Poisoning

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.
 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)
 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

Poisoning

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Poisoning

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Paracetamol-Normal Metabolism

 Paracetamol converted to:

Vitamins, dietary supplements, dental products (fluoridated

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

were treated in healthcare facility.

A few cases with life-threatening symptoms and DEATH

 thusworsening toxicity by allowing easy

 Pulmonary or cerebral edema

 Renal insufficiency that interferes with salicylate excretion

 Fluid overload that prevents the administration of sodium

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

 Clinical deterioration despite aggressive and appropriate

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