Retina

Retina starts at ora serrata & ends at optic disc

Layers of the retina

 Anatomy of retina
- Retina is the innermost layer of the globe.
- Retina is very thin & transparent showing the red color of choroid.
- It is sensitive only to light
Sudden traction on the retina stimulation of photoreceptors
patient complains of flashes of light

Gross anatomy
- Retina starts at ora serrata & ends at optic disc.
Minute anatomy = Layers of the retina
9 + 1 = 9 neuro-sensory retina + 1 retinal pigmented epithelium
Retinal pigmented epithelium (RPE)
- The outermost layer (in contact with Bruch's membrane)
- One layer of pigmented cubical cells.
- Attachment:
Firmly attached to Bruch's membrane, optic disc & ora serrata.
Loosely attached to sensory retina (potential space in between)
Clinical In retinal detachment, separation between RPE & sensory retina

Photoreceptors (rods & cones): light sensitive layer.

Rods Cones
Thin Thick
Contain rhodopsin Contain iodopsin
Maximum concentration at periphery Maximum concentration at center
Responsible for night vision & Responsible for color perception &
visual orientation detailed vision
120 millions 6 millions
Outer limiting membrane: made of the ends of Muller's fibers.
Outer nuclear layer: made of nuclei of photoreceptors.
Outer plexiform layer: made of synapses between the nuclear layers.
Inner nuclear layers: made of (bipolar, Muller, horizontal & amacrine) cells.
Inner plexiform layer: synapses between bipolar cells & ganglion cells.
Ganglion cell layer
Nerve fiber layer (NFL): axons of ganglion cells which converge to make the optic nerve
Inner limiting membrane: made of other end of Muller's fibers.
Blood supply to retina
 Fovea
a depression in the center of macula
Fovea gives the best visual acuity d.t. :
Contains only cones
Very thin, so light falls directly on cones
(The rest of retinal layers of fovea are displaced laterally)
Avascular: get its nutrition by diffusion from choroid capillaries around it
One-to-one transmission: one cone to one bipolar to one ganglion cell

Blood supply
Arteries
Inner layers of retina: from central retinal artery.
Outer layers of retina: Avascular
(They get their nutrition by diffusion form the choroidal capillaries)
In 10-15 % of population,
Cilio-retinal artery (originates from one of the posterior ciliary arteries)
supplies the macula

Veins
Inner layers of retina is drained into central retinal vein which is drained into
superior ophthalmic vein or directly to cavernous sinus.
Outer layers of retina is drained into choroid

Capillaries
Superficial plexus (in nerve fiber layer):
Hemorrhage in this plexus takes the distribution of nerve fiber layer
flame shaped hemorrhage

Deep plexus (in the inner nuclear layer):

Hemorrhage in this plexus dot shaped hemorrhage

 Fundus picture

Foveal avascualr zone (FAZ)

Located within the fovea (but extends beyond the foveola): devoid of capillaries.
 Normal fundus
How to examine the fundus? (see page 248)
Optic disc
Site: Nasal to posterior pole of the eye.
Shape: Rounded with physiological cup in its center (Normally Cup/Disc ratio = 0.3 )
Diameter: 1.5 mm
Color: light pink
Edge: well-defined.

Macula lutea
Site: Temporal to posterior pole of the eye (2 disc diameters from the edge of optic disc)
Diameter: 5.5 mm
Color: Yellow red d.t. high content of xanthophil pigments more than 1 layer of
ganglion cells.
Edge: ill-defined
Fovea centralis: a small dark red depression in the center of macula
& shows a bright foveal reflex.

Retinal vessels emerge from the cup then divide into upper & lower branches .These
branches subdivided into nasal & temporal branches
Artery is smaller than vein (A/V = 2/3) lighter & crosses over the vein without constricting it

Artery & vein are enclosed in one sheath,

So arteriosclerosis may lead to vein obstruction

Background Granular appearance

Choroidal vessels (red color) Choroidal pigment (dark areas)
In albinism (NO melanin pigment) Choroidal vessels can be seen
 Retinal vascular diseases
1. Vascular sclerosis
2. Vascular occlusion (CRAO CRVO)
3. Vascular retinopathy

