continuing education certification tulalip continuing education … · 2017-10-18 · continuing...

CONTINUING EDUCATION CERTIFICATION Tulalip Continuing Education

September 14, 2014 Tulalip Resort & Casino COPE EVENT #107876

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L Ryan Bulson, OD, MS Diabetic Retinopathy: An Evidence Based Approach (1 hr)

42551 SD

VERIFICATION STAMP

Dina Erickson, OD AMD Updates (2 Hrs)

42624 PS

VERIFICATION STAMP

Ryan Bulson, OD, MS The Effects of Smoking and the Eye (1 hr)

41520 PB

VERIFICATION STAMP

Ryan Bulson & Dina Erickson Grand Rounds (2 Hrs)

42625 PS

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.

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College of Optometry 2043 College Way Forest Grove, Oregon 97116 503-352-2202

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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 4th year optometry students.

Dina Erickson, OD Dr. Erickson has served as an adjunct faculty member since 1998 and assistant professor since 2004. 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 7th Annual Research Conference, Pacific University - 12 HOURS of Continuing Education January 10, 2015 Glaucoma Symposium, Willows Lodge, Woodinville, Washington 7 HOURS of Continuing Education. Information: [email protected] January 25 – 31, 2015 2015 Island Eyes Conference, Hilton Waikoloa Village, Hawaii Up to 29 HOURS of OD Continuing Education and 9 HOURS of Paraoptometric Education April 24 & 25, 2015 Coeur d’Alene CE, Coeur d’Alene Resort, Idaho - 10 HOURS of Continuing Education July 16 – 19, 2015 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 http://www.pacificu.edu/current-graduate-professional/academics/areas-study/optometry

Our new mobile app will be introduced soon

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http://www.pacificu.edu/sites/default/files/documents/2014%20BroxDraft7b.pdf

http://www.pacificu.edu/sites/default/files/documents/IslandEyes2015_Brochure_OPT_140806B_0.pdf

http://www.pacificu.edu/current-graduate-professional/academics/areas-study/optometry

http://www.pacificu.edu/current-graduate-professional/academics/areas-study/optometry

8/25/2014

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Diabetic Retinopathy: An Evidence Based

Approach Ryan Bulson, O.D., M.S., F.A.A.O.

[email protected]

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 2008. This number is expected to grow to 429 million by 2030.

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 140-199 mg/dl

• Impaired fasting glucose • Fasting glucose 100-125mg/dl

• Glycosolated Hemoglobin (A1C) • Measuring percentage of blood glucose attached to hemoglobin

• Average blood glucose level for the previous 2-3 months

• 5.7-6.4% is considered pre-diabetes

•

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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


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


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


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 2nd or 3rd 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 10-20 years


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/m2

• 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

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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


• 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 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

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• Image from Bresnick and Cuadros; EyePacs • Image from Bresnick and Cuadros; EyePacs

• Image from Bresnick and Cuadros; EyePacs • Image from Bresnick and Cuadros; EyePacs

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• 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

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• 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.

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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

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Image from Bresnick and Cuadros; EyePacs Image from Bresnick and Cuadros; EyePacs

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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.

• http://www.aoa.org/Documents/EBO/EyeCareOfThePatientWithDiabetesMellitus%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.”

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

Case 1

• 40yo White Male

• Type 2 DM

• x 10 years

• Meds: none, diet controlled

• HbA1C: 7.2%

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http://www.aoa.org/Documents/EBO/EyeCareOfThePatientWithDiabetesMellitus CPG3.pdf



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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.”

Case 2

• 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 16/16 @ 3:15pm

• DFE

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• 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.”

Case 3

• 21yo White Male

• Type 1 DM

• x 16 years

• Meds: insulin

• HbA1C: 10.2%


• OD 20/20 OS 20/20



• GAT 17/18 @ 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

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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”

Case 4

• 65yo Hispanic Male

• Type 2 DM

• x 20 years

• Meds: orals

• HbA1C: 10.8%


• OD 20/20 OS 20/20



• GAT 15/16 @ 11:15am

• DFE


• 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

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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.”

