Transcript ACUTE POISONING - University of Bristol

ACUTE POISONING
Major C J Porter RAMC
Army Medical Directorate
Emergency Medicine Registrar
Bristol Royal Infirmary
Outline of lecture
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Epidemiology
Toxidromes
History, examination and detective work
General management
Specific management
Antidotes
Scenarios
EPIDEMIOLOGY
• 4000 UK deaths per year (1/3 CO)
• Most deaths outside hospital
• 100,000 Hospital admissions (12%)
• Not just overdoses: Illicit drugs, Alcohol
EPIDEMIOLOGY
• Self poisoning:
• F>M
• 1/3 >one drug
• Taken with alcohol:
F: 40% M: 60%
• Repeated self-poisoning: 11% of
admissions
SUICIDE
• 2% of male deaths
• 1% of female deaths
• Method:
• Female:
• Male:
Poisoning 40%
Gas / Hanging / Suffocation
• Self-harm parasuicide:
• 1% dead after 12 months
• 3-5% dead after 5-10 years
Toxidromes
• Patterns of signs and symptoms
• Useful to help in diagnosis and treatment
of unknown poisons
Opiates
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Respiratory depression
Cardiovascular depression
Reduced level consciousness
Pinpoint pupils
Pulmonary oedema
Hypothermia
(Rapid response to Naloxone)
Common causes
• Opiates – heroin, morphine etc
Sympathomimetics / Stimulants
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Agitation/delusions/paranoia
Fight/Flight response
Tachycardia
Hypertension
Arrhythmias
Dilated pupils
Seizures
Hyperpyrexia
Common causes
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Cocaine
Amphetamines
Decongestants
Ecstasy
Anticholinergic
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Tachycardia
Arrhythmias
Pupils: mid-point or dilated / divergent
Confusion / drowsiness / coma
Seizures
Dry flushed skin
Urine retention
Hypertonia, Hyper-reflexia, Myotonic jerks
Anticholinergic signs
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Hot as a hare
Blind as a bat
Dry as a bone
Red as a beet
Mad as a hatter
Common causes
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Antidepressants-Tricyclics
Antihistamines
Atropine
Antipsychotics
Antispasmodics
Serotonin Syndrome
• Similar to anticholinergic syndrome
– loss of consciousness:
– sweating and tremor:
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Agitation
Delirium
Hypertonia / myoclonus
Tachycardia
Tachypnoea
uncommon
common
Common Causes
• SSRIs
• MAOIs (Hyperpyrexia / Hypertensive
crisis)
Cholinergic
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Brady/tachycardia
Confusion/reduced GCS
Pinpoint pupils
Seizures
Weakness
SLUDGE
Pulmonary oedema
SLUDGE
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sweating salivation
lacrymation
urinary frequency urgency
diarrhoea
gastrointestinal discomfort
eyes pinpoint
Common causes
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Organophosphates
Physostigmine
Some mushrooms
Nerve agents
Salicylism: Aspirin
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Impaired hearing
Tinnitus
Sweating
Warm skin
Hyperventilation
• Cinchonism: Quinine (salicylism +
blindness)
MANAGEMENT
Management Overview
• History & assessment of vital signs
• ANY concerns: move patient to RESUS
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DEFG
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Supportive care (O2, IV Fluids)
Prevent absorption
Increase elimination
Antidotes
PSYCHOLOGICAL ASSESSMENT
History
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What?
When?
How much? (mg/kg)
What else?
Why?
Collateral history
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Paramedics
Family / friends
Notes
Look in pockets – carefully!!!
Detective work
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BNF
Toxbase
Tablet identification aids: TICTAC
Poisons advice: NPIS
Plant identification books
National teratology information service
Initial examination
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Treat problems as you find them!!
Airway
Breathing
Circulation
Disability – GCS/AVPU and Pupils
DON’T EVER FORGET GLUCOSE
Observations
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Saturations and respiratory rate
Pulse and blood pressure
GCS
Pupils
Temperature
GLUCOSE
Investigations
• All Patients
– Glucose
– U&E
– Paracetamol & Salicylate
• As indicated
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LFT
Co-ag / INR
CK
ABG / VBG
ECG
CXR
• Urine toxicology screen
Reduce absorption
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Emesis – No role
Activated charcoal within 1 hour
Gastric lavage – rarely
Whole bowel irrigation - rarely
Increase elimination
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Urinary alkalinisation
Multi-dose Activated Charcoal
Haemodialysis
Haemoperfusion
Plasma exchange
• Forced alkaline diuresis (no longer recommended)
Paracetamol
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Very common: 40% poisons admissions
Often asymptomatic
Can be lethal – 200-300 deaths/year
Check blood level at 4 hours
Two treatment lines normal and high risk
Given IV N-acetylcysteine
Paracetamol metabolism
• Metabolised by glucuronidation (60%),
Sulphation (35%) and oxidation (10%)
• Cytochrome p450 produces NAPQI
• NAPQI toxic causes hepatocellular
necrosis – irreversible binding
• NAPQI detoxified by conjugation with
glutathione
Prescott Nomogram
High Risk
• Increased oxidation
– Chronic alcohol use
– Drugs
• Reduces glutathione stores
– Malnutrition
– Eating disorders
– Chronic liver disease
N-acetylcysteine
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Most effective within 8 hours
Precursor for glutathione production
Can cause anaphylactoid reactions
Consider starting before paracetamol
result if:
– Presenting > 8 hrs & >150mg/kg taken
– Staggered overdose
To treat or not to treat?
