Diabeticketoacidosis(DKA)emergencydepartmentofshengjinghospitalzhanghongleicase•Mrwang，M，52yearsold•chiefcomplaint：polydipsia,polyuria,weaknessfor1week，vomitingfor10hour•physicalexam: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/L•BUN:15.9mmol/L,Cr:147mmol/L•K+:8mmol/L,Na+:118mmol/L,Cl-:80mmol/L,Glu:33mmol/L•urinalysis:ketone:3+,gravity:1.024,glu:4+problem•whatisthediagnosis•whatisthereasonofhyperkalemiaandhyponatremia•whatisthereasonofMetabolicacidosis•howtodisposethediseaseifyouaretheERdoctoroncallIntroductionDKAisasyndromeinwhichinsulindeficiencyandglucagonexcesscombinetoproduceahyperglycemic,dehydrated,acidoticpatientwithprofoundelectrolyteimbalancePathophysiologyLiverMuscleAdiposetissueGluconeogenesisKetogenesisGlucoseUtilizationLipolysisInsulin↓↓↑↓Glucagon↑↑→→Epinephrine↑↑↓↑Cortisol↑↑↓↑Grownthhormone→↑↓↑PathophysiologyPathophysiology•Insulindeficiencyandglucagonelevationresultsinhyperglycemia,whichinturncauseglycosuria•Glucoseintherenaltubulesdrawswater,sodium,potassium,magnesium,calcium,phosphorus,andotherionsfromthecirculationintotheurine•ThisosmoticdiuresiscombinedwithpoorintakeandvomitingproducestheprofounddehydrationandelectrolyteimbalanceassociatedwithDKA•Asaresultofacidosisanddehydration,however,theinitialreportedvaluesfortheseelectrolytesmaybehigherthanactualbodystores.Pathophysiology•Insulindeficiencyresultsinactivationoflipasethatincreasescirculatingfreefattyacid(FFA)levels.•Long-chainFFAs,nowcirculatinginabundanceasaresultofinsulindeficiency,arepartiallyoxidizedandconvertedinthelivertoacetoacetateandβ-hydroxybutyrate.•ThisalterationoflivermetabolismtooxidizeFFAstoketonesratherthanthenormalprocessofre-esterificationtotriglyceridesappearstocorrelatedirectlywiththealteredglucagon/insulinratiointheportalblood.Pathophysiology•GlucagoniselevatedfourfoldtofivefoldinDKAandisthemostinfluentialketogenichormone.•Despitetheincreasedpathologicglucagon-mediatedproductionofketones,thebodyactsasitdoesinanyformofstarvation,todecreasetheperipheraltissue’suseofketonesasfuel.Thecombinationofincreasedketoneproductionwithdecreasedketoneuseleadstoketoacidosis.•TheacidosiscausethebodytoincreaselungventilationandridthebodyofexcessacidwithKussmaul’srespirationEtiologyDKAmaybecausedbycessationofinsulinintakeorbyphysicaloremotionalstressdespitecontinuedinsulintherapy.Mostoften,DKAoccursinpatientswithtype1diabetesandisassociatedwithinadequateadministrationofinsulin,infection,ormyocardialinfarction(MI).DKAcanalsooccurintype2patientsandmaybeassociatedwithanytypeofstress,suchassepsisorgastrointestinal(GI)bleedingDiagnosticStrategiesHistoryClinically,mostpatientswithDKAcomplainofarecenthistoryofpolydipsia,polyuria,polyphagia,visualblurring,weakness,weightloss,nausea,vomiting,andabdominalpain.DiagnosticStrategiesPhysicalExaminationTypicalfindingsincludetachypneawithKussmaul’srespiration,tachycardia,frankhypotension,theodorofacetoneonthebreath,andsignsofdehydrationDiagnosticStrategiesLaboratoryTestsOnthepatient’sarrivaltotheED,serumandurineglucoseandketones,electrolytes,andarterialbloodgases(ABGs)shouldbechecked.Glucoseisusuallyelevatedabove350mg/dL;however,euglycemicDKA(bloodglucose<300mg/dL)hasbeenreportedinupto18%ofpatients.ABGsdemonstratea...
