糖尿病酮症酸中毒英文PPT.ppt

Diabeticketoacidosis DKA emergencydepartmentofshengjinghospitalzhanghonglei case Mrwang 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 problem whatisthediagnosiswhatisthereasonofhyperkalemiaandhyponatremiawhatisthereasonofMetabolicacidosishowtodisposethediseaseifyouaretheERdoctoroncall Introduction DKAisasyndromeinwhichinsulindeficiencyandglucagonexcesscombinetoproduceahyperglycemic dehydrated acidoticpatientwithprofoundelectrolyteimbalance Pathophysiology Pathophysiology Pathophysiology Insulindeficiencyandglucagonelevationresultsinhyperglycemia whichinturncauseglycosuriaGlucoseintherenaltubulesdrawswater sodium potassium magnesium calcium phosphorus andotherionsfromthecirculationintotheurineThisosmoticdiuresiscombinedwithpoorintakeandvomitingproducestheprofounddehydrationandelectrolyteimbalanceassociatedwithDKAAsaresultofacidosisanddehydration however theinitialreportedvaluesfortheseelectrolytesmaybehigherthanactualbodystores Pathophysiology Insulindeficiencyresultsinactivationoflipasethatincreasescirculatingfreefattyacid FFA levels Long chainFFAs nowcirculatinginabundanceasaresultofinsulindeficiency arepartiallyoxidizedandconvertedinthelivertoacetoacetateand hydroxybutyrate ThisalterationoflivermetabolismtooxidizeFFAstoketonesratherthanthenormalprocessofre esterificationtotriglyceridesappearstocorrelatedirectlywiththealteredglucagon insulinratiointheportalblood Pathophysiology GlucagoniselevatedfourfoldtofivefoldinDKAandisthemostinfluentialketogenichormone Despitetheincreasedpathologicglucagon mediatedproductionofketones thebodyactsasitdoesinanyformofstarvation todecreasetheperipheraltissue suseofketonesasfuel Thecombinationofincreasedketoneproductionwithdecreasedketoneuseleadstoketoacidosis TheacidosiscausethebodytoincreaselungventilationandridthebodyofexcessacidwithKussmaul srespiration Etiology DKAmaybecausedbycessationofinsulinintakeorbyphysicaloremotionalstressdespitecontinuedinsulintherapy Mostoften DKAoccursinpatientswithtype1diabetesandisassociatedwithinadequateadministrationofinsulin infection ormyocardialinfarction MI DKAcanalsooccurintype2patientsandmaybeassociatedwithanytypeofstress suchassepsisorgastrointestinal GI bleeding DiagnosticStrategies HistoryClinically mostpatientswithDKAcomplainofarecenthistoryofpolydipsia polyuria polyphagia visualblurring weakness weightloss nausea vomiting andabdominalpain DiagnosticStrategies PhysicalExaminationTypicalfindingsincludetachypneawithKussmaul srespiration tachycardia frankhypotension theodorofacetoneonthebreath andsignsofdehydration DiagnosticStrategies LaboratoryTestsOnthepatient sarrivaltotheED serumandurineglucoseandketones electrolytes andarterialbloodgases ABGs shouldbechecked Glucoseisusuallyelevatedabove350mg dL however euglycemicDKA bloodglucose 300mg dL hasbeenreportedinupto18 ofpatients ABGsdemonstratealowpH Metabolicacidosiswithananiongapisprimarilytheresultofelevatedplasmalevelsofacetoacetateand hydroxybutyrate althoughlactatealsocontributetothiscondition DiagnosticStrategies LaboratoryTestsAcompleteurinalysishelpsinthedeterminationofurineketone Elevationsofurinespecificgravity BUN andhematocritsuggestdehydration DiagnosticStrategies LaboratoryTestsSodiumisoftenlowinthepresenceofsignificantdehydrationbecauseitisstronglyaffectedbyhyperglycemia hypertriglyceridemia salt poorfluidintake andincreasedGI renal andinsensiblelossesWhenhyperglycemiaismarked waterflowsfromthecellsintothevesselstodecreasetheosmolargradient therebycreatingdilutionalhyponatremia Lipidsalsodilutetheblood therebyfurtherloweringthevalueofsodium DiagnosticStrategies LaboratoryTestsAcidosisandthehyperosmolarityinducedbyhyperglycemiashiftpotassium fromtheintracellulartotheextracellularspace Dehydrationproduceshemoconcentration whichcontributestonormalorhighinitialserumpotassiumreadingsinDKA evenwithprofoundtotalbodydeficitsWhileinsulinisadministeredandthehydrogenionconcentrationdecreases thepatientneedsconsiderablepotassiumreplacement DiagnosticStrategies LaboratoryTestsAlllaboratorydeterminationsmustbeinterpretedwithcaution ThediagnosisofpancreatitisisconfoundedbytheusuallyelevatedurineandserumamylaselevelsinDKA Typically thisissalivaryamylase butmostlaboratoriesarenotequippedtomakethisdistinction Aserumlipasedeterminationhelpstodistinguishpancreatitisfromelevatedsalivaryamylaselevels