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DevelopmentsintheManagementofDiabetic
KetoacidosisinAdults
ImplicationsforAnaesthetists
AHallettMBChBFRCAAModiMBBSMDFRCANLevyMBBSBScFRCAFFICM
BJAEducation.201616(1):814.

Introduction
Diabeticketoacidosis(DKA)isamedicalemergency.Thediagnostictriadis:

i. Ketonaemia3.0mmollitre1orsignificantketonuria(morethan2+onurinesticks)

ii. Bloodglucose>11.0mmollitre1orknowndiabetesmellitus

iii. Bicarbonate<15.0mmollitre1,venouspH<7.3,orboth.

DKAcanoccurinbothtype1andtype2diabetesmellitusand,althoughpreventable,itremainsafrequentandlife
threateningcomplication.ErrorsinthemanagementofDKAarenotuncommonandareassociatedwithsignificant
morbidityandmortality.ThemajorityofmortalityandmorbidityinDKAareattributabletodelaysinpresentationand
initiationoftreatment.RapidrecognitionandtreatmentofDKAiscritical.

Toovercometheseconcernsandtohighlightcurrentmanagementstrategies,theJointBritishDiabetesSocieties
(JBDS)publishedguidelinesin2010.ThiswasupdatedinconsultationwiththeIntensiveCareSocietyinSeptember
2013.[1]

ThisarticlewillreviewthepathophysiologyofDKAandhighlightthemodernmanagementofDKAthatisrelevantfor
anaesthetists.AsummaryoftheJBDSguidelinespertinenttointensivistshasbeenpublished.[2]

Epidemiology
InEnglandin2010,therewere14375admissionstoacuteNHStrustswhereDKAwastheprimarydiagnosis.
Subsequently,itwasestimatedthat13%ofthesepatientswereadmittedtoIntensiveCareUnits(2%ofallgeneral
ICUadmissions).[3]Furthermore,theNationalDiabetesInpatientAudit2012foundthat0.5%ofinpatientswith
diabetesactuallydevelopedDKAasaninpatientwhilstinhospital.[4]

Themortalityratehasdecreasedinsomepatientpopulationshowever,intheelderlyandinpatientswith
comorbidities,itremains>5%.

Pathophysiology
DKAresultsfromarelativeorabsoluteinsulindeficiencywithaconcomitantincreaseincounterregulatory
hormonessuchasglucagon,catecholamines,cortisol,andgrowthhormone.Hyperglycaemiaensuesbecauseof
increasedgluconeogenesis,acceleratedglycogenolysis,andimpairedglucoseutilizationbyperipheraltissues.

Thisismagnifiedbytransientinsulinresistancebecauseofthehormoneimbalanceitself.Thecombinationofinsulin
deficiencyandincreasedcounterregulatoryhormonesleadstothereleaseoffreefattyacidsandtheirunrestrained
oxidationinthelivertoketones.Theseketonesincludeacetone,3betahydroxybutyrate,andacetoacetate.The
predominantketoneinDKAis3hydroxybutyrate.Hydrogenionsproducedbythedissociationoftheketone
bodiescausesthemetabolicacidosis.[5]

Hyperglycaemiacausesosmoticfluidshiftsfromintracellulartoextracellularcompartments.Theglucoseloadinthe
glomerulartubulesexceedstherenalthresholdleadingtoglucosuriaandanobligatoryosmoticdiuresis.This

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diuresiscausesalossofsodium,potassium,andphosphatealongwithwaterandglucose.

Causes
Thethreemostcommoncausesare:

i. Anunderlyinginfection

ii. Missedinsulintreatment

iii. Firstpresentationofdiabetesmellitus.[6]

InadequateinsulintherapyistherecognizedcauseofhospitalacquiredDKA.Thismaybecausedbyinadequate
prescriptionoradministrationofinsulin,orinsufficientmonitoringofcapillarybloodglucose(CBG).

Thecausemayoccasionallynecessitateemergencysurgicaltreatment(e.g.appendicitisinfarctedbowelincision
anddrainageofabscessectopicpregnancy).

