RETI

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Brief anatomy of Retina + Vitreous +Choroid
symptoms of retinal diseases

Retinal Vascular Diseases

Acquired Macular Disorders

Vitreous-related diseases & Choroid
 Retina right eye
• The innermost tunic of the eyeball, extends from
the optic disc to the ora serrata.

• Macula Lutea
o Temporal to the Optic Disc.
Macula right to the optic disc
o Btw the superior and inferior temporal arterial this is the right eye , and vice
branches versa
o Fovea Centralis is the central depressed part of the
macula, it’s the most sensitive part of the retina with
highest visual acuity, rich in cones.

• Optic Disc
o Where the optic nerve leave the eyeball.
o Contains Physiological Cup which is a depression
where retinal artery and vein enters and leaves the left eye
 Layers of Retina

Neuro
retina
 1. Retinal pigment epithelium (RPE) :
* A single layer of melanin-containing epithelial cells.
• Functions :
phagocytoses the redundant external
segments of the rods and cones.
passage of nutrients and metabolites
between the retina and choroid
regeneration of rhodopsin and cone
opsin , recycling vitamin A
 melanin granules absorb scattered light
2. Photoreceptive layer (Rods and Cones)

Rods Cones

Location of Retina Found around Found around center of

periphery the fovea

Optimal light conditions Dim light (Night vision) Bright light (Day vision)

Visual acuity Low resolution High resolution

(Many rods:one bipolar (One cone:one bipolar
cell) cell)

Color sensitivity All wavelengths Certain wavelengths

(Red, Green, Blue)

Type of vision Achromatic Chromatic

(Black & white) (Color)

No. of types One (All contain Three different

Rhodopsin) iodopsin pigments

Relative abundance Many Fewer

3)External limiting membrane : through which pass processes of the rods and
cones.
4) Outer nuclear layer : nuclei of the rods and cones.
5) Outer plexiform layer : connections with the dendrites of bipolar cells and
horizontal cells.
6) Inner nuclear layer :
- cell bodies of bipolar cells ( first order neurons ) + cell bodies of horizontal
amacrine and Muller’s cells + capillaries of central artery of retina ..
7) Inner plexiform layer : connections between the axons of bipolar cells
dendrites
of the ganglion cells and processes of amacrine cells.
8)Ganglion cell layer : contains the cell bodies of ganglion cells (the second order
neurons )
9) Nerve fibre layer (stratum opticum) : axons of the ganglion cells, which pass
through the lamina cribrosa to form the optic nerve.
10)Internal limiting membrane : the innermost layer and separates the retina from
vitreous body
layers of retina
mnemonic
 Retinal Blood Supply :
* Central retinal artery :
- Nourishes Inner six layers
- Branch of the ophthalmic artery , emerges from center of the physiological cup
-divides into 4 branches : superior-nasal ,superior-temporal, inferior-nasal and inferior-temporal .
• -the endothelial cells of the retinal capillaries are joined by tight junctions
(impermeable to proteins) >> this forms the Inner blood-retinal barrier .
• Blood-Retinal barrier:
* inner: tight junction in retinal capillaries.
* outer:tight junction in pigmented retinal epith (PRE).

* Choroidal vessels : (choriocapillaries)

- Nourish Outer four layers of the retina (including photoreceptors).
- The endothelial cells are fenestrated and leaky.
The retinal veins :
- follow the pattern of the retinal arteries
-The central retinal vein drains into the cavernous sinus directly or
through the superior ophthalmic vein
 Retinal venous
Due to: occlusion
1> central
- abnormal blood retinal vein
(hypercoagulability or occlusion (CRVO):
hyperviscosity)
- abnormal venous wall (inflammation)
- increased Intra-Ocular Pressure (IOP).

Types:
Non- ischemic (75%): milder, resolves or pregresses to the ischemic type.
Ischemic: severe; may be complicated by neovascular glaucoma & a painful blind eye.

