多脏器功能障碍综合征及监护

多脏器功能障碍综合征及监护MODSandintensivecare2Denominationvariation1973secondarysystemfunctionfailure---TilneySummarydataof18casesARFpatientsafterabdominalaorticaneurysmoperation,and17patientsdiedfromorganfailureduringdialysis.1975－1977MOFS，multipleorganfailuresyndrome-----Baue，1975（Yetthetreatmentdidnotsavethelives.)MOF，multipleorganfailure-----Eiseman，19771980‘sMSOF，multiplesystemorganfailure-----Fry38/533pointouttherelationshipbetweenMSOFandsevereinfection1990‘s※MODS,multipleorgandysfunctionsyndrome※3Case1Male26yPost-subtotalexcisionofcolonIleocolonicstomaleakageMultipleintestinalfistula4Abdominalabscess5Long-termapplicationofhighcaloriaparenteralnutrition(fatemulsion)livertumefactionliverdysfunctionSGPT36SGOT144TB167.9DB102.86HR170RR55PaCO223.8WBC18700Positivebloodcultivation7Jan16thsepticshockJan17thRenalfunctionBUN20.5Cr337needinhalationofoxygenwithmaskcontinuoushemofiltrationJan19thtracheotomyventilatorapplication8Case2male59yExtensiveanteriorwallMyocardialinfarction20daysafteronset(2002/3/6)continuousventriculartachycardia→ventricularfibrillationelectricdefibrillation5timesantiarrhythmicdrugscountershockdrugsventilatorapplication9HR120RR28PaCO226.8WBC1260010Repeatedlyventriculartachycardiaandfibrillation，totally21timeselectricdefibrillationContinuoushyperpyrexia、highWBC、HR≥90、RR≥22Cultivationnegative,antibioticsnoeffectivenessOrgandysfunctioncameincrowdsshockRespiratorydysfunctionDeteriorationofliverfunctionCastinurineroutinetest→BUN、Cr↑→oliguria、anuriaCoagulationabnormalitydeath11AcuteonsetManifestatinofexcessiveinflammationDeteriotationofpts’conditionsdespiteactivetherapyMultipleorgandysfunctionDifferentpts,SameprogressCase1:infectiousCase2:noninfectious12clinicalbehaviorAccumulativeSubstanceirreversibleMultipleorganlowfunctioncausedbyinteractionbetweenorgansChronicdiseaseMultipleorganlowfunction13MODSfollowedbyprimaryemergencydiseasein24hoursClinicalmanifestationburstoutSimultaneousdiequicklyprimaryMODSIschemiaischemiaandreperfusionphysicalandchemicalinjuryfactor14Sequentialorgandysfunctionafteremergencydisease,MODSClinicalbehaviorDelayedSequentialReversibleMODSExcessiveinflammatorymediators151.DirectinjuryofischemiaOxygen&nutrientinsufficiencyIntegrityofcellmembrane↓organelleinsult↓ATP↓Extracellularfluidin-flowHydrolaseactivationNatriumin-flowcalciumin-flow161.DirectinjuryofischemiaHypersensibitityinheartandbrainSelectiveischemiaEndothelialcellinjuryleadstohighvascularpermeabilityandlowvolume17permeabilityofcellmembrane↑Na+Ca++H2OADPAMPIMPadenosinexanthinehypoxanthinehypoxanthineribosideUricAcidoxygen-derivedfreeradidicalsxanthineoxidasexanthineoxidaseXanthinedehydrogenaseIntracellularacidosisLowerproteinsynthesisInjuryofischemiaandreperfusion18Vesselpermeability↑＋WBCchemotaxismonocyte/macrophageneutrophilelastinasePLA2ODFRTNFIL－8etalIL－1IL－6liver：acutephasereactionRemoteorganinjuryTissuedamageetiologicalfactorneutrophilAdherentmolecule2.ExcessiveinflammationSIRSMODSVascularendothelialcellSIRSMODS19ClinicalprogressuncontrolledstressSIRSCapillaryleakagesyndromeMODSMSOF20ImportantmoleculeinMODSPro-inflammatorycytokines:TNF-αβ,IL-1、2、6etcStimulatesynthesisandreleaseofothercytokinesActivateneutrophiles,eosinophilsandmonocytes;activateTandBcell;chemotaxisIncreasetheexpressionofadherentmoleculeActivatecomplementandcoagulationsystemIncreasepermeabilityofvessels,decreaseBPCausefeverandcatabolismofmuscle21ImportantmoleculeinMODSAnti-inflammatorycytokines:IL-4、10etcMaintainandenhancethefunctionofactivatedNKcells,monocytes,BandTcells，InhibitproliferationofT,BcellInhibitpro-inflammatorycytokinesproduction,receptorexpressionandcytotoxicityofmonocytesInhibitadherentmoleculeexpressionofvascularendothelialcells(VECs)InhibitH2O2、NOproductionofmacrophageInhibitantigenpresentationandotherassistantfunctionsofmonocytesandmacrophage22ImportantcellsinMODSPolymorphonuclearleucocyte（PMN）：Effectorcellofinflammatoryresponse.CouldreleaseseveralproteinenzymesandODFRtodestroyVECsandstromaVECs：Whenactivated,VECsexpresshigheradherencetoPMNandhigherclottingcompetence;alsotheyproducepro-inflammatorycytokinesandvasodilatingagenttomagnifyinflammatoryresponse;finally,capillaryleakagesyndromecomesifVECsweredestroyed.23ImportantorganinMODSIntestinesBecauseofstress,fastingandcatabolism,theblood-mucosabarrierofintestinescouldbedestructed,thebacteriaandtoxintranlocatetobloodcirculationandthelattercouldenhanceinflammatoryresponsetoformviciouscycle.Sointestinesarecalled“motor”ofinflammatoryresponse,andaresourcesoflatestageinfectonsofMODSpts.24uncontrolledstresscarbohydratemetabolismdysfunction,Insulintolerance,withoutKetonemiahyperkineticcirculatorystate,Hyperpyrexia,HighStrokevolume,HighoxygenconsumptionProteinmetabolismdysfunction,highkatabolism,acutephaseprotein25T＞38℃or＜36℃HR＞90beat/minRR＞20/minorPaCO2＜32mmHgWBC＞12000mm3or＜4000mm3orprematurecells＞10％SepsisSystemicInflammatoryResponseSyndrome(SIRS)(SIR+PositiveCulture)(SIRwithoutinfection)SystemicInflammatoryResponsesyndromeSIRS26Chaoticinter