Diseases of Retina
The 4th Affilitated Hospital of China Medical University
Eye Hospital of China Medical University
Introduction
Eyeball structure and retina
Macula lutea
Located 3mm temporally to the optic
papilla, right on the visual axis.
A concave central retinal depression is
called Fovea Centralis
macula lutea contains only cones; 1
cone synapes to 1 bipolar cell,which
synapes to 1 ganglion cell,leading to
the most sensitive vision.
In periferal retina ,600 rods connect to
1 ganglion.
Histology of retina
Internal limiting membrane
Nerve fiber layer
Ganglion cell layer
Inner plexiform layer
Inner nuclear layer
Outer plexiform layer
Outer nulear layer
External limiting membrane
photoreceptor
RPE
Bruchs membrane
Neuroconduction of retina
3 neurons: rod scotopic
vision
Photoreceptor cone photopic
vision
Bipolar Connecting cell between
photoreceptor and ganglion
Ganglion cell
Conduct to brain
Supporting tissue:
Mller cell
Vasculature of retina
inner layer central retinal vascular
system
outer layer choroid ciliary vascular
system
macula lutea choriocapillaries
Retina barrier
Inner barrier bloodretina barrier
dense connection of retinal capillary endothelium
Outer barrier choroid-retina barrier
zonula occludens between the RPE
RPE- Bruchs membrane- choriocapillaries
complex
Symptoms
Visual impairment Related to
lesion site
Metamorphopsia
Vitreous
Flickering traction to
the retina
Macropsia
Retina edema
fewer cones
Micropsia stimulated
micropsia
Signs
Retinal artery occlusion:
Intracellular edema ischemia leads to edema
of bipolar cell,ganglion and RNFL
Extracellular edemaCapillary endothelium injury and the
exudation
Cystoid macular edema
Henles fibers are radically located;
This pooling forms a flower-petal pattern
Intracellular edema Extracellular edema
Exudates
Hard exudate
Leakage of capillary absorb
deposition of lipid in outer plexiform layer
Cotton-wool spot
Since be calledsoft exudation
Precapillary arteriole occlusion
axoplasmic transport blockedorganelles stack
Cotton-wool spot Hard exudate (Hypertensive
retinopathy)
Heamarrhage
Between outer plexiform
layer and inner nuclear
Deep hemorrhage layer .Small round ,dark
red
Located in nerve fiber
layer
Superficial hemorrhage
line strip flame-
like bright red
Crescent-shaped
hematocele with
Preretinal hemorrhage transverse section
Profuse preretinal
hemorrhage into the
vitreous or hemorrhage
Vitreous hemorrhage of retinal neospastic
vasculature
Preretinal Subretianal hemorrhage
hemorrhage
Deep hemorrhage Superficial hemorrhage
Neovascularization
neovessels,NV
A large area of retinal ischemia
formation of vascular endothelial growth factor
neovascularization
neovessels membrane,NVM
Arise from small veins of optic disc and retina; grow along
retinal surface and into the vitreous
Neovacularizaton of optic disc
Retinal neovascularization
Blood vessel change
1,Atherosclerosis, stenosis,occlusion
2,Tortuous vein, dilated vein ,bead-like change
A-v cross sign
A-V cross sign
Vessel white Vessel white sheath
sheath
Microaneurysm
Microaneurysm
Changes of RPE
atrophy
Pigment loss atrophy
Pigment disorder
alteration
alteration
Osteocyte-like pigment deposition
Death
Death or
or proliferation
proliferation
Choroidal neovascularization
Inflammation , metabolic deposit of RPE or Bruchs
membrane break
CNV reach RPE or subsensory layer
Classification of retinal
diseases
Vascular diseases
Macular diseases
Retinal detachment
Retinal degeneration
Retinal tumor
Ocular manifestation of general
diseases
Retinal vascular disease
Retinal artery occlusion
Retinal venous occlusion
Diabetic retinopathy
Vasculitis
Coats disease
Central retinal artery
occlusion CRAO
Etiology
Common causes
atherosclerotic thrombosis of cribiform plate
systemic diseases,hemicrania, trauma, blood
coagulation disorder, inflammation, infectious
disease or connective tissue disease
Occasionally seen in
retrobulbar injection retinal detachment or
orbital operation
Clinical manifestation
Sudden painless vision
Symptoms lose of one eye
Direct light reflex disappear,
Signs indirect light reflex normal
Retinal edema cherry-red spot
Retina artery narrow mild hemorrhage
Normal eye fundus CRAO
21s after injection of
fluorescein ,a complete
absence in filling
central retinal artery,
except segment of
inferior temperal
branch and macular
branch FFA of CRAO
Treatment
Target: to reestablish retinal
circulation & function
Timing: the earlier the better
Drugs: vasodilator( tropical or
systemic)+ reduce IOP
1.Vasodilator :
antispasm or pushing thrombus to the
2.Reducing IOP:
smaller branch
1 massage
2 anterior chamber paracentesis
3 diamox 500mg st 250mg bid
NaHCO3 500mg bid tid
3.Oxgen inhalation:
mixture of 95% oxygen &5% carbon dioxide
4.Fibrolytic enzyme: for patients suspect of thrombosis
urokinase 5 000 10 000U iv qd
Prognosis
Depends on site ,severity and
duration.
