Organophosphate poisoning
Protect the airway, decontaminate, and give IV atropine fast, doubling the dose every 5 minutes until the chest is clear. Then watch the neck muscles for days.
A 22-year-old farm worker drank a pesticide after an argument at home. He is sweating, drooling and vomiting, with tiny pupils and a chest full of crackles. Pulse 48, BP 90/60, SpO₂ 86%. His clothes smell of kerosene.
What do you do first, and how much atropine?
- Airway and oxygenSuction the secretions, high-flow oxygen, recovery (left lateral) position if not intubated. Call your senior.
- Protect yourselfGloves and apron. Remove contaminated clothes into a sealed bag. Wash skin and hair with soap and water.
- IV atropine now1.8–3 mg IV, then double the dose every 5 minutes until atropinised.
- Check the five targets every 5 minutesClear chest, pulse above 80, systolic BP above 80, dry armpits, pupils no longer pinpoint.
- Atropine infusion once atropinised10–20% of the total loading dose per hour.
- MonitorECG, SpO₂, RR, GCS. Blood gas, sugar, electrolytes, CBC.
- Ask what was takenBottle or label photo. Other tablets, alcohol, wheat pills.
- Check neck flexion strengthEvery few hours for days: weakness warns of respiratory failure.
- Chest full of secretions with falling SpO₂
- Drowsy or unable to protect the airway
- Weak neck flexion or weak breathing
- Fits
- Large intentional ingestion
- Respiratory failure
- Too little atropine
- Intermediate syndrome (day 1–4)
- Aspiration pneumonia
- Co-ingestion: wheat pills, alcohol, paraquat
| Atropine start | 1.8–3 mg IV bolus |
| Doubling | Not atropinised after 5 minutes: double the previous dose. Keep doubling |
| Targets | Clear chest, pulse above 80, systolic BP above 80, dry armpits, pupils not pinpoint |
| Infusion | 10–20% of the total loading dose per hour, adjusted to targets |
| Fits | Diazepam 10 mg IV |
Check every dose against a current drug reference and your hospital protocol.
On this page
What is happening
Organophosphate and carbamate insecticides block the enzyme acetylcholinesterase, so acetylcholine builds up at nerve endings. In Pakistan these pesticides are cheap, kept in rural homes, and are a common means of self-poisoning.
- Drooling, sweating, tears
- Bronchorrhoea and bronchospasm: the chest fills with fluid
- Vomiting, diarrhoea, urination
- Slow pulse, small pupils
- Muscle twitching (fasciculations)
- Weakness, including breathing muscles
- Fast pulse and high BP sometimes
Patients die from respiratory failure: drowning in their own secretions early, or weakness of the breathing muscles later. Atropine treats the secretions. It does not treat the weakness, so keep watching.
Decontamination and safety
- Staff: gloves and an apron. Remove the patient's clothes and bag them. Wash skin and hair with soap and water.
- No induced vomiting.
- Gastric lavage is not routine. It may be considered by a senior only for a large ingestion within about an hour, with the airway protected.
- Activated charcoal is of uncertain benefit and must never delay atropine or airway care.
Atropine
- 1.8–3 mg IV bolusGive it fast. Do not wait for any test.
- Wait 5 minutes and check the five targetsChest, pulse, BP, armpits, pupils.
- Not atropinised? Double the dose3 mg, then 6 mg, then 12 mg, then 24 mg, every 5 minutes.
- Atropinised? Start an infusion10–20% of the total dose needed to atropinise, per hour.
- Check targets every 15 minutes, then hourlySecretions back: give a bolus and increase the rate. Signs of toxicity: stop for 30 minutes, then restart at a lower rate.
- Clear chest on listening (no crackles from secretions).
- Pulse above 80/min.
- Systolic BP above 80 mmHg.
- Dry armpits.
- Pupils no longer pinpoint.
Use all five together. Do not use pupil size or pulse rate alone, and do not aim for big pupils or a pulse of 140.
Confusion, agitation, hallucinations, fever, absent bowel sounds, urinary retention, very fast pulse. Stop the infusion for 30 minutes, then restart at about 70–80% of the previous rate. Catheterise if retaining urine.
Airway and ventilation
- Intubate if the patient cannot protect the airway, is tiring, has rising CO₂, or has weak breathing despite atropine.
- Avoid suxamethonium for intubation: its effect is greatly prolonged in organophosphate poisoning. The anaesthetist will choose another drug.
