1. Overdose Approach, Assessment and Management
Dr. Kirsty Dunn
FACEM
Emergency Department
Ballarat Health Services

2. Key Issues Heterogenous clinical presentation
Myriad toxins – ingestion, exposure
Risk assessment knows pt weight (?) and co-morbidities (?)
Dynamic medical illness (some anticipated clinical decline)
Tailored Mx plan for individual patient
Conventional resuscitation methods may not apply
GCS 12 vs 8 for ETT

3. Approach “RESUS RSI DEAD”
Typically management simultaneous with assessment. Coal face – no past medical history, limited drug history, reliant on bystanders/ ambulance officers / old notes.

4. Assessment Criticality Aetiology Impact on underlying comorbidities
Most likely
Most fatal
Impact on underlying comorbidities
Rule out non-accidental injury.
History
Examination
Investigations
Bedside
Labs
Imaging
Specialist

5. Management Resuscitate Specific Supportive Referral Disposition
RESUS RSI DEAD
Resuscitate + Antidote
Risk assess
Supportive care + monitoring
Investigations
Decontaminate
Enhance elimination
Disposition
Resuscitate
Specific
Supportive
Referral
Disposition
Education

6. RESUS RSI DEAD ABC…. DEFG Seek and treat Emergency antidote
hypoglycaemia
Seizures
Hypo/erthermia
Emergency antidote
Screening ECG
Bloods
Levels
ABG
glucose
alcohols, antiepileptics, paracetamol, salicylates, digoxin, lithium, methotrexate, iron

7. ABC’s in toxicology A – corrosive injury B – hyperV (acidosis) hypoV
Alkalis, acids, paraquat
B – hyperV (acidosis)
Salicylates, toxic alcohols
hypoV
Opiates, benzodiazepines
Increased secretions
Organophosphates, nerve agents, carbamates
Hypoxia w acidosis and MOFailure
Paraquat
imminent compromise so early ETT or surgical airway
avoid normoV iff ETT need to resp compensate with inc tidal vol. Soda bic 1-2 mmol/kg
naloxone 200mcg im, slow 200mcg iv titrate
NB do not give flumazenil (unless iatrogenic w nil PMH)
1 mouthful fatal - herbicide
Oxygen therapy injurious - aim SpO2 90 (PaO2 60)
Huge dose atropine - 1.2mg iv doubling every 3/60 titrate to drying secretions

8. ABC’s in toxicology C – VF VT Do ABG seeking hypocalcaemia
Systemic flurosis in hydrofluric acid vapourisation
(glass etching, chrome cleaning – mechanics) VT
Seek TCA o/d
Seek the Ia,c and III drugs (cocaine, lignocaine, flecainide, PROPRANOLOL, quinine
V ectopics
high dose iv calcium GLUCONATE (not chloride) not the usual "10ml 10% 10 mins" but 90ml 10% stat repeating every TWO mins with attempts at defibrillation
ammiodarone contraindicated (further prolongs blocks as cardiac domestos)
don't a/w VBG prior to sodabic 50mmol, intubate, hyperV, sodabic 50mmol.
immigrants
Bblock

9. ABC’s in Toxicology continued
C – refractory hypotension
Bblocker, CaCh blocker, local anaesthetics
Refractory hypertension / tachycardia
Amphetamines, cocaine, serotonin syndrome
Asystole
Digoxin
D – refractory seizure
Seek TCA w long QRS. Risk stratify for isoniazid (immigrant, Tb)
HIET, intralipid
benzo's+++, cyproheptadine. do not give BBlockers (unopposed alpha with ICH)
digibind . 5 vials and repeat
Calcium Chloride contraindicated despite looking like hyperkalaemia
benzo's, phenobarbitone, pyridoxine residue 1Giv.

