Retina for undergraduate students

• The innermost neuro sensitive layer of the eye
• Extends from the optic disc posteriorly to Ora serrata anteriorly.

• Round area at the posterior pole,
lying inside the temporal vascular
arcades

• 5 - 6 mm in diameter.
• Subserves the central 15 - 20º degrees of visual
field.
• Anatomical divisions:
A. Fovea: 1.5 mm diameter
B. Foveola: 0.35 mm diameter
C. Umbo: center of the foveola
• Central 0.6 mm area with
no blood vessels

1
• Single layer of Cubical cells
• Adherent to Bruchs membrane
• Functions:
1. Maintenance (Recycling) of the
photoreceptors
2. Absorption of stray light (contain
melanin)
3. Form the outer blood retinal barrier
4. Regeneration of the visual pigment
(Vitamin A)

Thin & Long Thick & Short
More numerous at
retinal periphery
More numerous
toward macula
Contain Rhodopsin Contain Iodopsin
Responsible for Dim
vision (Scotopic)
Responsible for Day
vision (Photopic),
Colour vision
Not in the fovea
The only receptors in
the fovea
2

6
• Contains nuclei of:
1. Bipolar cells: transmit signals from photoreceptors to
Ganglion cells
2. Muller cells: structural support, forms ELM, ILM
3. Amacrine, Horizontal cells: Interneurone connections

8
• Receive visual information from photoreceptors via the bipolar & amacrine
cells.
• Their axons form the retinal nerve finer layer (RNFL)

• Central retinal artery: supplies the inner 5 layers
• Choriocapillaris: supply the outer 5 layers
• Arises from Posterior ciliary arteries

• RPE: Become taller, more densely pigmented &more stacked together
• Photoreceptors: only Cones
• Bipolar & Ganglion cells: absent
• Foveal Avascular Zone (FAZ)

Indirect ophthalmoscope Direct ophthalmoscope
Slit lamp + Auxiliary lens
e.g. 90 D lens

1 • e.g. Snellen chart
2 • e.g. Pelli Robson chart
3 • e.g. Ishihara colour plates
4 • e.g. Perimetry

2
• A pseudo colour map of in vivo cut
section in all layers of the retina

3
• Used in case of media opacity e.g. opaque
cornea, cataract, vitreous haemorrhage

• Used to measure the massed electrical
response of the retina to brief flashes of light

Retinopathy Recurrent stye Pupil Light Near Dissociation
Unstable refraction Xanthelasma Papillopathy
Iris transillumination defects Accelerated senile cataract Orbital mucormycosis
Neovascular glaucoma
Ocular motor nerve palsies
Reduced corneal sensitivity

Ocular complications of diabetes mellitus:
Lid Cornea Iris Pupil Lens Refraction Retina Neuro Orbit
Common
Unstable
refraction
Diabetic
retinopathy
Uncommo
n
Recurrent
styes
Xanthelasm
a
Reduced
corneal
sensitivity
Rubeosis
irides
Accelerated
Senile
cataract
Ocular
motor nerve
palsies
Rare
Pupil Light
near
dissociation
Rhino
orbital
mucor-
mycosis

• The most important risk factor
• Has direct proportion with DR
• Raised HbA1c is associated with increased risk of Proliferative DR
• Due to poor control of DM, associated anaemia and elevated blood pressure
• Hyper lipidaemia
• Smoking
• Anaemia
• Cataract surgery

• Accumulation
of sorbitol &
free radicles
• Loss of pericytes
• Thickening of capillary basement
membrane
• Proliferation of endothelial cells
• Increase platelet stickiness
• Increase RBC abnormal forms
• Increase plasma viscosity
• Capillary non perfusion
• Retinal hypoxia
• Increase angiogenic factors
production by endothelial cells
e.g. Vascular Endothelial Growth
Factor (VEGF)
• Neovessel production
Microvascular Leakage Microvascular Occlusion

