EMCORE 2016...

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Introduction*Welcome*to*EMCORE*2016.*We*have*a*program*for*you*that*is*second*to*none.*The*teaching*is*fast,*to*the*point*and*practical.*This*is*Emergency*Medicine,*the*way*it*should*be.*

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Sit*back,*listen*and*enjoy!*

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The*EMCORE*TEAM*

ADULT*ADVANCED*LIFE*SUPPORT*SUMMARY*OF*CHANGES* Following(the(ILCOR(Consensus(on(Science(and(Treatment(Recommendations((CoSTR)(process(concluding(in(October(2015(a(number(of(ANZCOR(ALS(guidelines(have(been(reviewed(and(revised.(Treatment(recommendations(have(not(changed(unless(there(are(compelling(reasons(to(change(them.(The(ILCOR(systematic(reviews(showed(that(the(quality(of(evidence(for(many(ALS(interventions(is(low(or(very(low,(with(resultant(preKdominantly(weak(recommendations.(For(some(ALS(recommendations,(despite(low(quality(evidence,(AZCOR(has(made(strong(recommendation(consistent(with(ILCOR,(in(particular(when(there(was(consensus(that(not(doing(so(could(lead(to(harm.(

The(main(developments(and(recommendations(in(ALS(in(these(draft(guidelines(are:(

Defibrillation:*

If(the(first(shock(is(not(successful(and(the(defibrillator(is(capable(of(delivering(shocks(of(higher(energy,(it(is(reasonable(to(increase(the(energy(for(subsequent(shocks.(

Airway,*oxygenation,*and*ventilation:*

There(is(equipoise(between(the(choice(of(an(advanced(airway(or(a(bagKmask(device(for(airway(management(during(CPR,(and(the(choice(between(a(supraglottic(airway(or(tracheal(tube(as(the(initial(advanced(airway(during(CPR.(

The(role(of(waveform(capnography(during(ALS(is(further(emphasized,(including(its(use(to(confirm(and(continually(monitor(tracheal(tube(position,(the(quality(of(CPR,(and(to(provide(an(early(indication(of(return(of(spontaneous(circulation.(

Circulatory*support*during*CPR:*

ANZCOR(recommend(against(the(routine(use(of(the(impedence(threshold(device((ITD)(in(addition(to(conventional(CPR(

The(routine(use(of(automated(mechanical(chest(compression(devices(is(not(recommended(but(they(are(suggested(as(a(reasonable(alternative(in(situations(where(sustained(highKquality(manual(chest(compressions(are(not(feasible.(

Extracorporeal(cardiopulmonary(resuscitation(is(suggested(as(a(reasonable(rescue(therapy(for(select(patients(with(cardiac(arrest(when(conventional(CPR(is(failing.((

(

Physiological*monitoring*during*CPR:*

Cardiac(ultrasound(during(resuscitation(is(suggested(as(a(diagnostic(tool(to(identify(reversible(causes.(

Postresuscitation*care:*

Emphasis(is(placed(on(avoiding(hypoxia(and(hyperoxia(in(adults(with(ROSC(after(cardiac(arrest,(while(maintaining(normocarbia.(

ANZCOR(now(recommends(selecting(and(maintaining(a(constant(target(temperature(between(32◦C(and(36◦C(for(those(patients(in(whom(targeted(temperature(management(is(used(following(ROSC.(The(suggested(duration(for(TTM(should(be(at(least(24(hours.(

Fever(in(persistently(comatose(adults(after(completion(of(TTM(should(be(prevented(and(treated.(

Routine(seizure(prophylaxis(in(postKcardiac(arrest(patients(is(not(recommended.(

There(are(increased(suggestions(to(guide(prognostication(in(the(victims(who(remain(comatose(after(ROSC(whether(receiving(or(not(receiving(TTM(postresuscitation(care.(

Patients(who(have(restoration(of(circulation(after(CPR(and(who(subsequently(progress(to(death((by(brain(death(criteria(or(following(circulatory(death)(should(be(evaluated(for(organ(donation.(

There(is(an(excellent(summary(of(changes(booklet(produced(by(the(European(Resuscitation(Council(that(can(be(downloaded(at:(http://www.cprguidelines.eu/assets/downloads/ERC_summary_booklet_HRES.pdf(

I’M$ALLERGIC$TO$OXYGEN$$

Hypoxia(causes(anoxic(brain(injury(whereas(hyperoxia(is(said(to(cause(damage(to(the(brain(and(other(

organs(by(various(mechanisms.(((

(

During$Cardiac$Arrest:$Adults$$The(recommendation(by(the(Resuscitation(Guidelines(is(100%(oxygen(is(to(be(given(here.((This(is(a(

weak(recommendation(with(low(quality(evidence.((We(don’t(really(know(what(we(should(be(doing(

but(we(know(that(the(brain(requires(oxygen(to(function(and(as(the(oxygen(drops(it(causes(coma.((It(

therefore(makes(sense(that(we(should(be(supplying(oxygen(given(that(the(patients(cannot(ventilate(

on(their(own.((There(aren’t(many(studies(here(and(so(it(is(difficult(to(know(exactly(what(to(do.((

Spindelboek((Resuscitation(84;2013:770O775)(looks(at(an(end(point(of(admission(to(hospital(in(those(

patients(with(cardiac(arrest.((Patients(in(this(study(were(allocated(into(three(groups.(

(

1.! Low(oxygen(>60mmHg((

2.! Intermediate(61O300mmHg(

3.! High(>300mmHg(

(

There(were(145(patients(in(this(study(and(it(was(found(that(there(were(no(differences(in(baseline(

characteristics(or(in(CPR(interventions.(

(

There(is(a(linear(increase(in(hospital(admissions(related(to(increased(oxygen(given(to(the(patient.((It(

was(found(that(the(rates(of(hospital(admission(increased(with(more(oxygen(and(this(was(statistically(

significant.((However(there(was(no(direct(reflection(or(statistically(significantly(increases(in(

neurological(outcome.(((

(

Oxygen$and$Neonates$in$Resuscitation$$$Davis(et(al((The(Lancet,(2004)(conducted(a(meta(analysis(looking(at(air(versus(100%(oxygen(in(five(

trials.((No(individual(trial(showed(any(difference(in(mortality,(however(the(pooled(results(showed(a(

significant(benefit(in(infants(resuscitated(with(air.(

(

Mortality:(13%((oxygen)(–(8%((air).(((

(

How$About$PostECardiac$Arrest?$$Studies(have(shown(poor(neurological(outcome(where(hypoxia(is(used(postOROSC.((These(are(mainly(

animal(or(laboratory(studies.((Pilcher(et(al((Resuscitation(2012)(in(a(meta(analysis(of(animal(models,(

showed(that(100%(oxygen(resulted(in(worst(neurological(outcome(postOarrest.(((

(

How(does(this(relate(to(humans?(

(

Kuisma(et(al((Resuscitation(2006)(conducted(a(randomised(control(pilot(study(looking(at(patients(

with(out(of(hospital(cardiac(arrest.((Patients(were(ventilated(with(either(30%(of(100%(oxygen(for(60(

minutes.((Outcomes(measured(were(neuroprotein(leaks(up(to(48(hours(postOROSC,(which(would(

directly(determine(a(poorer(neurological(outcome.(((

(

The(study(found(adequate(oxygenation(at(30%(and(a(greater(leak(of(neuroproteins(at(100%.(((

( (

Septic Patient? Just Tell me What to do

((((((((((((((((((((((((((((((((((((((((

INVASIVE'RESUSCITATION''

We’ve%had%the%chain%of%survival%for%some%time%now,%we%know%that%good%CPR%is%paramount%and%we%also%know%that%defibrillation%works.%%%%Then%we%have%advanced%cardiac%life%support.%%What%is%this%really%all%about?%%It%certainly%adds%airway%and%drugs%to%the%picture%however,%the%reality%is%that%airway%(mostly%as%a%result%of%delaying%CPR)%probably%kills.%%Adrenalin%is%a%two%edged%sword,%that%hasn’t%really%been%shown%to%make%a%huge%difference.%%It%certainly%works%well%in%animal%models%but%it’s%not%as%convincing%in%humans.%%%%It%assists%with%peripheral%constriction%and%cardiac%vessel%dilatation%but%it%also:%%

1.! Increases%myocardial%oxygen%demand%2.! Increases%postIresuscitation%myocardial%dysfunction%3.! Increases%the%risk%of%ventricular%arrhythmias%4.! Causes%pulmonary%vasoconstriction%%

