1

Welcome to SECO 2011

SECO 2011March 2-6, 2011

Essentials in Posterior Segment DiseaseCarlo J. Pelino, OD

Joseph J. Pizzimenti, OD

DISCLOSURE STATEMENT

Please silence all mobile devices

At the conclusion of this course, please properlydispose of your trash as you leave this room

Dr. Pizzimenti is CEO of Optometryboardcertified.comDr. Pizzimenti has received honoaraia from Alcon, Reichert,Zeavision, and Carl Zeiss MeditecDr. Pelino has received honoraria from Carl Zeiss Meditec

Goals for This Course

Functional anatomy Recognize and

understand the telltalesigns of posteriorsegment disease.

Case examples New knowledge Interactive!

Identifying Signs of Retinal Disease

The Posterior Segment Functional Anatomy

– Vitreous– Choroid– Retina

Functional Anatomy of Posterior Segment

Clinical Landmark - Equator

2

Ora Serrata

Pars Plana

Peripheral vs Central Retina

Approx 6DiscDiameters

CentralRetina

Exit Site ofAmpulla

Cent. R

et. →Equator

Peripheral vs Central Retina

PosteriorPole

“Mid-Periphery”

The Vitreous

Vitreous cavity ~4 ml in volume– 80% of globe’s total volume

Composed of water, proteins, andmucopolysaccharides (MPS).

Protein– Type II c_______________

• Helps support shape

MPS– Hyaluronic acid

• Gives vitreous elastic and viscid qualities

The Vitreous

3

AscorbateAscorbate

Cloquet’s Canal

Area of Martegiani

Erggelet’s Space (Berger’s Space)

Vitreoretinal Vitreoretinal interface without PVDinterface without PVD

Posterior vitreous detachment initially occurs in thePosterior vitreous detachment initially occurs in thePerifovea Perifovea with a predilection for superior quadrant.with a predilection for superior quadrant.

Detachment extends widely in the Detachment extends widely in the perifovea perifovea withwithpersistent attachment to fovea and optic nerve head.persistent attachment to fovea and optic nerve head.

Detachment occurs in the fovea, persistentDetachment occurs in the fovea, persistentattachment of the posterior vitreous face to the opticattachment of the posterior vitreous face to the opticnerve head.nerve head.

Detachment is completed in with release of theDetachment is completed in with release of thevitreo-papillary vitreo-papillary adhesionadhesion.

Epiretinal Membrane SD-OCT Images

Fundus ImageFundus Image

ThicknessThicknessMap OverlayMap Overlay

ILM LayerILM Layer

ThicknessThicknessMapMap

Vitreoretinal Interface

Anomalous PVD Epiretinal

Membrane Macular Hole

Case Challenge

65 y/o WF CC: New floater OS x 3 wks

– Floater is bright

BCVA: OD 20/20 OS 20/25 Workup rules out vit cell, retinal breaks Lack of foveal depression OS

4

Diagnosis?

What is your plan?

Pharmacologic Pharmacologic vitreolysis vitreolysis - - MicroplasminMicroplasmin

Case Challenge

65 y/o WF CC: New floater OD x 3 wks

– Floater is bright

BCVA: OD 20/20 OS 20/25 Workup rules out vit cell, retinal breaks, but…

NFL or Pre-retinalFlame Hemeat ON 2° toAcute PVD

5

What is your plan?

Functional Anatomy: The Retina

RPE Neurosensory 6 million Cones

• Detailed vision• Color vision

120 million Rods• Peripheral retinal

receptors• Great sensitivity to

light

Retinal Pigment Epithelium

120 million cells inmonolayer

T____ junctions– Outer blood-retina

barrier

Functions of RPE– Phagocytosis of

renewable discs of PRs– O-2 diffusion to PRs– Provision of nutrients to

PRs

RPE

Describe That Fundus!

