Organophosphate Poisoning
Lesson Objectives
By the end of this lesson, learners should be able to:
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Identify common sources and routes of organophosphate poisoning in children.
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Explain the detailed pathophysiology of OP poisoning and its multi-system effects.
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Recognize early, moderate, and severe clinical manifestations across muscarinic, nicotinic, and CNS systems.
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Apply precise, stepwise treatment using atropine and pralidoxime, including dose titration, timing, and monitoring.
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Integrate seizure management and respiratory support within overall care.
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Anticipate complications and apply preventive and supportive strategies.
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Monitor patients closely and recognize indicators for escalation to intensive care.
Description
Organophosphate poisoning occurs primarily through accidental ingestion, dermal exposure, or inhalation of insecticides or rodenticides containing organophosphate compounds. These compounds irreversibly inhibit acetylcholinesterase, leading to accumulation of acetylcholine at muscarinic, nicotinic, and central synapses, causing overstimulation of multiple organ systems. Early recognition and aggressive management are essential to prevent respiratory failure, cardiovascular collapse, seizures, and death.
Pathophysiology
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Muscarinic receptor overstimulation:
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Excess acetylcholine binds to parasympathetic muscarinic receptors.
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Clinical effects: bronchorrhoea, bronchospasm, drooling, lacrimation, vomiting, diarrhea, urinary incontinence, hypotension, bradycardia, miosis, diaphoresis.
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Nicotinic receptor overstimulation:
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Affects skeletal muscles and neuromuscular junctions.
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Clinical effects: muscle weakness, fasciculations, tremors, respiratory muscle paralysis, hypertension, tachycardia.
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Central nervous system effects:
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Excess acetylcholine in the brain → malaise, irritability, confusion, delirium, seizures, coma.
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Complications: Respiratory failure (due to airway obstruction or paralysis), hypoxemia, aspiration, cardiovascular collapse, rhabdomyolysis, and secondary infections.
Clinical Features
| System | Early / Mild | Moderate | Severe / Life-threatening |
|---|---|---|---|
| Muscarinic | Diaphoresis, nausea, vomiting, miosis, mild salivation | Profuse secretions, hypotension, bradycardia, vomiting, diarrhea | Severe bronchorrhoea, bronchospasm, shock, extreme bradycardia |
| Nicotinic | Mild fasciculations, tremors | Progressive muscle weakness, ptosis, tachycardia, hypertension | Respiratory muscle paralysis, apnea, cardiovascular instability |
| CNS | Malaise, irritability | Confusion, delirium | Seizures, coma, stupor, loss of airway protection |
Investigations
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Diagnosis is primarily clinical, based on history of exposure and characteristic signs.
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Laboratory confirmation (if available): cholinesterase levels, electrolytes, renal and liver function tests, ABGs.
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Continuous monitoring of vital signs, oxygen saturation, respiratory rate, and neurological status is mandatory.
Stepwise Management
| Step | Intervention | Details / Rationale |
|---|---|---|
| Resuscitation | ABCDE approach | Airway management (suction secretions, consider intubation), breathing support (O2 or ventilation), circulatory support (IV fluids for hypotension). |
| Atropine therapy | Full atropinization | Dose titration: Administer repeated IV doses (0.05–0.1 mg/kg) every 5–10 minutes until heart rate and BP normalize for age, chest is clear, secretions stop, and pupils dilate. Muscarinic antagonist that reverses parasympathetic overstimulation. |
| Pralidoxime (2-PAM) | 20–50 mg/kg IV over 30 min | Reactivates acetylcholinesterase at nicotinic receptors. Repeat in 1–2 hours if muscle weakness persists, then every 10–12 hours if cholinergic signs recur. Consider continuous infusion in severe cases. |
| Seizure management | Benzodiazepines (e.g., diazepam) | Treat seizures promptly to prevent hypoxia, aspiration, and further neuronal injury. |
| Respiratory support | Oxygen therapy, mechanical ventilation if required | Indicated for hypoxemia, respiratory muscle weakness, or apnea. |
| Fluid and electrolyte management | IV fluids for hypotension or dehydration | Monitor for hyponatremia, hypokalemia, metabolic acidosis; correct accordingly. |
| Monitoring & supportive care | Continuous cardiac and neurological monitoring | Detect deterioration early; ICU referral if severe respiratory or cardiovascular compromise. |
Complications to Anticipate
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Respiratory failure due to bronchospasm or muscle paralysis
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Aspiration pneumonia
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Cardiovascular collapse (hypotension, arrhythmias)
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Seizures and status epilepticus
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Secondary infections due to prolonged ICU stay
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Rhabdomyolysis with acute kidney injury
Key Points Summary
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Organophosphate poisoning is a medical emergency requiring rapid identification and intervention.
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Muscarinic, nicotinic, and CNS signs may appear simultaneously and progress rapidly.
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Atropine addresses muscarinic symptoms; pralidoxime addresses nicotinic symptoms.
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Seizure management, respiratory support, and monitoring are critical components.
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Early and repeated monitoring reduces morbidity and mortality.