ClinicalPresentation
DKAoccurspredominantlyinpatientswithtype1diabetes,butitcanalsodevelopinpatientswithketonepronetype
2diabetes.ThereisawideclinicalspectruminthepresentationofDKA.DKAisarecognizedcauseoftheacute
abdomen,andthisinitselfcanactuallyresultinunnecessaryemergencysurgery.Presentationintype2diabetesis
thesameasintype1diabeteshowever,somestudieshavefoundtheretobeadifferentbiochemicalpresentation
withalesssevereacidosisandatendencyfornormalinitialserumpotassiumlevels.[7]

Investigations
Initialinvestigationsfallintothreecategories:

i. EstablishdiagnosisofDKA

ii. Baselineinvestigations

iii. Identifycause.

Ongoinginvestigationsarethenrequiredtomonitortheeffectoftreatment,andtoensuresuccessfulandsafe
treatment.

InvestigationstoEstablishDiagnosisofDKA

AsDKAisthetriadof:

i. Ketonaemia3.0mmollitre1orsignificantketonuria(morethan2+onurinesticks)

ii. Bloodglucose>11.0mmollitre1orknowndiabetesmellitus

iii. Bicarbonate<15.0mmollitre1,venouspH<7.3,orboth.

Thefollowinginvestigationsaremandatory.

i. Capillaryketonelevels/urinalysisforketones

ii. Bloodsugar

iii. BloodgasforpH,bicarbonate,orboth.

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KetoneMeters.Inthepast,diagnosisandsuccessfultreatmentofDKAwasguidedbyCBGwiththeerroneous
assumptionthatcorrectionofhyperglycaemiawouldbeamarkerforsuppressionofketogenesisandsuccessful
reversalofacidosis.However,CBGisbothapoordeterminantofseverityandapoorsurrogatemarkerfor
successfultreatment.Euglycaemicketoacidosisispossibledependingonthehepaticglycogenstoresbeforethe
onsetofDKA.Thisdemonstratesthenecessityforketonemonitoring.

Ketonemeters(Fig.1)arenowavailableforrapidtestingforhydroxybutyrateatthebedside.Handheldketone
metersareoperatedinanidenticalfashiontobedsideCBGmeters.Resultsareavailablewithin10sallowing
immediatedifferentiationbetweensimplehyperglycaemiaandketoticstates.

Figure1.

GlucoMenbloodglucosemeter
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Trialshavefoundthattheutilizationofbloodketonetestingismoreeffectivethanurineacetoacetatetestingin
improvingdiagnosisandtheiruseisassociatedwithareducedtimetorecoveryfromDKAandshorterhospitalstay.
[8]

BloodGas.Tomakethediagnosis,abloodgasisessentialfortheassessmentoftheacidosisandserum
bicarbonatelevels.RecentevidencehasshownlittledifferencebetweenarterialandvenouspHandbicarbonate.[9]
ThesesmalldifferencesareinconsequentialtothediagnosisormanagementofDKA,andthereforetheJBDS
guidelinesrecommendtheuseofvenousbloodgasesifthepatientismanagedontheward,inordertoprevent
repeatedarterialpunctures.

BaselineInvestigations

Theseincludefullbloodcount,urea,creatinine,potassium,sodium,chloride,CRP,andliverfunctiontests.

InvestigationstoIdentifyCause

ItisimperativetodiscoverthecauseoftheDKAandinvestigationsshouldbebasedontheclinicalfindings.
CommoninvestigationsincludeECG,bloodcultures,amylase,andpregnancytest.

OngoingInvestigations

Toassuresaferesponsetotreatment,thefollowingshouldoccurhourlytillresolutionoftheketosis:

i. CBG/arterialbloodglucose(ifarteriallinesited)

ii. Capillarybloodketones.

Toassuremetabolicstability,thefollowingshouldoccurataminimumof2hourlyintervalsuntilresolutionofthe
ketosis:

i. pH

ii. bicarbonate

iii. potassium.

InitialManagement
DKAisalifethreateningconditionandresuscitationalongwithinitialtreatmentmustoccursimultaneouslywith
clinicalassessment.Appropriatehistory,examination,andinvestigationsshouldbeundertakentodiagnosethe
condition,identifytheseverity,andidentifythecause.

Initialmanagementshouldfocuson:

i. Airwayprotection,ifrequired

ii. Fluidresuscitation

iii. Insulinadministration

iv. Assessmentofseverity

v. Identificationofcause.

Resuscitation
Anairway,breathing,circulation,disability,exposure(ABCDE)approachwillprovidestructuretotheinitial
resuscitation.Appropriatevenousaccessmustbeobtained.

