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Diabeticketoacidosis(DKA)emergencydepartmentofshengjinghospitalzhanghongleiDiabeticketoacidosis(DKA)emecaseMrwang，M，52yearsoldchiefcomplaint：polydipsia,polyuria,weaknessfor1week，vomitingfor10hourphysicalexam:tachypnea,BP150/90mmHg,HR:120bpm,SaO2:99%ABG:PH:7.06,PaCO2:12mmHg,PaO2:117mmmHg,HCO3-:3.4mmol/L,Lactate:3.1mmol/L,BE:-24.7mmol/L，AG:34.6mmol/LBUN:15.9mmol/L,Cr:147mmol/LK+:8mmol/L,Na+:118mmol/L,Cl-:80mmol/L,Glu:33mmol/Lurinalysis:ketone:3+,gravity:1.024,glu:4+caseMrwang，M，52yearsold2problemwhatisthediagnosiswhatisthereasonofhyperkalemiaandhyponatremiawhatisthereasonofMetabolicacidosishowtodisposethediseaseifyouaretheERdoctoroncallproblemwhatisthediagnosis3
IntroductionDKAisasyndromeinwhichinsulindeficiencyandglucagonexcesscombinetoproduceahyperglycemic,dehydrated,acidoticpatientwithprofoundelectrolyteimbalanceIntroductionDKAisa4PathophysiologyLiverMuscleAdiposetissueGluconeogenesisKetogenesisGlucoseUtilizationLipolysisInsulin↓↓↑↓Glucagon↑↑→→Epinephrine↑↑↓↑Cortisol↑↑↓↑Grownthhormone→↑↓↑PathophysiologyLiverMuscleAdip5PathophysiologyPathophysiology6Pathophysiology
Insulindeficiencyandglucagonelevationresultsinhyperglycemia,whichinturncauseglycosuriaGlucoseintherenaltubulesdrawswater,sodium,potassium,magnesium,calcium,phosphorus,andotherionsfromthecirculationintotheurineThisosmoticdiuresiscombinedwithpoorintakeandvomitingproducestheprofounddehydrationandelectrolyteimbalanceassociatedwithDKA
Asaresultofacidosisanddehydration,however,theinitialreportedvaluesfortheseelectrolytesmaybehigherthanactualbodystores.PathophysiologyInsulind7PathophysiologyInsulindeficiencyresultsinactivationoflipasethatincreasescirculatingfreefattyacid(FFA)levels.Long-chainFFAs,nowcirculatinginabundanceasaresultofinsulindeficiency,arepartiallyoxidizedandconvertedinthelivertoacetoacetateandβ-hydroxybutyrate.ThisalterationoflivermetabolismtooxidizeFFAstoketonesratherthanthenormalprocessofre-esterificationtotriglyceridesappearstocorrelatedirectlywiththealteredglucagon/insulinratiointheportalblood.PathophysiologyInsulind8Pathophysiology
GlucagoniselevatedfourfoldtofivefoldinDKAandisthemostinfluentialketogenichormone.Despitetheincreasedpathologicglucagon-mediatedproductionofketones,thebodyactsasitdoesinanyformofstarvation,todecreasetheperipheraltissue’suseofketonesasfuel.Thecombinationofincreasedketoneproductionwithdecreasedketoneuseleadstoketoacidosis.
TheacidosiscausethebodytoincreaselungventilationandridthebodyofexcessacidwithKussmaul’srespirationPathophysiology9Etiology
DKAmaybecausedbycessationofinsulinintakeorbyphysicaloremotionalstressdespitecontinuedinsulintherapy.
