Retina

DECANO, JOANNE APRIL

DOLOT, MIGUEL C.
RETINA

 MOST COMPLEX OF THE OCULAR TISSUES with a highly

organized structure
 Receives visual image produced by the optical system of
the eye →conversion of light energy into an electrical
signal → initial processing →transmission through the optic
nerve to the visual cortex →perception of structural and
spatial attributes
PHYSIOLOGY OF THE RETINA ROD AND CONE PHOTORECEPTORS
 For initial transformation through phototransduction of light stimuli into the nerve
impulses
 Located in the avascular outermost layer of the sensory retina
 Each rod photoreceptor cell contains RHODOPSIN (a photosensitive visual pigment
embedded in the double-membrane disks of the photoreceptor outer segment)
Opsin + chromophore = rhodopsin
o SCOTOPSIN serves as opsin
o RETINAL serves as chromophore
 When rhodopsin absorbs a photon of light, 11-cis terminal is isomerized to trans
retinal & eventually to → all-trans retinol
NIGHT (SCOTOPIC) VISION
o Mediated entirely by rod photoreceptors
o Dark-adapted form of vision where only varying shades of gray are seen
DAYLIGHT (PHOTOPIC) VISION
o Mediated primarily by cone photoreceptors
TWILIGHT (MESOPIC) VISION
o Combination of rods & cones
RETINAL PIGMENT EPITHELIUM
 Maintains photoreceptors
Function
o Phagocytosis of the outer segments of the photoreceptors
o Transport of vitamins
o Reduction of light scatter
o Providing a selective barrier between the choroid & retina
 Its basement membrane forms the inner layer of Bruch’s
membrane
 Have little capacity for regeneration
FOVEA
 In the foveola there is 1:1 relationship between each cone
photoreceptor, its ganglion cell, & the emerging nerve fiber
 Responsible for SPATIAL RESOLUTION (visual acuity) &COLORVISION,
both requiring high ambient light (photopic vision)
 Remaining retina is utilized primarily for MOTION, CONTRAST,
&NIGHT VISION(scotopic)
EXAMINATION
 Via Direct or indirect ophthalmoscope
 Via Slitlamp (biomicroscope)
 Handheld or contact biomicroscopylens
 Allows identification of the type, level, & extent of retinal disease
 Retinal imaging techniques are useful adjuncts to clinical
examination, enabling identification of anatomical, vascular
(retinal & choroidal), & functional abnormalities
Anatomy
 Pigment epithelium. It is the outermost layer of retina. It consists of a
single layer of cells containing pigment. It is firmly adherent to the
underlying basal lamina (Bruch’s membrane) of the choroid.
 Layer of rods and cones. Rods and cones are the end organs of
vision and are also known as photoreceptors. Layer of rods and
cones contains only the outer segments of photoreceptor cells
arranged in a palisade manner.
Photoreceptors
Rods- scotopic or dark vision (vision of low illumination)
Cones-photopic or day and color vision (highly discriminatory
central vision)
 External limiting membrane. It is a fenesterated membrane, through
which pass processes of the rods and cones.
 Outer nuclear layer. It consists of nuclei of the rods and cones.
 Outer plexiform layer. It consists of connections of rod spherules
and cone pedicles with the dendrites of bipolar cells and horizontal
cells.
 Inner nuclear layer. It mainly consists of cell bodies of bipolar cells. It also
contains cell bodies of horizontal amacrine and Muller’s cells and capillaries
of central artery of retina. The bipolar cells constitute the first order neurons.
 Inner plexiform layer. It essentially consists of connections between the
axons of bipolar cells dendrites of the ganglion cells, and processes of
amacrine cells.
 Ganglion cell layer. It mainly contains the cell bodies of ganglion cells (the
second order neurons of visual 7pathway). There are two types of ganglion
cells.
a. The midget ganglion cells are present in the macular region andthe dendrite of
each such cell synapses with the axon of single bipolar cell.
b. Polysynaptic ganglion cells lie predominantly in peripheral retina and each such
cell may synapse with upto a hundred bipolar cells.
 Nerve fibre layer (stratum opticum) consists of axons of the ganglion cells,
which pass through the lamina cribrosa to form the optic nerve.
 Internal limiting membrane. It is the innermost layer and separates the
retina from vitreous. It is formed by the union of terminal expansions of the
Muller’s fibres, and is essentially a basement membrane.
Gross anatomy
 Retina extends from the optic disc to the ora serrata.
Grossly it is divided into two distinct regions:
1. posterior pole
2. peripheral retina
separated by the retinal equator.
 Retinal equator is an imaginary line which is considered to lie in line with the
exit of the four vena verticose.
 Posterior pole refers to the area of the retina posterior to the retinal equator.
 includes two distinct areas: the optic disc
 and macula lutea
 Optic disc. It is a pink coloured, well-defined circular area of 1.5-mm
diameter. At the optic disc all the retinal layers terminate except the nerve
fibres, which pass through the lamina cribrosa to run into the optic nerve. A
depression seen in the disc is called the physiological cup. The central
retinal artery and vein emerge through the centre of this cup.
 Vitreous
 Transparent gel like structure
 Composed mainly of water and proteins
 Maintains the tone of the eyeball

