眼科学教学课件：03 Retina Disease

DiseasesofRetinaIntroduction

EyeballstructureandretinaMaculaluteaLocated3mmtemporallytotheopticpapilla,rightonthevisualaxisAconcavecentralretinaldepressioniscalledFoveaCentralis

maculaluteacontainsonlycones;

1conesynapesto1bipolarcell,whichsynapesto1ganglioncell,leadingtothemostsensitivevisionInperipheralretina,600rodsconnectto1ganglionHistologyofretinaInternallimitingmembraneNervefiberlayerGanglioncelllayerInnerplexiformlayerInnernuclearlayerOuterplexiformlayerOuternulearlayerExternallimitingmembranephotoreceptorRPEBruch’smembraneNeuroconductionofretina3neurons:

Photoreceptor

BipolarGanglioncellSupportingtissue:

Müllercell

rod（scotopicvision）

cone（photopicvision）ConnectingcellbetweenphotoreceptorandganglionConducttobrainVasculatureofretina

Innerlayer→centralretinalvascularsystem

Outerlayer→choroid（ciliaryvascularsystem）

Maculalutea→

choriocapillariesRetinabarrierInnerbarrier（blood–retinabarrier）

denseconnectionofretinalcapillaryendotheliumOuterbarrier（choroid-retinabarrier）

zonulaoccludensbetweentheRPE

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

fibersareradiallylocated;Thispoolingformsaflower-petalpatternRetinalEdemaIntracellularedemaExtracellularedemaExudatesHardexudateCotton-woolspotLeakageofcapillary→absorb→depositionoflipidinouterplexiformlayer

Alsocalled“softexudation”Precapillaryarterioleocclusion→

axoplasmictransportblocked→organellesstackExudatesCotton-woolspotHardexudateHemorrhage

DeephemorrhageSuperficialhemorrhage

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

formationofvascularendothelialgrowthfactor→

neovascularizationNeovascualrmembrane,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,

exceptsegmentofinferiortemperalbranchandmacularbranchBRAOBRAOFFABRANCH

retinalarteryocclusion

BRaOTreatmentTarget:toreestablishretinalcirculation&functionTiming:theearlierthebetterDrugs:vasodilator(tropicalorsystemic)+reduceIOPTreatment1.Vasodilator:antispasmorpushingthrombustothesmallerbranch2.ReducingIOP:（1）massage

（2）anteriorchamberparacentesis（3）diamox500mgst,250mgbid

NaHCO3500mgbid～tid3.Oxygeninhalation:mixtureof95%oxygen&5%carbondioxide4.Fibrinolyticenzyme:forpatientssuspectofthrombosisurokinase5000～10000Uiv

qdPrognosisDependsonsite,severityanddurationIrreversibleafter4hrs

ClinicalmanifestationNon-ischemictypeMildfunduschange:retinalhemorrhageandtortuousveinMildVAdecreasecapillarynonperfusionrareVisualfielddefectCentral

retinalVEINocclusion

CRVOIschemictype：MorecommonExtensiveretinalhemorrhageandtortuousvein，Multiplecotton-woolspotsSevereVAdecreaseWidespreadcapillarynonperfusion，60%casespresentiridalneovascularizationCentral

retinalVEINocclusion

CRVOCRVONonischemicCRVOischemicCentral

retinalVEINocclusion

CRVOCRVONon-ischemictypeIschemictypeVA≥0.05＜0.05PupilRAPD(-)RAPD(+)FundusMildhemorrhageandedemaExtensivehemorrhageandsevereedma,multiplecotton-woolspotsFFAcapillarynonperfusionrareWidespreadcapillarynonperfusionVFCentralvisualfielddefectPeripheralandcentralvisualfielddefectNVNoneCommonPrognosisGoodPoorBRVOBRVOFFABRANCH

retinalVEINocclusion

BRVOTreatmentChinesemedicineAnitplateletorantithromboticdrugs:unknowntherapeuticeffectsSystemicexaminationtofindoutcausesCorticosteroidifvasculitisexistGridpatternphotocoagulationofmacula,PRPLaserinducedretina-choroidvascularanastomosisDiabeticRetinopathyDiabeticretinopathyisaleadingcauseofnewcasesofblindnessinworkingagepeopleworldwideManyofthecomplicationsofdiabeticretinopathycanbepreventedordelayedbybloodglucosecontrolandtimelyinterventionDRDiseaseseverityscaleDiseaseSeverityLevelFindingsObservableuponDilatedOphthalmoscopyNoapparentretinopathyNoabnormalitiesMildNPDRMicroaneurysmsonlyModerateNPDRMorethanjustmicroaneurysmsbutlessthansevereNPDRSevereNPDRAnyofthefollowing(4-2-1rule)andnosignsofPDR:·Morethan20intraretinalhemorrhagesineachoffourquadrants·Definitevenousbeadingintwoormorequadrants·ProminentIRMAinoneormorequadrantsPDROneorbothofthefollowing:·Neovascularization·Vitreous/preretinalhemorrhageVEGFandDRVascularEndothelialGrowthFactorPromotesvasculargrowthandpermeabilityElevatedlevelsofcirculatingVEGFinconditionswithretinalischemiaAnatomicChangesMicroanerysmsDamagetoendothelialcellsleadstodilatedcapillariesandvenulesThesealteredvesselsallowserumandbloodtoleakintotheretinaNPDR

(non-proliferativediabeticretinopathy)IRMA

(intraretinal

microvascularabnormalities)

VENOUSBEADINGPDR

(proliferativediabeticretinopathy)PDR

(proliferativediabeticretinopathy)PDRFAVitreousHemorrhage(VH)VHultrasoundTRDultrasoundEpiretinalMembranePDRRetinalDetachmentIrisNeovascularizationMechanismsofVisionLossRetinalischemiaMacularedemaVitreoushemorrhageEpiretinalmembraneformationRetinaldetachmentNeovascularglaucomaScreeningofdrType1diabetics

Firstscreen5yearsafteronset,thenannuallyType2diabetics

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

decreasedVA,metamorphopsia,micropsiaVisualfield

centralscotomaFundus

Dry—drusen,RPEchange

Wet--gray-yellowCNVunderretinaofposteriorpole，associatedwithdarkredsubretinalhemorrhage,whichcoversCNVsometimes

FFACNVleakage，bleedingClassificationNonexudativeAMD:Drusen,RPEatrophy,Degenerationofphotoreceptor,ChoroidcapillaryatrophyExudativeAMD:Drusen,DamageofBruch’smembrane,CNV,Disciformscarformationundermacula,bleedingandleakageofCNVExudativeAMDTreatment