1. Micro aneurysms: due to loss of pericytes
2. Retinal edema & haemorrhage: due to increased capillary permeability
3. Retinal exudate: due to lipid accumulation
4. Retinal nerve fibre infarction (Cotton wool spots): because of capillary occlusion
5. Pathological neovessels: due to increased VEGF

• Micro aneurysms only
• Micro aneurysms
• Retinal haemorrhages
• Retinal Exudate
• Retinal haemorrhage > 20 per quadrant in 1-3 quadrants
• Venous beading
• Intra Retinal Microvascular Anomalies (IRMA)
• Cotton Wool Spots (CWS)
4 - 2 - 1 Rule
• Severe haemorrhage (>20/quadrant) in 4 quadrants
• Venous beading in 2 or more quadrants
• IRMA in 1 or more quadrants

Micro
Aneurysms
Retinal
Haemorrhage
Retinal
Exudate
Venous Changes IRMA CWS
very Mild 😏
mild 😏 😏 😏
moderate 😏 😏 😏 😏 😏 😏
severe 😏 😏
4 quadrants
😏 😏
> 2 quadrants
😏
> 1 quadrant
😏

• New vessels on the disc (NVDs)
• New vessels elsewhere (NVEs)
• NVDs > 1/3 disc area
• NVDs (any size) + Vitreous haemorrhage
• NVEs > 1/2 disc area + Vitreous haemorrhage
• Rubeosis Irides
• New vessels on the iris
• Usually start at pupillary
border, but may start at the
angle (NVA)

Microvascular Occlusion
The macula may look
relatively normal despite
reduced visual acuity

• Retinal thickening within 500 μm of the
centre of the macula
• Exudates within 500 μm of the centre of
the macula, if associated with retinal
thickening; the thickening itself may be
outside the 500 μm
• Retinal thickening one disc area (1500 μm)
or larger, any part of which is within one
disc diameter of the centre of the macula
• DME may exist in any stage of DR
Macular laser
treatment reduces
vision loss in presence
of CSME for 50%

• Causes Rapid Painless
diminution of vision

• Increased expression of
Transforming Growth Factors
(TGF) which transform
hyalocytes into fibroblasts.
• Epi retinal membrane formation.

• Pathological new vessels in the angle of AC causing 2ry OAG initially followed by a
fibrovascular membrane & 2ry ACG

• Hypertensive retinopathy
• Retinal vein occlusion
• Choroidal neovascularisation (CNV)
• Terson syndrome
• Post operative
• Topical PG
• Age Related Macular Degeneration
• Ocular ischaemic syndrome

• HbA1c%
• Lipid Profile
• Kidney Function Tests
• Full Blood Count
Hyper fluorescent lesions:
• Edema
• New vessels
• Micro Aneurysms
Hypo fluorescent lesions:
• Ischemia
• Haemorrhage

• Cystoid Macular Edema (CME): flower
petal appearance

Detect & Measure Retinal edema Study Vitreo Retinal interface:
• Traction
• Epi retinal membrane

In case of media opacity
• Vitreous haemorrhage
• Cataract
• Corneal opacity
To Exclude
• Retinal Detachment

• Diabetes
• Kidney functions
• Lipid profile
• Blood pressure
• Follow up the patient along with strict control of DM
• Pan Retinal Photocoagulation (PRP)
To destroy the ischemic retina thus decreasing VEGF
Improve retinal oxygenation by exposing it to choroidal
circulation

• Macular Grid laser for diffuse edema
• Focal laser for focal edema
Improve retinal oxygenation
by exposing it to choroidal
circulation
• Intra vitreal injection of anti VEGF
e.g. Bevacizumab (Avastin),
Ranibizumab (Lucentis)
In case of macular thickness > 350 microns • If DME Coexists with DR, DME should be
treated first.

• Alpha chymotrypsin, Aminocaproic
acid
• Intra vitreal anti VEGF
• Vitrectomy, When;
1. Non resolving vitreous haemorrhage
for 3 - 6 months
2. Pre macular haemorrhage
3. Vitreous haemorrhage combined with
retinal detachment

• Vitrectomy with peeling of the epi retinal membranes

• PRP
• Intra vitreal anti VEGF
• Topical anti glaucoma medications
• Topical steroids, cycloplegic eye drops
• Cyclodestructive therapy e.g. cyclodiode

• Increased rigidity, hardening and
loss of elasticity of small vessel
walls, manifested most obviously
at ArterioVenous crossing points.
• Presence of arteriosclerosis
indicates that hypertension
has been present for many
years even if BP is currently
controlled.

