Brian J. Mihok, D.O. Program Director Ophthalmology Grandview Hospital Common Eye Problems Brian J. Mihok, D.O. Program Director Ophthalmology Grandview Hospital

What is the most common cause of blindness in the United States? Macular Degeneration * Diabetic Retinopathy Cataract Glaucoma

Which of these potentially blinding diseases has early symptoms that the patient may recognize Macular Degeneration Diabetic Retinopathy Glaucoma None of the above*

Topics Anatomy Refresher Most Common Eye Problems The Big 3 Glaucoma, Macular Degeneration and Diabetes

Where 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

The Healthy Eye Light 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 eye Lens – responsible for the other 1/3 of the focusing power Iris – works to filter excess light Pupil – empty space in the middle of the iris which allows light transmission

The Healthy Eye The 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.

The Healthy Eye The retina consists of two main areas, the macula and peripheral retina. Macula Small 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.

The Healthy Eye Peripheral retina Everything that doesn’t fall into the macula Gives you your peripheral vision Important for night vision Better at detecting motion than the macula Normal retina

Retina

Macula and Foveal Importance Without the fovea the Best Visual potential is 20/200 The big E, qualifies as legally blind

What does 20/200 mean? 20/200 20/15 This 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 it Distance at which a patient with NORMAL VISION would need to be from an object to be able to see it

Legal Blindness Defined 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.

Overview of the Most Common Eye Diseases

World Health Organization Data Worldwide Most Common Causes of Blindness Cataract Glaucoma Macular Degeneration Corneal Opacities Diabetic Retinopathy Which of those diseases are preventable or curable?

What about in the US? The number one cause of blindness in the US and most developed nations is Macular Degeneration The most common cause of blindness of people under age 65 in the US is Diabetic Retinopathy The most common blinding diseases in the United States are Macular Degeneration, Glaucoma, Diabetic Retinopathy

The Big Three (Glaucoma, DM, AMD) None of these big 3 have early symptoms Screening is key to preventing vision loss By the time patients have perceived loss the disease is advanced.

Diabetes

Diabetes For Americans under the age of 65 Diabetes is the number one cause of blindness

Epidemiology 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 blind National Health and Nutrition Examination Survey III Rates of DR in diabetics over age forty is higher in AA (27%) & Mexican Americans (33%), than Caucasians (18%)

Diabetic Retinopathy Hyperglycemia leads to damaged and incompetent capillaries These capillaries can Leak (causing edema, hemorrhages, exudate) Shut down (ischemia, non-perfusion and neovascularization)

Findings in Diabetic Retinopathy Micro aneurysms Out pouching of diseased capillary endothelial cells Intra retinal hemorrhages Dot blot and flame Leakage through diseased capillary endothelial cells Hard exudates Lipid exudates from leakage out of diseased capillary endothelial cells Often associated with retinal edema

Micro aneurysms and Intra Retinal Heme

Hard Exudate

Findings in Diabetic Retinopathy Cotton Wool Spot Represents a local infarction of nerve fiber layer White areas with fluffy margins Have no predictive value in diabetic retinopathy Venous beading Tortuous veins and enlargement Used to determine severity of retinopathy and likely-hood of progressing to severe vision loss

Cotton Wool Spots

Venous Beading

Vision Threatening Changes Macular Edema Neovascularization Macular Ischemia

Retinal Edema Can occur anywhere in the retina but not clinically significant unless in the macula and meets certain criteria Occurs from leaky capillaries and is induced by vasoproliferative factors Treatment: Injections or lasers

Macular Edema

Neovascularization An attempt by the retina to reperfuse ischemic tissue Often a cause of vitreous hemorrhage Can lead to Tractional Retinal Detachments or Neovascular Glaucoma Treatment: PRP Kills ischemic tissue

Neovascularization

PRP

Macular Ischemia End result of decreased perfusion to the macula Causes permanent vision loss

Macular Ischemia

Initial 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 diagnosis Type I Initial exam should be with in the first 5 years of diagnosis then annually after 5 years Type II Initial visit at the time of diagnosis Follow up varies depending on degree of retinopathy Varies between annually down to monthly Pregnant Diabetics Seen during the 1st trimester and follow up as directed

Best Treatment of All Diabetic Retinopathy Prevention Diabetes 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 Retinopathy UKPDS also showed that strict blood pressure control in conjunction with intensive glycemic control slows the progression of DR and vision loss

Glaucoma

Glaucoma Anatomy Refresher Two main fluid compartments of the eye Aqueous humor Vitreous humor

Glaucoma 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 canal Aqueous is made at a rate that can completely turn over all the aqueous in about 90 minutes.

Glaucoma 2nd leading cause of blindness in the world Late detection is a major risk factor for blindness Tends to be inherited Number one risk factor for Glaucoma is AGE

Glaucoma Now 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 glaucoma Ocular hypertension Can have normal IOP and have glaucoma Normal Tension Glaucoma

Glaucoma Types Chronic problem Blindness typically over many years Open Angle Angle Closure Chronic problem Blindness typically over many years Painless and often symptomless VERY COMMON Acute problem Blindness can occur in hours Red painful eye, photophobia and fixed dilated pupil VERY UNCOMMON

Open Angle Glaucoma Findings Normal vision Normal or near normal visual fields +/- increased IOP Glaucomatous cupping of the optic disc

Angle Closure Findings “Hot” eye Red, painful Blurry vision Corneal edema Nausea, Vomiting and abdominal pain

What Causes the Increase in IOP? Open Angle Angle Closure Decreased drainage through the trabecular meshwork. Exact reason is unknown. Pupillary block Given the right circumstances the iris can limit the flow of aqueous through the pupil This causes the iris to bow forward, and narrow or completely occlude the drainage angle