Case 5

70yo White Male

• Type 2 DM

• x 40 years

• Meds: insulin and orals

• HbA1C: 12.1%


• OD 20/30 OS 20/40


• Anterior segment: grade 1 NSC OU

• GAT 18/19 @ 12:45pm

• DFE


• 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 “4-2-1” 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

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• 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. 20/4020/80)

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%

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• 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

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.”

Conclusions

• 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 http://www.aoa.org/Documents/EBO/EyeCareOfThePatientWithDiabetesMellitus%20CPG3.pdf

Thank You and Questions?

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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

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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

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• 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

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8/25/2014

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THE EFFECTS OF SMOKING ON

THE EYE

Ryan Bulson, O.D., M.S., F.A.A.O.

[email protected]

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

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

THE PROBLEM

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

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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

http://www.youtube.com/watch?v=X0tWONdhyO

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

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http://www.youtube.com/watch?v=X0tWONdhyO0&feature=related



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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


Conjunctivitis symptoms:

“Pink eye” (cosmesis)

Burning

Itching

Redness

Tearing

Foreign body sensation

Swollen eyelids

Increased sensitivity to light

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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:


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:


Cataract surgery

Vitamins/Supplements are inconclusive

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OPTIC NERVE

Responsible for conduction of sensory signal from

the retina to the visual cortex

Cranial nerve II

“Blind spot”

http://drugster.info/ail/pathography/2765/

http://drugster.info/ail/pathography/2765/

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 (minorprofound)

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

2nd 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

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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?

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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 60-90 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.

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8

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

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ONLINE RESOURCES

Government Resources

National Quit line: 1-800-QUITNOW

SmokeFree.gov http://www.smokefree.gov

National Cancer Institute http://www.cancer.gov/cancertopics/factsheet/Tobacco/cessation Telephone Hotline: 1-877-44U-QUIT (448-7848)

National Institutes of Health Smoking Cessation http://health.nih.gov/topic/SmokingCessation

Health Resources and Services Administration http://www.hrsa.gov/stopsmoking/

1-800-QUITNOW http://1800quitnow.cancer.gov/

Centers for Disease Control and Prevention http://www.cdc.gov/tobacco/quit_smoking/how_to_quit/index.htm

Agency for Healthcare Research and Quality http://www.ahrq.gov/consumer/tobacco/lowlit.htm

Womenshealth.gov http://www.womenshealth.gov/quit-smoking/

Healthfinder Tobacco Resources Page http://healthfinder.gov/scripts/SearchContext.asp?topic=860

MedlinePlus Tobacco/Smoking http://www.nlm.nih.gov/medlineplus/smoking.html

ONLINE RESOURCES

Outside Organizations

American Lung Association http://www.lungusa.org/site/c.dvLUK9O0E/b.22931/k.8550/Smoking_Cessation_Support.htm Telephone Hotline: 800-LUNG-USA (586-4872)

American Cancer Society http://www.cancer.org/docroot/subsite/greatamericans/content/Guide_to_Quitting_Smoking.asp Telephone Hotline: 800-ACS-2345 (228-2345)

American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=3048036

Become an Ex (project of the National Alliance for Tobacco Cessation) http://www.becomeanex.org/

American Legacy Foundation http://women.americanlegacy.org/quit/index.cfm Telephone Hotline: 866-66-START (667-8278) [for pregnant smokers]

Campaign for Tobacco Free Kids http://www.tobaccofreekids.org/index.php

American Association for Respiratory Care http://www.aarc.org/resources/tobacco/index.asp

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

http://eyemap.cistems.net

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. 2013 May 15;309(19):2005-15.

Asensio-Sánchez VM, Gómez-Ramírez V, Morales-Gómez I, Rodríguez-Vaca I. Clinically significant diabetic macular edema: systemic risk factors. Arch Soc Esp Oftalmol. 2008 Mar;83(3):173-6.

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. 2011 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. 2005 Jan;46(1):58-65.

