Presentation on theme: "How to Keep Your Sight For Life"— Presentation transcript:
1How to Keep Your Sight For Life The Aging Eye:How to Keep Your Sight For LifeNicholas J. Volpe, MDTarry Professor and ChairmanDepartment of OphthalmologyFeinberg School of MedicineNorthwestern University
2Strategies to Preserve Your Vision Prevention is our most potent tool in the quest to reduce disease (and healthcare costs)Choose your parents well and stop aging!!! ORDon’t SmokeWear Glasses that are UV protectiveSafety glasses for high risk activitiesPay Attention to Nutrition and VitaminsDon’t Ignore SymptomsGet Regular Eye Examinations
3Major Causes of Chronic Visual Loss Preventable and Treatable CataractsGlaucomaMacular degenerationDiabetic retinopathyOther IssuesDry eyePresbyopia near vision blurring
4Protective Eye Ware Avoid fireworks! Always if you have poor vision in one eyeHigh risk activitiesRacquet sportsSawingDrillingWorking overheadAny high speed toolfirearms
5Stop Smoking Clearly a risk factor for cataracts 3X the risk Clearly a risk factor for macular degeneration and its response to treatment
6Nutrition Healthy tear film Macular degeneration Fruits and Green Leafy VegetablesCarotenoid pigments (lutein) accumulate in macula and prevent light damageOmega fatty acidsLutein and ZeaxanthinStudied in AREDS 2Vitamins A,C, E
7Regular Check Ups Many diseases can be detected Every 2-3 years from age 40-65Every 1-2 years after age 65More frequently with diabetes or family history of glaucoma or macula degenerationYoung adults, in the absence of symptoms, do not require routine examinations
8Cataracts Symptoms Age Steroids (PSC) Trauma Inflammation Diabetes Expected if ≥ 60 years old50% years old70% > 75 years oldMost common cause of decreased visionSymptomsLoss of acuityDifficulty with colorsGlare at nightTrouble reading small printAgeSteroids (PSC)TraumaInflammationDiabetesOther drugs
10Nuclear cataract Progression Exaggeration of normal nuclear ageing changeIncreasing nuclear opacificationCauses increasing myopiaInitially yellow then brown
11Classification according to maturity ImmatureMatureHypermatureMorgagnian
12Drugs Systemic or topical steroids Chlorpromazine Other drugs - initially posterior subcapsular- central, anterior capsular granulesOther drugsLong-acting mioticsAmiodaroneBusulphan
13Cataract Surgery Outpatient Very successful > 95% Almost all with intraocular lensesMost common surgical procedure in U.S.>1.4 million/yearMost successful surgical interventionComplicationsuncommonsight threateningIOL technology continues to evolve for astigmatic correction and presbyopiaNewest modality is femtosecond laser
14Cataract Prevention Smoking cessation Reduces Vitamin C in the eye Vitamin C levels are high in the eye and this helps remove prooxidantsFruits and vegetables5 fold decrease at 3-4 servings per dayRegular alcohol consumption increases risk of cataractSteroids and inflammatory conditions are risks for cataractsObesity and radiation
15Ultraviolet Light Cataracts and Macular Degeneration Cataracts much more prevalent in equatorial climateAMD more common in light eyesSame rules as sun tan lotionsif you might tan or burn you should be wearing sunglasses10-30% transmission of lightWide brimmed hatAlso water, sand and snowPolarized not necessary but will cut glareDon’t assume expensive is UVA and B protectiveTest lens quality and fit to ensure successful use
16Age- Related Macular Degeneration Age-related macular degeneration (AMD) is the most common cause of severe, irreversible vision loss in older Americans and Europeans. (AMD Alliance International 2008; Ferris et al. 1984; National Society to Prevent Blindness 1980).Worldwide, AMD disease affects million people.Etiology is complex and poorly understoodFree-radical mediated damage to the photoreceptors and the RPE may disrupt the transport of metabolites from photoreceptors to choroidal capilariesAngiogenesis is a feature of neovascular AMDAMD may be associated with a systemic vascular disorderGenetic and environmental factorsVariation in the complement factor H gene
