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Overdose Approach, Assessment and Management

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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:

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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:

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

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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

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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

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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

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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+

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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 (


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