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多臟器功能障礙綜合征及監(jiān)護
MODSandintensivecare1多臟器功能障礙綜合征及監(jiān)護
MODSandintensiDenominationvariation1973secondarysystemfunctionfailure---Tilney
Summarydataof18casesARFpatientsafterabdominalaorticaneurysmoperation,and17patientsdiedfromorganfailureduringdialysis.1975-1977
MOFS,multipleorganfailuresyndrome-----Baue,1975
(Yetthetreatmentdidnotsavethelives.)
MOF,multipleorganfailure-----Eiseman,1977
1980‘s
MSOF,multiplesystemorganfailure-----Fry38/533
pointouttherelationshipbetweenMSOFandsevereinfection
1990‘s※MODS,multipleorgandysfunctionsyndrome※2Denominationvariation1973sCase1Male26yPost-subtotalexcisionofcolonIleocolonicstomaleakageMultipleintestinalfistula3Case13Abdominalabscess4Abdominal4Long-termapplicationofhighcaloriaparenteralnutrition(fatemulsion)
livertumefaction
liverdysfunction
SGPT36SGOT144TB167.9
DB102.8
5Long-termapplicationof5HR170RR55PaCO223.8WBC18700Positivebloodcultivation6HR170PositivebloodcultivJan16th
septicshockJan17thRenalfunction
BUN20.5Cr337needinhalationofoxygenwithmask
continuoushemofiltrationJan19th
tracheotomy
ventilatorapplication7Jan16th7Case2male59yExtensiveanteriorwallMyocardialinfarction20daysafteronset(2002/3/6)
continuousventriculartachycardia→ventricularfibrillation
electricdefibrillation5times
antiarrhythmicdrugs
countershockdrugs
ventilatorapplication8Case2male59y8HR120RR28PaCO226.8WBC126009HR1209Repeatedlyventriculartachycardiaandfibrillation,totally21timeselectricdefibrillationContinuoushyperpyrexia、highWBC、HR≥90、RR≥22Cultivationnegative,antibioticsnoeffectivenessOrgandysfunctioncameincrowdsshockRespiratorydysfunctionDeteriorationofliverfunctionCastinurineroutinetest→BUN、Cr↑
→oliguria、anuriaCoagulationabnormalitydeath10RepeatedlyventriculartachycaAcuteonsetManifestatinofexcessiveinflammationDeteriotationofpts’conditionsdespiteactivetherapyMultipleorgandysfunctionDifferentpts,SameprogressCase1:infectiousCase2:noninfectious11AcuteonsetDifferentpts,SameclinicalbehaviorAccumulativeSubstanceirreversibleMultipleorganlowfunctioncausedbyinteractionbetweenorgansChronicdiseaseMultipleorganlowfunction12clinicalbehaviorChronicdiseaMODSfollowedbyprimaryemergencydiseasein24hoursClinicalmanifestationburstoutSimultaneousdiequicklyprimaryMODSIschemiaischemiaandreperfusionphysicalandchemicalinjuryfactor13MODSfollowedbyprimaryemergSequentialorgandysfunctionafteremergencydisease,MODSClinicalbehaviorDelayedSequentialReversibleMODSExcessiveinflammatorymediators14Sequentialorgandysfunctiona1.DirectinjuryofischemiaOxygen&nutrientinsufficiencyIntegrityofcellmembrane↓organelleinsult↓ATP↓
Extracellularfluidin-flowHydrolaseactivationNatriumin-flowcalciumin-flow
151.DirectinjuryofischemiaOxy1.DirectinjuryofischemiaHypersensibitityinheartandbrainSelectiveischemiaEndothelialcellinjuryleadstohighvascularpermeabilityandlowvolume161.DirectinjuryofischemiaHyppermeabilityofcellmembrane↑Na+Ca++H2OADPAMPIMPadenosinexanthinehypoxanthinehypoxanthineribosideUricAcidoxygen-derivedfreeradidicalsxanthineoxidasexanthineoxidaseXanthinedehydrogenaseIntracellularacidosisLowerproteinsynthesisInjuryofischemiaandreperfusion17permeabilityofcellmembrane↑Vesselpermeability↑+WBCchemotaxis
monocyte/macrophage
neutrophil
elastinasePLA2ODFR
