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1 CONTINUING EDUCATION CERTIFICATION Tulalip Continuing Education September 14, 2014 Tulalip Resort & Casino COPE EVENT # Sunday, September 14, HOURS TOTAL Ryan Bulson, OD, MS Diabetic Retinopathy: An Evidence Based Approach (1 hr) Dina Erickson, OD AMD Updates (2 Hrs) Ryan Bulson, OD, MS The Effects of Smoking and the Eye (1 hr) Ryan Bulson & Dina Erickson Grand Rounds (2 Hrs) SD PS PB PS VERIFICATION STAMP VERIFICATION STAMP VERIFICATION STAMP VERIFICATION STAMP Therapeutic Hours: PB, SD, PS TOTAL HOURS OFFERED: 6 TOTAL HOURS ATTENDED: Name License # Mailing Address City/ST/ZIP Please keep a copy of this form for your records. Be advised that your individual state board makes the final determination of applicable hours. If you have an OE Tracker number, your hours will be added to their database. OE TRACKER captures and stores continuing education attendance data for optometrists. The information is retained in the secure ARBO database and can be accessed online by you and your licensing board. OE TRACKER can save you time and reduce your paperwork by tracking all your CE credits electronically. College of Optometry 2043 College Way Forest Grove, Oregon of 46

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3 TULALIP CE FACULTY Ryan Bulson, OD, MS Dr. Bulson is a native of Barneveld, New York and he completed his OD and MS at State University of New York. His residency training in Hospital Based Primary Care Optometry at the Portland VA Medical Center brought him to the Pacific Northwest. He is an Assistant Professor at Pacific University where he teaches clinical procedures and is an attending optometric physician for 4 th year optometry students. Dina Erickson, OD Dr. Erickson has served as an adjunct faculty member since 1998 and assistant professor since Dr. Erickson is co-instructor in the Ocular Disease and Clinical Procedures courses and also advises third- and fourth-year students in the Pacific University EyeClinics. In addition to her teaching responsibilities at the college, Dr. Erickson is in an optometric physician in a primary care private practice and is an active member of the Portland Metro Optometric Society. She earned her O.D. from Southern California College of Optometry and completed a residency in Hospital Based Optometry at the San Francisco VA Medical Center. October 2 4, 2014 January 10, 2015 January 25 31, 2015 April 24 & 25, 2015 July 16 19, th Annual Research Conference, Pacific University - 12 HOURS of Continuing Education Glaucoma Symposium, Willows Lodge, Woodinville, Washington 7 HOURS of Continuing Education. Information: frederim@pacificu.edu 2015 Island Eyes Conference, Hilton Waikoloa Village, Hawaii Up to 29 HOURS of OD Continuing Education and 9 HOURS of Paraoptometric Education Coeur d Alene CE, Coeur d Alene Resort, Idaho - 10 HOURS of Continuing Education 2015 Victoria Conference, Inn at Laurel Point, Victoria, BC, Canada 20 HOURS of Continuing Education and 4 HOURS of Paraoptometric Education Can t get away? Try our ONLINE CONTINUING EDUCATION Our new mobile app will be introduced soon 3 of 46

4 Diabetic Retinopathy: An Evidence Based Approach Ryan Bulson, O.D., M.S., F.A.A.O. Overview Review the impact of diabetes on the healthcare system Review the most common forms of diabetes and their risk factors Review standards for grading diabetic retinopathy Review newly revised (February 2014) AOA Clinical Practice Guidelines for managing diabetic retinopathy The Problem Diabetes mellitus is a group of chronic metabolic diseases characterized Hyperglycemia Defects of insulin secretion Increased cellular resistance to insulin Microvascular and macrovascular disease Long term complications including diabetic nephropathy, neuropathy, and retinopathy The Problem An estimated 25.8 million Americans (~8.3 percent of the population) have diabetes ~2 million adults newly diagnosed in 2010 As many as 40 percent of people with diabetes don t know they have the disease. If trends continue: one in three adults in the US will have diabetes by 2050 Seventh leading cause of death in the United States Direct and indirect costs: $245 billion annually The number of people with diabetes worldwide increased from 153 million in 1980 to 347 million in This number is expected to grow to 429 million by Diabetes Classification Pre-Diabetes Blood glucose is higher than normal, but not high enough for diabetes Impaired glucose tolerance On 75-g oral glucose tolerance test, the 2-hour plasma glucose value is mg/dl Impaired fasting glucose Fasting glucose mg/dl Glycosolated Hemoglobin (A1C) Measuring percentage of blood glucose attached to hemoglobin Average blood glucose level for the previous 2-3 months % is considered pre-diabetes 4 of 46 1

