Retinal vascular disease - Elseviersecure-ecsd.elsevier.com/uk/files/Bowling_Chapter... · Retinal vascular disease. 13. 521. widely used internationally. An abbreviated version is

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Chapter

Retinal vascular disease 13

RETINAL CIRCULATION 520

DIABETIC RETINOPATHY 520Introduction 520Pathogenesis 521Classification 521Signs 521Treatment 529Advanced diabetic eye disease 536Diabetic papillopathy 537

NON-DIABETIC RETINOPATHY 538

RETINAL VENOUS OCCLUSIVE DISEASE 538Introduction 538Risk factors 538Systemic assessment 538Branch retinal vein occlusion 539Impending central retinal vein

occlusion 541Non-ischaemic central retinal vein

occlusion 542Ischaemic central retinal vein

occlusion 542Hemiretinal vein occlusion 544Treatment of the complications of

CRVO 544

Systemic management in retinal vein occlusion 549

Papillophlebitis 549

RETINAL ARTERIAL OCCLUSIVE DISEASE 549Systemic assessment 550Amaurosis fugax 551Branch retinal artery occlusion 551Central retinal artery occlusion 552Cilioretinal artery occlusion 552Treatment of acute retinal artery

occlusion 552Systemic management following retinal

arterial occlusion 555Asymptomatic retinal embolus 556

OCULAR ISCHAEMIC SYNDROME 556

HYPERTENSIVE EYE DISEASE 557Retinopathy 557Choroidopathy 559

SICKLE-CELL RETINOPATHY 559Sickling haemoglobinopathies 559Anterior segment 560Non-proliferative retinopathy 560Proliferative retinopathy 560

THALASSAEMIA RETINOPATHY 561

RETINOPATHY OF PREMATURITY 561Active disease 563Cicatricial disease 565

RETINAL ARTERY MACROANEURYSM 565

PRIMARY RETINAL TELANGIECTASIA 569Idiopathic macular telangiectasia 569Coats disease 569

EALES DISEASE 569

RADIATION RETINOPATHY 572

PURTSCHER RETINOPATHY 572

VALSALVA RETINOPATHY 572

LIPAEMIA RETINALIS 574

RETINOPATHY IN BLOOD DISORDERS 574Leukaemia 574Anaemia 577Hyperviscosity 577

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520 Diabetic Retinopathy

RETINAL CIRCULATION

Arterial system• The central retinal artery,anendartery,enterstheoptic

nerveapproximately1cmbehindtheglobe.Itiscomposed

ofthreeanatomicallayers:

○ Theintima,theinnermost,iscomposedofasinglelayer

ofendotheliumrestingonacollagenouszone.

○ Theinternalelasticlaminaseparatestheintimafromthe

media.

○ Themediaconsistsmainlyofsmoothmuscle.

○ Theadventitiaistheoutermostandiscomposedofloose

connectivetissue.

• Retinal arteriolesarisefromthecentralretinalartery.Their

wallscontainsmoothmuscle,butincontrasttoarteriesthe

internalelasticlaminaisdiscontinuous.

CapillariesRetinalcapillariessupplytheinnertwo-thirdsoftheretina,with

theouterthirdbeingsuppliedbythechoriocapillaris.The inner

capillarynetwork(plexus)islocatedintheganglioncelllayer,with

anouterplexusintheinnernuclearlayer.Capillary-freezonesare

presentaroundarterioles(Fig.13.1A)andatthefovea(fovealavas-

cularzone–FAZ).Retinalcapillariesaredevoidofsmoothmuscle

andelastictissue;theirwallsconsistofthefollowing(Fig.13.1B):

• Endothelial cellsformasinglelayeronthebasement

membraneandarelinkedbytightjunctionsthatformthe

innerblood–retinalbarrier.

• The basement membraneliesbeneaththeendothelialcells

withanouterbasallaminaenclosingpericytes.

• Pericyteslieexternaltoendothelialcellsandhavemultiple

pseudopodialprocessesthatenvelopthecapillaries.Pericytes

havecontractilepropertiesandarethoughttoparticipatein

autoregulationofthemicrovascularcirculation.

