Transcript aging america updated fall segu 2013

Aging America:
Clinical
Management of the
Elderly Patient
Pat Segu, OD FAAO
Clinical Associate Professor
Cornea

Corneal Sensitivity
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Pros


Decreases with age
Threshold for touch doubles between the ages of
10 and 80
Etiology: unknown
Better adaptation to CLs
Cons

Lesions/abrasions may not cause a significant
subjective complaint
Cornea

Curvature
Horizontal meridian steepens with age
 Increasing lid laxity
 Shift from WTR to ATR


Transparency
Not affected greatly by age
 Endothelial cell count decreases

 Below
400-700 cells/mm3 difficulty with
maintenance of hydration

Decreased corneal luster
Pupil

Decrease in Size

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Reduction in amount of light
Etiology: unknown
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Decreased elasticity
Changes innervation & vascular supply
Possible atrophy of the dilator muscle
Delayed Pupil Response
May be irregularly shaped
Almost the same size in light-and dark-adapted
states
Iris

Pupil Size Smaller


Pigmentary Atrophy


Look for Iris Transillumination
Flattening of Iris Crypts


Average Size 2 mm ( vs. 4 mm for a younger patient)
Partial Color Change
Decrease in Elasticity

Slower Pupil Dilation
Anterior Chamber

Depth
Decreases with age
 15-20yrs
3.6mm
 70 yrs
3.0mm
 Due to growth of the lens

 Increase
in lens thickness
 May cause iris to bow forward
Anterior Chamber

May account for…..

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Narrower angle (caution with dilation)
Aqueous – chemical composition

appear to be independent of age
Crystalline Lens
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Increase in Lens Density
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Clarity

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3X Weight
decreases
Axial length
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Slowly increases throughout life
15-20 yrs
3.6mm
70 yrs
4.6mm (28%)
Crystalline Lens

Transverse/Equatorial Diam. vs. Axial
Length

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Anterior Curvature vs. Posterior
Curvature
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Axial length increases faster
Anterior curvature increases
Posterior remains relatively constant
Decrease Retinal Illumination


Crystalline lens absorption
60 yrs vs. 20 yrs ( 1/3 amount of light)
Crystalline Lens

Increased high MW proteins in nucleus
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Increased light scatter
Increase in Yellow Color
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Decreased transmission of visible and UV light (esp.
blue light)
Decrease sensitivity to blue – green wavelengths
Elders see Reds and Yellows the best
Crystalline Lens
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Index of refraction
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Decreased elasticity?
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Relatively stable
Increased optical density
More likely due to decreased elasticity of the
lens capsule
Loss of accommodation
Cataract
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“ADL’s”-activities of daily living
Cortical
Nuclear Sclerosis
PSC

Steroid
What is 20/20?
Vitreous
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Consistency
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Liquefaction and syneresis
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Monitor for retinal breaks and/or tears
Epiretinal membrane (ERM)
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Shrinkage
Posterior vitreous detachment (PVD)
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Increased speed and amplitude of movements of
floaters
Cellophane maculopathy
Traction @ ILM
Metamorphopsia
Vitreomacular Traction (VMT)
Vitreous Syneresis & Detachment
With aging, reduction in
hyaluronic acid causes loss of
support to the collagen.
www.brendanmoriarty.com
www.brendanmoriarty.com
The vitreous may collapse, with
detachment of the posterior
hyaloid face from the retina.
PVD is a process

Eye movements  tractional forces on areas
of vitreoretinal adhesion

2 - 4% develop retinal break
High risk period = 1st 6 weeks after onset
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Follow-up 1-4 wks initially
1 month later
> 6 months after onset risk of RD is low
90% bilaterality
Fellow eye involvement within 2 yrs
Weiss Ring
(peripapillary glial ring)
© Online Journal of Ophthalmology - Robert Machemer
Vitreomacular Traction (VMT)
Vitreous gel strong adhesion to
retina
 OCT scan to confirm diagnosis
 Vitrectomy if VA 20/40 or worse

Choroid
Supplies Outer ½ of the retina
 Decrease in Thickness


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Atrophic Changes

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Secondary to arteriolar sclerosis
ONH (peripapillary atrophy)
Pigment Changes
Retina

Decrease in Thickness

Loss # of Neural Cells

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Decrease # of Photoreceptors

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Decrease # of ganglion cell axons
25% loss of axons 70 yr ONH
Drusen Formation
Natural decline in contrast sensitivity
with age b/c decrease in the # of
neural cells