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FluidResuscitation

ThemostimportantinitialtherapeuticinventioninDKAisfluidreplacementfollowedbyinsulinadministration.Itis
nowuniversallyagreedthatcrystalloidswithasodiumconcentrationintherangeof130154mmollitre1shouldbe
usedastheresuscitationfluid.IntheUK,thisisgenerallyeither0.9%salineorHartmann'ssolution.Thereis
ongoingdebateonwhichcrystalloidissuperior.Thereisevidencetosuggestthattheuseofbalancedcrystalloid
solutionsareassociatedwithafasterresolutionofthemetabolicacidosisandlesshyperchloraemicmetabolic
acidosis.[10,11]However,balancedsolutionssuchasHartmann'ssolutioncontainsinsufficientpotassium,andunder
NPSArules,3%potassiumchlorideshouldnotbestored/addedtofluidsonthegeneralwards.[12]Therefore,the
useof0.9%salinewithpremixedpotassiumchlorideisadvocatedforwardandtheatreuse.Criticalcarecanboth
administerconcentratedpotassiumcentrally,andaddpotassiumtoHartmann'ssolution.Thus,criticalcaremay
choosetouseHartmann'ssolutionastheprimaryfluidforresuscitation.

isanexampleofatypicalfluidreplacementregimenforapreviouslywell70kgadult.However,theexactrateof
infusionshouldbeformulatedafterclinicalassessmentoftheindividualpatient.Ifthepatientisshocked,thepatient
shouldreceiveaninitialbolusof500mlover<15min,andfurtherfluidbolusesdependentonclinicalre
assessment.

Table1.Typicalfluidreplacementregimenforapreviouslywell70kgadultonthegeneralward

Fluidnumber Fluid Rate

Initialbag 1litre0.9%saline 1000mlh1

2ndbag 1litre0.9%salinewithpremixedpotassiumchloride 500mlh1

3rdbag 1litre0.9%salinewithpremixedpotassiumchloride 500mlh1

4thbag 1litre0.9%salinewithpremixedpotassiumchloride 250mlh1

5thbag 1litre0.9%salinewithpremixedpotassiumchloride 250mlh1

6thbag 1litre0.9%salinewithpremixedpotassiumchloride 150mlh1

Furtherfluid 1litre0.9%salinewithpremixedpotassiumchloride Clinicalassessment

Withregularreassessment
InsulinAdministration

Administrationofi.v.humansolubleinsulinismandatory.Classicallytheinsulinhasbeentitratedagainstthe
surrogatemarkerofthebloodglucoseusingavariableratei.v.insulininfusion(VRIII).Theterm'variableratei.v.
insulininfusion'hasnowreplacedtheambiguousandobsoleteterm'slidingscale'.Itisnowrecognizedthatglucose
levelsareapoorsurrogatemarkerforresolutionofketosis,andusingthebloodglucoseasamarkertoguideinsulin
therapymay(anddoes)leadtotheerroneousactionofreducinginsulinwhilstthepatientisstillhighlyketotic.A
fixedrateadministrationofi.v.insulinwhilstthepatientremainsketoticavoidsthisrisk.Thus,recentevidenceand
guidelinessuggestthataweightdependentfixedratei.v.insulininfusion(FRIII)shouldbeadministered,ratherthan
thevariableratei.v.insulininfusion(VRIII).summarizestheadvantagesanddisadvantagesofanFRIII.

Table2.AdvantagesanddisadvantagesofanFRIII

Advantages Disadvantages

(i)FasterresolutionofDKA
(ii)Notitrationoftheinsulinagainstthefalse
surrogatemarkerofcapillaryglucose
RiskofhypoglycaemiaifCBGisnotmeasuredhourlyand
additionalglucosecontainingsolutionsnotadministered
onceCBG<14mmollitre1

(iii)CompleteresolutionofDKAprovidedthe
FRIIIisturnedoffoncetheketonelevelsare
<0.6mmollitre1

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PreparationandAdministrationoftheFixedRatei.v.InsulinInfusion.TheFRIIIisadministeredviaaninfusion
pump.TheFRIIIisconstitutedbyadding50unitsofhumansolubleinsulin(Actrapid,HumulinS)to0.9%sodium
chloridetomakeafinalvolumeof50ml(1unitml1).Ideallythisshouldbeprovidedasareadymadeinfusion.The
FRIIIisthenadministeredatafixedrateof0.1unitkg1h1(i.e.7mlh1ifweightis70kg).Weightshouldbe
estimatedifnotavailable,andpregnantpatientsshouldhavetheircurrentweightused.