6

Outcome:

• Congenital Hypertrophy of Retinal Pigment Epithelium (CHRPE)

• Photos taken

• Patient referred back to Optometrist

• Monitor 1 year

The Real Deal on CHRPE

Dark black, only slightly raised No malignant potential When present in multiple locations, investigate for

Gardner’s Syndrome– This is familial polyposis coli, which can lead to colorectal

carcinoma.– Autosomal dominant condition– Probe family history, patient GI symptoms– Consider gastroenterology consult if symptomatic or +

family history

CHRPE

The Macula X___________ pigment in

NFL absorbs blue WL,“macula lutea”

Fovea– Shallow depression in middle of

macula, 1.5 DD– Retinal cells displaced exposing

only the PR– Has the highest concentration of

cones– Capillary free zone 500 microns

(FAZ)

Note yellowmacular pigment

Fovea

7

OSOSIS/OSIS/OSELMELM RPERPEISIS

NFL: Nerve Fiber LayerNFL: Nerve Fiber Layer OPL: Outer OPL: Outer Plexiform Plexiform Layer Layer IS/OS: Junction of inner and outerIS/OS: Junction of inner and outerILM: Inner Limiting MembraneILM: Inner Limiting Membrane ONL: Outer Nuclear LayerONL: Outer Nuclear Layer photoreceptor segmentsphotoreceptor segmentsGCL: Ganglion Cell LayerGCL: Ganglion Cell Layer ELM: External limiting membraneELM: External limiting membrane OS: Photoreceptor Outer SegmentOS: Photoreceptor Outer SegmentIPL: Inner IPL: Inner Plexiform Plexiform Layer Layer IS: Photoreceptor Inner Segment IS: Photoreceptor Inner Segment RPE: Retinal Pigment EpitheliumRPE: Retinal Pigment EpitheliumINL: Inner Nuclear Layer INL: Inner Nuclear Layer

ILMILM GCLGCLNFLNFL

ChoroidChoroid

IPLIPL INLINL OPLOPL ONLONL

SD-OCT Healthy Macula Retinal VasculatureRetinal Vasculature

2 main sources of blood2 main sources of bloodsupply:supply:Choroidal Choroidal BVBV–– Supplies outer retinalSupplies outer retinal

layers, including layers, including PRsPRs

CRACRA–– 4 branches nourish inner4 branches nourish inner

retinaretina–– Run Run radially radially toward foveatoward fovea

The The ChoriodChoriod

Loose connectiveLoose connectivetissuetissueMelanocytesMelanocytesChoriocapillarisChoriocapillaris–– FenestratedFenestrated

endothelium allowsendothelium allowsdiffusion of proteinsdiffusion of proteins

–– S__________S__________regulationregulation

–– High blood flowHigh blood flow–– Very little O-2Very little O-2

extracted, so highextracted, so highvenous O-2venous O-2

BM

CC

Mel.

thicknessRPE

sclera

Anatomic Anomaly #1Anatomic Anomaly #1

Cilioretinal Cilioretinal arteryartery10-30% have it10-30% have it

May spare centralMay spare centralvision in CRAOvision in CRAO

If occluded, centralIf occluded, centralvision lossvision loss

Cilioretinal Cilioretinal Artery in CRAOArtery in CRAO Cilioretinal Cilioretinal ArteryArtery OcclusionOcclusion

8

Cilioretinal Cilioretinal ArteryArtery OcclusionOcclusion Venous System AnatomyVenous System Anatomy

Central Retinal VeinCentral Retinal Vein–– Retinal veins join atRetinal veins join at

disc to form CRVdisc to form CRV–– Drains into superiorDrains into superior

ophthalmic v.ophthalmic v. CRA

CRV

Anatomic Anomaly #2Anatomic Anomaly #2

"Dual Trunk" anomaly"Dual Trunk" anomaly–– Retro-laminarRetro-laminar

bifurcationbifurcation–– 2 central retinal veins2 central retinal veins

CV CV DxDx. can lead to a. can lead to aspecial type of sup orspecial type of sup orinf inf hemispheric RVOhemispheric RVO