TNFIL-8etal
IL-1IL-6
liver:acute
phasereactionRemoteorganinjuryTissuedamageetiologicalfactor
neutrophilAdherentmolecule2.ExcessiveinflammationSIRSMODSVascularendothelialcellSIRSMODS18Vesselpermeability↑+WBCchemClinicalprogressuncontrolledstressSIRSCapillaryleakagesyndromeMODSMSOF19ClinicalprogressuncontrolledImportantmoleculeinMODS
Pro-inflammatorycytokines:TNF-αβ,IL-1、2、6etcStimulatesynthesisandreleaseofothercytokinesActivateneutrophiles,eosinophilsandmonocytes;activateTandBcell;chemotaxisIncreasetheexpressionofadherentmoleculeActivatecomplementandcoagulationsystemIncreasepermeabilityofvessels,decreaseBPCausefeverandcatabolismofmuscle20ImportantmoleculeinMODSPrImportantmoleculeinMODS
Anti-inflammatorycytokines:IL-4、10
etcMaintainandenhancethefunctionofactivatedNKcells,monocytes,BandTcells,InhibitproliferationofT,BcellInhibitpro-inflammatorycytokinesproduction,receptorexpressionandcytotoxicityofmonocytesInhibitadherentmoleculeexpressionofvascularendothelialcells(VECs)InhibitH2O2、NOproductionofmacrophageInhibitantigenpresentationandotherassistantfunctionsofmonocytesandmacrophage21ImportantmoleculeinMODSAnImportantcellsinMODSPolymorphonuclearleucocyte(PMN):Effectorcellofinflammatoryresponse.CouldreleaseseveralproteinenzymesandODFRtodestroyVECsandstromaVECs:Whenactivated,VECsexpresshigheradherencetoPMNandhigherclottingcompetence;alsotheyproducepro-inflammatorycytokinesandvasodilatingagenttomagnifyinflammatoryresponse;finally,capillaryleakagesyndromecomesifVECsweredestroyed.22ImportantcellsinMODSPolymorImportantorganinMODSIntestinesBecauseofstress,fastingandcatabolism,theblood-mucosabarrierofintestinescouldbedestructed,thebacteriaandtoxintranlocatetobloodcirculationandthelattercouldenhanceinflammatoryresponsetoformviciouscycle.Sointestinesarecalled“motor”ofinflammatoryresponse,andaresourcesoflatestageinfectonsofMODSpts.23ImportantorganinMODSIntestiuncontrolledstresscarbohydratemetabolismdysfunction,Insulintolerance,withoutKetonemiahyperkineticcirculatorystate,Hyperpyrexia,HighStrokevolume,HighoxygenconsumptionProteinmetabolismdysfunction,highkatabolism,acutephaseprotein24uncontrolledstresscarbohydratT>38℃or<36℃HR>90beat/minRR>20/minorPaCO2<32mmHgWBC>12000mm3or<4000mm3orprematurecells>10%SepsisSystemicInflammatoryResponseSyndrome(SIRS)(SIR+PositiveCulture)(SIRwithoutinfection)SystemicInflammatoryResponsesyndrome
SIRS25T>38℃or<36℃SepsisSystemicInChaoticinternalmilieuduringacutephaseDisturbanceofelectrolytesandacid-basebalanceFeverCatabolism:emaciated,anemiaAcutedisseminatedintravascularcoagulationArrhythmiaHyperglycemia,noketonemia26ChaoticinternalmilieuduringSecondaryaldosteronism---highdensityurinewithoutProteinuria,oliguria
---prerenalazotemia---swollenPlasmaproteinleakage---Interstitialedema
---Hypoproteinemia
---bloodinspissasion---HypovolemiaCapillaryleakagesyndrome,CLS27SecondaryaldosteronismPlasmaDiagnosisofCLSPositivebodyfluidbalanceBloodvolumedeficiencyHypoproteinemiaOrganandtotalbodyInterstitialedemalungInterstitialedemacerebralInterstitialedema28DiagnosisofCLSPositivebodyOrgansdysfunctionorfailureOrganorsystemdysfunctionfailurelungLiverkidneyintestineBloodHypoxemia,respiratoratlist3-5daysARDS,PEEP>10cmH2O,FiO2>0.5Bilirubin>2-3mg/dL,Liverfunction>2normalvalueBilirubin>2-3mg/dL,icterusoliguriadialysisUntoleranceofenteralnutrition>5daysCurlingl'sulcerneedsbloodtransfusion,AcalculouscholecystitisPTorPTTelongation,platelet<50-80thousand,HypercoagulablestateDICcentralnervoussystemcardiovascularsystemInsanity,lightorientationdisorderProgressivedeepencoma
