Organophosphorus Poisoning
On this page
Direct answer
Irreversible inhibition of acetylcholinesterase by an organophosphorus pesticide — a bottle swallowed on an Indian farm — floods muscarinic and nicotinic receptors with acetylcholine and produces the fastest "toxicology stem to diagnosis" in the paper: pinpoint pupils, frothing chest, fasciculations and bradycardia in a farmer who smells of pesticide. Muscarinic effects give the SLUDGE/DUMBBELS picture (salivation, lacrimation, urination, diarrhoea, miosis, bronchorrhoea, bradycardia, emesis), nicotinic effects give fasciculations and flaccid weakness, and severe cases progress to coma and seizures. Treatment is generous intravenous atropine titrated to chest clearance, pralidoxime to reactivate the enzyme, decontamination and meticulous intensive care.
What you must remember
- Muscarinic (DUMBBELS): diarrhoea, urination, miosis, bronchorrhoea and bronchospasm, bradycardia, excitation of glands (salivation, lacrimation, sweating), emesis; the chest full of secretions is the target of atropine.
- Nicotinic effects: muscle fasciculations, cramps, flaccid weakness and respiratory failure from depolarising blockade — atropine does not correct these; pralidoxime does, given early before the enzyme-inhibitor bond "ages".
- Atropinisation: give atropine 1 to 2 mg intravenously, doubling every five minutes until the chest is clear of secretions, heart rate above 80 and systolic pressure above 80; pupils and tachycardia are not endpoints; then start an infusion at 10 to 20 per cent of the total loading dose hourly.
- Pralidoxime: 1 to 2 g intravenously over 15 to 30 minutes, then infusion (about 8 mg per kg per hour in many protocols) for 24 to 48 hours in symptomatic cases; it is most effective when given early, and also treats nicotinic (muscle) manifestations.
- Decontamination: remove clothing, wash skin, gastric lavage within one hour of ingestion if airway is protected; staff wear gloves and aprons — dermal absorption poisons carers.
- Intermediate syndrome: proximal limb, neck-flexor, cranial nerve and respiratory muscle weakness appearing 24 to 96 hours after exposure, needing anticipatory ventilation — it is a neuromuscular junction disorder, not a recurrence of cholinergic crisis.
- Organophosphate-induced delayed polyneuropathy appears 1 to 4 weeks later as a distal symmetrical motor axonopathy. Avoid succinylcholine in these patients — prolonged apnoea results from plasma cholinesterase inhibition.
- Red cell (erythrocyte) acetylcholinesterase reflects synaptic enzyme and correlates better with severity than plasma pseudocholinesterase.
The first hours, antidote by antidote
A 28-year-old is brought in drowsy, sweating profusely, pupils pinpoint, chest audible with secretions, heart rate 48, fasciculations over his shoulders; an empty chlorpyrifos bottle is in the relative's hand. Protect yourself first — gloves and apron, remove and bag the clothes, wash the skin, since dermal absorption poisons carers; gastric lavage only within an hour and only with the airway protected. Now the two antidotes, in parallel and for different targets. Atropine 1 to 2 mg intravenously, doubled every five minutes, aims at the muscarinic chest: the endpoints are dry lungs, heart rate above 80 and systolic above 80 — deliberately not the pupils — after which an infusion runs at 10 to 20 per cent of the loading dose per hour. Pralidoxime 1 to 2 g over 15 to 30 minutes, then about 8 mg per kg per hour, aims at the nicotinic muscle: the fasciculations and weakness that atropine never fixes, and it must arrive before the bond ages. Watch the clock for what follows: If he needs intubation, succinylcholine is forbidden: plasma cholinesterase inhibition makes its paralysis dangerously prolonged. Red cell acetylcholinesterase is the assay that correlates with severity.
Where students slip
The syndromes blur when they should sit on a timeline: cholinergic crisis at presentation, intermediate syndrome at one to four days, delayed polyneuropathy weeks later — the stem's hidden clue is the interval. The atropine endpoint is the second guaranteed trap: chasing pupil dilatation overdoses the patient. Third, carbamate poisoning resembles this picture but is milder and self-limiting because its inhibition is reversible, so pralidoxime is often omitted there — a nuance the options exploit. And the muscarinic-nicotinic division answers the "which drug for which sign" question: atropine for secretions, pralidoxime for the muscles that atropine cannot reach.
Frequently asked questions
What is the antidote for organophosphorus poisoning?
Atropine for muscarinic effects plus pralidoxime to reactivate inhibited acetylcholinesterase, especially for nicotinic muscle weakness.
How is atropinisation judged?
By drying of chest secretions with heart rate above 80 and systolic pressure above 80 — pupil size is deliberately ignored as a target.
What is the intermediate syndrome?
Proximal and respiratory muscle weakness with cranial nerve involvement at 24 to 96 hours, requiring elective ventilation.
Why avoid succinylcholine here?
Its hydrolysis depends on plasma cholinesterase, which the poison inhibits, causing dangerously prolonged paralysis.
Which measurement correlates best with severity?
Red cell acetylcholinesterase, which mirrors the synaptic enzyme; plasma butyrylcholinesterase falls first but correlates less well.
When is pralidoxime most effective?
Given early, before the organophosphate-enzyme bond ages and becomes irreversible; it also reverses fasciculations and muscle weakness.