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HepaticEncephalopathyHepaticEncephalopathy1Definition(1)
Hepaticencephalopathy(HE)Itrepresentsareversibledecreaseinneurologicalfunction,baseduponthedisorderofmetabolismwhichiscausedbyseveredecompensatedliverdisease.嚴(yán)重肝病引起的以代謝紊亂為基礎(chǔ)的神經(jīng)、精神綜合征。主要臨床表現(xiàn)為意識(shí)障礙、行為失常和昏迷Definition(1)Hepaticenceph2Definition(2)SubclinicalorlatentHE
diagnosedonlybyprecisementaltestsorEEG,noobviousclinicalandbiochemicalabnormalities
Definition(2)Subclinicalorl3Incidence/prevalence
Universalfeatureofacuteliverfailure
50%~70%inchronichepaticfailureDifficulttoestimateIncidence/prevalence4EtiologyFulminanthepaticfailure
acutesevereviralhepatitis,drug/toxin,acutefattyliverofpregnancy
Duetoacutehepatocellularnecrosis
Chronicliverdiseasecirrhosisofalltypes,surgicallyinducedportal-systemicshunts,primarylivercancer
DuetooneormorepotentiallyreversibleprecipitatingfactorsEtiologyFulminanthepaticfai5CommonprecipitatingfactorDeteriorationinhepaticfunctionDrugs
SedativespotentiallyhepatotoxicagentsGastrointestinalbleedingExcessivedietaryproteinUremia/azotemiaInfectionConstipationAnesthesiaandsurgeryHypoxiaDiuretics
hypokalemia,AlkalosishypovolemiaNitrogenousEncephalopathyNon-NitrogenousEncephalopathyCommonprecipitatingfactorDet6肝性腦病-課件7Pathogenesis(1)
ToxicmaterialsderivedfromnitrogeneoussubstrateinthegutandbypasstheliverHEiscausedbyseveralfactorsactsynergisticallySeveralputativegut-derivedtoxinsidentifiedPathogenesis(1)Toxicmateria8Pathogenesis(2)Postulatedfactors/mechanisms:
AmmonnianeurotoxicitySynergisticneurotoxinsExcitatoryinhibitoryneurotransmittersandplasmaaminoacidimbalancehypothesisγ-Aminobutyricacid（GABA）/BZhypothesisPathogenesis(2)Postulatedfac9肝性腦病-課件10Ammonianeurotoxicity
Overproductionand/orhypoeccrisis
Poorhepato-cellularfunction:incompletemetabolismPortal-systemicencephalopathy:bypass
AmmoniaintoxicationInterferewithcerebralmetabolism:
Depletionofglutamicacid,asparticacidandATPDepressioncerebralbloodflowandoxygenconsumption
AmmonianeurotoxicityOverpro11Ammonianeurotoxicity
Elevationofammonia:detectedin60%~80%Absoluteconcentrationofammonia,ammoniametabolitesinbloodorcerebrospinalfluids,correlatesonlyroughlywiththepresenceorseverityofHEFewcases:withinnormalrangeAmmonianeurotoxicityElevatio12Synergisticneurotoxins
AmmoniaMercaptans(硫醇)
Short-chainfattyacidsSynergisticneurotoxinsAmmoni13Excitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceNeurotransmission:
MediatedbybothexcitatoryandinhibitoryneurotransmittersTheirsynthesiscontrolledbybrainconcentrationoftheprecursoraminoacidsExcitatoryinhibitoryneurotra14
Increasedaromaticaminoacids(AAAs)
Tyrosine（酪氨酸）Phenylalanine（苯丙氨酸）
Tryptophan（色氨酸〕
DuetothefailureofhepaticdeaminationDecreasedbranched-chainaminoacids(BCAAs)
Valine（纈氨酸）
Leucine（亮氨酸）
Isoleucine（異亮氨酸）
DuetoincreasedmetabolismbyskeletalmuscleandkidneysorincreasedinsulinExcitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceIncreasedaromaticaminoacid15Imbalanceofplasmaaminoacid:MoreAAAsenterintoblood-brainbarrierandCNSDecreasedsynthesisofnormalneurotransmittersEnhancedsynthesisoffalseneurotransmitters
Octopamine(苯乙醇胺)Tryptophan(-羥酪胺)
Excitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceImbalanceofplasmaaminoacid16γ-Aminobutyricacidhypothesisγ-Aminobutyricacid(GABA):
