Code Ready
Log inSign up free

Level 2 of 6Must-remember

Organophosphate and carbamate poisoning

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Ask about the route and the container: organophosphate and carbamate 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.
  • Smell the patient: most agricultural formulations are dissolved in hydrocarbon (kerosene-type) solvents that give a characteristic petroleum or garlicky odour on the breath and clothing, and carry their own risk of aspiration pneumonitis.
  • 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.
  • The illness is heralded by anxiety and restlessness, followed by nausea, vomiting, abdominal colic, diarrhoea, tenesmus, 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 heart rate is unreliable: 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, while hyperglycaemia is common in organophosphate poisoning and may reflect pancreatic involvement.
  • Get an ECG and monitor: sinus bradycardia and atrioventricular block are recognised effects, and look also for QT prolongation, repolarisation abnormalities 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; activity is below 50% of normal in anticholinesterase poisoning and depressed at least 50% below baseline in severe intoxication, but values correlate poorly and a normal result in a wet, miotic patient does not exclude the diagnosis.
  • Score the severity with the Peradeniya (POP) scale if you wish — pupil size, respiratory rate, heart rate, fasciculation, conscious level and seizures, total 0–11, mild 0–3, moderate 4–7, severe 8–11 — but treat it as a structured description and never let any cut-off delay atropine.
  • Recognise the 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 or extraocular muscle paralysis; declining conscious level, seizures or coma; bradycardia with hypotension unresponsive to volume; prolonged QT, ventricular ectopy or torsades; and a persistent or escalating atropine requirement.
  • 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.Doctor / Nurse
  • Remember the atypical patients: children may show only excessive salivation, drowsiness, seizures or coma with miosis as the only sign; older patients may present with an isolated confusional state, falls or unexplained bradycardia; and chronic low-grade occupational exposure gives headache, fatigue, anorexia, nausea, blurred vision, muscle cramps and depressed mood, often without miosis.

Management— 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 quantities of lukewarm water or saline, and for oily substances such as pesticides wash the skin 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 undissolved 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.Doctor / Nurse
  • 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.
  • 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.Doctor / NurseNot available at your setup — Infusion pump. Give intermittent atropine boluses at the frequency the patient demands and record the cumulative dose.
  • 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.Doctor / Nurse
  • Seizures — diazepam 10–20 mg intravenously, repeated as required, is useful for apprehension, agitation, fasciculation and convulsions; alternatives are 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.Doctor / Nurse
  • 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.
  • 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.Not available at your setup — Mechanical ventilator.
  • 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.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Activated charcoal may be considered if the patient presents sufficiently early — adult 50–100 g orally or by gastric tube as an aqueous slurry, child 1 g/kg to a maximum of 50 g — but it must never take precedence over atropine.
  • Torsades de pointes and prolonged QT: intravenous magnesium, 2 g over about 2 minutes in an adult, or overdrive pacing, alongside correction of potassium and magnesium.Doctor / Nurse
  • Replace fluid losses guided by pulse, blood pressure, urine output and repeated electrolytes, monitor creatine kinase and potassium, and keep urine output above 0.5 mL/kg per hour to reduce the risk of myoglobinuric acute kidney injury.Not available at your setup — Serum electrolytes.
  • When the patient will not dry, work through the list before concluding atropine has failed: the dose is too small (by far the commonest reason — there is no ceiling); continuing dermal absorption; continuing gastrointestinal absorption; hypoxia and acidosis; the wrong diagnosis or a co-ingestion; nicotinic failure misread as muscarinic failure (weakness and hypoventilation need ventilation, not more atropine); and atropine toxicity mistaken for persistent poisoning.

Caution— what harms

  • Never titrate atropine to the pupil: miosis may persist for many hours after adequate systemic atropinisation, particularly after dermal or ocular exposure, and titrating to pupil size produces atropine toxicity.
  • Never use suxamethonium: plasma (butyryl)cholinesterase, the enzyme that metabolises it, is precisely the enzyme this poison has inhibited, so its action is markedly and unpredictably prolonged — hours rather than minutes; if it has already been given, ventilation must continue until neuromuscular function objectively returns.Doctor / Nurse
  • 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.
  • Do not treat the frothing chest as cardiogenic pulmonary oedema: diuretics and nitrates do nothing for bronchorrhoea, which responds to atropine and suction.
  • A normal or fast pulse never excludes the diagnosis, and fasciculation is often absent even in serious poisoning — do not require either to start treatment.
  • An asymptomatic patient at 30 minutes is not a safe patient: many organophosphate insecticides are thions requiring hepatic oxidative desulfuration to the active oxon, so the features of intoxication may be delayed.
  • A rising atropine requirement usually means continuing absorption from unwashed skin, hair or clothing — re-inspect and re-wash, and check contaminated clothing and bedding have gone.
  • Recognise atropine toxicity: agitated delirium, hyperthermia, hot dry flushed skin, urinary retention, ileus and 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.
  • Cholinesterase results confirm and prognosticate; they never gate treatment — the antidote is never delayed pending results, and plasma cholinesterase is also reduced in liver disease, malnutrition, pregnancy and by genetic variants.
  • Charcoal must not be given to a comatose or convulsing patient unless it can be delivered by gastric tube with the airway protected by a cuffed endotracheal tube; routine gastric lavage is not recommended here because it risks aspiration of hydrocarbon solvent into the lungs of an already hypoxic, vomiting patient, and induced emesis has no place.
  • The patient who looks better at 24–48 hours is not safe: about 20% develop the intermediate syndrome at 1–4 days — ocular, bulbar, neck, proximal limb and respiratory weakness that neither atropine nor an oxime reverses — so document bedside respiratory-muscle assessment regularly for at least four days.
  • Phenytoin is a poor choice for a cholinergically driven seizure; escalate instead to phenobarbital 15–20 mg/kg or levetiracetam if seizures continue.Doctor / Nurse
  • Do not assume carbamate poisoning is benign: the acute picture is indistinguishable and, although it usually resolves within about 24 hours, severe cases give muscle twitching, profound weakness, profuse sweating, incontinence, mental confusion and progressive cardiorespiratory failure, and case fatality can be high.
  • Assume any arrhythmia is hypoxic until the airway, suction and oxygenation have been checked, and remember bradycardia with hypotension indicates more atropine, not an antiarrhythmic.

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.

PreviousNext

Read the full lesson free

Create a free account to unlock every page, the level exams, and progress tracking.

Sign up freeLog in