5 Diabetes Classification Diabetes HbA1C 6.5% Random (without regard to last meal) plasma glucose level 200 mg/dl in a person with classic symptoms of hyperglycemia (polyuria, polydipsia, and weight loss) or hyperglycemic crisis Fasting (no caloric intake for at least 8 hours) plasma glucose level 126 mg/dl Two-hour plasma glucose level 200 mg/dl on oral glucose tolerance test Diabetes Classification Type 1 Diabetes (formerly called insulin-dependent or juvenile diabetes) Body s immune system attacks and destroys insulin-producing beta-cells in the pancreas Rate of beta cell destruction varies In early stages may have sufficient beta cell function to prevent ketoacidosis, but will eventually require insulin Tend to be acutely symptomatic at onset, often complaining of polydipsia, polyphagia, polyuria, unexplained weight loss and dry mouth. Accounts for ~5-10 percent of diabetes in US Generally diagnosed in children and young adults, but can occur at any age Likely genetic with possible environmental component Diabetes Classification Type 2 Diabetes (formerly termed non-insulin dependent or adult-onset diabetes) occurs due to Insulin deficiency (insufficient insulin production) Insulin resistance (inability to use insulin efficiently) Initial compensatory mechanism involves increased insulin production to normalize glucose levels, which eventually leads to insulin resistance As insulin resistance worsens, body has more difficulty producing insulin Process develops over decades Initially asymptomatic Insulin resistance Hyperglycemia only following meals Diabetes Diabetes Classification Gestational Diabetes Glucose intolerance associated with onset during pregnancy Caused by hormones secreted during pregnancy and/or shortage of insulin Affects 5 to 10 percent of all pregnancies Usually diagnosed in 2 nd or 3 rd trimester Glucose tolerance typically returns to normal within 6 weeks after pregnancy ends Generally does not lead to retinopathy due to limited nature Women with GD has 35 to 60 percent chance of developing type 2 diabetes in years Diabetes Classification Other Forms of Diabetes Secondary to: Genetic defects in beta-cell function or insulin action Pancreatic diseases Other endocrinopathies Medication Toxic chemicals Infections Uncommon (1-5% of all diabetes) Risk Factors for Diabetes Type 1 Family history Viral exposure (Epstein-Barr, Coxsackie, Mumps, CMV) Autoimmune disease (Grave s, Crohn s, RA) Type 2 Family history (BMI) 25 kg/m 2 Age >45 years Ethnic Background: American Indian, Alaska Native, Black, Hispanic/Latino, Asian American, Native Hawaiian and other Pacific Islander adults are nearly twice as likely as Caucasian adults to have type 2 diabetes H/o gestational diabetes or delivering baby > 9 lbs Blood pressure >140/90 Abnormal cholesterol levels: HDL level < 35 mg/dl and/or a triglyceride level > 250 mg/dl 5 of 46 2

6 Diabetic Retinopathy Diabetic retinopathy is leading cause of new blindness and visual impairment among Americans 20 to 74 years old Accounts for approximately 12 percent of all new cases of blindness each year Nearly 86 percent of individuals with type 1 diabetes mellitus and 40 percent of those with type 2 diabetes mellitus have some form of clinically evident diabetic retinopathy 20-40% of patients have signs of retinopathy at diagnosis 33-50% of patients with DM do not receive annual eye exams Diabetic Retinopathy Diabetes duration and sustained hyperglycemia are among the primary risk factors for the development of diabetic retinopathy Intensive treatment to maintain blood glucose concentrations close to the normal range has been shown to decrease the risk of the development of diabetic retinopathy by as much as 76 percent. Diabetic Retinopathy Diabetic Retinopathy Findings Microaneurysms (MA) Outpouching of retinal capillaries resulting from the loss of intramural pericytes within the capillary walls Face into areas of non-perfusion Retinal hemorrhages (H) Ruptured or leaking microaneurysms or retinal capillaries Typically occur within the inner nuclear and outer plexiform layers creating a pinpoint or dot appearance Hemorrhages >2A in all quadrants is associated with 48% chance of developing neovascularization within 1 year Hard exudates Lipoproteins from leaking retinal vasculature Often associated with retinal edema Cotton wool spots Localized infarct of the nerve fiber layer Indicative of ischemia CWS not associated with increased risk for neovascularization Image from Bresnick and Cuadros; EyePacs 6 of 46 3

7 Image from Bresnick and Cuadros; EyePacs Image from Bresnick and Cuadros; EyePacs Image from Bresnick and Cuadros; EyePacs Image from Bresnick and Cuadros; EyePacs 7 of 46 4

8 Diabetic Retinopathy Findings Intraretinal microvascular anomalies (IRMA) New vessel growth within the retina or pre-existing vessels with endothelial cell proliferation that serve as shunts through areas of nonperfusion Indicates severe ischemic and neovascularization is likely to develop within a short time IRMA is associated with associated with 44% chance of developing neovascularization within 1 year Venous caliber abnormalities Venous dilation, venous beading (VB), or loop formation Large areas of nonperfusion can appear adjacent to these abnormal veins and are indicative of a substantial risk factor for neovascularization Also serve as strong indicators of severe retinal hypoxia VB associated with a 51% chance of developing neovascularization within 1 year 8 of 46 5

9 Diabetic Retinopathy Findings Neovascularization (NV) The growth of new vessels, either at or near the optic disc (NVD), or elsewhere in the retina (NVE) Increased risk for vitreous hemorrhage or traction retinal detachment resulting in severe vision loss Diagnosis and treatment of PDR can prevent 50% of severe vision loss in advanced diabetic retinopathy EARLY diagnosis and treatment of PDR can prevent 90% of severe vision loss. 9 of 46 6

10 Diabetic Retinopathy Findings Diabetic Macular Edema (DME) Most common cause of vision loss in persons with diabetes May be present at any severity level of diabetic retinopathy Represents breakdown of blood-retina barrier when tight junctions of vascular endothelial cells break down Causes intraretinal fluid accumulation in the macula, causing photoreceptor disruption, and if untreated, increased risk of loss of vision 50% reduction in visual loss compared non-treatment after 1 year 10 of 46 7

11 Image from Bresnick and Cuadros; EyePacs Image from Bresnick and Cuadros; EyePacs 11 of 46 8

12 Clinical Practice Guidelines The AOA has developed the Evidence-Based Clinical Practice Guideline to provides ODs with examination and management recommendations designed to preserve vision and reduce the risk of vision loss in persons with diabetes, through timely diagnosis, appropriate management and referral. ithdiabetesmellitus%20cpg3.pdf Clinical Practice Guidelines Institute of Medicine: Clinical Practice Guidelines are statements that include recommendations intended to optimize patient care that are informed by a systematic review of the evidence and an assessment of the benefits and harms of alternative care options. Case 1 40yo White Male Type 2 DM x 10 years Meds: none, diet controlled HbA1C: 7.2% Guidelines should: Be based on a systematic review of existing evidence Be developed by a knowledgeable, multidisciplinary panel of experts and key stakeholders. Be revised as appropriate when new evidence warrants modifications of recommendations 12 of 46 9