Mostoften,DKAoccursinpatientswithtype1diabetesandisassociatedwithinadequateadministrationofinsulin,infection,ormyocardialinfarction(MI).DKAcanalsooccurintype2patientsandmaybeassociatedwithanytypeofstress,suchassepsisorgastrointestinal(GI)bleedingEtiologyDKAmaybec10DiagnosticStrategiesHistory
Clinically,mostpatientswithDKAcomplainofarecenthistoryofpolydipsia,polyuria,polyphagia,visualblurring,weakness,weightloss,nausea,vomiting,andabdominalpain.DiagnosticStrategiesHistory11DiagnosticStrategiesPhysicalExamination
TypicalfindingsincludetachypneawithKussmaul’srespiration,tachycardia,frankhypotension,theodorofacetoneonthebreath,andsignsofdehydrationDiagnosticStrategiesPhysical12
DiagnosticStrategies
LaboratoryTestsOnthepatient’sarrivaltotheED,serumandurineglucoseandketones,electrolytes,andarterialbloodgases(ABGs)shouldbechecked.Glucoseisusuallyelevatedabove350mg/dL;however,euglycemicDKA(bloodglucose<300mg/dL)hasbeenreportedinupto18%ofpatients.ABGsdemonstratealowpH.Metabolicacidosiswithananiongapisprimarilytheresultofelevatedplasmalevelsofacetoacetateandβ-hydroxybutyrate,althoughlactatealsocontributetothiscondition
DiagnosticStrategies
Laborat13DiagnosticStrategies
LaboratoryTestsAcompleteurinalysishelpsinthedeterminationofurineketone.Elevationsofurinespecificgravity,BUN,andhematocritsuggestdehydrationDiagnosticStrategiesLaborato14DiagnosticStrategies
LaboratoryTests
Sodiumisoftenlowinthepresenceofsignificantdehydrationbecauseitisstronglyaffectedbyhyperglycemia;hypertriglyceridemia;salt-poorfluidintake;andincreasedGI,renal,andinsensiblelossesWhenhyperglycemiaismarked,waterflowsfromthecellsintothevesselstodecreasetheosmolargradient,therebycreatingdilutionalhyponatremia.Lipidsalsodilutetheblood,therebyfurtherloweringthevalueofsodium
DiagnosticStrategiesLaborato15DiagnosticStrategiesLaboratoryTestsAcidosisandthehyperosmolarityinducedbyhyperglycemiashiftpotassium,fromtheintracellulartotheextracellularspace.Dehydrationproduceshemoconcentration,whichcontributestonormalorhighinitialserumpotassiumreadingsinDKA,evenwithprofoundtotalbodydeficitsWhileinsulinisadministeredandthehydrogenionconcentrationdecreases,thepatientneedsconsiderablepotassiumreplacement.
DiagnosticStrategiesLaborator16DiagnosticStrategiesLaboratoryTestsAlllaboratorydeterminationsmustbeinterpretedwithcaution.ThediagnosisofpancreatitisisconfoundedbytheusuallyelevatedurineandserumamylaselevelsinDKA.Typically,thisissalivaryamylase,butmostlaboratoriesarenotequippedtomakethisdistinction.Aserumlipasedeterminationhelpstodistinguishpancreatitisfromelevatedsalivaryamylaselevels.DiagnosticStrategiesLaborator17DifferentialConsiderations
Alcoholics,especiallythosewhohaverecentlyabstainedfromdrinking,withKussmaul’srespiration,andacidemicABGvaluesmayhavealcoholicketoacidosis.Thesepatientsmaybeeuglycemicorhypoglycemic,Alcoholicketoacidosisaccountsforapproximately20%ofallcasesofketoacidosis.KetoacidosiscanalsodevelopwithfastinginthethirdtrimesterofpregnancyandinnursingmotherswhodonoteatDifferentialConsiderations18DifferentialConsiderations
Otherentitiesthatmaymanifestwithvariouscombinationsofalteredmentalstatus,acidosis,andabdominalpainincludehypoglycemia,cerebrovascularaccident(stroke),trauma,sepsis,hyperglycemichyperosmolarnonketoticcoma,postictalstates,lacticacidosis,uremicacidosis,andabdominalemergencies.Intoxicationsbyethanol,salicylates,methanolallsharesomefeaturesofDKA.DifferentialConsiderations19ManagementGeneralMeasuresThecomatosepatient,especiallyifvomiting,requiresintubation.Thepatientinhypovolemicshockrequiresaggressivefluidresuscitationwith0.9%salinesolution.
Whenhyperglycemia,ketosis,andacidosishavebeenestablished,fluid,electrolyte,andinsulintherapyshouldbeginManagementGeneralMeasures20ManagementDehydrationTheseverelydehydratedpatientislikelytohaveafluiddeficitof3to5L.
