INFECTIVEENDOCARDITIS感染性心內膜炎某章(或某三級學科)教學大綱要求要求內容學時掌握1、感染性心內膜炎的臨床表現、診斷及治療30分鐘熟悉1、感染性心內膜炎的病因5分鐘了解1、感染性心內膜炎的發病原理5分鐘注：適當標記重點和難點。InfectiveEndocarditisEssentialcharacteristicsGeneraldefinitionsandepidemiologyNVEI.V.drugabusePVEPathogenesisPathophysiologyClinicalfeaturesTreatmentEssentialcharacteristicsFebrileillnessPersistentbacteremiaCharacteristiclesionofmicrobialinfectionoftheendothelialsurfaceoftheheartVariableinsizeAmorphousmassoffibrin&plateletsAbundantorganismsFewinflammatorycellsthevegetationEssentialcharacteristicsTypicallyinvolvesthevalvesMayinvolveallstructuresoftheheartChordaetendinaeSitesofshuntingMurallesionsMajorityofcasescausedbystreptococcus,staphylococcus,enterococcus,orfastidiousgramnegativecocco-bacillaryformsClinicalclassificationNVEI.V.drugabusePVEEpidemiology55-75%ofpatientswithnativevalveendocarditis(NVE)haveunderlyingvalveabnormalitiesMVPRheumaticCongenitali.v.drugabuseEpidemiologyIntravenousDrugAbuseRiskis2–5%perpt./yearTendencytoinvolveright-sidedvalvesDistributioninclinicalseries46–78%tricuspid24–32%mitral8–19%aorticUnderlyingvalvenormalin75–93%S.aureuspredominantorganism(>50%,60-70%oftricuspidcases)EpidemiologyIntravenousDrugAbuseIncreasedfrequencyofgramnegativeinfectionsuchasP.aeruginosa&fungalinfectionsHighconcordanceofHIVpositivity&IE(27-73%)HIVstatusdoesnotinitselfmodifyclinicalpictureSurvivalisdecreasedifCD4count<200/mm3EpidemiologyProstheticValveEndocarditis(PVE)10–30%ofallcasesindevelopednationsCumulativeincidence1.4–3.1%at12months3.2–5.7%at5yearsEarlyPVE–within60daysNosocomial(s.epipredominates)LatePVE–after60daysCommunity(sameorganismsasNVE)InfectiveEndocarditisPathology NVEinfectionislargelyconfinedtoleafletsPVEinfectioncommonlyextendsbeyondvalveringintoannulus/periannulartissueRingabscessesSeptalabscessesFistulaeProstheticdehiscenceInvasiveinfectionmorecommoninaorticpositionandifonsetisearlyInfectiveEndocarditisPathogenesisEndothelialdamagePlatelet-fibrinthrombiMicroorganismadherenceInfectiveEndocarditisNonbacterialThromboticEndocarditisEndothelialinjuryHypercoagulablestateLesionsseenatcoaptationpointsofvalvesAtrialsurfacemitral/tricuspidVentricularsurfaceaortic/pulmonicModesofendothelialinjuryHighvelocityjetFlowfromhighpressuretolowpressurechamberFlowacrossnarroworificeofhighvelocityBacteriadepositedonedgesoflowpressuresinkorsiteofjetimpactionVenturiEffectPlatelet-fibrinthrombiVenturiEffectConversionofNBTEtoIEFrequency&magnitudeofbacteremiaDensityofcolonizingbacteriaOral>GU>GIDiseasestateofsurfaceInfectedsurface>colonizedsurfaceExtentoftraumaResistanceoforganismtohostdefensesMostaerobicgramnegativessusceptibletocomplement-mediatedbactericidaleffectofserumTendencytoadheretoendotheliumDextranproducingstrepFibronectinreceptorsonstaph,enterococcus,strep,CandidaCase:InfectionandShockVegetationsOpenedrightatrium

