2. 2
Poisoning
• POISON is any substance that is injurious to
health or cause death either taken internally or
applied locally.
• POISONING is the condition produced by a
poison.
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3. 3
Acute poisoning
• Acute poisoning is common.
• The most frequent cause is …
– intentional drug overdose in the context of self-harm
(eg, paracetamol , insecticide).
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4. 4
Accidental poisoning
• Household and agricultural products are commonest…
– pesticides and herbicides
– freely available
– common sources of poisoning
– associated with a much higher case fatality
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When to suspect poisoning
Unexplained illness in previously
healthy person
History of psychiatric problem
History of suicidal attempt
Recent change in economic and social
relationship
Working with chemicals
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Assessment of patient
• Triage and resuscitation
– immediate assessment of vital signs
– identifying the poison(s) involved and obtaining
adequate information about them
– identifying patients at risk of further attempts at
self-harm and removing any remaining hazards.
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Resuscitation
• Airway
• Breathing
• Circulation
• Admission to ICU/HDU
• if cardio-respiratory support is needed
• recurrent seizure
• GCS ↓, paO2 ↓ (< 7 kpa) & paCO2 ↑( > 6 kpa)
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Identification of poison: History
• Taking a history in poisoning
– What toxin have been taken and how much?
– What time were they taken and by what route?
– Has alcohol or any drug of misuse been taken as well?
– Obtain details of circumstances of the overdose from
family friends and ambulance personnel
– Assess suicide risk (full psychiatric evaluation)
– Past medical, drug, allergies, social and family history
• Record all information carefully
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16. Body temperature
16
Hypothermia (COOLS)
• C CO
• O opiates
• O oral hypoglycemic, insulin
• L liquor (Alcohols)
• S sedatives, hypnotics
Hyperthermia (NASA)
• N neuroleptic malignant
syndrome
• A antihistamines
• S salicylates,
sympathomimetics
• A anticholinergic,
antidepressant
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17. Skin findings
Diaphoretic skin
• Sympathomimetics
• Organophosphates
• Salicylates
Red skin
• CO
• Boric acid
Blue skin
• Cyanosis
• Methemoglobinemia
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23. Blood pressure
23
Hypotension (CRASH)
• C clonidine
• R reserpine
• A antidepressants
• S sedative hypnotics
• H heroin (opiates)
Hypertension (CT SCAN)
• C cocaine
• T theophylline
• S sympathomimetics
• C caffeine
• A anticholinergics, amphetamine
• N nicotine
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24. Heart rate
Bradycardia (PACED)
• P propranolol
• A anticholinesterase
• C clonidine, CCB
• E ethanol + alcohols
• D digoxin, dravon (opiates)
Tachycardia (FAST)
• F free base (cocaine)
• A anticholinergic, antihistamine
• S sympathomimetic
• T theophylline
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Investigations
• Urea, electrolytes and creatinine
– in most patients
• Arterial blood gasses
– with significant respiratory or circulatory
compromise
– poisoning with substance likely to affect acid-base
status
• Anion and osmolar gaps
• Identification of poisons in vomitus, blood and urine
samples
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Osmolal Gap
• OG = Measured serum osmolality – Calculated osmolality
• Calculated osmolality = (2Na)+ (Glucose/18) +(BUN/2.8)
• Normal serum osmolality is 285-300 mOsm/kg.
• Normal osmolal gap is 8-12 mOsm/kg.
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• Elevation due to presence of unmeasured, low-molecular
weight molecules that are osmotically active:
Methanol
Ethylene glycol
Diuretics, such as glycerol, manitol, sorbitol
Isopropanol
Ethanol
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Osmolal Gap
33. 33
Anion Gap
• AG is an indirect measure of phosphates, sulfates, & organic
acids.
• Na + unmeasured cations = (Cl + HCO3) + unmeasured anions
• Na – (Cl + HCO3) = unmeasured anions – unmeasured cations
• Anion gap = (Na ) – (Cl + HCO3)
• Normal anion gap is 12-16 mEq/L.
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34. Causes of high anion gap
metabolic acidosis:
• Carbon monoxide,
• Cyanide.
• Alcoholic ketoacidosis
• Toluene
• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde, Phenformin
• Iron, Isoniazid
• Lactic acidosis
• Ethylene glycol
• Salicylates
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Excessive acid production or with addition of exogenous acids:
35. Causes of low anion gap
metabolic acidosis:
• Acetazolamide
• Amiloride
• Ammonium chloride
• Amphotericin B
• Bromide
• Iodide
• Lithium
• Polymyxin B
• Spironolactone
• Toluene
• times
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Oxygen Saturation Gap
• Oxygen saturation calculated from routine blood gas analysis
- Oxygen saturation measured by pulse oximetry.
• Others use this term for the difference between the calculated
oxygen saturation from a standard blood gas machine and the
measured value from a co-oximeter.
