Organophosphate Poisoning
Summary
Organophosphate (OP) poisoning results from exposure to pesticides (agricultural) or nerve agents (chemical warfare). OPs irreversibly inhibit acetylcholinesterase, causing excess acetylcholine accumulation at muscarinic and nicotinic receptors. This produces the classic SLUDGE/BBB syndrome (salivation, lacrimation, urination, defaecation, GI upset, emesis / bronchospasm, bradycardia, bronchorrhoea). Treatment is atropine (muscarinic blockade), pralidoxime (oxime — reactivates AChE), and supportive care including ventilation.
Key Facts
- Mechanism: Irreversible acetylcholinesterase inhibition → cholinergic crisis
- SLUDGE: Salivation, Lacrimation, Urination, Defaecation, GI upset, Emesis
- BBB: Bronchospasm, Bradycardia, Bronchorrhoea
- Nicotinic effects: Muscle fasciculations, weakness, paralysis
- CNS effects: Agitation, seizures, coma
- Treatment: Atropine (high doses) + Pralidoxime + supportive care
Clinical Pearls
"SLUDGE + miosis + bradycardia = cholinergic toxidrome = OP poisoning"
Atropine doses in OP poisoning are MUCH higher than standard doses — titrate to dry secretions
Pralidoxime must be given early (before "ageing" of enzyme-OP complex)
Why This Matters Clinically
OP poisoning is a common cause of death from poisoning in agricultural regions. Rapid recognition and aggressive atropinisation saves lives. Delayed treatment leads to respiratory failure and death.
Visual assets to be added:
- SLUDGE/BBB mnemonic diagram
- Cholinesterase inhibition mechanism
- Atropine titration algorithm
- OP poisoning management flowchart
Incidence
- Over 3 million poisoning cases/year globally
- Over 200,000 deaths/year (mostly in Asia, Africa)
- Common in agricultural communities
Demographics
- Agricultural workers (occupational exposure)
- Rural areas (developing countries)
- Intentional self-harm (suicide attempt)
Sources
| Type | Examples |
|---|---|
| Agricultural pesticides | Parathion, malathion, chlorpyrifos |
| Nerve agents | Sarin, VX, novichok (chemical warfare) |
| Domestic | Household insecticides (rare severe toxicity) |
Mechanism
- OP binds and inhibits acetylcholinesterase (AChE)
- Acetylcholine accumulates at synapses
- Overstimulation of muscarinic, nicotinic, and CNS receptors
- "Ageing" — OP-enzyme bond becomes irreversible over time
Receptor Effects
| Receptor | Location | Effects |
|---|---|---|
| Muscarinic | Parasympathetic (smooth muscle, glands) | SLUDGE, miosis, bradycardia, bronchospasm |
| Nicotinic (NMJ) | Skeletal muscle | Fasciculations, weakness, paralysis |
| Nicotinic (ganglia) | ANS ganglia | Tachycardia, hypertension (can confuse picture) |
| CNS | Brain | Agitation, confusion, seizures, coma |
"Ageing"
- OP-enzyme bond undergoes chemical change
- Becomes irreversible after hours-days (depending on OP)
- Pralidoxime only effective before ageing
Muscarinic Effects — SLUDGE/BBB
| Mnemonic | Symptom |
|---|---|
| S | Salivation |
| L | Lacrimation |
| U | Urination |
| D | Defaecation/Diarrhoea |
| G | GI upset |
| E | Emesis |
| B | Bronchospasm |
| B | Bradycardia |
| B | Bronchorrhoea (excessive secretions) |
Nicotinic Effects
CNS Effects
Examination Findings
Red Flags
| Finding | Significance |
|---|---|
| Respiratory failure | Life-threatening; needs intubation |
| Severe bronchorrhoea | Atropine urgently needed |
| Coma/seizures | Severe toxicity |
| Fasciculations + weakness | Nicotinic; may need pralidoxime |
Vital Signs
- Bradycardia (muscarinic) or tachycardia (nicotinic)
- Hypotension or hypertension
- Tachypnoea
Eyes
- Miosis (pinpoint pupils)
- Lacrimation
Respiratory
- Bronchospasm
- Copious secretions
- Respiratory failure
Neurological
- Fasciculations
- Weakness
- Altered consciousness
- Seizures
Skin
- Sweating
- Odour of pesticide (garlic-like in some OPs)
Clinical Diagnosis
- Primarily clinical (history + cholinergic syndrome)