13 Case 2 No Retinopathy Individuals with diabetes should receive at least annual dilated eye examinations. More frequent examination may be needed depending on changes in vision and the severity and progression of diabetic retinopathy. The individual s primary care physician should be informed of eye examination results following each examination, even when retinopathy is minimal or not present. 35yo Hispanic Female Type 2 DM x 10 years Meds: none, diet controlled HbA1C: 6.8% Pregnant x 10 weeks Best corrected Distance VA OD 20/20 OS 20/20 Full motilities, PERRL (-)APD Anterior segment unremarkable GAT 3:15pm DFE 13 of 46 10

14 Case 3 Diabetes and Pregnancy Women with pre-existing diabetes who are planning pregnancy or who become pregnant should have a comprehensive eye examination prior to a planned pregnancy or during the first trimester, with follow-up during each trimester of pregnancy. Clinicians should use caution in administering topically applied drugs for pupillary dilation in pregnant women. Topically applied drugs for pupillary dilation, such as tropicamide, hydroxyamphetamine and phenylephrine are Pregnancy Category C drugs. When evaluation through a dilated pupil is necessary to assess diabetic retinal changes or unexplained decreased vision during pregnancy, the benefits of dilation may outweigh any potential risks. The use of digital punctual occlusion can minimize systemic absorption. 21yo White Male Type 1 DM x 16 years Meds: insulin HbA1C: 10.2% Best corrected Distance VA OD 20/20 OS 20/20 Full motilities, PERRL (-)APD Anterior segment unremarkable GAT 10:05am DFE Case 1 ETDRS Classification Mild Non-Proliferative Diabetic Retinopathy At least 1 retinal microaneurysm Severity of hemorrhage or microaneurysm less than standard photo 2A 14 of 46 11

15 Case 4 Mild NPDR An annual dilated eye examination is generally sufficient for monitoring the patient with mild NPDR, as long as there are neither DME nor coincident medical risk factors such as hypertension, renal disease or pregnancy, that may predispose patients to progression 65yo Hispanic Male Type 2 DM x 20 years Meds: orals HbA1C: 10.8% Best corrected Distance VA OD 20/20 OS 20/20 Full motilities, PERRL (-)APD Anterior segment unremarkable GAT 11:15am DFE ETDRS Classification Moderate Non-Proliferative Diabetic Retinopathy Hemorrhage or microaneurysm greater than that depicted in standard photograph 2A in one to three retinal quadrants CWS, VB, or IRMA definitely present 15 of 46 12

16 Case 5 Moderate NPDR For patients with moderate NPDR, fundus photography is strongly suggested, and repeat evaluation in 6 to 8 months is appropriate in the absence of DME or complicating medical or risk factors. If DME is present, but does not meet the criteria for CSME, follow-up every 2 to 4 months is advisable. 70yo White Male Type 2 DM x 40 years Meds: insulin and orals HbA1C: 12.1% Best corrected Distance VA OD 20/30 OS 20/40 Full motilities, PERRL (-)APD Anterior segment: grade 1 NSC OU GAT 12:45pm DFE ETDRS Classification Severe Non-Proliferative Diabetic Retinopathy Hemorrhage or MA standard photograph 2A in four quadrants VB (standard photograph 6B) in two or more quadrants Prominent IRMA ( than standard photograph 8A) in at least one quadrant. Sometimes referred to as rule Hemorrhages >2A in all quadrants is associated with 48% chance of developing neovascularization within 1 year VB in 2 quadrants associated with a 51% chance of developing neovascularization within 1 year IRMA is associated with associated with 44% chance of developing neovascularization within 1 year CWS not associated with increased risk for neovascularization Very Severe Non-Proliferative Diabetic Retinopathy Two or more criteria for severe NPDR are met, in the absence of frank neovascularization 16 of 46 13

17 ETDRS Classification Diabetic Macular Edema (DME) Retinal thickening within two disk diameters (DD) of the center of the macula Clinically Significant Macular Edema (CSME) Thickening of the retina 500 microns (1/3 DD) from the center of the macula Hard exudates 500 microns (1/3 DD) from the center of the macula with thickening of the adjacent retina. A zone or zones of retinal thickening 1 DA in size, any portion of which is 1 DD from the center of the macula. Hard exudate within one disc diameter (1DD) (1500 microns) of the center of the macula will identify CSME with 94% sensitivity CSME associated with 10 fold increased risk for moderate visual loss (defined as doubling of the visual angle, e.g. 20/40 20/80) Severe/Very Severe NPDR Follow-up every 2 to 3 months in consultation with an ophthalmologist experienced in the management of diabetic retinal disease is advisable for patients with severe or very severe NPDR. CSME Consultation with an ophthalmologist experienced in the management of diabetic retinal disease is indicated if PDR or DME is suspected or if there is an unexplained loss of visual acuity. Case 6 35yo White Male Type 1 DM x ~30 years Meds: insulin HbA1C: 15.3% 17 of 46 14

18 ETDRS Classification Proliferative Diabetic Retinopathy (PDR) New vessels on or within one disc diameter of the disc (NVD) or new vessels elsewhere on the retina (NVE) < standard photo 10A Fibrous proliferation on or within one disc diameter of the optic disc (FPD) or elsewhere on the retina (FPE) Preretinal hemorrhage (PRH) or NVE < ½ disc area without NVD High Risk Proliferative Diabetic Retinopathy NVD > one-fourth to one-third disc area in size (standard photograph 10A) NVD < one-fourth disc area in size with fresh vitreous hemorrhage (VH) or preretinal hemorrhage (PRH) present NVE > one-half disc area in size with VH or PRH present. Without treatment 50% of eyes with PDR are blind within 5 years Conclusions PDR Consultation with an ophthalmologist experienced in the management of diabetic retinal disease is indicated if PDR or DME is suspected or if there is an unexplained loss of visual acuity. Prompt referral to a vitreo-retinal surgeon is indicated when a vitreous hemorrhage, a retinal detachment or other evidence of proliferative diabetic retinopathy is present. Diabetes and management of diabetic retinopathy will continue to be a major issue in healthcare ODs should continue to be at the forefront of screening for and monitoring diabetic retinopathy When in doubt, don t be afraid to refer anything outside your comfort level Stay current with the AOA s Clinical Practice Guidelines ithdiabetesmellitus%20cpg3.pdf Thank You and Questions? 18 of 46 15

