Organophosphate Toxicity Flashcards
Which muscle relaxant should be used to intubate a patient with organophosphate toxicity and why
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.
Why can mydriasis, tachycardia, hypertension and bronchospasm counterintuitively occur in a cholinergic toxidrome?
Some SNS ganglia also contain nicotinic receptors –> SNS effects
Why does sweating sometimes occur in cholinergic toxidrome
Sweating occurs because sweat glands are regulated through SNS activation of postganglionic MUSCARINIC receptors
How can the diagnosis of organophosphate toxicity by made
- Clinical toxidrome
- Atropine: 1mg –> absence of anticholinergic effects = highly supportive of diagnosis
- measure RBC Achesterase (poor availability)
What is the mechanism of action of atropine in organophosphate poisoning
Atropine competes with acetylcholine at muscarinic receptors, preventing cholinergic activation.
What is the dose and method of adminstration of atropine to a patient with organophosphate poisoning?
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
Tachycardia and mydriasis are not appropriate markers for therapeutic improvement, why
They may indicate ongoing:
1. Hypoxia
2. Hypercapnoea
3. Hypovolaemia
4. SNS activation
What are the goals of atropine infusion in patients with organophosphate poisoning
- Clear lung auscultation
- HR > 80 bpm
- SBP > 80 mmHg
- Dry axillae
- Miosis resolved
without causing atropine toxicity
1. Confusion
2. Pyrexia
3. Absent bowel sounds
4. Urinary retention
What should be done if the patient becomes atropine toxic
Hold the infusion until the patient is no longer atropine toxic and then restart the infusion at 70 - 80 % of the rate
How should organophsophate related seizures be treated
- Supportive Rx
- Benzodiazepines
(Phenytoin not indicated)
How and when is activated charcoal administered in organophosphate poisoning
If patient presents within 1 hour of ingestion
dose 1 g/kg (max 50g)
Explore the options for decontamination in OP poisoning
- < 1 hr - activated charcoal
- , 1 hr - may gastric lavage after ETT/Atropine
- Never forced emesis
- Urinary alkalinization - no evidence