV regimen is 150 mg/kg loading, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours.

Flumazenil should not be used in seizure disorder, mixed overdose, benzodiazepine tolerance or prolonged QRS. It can provoke seizures when benzodiazepines are masking a tricyclic antidepressant overdose and can cause withdrawal in dependent patients.

Fomepizole is preferred, with ethanol as the alternative. Both inhibit alcohol dehydrogenase so that toxic metabolites do not form. Haemodialysis is the definitive treatment.

Giving EDTA first can redistribute lead into the brain. Dimercaprol is started first to avoid this, and CaNa2 EDTA follows.

No. It is likely to be ineffective in presynaptic envenoming such as krait or Russell's viper bites, and effective in postsynaptic envenoming such as cobra bites. It is given after atropine as a test and treatment for neurotoxic bites.

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