17Free radicals and antioxidants in CNV lightfree radical productiondamage blocked by antioxidantsPrevention of CNV is an especially desirable goal. No effective strategies have yet been identified, but several ideas focus on avoiding or lessening the impact of postulated risk factors.Free radicals, which are known to damage photoreceptors and the RPE, may have a role in CNV. Because antioxidants such as vitamins A, C, and E scavenge free radicals, vitamin supplements have been investigated for preventing AMD. Animal studies show that vitamin A, C, and E deficiencies can lead to damaged RPE or retina, but clinical studies have yet to show conclusive benefits of supplements.The high concentration of antioxidants found in wine may play a role in the link between moderate wine consumption and a decreased risk of developing AMD. Few studies have been conducted in this area, however, and further investigation is needed to confirm these initial findings.A growing body of evidence suggests that smokers have an increased risk of developing AMD. Epidemiologic data collected from thousands of patients worldwide show that cigarette smokers, especially current smokers, have a higher risk of developing AMD than non-smokers. Research on levels of macular pigment density supports the view that smoking may be causally linked to AMD: pigmentation in the fovea, which may protect the macula from damage, is depleted in smokers compared with non-smokers.photoreceptors and RPE damage
18AMD Risk Factors Gender ♀ > ♂ Race/Ethnicity Smoking Family History Symptomsearly = None, mild distortionlate = acute loss of visionGender ♀ > ♂Race/EthnicitySmokingFamily HistoryAtherosclerosisHypertension
19Atrophic AMD Progression Initially drusen and non-specific RPE changes Late RPE (geographic) atrophy
20Atrophic AMD Fluorescein angiogram Management Hyperfluorescence from RPE window defectLow-vision aids if appropriate
21Pathophysiology: Penetration of Bruch’s Membrane Breaks in Bruch’s membrane provide sites through which CNV may grow and proliferate. This process often causes rapid, widespread and progressive damage to photoreceptors. It is accompanied by a build-up of fibrous tissue.The RPE can detach from the outer aspect of Bruch’s membrane with or without ingrowth of fibrovascular tissue. These processes can damage the RPE and photoreceptors, leading to significant loss of vision. Damaged RPE may produce angiogenic growth factors, which stimulate growth of new blood vessels from the choroid.schematicfundus photographNew blood vessels penetrateBruch’s membrane
22Choroidal Neovascularization (CNV) Less common than atrophic AMD but more seriousMetamorphopsia is initial symptomMany lesions are not visible clinicallySuspicious clinical signsSubretinal blood or lipidGray-yellow subretinal lesion with fluid
23Current Status of Therapies for CNV Antiangiogenic therapyLucentis, Avastin, MacugenCATT trial (Avastin vs Lucentis)Photodynamic therapy with verteporfinSteroidsThermal LaserChoroidal neovascularization (CNV) has proved difficult to treat. Laser photocoagulation reduces vision loss in some forms of CNV in the long term, but the technique has many limitations. It is suitable for only a minority of patients, and around half of all treated eyes have persistent or recurrent CNV within 2 years.Most other approaches to treatment of CNV – such as radiation, antiangiogenic drugs including steroids , transpupillary thermotherapy  and surgery  – are under investigation. Progress in patient selection and development of new drugs and operating techniques may bring about benefits in other therapies in the future. At present, however, only photodynamic therapy (PDT) with verteporfin has been proven effective for treatment of CNV in clinical trials,  and may be suitable for a larger proportion of patients than laser photocoagulation.
26Treatment for Dry AMD-Age-related Eye Disease Study (AREDS) –role of antioxidantsvitamin E, 400 IUvitamin C, 500 mgbeta carotene, 15 mg (approximately 25,000 IU Vitamin A)zinc 80 mg as zinc oxidecopper, 2 mg, as cupric oxideCopper should be taken with zinc, because high-dose zinc is associated with copper deficiency.(Category 3: extensive intermediate size drusen, or at least 1 large druse (> 125 ?m), or noncentral geographic atrophy in 1 or both eyes)(Category 4: advanced or neovascular AMD in 1 eye or vision loss due to AMD in 1 eye) should consider taking high-dose anti-oxidants plus zinc on a daily basis.
27Established Age Related Macular Degeneration Use Amsler Grid to monitor central visionAREDS-Occuvite PreservisionB carotene vs. Lutein and Zeaxanthin (AREDS 2)Vitamin CVitamin EZinc Oxide (?necessary and ? Stomach upset)CopperNB: No beta carotene for smokers and others at risk for lung cancerOthers??? Lutein Eyes, PhoVision, Perspective, Ocu-force
28AREDS Results Recommendations Evaluation:Persons over 55 years old receive a dilated eye exam to assess risk of advanced AMD.Contraindications to Treatment:Smokers and ex-smokers should not use beta carotene, because previous studies have suggested an association with lung cancer and beta carotene in smokers.There were no benefits from treatment shown in the AREDS for patients with no AMD (Category 1) and early AMD (Category 2).
