Age-Related Macular

Degeneration
Aoife Smyth
 most comon cause of blindness in
ppl in western wpr;d?
– ARMD
– Common
– Mostly affecting the elderly over 50 yrs old
– Loss of central vision and visual distortion
Age-Related (metamorphopsia) - peripheral vision remains
Macular – Disease of the central retina (macula)
Degeneration – Gradual onset and progressive
– Genetic component (positive family history)
– Smoking is a risk factor
2 -3 x
 – Two forms - Dry (non exudative) & Wet (exudative)
gradually
– Dry form - least aggressive in terms of vision loss
rapidly progressive – Wet form - 90% of vision loss due to this form
ARMD and marked visual
distortion
– No definitive cure for Dry or Wet forms
– Treatments available to slow progression only
 – Non-neovascular / non-exudative
– 90% of ARMD (UK) (more common than wet form)
– 10% of blindness registration from dry ARMD (UK)
– Gradual reduction in visual acuity cant do daily things like
Dry ARMD – Metamorphopsia (Amsler grid) reading
lose central vision
– ? family history family hx and smoking
– ? smoker v hihg risk factor

– Drusen yellow dposit = drusen

– Loss of photoreceptors
– Retinal pigment epithelial (RPE) atrophy
– Geographic atrophy
bruch and choroid - maintain normal function of
photoreceptors remove waste

oxd stress - cell damage and cell death of RPE

and photoreceptors
waste products build up and activate complement
system - chronic inflammation and further impaired
retinal epithlium - drusen - inflamm deposits,
atrophy = black ditd, geo atrophy = spots missinfg

maintains blood
occular membrane
 darker = RPE
atrophy
yellow drusen
RPE atrophy and drusen
 Geographic atrophy

thinning of
retinal
photoreceptor
layer allows
visualisation of
underlying
choroid layer
 measures 10
degrees of
their vision
each square is
1 degree • An important symptom of ARMD
• Visual distortion - particularly of straight lines
• Use an Amsler grid to detect it in the clinic
Metamorphopsia • Horizontal and vertical lines
• Ask patient to stare at target in centre
• Test one eye at a time
• Patient can take a copy home and draw on the chart
where they see the distortion - can monitor progression
Amsler Grid
Central
scotoma

Distortion
of straight
lines
impact ability to see
faces
 – No cure available - no further investigation needed
only modifable risk
25% reduced
– Stop smoking factors chance of
progression - not
– Treatment consists of oral Vitamin C and E, lutein, B-carotene
stop it happening
and zinc (OCUVITE LUTEIN) - antioxidant effect shown to
all togeth

slow progression of dry ARMD

Treatment – Newer treatment with meso-zeaxanthin, carotenoids, lutein
for Dry and zeaxanthin- MACUSHIELD
– Give patient Amsler grid to take home and check on a
ARMD monthly basis themselves for progression

– Reassurance that they will not go completely blind from this

condition I.e. they will always have peripheral vision. Mention
also that it is very slow to progress
– Referral to NCBI or low vision aid clinic PRN
 causes leakage of
fluids as are v
weaky
– Neo vascular / exudative
– 10% of ARMD (UK) (less common than dry form)
– 90% of blindness registration from wet ARMD (UK)
– Gradual or sudden reduction in visual acuity
– Sudden reduction in vision happens due to a sub retinal bleed
Wet ARMD from a CNV can get metamophopsia

– Choroidal neovascular membrane

hallmark(CNV)
CNV - immature + leaky in or
below retina btwn retinal pgiment epith
– Retinal pigment epithelial detachment
and bruchs membrane- can cause
– Intra retinal haemorrhage pigment epithlium detachment
– Disciform scar (end stage) old fluid canc ause cause scarring - end
stage
see CNV creeping up from the choroid
btwn Bruch and RPE and in btwn
photoreceptors cusing detachment,
bleeding hemorr, and fluid leakage can
cause deciform scar
–
Fresh CNV with
overlying
haemorrhage

Disciform scar from

previous CNV
 – Fundus fluorescein angiography (FFA)
– Optical coherence tomography (OCT)

Investigation WHY?
of Wet ARMD
– Help diagnosis and characterisation of the particular
sub type of wet AMD
 – Injection of fluorescein dye through I.V. line
– Dye travels to eye stays within the choroidal
and retinal vessels
– Emits yellow light when excited with a blue
FFA light
– Visualisation of normal vessels and abnormal
vasculature possible (CNV)
– Photographs taken with a fundus camera -
black and white image can show
leakage or loss
of RPE cells
Hyperfluorescence from a choroidal
neovascular membrane (CNV)
 cross sectional image look at
different layers to see if blood
between them

– Non invasive imaging of the retinal layers

– Uses laser light
– Exploits differences in interferometric properties of the
OCT retinal layers
– Demonstrates retinal pigment epithelial detachment
due to underlying CNV
 vitreous humour
if was any fluid from
cnv would see
fovea
pockets of block

retina

sclera
 – No cure available

– Treatments slow progression and produce moderate

improvement in vision only

Treatment of – Intra vitreal injection of anti-VEGF antibody (Avastin) -

diffuses through vitreous to retina - blocks neovascularisation
wet ARMD and induces regression of CNV by neutralising VEGF activity
– Focal laser photocoagulation – limited utility now
– Photodynamic therapy – verteporfin – largely replaced by
anti-VEGF causes thrombosis
but doesnt improve
vision as causes
retina damage
 – National council for the blind (NCBI)
– Low vision aids
– CCTV
Visual – Large print
– Magnifiers / telescopes
rehabilitation
– Talking clocks / books
– Initiate community care
Diabetic retinopathy
(DR)
 Diabetic Retinopathy

uLeading cause of blindness in the working population

vascular
uEpidemiology – 460,000,000 adults with diabetes.
diasease of
uPrevalence with diabetic retinopathy (DR): 35-40%
the retina one
more likely to get it
of 3 main
uType I: rare at diagnosis and 90% at 30 years comps of
uType II: 20% at diagnosis and 60% at 15 years diabetes

uBest predictor - duration of the disease

uVery rare before puberty
Risk factors

– Increased duration of diabetes one of main risk

factor
– Poor glycemic control can decrease
progression with
better glycemic
– Hypertension control