Clinical picture:
Sudden partial or complete painless loss of vision Onset may
be less acute than that of arterial occl

Signs:
Marked diffuse(4 quadrants) hemorrhages Great
tortousity & swelling of the veins , exudates
2> Branched Retinal vein occlusion (BRVO):
- More common than CRVO
-Occurs at a crossing point of arteriole (atherosclerotic) & vein, as they share same
adventitia.
- can be ischemic or non-ischemic
* HTN is most important predisposing factor (AV Nicking)

Clinical picture:
Unilateral painless blurred vision Metamorphopsia ± field defect
Asymptamatic (especially if the occlusion was peripheral)
Vision loss  macula affected

Signs:
- vascular dilation and tortuosity ± Hemorrhage in the affected
area

*If the branched retinal venous occlusion was ischemic, that will
result in new vessel
growth in:
Retinal & optic disc >> vitreous hemorrhage "because the new vessels are weak" Iris >> Rubeosis "new vessel
formation in the iris" and Rubeotic glaucoma
*complications (sudden loss of vision both types )...macular edema , macular ischemia , neovascularization
(lead to hemorrhage).. Optical coherence tomography 
Case: 40-yr old hypertensive patent present with this retina on
slit lamp examination
1. Diagnosis: BRVO
2. Most important risk factor: HTN
3.Complication leads to visual loss : macular edema ,
macular ischemia , neovascularization
 Signs/complications that result from "occlusion" … ischemia“

* Cotton wool spots "Soft exudate" * New blood vessels

-white in color with indistinct(not well an ischemic retina release
defined) borders, more superficial vasogenic factors (e.g.VEGF)
-caused by a build-up of axonal debris in →  growth of abnormal
the nerve fiber layer of the retina, blood vessels and fibrous tissue
-found at the margins of ischemic onto the retinal surface and
infarcts,
forward into the vitreous
v e s s e l s → they are permeable,
-seen usually close to the optic disc and in abnormal position 
"thick layer of nerve fibers", not in the break and bleed
periphery "thin layer of nerve fibers"
Blood and thunder appearance
 Retinal arterial
occlusion
>> Usually embolic in origin.
>> Retinal artery occlusion is an eye emergency. Patients should be referred to
the nearest stroke center for further immediate management.
(a careful vascular work –up & a search for carotid artery disease should be made..)

>> Presentation : a sudden painless loss of all or part of the vision (depend where the
embolus close).

>> Acute treatment of central and branch artery occlusions is aimed at dilating the arteriole to
permit the embolus to pass more distally and limit the damage .

>>Complications >> neovascular glaucoma ,macular edema ,macular ischemia..

-While NVG is most commonly observed after Central Retinal VEIN Occlusions, it also occasionally occurs after retinal
artery occlusions and should be monitored.
usually embolic in
origin:
>fibrin-platelet emboli
typically cause a fleeting loss of vision as the emboli passes through the retinal circulation
(Amaurosis fugax). This may last for some minutes and then clears. In young pts, transient loss of
vision may be caused by
>cholesterol emboli migrane..
>calcific emboli
• Cholesterol and calcific emboli may result in permanent obstruction with no recovery
in vision (they may also be seen in the retinal vessels of asymptomatic individuals.
Central retinal artery occlusuin .. One of the top eye emergent cases
Funduscopic evaluation will reveal retinal ischemia. the entire retina (often
including the optic nerve) will appear pale , white &edematous except the macula,
which will look bright red.

Sudden painless loss of vision :

Arterial occlusion
Venous occlusion
Vitreous hemorrhage
Retinal detachment
 The characteristic
Branch retinal artery occlusion .. wedge of pale, ischemic
The obstruction of a branch of the central retinal artery retina should be what
results in focal ischemia of the wedge-shaped area you’re looking for when
supplied by that particular branch. a patient presents with
sudden, partial vision
Same complications
loss.

pan-retinal photocoagulation (PRP)  manage the new vessels on the

retina regardless the cause
Acquired Macular Disorders

Signs and symptoms

Investigations

Age-Related Macular Degenration

Macular hole and epimacular membrane

Central Serous chorioretinitis

Cystoid macular edema

Degenerative myopia
Signs & symptoms of macular diseases >>
- Blurred central vision
- Metamorphopsia (distorted vision)
- Scotomata central (blind spot in visual field) partially
diminished or entirely degenerated visual acuity that is
surrounded by a field of normal or relatively well-preserved
vision. if part of the photoreceptor layer becomes covered,e.g.
by blood, or if the photoreceptors are destroyed.
 Amsler grid
- is a tool used to detect vision problems resulting from damage to the
macula or the optic nerve
No macular disease  no abnormalities in this test egardless of
other diseases present
.
FLUORESCEIN ANGIOGRAPHY
provides detailed information about the retinal circulation
…investigation of choice in CRVO

https://www.youtube.com/watch?v=GI2_SMH9aX8
https://www.youtube.com/watch?v=3QxAIGRTx50
Optical coherence tomography (OCT)
- a non-invasive imaging test. OCT uses light waves to take
cross-section pictures of your retina.
- No contrast material needed to be introduced to the pt
body.