29AREDS 2 Adding omega 3’s did not help Taking away B Carotene did not hurt and lutein and zexanthine may have been a bit more protectiveReducing zinc dose did not hurt and less side effectsNo prevention of cataracts
30Diabetic Retinopathy most common cause of new blindness among adults yoBlindness in working adultsaffects over 5.3 million Americans age >18 (2.5% of this population)Prevention- worse in HTN, obesity, renal failure, hyperlipidema, smoking, anemia, pregnancy and POOR glycemic controlDiabetic retinopathy develops, to some degree, in nearly all patients with diabetes, and is the most common cause of new cases of blindness among adults. The most predominant causes of vision loss are clinically significant macular edema (CSME) and proliferative diabetic retinopathy (PDR). Vision loss can be avoided or minimized with proper ophthalmic care and examination to identify retinopathy in its early stages.
31Clinical Findings in NPDR MicroaneurysmsEarliest clinical sign of diabetic retinopathyAppear as small red dots in the superficial retinal layersRupture produces blot/flame hemorrhages
32Macular Edema (CSME)Leading cause of visual impairment in patients with diabetes
34Macular Edema Treatments ETDRSfocal laser surgery for CSME reduces the incidence of moderate visual loss (doubling of visual angle or roughly a 2-line visual loss) from 30% to 15% over a 3-year periodSteroids-peri-ocular-intraocularAnti-VEGF agentsFavorable prognostic factorsCircinate exudates of recent onsetWell-defined leakageGood perifoveal perfusionUnfavorable prognostic factorsDiffuse edema/multiple leaksLipid deposition in the foveaMacular ischemiaCystoid macular edemaPreoperative vision of less than 20/200HypertensionIf specific microaneurysms leak- they are treated directly with focal laser photocoagulation.Diffuse leakage - grid pattern of laserMedium intensity burns ( µm) are placed at least 1 burn size apartIntravitreal or sub-tenons steroid injections- when edema persists after multiple focal laser treatments.CSME should be treated and observed closely (every 2-3 mo)
35Ischemic diabetic maculopathy Macula appears relatively normalCapillary non-perfusion on FAPoor visual acuityTreatment not appropriate
36PDR Proliferation of new blood vessels due to ischemia NVD Disc NVE ElsewhereNVI IrisNVA AngleWhen proliferation of new blood vessels occurs, the patient is diagnosed as having PDR. New blood vessel formation is caused by retinal ischemia. Neovascularization can occur at the optic disk (NVD) or elsewhere in the retina (NVE). These new vessels are weak and, when they break, can cause vitreous hemorrhage. They can also cause retinal traction, retinal tears, and retinal detachment over time.
37PDR - cont. Treatment Options Pan-retinal photocoagulation Peripheral Retinal CryotherapyVitrectomyAnti-VEGFDRS proved that xenon and argon laser decreases to chances of visual loss in eye with high risk characteristics (HRC)High risk characteristics (HRC) was defined as:NVD > ½ the disc areaAny NVD and VHNVE > ½ the disc area and VH or pre-retinal hemorrhagePeripheral Retinal CryotherapyEmployed when HRC is present but the media are too hazy for laserMajor complication is increased risk of traction RD, seen in 25-38%VitrectomyMajor indications: non-clearing vitreous hemorrhage, macular involving or threatening TRD, or combined traction-rhegmatogenous RDOther indications: ME with a thickened and taut posterior hyaloid, macular heterotopia, ERM, severe pre-retinal hemorrhage, and NVG with cloudy media
38Retinopathy Screening Type 1 diabetes - screen within 3-5 years of diagnosis after age 101Type 2 diabetes - screen at time of diagnosis1Pregnancy - women with preexisting diabetes should be screened prior to conception and during first trimester1Follow-up depends on severity of diseaseA comprehensive eye exam should be given to all patients with diabetes. The exam should include all of the components recommended by the American Academy of Ophthalmology and the American Optometric Association for non-diabetic patients, however additional attention should be given to assess abnormalities of the retina and vitreous fluid. Dilated indirect ophthalmoscopy, slitlamp biomicroscopy, and fundus examination should be used to identify retinal or vitreous hemorrhages, microaneurysms, retinal tears or detachment, intraretinal microvascular abnormality (IRMA), neovascularization at the optic disk (NVD) and elsewhere in the retina (NVE).Patients with type 1 diabetes should be screened for NPDR (non-proliferative diabetic retinopathy) within three to five years of diagnosis after age 10. Retinopathy leading to vision loss rarely develops in children prior to puberty, regardless of how long the child has had diabetes. Patients with type 2 diabetes should be screened at time of diagnosis.Finally, women with preexisting diabetes should be screened prior to conception and during the first trimester. Follow-up exams should be scheduled at the physicians discretion based on the results of the first trimester exam.Note that follow-up exams should be conducted yearly, however new ADA Clinical Practice Recommendations state that less frequent exams every 2-3 years can be considered in the setting of a normal eye exam upon the advice of an eye care professional.
