Age

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The Aging Eye:
How to Keep Your Sight For Life
Nicholas J. Volpe, MD
Tarry Professor and Chairman
Department of Ophthalmology
Feinberg School of Medicine
Northwestern University
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Strategies to Preserve Your Vision
• Prevention is our most potent tool in the quest to
reduce disease (and healthcare costs)
• Choose your parents well and stop aging!!! OR
• Don’t Smoke
• Wear Glasses that are UV protective
– Safety glasses for high risk activities
• Pay Attention to Nutrition and Vitamins
• Don’t Ignore Symptoms
• Get Regular Eye Examinations
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Major Causes of Chronic Visual Loss
Preventable and Treatable
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Cataracts
Glaucoma
Macular degeneration
Diabetic retinopathy
• Other Issues
– Dry eye
– Presbyopia near vision blurring
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Protective Eye Ware
• Avoid fireworks!
• Always if you have poor vision in one eye
• High risk activities
– Racquet sports
– Sawing
– Drilling
– Sawing
– Working overhead
– Any high speed tool
– firearms
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Stop Smoking
• Clearly a risk factor for cataracts
– 3X the risk
• Clearly a risk factor for macular degeneration and its
response to treatment
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Nutrition
• Healthy tear film
• Macular degeneration
• Fruits and Green Leafy Vegetables
– Carotenoid pigments (lutein) accumulate in macula and
prevent light damage
• Omega fatty acids
• Lutein and Zeaxanthin
– Studied in AREDS 2
• Vitamins A,C, E
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Regular Check Ups
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Many diseases can be detected
Every 2-3 years from age 40-65
Every 1-2 years after age 65
More frequently with diabetes or family history of
glaucoma or macula degeneration
• Young adults, in the absence of symptoms, do not
require routine examinations
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Cataracts
• Expected if ≥ 60 years old
50% - 65 - 75 years old
70% > 75 years old
• Most common cause of
decreased vision
• Symptoms
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Loss of acuity
Difficulty with colors
Glare at night
Trouble reading small print
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Age
Steroids (PSC)
Trauma
Inflammation
Diabetes
Other drugs
Subcapsular cataract
Anterior
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Posterior
Nuclear cataract
Progression
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Exaggeration of normal nuclear
ageing change
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Increasing nuclear opacification
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Causes increasing myopia
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Initially yellow then brown
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Classification according to maturity
Immature
Hypermature
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Mature
Morgagnian
Drugs
Systemic or topical steroids
- initially posterior subcapsular
Chlorpromazine
- central, anterior capsular
granules
Other drugs
Long-acting miotics
• Amiodarone
• Busulphan
•
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Cataract Surgery
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Outpatient
Very successful > 95%
Almost all with intraocular lenses
Most common surgical procedure
in U.S.
>1.4 million/year
Most successful surgical
intervention
Complications
uncommon
sight threatening
IOL technology continues to evolve
for astigmatic correction and
presbyopia
• Newest modality is femtosecond
laser
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Cataract Prevention
• Smoking cessation
– Reduces Vitamin C in the eye
– Vitamin C levels are high in the eye and this helps
remove prooxidants
• Fruits and vegetables
– 5 fold decrease at 3-4 servings per day
• Regular alcohol consumption increases risk of cataract
• Steroids and inflammatory conditions are risks for
cataracts
• Obesity and radiation
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Ultraviolet Light
• Cataracts and Macular Degeneration
– Cataracts much more prevalent in equatorial climate
– AMD more common in light eyes
• Same rules as sun tan lotions
– if you might tan or burn you should be wearing
sunglasses
• 10-30% transmission of light
• Wide brimmed hat
• Also water, sand and snow
• Polarized not necessary but will cut glare
• Don’t assume expensive is UVA and B protective
• Test lens quality and fit to ensure successful use
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Age- Related Macular Degeneration
• Age-related macular degeneration (AMD) is the most
common cause of severe, irreversible vision loss in older
Americans and Europeans. (AMD Alliance International 2008;
Ferris et al. 1984; National Society to Prevent Blindness 1980).
• Worldwide, AMD disease affects 25-30 million people.
