RETINA

Ding JianGuang
Anatomy of Retina:

 Thin, semitransparent, inner layer

of the wall of the eyeball.
 Anterior margin: ora serrata
ciliary body
Posterior margin: round the optic
disc
Outside: closely neighbors with
the choroid
Inside: vitreous
Anatomy of Retina (Histology):

 10 layers, Retina pigment epithelium(RPE) are

firmly bound to Bruch’s membrane (basement
membrane of the RPE, its outside is choroid),
 RPE : tidy arranged, hexagonal cells, transport
nourishment from the choroid to the external layer
of the retina(5 layers)
 Photoreceptor layer ( rods and cones) separate
from the RPE layer --Retina detachment.
 Visual message visual never pulse.transmitted
by 3 neurons: Photoreceptor - bipolar cell –
ganglion cell.
 Photoreceptor cells : Rods (function)—dark vision
Cones—strong light and color
vision
Anatomy of Retina:
 Macula: the center of the posterior retina
no blood vessel, responsible for
the best visual acuity and color
vision.
 Fovea: the center of the macula
only cones
 Optic disc: 4mm lateral to the fovea
no photoreceptor cells
 The retinal artery: from ocular
artery
 The retinal vein
 Peripheral retina: mainly rod
photoreceptors, for peripheral and night
vision.
Examine the Retina:
 Direct ophthalmoscopy
 Indirect ophthalmoscopy
 Goldman three-mirror lens
 Fundus photography
Examine the Retina:
 Fundus Fluorescein
Angiography(FFA)—take pictures
 Indocyanine green
angiography(ICG)
 Electrophysiologic testing
ERG (Electroretinography)
—F-ERG : reflect the whole
retina (various retinopathies)
—P-ERG : reflect never ganglion
cell layer
EOG (Electro-oculography)—reflect
the diseases of RPE
VEP (Visual Evoked Response)—
above the ganglion cells
 Diseases of the Retina:
 Diseases of the macula:
Age- related macular degeneration ( AMD)
Central serous chorioretinopathy ( CSC)
 Diseases of the peripheral retina:
Retina detachment (RD)
 Retinal vascular diseases:
Retinal artery occlusion (Central , CRAO; Branch , BRAO)
Retinal vein occlusion (CRVO; BRVO)
Diabetic retinopathy (DR)
 Tumors of the retina:
Retinoblastoma(RB)
 Age- related macular degeneration
( AMD)
 Age-related macular degeneration is the
leading cause of permanent blindness in the
elderly. The exact cause is unknown, but
the incidence increases with each decade
over age 50.
 classified into two groups: nonexudative
("dry") and exudative ("wet").
 Nonexudative Macular
Degeneration
 Nonexudative age-related macular degeneration is
characterized by variable degrees of atrophy and
degeneration of the outer retina, retinal pigment
epithelium, Bruch's membrane and
choriocapillaris.
 Drusen are discrete, round, yellow-white deposits
of variable size beneath the pigment epithelium
and are scattered throughout the macula and
posterior pole.
Nonexudative age-related macular degeneration. Typical signs
include drusen (arrow) and geographic central atrophy
(arrowhead).
 Nonexudative Macular
Degeneration
 In addition to drusen, clumps of pigment
irregularly dispersed within depigmented
areas of atrophy may progressively appear
throughout the macula.
 There is no generally accepted means of
preventing of this type of macular
degeneration.
Exudative Macular Degeneration
 the majority of patients who experience severe
vision loss from this disease do so from the
development of subretinal neovascularization and
related exudative maculopathy
 Ingrowth of new vessels from the choroid into the
subretinal space is the most important change that
predisposes patients with drusen to macular
detachment and irreversible loss of central vision.
Exudative age-related macular degeneration. A typical finding
is the intraretinal serous fluid (arrows), which is extravasating
from the choroidal neovascularization.
a Fluorescein angiogram.
A classic
choroidal
neovascularization
is visible
under the fovea
(arrows). This is
therefore a late,
exudative stage
of age-related
macular
degeneration.
Exudative Macular Degeneration
Treatment
a well-defined extrafoveal (≥200um from
the center of the foveal avascular zone)
subretinal neovascular membrane----laser
photocoagulation
Central Serous Chorioretinopathy