Fluidrateshouldbeadjustedaccordingtoage,cardiacstatus,anddegreeofdehydrationtoachieveaurineoutputof1to2mL/kg/hr.Fluidresuscitationalonemayhelptolowerhyperglycemia.ManagementDehydration21ManagementInsulin
DKAcannotbereversedwithoutinsulin,andinsulintherapyshouldbeinitiatedassoonasthediagnosisiscertain.Inthepast,veryhighdosagesofinsulinwereadministeredtodiabeticpatientsinDKAbecausetheywerethoughttobeextremelyinsulin-resistant.However,low-dosageinsulintherapyhasprovedaseffectiveashigh-dosagetherapy
Highdosagesofinsulinhavepotentiallyharmfuleffects,includingagreaterincidenceofiatrogenichypoglycemiaandhypokalemia.Thecurrenttherapyofchoiceisregularinsulininfusedat0.1U/kg/hrupto5to10U/kg/hr,mixedwiththeIVfluids.ManagementInsulin22ManagementInsulin
Becausethehalf-lifeofregularinsulinis3to10minutes,IVinsulinshouldbeadministeredbyconstantinfusionratherthanbyrepeatedbolus.Whenthebloodglucosehasdroppedto250to300mg/dL,dextroseshouldbeaddedtotheIVfluidstopreventiatrogenichypoglycemiaandcerebraledema.InpatientswitheuglycemicDKA,dextroseshouldbeaddedtotheIVfluidsatthestartofinsulintherapyManagementInsulin23ManagementPotassiumPotassiumreplacementisinvariablyneededinDKA.Theinitialpotassiumlevelisoftennormalorhighdespitealargedeficitbecauseofsevereacidosis.Potassiumlevelsoftenplummetwithcorrectionofacidosisandadministrationofinsulin.Potassiumshouldbeadministeredwiththefluidswhilethelaboratoryvalueisintheupperhalfofthenormalrange.Renalfunctionshouldbemonitored.Inpatientswithlowserumpotassiumatpresentation,hypokalemiamaybecomelife-threateningwheninsulintherapyisadministered.
IVpotassiumshouldbevigorouslyadministeredinconcentrationsof20to40mEq/Lasrequired.ManagementPotassium24ManagementMagnesiumMagnesiumdeficiencyisacommonprobleminpatientswithDKAwithoutrenaldisease.BoththeinitialpathophysiologyandthetherapyforDKAinduceprofoundmagnesiumdiuresis.Magnesiumdeficiencymayexacerbatevomitingandmentalchanges,promotehypokalemiaandhypocalcemia,orinducefatalcardiacdysrhythmia.itisreasonabletoinclude0.35mEq/kgofmagnesiuminthefluidsofthefirst3to4hours,withfurtherreplacementdependentonbloodlevelsandtheclinicalpicture.ManagementMagnesium25Management
Acidosis
Acidosisalsodecreasesafterfluidinfusionalone.Increasedperfusionimprovestissueoxygenation,thusdiminishingtheformationoflactate.Increasedrenalperfusionpromotesrenalhydrogenionloss,theimprovedactionofinsulininthebetter-hydratedpatientinhibitsketogenesis.Bicarbonatetherapymaybeindicatedinseverelyacidemicpatients(pH≤7.0).TheuseofbicarbonateisnotwarrantedinlessillpatientsWhenbicarbonatetherapyisdeemednecessary,thepHshouldnotbecorrectedabove7.1.ManagementAcidosis26Prognosis
TheprecipitatingcausesofDKAmayhaveassociatedmorbidityandmortalityratesequaltoorworsethanthoseforDKAitself.TheseincludeiatrogeniccausesaswellasinfectionandMI.MorbidityinDKAislargelyiatrogenic:(1)hypokalemiafrominadequatepotassiumreplacement,(2)hypoglycemiafrominadequateglucosemonitoringandfailuretoreplenishglucoseinIVsolutionswhenserumglucosedropsbelow250to300mg/dL(3)alkalosisfromoveraggressivebicarbonatereplacement,(4)congestiveheartfailurefromoveraggressivehydration,(5)cerebraledemaprobablycausedbytoorapidosmolalshifts.Poorprognosticsignsincludehypotension,azotemia,coma,andunderlyingillnessPrognosisTheprecipitati27
Summary