Normal retinal Arteriovenous (AV) crossing:
The artery crosses to the vitreal side of the
vein
The artery causes no compression over the
vein.
In arteriosclerosis:
The artery wall is thickened
The artery causes compression over
the vein.

• Mild generalised arteriolar narrowing
• This is the 1ry response of retinal
arterioles to systemic hypertension

• Focal arteriolar
narrowing
• Arteriovenous nipping
(Squeezing)
• Copper wiring
appearance of
arteriolar wall
Deflection of vein at
AV crossing

• As Grade 2 Plus:
A. Retinal haemorrhage (dot, blot, flame shaped)
B. Retinal exudate (Macular star; exudate in foveal
area)
C. Cotton wool spots
Banking of vein distal
to AV crossing
Tapering of vein on either
side of AV crossing

• As Grade 3 Plus:
A. Silver wiring appearance of retinal arterioles
B. Optic disc swelling

• The most important risk factor (>50 years)

• Younger than 50 years
• Polycythemia, Myeloma
• Lupus anticoagulant, Antiphospholipid syndrome
• Protein C deficiency, Antithrombin deficiency
• Behcet syndrome, Sarcoidosis
• Chronic renal failure, dehydration

The central retinal vein and artery share a common adventitial sheath
at arteriovenous crossings posterior to the lamina cribrosa so that
atherosclerotic changes of the artery may compress the vein and
precipitate CRVO

The more anterior the post-laminar thrombus
in CRVO, the more ischemic the occlusion
because there are fewer collaterals available to
bypass the thrombus.

• Nothing; if Macula is not affected
• Sudden, Painless diminution of vision
• Visual field loss (BRVO)
• Normal
• Diminuted • 6/60 or better
• Less than 6/60

• Normal reactivity
• RAPD
Risk factor for RVO Neovascular Glaucoma

• New vessels in ischemic RVO
• More common in CRVO than BRVO
• Develop at pupillary border
• May develop at the AC angle within 2
- 4 months (100 day glaucoma)

• Tortuosity & engorgement of all
branches of CRV
• Blot & flame shaped retinal
haemorrhage
• Cotton wool spots
• ONH swelling & hyperaemia
• Macular edema
• Tortuosity & engorgement of the occluded
branches of BRV (Upper temporal quadrant is
most commonly affected) due to larger number
arteriovenous crossings in that quadrant.
• Blot & flame shaped retinal haemorrhage
• Cotton wool spots
• ONH swelling & hyperaemia
• Macular edema

• NVDs, NVEs
• NVI
• more in BRVO
• more in CRVO
• the leading cause of vision loss in RVO
• within 2 - 4 months of RVO (100 day glaucoma)
VEGF

• CBC
• HbA1c
• Lipid profile
• Kidney function tests
• Chest X ray; sarcoidosis
• Thrombophilia screen
• Auto antibodies; ANA, ANCA
• ESR, CRP

• Delayed venous filling
• Hypo fluorescence
A. capillary drop out (ischemia)
B. Retinal haemorrhage
• Hyper fluorescence
Macular edema

ISCHEMIC
CRVO
NON ISCHEMIC
CRVO
VA < 6/60 > 6/60
PUPIL RAPD RRR
FUNDUS
SEVERE TORTUOS,
ENGORGED RETINAL VEINS
LESS SEVERE TORUOSITY &
VEIN ENGORGEMENT
FFA
Areas of capillary drop out
(ischemia)
No capillary drop out

• Control of the systemic risk factors e.g. DM, Hypertension, …
• Intra vitreal anti VEGF injection
• Macular Argon laser photocoagulation
• Intra vitreal dexamethasone implant