Venous systemRetinalvenulesandveinsdrainbloodfromthecapillaries.

• Small venulesarelargerthancapillariesbuthaveasimilar

structure.

• Larger venulescontainsmoothmuscleandmergetoform

veins.

• Veinscontainasmallamountofsmoothmuscleandelastic

tissueintheirwallsandarerelativelydistensible.Their

diametergraduallyenlargesastheypassposteriorlytowards

thecentralretinalvein.

DIABETIC RETINOPATHY

Introduction

Ophthalmic complications of diabetes• Common

○ Retinopathy.

○ Iridopathy(minoriristransilluminationdefects).

○ Unstablerefraction.

• Uncommon○ Recurrentstyes.

○ Xanthelasmata.

○ Acceleratedsenilecataract.

○ Neovascularglaucoma(NVG).

○ Ocularmotornervepalsies.

○ Reducedcornealsensitivity.

• Rare.Papillopathy,pupillarylight-neardissociation,

Wolframsyndrome(progressiveopticatrophyandmultiple

neurologicalandsystemicabnormalities),acute-onset

cataract,rhino-orbitalmucormycosis.

PrevalenceThereportedprevalenceofdiabeticretinopathy(DR)indiabetics

variessubstantiallybetweenstudies,evenamongstcontemporary

populationsinthesamecountry,butisprobablyaround40%.It

is more common in type 1 diabetes than in type 2 and sight-

threateningdiseaseispresentinupto10%.Proliferativediabetic

Fig. 13.1 Normal retinal capillary bed. (A) Periarteriolar capillary-free zone – flat preparation of Indian ink-injected retina; (B) endothelial cells with elongated nuclei and pericytes with rounded nuclei – trypsin digest preparation (Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001)

AA

B



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CHAPTER

Retinal vascular disease 52113widelyused internationally.Anabbreviatedversion is setout in

Table13.1, inconjunctionwithmanagementguidelines.Thefol-

lowingdescriptivecategoriesarealsoinwidespreaduseinclinical

practice:

• Background diabetic retinopathy (BDR)ischaracterizedby

microaneurysms,dotandblothaemorrhagesandexudates.

ThesearegenerallytheearliestsignsofDR,andpersistas

moreadvancedlesionsappear.

• Diabetic maculopathystrictlyreferstothepresenceofany

retinopathyatthemacula,butiscommonlyreservedfor

significantchanges,particularlyvision-threateningoedema

andischaemia.

• Preproliferative diabetic retinopathy (PPDR)manifests

withcottonwoolspots,venouschanges,intraretinal

microvascularanomalies(IRMA)andoftendeepretinal

haemorrhages.PPDRindicatesprogressiveretinalischaemia,

withaheightenedriskofprogressiontoretinal

neovascularization.

• PDRischaracterizedbyneovascularizationonorwithinone

discdiameterofthedisc(NVD)and/ornewvessels

elsewhere(NVE)inthefundus.

• Advanced diabetic eye diseaseischaracterizedbytractional

retinaldetachment,significantpersistentvitreous

haemorrhageandneovascularglaucoma.

Signs

MicroaneurysmsMicroaneurysmsare localizedoutpouchings,mainly saccular,of

thecapillarywall thatmayformeitherby focaldilatationof the

capillarywallwherepericytesareabsent,orbyfusionoftwoarms

ofacapillaryloop(Fig.13.2A).Mostdevelopintheinnercapillary

plexus(innernuclearlayer),frequentlyadjacenttoareasofcapil-

larynon-perfusion(Fig.13.2B).Lossofpericytes(Fig.13.2C)may

also lead to endothelial cell proliferation with the formation of

‘cellular’microaneurysms(Fig.13.2D).Microaneurysmsmayleak

plasmaconstituentsintotheretinaasaresultofbreakdowninthe

blood–retinal barrier, or may thrombose. They tend to be the

earliestsignofDR.