• Etiology is complex and poorly understood
– Free-radical mediated damage to the photoreceptors
and the RPE may disrupt the transport of metabolites
from photoreceptors to choroidal capilaries
– Angiogenesis is a feature of neovascular AMD
– AMD may be associated with a systemic vascular
disorder
– Genetic and environmental factors
– Variation in the complement factor H gene
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Free radicals and antioxidants in
CNV
light
damage
blocked by
antioxidants
free radical
production
photoreceptors and RPE damage
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AMD Risk Factors
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Gender ♀ > ♂
Race/Ethnicity
Smoking
Family History
Atherosclerosis
Hypertension
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• Symptoms
• early = None, mild distortion
• late = acute loss of vision
Atrophic AMD
Progression
Initially drusen and non-specific RPE
changes
Late RPE (geographic) atrophy
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Atrophic AMD
Fluorescein angiogram
Management
Hyperfluorescence from RPE window defect Low-vision aids if appropriate
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Pathophysiology: Penetration of
Bruch’s Membrane
schematic
fundus photograph
New blood vessels penetrate
Bruch’s membrane
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Choroidal Neovascularization (CNV)
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Less common than atrophic AMD but more serious
Metamorphopsia is initial symptom
Many lesions are not visible clinically
Suspicious clinical signs
Gray-yellow subretinal lesion
with fluid
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Subretinal blood or lipid
Current Status of Therapies
for CNV
• Antiangiogenic therapy
• Lucentis, Avastin, Macugen
– CATT trial (Avastin vs
Lucentis)
• Photodynamic therapy with
verteporfin
• Steroids
• Thermal Laser
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Treatment w/Anti VEGF
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Treatment for Dry AMD
-Age-related Eye Disease Study
(AREDS) –role of antioxidants
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vitamin E, 400 IU
vitamin C, 500 mg
beta carotene, 15 mg (approximately 25,000 IU Vitamin A)
zinc 80 mg as zinc oxide
copper, 2 mg, as cupric oxide
– Copper should be taken with zinc, because high-dose zinc is
associated with copper deficiency.
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Established Age Related Macular
Degeneration
• Use Amsler Grid to monitor central vision
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AREDS-Occuvite Preservision
B carotene vs. Lutein and Zeaxanthin (AREDS 2)
Vitamin C
Vitamin E
Zinc Oxide (?necessary and ? Stomach upset)
Copper
• NB: No beta carotene for smokers and others at risk
for lung cancer
• Others??? Lutein Eyes, PhoVision, Perspective, Ocuforce
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AREDS Results
Recommendations
• Evaluation:
• Persons over 55 years old receive a dilated eye exam to
assess risk of advanced AMD.
• Contraindications to Treatment:
• Smokers and ex-smokers should not use beta carotene,
because previous studies have suggested an association
with lung cancer and beta carotene in smokers.
• There were no benefits from treatment shown in the
AREDS for patients with no AMD (Category 1) and early
AMD (Category 2).
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AREDS 2
• Adding omega 3’s did not help
• Taking away B Carotene did not hurt and lutein and
zexanthine may have been a bit more protective
• Reducing zinc dose did not hurt and less side effects
• No prevention of cataracts
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Diabetic Retinopathy
•most common cause of
• new blindness among adults 20-64 yo
• Blindness in working adults
•affects over 5.3 million Americans age >18 (2.5%
of this population)
•Prevention- worse in HTN, obesity, renal failure,
hyperlipidema, smoking, anemia, pregnancy and
POOR glycemic control
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Clinical Findings in NPDR
• Microaneurysms
• Earliest clinical sign of diabetic
retinopathy
• Appear as small red dots in the
superficial retinal layers
• Rupture produces blot/flame
hemorrhages
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Macular Edema (CSME)
•
Leading cause of
visual impairment in
patients with diabetes
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Macular Edema Treatments
• ETDRS
– focal laser surgery for CSME reduces the incidence of moderate
visual loss (doubling of visual angle or roughly a 2-line visual loss)
from 30% to 15% over a 3-year period
• Steroids
-peri-ocular
-intraocular
Anti-VEGF agents
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Ischemic diabetic maculopathy
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Macula appears relatively normal
Poor visual acuity
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Capillary non-perfusion on FA
Treatment not appropriate
PDR
• Proliferation of new
blood vessels due to
ischemia
• NVD Disc
• NVE Elsewhere
• NVI Iris
• NVA Angle
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PDR - cont.
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Treatment Options
Pan-retinal photocoagulation
Peripheral Retinal Cryotherapy
Vitrectomy
Anti-VEGF
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Retinopathy Screening
• Type 1 diabetes - screen within 3-5
years of diagnosis after age 101
• Type 2 diabetes - screen at time of
diagnosis1
• Pregnancy - women with preexisting
diabetes should be screened prior to
conception and during first trimester1
• Follow-up depends on severity of
disease
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Diabetic Eye Care
• Like glaucoma, you will NOT HAVE SYMPTOMS UNTIL
IT IS TOO LATE!