• PRP in CRVO
• Sector Argon laser photocoagulation on BRVO

development of disc collaterals
and the resolution of macular
oedema for at least 6 months
should allow the discharge of the
patient from clinical supervision.
Based on the Branch Retinal Vein Occlusion study (BVOS), the prognosis
of BRVO is better than CRVO with approximately 50 – 60% of
untreated BRVO cases retaining a visual acuity ≥ 6/12 after one year
non-ischaemic
CRVO
ischaemic
30%
3 years
Follow-up of non-
ischemic CRVO for at
least two years is
usually recommended

If no iris or angle NV and there is OCT evidence of MO
commence on
either intravitreal
anti-VEGF therapy
or Ozurdex
implant
the potential for significant
improvement in visual acuity is
minimal and the risk of ocular
neovascularisation is high.
However, eyes with VA< 6/96
may be offered treatment as
some of these eyes may
respond. The patients should be
watched for NVI/NVA
it is reasonable to
observe the patient for
spontaneous resolution
as per the judgment of
the treating
ophthalmologist
Treatment
Algorithm of
CRVO

0.5mg/0.05ml given as a
single intravitreal injection
monthly intravitreal injections
•If no improvement in VA (at least 5 ETDRS letters) cessation
of treatment may be considered and is recommended after 6
injections.
•Patients who achieve visual acuity stability should be monitored monthly
•Treatment is resumed when monitoring indicates loss of visual acuity due
to MO secondary to CRVO. Monthly injections should then be administered
again until stable visual acuity is reached for three consecutive monthly
assessments (implying a minimum of two injections).
•Maximum visual acuity is achieved, which is defined as stable
visual acuity for 3 consecutive monthly assessments
2mg/0.05ml given as a
single intravitreal injection

0.7 mg single-use, sustained release with a biodegradeable implant (Ozurdex)
at 4-6 monthly intervals until visual stability is obtained
Patients should be monitored for raised intraocular pressure
(IOP) and formation or progression of cataract

Reduction in retinal edema without VA improvement or
deterioration (i.e stable VA) may be accepted as a
favorable, but suboptimal outcome
The CVOS study failed to indicate benefit from laser grid treatment,
although a trend in favor of treatment was observed in younger patients.
There is also no evidence to suggest any benefit from a
combination of macular grid laser and intravitreal anti-VEGF
or steroids for MO secondary to CRVO.

๏ If an anti-VEGF agent is stopped due to lack of efficacy, there are no
randomised controlled trials that provide evidence that switching to
another anti-VEGF agent may be effective.
๏ However, given our experience with switching anti-VEGF agents in
neovascular ARMD, it may be worthwhile switching to another anti-VEGF
agent and further monthly injections for 3 months may be given to assess the
efficacy of the switch.
๏ There is a good rationale to switch from Ozurdex to an anti-VEGF agent
and vice versa as the different mode of actions of these agents may aid in
resolution of MO.
๏ However, the long term outcomes of sequential or combination treatment of
anti-VEGF agents and steroids remain unclear.

Urgent PRP
review at 2 weeks initially
and then less frequently as
regression occurs
PRP + intravitreal
bevacizumab (off
license) can be repeated
if NVI/NVA persist.
Urgent PRP
cyclodiode laser
therapy / tube
shunt surgery
Normal or normalizes
intravitreal
bevacizumab
High add medical treatment
to control IOP

it is reasonable to
regularly observe
progress for 3 months
mild to moderate
macular
ischaemia
ranibizumab
or Ozurdex
severe
macular
ischaemia
no treatment is recommended,
and regularly observe for NV
formation
a) Monthly ranibizumab or baseline
Ozurdex for three months.
b) Perform FFA at 3 months to assess
foveal integrity
c) If severe macular ischaemia is found
to be present at 3 months, no treatment
will likely be beneficial and further
therapy should be carefully considered
Treatment Algorithm of
BRVO