19 AMD Update Dina Erickson, OD, FAAO Outline: Background: Geographic atrophy and neovascular age related macular degeneration Treatment options: Dry AMD: AREDS II o Study criteria o Nutritional changes from AREDS I formula o Major outcomes o Possible study weaknesses o What have we learned and how should we advise our patients based on AREDS II outcomes Wet AMD: Current FDA approved treatments Photocoagulation PDT Anti-VEGF tx: o Macugen o Lucentis o Avastin? o Eylea o Patient education regarding Anti VEGF treatment o Potential side effects Case presentation: o 75 year old Caucasian male seeing white lines on the road as sheep jumping with OD for 3 weeks. Recent Studies and their outcomes: o CATT, o IVAN o View I and View II Current therapy strategy: o Monthly treatment o Monthly then as needed 19 of 46

20 o Treat and extend Potential new strategies: o Extended delivery methods for anti VEGF Tx o Anti PDGF: Fovista o Combination Tx: VEGF/PDGF Injections Potential oral combination on the horizon How may this affect the practice of optometry Eye Drops to treat wet AMD: o Pazopanib Eye Drops A Randomised Trial in Neovascular Age-related Macular Degeneration Genetics and AMD: o Is AMD in our DNA? o Genetic testing: Macular Risk RetnaGene o To test or not to test? o Genetic therapy Genzyme gene therapy for AMD Future of genetic Tx Stem Cell therapy o What is stem cell therapy o Where we are and where we are headed with AMD and stem cell therapy How to get reimbursed for your AMD patients o ICD-9 for insured patients What to tell your patients about: o AMD and aspirin To use or not to use o AMD and homocysteine level Association of Homocysteine levels to AMD progression o Blue light and link to AMD FDA approved Implantable miniature telescope for end stage AMD When is it used How is it used How does it work 20 of 46

21 Who can benefit from this device Final thoughts on the care and education of your AMD patient When recommending treatment consider the patient s: o Age o Level of activity o Transportation issues o General health o Visual goals 21 of 46

22 THE EFFECTS OF SMOKING ON THE EYE LEARNING OBJECTIVES Be able to describe the most common ocular effects of smoking Be able to discuss management options for the most common ocular conditions found in smokers Be able to provide a list of resources for patients interested in quitting Be able to discuss the most common smoking cessation strategies with patients Ryan Bulson, O.D., M.S., F.A.A.O. Ryan.Bulson@pacificu.edu THE PROBLEM THE PROBLEM Tobacco smoke is known to have 4,000 active compounds, including 40 known chemical carcinogen Cigarette smoking is the primary preventable cause of disease, disability, and premature death in the United States According to the CDC, ~20% of Americans are smokers ~15% of Canadians over age 15 are smokers Nearly 70% of smokers report a desire to quit Kennedy et al (2014) Survey sent to 4528 optometrists in Canada regarding their knowledge and practices for patients who smoke 98% believed that smoking cigarettes was a risk factor for AMD, however, knowledge levels of associations were lower for other eye diseases Only 55% assessed the smoking status of patients during their initial visit 33% reported that they always or regularly assess their patients interest in quitting smoking. 7% reported that they discussed the benefits of tobacco use prevention with patients younger than 19 years 22 of 46 1

23 WHY ARE WE NOT EDUCATING PATIENTS ON THE EFFECTS OF SMOKING? WHY YOU ARE HERE! 90% were interested in a continuing education program about the impact of smoking on vision and eye health as well as strategies for discussing tobacco cessation and prevention Study Conclusion: Opportunities for continuing education around cessation--including training specifically for optometrists--need to continue to increase. SMOKING AND THE EYE Toxic effects of smoking related to Cell damage from free radicals Decrease blood flow to ocular vasculature Increased formation of clots with ocular vasculature THE DOCTOR S REPORT 0&feature=related CORNEA AND TEAR FILM Very thin (~0.5mm) transparent front surface layer of the eye Responsible for ~2/3 of the eye s refractive power No vasculature Receives oxygen passively from environment Receives nutrition/waste removal via aqueous humor One of the body s most densely innervated tissues Tear film coats the most anterior layer of the cornea (epithelium) and maintains moisture Lipid layer (prevent evaporation) Aqueous layer (maintain moisture) Mucin layer (adherence to the cornea) SMOKING AND THE CORNEA/TEAR FILM Increases risk of dry eye syndrome Symptoms include: Burning Itching Redness Tearing Foreign body sensation Intermittent blurred vision Second hand smoke increases dry eyes in children Mechanism: free radicals and other pro-oxidants in smoke/tar cause lipid peroxidation (break down of lipid layer) and alteration of tear proteins Results in a reduced tear break up time 23 of 46 2