Fovea?
 Commonest cause of irreversible visual loss in
the developed world. progressive painless loss of vision

 Two types:
1. Exudative(wet)→ less common
2. Non-exudative(dry)

Progressive painless loss of vision

Cataract
Diabetic retinopathy
Open angle glaucoma
age related macular degeneration
 Drusen
Failure of RPE to remove lipid products

accumulate in Bruch’s membrane→

Degenerative changes may happen in RPE &
photoreceptors
Dry (nonexudative, > 80%)—Deposition of yellowish
extracellular material (“Drusen”) in between Bruch membrane
and retinal pigment epithelium
1. Non-exudative(dry)
 Hemorrhage
new vessels from the choroid
Choroidal blood vessels

sub-retinal neovascular
membrane→ haemorrhage into the sub-retinal
space or through retina into
the vitreous rapid loss of vision
Left eye
 Symptoms :
 Macular dysfunction symptoms

•  SIGNS
1. usual foveal reflex is absent.
2. Yellow, well-circumscribed drusen
3. In exudative > haemorrhages
4. areas of hypo- and hyper-pigmentation.
5. Stereoscope > elevation of the retina

*Presentation > progressive painless loss of vision.

>> Dry ... just observe , no proved tt.
Elderly pts with dry AMD should be regularly self-tested by Amsler charts
to allow for earlier detection of any abnormal changes in their vision (it
could indicates that dry AMD is progressing toward wet AMD!)

>> Wet... anti VEGF , OCT to follow resolution

if left untreated it can end up with subretinal fibrosis /irreversible
Macular hole/membrane
Presentation: progressive painless blurred and distorted
vision ,
scotoma… in elderly
Female , 30-40 years
, nervous
• Cystoid macular edema
• multiple cyst-like (cystoid) areas of fluid appear in the
macula and cause retinal swelling or edema.
• Presentation : progressive painless decline of vision
• On ophthalmoscopy >> loss of normal foveal reflex,
• If the dx is in doubt >> OCT or fluorescence angio

• Q) Macular edema is a sign ,mention 2 diseases can

cause it?
-Diabetic retinopathy (most common cause) ,uveitis ,
intraocular surgery ,retinitis pigmentosa, any vascular
occlusion (ex.CRAO).

Note:
In central serous retinopathy : fluid accumulates under the retina /
retinal layers
are still packed together ..
 High degree

Retinal tear
Vitreous-related & Choroid Diseases

Clinical examination..

Posterior vitreous detachment

Vitreous hemorrhage

Retinal detachment

Inherited retinal dystrophies

Retinal & choroid tumors

Vitreous Body anatomy
Choroidis the vascular layer of the eye, containing connective tissues, and lying between
the retina and the sclera. The choroid provides oxygen and nourishment to the It nourishes the
deep, outer two-thirds of the retina and may have a role in its temperature homeostasis.

Arterioles, venules and a dense fenestrated capillary network

Along with the ciliary body and iris, the choroid forms the uveal tract. Remember
Uveitis
Ultrasonograp
hy
• Indications
The most prevalent use of ocular ultrasonography is to obtain globe length in order
to calculate corrective lens power requirements. Other uses include the
measurement of tumors including choroidal melanomas , visualization of lens
dislocation,and detection of retinal detachment (specially in case of vetrious
hemorrhage) . Ultrasonography is especially useful in cases in which the fundus is
obscured from visualization by slit lamp and laser interferometry (IOL Master), as in
patients with dense cataracts,vitreous hemorrhage and corneal opacities or
corneal hypae , retinal tumors
**Important in diagnosing choroidal masses or posterior scleritis
 Posterior Vitreous Detachment
• The most common age-related event in the vitreous after Age of 65 .
• defined as separation between the posterior vitreous cortex and
the Inner Limiting Membrane of the retina.
• With age, the vitreous becomes progressively liquefied (syneresis).
this results in optically empty spaces (lacunae) and a reduction in its
shock absorbing capability
•Progressively , can be acute or chronic