Metabolictargetsforthecontinuationofthecurrentfixedrateinsulininfusionare:

i. Reductionofbloodketoneconcentrationby>0.5mmollitre1h1

ii. Ifbloodketonemeasurementisnotavailable,thevenousbicarbonateshouldincreaseby3.0mmollitre1h
1

iii. ReductioninCBGby3.0mmollitre1h1.

Iftheabovetargetsarenotbeingachieved,itisnecessarytoreassessthepatientandconsiderthecausesofnon
successfultreatment.Thismayinclude:

i. Nonadministrationoftheinsulinforanyreason(e.g.tissuedcannula,pumpnotrunning,antisyphonvalve
notused,etc.).

ii. Ongoingcomorbiditythatwillneedseniorreview

iii. Insufficientinsulin.

Ifitisdeemedthatunsuccessfultreatmentissecondarytoinsufficientinsulin,theFRIIIwillneedtobeincreasedin
incrementsof1unith1untilthetargetsaremet.Amaximumrateof15unitsh1isrecommended.

SafeCessationoftheFRIII.TheFRIIIshouldbecontinueduntilresolutionoftheketosis.ResolutionofDKAis
definedas:

i. pH>7.3

ii. bicarbonate>15.0mmollitre1

iii. bloodketonelevel<0.6mmollitre1.

BeforestoppingtheFRIII,itisnecessarytoadministerinsulininanotherformotherwise,thepatientwillredevelop
ketosis.Thepatientcaneitherberecommencedontheirusualregimen(iftheyareeatinganddrinking)orconverted
toavariableratei.v.insulininfusionwithconcurrentadministrationof5%dextrosein0.45%salinewith0.15%
potassiumchloride.Thistransitionshouldideallybemanagedbythediabetesspecialistteam.

Toaidthetransitionfromi.v.insulintosubcutaneousinsulins,itnowadvisedthatthelongactinganalogueinsulins
arecontinued.ThelongactinganalogueinsulinsareLevemir,Lantus,andTresiba.Someunitsarealso
beginningtoexperimentwiththecontinuationofthelongactinghumanbasalinsulinssuchasHumulinI,
Insulatard,andInsumanBasal.Continuationofthelongactinginsulinsavoidsreboundhyperglycaemiawhenthe
i.v.insulinisstoppedandmaysubsequentlyreducethelengthofstay.[13]

ManagementofBloodGlucose<14mmolLitre1

TheFRIIIshouldbecontinueduntilthereisresolutionoftheketosishowever,itmaycausehypoglycaemiabefore
resolutionoftheketosis.Therefore,itismandatorytoperformhourlyCBGsandtobepreparedtogiveadditional
glucoseoncetheCBGis<14mmollitre1.Itisrecommendedthat10%glucoseat125mlh1shouldbe
administered.Intheatre,20%glucoseat50mlh1or50%glucosemaybeadministered.Therateoftheprimary
resuscitationfluidmayneedtobealteredtopreventfluidoverload.

ManagementofContinuousSubcutaneousInsulinInfusion(CSII)Pumps

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Becauseoferraticandunpredictableinsulinabsorption,thesedevicesshouldprobablybestoppedand
disconnectedduringanepisodeofDKA,andonlyreinstatedwithdiabetesspecialistteaminput.

CriticalCareReferral
Patientsshouldbeconsideredforcriticalcarereferralifanyofthefollowingcriteriaarepresent:

i. GlasgowComaScore(GCS)<12orabnormalAVPU(alert,voice,pain,unresponsive)scale

ii. Bloodketones>6mmollitre1

iii. Bicarbonatelevel<5mmollitre1

iv. Venous/arterialpH<7.0

v. Hypokalaemiaonadmission(<3.5mmollitre1)

vi. Oxygensaturation<92%onair(assumingnormalbaselinerespiratoryfunction)

vii. SystolicBPbelow90mmHg

viii. Pulseover100orbelow60beatsmin

ix. Aniongap>16[Aniongap=(Na++K+)(Cl+HCO3)].

Itisoftennecessarytoadmitemergencysurgicalpatientstoalevel2or3facility,bothpreandpostsurgery.