24 SMOKING AND THE CORNEA/TEAR FILM Treatment: Eliminate offending agent Lubrication (artificial tears, ophthalmic ointments) Restasis Punctal occlusion Omega-3s Mechanism Anti-inflammatory? Enhancement of lipid layer of tear film? How much? No FDA recommendation (1g-6g/day) EXTRAOCULAR MUSCLES Six muscles responsible for movement and alignment of the eyes EXTRAOCULAR MUSCLES Cigarette smoking is a risk factor for Graves disease Development Progression Severity (increased risk of diplopia and exophthalmos) Poorer outcomes with immunosuppressive therapies in the active phase Increases risk of progression following radiotherapy The relationship between smoking and effect may be dose dependent EXTRAOCULAR MUSCLES Graves Disease Signs/Symptoms Ocular irritation, redness, tearing, photophobia Diplopia Stare due to lid retraction Exophthalmos EOM restriction Dry eyes/exposure keratopathy Lagophthalmos Elevated IOP Compressive optic neuropathy (~5%) Management Copious lubrication, nocturnal lid taping Systemic steroids, radiotherapy, surgery CONJUNCTIVA AND SCLERA Conjunctiva is the thin cellophane-like layer that lines the sclera and inner eyelids Responsible for maintaining moisture of the ocular surface Sclera is the white/opaque, fibrous, layer of the eye located directly posterior to the conjunctiva Primary role is protective in nature Smoking increases the risk of conjunctivitis Bacterial Viral Allergic CONJUNCTIVA AND SCLERA Conjunctivitis symptoms: Pink eye (cosmesis) Burning Itching Redness Tearing Foreign body sensation Swollen eyelids Increased sensitivity to light 24 of 46 3

25 CONJUNCTIVA AND SCLERA Mechanism: toxins and irritants in smoke causes allergic response that results in inflammation Higher amount of squamous metaplasia in the conjunctival epithelium Reduction or absence of conjunctival growth factors Treatment: Eliminate offending agent Lubrication ANTERIOR CHAMBER Space between cornea and iris that houses aqueous Plays a nutritional role with posterior cornea, trabecular meshwork, lens, and anterior vitreous Maintains intraocular pressure Smoking doubles the risk for infectious and inflammatory uveitis Symptoms Eye pain Redness Photophobia Tearing ANTERIOR CHAMBER Mechanism: pro-inflammatory components of tobacco smoke cause vascular inflammation (via hydrogen peroxide and upregulation of cytokines), which promotes organism entry to intraocular tissue Tobacco smoke may also enhance the response of inflammatory cells to the microorganism Treatment Topical steroids Topical cycloplegic Systemic work up as indicated LENS Crystalline lens is a transparent refractive medium that provides ~1/3 of the eye s power In young patients (<45), changes shape to change focus (accommodation) Cloudiness of the lens is called a cataract LENS Cataract symptoms Blurred vision (distance and near) Difficulty night driving (pupil dilates) Glare/haloes around lights Poor glare recovery (oncoming headlights) Mechanism: Systemic absorptions of smoke constituents produces oxidative stress Accumulation of metals such as Cd and Fe and the reduction in levels of vitamin C in the lens and blood LENS Treatment: Eliminate offending agent Cataract surgery Vitamins/Supplements are inconclusive 25 of 46 4

26 OPTIC NERVE Responsible for conduction of sensory signal from the retina to the visual cortex Cranial nerve II Blind spot OPTIC NERVE Smoking has been associated with increased risk of Optic neuritis Poor recovery than non-smokers (more R/G color defects) May speed progression and/or increase relapses Ischemic optic neuropathy Toxic optic neuropathy OPTIC NERVE Symptoms of optic neuritis/neuropathy Blurred vision (minor profound) Visual field defect Pupillary abnormality Color deficiency Pain (in acute inflammatory phase) Treatment of optic neuritis/neuropathy Remove offending agent IV/Oral steroids in acute inflammatory phase Speeds resolution but does not improve outcome Low vision rehabilitation OPTIC NERVE Glaucoma is a bilateral, progressive death of the optic nerve 2 nd leading causes of blindness worldwide Affects 2-3 million in the US; ~10% of blindness in the US Exact pathogenesis is unclear Treatment involves controlling the disease there is no cure Smoking increases the risk and progression of glaucoma and worsens surgical outcomes OPTIC NERVE Mechanisms Smoking produces ischemia and oxidative stress Smoking increases risk of vascular disease and glaucoma likely has an underlying vascular perfusion component Toxic substances that increase in free radicals and decrease in antioxidants Mitochondrial dysfunction Treatment Remove offending agent Reduce intraocular pressure Topical medication Surgery RETINA Sensory portion of the eye Contains rod and cone photoreceptors Transmits visual sensory information to the brain via optic nerve 26 of 46 5

27 RETINA Smoking is associated with increased risk of Diabetic retinopathy (DR) and Diabetic Macular Edema (DME) Age related macular degeneration (ARMD/AMD) RETINA Diabetic retinopathy and diabetic macular edema Leading cause of blindness in people <65 10% of world will be diabetic by 2035; 11% of US DME is the most frequent cause of severe vision impairment in diabetic patients Vision loss is secondary to the accumulation fluid within the macula (most sensitive part of vision) Treatment Glycemic control Laser Photocoagulation Anti-VegF injection RETINA Age related macular degeneration Affects ~10 million in US Accounts for 50% of severe and irreversible vision loss in the US, particularly those >65 Expected to rise to nearly ~20 million by 2050 Population attributable risk percent for smoking and AMD is 13.8% Dry AMD Wet AMD RETINA Mechanism: Oxidative damage to retinal pigment epithelial cells Depression of serum antioxidant levels Alterations of choroidal blood flow and of retinal pigment epithelium drug detoxification pathways Decrease luteal pigments to increase, increasing damage to the macula by light and oxidative damage, RETINA Treatment: Early Dry AMD-No treatment Intermediate/Late Dry AMD-AREDS formula vitamins 500mg Vitamin C 400mg Vitamin E 15mg Beta carotene* 80mg Zinc 2mg Copper Reduces risk of progression to advanced (exudative/wet) by 25% in patients with intermediate/late dry AMD Wet AMD-Anti-VegF (Lucentis/Avastin) injections REFRACTIVE CONSIDERATIONS Smoking does not appear to influence refractive error of smokers, but can second hand smoke influence children s refractive error? Study of ~4000 children age 1-6 years (STARS) Inverse relationship between child myopia and H/o maternal smoking Smoking during child s life Smoking during pregnancy H/o paternal smoking Previous study of older children (mean 8.7)in the US found similar inverse relationship Mechanism: nicotinic acetylcholine receptors? 27 of 46 6