CRVO AnatomyCRVO Anatomy

Anatomy of HCRVOAnatomy of HCRVO Fluorescein Angiography HCRVOFluorescein Angiography HCRVO

9

Identifying Signs ofIdentifying Signs ofRetinal DiseaseRetinal Disease

Signs of vascularSigns of vasculardiseasediseaseSigns of degenerativeSigns of degenerativediseasediseaseSigns of other diseaseSigns of other disease–– InfectiousInfectious–– InflammatoryInflammatory–– Retina/Optic N.Retina/Optic N.–– HereditaryHereditary–– NeoplasticNeoplastic–– TraumaTrauma

69 year old Caucasian Female

CC: Reduced central vision OD x 3 weeks @ distance and near

Ocular History: Unremarkable

Systemic History: Unremarkable ; Last PCP exam 15 years ago

Social History: Smokes ½ pack of cigarettes a day Alcohol 5-10 drinks a day

Meds: Multivitamin

Allergies: +Penicillin

VA: s Rx 20/60 OD 20/20 OS

EOM: Smooth / Full

Pupils: PERRLA - APD

CF: Central blur OD Full Periphery OU

SLE: Unremarkable OU

TA : 20 mm Hg OU

Vitreous: PVD OU

BP: 168 / 98 RAS

Describe That Fundus!

Fluorescein Angiography

10

What is your assessment?

Hemispheric Retinal VeinOcclusion

What is your plan?

BRVO

CRVO

1

2

11

•• Central Retinal Vein Occlusion Central Retinal Vein Occlusion •• Hemispheric Retinal Vein Occlusion Hemispheric Retinal Vein Occlusion•• Branch Retinal Vein Occlusion Branch Retinal Vein Occlusion

•• Ischemic Ischemic •• Non-ischemic Non-ischemic

Outcome:

•Diagnosis: Inferior Hemi-Central Retinal Vein Occlusion OD

•Treated as a non-ischemic CRVO (Why?)

•Follow-Up in 1 month

•Patient sent to PCP to rule out Diabetes, Hypertension, Cholesterol

•Hypertension diagnosed

•Treatment: intravitreal injection of Kenalog at 4 months for CME

•Patient had IOP spike after Kenalog injection – given Alphagan P

•No NVD or NVE occurred

•Vision at 1 year was OD 20/25

Hemi-Central Retinal Vein Occlusion

Uncommon type of hemispheric RVO– Occurs in "Dual Trunk" anomaly

Same pathophysiology as CRVO. May affect either the superior or inferior CRV

before they unite into common central retinalvein.

Usually occurs at or near the optic disc.

The Real Deal on CRVOs

T__________ in CRV at lamina CRVO Study

– Prophylactic PRP did not prevent NVI/NVA in ischemic CRVO• Therefore, wait for development of NVI/NVA before PRP

– No real benefit of macular grid laser for ME Follow-up

– Observe monthly for first 4-6 mon– Angiography when heme, retinal edema reduces– Monitor for NVI/NVA PRP– Medical workup

• CV Dx, DM, hyperviscosity, lipids– Non-ischemic CRVO may convert to ischemic (30%)!

Modern Retinal Specialist Retinal Vein Occlusion

Observe for short period for spontaneousimprovement of ME– 2-4 weeks

Eval. For HTN, DM, Chol, TGs, smoking– Use RVO as life modifier

If patient > 50 y/o and w/o above RF– ESR, CRP

If patient < 50 y/o and w/o above RF– Eval. For hyperviscosity

• Antiphospholipid antibody• Factor V Leiden

12

Thrombus vs. Embolus

Thrombus– A hardened clump of blood within a vessel.

Embolus– Sudden blockage of an artery by a blood clot (thrombus) or

a_____________ material. Both are common causes of stroke.