DiabeticKetoacidosis（DKA）manifestsclinicallyasatriad:hyperglycemia(usually>200mg/dL),ketonemia,acidemia(pH<7.3).DKAcanbecausedbyanyconditionthatreducesinsulinavailabilityoractivityorthatincreasesglucagon.Precipitatingeventsusuallyincludeinfections,surgery,andemotionalorphysicalstressors.Treatmentisaimedatfluidreplacementoverthefirst24to48hours,insulinreplacement,andpotassiumreplacement.SummaryDiabeticKetoaci28keywhatisthediagnosisDKAwhatisthereasonofhyperkalemiaandhyponatremiaAsaresultofacidosisanddehydration,however,theinitialreportedvaluesforpotassiummaybehigherthanactualbodystores.Sodiumisoftenlowinthepresenceofsignificantdehydrationbecauseitisstronglyaffectedbyhyperglycemia;hypertriglyceridemia;salt-poorfluidintake;andincreasedGI,renal,andinsensiblelosseswhatisthereasonofMetabolicacidosisMetabolicacidosiswithananiongapisprimarilytheresultofelevatedplasmalevelsofacetoacetateandβ-hydroxybutyrate,howtodisposethediseaseifyouaretheERdoctoroncallTreatmentisaimedatfluidreplacementoverthefirst24to48hours,insulinreplacement,andpotassiumreplacementkeywhatisthediagnosis29
thanksforattentionthank30Diabeticketoacidosis(DKA)emergencydepartmentofshengjinghospitalzhanghongleiDiabeticketoacidosis(DKA)emecaseMrwang，M，52yearsoldchiefcomplaint：polydipsia,polyuria,weaknessfor1week，vomitingfor10hourphysicalexam:tachypnea,BP150/90mmHg,HR:120bpm,SaO2:99%ABG:PH:7.06,PaCO2:12mmHg,PaO2:117mmmHg,HCO3-:3.4mmol/L,Lactate:3.1mmol/L,BE:-24.7mmol/L，AG:34.6mmol/LBUN:15.9mmol/L,Cr:147mmol/LK+:8mmol/L,Na+:118mmol/L,Cl-:80mmol/L,Glu:33mmol/Lurinalysis:ketone:3+,gravity:1.024,glu:4+caseMrwang，M，52yearsold32problemwhatisthediagnosiswhatisthereasonofhyperkalemiaandhyponatremiawhatisthereasonofMetabolicacidosishowtodisposethediseaseifyouaretheERdoctoroncallproblemwhatisthediagnosis33
IntroductionDKAisasyndromeinwhichinsulindeficiencyandglucagonexcesscombinetoproduceahyperglycemic,dehydrated,acidoticpatientwithprofoundelectrolyteimbalanceIntroductionDKAisa34PathophysiologyLiverMuscleAdiposetissueGluconeogenesisKetogenesisGlucoseUtilizationLipolysisInsulin↓↓↑↓Glucagon↑↑→→Epinephrine↑↑↓↑Cortisol↑↑↓↑Grownthhormone→↑↓↑PathophysiologyLiverMuscleAdip35PathophysiologyPathophysiology36Pathophysiology
Insulindeficiencyandglucagonelevationresultsinhyperglycemia,whichinturncauseglycosuriaGlucoseintherenaltubulesdrawswater,sodium,potassium,magnesium,calcium,phosphorus,andotherionsfromthecirculationintotheurineThisosmoticdiuresiscombinedwithpoorintakeandvomitingproducestheprofounddehydrationandelectrolyteimbalanceassociatedwithDKA
Asaresultofacidosisanddehydration,however,theinitialreportedvaluesfortheseelectrolytesmaybehigherthanactualbodystores.PathophysiologyInsulind37PathophysiologyInsulindeficiencyresultsinactivationoflipasethatincreasescirculatingfreefattyacid(FFA)levels.Long-chainFFAs,nowcirculatinginabundanceasaresultofinsulindeficiency,arepartiallyoxidizedandconvertedinthelivertoacetoacetateandβ-hydroxybutyrate.ThisalterationoflivermetabolismtooxidizeFFAstoketonesratherthanthenormalprocessofre-esterificationtotriglyceridesappearstocorrelatedirectlywiththealteredglucagon/insulinratiointheportalblood.PathophysiologyInsulind38Pathophysiology
GlucagoniselevatedfourfoldtofivefoldinDKAandisthemostinfluentialketogenichormone.Despitetheincreasedpathologicglucagon-mediatedproductionofketones,thebodyactsasitdoesinanyformofstarvation,todecreasetheperipheraltissue’suseofketonesasfuel.Thecombinationofincreasedketoneproductionwithdecreasedketoneuseleadstoketoacidosis.