• Signs.Tinyreddots,ofteninitiallytemporaltothefovea

(Fig.13.3A);maybeindistinguishableclinicallyfromdot

haemorrhages.

• Fluorescein angiography (FA)allowsdifferentiation

betweendothaemorrhagesandnon-thrombosed

microaneurysms.Earlyframesshowtinyhyperfluorescent

dots(Fig.13.3B),typicallymorenumerousthanvisible

clinically.Lateframesshowdiffusehyperfluorescencedueto

leakage.

Retinal haemorrhages• Retinal nerve fibre layer haemorrhagesarisefromthelarger

superficialpre-capillaryarterioles(Fig.13.4A)andassume

theircharacteristicshape(Fig.13.4B)becauseofthe

architectureoftheretinalnervefibrelayer.

retinopathy(PDR)affects5–10%ofthediabeticpopulation;type

1diabeticsareatparticularrisk,withanincidenceofupto90%

after30years.

Risk factors• Duration of diabetesisthemostimportantriskfactor.In

patientsdiagnosedwithdiabetesbeforetheageof30years,

theincidenceofDRafter10yearsis50%,andafter30years

90%.DRrarelydevelopswithin5yearsoftheonsetof

diabetesorbeforepuberty,butabout5%oftype2diabetics

haveDRatpresentation.Itappearsthatdurationisastronger

predictorforproliferativediseasethanformaculopathy.

• Poor control of diabetes.Ithasbeenshownthattightblood

glucosecontrol,particularlywheninstitutedearly,can

preventordelaythedevelopmentorprogressionofDR.

However,asuddenimprovementincontrolmaybe

associatedwithprogressionofretinopathyinthenearterm.

Type1diabeticpatientsappeartoobtaingreaterbenefit

fromgoodcontrolthantype2.RaisedHbA1cisassociated

withanincreasedriskofproliferativedisease.

• Pregnancyissometimesassociatedwithrapidprogressionof

DR.Predicatingfactorsincludegreaterpre-pregnancy

severityofretinopathy,poorpre-pregnancycontrolof

diabetes,controlexertedtoorapidlyduringtheearlystages

ofpregnancy,andpre-eclampsia.Theriskofprogressionis

relatedtotheseverityofDRinthefirsttrimester.If

substantialDRispresent,frequencyofreviewshouldreflect

individualrisk,andcanbeuptomonthly.Diabeticmacular

oedemausuallyresolvesspontaneouslyafterpregnancyand

neednotbetreatedifitdevelopsinlaterpregnancy.

• Hypertension,whichisverycommoninpatientswithtype2

diabetes,shouldberigorouslycontrolled(<140/80mmHg).

Tightcontrolappearstobeparticularlybeneficialintype2

diabeticswithmaculopathy.Cardiovasculardiseaseand

previousstrokearealsopredictive.

• Nephropathy,ifsevere,isassociatedwithworseningofDR.

Conversely,treatmentofrenaldisease(e.g.renal

transplantation)maybeassociatedwithimprovementof

retinopathyandabetterresponsetophotocoagulation.

• Other risk factorsincludehyperlipidaemia,smoking,

cataractsurgery,obesityandanaemia.

PathogenesisDR is predominantly a microangiopathy in which small blood

vessels are particularly vulnerable to damage from high glucose

levels.Directhyperglycaemiceffectsonretinalcellsarealsolikely

toplayarole.

Manyangiogenicstimulatorsand inhibitorshavebeen identi-

fied;vascularendothelialgrowthfactor(VEGF)appearstobeof

particularimportanceintheformercategory.

ClassificationTheclassificationusedintheEarlyTreatmentDiabeticRetinopa-

thyStudy(ETDRS– themodifiedAirlieHouseclassification) is



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bychroniclocalizedretinaloedema;theydevelopatthejunction

ofnormalandoedematousretina.Theyarecomposedoflipopro-

teinandlipid-filledmacrophageslocatedmainlywithintheouter

plexiform layer (Fig. 13.5A). Hyperlipidaemia may increase the

likelihoodofexudateformation.