• 95-100% treatable with early detection
• Regular eye exams at 6 or 12 month interval depending
on what MD sees
• Bleeding, swelling and growth of blood vessels
• Diabetes control (Hemoglobin A1c) is the most important
way to reduce your risk
• High blood pressure is a risk
• Diet and exercise
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Glaucoma
• Optic nerve
• 1.2 million nerve fibers
• Ganglion cells in retina
exit to brain as optic nerve
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Definition of Glaucoma
• A group of optic neuropathies in which retinal ganglion
cells die by apoptosis with resultant optic disc cupping and
characteristic visual field deficits
– Optic neuropathy
– Retinal ganglion cell apoptosis
– Optic disc cupping or excavation
– Loss of visual function
-IOP is too high for the nerve???
• Most common cause blindness:
• African-Americans
COMPLETE/TOTAL BLINDNESS
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Glaucoma
• Loss of visual field
• Site of visual field loss
corresponds to area of
damage on optic disc,
e.g., “cupping”
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Classification of the Glaucomas
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RISK FACTORS
Open-angle glaucomas (90%)
IOP  21 mm Hg
Angle-closure glaucomas (10%)
Family history
Risk is increased
Primary glaucomas
by x2 if parent has
Secondary glaucomas
POAG
Risk is increased
x4 if sibling has
POAG
African American
C:D ratio > 0.5
Asymmetric cupping
Myopia
Diabetes
Age > 75 years
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Angle Closure Glaucoma
• Acute pain, redness, tearing
• Associated with dilation of
pupil
• Natural (e.g., movie theater)
• Pharmacologic
• Nausea & vomiting
often in ER with “acute abdomen”
Risk factor of narrow angle can be
detected on screening exam
(esp hyperope) and
prophylactic iridotomy is
preventative of attack in 100%
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Acute angle-closure glaucoma
Signs
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Severe corneal edema
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Ciliary injection
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Dilated, unreactive,
vertically oval pupil
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Shallow anterior
chamber
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Complete angle closure
Medical rx to lower IOP, followed by laser (Yag) iridotomy
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Primary Open-Angle Glaucoma
• The most prevalent type of glaucoma in the United States
• Elevated intraocular pressure is not part of the diagnostic
criteria
– 25% of patients with primary open-angle glaucoma in
the US have normal intraocular pressure
• Asymptomatic
– Some loss of visual field
– Most common type
– Familial, bilateral
– “Sneak thief of sight”
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Primary Open-Angle Glaucoma
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Evidence that IOP reduction is beneficial
Collaborative Normal-Tension Glaucoma Study (CNTGS)
Advanced Glaucoma Intervention Study (AGIS)
Early Manifest Glaucoma Study (EMGT)
– 25% IOP reduction RoP 62% to 45% at a median of 6
years.
• Ocular Hypertension Treatment Study (OHTS)
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Treatment for POAG
• Lower the IOP
• Medical therapy
• Prostaglandin , Bblockers,Sypathomimetic
s, Carbonic-anyhrase
inhibitors
• Laser surgery (ALT, SLT)
• Incisional surgery (Trab,
shunt)
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Incisional Surgey
Most glaucoma specialists use
an anti-fibrosis agent for every
case in the year 2003
Limit episcleral fibrocellular
proliferation
Mitomycin C (MMC) antitumor antibiotic 0.2 to 0.5
mg/mL for 1 to 5 minutes
5-Fluorouracil (5-FU)
antimetabolite 50 mg/mL for 5
minutes
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Tube Shunts
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Eye Strain
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Myth??
Often dry eye
Maybe the muscles around the eye
Worse with misalignment issues
Cant do any harm
Take breaks often and focus at distance
A few extra blinks
Lubricate before long drives, plane trips, windy or smoke
filled environments
• Careful not to dismiss Headaches as “eye strain”
• Seek care if not responsive to behavioral strategies
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Summary
• Diabetic Retinopathy
•Prevention, treatment
• Cataract
–Surgical treatment continues to improve
• Glaucoma
–Silent blindness, family history
–Medical and surgical rx
• ARMD
–New age of available prevention strategies and treatments exudative
variety
Volpe Healthy Transitions ‘13
Strategies to Preserve Your Vision
• Prevention is our most potent tool in the quest to
reduce disease (and healthcare costs)
• Choose your parents well and stop aging!!! OR
• Don’t Smoke
• Wear Glasses that are UV protective
– Safety glasses for high risk activities
• Pay Attention to Nutrition and Vitamins
• Don’t Ignore Symptoms
• Get Regular Eye Examinations
Volpe Healthy Transitions ‘13
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