PrincipalinhibitoryneurotransmittersGeneratedinthegutbybacteriaBypassesthediseasedorshuntedliverIncreasedblood-brainbarrierpermeabilityγ-Aminobutyricacidhypothesi17肝性腦病-課件18Pathohistology
Brainmaybenormalorcerebraledema
ParticularlyinfulminanthepticfailureCerebraledemaislikelythesecondlychangesInpatientswithchronicliverdisease
Astrocytes:increaseinnumberandenlargementInaverylong-standingcase
Thincortex,lossofneuronsfibers,laminarnecrosis
,pyramidaltractsdemyelinationPathohistologyBrainmaybeno19肝性腦病-課件20Clinicalmanifestation
Clinically,HEmanifestsdiversesignsandsymptoms.Earlyforms,quitesubtlechangesinpersonalityorlevelofperformance.AsHEadvances,adisturbanceofconsciousness,impairedintellectualfunction,neuromuscularabnormalities,moodchanges,inversionofthesleepcycle,andslowedreactiontime.Day-nightreversalisoftenanearlymanifestation.ClinicalmanifestationClinica21ClinicalmanifestationCriteriaforclinicalstages
PersonalityandmentalchangesAsterixisAbnormalEEGpatternsClinicalmanifestationCriteria22肝性腦病-課件23ClinicalGradingofHEGradeSymptomsSignEEGAbnormalitiesI-ProdromeAlteredsleeppatternsFluctuatingmood-
euphoria,depressionInappropriatebehaviorApathyLossofaffectWritingdifficultConstructionalapraxiaAsterixismaybepresentMaybepresentII-MildHEMildconfusionDisorientationDrowsiness（嗜睡）Asterixis(easilyelicitated)Ataxia（共濟(jì)失調(diào)）Fetorhepaticus肝臭AbnormalSlowerrhythmsClinicalGradingofHEGradeSym24ClinicalGradingofHEGradeSymptomsSignEEGAbnormalitiesIII-ModerateHEMarkedconfusionArousablefromsleepResponsiveAsterixisRigidityoflimbsHyperflexiaClonusGraspingandsuckingreflexesBabinskiModerateIV-ComaUnconsciousnessUnresponsivetostimuliFlaccidlimbsDiminishedreflexesNomuscletonesignificantClinicalGradingofHEGradeSym25Laboratoryandothertests
Serumammonia
Elevationofserumammonia:60%~80%
particularlyinchronicHE(withportosystemicshunting)Electroencephalogram(EEG)
Severeslowingwithfrequenciesinthethetaanddelta
EvokedpotentialsVariation,lackofspecificityandsensitivityLaboratoryandothertestsSer26
Reitantrail-makingtestPsychometrictests----NumberconnectiontestReitantrail-makingtestPs27WritingchartPsychometrictests----DigitsymboltestWritingchartPsychometrictest28Diagnosisand
differentialdiagnosisDiagnosisand
differentialdi29Diagnosis
Patientswithsevereliverdiseaseand/orportalhypertension,portosystemicshuntingMentalchanges:confusion,somnolence,coma
FactorsprecipitatingoraggravatingHEexist
Severelyimpairedliverfunctionand/orhyperammonemia
FlappingtremorandtypicalEEGchangesDiagnosisPatientswithsevere30Diagnosis
Recognitionofthelatentand/orsubclinicalHEImportantforviewoftheprevalenceofcirrhosisIntheabsenceofcharacteristicfeatures
Abnormalneuropsychiatricfunction:NumberconnectiontestDigitsymboltestsBlockdesignVisualreactiontimesDiagnosisRecognitionofthel31Differentialdiagnosis
Hypoglycemia（低血糖）UremiaDiabeticketoacidosis（糖尿病酮癥酸中毒）Nonketotichyperosmolarsyndrome（非酮癥高滲綜合癥）Subduralhematoma（硬膜下血腫）Cerebrospinalinfection（腦脊髓感染）Differentialdiagnosis32TreatmentTreatment33ThegoalsoftherapyTotreattheunderlyingliverdiseaseandimprovemental.Themostimportantinitialaspectsofcarearetodiagnosetheconditionproperly,excludeothercausesofencephalopathy,andsearchforprecipitatingfactors