TheacidosiscausethebodytoincreaselungventilationandridthebodyofexcessacidwithKussmaul’srespirationPathophysiology39Etiology
DKAmaybecausedbycessationofinsulinintakeorbyphysicaloremotionalstressdespitecontinuedinsulintherapy.
Mostoften,DKAoccursinpatientswithtype1diabetesandisassociatedwithinadequateadministrationofinsulin,infection,ormyocardialinfarction(MI).DKAcanalsooccurintype2patientsandmaybeassociatedwithanytypeofstress,suchassepsisorgastrointestinal(GI)bleedingEtiologyDKAmaybec40DiagnosticStrategiesHistory
Clinically,mostpatientswithDKAcomplainofarecenthistoryofpolydipsia,polyuria,polyphagia,visualblurring,weakness,weightloss,nausea,vomiting,andabdominalpain.DiagnosticStrategiesHistory41DiagnosticStrategiesPhysicalExamination
TypicalfindingsincludetachypneawithKussmaul’srespiration,tachycardia,frankhypotension,theodorofacetoneonthebreath,andsignsofdehydrationDiagnosticStrategiesPhysical42
DiagnosticStrategies
LaboratoryTestsOnthepatient’sarrivaltotheED,serumandurineglucoseandketones,electrolytes,andarterialbloodgases(ABGs)shouldbechecked.Glucoseisusuallyelevatedabove350mg/dL;however,euglycemicDKA(bloodglucose<300mg/dL)hasbeenreportedinupto18%ofpatients.ABGsdemonstratealowpH.Metabolicacidosiswithananiongapisprimarilytheresultofelevatedplasmalevelsofacetoacetateandβ-hydroxybutyrate,althoughlactatealsocontributetothiscondition
DiagnosticStrategies
Laborat43DiagnosticStrategies
LaboratoryTestsAcompleteurinalysishelpsinthedeterminationofurineketone.Elevationsofurinespecificgravity,BUN,andhematocritsuggestdehydrationDiagnosticStrategiesLaborato44DiagnosticStrategies
LaboratoryTests
Sodiumisoftenlowinthepresenceofsignificantdehydrationbecauseitisstronglyaffectedbyhyperglycemia;hypertriglyceridemia;salt-poorfluidintake;andincreasedGI,renal,andinsensiblelossesWhenhyperglycemiaismarked,waterflowsfromthecellsintothevesselstodecreasetheosmolargradient,therebycreatingdilutionalhyponatremia.Lipidsalsodilutetheblood,therebyfurtherloweringthevalueofsodium
DiagnosticStrategiesLaborato45DiagnosticStrategiesLaboratoryTestsAcidosisandthehyperosmolarityinducedbyhyperglycemiashiftpotassium,fromtheintracellulartotheextracellularspace.Dehydrationproduceshemoconcentration,whichcontributestonormalorhighinitialserumpotassiumreadingsinDKA,evenwithprofoundtotalbodydeficitsWhileinsulinisadministeredandthehydrogenionconcentrationdecreases,thepatientneedsconsiderablepotassiumreplacement.