The days after
After the cholinergic crisis settles, some patients develop weakness of the neck, the muscles near the trunk, cranial nerves and the breathing muscles, while fully conscious. It can lead to sudden respiratory arrest.
- Test neck flexion (lifting the head off the pillow against your hand) every few hours.
- Measure breathing strength (single-breath count or peak flow) if possible.
- Weakness appearing: call your senior and ICU before the patient stops breathing.
- Aspiration pneumonia is common. Treat if fever, new crackles or X-ray changes.
- Delayed neuropathy can appear weeks later (weakness of feet and hands).
- Psychiatric review for every intentional ingestion before discharge. Ask about safety at home, and advise the family to lock away pesticides.
Investigations
| Test | Why |
|---|---|
| Blood gas, sugar, electrolytes | Acidosis, respiratory failure, low potassium |
| CBC, urea, creatinine, LFTs, amylase | Baseline and complications |
| ECG | Slow pulse, QT prolongation, arrhythmias |
| Chest X-ray | Aspiration |
| Paracetamol and other levels | If co-ingestion is possible |
| Cholinesterase level | If available, helps confirm the diagnosis. Never wait for it to treat |
Common mistakes
- Giving small repeated doses (0.6 mg) instead of doubling.
- Stopping atropine as soon as the pupils dilate.
- Chasing a pulse of 140 and causing atropine toxicity.
- Sending the patient to the ward without checking neck strength for the next days.
- Forgetting to protect staff from contaminated clothing.
- Using suxamethonium for intubation.
Frequently asked questions
What is the dose of atropine in organophosphate poisoning?
1.8–3 mg IV, then double the dose every 5 minutes until atropinised (clear chest, pulse above 80, systolic BP above 80, dry armpits, pupils not pinpoint), then an infusion of 10–20% of the total loading dose per hour.
What are the signs of atropinisation?
A clear chest, pulse above 80, systolic BP above 80 mmHg, dry armpits, and pupils no longer pinpoint.
What is intermediate syndrome?
Weakness of the neck, proximal limb, cranial nerve and breathing muscles 1–4 days after organophosphate poisoning, after the acute crisis. It can cause sudden respiratory failure.
Is pralidoxime effective?
Evidence is mixed. It may help some patients if given early. Atropine and airway support are the essential treatments.
What is the antidote for organophosphate poisoning?
Atropine is the main antidote. It is given IV in doubling doses every 5 minutes until the chest is clear, pulse above 80, systolic BP above 80, armpits dry and pupils no longer pinpoint. Pralidoxime may be added if available.
Test yourself
Exam-style questions on this guide, from our two question banks. Choose an answer to see why each option is right or wrong.
1. A farmer with organophosphate poisoning has had atropine 2 mg, then 4 mg, then 8 mg IV at 5-minute intervals. He still has crackles in the chest and a pulse of 60. What is the next atropine dose?
Answer: 16 mg IV. Atropine is doubled every 5 minutes until the targets are met: clear chest, heart rate above 80, systolic BP above 80, dry axillae and pupils no longer pinpoint. Then an infusion of 10–20% of the total loading dose per hour.
- 2 mg IV: Too small; restarting low wastes time.
- 1 mg IM: Too slow and too small.
- Stop atropine and give pralidoxime only: Atropine is the life-saving drug for muscarinic effects.
- 8 mg IV again: Doses are doubled until atropinisation targets are met.
2. A patient needed a total of 40 mg of atropine to become atropinised after organophosphate poisoning. What hourly infusion rate is usually started?
Answer: 4–8 mg per hour. The atropine infusion is usually 10–20% of the total dose needed for atropinisation, per hour, then adjusted to the clinical targets.
- 0.5 mg per hour: Too low; secretions will return.
- No infusion is needed: Organophosphates keep acting for hours to days.
- 20 mg per hour: Likely to cause atropine toxicity.
- 40 mg per hour: The infusion is a fraction of the loading total.
3. On day 2 after organophosphate poisoning, a man is alert but cannot lift his head off the pillow and his neck flexion is weak. What is the likely problem?
Answer: Intermediate syndrome. Intermediate syndrome develops 24–96 hours after poisoning with weakness of neck flexors, proximal limbs and respiratory muscles. Monitor breathing closely and involve ICU.
- Normal recovery: Neck flexor weakness is a warning sign.