Central retinal artery & vein

CRAO Cherry red spot

CRAO with cilio-retinal sparing

 Central retinal artery occlusion
Etiology
In
Thrombosis: d.t atherosclerosis
Risk factors of atherosclerosis: old age, hypertension, D.M., cholesterol & smoking
Embolism (most common as the ophthalmic artery is the 1st branch of internal carotid artery)
Detached thrombus from:
- Large arteries: as atheromatous plaque of carotid artery
- Heart: vegetations on heart valves as in infective endocarditis.
Left eye is more commonly affected with emboli than the right eye;
as left carotid is directly connected with aorta
Wall
Spasm: as in
- Migraine Spasm causes
- Raynaud's disease transient loss of vision
- Malignant hypertension (amarousis fugax)
Inflammation: e.g. giant cell arteritis
Out
rare
Acute congestive glaucoma
IOP during retinal detachment surgeries e.g. scleral buckling or pneumatic retinopexy
Orbital cellulitis
Clinical picture
Symptoms Sudden painless loss of vision
as occlusion of central retinal artery (which is an end artery) coagulative necrosis of the
inner layers of retina
In 10-15 % of population,
Cilio-retinal artery (NOT CRA) supplies the macula
So, central vision is preserved (tubular vision)

Signs
1. Visual acuity: NO P.L
2. Pupil reflex: ( Total afferent pupillary defect )
Affected side: Absent (direct & consensual)
Healthy side: Reactive (direct & consensual)
3. Fundus :
Early (at the time of occlusion)
Blood vessels
Arteries: attenuated (thread like)
Veins: segmented blood column (cattle truck appearance)
Background: Cherry red spot d.t.:
Coagulative necrosis in ganglion cells milky white appearance (obscuring choroid)
Fovea do NOT contain ganglion cells remains red

Late (several weeks after occlusion)

Blood vessels: arteries are attenuated & sheathed (white threads)
Background: disappearance of white color of retina & cherry red spot.
(as macrophages engulf the dead ganglion cells )
Disc: Consecutive optic atrophy

D.D.
1] Causes of cherry red spot
C.R.A.O
Quinine idiosyncrasy
Macular hole surrounded by R.D
Commitio retinae
Amaurotic family idiocy = Tay Sacks disease
2] Causes of sudden loss of vision
C.R.A.O Amaurosis fugax
Hysteria Malingering
Rupture globe
3] Causes of tubular vision
Open angle glaucoma Retinitis pigmentosa
C.R.A.O with preserved cilio-retinal artery Quinine idiosyncrasy
 Treatment
It is an emergency
It should be treated within 30 minutes
Treatment is useless if delayed, as irreversible damage will occur
Aim of treatment Dilatation of central retinal artery
- If the cause is spasm vasodilatation relieve the spasm
- If the cause is embolus vasodilatation dislodge the embolus to from the large
artery (big damage) to a smaller (peripheral) branch (small damage)
Methods
Local: as
- Paracentesis I.O.P V.D.
- Ocular massage I.O.P V.D.
- Retro-bulbar injection of priscolin V.D
General: as
- Inhalation or sublingual nitrate V.D.
- Breathing in a bag ( concentration of CO2 in blood V.D.)
- I.V. carbonic anhydrase inhibitor I.O.P V.D

Refer the patient to a cardiologist to search for the cause

 CRVO

Artery & vein are enclosed in one sheath,

So arteriosclerosis may lead to vein obstruction

RAPD = Marcus Gunn pupil

 Central retinal vein occlusion
Incidence CRVO is more common than CRAO
Etiology
In
Blood viscosity d.t. :
R.B.Cs (Polycythemia)
W.BCs (Leukemia)
Platelet (Thrombocytosis)
Plasma (dehydration)
Wall
Inflammation of vein (phlebitis) more common at young age, as in Behcet's syndrome
Out
Cause from outside pressing on the vein
Orbital mass: as orbital tumor
Orbital cellulitis
Retro-bulbar hematoma
I.O.P
Atherosclerosis: sclerosed artery presses on the vein as they are enclosed in one sheath
Risk factors of atherosclerosis: old age, hypertension, D.M., cholesterol & smoking
Clinical picture ischemic type
Symptoms
Rapid painless drop of vision
d.t. ischemia of inner layers of retina & macular odema - hemorrhage
(The drop of vision is usually noticed at the morning d.t. venous stasis during sleep)
Signs
Visual acuity: down to H.M
Pupil reflex: R.A.P.D [Marcus Gunn pupil] best elucidated by swinging flash light test
Fundus: "Stormy sunset appearance"
Blood vessels: veins are engorged & tortuous
Background: retinal odema, cotton-wool spots & hemorrhage
Disc oedema
Color: hyperemic Cup: elevated Edge: ill-defined
Macular oedema
 OCT macula