%…..%and%so%much%more.%%Imagine%what%the%heart%is%like%after%a%cardiac%arrest.%%It’s%not%functioning%properly%and%we%need%to%give%it%the%rest%it%needs%and%the%assistance%it%needs%to%start%producing%appropriate%cardiac%output.%%However,%that’s%not%possible%with%adrenalin.%%A%wounded%heart%tries%to%pump%against%an%increased%after%load%increasing%the%work%it%has%to%do%at%the%same%time%we%are%increase%its%rate%and%its%force%of%contraction.%%It’s%no%wonder%that%in%many%cases%the%heart%will%fail%again.%%What%if%we%didn’t%need%to%use%as%much%adrenalin%but%assist%the%heart%with%better%CPR.%%The%quality%of%CPR%is%directly%related%to%survival.%%Increased%pauses,%inadequate%depth%and%incorrect%rates,%decrease%survival%(Resuscitation%2013;128:417I35).%%The%important%elements%of%CPR%are:%%

1.! Chest%compression%fraction%2.! Chest%compression%rate%3.! Chest%compression%depth%4.! Chest%recoil%5.! Ventilation%in%coordination%with%chest%compression%

%Whilst%performing%CPR%we%need%real%time%feedback%to%its%quality%and%effectiveness.%%We%need%to%move%from%a%rescuer%focused%to%a%patient%focused%approach.%%%%Our%current%measures%of%how%effective%CPR%include:%%

1.! Pulse%check:%this%is%considered%next%to%useless%2.! EtC02:%we%use%this%as%a%surrogate%marker%for%cardiac%output.%%It%doesn’t%really%reflect%

coronary%perfusion%it%reflects%cardiac%output%as%it%correlates%with%pulmonary%blood%flow.%%What%measures%as%coronary%perfusion?%%At%coronary%perfusion%pressures%of%greater%than%20I30mmHg%we%get%return%of%spontaneous%circulation%(ROSC).%%%% (

When%to%stop%!Shane!Curran!!When!to!stop!is!both!a!simple!and!a!difficult!question!!Most!people!take!it!to!mean!when!to!stop!cardiac!compressions!and!believe!it!is!an!easy!decision!,!ie!when!the!likelihood!of!recovery!is!either!nil!or!such!low!likelihood!that!significant!!recovery!will!not!occur!!However!resuscitation!is!a!dynamic!continuum!and!is!carried!out!in!a!number!of!settings!with!involvement!of!a!significant!number!of!stakeholders!,!namely!the!patients!!,!their!relatives!and!health!care!providers.!!Resuscitation!can!also!include!the!continuance!or!otherwise!of!other!therapies!!When!to!stop!involves!consideration!of!a!number!of!factors!including!!the!!location!,!eg!prehospital!will!involve!different!factor!that!an!ICU!setting!!!Other!factors!that!are!involved!include!!! !

D! Patient!wishes!,!e.g.!is!there!a!valid!advanced!care!directive!that!is!known!!D! Family!wishes!D! Knowledge!or!otherwise!of!any!premorbid!or!coDexisting!conditions!D! Social!dynamics!of!the!setting!!D! “down!time”!D! Cardiac!rhythm!on!arrival!D! Treatments!already!undertaken!and!the![patient!response!to!those!therapies!D! Anecdote!!

!!Some!traditional!markers!of!when!to!stop!cardiac!compressions!do!not!have!100%!reliability!and!the!pitfalls!of!using!these!will!be!discussed! (((((((((((

Post%arrest%debrief%–%still%done?%J%Cruickshank%!Cardiac!arrest!survival!rates!remain!poor!&!performance!is!often!reported!as!less!than!optimal!!

•! Incorrect!rate!•! Incorrect!depth!•! Incorrect!ventilations!•! Incorrect!decisions!

There% is% some% evidence% that% post% arrest% debrief% and% real% time% feedback%improves%%

•! Subsequent!quality!of!CPR!depth!and!compressions!•! ROSC…!but!not!mortality,!but!there!is!potential…!

The!fact!is!that!national!standards!and!colleges!and!employers!are!still!debating!recommendations!due!to!the!lack!of!evidence,!but!surely!further!research,!to!inform!guidelines,!training,!competency!and!real!time!performance!feedback!is!the!future.!!

Features%of%real%time%feedback%Debriefing!!D!!CPR!depth!38%!to!68%!P=0.015!Feedback!–!!CPR!depth!19%!to!58%!p=!0.002!Compression!=!ns!!Debriefing!+!feedback!D!compressions!45%!to!84%!p=0.001!!Debriefing!+!feedback!–!compressions!AND!depth!29%!to!64%!p=0.005!!!

!

References/suggested%further%reading%http://www.safetyandquality.gov.au/wpDcontent/uploads/2014/11/TrainingDandDcompetenciesDforDrecognisingDandDrespondingDtoDclinicalDdeteriorationDConsultationDreportDandDoptionsDforDactionDNovD2014.pdf!! (((

Traumatic*Cardiac*Arrest*Resuscitation*(

(

Troponin'and'Rule.Out'Acute'Myocardial'Infarction'strategies:''Summary'Only 10-20% of patients who present to emergency departments (EDs) with suspected cardiac-related chest pain are finally diagnosed with an AMI.(1) This observation has driven development of strategies to identify patients without an AMI for safe, early discharge to outpatient management (including further investigations where indicated).(2-6)

Cardiac troponins are the most sensitive and specific biomarker for myocardial injury and necrosis caused by myocardial infarction. The detection of rise and/or fall of troponin with at least one value greater than the 99th percentile is a key criteria for diagnosis of MI according to the 2012 Third Universal Definition of MI (7). Five clinical presentations of MI on the basis of pathological, clinical, and prognostic factors have been defined. In the clinical setting of patients with chest pain and identification of possible AMI, type 1 AMI (an event related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries) is the main focus of ED testing strategies.

Current Australian guidelines recommend serial measurements of cardiac troponin between 6 and 8 hours after patient presentation to the ED when using a sensitive troponin assay and as short as 3 hours when using highly sensitive troponin results. There is significant variety though in other international recommendations. (8, 9) The majority of patients require prolonged assessment prior to safe discharge, despite only 10-15% of these having a final diagnosis of acute coronary syndrome (ACS)(10). This diagnostic approach leads to a large number of potentially avoidable, and costly, hospital admissions. Strategies that could safely identify a large proportion of patients suitable for discharge after early or even a single blood draw on arrival in the ED would have major benefits to healthcare systems.

Improvements on the ability of assays to detect low concentrations of troponin have allowed the earlier identification of abnormal troponin results in the setting of myocardial necrosis. In addition, the structured combination of sensitive or highly sensitive troponin assay results with clinical risk assessment and ECG findings support the early rule-in and rule-out of AMI. Serial measurement of troponin levels is recommended to accommodate differences in time of presentation and may identify those instances of elevated troponin which are attributable to factors other than acute coronary syndrome.

It is essential that clinicians know the local assay used, and understand the specific evidence about early Ro or RI strategies evaluated with this assay. This may determine what options for accelerated assessment strategies are possible in the local setting. The analytical and performance characteristics of assays vary significantly and so adherence to evidence-based specific strategies is recommended. It is particularly important for clinicians to recognise that quantitative comparison cannot be made between troponin I and troponin T, nor should it be attempted between point-of-care devices and laboratory based highly sensitive immunoassays.

A number of different troponin sampling intervals have been reported for ED patient with a possible AMI. These include:

•! 0 h – RO AMI with values <Limit of Detection (LoD) in patients with symptom onset > 3hours (hs-assays) (11-13)