28 MARIJUANA 23 States and DC have legalized medical use of marijuana 2 States have legal recreational marijuana THC is the primary compound marijuana s neurogenic and psychotropic effects Stimulate specific dopamine receptors in the central nervous system, resulting in an induced state of euphoria or relaxation Kabat and Sowka MARIJUANA Initial studies in the 1970s (Hepler and Frank) showed IOP lowering effect peaking at minutes and lasting only 3-4 hours Prostaglandin analog may have IOP lowering effect 80+ hours Side effects Conjunctival hyperemia Diminished tear production (leading to dry eye) Pupillary mydriasis Alteration of blood pressure Cardiac arrhythmias Psychogenic effects: disruption of short-term memory, cognitive impairment, a sense of time distortion, reduced motor coordination and sleepiness MARIJUANA Mariol-synthetic version of THC available by Rx in 2.5mg, 5mg or 10mg capsules Topical routes are challenging due to the hydrophobic/ lipophilic nature of cannabinoids, which make them insoluble in water. Canasol-topical glaucoma medication marketed in Jamaica MARIJUANA Position from American Academy of Ophthalmology: Based on analysis by the National Eye Institute and the Institute of Medicine, the Academy finds no scientific evidence that marijuana is an effective long-term treatment for glaucoma, particularly when compared to the wide variety of prescription medication and surgical treatments available. SMOKING CESSATION Nearly 70% of smokers report a desire to quit, but many lack access to resources to help Physician involvement greatly increases success rates, but physicians are not being as effective as they could be in helping patients quit Long term abstinence alone: 7% Long term abstinence with help of physician: 30% Less than 3 minutes of counseling by health care providers has been shown to increase quit rates by 30% (US DHS) Ophthalmologists are more likely to counsel on smoking cessation than Optometrists (Lawrenson, 2013) SMOKING CESSATION BY EYE CARE PROVIDERS Caban-Martinez et al Cessation counseling for patients with AMD Most patients who smoke reported never being advised to quit smoking Most eye care providers reported that they had advised smokers to quit. Two-thirds of providers expressed a desire for additional training and resources to support patient quit attempts, indicating the need for the integration of smoking cessation opportunities in the clinic setting. 28 of 46 7

29 SMOKING CESSATION BY PCPS (AAMC) All physicians surveyed believe it is their role to help patients quit smoking. 86% ask patients who smoke about their smoking status and advise them to stop 13% usually refer smokers to others for appropriate treatment 17% arrange for follow-up visits to address smoking. Five factors cited most often by physicians as significant barriers to successful intervention: (1) lack of patient motivation (63%) (2) limited coverage for interventions (54%) (3) limited reimbursement for a physician s time (52%) (4) time with patients is limited (41%) (5) too few available cessation programs (39%) SMOKING CESSATION OPTIONS According to PCPs, highly effective interventions include Bupropion with nicotine replacement (29%) Nicotine replacement with counseling (21%) Family support (19%) Evidence based studies have suggested these interventions have success rates (long term abstinence) up to 38% NICOTINE REPLACEMENT Designed to wean the body off cigarettes Supply nicotine in controlled amounts without chemicals found in cigarettes OTC nicotine replacement products include Skin patches-transdermal nicotine patches brand names Habitrol and Nicoderm Chewing gum Brand name Nicorette Lozenges Brand name Commit Rx only product Nasal spray or inhaler E-cigarettes-controversial NON-NICOTINE MEDICAL THERAPY Chantix (varenicline tartrate) Acts at sites in the brain affected by nicotine. It provides some nicotine effects to ease withdrawal symptoms and blocks the effects of nicotine from cigarettes if users resume smoking. Side effects include Nausea Constipation Gas Vomiting Trouble sleeping Vivid, unusual, or strange dreams. Changes in behavior, depressed mood, hostility, and suicidal thoughts NON-NICOTINE MEDICAL THERAPY Zyban (buproprion) Aids in cessation; precise mechanism unknown Same active ingredient as the antidepressant Wellbutrin Side effects include Insomnia Dry mouth Changes in behavior, depressed mood, hostility, and suicidal thoughts COUNSELING & FAMILY SUPPORT Mentoring programs and smoking counselors Support groups Helplines Smokefree Text Encouragement, tips, and advice via text Apps QuitSTART-free-tracks cravings and moods, monitors and milestones, identifies smoking triggers, personalized "pick me ups" for challenging times to QuitPal-not yet available-integrates calendar to set date goals, tracks monetary savings and financial goals, personalized messages from loved ones, social networking QuitGuide-designed to help prepare quitting and provides support in the days and weeks after quitting via information and social networking 29 of 46 8