 Vitreous Base
 An area of vitreoretinal adhesion which
straddles the pars plana , oro serrata, and
most peripheral retina(3-4mm width)
 Anterior hyaloid- anterior border of the
vitreous
 Posterior hyaloid- post. border of the
vitreous
Retina and Areas

 Optic disc
 Macula
 Central/peripheral retina
 Retinal Vasculature
 Choroidal Vessels
Normal Retina
 The retina is approximately 0.5 mm thick and lines
the back of the eye.
Optic Nerve and Vessels
 Circular to oval
white area
 Measures about
2 x 1.5 mm
across.
 Major blood
vessels of the
retina radiate
from the center
of the nerve
Optic Nerve
 Transmits visual
impulses from
the retina to
the brain.
 Visible part of
the optic nerve
is the optic
disc, or optic
nerve head.
 Optic Nerve
 ON goes through
the lamina
cribrosa, a
fibrous, sieve-like
structure
 Lamina cribrosa
forms the base of
the physiologic
cup, the
depression in the
disc.
Cup/Disc
C/D ratio
Rim of ON is
compared in
size with the
cup to get
C/D ratio.
Scale from
0.1 to 0.9
Normal 0.3 or
less
Optic Nerve

 Peri = around  papilledema

 Papillary =
ON
 Peripapillary
= area of the
retina around
ON.
Optic Nerve disease
 Drusens are intrapapillary
refractile bodies, which
 Optic disc usually lie deep beneath the
surface of the disc tissue in
drusen childhood and emerge out by
the early teens.
 Thus, in children they present
as pseudo-papilloedema and
by teens they can be
recognized
ophthalmoscopically
 as waxy pea-like irregular
refractile bodies.
Optic Nerve Disease

 Optic disc pit  Optic nerve

hypoplasia
Optic Nerve Disease
 Coloboma  It results from
the failure in
closure of the
embryonic
fissure.
 Defect on the
inferior aspect
of the ON
Optic Nerve Disease
 Optic atrophy  Leber’s optic
neuropathy
Macular Area

 “Straight ahead”
vision
 Best visual acuity
 Cones form a
concentrated area
known as the fovea,
 Fovea is center of the
macula
Fovea

 Located 2 1/2
disc diameters
to the left of
the disc,
 slightly oval-
shaped
 blood vessel-
free reddish
spot
Macula

 The center of the fovea is known as the foveal pit

Macula
 The whole foveal area
 foveal pit,
 foveal slope,
 parafovea and
 perifovea is considered the MACULA
area
 A yellow pigmentation to the
macular area is known as the macula
lutea.
Macula lutea

 Yellow pigmentation
 Acts as a short wavelength
filter,
 (Lens also a filter)
 Protective mechanism for
avoiding bright light and
especially UV irradiation
damage
Macular Disease