• Signs○ Waxyyellowlesions(Fig.13.5B)withrelativelydistinct

marginsarrangedinclumpsand/orringsattheposterior

pole,oftensurroundingleakingmicroaneurysms.

○ Withtimethenumberandsizetendtoincrease(Fig.

13.5C),andthefoveamaybeinvolved.

○ Whenleakageceases,exudatesabsorbspontaneouslyover

aperiodofmonths,eitherintohealthysurrounding

capillariesorbyphagocytosis.

• Intraretinalhaemorrhagesarisefromthevenousendof

capillariesandarelocatedinthecompactmiddlelayersof

theretina(seeFig.13.4A)witharesultantred‘dot/blot’

configuration(Fig.13.4C).

• Deeperdarkroundhaemorrhages(Fig.13.4D)represent

haemorrhagicretinalinfarctsandarelocatedwithinthe

middleretinallayers(seeFig.13.4A).Theextentof

involvementisasignificantmarkerofthelikelihoodof

progressiontoPDR.

ExudatesExudates,sometimestermed‘hard’exudatestodistinguishfrom

theoldertermforcottonwoolspots–‘soft’exudates,arecaused

Table 13.1 Abbreviated Early Treatment Diabetic Retinopathy Study (ETDRS) classification of diabetic retinopathy

Category/description Management

Non-proliferative diabetic retinopathy (NPDR)

No DR Review in 12 months

Very mild NPDR Review most patients in 12 months

Microaneurysms only

Mild NPDR Review range 6–12 months, depending on severity of signs, stability, systemic factors, and patient’s personal circumstancesAny or all of: microaneurysms, retinal haemorrhages,

exudates, cotton wool spots, up to the level of moderate NPDR. No intraretinal microvascular anomalies (IRMA) or significant beading

Moderate NPDR Review in approximately 6 monthsProliferative diabetic retinopathy (PDR) in up to 26%,

high-risk PDR in up to 8% within a year• Severe retinal haemorrhages (more than ETDRS standard photograph 2A: about 20 medium–large per quadrant) in 1–3 quadrants or mild IRMA

• Significant venous beading can be present in no more than 1 quadrant

• Cotton wool spots commonly present

Severe NPDR Review in 4 monthsPDR in up to 50%, high-risk PDR in up to 15% within a

yearThe 4–2–1 rule; one or more of:• Severe haemorrhages in all 4 quadrants• Significant venous beading in 2 or more quadrants• Moderate IRMA in 1 or more quadrants

Very severe NPDR Review in 2–3 monthsHigh-risk PDR in up to 45% within a year

Two or more of the criteria for severe NPDR

Proliferative diabetic retinopathy (PDR)

Mild–moderate PDR Treatment considered according to severity of signs, stability, systemic factors, and patient’s personal circumstances such as reliability of attendance for review. If not treated, review in up to 2 months

New vessels on the disc (NVD) or new vessels elsewhere (NVE), but extent insufficient to meet the high-risk criteria

High-risk PDR Treatment advised – see textShould be performed immediately when possible, and

certainly same day if symptomatic presentation with good retinal view

• New vessels on the disc (NVD) greater than ETDRS standard photograph 10A (about 1

3 disc area)• Any NVD with vitreous haemorrhage• NVE greater than 1

2 disc area with vitreous haemorrhage

Advanced diabetic eye disease See text

See text for description



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Fig. 13.2 Microaneurysms – histopathology. (A) Two arms of a capillary loop that may fuse to become a microaneurysm – flat preparation of Indian ink-injected retina; (B) an area of capillary non-perfusion and adjacent microaneurysms – flat preparation of Indian ink-injected retina; (C) eosinophilic (dark pink) degenerate pericytes – trypsin digest preparation; (D) microaneurysm with endothelial cell proliferation (cellular microaneurysm) – trypsin digest preparation (Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – figs A and C; J Harry – figs B and D)

A B

C

D

Fig. 13.3 Microaneurysms. (A) Microaneurysms and dot/blot haemorrhages at the posterior pole; (B) FA shows scattered hyperfluorescent spots in the posterior fundus

A

B



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oedematous.Withcentralaccumulationoffluidthefoveaassumes

a cystoid appearance – cystoid macular oedema (CMO) that is

readilydetectableonopticalcoherencetomography(OCT)(Fig.