Retina Quiz

In an ischemic CRVO, which is false?

a. it carries high risk of NVI/NVAb. complications may include ME,

ischemic damagec. risk of NVG is 5%d. it carries some risk for NVD, NVE,

leading to vitreous heme

Retina Quiz

In an ischemic CRVO, which is false?

a. it carries high risk of NVI/NVAb. complications may include ME,

ischemic damagec. risk of NVG is 5%d. it carries some risk for NVD, NVE,

leading to vitreous heme

Non-ischemic vs. Ischemic CRVO

Functional Tests

VA Pupil testing Visual fields Electroretinography

Structural Tests

Ophthalmoscopy– SL Fundoscopy– BIO

Fluoresceinangiography

Ischemic CRVO

• Note disc edema, several CWS

• Capillary non-perfusion on FA

• VA < 20/200, +APD, retinal/macular edema

• More likely to result in NVI/NVA than non-is

• 45% of cases result in NVG

Should Ischemic VenousOcclusions be Referred to a

Retinologist Before NVI/NVA?

13

Macular Edemain CRVO

The Real Deal on BRVOs

Caused by a______________of overlying artery BRVO Study

– Observe monthly for first 6 mon• DFE, (OCT)• Gonio

– Chronic findings include ME, collateral BVs– Macular grid laser helpful for ME > 6 mon– Lucentis/Avastin off-label for ME– After initial 6 mon, observe q 3-4 mon for RNV, NVI/A– Scatter laser for RNV, VHeme

Medical workup• CV Dx, DM, hyperviscosity, lipids

Arteriosclerosis with calcification ofvessel wall

Emerging Treatments forEmerging Treatments forBRVO/CRVOBRVO/CRVO

Intravitreal KenalogIntravitreal Kenalog–– Intravitreal injection for MEIntravitreal injection for ME–– The The SStandard Care versus tandard Care versus COCOrticosteroid forrticosteroid for

REREtinal Vein Occlusion (SCORE) Study: tinal Vein Occlusion (SCORE) Study: TwoTwoRandomized TrialsRandomized Trials to Compare the Efficacy and to Compare the Efficacy andSafety of Intravitreal Injections(s) ofSafety of Intravitreal Injections(s) ofTriamcinolone Acetonide with Standard Care toTriamcinolone Acetonide with Standard Care toTreat Treat Macular EdemaMacular Edema

–– One for One for CRVOCRVO and One for and One for BRVOBRVO–– IVK found useful for ME in CRVO, IVK found useful for ME in CRVO, notnot BRVO BRVO

when compared to CRVOS/BRVOS standardwhen compared to CRVOS/BRVOS standard

SCORE84 clinics and sponsored by the National Eye Institute

One group received the standard clinical care for the conditionOne group got 4 milligramOne group got 1 milligram

Results: SCORE (CRVO) – 27%(1milligram) group and 26%(4milligram) groupExperienced a substantial visual gain of 3 or more lines. The results up to 2 years.

The 4 milligram group had the highest rates of cataract formation, cataractSurgery, and elevated pressure. The 1 milligram dose is safer for patients.

SCORE (BRVO) – 29%(laser), 26%(1mg), 27%(4mg) gained 3 or more lines. 3 yr.Laser treatment may have fewer side effects for patients.

14

Emerging Treatments forEmerging Treatments forBRVO/CRVOBRVO/CRVO

Dexamethasone Dexamethasone Drug Delivery SystemDrug Delivery System–– OZURDEX (OZURDEX (intravitreal intravitreal implant) 0.7mgimplant) 0.7mg

((AllerganAllergan))–– Intraocular, biodegradable implant for theIntraocular, biodegradable implant for the

treatment of persistent MEtreatment of persistent ME–– Clinical trial validatedClinical trial validated OzurdexOzurdex

for ME in CRVOfor ME in CRVO

DR: CSME DR: CSME TreamentTreament

Iluvien Iluvien (formerly known as(formerly known asMedidureMedidure))–– Tube 3.5mm x 0.37mmTube 3.5mm x 0.37mm

containing containing fluocinolonefluocinolone–– Implanted into vitreousImplanted into vitreous w/ w/ 25g25g