39Diabetic Eye CareLike glaucoma, you will NOT HAVE SYMPTOMS UNTIL IT IS TOO LATE!95-100% treatable with early detectionRegular eye exams at 6 or 12 month interval depending on what MD seesBleeding, swelling and growth of blood vesselsDiabetes control (Hemoglobin A1c) is the most important way to reduce your riskHigh blood pressure is a riskDiet and exercise
40Glaucoma Optic nerve 1.2 million nerve fibers Ganglion cells in retina exit to brain as optic nerve
41Definition of Glaucoma A group of optic neuropathies in which retinal ganglion cells die by apoptosis with resultant optic disc cupping and characteristic visual field deficitsOptic neuropathyRetinal ganglion cell apoptosisOptic disc cupping or excavationLoss of visual function-IOP is too high for the nerve???Most common cause blindness:African-AmericansCOMPLETE/TOTAL BLINDNESS
44Glaucoma Loss of visual field Site of visual field loss corresponds to area of damage on optic disc,e.g., “cupping”
45Classification of the Glaucomas RISK FACTORSIOP 21 mm HgFamily historyRisk is increased by x2 if parent has POAGRisk is increased x4 if sibling has POAGAfrican AmericanC:D ratio > 0.5Asymmetric cuppingMyopiaDiabetesAge > 75 yearsOpen-angle glaucomas (90%)Angle-closure glaucomas (10%)Primary glaucomasSecondary glaucomas
46Angle Closure Glaucoma Acute pain, redness, tearingAssociated with dilation of pupilNatural (e.g., movie theater)PharmacologicNausea & vomitingoften in ER with “acute abdomen”Risk factor of narrow angle can be detected on screening exam (esp hyperope) and prophylactic iridotomy is preventative of attack in 100%
47Acute angle-closure glaucoma SignsCiliary injectionComplete angle closureSevere corneal edemaDilated, unreactive,vertically oval pupilShallow anteriorchamberMedical rx to lower IOP, followed by laser (Yag) iridotomy
48Primary Open-Angle Glaucoma The most prevalent type of glaucoma in the United StatesElevated intraocular pressure is not part of the diagnostic criteria25% of patients with primary open-angle glaucoma in the US have normal intraocular pressureAsymptomaticSome loss of visual fieldMost common typeFamilial, bilateral“Sneak thief of sight”
49Primary Open-Angle Glaucoma Evidence that IOP reduction is beneficialCollaborative Normal-Tension Glaucoma Study (CNTGS)Advanced Glaucoma Intervention Study (AGIS)Early Manifest Glaucoma Study (EMGT)25% IOP reduction RoP 62% to 45% at a median of 6 years.Ocular Hypertension Treatment Study (OHTS)
50Treatment for POAG Lower the IOP Medical therapy Prostaglandin , B-blockers,Sypathomimetics, Carbonic-anyhrase inhibitorsLaser surgery (ALT, SLT)Incisional surgery (Trab, shunt)
51Most glaucoma specialists use an anti-fibrosis agent for every case in the year 2003 Limit episcleral fibrocellular proliferationMitomycin C (MMC) anti-tumor antibiotic 0.2 to 0.5 mg/mL for 1 to 5 minutes5-Fluorouracil (5-FU) antimetabolite 50 mg/mL for 5 minutesIncisional Surgey
53Eye Strain Myth?? Often dry eye Maybe the muscles around the eye Worse with misalignment issuesCant do any harmTake breaks often and focus at distanceA few extra blinksLubricate before long drives, plane trips, windy or smoke filled environmentsCareful not to dismiss Headaches as “eye strain”Seek care if not responsive to behavioral strategies
54Summary Diabetic Retinopathy Cataract Glaucoma ARMD Prevention, treatmentCataractSurgical treatment continues to improveGlaucomaSilent blindness, family historyMedical and surgical rxARMDNew age of available prevention strategies and treatments exudative variety
55Strategies to Preserve Your Vision Prevention is our most potent tool in the quest to reduce disease (and healthcare costs)Choose your parents well and stop aging!!! ORDon’t SmokeWear Glasses that are UV protectiveSafety glasses for high risk activitiesPay Attention to Nutrition and VitaminsDon’t Ignore SymptomsGet Regular Eye Examinations