EjectionFraction
↓,capillaryleakageIrresponsivitytomusclestrengthdrugs29OrgansdysfunctionorfailureOGlasgowScore30GlasgowScore30InfluencedorganLung——ARDS>95%Kidney——ARF
onlyafew31InfluencedorganLung——ARDS31AcuteRespiratoryDistressSyndrome,ARDSPathologyoflungHighcapillarypermeability——InterstitialedemaVasoconstriction,microthrombosis——communicatingbranchopeningAlveolarandsmallbronchus——AtelectasisDecreasedalveolarsurfactantEdemaItypeepithelialcellsinsteadbyIItypecellSymptomTachypnea,respiratorydistresscannotbeeasedbyoxygeninhalationNoralesNolungx-rayabnormality1.Theearlystage32AcuteRespiratoryDistressSynPathologyDeterioratedlungInterstitialinflammation,usuallycomplicatedwithSEPSISSymptomObviouslydyspnoeaandcyanosis——needsventilatorIncreasedrespiratorytractsecretion,ralesLungx-ray——infiltratesDisturbanceofconsciousnessFebrileorhighleucocyte↑.Thesecondstage33Pathology.Thesecondstage333.Telophase
PathologyLungparenchymafibrosisMicrovascularocclusionIncreasedpreload,hypoxiaSymptomDeepcomaArrhythmia—bradycardia—cardiacarrest343.TelophasePathology34Diagnosis35Diagnosis35AcuteRenalFailure,ARFEtiologyPrerenalHemorrhage,shock,fluidlosingwithoutappropriatefluidresuscitationpostrenalbothsideureterorurinaryflowblockedrenalkidney
ischemia(hematorrhea,sepsis,allergicreaction)intoxication(aminoglycosideantibiotic,biotictoxin,chemical)36AcuteRenalFailure,ARFEtiolo1.HistoryandphysicalexaminationEtiologyprerenalpathogenpostrenalpathogenDiagnosisofARF371.Historyandphysicalexamina2.DifferentiationDiagnosiswithprerenalARF382.DifferentiationDiagnosiswi3.DifferentiationDiagnosiswithPostrenalARFBtypeultrasound(renalenlargement,ureter)Abdominalx-rays(calcification,calculusorObstruction)393.DifferentiationDiagnosiswi4.LaboratoryUrinetestUrinarycathetertorecordurinevolumeUrineacidity/density(1.010-1.014)UrinemicroscopicexaminationRBCandrenaltubuleepithelia(renalcortexandrenalmedullanecrosis)LargeBrowncasts(renalfailurecasts)Eosinophil↑(interstitialnephritis)Redcellcast(glomerulonephritis)Normal(prerenalorpostrenalfailureearlierperiod)404.LaboratoryUrinetestUrinar5.renalfunctionexaminationUrineureanitrogen↓
(<180mmol/24)UrineNa↑(>175mmol/24h)Fractionalexcretionoffiltratedsodium>1
FENa(%)=(UNa/PNa)×(PCr/UCr)×100osmoticpressureofurine
*ARF------<400mOsm/L
*prerenalARForglomerulonephritis------>400mOsm/LBUN(morethan
3.8-9.4mmol/Lperday),Cr↑Urine/PlasmaCr------<20renalfailureindex,RFIRFI=Una×(PCr/UCr)
*>1------ARF*<1------prerenal415.renalfunctionexaminationUIntensivecareOrganandsystemfunctionMonitoringandsupportObjectameliorateoxygenmetabolismamelioratenutrienstateTherapyaimedatstressandinflammatoryMediatorsTreatmentofcapillaryleakageTreatmentofprimarydisease42IntensivecareOrganandsystemOxygenmetabolismMonitoringCriticalDO2Assayofplasmalacticacid/pyruvicacid43OxygenmetabolismMonitoringCrOxygenassociatedindexDO2OxygenDelivery---OxygenofferedtothebodyinacertainperiodbycirculatorysystemDO2=CO×(1.38×SaO2+0.003×PaO2)VO2OxygenConsumption---Oxygenconsumptedbyallcellsinacertainperiod.VO2=Ca-vDO2×CO×1044OxygenassociatedindexDO2OxyCriticalDO2VO2DO2SepsisARDSMODSNormalCriticaldeliveryoxygen45CriticalDO2VO2DO2SepsisNormaLacticAcidandcellshypoxiaLacticAcid↑--latentcellshypoxia
