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ORGANOPHOSPHORUS POISIONING.pptx
This document discusses organophosphorus poisoning. It covers the types and uses of organophosphates, their metabolism and mechanism of action by inhibiting acetylcholinesterase, and the resulting clinical features. Diagnosis involves looking for a history of exposure and measuring plasma butyrylcholinesterase and red blood cell acetylcholinesterase levels. Treatment consists of atropine to block muscarinic receptors, pralidoxime as a cholinesterase reactivator, and supportive care.
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ORGANOPHOSPHORUS POISIONING.pptx
- 1. ORGANOPHOSPHORUS POISIONING DR ANKIT GAJJAR MD,IDCCM, IFCCM, EDIC CONSULTANT INTENSIVIST
- 2. • USE • CLASSIFICATION •TYPES • METABOLISM • CLINICAL FEATURES • DIAGNOSIS • MANAGEMENT
- 3. USE • Agriculture asa pesticide • Household chemical • Nerve agents in chemical warfare
- 4. CLASSIFICATION • Based ontoxicity & clinical use • Highly Toxic: Agriculture insecticides (parathion) • Intermediate toxic: Animal insecticides (trichlorfon) • Low toxic: Household application & Field spray (malathion, diazinon)
- 5.
- 6. ABSORPTION ROUTE • Ingestion(Accidental or Suicidal) • Cutaneous • Inhalation
- 7. PHARMACOKINETICS • Most ofare highly lipid soluble • Well absorbed from skin, mucous membrane, conjunctiva, GI tract and Respi tract • Easily cross BBB • Metabolism by oxidation in liver & esterase hydrolysis • Redistribution is common
- 8.
- 9. MOA • OP inactivatesAChE by phosphorylation in synapses, on RBC membrane & butyrylcholinesterase in plasma • Accumulation of Ach throughout the Nervous system – overstimulation of muscarinic & nicotinic receptors • Aging occurs when phosphorylated AChE loses alkyl side chain OP vs Carbamates • Same MOA but in carbamtes binding occurs reversible so no Aging
- 10. AGEING • DIETHYL –50% by 33 hrs - PAM useful for 5 days • DIEMETHYL – 50 % by 3 hrs - PAM useful for 12 hrs • 5-ALKYL GROUP – no use of PAM
- 11. MOA Sequelae of AchE •Spontaneous reactivation • Reactivation by PAM • Irreversible binding by permanent enzyme inactivation (Aging) • Onset and severity depends on compound, route of exposure and metabolism
- 12.
- 13.
- 14. CNS Type 1 Paralysis/ Acute Paralysis • During initial cholinergic phase • Due to large number of Ach at muscarinic & nicotinic receptor • Patient may need venti support • Fasciculation, twitching, weakness
- 15. CNS • Type 2Paralysis / Intermediate Syndrome (IMS) - Downregulation of presyneptic & postsyneptic receptor - Inadequate oxime treatment • Lipid soluble agents • 24-96 hours after ingestion • Progressive muscle weakness – Ocular, Neck, Proximal limb, Respiratory muscle • Treatment – supportive (3-4 weeks)
- 16. CNS • Type 3Paralysis / OP Induced delayed Polyneuropathy (OPIDN) • After 2-4 weeks • Distal limb weakness • Sensory loss • Weakness & ataxia • Recovery takes 1-2 yrs
- 17. CNS • Delayed OPEncephalopathy (DOPE) • Normal sensorium to progressive coma • Can be extrapyramidal side effects • Clinically brain dead • Neuroimaging & CSF normal • Prognosis good
- 18. DIAGNOSIS • H/O exposure •Typical garlic smell • SLUDGE • Plasma butyryl cholinesterase / RBC AChE
- 19. DIAGNOSIS PLASMA BUTYRYLCHOLINESTERASE RBC CHOLINESTERASE Easily assesNot readily available Does not correlate with clinical severity Correlate with the neuronal activity & severity Used to detect exposure to OP Marker of severity Rising trend suggest that OP is eliminated Slow recovery (1% / day) Response to Antidote therapy is less Increase activity after PAM therapy Levels altered in malnutrition, chronic illness & chronic liver disease Levels altered in Hbpathies & Thalassemia
- 20. TREATMENT • ABC • DECONTAMINATION •Gastric Lavage – 1-2 hrs • Activated Charcoal – 1-2 hrs • Atropine • PAM
- 21. TREATMENT • ATROPINE • Blocksmuscarinic receptors • Incremental dose regimen – double the dose every 5 minutes – 10-20% infusion • Intermittent bolus – 2-5 mg / 10-15 minutes • Continuous infusion • End point of atropine - Reduce secretion - SBP > 80 - HR > 80
- 22. TREATMENT • Atropine toxicity -Fever, Delirium, urinary retention, tachycardia • Discontinue if toxicity • Restart with 70-80% of previous rate • Glycopyrrolate can be used
- 23. TREATMENT • PRALIDOXIME • Reactivationof AChE • MOA – PAM binds to OPC causing the compound to break its bond with AChE • Mainly affect PNS only, CNS penetration is limited • Enhance recovery of NM transmission at nicotinic synapses • Enhance activity at muscarinic site as well, reducing Atropine requirement
- 24. TREATMENT • DOSE –30 mg/kg bolus f/b 8 mg/kg/hr • End Point - Clinical recovery or 12-24 hrs after atropine stopped • Rapid infusion – tachycardia, laryngospasm
- 25. TREATMENT • MgSO4 Reduce Achat motor end plate • CLONIDINE Reduce Ach synthesis & release • FFP