At three months follow-up
1. Consider modified grid laser photocoagulation if:
Further Follow-up
1. If under observation only, follow-up three monthly intervals for 18 months
2. In case of recurrence or new macular oedema, consider re-initiating
intravitreal ranibizumab or Ozurdex therapy
2. If VA >6/9 or no macular oedema detected, continue
to observe if initially observed. If on anti-VEGF or
Ozurdex therapy, continue as suggested in MO due to
CRVO.
persistent macular
oedema
no or minimal macular
ischaemia and other
treatments
unsuccessful or
unavailable

a) Watch carefully for NV
b) If NVE — consider sector laser photocoagulation applied to all ischaemic
quadrants. Intravitreal bevacizumab (off-license) may also be given in
combination with laser.
c) Follow-up at three monthly intervals for up to 24 months.

1. Thrombus (Atherosclerosis related)
2. Embolus (cholesterol, calcific, fibrin platelet)
3. Arterial wall disease:
A. retinal migraine
B. Peri arteritis (SLE, PAN, GCA)

RAO
• Retinal Artery supplies the
inner 5 layers of the retina
• Cherry Red spot;
A. No Ganglion cells in fovea
B. Accentuation of fovea red colour due to
increased colour contrast

A cilioretinal artery is present in 15–50% of eyes,
providing the central macula with a second arterial
supply derived from the posterior ciliary
circulation.

• Sudden painless diminution of vision
• Except if macula is not affected or the
presence of a patent Cilioretinal artery
• Severely diminished, up to No PL
• Except in the presence of a patent
Cilioretinal artery
• Might be preceded by transient attacks of
loss of vision (Amaurosis fugax)

• RAPD
•Attenuation of arteries and veins with sludging and
segmentation of the blood column (‘cattle trucking
•Cloudy white oedematous (ground glass) retina
corresponding to the area of ischaemia.
•One or more occluding emboli may be seen, especially
at bifurcation points.
The orange reflex from the intact choroid stands out
at the thin foveola, in contrast to the surrounding pale
retina, giving rise to a ‘cherry-red spot’ appearance.

• CBC
• ESR
• CRP
• Carotid duplex
• ECG
• Chest X ray; sarcoidosis
• MRI brain
• Echocardiography
• Thrombophilia screen

• Delayed arterial filling
• Hypo fluorescence:
of the involved segment due to
blockage of background
fluorescence by retinal swelling

• Sphingolipids accumulation in Ganglion cells
• Retinal edema
• Lipid storage disease

Should be tried in the 1st 24-48 hours of artery occlusion
• Might improve ocular perfusion
• Using a 3 mirror contact lens
• In order to dislodge the embolus or thrombus
• To lower the IOP thus allowing forward translocation of the embolus or thrombus
• Topical or systemic Anti Glaucoma medications

• Sublingual Isosorbide dinitrate
• Rebreathing into a paper bag (rising CO2 level)
• Breathing Carbogen (O2 95% + CO2 5%)
• Using trans luminal YAG laser shots
• Fibrinolysis using rTPA (recombinant Tissue Plasminogen Activator)

• Aspirin
• Warfarin
• In patients with carotid obstruction > 70%)

• 4th month gestation: Onset of retinal vascular growth, from center
toward periphery.
• 8th month gestation: nasal retina is fully vascularized,
• 10th month gestation: the temporal periphery is fully vascularized.
• Vascular endothelial growth factor (VEGF) is believed to play an
important role in the vascularization process.

• Gestational age ≤ 32 weeks
• Birthweight ≤ 1500 g
• Exposure to high ambient oxygen concentrations (100%)

• Early exposure to high ambient oxygen retards retinal vascular growth
due to hyperoxia
• After weaning from the incubator Exposure to the atmospheric Oxygen
(20%) which is relatively hypoxic promotes excess VEGF expression and
anomalous retinal vascularization

• Demarcation line: a thin, flat,
tortuous, grey-white line
running parallel with the ora
serrata.
• It is more prominent in the
temporal periphery
• It demarcates the boundary
between mature and
immature retina
Stage 1

Ridge: arises in the region of
the demarcation line, has height
and width, and extends above
the plane of the retina.
Stage 2

