Organophosphate Poisoning

Organophosphates are substances bind irreversibly to acetylcholinesterase, causing cholinergic excess. Examples include fertilisers and sarin gas.

Toxicity

Effects (as expected) are signs of muscarinic and nicotinic over-activation. This can be remembered by 'BLUDGES' for the muscarinic effects:

• Bradycardia (and subsequent hypotension)
• Lacrimation
• Urination
• Defecation
• GIT upset
• Emesis
• Sweating and Salivation

and 'M' for the nicotinic effects:

• Muscular spasm

Management

Management is aimed at reducing ACh burden:

• Atropine
  Competitive antagonises ACh at the muscarinic receptor.
  • Atropine is preferred over glycopyrrolate as it will cross the blood brain barrier and treat central ACh toxicity
• Pralidoxime
  Reactivates acetylcholinesterase by luring the organophosphate away from the enzyme with a tantalising oxime group.
  • Pralidoxime must be used within the first few hours of poisoning
    After which the organophosphate-enzyme group 'ages' and is no longer susceptible.
  • Does not cross the blood-brain barrier and so cannot treat central effects

References

1. CICM March/May 2009
2. Rang HP, Dale MM, Ritter JM, Flower RJ. Rang and Dale's Pharmacology. 6th Ed. Churchill Livingstone.