Organophosphate Poisoning
What is the dose of Atropine in children in the management of OP poisoning?
- 50mcg/kg - double dose every FIVE minutes until resolution of bradycardia, drying of secretions and good air entry
What is the result of OP action in the brain and brain stem?
- LOC - seizures
Why the duration of toxicity with carbamate compounds of OP is shorter than organophosphate compounds?
- OP permanently bind to AChE (ageing). this prevents reactivation of AChE by antidote - ageing DOES NOT OCCUR with carbamates
What are the four important syndromes in OP poisoning in relation to the time of exposure?
- acute intoxication - intermediate syndrome (2-5 days post exposure) - delayed neurotoxocity - chronic exposure leading to neuropsychiatric disorder
What are the killer B's in OP poisoning?
- bronchorrhoea - bronchospasm
What factors determine onset of symptoms following exposure to OP?
- dose - route - agent used
What enhanced elimination techniques in OP toxicity are of benefit in the emergency department?
- enhanced elimination is not clinically useful in the management of OP poisoning
How do you manage Atropine administration in adults in the setting of OP poisoning?
- initial dose 1.2mg - double dose five minutely until secretions dry, bradycardia corrected and good air entry - IVI Atropine may be required
What are the most important initial manifestations of OP poisoning?
- killer B's - bronchorrhoea - bronchospasm
What are the main principles in the management of OP poisoning?
- manage in area fit for cardiorespiratory monitoring and resuscitation - simultaneous decontamination and resusscitation - universal precautions for staff - if poor air entry, bradycardia, hypotension, killer B's, -start escalating doses of Atropine - control agitation with BZD - general supportive care
What receptors are targeted in OP poisoning?
- muscarinic - nicotinic
What are the three main sites of action of OP?
- muscarinic receptors - nicotinic receptors - central action
What is the fundamental difference between organophosphates and carbamates in deliberate self-poisoning as related to the outcomes?
- organophosphate poisoning is LONGER lasting and almost ALWAYS leads to life threatening poisoning - carbamate poisoning is usually shorter in duration
What are the useful tests to determine AChE activity?
- plasma ChE activity - RBC ChE activity
What are the results of action of OP on muscarinic receptors?
- salivation - lacrimation - urination - GI emptying (diarrhoea and vomiting) - bronchorrhoea/ bronchospasm (killer be's) - abdominal distress - miosis
TRUE or FALSE Activated charcoal, provided given within two hours of poisoning with OP, allows to reduce severity of toxicity.
FALSE Activated charcoal confers no benefit in the management of OP toxicity.
TRUE or FALSE. Significant secondary staff poisoning with organophosphates may occur.
FALSE Significant secondary poisoning of staff does not occur.
TRUE or FALSE OP have very specific smell.
FALSE the smell is is due to hydrocarbons which are used as a vehicle for OP delivery
TRUE or FALSE Use of pralidoxime improves survival and allows to decrease rate of intubation in patients with OP poisoning.
FALSE there is no evidence the Pralidoxime reduces rate of intubation or improves mortality in acute OP poisoning
What is the advantage of using Pralidoxime in OP poisoned patients?
Pralidoxime reactivates AChE in RBC
Is there a mnemonic for muscarinic receptor effects in OP poisoning?
SLUGBAM
What is the mechanism of action of OP?
acetylcholine esterase inhigitor (AChEi)
What are the results of action of OP on nicotinic receptors?
hyperactivity - voluntary muscle fasciculations - tremor - weakness - flaccid paralysis - respiratory muscle paralysis
