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Organophosphate and Carbamate Poisoning
Epidemiology: 200K fatalities worldwide every year
DDx: Cholinesterase inhibitors, Cholinomimetics, Nicotine alkaloids
Kinetics: Absorption via ingestion, inhalation or topical contact. Minutes to hours depending on lipophilicity, metabolism and toxicity of compound
Pathophysiology: Inhibition of AChE by phosphorylating active site > Cholinergic crisis > If inhibition is prolonged AChE can be irreversibly inhibited (“aging” which does not occur with carbamates)
Clinical features: Miosis most commonly encountered symptom. Fatality usually due to respiratory failure.
Cholinergic effects at post ganglionic muscarinic fibers:
SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
DUMBELS – Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation
Cholinergic effects at postganglionic sympathetic fibers: tachycardia. mydriasis, bronchodilation, leukocytosis, urinary retention, hyper or hypotension, hyper or hypoglycemia, and ketosis
Nicotinic effects at NMJ and postganglionic sympathetic fibers: fasciculations, muscle weakness, paralysis
Delayed Syndromes: Intermediate Neurologic Syndrome, Organophosphorus agent induced delayed neuropathy
Diagnosis: Largely clinical, Atropine challenge 1mg of Atropine in adults, 0.1-0.2mg atropine in children, serum or rbc cholinesterase levels
Management: IV, O2, Monitor
Atropine: Competitive muscarinic receptor antagonist. Treats muscarinic symptoms, most importantly bronchorrhea and bronchospasm
Adults 2-5mg doubling dose q 3-5 minutes until atropinization occurs
Children 0.05-0.1 mg/Kg dose q 3-5 minutes until atropinization occurs
After atropinization give 10-20% total loading dose per hour. If anticholinergic symptoms occur, pt likely has atropine toxicity
Pralidoxime (2-Pam): Reactivates AChE. Treats both muscarinic and nicotinic symptoms
Adults 30mg/kg bolus followed by 8mg/kg/hr infusion
Children 20-50mg/kg bolus followed by 10-20mg/kg/hr infusion
Intubation: Avoid Succinlycholine, Use non-depolarizing agents
Seizures: Benzodiazepines
Decontamination: Remove and discard clothes. Consider activated charcoal if within one hour of ingestion
Poison control
Prognosis: GCS less than 13, lipophilic OPs such as fenthion and parathion, all associated with poor prognosis
Disposition: ICU.
References
- Eddleston, M., Buckley, N. A., Eyer, P., & Dawson, A. H. (2008). Management of acute organophosphorus pesticide poisoning. The Lancet, 371(9612), 597-607.
- RF Clark (2002),Insecticides: organic phosphorus compounds and carbamates
- Goldfrank’s Toxicological Emergencies (7th edn.), McGraw-Hill Professional, New York pp. 1346–1360
- Sungur, M., & Güven, M. (2001). Intensive care management of organophosphate insecticide poisoning. Critical care, 5(4), 211.
- Worek, F., Koller, M., Thiermann, H., & Szinicz, L. (2005). Diagnostic aspects of organophosphate poisoning. Toxicology, 214(3), 182-189.
- Lee, P., & Tai, D. Y. H. (2001). Clinical features of patients with acute organophosphate poisoning requiring intensive care. Intensive care medicine, 27(4), 694-699.
- Rusyniak, D. E., & Nanagas, K. A. (2004, June). Organophosphate poisoning. In Seminars in neurology (Vol. 24, No. 2, pp. 197-204).
Jay Khadpe MD
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