ViewoftheTricuspidValve(fromAtrialSide)InfectiveendocarditisMitralvalveinvolvedAorticvalveinvolvedInfectiveendocarditisTricuspidvalveinvolvedPathophysiologyClinicalmanifestationsDirectConstitutionalsymptomsofinfection(cytokine)IndirectLocaldestructiveeffectsofinfectionEmbolization–septicorblandHematogenousseedingofinfectionN.B.maypresentaslocalinfectionorpersistentfever,metastaticabscessesmaybesmall,miliaryImmuneresponseImmunecomplexorcomplement-mediatedPathophysiologyLocaldestructiveeffectsValvulardistortion/destructionChordalrupturePerforation/fistulaformationParavalvularabscessConductionabnormalitiesPurulentpericarditisFunctionalvalveobstructionPathophysiologyEmbolizationClinicallyevident11–43%ofpatientsPathologicallypresent45–65%HighriskforembolizationLarge>10mmvegetationHypermobilevegetationMitralvegetations(esp.anteriorleaflet)Pulmonary(septic)–65–75%ofi.v.drugabuserswithtricuspidIEClinicalFeaturesFevermostcommonsignMaybeabsentinelderly/debilitatedpt.Murmurpresentin80–85%GenerallyindicationofunderlyinglesionFrequentlyabsentintricuspidIEChangingmurmurClassicalPeripheralManifestationsLesscommontodayNotseenintricuspidendocarditisPetechiaemostcommonJanewayLesionsSplinterHemorrhageOsler’sNodesSubconjunctivalHemorrhagesRoth’sSpotsClinicalFeaturesSystemicemboliIncidencedecreaseswitheffectiveanti-microbialRxNeurologicalsequelaeEmbolicstroke15–20%ofpatientsMycoticaneurysmCerebritisCHFDuetomechanicaldisruptionHighmortalitywithoutsurgicalinterventionRenalinsufficiencyImmunecomplexmediatedImpairedhemodynamics/drugtoxicityTests:RepeatedbloodcultureandsensitivityESRCBCmayshowlowgrade,microcytic(smallredbloodcells)anemiaEchocardiogramTTE–60%sensitivityTEE–80–95%sensitivechestX-rayCTscanofthechestASO臨床警惕IE器質性心臟病患者出現原因不明發熱一周以上；新出現的心臟雜音，或原有雜音性質發生明顯改變動脈栓塞癥而無原因解釋；原因不明的心力衰竭；心臟手術后伴持續性發熱超過1周。DiagnosticCriteriaDefinitiveinfectiveendocarditispathologiccriteriaclinicalcriteria(seebelow)twomajorcriteria,oronemajorandtwominorcriteria,orfiveminorcriteriaIE診斷（病理學依據）（1）

微生物：在贅生物、發生栓塞的贅生物或心內膿腫中經培養或組織學檢查證實有微生物（2）

病理改變：贅生物或心內膿腫經組織學證實有活動性心內膜炎。IE診斷（臨床依據）主要指標：1.血培養兩次陽性，提示為典型微生物，如草綠色鏈球菌、HACEK組菌

2.間隔>12h兩次血培養持續菌血癥，或培養3次陽性為金黃色葡萄球菌、腸球菌或表皮葡萄球菌

3.伯氏立克次體、鸚鵡熱衣原體等感染的血清學檢測陽性

4.特殊的基因靶點分子生物學檢測陽性

5.超聲檢測發現贅生物、膿腫，或新出現的瓣膜反流、穿孔、人工瓣膜或缺損補片有新的開裂

6.血管征象：重要的動脈栓塞、膿毒性肺梗死或感染性動脈瘤

IE診斷（臨床依據）次要指標：l.易致IE的基礎疾病，包括基礎心血管病或靜脈毒癮2.發熱，體溫≥38℃伴貧血

3.原有心臟雜音改變、出現新的反流性雜音或心功能不全

4.血管征象：脾大、結膜出血、鏡下血尿、顱內出血、Janeway結節、杵狀指、瘀點瘀斑等5.免疫現象：腎小球腎炎、Osler結節、Roth斑、類風濕因子陽性6.微生物學證據：血培養陽性但不符合上述主要標準，或血清學證據符合可致IE的微生物活動性感染7.CRP升高，ESR加快GoalsofTherapy EradicateinfectionDefinitivelytreatsequelaeofdestructiveintra-cardiacandextra-cardiaclesionsAntibioticTherapyTreatmenttailoredtoetiologicagentImportanttonoteMIC/MBCrelationshipforeachcausativeorganismandtheantibioticusedHighserumconcentrationnecessarytopenetrateavascularvegetationAntibioticTherapy

.Intravenousantibiotics..Long-termhigh-doseantibiotictherapyisrequired,Therapyupto6weeksisnotuncommon..Thechosenantibioticmustbespecificfortheorganismcausingthecondition.Thisisdeterminedbythebloodcultureandthesensitivitiestests..Ifheartfailuredevelopsasaresultofdamagedheartvalves,surgerytoreplacetheaffectedheartvalvemaybeindicated.SurgicalTreatmentofIntra-CardiacComplicationsNYHAClassIII/IVCHFduetovalvedysfunctionSurgicalmortality–20-40%Medicalmortality–50-90%UnstableprostheticvalveSurgicalmortality–15-55%Medicalmortality–near100%at6monthsUncontrolledinfectionSurgicalTreatmentofIntra-CardiacComplicationsUnavailableeffectiveantimicrobialtherapyFungalendocarditisBrucellaS.aureusPVEwithanyintra-cardiaccomplicationRelapseofPVEafteroptimaltherapyPreventionProphylacticregimentargetedagainstlikelyorganismStrep.viridans–oral,respiratory,eosphogealEnterococcus–genitourinary,gastrointestinalS.aure