Iyer JV, Low WC, Dirani M, Saw SM. Parental smoking and childhood refractive error: the STARS study. Eye (Lond). 2012 Oct;26(10):1324-8

Lawrenson JG, Evans JR. Advice about diet and smoking for people with or at risk of age-related macular degeneration: a cross-sectional 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;117:585-90.

Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106:336-56.

Physician behavior and practice patterns related to smoking cessation summary report. Washington (DC): American Association of Medical Colleges; May 2007. http://www.aamc.org/workforce/smoking-cessation-summary.pdf.

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: http://www.ahrq.gov/professionals/clinicians-providers/guidelines-recommendations/ 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. 1996 Oct;114(10):1193-6.

30 of 46

http://www.smokefree.gov/

http://www.cancer.gov/cancertopics/factsheet/Tobacco/cessation

http://health.nih.gov/topic/SmokingCessation

http://www.hrsa.gov/stopsmoking/

http://1800quitnow.cancer.gov/

http://www.cdc.gov/tobacco/quit_smoking/how_to_quit/index.htm

http://www.ahrq.gov/consumer/tobacco/lowlit.htm

http://www.womenshealth.gov/quit-smoking/



http://healthfinder.gov/scripts/SearchContext.asp?topic=860

http://www.nlm.nih.gov/medlineplus/smoking.html

http://www.nlm.nih.gov/medlineplus/smoking.html

http://www.lungusa.org/site/c.dvLUK9O0E/b.22931/k.8550/Smoking_Cessation_Support.htm

http://www.lungusa.org/site/c.dvLUK9O0E/b.22931/k.8550/Smoking_Cessation_Support.htm

http://www.cancer.org/docroot/subsite/greatamericans/content/Guide_to_Quitting_Smoking.asp

http://www.cancer.org/docroot/subsite/greatamericans/content/Guide_to_Quitting_Smoking.asp

http://www.americanheart.org/presenter.jhtml?identifier=3048036

http://www.becomeanex.org/

http://women.americanlegacy.org/quit/index.cfm

http://www.tobaccofreekids.org/index.php

http://www.aarc.org/resources/tobacco/index.asp

8/29/2014

1

Grand Rounds

Ryan Bulson, O.D., M.S., [email protected]

Dina Erickson, O.D., [email protected]

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 lifeDenied neurological symptoms

Ocular History: UnremarkableROS: UnremarkableMedication: NoneFamily Ocular History: Glaucoma (maternal aunt)

Case #1

Uncorrected distance visual acuityOD 20/15 OS 20/15

PERRL (-)APDMotilities full and comitant without pain/diplopiaConfrontation fieldsSuperior nasal constriction OD and OS

Refraction: +1.00 DS OUAnterior Segment: UnremarkableGAT (@2:32pm): 24mmHg OD/OSPosterior Segment:

Follow up 1 week later

No changes in vision, no new visual/ocular/neurological complaintsUncorrected distance acuity20/15 OD/OS

Motilities full and comitantPERRL (-)APD Ishihara Color Testing10/10 plates correct OD/OS

GAT @ 1:29pm: 22/23 mmHgPachymetry: 586/581 micronsGonioscopy: flat approach, open to CB 360 OU, tr pigment

http://www.westcoastretina.com/WestCoastRetina/Nov-2010.html

Follow up over ~ 3 years

No new ocular/visual/neurological complaintsNo treatment has been electedUncorrected visual acuityOD 20/15 OS 20/15

Tmax 25/25, range: 22-25

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%


In young patients, drusen typically “buried”With age, “buried” drusen enlarge due to calcium apposition and extend anteriorlyAs 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 edemaBlurring of disc marginsObscuration of retinal vesselsPeripapillary hemorrhages Retinal/choroidal folds

B-scan continues to be the gold standard for detecting drusenOCT (and AF) gaining popularity

Optic Nerve Edema or Optic Nerve Drusen?

Lee et al

Treatment

No universally accepted treatment protocolContrasting 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 effectsReceptors on target tissueAdequate penetration to the retinaInduction of intracellular changes that enhance neuronal resistance to insult in

animals studiesTo date, has yet to satisfy the fourth criterion: demonstrated efficacy in human

clinical trials.