Irreversible after 4 hrs
Central retinal vein
occlusion
Clinical manifestation
Non-ischemic type
Mild fundus change :
retinal hemorrhage and
tortuous vein
Mild VA decrease
capillary nonperfusion
rare
Visual field defect
(retinal hemorrhage)
Ischemic type
More common
Extensive retinal
hemorrhage and
tortuous
vein Multiple
cotton-wool spots
Severe VA decrease
Widespread capillary
nonperfusion 60%
cases present iridal
neovascularization.
CRVO CRVO
Nonischemic ischemic
Branch retinal vein
occlusion
BRVO BRVO
FFA
Treatment
Chinese medicine
Anitplatelet or antithrombotic drugs: unknown
therapeutic effects
Systemic examination to find out causes
Corticosteroid if vasculitis exist
Grid pattern photocoagulation of macula PRP
Laser induced retina-choroid vascular
anastomosis
Vasculitis
Idiopathic retinal vasculitis
Eales disease(Retinalperiphlebitis)
Both A. and V. are involved
Causes is unclear patient tuberculin
reaction (+)
Seen in 20-40 years old men
Bilateral peripheral small vessels
occlusion recurrent vitreous
hemorrhage retinal neovascularization
Ealesdisease:
Grey exudate, vessel
white shealth and
pigment scar is
seen near the
temperal periferal
vein.
Clinical manifestation:
early stage: no symptoms
mild hemorrhage: floaters
moderate hemorrhage: visual defect
severe hemorrhage: retinal detachment.
Chinese medicine
Nutrition reinforcement:
vitamin
Remove causes
Corticosteroid
laser photocoagulation
Surgery: vitrectomy
Coats disease
Or retinal telangiectasia external exudative
retinopathy
Often seen in boy unilateral
Youngsters and adults may also suffer
No heredity no relation with systemic angiopathy
Etiology: unknown
Malformation and telangiectasia of capillary in external
plexiform layer Permeability alteration and vessel
rupture
Exudation
Clinical manifestation
Visual
disturbance strabismus leucoria
Fundus
extensive yellow-white lipid exudation
with faring cholesterol crystal capillary
and vein dilate microaneurysm
capillary nonfusion Secondary
glaucoma, exudative RD, uvitis,
complicated cataract
Rare neovascularization
Differential diagnosis
RB
ROP
FEVR
Treatment
Photocoagulation or
cryocoagulation of capillary dilation
Macular diseases
Central serous chorioretinopathy
Age-related macular degeneration
Central exudative chorioretinopathy
Central serous
chorioretinopathy
Often seen in 20-45 years old men
Self-limitted
Related to stress reaction
Etiology unknown
Anxiety,allergy,infection,
insufficient reflux of choroid
vein,thermal regulation
dysfunction
Clinical manifestation
Metamorphopsia
blurred vision,
micropsia
OCT
serous
detachment of the
sensory retina in
the macular area
Subretinal yellow
deposit in the
macular area
FFA shows dye leakage under RPE
Treatment
80% -90%undergo spontaneous
recovery
Corticosteroid is forbidden
Laser photocoagulation may be
considered when the leakage more than
200um away from macula
Age-related macular
degeneration
The incidence increase with each decade over age 50
Main blind-causing disease in elderly
Severe central visual loss
Etiology:
Long-term chronic macular light damage heredity metabolism
nutrient factors
Mechanism:
Decreased phagocytosis of RPE leading to dusen.
