5Topics Anatomy Refresher Most Common Eye Problems The Big 3 Glaucoma, Macular Degeneration and Diabetes
6Where to Start?Recent study done at Georgetown University revealed that about 2/3 of internal medicine residents admit to not being comfortable with their ophthalmologic examination.Also showed that when given a fundus photo 60% could not properly identify the optic nerve
7The Healthy EyeLight rays enter the eye through the cornea, pupil and lens. These structures all work to focus light on the retina.Cornea – clear watch glass in the front of the eye responsible for 2/3 of focusing power of the eyeLens – responsible for the other 1/3 of the focusing powerIris – works to filter excess lightPupil – empty space in the middle of the iris which allows light transmission
8The Healthy EyeThe retina is a transparent multilayered structure that converts light rays into electrical impulses. This electrical signal is then sent through the optic nerve and eventually to the brain.The brain then analyzes the information and produces what we perceive as our sight.
9The Healthy Eye The retina consists of two main areas, the macula and peripheral retina.MaculaSmall area in center of retina that is located between the retinal arcades.It allows you to see fine details clearly.At its center is the fovea, which allows activities like reading small print and recognizing a face.
10The Healthy Eye Peripheral retina Everything that doesn’t fall into the maculaGives you your peripheral visionImportant for night visionBetter at detecting motion than the maculaNormal retina
12Macula and Foveal Importance Without the fovea the Best Visual potential is 20/200The big E, qualifies as legally blind
13What does 20/200 mean?20/20020/15This patient can see at twenty feet what a normal vision person can see at 15.Distance at which THIS patient would need to be from an object to be able to see itDistance at which a patient with NORMAL VISION would need to be from an object to be able to see it
14Legal BlindnessDefined as best corrected visual acuity of 20/200 or less in the better eye; or a visual field limitation such that the widest diameter of the visual field, in the better eye, subtends an angle no greater than 20 degrees.
18What about in the US?The number one cause of blindness in the US and most developed nations is Macular DegenerationThe most common cause of blindness of people under age 65 in the US is Diabetic RetinopathyThe most common blinding diseases in the United States areMacular Degeneration, Glaucoma, Diabetic Retinopathy
19The Big Three (Glaucoma, DM, AMD) None of these big 3 have early symptomsScreening is key to preventing vision lossBy the time patients have perceived loss the disease is advanced.
21DiabetesFor Americans under the age of 65 Diabetes is the number one cause of blindness
22Epidemiology As duration of DM increases so does the prevalence of DR At 20 years 99% Type I and 60% of Type II have some diabetic retinopathy, with 3.6% of Type I and 1.6% of Type II being legally blindNational Health and Nutrition Examination Survey IIIRates of DR in diabetics over age forty is higher in AA (27%) & Mexican Americans (33%), than Caucasians (18%)
23Diabetic RetinopathyHyperglycemia leads to damaged and incompetent capillariesThese capillaries canLeak (causing edema, hemorrhages, exudate)Shut down (ischemia, non-perfusion and neovascularization)
24Findings in Diabetic Retinopathy Micro aneurysmsOut pouching of diseased capillary endothelial cellsIntra retinal hemorrhagesDot blot and flameLeakage through diseased capillary endothelial cellsHard exudatesLipid exudates from leakage out of diseased capillary endothelial cellsOften associated with retinal edema
27Findings in Diabetic Retinopathy Cotton Wool SpotRepresents a local infarction of nerve fiber layerWhite areas with fluffy marginsHave no predictive value in diabetic retinopathyVenous beadingTortuous veins and enlargementUsed to determine severity of retinopathy and likely-hood of progressing to severe vision loss
31Retinal EdemaCan occur anywhere in the retina but not clinically significant unless in the macula and meets certain criteriaOccurs from leaky capillaries and is induced by vasoproliferative factorsTreatment: Injections or lasers
33NeovascularizationAn attempt by the retina to reperfuse ischemic tissueOften a cause of vitreous hemorrhageCan lead to Tractional Retinal Detachments or Neovascular GlaucomaTreatment: PRPKills ischemic tissue
38Initial Screening and Follow up Type I rarely have DR within the first 5 years of diagnosis however a number of Type II patients have retinopathy at the time of diagnosisType IInitial exam should be with in the first 5 years of diagnosis then annually after 5 yearsType IIInitial visit at the time of diagnosisFollow up varies depending on degree of retinopathyVaries between annually down to monthlyPregnant DiabeticsSeen during the 1st trimester and follow up as directed
39Best Treatment of All Diabetic Retinopathy PreventionDiabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) showed that intensive glycemic control decreased rate of onset and progression of Diabetic RetinopathyUKPDS also showed that strict blood pressure control in conjunction with intensive glycemic control slows the progression of DR and vision loss
41Glaucoma Anatomy Refresher Two main fluid compartments of the eyeAqueous humorVitreous humor
42Glaucoma Anatomy Refresher Aqueous Humor is made by the ciliary body and travels through the pupil and drains our of our trabecular meshwork and into Schlems canalAqueous is made at a rate that can completely turn over all the aqueous in about 90 minutes.
