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    Current Management Guidline in Organophosphors Poisoning: DR - Surendra Khosya Guided by Dr. S.R Meena Dr. Meenaxi Sharda

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    Organophosphates and carbamates are potent cholinesterase inhibitors that can cause severe toxicity through cutaneous, inhalation, or ingestion exposure. Management involves initial resuscitation with oxygen, ventilation if needed, and atropine administration. Atropine is the primary antidote and aims to compete with acetylcholine at muscarinic receptors. Pralidoxime may also be given to reactivate cholinesterase within 48 hours. Gastric decontamination, benzodiazepines for seizures, and supportive care are also important aspects of management. Complications include intermediate syndrome, delayed neuropathy, and atropine toxicity requiring careful monitoring.

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    Current Management Guidline in Organophosphors Poisoning: DR - Surendra Khosya Guided by Dr. S.R Meena Dr. Meenaxi Sharda

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    Organophosphates and carbamates are potent cholinesterase inhibitors that can cause severe toxicity through cutaneous, inhalation, or ingestion exposure. Management involves initial resuscitation with oxygen, ventilation if needed, and atropine administration. Atropine is the primary antidote and aims to compete with acetylcholine at muscarinic receptors. Pralidoxime may also be given to reactivate cholinesterase within 48 hours. Gastric decontamination, benzodiazepines for seizures, and supportive care are also important aspects of management. Complications include intermediate syndrome, delayed neuropathy, and atropine toxicity requiring careful monitoring.

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    OPC POISOINING

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    Organophosphates and carbamates are potent cholinesterase inhibitors that can cause severe toxicity through cutaneous, inhalation, or ingestion exposure. Management involves initial resuscitation with oxygen, ventilation if needed, and atropine administration. Atropine is the primary antidote and aims to compete with acetylcholine at muscarinic receptors. Pralidoxime may also be given to reactivate cholinesterase within 48 hours. Gastric decontamination, benzodiazepines for seizures, and supportive care are also important aspects of management. Complications include intermediate syndrome, delayed neuropathy, and atropine toxicity requiring careful monitoring.

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    30 views28 pages

    Current Management Guidline in Organophosphors Poisoning: DR - Surendra Khosya Guided by Dr. S.R Meena Dr. Meenaxi Sharda

    Uploaded by

    surendrakhosya
    Organophosphates and carbamates are potent cholinesterase inhibitors that can cause severe toxicity through cutaneous, inhalation, or ingestion exposure. Management involves initial resuscitation with oxygen, ventilation if needed, and atropine administration. Atropine is the primary antidote and aims to compete with acetylcholine at muscarinic receptors. Pralidoxime may also be given to reactivate cholinesterase within 48 hours. Gastric decontamination, benzodiazepines for seizures, and supportive care are also important aspects of management. Complications include intermediate syndrome, delayed neuropathy, and atropine toxicity requiring careful monitoring.

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    of 28

    CURRENT MANAGEMENT

    GUIDLINE IN ORGANOPHOSPHORS
    POISONING
    Dr.Surendra Khosya
    Guided By
    Dr. S.R MEENA
    Dr. Meenaxi Sharda
    COMMONLY AVAILABLE OPC
    ORGANOPHPHOSPHATES
    PHARMACOLOGICAL NAME BRAND NAME
    1. FENTHION BAY-TEX
    2. MALATHION FLIT,FINIT,KILL BUG BUGSOLIN
    3. FENTHRITHION
    4. ETHYL PARATHION PARATHION
    5. DIMETHOATE
    6. DICHLORVOS
    7. DIAZINON TIK 20
    8. HETP ,,TEPP
    9. ROGOR NUVON
    1O. PHORAT
    11.CHLOPYRIFOS
    .ORGANOCARBAMATES
    1. ISOPROPOXYPHENYL (APOCARB) BAYGON
    N-METHYL CARBAMATES
    2. NAPHTHYL-NMETHYL CARBAMATES CARBARYL(SEVIN)
    3. PROPOXUR HIT
    Introduction

     Organophosphates and carbamates are


    potent cholinesterase inhibitors capable
    of causing severe cholinergic toxicity
    following cutaneous exposure,
    inhalation, or ingestion.
     World Wide:
     3,000,000 per yr people are exposed.
     up to 300,000 fatalities.