 Central serous chorioretinopathy is

characterized by serous detachment of the
sensory retina as a consequence of focal
leakage of fluid from the choriocapillaris
through a defect in the retinal pigment
epithelium.
 Young to middle-aged men, may be related
to life stress events.
Central Serous Chorioretinopathy
Central Serous Chorioretinopathy
A sudden onset of blurred vision, micropsia,
metamorphopsia, and central scotoma.
 Visual acuity is often moderately decreased.
 FFA: Fluorescein dye leaking from the
choriocapillaris may accumulate below the
pigment epithelium or sensory retina, resulting in
a variety of patterns including the well-recognized
smokestack configuration.
Central Serous Chorioretinopathy
Central Serous Chorioretinopathy
 80% of eyes undergo spontaneous resorption of
subretinal fluid and recovery of normal visual
acuity within 6 months.
 Many patients have a mild permanent visual
defect.
 Argon laser photocoagulation shortens the
duration of the sensory detachment and hastens
the recovery of central vision, but can not reduce
the chance of permanent loss of visual function.
Myopic Macular Degeneration
 Pathologicmyopia is one of the leading
causes of blindness and characterized by
progressive elonggation of the eye with
subsequent thinning and atrophy of the
choroid and pigment epithelium in the
macular.
Myopic Macular Degeneration
 Perpapillary chorioretinal atrophy and linear
breaks in Bruch’s membrane are characteristic
findings on ophthalmoscopy.
 A characteristic lesion
of this disease is a
raised, circular,
pigmented macular
lesion called a Fuchs
spot.
Myopic Macular Degeneration
 Most patients are in the fifth decade when
the degenerative macular changes cause a
slowly progressive loss of vision; rapid loss
of visual acuity is usually caused by serous
and hemorrhagic macular
degeneration overlying a
subretinal neovascular
membrane.
Myopic Macular Degeneration
 Peripheral retinal findings may include
paving stone degeneration, pigmentary
degeneration, and lattice degeneration.
 Some retinal breaks

will progress to
Rhegmatogenous
retinal detachment.
 Macular Hole
A macular hole is a partial
or full-thickness absence of
the sensory retina in the
macula.
Tangential traction from
epiretinal vitreous cortex
plays an important role in
the pathogenesis.
Retinal detachment:
 Retinal detachment:
Separation of the sensory retina
(photoreceptors and inner tissue
layers) from the underlying retinal
pigment epithelium (RPE).
Retinal detachment:
 Three main types:

 Rhegmatogenous detachment
 Traction detachment
 Serous or hemorrhagic detachment
Rhegmatogenous retinal
detachment:
 Most common of the three types
 Tear: full-thickness break in sensory retina
horseshoe tear,round atrophic hole,etc
 Blurred vision: one part(nasal 、 temporal)
extend
 Variable degrees of vitreous traction
 Liquefied vitreous through the sensory retina
defect(tear) into the subretinal space
 Usually accompanied by a posterior vitreous
detachment
 Myopia,ocular trauma, aphakia associated with
this type
Posterior vitreous detachment:

 Normal vitreous is bounded by the retina,optic

disk,pars plana, zonule, and lens.
 It’s firmly attached to the retina and pars plana
near the ora serrata
 Support the retina
 With age,the center of the vitreous may undergo
syneresis and become filled with liquid.The liquid
contents of the cavity can migrate into the
preretinal space .The heavier vitreous gel
collapses.
 Vitreous shrinkage:
 Vitreoretinal traction—retinal tear
Rhegmatogenous retinal detachment treatment:

Close the hole(key)

 Cryotherapy
 Laser photocoagulation
 surgery
 Retinitis Pigmentosa
 Retinitispigmentosa is a group of
hereditary retinal degenerations
characterized by progressive dysfunction of
the photoreceptors and associated with
progressive cell loss and eventual atrophy
of several retinal layers.
 Retinitis Pigmentosa
 This disease can be inherited as an
autosomal recessive, autosomal dominant,
or X-linked recessive trait.
 The hallmark symptoms

are night blindness and

gradually progressive
peripheral visual field loss.
 Retinitis Pigmentosa
 The most characteristic ophthalmoscopic findings
are narrowing of the retinal arterioles, mottling of
the retinal pigment
epithelium, and
peripheral retinal
pigment clumping,
referred to as
“bone-spicule formation”.
 Retinitis Pigmentosa
 The electroretinogram usually shows either
markedly reduced or absent retinal function.
 No effective therapy.
 Diabetic retinopathy(RD)
Diabetic patient
 One of the leading causes of blindness in the Western world
 Damage of pericyte and endothelial cell of retinal capillary