 AMD  Stargardts
AGE RELATED MACULAR
DEGENERATION (AMD)
 Affects people over 55 years
 LEADING CAUSE OF IRREVERSIBLE BLINDNESS IN THE DEVELOPED
WORLD
 A complex multifactorial progressive disease
 May be genetic, involving the complement pathway &
environmental risk factors, including increasing age, white race, &
smokers
CLASSIFICATION OF AMD
1. Early AMD
 Characterized by limited drusen, pigmentary change, or retinal
pigment epithelial atrophy
 Fluorescein angiography – irregular patterns of RPE hyperplasia &
atrophy
 DRUSEN
o Yellow deposits w/in Bruch’s membrane
o Discrete or confluent
o May also be detected as diffuse subretinal deposits, either:
basal laminar deposits formed mainly of collagen-based
material & situated between the plasma & basement
membranes of the retinal pigment epithelium, or basal linear
deposits, consisting of granular lipid-rich material located w/in
the Bruch’s membrane
2. Late AMD
 GEOGRAPHIC ATROPHY (“dry”AMD)
o 20% of legal blindness attributable to AMD
o Manifests as well-demarcated areas, larger than 2 disk diameters,
of atrophy of the RPE & photoreceptor cells, allowing direct
visualization of the underlying choroidal vessels
o Accumulation of LIPOFUSCIN– thought to contribute to strophic
changes
o Visual loss – occurs once the fovea is affected
 NEOVASCULAR (“wet” AMD)
o Development of choroidal neovascularization or serous retinal
pigment
epithelium detachment
o Choroidal new vessels may grow in a flat cartwheel or sea-fan
configuration
o Permanent loss of central vision ensues.
o Fluorescein angiography should be performed on all patients w/
AMD w/ new onset of reduced vision or distortion, as the most
sensitive method
Prophylactic Therapy
o Oral vitamins and antioxidants daily comprising
500g vitamin C
400 IU vitamin E
15mg betacarotene
80mg zinc
2mg copper
o Smokers taking betacarotene has an increased risk of
developing lung cancer
o Smoking
Risk factor for development of all forms of macular
degeneration
Cessation is thought to reduce the rate of progression
o RETINAL LASER PHOTOCOAGULATION
Reduces the extent of drusen but increases the rate of
choroidal neovascularization
Treatment of Neovascular AMD
o ANTI-VEGF THERAPY – preferred tx for neovascular AMD
o RANIBIZUMAB
Treatment of choice for all forms of neovascular AMD
o ANCHOR trial
Significant benefit over photodynamic therapy (PDT) for
predominant classic lesions
o PEGAPTANIL
Binds the major pathogenic isoform of VEGF
Intravitreal injection administration
o BEVACIZUMAB
Humanized full length monoclonal antibody to VEGF
o CONVENTIONALRETINAL LASER PHOTOCOAGULATION
Direct destruction of a choroidal neovascular membrane
PHOTODYNAMIC THERAPY
intravenous infusion of a photosensitive dye, VERTEPORFIN
Stargardt disease
 The ABCR gene produces a
protein involved in energy
transport to and from
photoreceptor cells in the
retina.
 Mutations in the ABCR gene,
which cause stargardt
disease, produce a
dysfunctional protein that
cannot perform its transport
function. As a result,
photoreceptor cells
degenerate and vision loss
occurs
Macular Disease

 Best’s juvenile,
adult
 Best disease, also termed 
vitelliform macular
dystrophy, is typically an
autosomal dominant
disorder, which classically
presents in childhood with
the striking appearance of
a yellow or orange yolklike
lesion in the macula.
Abnormalities in the eye
result from a disorder in
the retinal pigment
epithelium (RPE). A
dysfunction of the protein
bestrophin results in
abnormal fluid and ion
transport by the RPE.
Macular Disease

 Coat’s  CME
Macular Disease

 Drusen  Macular hole

Central and Peripheral
Retina
 Central retina = circular
field 6 mm around fovea
 Peripheral retina
stretches to the ora
serrata, 21 mm from the
center of the optic disc.
Ora Serrata
 Anterior
termination of
the retina
 Junction of the
retina and the
ciliary body.
 Retina attaches
to the choroid at
ora serrata.
Peripheral Retinal Disease

 Retinitis  Sickle Cell

Pigmentosa Retinopathy
Peripheral Retinal Disease

 Lattice  Retinal tear

Degeneration
2 sources of retinal blood
supply
 CHOROIDAL
BLOOD VESSELS

 65-85% of blood flow

 Nourishes outer retina
(photoreceptors = rods
and cones)
2 sources of retinal blood
supply
 CENTRAL
RETINAL ARTERY