lacticacidosis--tissueperfusiondeficiencyandcellshypoxia
LacticAcidnormalvalue---0.5-1.5mmol/L
>4-5mmol/L→SBandPH↓→lacticacidosisL/Prate↑--cellshypoxia
L/Prate
normalvalue---10:146LacticAcidandcellshypoxiaLStrategyofameliorateoxygenmetabolism
Improvementofoxygendeliveryrespiratorysupport---toimprovearterialbloodoxygencontenthigherinhalatedoxygenconcentration,ventilatorincreasecardiacoutput
Heartrate,cardiacrhythm,cardiaccontractility,preload/afterloadBloodsystemrisehemoglobinconcentration47StrategyofameliorateoxygenStrategyofameliorateoxygenmetabolismIncrease
oxygenextractionratioAmeliorateinterstitialedemaReducebloodcapilarypermeabilityAmeliorateoxygenextractionofcells48StrategyofameliorateoxygenTreatmenofCLSLimitationofwater-intakepremise:nevergetCOdownInfusionvolumedecidedbyurinevolumeperhourwhenlungandbraininterstitialedemahappen.RisecolloidosmoticpressureUsepowerfuldiureticUseglucocorticoid49TreatmenofCLSLimitationofwNutritionalsupportMetabolismsupportOffernutritionalsubstratebutneverincreaseorganloading.MetabolismmodulationInhibitionofcatabolismhormonesPromoteproteinsynthesis,easenegativenitrogenbalance50NutritionalsupportMetabolismNutritionalsupportAddaccessoriesPromoteproteinsynthesisandcellgrowthModulateimmunologicresponse
EnteralnutritionProtectbowelblood-mucosabarrier(preventfrominfection)51NutritionalsupportAddaccessoDiscussionoftherapyforstressandinflammatorymediatorsAntagonismandclearanceAimatexcessivecytokines---post-translationlevelsReductionofsynthesis
keepthebalancebetweenpro-andanti-cytokines---intranscriptionlevels
---intranslationlevel52DiscussionoftherapyforstrCytokinesmodulationIntranscriptionlevelAnti-mRNAexpression
(NF-κBisinchargeofmanykindsofcytokineexpression.)TranslationlevelReducecytokinessynthesisPosttranslationlevelAnti-cytokines(antibodyorsolublereceptor)BlockreceptorofcytokinesClearanceofcytokines(plasmapheresis)53CytokinesmodulationIntranscrTreatmenofARDSCorrecthypoxemiaquicklyuseventilatorassoonaspossibleappropriatePEEP(regainalveolarfunctionandfunctionalresidualcapacity)54TreatmenofARDSCorrecthypoxeTreatmenofARDSMaintainCirculationandlunginterstitialedemaPropercrystal/colloidrateDiureticNegativewaterbalance(accordingtoCVP/PAWP,urineoutputandlungauscultation)55TreatmenofARDSMaintainCircuTreatmenofARDSPreventandtreatinfectionBlockSIRScorticoidintheinitialstagemediatorsinhibitor(Ibuprofen,Dentoxifylline,TNFantibody)56TreatmenofARDSPreventandtrTreatmentofARFOliguriaoranuriastage
(7-10days,average5-6andmax.morethan1month)confinewaterintakeEqualwaterintakeandoutputfluidintakeperday=(dominantwaterlosing)+(nondominantwaterlosing)-(endogeneouswater)or0.5kgnutrientLowprotein,highcalorie,highVitaminproteinsynthesishormones57TreatmentofARFOliguriaoranTreatmentofARFcorrectelectrolytesimbalaHyperkalemiaHyponatremiaHypocalcemiaAcidosisCounterinfectionbloodpurification(CHF)58TreatmentofARFcorrectelectrProperfluidintaketopreventexcessivelosingofextracellularfluid:about