NVD & NVE

NVI & NVA
 Types
Non-ischemic Ischemic
Site of Posterior to lamina cribrosa Anterior to lamina cribrosa
obstruction ( Good collaterals ) ( NO collaterals )
Incidence More common Less common
Symptoms Blurring of vision Marked drop of vision
Pupil reflex Reactive R.A.P.D
Odema Mild Extensive
Exudate Hard Soft (cotton wool spots)
Hemorrhage Mild Extensive
Complications Rare Common
Prognosis Good Poor

Complications
1. Chronic macular oedema: up to cystoid macular oedema macular degeneration
permanent affection of vision
2. Neo-vessels formation (in ischemic type) d.t. release of V.E.G.F (vaso-endothelial growth
factors) which stimulates new vessels formation
Retina (N.V.D & N.V.E) (Neovessels at disc & neovessels elsewhere) recurrent
attacks of vitreous hemorrhage fibro-vascular proliferation tractional R.D.
Iris (Rubeosis irides) (NVI = Neovessels at iris) hyphema
Angle (NVA = Neovessels at angle) neovascular glaucoma

Neovascular glaucoma
d.t. neovessels & proliferation of fibro-vascular tissue at angle
It takes about 3-4 months to develop [100-day glaucoma]

D.D.
Causes of rapid drop of vision (see page 228)
Investigations
Fluorescein angiography:
Delay in arterio-venous transit [Diagnostic]
Differentiate between ischemic & non-ischemic types.
Differentiate between and inflammatory from thrombotic.
OCT (Optical coherence tomography): for macular odema
 Intravitreal injection

PRP (pan retinal photocoagulation) by argon laser

Shunt operation
 Treatment
1. Control of risk factors
2. Macular odema
o Intra-vitreal anti-VEGF
o Intra-vitreal steroid (Triamcinolone acetonide) stabilization of blood retinal barrier
Side effects: 2ry glaucoma, cataract, endophthalmitis & R.D
3. Follow up (by fundus examination & gonioscopy) to detect neovascularization

If neovascularization occurs
o P.R.P (pan-retinal photo-coagulation)
Pan-retinal photo-coagulation (P.R.P)
Destroy the hypoxic area NO VEGF release
Regression of the neo-vessels
Improvement of circulation of the central part of retina.

o Anti-VEGF

If neovascular glaucoma occurs Anti VEGF + PRP +

Medical:
o IOP: Beta blockers + carbonic anhydrase inhibitor
o Inflammation: steroid + atropine
Miotics & PG are contraindicated as they permeability of blood vessels & inflammation
Surgical: Trabeculectomy with mitomycin C or shunt operation
Absolute glaucoma (blind painful eye): Cyclo-destruction

If vitreous hemorrhage occurs Anti VEGF + wait for absorption

When to do vitrectomy?
Severe persistent or recurrent vitreous hemorrhage.
Dense pre-macular sub-hyaloid hemorrhage.
Tractional R.D. threatening the macula.

Systemic steroid is used in phlebitis e.g. Behcet syndrome

 Vascular sclerosis
Definition Degenerative aging process affecting the central retinal artery & its branches.

Atherosclerotic changes in retinal vessels seen by fundus examination

give an idea about the condition of cerebral & renal vessels.

