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Dr Chris Cresswell
FACEM
Whanganui
New Zealand
The Bible
 TOXINZ.com
General approach
Resuscitate if needed
Risk assessment – is what they have taken dangerous?
Supportive Care and Monitoring
 depending on your risk assessment
Investigations
 Everyone:
 Paracetamol level
 ECG
 Other as indicated
Decontamination – very rare
Antidotes
Enhanced elimination - rare
Seek and treat complications
Disposition – usually psych. Psych does the psych risk assessment for
us.
Toxinology
Critters rather than drugs/chemicals
We have one rare annoying, non-life threatening
spider in NZ.
Katipo = red back – painful bite and sweating +/-
back pain -> analgesia + antivenom.
Controversial whether antivenom actually works.
Toxicology
Drugs and chemicals
Not going to cover them all!
Toxidrome
What’s a toxidrome?
What are some examples?
Toxidrome
Clinical toxicological syndrome
ie you can examine a patient +/- look at their ECG or
other bedside tests and get a good idea of what they
have taken
Eg
Opioid
Anticholinergic
Cholinergic syndrome
Serotonin syndrome
Na channel blockade
Toxidromes
Opioid: resp depression, decr LOC, miosis
Anticholinergic: hot as a hare, mad as a hatter, red as a beet,
dry as a bone eg datura
Cholinergic syndrome eg organophosphate, nerve gas
 SLUDGEM: salivation, lacrimation, urinarination,
diarrhoea, GI upset, emesis, miosis + muscle spasm
 Or DUMBELLS: diarrhoea, urination, miosis/muscle
weakness, bronchorrhoea/bradycardia, emesis,
lacrimation, salivation/sweating
Serotonin syndrome eg SSRI: sweating, agitation, increase
muscle tone, fever
Na channel blockade eg tricyclic: hypotension, decr LOC,
widened QRS
Rapidly alternating apnoea and coma eg GHB
Tox exam
HR
RR
Pupil size and reactivity and look for nystagmus
Armpits for sweat
Reflexes and test for clonus
Temp
ECG
BSL
Labs: almost everyone gets a paracetamol level
 Cheap test. Treatment very efficacious.
Some specific drugs / chemicals
Common or important ones.
Paracetamol/acetominphen
NB different units from UK
Common
Almost always reversible with antidote
High survival even from liver failure
How to you risk stratify and treat these ingestions?
What is the antidote?
Paracetamol/Acetominophen
 Most common scenario: single ingestion, reasonable idea of time.
 < 10g or 200mg/kg ingested within 8 hours does not need investigation
 Otherwise or unknown:
 < 2 hours post ingestion of non-liquid and cooperative patient ->
single dose activated charcoal.
 < 4 hours post ingestion: wait and take blood for paracetamol level at
4 hours post ingestion. N-acetylcysteine (NAC) if over 1000µmol/L.
 4-8 hours. Take level. NAC if over threshold on nomogram.
 8-24 hours. Take level and start NAC. Stop treatment if under
treatment threshold.
 24+ hours or unknown. Take level, VBG, LFT, glucose, INR, renal
function. Start NAC. Stop NAC if ALT normal. If liver failure d/w
liver unit
Paracetamol
Multiple doses
Look it up
NAC
N-acetylcysteine
Very safe and effective
Boxes in ED with dose schedule written on them
3 different rates over 24 hours
Fairly frequent anaphylactoid reaction
Eg erythema, urticaria, pruritis, hypotension
Thought to be from histamine release rather than true
anaphylaxis
If mild reaction half rate +/- give IV antihistamine
If severe reaction. Stop infusion. Give IV antihistamine +/-
bronchodilators, fluids etc. Once asymptomatic for 1 hour
restart infusion at ¼ rate and titrate up
Disposition
In this hospital all patients requiring NAC get
admitted to ward under medical team.
Inform psych of admission. They say they will see
patient before “medically cleared”
SSRIs
What do you need to know about these?
SSRIs
Usually no significant toxicity
Main risk is serotonin syndrome
What is serotonin sydrome?
