Anticholinesterase Poisoning

Reza Gorji, MD
Reza Gorji, MD
Fenghua Li, MD

Fenghua Li, MD

Reza Gorji, MD
Fenghua Li, MD

SUNY Upstate Medical University

Anticholinesterase poisoning can occur in a variety of situations:

  1. Insecticides (parathion, isulfoton, malathion, diazinon)
  2. Herbicides (tribufos)
  3. Aerosols or dust particles
  4. Nerve gas in chemical warfare (sarin, soman, tabon, VX)

Mechanism of toxicity:

  1. Absorption is through skin, mucous membranes or via inhalation thru lungs
  2. Organophosphates are acetylcholine inhibitors which form a covalent bond to the enzyme acetylcholinesterase
  3. Location:
    1. parasympathetic postganglionic junctions (muscarinic receptors)
    2. Autonomic ganglia and neuromuscular junctions (nicotinic receptors)
    3. Some CNS receptors

Acetylcholinesterase is the enzyme responsible for the degradation of acetylcholine at cholinergic junctions. Therefore, organophosphates inhibit acetylcholinesterase and allow increased amounts of acetylcholine at noted above resulting in excessive stimulation and then depression.

Signs and Symptoms:

  1. Muscarinic effect: miosis, SLUDGE (Salivation, lacrimation, urination, diaphoresis, gastrointestinal upset, emesis), bronchospasm, bradycardia or tachycardia, blurred vision, hypotension, confusion, shock.
  2. Nicotinic effect: muscle fasciculations, weakness or paralysis. Severe reactions can result in ventilatory failure and death.
  3. CNS effect: anxiety, restlessness, headache, withdrawal and depression, impaired concentration, depression CV and respiratory centers


  1. Atropine: 1-5 mg IV (IM, SC) q 15 min PRN to drying of secretions
  2. Pralidoxime: 1 gm IV (PO) over 15-30 mins q8-12 hX3 doses PRN


  1. Miller’s Anesthesia, 6th edition
  2. Washington Manual of Medical Therapeutics, 30th edition

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