• An oxygen saturation gap is present when there is more than a
5% difference.
• Causes of elevated oxygen saturation gap include carbon
monoxide poisoning.
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42. 42
Steps in Mx of poisoning
Counseling, education and psychiatrist referral
Supportive Rx
Specific Rx to ↓ the toxic effect on the body (antidotal Rx)
Non specific Rx to ↓ the level of toxins in the body
Diagnosis of type of poison
Resuscitation and initial stabilization
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Prevention of further absorption
A- Dermal Exposure
• Remove all clothing.
• Washing skin gently with soap and water for at least
30 minutes.
• Forceful washing may damage skin and promotes further
absorption.
• Protection of medical staff
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B- Eye Exposure
• Washing conjunctiva with running water or normal
saline for 20 minutes.
Solid corrosives should be removed by forceps.
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C- GIT Exposure : GI decontamination
Single-dose activated charcoal (up to 1 hr)
Multiple-dose activated charcoal
• Carbamazepine, dapsone, phenobarbital, quinine or
theophylline
• It is not digested; it stays inside the GI tract and eliminates
the toxin when the person has a bowel movement.
• Adult dose is 1 gm/kg.
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Contraindications of AC
• Coma
• Intestinal obstruction.
• Corrosives
• If an oral antidote is given
• Hydrocarbons
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48. 48
Gastric Lavage
• Used only for life threatening overdose of substance not
absorbed by activated charcoal.
• Not usually indicated.
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49. Contraindications of gastric lavage
Absolute contraindications:
• Corrosives
• Froth producing substances as
shampoo or liquid soap
• Oesophageal varices or peptic
ulcer
Relative contraindications
• Coma
• Convulsions
• Petroleum distillates
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Induction of emesis
Syrup Ipecac
• The only safe method for induction of vomiting.
• From the root of Cephalus Ipecachuana: emetine &
cephaline
• Early phase: within 30 minutes by direct GIT stimulation.
• Late phase: after 30 minutes through action on CTZ.
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51. Contraindications for
induction of emesis
1. Convulsions.
2. Corrosives.
3. Hydrocarbons.
4. Sharp objects (e.g. needles).
5. Coma or impending coma
6. Decreased gag reflex.
7. Severe CVS disease or respiratory
distress or emphysema.
8. Recent surgical intervention.
9. Hemorrhagic tendencies (varices,
active peptic ulcer,
thrombocytopenia).
10. Previous significant vomiting
(spontaneously).
11. Less than 6m of age (not well
developed gag reflex).
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Whole bowel irrigation
• For ingested packet or slow release tablet
• But the use is controversial.
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53. 53
Cathartics or Laxatives
• These are substances that enhance the passage of material
through GIT and decrease the time of contact between the
poison and the absorptive surfaces of the stomach and
intestine.
a) Osmotic cathartics: increase osmotic pressure in the
lumen, as Mg sulfate.
b) Irritant cathartics: act by increasing motility, such as
caster oil.
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55. Enhancement of excretion of
absorbed poisons
Forced Diuresis
• It is a simple method for some poisons.
• It is effect is increase with manipulation of urine pH.
• It is efficient only in poisons with the following properties:
Substances excreted mainly by kidneys.
Substances with low volume distribution.
Substances with low protein binding.
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56. Types:
1- Fluid Diuresis
2- Osmotic Diuresis: mannitol 10%, which is excreted by renal tubules
leading to increases in its osmotic pressure
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57. 57
Manipulation of Urine pH
Urinary alkalinisation
– alkalinised (pH >7.5) with sodium bicarbonate
– Weak acids (salicylates, methotrexate and herbicides-
2,4-dichlorophenoxyacetic acid) are highly ionised and
so their urinary excretion enhanced
– Currently recommended for salicylate poisoning when
HD are not met
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Haemodialysis (HD) and haemoperfusion
– For poisons with small volume of distribution and
long half-life
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Lipid emulsion therapy
– Lipid emulsion therapy, or ‘lipid rescue’, is being
used increasingly for the management of poisoning
with lipid-soluble agents,
• local anaesthetics, tricyclic antidepressants,
calcium channel blockers and lipid soluble
β-blockers such as propranolol.
– Intravenous infusion of 20% lipid emulsion
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61. Digoxin Digoxin specific antibody
Ethylene glycol ethanol, fomepizole
Methanol ethanol, fomepizole
Iron Desferroxamine
Lead / Mercury Di mercaprol, penicillamine,
sodium calcium edetate
Opoids Naloxone
Organophosphates Atropine, Pralidoxime
Paracetamol N acetylcysteine
Warfarin Vit k, FFP
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Supportive care
• For most poisons antidotes and methods to accelerate
elimination are inappropriate or unavailable.
• Outcome depend on …
– appropriate nursing
– careful monitoring
– supportive care
– treatment of complications
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