Retina

Anatomy
 Gross anatomy:- MCQ
1) it is the inner most layer of the eye ball.
2) it is develop from neural-ectoderam(mesenchyme).
3) it start at ora serrata ( anteriorly) where it continus with the pigment
epith. Of the ciliary body & iris. It end at optic disc ( posteriory).
4) it is very thin & transparent showing red color of choroid.
5) it is sensitive only to the light.
6) it shows dark area 3-4mm temporal to optic disc called macula lutea
which has avascular depression called fovea centralis & insid the fovea
there is fovula.
 The retina divided into :-
1- central retina:-(macula lutea)
 Size:- 5-5.5 mm.
 The central of macula is avascular depression called fovea
centralis=1.5mm.
 Function:-(mainly cones). MCQ& OSCE
responsible for visual acuty &color vision (photopic vision)(day vision).
2- peripheral retina:-end at the ora serrata.( mainly rods).
Function:-responsible for night vision & peripheral field(scotopic vision).
 Microscopic anatomy:- the retina composed of 10 layers.
1- retinal pigment epithelium :- (RPE).
- It is outer most layer (contact with bruchs membrane of choroid).
- It is one layer of pigmented cubical cells.
2- photo-receptors.(rods & cones)( contains visual pigments). MCQ
Rodes (more sensitive) Cones
Thin Thick
Contain rhodopsin Contain iodopsin
Responsible for night vision. Responsible for day &color vision.
Identification of movement of Identification of details of object.
objects
Maximum concentration in Maximum concentration in center
peripheral

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 Number 120 million Number 6 million.
3- outer limiting membrane end of Mullers fibers.
4- outer nuclear layer nuclei of rods & cones.
5- outer plexiform layersynapes between photo-receptor&bipolar cell.
6- inner nuclear layer  bipolar & Mullers cells+amacrine +horizontal cell
7- inner plexiform layer synapse between bipolar &ganglion cells.
8- ganglion cell layer.
9- nerve fiber layer axons of ganglion cells which form optic nerve.
10- inner limiting membrane  end of Mullers fiber & contact with the
vitreous.
N.B:-
 the layers 2-10 are sensory retina (neural layers).
 The adhesion between RPE & bruchs membrane is strong.
 The adhesion between RPE & sensory retina is weak potential space.
SO the separation occure at this space caused retinal detachment.
 The fovea:-
Composed of auter 3 layers only. MCQ& OSCE
Gives the best vision (6/6) why??
1- Very thin ( 3 layer),so light falls directly on cones.
2- Avascular (nutrition by diffusion from choroid)
3- High concentration of receptor ( only cones).
 Blood supply :-
 Arteries:- MCQ
 inner 5 layers central retinal artery ( from ophthalmic a.)
 outer 5 layers avascular(nutrition by diffusion from chorio-capillaries
NB:- in 20% of normal people :-the macula supply by cilio-retinal artery
originated from posterior ciliary arteries( choroidal circulation).
 Veins:-
 Inner 5 layes drain  central retinal vein cavernous sinus.
 Outer 5 layer drainby diffusion through chorio-capillaries.
NB:- retinal capillaries:- OSCE
- Superficial plexus:-(in nerve fiber layer ):-hge in this plexus takes the
distribuation of the nerve fiber flame shaped hge.
- Deep plexus:- ( in inner nuclear layer & outer plexiform):- hge dot
blot hge.

 Fundus examination:- OSCE

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 Includes:- 1- retina 2-optic disc 3-choroid 4-vitreous.
Examination by:-
1- Direct ophthalmoscope. OSCE& SLID
2- Indirect ophthalmosope. OSCE& SLID
3- Slit lamp bio-microscopy +fundus lens:-
*non contact lens :- volk lens ( +90 ,+78 ,+60) ,hruby lens.
*contact lens:- Goldmann 3-mirror.
4-Fluorescein Angiography (FA):- OSCE
- It is useful investigation to evaluated the retinal & choroidal
circulation.
- Areas of vascular occlusion  black = hypoflourescence.
- New BVs &he  leakagewhite  hyperflourescence.
Direct ophthalmoscope Indirect ophthalmoscope
Erect image. Inverted image.
Magnification:- 15 x Magnification:- 5x
Uniocular Binocular
No steroposis Steroposis(to see elevated lesion)
Small field. Larger field.

