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    Paracetamol Poisoning

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    Ooi Ah Guan
    Paracetamol is commonly used for self-poisoning and can cause liver damage and death. A single toxic dose is over 150mg/kg for adults or children. Risk is increased with alcohol abuse, malnutrition, or liver enzyme inducing drugs. Paracetamol is metabolized in the liver, but an overdose overwhelms pathways, producing the toxic metabolite NAPQI which depletes glutathione stores and causes liver necrosis. Treatment involves emptying the stomach, administering activated charcoal or N-acetylcysteine as an antidote to replenish glutathione within 10 hours of ingestion to prevent liver injury.

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    Paracetamol Poisoning

    Uploaded by

    Ooi Ah Guan
    259 views12 pages
    Paracetamol is commonly used for self-poisoning and can cause liver damage and death. A single toxic dose is over 150mg/kg for adults or children. Risk is increased with alcohol abuse, malnutrition, or liver enzyme inducing drugs. Paracetamol is metabolized in the liver, but an overdose overwhelms pathways, producing the toxic metabolite NAPQI which depletes glutathione stores and causes liver necrosis. Treatment involves emptying the stomach, administering activated charcoal or N-acetylcysteine as an antidote to replenish glutathione within 10 hours of ingestion to prevent liver injury.

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    Paracetamol Poisoning

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    Paracetamol is commonly used for self-poisoning and can cause liver damage and death. A single toxic dose is over 150mg/kg for adults or children. Risk is increased with alcohol abuse, malnutrition, or liver enzyme inducing drugs. Paracetamol is metabolized in the liver, but an overdose overwhelms pathways, producing the toxic metabolite NAPQI which depletes glutathione stores and causes liver necrosis. Treatment involves emptying the stomach, administering activated charcoal or N-acetylcysteine as an antidote to replenish glutathione within 10 hours of ingestion to prevent liver injury.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    259 views12 pages

    Paracetamol Poisoning

    Uploaded by

    Ooi Ah Guan
    Paracetamol is commonly used for self-poisoning and can cause liver damage and death. A single toxic dose is over 150mg/kg for adults or children. Risk is increased with alcohol abuse, malnutrition, or liver enzyme inducing drugs. Paracetamol is metabolized in the liver, but an overdose overwhelms pathways, producing the toxic metabolite NAPQI which depletes glutathione stores and causes liver necrosis. Treatment involves emptying the stomach, administering activated charcoal or N-acetylcysteine as an antidote to replenish glutathione within 10 hours of ingestion to prevent liver injury.

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    Download as ppt, pdf, or txt
    of 12

    PARACETAMOL POISONING

    Paracetamol commonest drug used


    50% of all self-poisoning episodes
    100-200 deaths per year
    Max daily dose is 4g in adults and 90mg/kg in
    children
    Toxic dose after a single acute ingestion is
    150mg/kg or about 7g in adults
    Toxic dose may be lower in susceptible pt e.g.
    alcohol abuse, malnourishment, viral illness or
    dehydration
    Chronic paracetamol overdose occurs with
    ingestion of 4g or more per 24 hours

    Paracetamol Normal
    Metabolism
    Metabolized in the liver by conjugation with
    glucuronide & sulphate groups to form inactive
    metabolites which are excreted in urine
    A small portion of pcm is hydroxylated via the
    cytochrome P450 enzymes to produce NAPQI ( Nacetyl-p-benzoquinoneimine )
    NAPQI is a toxic metabolite
    NAPQI reacts with sulphydryl group of
    glutathione in the liver to produce a non-toxic
    metabolites

    Paracetamol Metabolism In
    Overdose
    In overdose normal conjugation pathways are saturated

    More pcm is metabolised to NAPQI


    Glutathione stores are used up by the excess NAPQI
    Toxic metabolite build up
    NAPQI binds irreversibly to hepatic cell membranes
    results in liver necrosis
    Higher risk in :
    Chronic alcoholics ( > 3 drinks/day )
    Induce liver
    Certain drugs e.g. rifampicin, isoniazid,
    enzymes
    phenytoin,phenobarbital,carbamazepine
    Malnutrition
    Reduced Glutathione
    Eating disorder
    Stores
    Chronic Liver Disease

    Paracetamol Metabolism

    Signs & Symptoms Of Paracetamol


    poisoning
    Initial Phase ( >150mg/kg, 12-24 hr )
    - nausea & vomiting
    - pallor
    - malaise
    Latent Phase ( about 4 days)
    - feeling relatively well
    - may recover
    Third Phase ( 4 days to a week )
    - hepatic failure (jaundice)
    - coma
    - death

    Management Of Paracetamol
    Poisoning
    Primary Survey
    - Airway
    - Breathing
    - Circulation
    Stomach Emptying
    - induce vomiting
    - gastric lavage
    Activated Charcoal useful for removing unabsorbed drug up
    to 4 hour after ingestion
    - 1g/kg p.o. or via NG tube
    - not useful in pcm syrup poisoning ( absorbed in 30 minutes )
    Antidote N-acetylcysteine (NAC )- Parvolex
    Methionine can be given orally as an alternative if NAC not
    available
    Dose : adult & child over 6 yr : 2.5g initially followed by 3 more
    doses of 2.5g q4h. Below 6 yr : 1g (same regime)

    Management Of Paracetamol
    Poisoning- continue
    Depends on :

    Time of ingestion
    Amount taken
    Risk factors for liver enzyme induction
    Blood level at 4 hour after ingestion
    Blood level dictate use of antidote
    Use the pcm graph
    If in doubt or late presentation give treatment
    first

    Paracetamol Treatment Graph

    N-acetylcysteine ( NAC )
    Specific antidote for pcm poisoning
    Most effective within 10 hours
    Treatment should be initiated after 4 hours following
    ingestion ,when blood level exceeds threshold for risk
    NAC is usually given orally diluted with juice
    If vomiting occurs within an hour, repeat the dose or use
    NG tube
    Can also be given by IV close monitoring of anaphylaxis
    is needed for the 1st hour after IV loading dose
    Consider starting NAC before pcm result if
    - presenting > 10 hr & > 150mg/kg taken
    - staggered overdose

    Mechanism Of Action Of NAC


    NAC increases the available glutathione to
    conjugate with NAPQI
    NAC is a precursor in production of
    glutathione
    NAC is converted to cysteine which is then
    converted to glutathione

    Dose Of NAC
    ROUTE
    ORAL

    I.V.

    LOADING DOSE
    140mg/kg

    150mg/kg over
    15 min

    MAINTENANCE
    DOSE
    70mg/kg Q4H
    17 doses
    50mg/kg over 4
    hr followed by
    100mg/kg over
    16 hr

    COURSE
    72 hours

    20 hours

    NAC Therapy - continue


    When to stop NAC
    Pcm level is non-detectable & the absence of liver
    injury at 24 hr
    Pt with evidence of injury are treated for full 72 hourcourse

    NAC therapy : P.O Vs IV


    Oral 1st choice
    - low risk of anaphylaxis
    - S/E vomiting
    IV useful in intractable vomiting
    - can be used in pregnancy, hepatic failure
    - S/E urticaria, anaphylatoid reaction

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