Serotonin Syndrome
Rare
Excess serotonin usually from over dose of SSRI or
combination of serotonergic agents
Eg
SSRI, St John’s wort
Antipsychotics
Lithium
Pethidine
Tramadol
LSD
Ecstacy and other amphetamines
Serotonin Syndrome
Serotonergic drug +
Mild: Tremor, anxiety, nausea
Moderate: agitation and hyperreflexia and clonus
Severe: severe: fever, seizures, respiratory failure,
rhabdomyolysis, renal failure, DIC
Serotonin syndrome
Management
Mild: observe for 4-6 hours
Moderate: IV fluids, benzodiazepine, +/-
cyproheptadine
Severe: cooling, IV benzodiazepine, IV fluid. May need
RSI
So for all overdoses of serotonergic
agent need ...
Record
Temperature
Tone
Reflexes
Clonus
CCB and Beta Blocker
Cause ?
CCB or Beta Blocker
Hypotension and bradycardia
Most beta blockers fairly benign
Exception: propranolol: Na channel blocking effect:
manage as for tricyclic + Beta blocker
Calcium channel blockers: nasty
Treatment?
Beta blocker + CCB
Resuscitate if required: ABCs
Risk assessment: look up to see how toxic the dose could be.
Supportive care and monitoring: if moderate risk: resus bay, IV
access, cardiac monitoring, IV fluids, trial of atropine, calcium
gluconate, pressors eg dopamine. If high risk likely to need
intubation
Investigations: ECG, paracetamol level, lactate, glucose.
Decontamination: Whole bowel irrigation likely to be needed
eg Polyethylene glycol via NG tube
Beta blocker + CCB
Antidote/specific treatments: could call calcium an
antidote to CCB, glucagon 5mg IV, high dose insulin 1
unit/kg then 1unit/kg/hour
Enhanced elimination: dialysis ineffective. Multidose
activated charcoal may be effective for CCB.
Seek and treat complications: Likely to need ICU
care. Monitor for MOF, rhabdo etc
If all of the above wasn’t working what else could be
done?
Intraarterial balloon pump
Bypass/ECMO
Most life threatening drug ingestions cause
temporary CVS collapse – if we can support them
through this the patient should do well
Sulphonylureas
Life threatening
Antidote?
Sulphonylureas
Antidote: IV glucose then IV octreotide
Iron
What’s important about iron
What’s the antidote
Iron
Can be life threatening and yet the patient is
asymptomatic, or has recovered
Look it up
Most accidental ingestions not harmful
Over a threshold ingestion -> iron levels useful
Low threshold for whole bowel irrigation
Antidote: desferoxamine
Digoxin
What are the 2 main types of toxicity?
What are the classic signs and symptoms?
What is the antidote?
Digoxin
2 main types of toxicity:
 Acute ingestion – rare
 Chronic – usually due to dehydration/renal impairment
 Consider this in any patient on digoxin who is unwell. Check ECG, K+ and
digoxin level
Classic signs and symptoms
 Yellowed vision
 Nausea and vomiting
 Confusion
 Cardiac automaticity (ectopics or tachyarrythmia) and block
What is the antidote?
 Digoxin FAB fragments – “digibind”
 Expensive but cost effective
Indications for Digoxin FAB
Hemodynamically unstable or life-threatening
dysrhythmia,
Hyperkalemia > 6 mmol/L (6 mEq/L)
Plasma digoxin level > 20 nmol/L (15.6 ng/mL) at 6
hours post-ingestion
Digoxin level > 10 nmol/L (7.8 ng/mL) or elevated
digoxin level + renal impairment + symptoms in
chronic toxicity
Local anaesthetic
Eg femoral nerve block -> intraarterial
Classic signs?
Local anaesthetic
Perioral tingling
Others:
Visual disturbance
Seizure
VT
Antidote?
Local anaesthetic
Intralipid
? Lipid sink
? Cardiac fuel
Tricyclic / propranalol
Na channel blockade
Nasty
Hypotension
Decr LOC
Seizure
Dysrhythmias
Antidote?
Na channel blockade
"Prompt intubation, hyperventilation and
administration of administration of sodium
bicarbonate at the first evidence of severe toxicity is
life-saving"
Na channel blockade from TCA
Blue apnoeic patient dumped at the front door.