Retinal detachment (RD)

 Def:-it is separation of sensory retina from retinal pigment epith.(RPE) by
subretinal fluid .
 Types:- OSCE& SLID
1- Rhegmatogenous RD.(1ry or simple RD.)common.
2- Non-Rhegmatogenous RD.( 2ry RD.)less common.
a- Traction RD.
b- Exudative RD.
Rhegmatogenous RD
*Def:-it is due to formation of retinal breaks,which allow the liquefied
vitreous to enter between the retinal layer causing retinal separation(RD).
*Risk factors:- OSCE
1- Chorio- retinal degeneration in high myopia ( lattice degeneration)
2- Blunt trauma.
3- Cat extraction( ECCE with vit. Loss.).
4- +Ve family history of RD or history of RD in follow eye.
*Incidence:-
- age :>40yrs sex:- >male
bilateral > 10% of cases.
*Types & shape of retinal breaks:-(tear & hole).

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 1- Horse-shoe tear ( most common). SLID
2- Irregular or linear tear.
3- Retinal dialysis:- separation of retina from its root at ora serrata.
4- Giant tear :- 90 degree.
5- Retinal hole.(high myopia)
NB:- *Retinal hole :- - more common in high myopia.
- rounded or oval.
- common site : upper & temporal ------why??
Retinal breaks : more danger if superior ( upper) why? Due to gravity
 C/P:-
*symptoms:- MCQ
1- photopsia ( flashing of light):- due to irritation of rods &cones by
vitreous traction.
3- Floaters ( musca volitans ).
4- Metamorphopsia , micropsia or macropsia ( distortion of odjects)
5- Field defect (black curtain)
6- Poor vision ( painless). If macula involved.
*Signs:-
1- Marcus Gun pupil (relative afferent pupillary defect). MCQ
2- Red reflex gray ( grayish flap.). MCQ
3- IOP low:-soft globe due to absorption of fluid by choroidal BVs.
4- Iridocyclitis flare A/C.
5- Fundoscopy:-
a- Retinal flap:-wavy,thick , grayish,convex ,tremulous retina.
b- Retinal BVs:-wavy & darker .
c- Retinal tear :-red in color  show the choroid.
d- Retinal he ;- may be seen
 Investigation:-( if opaque media  as cataract or vit he.)
1- U/S B-scan .MCQ
2- OCT. MCQ
 Complication:- MCQ
1- Iridocyclitis.
2- Complicated cataract.
3- Rubeosis iridis  NVG.
4- Atrophia bulbi No pl.
5- Phthisis bulbi.
Treatment:-

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 I. Prophylaxis ; retinal tear sealing
* Indication :-
a- Flat retinal tear.
b- High myopia.
c- RD in the others eye.
*Technique of sealing :-
1- Argon laser:-(trans-pupillary): if the media is clear&the tear is central.
2- Cryotherapy:(trans-scleral): if the media is hazy OR peripheral tear.
II. Sclera buckling(+/-)intra-vitreal injection of air or gases like(sulpher
hexafluoride).
Complications:-
1- Axial length of the globe more myopia.
2- Glaucoma
3- Metamorphopsia
4- Tight  ant. Segment ischemia.
III. Pars-plana vitrectomy+ endo laser+ intra-vitreal inj. Of silicon oil +PI
at 6 O”clock.------why?? ( to prevent inverted hypopyon) OSCE
Inducation:-
1- RD with vitreous traction.
2- Posterior retinal breaks.
3- Giant retinal breaks.
NB:- silicon oil removed after 6 months :-
complication:-(cataract , glaucoma , inverted hypopyon.)
Non –rhegmatogenous RD( No breaks)
Traction RD Exudative RD
Def:- It is pulling of retina(vitreous It is pushing of retina.
fibrosis) (choroidal defect)
Causes: -proliferative diabetic retinopathy -choroiditis ( harada disease)
- (PDR)(common) -choroidal tumore (melanoma)
MCQ -Cyclitic membrane -posterior scleritis.
-organized vit hge. -choroidal neovascularization.
-traumavit hge  fibrosis. - toxaema in pregnancy.
-retinopathy of prematurity(ROP). -sever hypertension.
C/P -poor vision. -poor vision.
-Floatera. -Floatera.
-Concave retina & no mobile -convex & mobile-
- U/S B-scan (diagnosis) -U/S B-scan (diagnosis)
TTT P-P viterctomy -Steroid  inflammation

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 -enucleation.

