Level 1 of 6Core
Organophosphate and carbamate poisoning
The core to-do list — diagnose and manage, at a glance
Diagnose— recognise it
- The cardinal pattern is miosis with hypersalivation, rhinorrhoea and bronchorrhoea — a wet patient with small pupils; that cluster in a patient who smells of solvent is an anticholinesterase poisoning until proven otherwise. Smell the patient: most agricultural formulations are dissolved in hydrocarbon (kerosene-type) solvents giving a petroleum or garlicky odour on the breath and clothing.
- Ask about the route and the container: intoxication may follow ingestion, inhalation or dermal absorption — deliberate ingestion accounts for most hospital deaths, and occupational spraying, re-entry into treated fields, contaminated clothing and contaminated foodstuffs account for the rest. The illness is heralded by anxiety and restlessness, followed by nausea, vomiting, abdominal colic, diarrhoea, sweating, hypersalivation and chest tightness.
- Separate muscarinic from nicotinic features: muscarinic gives bronchorrhoea, bronchoconstriction, bradycardia, hypotension, miosis, lacrimation, salivation, vomiting, colic, profuse diarrhoea, involuntary micturition, sweating and fever; nicotinic gives tachycardia, hypertension, mydriasis, fasciculation, weakness and flaccid paralysis. Look for fasciculation tangentially across the undressed chest wall and thighs — its presence strongly suggests the diagnosis, although it is often absent even in serious poisoning.
- The pupil and the pulse both lie: bradycardia and tachycardia both occur depending on whether muscarinic or nicotinic effects predominate, so a normal or fast pulse never excludes the diagnosis; mydriasis may replace miosis, so the pupil is unreliable as a treatment endpoint. Auscultate: widespread coarse crackles and wheeze with frothing at the mouth is bronchorrhoea, not cardiogenic pulmonary oedema, and it responds to atropine and suction, not to diuretics or nitrates.
- Assess the respiratory muscles at the bedside and repeatedly: respiratory rate, oxygen saturation, single-breath count, ability to lift the head from the pillow, to swallow saliva and to complete a sentence — shallow or paradoxical breathing is pre-terminal. Measure the capillary glucose (hypoglycaemia mimics and complicates the picture; hyperglycaemia is common) and get an ECG — sinus bradycardia and atrioventricular block are recognised, as are QT prolongation and torsades de pointes.
- Send cholinesterase but never wait for it — activity below 10% of normal indicates severe poisoning, 20–50% moderate and above 50% subclinical, but values correlate poorly and a normal result in a wet, miotic patient does not exclude the diagnosis. If the diagnosis is genuinely uncertain, use the atropine test dose: record the pulse before and three minutes after atropine 1 mg intravenously — a marked increase in heart rate with skin flushing makes organophosphate poisoning unlikely; in an obviously cholinergic patient omit it and go straight to full antidotal treatment. Red flags: secretions accumulating faster than they can be suctioned or an audibly bubbling airway; falling saturation on high-flow oxygen or any rise in arterial carbon dioxide; inability to lift the head, swallow saliva or complete a sentence; generalised fasciculation progressing to flaccid weakness; declining conscious level, seizures or coma; bradycardia with hypotension unresponsive to volume; prolonged QT or torsades; and a persistent or escalating atropine requirement.
Manage now— do this, in order
- Protect yourself first: the agent crosses intact skin and is present in secretions, vomit and sweat, so wear gloves, an impermeable apron and eye protection from the outset, and remove and assess any staff member who develops headache, nausea, blurred vision, sweating or miosis.
- Decontaminate — it is treatment: remove all clothing including underwear, footwear, watch straps and leather items, cutting garments off rather than pulling them over the face, and double-bag them. Wash the skin with copious lukewarm water or saline, and for pesticides wash at least twice with plain soap and shampoo the hair, cleaning behind the ears, under the nails and in skin folds — hot water increases dermal absorption and cold water causes hypothermia, and alcohol and other solvents may paradoxically enhance absorption. Eyes: instil local anaesthetic drops if available, remove contact lenses, lift the tarsal conjunctiva to look for particles, and irrigate each eye with at least 1 litre of saline or water over 15 minutes.
- High-flow oxygen to every symptomatic patient, and suction the airway continuously in the severely poisoned patient — suction is a therapeutic intervention here; nebulised ipratropium may be added for bronchospasm but does not replace intravenous atropine.
