aging america updated fall segu 2013
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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
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
Reduction in amount of light
Etiology: unknown
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…..
Narrower angle (caution with dilation)
Aqueous – chemical composition
appear to be independent of age
Crystalline Lens
Increase in Lens Density
Clarity
3X Weight
decreases
Axial length
Slowly increases throughout life
15-20 yrs
3.6mm
70 yrs
4.6mm (28%)
Crystalline Lens
Transverse/Equatorial Diam. vs. Axial
Length
Anterior Curvature vs. Posterior
Curvature
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
Increased light scatter
Increase in Yellow Color
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
Index of refraction
Decreased elasticity?
Relatively stable
Increased optical density
More likely due to decreased elasticity of the
lens capsule
Loss of accommodation
Cataract
“ADL’s”-activities of daily living
Cortical
Nuclear Sclerosis
PSC
Steroid
What is 20/20?
Vitreous
Consistency
Liquefaction and syneresis
Monitor for retinal breaks and/or tears
Epiretinal membrane (ERM)
Shrinkage
Posterior vitreous detachment (PVD)
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
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
Atrophic Changes
Secondary to arteriolar sclerosis
ONH (peripapillary atrophy)
Pigment Changes
Retina
Decrease in Thickness
Loss # of Neural Cells
Decrease # of Photoreceptors
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
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
Sclerotic vasculature
Drusen
Pigmentary changes
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?
Vergence
Fusional – decreased (+) fusional
vergence
Aging Eye –
Adnexa & Anterior
Segment
Xanthelasma
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
Treatment
Excision
Laser ablation
Actinic Keratosis
Most Common PRE-Malignant lesion
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
Metastasis in 3%
Lymph Nodes
Fair Skinned
SECO #153
HX of Chronic Sun Exposure
Spontaneous or from pre-existing AK
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
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
Rare Tumor
Frequently Affects Elderly
Arises from MG or glands of Zeis
More common location Upper Lid
Unlike BCC & SCC
HX of recurrent Hordeolum/Chalazion
Difficult to Diagnosis
Poor Prognosis
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:
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
Hair dryer held at arms length
Dry out the corneal surfaces
Decrease the time the blur persists
bandage soft contact lens
1 gt qid
Ung qhs
Comfort
Flat, High water content SCL, Loose Fitting
PKP
Advanced cases
Account 10% of all corneal grafts performed
Map/Dot/Fingerprint
Dystrophy
Map/Dot/Fingerprint
Dystrophy
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
DIABETES MELLITUS
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
Multi-factorial Disease
90 -95 % Essential HTN
Asymptomatic
AA > Caucasians
Long Standing HTN
Blood Retinal Barrier
Degeneration of Pericytes & Muscle Cells
Arteriolosclerosis of Vessel Walls
Hypertensive Retinopathy
Grade I
Bilateral Attenuation of
Arterioles
Grade II
Greater Attenuation
A/V nicking
Hypertensive Retinopathy
Grade III
Grade II changes
CWS
NFL hemorrhages
Exudates
CWS
24-48 hrs of elevated BP
Diastolic >110mmHg
Hypertensive Retinopathy
Grade IV
Grade III
Bilateral Disc Edema
Macular Star
Papilledema from HTN
Malignant HTN
BP range 250/150 mmHg
Medical Crisis - ER
Amaurosis Fugax
Transient monocular blindness
Sudden
Unilateral blindness
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)
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
Pseudoexfoliation Glaucoma
“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
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