•! 0 & 1h – RO and RI AMI algorithms (hs-assays) (14-16) (

You can use lactate for that...? !Detergent?........Mosquito!attractant?............Window!on!the!metabolic!soul....?!!This!talk!will!focus!first!on!the!basic!physiology!and!biochemistry!of!lactate,!and!then!the!clinical!applications!!?!The!lactate!shuttle!concept!Lactate!has!a!physiologic!role!in!transferring!energy!from!tissues!unable!to!effect!aerobic!metabolism!of!glucose!to!other!tissues!which!can!extract!remaining!energy!from!the!molecule.!!This!is!either!through!hepatic!gluconeogenesis!or!conversion!to!pyruvate!which!enters!the!Cori!cycle.!!?!The!lactate!threshold!In!exercise!physiology!the!concept!of!the!lactate!threshold!is!used!to!describe!the!point!at!which!blood!lactate!rises!exponentially!with!increased!work!of!exercise.!!It!has!been!shown!that!this!is!the!point!at!which!the!balance!between!oxygen!supply!and!demand!leads!to!increased!anaerobic!metabolism!increases!and!decreased!ability!of!tissues!to!utilise!lactate!as!an!energy!source.!!In!effect,!it!is!the!point!at!which!the!lactate!shuttle!gets!a!flat!tire.!!It!is!seen!in!exercising!subjects!at!a!lactate!of!4!mmol/L.!!?!Epidemiologic!data!on!what!levels!of!lactate!mean!for!mortality!Mortality!from!a!number!of!conditions!increases!with!increasing!lactate.!!Interestingly,!the!level!of!lactate!described!in!the!sports!science!literature!as!the!point!at!which!the!lactate!shuttle!ceases!to!work!efficiently!is!the!same!point!?!at!which!cryptogenic!shock!is!described!?!at!which!a!markedly!increased!mortality!is!seen!!?!Lactate!clearance!One!could!conceive!of!the!role!of!a!resuscitationist!as!being!the!mechanic!for!a!cellular!energy!delivery!system.!!Given!the!role!of!lactate!as!an!energy!shuttle,!and!that!it!increases!when!oxygen!delivery!is!compromised!relative!to!demand!and!significantly!increases!when!lactate!consumption!also!becomes!inhibited,!it!makes!sense!to!consider!management!of!lactate!as!a!potential!endpoint!in!resuscitation.!!!!?!Clinical!trial!evidence!exists!for!the!use!of!lactate!clearance!as!a!relatively!noninvasive!endpoint!in!resuscitation!of!the!shocked!patient,!and!this!will!be!reviewed.!!?!Other!things!can!increase!the!blood!lactate!–!beta!agonists!and!biquanides!being!prominent.!!One!of!the!more!interesting!uses!for!lactate!is!to!contrast!the!diagnosis!of!Metformin!induced!lactic!acidosis!with!the!Cochrane!collaboration!conclusion!of!it’s!nonexistence.!!Hepatic!failure,!regional!ischaemina!(compartment!syndrome,!dead!gut)!! (

DVT$Diagnosis$!Diagnosing!DVT,!is!like!everything!else!in!emergency!medicine,!it's!about!risk!stratification.!!The!important!thing!to!understand!is!the!Wells!score!and!know!that!there!is!a!difference!between!the!score!for!DVT!and!PE.!!As!Wells!himself!states:!!

1.! It!should!only!be!used!if!DVT!is!a!possibility!after!history!and!examination.!2.! The!DGdimer!should!never!be!done!before!history!and!examination,!due!to!the!large!

number!of!other!causes!of!a!raised!DGdimer.!!There!are!three!risk!groups!and!two!risk!groups,!alternative!models.!!The!two!risk!group!models!state!that:!!

1.! If!Wells!score!is!<2!DVT!is!unlikely!2.! If!Wells!core!is!≥2!DVT!is!likely!

!The!DGdimer!then!becomes!very!important!in!our!decision!making.!!A!Wells!score!of!less!than!2!in!a!negative!quantitative!DGdimer!and!you!can!rule!out!DVT.!!The!key!with!the!DGdimer!is:!!

1.! If!the!Wells!score!is!<2!and!the!DGdimer!is!positive!and!your!ultrasound!is!negative,!it's!ruled!out.!

2.! If!the!Wells!score!is!≥2!and!the!DGdimer!is!positive!and!your!ultrasound!is!negative,!you!still!need!to!repeat!the!ultrasound!in!one!week.! (

(((((((((((((((((((

The ABG: A Case Study A multifactorial case of metabolic acidosis A 76 year old male presented with 3-4 days feeling unwell with fevers and cough productive of brown sputum, after visiting a sick relative interstate. Past history includes nephrectomy for renal cell carcinoma, atrial fibrillation on NOAC, heart failure, pacemaker in situ, and insulin-requiring type II diabetes. He had had a previous admission several months earlier at another hospital with a respiratory illness and at the time was specifically taken off metformin. Initial findings were temperature at 38, with marked tachypnoea (RR >40). Initial ABGS are as follows: pH 7.11 pO2 586 pCO2 10 Std HCO3 7 Other investigations: Lactate 5.0 Hb 21.1, Hct 69.6 K 6.0 glucose 3.1 Soon after arrival in the ED he had a respiratory arrest and was transferred to ICU. It was noted he was anuric and was commenced on haemofiltration. Initial ABGs in ICU: pH 6.98 pO2 170 pCO2 33 Std HCO3 8 Other investigations: Hb 18.0, Hct 54.9 Lactate 12.0 Glucose 6.8 (

Clinical Gestalt and Chest pain assessment: Summary

“an organized whole that is perceived as more than the sum of its parts” The$synthesis$of$a$patient’s$clinical$history$and$examination$leads$us$to$our$determination$of$risk$of$disease.$This$is$a$complex$task,$with$often$intangible$components$contributing$to$our$assessment.$On$any$given$day$in$the$Emergency$Department$physicians$appraise$the$risk$of$many$patients$with$chest$pain$and$other$symptoms$of$possible$acute$coronary$syndromes.$With$the$seriousness$of$the$condition,$and$the$risk$of$serious$harm$in$misdiagnoses,$accuracy$of$this$assessment$process$is$fundamental$to$good$clinical$care.$$$$In$the$assessment$of$patients$with$possible$acute$coronary$syndrome,$historical$and$examination$findings$are$usually$limited$in$both$sensitivity$and$specificity.$(1D3).$From$the$ED$perspective$where$the$ability$to$exclude$or$ruleDout$a$diagnosis$is$key,$no$single$historical$feature$nor$examination$finding$has$the$sensitivity$required$to$be$100%$confident$that$a$diagnosis$of$ACS$can$be$excluded.$Risk$factors$are$commonly$assessed$in$patients$presenting$with$possible$ACS.$While$risk$factors$are$useful$when$looking$at$populationDlevel$risk,$on$an$individual$basis,$they$add$little$to$the$assessment$of$ED$patients,$especially$for$patients$aged$over$65$years.$(4,$5)$$Objective$tools$such$as$the$electrocardiogram$(ECG)$is$essential$in$initial$management$and$risk$stratification.$The$presence$of$STDsegment$elevation$identifies$patients$who$will$benefit$from$urgent$reperfusion$therapy.$(6)$Other$ECG$changes$such$as$ST$depression$(STD),$TDwave$inversion$(TWI),$pathological$Q$waves,$and$bundle$branch$blocks,$confer$an$increased$likelihood$of$nonDST$segment$myocardial$infarction$(NSTEMI)$(7,$8)$and$are$used$in$the$ED$to$risk$stratify$patients$with$possible$acute$coronary$syndromes$(ACS).$However,$up$to$8%$of$patients$with$an$acute$myocardial$infarction$(AMI),$and$even$larger$proportions$of$patients$with$unstable$angina,$have$a$reportedly$normal$ECG.$(7,$9)$$$

The$advent$of$troponin$assays$has$allowed$improved$identification$of$patients$with$myocardial$necrosis.$The$assays$in$clinical$use$for$troponin$testing$have$improved$exponentially$over$the$past$decade,$allowing$very$low$concentrations$of$troponin$to$be$detected.$One$advantage$of$this,$is$that$we$can$detect$abnormalities$in$troponin$at$earlier$time$points$after$coronary$occlusion,$however$we$are$also$identifying$more$conditions$associated$with$myocardial$necrosis$or$injury$that$also$cause$elevated$values.$Elevated$troponin$values$are$seen$in$acute$myocardial$infarction,$but$also$in$other$conditions$causing$myocardial$necrosis$such$as$tachyarrhythmia,$myocarditis,$and$pulmonary$embolism.$Also$there$is$a$timeDdependent$release$of$troponin$after$injury$and$so$at$early$time$points$after$coronary$occlusion,$an$elevation$of$troponin$may$not$be$seen.$It$is$important$to$recognise$that$in$unstable$angina,$associated$with$ischemia$without$infarction,$no$elevation$in$troponin$will$occur.$Some$have$speculated$that$since$the$advent$of$hsDassays,$the$diagnosis$of$unstable$angina$may$no$longer$exist.$Unfortunately,$this$has$not$been$the$case$in$countries$using$such$assays.$

$So$how$about$clinical$gestalt?$While$this$has$been$addressed$even$in$the$current$era,$we$are$in$a$situation$where$our$best$assessment$of$the$probability$of$disease$is$not$accurate$enough$in$isolation$to$allow$rapid$safe$discharge.$(10)$$We$have$some$understanding$about$ED$physicians$risk$tolerance,$with$the$majority$not$accepting$of$a$risk$greater$than$1$in$100$risk$ (