     Chemical
    weapons (nerve gases) are
    organophosphate agents.
    Mechanism Of Action
     Organ phosphorous compounds bind to acetyl
    cholinesterase
     overabundance of acetylcholine in the synapse
     By time the compound undergoes a
    conformational change (aging) renders the
    enzyme irreversibly resistant to reactivation.
     Carbamate compounds unlike
    organophosphates, are transient
    cholinesterase inhibitors.
    Clinical Features

     Generally oral or respiratory exposures


    result in signs or symptoms within three
    hours.

     while
    symptoms of toxicity from dermal
    absorption may be delayed up to 12 hours.
    Niccotinic , Muscarinic & Central
    syndrome
    Manifestations
     Cholinergic phase
    central
    peripheral muscarinic
    peripheral nicotinic
     Intermediate syndrome
     Delayed neuropathy
     Behavioral effects
    Clinical Features (Acute Toxicity)
     Generally manifests in minutes to hours
     Evidence of cholinergic excess

    ◦ SLUDGE = Salivation,
    Lacrimation,
    Urination,
    Defecation,
    Gastric Emptying.
    ◦ BBB = Bradycardia,
    Bronchorrhea,
    Bronchospasm.
    Clinical Features (Acute Toxicity)

     Respiratory insufficiency can result from


    muscle weakness, decreased central
    drive, increased secretions, and
    bronchospasm and it is the lead cause of
    death.

     Cardiac arrhythmias, including heart


    block and QTc prolongation may be due
    to hypoxemia.
    Clinical Features (Acute Toxicity)

     In children
    Seizures are more common (22%-25%).
    Lethargy and coma (54%-96%).
    Flaccid muscle weakness,
    miosis,
    excessive salivation
    are common presenting signs.
    Clinical Features (Intermediate Syndrome)

     10to 40 % of organophosphorous agent


    poisoned patients.
     Occurs 24-96 hours after exposure
     Bulbar,
    respiratory, and proximal muscle
    weakness are prominent features.
     Generally resolves completely in 1-3 weeks.
    Clinical Features (Delayed Neurotoxicity)

     Organophosphate Induced Delayed


    Neuropathy (OPIDN).
     Usually occurs several weeks after exposure.
     Primarily motor involvement (symmetrical
    motor polyneuropathy) flaccid weakness of lower
    extremities, ascends to involve upper extremities.
     Sensory disturbances are usually mild.
     May resolve spontaneously, but can result in
    permanent neurologic dysfunction.
    Grading Severity of organophosphate poisoning
    Normal serum acetyl cholinesterase/RBC Cholinesterase-8-20 U/I
    MILD Level isMODERATE
    8-20U/L SEVERE

    Walk ,talk Cannot walk Unconscious,no pupillary


    Headache,dizzy Soft voice reflex
    Nausea,vomiting Musle twitching Muscle twitching,flaccid
    Abdominal pain (fasiculation) paralysis
    Sweating, salivation Anxity restlessness Increased bronchial secr
    Rhinorrhoea Small pupil(miosis) dyspnoea
    Crackles /wheeze
    convulsion, respiratory
    failure
    AChE 1.6-4.0U/I AChE .8-2.0U/I AchE <.8u/l
    DIAGNOSIS (Clinical findings)

     88% of parents initially deny any exposure history.

     petroleum or garlic-like odor.