ThegoalsoftherapyTotreat34一、IdentificationandtreatmentofprecipitatingfactorsTheseprecipitatingeventsmaybereadilyapparentorsubtle.Therefore,detaileddiscussionsandacarefulassessmentofchangesinlaboratoryvaluesarenecessary.SupportivecareCorrectionoffluid,electrolyte,glucose,acid-alkalineabnormalitiesManagementofcerebraledema,bacteremia
一、Identificationandtreatment35二、DecreasingnitrogenloadandammoniaproductionsandabsorptionofenterictoxinsDecreasingammoniaproductionsDietaryproteinrestrictionBowelcleaning(clysis灌腸,catharsis導(dǎo)瀉)NonabsorbabledisaccharidesAntibioticseradicationofHpIncreasingammoniametabolisms二、Decreasingnitrogenloadand36DietaryproteinrestrictionRestrictionofdietaryproteinatthetimeofacuteHEwithsubsequentincrementstoassessclinicaltoleranceisaclassiccornerstoneoftherapyProteinrestriction:0.81.0g/kg.dVegetableanddairysourcesarepreferabletoanimalproteinApositivenitrogenbalancepositiveefectsDietaryproteinrestrictionRes37BowelcleaningClysisLaxative(e.g.magnesiumcitrate硫酸鎂)
Notes:allenemasmustbeneutraloracidictoreduceammoniaabsorptionBowelcleaningClysis38NonabsorbabledisaccharidesLactulose（乳果糖）
SyntheticdisaccharideFirst-linepharmacologicaltreatmentReleaselacticandaceticacidsbycolonicbacteriaDecreasingstoolpHtoabout5.5ReduceportionofammoniaanditsabsorptionEffectivein80%ofpatientsCause2~3softstool/dNonabsorbabledisaccharidesLac39AntibioticsNeomycin（新霉素）:2~4g/DLitterisabsorbedImpairedhearingordeafness(longtermuse)Longtermuse(>1month)isnotadvisableMetronidozol（甲硝唑）:0.2gqidaseffectiveasneomycinRifaximin（利福昔明）AntibioticsNeomycin（新霉素）:2~40IncreasingammoniametabolismsL-Ornithine-L-asparagicacid（L-鳥(niǎo)氨酸-L-天冬氨酸）Benzoate（苯甲酸鹽），Phenylaceticacid（苯乙酸）Zinc(鋅)Potassiumglutamate(谷氨酸鉀)，sodiumglutamate(谷氨酸鈉)Arginine(精氨酸)Increasingammoniametabolisms41三、Drugsthataffectneurotransmission
AdministrationofBCAAsOralorparenteraladministration
L-dopa（左旋多巴）Precursoroftheneurotransmitternorepinephrinedopaminepenetrateblood-brainbarrierIncreasethenormalneurotransmitter三、Drugsthataffectneurotrans42四、GABA/BZreceptorantagonistsFlumazenil（氟馬西尼）
andothers:mayhaveatherapwuticroleinselectedpatientsAformalrecommendationontheuseofthesedrugscannotbemadeonthebasisofevidence-baseddata四、GABA/BZreceptorantagonists43LivertransplantationUltimateanswertotheproblemofchronicHELivertransplantation44Summary
KeyissuesoftheHEtopicClinicalmanifestations------ClinicalstagesofHEDiagnosisanddifferentialdiagnosisFactorsprecipitatingand/oraggravatingHESummary
Keyissu45HepaticEncephalopathyHepaticEncephalopathy46Definition(1)
Hepaticencephalopathy(HE)Itrepresentsareversibledecreaseinneurologicalfunction,baseduponthedisorderofmetabolismwhichiscausedbyseveredecompensatedliverdisease.嚴(yán)重肝病引起的以代謝紊亂為基礎(chǔ)的神經(jīng)、精神綜合征。主要臨床表現(xiàn)為意識(shí)障礙、行為失常和昏迷Definition(1)Hepaticenceph47Definition(2)SubclinicalorlatentHE
diagnosedonlybyprecisementaltestsorEEG,noobviousclinicalandbiochemicalabnormalities
Definition(2)Subclinicalorl48Incidence/prevalence
Universalfeatureofacuteliverfailure
50%~70%inchronichepaticfailureDifficulttoestimateIncidence/prevalence49EtiologyFulminanthepaticfailure
acutesevereviralhepatitis,drug/toxin,acutefattyliverofpregnancy
Duetoacutehepatocellularnecrosis