43Glaucoma 2nd leading cause of blindness in the world Late detection is a major risk factor for blindnessTends to be inheritedNumber one risk factor for Glaucoma is AGE
44GlaucomaNow defined as an “Optic Neuropathy” which is often associated with increased intraocular pressure (IOP)Increased IOP doesn’t mean glaucoma!!!!Can have high IOP and never have glaucomaOcular hypertensionCan have normal IOP and have glaucomaNormal Tension Glaucoma
45Glaucoma Types Chronic problem Blindness typically over many years Open AngleAngle ClosureChronic problemBlindness typically over many yearsPainless and often symptomlessVERY COMMONAcute problemBlindness can occur in hoursRed painful eye, photophobia and fixed dilated pupilVERY UNCOMMON
46Open Angle Glaucoma Findings Normal visionNormal or near normal visual fields+/- increased IOPGlaucomatous cupping of the optic disc
48What Causes the Increase in IOP? Open AngleAngle ClosureDecreased drainage through the trabecular meshwork.Exact reason is unknown.Pupillary blockGiven the right circumstances the iris can limit the flow of aqueous through the pupilThis causes the iris to bow forward, and narrow or completely occlude the drainage angle
49Treatment Medications: Either increase outflow or decrease production Open AngleAngle ClosureMedications: Either increase outflow or decrease productionLaser: Thought to cause inflammatory response which “cleans” out the drainSurgery: Create a fistulous passage for aqueousMedications:Used to help lower IOP in an the acute attack.Pilocarpine may help prevent closure from startingLaser: Create a new passage for fluidSurgery: Cataract removal will provide more space between iris and lens
50Treatment Early identification is key If treated early most open angle glaucoma will never lead to significant visual dysfunctionIf at risk patients are identified by screening angle closure can be prevented
51Age-Related Macular Degeneration Insert name/Practice name/Logo here if desiredAge-Related Macular Degeneration
52AMD Facts #1 cause of blindness in the US Affects more than 30 Million people world wideInherited (multiple genes most as AD)Twice as common as Alzheimer's in people over 60Responsible for 50% of all blindness in developed nations
53AMD FactsIn 2010 the world wide direct health care expenditure because of AMD was 255 billion dollars.Smokers are 2-3x’s more likely to have AMDObesity and Hypertension are also risk factors for AMD
55Macular DegenerationA disease primarily of the Retinal Pigmented Epithelium.The retina is secondarily injured
56Retinal Pigmented Epithelium (RPE) Primary function is to serve as a support cell to the metabolically active photoreceptorsHelps supply nutrients to the photoreceptorsHelps remove wastePhagocytize old outer segments of the photoreceptorsVitamin A cycleOther functionsAbsorb scatteredlight and heat
57Bruch’s MembraneThe anatomical barrier between the highly vascular Choroid and the RPE and RetinaThe Choroid has more blood vessels per square mm than any where else in the body
58What is age-related macular degeneration (AMD)? Over time the RPE has difficulty keeping up with the high metabolic demand of the photoreceptors.Waste materials from the retina accumulate between the RPE and the underlying Bruchs’ Membrane.These are clinically seen as drusenThese drusen lead to inflammationThe drusen and inflammatory mediators are toxic to both the overlying RPE and the underlying Bruch’s membrane.