     If doubt exists a trial of Atropine (0.01 to
    0.02 mg/kg) may be employed.
    The absence of signs or symptoms of
    anticholinergic effects following atropine
    challenge strongly supports the diagnosis
    DIAGNOSIS (Laboratory abnormalities)

     RBC acetylcholinesterase activity:


    ◦ provides a measure of the degree of toxicity.
    ◦ determine the effectiveness of antidote therapy.

     plasma (or pseudo-) cholinesterase activity:


    ◦ more easily performed.
    ◦ not correlate well with the severity of poisoning.
    ◦ a depression of 25% or more is strong evidence of
    excessive organophosphate absorption.
    MANAGEMENT (Initial resuscitation)

     Deliver 100 % oxygen via facemask


     Strongly consider intubation:

     patients who appear mildly poisoned may rapidly develop


    respiratory failure.
     Consider volume resuscitation with normal saline or
    ringer to treat Bradycardia and hypotension.
     Use activated charcoal within one hour of an

    ingestion.
      In cases of dermal exposure aggressive

    decontamination with complete removal of the


    patient's clothes and vigorous irrigation of the
    affected areas should be performed.
    GASTRIC DECONTAMINATION
     Forced emesis have no role
     Gastric lavage is indicated once patient is

    stabilsed,
     in unconcious, intubated patient repeated

    after 2-3 hrs. and within 1-2 hrs of ingetion


    of op/ carbamate or started even after 12 hr
    of ingestion and repeated thrice at an interval
    of 4 hrs
     Repeat stomach wash will remove residul

    poison
    ANTIDOTE(atropine is only life
    saving)
     Competes with acetylcholine at
    muscarinic receptors.

     Initial
    dose 0.05 mg/kg IV bolous.
     Doubled every 3 to 5 min until bronchial
    secretions and wheezing stop (SaO2).
     Repeat every 10 to 30 min until all
    absorbed organophosphate metabolized
    (few hours to several days; usually 2 to
    12 hours).
    TARGET END POINT OF ATROPINISATION

    Chest clear on auscultation with no wheeze

    Heart rate>80 beats/min

    Dry axilla

    Systolic blood pressure >80 mmhg


    MANAGEMENT (Atropine)

     Keep a maintenance dose of atropine for 2-3


    days after disappearing of manifestation.
     10-20 % of loading every hrs
     Tachycardia and mydriasis are not appropriate
    markers for therapeutic improvement, as they
    may indicate continued hypoxia, hypovolemia,
    or sympathetic stimulation.

     Fever,muscle fibrillation, and delirium are the


    main signs of atropine toxicity that indicate that
    atropine administration should be discontinued,
    at least temporarily.
    ATROPINE TOXICITY
    Dry Mouth

    Dysphagia

    Dilated pupils

    Drunken gait

    Delirium

    Drowsiness

    Death due to respiratory failure

    Dry hot skin

    Carphologia

    Hallucination and delusion


    MANAGEMENT (Pralidoxime)

     Cholinesterase reactivating agent that are


    effective in treating both muscarinic and
    nicotinic symptoms.
     Use within 48 hours after poisoning.
     Use with concurrent of atropine.
     Use only for moderate to severe
    Organophosphate poisoning and not
    carbamate.
     Use if neuromuscular dysfunction is present.
    MANAGEMENT (Pralidoxime)

     30 mg/kg over 10 -20 min f/b


     Continuous infusion at 8-1o mg/kg/hour.
     Until clinical recovery or 7 day which have
    elapsed whichever is later
     Obidoxime 250 mgf/b infusion750
    mg/24hrs
     Monitor Blood pressure during
    administration
    MANAGEMENT (Benzodiazepines )

     Prophylactic diazepam has been shown to


    decrease neurocognitive dysfunction after
    poisoning.
     Diazepam 0.1-0.2 mg/kg IV, repeat as
    necessary if seizures occur.

     phenytoin
    has no effect on
    organophosphate agent-induced seizures.
    OTHER DURG

    Magnesium Therapy –may inhibit AChE andOP antagonism

    Glycopyrolate is equally effective and lessr CNS side effect


    With better control of secretion then atropine

    Furosemide –if pulmonary edema persist after full atropinisation


    Antibiotics –consider risk of infection

    DURG SHOUID BE AVOIDED


    Morphine
    Succinyl choline
    Theophylline
    Phenothiazine, reserpine
    Adrenergic amine only if maked hypotenmsion
    Special Considerations

    Organophosphates are usually dissolved in


    hydrocarbon bases; thus, the clinician
    should consider hydrocarbon pneumonitis .
    Thanks
    For
    Listening

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