The Essentials for Paraoptometric Personnel in Understanding Medical Optometry Jeff D. Miller, O.D. Stillwater, Oklahoma firstname.lastname@example.org Baby Boomers • Approximately 80 Million • 7,918 people turn 60 each day in 2006 • That’s 330/hour • Every day until 2014, 10,000 Americans turn 50 • 1/8 Americans are 65 or older Health of Americans • Diabetes –epidemic in children • HTN – steep rise • CVD – linked w/HTN • Obesity – 15% in 1980 - 33% in 2004 • Obesity doubles the risk of vision loss AMD, Glaucoma, Cataracts, Diabetes Ocular Disease -TODAY • Diabetic Retinopathy is the leading cause of blindness ages 25-74 • AMD is the most common cause of blindness in Americans 60 and older • Cataracts are the leading cause of blindness in the world Ocular Disease-TODAY • Glaucoma – 2.2 million cases diagnosed, 2 million undiagnosed • 1 Million blind, 2.4 million visually impaired (2/3 are female) • By far the most common ocular disorder: “Ocular Surface Disease” or OSD Ocular Disease Estimates In The Year 2020 • NEI Eye Prevention Research Group • Diabetic Retinopathy – 50% increase • AMD – 70% increase • Glaucoma – 3.36 million – 53% increase • Legal Blindness – 70% increase • In 2036 all today’s numbers will double REMEMBER- OF THE EYE DISEASES WE ARE COVERING TODAY THEY REPRESENT: A. THE LEADING CAUSE OF BLINDNESS IN THE USA AGES 25-74. B. THE LEADING CAUSE OF CENTRAL VISION LOSS IN PATIENTS OVER 60 C. THE SECOND LEADING CAUSE OF PREVENTABLE BLINDNESS IN THE USA (CATARACTS ARE FIRST) AND THERE IS NO WAY TO TELL YOU HAVE THEM BASED ON THE WAY YOU FEEL! THEY ARE ONLY DETECTABLE THROUGH AN EYE HEALTH EVALUATION GLAUCOMA • Glaucoma is a group of diseases that can damage the eye’s optic nerve and result in irreversible vision loss and blindness. • Glaucoma is multifactorial – it is not a single disease process. Rather it is a large group of disorders. • The term glaucoma should only be used in reference to the entire group of disorders, just as the term cancer is used to encompass many clinical entities with certain common denominators. GLAUCOMA • The common denominator in glaucoma is optic nerve damage/death which derives from various risk factors. • Glaucoma is the leading cause of preventable blindness in the US. • There are several forms of glaucoma, the most common is Primary Open Angle Glaucoma or POAG. Forms of Glaucoma • POAG, Primary Open Angle Glaucoma • LTG or NTG, Low Tension or Normotensive Glaucoma • Angle Closure Glaucoma • Congenital Glaucoma • Secondary Glaucoma’s – Pigmentary Glaucoma, Neovascular Glaucoma, and Inflammatory or Uveitic Glaucoma, Angle Recession Glaucoma Risk Factors for Glaucoma • Intraocular Pressure, IOP • Genetics - Family History • Age (increases after 40yrs and 60 yrs) • Race (African American, Hispanics) • Gender (men or women?) • Diabetes Mellitus • Cardiovascular Disorders • Obstructive Sleep Apnea Glaucoma Diagnosis • Traditionally: IOP, optic nerve changes, visual field defect – treat or monitor. • Risk factors are better known today and play a large role in treatment initiation. • Today’s technology also allows much earlier diagnosis and treatment initiation through various tests/technology:IOP, stereoscopic optic nerve evaluation, optic nerve topography, nerve fiber layer analysis with scanning lasers and OCT, central corneal thickness, gonioscopy, Visante OCT, blood flow analysis, and visual fields. Diagnosis • IOP – “normal” 10-22mmHg • Remember LTG or NTG, IOP appears in the normal range • ONH evaluation –characteristic changes • CCT - central corneal thickness obtained via pachymetry - normal is 555 microns • Gonioscopy – evaluates where the aqueous fluid drains • Nerve Fiber layer Analysis: GDx VCC, HRT II and III, OCT (i.e.Stratus,Cirrus) • Visual