Hartmans vs saline; a fluid grudge match…? !0.9%!sodium!chloride!is!a!solution!rich!not!only!in!salt,!but!also!in!history.!!An!exploration!of!this!history,!answering!such!questions!as!“who!put!the!normal!in!normal!saline”!raises!other!questions!as!to!whether!it!is!the!best!crystalloid!to!be!using!for!our!patients.!!Infusion!of!0.9%!NaCl!vs!a!balanced!electrolyte!solution!in!normal!subjects!results!in!a!lesser!increase!in!renal!blood!flow!and!urine!output.!!This!is!likely!due!to!glomerular!afferent!arteriolar!vasoconstriction!in!response!to!an!increased!chloride!load!at!the!macula!densa.!!!The!hypothesis!that!hyperchloraemia,is,nephrotoxic!holds!biologic!plausibility.!!Additionally,!observational!data!suggest!increased!rates!of!renal!complications,!post!surgical!complications!and!death!when!saline!is!used!vs!balanced!electrolyte!solutions.!!Perhaps!even!more!fascinating,!large!amounts!of!intravenous!saline!versus!balanced!electrolyte!solution!made!American!surgical!registrars!cognitively!slower.!!Hyperchloraemia!causes!acidosis.!!The!basic!science!behind!this!is!very!complex.!!A!simple!and!understandable!analogy!is!that!NaCl!dissolves!into!solution!more!readily!than!other!Na!salts!(for!example,!sodium!bicarbonate).!!When!an!increased!concentration!of!NaCl!is!introduced!there!is!an!electrostatic!force!toward!other!anions!associating!with!Na!to!exit!!that!same!solution.!!This!concept!is!embodied!in!the!“strong!ion!difference”!concept!and!equation.!!While!not!clearly!evidenced!as!causing!harm,!understanding!the!impact!of!hypercholraemia!on!the!acid!base!state!can!aid!in!management.!!For!example,!it!has!been!demonstrated!that!using!Hartmanns!more!readily!corrects!acidosis!in!DKA.!!As!ever,!the!most!beautiful!theories!in!medicine!do!not!always!equate!with!the!known!facts.!!The!SPLIT!trial!in!ICU!patients!is!the!only!major!RCT!in!this!area.!!It!was!primarily!designed!to!pilot!a!type!of!trial!methodology,!!however!the!issue!investigated!saline!vs!balanced!electrolyte!solution.!!No!difference!in!the!primary!endpoints!of!death!or!renal!dysfunction!were!seen.!!However,!interesting!patterns!were!seen!in!the!subgroup!analysis!and!in!the!most!sick!patients!there!was!a!5%!nonsignificant!mortality!increase!with!saline.!!An!8000!patient!trial!is!planned!in!this!subgroup!to!definitively!investigate.!!Watch!this!space.!!!! ((((((

(

Massive Transfusion Protocol

Peripheral Vasopressors

(((((((((((((((((((((((((

Pills%that%kill%%!Shane!Curran!!All!medications!can!kill.!!Drug!related!deaths!can!be!classified!as!intentional!or!avoidable!!Intentional!overdoses!are!managed!according!to!standard!risk!stratification!with!the!appropriate!use!of!decontamination!strategies!,!supportive!therapy!and!antidotes!as!needed!!Avoidable!drug!deaths!fall!onto!the!categories!of!drug!reaction!or!!inadvertent!!!!!Approximately!3%!!of!!hospital!admissions!are!related!to!medication!side!effects!or!interactions,!with!the!number!increasing!with!age!and!the!number!of!medications.!!Some!reactions!are!idiosyncratic!and!can!range!from!mild!to!life!threatening!!!There!are!a!number!of!medications!!and!substances!that!are!potentially!lethal!in!small!doses!,!particularly!to!children.!This!list!of!toxins!has!not!really!changed!over!20!years!with!respect!to!drug!categories!,!but!the!profile!within!each!category!!has!changed!!!Mots!publicity!relates!to!the!emergence!of!“party”!drugs!and!the!well!publicised!deaths!of!young!people!at!music!festivals!,!usually!related!to!idiosyncratic!reactions!to!an!ingested!!!substance!!!.!!!! ((((((((((((

Anticoagulants and Antidotes (

(((((((((((((((((((((((((((((((((((((((((

New tox on the block !Reviewed!in!this!presentation!is:!!The!changes!to!the!management!of!paracetamol!toxicity!in!the!2015!Australasian!guidelines!–!changes!in!massive!OD,!repeated!supratherapeutic!dose!and!modified!release!ingestion.!!The!changes!to!recommendations!around!the!use!of!activated!charcoal!are!reviewed!in!light!of!recent!gastroscopic!evidence!around!the!duration!of!time!intoxicant!remains!in!the!stomach!after!poisoning.!!From!black!charcoal!to!white!lipid!emulsion!–!2015!ACLS!guidelines!suggesting!lipid!emulsion!may!be!reasonable!in!lipophilic!drug!induced!arrest!are!reviewed.!!!The!relatively!rare!indications!for!the!use!of!lipid!emulsion!are!reviewed,!along!with!guidelines!for!dosage!and!administration.!!While!THC!is!not!new,!it’s!presentations!seem!to!always!be!evolving.!!Vignettes!and!evidence!around!THC!interactions!and!the!use!of!capsaicin!in!cannabinoid!hyperemesis!are!presented.! (((((((((((((((((((((((((((

Things that Crawl and Slither (

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Atrioventricular Nodal Re-entrant Tachycardia: Summary

!

Atrioventricular-nodal-re/entrant-tachycardia-(AVNRT)-represents-the-most-common-regular-supraventricular-arrhythmia-in-humans.(1)-By-definition,-it-originates-above-the-Bundle-of-His,-but-the-precise-anatomic-site-and-nature-of-the-pathways-involved-have-not-yet-been-established.-The-rentry-circuit-is-in-or-around-the-AV-node,-and-formed-by-a-slow-and-a-fast-pathway.-

-

ECG!Presentation!

Typically,-AVNRT-is-a-narrow/complex-tachycardia-(rates-140/280-bpm),-ie,-QRS-duration-<120-ms,-unless-aberrant-conduction,-which-is-usually-of-the-right-bundle/branch-type,-or-a-previous-conduction-defect-exists.-Tachycardia/related-ST-depression-may-be-seen-and-concerns-about-ischemia-may-be-present.-RR/interval-variation-may-be-seen.--

There-are-3-different-types-and-so-ECG-findings-include:-

•! No-visible-P-waves-(within-the-QRS-complex)-•! P-waves-immediately-before-the-QRS-•! P-waves-immediately-after-the-QRS-

-

In-the-typical(form(of(AVNRT((slow5fast),-abnormal-(retrograde)-P’-waves-are-constantly-related-to-the-QRS-and-in-the-majority-of-cases-are-indiscernible-or-very-close-to-the-QRS-complex.-Thus,-P’-waves-are-either-masked-by-the-QRS-complex-or-seen-as-a-small-terminal-P’-wave-that-is-not-present-during-sinus-rhythm-(Figure-1).-This-accounts-for-80/90%-of-AVNRT-and-in-most-cases-the-ECG-looks-like-the-‘typical’-SVT-appearance-with-absent-P-waves.-

-

-

Figure-1.-(2)-(

Blood Pressure Control in Brain Bleeds !Autoregulation!maintains!cerebral!blood!flow!by!maintaining!a!MAP!at!609150!mmHg.!!In!patients!with!chronic!hypertension!the!autoregulation!curve!may!undergo!a!right!sided!shift.!!What!does!this!mean!in!real!terms?!!These!patients!may!have!symptoms!of!hypotension!at!higher!blood!pressures.!!Our!goal!is!to!keep!the!haematoma!volume!as!small!as!possible!by:!!

•! Reversing!any!bleeding!•! Blood!pressure!control!to!decrease!the!volume!of!the!bleed!

