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ACUTE POISONING Major C J Porter RAMC Emergency Medicine Registrar

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Presentation on theme: "ACUTE POISONING Major C J Porter RAMC Emergency Medicine Registrar"— Presentation transcript:

1 ACUTE POISONING Major C J Porter RAMC Emergency Medicine Registrar
Army Medical Directorate Emergency Medicine Registrar Bristol Royal Infirmary

2 Outline of lecture Epidemiology Toxidromes
History, examination and detective work General management Specific management Antidotes Scenarios

3 EPIDEMIOLOGY 4000 UK deaths per year (1/3 CO)
Most deaths outside hospital 100,000 Hospital admissions (12%) Not just overdoses: Illicit drugs, Alcohol

4 EPIDEMIOLOGY Self poisoning:
F>M 1/3 >one drug Taken with alcohol: F: 40% M: 60% Repeated self-poisoning: 11% of admissions

5 SUICIDE 2% of male deaths 1% of female deaths Method:
Female: Poisoning 40% Male: Gas / Hanging / Suffocation Self-harm parasuicide: 1% dead after 12 months 3-5% dead after 5-10 years

6 Toxidromes Patterns of signs and symptoms
Useful to help in diagnosis and treatment of unknown poisons

7 Opiates Respiratory depression Cardiovascular depression
Reduced level consciousness Pinpoint pupils Pulmonary oedema Hypothermia (Rapid response to Naloxone)

8 Common causes Opiates – heroin, morphine etc

9 Sympathomimetics / Stimulants
Agitation/delusions/paranoia Fight/Flight response Tachycardia Hypertension Arrhythmias Dilated pupils Seizures Hyperpyrexia

10 Common causes Cocaine Amphetamines Decongestants Ecstasy

11 Anticholinergic Tachycardia Arrhythmias
Pupils: mid-point or dilated / divergent Confusion / drowsiness / coma Seizures Dry flushed skin Urine retention Hypertonia, Hyper-reflexia, Myotonic jerks

12 Anticholinergic signs
Hot as a hare Blind as a bat Dry as a bone Red as a beet Mad as a hatter

13 Common causes Antidepressants-Tricyclics Antihistamines Atropine
Antipsychotics Antispasmodics

14 Serotonin Syndrome Similar to anticholinergic syndrome Agitation
loss of consciousness: uncommon sweating and tremor: common Agitation Delirium Hypertonia / myoclonus Tachycardia Tachypnoea

15 Common Causes SSRIs MAOIs (Hyperpyrexia / Hypertensive crisis)

16 Cholinergic Brady/tachycardia Confusion/reduced GCS Pinpoint pupils
Seizures Weakness SLUDGE Pulmonary oedema

17 SLUDGE S sweating salivation L lacrymation U urinary frequency urgency
D diarrhoea G gastrointestinal discomfort E eyes pinpoint

18

19 Common causes Organophosphates Physostigmine Some mushrooms
Nerve agents

20 Salicylism: Aspirin Impaired hearing Tinnitus Sweating Warm skin
Hyperventilation Cinchonism: Quinine (salicylism + blindness)

21 MANAGEMENT

22 Management Overview A B C D DEFG Supportive care (O2, IV Fluids)
History & assessment of vital signs ANY concerns: move patient to RESUS A B C D DEFG Supportive care (O2, IV Fluids) Prevent absorption Increase elimination Antidotes PSYCHOLOGICAL ASSESSMENT

23 History What? When? How much? (mg/kg) What else? Why?

24 Collateral history Paramedics Family / friends Notes
Look in pockets – carefully!!!

25

26 Detective work BNF Toxbase Tablet identification aids: TICTAC
Poisons advice: NPIS Plant identification books National teratology information service

27

28

29 Initial examination Treat problems as you find them!! Airway Breathing
Circulation Disability – GCS/AVPU and Pupils DON’T EVER FORGET GLUCOSE

30 Observations Saturations and respiratory rate Pulse and blood pressure
GCS Pupils Temperature GLUCOSE

31 Investigations All Patients As indicated Urine toxicology screen
Glucose U&E Paracetamol & Salicylate As indicated LFT Co-ag / INR CK ABG / VBG ECG CXR Urine toxicology screen

