Toxicology pgy 1+2 2013


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Toxicology pgy 1+2 2013

  1. 1. Dr Chris CresswellFACEMWhanganuiNew Zealand
  2. 2. The Bible
  3. 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 forus.
  4. 4. ToxinologyCritters rather than drugs/chemicalsWe have one rare annoying, non-life threateningspider in NZ.Katipo = red back – painful bite and sweating +/-back pain -> analgesia + antivenom.Controversial whether antivenom actually works.
  5. 5. ToxicologyDrugs and chemicalsNot going to cover them all!
  6. 6. ToxidromeWhat’s a toxidrome?What are some examples?
  7. 7. ToxidromeClinical toxicological syndromeie you can examine a patient +/- look at their ECG orother bedside tests and get a good idea of what theyhave takenEgOpioidAnticholinergicCholinergic syndromeSerotonin syndromeNa channel blockade
  8. 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/muscleweakness, bronchorrhoea/bradycardia, emesis,lacrimation, salivation/sweatingSerotonin syndrome eg SSRI: sweating, agitation, increasemuscle tone, feverNa channel blockade eg tricyclic: hypotension, decr LOC,widened QRSRapidly alternating apnoea and coma eg GHB
  9. 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. 10. Some specific drugs / chemicalsCommon or important ones.
  11. 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. 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 at4 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 undertreatment threshold. 24+ hours or unknown. Take level, VBG, LFT, glucose, INR, renalfunction. Start NAC. Stop NAC if ALT normal. If liver failure d/wliver unit
  13. 13. Paracetamol
  14. 14. Multiple dosesLook it up
  15. 15. 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 trueanaphylaxisIf mild reaction half rate +/- give IV antihistamineIf severe reaction. Stop infusion. Give IV antihistamine +/-bronchodilators, fluids etc. Once asymptomatic for 1 hourrestart infusion at ¼ rate and titrate up
  16. 16. DispositionIn this hospital all patients requiring NAC getadmitted to ward under medical team.Inform psych of admission. They say they will seepatient before “medically cleared”
  17. 17. SSRIsWhat do you need to know about these?
  18. 18. SSRIsUsually no significant toxicityMain risk is serotonin syndromeWhat is serotonin sydrome?
  19. 19. Serotonin SyndromeRareExcess serotonin usually from over dose of SSRI orcombination of serotonergic agentsEgSSRI, St John’s wortAntipsychoticsLithiumPethidineTramadolLSDEcstacy and other amphetamines
  20. 20. Serotonin SyndromeSerotonergic drug +Mild: Tremor, anxiety, nauseaModerate: agitation and hyperreflexia and clonusSevere: severe: fever, seizures, respiratory failure,rhabdomyolysis, renal failure, DIC
  21. 21. Serotonin syndromeManagementMild: observe for 4-6 hoursModerate: IV fluids, benzodiazepine, +/-cyproheptadineSevere: cooling, IV benzodiazepine, IV fluid. May needRSI
  22. 22. So for all overdoses of serotonergicagent need ...RecordTemperatureToneReflexesClonus
  23. 23. CCB and Beta BlockerCause ?
  24. 24. 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?
  25. 25. 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, IVaccess, cardiac monitoring, IV fluids, trial of atropine, calciumgluconate, pressors eg dopamine. If high risk likely to needintubationInvestigations: ECG, paracetamol level, lactate, glucose.Decontamination: Whole bowel irrigation likely to be neededeg Polyethylene glycol via NG tube
  26. 26. Beta blocker + CCBAntidote/specific treatments: could call calcium anantidote to CCB, glucagon 5mg IV, high dose insulin 1unit/kg then 1unit/kg/hourEnhanced elimination: dialysis ineffective. Multidoseactivated charcoal may be effective for CCB.Seek and treat complications: Likely to need ICUcare. Monitor for MOF, rhabdo etc
  27. 27. If all of the above wasn’t working what else could bedone?