1/3-1/2waterloseCorrectelectrolyteimbalanceElectrolytestesteverydayIncreaseproteinintakeCounterinfectionDiuresisstage59ProperfluidintaketopreventSummary(1)DifferencesbetweenMODSandmultipleorganlowfunctionLowfunctionMODSprimaryillnessChronicacutePathogenesisinteractionamongorganshypoxiaandMediatorsPathologyNOcapillarydysfunctioncapillarydysfunctionOrganlesionaccumulativesubclinicalsubstantialfunctionalirreversiblereversible60Summary(1)Differencesbetween(2)DifferencesbetweenMODSandprimaryMODSTheeffectofischemia,ischemia-reperfusionorotherinjuryfactoroncellsThefirststrike→primaryMODSOrganellinjuryCelledemaandnecrosisCellinjurymediatedbyinflammatorymediatorsThesecondstrike→secondaryMODSCellmembraneinjuryCellmetabolismdysfunction,apoptosis
61(2)DifferencesbetweenMODSa(3)ModernopinionofMODSdevelopmentExcessiveinflammatoryresponserunsthroughthecourse,andisthemainthreatentolife.OnceSIRStriggerssingleorgandysfunction,thepathophysiologicalstatewillgetworseprogressively,andfinallyMODScomeup.SIRS,sepsisandtheircomplicationsconstructaCONTINUM,andMOFisthemostsevereconsequence.62(3)ModernopinionofMODSdeve多臟器功能障礙綜合征及監(jiān)護
MODSandintensivecare63多臟器功能障礙綜合征及監(jiān)護
MODSandintensiDenominationvariation1973secondarysystemfunctionfailure---Tilney
Summarydataof18casesARFpatientsafterabdominalaorticaneurysmoperation,and17patientsdiedfromorganfailureduringdialysis.1975-1977
MOFS,multipleorganfailuresyndrome-----Baue,1975
(Yetthetreatmentdidnotsavethelives.)
MOF,multipleorganfailure-----Eiseman,1977
1980‘s
MSOF,multiplesystemorganfailure-----Fry38/533
pointouttherelationshipbetweenMSOFandsevereinfection
1990‘s※MODS,multipleorgandysfunctionsyndrome※64Denominationvariation1973sCase1Male26yPost-subtotalexcisionofcolonIleocolonicstomaleakageMultipleintestinalfistula65Case13Abdominalabscess66Abdominal4Long-termapplicationofhighcaloriaparenteralnutrition(fatemulsion)
livertumefaction
liverdysfunction
SGPT36SGOT144TB167.9
DB102.8
67Long-termapplicationof5HR170RR55PaCO223.8WBC18700Positivebloodcultivation68HR170PositivebloodcultivJan16th
septicshockJan17thRenalfunction
BUN20.5Cr337needinhalationofoxygenwithmask
continuoushemofiltrationJan19th
tracheotomy
ventilatorapplication69Jan16th7Case2male59yExtensiveanteriorwallMyocardialinfarction20daysafteronset(2002/3/6)
continuousventriculartachycardia→ventricularfibrillation
electricdefibrillation5times
antiarrhythmicdrugs
countershockdrugs
ventilatorapplication70Case2male59y8HR120RR28PaCO226.8WBC1260071HR1209Repeatedlyventriculartachycardiaandfibrillation,totally21timeselectricdefibrillationContinuoushyperpyrexia、highWBC、HR≥90、RR≥22Cultivationnegative,antibioticsnoeffectivenessOrgandysfunctioncameincrowdsshockRespiratorydysfunctionDeteriorationofliverfunctionCastinurineroutinetest→BUN、Cr↑
→oliguria、anuriaCoagulationabnormalitydeath72RepeatedlyventriculartachycaAcuteonsetManifestatinofexcessiveinflammationDeteriotationofpts’conditionsdespiteactivetherapyMultipleorgandysfunctionDifferentpts,SameprogressCase1:infectiousCase2:noninfectious73AcuteonsetDifferentpts,SameclinicalbehaviorAccumulativeSubstanceirreversibleMultipleorganlowfunctioncausedbyinteractionbetweenorgansChronicdiseaseMultipleorganlowfunction74clinicalbehaviorChronicdiseaMODSfollowedbyprimaryemergencydiseasein24hoursClinicalmanifestationburstoutSimultaneousdiequicklyprimaryMODSIschemiaischemiaandreperfusionphysicalandchemicalinjuryfactor75MODSfollowedbyprimaryemergSequentialorgandysfunctionafteremergencydisease,MODSClinicalbehaviorDelayedSequentialReversibleMODSExcessiveinflammatorymediators76Sequentialorgandysfunctiona1.DirectinjuryofischemiaOxygen&nutrientinsufficiencyIntegrityofcellmembrane↓organelleinsult↓ATP↓