Diabetic retinopathy(DR) OSCE

 Def:- it is micro-angiopathy affecting retinal arterioles , capillaries
,venules, always bilateral but asymmetrical.
NB: -common in insulin dependent= juvenile DM= type 1 DM.
-Main cause of blindness.
 risk factors:- MCQ& OSCE
1- Duration of disease:- long duration  DR
- After 7yrs - 50%-DR
- After 15yrs 90%-DR
2- Metabolic control :- dose not prevent DR ,but delays DR
3- Other factors :-
a- Pregnancy.
b- Hypertension.
c- Anemia
d- Renal disease
e- Smoking
f- Obesity & hyperlipidemia
 Pathogenesis:- MCQ & OSCE
1- Micro-vascular leakage:-(disturbance of blood- retinal barrier): lead to
a- Retinal odema.
b- Retinal hge.
c- Hard exudateslipoprotine
d- Micro-aneueysm( capillary distension).
2- Micro –vascular occlusion:- due to
-aggregation of platelats.
-depostion of lipid & cholesterol.
-RBCs deformability.
*lead to:-
retinal ischemia release vasogenic factors neovascularization
vit hge.
 C/P:-OSCE, MCQ & SLID 100%
Symptoms: poor vision only in maculopathy or lat stage .
Signs:- ( stages)
Non- proliferative DR( Background DR) good vision if no macular odema.
 Retinal He  dot ,blot hge

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  Retinal exudates.
 Retinal odema.
 Micro- aneurysme
 (+_ )macular odemapoor vision
TTT:--argon laser micro- aneurysms.
-argon laser( focal & grid)  macular odema( CMO).
-control DM& hypertension.
Pre-proliferative:-( short duration )
 Retinal hge dot,blot hge
 Cotton wool spots (soft exudates)
 IRMA= intra retinal micro-vascular abnormalities.
TTT: control DM & hypertension
Proliferative DR:-( Pre-proliferative + new vessels )at:-
 NVDs =new vessels at disc.
 NVEs = new vessels elsewhere.
 NVIs =new vessels at iris ( rubeosis iridis).
TTT:-
1- pan-retinal photocoagulation ( PRP ) Argon laser .
NB: Done flurescein angiography befor laser( SLID,OSCE)
2- Alpha-chemotrypsinretinal hge.
3- Intra-vitreal steroid or Avastin.
Diabetic maculopathy:-( may be with any stage).
-focal odema dut micro-aneurysm.
- CMO:- may lead to foveal cystruptur  macular hole RD.
Investigation:- FA , OCT,
TTT: - focal & Grid argon laser
Advanced DR:- ( Complicated stage )
- Vitreous hge& sub-hyaloid  fibrosis vittraction RD
- Rubeosis iridis  NVG
- Complicated cataract.
TTT:-
- Vit hge+ traction RD vitrectomy + endo-laser .
- NVGanti- glaucoma drugs +trab.

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 Ocular manifestation(OSCE)
 Lid:- blepharitis , sty & Xanthelasma.
 Conj:- conjunctivitis
 Cornea:- keratitis ( ulcer)
 AC:-hyphaema  due to NVIs
 Iris:-Rubeosis.
 Lens:- complicated cataract (snow flaken)
 Vitreous:- vit. He
 Retina:- DR, CRVO retinal he
 Optic nerve:- optic neuritis
 Orbital:- orbital cellulitis.
 EOMs:- paralytic squint ( LR ms palsy)
 Post operative :- infection , delayed wound healing ,Hge.