Chronicliverdiseasecirrhosisofalltypes,surgicallyinducedportal-systemicshunts,primarylivercancer
DuetooneormorepotentiallyreversibleprecipitatingfactorsEtiologyFulminanthepaticfai50CommonprecipitatingfactorDeteriorationinhepaticfunctionDrugs
SedativespotentiallyhepatotoxicagentsGastrointestinalbleedingExcessivedietaryproteinUremia/azotemiaInfectionConstipationAnesthesiaandsurgeryHypoxiaDiuretics
hypokalemia,AlkalosishypovolemiaNitrogenousEncephalopathyNon-NitrogenousEncephalopathyCommonprecipitatingfactorDet51肝性腦病-課件52Pathogenesis(1)
ToxicmaterialsderivedfromnitrogeneoussubstrateinthegutandbypasstheliverHEiscausedbyseveralfactorsactsynergisticallySeveralputativegut-derivedtoxinsidentifiedPathogenesis(1)Toxicmateria53Pathogenesis(2)Postulatedfactors/mechanisms:
AmmonnianeurotoxicitySynergisticneurotoxinsExcitatoryinhibitoryneurotransmittersandplasmaaminoacidimbalancehypothesisγ-Aminobutyricacid（GABA）/BZhypothesisPathogenesis(2)Postulatedfac54肝性腦病-課件55Ammonianeurotoxicity
Overproductionand/orhypoeccrisis
Poorhepato-cellularfunction:incompletemetabolismPortal-systemicencephalopathy:bypass
AmmoniaintoxicationInterferewithcerebralmetabolism:
Depletionofglutamicacid,asparticacidandATPDepressioncerebralbloodflowandoxygenconsumption
AmmonianeurotoxicityOverpro56Ammonianeurotoxicity
Elevationofammonia:detectedin60%~80%Absoluteconcentrationofammonia,ammoniametabolitesinbloodorcerebrospinalfluids,correlatesonlyroughlywiththepresenceorseverityofHEFewcases:withinnormalrangeAmmonianeurotoxicityElevatio57Synergisticneurotoxins
AmmoniaMercaptans(硫醇)
Short-chainfattyacidsSynergisticneurotoxinsAmmoni58Excitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceNeurotransmission:
MediatedbybothexcitatoryandinhibitoryneurotransmittersTheirsynthesiscontrolledbybrainconcentrationoftheprecursoraminoacidsExcitatoryinhibitoryneurotra59
Increasedaromaticaminoacids(AAAs)
Tyrosine（酪氨酸）Phenylalanine（苯丙氨酸）
Tryptophan（色氨酸〕
DuetothefailureofhepaticdeaminationDecreasedbranched-chainaminoacids(BCAAs)
Valine（纈氨酸）
Leucine（亮氨酸）
Isoleucine（異亮氨酸）
DuetoincreasedmetabolismbyskeletalmuscleandkidneysorincreasedinsulinExcitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceIncreasedaromaticaminoacid60Imbalanceofplasmaaminoacid:MoreAAAsenterintoblood-brainbarrierandCNSDecreasedsynthesisofnormalneurotransmittersEnhancedsynthesisoffalseneurotransmitters
Octopamine(苯乙醇胺)Tryptophan(-羥酪胺)
Excitatoryinhibitoryneurotransmitter&plasmaaminoacidsimbalanceImbalanceofplasmaaminoacid61γ-Aminobutyricacidhypothesisγ-Aminobutyricacid(GABA):
PrincipalinhibitoryneurotransmittersGeneratedinthegutbybacteriaBypassesthediseasedorshuntedliverIncreasedblood-brainbarrierpermeabilityγ-Aminobutyricacidhypothesi62肝性腦病-課件63Pathohistology
Brainmaybenormalorcerebraledema
ParticularlyinfulminanthepticfailureCerebraledemaislikelythesecondlychangesInpatientswithchronicliverdisease
Astrocytes:increaseinnumberandenlargementInaverylong-standingcase
Thincortex,lossofneuronsfibers,laminarnecrosis
,pyramidaltractsdemyelinationPathohistologyBrainmaybeno64肝性腦病-課件65Clinicalmanifestation