• RF can accelairate this condition : Myopia, Trauma, Inflammation ,

connective tissue and collagen disorders
Presentation : Symptoms are most marked on bright days,
when the small pupil throws a sharper image on the
retina.
floaters : These take the form of spots or cobwebs which obscure vision only
slightly
photopsia (Flashes)  more dangerous

Usually, it should happen with no

symptoms
Any of these present mean that
you should refer to ophthalmologist
 Sign on examination :
Vitreous: Weiss ring (indicates detachment at the optic disc)

Complications: retinal break(s), vitreous hemorrhage, retinal detachment.

 Need regular check ups
 Disease
Vitreous Hemorrhage is a relatively common cause of acute vision loss, It is
frequently encountered by ophthalmologists and Emergency Room professionals
alike due to its often rapid onset which causes painless, but substantial vision
loss. Although the diagnosis of vitreous hemorrhage is often straightforward to
make on fundoscopic examination/slit lamp exam or ultrasonography, further
investigation may be required to determine the underlying etiology.
Symptoms depend on the severity

Sudden, painless visual loss or haze is a common presentation

 Vitrous hemorrhage
The three most common causes include
proliferative diabetic retinopathy,
posterior vitreous detachment (PVD) with or without retinal tear,
and ocular trauma.

Less commonly being a result of retinal vein occlusion or

neovascularization with AMD.

- Vitreous hemorrhage sometimes goes away by itself, or it can be removed

with vitrectomy surgery , which may also be required to treat the cause of
the hemorrhage.
 Retinal detachment
A retinal detachment is an ophthalmic emergency requiring urgent diagnosis and treatment.
The potential space between the neuroretina and its pigment epithelium corresponds to the cavity of the
embryonic optic vesicle. The two tissues are loosely attached in the mature eye and may become separated:
most commonly associated with the onset of a posterior vitreous detachment
•If a tear occurs in the retina, allowing
liquefied vitreous to gain entry to the
sub-retinal space.
This causes a progressive,
Rhegmatogenous
Retinal detachment which may be partial or
total.

•If it is pulled off by contracting fibrous tissue on the

retinal surface, for example in the proliferative retinopathy
of diabetes mellitus (traction retinal
detachment).
•When, rarely, fluid accumulates in the sub-retinal space
as a result of an exudative process, which may occur with
 1)Rhegmatogenous retinal detachment TOP EMERGENCY
- A tear in the neurosensory retina permits to the liquified vitreous fluid enter
to the subretinal space causing a progressive detachment separation between
the neurosensory retina and retinal pigment epithelium.

- Usual site for tear superior temporal.

- RF: trauma , posterior vitreous detachment , Lattice Degeneration and Pts with
high myopes or undergo cataract surgery have more risk

 tear level  can see floaters

May be preceded by symptoms of a posterior vitreous detachment,
including floaters and flashing lights.

With the onset of the retinal detachment itself the patient notices the
progressive development of a field defect, often described as a ‘shadow’
or ‘curtain’.

- If the macula becomes detached there is a marked fall in visual acuity

Signs On ophthalmoscope :
- Detached retina → pinkish grey membrane
-“bullous retinal detachment” : marked accumulation of fluid in the sub-retinal space →
undulating movements of the retina
- tear in the retina → reddish pink (underlying choroidal vessels)
- May be ass. with debris in the vitreous comprising blood (vitreous hemorrhage ) .

bullous retinal
detachment
 INVESTIGATION
S ?!
• Rhegmatogenous retinal detachment is a
clinical diagnosis.
•it is sometimes appropriate to examine and document
macula status with ocular coherence tomography and/or
wide field fundus photography.
•Additionally, in cases of media opacities, B-scan ultrasound is
indicated and may be a critical diagnostic tool.
MANAGEMENT :
principle behind the treatment is to :
- close the causative break in the retina
- increase the strength of attachment ( cryoprobe or laser )

Surgically by
1 -external (conventional approach);
2 - internal (vitreoretinal surgery).

Retinal tears not associated with subretinal fluid are

treated prophylactically with a laser or cryoprobe .

