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    Poisoning

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    Paracetamol is normally metabolized into non-toxic compounds through conjugation with glutathione, but excess paracetamol can deplete glutathione stores leading to a toxic metabolite that binds irreversibly to hepatic cells and causes liver necrosis. Paracetamol overdose is managed with N-acetylcysteine, which provides sulphydryl groups to increase glutathione availability and convert the toxic metabolite into a non-toxic form to prevent liver damage. The clinical features of paracetamol overdose progress from mild symptoms initially to potential liver failure, coagulopathy, and death if left untreated.

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    Poisoning

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    Paracetamol is normally metabolized into non-toxic compounds through conjugation with glutathione, but excess paracetamol can deplete glutathione stores leading to a toxic metabolite that binds irreversibly to hepatic cells and causes liver necrosis. Paracetamol overdose is managed with N-acetylcysteine, which provides sulphydryl groups to increase glutathione availability and convert the toxic metabolite into a non-toxic form to prevent liver damage. The clinical features of paracetamol overdose progress from mild symptoms initially to potential liver failure, coagulopathy, and death if left untreated.

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    Paracetamol is normally metabolized into non-toxic compounds through conjugation with glutathione, but excess paracetamol can deplete glutathione stores leading to a toxic metabolite that binds irreversibly to hepatic cells and causes liver necrosis. Paracetamol overdose is managed with N-acetylcysteine, which provides sulphydryl groups to increase glutathione availability and convert the toxic metabolite into a non-toxic form to prevent liver damage. The clinical features of paracetamol overdose progress from mild symptoms initially to potential liver failure, coagulopathy, and death if left untreated.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    16 views23 pages

    Poisoning

    Uploaded by

    seed1876
    Paracetamol is normally metabolized into non-toxic compounds through conjugation with glutathione, but excess paracetamol can deplete glutathione stores leading to a toxic metabolite that binds irreversibly to hepatic cells and causes liver necrosis. Paracetamol overdose is managed with N-acetylcysteine, which provides sulphydryl groups to increase glutathione availability and convert the toxic metabolite into a non-toxic form to prevent liver damage. The clinical features of paracetamol overdose progress from mild symptoms initially to potential liver failure, coagulopathy, and death if left untreated.

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    © All Rights Reserved
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    of 23

    Paracetamol-Normal Metabolism

     Paracetamol converted to:


     N-Acetyl-p-benzoquinonamine (TOXIC)
     This is conjugated with Glutathione
     Glutathione stored in the body
     Produces a NON TOXIC metabolite.
     Glutathione stores are used up by the excess Paracetamol
     Toxic Metabolite build up
     Binds IRREVERSIBLY to Hepatic Cell membranes
     Resulting in LIVER NECROSIS
    Clinical features of Paracetamol Overdose
     Stage I (0.5 to 24 hours)
    No symptoms; N&V Malaise
     Stage II (24 to 72 hours)
    Subclinical elevations of hepatic aminotransferases (AST, ALT)
    right upper quadrant pain, with liver enlargement and tenderness. Elevations
    of prothrombin time (PT), total bilirubin, and oliguria and renal function
    abnormalities may become evident
     Stage III (72 to 96 hours)
    Jaundice, confusion (hepatic encephalopathy), a marked elevation in hepatic
    enzymes, hyperammonemia, and a bleeding diathesis hypoglycemia, lactic
    acidosis, renal failure 25%, death
     Stage IV (4 days to 2 weeks)
    Recovery phase that usually begins by day 4 and is complete by 7 days after
    overdose
    Paracetamol Overdose-management
     Initial ABC ( usually well systemically)
     Get a good history
     TIME TAKEN, AMOUNT
     Any other medication
     History of Liver disease
     N-Acetylcysteine. Shown to be advantageous if given in
    the first 10 hours.
    Paracetamol Overdose-management
     N - Acetylcysteine
     Specific antidote used for Paracetamol
     Provides the Sulphydryl groups needed to increase the
    availability of Glutathione
     So that Body can turn the TOXIC metabolite into the non
    toxic form and prevent Liver Cell Damage and
    NECROSIS
     (Not shown to be effective after 15 hours)
    Paracetamol Overdose-management
     Able to measure levels of Paracetamol in the blood.
     Helps to guide whether amount taken is enough to be
    Hepatotoxic
     IF IN DOUBT start treatment before the Paracetamol
    levels get back to save time
    Fluoride Toxicity
     Excessive ingestion / short time
     Acute toxic effects

    A- Gastric disturbance
    B- Nausea, vomiting
    C-Death
    Excessive ingestion / long period during tooth development
     Dental fluorosis;
     The effect of long term fluoride exposure on
    bone is still controversial
    Historical perspective of fluoride toxicity
    Fluoride was used as a pesticide
    Mistaken for powder milk, salt, baking soda, flour
    1933-1955: 607 fatal cases in the US.
    Pittsburgh 1940:
    Salvation Army service center.Mistaken NaF for flour in pancake
    40 poisoning cases & 12 deaths .
    Oregon 1943:
    State hospital,Mistaken roach powder for powder milk.10 gallons
    of scrambled eggs + 17 lbs NaF 263 poisoning cases & 47 deaths
    Current incidences of F toxicity
    USA poison control centers ;>20,000 reports/year of over-
    ingestion of fluoride.
    Sources of fluoride

    Vitamins, dietary supplements, dental products (fluoridated

    toothpastes or mouthwashes).

