Poisoning Emergency Care
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Direct answer
Poisoning care in India runs through three giants — organophosphorus pesticides, aluminium phosphide (the "rice tablet"), and drug overdoses led by paracetamol and benzodiazepines — and its principles are simultaneous resuscitation, identification by toxidrome, selective decontamination, and specific antidote where one exists. Airway and breathing come first because most lethal pesticides kill by secretion and respiratory failure; activated charcoal at about 1 g/kg within an hour benefits most oral overdoses, while gastric lavage is selective, early and contraindicated with corrosives or petroleum products. The telephone number of a poison information centre belongs on the wall: its advice changes management more than any single test.
What you must remember
- Resuscitation before antidote always: C-ABCDE with gloves — a pesticide-soaked patient is a staff hazard; undress and wash before crowded resuscitation.
- Organophosphorus toxidrome: salivation, lacrimation, urination, diarrhoea, GI upset, emesis — the SLUDGE mnemonic — plus miosis, bronchorrhoea and bradycardia, with fasciculations from nicotinic overstimulation; the cardiorespiratory killer is bronchorrhoea with respiratory failure.
- OP treatment pair: atropine (adult bolus commonly 2-4 mg IV, doubling every few minutes until the chest is dry and the rate above 80 — "atropinisation") plus an oxime such as pralidoxime per local protocol for the nicotinic findings; organic carbamate poisoning looks identical but shorter-acting — atropine alone usually suffices; beware the intermediate syndrome at 24-96 hours.
- Aluminium phosphide: the fumigant "rice tablet" releases phosphine — refractory shock, arrhythmia, metabolic acidosis; no proven antidote, magnesium and supportive care used, mortality remains high.
- Paracetamol: antidote N-acetylcysteine, the classical regimen 150 mg/kg over one hour, 50 mg/kg over four hours, 100 mg/kg over sixteen; the Rumack-Matthew line guides treatment from about 4 hours post-ingestion, and late presentations are treated regardless of level.
- Decontamination rules: charcoal about 1 g/kg within roughly an hour for most drugs (not lithium, iron, alcohols, hydrocarbons, corrosives); lavage within an hour for life-threatening ingested amounts; whole-bowel irrigation for sustained-release and body-packer scenarios.
- Cheap tests that steer everything: glucose (the comatose alcoholic), ECG (sodium-channel blockers widen the QRS), paracetamol and salicylate levels where available.
- Psychosocial closure: every intentional overdose earns a psychiatric assessment before discharge — a legal expectation in Indian practice, not a courtesy.
A dusk arrival from the fields
A 34-year-old is carried in two hours after drinking an unknown liquid; he is drowsy, soaked with sweat, pinpoint pupils, breathing 30 with audible chest secretions, and his heart rate is 54. The staff glove and gown; his clothes go into a bag and the skin is washed — in Indian pesticide exposure the family and the trolley also carry toxin. Two cannulae go in while the airway is suctioned; atropine 3 mg is given intravenously, doubled every five minutes against the endpoints — chest clearing, secretions drying, rate above 80 — reaching control at roughly 12 mg, then an infusion; mydriasis is a dangerously late endpoint. Pralidoxime is prepared and run per the hospital's protocol for his fasciculations, and the team writes on the board the two dates that matter: today's resuscitation, and day 2 to 4 for the intermediate syndrome — neck flexor weakness and respiratory decline that will need ventilator readiness, not more atropine. A glucose, ECG and chest film complete the first thirty minutes, and the poison centre is called to identify the compound.
Where students slip
The atropine endpoint is the perennial trap: dry chest and heart rate above 80 are the targets; waiting for dilated pupils guarantees over-atropinisation with delirium and hyperthermia. The second is antidote reflexes — charcoal for everything (useless for hydrocarbons, corrosives, iron, lithium, alcohols), or an oxime for every cholinergic-looking picture without confirming the class. And the sequencing error of antidote before airway: the poisoned patient dies of secretion-filled airways first. The aluminium phosphide stem is tested precisely because no antidote exists — the honest answer is aggressive supportive care, magnesium per local practice, and early referral. Indian viva examiners extend to pesticide storage rules, poison centre usage, and medico-legal documentation with police intimation for every suspected suicidal or homicidal poisoning — as examinable as the pharmacology.
Frequently asked questions
What marks the cholinergic (organophosphorus) toxidrome?
Salivation, lacrimation, urination, diarrhoea, vomiting, miosis, bradycardia and bronchorrhoea, with fasciculations from nicotinic overstimulation — the secretion-loaded airway kills first.
What endpoints define adequate atropinisation?
Dry chest with cleared secretions and heart rate above 80 — pupillary dilatation is a late, dangerous endpoint.
What is the classical N-acetylcysteine regimen for paracetamol?
150 mg/kg over one hour, 50 mg/kg over four, 100 mg/kg over sixteen — guided by the treatment line from about four hours post-ingestion.
Why is gastric lavage selective rather than routine?
Benefit is confined to early, life-threatening ingestions; lavage is contraindicated after corrosives and hydrocarbons and carries aspiration risk — charcoal within the hour helps more patients.
What is the intermediate syndrome of organophosphorus poisoning?
Weakness of neck flexors, proximal limbs and respiratory muscles appearing 24-96 hours after recovery, requiring ventilator preparedness — it does not respond to more atropine.