Fields ONH EVALUATION Normal Healthy Optic Nerve Grading cup to disc ratio Normal Healthy Optic Nerve with small C/D Ratio SUSPICIOUS ONH GLAUCOMATOUS ADVANCED GLAUCOMA WITH OPTIC ATROPHY ADVANCING GLAUCOMA WITH NOTCHING OF SUPERIOR RIM EMGTS-patients with exfoliation or recurrent disc hemorrhage may have worse prognosis and need greater tx and closer observation. CNTGS-”strongly predictive of disease progression” OHTS-detection of disc hemorrhages- 84% were detected only by photos 16% by exam and photos. Increased risk of glaucoma development found however, 86.7% w/disc hem have not converted to glaucoma. Grading cup to disc ratio Optic Nerve Head Analysis Key parameters Disc edge is are Horizontal determined by Integrated Rim the end of the Volume* and RPE -shown by Cup/Disc blue marker ratios Yellow line on composite diagram Fundus image indicates for verification individual radial of scan scan selected and displayed placement *Comparison of three optical coherence tomography scanning areas for detection of glaucomatous damage. Wollstein G, Ishikawa H, Wang J, Beaton SA, Schuman JS. Am J Ophthalmol. 2005 Jan;139(1):39-43 xxx CCT-Central Corneal Thickness • Ultrasound Pachymetry (sound waves) • Visante OCT Pachymetry (light waves) • Ocular Hypertensive Treatment Study OHTS – CCT can suggest/determine risk >588 microns (low risk) =555-588 microns (mod. risk) <555 microns (high risk) Gonioscopy Virtual Gonioscopy Scanning Laser Polarimetry: GDx VCC Retinal Nerve Fiber Layer GDx VCC Printout Normal Glaucoma Fundus Image Parameters Thickness Map Deviation Map TSNIT Graph Comparisons of each scan to the Normative Database allows accurate and rapid interpretation in one exam Correlation of the Deviation Map and Thickness Map with Visual Field Pattern Deviation is shown below These are examples from normal to advanced glaucoma • A normal eye with normal thickness and deviation maps and normal visual field • An eye with focal Retinal Nerve Fiber Layer loss prior to visual field loss • A moderate glaucoma eye with superior RNFL loss and inferior visual field loss • An advanced glaucoma eye with advanced RNFL and visual field loss Stratus OCT™ Cirrus™HD-OCT Glaucoma – RNFL Thickness Analysis An OU analysis example (2) VISUAL FIELDS • Helps to confirm a definitive diagnosis of glaucoma. • Determines the degree of vision loss associated with glaucoma. • Helps to monitor the progression of the disease and determine treatment strategies and if the medications and/or surgeries are working. Treatment • Treatment – ultimate goal is to lower IOP by reducing the production of the fluid in the eye or increasing the outflow of the fluid (Aqueous) • Medical Treatment • Topical Glaucoma Drops • Various Classes: reduce aqueous production or increase aqueous outflow • Neuro-protection (now and future) • Blood flow enhancers (future) • Timoptic, Betimol, Betagan, Betoptis S, Azopt, Trusopt Travatan, TravatanZ, Lumigan, Xalatan, Alphagan, Alphagan-P, Cosopt, Combigan, Pilocarpine • What about oral meds ? (Diamox, Neptazane) Surgical Treatment • Laser treatment: The laser treats the tissue that the aqueous fluid drains through such that it opens or “cleans” it out increasing drainage ALT - Argon Laser Trabeculoplasty SLT - Selective Laser Trabeculoplasty • Other Lasers • Trabeculectomy - creates drainage canal • Glaucoma valve – creates drainage canal Glaucoma Management • Once diagnosed patients should be monitored on a quarterly basis for IOP and yearly (at minimum) for changes in VF, optic nerve, nerve fiber layer damage and gonioscopy. • The more advanced the more often VF, and other testing should be performed. • Glaucoma suspects should be monitored yearly or on a 6 month basis depending on their findings