(~0.5mm) inserter(~0.5mm) inserterSuturelessSutureless

–– Designed to provideDesigned to provide sustained sustainedeffect up to 24 monthseffect up to 24 months

–– FAMEFAME ( (fluocinolone acetonidefluocinolone acetonidein DME)in DME) results favorableresults favorable

Emerging Treatments forEmerging Treatments forBRVO/CRVOBRVO/CRVO

BRAVO and CRUISE studies BRAVO and CRUISE studies –– Lucentis Lucentis clinical trials for RVOclinical trials for RVO

BRAVOBRAVO –– Phase III study (12 month study) 0.3 or 0.5 mg of Phase III study (12 month study) 0.3 or 0.5 mg of LucentisLucentis

Safety and effectiveness of Safety and effectiveness of Lucentis Lucentis in macular edema secondary to BRVOin macular edema secondary to BRVO

CRUISECRUISE –– Phase III study (12 month study) 0.3 or 0.5 mg of Phase III study (12 month study) 0.3 or 0.5 mg of LucentisLucentis

Safety and efficacy of Safety and efficacy of Lucentis Lucentis in macular edema secondary to CRVOin macular edema secondary to CRVO

An analysis of the 6 month data from both studies showed a safety profileAn analysis of the 6 month data from both studies showed a safety profileconsistent with previous consistent with previous Lucentis Lucentis Phase III trials in wet ARMD.Phase III trials in wet ARMD.

As early as seven days after the first injection, patients who received monthlyAs early as seven days after the first injection, patients who received monthlyinjections of injections of Lucentis Lucentis had, on average, a statistically significant improvementhad, on average, a statistically significant improvementin their vision that lasted 6 months.in their vision that lasted 6 months.

Final thoughts on CRVOFinal thoughts on CRVOWhen NV occurs in ischemic CRVO, it most often occursWhen NV occurs in ischemic CRVO, it most often occursin the anterior segment.in the anterior segment.Neovascular Neovascular glaucoma is seen in ~ 45% of eyes withglaucoma is seen in ~ 45% of eyes withischemic CRVO.ischemic CRVO.M______ e_____ may occur in either ischemic or non-M______ e_____ may occur in either ischemic or non-ischemic CRVO, leading to permanent central scotoma.ischemic CRVO, leading to permanent central scotoma.–– Referral for steroid or Anti-VEGFReferral for steroid or Anti-VEGF

Non-ischemic CRVO may convert to ischemic (30%)!Non-ischemic CRVO may convert to ischemic (30%)!2/3 of non-ischemic CRVO will have 20/40 or better w/o2/3 of non-ischemic CRVO will have 20/40 or better w/oocular ocular TxTx..

Questions and Comments?Questions and Comments?

15

Arterial Occlusive Disease

Central Retinal Artery (CRAO)– CRAO with retinal whitening and “cherry-red” spot in the fovea– May be embolic, “ischemic”, thrombotic (GCA), or due to NVG

Retina Quiz

In CRAO of < 24 hrs duration, best initialmanagement is:a. digital ocular massage, STAT retinal

consultb. IV methylprednisonec. po steroidd. observe without treatment; prognosis

excellent for visual recovery

Retina Quiz

In CRAO of < 24 hrs duration, best initialmanagement is:a. digital ocular massage, STAT retinal

consultb. IV methylprednisonec. po steroidd. observe without treatment; prognosis

excellent for visual recovery

The Real Deal on CRAO

CRAO can be embolic or thrombotic– Atherosclerotic changes, inflammatory endarteritis– BP, carotid auscultation

Acute management (< 24 hours)– Ocular Massage: 10 seconds/release Retinal consult **

• AC paracentesis (<24 hr)• IV Acetazolamide• Carbogen (95% O-2, 5% CO-2)

– Medical evaluation to ID and treat underlying cause• Carotid, cardiac studies• ESR if > 55 y/o, no visible emboli• If suspect GCA, hi-dose steroids

Follow-up– Monitor for NVI/NVA PRP

Arterial Occlusive Disease

Branch Retinal Artery (BRAO)– Almost always embolic

Color (left) and red-free (middle) photographs with retinal whitening.Fluorescein angiography (right) with delay in A-V transit time alonginferior arcade.