DKAComplications
MortalityfromDKAintheUKhasfallensignificantlyinthelast20yrfrom7.96to0.67%.[1]Hypokalaemia,acute
lunginjury,andcomorbidstatessuchaspneumonia,sepsis,andmyocardialinfarctionareassociatedwith
increasedmortality.CerebraloedemaremainsthemostcommoncauseofdeathinDKAinchildren.Theexact
mechanismisuncertainhowever,itisfeltthatcerebraloedemamayberelatedtocerebralhypoperfusionbefore
treatment,withsubsequentvasogenicoedemaoccurringduringDKAtreatmentasaresultofreperfusionof
previouslyischaemicbraintissue(i.e.theosmoticfluctuationsduringDKAtreatmentdonotplaytheprimarycausal
role).[14]

summarizestheriskfactors,signsandsymptoms,immediatetreatmentandalsothedifferentstrategiesthatare
utilizedbypaediatricianstoreducetheriskofcerebraloedema.[15]

Table3.Summaryofriskfactors,signsandsymptoms,initialtreatmentofcerebraloedema,andthestrategies
usedtominimizetheriskofcerebraloedemainchildren

Majordifferencesintreatmentof
Riskfactorsfor Initialtreatmentof
Signsandsymptoms paediatricDKAtominimizeriskof
cerebraloedema cerebraloedema
cerebraloedema

(i)Youngerage
(ii)Newonset
diabetes
(iii)Longerdurationof
symptoms
(iv)Greater
hypocapniaat
presentationafter
adjustingfordegreeof (i)Headache
(i)Immediatei.v.
acidosis (ii)Slowingofheartrate
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(v)Increasedserum (iii)Changein mannitolor

(i)Noi.v.bolusesofinsulin
ureanitrogenat neurologicalstatus hypertonic3%
(ii)Commencementofi.v.insulin
presentation (restlessness,irritability, saline
after1hoffluidtreatment
(vi)Moresevere increaseddrowsiness, (ii)Reducefluids
(iii)Gradualratherrapidrestoration
acidosisat incontinence) by1/3
ofnormovolaemia(>48h)
presentation (iv)Specificneurological (iii)Intubationand
(iv)Useof0.9%salineinitially(1st
(vii)Bicarbonate signs(e.g.cranialnerve ventilationand
46h)andthenconsiderationof
treatmentfor palsies) avoidanceof
salinewithtonicity>0.45%according
correctionofacidosis (v)Increaseinblood aggressive
toserumsodiumandosmolality.
(viii)Anattenuated pressure hyperventilation
increaseinmeasured (vi)DecreasedO2 (iv)CTtoruleout
serumsodium saturation otherpathology
concentrationsduring
therapy
(ix)Greatervolumes
offluidgiveninthe
first4h
(x)Administrationof
insulininthefirsthour
offluidtreatment

FurtherManagement
MonitoringandReplacementofElectrolytes

Initialserumpotassiummaybenormal,raisedorlowinDKA.However,thereisatotalbodypotassiumdeficit.
Potassiumlossiscausedbyashiftfromtheintracellulartoextracellularspaceinexchangeforhydrogenionswhich
accumulateinacidosis.Theextracellularpotassiumisthenlostthroughosmoticdiuresis.

Theinitiallitreoffluidshouldnothavepotassiumadded.Providedtheserumpotassiumis<5.5mmollitre1,andthe
patientisnotoliguric,subsequentfluidsshouldhave40mmollitre1ofpotassiumchloride.

Adequatefluid,potassiumandinsulintherapywillresolvetheacidosisinDKA,buttheremaybedisturbancesof
otherelectrolytesincludingbicarbonate,sodium,andphosphate.Generally,theseelectrolyteimbalancesimproveas
theDKAistreatedeffectively.Typicalfluidandelectrolytedeficitsaresummarizedin.

Table4.TypicalfluidandelectrolytedeficitsinadultswithDKA

Water 100mlkg1

Sodium 710mmlkg1

Chloride 35mmolkg1

Potassium 35mmolkg1
NasogastricTube

Ketosiscausesdelayedgastricemptyingtherefore,theuseofnasogastrictubemayhelpprotecttheairwayinthose
patientswithanalteredmentalstate,andthosewhorequiresurgeryandanaesthesia.