Extracellularfluidin-flowHydrolaseactivationNatriumin-flowcalciumin-flow
771.DirectinjuryofischemiaOxy1.DirectinjuryofischemiaHypersensibitityinheartandbrainSelectiveischemiaEndothelialcellinjuryleadstohighvascularpermeabilityandlowvolume781.DirectinjuryofischemiaHyppermeabilityofcellmembrane↑Na+Ca++H2OADPAMPIMPadenosinexanthinehypoxanthinehypoxanthineribosideUricAcidoxygen-derivedfreeradidicalsxanthineoxidasexanthineoxidaseXanthinedehydrogenaseIntracellularacidosisLowerproteinsynthesisInjuryofischemiaandreperfusion79permeabilityofcellmembrane↑Vesselpermeability↑+WBCchemotaxis
monocyte/macrophage
neutrophil
elastinasePLA2ODFR
TNFIL-8etal
IL-1IL-6
liver:acute
phasereactionRemoteorganinjuryTissuedamageetiologicalfactor
neutrophilAdherentmolecule2.ExcessiveinflammationSIRSMODSVascularendothelialcellSIRSMODS80Vesselpermeability↑+WBCchemClinicalprogressuncontrolledstressSIRSCapillaryleakagesyndromeMODSMSOF81ClinicalprogressuncontrolledImportantmoleculeinMODS
Pro-inflammatorycytokines:TNF-αβ,IL-1、2、6etcStimulatesynthesisandreleaseofothercytokinesActivateneutrophiles,eosinophilsandmonocytes;activateTandBcell;chemotaxisIncreasetheexpressionofadherentmoleculeActivatecomplementandcoagulationsystemIncreasepermeabilityofvessels,decreaseBPCausefeverandcatabolismofmuscle82ImportantmoleculeinMODSPrImportantmoleculeinMODS
Anti-inflammatorycytokines:IL-4、10
etcMaintainandenhancethefunctionofactivatedNKcells,monocytes,BandTcells,InhibitproliferationofT,BcellInhibitpro-inflammatorycytokinesproduction,receptorexpressionandcytotoxicityofmonocytesInhibitadherentmoleculeexpressionofvascularendothelialcells(VECs)InhibitH2O2、NOproductionofmacrophageInhibitantigenpresentationandotherassistantfunctionsofmonocytesandmacrophage83ImportantmoleculeinMODSAnImportantcellsinMODSPolymorphonuclearleucocyte(PMN):Effectorcellofinflammatoryresponse.CouldreleaseseveralproteinenzymesandODFRtodestroyVECsandstromaVECs:Whenactivated,VECsexpresshigheradherencetoPMNandhigherclottingcompetence;alsotheyproducepro-inflammatorycytokinesandvasodilatingagenttomagnifyinflammatoryresponse;finally,capillaryleakagesyndromecomesifVECsweredestroyed.84ImportantcellsinMODSPolymorImportantorganinMODSIntestinesBecauseofstress,fastingandcatabolism,theblood-mucosabarrierofintestinescouldbedestructed,thebacteriaandtoxintranlocatetobloodcirculationandthelattercouldenhanceinflammatoryresponsetoformviciouscycle.Sointestinesarecalled“motor”ofinflammatoryresponse,andaresourcesoflatestageinfectonsofMODSpts.85ImportantorganinMODSIntestiuncontrolledstresscarbohydratemetabolismdysfunction,Insulintolerance,withoutKetonemiahyperkineticcirculatorystate,Hyperpyrexia,HighStrokevolume,HighoxygenconsumptionProteinmetabolismdysfunction,highkatabolism,acutephaseprotein86uncontrolledstresscarbohydratT>38℃or<36℃HR>90beat/minRR>20/minorPaCO2<32mmHgWBC>12000mm3or<4000mm3orprematurecells>10%SepsisSystemicInflammatoryResponseSyndrome(SIRS)(SIR+PositiveCulture)(SIRwithoutinfection)SystemicInflammatoryResponsesyndrome