Pregnancy and Glaucoma

Conventional wisdom is to defer treatment during pregnancyThere is a statistically significant drop in IOP during pregnancy (from 1st to 3rd

trimester) (Dinh; Marris)Mechanisms?Increase in outflow facilityDecrease in episcleral venous pressureDevelopment of a mild metabolic acidosis

Pregnancy Categories-Glaucoma

Category B: BrimonidineCategory 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 HFCC: blurred distance vision x 1-2 monthsEstablished patient, LEE 2 years ago: unremarkableROS: unremarkableMedication: NoneOcular history: unremarkableFamily ocular history: unremarkable

Case #2

Uncorrected distance visual acuityOD 20/150 PH 20/50 OS 20/200 PH 20/50

PERRL (-)APDMotilities full and comitant without pain/diplopiaConfrontation fields: Generalized constriction OD/OSRefraction: OD: -1.25 DS 20/50 OS: -1.00-0.75x005 20/50

Anterior Segment: UnremarkableGAT (@2:55pm): 12 mmHg OD/OSPosterior Segment:


No new visual/neurological complaintsUncorrected distance visual acuityOD 20/150 PH 20/50 OS 20/200 PH 20/50

PERRL (-)APDMotilities full and comitant without pain/diplopiaColor Vision: OD/OS: test plate correct, 7/11 correctBlood Pressure: 104/50

Ordered labs, f/u 1-2 weeks

CBCSerum levels of B1 (thiamine), B9 (folate), B12 (cobalamin) If normal, may considerFTA-ABS/VDRLHeavy 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 energyCorrected distance visual acuityOD 20/20- OS 20/20-

Color vision: 17/17 OD/OS

Common Causes of Anemia

Common Causes of Vision Loss in Teenagers

Anemia

Condition in which the body does not possess enough healthy red blood cellsVarious classification typesMorphological-Based on size (mean corpuscular volume)Microcytic-MCV <80 fLMacrocytic-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: +0.75-1.75x180 OS: -0.50sph

BCVA OD/OS/OU: 20/60SLE/DFE: unremarkableA/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 nightAll visual difficulties began around age 5

Mild speech impairment and learning disabilityMildly overweightNormal pregnancy and birth. (+) PolydactylNo FHx of any visual/ocular conditions

Patient K.H.

Corrected Distance Visual AcuityOD/OS/OU: 20/60 PH:NI

Motilities full and comitantPERRL (-)APDRefraction: OD: +0.75-1.75x180 OS: -0.50sph20/60 OD/OS/OU

Ishihara: Test plate correct, all others missedAnterior segment: unremarkableGAT: 12/12 @ 10:30amPosterior Segment:

Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.

Summary of relevant findings:Reduced BCVA (20/60)Reduced color visionh/o excessive sunlight sensitivity and difficulty functioning at night, polydactyl, LD,

overweightClinically excessive retinal sheen confirmed by thickened RNFL, possible arteriolar

attenuationAbsence of PIL centrally and peripherally

Patient K.H.

A/PPresumed 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.



attenuationAbsence of junction centrally and peripherally

Patient K.H.

Is there more to this case than a cone-rod dystrophy?

Laurence-Moon-Bardet-BiedlSyndrome

Primary Features

Rod-Cone DystrophyPolydactylyObesity Learning DisabilitiesHypogonadism in MalesRenal Anomalies

Secondary Features

Speech DisorderBrachydactylyDevelopmental DelayPolyuriaAtaxia

Secondary Features

Poor CoordinationDM Left Ventricle HypertrophyHepatic FibrosisSpasticity

Diagnosis

Must exhibit 4 primary characteristics or 3 primary and 2 secondary. Primary:Rod-Cone DystrophyPolydactylyObesityLearning Disabilities

Secondary:Speech DisorderDevelopmental DelayAtaxiaPoor Coordination

Treatment

The only treatment is the management of symptoms. Vision- Low Vision ServicesObesity- DieticianKidney Problems-Medication/TransplantPolydactyly- surgical removal

Demographics

Prevalence rate in North America/Europe ranges from 1:14,000 to 1:16,000 live births (Sharifian et al)

However, in some regions such as Kuwait, the rate is higher, with an estimated incidence of 1:13,500 due to a high frequency of consanguine marriages.