UrinaryCatheter

Aurinarycathetershouldbeinsertedinallpatientswithanalteredmentalstate,thoseinacriticalcaresettingor
undergoinganaesthesiaformonitoringofurineoutputandfluidbalance.Oliguriaisasignofacutekidneyinjury.

VenousThromboembolismRiskAssessmentandProphylaxis

Allpatientsshouldreceiveappropriatevenousthromboembolism(VTE)riskassessmentandsubsequent

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prophylaxis.DehydratedpatientswithDKAareathighriskofVTE.Bothchemical(e.g.lowmolecularweight
heparin)andphysical(e.g.antiembolicstockings)thromboprophylaxisshouldbeconsidered.

Antibiotics

Ifinfectionissuspectedappropriateantibiotictherapyshouldbecommencedaccordingtolocalpolicy.

InvolvementofDiabetesSpecialistTeams

ThediabetesspecialistteammustbeinvolvedinthecareofthosewithDKAassoonaspossibleintheacutephase.
Theirinvolvementhasbeenshowntoreducethelengthofstayandimprovepatientsafety.

PerioperativeManagementofDKA
Ifasurgicalcauseisidentified,seniormultidisciplinaryreviewtodiscusstheoptimaltimingofsurgeryisrequired.It
isalsoimportanttotryandensurethattheclinicalpictureofan'acuteabdomen'isnotsecondarytotheDKAin
ordertopreventneedlesssurgery.TheRoyalCollegeofSurgeons(RCS)document'EmergencySurgery,
Standardsforunscheduledsurgicalcare'providesausefulframeworkthatpromotestimelysurgerybutallowstime
foraccuratediagnosis,initialtreatment,andresuscitation.[16]Thestandardsaresummarizedbelow.

TimeframetoTheatreasSuggestedbyRoyalCollegeofSurgeons

i. Patientswithongoinghaemorrhagerequireimmediatesurgery.

ii. Patientswithsepticshockwhorequireimmediatesurgeryareoperatedonwithin3hofthedecisionto
operateasdelayincreasesmortalitysignificantly.

iii. Patientswithseveresepsis(withorgandysfunction)whorequiresurgeryareoperatedonwithinamaximum
of6htominimizedeteriorationintosepticshock.

iv. Patientswithsepsis(butnoorgandysfunction)whorequiresurgeryshouldhavethiswithinamaximumof18
h.

v. Patientswithnofeaturestoindicatesystemicsepsiscanbemanagedwithlessurgencybutintheabsenceof
modernandstructuredsystemsofcare,delaywillresultinunnecessaryhospitalstay,discomfort,illness,and
cost.

Eachpatientmustbemanagedindividually,includingtheoptimaltimetooperate.Unlessthepatientrequires
immediatesurgery,preoperativeresuscitationshouldoccurwithcorrectionofthehypovolaemia,themetabolic
acidosis,andtheelectrolyteimbalances.

PreoperativePreparation

Preoperativemanagementshouldbefocusedonoptimizingthepatientforsurgery.Furthermore,thesenior
anaesthetistmustdecidewhetheraVRIIIoraFRIIIwillbeusedintraoperatively.Iftheanaesthetistdecidestouse
theFRIIIintraoperatively,asaminimum,provisionmustbemadetohavesufficientvascularaccessforthe
following:

i. Administrationofthefixedratei.v.insulininfusionviaapump

ii. AdministrationoftheDKAresuscitationfluid(0.9%salinewith0.3%premixedpotassiumchlorideviaapump
maybethemostappropriate)attherateasguidedby.

Table1.Typicalfluidreplacementregimenforapreviouslywell70kgadultonthegeneralward

Fluidnumber Fluid Rate

Initialbag 1litre0.9%saline 1000mlh1

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2ndbag 1litre0.9%salinewithpremixedpotassiumchloride 500mlh1

3rdbag 1litre0.9%salinewithpremixedpotassiumchloride 500mlh1

4thbag 1litre0.9%salinewithpremixedpotassiumchloride 250mlh1

5thbag 1litre0.9%salinewithpremixedpotassiumchloride 250mlh1

6thbag 1litre0.9%salinewithpremixedpotassiumchloride 150mlh1

Furtherfluid 1litre0.9%salinewithpremixedpotassiumchloride Clinicalassessment

Withregularreassessment

iii. Administrationoftheintraoperativeresuscitationfluid

iv. Administrationofanaestheticbolusdrugs

v. Administrationof20%glucoseat50mlh1iftheCBGis<14mmollitre1.

vi. Abilitytocheckbloodglucose,potassium,andpHatregularintervals(minimumhourly).

