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A 28-year-old farmer is brought to the emergency department unconscious. He was found in a storeroom beside an empty 250 mL bottle of chlorpyrifos, an organophosphate insecticide, approximately 90 minutes after ingestion. On examination he is unresponsive (GCS 8), with pinpoint (1 mm) pupils, copious oral and bronchial secretions, generalised wheeze, visible muscle fasciculations over the tongue, eyelids and proximal limbs, a respiratory rate of 8/min with accessory-muscle use, SpO2 of 84 percent on room air, heart rate 38/min, blood pressure 76/46 mmHg, and a smell of solvent/garlic on his clothing. Two nurses in the bay have begun to develop watering eyes and a headache. A finger-prick glucose is 9.2 mmol/L.
Questions
a) What is the clinical diagnosis, and name the three receptor families at which the underlying toxin produces its effects? (2 marks)
The diagnosis is acute organophosphate (OP) cholinergic crisis from chlorpyrifos ingestion — the combination of miosis, bronchorrhoea, bronchospasm, fasciculations, bradycardia and a clear history of organophosphate exposure is pathognomonic. The OP irreversibly phosphorylates acetylcholinesterase, so acetylcholine accumulates at three receptor families: muscarinic (exocrine glands, smooth muscle, heart), nicotinic (skeletal neuromuscular junction and autonomic ganglia) and central (cortical and brainstem receptors). The two nurses have secondary healthcare-worker contamination from off-gassing/dermal contact — they need PPE and removal from the bay.
b) Outline the immediate resuscitation bundle in the correct order, including staff protection, airway/breathing, and the first antidote with its dose and end-point. (4 marks)
- Protect the staff FIRST — all staff don PPE (gown, double gloves, mask with eye protection); remove and double-bag the patient's clothing; wash skin and hair with soap and water; ventilate the bay. Atropine protects the patient, NOT the staff.
- Airway and breathing — suction the copious secretions; high-flow oxygen; intubate and ventilate early for respiratory failure (GCS 8, RR 8, SpO2 84 percent, falling effort). Use rocuronium, NOT suxamethonium (butyrylcholinesterase is depleted by the OP, causing prolonged apnoea with suxamethonium).
- Atropine IV — first-line antidote (muscarinic) — 1.2 to 3 mg IV bolus, doubled every 5 minutes until atropinisation (dry mouth and axillae, clear chest on auscultation, HR over 80, SBP over 80, pupils no longer pinpoint), then an infusion at 10 to 20 percent of the loading dose per hour. End-point is a DRY PATIENT — not dilated pupils or dry flushed skin (those are atropine toxicity).
- Pralidoxime (2-PAM) — second antidote (nicotinic) — give early, before the enzyme ages: 30 mg/kg IV bolus over 15 to 30 min, then 8 mg/kg/h infusion for at least 24 to 48 h (the WHO high-dose regimen).
- GI decontamination — airway protected: gastric lavage within 1 h of ingestion, then activated charcoal 50 g NG.
- Treat seizures if they occur with lorazepam 4 mg IV.
c) Why must pralidoxime be given EARLY, and what is 'ageing'? (2 marks)
Pralidoxime reactivates AChE by nucleophilic attack on the phosphorylated serine-203, restoring the enzyme — but only before the enzyme has aged. Ageing is the time-dependent dealkylation of the phosphorylated AChE, leaving a negatively charged species that pralidoxime can no longer displace. The enzyme is then permanently inactivated and recovery depends on de novo synthesis (only 1 to 2 percent new AChE per day). Ageing half-life is minutes for soman, hours for sarin and dimethoate, days for parathion/malathion — so the earlier pralidoxime is given the better. This patient should receive pralidoxime immediately alongside atropine.
d) Name the two delayed neurological complications, with their typical timing and one hallmark feature of each. (2 marks)
- Intermediate syndrome — at 24 to 96 hours after exposure. Hallmark: proximal and cranial-nerve weakness with respiratory-muscle involvement (ptosis, neck-flexor weakness, dysphagia, falling vital capacity) WITHOUT recurrent muscarinic features. Managed with supportive ventilation (often 7 to 21 days), continued pralidoxime and atropine.
- Organophosphate-induced delayed polyneuropathy (OPIDP) — at 1 to 3 weeks after exposure. Hallmark: symmetrical distal sensorimotor polyneuropathy (cramping calf pain, distal paraesthesia, foot-drop, wrist-drop) caused by inhibition and ageing of neuropathy target esterase (NTE) in axons. No specific antidote; supportive rehabilitation and physiotherapy.
Monitor daily for both during admission (vital capacity, neuro exam); all deliberate self-harm cases require psychiatric assessment once stable.