    90% are young children, ~5% had minor symptom, ~2%

    were treated in healthcare facility.

    A few cases with life-threatening symptoms and DEATH


    Symptoms of fluoride toxicity
    Low Dosage
    Nausea,Vomiting,Abdominal pain,Diarrhea,
    Hypocalcemia and Hyperkalemia
     Hypersalivation,Tears,Discharge from nose and mouth and
    Headache.
     High Dosage; Convulsion,Spasm of the
    extremitie,Generalized weakness,Blood pressure drop.
    Cardiac arrhythmias ,Respiratory acidosis ,Extreme
    disorientation
     Coma and Death May occur within
     the first few hours
    Treatment of Fluoride Toxicity
    Reduce absorption; Induce vomiting immediately (providing no
    risk of aspiration)
    Reduce bioavailability : 1% CaCl2 or calcium gluconate, milk .
    Additional washing of stomach with lime water .
    IV fluid replacement,add calcium gluconate .
    Blood calcium level ,Plus sodium bicarbonate : urine flow rate &
    urinary pH
    Other monitoring and supportive therapies
     Generally, if death has not occurred in 1-2 days the prognosis is good.
     Exception: 2 year-old boy died 5 days after ingesting 100 tablets 0.5
    mg Fuoride.
    Salicylate overdose
     Aspirin (acetylsalicylic acid)
     Methyl salicylate (Oil of Wintergreen)
     5 ml = 7g salicylic acid
     Herbal remedies
     Fatal intoxication can occur after the ingestion of 10
    to 30 g by adults and as little as 3 g by children
    Salicylate levels
     Rapidly absorbed; peak blood levels usually occur within one
    hour but delayed in overdose 6-35 hrs
     Measure 4 hrs post ingestion & every 2 hrs until they are
    clearly falling
     Most patients show signs of intoxication when the plasma level
    exceeds 40 to 50 mg/dL (2.9 to 3.6 mmol/L)
    Salicylate overdose
     Inhibition of cyclooxygenase results in decreased
    synthesis of prostaglandins, prostacyclin, and
    thromboxanes
     Stimulation of the chemoreceptor trigger zone in the
    medulla causes nausea and vomiting
     Direct toxicity of salicylate species in the CNS, cerebral
    edema, and neuroglycopenia
     Activation of the respiratory center of the medulla results
    in tachypnea, hyperventilation, respiratory alkalosis
     Uncoupled oxidative phosphorylation in the mitochondria
    generates heat and may increase body temperature
     Interference with cellular metabolism leads to metabolic
    Clinical features of Salicylate overdose
     Early symptoms of aspirin toxicity include
    tinnitus, fever, vertigo, nausea,
    hyperventilation, vomiting, diarrhoea
     More severe intoxication can cause altered
    mental status, coma, non-cardiac pulmonary
    oedema and death
    Metabolic abnormalities Salicylate overdose
     Stimulate the respiratory center directly, early fall in
    the PCO2 and respiratory alkalosis
     An anion-gap metabolic acidosis then follows, due
    to the accumulation of organic acids, including
    lactic acid and ketoacids
     Mixed respiratory alkalosis and metabolic acidosis
    with ↑ anion gap
     Arterial Ph variable depending on severity
    Metabolic abnormalities
     Metabolicacidosis increases the plasma
    concentration of protonated salicylate

     thusworsening toxicity by allowing easy


    diffusion of the drug across cell membranes
    Salicylate overdose - treatment
     Directed toward increasing systemic pH by the
    administration of sodium bicarbonate .
     IV fluids +/- vasopressors
     Avoid intubation if at all possible (↑ acidosis)
     Supplemental glucose (100 mL of 50 percent dextrose
    in adults) to patients with altered mental status
    regardless of serum glucose concentration to
    overcome neuroglycopaenia

     Hemodialysis
    Alkalinization of plasma and urine
     Alkalemia from a respiratory alkalosis is not a
    contraindication to sodium bicarbonate therapy.
     A urine pH of 7.5 to 8.0 is desirable
     Blood gas analysis every two hours
     Avoid severe alkalemia (arterial pH >7.60)
    Haemodialysis - indications
     Altered mental status

     Pulmonary or cerebral edema

     Renal insufficiency that interferes with salicylate excretion

     Fluid overload that prevents the administration of sodium


    bicarbonate .

     A plasma salicylate concentration >100 mg/dL (7.2 mmol/L)

     Clinical deterioration despite aggressive and appropriate


    supportive care
    Antidotes
     Acetaminophen N-acetylcysteine
     Organophosphates Atropine, pralidoxime
     Anticholinergic physostigmine
     Arsenic, mercury, gold dimercaprol
     Benzodiazepines flumazenil
     Beta blockers glucagon
     Calcium channel block calcium
     Carboxyhemoglobin 100% O2
     Cyanide nitrite, Na thiosulfate
     Digoxin digoxin antibodies
    Antidotes
     Ethylene glycol fomepizole, HD
     Heparin protamine
     Iron deferoxamine
     Isoniazid pyridoxime
     Methanol fomepizole, HD
     Methemoglobin methylene blue
     Opioids naloxone
     Salicylate alkalinization, HD
     TCA’s sodium bicarbonate
     Warfarin FFP, vitamin K
    Decontamination

     Skin
     Protect yourself and other HC
    workers
     Remove clothing
     Flush with water or normal saline
     Use soap and water if oily
    substance
     Chemical neutralization can
    potentiate injury
     Corrosive agents injure skin and
    can have systemic effects

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