Aspheric IOLS designed to increase
contrast sensitivity
Retinal and Neural
Connections

In the absence of pathology, little decline
in VA up to the age of 70
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20/10
52-64
65-74
75-85
to 20/25 acuity:
yrs
95.4%
yrs
91.9%
yrs
69.1%
Retinal and Neural
Connections

Major causes of acuity decline in
75-85 yrs
Cataract
 ARMD
 Glaucoma
 Unknown

46%
28%
7.2%
10%
Retinal and Neural
Connections

Ophthalmoscopy findings

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Sclerotic vasculature
Drusen
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Pigmentary changes
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AMD
grainy or reticular-like in periphery
peripapillary atrophy (PPA)
Loss of foveal reflex
Loss of luster
Retinal and Neural
Connections

Retinal Recovery Time


increases
Visual Field
Constriction – after controlling for pupil
size
 Decline Peripheral VF vs. Central VF

 Loss

of Neurosensory Cells
Automated fields - may need to perform
while dilated
Dark Adaptation

Absolute level of dark adaptation

Probably less than in younger people

Likely attributable to miosis and lens
growth/density

Difficulty in poor lightening
Motilities

Versions
Increased lag
 Dynamic VA

 Slower
eye movements VA for moving targets
 Decreases (proportional to the speed of the
target)
 Perhaps due to decreased smooth pursuits?
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Vergence
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Fusional – decreased (+) fusional
vergence
Aging Eye –
Adnexa & Anterior
Segment
Xanthelasma
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Common
Bilateral
HX of elevated cholesterol
Yellowish subcutaneous plaques
Located Medial
Flat oval shaped deposits of cholesterol
Can be removed by excision or CO2 laser

tend to re-occur
Benign Squamous Papilloma
Most common benign eyelid lesion
 Clinical Features:

Pedunculated or sessile
 Finger-like projections
 Raspberry-like surface

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Treatment
Excision
 Laser ablation
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Actinic Keratosis

Most Common PRE-Malignant lesion
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Pre-cancerous to squamous cell carcinoma
Up to 10% progress to SCC
> 5 million Americans have at least one AK lesion

Light Skinned & HX of excessive sun exposure

Flat, scaly, or papillary lesions

Nodular or Wart

Occur in sun-exposed area

Rarely develops around eyelid
Squamous Cell Carcinoma

Less common than BCC (5-10% eyelid tumors)

Biologically Aggressive
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Metastasis in 3%
Lymph Nodes
Fair Skinned
SECO #153

HX of Chronic Sun Exposure

Spontaneous or from pre-existing AK
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Absence of Surface Vascularization
SECO #158
Basal Cell Carcinoma
Accounts for about 75% of all skin
cancers USA
 Most common malignant eyelid
tumor
 Locally Invasive
 Rarely Metastatic
 TX: excisional surgery

Basal Cell Carcinoma
Caucasians
 Occurs on inner lower portion of lids
and tops and backs of ears
 Persons over 50
 Related to Sunlight Exposure
 Must Biopsy
 Maybe pigmented
 Irregular borders, central
depression, white rolled margins

Seborrhoeic Keratosis
(Basal Cell Papilloma)

AA pts known as
Dermatosis Papulosis Nigra
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Benign overgrowth of basal cells of
epithelium
Common slow-growing condition face &
eyelids
Grayish or darker color
Crumbly texture
“Stuck on Appearance”
Sun Exposed Areas
Treatment - Removal
Sebaceous Cell Carcinoma
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Rare Tumor
Frequently Affects Elderly
Arises from MG or glands of Zeis
More common location Upper Lid
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Unlike BCC & SCC
HX of recurrent Hordeolum/Chalazion
Difficult to Diagnosis
Poor Prognosis

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UL
>10mm diameter
Symptoms >6months
HERPES ZOSTER

Reactivation varicella zoster virus from
latency
“Shingles”
Localized lesions
HZO occurs when the ophthalmic branch of
the trigeminal nerve is involved (Hutchinson
sign)
Disease of the elderly

Standard treatment:
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Acyclovir 800mg 5 x daily for 1 wk
72 hours of onset
Arcus Senilis (Gerontoxon)

Hazy ring of yellow-white
deposits in the peripheral
cornea without thinning

Cholesterol esters,
cholesterol and neutral
glycerides in the extracellular
stroma

Lucid interval @ limbus
Fuch’s Dystrophy
Accumulation of guttata which
coalesce and cause cornea edema
 Progressive metabolic defect of the
endothelium which can lead to
serious vision loss
 Inherited and found 4x more often
in women than men, after the age
of 40
 Usually bilateral and asymmetric
 Autosomal Dominant