Fundus picture
Changes in vascular light reflex:
(Reflection of light from vessel wall with thickening of vessels)
Copper wire (d.t thickening of vessel wall)
Silver wire (d.t more thickening of vessel wall)
Sheathing of vessels: d.t. fibrosis of the wall.
Change in:
Course: tortuous
Diameter: attenuation (generalized or localized)
Arterio-venous (A/V) crossing changes:
Concealment of vein: obscuration of a part of vein (as artery lost its transparency)
Gunn's sign (nicking of vein): compression of the underlying vein
Banking: distension of the vein distal to crossing & tapering on the other side.
Salus sign: deflection of the course of the vein by rigid artery (being enclosed in one sheath)
Vertical deflection: Veins make "U" shaped arch avoiding the artery
Lateral deflection: Veins changes its course to cross the artery at right angle
 Vascular retinopathy
Definition Bilateral retinal affection 2ry to systemic vascular diseases e.g.
Benign hypertension
Malignant hypertension
Renal retinopathy
Pre-eclampsia (toxemia of pregnancy)
Diabetic retinopathy
Fundus picture
Retinal vessels sclerosis or spasm (according to the cause)
Background
Hemorrhage:
Superficial: Flame shaped hemorrhage (hemorrhage in the nerve fiber layer)
Deep: Dot shaped hemorrhage (hemorrhage in the inner nuclear layer)
Exudate:
Soft exudate (Cotton wool patches): white, large, ill-defined patches
[Retinal infarction in the N.F.L d.t. micro-vascular occlusion]
Hard exudate: yellowish white, small rounded, well-defined spots.
[Leakage of lipids in the inner nuclear layer d.t. disturbance of inner retinal barrier]
Macula oedema (severe cases) exudate (macular fan or macular star)
Optic disc oedema (severe cases)
Benign HTN Malignant HTN Pre-eclampisa
Blood pressure > Pregnancy induced
Definition Blood pressure >200/120
140/90 HTN
Vessels Sclerosis Spasm Spasm
Hemorrhage Flame-shaped Flame-shaped Flame-shaped
Exudate Hard Soft Soft
Macular &
Absent Present Present
disc odema
Retinal Present Present
Absent or mild
oedema (up to exudative R.D.) (up to exudative R.D.)
Patient is liable to Patient rarely live more Termination of
cardiac & cerebral than 2 years. pregnancy must be done
Significance
accidents. so, medical Death is usually d.t. to save life vision
care is needed renal failure of the mother
 Disturbance of blood retinal barrier by damage of pericyte

Pathogenesis (Leakage & occlusion)

Micro-vascular leakage Micro-aneurysm - odema exudate - hemorrhage

Micro-vascular occlusion IRMA - neovessels

 Diabetic retinopathy
Definition Micro-angiopathy affecting the retinal arterioles, capillaries & venules.
Incidence bilateral (asymmetrical)
One of the most common causes of visual impairment in middle age group all over the world
Risk factors
Long duration of D.M. (most important risk factor)
Uncontrolled D.M.
Hypertension
Lipids
Anemia
Smoking
Pregnancy
Renal disease

Pathogenesis
Micro-vascular leakage
- Cause: Loss of pericytes disturbance of inner blood retinal barrier
- Resulting in: Micro-aneurysm, oedema, exudate & hemorrhage.

Micro-vascular occlusion
- Cause:
1. Change in the vessels wall
i. Thickening of basement membrane.
ii. Endothelial cell proliferation.
2. Change in the blood contents
i. Aggregation & stickiness of platelets.
ii. RBCs changes (glycosylated hemoglobin & lack of deformability)
- Resulting in: retinal ischemia (hypoxia)
Arterio-venous shunt (I.R.M.A) (Intra-retinal micro-vascular abnormality)
Release of vaso-genic materials (VEGF) neo-vessel formation.
 OCT macula

Non proliferative diabetic retinopathy

NVI = Rubeosis irides

NVA

NVD & NVE Tractional RD

 Clinical picture
Symptoms
- Asymptomatic
- If macular affection gradual of vision micropsia macropsia metamorphopsia
- If vitreous hemorrhage floaters or rapid painless drop of vision
Signs = Classification of diabetic retinopathy
1. Non-proliferative diabetic retinopathy (NPDR): (Simple = Background)
A. Mild N.P.D.R: Micro-aneurysms only
B. Moderate N.P.D.R: Micro-aneurysms + retinal hemorrhage (dot & blot) + exudate
C. Severe N.P.D.R (Pre-proliferative D.R.): 1:2:4 rule, anyone of these features:
I.R.M.A (in 1 quadrant)
Venous beading (in 2 quadrants)
Retinal hemorrhage (in 4 quadrants)
2. Proliferative diabetic retinopathy [PDR]
Neovessels at disc (NVD) & neovessels elsewhere (NVE)
3. Advanced proliferative diabetic retinopathy
Retina (N.V.D & N.V.E) recurrent attacks of vitreous hemorrhage fibro-vascular
proliferation tractional R.D.
Iris (Rubeosis irides) (NVI = Neovessels at iris) starts at pupillary margin hyphema
Angle (NVA = Neovessels at angle) neovascular glaucoma
Diabetic maculopathy
Most common cause of visual impairment in D.M.
Diabetic maculopathy can occur with any stage of diabetic retinopathy.
Types:
Focal: d.t. focal leakage: focal odema (thickening) + hard exudates
Diffuse: d.t. diffuse leakage: diffuse odema (thickening) + hard exudates
odema may take cystoid pattern
Ischemic: area of capillary non-perfusion (detected by fluorescein angiography)
Mixed

