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MultipleorgandysfunctionSyndrome大綱多器官功能障礙的定義和特點掌握多器官功能障礙的臨床演進(jìn)熟悉多器官功能障礙的診斷熟悉急性腎功能衰竭的病因熟悉急性腎功能衰竭的定義和病因熟悉腎功能衰竭的臨床表現(xiàn)、診斷和防治方法熟悉急性呼吸窘迫綜合征的定義和病因熟悉急性呼吸窘迫綜合征的臨床表現(xiàn)、診斷和治療熟悉CascliniqueM.26years,whohashadacolectomywithananastomosisFeverat40degree,abdominaltendernessHemoculture:EscherichiacoliT40℃HR170RR55PaCO223.8Whitecell18700Hemoc+1stday

chocSeconddya

anuriaetdyspnea (BUN20.5Crea337)

ThirddaymechanicalventilationHe+patomegalybecauseoflongtermparenteralnutrition

SGPT36SGOT144TB167.9DB102.8

MODSName1973sequentialdysfunction1977Remoteorgandysfunction1986post-traumaticmultipleorgandysfunction1991MultipleorgandysfunctionsyndromeDefinition

sequentialorsimultaneous>2organsdysfunctioncausedbyprimitiveillnessoragression(inflammation)EtiologySepsisetsepticshockTraumaandburnsMajorbleedingIschemiaandreperfusionIntra-abdominalinfectionAcutepancreatitisDifferentfromdeathTerminalstage:StressabsentNaturalorgandegradationIrreversibleMODS:AcutestressInflammatorydamageReversibleExempleRespiratoryandcirculatoryfailureleadingfromsepticshockheptorenalsyndromepulmonary

heart

diseasePulmonaryedemaPhysiopathologyPolytraumaSepticshock?MODS?=SIRS

SystemicInflammatoryResponseSyndromeMorethan2pointsHRmorethan90RRmorethan20/minorPaCO2lessthan32mmHgBodytemperaturemorethan38℃orlessthan36℃;Whitecell>12000/mm3

or<4000/mm3,orprematureratiomorethan10%inflammationBodydefenseresponsetobacteria,foreignbodyanddamageProandanti-inflammatorybalanceDolor,calor,rubor,tumor,functiolaesaCytokinendotheliumneutrophilemono-macrophageTNF-aIL-1、2、6v.sIL-10Amplifiedinflammation--SIRSDamageintroducedbyneutrophilandcytokinviolentstressresultendotheliumdamageEndothéliumcontractionCapillaryleakhemodynamicinstabilitycoagulationminithrombosismicrocirculationfailureIschemiareperfusionorganinvolvedLungCardiovascularsystemkidneyliverdigestiveImmunologyhematologyneurology

PreventionEtiologictreatmentEarlyidentificationTachypneashockOliguriaAntibioticAbdominalabces

IntestinalfistulaAcutekidneyinjurySyndromeofazotemia,hydro-electroliticdisturbancecausedbyfunctionalororganicrenaldysfunctionetiologypre-renalhypovolemiaandhypoperfusionshockBleedingExtracellulardehydrationabdominalcompartmentsyndromeetiologyrenalAcutetubularnecrosisGlomerulonephritisRhabdomyolysisMedicinepost-renalobstructionmechanismeischemieTubularnecrosisObstructionischemiareperfusioninfection,medicine,endotoxineClinicalManifestationoliguricSeveraldaysto3weekshydro-electrolticetacido-basicdisturbanceazotemiableeding:subcutaneous,gums,post-operativeManifestationpolyuric(14

days)RecoverstylerapidprogressiveslowHomeostasisdisturbanceDiagnostic

historydehydrationVomiting,diarrhea,sweatbleedingCapillaryleakIatrogenicfactorHeartfailureSeveresepsis,septicshockDiagnosticPre-renalTachycardiashockCVPdecreaseSkinmarbleandcoldMoistralesAbdominalhypertensionDiagnosticRenalemedicineHistoryofrenaldiseaseInsuffisancecardiaqueouhépatiquechroniqueSepsisProlongedischemia

DiagnosticDifferentialIRfonctionnelleIRorganiqueetiology HypoperfusionInfectionConcentrationBaruriaIsosthenuriaNatriuriadecreased>40mmol/LbunIncreasealoneIncreasewithcreatininHydratationrecoverOliguriaLasilixeffectivenoneeffectiveLaboratoryUrinaryUrinevolumepH,pycnometerMicroscopieBiochemistryazotemiaCreatinineclearanceratedecreaseLaboratoryHyperkaliemiaHypermagnesemiaHyperphosphoremiaHyponatremiaHypochloremiaHypocalcemiaAcidosisWaterIntoxicationPreventionresuscitationAlkalinizationofbloodDecompressionInotropicTreatmentOliguriaLiquidrestrictionAvoidhypoperfusionAdequatecalorieProteinatleast1g/kg/dTreatmentHomeostasisHyperkaliemiaacidosisAntibiotherapyAvoidnephortoxicmedicineTreatmentContinuousrenalreplacetreatmentHemodialysisHemofiltrationHemodiafiltrationPeritonealDialysisTreatmentPolyuriaAvoidhypovolemiaMaintainelectrolyticbalanceProteinAntibiotherapyAcuterespiratorydistresssyndromeARDSAcuterespiratoryfailurewithprogressivehypoxia,bilateralinfiltration,pulmonarycompliancedecreasecausedfromtrauma,sepsis,pancreatitis.EtiologydirectedamageaspirationPulmonarycontusionInhalation:hotortoxicgasdrowningEtiologyIndirectedamageSepsisorsepticshock

AcutepancreatitisVasttransfusionofbloodproductsTrauma

PolyfracturemechanismeSIRSCapillaryleakAlveolarandinterstitialdestructionbyneutrophiloxygenationdysfunctionPulmonarycompliancedecreasePulmonaryhypertensionmechanismeshuntingAlveolarcollapseDeadspacevasoconstrictionandminithrombosisPneumocytedestructionsurfactantdecreaseHyalinemembraneFunctionalresidualcapacitydecreaseManifestationHypoxemiaprogressiveAcutestageTachypnea

l’oxygenotherapynotworkAuscultation:normalChestradio:normalProgressivestageSevererespiratoryfailure:mechanicalventilationRespiratorysecretion:raleandwheezeRadio─bilateralopacityObnubilationFeverandhyperleucocytosisTerminalstageComaArrhythmia→bradycardia→cardiacarrestDiagnosticBloodgasHypoxemiaPaO2decreasePaO2/FiO2decreaseHypercapniaMorecriticalHemodynamicSwan-Ganz,echocardiographyTreatmentetiologyInterstitialedemaCristalloidetcolloidDiuresisLiquidrestrictionTreatmentOxygenotherapyCannulaMaskVentilatio

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