!THE$PENUMBRA$CONUNDRUM$This!is!a!term!that!I've!coined,!to!describe!the!difference!between!ischemic!and!haemorrhagic!strokes.!!In!ischemic!strokes,!the!ones!we!give!lytics!to,!there!is!a!necrotic!area.!!There!is!an!area!of!dead!tissue!surrounding!the!stroke.!!There!is!an!ischemic!penumbra.!!In!ischemic!strokes!if!the!penumbra!is!reperfused!the!cells!live.!!This!is!what!all!the!fuss!is!about!with!lytics.!!Bleeds!are!different!to!ischemic!strokes.!!There!is!no!ischemic!penumbra.!!Because!of!this!significant!blood!pressure!reduction!appears!safe!in!the!intracranial!haemorrhage.!!INTRACEREBRAL$HAEMORRHAGE$It!appears!safe!for!patients!presenting!with!a!systolic!blood!pressure!greater!than!180!mmHg!to!reduce!the!blood!pressure!to!160!mmHg.!!In!patients!with!a!systolic!blood!pressure!less!than!220!mmHg,!140!may!be!a!safe!level!to!reduce!to.!!You!will!be!guided!by!your!patients!behaviour.!!If!the!patient!starts!to!show!signs!of!hypotension!or!show!signs!of!neurological!impairment!as!you!decrease!the!blood!pressure,!that!blood!pressure!needs!to!be!increased.!!SUBARACHNOID$HAEMORRHAGE$The!aim!here!is!to!reduce!the!blood!pressure!to!less!than!160!mmHg.!!This!is!important!due!to!the!potential!early!rebleeds.! ((((((((((((((

Communication*in*the*ED.*J*Cruickshank*

Here*is*the*case*You$ have$ a$ colleague$ that$ you$ occasionally$ have$ disagreements$with.$ You$walk$ up$ to$ them$ in$ the$cafeteria,$and$note$that$you$have$not$had$an$argument$in$ages.$You$ask$them$if$they$want$to$know$why?$$$It’s$ the$ last$ talk$of$Saturday.$You’ll$have$ to$stay$until$ the$end$to$discover$ the$secret.$Peter$Kas$ told$people$in$the$past$to$“find$your$bliss”.$This$year$we$discover$“the*secret”$that$goes$beyond$the$golden$rule$and$beyond$the$platinum$rule$of$communication.$$Teaching$you$talk$is$like$teaching$you$to$walk.$You$know$how$to$do$that.$$

Talk%the%talk%you’ll%have%to%walk%the%walk%Talk%the%talk%you’ll%have%to%….%

$50%*talking*and*50%*listening*–*what*could*go*wrong*

$

The*power*of*Positive*feedbackE*as*easy*as*ABCD*“I’ll%take%any%positive%feedback%I’ll%get”%“Relearn%the%attitude%of%gratitude”%

$$

Can*I*get*in*trouble*for*what*I*am*thinking?**

Constructive*criticism*rules*•! Do$it$now$&$Do$it$face$to$face$•! Do$it$in$private$•! Ask$questions$and$listen$to$the$answers$•! Agree$the$facts$•! Criticise$the$action$not$the$person$•! Explain$why$it$matters$•! Agree$a$remedy$•! Finish$on$a$positive$

$$

The*secret.$You’ll$have$to$wait$and$see…$or$wait$and$listen.$$$$You’ll$make$mistakes$when$under$pressure$and$everyone’s$watching,$so$some$skills$require$practice.$$https://youtu.be/2ZqKtaNmKfY ((((((

((

AIRWAYAdvances)in)airwayDifficult)airway)kitKetamine/sedation

Roc)vs)sux

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29/05/2016 12:14 am5 Things To Help You Get The Airway | Resus.com.au | Emergency Medicine Blog

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Home Airway 5 Things To Help You Get The Airway

5 Things To Help You Get The Airway

1. Know When To IntubateIt may sound strange, but we should have an approach as to when it’s appropriate to intubate. Mychoice is when there is failure of ( whether this is now or imminent) of oxygenation and ventilation,maintenance of airway or airway protection.

I then also ask the questions:1. Will I be able to oxygenate and ventilate?2. Will I be able to intubate?3. Will I be able to perform a surgical airway if needed?

2. Know your drugs and equipment

EquipmentThe basics are: 1. A Bag Valve Mask(BVM) to oxygenate and ventilate2. The laryngeal mask3. The curved blade laryngoscope- size 3 in most cases4. The endotracheal tube(ETT). I use a size 7.5 for everyone then can change if I need to.5. A stylette or introducer. I insert this into the ETT and curve the end like a hockey stick (seebelow)6. A bogie if I need this.7. A scalpel if I need to perform a surgical airway

Curving the end of the ETT can be very helpful. Rememberthat the trachea is anterior to the oesophagus and thisallows us to intubate anteriorly.

This angle is the angle we see in the bougie. My reasoning,why use the bougie, when I can create a bougie-like devicewith my ETT.

Drugs

I really think of 4 main drugs to keep it simple. I will use others of course, but get good at usingsome agents.

KETAMINECurrently my favourite drug for sedation and induction. In intubation, 1-2mg/kg will do the job. Ifyou give it over a minute, the patient will slip into a dissociative state, if you give it fast, they’lldevelop apnoea.

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29/05/2016 12:18 amApnoeic Oxygenation | Resus.com.au | Emergency Medicine Blog

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Home Airway Apnoeic Oxygenation

Apnoeic Oxygenation…or how can I stop my sedated patient from desaturating?

This is simple; a 7 minute video that briefly explains the use of apnoeic oxygenation. I use it tohelp keep saturations up in patients that I’m about to intubate, or in those that are sedated for aprocedure. I use it in adults.

It suits a patient group that has good pre-oxygenation and that is not hypoxic to begin with.

The technique is simple:

1 Attach nasal prongs.

2 Pre-oxygenate the patient as you normally would

3 When the sedation is in place, increase the flow in the nasal prongs to>15L/min(remember thatawake patients can’t tolerate this from normal nasal prongs.

4 The result will be increased and maintained oxygen saturations (there is a potential forhypercarbia- but we accept this)

The effects is more time before desaturation occurs.

I use this all the time. I love this technique.

More in this at the Advanced Airway Workshop at EMCORE 2013.

Watch the video.

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29/05/2016 12:16 amDelayed Sequence Intubation | Resus.com.au | Emergency Medicine Blog

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Home Airway Delayed Sequence Intubation

Delayed Sequence IntubationThere’s been a lot of talk around aboutDelayed Sequence Intubation and a little bitof confusion about it, so I thought I’d clearup a couple of things.

Is there a lot of evidence for it?No- there is very little, but we will see theevidence coming out soon. The currentevidence is mostly anecdotal.

What is it?It is really procedural sedation, where theprocedure is improved oxygenation. What

you say? Thinks of it this way, you have a patient that will need intubation, but they are notobtunded and you are having a difficult time pre-oxygenating them, to allow you to give paralysisand intubate. They can be difficult to pre-oxygenate because they are cerebrally agitated, orsimply because they can’t tolerate CPAP or BiPAP.

Is it for everyone?No. Its not suitable for your obtunded patients. They just need the tube. It’s probably not neededfor those with Oxygen saturations >95%, although can be used in those patients. I use it for thosepatients that have oxygen sats of <95% and in whom I have difficulty pre-oxygenating.

How do I actually do it?The key is apnoeic oxygenation and Ketamine.

Use Ketamine at a dose of 1-2mg/kg. I wouldn’t use more than 2mg/kg. Ketamine results indissociative anaesthesia, but maintains airway reflexes and doesn’t affect respiratory drive atthese doses. This means your patient is breathing, maintaining their airway and now calm andtolerating pre-oxygenation.

Unless it’s a trauma, I have the patient head-up 20 degrees.

I use the apneic oxygenation technique, of nasal prongs at 15L/min and then I add either CPAP orI use a bag valve mask on the patient with a PEEP valve set at 5-10cm H2O. I don’t actively bagthe patient, but let them breathe through the mask. The sats should rise in a couple of minutes.

Then, whilst still maintaining apneic oxygenation, give the paralysing agent and intubate.

It may get us out of trouble, but remember it doesn’t always work. It’s something else to have inyour bag of tricks.

Peter Kas

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29/05/2016 12:17 amAre you still using cricoid pressure? STOP IT! | Resus.com.au | Emergency Medicine Blog

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Home Airway Are you still using cricoid pressure? STOP IT!

Are you still using cricoid pressure? STOP IT!For years we have been using cricoid pressure in the emergency airway, so as to minimiseregurgitation when the neuromuscular blocker is given and the gastro-oesophageal sphincterrelaxes. The theory is that we use the trachea to compress the posterior lying oesophagus.Weneed to stop. The only real indication for cricoid pressure is when there is bag valve masking of apatient for a prolonged period.

In a study in Anesthesiology 2003;99:60-64, it was found that:

When cricoid was applied, IN 90.5% of cases theoesophagus was displaced, n 66.7% of cases,cricoid resulted in lateral laryngeal compressionand in 81% of cases cricoid resulted in AIRWAYCOMPRESSION. So beware!

One of the reasons that compression occurs isthat the person doing the compression, doesn’tknow how much pressure to apply.

So intubate without cricoid, but still using all thosegreat techniques you all have.

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29/05/2016 12:15 amRoc Rocks, I’ll miss you Sux | Resus.com.au | Emergency Medicine Blog

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Home Airway Roc Rocks, I’ll miss you Sux

Roc Rocks, I’ll miss you SuxRocuronium vs Suxamethonium(Succinylcholine)

I remember teaching the Advanced Airway Workshop and having oneslide with “SUX is KING”. Times have changed!Which is the better paralytic agent to use in the EmergencyDepartment; Suxamethonium(Succinylcholine for our US colleagues)or Rocuronium? This argument has been ongoing for some time, withdebates, podcasts and written reviews by proponents each takingstrong positions, sometimes quite belligerently. Here is the evidence. Ihave highlighted the important points to save you reading time.

