多臟器功能障礙綜合征及監(jiān)護課件_第1頁
多臟器功能障礙綜合征及監(jiān)護課件_第2頁
多臟器功能障礙綜合征及監(jiān)護課件_第3頁
多臟器功能障礙綜合征及監(jiān)護課件_第4頁
多臟器功能障礙綜合征及監(jiān)護課件_第5頁
已閱讀5頁,還剩119頁未讀, 繼續(xù)免費閱讀

下載本文檔

版權(quán)說明:本文檔由用戶提供并上傳,收益歸屬內(nèi)容提供方,若內(nèi)容存在侵權(quán),請進行舉報或認領(lǐng)

文檔簡介

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

溫馨提示

  • 1. 本站所有資源如無特殊說明,都需要本地電腦安裝OFFICE2007和PDF閱讀器。圖紙軟件為CAD,CAXA,PROE,UG,SolidWorks等.壓縮文件請下載最新的WinRAR軟件解壓。
  • 2. 本站的文檔不包含任何第三方提供的附件圖紙等,如果需要附件,請聯(lián)系上傳者。文件的所有權(quán)益歸上傳用戶所有。
  • 3. 本站RAR壓縮包中若帶圖紙,網(wǎng)頁內(nèi)容里面會有圖紙預(yù)覽,若沒有圖紙預(yù)覽就沒有圖紙。
  • 4. 未經(jīng)權(quán)益所有人同意不得將文件中的內(nèi)容挪作商業(yè)或盈利用途。
  • 5. 人人文庫網(wǎng)僅提供信息存儲空間,僅對用戶上傳內(nèi)容的表現(xiàn)方式做保護處理,對用戶上傳分享的文檔內(nèi)容本身不做任何修改或編輯,并不能對任何下載內(nèi)容負責(zé)。
  • 6. 下載文件中如有侵權(quán)或不適當(dāng)內(nèi)容,請與我們聯(lián)系,我們立即糾正。
  • 7. 本站不保證下載資源的準(zhǔn)確性、安全性和完整性, 同時也不承擔(dān)用戶因使用這些下載資源對自己和他人造成任何形式的傷害或損失。

評論

0/150

提交評論