Investigation
Fluorescein angiography: evaluation of extent of retinal ischemia, neovessels & macular
odema
Optical coherence tomography (O.C.T): evaluation of macular oedema & detects
abnormalities at the vitreo-retinal interface
 Intravitreal injection

PRP (pan retinal photocoagulation) by argon laser

Pars plana vitrectomy

Shunt operation
 Treatment
1. Control of risk factors
2. Non-proliferative diabetic retinopathy
* Mild: follow up every 6-12 months
* Moderate: follow up every 6 months
* Severe: follow up every 3 months (In Egypt Pan retinal photo-coagulation)
Pan-retinal photo-coagulation (P.R.P)
Destroy the hypoxic area NO VEGF release
Regression of the neo-vessels
Improvement of circulation of the central part of retina.

3. Proliferative diabetic retinopathy Pan retinal photo-coagulation

4. Advanced diabetic retinopathy = Complications

If neovascular glaucoma occurs Anti VEGF + PRP +

Medical:
o IOP: Beta blockers + carbonic anhydrase inhibitor
o Inflammation: steroid + atropine
Miotics & PG are contraindicated as they permeability of blood vessels & inflammation
Surgical: Trabeculectomy with mitomycin C or shunt operation
Absolute glaucoma (Blind painful eye): Cyclo-destruction
If vitreous hemorrhage occurs Anti VEGF + wait for absorption
When to do vitrectomy?
Severe persistent or recurrent vitreous hemorrhage
Dense pre-macular sub-hyaloid hemorrhage
Tractional R.D. threatening the macula
5. Diabetic maculopathy
Focal odema: Focal laser
Diffuse odema: Grid laser
+ intra-vitreal anti-VEGF or intra-vitreal? steroid (Triamcinolone acetonide)
Ischemic maculopathy: NO TTT
 Effects of diabetes mellitus (D.M.) on the eye
Ocular manifestations of diabetes are related to the duration of the disease more than the severity
The effects of D.M can extend to all ocular tissues
1. Lids: blepharitis recurrent styes xanthelasma
2. Conjunctiva: conjunctivitis Glaucoma & D.M
3. Cornea: Neovascular glaucoma
- Neurotrophic ulcer Ghost cell glaucoma
- Resistant corneal ulcers Pigmentary glaucoma
- Recurrent corneal erosions 1ry open angle glaucoma (risk factor)
4. Iris
- Rubeosis irides (NVI = neovessels at iris): neovessels starts at the pupillary margin
It may reach the angle neovascular glaucoma
- Diabetic iridopathy = Diabetic vacuolation of the iris pigment epithelium
easy scattering of iris pigment on mild trauma
5. Lens
- Complicated cataract
1. True diabetic cataract = Snowflake cataract: occurs in juvenile uncontrolled D.M
Milky white cataract as flakes under the anterior capsule with multiple vacuoles inside lens
2. Pre-senile cataract: Cataract occurs earlier < 45years & matures rapidly
- Change in refractive index (by the variation in the state of lens hydration)
Hypoglycemia Hyperopia
Hyperglycemia Myopia
It is NOT advised to prescribe glasses to an uncontrolled diabetic patient
until blood sugar level remains stable for months.

- Weakness of accommodation
6. Retina: diabetic retinopathy clinical picture
7. Diabetic neuropathy:

- 2nd nerve: optic neuritis (bilateral painless - rapid onset)

- 3rd, 4th, 6th nerves: E.O.Ms palsy

3th nerve palsy is the most common cause of EOMs palsies with D.M.

- 5th nerve: neurotrophic keratitis

 For those who are interested

Clinically significant macular oedema (CSMO)

Clinically significant macular oedema (CSMO)

A. Retinal thickening within 500 m of the fovea.
B. Hard exudates within 500 m of the fovea with adjacent retinal thickening.
C. Retinal thickening at least one disc area in size, part of which is located within one disc
diameter of the fovea.