32 Reduce absorption Emesis – No role Activated charcoal within 1 hour
Gastric lavage – rarely Whole bowel irrigation - rarely

33 Increase elimination Urinary alkalinisation
Multi-dose Activated Charcoal Haemodialysis Haemoperfusion Plasma exchange Forced alkaline diuresis (no longer recommended)

34 Paracetamol Very common: 40% poisons admissions Often asymptomatic
Can be lethal – deaths/year Check blood level at 4 hours Two treatment lines normal and high risk Given IV N-acetylcysteine

35 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

36 Prescott Nomogram

37 High Risk Increased oxidation Reduces glutathione stores
Chronic alcohol use Drugs Reduces glutathione stores Malnutrition Eating disorders Chronic liver disease

38 N-acetylcysteine 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

39 To treat or not to treat?

40 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

41 No need to treat Patient is not high risk
Level at 4 hours is below even the high risk line

42 Patient 2 70 year old man Takes 20 paracetamol 6 hours before presenting Alcoholic No drug history Blood level 100mg/l

43 Treat Patient is high risk Level is above the high risk line
Delayed presentation means need to act fast

44 Patient 3 17 year old epileptic
25 codydramol 2 hours before attendance Taking carbamazepine Blood level at 4 hours is 120mg/l

45 Treat High risk patient Level above the high risk line

46 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

47 Treat 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

48 PARACETAMOL DEADLY PITFALLS The Prescott Nomogram High Risk Line
Staggered Overdoses Management of late presentation Recheck U&E, LFT, INR after N-acetylcysteine

49 Tricyclics Antidepressants Dangerous: US 60-70% fatal ODs
UK commonest fatal OD per prescription 10% unconscious patient will fit Treat fits with diazepam/lorazepam

50 Tricyclic effects Anticholinergic toxidrome The 3 C’s Coma Convulsion
Cardiac

51 Tricyclics cardiac effects
Quinidine effects lead to arrhythmias ECG 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

52 Tricyclics ABG Hypoxaemia Metabolic acidosis Respiratory acidosis

53 Tricyclics Management: EARLY ITU REFERRAL SODIUM BICARBONATE
If hypotension resistant to fluid challenge Dysrhythmias Convulsions Consider IV Magnesium for resistant dysrhythmia

54 Salicylate Salicylism Dehydration Confusion /coma Seizures
Haemetemesis Hypoglycaemia

55 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

56 Salicylate Severity of ingested dose: >150 mg/kg: mild
>250 mg/kg: moderate >500 mg/kg: severe

57 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

58 Salicylate management
<350mg/L: oral fluids >350mg/L: urinary alkalinisation >700mg/L: haemodialysis DISCUSS WITH NPIS

59 Salicylate DEADLY PITFALL
Salicylate levels can continue to rise following admission (10% of cases) Repeat levels every until peaked

60 Opiates 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

61 Antidotes Opiates – naloxone Paracetamol – acetylcysteine/methionine
Beta-blockers – glucagon Insulin – glucose Iron – desferrioxamine Carbon monoxide – oxygen Methanol - ethanol (Benzodiazepines – flumazenil)

62

63 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

64 What next? A – Give naloxone B – Check airway C – Take history
D – Give flumazenil

65 Check airway Check airway patent Give oxygen Call for senior help
Check glucose Give naloxone IM and IV

66 Scenario 2 30 year old woman Taken some white tablets 4 hours earlier
Feels completely well Felt depressed after argument with partner Usually fit and well

67

68 What next? A – Start N-Acetylcysteine
B – Discharge as she is obviously well C – Find out what the tablets are D –Take blood for paracetamol levels

69 Take bloods Early treatment is essential in paracetamol overdose
Need to know what her levels are as soon as possible

70

71 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

72 Lion fish

73 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!

74 Toxbase 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

75 Summary Common Approach using: A B C D DEFG Consider the toxidromes
Early senior help / Early ITU referral Supportive Care Antidotes Psychological assessment

76 Questions ?


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