Clinically,HEmanifestsdiversesignsandsymptoms.Earlyforms,quitesubtlechangesinpersonalityorlevelofperformance.AsHEadvances,adisturbanceofconsciousness,impairedintellectualfunction,neuromuscularabnormalities,moodchanges,inversionofthesleepcycle,andslowedreactiontime.Day-nightreversalisoftenanearlymanifestation.ClinicalmanifestationClinica66ClinicalmanifestationCriteriaforclinicalstages
PersonalityandmentalchangesAsterixisAbnormalEEGpatternsClinicalmanifestationCriteria67肝性腦病-課件68ClinicalGradingofHEGradeSymptomsSignEEGAbnormalitiesI-ProdromeAlteredsleeppatternsFluctuatingmood-
euphoria,depressionInappropriatebehaviorApathyLossofaffectWritingdifficultConstructionalapraxiaAsterixismaybepresentMaybepresentII-MildHEMildconfusionDisorientationDrowsiness（嗜睡）Asterixis(easilyelicitated)Ataxia（共濟(jì)失調(diào)）Fetorhepaticus肝臭AbnormalSlowerrhythmsClinicalGradingofHEGradeSym69ClinicalGradingofHEGradeSymptomsSignEEGAbnormalitiesIII-ModerateHEMarkedconfusionArousablefromsleepResponsiveAsterixisRigidityoflimbsHyperflexiaClonusGraspingandsuckingreflexesBabinskiModerateIV-ComaUnconsciousnessUnresponsivetostimuliFlaccidlimbsDiminishedreflexesNomuscletonesignificantClinicalGradingofHEGradeSym70Laboratoryandothertests
Serumammonia
Elevationofserumammonia:60%~80%
particularlyinchronicHE(withportosystemicshunting)Electroencephalogram(EEG)
Severeslowingwithfrequenciesinthethetaanddelta
EvokedpotentialsVariation,lackofspecificityandsensitivityLaboratoryandothertestsSer71
Reitantrail-makingtestPsychometrictests----NumberconnectiontestReitantrail-makingtestPs72WritingchartPsychometrictests----DigitsymboltestWritingchartPsychometrictest73Diagnosisand
differentialdiagnosisDiagnosisand
differentialdi74Diagnosis
Patientswithsevereliverdiseaseand/orportalhypertension,portosystemicshuntingMentalchanges:confusion,somnolence,coma
FactorsprecipitatingoraggravatingHEexist
Severelyimpairedliverfunctionand/orhyperammonemia
FlappingtremorandtypicalEEGchangesDiagnosisPatientswithsevere75Diagnosis
Recognitionofthelatentand/orsubclinicalHEImportantforviewoftheprevalenceofcirrhosisIntheabsenceofcharacteristicfeatures
Abnormalneuropsychiatricfunction:NumberconnectiontestDigitsymboltestsBlockdesignVisualreactiontimesDiagnosisRecognitionofthel76Differentialdiagnosis
Hypoglycemia（低血糖）UremiaDiabeticketoacidosis（糖尿病酮癥酸中毒）Nonketotichyperosmolarsyndrome（非酮癥高滲綜合癥）Subduralhematoma（硬膜下血腫）Cerebrospinalinfection（腦脊髓感染）Differentialdiagnosis77TreatmentTreatment78ThegoalsoftherapyTotreattheunderlyingliverdiseaseandimprovemental.Themostimportantinitialaspectsofcarearetodiagnosetheconditionproperly,excludeothercausesofencephalopathy,andsearchforprecipitatingfactors
ThegoalsoftherapyTotreat79一、IdentificationandtreatmentofprecipitatingfactorsTheseprecipitatingeventsmaybereadilyapparentorsubtle.Therefore,detaileddiscussionsandacarefulassessmentofchangesinlaboratoryvaluesarenecessary.SupportivecareCorrectionoffluid,electrolyte,glucose,acid-alkalineabnormalitiesManagementofcerebraledema,bacteremia
一、Identificationandtreatment80二、DecreasingnitrogenloadandammoniaproductionsandabsorptionofenterictoxinsDecreasingammoniaproductionsDietaryproteinrestrictionBowelcleaning(clysis灌腸,catharsis導(dǎo)瀉)NonabsorbabledisaccharidesAntibioticseradicationofHpIncreasingammoniametabolisms二、Decreasingnitrogenloadand81DietaryproteinrestrictionRestrictionofdietaryproteinatthetimeofacute
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