Treatment Medications: Either increase outflow or decrease production Open Angle Angle Closure Medications: Either increase outflow or decrease production Laser: Thought to cause inflammatory response which “cleans” out the drain Surgery: Create a fistulous passage for aqueous Medications: Used to help lower IOP in an the acute attack. Pilocarpine may help prevent closure from starting Laser: Create a new passage for fluid Surgery: Cataract removal will provide more space between iris and lens

Treatment Early identification is key If treated early most open angle glaucoma will never lead to significant visual dysfunction If at risk patients are identified by screening angle closure can be prevented

Age-Related Macular Degeneration Insert name/ Practice name/ Logo here if desired Age-Related Macular Degeneration

AMD Facts #1 cause of blindness in the US Affects more than 30 Million people world wide Inherited (multiple genes most as AD) Twice as common as Alzheimer's in people over 60 Responsible for 50% of all blindness in developed nations

AMD Facts In 2010 the world wide direct health care expenditure because of AMD was 255 billion dollars. Smokers are 2-3x’s more likely to have AMD Obesity and Hypertension are also risk factors for AMD

Retinal Anatomy

Macular Degeneration A disease primarily of the Retinal Pigmented Epithelium. The retina is secondarily injured

Retinal Pigmented Epithelium (RPE) Primary function is to serve as a support cell to the metabolically active photoreceptors Helps supply nutrients to the photoreceptors Helps remove waste Phagocytize old outer segments of the photoreceptors Vitamin A cycle Other functions Absorb scattered light and heat

Bruch’s Membrane The anatomical barrier between the highly vascular Choroid and the RPE and Retina The Choroid has more blood vessels per square mm than any where else in the body

What 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 drusen These drusen lead to inflammation The drusen and inflammatory mediators are toxic to both the overlying RPE and the underlying Bruch’s membrane.

Drusen

Two types of AMD Atrophic (“dry”) macular degeneration. Exudative (“wet”) macular degeneration.

Dry AMD The most common form of AMD Wet AMD arises out of Dry AMD so everyone with Wet AMD also has Dry AMD Vision loss is slow Over many years

Dry AMD Drusen formation and RPE changes are the first signs of AMD. Asymptomatic to the patient As the process continues the waste products slowly cause death of photo receptors This is irreversible. Small central scotoma Metamorphopsia

Dry AMD Eventually enough RPE is damaged that patient ends up with geographic atrophy

Wet 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 AMD Vision loss may be rapid and severe. Causes about 80% of blindness because of AMD

With wet AMD, abnormal blood vessels are present under the retina If Bruch’s membrane gets damaged enough it can form small breaks These 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

Wet AMD

Age Related Eye Disease Study (AREDS) AREDS investigated whether or not anti-oxidants had an effect on cataracts and macular degeneration. No effect on cataracts Slows progression of dry AMD and decrease risk of conversion to wet AMD in moderate to severe AMD: Vitamins C, E, Beta Carotene, Zinc 500mg Vitamin C, 400 IU Vitamin E, 15mg Beta Carotene (25,000 IU Vitamin A), 80mg Zinc, 2mg of Copper Zinc only group did almost as well Lutein and Xeazanthine now replace beta carotene and have been shown to be equally beneficial AREDS 2 showed no benefit from Omega 3 FA’s on top of antioxidants

Treatment of Dry AMD Currently the only thing we can do are preventative Smoking cessation Vitamin supplementation AREDS vitamins (I-Caps, PreserVision, Ocuvite) Diet full of dark green vegetables Exercise and weight loss Blood pressure control MANY new investigational therapies including injections.

Anti-VEGF treatment for wet AMD Currently the gold standard treatment Largest drawback is frequency of treatment Q monthly injections for as long as it takes Earlier 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 get improvement Given via a pars plana intravitreal injection

Recommendations for patients with AMD Change Modifiable Risk Factors Smoking cessation Vitamin supplementation AREDS vitamins (I-Caps, PreserVision, Ocuvite) Diet full of dark green vegetables Exercise and weight loss Blood pressure control Daily Monitoring with Amsler Grid. Early detection to stabilize at a higher start point Amsler Grid, as seen through a normal eye Amsler Grid, as might be seen through an eye with AMD

Blindness From the Big 3 AMD – leads to loss of central vision. Despite poor central vision most maintain full peripheral vision Have difficulty with reading, watching TV, recognizing faces Worst case: no central vision, but preserved periphery Glaucoma – leads to loss of peripheral vision and if severe enough central vision. Can have “legal blindness” and still have 20/20 vision Worst case: Lights Out Dark Blind. Diabetes – can cause loss of both peripheral vision and central vision. Worst case: Lights Out Dark Blind

An Ounce of Prevention Whether we are talking about Diabetes, AMD, or Glaucoma the best and most important thing we can do is screening exams Most 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.

American Academy of Ophthalmology guidelines for eye exams Age 20-29 years: At least once during this period Those with risk factors for glaucoma (African Americans or people with a family history of glaucoma) should be seen every 3-5 years. Age 30-39 years: At least twice during this period Those with risk factors for glaucoma should be seen every 2-4 years. Age 40-64 years: Every 2-4 years. Age 65 years or older: At least once a year.

Conclusions AMD is the #1 cause of blindness in the US Control modifiable risk factors Screening exams are vital as disease is often asymptomatic until conversion to wet AMD Diabetes is the # 1 cause of blindness in the US for 25-65 year olds Screening exams are vital as disease is often asymptomatic until there is proliferative retinopathy Glaucoma is the #2 cause of blindness worldwide Most people with Open angle glaucoma have no idea they have a problem With screening angle closure is preventable!