Causes of neo-vascularization
C.R.V.O
Proliferative diabetic retinopathy
C.R.A.O
R.O.P
 P.V.D

Retinal break

Retinal detachment
 Retinal detachment
Definition Separation of the sensory retina from the R.P.E by sub-retinal fluid (SRF)
Types
1ry R.D.= Rhegmatogenous R.D.
2ry R.D.: Exudative Tractional
1ry R.D. = Rhegmatogenous R.D.
Definition Full-thickness break in the sensory retina separation of the sensory retina
from the R.P.E by sub-retinal fluid
Incidence
Age: more at age > 40 years
Sex: > (more liable to trauma)
Laterality: Bilateral 20%
Predisposing factors
High myopia: RD is more common d.t.:
- High incidence of posterior vitreous detachment (P.V.D)
- Thin retina
- Peripheral retinal degenerations (lattice degeneration)
Trauma
Aphakia vitreous herniation PVD
Intra-ocular surgery: manipulation may lead to R.D.
Pathogenesis
Vitreous liquefaction vitreous collapse posterior vitreous detachment (P.V.D.) traction
on the retina retinal break movement of the liquefied vitreous through the break
separation between sensory retina & RPE.
Clinical picture
Symptoms 2F + 2F NOT painful
1. Symptoms d.t. retinal break
o Floaters (musca volitantes) d.t collapse of vitreous, minute vitreous hemorrhage &
pigment dispersion into vitreous from the break
o Flashes of light (Photopsia) d.t sudden traction on the photoreceptors of retina
2. Symptoms d.t. retinal detachment
o Field defect: (Black curtain) corresponding to the detached retina
o Falling of vision (if macula is detached = macula OFF)
 Retinal breaks

Horse-shoe tear Hole Retinal dialysis

Rhegmatogenous RD

PVR (Proliferative vitreo-retinopathy)

 Signs
Visual acuity: Normal! except if macula is detached (macula OFF)
Pupil reflex: Reactive! except if extensive RD RAPD (Marcus Gunn pupil)
Red reflex: Grey; as the detached retina lost its transparency prevent light from reaching
the choroid
IOP: mild d.t. absorption of S.R.F by choroidal blood vessels
Fundus:
1. Retinal break Red in color d.t. appearance of underlying choroid in contrast with
grayish detached retina.
Shapes:
Horse shoe tear (U-shaped tear): indicates persistent vitral traction (usually peripheral)
Giant retinal tear: tear involving > 90o of retinal circumference.
Rounded hole (ususally peripheral, rarely affecting the macula)
Retinal dis-insertion (Retinal dialysis) : Retina is separated from the ora serrata
2. Detached retina
Recent RD
Convex surface
Grayish in color
Corrugated appearance
Freely mobile
Wavy blood vessels
Old RD = RD not treated
Retinal thinning d.t. atrophy
Demarcation line d.t. proliferation of R.P.E at the junction between attached &
detached retina
Proliferative vitreo-retinopathy (P.V.R) d.t. proliferation of membranes
restriction of retinal movement
Retinal cyst & subretinal fibrosis
Complications
1. Iridocyclitis
2. Complicated cataract.
3. Atrophia bulbi (in neglected cases) d.t. absorption of SRF & cyclitis aqueous formation
4. Old RD = = RD not treated ..
 Horse-shoe tear treated by argon laser

Pneumatic retinopexy Scleral buckling

 Treatment
A. Prophylactic treatment
Meticulous follow up: for patients having symptoms of acute PVD (flashes of light &
floaters) to detect early retinal breaks
Who are at risk to develop retinal break?
1. Patients with predisposing factors . or
2. Patients with previous history of RD in the other eye

In order not to miss breaks at retinal periphery

1. Examine the eye with dilated pupils
2. Use scleral depressor

If retinal break is formed: seal the breaks as soon as possible:

Mechanism of sealing: induce aseptic (sterile) chorio-retinitis around the tear to seal it
Methods of sealing:
o If central break with clear media seal break with argon laser
o If peripheral break with opaque media seal break with cryotherapy by -70 cryo probe

B. Curative treatment

Aim: seal the break + repositioning of the retina to adhere to underlying choroid

Pneumatic retinopexy intra-vitreal injection of expansile gas e.g. SF6 (sulphur hexafluoride)
to stretch the detached retina against the underlying choroid
+ Seal of the break by: cryotherapy during the procedure or laser photocoagulation after
retinal attachment
Indication: Simple R.D. with single small superior break

Scleral buckling (Conventional RD surgery)

1. Cryotherapy of the peripheral breaks
2. Buckle implant: by suturing a silicon rubber or sponge on the sclera (over the region of
retinal tear) indentation of sclera pushing the choroid against the retina.
+ Trans-scleral drainage of sub-retinal fluid (SRF) using diathermy needle over the
most dependent area of SRF
 Pars plana vitrectomy