Patient 1
• 20 year old woman
who takes a handful
of paracetamol tablets
• No drug history
• No alcohol use
• Fit and well
• Blood level is 80mg/l
No need to treat
• Patient is not high risk
• Level at 4 hours is below even the high risk
line
Patient 2
• 70 year old man
• Takes 20 paracetamol
6 hours before
presenting
• Alcoholic
• No drug history
• Blood level 100mg/l
Treat
• Patient is high risk
• Level is above the high risk line
• Delayed presentation means need to act fast
Patient 3
• 17 year old epileptic
• 25 codydramol 2
hours before
attendance
• Taking
carbamazepine
• Blood level at 4 hours
is 120mg/l
Treat
• High risk patient
• Level above the high risk line
Patient 4
• 35 year old man who
presents after taking
24 paracetamol over
a period of 24 hours
• No drug history
• Fit and well
• Blood level 20mg/l
Treat
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Staggered overdoses are difficult
Poisons advice is to give IV acetylcysteine
Levels are not that helpful
Need to monitor Liver function, clotting and
renal function
• May need discussing with Liver Unit if
abnormal
PARACETAMOL
DEADLY PITFALLS
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The Prescott Nomogram High Risk Line
Staggered Overdoses
Management of late presentation
Recheck U&E, LFT, INR after N-acetylcysteine
Tricyclics
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Antidepressants
Dangerous: US 60-70% fatal ODs
UK commonest fatal OD per prescription
10% unconscious patient will fit
– Treat fits with diazepam/lorazepam
Tricyclic effects
• Anticholinergic toxidrome
• The 3 C’s
– Coma
– Convulsion
– Cardiac
Tricyclics cardiac effects
• Quinidine effects lead to arrhythmias
• ECG
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Sinus tachycardia
Broad QRS: RBBB
Prolonged QT interval
Right axis deviation
• Severe poisoning – VT, bradycardia, heart block
• QRS > 160mS = ↑↑risk of seizures and cardiac
toxicity
Tricyclics
• ABG
– Hypoxaemia
– Metabolic acidosis
– Respiratory acidosis
Tricyclics
• Management:
– EARLY ITU REFERRAL
– SODIUM BICARBONATE
• If hypotension resistant to fluid challenge
• Dysrhythmias
• Convulsions
– Consider IV Magnesium for resistant dysrhythmia
Salicylate
• Salicylism
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Dehydration
Confusion /coma
Seizures
Haemetemesis
Hypoglycaemia
Salicylate
• Metabolic and acid-base disturbance
• Complex
• Respiratory alkalosis – direct stimulation to
over breathe
• Metabolic acidosis- acid, impaired normal
metabolism, production of lactic acid
• Check ABG / VBG
Salicylate
• Severity of ingested dose:
• >150 mg/kg:
• >250 mg/kg:
• >500 mg/kg:
mild
moderate
severe
Salicylate management
• Tailor treatment to symptoms
• Fluids
• Reduce absorption:
• Activated charcoal
• Gastric lavage (>500 mg/kg and <1 hour)
• Increase elimination:
• Urinary alkalinisation
• Cooling
• Glucose if hypoglycaemic
Salicylate management
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<350mg/L:
oral fluids
>350mg/L:
urinary alkalinisation
>700mg/L:
haemodialysis
DISCUSS WITH NPIS
Salicylate
DEADLY PITFALL
• Salicylate levels can continue to rise
following admission (10% of cases)
– Repeat levels every until peaked
Opiates
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Common
Act on μ-receptors
Reversible with Naloxone
Naloxone pure opioid antagonist
Naloxone
• Short half life: may need repeated doses
• Give IV +/- IM & may need IVI
Antidotes
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Opiates – naloxone
Paracetamol – acetylcysteine/methionine
Beta-blockers – glucagon
Insulin – glucose
Iron – desferrioxamine
Carbon monoxide – oxygen
Methanol - ethanol
(Benzodiazepines – flumazenil)
Scenario 1
• 20 year old IVDU found by ambulance
crew unconscious
• Needle lying by side
• Resp rate 6, Sats 94% on air
• 60bpm BP 100/55
• Responds to pain
What next?
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A – Give naloxone
B – Check airway
C – Take history
D – Give flumazenil
Check airway
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Check airway patent
Give oxygen
Call for senior help
Check glucose
Give naloxone IM and IV
Scenario 2
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30 year old woman
Taken some white tablets 4 hours earlier
Feels completely well
Felt depressed after argument with partner
Usually fit and well
What next?
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A – Start N-Acetylcysteine
B – Discharge as she is obviously well
C – Find out what the tablets are
D –Take blood for paracetamol levels
Take bloods
• Early treatment is essential in paracetamol
overdose
• Need to know what her levels are as soon
as possible
Scenario 3
• 45 year old man works in local aquarium
• Put right hand into tank and got stung by a
lion fish
• Respiratory rate 16 sats 100% on air
• Pulse 100 bpm 160/80
• Fully conscious
• Extreme pain in hand
Lion fish
What next?
• A – Panic you know nothing about lion
fish!
• B – Look on Toxbase
• C – Ring local zoo
• D – Ask a senior who also knows nothing
about Lion fish!
Toxbase
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Patient needs cardiovascular monitoring
Analgesia
Hand in water as hot as can tolerate
Lion fish toxin is heat labile
Carefully remove spines if present
• Few hours later patient feels much better
goes home
Summary
• Common
• Approach using:
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ABCD
DEFG
Consider the toxidromes
Early senior help / Early ITU referral
Supportive Care
Antidotes
Psychological assessment
Questions
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