There are a list of what I call light concerns, ‘fluff’ if you like, thatdistract from real concerns and then there is the evidence basedmaterial, that makes a difference. Let’s get rid of the fluff first.

One of the first arguments against Suxamethonium, is its fasciculation-induced muscleaches and pains that the patient may experience when woken, in ICU. They are real and weshould certainly care that the patient may have discomfort down the track. However I have asingle goal; to establish/protect the airway. No-one will thank you if you can’t get this right. Solets not spend too much time on the aches and pains. Rhabdomyolysis is a different matter,which will be discussed later. A further concern relates to what we do, if we can’t intubate andhave used a long- lasting paralytic agent, such as Rocuronium? The approach of letting thepatient wake up, has no place in the emergency department. This statement belongs toanaesthetics and elective procedures, where they can wake them up and play another day. In theemergency department, the reason we needed to intubate in the first place is still there.

With the introduction of ‘Sugammadex’, a rapid reversal agent for Rocuronium, thisshould no longer be of concern.Proponents in favour of suxamethonium use the head injured patient with an intracranial bleed asan example. Their main argument is that the Neurosurgeon may need to examine them, so it isappropriate to wake them up.Neurosurgeons care about what the patient was doing when they came in, their co-morbiditiesand the single most important thing, the CT brain. The examinations are usually very basic andinvolve movement of the limbs, pupil size and reactivity and test for doll’s eyes, or the oculocephalicreflex. This examination should be done prior to intubation, but sometimes this isn’t possible.In the rare occasion where this can be done, Suxamethonium will wear off and Rocuronium canbe completely reversed.

What are the things that matter? What are those things important to establishing anairway? Here is my list.

ADVERSE REACTIONS: SUX vs ROC

1. How quickly will I induce paralysis to allow intubation and how good will myintubation conditions be?2. Will any of these drugs reduce my available apnoeic time? This means, will my patientdesaturate faster on one drug rather than the other and will this matter in the real world?3. Will any of these drugs have adverse reactions?

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NON-INVASIVE VENTILATION Approach(to(the(Dyspnoeic(patient((

Shane(Curran(

(

Patients(present(with(dyspnoea(of(all(shapes(sizes(ages(and(causes.(

The(initial(assessment(and(management(of(a(patient(with(dyspnoea(does(not(vary(from(any(other(ED(patients(and(involves(the(classical(order(of(history,(examination(,(differential(diagnosis(,(tests(and(treatment((

For(some(patients(with(dyspnoea(however(this(may(be(inappropriate(with(immediate(interventions(needed(in(patients(with(life(threatening(or(imminently(life(threatening(causes.(

Emergency(Medicine(history(and(examination(techniques(vary(between(levels(of(clinical(staff(in(an(ED((

Beginners(and(experts(in(emergency(medicine(((have(differing(styles(of(diagnosis(and(use(either(system(1(or(system(2(thinking(to(get(to(a(diagnosis((

Each(system(can(be(open(to(errors(which(may(be(predictable(

History(and(examination(findings(relevant(to(the(causes(of(dyspnoea(are(aimed(at(getting(the(most(information(available(in(a(short(time((

Non(respiratory(causes(of(dyspnoea(also(need(to(be(included(in(any(differential(diagnosis((

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Violent(and(psychotic–(sedation(anyone?(J(Cruickshank(

Introduction(When%you%see%this%topic%is%the%first%thing%you%think%of%“delivering%compassionate%care%in%a%compassionate%and%safe%workplace?”%%%

The(best(approach(to(the(aggressive(patient(is(Know%that%many%patients%are%likely%to%be%seriously%ill%or%injured%%

•! Exclude%hypoxia%and%Don’t%Ever%Forget%Glucose%–%hypoglycaemia%•! Organic( causes( are( most( likely,( including( trauma,( drug( and/or( alcohol(

intoxication( or( withdrawel,( look( for( delirium( due( to( infections( and( other(medical(illnesses(

%Work%in%a%hospital%with%well%developed%aggressive%patient%systems%All%staff%should%have%basic%training%in%management%of%clinical%aggression%Orientation%and%education%includes%

•! Medico%legal%principles%%•! Mental%Health%literacy%%•! Recognition%of%early%signs%%•! Verbal%deIescalation%techniques%%•! Know%where%the%exits%and%panic%buttons%are.%•! Least%restrictive%options%

(Have%a%strategy:%mechanical%restraint%and%therapeutic%sedation%%

Evidence%supports%Midazolam%plus%either%droperidol%or%olanzepine%is%superior%to%midazolam%alone,%

%•! There%has%been%research%in%Victoria%and%Australia.%•! Cochrane%database%describes%evidence%and%low%quality.%•! No%international%consensus%–%refer%to%locally%published%guidelines%and%be%

familiar%with%your%usual%strategy.%Your%expertise%and%local%capacity%to%deal%with%complications%is%important.%

%Early%psychiatric%assessment%and%intervention%

•! Ensure% your% ED% and% psychiatric% department% have% an% agreed% policy% on%“medical%clearance”%vs%“medically%stable%and%fit%for%interview”%

•! Agree%that%a%reduced%length%of%time%in%the%ED%is%best%for%all,%and%work%on%safe%discharge%strategies%both%to%home%and%inpatient%settings.%%

References/suggested(further(reading(Article:%Compassionate%Approaches%to%prevent%patient%violence%Article%–%Management%of%the%acutely%violent%patient%Article%http://www.ncbi.nlm.nih.gov/pubmed/19527279%This%highlights%that%organic%causes%are%common%%%

Is#that#joint#septic##Shane#Curran##Diagnosis#of#a#septic#joint#can#be#difficult###Symptoms#suggestive#of#a#joint#infection#include#pain#and##diminution#or#loss#of#function#,#particularly#if#associated#with#a#fever##Clinical#findings#include#limitation#of#range#of#movement#and#pain#in#both#active#and#passive#movement###Imaging#will#show#the#presence#of#fluid#but#is#limited#in#the#early#phases##Inflammatory#markers#can#assist#in#the#diagnosis#but#may#in#fact#be#normal###Native#Joints#have#a#number#of#defence#mechanisms#against#infection##with#the#joint#capsule#being#a#barrier#and#synovial#fluid#having#some#anti@bacterial#properties##Damage#to#a#natural#joint##eg##rheumatoid#arthritis#can#predispose#to#the#development##of#sepsis###Definitive#diagnosis##is#made#on#aspiration#of#joint#contents#with#a#value#of#greater#than#50000#white#cells#with#a#polymorph#predominance##indicative#of#a#joint#infection#,#along#with#visualisation#of#bacteria####### ((

Osteomyelitis*

Aspiration of the Ankle, Knee of Shoulder Joint

Indications

Diagnostic Indications Therapeutic Indications • Evaluation of mono-arthritis • Evaluation of suspected septic arthritis • Evaluation of joint effusion • Identification of intra-articular fracture • Identification of crystal arthropathy

• Relief of pain by aspirating effusion or blood (limited evidence)

• Injection of medications (eg. corticosteroids, antibiotics, or anaesthetics) (conflicting evidence)

• Drainage of septic effusion

Interpretation of Aspirate

Pathology Appearance WCC/mcL PMN cells %

Glucose Protein g/dL

Crystals

None Clear < 150 25% Normal 1.3-1.8 none Noninflammatory Clear < 3000 25% Normal 2-3.5 none Inflammatory 3-5 R.A Cloudy > 2000 < 75% Low none Gout Cloudy > 2000 < 75% Normal Present

Negative birefringent

Pseudogout Cloudy > 2000 < 75% Normal Present Positive birefringent

O.A. Cloudy < 2000 Normal none Septic Cloudy > 50 000 > 90% Low 3-5 none Haemorrhagic Boody > 2000 50-75% Normal 4-6 none Adapted from: Introduction to Rheumatic Diseases and Joint Physiology . Robert Kalish. 2005 and Knee Arthrocentesis Technique. Gil Z Shlamovitz. Medscape 2014 Evidence for Diagnosis of Septic Arthritis Variable Sensitivity Specificity Total WCC > 25 000 77% 73% Total WCC > 50 000 62% 92% Total WCC >100 000 22% 99% PMN >90% 73% 79% Glucose < 0.5 serum glucose 51% 85% Protein > 3 g/dL 48% 46% Lactate dehydrogenase >250 U/L 100% 51% Adapted from: McGillicuddy DC, Shah KH, Friedberg RP, Nathanson LA, Edlow JA. How sensitive is the synovial fluid white blood cell count in diagnosing septic arthritis?. Am J Emerg Med. Sep 2007;25(7):749-52.