Emulsified silicon oil Band-shaped keratopathy

inverted hypopyon

Complications of silicon oil

 Vitrectomy
Removal of the vitreous gel in order to gain access to manage the detached retina
Indications:
1. Rhegmatogenous R.D. in which retinal breaks can NOT be visualized e.g. in vitreous
hemorrhage .
2. Rhegmatogenous R.D. in which retinal breaks can NOT be closed by scleral buckling as:
o Giant tear
o Multiple breaks
o Central break
o PVR (proliferative vitreo-retinopathy)
3. Pseudophakic RD
Technique:
1. 3 separate incisions at pars plana :
1st incision for: fluid infusion
2nd incision for: illumination
3rd incision for: vitrectomy cutter
2. After vitreous removal: breaks are identified & sealed by endo-laser probe.
3. Inner temponade is used to maintain the retinal attachment. :
Short acting temponade: as SF6 (sulphur hexa-fluoride) gas
Intermediate acting temponade: as C3F8 (octa-fluoropropane) gas
Long acting temponade: as silicon oil

Silicon should be removed later on, as leaving it in eye for long time
Corneal decompensation band keratopathy
2ry glaucoma
Complicated cataract
 2ry retinal detachment

Tractional R.D. Exudative R.D.

The SRF (derived from the
Vitreous hemorrhage vitreous
choriocapillaries) gains access to the
Pathogenesis fibrosis pulls of the sensory retina
subretinal space through the damaged
away from R.P.E.
RPE
Choroidal inflammation: e.g.
Proliferative diabetic
Harada syndrome, sympathetic
retinopathy
ophthalmitis or posterior scleritis
Retinopathy of prematurity
Causes Choroidal tumor (melanoma)
Proliferative sickle retinopathy
Choroidal neo-vascularization
Penetrating posterior segment
(CNV) sub-retinal hemorrhage.
trauma
Systemic causes: as pre-eclampsia
Cyclitic membrane
& malignant hypertension
Symptoms
absent
absent
Flashes of light [as the vitro-retinal traction is
[as there is NO vitro-retinal traction ]
gradual]
Floaters if associated with vitritis
Field defect
Falling of vision If macula is affected
Signs
Retinal break NO breaks
Detached Concave
Convex NO corrugation
retina Highest elevation is at the point of traction

Shifting of
NO Shifting of fluid (characteristic)
fluid
Retinal
Severely restricted
motility
Treatment of the cause +
Treatment Treatment of the cause
Vitrectomy
 Retinopathy of prematurity (ROP)
Definition proliferative retinopathy occurs in premature infant of (very low birth weight) d.t.
sudden in O2 pressure [40 mmHg (intrauterine) to 100 mmHg (after birth in room air)].
Pathogenesis
Blood vessels of retina grow from optic disc towards the periphery:
Blood vessels reach nasal end at 8th month of gestation.
Blood vessels reach temporal end 1 month after birth!
The non-vascularized retina suffers from ischemia V.E.G.F release proliferative
retinopathy.
Stages
o Stage 1 (Demarcation line) between vascularized & non-vascularized retina
o Stage 2 (Ridge) at site of demarcation line (have height & width)
o Stage 3 (Extra-retinal fibro-vascular proliferation) extends from ridge into vitreous
o Stage 4 (Sub-total R.D)
o Stage 5 (Total R.D)
 Retinitis pigmentosa
(Attenuated vessels spider-like pigments waxy disc)
 1ry retinal dystrophy (Retinitis pigmentosa)
Definition Progressive retinal dystrophy affecting photoreceptors (rods then cones) & R.P.E
Inheritance autosomal recessive (AR) & X-linked are more severe than autosomal
dominant (AD) type
Pathology
Degeneration affecting the photoreceptors (rods then cones) & R.P.E.
Degeneration starts at the equator (least blood supply) then progress centrally &
peripherally complete blindness.
R.P.E proliferates & migrates towards the inner retinal layers along small arterioles &
venules
Clinical picture
Symptoms
Night blindness
Progressive visual filed contraction then complete loss of vision
Signs
1. Fundus: Triad
Attenuated blood vessels (1st sign)
Spider-like pigmented spots (bone corpuscles) starting at equator.
Consecutive optic atrophy (waxy disc)
2. Field changes:
Early: Ring scotoma d.t. equatorial degeneration
Late: Tubular field then complete loss of vision
Investigation EOG & scotopic ERG are markedly affected (sometimes extinguished)
D.D.
Night blindness Tubular field defect Ring scotoma
Types of retinitis pigmentosa
1. Typical retinitis pigmentosa
2. Atypical retinitis pigmentosa:
- Associated with syndromes e.g. BardetBiedl syndrome .
- Unilateral
- Central
- Sector
- Retinitis pigmentosa sine pigmento
- Retinitis punctata albescens
 Extra notes