 20-30% blood flow

 Nourishes inner retinal
layers
 Has 4 main branches
Retinal vessels

 Arteries cross  Arteriole

over veins narrowing in
hypertension
RETINAL VASCULAR
DISEASE
1. DIABETIC RETINOPATHY (DR)
 Chronic hyperglycemia,
hypertension,
hypercholesterolemia, & smoking
are all risk factors for
development & progression of
retinopathy
o Type 1 DM (insulin dependent)
 Does not develop retinopathy for
at least 3-5 years after the onset
of the systemic disease
o Type II DM (non-insulin dependent)
 May have retinopathy at the time
of diagnosis,
 May be the presenting
manifestation
Screening
o Readily detectable
changes occur before
vision is affected
o Screening should be
performed w/in 3 years
from diagnosis in type I
diagnosis, on diagnosis in
type II diabetes, &
annually thereafter in
both types
o Digital fundal
photography
Effective & sensitive
method for screening
o Seven-field photography
GOLD STANDARD
However, two 45o
fields, one centered on
the macula & the other
centered on the disk,
are becoming the
method of choice in
most screening
programs
Mydriasis is necessary for
best quality photographs,
especially if there is
cataract
Treatment
o Good control of hyperglycemia, systemic hypertension, &
hypercholesterolemia
MAINSTAY OF PREVENTION OF PROGRESSION TO RETINOPATHY
o Clinically significant macular edema requires:
Focal laser – if focal macular edema
Grid laser – if diffuse macular edema
o Intravitreal injections of TRIAMCINOLONE or ANTI-VEGF agents are also
effective
o VITRECTOMY
Able to clear vitreous hemorrhage & relieve vitreoretinal traction
Classification of Diabetic
retinopathy

 Nonproliferative retinopathy
 Maculopathy
 Proliferative retinopathy
2. RETINAL VEIN OCCLUSION
A common and easily diagnosed w/ potentially blinding
complications
Presents w/ sudden painless loss of vision
Clinical appearance varies from a scattered retinal
hemorrhages and cotton-wool spots to a marked hemorrhagic
appearance w/ both deep and superficial retinal hemorrhage,
CENTRAL RETINAL VEIN OCCLUSION (CRVO)
o Retinal abnormalities involve all 4 quadrants of the fundus
BRANCH RETINAL VEIN OCCLUSION (BRVO)
o Confined to one quadrant
o May involve the upper or lower half or just the macula
Major complications
o Reduced vision from macular edema
o Neovascular glaucoma secondary to iris neovascularization
o Retinal neovascularization
Vein Disease

 CRVO  BRVO
2. RETINAL VEIN OCCLUSION
A common and easily diagnosed w/ potentially blinding
complications
Presents w/ sudden painless loss of vision
Clinical appearance varies from a scattered retinal
hemorrhages and cotton-wool spots to a marked
hemorrhagic appearance w/ both deep and superficial
retinal hemorrhage, w/c rarely may break through into the
vitreous cavity
o Retinal neovascularization
CENTRAL RETINAL VEIN OCCLUSION
o Retinal abnormalities involve all 4 quadrants of the fundus
BRANCH RETINAL VEIN OCCLUSION
o Confined to one quadrant because the occlusion usually
occurs at the site of an arteriovenous crossing o May
involve the upper or lower half (hemispheric branch
retinal vein occlusion), or just the macula (macular
branch retinal vein occlusion)
Major complications
o Reduced vision from macular edema
o Neovascular glaucoma secondary to iris
neovascularization
Treatment
 In branch retinal vein occlusion, grid-pattern macular argon
laser photocoagulation may be indicated when vision loss due
to macular edema persists for several months w/o an
spontaneous improvement
Intravitreal injection of anti-VEGF agents or steroids may
be useful
Monthly renibizumab injections for macular edema
secondary to branch and central retinal vein occlusion
Ozurdex (Allergan) with dexamethasone
Increased IOP
o Most commonly reported adverse events during the first
6 months after treatment
IRIS AND RETINAL NEOVASCULARIZATION IN
RETINAL VEIN OCCLUSION

Pan-Retinal laser Photocoagulation (PRP)

o Standard treatment for iris neovascularization
May also be controlled w/ intravitreal anti-VEGF
agents
Sectoral retinal laser photocoagulation
Laser Panretinal
Photocoagulation
Arteriole Disease

 CRAO  BRAO
RETINAL ARTERY OCCLUSION (CRAO)
o Causes painless catastrophic visual loss occurring over a period of
SECONDS;
o Caused by antecedent transient visual loss (amaurosis fugax)
o Other causes of central retinal artery occlusion
Arteriosclerosis
Emboli from carotid or cardiac sources
 Branch retinal artery occlusion (BRAO)
o Also causes sudden painless visual loss but usually manifesting as
impairment of visual field
o Visual acuity is only reduced if there is foveal involvement
o With retinal opacification is the same as central retinal artery occlusion, but
sometimes accompanied by cotton-wool spots along its border
o Determined by the extent of retinal infarction
o Most often cause is embolic disease
Treatment