Extra retinal fibro-vascular
proliferation: extends from the
ridge into the vitreous.
It is continuous with the
posterior aspect of the ridge,
causing a ragged appearance
as the proliferation becomes
more extensive.
Stage 3

Partial RD: Foveal or Extra
foveal
Stage 4
Total RD
Stage 5

UK ROP Screening guidelines
• Gestational age ≤ 32
weeks
• Birthweight ≤ 1500 g
 Who to screen:
All babies with
 When to screen (1st exam):
Between 4 to 5 weeks postnatal age
 How to examine:
- Indirect ophthalmoscope (+ 28D lens  wide
field of view)
- Cyclopentolate 0.5% + phenylephrine 2.5% E.D
- Lid speculum + scleral indentation

 Argon laser photocoagulation:
For the avascular peripheral retina
 Intra vitreal anti VEGF:
 Pars Plana Vitrectomy:
- For tractional RD not involving the macula
Bevacizumab (Avastin) has been used for the
treatment of ROP, but an optimal regimen is yet to
be established.

• Inherited diffuse retinal degenerative diseases initially predominantly affecting the rod
photoreceptors, with later degeneration of cones.
• Sporadic, AD, AR or XLR
• Mutation of rhodopsin gene
• Visual pigment dysfunction

• Defective Night vision (Nyctalopia)
• Peripheral visual field difficulties
• Reduced Central vision (Later on)
• Family history of RP
• Not affected except late
• Contrast sensitivity is affected earlier

• Bilateral mid-peripheral
intraretinal perivascular
‘bone-spicule’ pigmentary
changes and RPE atrophy
associated with arteriolar
narrowing

• Gradual increase
in density of the
pigment with
anterior & posterior
spread

• Marked arteriolar narrowing,
• Waxy yellow optic disc pallor,
• Severe Pigmentary changes

• Early; reduced Scotopic responses
• Then; reduced Scotopic & Photopic responses
• Finally; Extinguished ERG
• To detect macular edema
• Mid peripheral field changes
• To identify the mutation

• Advanced Glaucoma, PRP
• 1ry, 2ry, post Glaucoma
• Advanced Glaucoma, PRP

• In early stages of the disease
• e.g. PSCC, macular edema

• An acquired degenerative disorder affecting the macula. It is characterised by the
presence of specific clinical findings, including drusen and RPE changes, in the absence
of another disorder.
• The most important risk factor
• More common in white race
• increase risk by 3 times in 1st degree relative
• Doubles the risk of AMD
• High fat intake
AMD is the most common cause of
irreversible visual loss in industrialized
countries.

• Immune-mediated and metabolic processes in the RPE
• They accumulate between Bruch membrane & RPE
• They disrupt the intimate relationship between RPE & choriocapillaris
resulting in hypoxia & oxidative stress
• A resultant inflammation with subsequent inflammatory mediators & growth
factor release e.g. VEGF

• New blood vessels (Choroidal Neovascularisation; CNV) sprout & grow
through the weekend Bruch membrane
• These new vessels are abnormally leaky which allows fluid & blood to seep
into the layers of he macula
• Resulting in damage of the photoreceptors & vision loss

More common Less common
Drusen
Geographic RPE atrophy
CNV
Pigment Epithelium Detachment
(PED)

• Gradual painless impairment of central vision
• Metamorphopsia
• Micropsia
• Macropsia

A. Well defined, yellow-white focal deposits at the level of
RPE i.e deep to retinal vessels
B. +/- dystrophic calcification
C. +/- retinal pigmentary changes
D. Geographic atrophy of RPE in late cases

1. Serous PED detachment; orange dome shaped macular
elevation
2. Fibrovascular PED; much more macular elevation
3. Haemorrhagic PED; elevated, dark red, well defined, dome
shaped macular lesion
4. CNV; greyish green subfoveal membrane

• Drusen show Auto
Fluorescence
• RPE atrophy show hyper
fluorescence (Window defect)

• PED shows hyper fluorescence (Pooling)
• CNV shows hyper fluorescence (Leak)