He has pin point pupils
How will you manage this patient?
IV opioid toxicity
Lots of techniques
BVM ventilate
400mcg IM naloxone
200mcg IN naloxone
Oral opioid toxicity
If significant respiratory/LOC depression usually
require naloxone infusion
Titrate IV nalaxone boluses to get just adequate
reversal – don’t make the patient withdraw and run
Infusion of 2/3 of reversal dose/hour
Rare but nasty
Theophylline -> vomiting +++ -> needs urgent
dialysis
Ethylene glycol
Neuroleptic Malignant Syndrome
What is it?
What do you do about it?
Neuroleptic malignant syndrome
Rare
Usually an idiosyncratic reaction to standard/high
doses of antispychotic rather than a result of
overdosage.
Life threatening
“Malignant Parkinson’s”
Parkinsonism + fever + autonomic instability
Doesn’t have the agitation, hyperreflexia or clonus of
serotonin syndrome
Neuroleptic malignant syndrome
If temp > 39.5 or rigidity compromising ventilation ->
RSI
Cool to 38-39˚
Benzodiazepines
Treat hypoglycaemia
Bromocriptine +/or dantrolene
“My child might have taken some of granny’s
pills”
Try to work out what Granny is on
Default
Blood sugar
BP
ECG
If abnormal or toxidrome: IV line and treat empirically.
If normal: Observe 12 hours. Discharge if BP and BSL
normal
Benzodiazepines
Antidote – when do we use it?
Flumazenil
Antidote to benzos
Almost never used
Only used if we caused the OD
For chronic benzo users or coingestion with a
proconvulsant (eg TCA) flumazenil may cause seizure
Benzos almost never need treatment or intubation
Recovery position, wait for them to wake up
Alcohol
Almost never needs intubation
Recovery position and observe
LOC should improve hourly – if not consider other
diagnosis eg head injury
Activated charcoal
Almost never used
Little proof of efficacy
Has killed people - aspiration
Hydrofluoric acid
Nasty. 2% BSA exposure can kill
Warfarin
Vitamin K and prothrombin complex
(prothrombinex)
Insulin
Glucose + food
Occasionally 10% glucose infusion
CO and cyanide
High flow oxygen then look it up
Cyanide ? Amyl nitrate, Sodium nitrite, sodium
thiosulphate (or dicobalt EDTA where available)
Questions?
Comments?
Suggestions?
chris.cresswell@wdhb.org.nz

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Toxicology pgy 1+2 2013

  • 3. General approach Resuscitate if needed Risk assessment – is what they have taken dangerous? Supportive Care and Monitoring  depending on your risk assessment Investigations  Everyone:  Paracetamol level  ECG  Other as indicated Decontamination – very rare Antidotes Enhanced elimination - rare Seek and treat complications Disposition – usually psych. Psych does the psych risk assessment for us.
  • 4. Toxinology Critters rather than drugs/chemicals We have one rare annoying, non-life threatening spider in NZ. Katipo = red back – painful bite and sweating +/- back pain -> analgesia + antivenom. Controversial whether antivenom actually works.
  • 5. Toxicology Drugs and chemicals Not going to cover them all!
  • 7. Toxidrome Clinical toxicological syndrome ie you can examine a patient +/- look at their ECG or other bedside tests and get a good idea of what they have taken Eg Opioid Anticholinergic Cholinergic syndrome Serotonin syndrome Na channel blockade
  • 8. Toxidromes Opioid: resp depression, decr LOC, miosis Anticholinergic: hot as a hare, mad as a hatter, red as a beet, dry as a bone eg datura Cholinergic syndrome eg organophosphate, nerve gas  SLUDGEM: salivation, lacrimation, urinarination, diarrhoea, GI upset, emesis, miosis + muscle spasm  Or DUMBELLS: diarrhoea, urination, miosis/muscle weakness, bronchorrhoea/bradycardia, emesis, lacrimation, salivation/sweating Serotonin syndrome eg SSRI: sweating, agitation, increase muscle tone, fever Na channel blockade eg tricyclic: hypotension, decr LOC, widened QRS Rapidly alternating apnoea and coma eg GHB
  • 9. Tox exam HR RR Pupil size and reactivity and look for nystagmus Armpits for sweat Reflexes and test for clonus Temp ECG BSL Labs: almost everyone gets a paracetamol level  Cheap test. Treatment very efficacious.