and other health issues. GLAUCOMA QUESTIONS ? MACULAR DEGENERATION • Leading cause of severe irreversible central vision loss and legal blindness in individuals 60 and older in the US. • Predominantly Caucasian (Hispanics on the rise) • Approximately 30% of those over 75 have early AMD • 23% of the remainder of those will develop it with in five years • By 2020 the incidence is estimated to rise by 70% • By 2036 all today’s numbers will double (Baby Boomers) Macular Degeneration- Two Forms • Non-neovascular, dry or atrophic macular degeneration • Neovascular, wet or exudative macular degeneration Dry or Atrophic Macular Degeneration-AMD • The retina is 10 layers thick. The last layer is called the RPE - Retinal Pigment Epithelium • The RPE is responsible for providing nourishment to the retinal visual cells and maintains the retinal environment • If the RPE is sick or damaged the retina degenerates • AMD is characterized by abnormalities in the retinal pigment epithelium (RPE) with drusen formation • Drusen are tiny white or yellow accumulations in Bruch’s membrane, a membrane between the final layer of the retina (RPE) and its blood supply in the choriocapillaris. Wet or Exudative Macular Degeneration • The wet form of AMD is defined by the appearance of “new” blood vessel growth, neovascularization, originating in the layer below the retina called the choricapillaris. • These new blood vessels are abnormal and leak fluid and blood into the subretinal space causing disruption of the RPE with subsequent fibrosis and scarring • The damage to the RPE is irreversible Macula ### RNFL RGC Rods & Cones Retinal RPE Anatomy Cirrus HD-OCT Healthy Macula NFL ILM GCL IPL INL OPL ONL ELM IS IS/OS OS RPE Choroid NFL: Nerve Fiber Layer OPL: Outer Plexiform Layer IS/OS: Junction of inner and outer ILM: Inner Limiting Membrane ONL: Outer Nuclear Layer photoreceptor segments GCL: Ganglion Cell Layer ELM: External limiting membrane OS: Photoreceptor Outer Segment IPL: Inner Plexiform Layer IS: Photoreceptor Inner Segment RPE: Retinal Pigment Epithelium INL: Inner Nuclear Layer DIAGNOSIS • Primarily observation • Patients must be seen yearly for eye health exams • Retinal evaluation with various lenses and photographic devices • OCT/HRT scans (Stratus,Cirrus,HRT-II,III) • Fluorescein Angiography (RSFA) • Macular pigment optical density DRUSEN Drusen and RPE Changes Drusen and RPE Changes SOFT DRUSEN FLOURESCEIN ANGIOGRAPHY- RSFA xx DRUSEN DRUSEN WITH PROGRESSIVE RPE DISRUPTION/DROPOUT RSFA OF DRUSEN AND RPE CHANGES EXUDATIVE OR WET MACULAR DEGENERATION WET AMD RSFA OF WET MACULAR DEGENERATION WET OR EXUDATIVE MACULAR DEGENERATION EXTENSIVE WET MACULAR DEGENERATION Macular Pigment RISK FACTORS Diets high in antioxidants and lutein have been shown • Age to have a positive effect on • Smoking controlling the formation and • Family History advancement of dry AMD • Exposure to UV (sunlight) • Females • Caucasian • Hyperopia • HTN • Diabetes • Cardiovascular Risk Factors • High Fat Intake • Diets with foods that have a high glycemic index, refined sugars starchy foods “the white stuff” Atrophic and Exudative Macular Degeneration Patient Education • The leading cause of blindness in people over 60 • To avoid: don’t smoke, UV protection, diet high in lutein/antioxidants • Carrots vs. broccoli, peas and spinach • Dry accounts for 90%, Wet 10% • “New abnormal blood vessels” – CNV membranes, grow at a rate of 20 microns/day • Wet AMD patients prompted to seek exam when membranes are on avg. 3300 microns Lutein Concentration mcg/100g • Kale 39,550 • Yellow corn 764 • Turnip Gr. 12,825 • Asparagus 710 • Spinach 12,198 • Green Beans 640 • Mustard Gr. 9,900 • Artichokes 464 • Collard Gr. 8,932 • Red Cabbage 329 • Green Peas 