DifferentialConsiderations Alcoholics especiallythosewhohaverecentlyabstainedfromdrinking withKussmaul srespiration andacidemicABGvaluesmayhavealcoholicketoacidosis Thesepatientsmaybeeuglycemicorhypoglycemic Alcoholicketoacidosisaccountsforapproximately20 ofallcasesofketoacidosis Ketoacidosiscanalsodevelopwithfastinginthethirdtrimesterofpregnancyandinnursingmotherswhodonoteat DifferentialConsiderations Otherentitiesthatmaymanifestwithvariouscombinationsofalteredmentalstatus acidosis andabdominalpainincludehypoglycemia cerebrovascularaccident stroke trauma sepsis hyperglycemichyperosmolarnonketoticcoma postictalstates lacticacidosis uremicacidosis andabdominalemergencies Intoxicationsbyethanol salicylates methanolallsharesomefeaturesofDKA Management GeneralMeasuresThecomatosepatient especiallyifvomiting requiresintubation Thepatientinhypovolemicshockrequiresaggressivefluidresuscitationwith0 9 salinesolution Whenhyperglycemia ketosis andacidosishavebeenestablished fluid electrolyte andinsulintherapyshouldbegin Management DehydrationTheseverelydehydratedpatientislikelytohaveafluiddeficitof3to5L Fluidrateshouldbeadjustedaccordingtoage cardiacstatus anddegreeofdehydrationtoachieveaurineoutputof1to2mL kg hr Fluidresuscitationalonemayhelptolowerhyperglycemia Management InsulinDKAcannotbereversedwithoutinsulin andinsulintherapyshouldbeinitiatedassoonasthediagnosisiscertain Inthepast veryhighdosagesofinsulinwereadministeredtodiabeticpatientsinDKAbecausetheywerethoughttobeextremelyinsulin resistant However low dosageinsulintherapyhasprovedaseffectiveashigh dosagetherapyHighdosagesofinsulinhavepotentiallyharmfuleffects includingagreaterincidenceofiatrogenichypoglycemiaandhypokalemia Thecurrenttherapyofchoiceisregularinsulininfusedat0 1U kg hrupto5to10U kg hr mixedwiththeIVfluids Management InsulinBecausethehalf lifeofregularinsulinis3to10minutes IVinsulinshouldbeadministeredbyconstantinfusionratherthanbyrepeatedbolus Whenthebloodglucosehasdroppedto250to300mg dL dextroseshouldbeaddedtotheIVfluidstopreventiatrogenichypoglycemiaandcerebraledema InpatientswitheuglycemicDKA dextroseshouldbeaddedtotheIVfluidsatthestartofinsulintherapy Management PotassiumPotassiumreplacementisinvariablyneededinDKA Theinitialpotassiumlevelisoftennormalorhighdespitealargedeficitbecauseofsevereacidosis Potassiumlevelsoftenplummetwithcorrectionofacidosisandadministrationofinsulin Potassiumshouldbeadministeredwiththefluidswhilethelaboratoryvalueisintheupperhalfofthenormalrange Renalfunctionshouldbemonitored Inpatientswithlowserumpotassiumatpresentation hypokalemiamaybecomelife threateningwheninsulintherapyisadministered IVpotassiumshouldbevigorouslyadministeredinconcentrationsof20to40mEq Lasrequired Management MagnesiumMagnesiumdeficiencyisacommonprobleminpatientswithDKAwithoutrenaldisease BoththeinitialpathophysiologyandthetherapyforDKAinduceprofoundmagnesiumdiuresis Magnesiumdeficiencymayexacerbatevomitingandmentalchanges promotehypokalemiaandhypocalcemia orinducefatalcardiacdysrhythmia itisreasonabletoinclude0 35mEq kgofmagnesiuminthefluidsofthefirst3to4hours withfurtherreplacementdependentonbloodlevelsandtheclinicalpicture Management AcidosisAcidosisalsodecreasesafterfluidinfusionalone Increasedperfusionimprovestissueoxygenation thusdiminishingtheformationoflactate Increasedrenalperfusionpromotesrenalhydrogenionloss theimprovedactionofinsulininthebetter hydratedpatientinhibitsketogenesis Bicarbonatetherapymaybeindicatedinseverelyacidemicpatients pH 7 0 TheuseofbicarbonateisnotwarrantedinlessillpatientsWhenbicarbonatetherapyisdeemednecessary thepHshouldnotbecorrectedabove7 1 Prognosis TheprecipitatingcausesofDKAmayhaveassociatedmorbidityandmortalityratesequaltoorworsethanthoseforDKAitself TheseincludeiatrogeniccausesaswellasinfectionandMI MorbidityinDKAislargelyiatrogenic 1 hypokalemiafrominadequatepotassiumreplacement 2 hypoglycemiafrominadequateglucosemonitoringandfailuretoreplenishglucoseinIVsolutionswhenserumglucosedropsbelow250to300mg dL 3 alkalosisfromoveraggressivebicarbonatereplacement 4 congestiveheartfailurefromoveraggressivehydration 5 cerebraledemaprobablycausedbytoorapidosmolalshifts Poorprognosticsignsincludehypotension azotemia coma andunderlyingillness Summary DiabeticKetoacidosis DKA manifestsclinicallyasatriad hyperglycem