  • 10. Some specific drugs / chemicals Common or important ones.
  • 11. Paracetamol/acetominphen NB different units from UK Common Almost always reversible with antidote High survival even from liver failure How to you risk stratify and treat these ingestions? What is the antidote?
  • 12. Paracetamol/Acetominophen  Most common scenario: single ingestion, reasonable idea of time.  < 10g or 200mg/kg ingested within 8 hours does not need investigation  Otherwise or unknown:  < 2 hours post ingestion of non-liquid and cooperative patient -> single dose activated charcoal.  < 4 hours post ingestion: wait and take blood for paracetamol level at 4 hours post ingestion. N-acetylcysteine (NAC) if over 1000µmol/L.  4-8 hours. Take level. NAC if over threshold on nomogram.  8-24 hours. Take level and start NAC. Stop treatment if under treatment threshold.  24+ hours or unknown. Take level, VBG, LFT, glucose, INR, renal function. Start NAC. Stop NAC if ALT normal. If liver failure d/w liver unit
  • 14.
  • 16. NAC N-acetylcysteine Very safe and effective Boxes in ED with dose schedule written on them 3 different rates over 24 hours Fairly frequent anaphylactoid reaction Eg erythema, urticaria, pruritis, hypotension Thought to be from histamine release rather than true anaphylaxis If mild reaction half rate +/- give IV antihistamine If severe reaction. Stop infusion. Give IV antihistamine +/- bronchodilators, fluids etc. Once asymptomatic for 1 hour restart infusion at ¼ rate and titrate up
  • 17. Disposition In this hospital all patients requiring NAC get admitted to ward under medical team. Inform psych of admission. They say they will see patient before “medically cleared”
  • 18. SSRIs What do you need to know about these?
  • 19. SSRIs Usually no significant toxicity Main risk is serotonin syndrome What is serotonin sydrome?
  • 20. Serotonin Syndrome Rare Excess serotonin usually from over dose of SSRI or combination of serotonergic agents Eg SSRI, St John’s wort Antipsychotics Lithium Pethidine Tramadol LSD Ecstacy and other amphetamines
  • 21. Serotonin Syndrome Serotonergic drug + Mild: Tremor, anxiety, nausea Moderate: agitation and hyperreflexia and clonus Severe: severe: fever, seizures, respiratory failure, rhabdomyolysis, renal failure, DIC
  • 22. Serotonin syndrome Management Mild: observe for 4-6 hours Moderate: IV fluids, benzodiazepine, +/- cyproheptadine Severe: cooling, IV benzodiazepine, IV fluid. May need RSI
  • 23. So for all overdoses of serotonergic agent need ... Record Temperature Tone Reflexes Clonus
  • 24. CCB and Beta Blocker Cause ?
  • 25. CCB or Beta Blocker Hypotension and bradycardia Most beta blockers fairly benign Exception: propranolol: Na channel blocking effect: manage as for tricyclic + Beta blocker Calcium channel blockers: nasty Treatment?
  • 26. Beta blocker + CCB Resuscitate if required: ABCs Risk assessment: look up to see how toxic the dose could be. Supportive care and monitoring: if moderate risk: resus bay, IV access, cardiac monitoring, IV fluids, trial of atropine, calcium gluconate, pressors eg dopamine. If high risk likely to need intubation Investigations: ECG, paracetamol level, lactate, glucose. Decontamination: Whole bowel irrigation likely to be needed eg Polyethylene glycol via NG tube
  • 27. Beta blocker + CCB Antidote/specific treatments: could call calcium an antidote to CCB, glucagon 5mg IV, high dose insulin 1 unit/kg then 1unit/kg/hour Enhanced elimination: dialysis ineffective. Multidose activated charcoal may be effective for CCB. Seek and treat complications: Likely to need ICU care. Monitor for MOF, rhabdo etc
  • 28. If all of the above wasn’t working what else could be done?