2,477 • Tomatoes 123 • Brussel Sprouts 1,819 • White Onion 5 • Broccoli 1,403 Injections for Exudative AMD • Block Vascular Endothelial Growth Factor – Anti-VEGF drugs stop the growth of neovascularization in and beneath the retina restoring vision in many cases. Prior to 2005 these drugs were not available and most with wet macular degeneration lost significant vision if laser treatment was not an option. • Lucentis $1500 to $ 2500 per injection • Avastin $70 to $400 per injection AMD/Cataracts and Carbohydrate Consumption • Carbohydrates – high glycemic index • American Journal of Clinical Nutrition – followed 1036 women over 10 years. Carbohydrate intake directly correlated to incidence of early AMD. • Dietary glycemic index was also linked with higher incidence of cataracts. AMD/Cataracts and Carbohydrate Consumption • Annals of Internal Medicine – Study demonstrated women with early AMD were twice as likely to suffer a stroke vs. those who didn’t have AMD. • This finding was noted after factoring out smokers, Diabetics, and HTN patients. MACULAR DEGENERATION QUESTIONS ? DIABETIC EYE DISEASE • DIABETES IS THE LEADING CAUSE OF NEW BLINDNESS IN THE US AGES 25-74. • Accounts for 5800 new cases a year of legal blindness. • Approximately 25% of diabetics have some degree of retinopathy. • A significant increased risk of cataracts and glaucoma is seen in patients with both Type I and Type II diabetes. • At minimum, a diabetic should be seen yearly for a full eye health exam. DIABETIC EYE DISEASE • The prevalence of retinopathy increases with the duration of diabetes and in those with uncontrolled blood sugar. • Patients are usually spared of diabetic retinopathy for 3-5 years following the onset of the disease. • Diabetic retinopathy is broadly classified as nonproliferative and proliferative diabetic retinopathy – NPDR, PDR. • NPDR – bleeding and exudates (by-products) present in the retina • PDR – the growth of “new and abnormal” blood vessels or neovascularization DIABETIC EYE DISEASE • Macular Edema – diabetic cystoid macular edema (DCME) can occur in any stage of retinopathy and results in decreased visual acuity. • Retinal treatment other than diet, oral meds and insulin is considered when patients have NPDR with clinically significant DCME to avoid permanent vision loss and progression to PDR TREATMENT • Control of blood sugar is always paramount; daily evaluation as well as regular Hemaglobin A1C. • Laser Treatment: Macular Grid - for Diabetic Cystoid Macular Edema (DCME) Pan-Retinal Laser Photocoagulation – or “PRP” to prevent or treat PDR which is characterized by the growth and extension of new blood vessels in the retina and vitreous. NONPROLIFERATIVE DIABETIC RETINOPATHY - NPDR NPDR NPDR NPDR NONPROLIFERATIVE DIABETIC RETINOPATHY WITH MACULAR EDEMA AND COTTON WOOL SPOTS (CWS) PROLIFERATIVE DIABETIC RETINOPATHY PROLIFERATIVE DIABETIC RETINOPATHY WITH PRE-RETINAL HEMORRHAGE PROLIFERATIVE DIABETIC RETINOPATHY WITH NEOVASCULARIZATION OF THE DISC TERMED “NVD” PDR WITH NEOVASCULARIZATION IN THE RETINA TERMED “NVE” NEOVASCULARIZATION ELSEWHERE PAN-RETINAL PHOTOCOAGULATION “PRP” RETINAL FIBROSIS RETINAL FIBROSIS RETINAL FIBROSIS WITH SUBSEQUENT RETINAL DETACHMENT RETINAL DETACHMENT PATIENT MANAGEMENT • Diabetics should be examined yearly at minimum. • Visit schedule should be adjusted when patients are suspect for progression of retinopathy and or Diabetic Cystoid Macular Edema (DCME). • Photodocumentation, IOP checks, retinal imaging (OCT, HRT), and gonioscopy should all be considered based on the patients clinical presentation. • Education should include other ocular complications; glaucoma and cataracts. DIABETIC EYE DISEASE QUESTIONS ?
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