- Atropine 2 mg intravenously, doubled every 5–10 minutes until clinical improvement — 2, 4, 8, 16, 32, 64 mg and beyond, reassessing after each dose; as much as several hundred milligrams may be needed and there is no ceiling. Paediatric atropine 0.02 mg/kg intravenously with a minimum dose of 0.1 mg, doubled every 5–10 minutes against the same endpoints, targeting an age-appropriate heart rate; dilute an adult ampoule (for example 1 mL to 10 mL with 0.9% sodium chloride) before drawing paediatric volumes.Doctor / Nurse
- The endpoints of atropinisation are four: secretions controlled (the chest clears of coarse bubbling crackles and the suction yield falls), skin dry at the axilla and sternum, blood pressure adequate, and heart rate above 80 beats per minute. The pupil is not one of them — never titrate atropine to the pupil, because miosis may persist for many hours after adequate systemic atropinisation and titrating to pupil size produces atropine toxicity (agitated delirium, hyperthermia, hot dry flushed skin, retention, ileus, marked tachycardia). A confused patient with a wet chest needs more atropine; a confused patient with a bone-dry chest, a silent abdomen and a temperature of 39°C needs less — stop the infusion, reassess after 30 minutes and restart at half the previous rate when secretions return.
- Maintain atropine after loading: the acute cholinergic phase lasts 48–72 hours, so run an infusion delivering approximately 10–20% of the total loading dose per hour, titrated hourly against the same four endpoints — a patient who needed 20 mg to atropinise starts at roughly 2–4 mg per hour — or give intermittent boluses at the frequency the patient demands, recording the cumulative dose. A rising atropine requirement usually means continuing absorption from unwashed skin, hair or clothing — re-inspect and re-wash.Doctor / NurseNot available at your setup — Infusion pump. Where no infusion device is available, give intermittent boluses at the frequency the patient demands.
- Give an oxime early to every patient who needs atropine: pralidoxime chloride 30 mg/kg by slow intravenous injection (about 2 g in a 70 kg adult), diluted in 100 mL of 0.9% sodium chloride over 20–30 minutes, then 8–10 mg/kg per hour by infusion (about 560–700 mg/hour in a 70 kg adult) or 30 mg/kg intravenously every 4–6 hours, continued as long as there is any evidence of acetylcholine excess. Never allow the oxime to delay atropine, and monitor blood pressure through the loading dose since oximes may provoke hypotension if given rapidly.Doctor / Nurse
- Ventilatory support is instituted before the patient develops respiratory failure, judged on trajectory: falling saturation on high-flow oxygen, a rising or even normalising PaCO2 in a tiring patient, a falling single-breath count, new head lag, inability to swallow saliva, declining conscious level, or secretions outrunning suction. Intubate safely in this poisoning: suction thoroughly before laryngoscopy because the cords cannot be seen through bronchorrhoea, atropinise before induction or the patient becomes profoundly bradycardic on laryngoscopy, and use a non-depolarising agent such as rocuronium. Never use suxamethonium — the enzyme that metabolises it is precisely the enzyme this poison has inhibited, so its action is markedly and unpredictably prolonged. Atropine has no effect on fasciculation, muscle weakness or respiratory muscle failure, which are nicotinic — escalating atropine for a weak patient wastes the time in which they should be ventilated.Doctor / NurseNot available at your setup — Endotracheal intubation kit, Mechanical ventilator.
- Seizures — diazepam 10–20 mg intravenously, repeated as required (alternatives lorazepam 2–4 mg IV or midazolam 5–10 mg IV/IM; child diazepam 0.1–0.3 mg/kg IV slowly to a maximum of 10 mg per dose, or midazolam 0.1 mg/kg IV) — have a bag-valve-mask ready before the first dose, and give pralidoxime and atropine in addition to the anticonvulsant; escalate to phenobarbital 15–20 mg/kg or levetiracetam, since phenytoin is a poor choice for a cholinergically driven seizure. Hypotension — 0.9% sodium chloride 500 mL to 1 litre in an adult or 10–20 mL/kg in a child, then reassess; in the wet, bradycardic, hypotensive patient atropine is the pressor, and only if hypotension persists despite adequate volume and full atropinisation should noradrenaline be used. Torsades or prolonged QT: magnesium 2 g IV over about 2 minutes, with correction of potassium and magnesium. Keep urine output above 0.5 mL/kg per hour and monitor creatine kinase and potassium. Activated charcoal may be considered if the patient presents sufficiently early — adult 50–100 g orally or by gastric tube, child 1 g/kg to a maximum of 50 g — but it must never take precedence over atropine, and routine gastric lavage is not recommended because of the risk of aspirating hydrocarbon solvent.Doctor / Nurse
Refer / escalate
Call for help and arrange ventilation or transfer to a ventilated bed as soon as secretions outrun suction, the saturation falls on high-flow oxygen, the carbon dioxide rises or even normalises in a tiring patient, the single-breath count or head lift deteriorates, the conscious level declines, seizures occur, or the atropine requirement keeps escalating — case fatality after deliberate ingestion is 5–20% and is decided chiefly by access to mechanical ventilation; and remember about 20% develop the intermediate syndrome at 1–4 days, which neither atropine nor an oxime reverses.
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