Fuch’s Dystrophy

Three phases of disease
Guttata
 Bullous Keratopathy -edema, blurred
vision, glare, pain. Descemet’s
thickens and wrinkles and cornea
appears hazy
 Corneal scarring - severe vision loss,
high IOP, peripheral vascularization,
pain subsides

Fuch’s Dystrophy

Management depends on the stage

5% NaCL to draw out edema
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Hair dryer held at arms length

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Dry out the corneal surfaces
Decrease the time the blur persists
bandage soft contact lens

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1 gt qid
Ung qhs
Comfort
Flat, High water content SCL, Loose Fitting
PKP

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Advanced cases
Account 10% of all corneal grafts performed
Map/Dot/Fingerprint
Dystrophy
Map/Dot/Fingerprint
Dystrophy

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Epithelial dystrophy
Most patients are between age 40 to 70
May or may not be symptomatic
Due to abnormal BM
Dots are microcysts which can migrate to
the epithelial surface and burst


This causes recurrent erosions
After the erosions start symptoms occur
Map/Dot/Fingerprint
Dystrophy
Lubricate the cornea with
hypertonic drops and ointments
 Scrape the edges of the erosion and
use a soft bandage contact lens
 Laser is useful for erosions if they
are very severe

Aging Eye:
Posterior
Segment
AMD
Leading cause of blindness over age 65
 Changes “Bruch’s” membrane
 “Dry” vs. “Wet” Form of AMD
 Painless loss of VA
 Metamorphopsia
 Risk of Choroidal Neovascular
Membrane
 TX: Oral antioxidants, anti-VEGF

CME
“Swelling” center of macula
 Associated with inflammatory
conditions
 Increase leakage of capillaries
 Painless decrease in VA
 8-12% of cataract patients

DM maybe predisposition
 2-8 weeks after cataract surgery
 OCT scan
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DIABETES MELLITUS
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Chronic Disease
Macro & Micro vascular changes
Nephropathy, Neuropathy & Retinopathy
DM Retinopathy Leading Cause of New Blindness in
20 - 74 patient population
________
Early Intervention = Lower risk for Blindness
Type I vs. Type II
Controlled vs. Uncontrolled
Absence or Presence of retinopathy/ CSME
Consider a baseline OCT scan to document MT
Diabetic Retinopathy

NPDR +/- CSDME

PDR +/- CSDME

Macular Ischemia

Vitreous Hemorrhage

Tractional Retinal Detachment

Neovascular Glaucoma
Hypertension

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Multi-factorial Disease
90 -95 % Essential HTN
Asymptomatic
AA > Caucasians
Long Standing HTN

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Blood Retinal Barrier
Degeneration of Pericytes & Muscle Cells
Arteriolosclerosis of Vessel Walls
Hypertensive Retinopathy

Grade I

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Bilateral Attenuation of
Arterioles
Grade II
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Greater Attenuation
A/V nicking
Hypertensive Retinopathy
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Grade III
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Grade II changes
CWS
NFL hemorrhages
Exudates
CWS


24-48 hrs of elevated BP
Diastolic >110mmHg
Hypertensive Retinopathy

Grade IV

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Grade III
Bilateral Disc Edema
Macular Star
Papilledema from HTN

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
Malignant HTN
BP range 250/150 mmHg
Medical Crisis - ER
Amaurosis Fugax

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
Transient monocular blindness
Sudden
Unilateral blindness

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
Sector or total loss of vision
Short period (up to 2 hours)
Vision returns back to normal
10-15% risk to develop a CRAO
Initial sign of GCA- elderly patient
Transient Ischemic Attacks
(TIA)
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Sudden numbness or weakness one side
of body
Temporary loss of speech or difficulty
talking
Temporary difficulty understanding
speech, particularly with right side
weakness
5 minutes – several hours
Amaurosis Fugax
Diagnoses is made based on history and
not clinical examination
Pending STROKE
TYPES OF EMBOLI
Cholesterol
 Calcium
 Platelets
 Fibrin
 Talc

Cholesterol Emboli
Shiny yellow-orange
 Bifurcations
 Mobile
 Carotid
 (-) Infarction

Calcium Emboli
Gray-white
 Unbranched arterioles
 Nonmobile
 Origin Cardiac & Artificial heart
valves
 BRAO

Platelets Emboli
Dull white long plugs
 Arterioles
 Carotid & thrombocytopenia
 BRAO

