Pinpoint Pupils and a Failing Chest: Organophosphate Poisoning at 02:00
A 34-year-old wheat farmer is brought to a district hospital emergency department at 02:00, about 90 minutes after spraying chlorpyrifos for four hours without gloves or a mask. He is drowsy but rousable, with profuse bronchorrhea, bilateral coarse crackles, pinpoint pupils, heart rate 48/min, blood pressure 92/58 mmHg, respiratory rate 12/min and SpO2 84% on room air. Coarse fasciculations are visible over both thighs and the abdomen. The ambulance crew gave atropine 2 mg IV 20 minutes ago with no visible change. Stock on hand: atropine 1 mg/mL ampoules (14 available), pralidoxime 500 mg vials (8 available), one functioning ventilator, and no ICU bed. The nearest tertiary centre with a toxicology unit is a three-hour road transfer, and the ambulance is shared with two other calls. A medical officer asks you whether to keep pushing atropine, intubate now, or arrange immediate transfer.
1. Explain, receptor by receptor, why atropine relieves the bronchorrhea and bradycardia but will not correct the fasciculations or the muscle weakness, and what that implies for your choice of neuromuscular blocker if you intubate.
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Chlorpyrifos inhibits acetylcholinesterase, so acetylcholine accumulates at every cholinergic synapse.
- Muscarinic (M2/M3) excess produces bronchorrhea, bronchospasm, bradycardia, salivation and miosis. Atropine is a competitive muscarinic antagonist, so it reverses these - and these are the effects that kill the patient in the first hour.
- Nicotinic (neuromuscular junction) excess produces fasciculations followed by depolarising block and weakness, including weakness of the respiratory muscles. Atropine has no nicotinic action, so the fasciculations and the weakness will not budge. They require reactivation of the enzyme with an oxime (pralidoxime) before ageing occurs, plus ventilatory support.
Consequence for the airway: succinylcholine is hydrolysed by plasma cholinesterase, which is also inhibited here, so its block is unpredictable and prolonged. Avoid it for rapid sequence intubation. Use rocuronium (e.g., 0.6 mg/kg) or vecuronium with adequate sedation, and plan for a period of mechanical ventilation rather than a quick extubation.
Also remember that the bradycardia of muscarinic excess can be replaced by tachycardia once hypoxia sets in, so do not use heart rate alone to judge severity.
2. Give a concrete atropine titration plan using the stock available, state the endpoints you will use to stop escalating, and say what you will do about the airway.
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Titration: give 2 mg IV now and reassess within 2–5 minutes. If secretions persist, double to 4 mg, then 8 mg, then 16 mg - geometric escalation every 5 minutes until the endpoints are met. With only 14 ampoules (14 mg total) you cannot sustain this for more than a few doses, so send someone to borrow atropine from other wards and the district store immediately; do not under-dose to conserve stock. A patient who needs 40 mg is not unusual.
Endpoints: dry chest on auscultation, heart rate above 80/min, systolic pressure above 90 mmHg, no fresh secretions, warm dry skin. Pupil size and flushing are unreliable and must not be used to stop escalating.
Oxime: pralidoxime 30 mg/kg (about 2 g) IV over 30 minutes, then 8–10 mg/kg/hour. Eight vials of 500 mg gives only 4 g - enough for the loading dose. Obtain more, or accept a short course and prioritise transfer.
Airway: intubate early. He is hypoxic at 84% with copious secretions and a falling respiratory rate; he will tire. Suction, pre-oxygenate, ketamine plus rocuronium (not succinylcholine), cuffed tube, and ventilate. Decontaminate him - remove clothes, wash skin - and wear gloves and apron yourself.
3. Justify your disposition decision: keep and stabilise, or transfer immediately? What must be documented and communicated?
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Keep him until the secretions are controlled. Transferring a patient who is still pouring secretions at SpO2 84% invites an arrest in the back of a shared ambulance three hours from help.
Criteria before the wheels move: atropinised (dry chest, heart rate above 80/min, systolic above 90), intubated and ventilated with a secured tube, oxime infusing, no recurrent fasciculations, a doctor escort with a bag-valve and suction, and a receiving hospital that has already accepted him by name.
Documentation: time and dose of every atropine bolus, which endpoints were reached, GCS, pupil size, SpO2 trend, oxime dose and rate, airway grade and tube size, decontamination performed, staff PPE used. This record is both clinical and medico-legal.
Communication with the family: the diagnosis is organophosphate poisoning, prognosis depends on how quickly the enzyme is reactivated and on respiratory support, and he may need ventilation for days. Counsel them on protective equipment for future spraying, and make sure someone stays with him - he should not be left alone while still requiring repeated atropine.