While this syndrome is considered rare, it is suspected that there is a major problem with its under-diagnosis

Genetics and Types

Type 1 11q13-- Most CommonType 2 16q21Type 3 3p12-- Least CommonType 4 15q22There are patients with the disease that do not have any of the genes listed above.

Case 4

53 yo WFCC: blurred distance and near vision OUOHx: glaucoma suspect x many years, h/o corneal abrasion OD age 20, h/o dry eyes FOHx: strabismus (sister), cataracts (parents)PMx: asthma (albuterol), bipolar/depression (tegretol,wellbutrin), h/o astrocytoma

right side s/p surgery, radiation, and chemotherapy (~20 years ago)

Case 4


PERRL (-)APDMotilities full and comitant without pain/diplopiaConfrontation fields?superior restriction OD/OSFDT 30-5 screener: scattered non-specific defects superior>inferior

Refraction: -0.50DS to 20/20 OD/OSAnterior Segment: UnremarkableGAT (@10:53am): 15mmHg OD/OSPosterior Segment:

A/P

Low risk normotensive glaucoma suspect Moderate physiological cupping with healthy appearance Possible superior constriction on confrontation fields OD/OS; FDT demonstrates

non-specific defects superior>inferiorOCT demonstrates thinning superior OD, no thinning OSH/o right side astrocytoma status post radiation, surgery, and chemotherapy that

may confound visual fieldNo known family history of glaucoma

Follow up 2 weeks later


PERRL (-)APDMotilities full and comitant without pain/diplopiaAnterior Segment: UnremarkableGAT (@10:44am): 17mmHg OD/OSPachymetry: 527/529Gonioscopy: flat approach, open to CB 360 OU Visual Field

Moderate risk normotensive glaucoma suspect Moderate physiological cupping with healthy appearance Suspicious glaucomatous field defects OS>ODOCT demonstrates thinning superior OD, no thinning OSH/o right side astrocytoma status post radiation, surgery, and chemotherapy that


Follow up 3-4 weeks later


PERRL (-)APDMotilities full and comitant without pain/diplopiaAnterior Segment: UnremarkableGAT (@11:21am): 16/13mmHg Visual Field

Astrocytoma

Tumor arising from star shaped astrocytes in the brainAlong with oligodendrocytes and ependymal cells, serve as glial tissue that

provides support to brainAstrocytomas are a form of glioma

More common in men than womenTend to affect cerebral hemispheres in adultsGraded on a scale from I-IVI-slow growing, non-invasive (more common in children)IV-rapid growing, infiltrative (more common in adults)

Astrocytoma

Grade I Generally non-infiltratingThe most common type is pilocytic astrocytoma, which grows slowly but can grow

largeMost common in the cerebellum, cerebrum, optic nerve pathway and brainstem. Occurs mostly in children and teenagersAccounts for 2% of all brain tumors.

Grade IIUsually infiltrative, but grows slowlyMost common in adults 20-40 years old

Grade IIIInfiltrative and grows more quickly, aka malignant astrocytoma astrocytomaMost common in adults 30-50 years oldAccounts for 4% of all brain tumors.

Grade IV Most aggressive nervous system tumor, aka glioblastomaMost common in adults 50-80Accounts for 23% of all primary brain tumors.

References

Aizawa S, Mitamura Y, Baba T, Hagiwara A, Ogata K, Yamamoto S. 2008. Correlation between visual function and photoreceptor inner/outer segment junction in patients with retinitis pigmentosa. Eye.

Auw-Haedrich C, Staubach F, Witschel H. Optic disk drusen. Surv Ophthalmol 2002; 47: 515-532.

Biousse V, Rucker JC, Vignal C, et al. Anemia and papilledema. Am J Ophthalmol2003;135(4):437-46.

Bunn HF. Approach to the anemias. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:Chap 161.

