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The document discusses the use and effects of organophosphates (OP) in poisoning cases, including symptoms, diagnosis, and treatment protocols. It highlights the clinical manifestations arising from acute, intermediate, and delayed exposure, emphasizing the need for immediate management and specific agents like atropine and oximes for treatment. Long-term exposure risks and strategies for recovery and prevention of complications are also addressed.
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- 5. Organophosphates are used insuicidal cases • Deliberate Use of OP : • Accidental OP : taken in suicidal cases • Accidentally taken by a child or adult when they are kept in unknown container
- 7. Mechanism of Actionof OP
- 8. Clinical Manifestations • Theonset , severity and duration of Poisoning depend on the route of exposure And the agent used • Triphasic illness follows OP intoxication : • Acute cholinergic Crisis • Intermediate syndrome ( IMS) • OPIDN ( organophosphate –induced Delayed polyneuropathy
- 9. Long – termoccupational exposure to op pesticides Nonspecific SMX • H/A • Nausea • Fatigue • Muscle twitching • Visual disturbances Chronic exposure to OP Development of blood dyscrasias including aplastic anemia and leukemia Other Manifestation of chronic exposure : • Anorexia • Hepatotoxicity • Renal toxicity • CNS disturbances
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- 12. Various MNEMONICS havebeen used to describe the Muscarinic signs of OPP SLUDGE • Salivation • Lacrimation • Urinary incontinence • Diarrhea • Gastrointestinal cramps • Emesis DUMBELS • Diarrhea • Urination • Miosis • Bronchospasm Bronchorrhea • Emesis • Lacrimation • Salivation
- 13. Intermediate syndrome • Occurs24 to 96 hrs. after ingestion of an OP compound • Approx. 10-40 % of pts. treated for acute poisoning develop this illness • The onset of the IMS is often rapid , with progression of muscle weakness From the • Ocular muscles to neck • Proximal limbs • Respiratory muscles
- 14. Proposed Mechanism include: • Persistent inhibition of ACHE - leading to functional paralysis of NMT • Muscle necrosis • Oxidative free radical damage to the receptors
- 15. Organophosphate – induceddelayed polyneuropathy (OPIDN) Occurs abt 1-3 wks. after acute exposure and uncertain period following Chronic exposure , due to degeneration of long myelinated nerve fibers MECHANISM Inhibition of neuropathy target esterase (NTE) enzyme in NT by certain OP i.e Chloropyriphos
- 16. Sign and symptoms ofOPIDN • Cramping muscle pain • Numbness and paraesthesia • Acute limb weakness • Muscle wasting & deformity such as clawing of the hands • Symmetrical flaccid weakness • Tendon reflexes are reduced or lost • Later , mild pyramidal tract sign
- 17. Diagnosis : • Hxof exposure to OP compound • Characteristic manifestation of toxicity to OP • Improvement of sign and smx after atropine administration • Search of container of the poison in the vicinity of the pt by asking the attaindents • Garlic like smell – sulphur containing OP Confirmatory investigations : • CHE estimation (plasma Butyryl cholinesterase and Red cell ACHE ) useful biochemical • Tool but poor guide to tx and px
- 18. Treatment Acute Cholinergic Crisis Decontaminationand supportive • Decontimation • Supportive • Blockade of Muscaric activity by ATROPINE • Reversal of cholinesterase inhibition with OXIME • Correction of metabolic abnormalities • Protection of health care staff • Maintain ABC • Keep pt in lateral position if comatose or vomiting • Frequent suction • O2 therapy
- 19. DECONTAMINATION • SKIN DECONTAMINATION •GASTRIC LAVAGE • ACTIVATED CHARCOAL • AVOID INDUCED EMESIS
- 20. Presenting with in 2hrsof ingestion Presenting after 2hrs of ingestion Conscious Altered Conscious Gastric Lavage Activated charcoal Secure Airway e.g. intubation Gastric lavage Activated Charcoal Conscious Altered Conscious OPP procedure of decontamination Activated charcoal ? Secure Airway ABC ?
- 21. ATROPINE : • SpecificAntidote - Muscaric no effect on Nicotinic smx • Reverses life threatening features that can result in Death e.g • Central Respiratory depression • Bronchospasm • Excessive Bronchosecretion • Severe Bradycardia • Hypotension
- 24. CURRENT GUIDELINES OFATROPINE ADMINSTRATION : • Bolus dose to attain target End points followed by setting up an infusion to maintain these end points Target End points for Atropine Rx HR > 80 / min Dilated pupils Dry Axilla Sys B.p > 80 mmHg Clear chest on auscultation of Bronchorrhea
- 25. Recommended Dose ofAtropine : • Initial I/V bolus of 1.8 – 3mg with subsequent doses • Dose is doubled every 5 mints until atropinization is achieved Maintenance Dose : • 20% of initial atropinizing dose /hr. for 1st 48hrs • Gradually taper over 5-10 days . Continuously monitoring the adequacy of RX
- 26. Atropine Toxicity • Agitation •Confusion • Hyperthermia • Urinary Retention • Severe Tachycardia – ischemic events – CAD • Close observation & dose adjustment is essential – to avoid features of under and over atropinization Anticholinergic Agent : Glycopyrrolate along with atropine can be used in order to limit the central stimulation produced by atropine
- 27. OXIMES : Reactivating ACHE– that has been bound to the OP molecule Pralidoxime : - • Frequent used oximes worldwide • Effective in restoring SM strength and improves diaphragmatic weakness- where atropine has virtually no effect Therapeutic window for Oxime Limited – by the time taken for ageing of the enzyme – OP complex because aged Enzyme can no longer be reactivated by oximes
- 28. WHO RECOMMENDATION OFOXIMES DOSE • 30 mg / kg bolus IV followed by continuous infusion of 8mg/kg/hr Infusion – continued until recovery : Common S/E of OXIMES : • Dizziness • H/A • Blurred vision • Diplopia Rapid Administration of OXIMES • Tachycardia • Laryngospasm • Muscle spasm • Transient NM blockade
- 29. Rx of IMS •Ventilatory support • Diazepam or Midazolam • PTN unless OPIDN develops recovery of IMS is complete with adequate ventilatory care
- 30. Rx of OPIDN:- • No specific Rx Measures • Regular physiotherapy – reduce deformity caused by muscle wasting Recovery from OPIDN :- • incomplete • May be limited to hands and feet Although substantial functional recovery after 1-2 yr. may occur in younger pts.
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- 32. Home Message • OPare dangerous chemicals • OP can be misused by antisocial elements . • It should be remembered OP may be used in future wars and that war will be the war of Nerves . • Immediate management of a pt. • Treatment must not be delayed . • Proper observation of treatment .