o anterior chamber paracentesis & intravenous acetazolamide

for Sudden decrease in IOP resulting in increased retinal perfusion

o Inhaled oxygen-carbon dioxide mixture

o Thombolytic therapy
o Systemic anticoagulants
RETINAL DETACHMENTS
RHEGMATOGENOUS RETINAL DETACHMENT
o MOST COMMON type
o Characterized by:
Full-thickness break in sensory retina such as:
Horseshoe tear
Round atrophic hole
Anterior circumferential tear (retinal dialysis)
Vitreous traction
Passage of liquefied vitreous
o Accompanied by: posterior vitreous detachment
o Associated with: myopia, aphakia, lattice degeneration, and
ocular trauma
o Ophthalmoscopy reveals: elevation of translucent detached
sensory retina with full thickness sensory retinal breaks
Retinal Detachment
 Treatment of Retinal Detachment
 Lasers
 Cryotherapy
 Expansile gas
 Scleral buckles
 Vitrectomy surgery
 Silicone oils
Choroid

 Layer in-between the

retina and the sclera
 Mainly composed of
blood vessels
 Function is to supply
nourishment to the outer
portion of the retina
Choroidal Disease

 Choroidal
neovasc
Choroidal Disease
 Chorioderemia  Choroideremia is a
condition characterized
by progressive vision
loss that mainly affects
males. The first
symptom of this
condition is usually an
impairment of night
vision (night blindness),
which can occur in early
childhood.
Bruch’s Membrane

 Separates the retina

and choroid
 Permeable
membrane
 Water-soluble
nutrients diffuse from
the choroid to the RPE
and retina
Bruch’s membrane

 If Bruch’s membrane
compromised,
nutrients such as
vitamin A, might not
be able to reach rods
and cones.
 Drusen deposits of
extracellular material
 Provide space for
SRNV by lifting up the
RPE
Subretinal
neovascularization
 SRNV  SRNV
 abnormal vessels
develop and penetrate
Bruch’s membrane after
it is first damaged by
something else.
Subretinal
neovascularization
 SRNV  SRNV
 AMD correlates with a
thickening of the
membrane with extra-
cellular material
Retinal Pigment Epithelium

 RPE
 layerof dark tissue
 absorbs excess light so that
the photoreceptors can
give a clearer signal
(reduces scattering)
Retinal Pigment Epithelium
 Plays a role in "trimming"
photoreceptors -- cones are
"trimmed" at dusk, and rods are
"trimmed" at dawn
 Move nutrients to (and waste
from) the photoreceptors to the
choroid.
 Bruch's membrane separates the
choroid from the RPE.
Diseases of RPE

 Central serous  Central serous

Sensory Retina: Rods and
Cones

RPE
Retinitis Pigmentosa

 Degeneration
of rods
 Loss of
peripheral
vision
External Limiting
Membrane
Outer Nuclear Layer
 Theouter nuclear layer
contains cell bodies of the
rods and cones
Outer Plexiform Layer

 The outer
plexiform
layer (OPL)
 Connections
between rod
and cones,
 and bipolar
cell dendrites
Inner Nuclear Layer

 Contains:
 Nuclei of bipolar cells
 MÜller cells (synthesize and
store glycogen)
 Amacrine cell bodies (act
as condensers, as in an
electric circuit)
Inner Plexiform Layer

 Relay station for

the bipolar cells,
to connect to
ganglion cells.
 Amacrine cells
also interact in
networks to
influence and
integrate ganglion
cell signals
Ganglion Cell Layer

 Ganglion
cell axons
are fibers
that carry
electrical
signal to
the optic
nerve
Nerve Fiber Layer

 Located above the

ganglion cell layer
 Fibers radial to the optic
nerve
 Distribution plays role in VF
defect patterns
 Major blood vessels
embedded in this layer
Nerve Fiber Pattern
Blood vessels in NFL

 Flame  located in NFL

hemorrhage
Internal Limiting
Membrane
 Layer right
next to the
vitreous.
 Forms a
diffusion
barrier
between
neural retina
and vitreous
humor.
Internal Limiting
Membrane
 Wrinkling of the ILM can cause
distorted central VA
ILM

 Standard surgery  Membrane Peel

for macular
pucker or macular
hole repair
 Peeling away the
ILM with
microsurgical
forceps.
 Time-sensitive
delicate and
difficult operation
ILM
 New technique
Fluidic Internal
 Removes the 
Limiting Membrane
abnormal macular Separation
tissue and wrinkled
ILM
 Fluid pressure lifts
ILM and separates
tissue
 Also smoothes
underlying distorted
retinal layer
Neovascularization

 neovasc  New blood

vessels
Blood in front of retina