Femoral Nerve Block

Ultrasound in the ED: Fad or Fantastic? Introduction Ultrasound is commonly available across Emergency Departments in Australasia. This has evolved rapidly within the past 20 years. ACEM embraced the potential of Ultrasound early in the development with guidelines and course requirements in 1999 and an ongoing structure through an Ultrasound sub-committee that has helped to oversee improved training and programmes within Emergency departments. In 2016 there are several course providers for basic and advanced ultrasound education with no specific requirement for ongoing CPD in those using ultrasound. There remains anxiety about clinician accreditation as well as the appropriate scope of practice. One of the main original roles for ultrasound in the Resuscitation room was for the detection of free fluid in blunt trauma. Now with the greater availability of rapid CT for trauma patients the benefit of this specific ultrasound practice can be debated. However other uses of ultrasound such as for difficult venous access, drainage of fluid collections, abscess or cellulitis confirmation, detection of DVT have greatly developed. We surmise that Ultrasound may well have started its life in the ED as a fad but is now truly fantastic. Methods A review of recent literature 2010-current is performed to provide recent literature evidence into specific roles and functions for Point of Clinical Care Ultrasound (POCUS). This review provides examples of clinical practice as well as training programmes provided to doctors and undergraduates. Results The Emergency Department literature demonstrates the benefits of ultrasound within the ED. The challenge remains ensuring that the practitioner has sufficient training and understanding as to how to optimally utilise the skill within any specific clinical setting. The risk of over-diagnosis and potential inefficiency is identified. This is a common challenge to many aspects of Clinical Medicine’s interface with technology where the context is crucial to determining the optimal decision making by the medical practitioner. Discussion Ultrasound provides the clinician within ED with the benefit of an additional perspective when assessing a patient. Point of Care Ultrasound (POCUS) complements the history and physical examination and assists in narrowing a differential diagnosis earlier within the Emergency clinical journey. The original big six (Trauma, AAA, IUP, Cholecystitis, pericardial effusion, DVT-PE) remain core and form the ‘RESUS-Ultrasound’ assessment. Often the role of supporting interventional practices- venous access, drainage of fluid collections, nerve blocks etc. is why clinicians may reach for the ultrasound. Ultrasound helps to make the intervention easier and so safer for patients. Conclusion Ultrasound is fantastic. If you have some experience develop it further and if you have none then get in contact to start the short journey to learn the basics and revolutionise your clinical practice and bedside decision-making.

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• PETER KAS

UNSTABLE PATIENT AND SURGEON WANTS A CT

PAN$Scan$$Shane$Curran$$The$pan$scan$is$a$term$that$is$used$most$in$relationship$to$trauma$where$a$patient$with$multiple$or$severe$trauma$undergoes$a$series$of$scans$$with$the$aim$being$to$ensure$that$no$serious$injury$is$missed.$$The$original$total$body$scan$originated$in$diamond$mines$to$ensure$no$theft$was$occurring$$$Trauma$is$not$the$only$indicator$for$total$body$scans$with$$oncology$in$particular$embracing$the$total$body$scan$$Concerns$with$the$pan$scan$include$the$amount$of$radiation$involved$with$a$widely$quoted$figure$of$1:2000$new$cancers$for$$each$total$body$scan.$This$number$is$a$lifelong$risk$,$with$$a$greater$lifelong$risk$for$younger$patients$$$Proponents$of$the$panscan$point$to$the$number$of$injuries$that$are$found$and$the$fact$that$$the$patient$$population$who$have$pan$scans$have$a$decreased$mortality$,$especially$with$the$$Patient$who$may$have$a$distracting$injury$$$Opponents$of$the$pan$scan$point$to$the$number$of$$incidental$findings$that$are$discovered$and$that$not$all$of$these$findings$are$communicated$to$the$patients$.$$$There$are$alternative$diagnostic$tools$to$assist$in$the$management$of$the$trauma$patient$$including$clinical$decision$rules$and$the$expanded$use$of$ultrasound$$$$$$

CERVICAL(SPINE(CLEARANCE(IN(CHILDREN(!The!paediatric!cervical!spine!can!be!difficult!to!clear,!especially!if!we!don't!see!a!lot!of!patients!with!this!condition.!!When!it!comes!to!cervical!spine!injuries!there!is!some!distinct!differences!between!adults!and!children.!!Injuries!in!children!tend!to!be!high,!ie.!C1!to!C2!levels.!!This!is!as!a!result!of!children!having!comparably!larger!head,!which!produces!different!forces!on!the!cervical!spine.!!The!mechanism!of!injury!also!differs!in!children.!!Children!and!major!trauma!are!usually!car!occupants!or!pedestrians.!!Specific!problems!related!to!children!include:!!

•! Less!than!3!years!of!age!children!tend!to!be!nonEverbal,!thus!it!is!difficult!to!ascertain!if!there!is!pain!and!exactly!where!it!is.!!At!this!age!it!is!difficult!to!obtain!a!PEG!view!as!children!not!able!to!keep!their!mouth!open!for!prolonged!periods!for!this!view.!

•! The!paediatric!cervical!spine!does!not!become!adult!like!until!approximately!8!years!of!age.!•! The!developing!tissues!are!more!prone!to!ionising!radiation.!!A!CT!scan!of!the!cervical!spine!

can!expose!children!to!the!equivalent!of!100!chest!xErays.!!In!the!adult!population!we!have!two!validated!clinical!rules:!!

•! The!Canadian!CEspine!rule!(Stiell!et!al!JAMA!2001;!286!(15)!1841E1848)!•! The!National!Emergency!XEradiography!Utilisation!Study!(NEXUS)!Hoffman!et!al,!NEJM!2000;!

343!(2);!94E9!!There!is!no!decision!rule!available!for!use!with!children.!!We!know!that!there!are!some!risk!factors!that!increase!the!likelihood!of!cervical!injury!and!these!include:!!

•! Altered!mental!status!•! Focal!neurology!•! Neck!pain!•! Torticollis!•! Substation!torso!injury!•! Diving!injury!•! High!risk!motor!vehicle!crash!•! Inherited!genetic!disorders!or!bone!and!connective!tissue!

!In!terms!of!clinical!decision!rules!the!validation!of!the!NEXUS!rule!includes!patients!less!than!18!years!old.!!There!is!a!total!of!3065!patients!under!18!years!of!age.!!In!that!group!there!were!26!cervical!injuries.!905!patients!were!≤!8!years!old.!!Only!4!injuries!were!found!in!this!group!and!all!were!high!cervical.!!We!can!use!this!rule!however!the!number!of!injuries!were!small.!!The!authors!therefore!cautiously!endorsed!it.!!The!Canadian!CEspine!rule!is!more!specific!for!those!≥!16!year!old!group.!!Trying!to!apply!two!different!rules!may!be!quite!confusing.!!My!recommendation!is!we!apply!one!rule!and!that!is!the!NEXUS!rule.!!

EMCORE 2016

Beware the Flail Chest Dr. Sam Bendall

Definition: Anatomical: Flail chest occurs when two or more ribs are broken in at least two places – results in a free segment of chest wall that can move independently of the remainder of the chest during ventilation. 3 This segment can move paradoxically – indraws during inspiration due to the negative intrathoracic pressure. Flail chest produces mechanical AND physiological abnormalities. Usually indicates LARGE FORCES (energy transfer) involved in the injury. Therefore, you need to LOOK HARD for other associated injuries. Some may be life threatening. Caveats to this:

• Elderly – can occur with minimal force such as a fall from standing height.

• Children – elastic chest wall – may not see flail but will have injury to underlying structures.