Centralvenousaccessshouldbeobtainedtoguidefluidtherapyandtofacilitatetheadministrationofmultipledrugs
andfluids.

ConductofAnaesthesia

Patientsshouldbeanaesthetizedwithfullmonitoring,withanarteriallineinsitu,andintheatretofacilitate
continuousbloodpressuremonitoringpostinduction.Anarterialbloodgas(ABG)shouldbeobtainedbefore
inductiontogiveanindicationofthedegreeofacidosis,andtoensurenohyperkalaemia,assuccinylcholineisoften
usedtofacilitateintubationaspartofarapidsequenceinduction.Becauseofgastricstasis,thenasogastrictube
shouldbeaspiratedbeforeinductionofanaesthesia.

Patientsshouldbeintubatedwitharapidsequenceinductionwithcricoidpressure.Inviewofthehypovoalemic
stateandtheacidosis,anaesthesiamustbeinducedwithacombinationofdrugsthatpromotecardiovascular
stability.

Regular(minimumhourly)monitoringofABGsandbloodglucoseismandatory.Patientsshouldbeventilatedto
ensurenoiatrogenicrespiratoryacidosis.Potassiumneedstobekeptwithinthenormalrange,andreplacedas
indicated.Bloodglucoseneedstobekept>14mmollitre1whilstthepatientisbeingtreatedwiththeFRIII.

Considerationshouldbegiventoflow/cardiacoutputdirectedguidedfluidtherapygiventhecomplexintraoperative
fluidrequirementsofthesurgicalpatientwithDKA.

PostoperativeCare

Afteroperationpatientsshouldreceivenursingcareinalevel2/3environmentuntilresolutionoftheDKA.The
patientshouldreceivetheirnormallongactinginsulinanalogueatthenormaltime.TheDiabetesspecialistteams
willbeabletoassistinthetransitionfromi.v.insulintosubcutaneousinsulinandcanprovidefurthereducationand
reinforcethe'sickdayrules'tothepatient.

Summary

i. DKAisalifethreateningmedicalemergencycharacterizedbythebiochemicaltriadofketonaemia,
hyperglycaemia,andacidaemia.

ii. Bedsidemonitoringofcapillaryketones,glucose,bloodgases,andelectrolytesshouldbeusedtomakethe
initialdiagnosisandguidesubsequentmanagement.

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iii. Weightbasedfixedratei.v.insulininfusion(FRIII)isnowrecommendedratherthanavariableratei.v.insulin
infusion(VRIII),andthebloodglucosemustbekept>14mmollitre1withtheFRIII.

iv. 0.9%Salinewithpremixedpotassiumchlorideshouldbethemainresuscitationfluidonthegeneralwards
andintheatre.ThisisbecauseitcomplieswithNationalPatientSafetyAgencyrecommendationson
administrationofpotassiumchloride.

v. Balancedelectrolytesolutionsareassociatedwithafasterresolutionofacidosis,butcontaininsufficient
potassiumtojustifytheirsafeuseexceptincriticalcare.

vi. ThecauseoftheDKAmustbesoughtandsurgerymayberequired.

vii. Criticalcaremayberequired.

viii. Continuationoflongactinginsulinsmayreducecomplicationsduringtransitionfromi.v.tosubcutaneous
insulin.

ix. Earlyinvolvementofdiabeticspecialistteamsismandatory.

Sidebar
KeyPoints

Diabeticketoacidosis(DKA)isamedicalemergencyandbedsidecapillaryketonetestingallowstimely
diagnosisandidentificationofsuccessfultreatment.

0.9%salinewithpremixedpotassiumchlorideshouldbethemainresuscitationfluidonthegeneralwards
andintheatrethisisbecauseitcomplieswithNationalPatientSafetyAgencyrecommendationsonthe
administrationofpotassiumchloride.

Weightbasedfixedratei.v.insulininfusion(FRIII)isnowrecommendedratherthanavariableratei.v.insulin
infusion(VRIII).

Thebloodglucosemustbekeptabove14mmollitre1withtheFRIII.

Precipitatingfactor(s)needstobeidentifiedandtreated.Surgeryandalsocriticalcaremaybeindicatedto
managethepatientpresentingwithDKA.

References

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