13.7A) and assumes a central flower petal pattern on FA (Fig.

13.7B).

• Focal maculopathy:well-circumscribedretinalthickening

associatedwithcompleteorincompleteringsofexudates

(Fig.13.8A).FAshowslate,focalhyperfluorescencedue

toleakage,usuallywithgoodmacularperfusion

(Fig.13.8B).

• Diffuse maculopathy:diffuseretinalthickening,whichmay

beassociatedwithcystoidchanges;therearetypicallyalso

scatteredmicroaneurysmsandsmallhaemorrhages(Fig.

13.9A).Landmarksmaybeobscuredbyoedema,whichmay

renderlocalizationofthefoveaimpossible.FAshows

mid-andlate-phasediffusehyperfluorescence(Fig.13.9B),

anddemonstratesCMOifpresent.

○ Chronicleakageleadstoenlargementandthedeposition

ofcrystallinecholesterol(Fig.13.5D).

• FAwillcommonlyshowhypofluorescenceonlywithlarge

denseexudates,asalthoughbackgroundchoroidal

fluorescenceismasked,retinalcapillaryfluorescenceis

generallypreservedoverlyingthelesions(Fig13.6).

Diabetic macular oedema (DMO)Diabeticmaculopathy(fovealoedema,exudatesor ischaemia) is

themostcommoncauseofvisualimpairmentindiabeticpatients,

particularlytype2.Diffuseretinaloedemaiscausedbyextensive

capillary leakage, and localized oedema by focal leakage from

microaneurysmsanddilatedcapillarysegments.Thefluidis ini-

tially located between the outer plexiform and inner nuclear

layers;lateritmayalsoinvolvetheinnerplexiformandnervefibre

layers,untileventuallytheentirethicknessoftheretinabecomes

Fig. 13.4 Retinal haemorrhages. (A) Histology shows blood lying diffusely in the retinal nerve fibre and ganglion cell layers and as globules in the outer layers; (B) retinal nerve fibre layer (flame) haemorrhages; (C) dot and blot haemorrhages; (D) deep dark haemorrhages (Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – fig. A)

A B

C D



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Fig. 13.5 Exudates. (A) Histology shows irregular eosinophilic deposits mainly in the outer plexiform layer; (B) small exudates and microaneurysms; (C) more extensive exudates, some associated with microaneurysms; (D) exudates involving the fovea, including central crystalline cholesterol deposition – focal laser has recently been applied superotemporal to the fovea (Courtesy of J Harry – fig. A; S Chen – figs C and D)

A B

C D

Fig. 13.6 FA of exudates. (A) Clinical appearance; (B) exudates not shown on FA

A B



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Cotton wool spotsCotton wool spots are composed of accumulations of neuronal

debris within the nerve fibre layer. They result from ischaemic

disruptionofnerveaxons,theswollenendsofwhichareknown

ascytoidbodies,seenonlightmicroscopyasglobularstructures

in the nerve fibre layer (Fig. 13.12A). As cotton wool spots heal,

debrisisremovedbyautolysisandphagocytosis.

• Signs.Smallfluffywhitishsuperficiallesionsthatobscure

underlyingbloodvessels(Fig.13.12BandC).Theyare

clinicallyevidentonlyinthepost-equatorialretina,where

thenervefibrelayerisofsufficientthicknesstorenderthem

visible.

Ischaemic maculopathy• Signsarevariableandthemaculamaylookrelatively

normaldespitereducedvisualacuity.InothercasesPPDR

maybepresent.

• FAshowscapillarynon-perfusionatthefovea(anenlarged

FAZ)andfrequentlyotherareasofcapillarynon-perfusion

(Fig.13.10)attheposteriorpoleandperiphery.