DiagnosticStrategiesLaborator46DiagnosticStrategiesLaboratoryTestsAlllaboratorydeterminationsmustbeinterpretedwithcaution.ThediagnosisofpancreatitisisconfoundedbytheusuallyelevatedurineandserumamylaselevelsinDKA.Typically,thisissalivaryamylase,butmostlaboratoriesarenotequippedtomakethisdistinction.Aserumlipasedeterminationhelpstodistinguishpancreatitisfromelevatedsalivaryamylaselevels.DiagnosticStrategiesLaborator47DifferentialConsiderations
Alcoholics,especiallythosewhohaverecentlyabstainedfromdrinking,withKussmaul’srespiration,andacidemicABGvaluesmayhavealcoholicketoacidosis.Thesepatientsmaybeeuglycemicorhypoglycemic,Alcoholicketoacidosisaccountsforapproximately20%ofallcasesofketoacidosis.KetoacidosiscanalsodevelopwithfastinginthethirdtrimesterofpregnancyandinnursingmotherswhodonoteatDifferentialConsiderations48DifferentialConsiderations
Otherentitiesthatmaymanifestwithvariouscombinationsofalteredmentalstatus,acidosis,andabdominalpainincludehypoglycemia,cerebrovascularaccident(stroke),trauma,sepsis,hyperglycemichyperosmolarnonketoticcoma,postictalstates,lacticacidosis,uremicacidosis,andabdominalemergencies.Intoxicationsbyethanol,salicylates,methanolallsharesomefeaturesofDKA.DifferentialConsiderations49ManagementGeneralMeasuresThecomatosepatient,especiallyifvomiting,requiresintubation.Thepatientinhypovolemicshockrequiresaggressivefluidresuscitationwith0.9%salinesolution.
Whenhyperglycemia,ketosis,andacidosishavebeenestablished,fluid,electrolyte,andinsulintherapyshouldbeginManagementGeneralMeasures50ManagementDehydrationTheseverelydehydratedpatientislikelytohaveafluiddeficitof3to5L.
Fluidrateshouldbeadjustedaccordingtoage,cardiacstatus,anddegreeofdehydrationtoachieveaurineoutputof1to2mL/kg/hr.Fluidresuscitationalonemayhelptolowerhyperglycemia.ManagementDehydration51ManagementInsulin
DKAcannotbereversedwithoutinsulin,andinsulintherapyshouldbeinitiatedassoonasthediagnosisiscertain.Inthepast,veryhighdosagesofinsulinwereadministeredtodiabeticpatientsinDKAbecausetheywerethoughttobeextremelyinsulin-resistant.However,low-dosageinsulintherapyhasprovedaseffectiveashigh-dosagetherapy
Highdosagesofinsulinhavepotentiallyharmfuleffects,includingagreaterincidenceofiatrogenichypoglycemiaandhypokalemia.Thecurrenttherapyofchoiceisregularinsulininfusedat0.1U/kg/hrupto5to10U/kg/hr,mixedwiththeIVfluids.ManagementInsulin52ManagementInsulin
Becausethehalf-lifeofregularinsulinis3to10minutes,IVinsulinshouldbeadministeredbyconstantinfusionratherthanbyrepeatedbolus.Whenthebloodglucosehasdroppedto250to300mg/dL,dextroseshouldbeaddedtotheIVfluidstopreventiatrogenichypoglycemiaandcerebraledema.InpatientswitheuglycemicDKA,dextroseshouldbeaddedtotheIVfluidsatthestartofinsulintherapyManagementInsulin53ManagementPotassiumPotassiumreplacementisinvariablyneededinDKA.Theinitialpotassiumlevelisoftennormalorhighdespitealargedeficitbecauseofsevereacidosis.Potassiumlevelsoftenplummetwithcorrectionofacidosisandadministrationofinsulin.Potassiumshouldbeadministeredwiththefluidswhilethelaboratoryvalueisintheupperhalfofthenormalrange.Renalfunctionshouldbemonitored.Inpatientswithlowserumpotassiumatpresentation,hypokalemiamaybecomelife-threateningwheninsulintherapyisadministered.
IVpotassiumshouldbevigorouslyadministeredinconcentrationsof20to40mEq/Lasrequired.ManagementPotassium54ManagementMagnesiumMagnesiumdeficiencyisacommonprobleminpatientswithDKAwithoutrenaldisease.BoththeinitialpathophysiologyandthetherapyforDKAinduceprofoundmagnesiumdiuresis.Magnesiumdeficiencymayexacerbatevomitingandmentalchanges,promotehypokalemiaandhypocalcemia,orinducefatalcardiacdysrhythmia.itisreasonabletoinclude0.35mEq/kgofmagnesiuminthefluidsofthefirst3to4hours,withfurtherreplacementdependentonbloodlevelsandtheclinicalpicture.ManagementMagnesium55Management
Acidosis
Acidosisalsodecreasesafterfluidinfusionalone.Increasedperfusionimprovestissueoxygenation,thusdiminishingtheformationoflactate.
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