 Two types: nonproliferative diabetic retinopathy(back-ground

preproliferative)
proliferative diabetic retinopathy
 Diabetic retinopathy(RD)
Back-ground diabetic retinopathy
 Microaneurysms—the capillaries develop tiny dot-like outpouchings, the
retinal veins become dilated and tortuous .
 Hemorrhages—flame-shaped, dot, blot.
 Macular edema—most frequent cause of visual loss among patients with
background diabetic retinopathy.It is caused primarily by a breakdown of the
inner blood-retinal barrier at the level of the retinal capillary endothelium,
allowing leakage of fluid and plasma constituents into the surrounding retina.
 Diabetic retinopathy(RD)
Preproliferative diabetic retinopathy
 Cotton-wool spots— the most typical finding. microvascular occlusion.
Beading of the retinal veins, and irregular segmental dilation of the retinal
capillary bed.
 FFA: Large filling defects of capillary beds — “capillary nonperfusion” —
show the extent of retinal ischemia, most prominent in the midperiphery.
 No macular edema — treatment of hyperglycemia and intercurrent systemic
disease.
 Macular edema — Focal argon laser treatment of discrete points of retinal
leakage, reduces the risk of visual loss and increases the likelihood of visual
improvement.
 Diabetic retinopathy(RD)
Proliferative diabetic retinopathy
 Neovascularization—progressive retinal ischemia eventually stimulates
the formation of delicate new vessels that leak serum proteins profusely.
The fragile new vessels bleed, massive vitreous hemorrhage may cause
sudden visual loss.
 Diabetic retinopathy(RD)
Proliferative diabetic retinopathy
 Traction retinal detachment —elevated neovascular fronds may undergo fibrous
change and form tight fibrovascular bands that tug on the retina, cause a
progressive traction retinal detachment or rhegmatogenous retinal detachment.
 Diabetic retinopathy(RD)
Treatment of proliferative diabetic retinopathy
 Argon laser panretinal photocoagulation—reduce the chance of
massive vitreous hemorrhage and retinal detachment.
 Vitreoretinal surgery—severe vitreous hemorrhage and proliferative
diabetic retinopathy.
Retinal artery occlusion:
Pathogeny:
 Narrow blood vessel and spasm
 vascular inflammation
 Operation of RD or intraorbital
operation(sometimes)
 Arteriosclerosis
 Retinal artery occlusion clinical finding:
 Not common but very serious
prognosis
 Two types:
Central, branch
 History:
 Painless catastrophic visual loss occurring over a
period of seconds for one eye
 Antecedent transient visual loss
 Examination:
 Visual acuity :
between counting fingers and light perception
(no light perception)
 Light reflex of pupil:
direct: ill eye—disappears
indirect: ill eye—exists
 Retinal artery occlusion clinical finding:
 Examination:
 Fundus: (Ophthalmoscopically)
1. The superficial retina becomes opacified (The
inner layer loses transparence to become grayish-
white edema due to ischemia).
2. Cherry-red spot: in the foveola
Because the retina in macular area is
thinner and without inner layer,so the edema is
no obvious.The choroidal red background
3. BRAO: The retina in distributed area of the
artery is in grayish(retina edema)
4. Retinal artery becomes narrow, with segmental
fluxion of the blood
 Retinal artery occlusion clinical finding:
 FFA
 The filling time of retinal artery is prolonged
 The fluorecein is no filling in obstructed blood
vessel or filling peak prolonged than the others
 A few cases: see doctor quite late
In FFA, the sign of artery occlusion may
not be seen,but the fundus change is very
typical
 Retinal artery occlusion clinical finding:
 After few weeks:
 The function of the retina lost almost at all.
 The retina restores to transparency, but the
ganglions and nerve fibers at occlusion area are
dead.
 Optic atrophy and pale of the disk may be
appeared in the trunk occlusion(CRAO)
 FFA: Artery blood flow had been restored to
unobstructed, but the filling peak prolong than
the other eye or other branch
 Some fundus are normal
 Retinal artery occlusion Treatment:
Retina ischemia is longer than 90 minutes:
retina damage is irreversible (photoreceptor die)
When diagnosis is clear:
4. Massage eyeball by himself at once: Close the eye--use the
finger --press the eyeball for seconds--then loose finger for
seconds--repeat.
5. Anterior chamber paracentesis (puncture)
6. Inhalation with mixed gas(95% oxygen+5%carbon
dioxide),10 minutes every hour
7. Or inhalation of isoamyl nitrite
8. Retrobulbar injection: drugs:Tolazoline,
papaverine(with the use of promote angiectasis )
9. Treat systemic disorder: carotid and heart system(risk of
cerebral infarction)
10. It must be performed within 8 hours
 Retinal vein occlusion:
 Common fundus disease
 Pathogeny:
 Extravascular compression: retina artery
compress the neighbor vein at the
arteriovenous crossing
 Insufficient perfusion pressure or increased
intraocular pressure or high blood viscosity.
1.Olds with hypertension and arteriosclerosis
is commonly seen
2. Often complicated by insufficient blood
erythrocytosis, glaucoma,diabetes,etc.
Retinal vein occlusion clinical finding:
 Two types: BRVO is much common
than CRVO
 Clinical finding depend on
the types
 Easily diagnose
 With potentially blinding
complication
 History:sudden painless loss of
vision,often at about 0.1
Retinal vein occlusion clinical finding:

Fundus
Varies from a few small scattered retinal
hemorrhages and cotton-wool spots to a
marked hemorrhagic appearance with both
deep and break through into vitreous cavity.
Retinal vein –dilated tortuous with deep color
Hemorrhages –flame-shape
Optic disk—edema(severe cases)
Yellowish-white hard lipid exudates—cystoid
macular edema(CMD)with long ill course
Retinal vein occlusion FFA:
 Ischemia: capillary occlusion in large area
leading to extensive retinal ischemia
 Non-ischemia: prognosis is quite good
 Venous vascular walls—staining(In later stage of
FFA)
 Two major complications:
Reduced vision from macular edema
Neovascular glaucoma secondary to iris
neovascularization.
Retinal vein occlusion FFA:
Retinal vein occlusion treatment:

*No specific therapy for RVO

*Chinese traditional medicine
*Careful follow-up evaluation is warranted
*When develop anterior segment
neovascularization, prompt panretinal laser
photocoagulation
 Retinoblastoma(RB)

 RB is a rare(morbidity rate is 1/15000-1/28000) but life-

endangering tumor of childhood.Two-thirds of cases appear before
the end of third year.
 Bilateral disease occurs in 30% of cases.
 Generally a sign of heritable disease.An allele within chromosomal
band 13q14(band 14 of long arm of chromosome) controls both the
heritable and nonheritable forms of the tumor. The normal
retinoblastoma gene is a suppressor gene or anti-oncogene. Gene
defect or inactivation----tumor happen.
 Retinoblastoma(RB) clinical
findings:
 RB may exhibit outward or inward
growth---either or both, gradually fill
the eye and extend through the optic
nerve to the brain. Less commonly, to the
orbital tissue.
 Occasionally, discharging malignant cells

into vitreous or anterior chamber,

producing a psedoinflammatory process.
Early symptom isn’t obvious.
RB usually remains unnoticed until
it has advanced far enough to
produce a white pupil (leukocoria).

Simulate symptom: retrolental

fibroplasia, persistence of the
primary vitreous, retinal dysplasia,
Coats’ disease, and nematode
endophthalmitis.
 Retinoblastoma(RB) clinical
findings:
 B-scan ultrasonic
 MRI
 X-ray: show calcific focus
in the tumor
 CT
Retinoblastoma(RB) treatment:
First of all, Rescue the baby’s life
Then saved the eyeball
 Laser photocoagulation or cryotherapy—small tumor,
localized at the retina, early stage, make the tumor necrosis and
atrophy
 Radiotherapyof sclera—60Co, 125I
 Enucleation—over a quadrant, Operative manipulation should be
gentle; cutting of the optic nerve should be as long as you
can(should not less than 10mm)
 Evisceration
of orbit combined with radiotherapy or
chemotherapy—extraocular stage, prognosis is quit worse
 Retinoblastoma(RB) prevention:

 Not effective preventive

 High-risk family(got RB)—for every newborn baby should examine
the fundus with mydriasis