Clinically significant macular oedemaClinically significant macular oedema (CSMO) is detected on

clinicalexaminationasdefinedintheETDRS(Fig.13.11):

• Retinalthickeningwithin500µmofthecentreofthe

macula(Fig.13.11,upperleft).

• Exudateswithin500µmofthecentreofthemacula,if

associatedwithretinalthickening;thethickeningitselfmay

beoutsidethe500µm(Fig.13.11,upperright).

• Retinalthickeningonediscarea(1500µm)orlarger,any

partofwhichiswithinonediscdiameterofthecentreofthe

macula(Fig.13.11,lowercentre).

Fig. 13.7 Cystoid macular oedema. (A) OCT shows retinal thickening and cystoid spaces; (B) FA shows leaking microaneurysms and central diffuse hyperfluorescence with a flower-petal configuration – same patient as Fig. 13.6

A

B

Fig. 13.8 Focal diabetic maculopathy. (A) A ring of hard exudates temporal to the macula; (B) FA late phase shows focal area of hyperfluorescence due to leakage corresponding to the centre of the exudate ring

A

B



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Fig. 13.9 Diffuse diabetic maculopathy. (A) Dot and blot haemorrhages – diffuse retinal thickening is present; (B) late-phase FA shows extensive hyperfluorescence at the posterior pole due to leakage (Courtesy of S Chen – fig. B)

A

B

Fig. 13.10 Ischaemic diabetic maculopathy. FA venous phase shows hypofluorescence due to capillary non-perfusion at the central macula and elsewhere (Courtesy of S Chen)

Fig. 13.11 Clinically significant macular oedema

Fovea

• FAshowsfocalhypofluorescenceduetolocalischaemiaand

blockageofbackgroundchoroidalfluorescence.

Venous changesVenousanomaliesseeninischaemiaconsistofgeneralizeddilata-

tionandtortuosity,looping,beading(focalnarrowinganddilata-

tion)andsausage-likesegmentation(Fig.13.13).Theextentofthe

retinal area exhibiting venous changes correlates well with the

likelihoodofdevelopingproliferativedisease.

Intraretinal microvascular abnormalitiesIntraretinal microvascular abnormalities (IRMA) are arteriolar–

venular shunts that run from retinal arterioles to venules, thus

bypassingthecapillarybedandarethereforeoftenseenadjacent

toareasofmarkedcapillaryhypoperfusion(Fig.13.14A).

• Signs.Fine,irregular,redintraretinallinesthatrunfrom

arteriolestovenules,withoutcrossingmajorbloodvessels

(Fig.13.14B).

• FAshowsfocalhyperfluorescenceassociatedwithadjacent

areasofcapillaryclosure(‘dropout’)butwithoutleakage.

Arterial changesSubtle retinal arteriolar dilatation may be an early marker of

ischaemic dysfunction. When significant ischaemia is present

signs include peripheral narrowing, ‘silver wiring’ and oblitera-

tion, similar to the late appearance following a branch retinal

arteryocclusion.



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Fig. 13.12 Cotton wool spots. (A) Histology shows cytoid bodies in the retinal nerve fibre layer; (B) clinical appearance; (C) red-free photography showing differing appearance of cotton wool spots and haemorrhages, the latter appearing black – the smaller well-defined white lesions are exudates (Courtesy of J Harry – fig. A)

A

B

C

Fig. 13.13 Venous changes. (A) Looping; (B) beading; (C) severe segmentation

A

B

C



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Proliferative retinopathyIthasbeenestimatedthatoverone-quarteroftheretinamustbe

non-perfused before PDR develops. Although preretinal new

vesselsmayariseanywhereintheretina,theyaremostcommonly

seenat theposteriorpole.Fibroustissue, initiallyfine,gradually

developsinassociationasvesselsincreaseinsize.

• New vessels at the disc(NVD)describesneovascularization

onorwithinonediscdiameteroftheopticnervehead(Fig.

13.15).

