Pralidoxime
Brand names: P2S, Pralidoxime Mesylate
Pralidoxime is a cholinesterase reactivator used, alongside atropine, in the treatment of poisoning by organophosphate insecticides and nerve agents.
Adult dose
Paediatric dose
Dose adjustments
Because pralidoxime is excreted in the urine, a decrease in renal function will result in increased blood levels of the drug; the dosage of pralidoxime chloride should be reduced in the presence of renal insufficiency (the retrieved US label gives no numeric renal dose adjustment).
Not stated in the product information we used — check the full SPC.
Dose independently re-sourced from US FDA prescribing information (openFDA / DailyMed) — cross-check; US labelling may differ from UK — clinician-reviewed. Always confirm against the product SmPC and your local formulary before prescribing.
Contraindications
- No known absolute contraindications; relative contraindications include known hypersensitivity to the drug and other situations in which the risk of its use clearly outweighs possible benefit
- Not effective in poisoning due to phosphorus, inorganic phosphates, or organophosphates not having anticholinesterase activity
- Not indicated as an antidote for intoxication by carbamate-class pesticides - it may increase the toxicity of carbaryl
- Use with great caution in organophosphate overdosage in patients with myasthenia gravis - it may precipitate a myasthenic crisis
Side effects
- Mild to moderate pain at the injection site 40 to 60 minutes after intramuscular injection
- In normal volunteers given parenterally: blurred vision, diplopia and impaired accommodation, dizziness, headache, drowsiness, nausea, tachycardia, increased systolic and diastolic blood pressure, hyperventilation and muscular weakness
- Too-rapid intravenous administration: temporary worsening of cholinergic manifestations (tachycardia, cardiac arrest, laryngospasm, muscle rigidity or paralysis)
- Elevations in SGOT and/or SGPT (observed in normal volunteers given 1200 mg or 1800 mg intramuscularly; returned to normal in about 2 weeks) and transient creatine phosphokinase elevations
- Excitement and manic behaviour immediately following recovery of consciousness (also seen in organophosphate poisoning not treated with pralidoxime)
- In patients it is very difficult to differentiate toxic effects of atropine or the organophosphate compounds from those of the drug
Interactions
- Atropine - signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than expected, especially if the total atropine dose has been large and pralidoxime delayed
- Morphine, theophylline, aminophylline, reserpine and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning
- Barbiturates are potentiated by anticholinesterases - use cautiously in the treatment of convulsions
- Succinylcholine - prolonged paralysis has been reported with drugs having anticholinesterase activity; use with caution
Monitoring
- Observe the patient for at least 48 to 72 hours after organophosphate poisoning
- Muscle weakness and respiratory depression (the principal indications for use) and recurrence of signs of poisoning
- Red blood cell and plasma cholinesterase, and urinary paranitrophenol (parathion exposure), may help confirm the diagnosis and follow the course, but may be normal despite clinically significant poisoning - do not delay treatment for results
- Maintain some degree of atropinization for at least 48 hours and until any depressed blood cholinesterase activity is reversed
- Renal function - dosage should be reduced in renal insufficiency
Clinical monograph
How it works
It reactivates acetylcholinesterase by displacing the organophosphate from the enzyme, restoring acetylcholine breakdown, but only before irreversible 'ageing' of the enzyme-organophosphate bond occurs.
Prescribing in practice
- It must be given as early as possible and always in addition to, not instead of, atropine, which remains the primary antidote for muscarinic effects.
- Efficacy falls once the inhibited enzyme has aged, so it is most useful when started promptly after exposure.
- Administer by slow intravenous infusion and follow UK poisons information advice on its use and continuation.
Monitoring
Monitor neuromuscular and respiratory function, atropinisation and, where available, cholinesterase activity to guide ongoing treatment.
Counselling the patient
- Explain to the team that this drug reactivates the poisoned enzyme but works together with atropine.
- Stress that it should be started as early as possible after organophosphate exposure.
- Note that decontamination and airway support are essential parts of management.
Evidence & guidelines
Pralidoxime with atropine is the standard antidotal regimen for organophosphate and nerve-agent poisoning, with use guided by UK poisons information (TOXBASE).
Reference: NPIS Toxbase; WHO Guidelines for Organophosphate Poisoning; Lancet 2009; 374(9694):992-1000; Drug verified in RxNorm (NLM); confirm dosing against the manufacturer SPC (eMC). Verify against your local formulary and current prescribing references before prescribing. The structured dose values shown have been reviewed by a clinician. Monograph status: clinician-reviewed (2026-07-04).
Related
Curated clinical cross-links plus same-class fallbacks.
- Paracetamol overdose · TOXBASE/NPIS; MHRA DSU 2012/2024; SNAP regimen (Lancet 2014)
- TCA overdose · TOXBASE/NPIS; AACT/EAPCCT position statements; Resuscitation Council UK ALS
- Opioid overdose · TOXBASE/NPIS; Resuscitation Council UK
- Anticholinergic toxidrome · TOXBASE/NPIS; AACT/EAPCCT
- Benzodiazepine overdose · TOXBASE/NPIS; AACT/EAPCCT
- β-blocker overdose · TOXBASE/NPIS; AACT/EAPCCT; ESC
Featured in these MRCEM clinical pathways
Pralidoxime is a core drug in the following exam-focused workups on our sister siteReviseMRCEM.
MRCEM Primary / Intermediate / OSCE candidates: each pathway includes exam-style questions, RCEM/NICE citations, and FAQ summaries.