10. ABC’s in toxicology E – febrile G – hypoglycaemia Hyperglycaemia
Serotonin syndrome, neuroleptic malignant syndrome, (malignant hyperthermia)
G – hypoglycaemia
Gliclazide, insulin, Bblockers
Hyperglycaemia
Salicylates (CNS gluc zero)
benzo's +++, cyproheptadine 4mg NG or PO 4/24, cease offending agents, active cooling, seek rhabdo.
octreotide

11. Risk assessment Agent (s) Dose Time ingested Time lapsed
Clinical features and course
Patient factors (Wt, liver and renal F, anorexia, cardiac)

12. Toxic Drug Levels Paracetamol >200mg/kg Iron 60mg/kg elemental iron
Colchicine >500mg/kg
Digoxin > 4mg (16 x 250 mic tabs)
Warfarin or rat sac >1 sachet
Aspirin >300mg / kg
Paeds 1 pill (CCB, BB, amphetamines, TCA, propranolol, gliclazide, opioids)

13. Decontamination PROS Improved morb / mortality
More benign clinical course
Reduce need for hazardous intervention
Reduce hosp LOS
CONS
Aspiration
GIT obstruction / perf
Distraction from supportive Mx
Resource intense

14. Decontamination Charcoal (“activated”)
steamed wood pulp
to increase surface area for binding
Charcoal (“activated”)
50G adults, 1G/kg kids (mixed w ice cream)
Benefit must outweigh risk (aspirn)
Ci Altered or anticipated drop in GCS / Seizure risk
Safe in pregnancy

15. Poisons Information Hotline
Charcoal
Indications….(*dubious)
Almost everything else
But never really used
Paracetamol (*)
Benzo’s (*)
Barbiturates (*)
TCA’s (*)
Phenothiazines
Anticonvulsants (*)
Aspirin
Theophylline
Digoxin
Amphetamines (*)
Quinine
Blockers
Contraindications
PHAILS
Pesticides
Hydrocarbons
Acids / alkalis / alcohols /arsenic
Iron / lead
Lithium or ionic elements
Solvents
Patient:
unstable,
non-toxic ingestion,
antidote available,
ACS,
will require gastroscopy, bowel obstruction
Poisons Information Hotline

16. Whole bowel irrigation
PEG
Takes 1 nurse 6 hours as sole job
Needs commode and antiemetics (and lots of toilet paper)
When charcoal ineffective and poor prognosis with no antidote and not amenable to purely supportive care
Eg enteric coated or slow release preps.
IRON, slow K, SR CaCh Block, arsenic, lead, body packers.
Poisons Information Hotline

17. Poisons Information Hotline
Elimination
Never carried out to the detriment of resuscitation or antidote.
Multi-dose activated charcoal
Urinary alkalinisation
Haemodialysis / CVVHDF
Charcoal haemoperfusion
Poisons Information Hotline

18. Pearls for Elimination
MDAC causes aspiration, bowel obstruction, corneal abrasions
listen for bowel sounds every 2/24 50g bottle. Takes up to 6 hours.
Urinary alkalinisation
Aim urine pH >7.5
1-2 mmol soda bic / Kg then 100mmol over 4/24. give KCl and monitor K. Stop when tox resolving.

19. Scenarios FACEM Q7
A 46 year old man is brought to your emergency department by ambulance following an overdose of unknown medications. He has had a brief generalized seizure en route.
On arrival his observations are:

22. I-V conduction delay (QRS) ® Terminal R wave aVR >3mm
Broad complex tachy
LAD
I-V conduction delay (QRS) ®
Terminal R wave aVR >3mm
Prolonged QTc >550ms
RSR in V1, slurred upstroke V6
Critical TCA overdose. QRS seizure. QT torsades / VT

23. Management
Mx in resus area, treatment with NaHCo mmol aiming to reduce R wave and shorten QRS. pH 7.55,
Fluid Mx for hypotension and Benzodiazepines for seizures.
Use of RSI to assist is accepted but was felt that in this Stem was secondary to above
Features of unsuccessful answers
Lack of detail & precision or systematic approach to part A
Inadequate management – focus was NaHCo3 is the antidote and 1st line treatment.
No titration or endpoints – to pH 7.55 & QRS , and no detail in doses or utalising cardioversion in Mx

24. Scenario 2 FACEM 2013/1. Q1 Observations:
A 20 year old man is brought to your ED by ambulance after being found collapsed at home following a large polypharmacy drug overdose that included Venlafaxine. He has been intubated and received 500mls of normal saline prior to arrival. The time of ingestion is not known.
Observations:

26. no mans land axis - ventricular origin
capture
broad complex tachycardia, rate 180 bpm
peaked T waves
no mans land axis - ventricular origin

28. FACEM VAQ Exam 2013.1 - Question 6
The overall pass rate for this question was 68/134 (50.7%)
Pass Criteria ECG
Broad complex tachycardia with differential of VT and possible Na channel blockade. May pass if Na blockade not mentioned but management includes appropriate use of NaHCO3
Pass Criteria Treatment
Hyperventilation (patient intubated, key initial therapy) or ventilation strategy to achieve this
Use of NaHCO3 with initial bolus of minimum mmol aiming pH 7.55, narrowing of QRS
DO NOT use amiodarone. Safe to try DC cardioversion however.
Fluid loading with minimum 1 litre stat (in view of initial 500 ml bolus, further min 500ml required though more ideal)

29. Features of Higher level answers
Description of ECG features supporting VT.
Recognition of potential Na Channel blockade/ coingestion (eg TCA).
Recognition that atypical for Venlafaxine.
Consideration of hyperkalaemia
Aggressive management of possible Na channel blockade with alkalinisation
Hyperventilation of intubated patient. pH
NaHCO3 (100mmol or 2 mmol/kg repeated to end points of ECG, cardiovascular stability, pH)
Description of measures to improve BP (fluids + 2nd line of pressors) + endpoints
DCCV likely ineffective. Appropriate to delay until after NaHO3, hyperventilation, fluids.
Recognition of hyperthermia, concern for serotonin syndrome. Sedation with benzodiazepines, probable paralysis, simple cooling measures, core temp. Consideration possible differential for this re other causes (other toxidromes, sepsis, aspiration etc)
Recognition of significant seizure risk due to Venlafaxine with mention of management with benzodiazepines 1st line, and consideration of monitoring implications.
Consideration of co-ingestants, hyperkalaemia, rhabdomyolysis, renal failure etc.

30. Fail criteria
Inappropriate use of anti-arrhythmics. Class I agent use is contraindicated and dangerous (=Fail).
Use of amiodarone is also inappropriate as 1st line = fail if used prior to hyperventilation, NaHCO3, DCCV
Displaying no significant knowledge of the management of an unstable broad complex tachyarrhythmia in a toxicological setting (managing along standard ALS lines with no use of NaHCO3 or hyperventilation).

31. Scenario 3 FACEM Q3
A 77 year old man presents to your emergency department feeling generally unwell for several days. He is noted to have a pulse rate of 36 beats / minute and is normotensive.
Arterial blood gases and serum biochemical tests are performed

34. Describe and Interpret
Life threatening metabolic acidaemia with a HAGMA likely related to Acute on CRF causing life threatening digoxin toxicity requiring urgent antidote and correction of acid base balance and renal supportive therapy.
Expected pCO2 = 1.5x HCo3 +8 = 29
Anion Gap = (Na +K) –(HCO3 +Cl) = 27
Ddx – LTKR or CATMUDPILES
Expected K = 3.5 +[0.1( ) x 0.5] = 4.3
winters formula
carbon monoxide, AKA, toluene, methanol, metformin, uraemia, DKA, paraldehyde [R], iron, isoniazid [seizure], lactate, ethylene glycol, salicylates
can also do Aa gradient, Delta gap, Ur:Cr ratio

35. Outline Management Resus: A/B fine. Allow to hyperV Specific:
Move to resus, full physiological monitoring with a team approach.
Resus: A/B fine. Allow to hyperV
C – gain IVC and commence aggressive rehydration 1 Lstat aiming for UO >1ml/kg/hr
D – do not sedate (avoid resp acidosis)
Specific:
Delegate staff for digibind 2 vials and repeat 15/60 aiming for HR >60
Hyperkalaemia
Ins dext / salbutamol / resonium / Soda bic. FAIL IF USE CALCIUM CHLORIDE
Monitor VBG 30/60, serial ECG’s seeking automaticity and peaked T waves.