Branch Retinal Artery Occlusion

• Monitor for NV

• Carotid Studies

• Echocardiogram

• “Baby Aspirin”

• Lower the Cholesterol

16

81 year old Caucasian female

CC: Decreased vision OU but OS getting much worse

Ocular History: + “Dry”AMD OU x 15 years, +Cataracts OU

Medical History: + Hypertension x 27 years (controlled with meds)

Allergies: +Sulfa drugs Meds: Ocuvite

VA: 20/100 OD 10/400 FB OS

EOMS: smooth/full TA: 12 mm Hg OU

Pupils: PERRLA – APD BP: 135/90 RAS

CF: Full periphery OU Central scotoma OU, confirmed w/Amsler

SLE: Unremarkable Vitreous: PVD OU

Describe That Fundus!Describe That Fundus!

17

Fluorescein AngiographyFluorescein AngiographyOutcome:

• Diagnosis:• Geographic Atrophy (End-stage Dry AMD) OD• Choroidal Neovascularization (Wet AMD) OS

• FA ordered

• Avastin injections OS

• Subsequent PDT (“double therapy”)

• 20/200 VA (OD) 20/200 (OS) at 1 year

• Low Vision Referral

• D/C Ocuvite; switch to BS MV w/L & Z

Soft DrusenSoft Drusen

Soft, confluent more inclined to lead toSoft, confluent more inclined to lead to_______________ AMD *_______________ AMD *

soft drusen

Stages of AMD

EarlyAMD

Intermed.AMD

AdvancedAMD

“wet”

“dry”

Retina QuizRetina Quiz

The clinical feature of Wet AMD thatThe clinical feature of Wet AMD thatdistinguishes it from Dry is:distinguishes it from Dry is:a.a. Geographic atrophy of the RPEGeographic atrophy of the RPEb.b. soft, confluent soft, confluent drusendrusenc.c. vision 20/60 or worsevision 20/60 or worsed.d. Choroidal neovascular Choroidal neovascular membranemembrane

(CNVM) formation(CNVM) formation

Retina QuizRetina Quiz

The clinical feature of Wet AMD thatThe clinical feature of Wet AMD thatdistinguishes it from Dry is:distinguishes it from Dry is:a.a. Geographic atrophy of the RPEGeographic atrophy of the RPEb.b. soft, confluent soft, confluent drusendrusenc.c. vision 20/60 or worsevision 20/60 or worsed.d. Choroidal neovascular Choroidal neovascular membranemembrane

formationformation

18

AMD Risk FactorsAMD Risk FactorsAgeAge

Gender - Gender - F > MF > M

SmokingSmoking

Iris Color - Iris Color - lighter irislighter iris

ObesityObesity

CV DiseaseCV Disease

AMD Family HistoryAMD Family History

Poor nutritionPoor nutrition

Low Macular PigmentLow Macular Pigment

Dietary and Serum Levels -Dietary and Serum Levels -Complex analyses (most, butComplex analyses (most, butnot all) show a relationship.not all) show a relationship.

MPOD-MPOD- Most (but not all)Most (but not all)studies have shown reducedstudies have shown reducedMPOD in AMD (by multipleMPOD in AMD (by multiplemeasurement techniques).measurement techniques).

Nutritional Factors

AREDSAREDS 2

AREDS 1 and 2Formulations

Vitamin C: 500 mg* Vitamin E: 400 IU* Beta-carotene: 15 mg (May be listed on the label as

“25,000 IU vitamin A as beta-carotene”) (eliminated) Why?