SIRS87T>38℃or<36℃SepsisSystemicInChaoticinternalmilieuduringacutephaseDisturbanceofelectrolytesandacid-basebalanceFeverCatabolism:emaciated,anemiaAcutedisseminatedintravascularcoagulationArrhythmiaHyperglycemia,noketonemia88ChaoticinternalmilieuduringSecondaryaldosteronism---highdensityurinewithoutProteinuria,oliguria
---prerenalazotemia---swollenPlasmaproteinleakage---Interstitialedema
---Hypoproteinemia
---bloodinspissasion---HypovolemiaCapillaryleakagesyndrome,CLS89SecondaryaldosteronismPlasmaDiagnosisofCLSPositivebodyfluidbalanceBloodvolumedeficiencyHypoproteinemiaOrganandtotalbodyInterstitialedemalungInterstitialedemacerebralInterstitialedema90DiagnosisofCLSPositivebodyOrgansdysfunctionorfailureOrganorsystemdysfunctionfailurelungLiverkidneyintestineBloodHypoxemia,respiratoratlist3-5daysARDS,PEEP>10cmH2O,FiO2>0.5Bilirubin>2-3mg/dL,Liverfunction>2normalvalueBilirubin>2-3mg/dL,icterusoliguriadialysisUntoleranceofenteralnutrition>5daysCurlingl'sulcerneedsbloodtransfusion,AcalculouscholecystitisPTorPTTelongation,platelet<50-80thousand,HypercoagulablestateDICcentralnervoussystemcardiovascularsystemInsanity,lightorientationdisorderProgressivedeepencoma
EjectionFraction
↓,capillaryleakageIrresponsivitytomusclestrengthdrugs91OrgansdysfunctionorfailureOGlasgowScore92GlasgowScore30InfluencedorganLung——ARDS>95%Kidney——ARF
onlyafew93InfluencedorganLung——ARDS31AcuteRespiratoryDistressSyndrome,ARDSPathologyoflungHighcapillarypermeability——InterstitialedemaVasoconstriction,microthrombosis——communicatingbranchopeningAlveolarandsmallbronchus——AtelectasisDecreasedalveolarsurfactantEdemaItypeepithelialcellsinsteadbyIItypecellSymptomTachypnea,respiratorydistresscannotbeeasedbyoxygeninhalationNoralesNolungx-rayabnormality1.Theearlystage94AcuteRespiratoryDistressSynPathologyDeterioratedlungInterstitialinflammation,usuallycomplicatedwithSEPSISSymptomObviouslydyspnoeaandcyanosis——needsventilatorIncreasedrespiratorytractsecretion,ralesLungx-ray——infiltratesDisturbanceofconsciousnessFebrileorhighleucocyte↑.Thesecondstage95Pathology.Thesecondstage333.Telophase
PathologyLungparenchymafibrosisMicrovascularocclusionIncreasedpreload,hypoxiaSymptomDeepcomaArrhythmia—bradycardia—cardiacarrest963.TelophasePathology34Diagnosis97Diagnosis35AcuteRenalFailure,ARFEtiologyPrerenalHemorrhage,shock,fluidlosingwithoutappropriatefluidresuscitationpostrenalbothsideureterorurinaryflowblockedrenalkidney
ischemia(hematorrhea,sepsis,allergicreaction)intoxication(aminoglycosideantibiotic,biotictoxin,chemical)98AcuteRenalFailure,ARFEtiolo1.HistoryandphysicalexaminationEtiologyprerenalpathogenpostrenalpathogenDiagnosisofARF991.Historyandphysicalexamina2.DifferentiationDiagnosiswithprerenalARF1002.DifferentiationDiagnosiswi3.DifferentiationDiagnosiswithPostrenalARFBtypeultrasound(renalenlargement,ureter)Abdominalx-rays(calcification,calculusorObstruction)1013.DifferentiationDiagnosiswi4.LaboratoryUrinetestUrinarycathetertorecordurinevolumeUrineacidity/density(1.010-1.014)UrinemicroscopicexaminationRBCandrenaltubuleepithelia(renalcortexandrenalmedulla
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