30 ONLINE RESOURCES ONLINE RESOURCES Government Resources National Quit line: QUITNOW SmokeFree.gov National Cancer Institute Telephone Hotline: U-QUIT ( ) National Institutes of Health Smoking Cessation Health Resources and Services Administration QUITNOW Centers for Disease Control and Prevention Agency for Healthcare Research and Quality Womenshealth.gov Healthfinder Tobacco Resources Page MedlinePlus Tobacco/Smoking Outside Organizations American Lung Association Cessation_Support.htm Telephone Hotline: 800-LUNG-USA ( ) American Cancer Society to_quitting_smoking.asp Telephone Hotline: 800-ACS-2345 ( ) American Heart Association Become an Ex (project of the National Alliance for Tobacco Cessation) American Legacy Foundation Telephone Hotline: START ( ) [for pregnant smokers] Campaign for Tobacco Free Kids American Association for Respiratory Care CONCLUSIONS AND THE GOOD NEWS! Smoking increases the risk for a variety of ocular conditions These ocular conditions range from nuisances to sight threatening BUT, studies suggest there is a dose dependent relationship between tobacco and tobacco use related eye diseases THEREFORE: risk of tobacco use related eye disease will likely decrease substantially after smoking cessation We play a valuable role in providing resources to assist patients in quitting Please complete your session evaluation using EyeMAP online at Tweet about this session using the official meeting hashtag #aaoptom14 REFERENCES Age-Related Eye Disease Study 2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA May 15;309(19): Asensio-Sánchez VM, Gómez-Ramírez V, Morales-Gómez I, Rodríguez-Vaca I. Clinically significant diabetic macular edema: systemic risk factors. Arch Soc Esp Oftalmol Mar;83(3): Caban-Martinez AJ, Davila EP, Lam BL, Dubovy SR, McCollister KE, Fleming LE, Zheng DD, Lee DJ. Age-related macular degeneration and smoking cessation advice by eye care providers: a pilot study. Prev Chronic Dis Nov;8(6):A147. Krishnaiah S, Vilas K, Shamanna BR, Rao GN, Thomas R, Balasubramanian D. Smoking and its association with cataract: results of the Andhra Pradesh eye disease study from India. Invest Ophthalmol Vis Sci Jan;46(1): Iyer JV, Low WC, Dirani M, Saw SM. Parental smoking and childhood refractive error: the STARS study. Eye (Lond) Oct;26(10): Lawrenson JG, Evans JR. Advice about diet and smoking for people with or at risk of age-related macular degeneration: a crosssectional survey of eye care professionals in the UK. BMC Public Health 2013;13:564. Lin P, Loh AR, Margolis TP, Acharya NR. Cigarette smoking as a risk factor for uveitis. Ophthalmology 2010;117: Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106: Physician behavior and practice patterns related to smoking cessation summary report. Washington (DC): American Association of Medical Colleges; May Timothy CO, Nneli RO. The effects of cigarette smoking onintraocular pressure and arterial blood pressure ofnormotensive young Nigerian male adults. Niger J PhysiolSci 2007; 22:31 35 US Department of Health and Human Services. Agency for Healthcare Research and Quality. Clinical Care Guideline. Treating Tobacco Use and Dependence: 2008 Update. Available at: tobacco/clinicians/update/treating_tobacco_use08.pdf. Vingerling JR, Hofman A, Grobbee DE, de Jong PT. Age-related macular degeneration and smoking. The Rotterdam Study. Arch Ophthalmol Oct;114(10): of 46 9

31 8/29/ Grand Rounds Ryan Bulson, O.D., M.S., F.A.A.O. Ryan.Bulson@pacificu.edu Dina Erickson, O.D., F.A.A.O. derickson@pacificu.edu Pacific University College of Optometry Case #1 27 yo Caucasian female CC: Possible visual field defect detected on confrontation testing Unaware of defects in daily life Denied neurological symptoms Ocular History: Unremarkable ROS: Unremarkable Medication: None Family Ocular History: Glaucoma (maternal aunt) Case #1 Uncorrected distance visual acuity OD 20/15 OS 20/15 PERRL (-)APD Motilities full and comitant without pain/diplopia Confrontation fields Superior nasal constriction OD and OS Refraction: DS OU Anterior Segment: Unremarkable GAT (@2:32pm): 24mmHg OD/OS Posterior Segment: Follow up 1 week later No changes in vision, no new visual/ocular/neurological complaints Uncorrected distance acuity 20/15 OD/OS Motilities full and comitant PERRL (-)APD Ishihara Color Testing 10/10 plates correct OD/OS 1:29pm: 22/23 mmhg Pachymetry: 586/581 microns Gonioscopy: flat approach, open to CB 360 OU, tr pigment of 46 1

32 8/29/ Follow up over ~ 3 years No new ocular/visual/neurological complaints No treatment has been elected Uncorrected visual acuity OD 20/15 OS 20/15 Tmax 25/25, range: Optic Nerve Head Drusen Congenital, acellular, calcific bodies commonly often found bilaterally and associated with small, crowded optic nerves It is believed that the formation of ONHD is associated with axonal transport alteration and degeneration. The prevalence of ONHD in the general population has been estimated at approximately 0.4%; however, histological studies have reported prevalence as high as 2.4% Optic Nerve Head Drusen In young patients, drusen typically buried With age, buried drusen enlarge due to calcium apposition and extend anteriorly As the drusen expand, the nerve fiber layer is disrupted, resulting in visual field loss in 24-87% of adults (Auw-Haedrich et al) Central visual acuity is generally spared, and thus this condition is often asymptomatic Pseudopapilledema Critical to differentiate pseudopapilledema from drusen from true optic nerve edema Blurring of disc margins Obscuration of retinal vessels Peripapillary hemorrhages Retinal/choroidal folds 32 of

33 8/29/ B-scan continues to be the gold standard for detecting drusen OCT (and AF) gaining popularity Optic Nerve Edema or Optic Nerve Drusen? Lee et al Treatment No universally accepted treatment protocol Contrasting views on whether nerve fiber layer loss occurs more rapidly in presence of ocular hypertension (Moussalli et al, Grippo et al) Some evidence that treatment with topical alpha-2 adrenergic agonist brimonidine may provide neuroprotection in addition to it s anti-hypertensive effect Brimonidine Believed to upregulate intrinsic cell survival signaling pathways, as well as antiapoptotic genes. In rat models, has been shown to reduce levels of intravitreal glutamate associated with optic nerve degeneration secondary to ischemia. Elevates neurotrophic factors important in preserving retinal ganglion cells after insult. Brimonidine In laboratory studies, has demonstrated three out of four criteria required to demonstrate neuroprotective effects Receptors on target tissue Adequate penetration to the retina Induction of intracellular changes that enhance neuronal resistance to insult in animals studies To date, has yet to satisfy the fourth criterion: demonstrated efficacy in human clinical trials. Pregnancy and Glaucoma Conventional wisdom is to defer treatment during pregnancy There is a statistically significant drop in IOP during pregnancy (from 1 st to 3 rd trimester) (Dinh; Marris) Mechanisms? Increase in outflow facility of 46 3

