Taking a history in poisoning What toxin(s) have been taken and

Dr.Dhaher JS Al-habbo
FRCP London UK
Assistant Professor in Medicine
Department of Medicine
College of Medicine
POISONING
Paracelsus (1493-1541)
‘Grandfather of Toxicology’
"All things are poison and
nothing is without poison, only
the dose permits something not
to be poisonous."
“The dose makes the poison”
therapeutic
effect
2
increasing dose
toxic
effect
Taking a history in poisoning What
toxin(s) have been taken and how much?
 Recognition
of poisoning
 Identification of agents involved
 Assessment of severity
 Prediction of toxicity
Taking a history in poisoning What
toxin(s) have been taken and how much?
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What time were they taken and by what route?
Has alcohol or any drug of misuse been taken as well?
Obtain details of the circumstances of the overdose from
family, friends and ambulance personnel
Ask the general practitioner for background and details of
prescribed medication
Taking a history in poisoning What
toxin(s) have been taken and how much?
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Assess suicide risk (full psychiatric evaluation when
patient has physically recovered)
Capacity to make decisions about accepting or refusing
treatment?
Past medical history, drug history and allergies, social and
family history?
Record all information carefully
EVALUATION OF THE ENVENOMED
PATIENT
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Neurotoxic paralysis
'Sleepy' or drooping eyelids
Difficulty swallowing, dysarthria and drooling
Limb weakness
Respiratory distress
Excitatory neurotoxicity.
Sweating, salivation, piloerection
Tingling around mouth, tongue or muscle twitching
Dyspnoea (pulmonary oedema)
Assessment of type and extent of
envenoming
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Coagulopathy.
Blood oozing from bite site and/or gums
Bruising
Melaena, haematemesis
Local effects :Pain, sweating, blistering, bruising etc.
Myolysis ; Muscle pain or weakness
Important substances involved in
poisoning
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IN UK
Analgesics, e.g. paracetamol and non-steroidal antiinflammatory drugs (NSAIDs)
Antidepressants, e.g. tricyclic antidepressants (TCAs),
selective serotonin re-uptake inhibitors (SSRIs) and
lithium
Cardiovascular agents, e.g. β-blockers, calcium channel
blockers and cardiac glycosides
Drugs of misuse, e.g. opiates, benzodiazepines, stimulants
(e.g. amphetamines, MDMA, cocaine)
Carbon monoxide
Alcohol
Important substances involved in
poisoning
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In South and South-east Asia.
Organophosphorus and carbamate insecticides(mostly
fatal)
Aluminium and zinc phosphide
Oleander
Snake venoms
Antimalarial drugs, e.g. chloroquine
Antidiabetic medication
Important substances involved in
poisoning
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Poisoning in old age
Aetiology: commonly results from accidental poisoning (e.g.
due to confusion or dementia) or drug toxicity as a
consequence of impaired renal or hepatic function or drug
interaction. Toxic prescription medicines are more likely to be
available.
Psychiatric illness: self-harm is less common than in
younger adults but more frequently associated with depression
and other psychiatric illness, as well as chronic illness and pain.
There is a higher risk of subsequent suicide.
Severity of poisoning: increased morbidity and mortality
result from reduced renal and hepatic function, reduced
functional reserve, increased sensitivity to sedative agents and
frequent comorbidity.
Epidemiology
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More than 2 million toxic exposures reported in 200
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Over half were children < 6 years
Poisoning third leading cause of death from 19851995
Incidence of toxin related deaths increase 300%.
All chemicals have potential to be poisons if given a
large enough dose
Poisoning occurs when exposure to a substance
adversely affects function of any organ system
Examination
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Physiologic excitation –
anticholinergic, sympathomimetic, or central hallucinogenic
agents, drug withdrawal
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Physiologic depression –
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cholinergic (parasympathomimetic), sympatholytic, opiate, or
sedative-hypnotic agents, or alcohols
Mixed state –
polydrugs, hypoglycemic agents, tricyclic antidepressants,
salicylates, cyanide
Physical Examination
 Oropharynx for increase salivation or
excessive dryness
 CV: rhythm, rate, regularity
 Lungs: bronchorrhea or wheezing
 Abd: bowel sounds, tenderness or rigidity
 Ext: fasiculations, tremor
 Neuro: CN, reflexes, muscle tone
coordination, cognition, ability to ambulate
Drug detection
Drug levels
General Management
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A (Airway)
B (Breathing)
C (Circulation)
D (Disability- /Glasgow Coma Scale)
DEFG ( Don’t ever forget the Glucose)
GET A SET OF BASIC OBSERVATIONS
Airway
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Airway obstruction can cause death after poisoning
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Evaluate mental status and gag/cough reflex
Airway interventions
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Flaccid tongue
Aspiration
Respiratory arrest
Sniffing position
Jaw thrust
Head-down, left-sided position
Examine the oropharynx
Clear secretions
Airway devices: nasal trumpet, oral airway
Intubation?
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Consider naloxone first
Breathing
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Determine if respirations are adequate
Give supplemental oxygen
Assist with bag-valve-mask
Check oxygen saturation, ABG
Auscultate lung fields
 Bronchospasm: Albuterol nebulizer
 Bronchorrhea/rales: Atropine
 Stridor: Determine need for immediate intubation
Circulation
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IV access
Obtain blood work
Measure blood pressure, pulse
Hypotension treatment:
 Normal saline fluid challenge, 20 mL/kg
 Vasopressors if still hypotensive
 PRBC’s if bleeding or anemic
Hypertension treatment:
 Nitroprusside, beta blocker, or nitroglycerin
Continuous ECG monitoring
 Assess for arrhythmias, treat accordingly
Supportive care
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Vital signs, mental status, and pupil size
Pulse oximetry, cardiac monitoring, ECG
Protect airway
Intravenous access
cervical immobilization if suspect trauma
Rule out hypoglycaemia
Naloxone for suspected opiate poisoning
Preventing absorption
Gastric lavage
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Not in unconscious patient unless intubated (risk aspiration)
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Flexible tube is inserted through the nose into the stomach
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Stomach contents are then suctioned via the tube
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A solution of saline is injected into the tube
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Recommended for up to 4hrs in Salicylate OD
Induced Vomiting
 Ipecac - Not routinely recommended
 Risk of aspiration
Preventing absorption
Activated charcoal
 Adsorbs toxic substances or irritants, thus
inhibiting GI absorption
 Addition of sorbitol →laxative effect
 Oral: 25-100 g as a single dose
 repetitive doses useful to enhance the
elimination of certain drugs (eg, theophylline,
phenobarbital, carbamazepine, aspirin, sustainedrelease products)
 not effective for cyanide, mineral acids, caustic
alkalis, organic solvents, iron, ethanol, methanol
poisoning, lithium
Elimination of poisons
Renal elimination
 Medication to stimulate urination or defecation may be given to try
to flush the excess drug out of the body faster.
Forced alkaline diuresis
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Infusion of large amount of NS+NAHCO3
Used to eliminate acidic drug that mainly excreted by the
kidney eg salicylates
Serious fluid and electrolytes disturbance may occur
Need expert monitoring
Hemodialysis or haemoperfusion:
 Reserved for severe poisoning
 Drug should be dialyzable i.e. protein bound with low volume of
distribution
 may also be used temporarily or as long term if the kidneys are
damaged due to the overdose.