Centers for Disease Control and Prevention. Recommendations to Prevent and Control Iron Deficiency in the United States. MWR 1998; 47(No. RR-3):25

Chopra KB, Banka NH, Chandalia HB. Bilateral optic nerve infarction following acute systemic hypotension and anemia--a case report. Indian J Ophthalmol1992;40(2):66-9.

Dinn RB, Harris A, Marcus PS. Ocular changes in pregnancy. Obstet Gynecol Surv. 2003;58(2):137-144.

Frith-Terhune AL, Cogswell ME, Khan LK, Will JC, Ramakrishnan U. Iron deficiency anemia: higher prevalence in Mexican American than in non-Hispanic white females in the third National Health and Nutrition Examination Survey, 1988-1994. Am J ClinNutr. 2000 Oct;72(4):963-68

Gerth C, Zawadzki RJ, Werner JS, Héon E. 2008 Retinal morphology in patients with BBS1 and BBS10 related Bardet-Biedl Syndrome evaluated by Fourier-domain optical coherence tomography. Vision Res. 48, 392-9.

Grippo TM, Shihadeh WA, Schargus M, Gramer E, Tello C, Liebmann JM, et al. Optic nerve head drusen and visual field loss in normotensive and hypertensive eyes. J Glaucoma 2008;17:100-104.

Green J.S. et al. 1989. The cardinal manifestations of Bardet-Biedl syndrome, a form of Laurence-Moon-Biedl syndrome. NEJM. 321, 002-9.

References

Kacer B, Hattenbach LO, Horle S, et al. Central retinal vein occlusion and nonarteriticischemic optic neuropathy in 2 patients with mild iron deficiency anemia. Ophthalmologica 2001;215(2):128-31.

Kahlon N, Gandhi A, Mondal S, et al. Effect of iron deficiency anemia on audiovisual reaction time in adolescent girls. Indian Journal of Physiology & Pharmacology 2011;55(1):53-9.

Lee KM, Woo SJ, Hwang JM. Differentiation of optic nerve head drusen and optic disc edema with spectral-domain optical coherence tomography. Ophthalmol2011;118:971-977.

Maris Jr. PJG, Mandal AK, Netland PA. Medical therapy of pediatric glaucoma and glaucoma in pregnancy. Ophthalmol Clin N Am. 2005;18:461-468.

Matsuoka Y, Hayasaka S, Yamada K. Incomplete occlusion of central retinal artery in a girl with iron deficiency anemia. Ophthalmologica 1996;210(6):358-60.

Moussalli MA, Sanseau A, Ebner R. Papillary drusen and ocular hypertension. IntOphthalmol 2001;23:275-278.

Onaran Z, Tan FU, Yılmazbaş P, Onaran Y. Bilateral non-arteritic anterior ischemic optic neuropathy following second-trimester spontaneous abortion-related haemorrhage. J Clin Neurosci. 2012 Aug 13.

Sharifian M, Dadkhah-Chimeh M, Einollahi B, Nafar M, Simforoush N, Basiri A, Otukesh H. 2007 Renal transplantation in patients with Bardet-Biedl syndrome. Arch. Iran Med. 10, 339-42

Trethowan BA, Gilliland H, Popov AF, Varadarajan B, Phillips SA, McWhirter L, Ghent R. A case report and brief review of the literature on bilateral retinal infarction following cardiopulmonary bypass for coronary artery bypass grafting. J CardiothoracSurg. 2011; 21(6):154.

http://www.webmd.com/cancer/brain-cancer/astrocytomaVillegas RB, Ilsen PF. Functional vision loss: a diagnosis of exclusion. Optometry

2007;78(10):523-33.

