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Basic Anatomy
Pre-retinal:
glaucoma
Retinal:
tumours
macular degeneration
Post-retinal:
Pre-retinal:
glaucoma
Retinal:
tumours
macular degeneration
Post-retinal:
VF testing
fluorescein angiography +/- other tests
**Remember
for exam:
Corneal Causes
-
dystrophy
- scarring
- edema
The Cornea
- allows light to enter the
eye
- provides most of the eyes
optical power
- 0.5-0.8 mm thick
- transparent due to its
uniformity, avascularity
and deturgescence
Epithelium
Stroma
Endothelium
Corneal Dystrophies
-
affect transparency
Corneal Dystrophies
-
divided into:
-
anterior dystrophies:
- epithelium
- may present with recurrent corneal erosions
stromal dystrophies:
- usually present with visual loss
posterior dystrophies:
- endothelium
- vision loss secondary to edema (endothelial dysfx)
Corneal Scarring
-
multiple causes:
-
trauma
post-surgical
Corneal Edema
-
dystrophy
trauma
post-surgical
Corneal
Transplantation
Corneal Transplantation
Lens-Related Causes
(cataract)
age-related
- traumatic
- steroid induced
-
The Lens
- biconvex, avascular,
transparent structure
- sits inside a thin
capsule, attached to the
ciliary body by the
zonules
- provides the
remainder of the eyes
optical power (along
with the cornea)
Lens
cataracts
Age-Related Cataract
-
eventually, liquefaction
Traumatic Cataract
-
concussion
Steroid-Induced Cataract
-
Glaucoma
Glaucoma
disease
Glaucoma
if
Glaucoma
by
increased IOP
optic nerve changes
visual field changes
Glaucoma
classification:
IOP
family history
myopia
heritage
Symptoms of Glaucoma
often
asymptomatic
with late disease, constriction of
peripheral, and later central visual field
with very high IOP, can have blurry
vision and halos around lights
cup:disc ratio
thinning of neural rim
progressive loss of nerve fiber layer
flame hemorrhages on disc
common (90%)
usually bilateral (can be asymmetric)
prevalence increases with age
angle is open, eye is quiet
increased resistance to aqueous drainage
at the level of the trabecular meshwork is
thought to be the main pathophysiologic
feature
Treatment options
goal
drops
laser
surgery
Glaucoma - Medications
mechanism
of action:
Glaucoma - Lasers
usually
fails
high
success rate
Glaucoma - Surgery
usually
Pre-retinal:
glaucoma
Retinal:
tumours
macular degeneration
Post-retinal:
THE RETINA
- neural tissue lining
the inside of the eye
- converts the visual
image into a
neurochemical
message and sends it
to the brain
- is made up of 10
anatomic layers
Diabetes
diabetic retinopathy
- diabetic macular edema
-
Diabetic Retinopathy
microangiopathy
affects pre-capillary arterioles, capillaries
and post-capillary venules
features of:
microvascular occlusion
leakage
Epidemiology
Wisconsin Epidemiologic Study of Diabetic Retinopathy
Between 1979-1980
1210 patients with Type 1
1780 patients with Type 2
predominantly white population
***Macular edema
May be present at any stage of DR
NPDR
typically asymptomatic
fluctuating visual acuity:
fluctuating blood sugar
decreased visual acuity:
CSME
macular ischemia
Mild NPDR
Moderate NPDR
Severe NPDR
Proliferative DR
affects 5-10% of the diabetic population
neovascularization is the hallmark
NVD: neovascularization of the disc
NVE: neovascularization elsewhere
new vessels are not only extremely fragile
(intraretinal or vitreous hemorrhage), but
often associated with fibrous proliferation,
leading to an increased risk of tractional retinal
detachment
Advanced PDR
Tractional retinal
detachment
resulting from
contraction of
the fibrovascular
proliferative
tissue on the
retina
goal is to induce
involution (or at
least arrest) of new
vessels by creating
areas of retinal
ischemia
1200-3000 burns
4 sessions
Treatment of CSME
Ophthalmological Follow-Up
Diabetic Screening
Type 1 diabetics:
Dilated funduscopic exam (DFE) 5 yrs after diagnosis
Newly diagnosed patients with Type 1 diabetes rarely
have retinopathy during the first 5 yrs
Type 2 diabetics:
Type 2 diabetics typically diagnosed yrs after initial
onset
DFE at the time of diagnosis
Significant portion of newly diagnosed Type 2
diabetics have established DR at the time of
diagnosis
Vascular Insufficiency
arterial occlusions (CRAO, BRAO)
- venous occlusions (CRVO, BRVO)
-
CRAO
CRAO
most
CRAO
presentation is with sudden and
profound loss of vision
RAPD is present
orange reflex from the choroid stands
out at the fovea, and contrasts with the
surrounding pale retina (cherry-red
spot)
must r/o temporal arteritis
CRAO
most commonly the result of
atherosclerosis (thrombosis) but may
also be caused by calcific emboli
often in older patients, with a hx of
arteriosclerosis
may have had a hx of amaurosis fugax
(transient visual loss)
CRAO
OPHTHALMOLOGIC EMERGENCY!!