  • 29. Intraarterial balloon pump Bypass/ECMO Most life threatening drug ingestions cause temporary CVS collapse – if we can support them through this the patient should do well
  • 32. Iron What’s important about iron What’s the antidote
  • 33. Iron Can be life threatening and yet the patient is asymptomatic, or has recovered Look it up Most accidental ingestions not harmful Over a threshold ingestion -> iron levels useful Low threshold for whole bowel irrigation Antidote: desferoxamine
  • 34. Digoxin What are the 2 main types of toxicity? What are the classic signs and symptoms? What is the antidote?
  • 35. Digoxin 2 main types of toxicity:  Acute ingestion – rare  Chronic – usually due to dehydration/renal impairment  Consider this in any patient on digoxin who is unwell. Check ECG, K+ and digoxin level Classic signs and symptoms  Yellowed vision  Nausea and vomiting  Confusion  Cardiac automaticity (ectopics or tachyarrythmia) and block What is the antidote?  Digoxin FAB fragments – “digibind”  Expensive but cost effective
  • 36. Indications for Digoxin FAB Hemodynamically unstable or life-threatening dysrhythmia, Hyperkalemia > 6 mmol/L (6 mEq/L) Plasma digoxin level > 20 nmol/L (15.6 ng/mL) at 6 hours post-ingestion Digoxin level > 10 nmol/L (7.8 ng/mL) or elevated digoxin level + renal impairment + symptoms in chronic toxicity
  • 37. Local anaesthetic Eg femoral nerve block -> intraarterial Classic signs?
  • 38. Local anaesthetic Perioral tingling Others: Visual disturbance Seizure VT Antidote?
  • 40. Tricyclic / propranalol Na channel blockade Nasty Hypotension Decr LOC Seizure Dysrhythmias Antidote?
  • 41. Na channel blockade "Prompt intubation, hyperventilation and administration of administration of sodium bicarbonate at the first evidence of severe toxicity is life-saving"
  • 43. Blue apnoeic patient dumped at the front door. He has pin point pupils How will you manage this patient?
  • 44. IV opioid toxicity Lots of techniques BVM ventilate 400mcg IM naloxone 200mcg IN naloxone
  • 45. Oral opioid toxicity If significant respiratory/LOC depression usually require naloxone infusion Titrate IV nalaxone boluses to get just adequate reversal – don’t make the patient withdraw and run Infusion of 2/3 of reversal dose/hour
  • 46. Rare but nasty Theophylline -> vomiting +++ -> needs urgent dialysis Ethylene glycol
  • 47. Neuroleptic Malignant Syndrome What is it? What do you do about it?
  • 48. Neuroleptic malignant syndrome Rare Usually an idiosyncratic reaction to standard/high doses of antispychotic rather than a result of overdosage. Life threatening “Malignant Parkinson’s” Parkinsonism + fever + autonomic instability Doesn’t have the agitation, hyperreflexia or clonus of serotonin syndrome
  • 49. Neuroleptic malignant syndrome If temp > 39.5 or rigidity compromising ventilation -> RSI Cool to 38-39˚ Benzodiazepines Treat hypoglycaemia Bromocriptine +/or dantrolene
  • 50. “My child might have taken some of granny’s pills” Try to work out what Granny is on Default Blood sugar BP ECG If abnormal or toxidrome: IV line and treat empirically. If normal: Observe 12 hours. Discharge if BP and BSL normal
  • 52. Flumazenil Antidote to benzos Almost never used Only used if we caused the OD For chronic benzo users or coingestion with a proconvulsant (eg TCA) flumazenil may cause seizure Benzos almost never need treatment or intubation Recovery position, wait for them to wake up
  • 53. Alcohol Almost never needs intubation Recovery position and observe LOC should improve hourly – if not consider other diagnosis eg head injury
  • 54. Activated charcoal Almost never used Little proof of efficacy Has killed people - aspiration
  • 55. Hydrofluoric acid Nasty. 2% BSA exposure can kill
  • 56. Warfarin Vitamin K and prothrombin complex (prothrombinex)
  • 57.
  • 59. CO and cyanide High flow oxygen then look it up Cyanide ? Amyl nitrate, Sodium nitrite, sodium thiosulphate (or dicobalt EDTA where available)