Neuro Anesthesia Keywords

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  1. Anticholinesterase poisoning
    • commercial insecticides (isulfoton, phorate,parathion,dimetonor)
    • as aerosols or dusts
    • chemical warfare (nerve gases such as tabun and sarin)
    • absorbed through skin and mucous membranes or by inhalation
    • Organophosphates are also used in ophthalmology – echothiopate is used to treat glaucoma.

  2. Organophosphate mechanism of toxicity:
    Acetylcholinesterase inhibitors that form a stable irreversible covalent bond to the enzyme.

    Occurs at cholinergic junctions of the nervous system including postganglionic parasympathetic junctions (sites of muscarinic activity), autonomic ganglia and the neuromuscular junctions (sites of nicotinic activity) and certain synapses in the CNS.

    Acetylcholine is the neurohumoral mediator at the cholinergic junctions. Since acetylcholinesterase is the enzyme that degrades acetylcholine following stimulation of a nerve, by inhibiting acetylcholinesterase, organophosphates allows acetylcholine to accumulate and result in initial excessive stimulation followed by depression.

  3. Anticholinesterase poisoning

    Signs and Symptoms
    • Muscarinic signs
    • (SLUDGE) salivation, lacrimation, urination, diaphoresis, gastrointestinal upset, emesis and progressing to bronchospasm, bronchorrhea, blurred vision, bradycardia or tachycardia, hypotension, confusion, and shock.
    • Nicotinic effects        
    • Skeletal muscle initially exhibits fasciculation (involuntary irregular, violent muscle contractions) followed by the inability to repolarize cell membranes resulting in weakness and paralysis. Severe reactions can lead to ventilatory failure and death (cholinergic crisis).
  4. Anticholinesterase poisoning


    Remove clothing and wash skin with soap and water

    Airway management (secretions are the main issue), avoid SCh (degraded by AChE)

    • Atropine (titrated to dried secretions, not HR) and pralidoxime (reactivates AChE)
      • Atropine - The endpoint for atropine is dried pulmonary secretions and adequate oxygenation. Tachycardia and mydriasis must not be used to limit or to stop subsequent doses of atropine. The main concern with OP toxicity is respiratory failure from excessive airway secretions. Start with a 1-2 mg IV bolus, repeat q3-5min prn for desire effects (drying of pulmonary secretions and adequate oxygenation). Consider doubling each subsequent dose for rapid control of patients in severe respiratory distress. An atropine drip titrated to the above endpoints can be initiated until the patient's condition is stabilized.
      • Pralidoxime - Nucleophilic agent that reactivates the phosphorylated AChE by binding to the OP molecule. Used as an antidote to reverse muscle paralysis resulting from OP AChE pesticide poisoning but is not effective once the OP compound has bound AChE irreversibly (aged). Current recommendation is administration within 48 h of OP poisoning. Because it does not significantly relieve depression of respiratory center or decrease muscarinic effects of AChE poisoning, administer atropine concomitantly to block these effects of OP poisoning. Start with 1-2 g (20-40 mg/kg) IV in 100 mL isotonic sodium chloride over 15-30 min; repeat in 1 h if muscle weakness is not relieved; then repeat q3-8h if signs of poisoning recur; other dosing regimens have been used, including continuous drip.
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