Associated Injuries:

• Pulmonary contusions (always!) • Pulmonary parenchymal damage • Haemothorax • Pneumothorax • Cardiac contusions (esp if sternal injury) • Associated great vessel injury – these are often lethal at the scene

The elderly are worse off:

• “Elderly patients with rib fractures have twice the morbidity and mortality of younger patients. For each additional rib fracture in the elderly, mortality increases by 19% and the risk of pneumonia by 27%. Improvements, in terms of hospital stay or mortality, have not been shown in patients treated using epidural analgesia but have trended towards significance, especially in the elderly population. Larger studies are required in this area (Bulger et al., 2000).” 1

Mechanical AND Physiological Problems:

Mechanical Problems – due to direct injury to the ribs and soft tissues:

• Pain – results in splinting and atelectasis +/- impairment of ventilation. • Muscle spasm may delay the appearance of the flail. • Inability to cough & clear secretions

Needle, Finger and Tube Thoracostomies Needle Thoracostomy

x Advantages: o Very quick o Easy to perform o Little training required o Minimal risk of damage to NV. bundle

x Disadvantages:

o Only a temporising measure o Only useful for gases o Easily dislodged or kinked o Requires replacement by a tube thoracostomy at the earliest convenience

Finger Thoracostomy

x Advantages: o Quite quick o Easy to perform o Little training required

x Disadvantages: o Prehospital only o Only a temporising measure o No ability to suction o Messy o I suggest replacement by a tube thoracostomy at the earliest convenience

Tube Thoracostomy

x Advantages: o Drains both liquids and gases (depending on the calibre) o Allows large volumes of drainage o Can be secured firmly o Can be attached to a valve such as underwater seal to allow for one way

drainage and application of suction. x Disadvantages:

o Technically more challenging o Requires a trained operator o Slight risk of vascular injury in inexperienced hands o Fear may lead to reluctance and fatal delay

Crush&syndrome&&Shane&Curran&&Crush&syndrome&was&originally&described&in&the&second&world&war&with&people&who&were&&trapped&in&bombed&buildings&and&the&subsequent&description&of&the&disease&course&&Crush&syndrome&is&a&crush&injury&with&associated&systemic&manifestations&related&to&rhabdomyolysis&and&the&subsequent&release&of&toxic&metabolites&,&in&particular&causing&renal&impairment&&&Rhabdomyolysis&management&includes&management&of&the&original&injury&and&supportive&treatment&of&the&renal&impairment&&including&renal&dialysis&&Only&10&%&of&cases&have&the&classical&triad&of&myalgia&weakness&and&myoglobinuria&Myoglobinuria&is&classically&described&as&tea&coloured&urine&&&Compartment&syndrome&occurs&when&there&is&swelling&in&a&limited&volume&fascial&compartment&.&Early&suspicion&and&investigation&is&paramount&to&reversibility&of&any&sustained&injury&&&Early&measurement&of&compartment&pressures&is&vital&.&&Use&of&a&pressure&transducer&similar&&to&&arterial&line&monitoring&is&the&easiest&way&&A&normal&pressure&is&8I10&MM&Hg&.A&pressure&of&30&mmHg&usually&indicates&the&need&for&operative&intervention&& &

EMCORE 2016

Resuscitating Kids – It’s all in your mind

Dr. Sam Bendall Resuscitating paediatric patients is challenging for most clinicians. We are told repeatedly that they are “not little adults” which makes them aliens. They come with parents and emotional triggers for most clinicians. It takes a strong willed clinician to not put themselves subconsciously in the same position as the parent in front of them. So how do we get around that as docs who have to resuscitate kids fortunately relatively infrequently? Well….. it’s all in the way you think about it.

“Whether you think you can, or you think you can't--you're right.” ― Henry Ford

So we need to reframe paediatric resuscitation to make it something we KNOW we can do: Here are my suggestions:

1. K.I.S.S Ken’s First Law: Air goes in and out, blood goes round and round – any variation on that is a bad thing!

• Airway management- Position ear to sternal notch, do the simple things well, focus on oxygenation not application of plastic.

• Trauma – a small amount of blood loss can be a lot (kids only have 80ml/kg to play with). Actively look for underlying injuries even if the bones are intact.

• Sepsis – Who knows whether it is viral or bacterial in the first instance. If they look toxic they are.

2. Know the peculiarities of aliens

• Anatomical differences • Circulation differences esp. neonates • What is “normal” for each age group and how you can communicate to get what

you want (PEMSoft app has some great videos on what is normal for each age group_

3. Mitigate the potential for bad maths & unnecessary errors

• Paediatric calculators – don’t rely on your mental maths • Have a system and make it idiot proof e.g. Broselow, drug cards, 1ml syringes • Cross check everything

Fluids'and'kids.'Jaycen'Cruickshank'Everything+you+need+to+calculate+is+available+online+RCH$website$–$guidelines$and$calculators$or$NSW$Health$guideline$–$or$local$–$paediatric$portal$http://www.rch.org.au/clinicalguide/forms/fluids?calculator/?LangType=3081$http://www.rch.org.au/clinicalguide/guideline_index/Intravenous_Fluids/$$Key+principles+

•! Reduce$ risk$ of$ hyponatraemia$ through$ increasing$ low$ sodium$ content$ and$ limiting$ low$Na$fluids$

•! Address$glucose$requirements$of$kids/neonates$through$increased$glucose$content$•! Consistent$addition$of$K+$as$early$as$considered$safe$and$appropriate$•! Recent$evidence$supports$isotonic$saline$solutions$•! Standardised$care$to$1000ml$bags$+$standard$labeling$•! Special$care$nursery$is$special$–$we$wont$cover$that$in$detail$here.$

$

$$For+Gastroenteritis+There+are+nasogastric+fluid+recommendations.++This+talk+covers+IV+fluids+The$RCH$guidelines$allow$you$to$calculate$maintenance$plus$losses$

•! In$the$past???$suggests$deficit$½$over$8$hours$½$over$16$hours$–$not$currently.$They$also$recommend$rapid$rehydration$10mls/kg/hr$for$4$hours$if$Age/4$They$also$recommend$Table$4$(for$your$reference)$of$gastroenteritis$guideline$Base'on'initial'weight'8'Example'10kg'child''Moderate?severe$dehydration$=$65$mls/hr,$noting$that$the$maintenance$recommendation$is$40mls/hr$This$equals$25mls/hr$to$cover$deficit$which$is$additional$600mls/24$hours,$because$they$are$aiming$re$replace$a$deficit$over$48$hours$and$avoid$sodium$issues$In+summary+After'initial'boluses,'give'maintenance'+'correct'deficit'slowly'Choose'an'appropriate'fluid'–'RCH'recommend'Plasmalyte8148'No'need'for'complex'Na'and'Cl'calculations.+ +

EMCORE 2016

Rashes that Kill Dr. Sam Bendall

Triage: Rash…… If this makes you groan because it doesn’t involve A, B C or D, think again. Here are 10 rashes you NEED to know so you can recognize them before the disease kills your patient….. Infections:

1. Purple is bad: Purpuric Rashes + Fever = NOT good Purpura Fulminans – life threatening disorder. Causes microvascular thrombosis leading to tissue necrosis, skin infarction and haemorrhage. DIC also often present. Characteristic appearance – erythema followed by central areas of black or blue haemorrhagic necrosis with an erythematous border Associated with: Bacterial Infections:

- Neisseria Meningitidis (about 170 cases in Australia per year) - Streptococcus Pneumoniae - Group A Streptococcus - Varicella

Congenital – neonatal purpura fulminans – Protein C or S deficiency. Occurs on 1st day of life. DIC & low protein C antigen. Other Causes of petechial/purpuric rashes: Viral infections:

- Parovirus - Enterovirus incl. echovirus & parechovirus - Adenovirus - Rickettsial disease (Rocky Mountain Spotted Fever) – mortality pre antibiotics = 30 up to

80%. Now 3 – 7%. Tick borne illness. Rash develops day 3-5. Absent in 10%. US & Sth America.

Haemorrhagic fevers:

- Dengue (arbovirus) – skin manifestations in 40-50% - maculopapular /petechiae /purpura /ecchymoses

- Ebola (filovirus)

Clostridial Enteritis Necrotans

Background: Pigbel was first described in PNG in the 1960s as a new disease (1), but was in reality a manifestation of a disease first noted in Germany and Denmark in the late 1940s and known as "Darmbrand," meaning " fire bowels" (2). Its appearance was limited to the early years after World War II; the highest incidence was in 1948, after which the disease disappeared. The overall mortality was about 40%. Clostridium perfringens type F, later shown to be a heat resistant variant of type C, was isolated from many cases. Pathophysiology: Heat stable E toxins of C perfringens type C are found in pig intestines. Poor butchering techniques and incomplete cooking with lack of cold storage, as commonly encountered at pig feasts, contributes a large bacterial and toxin load taken on during feasts. Under normal circumstances the gut trypsin inactivates the E toxin before it can cause damage to the small intestine. Unfortunately populations who are malnourished and subsist on a low protein diet have low trypsin levels. This was thought to be the cause of the post war outbreak in Lubeck, Germany (2). In Papua New Guinea there are 2 other variables that combine with a protein-malnutrition to produce a deadly triad of pigbel; sweet potato is very high in anti-trypsin, further supressing ant endogenous trypsin activity, ascaris worms produce anti-trypsin as part of a defence mechanism when they invade the gut. Given the high prevalence of ascaris infestation (up to 68% in one survey) (3) and a diet that comprises almost entirely of kaukau, the population of the Highlands are very susceptible to pigbel. Figure 1. Intraoperative photograph of patulous necrosis of the small bowel due to pigbel. (4)

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