36. Outline management Supportive
Renal failure – ivf. Cvvhdf. Monitor fluid balance, K and urea. Cease nephrotoxics.
Glucose – avoid hypoglycaemia (K Rx)
Antiemetics for nausea
Seek cause of ARF--- digoxin tox --N/V
?stroke / myocardial event / infection / change meds

37. Outline management Referral Disposition Education
ICU, renal med, poisons information, and cause initial illness – cardiol / neurol / etc
Disposition
ICU for monitoring, correction of fluid / elec’s/ treating cause
Education
NOK, GP, altering prescription

38. Scenario 4
A 27-year old female presents to ED one hour after swallowing 70 x 40mg propranolol tablets (= 2.8 grams) with suicidal intent.
At the time of assessment she is drowsy (GCS 13) with a heart rate of 46 bpm.
Fifteen minutes earlier she had been awake and able to give a history to paramedics… You need to act fast to save this patient. Are you up to the challenge?
LITFL

40. terminal R wave in aVR >3mm. Sodium channel blockade
RSR in V1 and slurred upstroke V6. broad complex RBBB pattern
1st degree heart block.
prolonged QTc
Basetts formula QTc = QT/square root of the R-R (medcalc.com)
general rate not as anticholinergic as expected in a TCA O/D.
rate = 13 x 6 = 78

42. Propranolol overdose

43. Question for Pharmacy Primary
Describe the toxicokinetics of propranolol.
Absorption: Rapidly absorbed orally. Peak blood levels occur at 1-3 hours following oral administration.
Distribution: Highly lipophilic agent with a wide volume of distribution. Rapidly distributed to all tissues, including CNS.
Protein Binding: Approximately 93% protein bound.
Metabolism: Undergoes extensive hepatic metabolism, with hydroxylation of the aromatic nucleus and degradation of the isoprenaline side-chain. Over 20 metabolites identified. The 4-hydroxy metabolite has active beta-blocking properties.
Elimination: % of an ingested dose is excreted in the urine as metabolites and their conjugates.
Half-life: Plasma half-life is around 3-6 hours. The pharmacological effects last much longer than this. Elimination half-life is 12 hours and may be prolonged following overdose.

44. Question for Pharmacy Primary
Describe the toxicokinetics of propranolol.
Absorption: Rapidly absorbed orally. Peak blood levels occur at 1-3 hours following oral administration.
Distribution: Highly lipophilic agent with a wide volume of distribution. Rapidly distributed to all tissues, including CNS.
Protein Binding: Approximately 93% protein bound.
Metabolism: Undergoes extensive hepatic metabolism, with hydroxylation of the aromatic nucleus and degradation of the isoprenaline side-chain. Over 20 metabolites identified. The 4-hydroxy metabolite has active beta-blocking properties.
Elimination: % of an ingested dose is excreted in the urine as metabolites and their conjugates.
Half-life: Plasma half-life is around 3-6 hours. The pharmacological effects last much longer than this. Elimination half-life is 12 hours and may be prolonged following overdose.

45. Propranolol O/D Behave like TCA but slower ventricular rate
Treated as per TCA
Excess beta-blockade causes:
Hypotension and bradycardia
Bradyarrhythmias, including sinus bradycardia, 1st-3rd degree heart block, junctional or ventricular bradycardia
Bronchospasm
Hyperkalaemia and hypo/hyperglycaemia
Sodium-channel blockade causes:
Cardiotoxicity – QRS widening, ventricular arrhythmias and cardiac arrest
Neurotoxicity – coma, seizures and delirium
Massive propranolol overdose typically presents with coma, seizures, bradycardia and progressive cardiogenic shock.
In TCA O/D anticholinergic effects create tachycardia - relative protection against prolonged QTc and torsades. BUT in propranolol O/D Bblockade means R-on-T a high risk.