Drusen can cause damage of Bruchs membrane CNV and fibrocyte
proliferation
Destruction of choroidal capillary Bruchs membrane RPE and
photoreceptor
Clinical presentation
Visual acuity: decreased VA, metamorphopsia,
micropsia
Visual field: central scotoma
Fundus:
Dry:
drusen, RPE change
Wet:
gray-yellow CNV under retina of posterior pole
associated with dark red subretinal hemorrhage which
covers CNV sometimes
FFA: CNV leakage bleeding
Nonexudate:
Drusen
RPE atrophy
Degeneration of photoreceptor
Choroid capillary atrophy
Exudate:
Dursen
Damage of Bruchs membrane
CNV
Disciform scar formation under
macula, bleeding and leakage of
CNV
Exudative AMD
Treatment
Anti-oxidation drug
CNVM located greater than 200 microns from
the center of the foveal avascular zone (FAZ)
Photodynamic therapy PDT
TTT
Surgically remove CNV
Macular translocation
Retinal detachment
Retinal detachment denotes
separation of the sensory retina from the
underlying RPE
There are three main types
rhegmatogenous traction exudative
Rhegmatogenous retinal
detachment formation
retinal degeneration
Basis liquified vitreous
retinal holeRD
aging
Incentives high myopia
ocular trauma
Clinical manifestation:
Flashes of light, floaters, a curtain or
shadow moving over the field of vision,
peripheral and/or central visual loss.
Normal IOP, then low IOP
Elevation of the retina and a flap tear or
break in the retina
Treatment
Close the tears by
photocoagulation condensation
electric coagulation
Scleral buckling
Vitrectomy
Retinitis Pigmentosa
Chronic ,progressive,inherited disease
Cone cell rod cell and RPE distrophy
Inheritance pattern: AD, AR,X-link
Onset age: childhood,
Bilateral eyes involved
Clinical manifestation
Constriction of visual field
Fundus :
optic disc waxcolor, "bone spicule" pigment
deposition
Nyctalopia is the first symptom
FFA:
window defect, blocked fluorescein in pigment
deposition at early stage, hypofluorescence and the
fluorescein of choroid is seen at late stage
optic disc waxcolor,
bone spicule" pigment
deposition
Treatment
Genetic counselling
Avoiding sunlight and UV
Vasodilator, Vitamins
Suppliment of taurine
Low vision aids
Grid laser coagulation is used with caution
for CME
Retinal tumor
Retinoblastoma
The most common primary intraocular
malignant tumor in children,of which
90%younger than 3 yrs
Heritable (AD)or sporadic
Etiology
parents are affected or gene carriers ,or germ
cell mutation
-----autosomal dominant 40%
patient with retinoblast mutation
-----uninherited 60%
patient with autosomal chromosome mutation
----- RB ,complicated with intelligent and
growth retardation.
Study shows:
loss of or unactivated RB gene is the key
factor of RB
Staging
intraocular stage
glaucomatous stage
extraocular stage
metastasis stage
Differential diagnosis
RB Coats disease
Onset age 90%<3 >6-8 yrs
yrs
Eyes involved 30%both 95%single
Microcirculati none Diffuse
on microanuerysm
abnormality
Cholesterol none Subretinal
cystal ,obvious
Calcification + -
B-us Solid Without solid
tumor tumor
RB Coats disease
Treatment
Small tumor localized in central retina
can be effectively treated with
photocoagulation
Small tumor localized in periferal retina
can be treated with cryotherapy
Moderate localized tumor:Plaque
radiation therapy
Big tumor: Enucleation
Extraocular stage: enucleation+
chemotherapy + radiation (bad
prognosis)
Metastasis : no specific treatment
Right afterLaser
photocoagulation
6 moths after
photocoagulation
RB
After plate radiation therapy