Zinc oxide: 80 mg (40 mg) Copper: 2 mg (needed to prevent Cu deficiency caused by

high dosage of zinc)* Lutein & Zeaxanthin (10 mg & 2 mg) Omega-3 fatty acids (1 gram)

Retina Quiz The AREDS 1 study found that in subjects with

intermediate AMD, or advanced AMD in one eye(but not the other):a. Zinc alone lowered risk of advanced AMD by about 25

percent.b. Lutein alone lowered risk of advanced AMD by about 25

percent.c. Antioxidants increased risk of advanced AMD by about 25

percentd. Antioxidants + zinc lowered risk of advanced AMD by

about 25 percent.

19

Retina Quiz The AREDS 1 study found that in subjects with

intermediate AMD, or advanced AMD in one eye(but not the other):a. Zinc alone lowered risk of advanced AMD by about 25

percent.b. Lutein alone lowered risk of advanced AMD by about 25

percent.c. Antioxidants increased risk of advanced AMD by about 25

percentd. Antioxidants + zinc lowered risk of advanced AMD by

about 25 percent.

AREDS Grading Scale

1. No drusen or a few small drusen.2. Pigment abnormalities or non-extensive small

or intermediate drusen.3. Extensive intermediate drusen or any large

drusen or non-central atrophy.4. Good acuity and no advanced AMD in the

study eye. Advanced AMD in the fellow eye(choroidal neovacularization or geographicatrophy).

Intermediate Stage AMD

•• AREDS Category 3 AREDS Category 3• Extensive intermediatedrusen (63-124µ indiameter)

• At least one large druse(>125µ in diameter)

• Geographic atrophy notinvolving the foveal center

Is There a Strategy ?Is There a Strategy ?USDA Food TriangleUSDA Food Triangle5+ daily portions of fruits5+ daily portions of fruits& veggies& veggies–– at least 1 dark green, leafyat least 1 dark green, leafy

veg (spinach, kale)veg (spinach, kale)Low fat, low cholesterolLow fat, low cholesterolAntioxidant forAntioxidant for““nutritionally-challenged nutritionally-challenged ““Address CardiovascularAddress CardiovascularDisease, exerciseDisease, exerciseAvoid smoking, UVAvoid smoking, UV

20

Available technologies for earlyAvailable technologies for earlydetection and monitoring of AMDdetection and monitoring of AMD

Non-invasive MethodsNon-invasive MethodsMacular Pigment Optical DensityMacular Pigment Optical Density–– MPODMPOD

Preferential Preferential Hyperacuity Hyperacuity PerimetryPerimetry–– PHPPHP

Optical Coherence Tomography Optical Coherence Tomography–– OCTOCT

Management of Dry AMDManagement of Dry AMD

Repeat Exams q3-4 Repeat Exams q3-4 monmonUV/blue WL Protection, Home AmslerUV/blue WL Protection, Home AmslerAntioxidants/Nutrition/Diet/SmokingAntioxidants/Nutrition/Diet/Smoking–– Contrast Sensitivity FunctionContrast Sensitivity Function–– AmslerAmsler–– Photostress Photostress RecoveryRecovery–– DFE, PhotosDFE, Photos–– MPODMPOD–– OCTOCT–– Hyperacuity PerimetryHyperacuity Perimetry(PHP)(PHP)

LV consultLV consult

Retina QuizRetina Quiz

Approximately what percentage of dryApproximately what percentage of dry((non-exudativenon-exudative) AMD eyes progress to wet) AMD eyes progress to wet((exudativeexudative) AMD?) AMD?

a. 37 %a. 37 %b. 50 %b. 50 %c. 2 %c. 2 %d.d. 15-20 %15-20 %

Clinical Features of Clinical Features of ExudativeExudative(Wet) AMD(Wet) AMD

______________________*______________________*________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

Available technologies for earlyAvailable technologies for earlydetection and monitoring of AMDdetection and monitoring of AMD