•The near-infrared light utilised in indocyanine green angiography (ICGA) penetrates
ocular pigments such as melanin and xanthophyll, making this technique preferable over
FFA in diagnosing Choroidal lesions.
•CNV shows focal hyper fluorescence (Hot spot)

• Thickening &
fragmentation of RPE &
choriocapillaris

• Taking high-dose antioxidant vitamins and minerals on a regular basis can decrease
the risk of the development of advanced AMD in individuals with certain dry AMD
features
• Vitamin C, vitamin E, the beta-carotene form of vitamin A, and 80 mg daily of zinc (with
copper to prevent zinc-induced copper deficiency)
• Stop Smoking
• Protective measures against exposure to excessive
sun light (UVR)
• Consumption of green leafy vegetables & fish oil

• Provided for home use
• self test on a regular basis to seek medical
advice urgently in case of any change
• In case of severe
vision loss e.g.
geographic RPE
atrophy
• e.g. Telescopes,
Magnifying lenses

• Macular translocation surgery
• Retinal prosthesis

• Avastin
• Lucentis
• Macugen
• VEGF trap-eye
• Eyelea

• Veteprofin (Photosensitive drug) is injected intra venous and taken
by dividing cells of the CNV
• A diode laser is used to activate this dye causing thrombosis of the
CNV

Separation of the neurosensory retina (NSR) from the RPE. This results in the accumulation of
SRF in the potential space between the NSR and RPE.

Rhegmatogenous (Greek rhegma – break) RD requires a full-thickness defect in the
sensory retina, which permits fluid derived from synchytic (liquefied) vitreous to gain
access to the subretinal space.

The NSR is pulled away from the RPE by contracting vitreoretinal membranes in the
absence of a retinal break.

Exudative RD (serous, secondary) RD. Sub retinal Fluid (SRF) is derived from the
vessels of the NSR and/or choroid.

• PVD; due to trauma, senility,
high myopia
• Peripheral Retinal
Degeneration; e.g. lattice
degeneration in high myopia

• PVR; due to retinal break, DR,
…
• Epiretinal membrane;
contraction

• In absence of retinal break or traction, a
variety of vascular, inflammatory
(Uveitis) and neoplastic (Choroidal
melanoma) diseases involving the
retina, RPE and choroid in which fluid
leaks outside the vessels and
accumulates under the retina.

• Of PVD: Floaters,
flashes of light
• Of RD: Field defect
(Black curtain)
• Of the risk factors:
trauma, high
myopia, …

• Diminished only if macula is affected
• Might be normal, low (due to escape of fluid in the sub retinal space) or high
(uveitis)
• RAPD in case of total RD
• Appears Grey

• Tobacco dust
(pigmented cells appear
in the anterior vitreous in
case of retinal break;
PVR)

• Retinal break
• Detached retina appears grey with corrugated surface with convex configuration

• Epi retinal membranes
• Corrugated retinal surface with
fixed retinal folds and limited
mobility

• Convex, smooth retinal surface
• The detached retina is freely
mobile with shifting fluid
• The cause may be obvious e.g.
choroidal melanoma

• In case of media opacity e.g. cataract

• Argon laser retinopexy for retinal breaks, or external cryotherapy

• In Rhegmatogenous
RD with no or
minimal PVR

• Intravitreal injection
of expanding gas
• Used in
rhegmatogenous RD
with minimal or no
PVR & in case of
upper retinal breaks

• In RD with severe
PVR, multiple retinal
breaks or giant
break
• A vitreous substitute
is used e.g. Silicone
oil

1. CRVO
2. CRAO
3. RD
4. Hysterical
5. Malingerer
1. Acute Congestive Glaucoma
2. Optic neuritis
3. Ruptured globe
1. DME
2. CRVO
3. Vitreo macular traction
4. Prostaglandin use
5. Post operative
1. PDR
2. CRVO
3. OIS

Retina for undergraduate students

Retina for undergraduate students

More Related Content

What's hot

Similar to Retina for undergraduate students

More from faculty of medicine -benha university

Recently uploaded

Retina for undergraduate students