Cholinesterase Levels
| Test | Notes |
|---|---|
| Plasma (butyryl) cholinesterase | Rapidly available; correlates with exposure |
| RBC (acetyl) cholinesterase | More specific for tissue AChE; slower turnaround |
Other Tests
| Test | Purpose |
|---|---|
| ABG | Respiratory failure assessment |
| ECG | Arrhythmias (QT prolongation) |
| U&E, glucose | Baseline |
| CXR | Aspiration, pulmonary oedema |
By Severity
| Severity | Features |
|---|---|
| Mild | Miosis, excessive secretions, no respiratory compromise |
| Moderate | SLUDGE, fasciculations, mild respiratory distress |
| Severe | Respiratory failure, coma, seizures, cardiovascular collapse |
By Agent Type
- Agricultural pesticides (common, variable toxicity)
- Nerve agents (highly toxic, rapid onset)
Immediate Resuscitation
| Action | Details |
|---|---|
| Decontamination | Remove clothing, wash skin with soap and water; protect staff (PPE) |
| Airway | Suction secretions; intubate early if needed |
| Oxygen | High flow |
| IV access | Large bore |
Atropine — Muscarinic Blockade
| Dosing | Details |
|---|---|
| Initial dose | 1-3 mg IV (adults); 0.05 mg/kg (children) |
| Repeat | Double dose every 5 minutes if no response |
| Endpoint | Clear chest (dry secretions), HR over 80 |
| Maintenance | Infusion may be needed (0.02-0.08 mg/kg/hr) |
Key point: Atropine doses are MUCH higher than usual — may need tens of milligrams
Pralidoxime (Oxime) — AChE Reactivation
| Dosing | Details |
|---|---|
| Loading | 30 mg/kg IV over 20 minutes (max 2g) |
| Maintenance | 8-10 mg/kg/hr infusion |
| Duration | Continue for 24-48 hours or until clinically improved |
Key point: Most effective if given early (before "ageing"); continue even if late
Other Treatments
| Treatment | Indication |
|---|---|
| Benzodiazepines | Seizures (diazepam, lorazepam) |
| Avoid succinylcholine | Prolonged paralysis |
| Avoid morphine, theophylline | Worsen toxicity |
| Gastric lavage | Only if very recent ingestion, protected airway |
| Activated charcoal | Only if within 1 hour |
ICU Care
- Mechanical ventilation if needed
- Prolonged monitoring (intermediate syndrome may occur days later)
Intermediate Syndrome
- Occurs 1-4 days after exposure
- Weakness of respiratory muscles, proximal limbs, neck flexors
- May need prolonged ventilation
Acute
- Respiratory failure
- Aspiration pneumonia
- Arrhythmias
- Seizures
- Death
Delayed
- Intermediate syndrome (paralysis days after exposure)
- Organophosphate-induced delayed neuropathy (OPIDN) — rare
Prognosis
- Mortality 10-20% with treatment (higher without)
- Survival depends on early treatment
Factors Affecting Outcome
- Type and dose of OP
- Time to treatment
- Access to ICU care
- Aspiration/respiratory failure
Key Guidelines
- WHO Clinical Management of Acute Pesticide Intoxication
- TOXBASE (UK National Poisons Information Service)
Key Evidence
- Atropine is life-saving
- Role of pralidoxime is debated but recommended in severe cases
What is Organophosphate Poisoning?
Organophosphate poisoning happens when someone is exposed to pesticides or chemicals that affect the nerves. This can happen by swallowing, breathing in, or skin contact.
Symptoms
- Too much saliva, tears, and sweat
- Difficulty breathing
- Muscle twitching
- Confusion or unconsciousness
Treatment
- Emergency treatment with specific antidotes
- May need help breathing with a machine
Prevention
- Use protective equipment when handling pesticides
- Store pesticides safely away from children
Resources
Primary Guidelines
- Eddleston M, et al. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597-607. PMID: 17706760
Key Reviews
- Jokanovic M, Kosanovic M. Neurotoxic effects in patients poisoned with organophosphorus pesticides. Environ Toxicol Pharmacol. 2010;29(3):195-201. PMID: 21787591
- Peter JV, et al. Oximes in organophosphate poisoning. Clin Toxicol. 2007;45(3):312-317. PMID: 17453878