Physical signs of retinal diseases

The retinal can react in limited ways to diseases and shows a limited range of physical signs
So that similar fundus appearance may be produced by different diseases

1) Micro-aneurysms Tiny rounded red dots represent capillary dilatation d.t. loss of its tone.
Causes: D.M and hypertension
2) Cotton wool spots (Soft exudates)
Origin: Micro-infarcts (denoting an ischemic micro-vascular disease)
Site: Nerve fiber layer of the retina.
Shape: White fluffy patches, most commonly in the posterior pole (thick nerve fiber layer).
[They become smaller and more circumscribed with time]
Causes:
Hypertension
D.M
Systemic lupus erythematosus.
Venous infarcts.
3) Hard Exudates
Origin: deposition of lipid and lipoproteins
(d.t. abnormal vascular permeability from either retinal or sub-retinal vessels)
Site: inner nuclear layer
Shape: Yellow white spots, well defined edges
Distribution:
Circinate pattern: Separated from the leaking vessel by a clear zone
(Forming complete or incomplete circle)
Macular star: Lipids accumulates in the N.F.L of Henle in malignant hypertension
(4) Retinal Hemorrhages Shape indicates their anatomical depth and etiology e.g.
Superficial retinal hemorrhages: flame-shaped (nerve fiber layer)
Deep retinal hemorrhages: rounded or blot hemorrhage (inner nuclear layer)
Vitreous hemorrhage: diffuse inside the vitreous
Sub-haloid hemorrhage: between retina and vitreous [Saucer shape with fluid level]
Sub-retinal hemorrhage
Hemorrhage under the RPE
5) Retinal membranes
Epi-retinal or pre-retinal membrane formation on the retinal surface at the vitreo-retinal
interface is due to physical disruption of the internal limiting membrane allowing glial cells to
spread from the retina on its surface and to proliferate traction and distortion.
Causes:
Vascular occlusive retinopathy
Excessive photocoagulation
Cryotherapy
Posterior uveitis
Idiopathic
6) Macular edema
The macula and the NFL of Henle are particularly susceptible to the accumulation of fluid and
lipid from leaking vessels lying adjacent to the macula.
Causes:
Posterior segment inflammation
Retinal ischemia
Retinal vascular leakage with hard exudation
7) Retinal pigment epithelium disturbances
RPE proliferation
Causes:
After retinal detachment surgery.
After trauma to the eye.
After laser application

During fluorescein angiography

Normal RPE partially masks the background choroidal fluorescence.
o Pigmentation blocks the background choroidal fluorescence.
o Pigmentation transmits the background choroidal fluorescence.
8) Neovascular response
Mechanism: Hypoxia release of V.E.G.F stimulate the formation of the neo-vessels.
Characters of the new vessels:
Lack the barrier properties leaks fluorescein dye during angiography.
Very fragile liable to bleed
(Associated with fibrosis and membrane formation tractional retinal detachment)
Neovascular tissue in the eye can be derived from:
Optic disc: Neo-vessels on the disc (NVD)
Retina: Neo-vessels elsewhere (NVE) as in diabetes, venous occlusion, retinopathy of
prematurity , or sickle cell disease
Iris: rubeosis irides (NVI)
Angle: (NVA) as in advanced diabetes and ischemic retinal venous occlusion.
Choroid: choroidal neovascular membrane.

Capillary dropouts: areas of retinal ischemia due to capillary occlusions

I.R.M.A (intra-retinal microvascular abnormalities): actually they are shunt vessels
from retinal arteriole to venules at the edge of ischemic retina.

Diagnostic procedure & technique to examine retina

Subjective tests
Visual acuity
Contrast sensitivity
Color vision
Visual field (static & kinetic)
Amsler grid
Objective tests
Direct ophthalmoscopy
Indirect ophthalmoscopy
Slit-lamp bio-microscopy
Fluorescein angiography (FA)
Optical coherence tomography (OCT)
Ultrasonongraphy (US)
Electro-retinography (ERG)
Electro-oculography (EOG)
Visual evoked potential (VEP)