Organophosphate Toxicity Flashcards

1
Q

Which muscle relaxant should be used to intubate a patient with organophosphate toxicity and why

A

Organophosphate toxicity is inactivation of acetylcholinesterase and abundant acetylcholine with resulting effects on ANS, PNS and CNS. In the PNS - acetylcholinesterase metabolizes succinylcholine. Hence use of sux for RSI will result in prolonged and unpredictable neuromuscular blockade.
Rocuronium can be used but as it is a competitive (with Ach) antagonist, larger doses are required for same clinical effect.

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2
Q

Why can mydriasis, tachycardia, hypertension and bronchospasm counterintuitively occur in a cholinergic toxidrome?

A

Some SNS ganglia also contain nicotinic receptors –> SNS effects

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3
Q

Why does sweating sometimes occur in cholinergic toxidrome

A

Sweating occurs because sweat glands are regulated through SNS activation of postganglionic MUSCARINIC receptors

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4
Q

How can the diagnosis of organophosphate toxicity by made

A
  • Clinical toxidrome
  • Atropine: 1mg –> absence of anticholinergic effects = highly supportive of diagnosis
  • measure RBC Achesterase (poor availability)
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5
Q

What is the mechanism of action of atropine in organophosphate poisoning

A

Atropine competes with acetylcholine at muscarinic receptors, preventing cholinergic activation.

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6
Q

What is the dose and method of adminstration of atropine to a patient with organophosphate poisoning?

A

Initial dose: 2 - 5 mg (0.05mg/kg kids)
Double dose every 5 minutes until pulmonary muscarinic signs and symptoms are alleviated (clear resp. secretions and resolve bronchoconstriction)

Followed by 10 - 20% of the total initial bolus as an infusion per hour

Adjust infusion until adequate response and then taper until recovery

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7
Q

Tachycardia and mydriasis are not appropriate markers for therapeutic improvement, why

A

They may indicate ongoing:
1. Hypoxia
2. Hypercapnoea
3. Hypovolaemia
4. SNS activation

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8
Q

What are the goals of atropine infusion in patients with organophosphate poisoning

A
  1. Clear lung auscultation
  2. HR > 80 bpm
  3. SBP > 80 mmHg
  4. Dry axillae
  5. Miosis resolved

without causing atropine toxicity
1. Confusion
2. Pyrexia
3. Absent bowel sounds
4. Urinary retention

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9
Q

What should be done if the patient becomes atropine toxic

A

Hold the infusion until the patient is no longer atropine toxic and then restart the infusion at 70 - 80 % of the rate

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10
Q

How should organophsophate related seizures be treated

A
  1. Supportive Rx
  2. Benzodiazepines
    (Phenytoin not indicated)
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11
Q

How and when is activated charcoal administered in organophosphate poisoning

A

If patient presents within 1 hour of ingestion
dose 1 g/kg (max 50g)

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12
Q

Explore the options for decontamination in OP poisoning

A
  1. < 1 hr - activated charcoal
  2. , 1 hr - may gastric lavage after ETT/Atropine
  3. Never forced emesis
  4. Urinary alkalinization - no evidence
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