It is ALWAYS IMPORTANT to check the peripheral retina in the FELLOW EYE, as

tears or an asymptomatic retinal detachment may be seen here too
 2) tractional
retinal
• ifdetachment
it is pulled off by contracting
fibrous tissue on the retinal
surface (e.g. as in the
proliferative retinopathy of
diabetes mellitus )

• ((the retina is pulled away

from the pigment epithelium
by contracting fibrous tissue
which has grown on the retinal
surface .))

• Vitreoretinal surgery is required

to remove the fibrous
membrane & to repair these
detachments
Inherited retinal dystrophies
• Retinitis pigmentosa :
presents with nyctalopia (poor night vision)
It is aninherited disorder of the photoreceptors.
isolation /association with other systemicdiseases.

Pathogenesis
The disease affects both types of photoreceptors, but
the rods are particularly affected. The
inheritance may be:
• autosomal recessive
• autosomal dominant;
• X-linked recessive.

due to mutations in the gene for rhodopsin.

• SYMPTOMS :
• AD >> later onset and milder degree;
• AR & XR >> present in infancy or childhood.
 poor night vision,
 visual fields become increasingly constricted
and central vision may ultimately be lost.
SIGNS : ( triad )

1) Peripheral clumps of
retinal pigmentation
(‘bone-
spicule’ pigmentation);

2) Attenuation(narrowing) of
the retinal arterioles

3) Disc pallor

Pts may have cataracts at an

early age and may develop
macular oedema.
• INVESTIGATION:

• Family Hx. >> mode of inheritance

• Dx. made clinically
• Electrophysiologic tests are useful in Dx. (early
disease / may be few clinical signs)
• Genetic mapping >> to determining disease
mechanism.
• Note that electroretinogram (ERG) may
be useless in early stages of the disease
• MANAGEMENT:
• Nothing can be done to prevent
the progression of the disease.
• Associated ocular problems can be treated
(cataract , macular edema).
• genetic counselling should be discussed with
the patient.

• PROGNOSIS :
• AR & XR disease produce the most severe
visual symptoms.
• 50% of retinitis pigmentosa will have an acuity
of less than 6/60 by the time they reach 50.
Cone dystrophy
This is less common than retinitis pigmentosa. It is usually autosomal
dominant, but many cases are sporadic.
Patients present in the first decade of life with poor vision. Examination reveals
an abnormal, banded macular appearance which has been likened to a bull’s-
eye target. No treatment is possible but it is important to provide appropriate
help, not only to maximize vision but also to help with educational problems.
Genetic counselling should be offered.
• Retinoblastoma :

• The commonest malignant tumour of the

eye in childhood
• Mostly sporadic ( may AD)
• Mean age of presentation is 8 mo if
inherited and
25 mo if :very
• SYMPTOMS sporadic.
imp
1. Leukocoria (white pupillary reflex , DDx:
retinoblastoma , congenital cataract..)
2. squint due to reduced vision.
3. painful red eye.
• SIGNS :
• Dilated fundoscopy shows a
whitish pink mass
protruding from the retina
into the vitreous cavity. • INVESTIGATIONS :
• Clinically

• CSF and BM >> check for

mets.
• TREATMENT :

1- Radiotherapy >> less

advanced disease
 2- Removal
(enucleation) of the
eye >>advanced cases.
3- chemotherapy
>> Metastatic disease
1) which eye is the
abnormal eye ?
left eye of the baby

2)what is the name of this

sign ?
Leukocoria

3)what is the most

dangerous
DDX ?
Retinoblastoma
• The most common malignant tumor in adults : metastatic
• The most common primary malignant tumor : choroidal melanoma

• Melanoma :
• In general Pigmented fundus lesions include:
 Retinal pigment hypertrophy;
 Old chorioretinitis;
 Choroidal naevi;
 Malignant melanoma (rarest).
Retinal pigment hypertrophy Old
chorioretinitis

DDx of
pigmented
leisions
on retina

M
a
l
i
g
n
a
Choroidal naevi n
t
In Advanced cases may present with a visual field defect or loss
of acuity (macula). If situated in the anterior part of the choroid,
the enlarging tumor may cause shallowing of the anterior
chamber, resulting in secondary angle closure glaucoma.

Presentation
depends on
the site