眼科學(xué)教學(xué)課件：06 Retina Disease（英文班終版）

DiseasesofRetinaIntroduction

EyeballstructureandretinaMaculaluteaLocated3mmtemporallytotheopticpapilla,rightonthevisualaxis.AconcavecentralretinaldepressioniscalledFoveaCentralis

maculaluteacontainsonlycones;

1conesynapesto1bipolarcell,whichsynapesto1ganglioncell,leadingtothemostsensitivevision.Inperipheralretina,600rodsconnectto1ganglion.HistologyofretinaInternallimitingmembraneNervefiberlayerGanglioncelllayerInnerplexiformlayerInnernuclearlayerOuterplexiformlayerOuternulearlayerExternallimitingmembranephotoreceptorRPEBruch’smembraneNeuroconductionofretina3neurons:

Photoreceptor

BipolarGanglioncellSupportingtissue:

Müllercell

rod（scotopicvision）

cone（photopicvision）ConnectingcellbetweenphotoreceptorandganglionConducttobrainVasculatureofretina

Innerlayer→centralretinalvascularsystemOuterlayer→choroid（ciliaryvascularsystem）Maculalutea→

choriocapillariesRetinabarrierInnerbarrier（blood–retinabarrier）

denseconnectionofretinalcapillaryendotheliumOuterbarrier（choroid-retinabarrier）

zonulaoccludensbetweentheRPE

RPE-Bruch’smembrane-choriocapillariescomplexSymptomsVisualimpairmentMetamorphopsiaFlickeringMacropsiaMicropsiaRelatedtolesionsiteVitreoustractiontotheretinaRetinaedema→fewerconesstimulated→micropsiaSignsIntracellularedemaExtracellularedemaCystoidmacularedemaRetinalarteryocclusion:ischemialeadstoedemaofbipolarcell,ganglionandRNFLCapillaryendotheliuminjury，andthenexudationHenle’s

fibersareradicallylocated;Thispoolingformsaflower-petalpattern.RetinalEdemaIntracellularedemaExtracellularedemaExudatesHardexudateCotton-woolspotLeakageofcapillary→absorb→depositionoflipidinouterplexiformlayer

Alsocalled“softexudation”Precapillaryarterioleocclusion→

axoplasmictransportblocked→organellesstackExudatesCotton-woolspotHardexudate(Hypertensiveretinopathy)Hemorrhage

DeephemorrhageSuperficialhemorrhage

PreretinalhemorrhageVitreoushemorrhageBetweenouterplexiformlayerandinnernuclearlayer.Smallround,darkredLocatedinnervefiberlayerLine,strip,flame-like,brightredCrescent-shapedhematocelewithtransversesectionProfusepreretinalhemorrhageintothevitreousorhemorrhageofretinalneospasticvasculaturePreretinalhemorrhageVitreoushemorrhageDeephemorrhageHemorrhageSuperficialhemorrhageNeovascularizationneovessels,NVAlargeareaofretinalischemia→

formationofvascularendothelialgrowthfactor→

neovascularizationneovesselsmembrane,NVMArisefromsmallveinsofopticdiscandretina;growalongretinalsurfaceandintothevitreousNeovascularization

RetinalneovascularizationNeovacularizatonofopticdiscBloodvesselchange1.Atherosclerosis,stenosis,occlusion2.Tortuousvein,dilatedvein,bead-likechangeA-VcrosssignVesselwhitesheathMicroaneurysmMicroaneurysmA-vcrosssignVesselwhitesheathBloodvesselchangeChangesofRPEPigmentlossPigmentdisorderOsteocyte-likepigmentdepositionChoroidal

neovascularizationInflammation,metabolicdepositofRPEorBruch’smembranebreak→CNVreachRPEorsubsensorylayerRetinalDiagnosticTestsRetinoscopyElectroretinographyFluoresceinAngiography(FA)OCTClassificationof

retinaldiseasesVasculardiseasesMaculardiseasesRetinaldetachmentRetinaldegenerationRetinaltumorOcularmanifestationofgeneraldiseasesRetinalvasculardiseaseRetinalarteryocclusionRetinalvenousocclusionDiabeticretinopathyVasculitisCoatsdiseaseCentral

retinalarteryocclusion

CRAO

Commoncauses：

atheroscleroticthrombosisofcribriformplate

systemicdiseases,hemicrania,trauma,

bloodcoagulationdisorder,inflammation,infectiousdiseaseorconnectivetissuedisease

Occasionallyseenin：retrobulbarinjection、retinaldetachmentororbitaloperationEtiologyClinicalmanifestation