treatment:
decrease IOP
paracentesis
ocular massage
goal: to send the embolus distally
**remember to r/o giant cell arteritis! (ESR, CRP, plt)
poor prognosis: 60% 20/400
BRAO
BRAO
sudden and profound altitudinal or
sectoral visual field loss
similar causes as CRAO
identify and treat associated medical
conditions (HTN, DM,
hypercholesterolemia, smoking,
vasculitis etc)
BRAO
retinal cloudiness in ischemic area
+/- visible embolus
also has a poor prognosis, unless the
obstruction can be dislodged within a
few hours
CRVO
CRVO
thrombosis
CRVO
underlying associations
advancing age
systemic conditions: HTN, DM, smoking,
obesity, hyperlipidemia
glaucoma
inflammatory diseases: sarcoidosis, Behcet
disease
thrombophilic disorders:
hyperhomocysteinaemia, antiphospholipid
antibody syndrome
CRVO
Treatment:
treat associated medical conditions
decrease IOP if elevated
pan-retinal photocoagulation
(laser) if:
neovascularization (iris, angle,
retina)
especially if ischemic CRVO
BRVO
BRVO
thrombosis
BRVO
obstruction often at arterio-venous
crossings: arteries and veins share
adventitial sheath thickening of the
arteriole (arteriosclerosis) compresses the
vein, eventually causing an occlusion
often associated with:
hypertension (75%)
diabetes (10%)
BRVO
prognosis: depends on amt of venous
drainage involved by the occlusion and
severity of macular ischemia: within 6 mos,
about 50% of eyes have a VA of 20/30 or
better
main complications:
chronic macular edema
neovascularization
Retinal Tumours
ocular
tumours:
ciliary body:
melanoma
choroid:
melanoma
hemangioma
metastases
Choroidal Melanoma
most
signs:
raised, usually pigmented lesion visible at
the back of the eye
may be associated with retinal detachment
optic nerve may be involved
Choroidal Melanoma
treatment:
Choroidal Metastases
with
CXR
Choroidal Metastases
usually
Choroidal Metastases
treatment:
prognosis
is poor
Retinoblastoma
most
Retinoblastoma
malignant
transformation of primitive
retinal cells before their final differentiation
can
Retinoblastoma
this
Retinoblastoma
prognosis:
Macular Degeneration
Macula
1.5
mm in diameter
central vision: BEST VISUAL ACUITY
colour vision
progressive destruction of the macular
area:
MACULAR DEGENERATION
Macular Degeneration
most
Non-exudative Macular
Degeneration
lipid
Exudative Macular
Degeneration
new
subsequent
Macular Degeneration
symptoms:
Macular Degeneration
rx:
Macular Degeneration
rx:
Pre-retinal:
glaucoma
Retinal:
tumours
macular degeneration
Post-retinal:
OPTIC NERVE
1.2
million cells
80 % visual fibres
20 % pupillary fibres
carries
visual
information from
the eye to the brain
OPTIC CHIASM
crossover
above
of nasal fibers
the pituitary
internal
lateral
from
optic chiasm:
optic
tract to the
lateral geniculate body
optic
radiation to the
primary visual cortex
Anterior to Optic
Chiasm
compressive optic neuropathies
- toxic/nutritional optic neuropathies
-
Compressive Optic
Neuropathies
INTRACRANIAL
MASSES:
THYROID
EYE DISEASE
no
loss from:
exposure keratopathy
due to severe proptosis resulting in incomplete lid
closure chronically exposed cornea corneal
ulceration & exposure keratopathy
optic neuropathy
affects 5% of pts
compression of ON or its blood supply by
congested (enlarged) EOMs
can lead to severe, permanent visual impairment
rx with steroids, surgery if needed
Toxic/Nutritional Optic
Neuropathies
nutritional
deficiencies
alcohol-tobacco amblyopia
Nutritional Deficiencies
Alcohol-Tobacco Amblyopia
pituitary adenoma
Pituitary Adenoma
presentation
middle age
symptoms:
h/a
visual symptoms: very gradual onset (often
not noticed by pt until very well-established)
VF defect: usually, bitemporal hemianopia, worst in
the superior field, and extending inferiorly
colour desaturation across vertical midline
optic atrophy: in 50% of cases with field defects
caused by pituitary lesions
Pituitary Adenoma
investigations:
Pituitary Adenoma
treatment
options:
observation
medical: dopamine agonists (bromocriptine)
surgery
radiotherapy: often used as an adjunct
gamma knife stereotactic radiotherapy
Merci