- Delayed peripheral neuropathy: That appears after 2–3 weeks.
- Atropine toxicity: Toxicity causes agitation, fever and dry skin, not neck weakness.
- Hypoglycaemia: Not this pattern.
4. A 28-year-old cotton farmer in southern Punjab is brought in after spraying pesticide. He is sweating, salivating and vomiting, with pinpoint pupils, HR 48/min, widespread wheeze and muscle twitching. What is the most important immediate drug treatment?
Answer: IV atropine, doubling until chest clear. This is organophosphate poisoning — acetylcholinesterase inhibition causing muscarinic (secretions, bradycardia, bronchospasm, miosis) and nicotinic (fasciculations, weakness) features. After airway support, give IV atropine and double the dose every few minutes until atropinised: clear chest on auscultation, HR > 80, systolic BP > 80, dry axillae. Pralidoxime is an adjunct in some protocols; it does not replace atropine. Remove contaminated clothes and wash the skin.
- IV pralidoxime alone, without atropine: Oximes are adjuncts at best; atropine reverses the life-threatening muscarinic effects.
- IV naloxone: Pinpoint pupils here are cholinergic, not opioid; the bradycardia and secretions point to organophosphate.
- IV physostigmine, then atropine: Physostigmine is a cholinesterase inhibitor — it would add to the cholinergic poisoning, not reverse it.
5. A farmer drank an organophosphate pesticide. After atropine his chest is dry and pulse 95, but 2 days later he develops neck flexion weakness, proximal limb weakness and cranial nerve palsies, then respiratory failure. What is this?
Answer: Intermediate syndrome. Intermediate syndrome develops 24–96 hours after organophosphate poisoning, after the cholinergic crisis has settled: weakness of neck flexors, proximal limbs, cranial nerves and respiratory muscles from prolonged nicotinic receptor dysfunction. It requires monitoring of neck flexion and ventilation. Organophosphate-induced delayed polyneuropathy occurs after 2–3 weeks (distal, motor). Atropine toxicity causes agitation, hyperthermia and tachycardia.
- OPIDN: Later — 2–3 weeks, distal.
- Atropine toxicity: Atropine toxicity causes agitation, fever and dry skin, not proximal and neck weakness.
- Guillain–Barré syndrome: GBS is unrelated to poisoning and has a different timing; weakness 1–4 days after organophosphate is intermediate syndrome.
6. A farmer is brought in unconscious with pinpoint pupils, bradycardia, sweating, drooling and wheezing. An empty pesticide bottle was found. What is the treatment?
Answer: Atropine and pralidoxime. Organophosphates irreversibly inhibit acetylcholinesterase, causing excess acetylcholine: muscarinic signs (salivation, sweating, miosis, bradycardia, bronchorrhoea, diarrhoea) and nicotinic weakness. Atropine is titrated until secretions dry. Pralidoxime reactivates the enzyme if given before 'ageing'. Decontaminate the skin.
- Naloxone infusion: Opioid antidote; would not dry secretions.
- Flumazenil injection: Benzodiazepine antidote.
- N-acetylcysteine: Paracetamol antidote.
- Physostigmine: Another cholinesterase inhibitor; would worsen it.
7. A woman with myasthenia gravis takes increasing doses of pyridostigmine. She now has worse weakness, sweating, drooling, small pupils and muscle twitching. What is happening?
Answer: Cholinergic crisis. Too much anticholinesterase causes excess acetylcholine: muscarinic signs (salivation, sweating, miosis, bradycardia) and depolarising block with fasciculations and weakness. Stop the drug, support breathing and give atropine for muscarinic effects. Myasthenic crisis is weakness from disease without these cholinergic signs.
- Myasthenic crisis: No cholinergic signs in myasthenic crisis.
- Botulism: Dilated pupils, descending paralysis.
- Guillain–Barré syndrome: Ascending weakness, areflexia.
- Hypokalaemic paralysis: No cholinergic signs.
References and dose sources
- Eddleston et al. Management of acute organophosphorus pesticide poisoning (Lancet 2008)
- Atropine dosing: Drugs.com: Atropine dosage (see also our atropine dose page)
- Pralidoxime dosing: Drugs.com: Pralidoxime dosage (see also our pralidoxime dose page)
- Diazepam dosing: Drugs.com: Diazepam dosage (see also our diazepam dose page)
International guidance is linked where it reflects good practice. Where your hospital’s protocol differs, follow your hospital.