Fibrin Emboli




Not readily observed
Laminar location
Thromboemboli after acute
mitral insufficiency
Arterial occlusions (CRAO)
Talc or Cornstarch Emboli
Shiny red-yellow
 Capillaries of Posterior Pole
 Self-injected drug users
 Microinfarcts in capillaries (CWS)

Ocular Ischemic Syndrome
Ocular Ischemic Syndrome
Elderly Patient (50s-80s)
 2:1 Males vs. Females
 Decreased VA
 HX of TIA or Amaurosis fugax
 Ocular or periorbital pain
 Unilateral
 “ASYMMETRIC PRESENTATION”

OIS

Etiology

Decreased ocular arterial inflow
secondary to severe carotid artery
obstruction (>90% stenosis)
HTN, DM, Ischemic heart disease,
stroke, peripheral vascular disease
 RISK OF NEO of iris, angles, disc
and retina

OIS – Anterior Segment
Iris Neovascularization
 Corneal edema from elevated IOP
 NVG
 Mild iritis
 Episcleral injection, iris atrophy and
cataracts

OIS – Posterior Segment

Dilated beaded retinal veins

NOT tortuous
Narrowed retinal arterioles
 MID-peripheral retinal dot-blot hem
(80%)
 NEO of ONH or retina
 CWS

OIS- Management

FA
Delayed choroidal filling
 Delayed retinal circulation


Cardiology consultation
Carotid duplex, EKG, Lipid profile
 Carotid endarterectomy


Manage NVG
Vitreomacular traction
Senile Macular Holes

Pre-foveal vitreal
shrinkage causes
tangential traction on
the fovea.


Photo by Dr.HD Riley

Separation of the sensory
retina from the
underlying RPE.
Sensory retina atrophy
results in a break.
Progression to a fullthickness hole or
spontaneous resolution.
Clinical Assessment
 VA
 Amsler
 Vitreous: ?
PVD
 Fundus
CL
 +/ - Watzke
Sign
 +/ - OCT
(+) (+)
Epiretinal Membrane
http://www.mrcophth.com/pd/epia.html
ERM - Etiology
Idiopathic
Retinal break or detachment
Post-surgical, Post-laser
Trauma
Inflammation
Retinal vascular disease
Congenital (e.g., RP)
ERM

Proliferation of glial cells and RPE
cells.

Contraction of cells along the
internal limiting membrane.

Puckering of the macula with
tortuosity of the small retinal
vessels.
Glaucoma

Pigmentary Dispersion Glaucoma


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Pseudoexfoliation Glaucoma

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“Mask” hypoglycemic event
Caution in patients taking calcium channel blockers-risk of
arrhythmia
Topamax


Caution with Cataract surgery
Beta Blocker


Decrease with age
Risk of increase IOP post-dilation
“Bilateral AAC event
Suprachoroidal effusion forward displacement of CB into the
angle
Issue of Compliance
10-2 HVF for endstage glaucoma
Most Common Type of Optic
Neuropathy in The Elderly

Ischemic optic neuropathy



NAAION
AAION
Associated with systemic condition



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Nocturnal hypotension
Hemotologic anomaly
Migraine
Auto-Immune
 SLE
Systemic hypoperfusion



Hypovolemic event
Cardiac insufficiency
Anemia
Ischemic Optic Neuropathy

Ischemia occurs at the optic nerve head

Nonarteritic (idiopathic) anterior ischemic optic
neuropathy- NAAION





95% of all AION cases
most frequent cause of disc edema in adults over the
age of 50
second most prevalent optic neuropathy in adults,
after glaucoma
Current theory: insufficiency of ONH circulation
exacerbated by “structural crowding” of nerve fibers
and supporting structures
Arteritic anterior ischemic optic neuropathy
(AAION)


5% of all AION cases
Short posterior ciliary artery vasculitis with ONH
infarction associated with Temporal arteritis
Role of the Optometrist

Primary care provider

May be the only health care professional
patient in contact with

Responsibility of DX, TX & management,
Referring patient
 always

take a thorough case history
remind pt to see M.D. when appropriate
 Co-management

Enhancement of vision
“New Elder”
Living longer, living better
 Increasingly healthy, active & working
 Knowledgeable about health & illness
 Better educated
 Economically stronger

Conclusion

The older population (65+) is not only
increasing in size but also living longer,
healthier and active lives

Visual Needs are Diverse


1 in 3 Older Americans Vision-limited Disease
ODs play an IMPORTANT role

management of ocular disease and enhancement of
vision