46. Beta Blocker O/D
Propranolol and sotalol are really the ones to worry about
Risk Assessment (what,where,when,how)
Prop / sotalol
Underlying cardiac or lung disease
Co-ingested CCB or digoxin
Elderly or children (1 pill can kill)
Even 1G propranolol is severe tox
Anticipate early DECLINE (unless SR sotalol)

47. Toxic Mechanism Inhibit B1 and B2 receptors
Inhibit response to catecholamines
Negative chronotropy, negative inotropy, hypoglycaemia
Sodium channel blockade
Lipid soluble so crosses BBB -seizure, coma, DEATH

48. Propranolol toxicity is associated with QRS widening and a positive R’ wave in aVR (signs of sodium channel blockade), which portend the onset of coma, seizures, hypotension and ventricular arrhythmias.
Sotalol blocks myocardial potassium channels, causing QT prolongation and Torsades de Pointes in overdose.

49. Management BB O/D In resus with INVASIVE monitoring Resus ABC’s
Antidote?

50. Management BB O/D In resus with INVASIVE monitoring Resus ABC’s
Antidote?
SODIUM BICARBONATE

51. Management BB O/D In resus with INVASIVE monitoring Resus ABC’s
Intubate, hyperventilate
Antidote?
SODIUM BICARBONATE
Dose?

52. Management BB O/D In resus with INVASIVE monitoring Resus ABC’s
Intubate, hyperventilate
Antidote?
SODIUM BICARBONATE
Dose?
100mmol IV and repeat 15/60

53. Management BB O/D In resus with INVASIVE monitoring Resus ABC’s
Intubate, hyperventilate
Antidote?
SODIUM BICARBONATE
Dose?
100mmol IV and repeat 15/60
Aims?

54. Management BB O/D In resus with INVASIVE monitoring and… Resus ABC’s
PACING PADS in situ
Resus ABC’s
Intubate, hyperventilate
Antidote?
SODIUM BICARBONATE
Dose?
100mmol IV and repeat 15/60
Aims?
Narrowing QRS, shortening R wave in aVR, pH 7.55

55. Management BB O/D
C – what are the options?

56. Management BB O/D C – what are the options?
Atropine 600mcg iv 2 minutely up to 3mg
Isoprenaline mcg / min
Adrenaline start at 10mcg/min and titrate aiming for BP and secretions
AVOID bradyarrythmia – torsades. ESP sotalol.
Isoprenaline
(magnesium)
Overdrive pacing

57. New Management BB O/D HIET INTRALIPID High Insulin Euglycaemic Therapy
What is it used for??
Propranolol, sotalol and any symptomatic BB O/D with anticipated decline (underlying cardiac or pulm)
CaCh Blocker O/D
INTRALIPID
(100ml iv)

58. HIET How to give HIET… 3 IV lines Monitor K+ 50ml 50% dextrose push
Allows glucose into myocytes eliminating FFacid metabolism
How to give HIET… 3 IV lines
50ml 50% dextrose push
After DXT give massive dose actrapid
1 unit/kg bolus
Infusion of 0.5 un/kg.
If ongoing HD instability can inc infusion to 1 un/kg
50ml 50% dextrose ivi titrated to BSL (hrly)
Monitor K+

60. p waves
nil correlation with atrium and ventricular impulses
rate is 5 x 6 =30bpm

61. Calcium Channel O/D Verapamil and diltiazem the ones to worry about
Risk Ax
Just TWICE the usual dose of v or d can cause tox in susceptible pt (liver F)
ALL taken seriously
10 tabs life threatening adult
1 pill can kill kids

62. Calcium Ch O/D
If altered consc state then due to profound hypoT or a co-ingestant
CCB do not Cross BBB
Cause hyperglycaemia as suppress insulin release
Must keep SR preps 16hrs for observation. Not the usual 4 hour rule.

63. Ix in CCB Screening ECG, paracetamol Cardiac monitor U+E CCa
ABG – lactate (shock),
Glucose (H)
CXR (APO)

64. Mx in CCB
Resus –
Anticipate rapid decline. Calamity of hypotension and brady arrythmia. Need concurrent resus, antidote and decontamination
A – early ETT if risk Assess high risk. Intubate anyone not responding to 20ml/kg IVF
C – Calcium. 20ml 10% 10mins CaChloride (x3 potency Ca gluconate). Aim CCa 2-3 mEq/L

65. PEG
ECMO
Balloon pump

66. Reading list Murray Toxicology Handbook Life in the fast lane EM RAP
Cameron
Resources:
Life in the Fast Lane (