62Dry AMD The most common form of AMD Wet AMD arises out of Dry AMD so everyone with Wet AMD also has Dry AMDVision loss is slowOver many years
63Dry AMD Drusen formation and RPE changes are the first signs of AMD. Asymptomatic to the patientAs the process continues the waste products slowly cause death of photo receptorsThis is irreversible.Small central scotomaMetamorphopsia
64Dry AMDEventually enough RPE is damaged that patient ends up with geographic atrophy
65Wet AMD Arises out of Dry AMD Vision loss may be rapid and severe. 10-15% of people with Dry AMD will go on to develop Wet AMDVision loss may be rapid and severe.Causes about 80% of blindness because of AMD
66With wet AMD, abnormal blood vessels are present under the retina If Bruch’s membrane gets damaged enough it can form small breaksThese breaks act as an entryway for new blood vessel growth under the retina from the vascular choroid.These new vessels leak blood/fluid into the retina and blur the central vision.With wet AMD, abnormal blood vessels are present under the retina
68Age Related Eye Disease Study (AREDS) AREDS investigated whether or not anti-oxidants had an effect on cataracts and macular degeneration.No effect on cataractsSlows progression of dry AMD and decrease risk of conversion to wet AMD in moderate to severe AMD:Vitamins C, E, Beta Carotene, Zinc500mg Vitamin C, 400 IU Vitamin E, 15mg Beta Carotene (25,000 IU Vitamin A), 80mg Zinc, 2mg of CopperZinc only group did almost as wellLutein and Xeazanthine now replace beta carotene and have been shown to be equally beneficialAREDS 2 showed no benefit from Omega 3 FA’s on top of antioxidants
70Treatment of Dry AMDCurrently the only thing we can do are preventativeSmoking cessationVitamin supplementationAREDS vitamins (I-Caps, PreserVision, Ocuvite)Diet full of dark green vegetablesExercise and weight lossBlood pressure controlMANY new investigational therapiesincluding injections.
71Anti-VEGF treatment for wet AMD Currently the gold standard treatmentLargest drawback is frequency of treatmentQ monthly injections for as long as it takesEarlier treatments worked to limit how bad final visual out come was. This works to halt progression from worsening from its current state.Some people will even getimprovementGiven via a pars planaintravitreal injection
72Recommendations for patients with AMD Change Modifiable Risk FactorsSmoking cessationVitamin supplementationAREDS vitamins (I-Caps, PreserVision, Ocuvite)Diet full of dark green vegetablesExercise and weight lossBlood pressure controlDaily Monitoring with Amsler Grid.Early detection to stabilize at a higher start pointAmsler Grid, as seen through a normal eyeAmsler Grid, as might be seen through an eye with AMD
73Blindness From the Big 3AMD – leads to loss of central vision. Despite poor central vision most maintain full peripheral visionHave difficulty with reading, watching TV, recognizing facesWorst case: no central vision, but preserved peripheryGlaucoma – leads to loss of peripheral vision and if severe enough central vision.Can have “legal blindness” and still have 20/20 visionWorst case: Lights Out Dark Blind.Diabetes – can cause loss of both peripheral vision and central vision.Worst case: Lights Out Dark Blind
74An Ounce of PreventionWhether we are talking about Diabetes, AMD, or Glaucoma the best and most important thing we can do is screening examsMost Ophthalmologic findings in Diabetic Retinopathy, AMD, and Glaucoma are asymptomatic to the patient. Patients don’t often times notice problems until the disease is advanced.
75American Academy of Ophthalmology guidelines for eye exams Age years: At least once during this periodThose with risk factors for glaucoma (African Americans or people with a family history of glaucoma) should be seen every 3-5 years.Age years: At least twice during this periodThose with risk factors for glaucoma should be seen every 2-4 years.Age years: Every 2-4 years.Age 65 years or older: At least once a year.
76Conclusions AMD is the #1 cause of blindness in the US Control modifiable risk factorsScreening exams are vital as disease is often asymptomatic until conversion to wet AMDDiabetes is the # 1 cause of blindness in the US for year oldsScreening exams are vital as disease is often asymptomatic until there is proliferative retinopathyGlaucoma is the #2 cause of blindness worldwideMost people with Open angle glaucoma have no idea they have a problemWith screening angle closure is preventable!