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31 of 46

8/29/2014

2

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4

53 yo WFCC: blurred distance and near vision OUOHx: glaucoma suspect x many years, h/o corneal abrasion OD age 20, h/o dry eyesFOHx: strabismus (sister), cataracts (parents)PMx: asthma (albuterol), bipolar/depression (tegretol,wellbutrin), h/o astrocytoma


Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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32 of 46

8/29/2014

3

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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33 of 46

8/29/2014

4

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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34 of 46

8/29/2014

5

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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35 of 46

8/29/2014

6

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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36 of 46

8/29/2014

7

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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37 of 46

8/29/2014

8

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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38 of 46

8/29/2014

9

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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39 of 46

8/29/2014

10

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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40 of 46

8/29/2014

11

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4

53 yo WFCC: blurred distance and near vision OUOHx: glaucoma suspect x many years, h/o corneal abrasion OD age 20, h/o dry eyesFOHx: strabismus (sister), cataracts (parents)PMx: asthma (albuterol), bipolar/depression (tegretol,wellbutrin), h/o astrocytoma


Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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41 of 46

8/29/2014

12

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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42 of 46

8/29/2014

13

Grand Rounds




Case #1




Case #1











Tmax 25/25, range: 22-25








asymptomatic

Pseudopapilledema




Lee et al

Treatment




Brimonidine




Brimonidine



clinical trials.












Case #2


Case #2









Follow up


1 month follow up





Anemia



Anemia






Case #3






Case #3




Patient K.H.




Mom

Mom

Dad

Dad

K.H.

Dad

GDX

Patient K.H.




Patient K.H.




Do We Need an ERG?




Patient K.H.




Patient K.H.



Primary Features


Secondary Features


Secondary Features


Diagnosis



Treatment


Demographics




Genetics and Types


Case 4



Case 4




A/P












Astrocytoma




Astrocytoma






References












References











2007;78(10):523-33.

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43 of 46

Grand Round Cases Dina Erickson, OD, FAAO

Outline: Central Retinal Vein Occlusion: Case #1:

• 59 year old Caucasian male presented to the office with visual disturbances after a car accident March 2014

o Post concussion • Findings • Scheduled for a F/U in 1 month for glaucoma F/U & DFE

o Fundus findings. • What is your ddx? • Sent to PCP to for blood work up

o Blood work up results • Returned for a F/U in 1 month.

o Fundus findings o What is your Dx?

• What does the OCT show • What would you do next?

CRVO Review:

• Risk Factors o Age o Systemic

The metabolic syndrome HTN DM Hyperlipidemia HLD Atherosclerosis associated Dz Others Drug Therapy

o Severity of systemic Dz: o Socioeconomic factors

AA 58% increased risk of CRVO compared to non-Hispanic whites.

o Smoking o Ocular Risk factors:

Glaucoma Drug treatments for CME secondary to CRVO:

• What are the treatment options?

44 of 46

• Anti VEGF therapy • Studies to support the above:

o COPERNICUS 2012 Aflibercept

o GALILEO 2012 Aflibercept

o Cruise 2010 Ranibizumab

o EPSTEIN 2012 Bevacizumab

• Steroid therapy: • Studies to support the above:

o GENEVA 2010 Dexamethasone

o SCORE 2009 Triamcinolone

• How do the above two therapy options compare? • Weaknesses of the studies • What are retina specialists doing? • What may work best for the patient • Further research.

Case #2: Age Related Macular Degeneration:

• A 77 year old Caucasian male presented with the chief complaint of “ white lines in middle of road appear as “sheep jumping”.

• Case history: • Entering VAs

o Funuds exam o TD OCT o DDx

• Referral • FA & PHP • Treatment • Progression and follow ups over the past 4 years

Current AMD Treatment:

• Avastin • Lucentis

o Long term potential side effects • Eyelea

o FDA approval vs clinical experience •

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Case #3 Macular Hole: Case report:

• A 39 year old Caucasian female presented with sudden painless vision loss in her left eye.

• No improvement with refraction • Photos • OCT

Macular hole review:

• Pathophysiology • Stages of macular hole • Risk factors

o Age o Gender o Elevated plasma fibrinogen

• Impact on quality of life • Treatment options:

o Observation o Vitrectomy

Advantages Disadvantages

o Ocriplasmin: Jetrea FDA approved Oct 2012 for the Tx of VMT How it works Patient selection Simulates surgery Clinical efficacy Safety Future potential

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