  28. 28. Intraarterial balloon pumpBypass/ECMOMost life threatening drug ingestions causetemporary CVS collapse – if we can support themthrough this the patient should do well
  29. 29. SulphonylureasLife threateningAntidote?
  30. 30. SulphonylureasAntidote: IV glucose then IV octreotide
  31. 31. IronWhat’s important about ironWhat’s the antidote
  32. 32. IronCan be life threatening and yet the patient isasymptomatic, 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
  33. 33. DigoxinWhat are the 2 main types of toxicity?What are the classic signs and symptoms?What is the antidote?
  34. 34. 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+ anddigoxin 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
  35. 35. Indications for Digoxin FABHemodynamically unstable or life-threateningdysrhythmia,Hyperkalemia > 6 mmol/L (6 mEq/L)Plasma digoxin level > 20 nmol/L (15.6 ng/mL) at 6hours post-ingestionDigoxin level > 10 nmol/L (7.8 ng/mL) or elevateddigoxin level + renal impairment + symptoms inchronic toxicity
  36. 36. Local anaestheticEg femoral nerve block -> intraarterialClassic signs?
  37. 37. Local anaestheticPerioral tinglingOthers:Visual disturbanceSeizureVTAntidote?
  38. 38. Local anaestheticIntralipid? Lipid sink? Cardiac fuel
  39. 39. Tricyclic / propranalolNa channel blockadeNastyHypotensionDecr LOCSeizureDysrhythmiasAntidote?
  40. 40. Na channel blockade"Prompt intubation, hyperventilation andadministration of administration of sodiumbicarbonate at the first evidence of severe toxicity islife-saving"
  41. 41. Na channel blockade from TCA
  42. 42. Blue apnoeic patient dumped at the front door.He has pin point pupilsHow will you manage this patient?
  43. 43. IV opioid toxicityLots of techniquesBVM ventilate400mcg IM naloxone200mcg IN naloxone
  44. 44. Oral opioid toxicityIf significant respiratory/LOC depression usuallyrequire naloxone infusionTitrate IV nalaxone boluses to get just adequatereversal – don’t make the patient withdraw and runInfusion of 2/3 of reversal dose/hour
  45. 45. Rare but nastyTheophylline -> vomiting +++ -> needs urgentdialysisEthylene glycol
  46. 46. Neuroleptic Malignant SyndromeWhat is it?What do you do about it?
  47. 47. Neuroleptic malignant syndromeRareUsually an idiosyncratic reaction to standard/highdoses of antispychotic rather than a result ofoverdosage.Life threatening“Malignant Parkinson’s”Parkinsonism + fever + autonomic instabilityDoesn’t have the agitation, hyperreflexia or clonus ofserotonin syndrome
  48. 48. Neuroleptic malignant syndromeIf temp > 39.5 or rigidity compromising ventilation ->RSICool to 38-39˚BenzodiazepinesTreat hypoglycaemiaBromocriptine +/or dantrolene
  49. 49. “My child might have taken some of granny’spills”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 BSLnormal
  50. 50. BenzodiazepinesAntidote – when do we use it?
  51. 51. FlumazenilAntidote to benzosAlmost never usedOnly used if we caused the ODFor chronic benzo users or coingestion with aproconvulsant (eg TCA) flumazenil may cause seizureBenzos almost never need treatment or intubationRecovery position, wait for them to wake up
  52. 52. AlcoholAlmost never needs intubationRecovery position and observeLOC should improve hourly – if not consider otherdiagnosis eg head injury
  53. 53. Activated charcoalAlmost never usedLittle proof of efficacyHas killed people - aspiration
  54. 54. Hydrofluoric acidNasty. 2% BSA exposure can kill
  55. 55. WarfarinVitamin K and prothrombin complex(prothrombinex)
  56. 56. InsulinGlucose + foodOccasionally 10% glucose infusion
  57. 57. CO and cyanideHigh flow oxygen then look it upCyanide ? Amyl nitrate, Sodium nitrite, sodiumthiosulphate (or dicobalt EDTA where available)
  58. 58. Questions?Comments?Suggestions?