34 8/29/ Decrease in episcleral venous pressure Development of a mild metabolic acidosis Pregnancy Categories-Glaucoma Category B: Brimonidine Category C: Beta blockers, prostaglandin analogues, CAIs, cholinergics, apraclonidine Pregnancy Categories Category A: Studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters). Category B: Animal studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women. Category C: Animal studies have shown an adverse effect on the fetus and there are no studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks. Category D: There is positive evidence of human fetal risk based on human studies, but potential benefits may warrant use of the drug in pregnant women despite potential risks. Category X: Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based human studies, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits Case #2 16yo HF CC: blurred distance vision x 1-2 months Established patient, LEE 2 years ago: unremarkable ROS: unremarkable Medication: None Ocular history: unremarkable Family ocular history: unremarkable Case #2 Uncorrected distance visual acuity OD 20/150 PH 20/50 OS 20/200 PH 20/50 PERRL (-)APD Motilities full and comitant without pain/diplopia Confrontation fields: Generalized constriction OD/OS Refraction: OD: DS 20/50 OS: x005 20/50 Anterior Segment: Unremarkable GAT (@2:55pm): 12 mmhg OD/OS Posterior Segment: of 46 4

35 8/29/ Follow up 1 week later No new visual/neurological complaints Uncorrected distance visual acuity OD 20/150 PH 20/50 OS 20/200 PH 20/50 PERRL (-)APD Motilities full and comitant without pain/diplopia Color Vision: OD/OS: test plate correct, 7/11 correct Blood Pressure: 104/ Ordered labs, f/u 1-2 weeks CBC Serum levels of B1 (thiamine), B9 (folate), B12 (cobalamin) If normal, may consider FTA-ABS/VDRL Heavy metal screen (e.g. Lead) MRI Follow up Patient placed on liquid multivitamin supplement Follow up 1 month 1 month follow up Vision improving, feeling better and has more energy Corrected distance visual acuity OD 20/20- OS 20/20- Color vision: 17/17 OD/OS Common Causes of Anemia Common Causes of Vision Loss in Teenagers Anemia 35 of 46 5

36 49 8/29/ Condition in which the body does not possess enough healthy red blood cells Various classification types Morphological-Based on size (mean corpuscular volume) Microcytic-MCV <80 fl Macrocytic-MCV >100 fl Pathogenic-Based on etiology Anemia Adolescent females are 10 times more likely to develop anemia than adolescent boys (CDC) Mexican heritage and poor socioeconomic status have been shown to increase risk for developing the condition While anemia is a rare cause of vision loss, it can produce optic nerve ischemia, particularly in the setting of hypotension. Ischemic optic neuropathies related to anemia have been reported in cases of repeated gastrointestinal bleeding, trauma involving excessive blood loss, spinal and cardiac bypass surgeries, nasal/sinus surgery, and spontaneous abortion. Iron deficiency anemia has been associated with other optic neuropathies, including NAION and papilledema Case #3 9 yo HF Previous Records: Subjective: OD: x180 OS: -0.50sph BCVA OD/OS/OU: 20/60 SLE/DFE: unremarkable A/P: New spectacle Rx given, RTO 1 month. F/U visit 1 month later: No change in vision-bcva remains 20/60. Ishihara: (?)Red-Green and Blue-Yellow Deficiencies A/P: Reduced BCVA/color. Refer to University Case #3 9 yo HF Case Hx (per parents): Difficulty localizing objects Excessive sensitivity to sunlight. Avoids outdoor activities. Difficulty functioning at night All visual difficulties began around age 5 Mild speech impairment and learning disability Mildly overweight Normal pregnancy and birth. (+) Polydactyl 36 of 46 6

37 8/29/ No FHx of any visual/ocular conditions Patient K.H. Corrected Distance Visual Acuity OD/OS/OU: 20/60 PH:NI Motilities full and comitant PERRL (-)APD Refraction: OD: x180 OS: -0.50sph 20/60 OD/OS/OU Ishihara: Test plate correct, all others missed Anterior segment: unremarkable GAT: 10:30am Posterior Segment: Mom Mom Dad Dad K.H. Dad GDX Patient K.H. Summary of relevant findings: Reduced BCVA (20/60) Reduced color vision h/o excessive sunlight sensitivity and difficulty functioning at night, polydactyl, LD, overweight Clinically excessive retinal sheen confirmed by thickened RNFL, possible arteriolar attenuation Absence of PIL centrally and peripherally Patient K.H. 37 of 46 7

38 8/29/ A/P Presumed Early Cone-Rod dystrophy. Educated on condition, potential for future progression of vision loss/visual impairment, sunglasses whenever outside. Parents encouraged to pursue educational services in school. Defer ERG at this time Do We Need an ERG? Microstructural retinal changes are commonly observed in patients with inherited retinal dystrophies using high definition OCT. (Gerth et al). Absence or interruption of the photoreceptor integrity line, as seen in inherited retinal dystrophies, is associated with reduced visual function. High resolution OCT images can be used to predict visual function through the presence, size, and integrity of the photoreceptor integrity line (Aizawa et al). Patient K.H. Summary of relevant findings: Reduced BCVA (20/60) Reduced color vision h/o excessive sunlight sensitivity and difficulty functioning at night, polydactyl, LD, overweight Clinically excessive retinal sheen confirmed by thickened RNFL, possible arteriolar attenuation Absence of junction centrally and peripherally Patient K.H. Is there more to this case than a cone-rod dystrophy? Laurence-Moon-Bardet-Biedl Syndrome Primary Features Rod-Cone Dystrophy Polydactyly Obesity Learning Disabilities Hypogonadism in Males of 46 8