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S
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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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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522 Diabetic Retinopathy
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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524 Diabetic Retinopathy
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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Retinal vascular disease 52513
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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526 Diabetic Retinopathy
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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Retinal vascular disease 52713
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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Retinal vascular disease 52913
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)
Bowling_Chapter 13_main.indd 529 2/25/2015 6:55:37 PM
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S
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
Bowling_Chapter 13_main.indd 530 2/25/2015 6:55:39 PM
To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter Toppan Best-set. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication.
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