• New vessels elsewhere(NVE)describesneovascularization

furtherawayfromthedisc(Fig.13.16);itmaybeassociated

withfibrosisiflong-standing.

• New vessels on the iris(NVI–Fig.13.17),alsoknownas

rubeosisiridis,carryahighlikelihoodofprogressionto

neovascularglaucoma(seeCh.10).

Fig. 13.14 Intraretinal microvascular abnormalities. (A) Histology shows arteriolar-venular shunt and a few microaneurysms within a poorly perfused capillary bed – flat preparation of Indian ink-injected retina; phase contrast microscopy; (B) clinical appearance (Courtesy of J Harry – fig. A)

A

B

• FA(seeFig.13.15C)highlightsneovascularizationduringthe

earlyphasesoftheangiogramandshowsirregularexpanding

hyperfluorescenceduringthelaterstagesduetointense

leakageofdyefromneovasculartissue.FAcanbeusedto

confirmthepresenceofnewvessels(NV)iftheclinical

diagnosisisindoubt,andalsodelineatesareasofischaemic

retinathatmightbeselectivelytargetedforlasertreatment.

Treatment

General• Patient educationiscritical,includingregardingtheneedto

complywithreviewandtreatmentschedulesinorderto

optimizevisualoutcomes.

• Diabetic controlshouldbeoptimized.

• Other risk factors,particularlysystemichypertension

(especiallytype2diabetes)andhyperlipidaemiashouldbe

controlledinconjunctionwiththepatient’sdiabetologist.

• Fenofibrate200mgdailyhasbeenshowntoreducethe

progressionofdiabeticretinopathyintype2diabeticsand

prescriptionshouldbeconsidered;thedecisionis

independentofwhetherthepatientalreadytakesastatin.

• Smokingshouldbediscontinued,thoughthishasnotbeen

definitivelyshowntoaffectretinopathy.

• Other modifiable factorssuchasanaemiaandrenalfailure

shouldbeaddressedasnecessary.

Treatment of diabetic macular oedemaUntil recently laserphotocoagulationwas themainstayof treat-

ment for DMO, reducing the risk of visual loss by 50% overall

compared with observation. The availability of newer treatment

modalitiesandincreasingevidencefortheirefficacyhasdramati-

cally altered the approach to management over recent years.

However, options should always be discussed fully with the

patient. In particular, patients with good vision who otherwise

meetcriteriafortreatmentmightpreferobservationoncetherisks

ofvariousinterventionsaretakenintoaccount.

• Laser photocoagulation(modifiedETDRSfocal/grid

treatment).

○ Focal(Figs13.18AandB).Diodeorargonburnsare

appliedtoleakingmicroaneurysms500–3000µmfrom

thefoveola;spotsize50–100µm,duration0.05–0.1swith

sufficientpowertoobtainagreyishreactionbeneaththe

microaneurysm.

○ Grid(Figs13.18C–F).Burnsareappliedtomacularareas

ofdiffuseretinalthickening,treatingnocloserthan

500µmfromthefoveolaand500µmfromtheopticdisc

usingaspotsizeof50–100µmandduration0.05–0.1

second,withpoweradjustedtogiveamildreaction.A

‘modified’gridincludesfocaltreatmenttofociofleakage,

usuallymicroaneurysms.

• Subthreshold micropulse diode laser.Thismodalityuses

veryshort(microsecondorder)laserpulseduration

combinedwithalongerinterval(e.g.5%dutycycle)



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Fig. 13.15 Disc new vessels. (A) Mild; (B) severe; (C) FA shows leaking disc vessels, with extensive peripheral capillary dropout and a small focus of leaking vessels elsewhere (Courtesy of S Chen – fig. B)

A

B

C

Fig. 13.16 New vessels elsewhere. (A) Mild; (B) severe; (C) associated with fibrosis

A

B

C



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Retinal vascular disease - Elseviersecure-ecsd.elsevier.com/uk/files/Bowling_Chapter... · Retinal vascular disease. 13. 521. widely used internationally. An abbreviated version is