SymptomsSignsSuddenpainlessvisionloseofoneeyeDirectlightreflexdisappear,indirectlightreflexnormalRetinaledema,cherry-redspotRetinaarterynarrow,mildhemorrhageNormaleyefundusCRAOFFAofCRAO21safterinjectionoffluorescein,acompleteabsenceinfillingcentralretinalartery,

exceptsegmentofinferiortemperalbranchandmacularbranchTreatmentTarget:toreestablishretinalcirculation&functionTiming:theearlierthebetterDrugs:vasodilator(tropicalorsystemic)+reduceIOPTreatment1.Vasodilator:antispasmorpushingthrombustothesmallerbranch2.ReducingIOP:

（1）massage

（2）anteriorchamberparacentesis（3）diamox500mgst,250mgbid

NaHCO3500mgbid～tid；3.Oxygeninhalation:

mixtureof95%oxygen&5%carbondioxide

4.Fibrolyticenzyme:forpatientssuspectofthrombosis

urokinase5000～10000Uiv

qd

PrognosisDependsonsite,severityandduration.Irreversibleafter4hrsCentralretinal

veinocclusion

ClinicalmanifestationNon-ischemictypeMildfunduschange:retinalhemorrhageandtortuousveinMildVAdecreasecapillarynonperfusionrareVisualfielddefectCentralretinal

veinocclusionIschemictype：MorecommonExtensiveretinalhemorrhageandtortuousvein，Multiplecotton-woolspotsSevereVAdecreaseWidespreadcapillarynonperfusion，60%casespresentiridalneovascularization.CentralretinalveinocclusionCRVONonischemicCRVOischemicBranchretinal

veinocclusionBRVOBRVOFFATreatmentChinesemedicineAnitplateletorantithromboticdrugs:unknowntherapeuticeffectsSystemicexaminationtofindoutcausesCorticosteroidifvasculitisexistGridpatternphotocoagulationofmacula,PRPLaserinducedretina-choroidvascularanastomosisDiabeticRetinopathyDiabeticretinopathyisaleadingcauseofnewcasesofblindnessinworkingagepeopleworldwideManyofthecomplicationsofdiabeticretinopathycanbepreventedordelayedbybloodglucosecontrolandtimelyinterventionVEGFandDRVascularEndothelialGrowthFactorPromotesvasculargrowthandpermeabilityElevatedlevelsofcirculatingVEGFinconditionswithretinalischemiaAnatomicChangesMicroanerysmsDamagetoendothelialcellsleadstodilatedcapillariesandvenulesThesealteredvesselsallowserumandbloodtoleakintotheretinaNPDRIRMAPDRPDRPDRFAVitreousHemorrhage(VH)VHultrasoundTRDultrasoundEpiretinalMembranePDRRetinalDetachmentIrisNeovascularizationMechanismsofVisionLossRetinalischemiaMacularedemaVitreoushemorrhageEpiretinalmembraneformationRetinaldetachmentNeovascularglaucomaScreeningofdrType1diabetics

Firstscreen5yearsafteronset,thenannuallyType2diabetics

FirstscreenupondiagnosisandthenannuallyTreatmentofdrNPDRwithoutmacularedemaObserveMacularedema1.Focal/Gridlaserphotocoagulation2.Vitrectomywithmembranepeeling3.IntraocularSteroid4.IntraocularVEGFinhibitorDMElasertreatmentDMElasertreatment************TreatmentofdrVitreousHemorrhage1.Pan-retinalphotocoagulation2.Vitrectomywithlaserphotocoagulation3.IntraocularVEGFinhibitorTractionRetinalDetachment1.Observationifnotinvolvingthemacula2.VitrectomywithmembranedissectionPan-retinalPhotocoagulationVitrectomyAge-relatedmaculardegenerationEtiologyLong-termchronicmacularlightdamage,heredity,metabolism,nutrientfactorsMechanismDecreasedphagocytosisofRPEleadingtodusenDrusencancausedamageofBruch’smembrane,CNVandfibrocyteproliferationDestructionofchoroidalcapillary,Bruch’smembrane,RPEandphotoreceptorClinicalpresentationVisualacuity

decreasedVA,metamorphopsia,micropsiaVisualfield

centralscotomaFundus

Dry—drusen,RPEchange

Wet--gray-yellowCNVunderretinaofposteriorpole，associatedwithdarkredsubretinalhemorrhage,whichcoversCNVsometimes

FFACNVleakage，bleedingClassificationNonexudate:Drusen,RPEatrophy,Degenerationofphotoreceptor,Choroidcapillaryatrophy;Exudate:Dursen,DamageofBruch’smembrane,CNV,Disciformscarformationundermacula,bleedingandleakageofCNVExudativeAMDTreatment

Anti-oxidationdrugCNVlocatedgreaterthan200micronsfromthecenterofthefovealavascularzone