– Hypercholesterolemia
– Nephropathy
– Pregnancy
 – Thickening of basement membrane
endothelial cell
– Loss of pericytes damage
– Leakage of fluid
– Microaneurysm formation
Pathology
– Platelets adhere to endothelium of small
vessels - leads to occlusion
– Ischaemia
– neovascularisation
2 main changes -
this and ischemia Hyperglycaemia

perycytes maintain
the blood retinal
barrier and BM wrap
around epithelial
cells of these
vessels and are
located on BM -
there to prevent
leakage - lose them
- get weakening of
capillary walls - get
micoraneurysm
outpouching of
vessel lumen -
leakge of plasma
and blood into retina
retina v metabolically active - very
sensitive to ischemia - damgwe to
endothelial cell, BMthickening and
plateltts - decrease perfusion - get
hypoxiaa - VEGF - angiogenesis - are
think weak leaky fragile and misdirected
 can evolve into
proliferative which
has
Stages neovascularisatio
and potential for
more serious
vision
— Non-proliferative diabetic retinopathy (NPDR) consequences
— Mild: microaneurysms only
— Moderate: above + haemorrhages, exudates, cotton wool
— Severe: above + venous beading, IRMA
— Proliferative diabetic retinopathy (PDR)
— New vessels at the disc (NVD)
— New vessels elsewhere (NVE)
fluid deposition under macula or macular odema can occur
— Maculopathy at any stage in both prolif and non prolif
main complaint as it affects their central vision -
— Macular oedema and exudates
in non proliferative - get microaneurisms - usually first
— Macular ischemia
things visualised on exam of retina

later leakage of fluid and blood. blot and dot hemorrahges -

dt appearance
resolution of fluid lakes
can leave behind sediment - lipid
bipdcts, waxy yellow pdct called
hard exudates

as non prolif diabetic retinopathy

progresses - affected vessels
become obstructed - can cause
infarction of nerve fibre layer -
which is one of the layer of the
retina - resulting in fluffy white
patches called - cotton woool
spots.

NON PROLIFERATIVE
Micro aneurysms, hard exudates, dot and blot haem
Underlined ones may be seen with ophthalmoscope
Micro aneurysms can only be seen on slit lamp exam
 must have neovascularisation
at optic disk or elsewhere

PROLIFERATIVE

– PROLIFERATIVE
– new vessels at the disc
– Lots of hard exudates at
macula
– microaneurysms etc
(features of non can grow off of retina into vitrous - vitreous
proliferative) shrink with age so can pull on new weak
vessels cause bleeding = vitreous
hemorrahage and sudden vision loss
can also scar down - and traction on retina -
tractional retinal detachment
PROLIFERATIVE
All features of non proliferative with new vessels at disc, elsewhere,
traction band and venous loops
Vitreous haemorrhage

in front of retina
can be watched and
resorbed or if is
recirring or blocking
vision - can do
vitrectomy - suction
out vitreous and
blood - of non
resolving
 Tractional retinal detachment

on left
traction by
neovascularis
ation

do votrectomy
- replace
vitreous with
oil or gas to
press retina
back down
and let it heal
Rubeosis

neovascularisation
into angle of ant
compartment -
obstructing outflow
- increased iop -
cause glaucome
 uRationale for Screening Programme –Wilson and
Jungner 1968
uFundus photography every 12 months- graded at
specialized centre.
uTimely referral for those needing intervention (R2,3,
M1)
Diabetic
uGrading – Rx Mx
Retina Screen uR0: no retinopathy
uR1: background retinopathy
uR2: pre-proliferative
uR3: proliferative
uM0: no maculopathy
uM1: Maculopathy
 – Lifestyle changes:
– Cessation of smoking
– Regular exercise
– Weight control
Treatment – Glycemic control: aim for HbA1c of 6.5-7.0%
– Blood pressure control
– Cholesterol control: Statin
non prolif - optimize px health
tight gluclose control
 if have macular oedema with
non proliferative retinopathy -
need to be tx - grid laser to the
macula - howeber intravitreal Maculopathy:
anti vegf injections
– Intravitreal anti-VEGF: Avastin, Lucentis
Treatment of – Focal laser photocoagulation
PDR:
diabetic retinopathy u Pan retinal
Photocoagulation (PRP)
 avoids macula killing off
parts of retina that is
ischemia and stops
can affect peripheral visual
fields

only used on– macula

The retina is ischaemic as indicated by the
if have
oedema ie cant see
neovascularisation
because of the fluid but
– Laser
usually injections for photocoagulates
that? (burns) and kills the
retinal tissue
Why use laser? – This reduces overall oxygen demand of the
retina
– Less stimulus for neovascularisation
– Implications for driving…PRP causes a field
defect
use anes drops
and contact lens
to magnify and
help concentrate
the beam
 Thank you!

Any questions – email

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