Non-invasive MethodsNon-invasive MethodsMacular Pigment Optical DensityMacular Pigment Optical Density–– MPODMPOD

Preferential Preferential Hyperacuity Hyperacuity PerimetryPerimetry–– PHPPHP

Optical Coherence Tomography Optical Coherence Tomography–– OCTOCT

21

Optical Coherence Tomography

Subfoveal Subfoveal CNVM w/ret thick, serous RDCNVM w/ret thick, serous RD

TD-OCTTD-OCT

CysticCysticchange inchange inWet AMDWet AMD

SD-OCTSD-OCT

Wet AMDWet AMD

Management of Exudative AMDManagement of Exudative AMDUV/blue WL protectionUV/blue WL protectionHome AmslerHome AmslerAntioxidants/Nutrition/Diet/Antioxidants/Nutrition/Diet/Smoking/ExerciseSmoking/ExerciseFA - Stat ! (ICG - as indicated) *FA - Stat ! (ICG - as indicated) *Retinal Consult and TreatmentRetinal Consult and Treatment–– Laser PhotocoagulationLaser Photocoagulation–– Photodynamic TherapyPhotodynamic Therapy–– Anti-angiogenic Anti-angiogenic TherapyTherapy–– Surgical or Other MedicalSurgical or Other Medical

InterventionInterventionLow Vision ConsultLow Vision Consult

Antiangiogenic Antiangiogenic Drugs: VEGFDrugs: VEGFInhibitorsInhibitors

VEGF binds to receptorVEGF binds to receptor

22

Targeting Vascular EndothelialGrowth Factor (VEGF)

• Macugen

• Lucentis

• Avastin

Lucentis

• Lucentis ™ (ranibizumab) .5 mg injection monthly treatment x 4 mon

• Genentech• Antibody-based• VEGF-A inhibition• (low) risk of thromboembolism• Requires re-treatments• $2,000.00

Lucentis

• Lucentis approved for treatment ofneovascular AMD in June 2006

• MARINA – 12 mon results, Min. classic 95% of patients treated maintained vision 40% of patients treated improved their vision

by at least 3 lines (or 15 letters) on the studyeye chart

• ANCHOR: Predom. Classic• Similar results to MARINA

Treatments for Wet AMD VEGF Inhibitors

• Bevacizumab- Avastin (Genentech) $40.00 Intravitreal injection “off-label” for Wet AMD 1 injection/mon x 3 mon Is being compared w/Lucentis in CATT

23

VA 55 L

VA 78 L

Pre and Post Avastin Treatment Antiangiogenesis

• Corticosteriods Kenalog

• Intravitreal triamcinolone combined withPDT showed mean VA improvement(Spaide 2004).

• Anti-VEGF agents

• Steroids

• PDT

Triple TherapyWhich therapy(ies) is/are“off-label” for Wet AMD?

a. Argon Laser Photocoagulationb. Visudyne Photodynamic Therapyc. Intravitreal Ranibizumab (Lucentis)d. Intravitreal Bevacizumab (Avastin)e. Intravitreal Triamcinolone (Kenalog)

24

VEGF Inhibitor not yetapproved

• VEGF-Trap (Regeneron) Intravitreal injection completed Phase II

• No adverse effects

Now entering Phase III Binds tightly to VEGF receptors Rapid decrease in foveal thickening,

improved VA Also in trials for DME

Conclusions

We have an importantrole in the diagnosis and(co-)management ofposterior segmentvascular, degenerative,and other diseases.

Don’t miss the telltalesymptoms and signs.

Used evidence-basedmanagement.

Questions?

????

Thank youFor spending your precious time with us!

Carlo J. Pelino

Cpelino@salus.edu

Joseph J. Pizzimenti, OD

pizzimen@nova.edu