Hypertensive retinopathy
 Def:-it is bilateral retinal affectiondue to sever hypertension(140/90)
 Risk factors:-
1- Age 2-Severity of HPT 3-Duration of HPT 4-Pregnancy.
 Grades:-
- Grade I:-generalized mild attenuation of the arteries
- broader vascular light reflex.
-veins no changed.
- Grade II:- gradeI+ focal attenuation arteries
A-V crosse salu”s signe. MCQ
- Grade III:-banking of veins .
- copper wire +A-V crosse gunn”s signe (nicking).MCQ
-flam hge+ retinal exudates +cotton wool spots.
- Grade IV:- grade III + sliver wire + papilloedema + macular star.
 Complication :- MCQ
a- CRVO.&CRAO.
b- 3rd nerve palsy.
c- Retinal macro-aneurysm.
 Treatment:- Control hypertension.

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 Retinopathy of prematurity (ROP)
 Pathogenesis:-
ROP is proliferativeaffect pre-term infants < 30wks or low birth
weight< 1500g  exposed to high O2 concentration lead to damage
of incompletely vascularized retina  temporal produce vasogenic
factore New BVs.
C/P:- Vit he  RD & Avascular area  leuckcoria. MCQ& SLID
TTT:- - P-P vitrectom .
Reinal vein occlusion(RVO)
Types:- Central retinal vein occlusion.( CRVO)
Branch retinal vein occlusion.(BRVO)
Predisposing factors:- MCQ
- Old age
- Systemic hypertension, DM , Blood diseaseanemia, polycythemia.
- Ocular hypertension.
- Periphlebitis  behcet disease.
- Hypermetropia BRVO
- Oral contraceptive pills.
Causes:-
- Inside the vein:-due to increased blood viscosity as:-(polycythemia
,leukaemia, dehydration, contraceptive pills.
- In the vein wall:- behcet disease & sarcoidosis.
- Outside the vein :-due to pressure on vein as:-increased IOP ,
A-V cross , orbital tumore . sclerosed artery.
NB: RVO usually at morning due to thrombus forms at night due
to venous stasis at night.

Central retinal vein occlusion

Types :-
1- Non- ischemic CRVO.

2- Ischemic CRVO.

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Non – ischemic CRVO:- most common
 C/P:-( common unilateral)
- Symptoms:- rapid painless loss of vision .( 6/60)
- Signs:-
o Mild dilated &tortuous BVs
o Mild flam hge.& hard exudates
o Mild macular odema & optic disc odema.
 Investigation:- OCT , FA.
 TTT:- argon laser to anastomosis between retinal vein & choroidal vein .
NB Good prognosis.
Ischemic CRVO:- less common
 C/P:-
- Symptoms :- sudden painless loss of vision. ( MCQ)
- Signs:-
o Fundus stormy sunset appearance.
o Marked dilated &tortuousBVs
o Extensive retinal Hge. ( flam , dot & blot )
o Cotton wool spots ( soft exudates).
o Afferent pupillary defect.
o CMO, optic disc odema.
o NVDs ,NVEs (OSCE& MCQ)
o NVIs (NVG) 100 – day- glaucoma. MCQ
 Investigation:- OCT ,FA
 Complication:-
1- Vit hge .& hyphaema red cell glaucom.
2- CMO macular hole  RD.
 Treatment:- ( Bad prognosis)
o Contral DM & hypertension.
o Argon laser  pan retinal photocoagulation( PRP).
o Intravitreal :-
1- steroids  in macular odema.
2- Avastin( anti vasogenic facters) in NVDs, NVEs.

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Branch retinal vein occlusion( MCQ)
 Occlusion of one branch of CRV.
 If peripheral branch occlusion the vision not impaired( good vision).
 If central branch occlusion ( macula affect ) the vision is impaired
( poor vision).
NB:- common site of occlusion :- bifurcation of vein.& A-V cross.
- common branch occlusion  supera –temporal quadrant.
 C/P:-
- symptoms:-
- vision affect if macula involved.
- Metamarphopsia.
-Field defect  if branch occlusion at periphery.
- Signs:-
o Dilated & tortuous of branch.
o Flam hge & dot ,blot hge.
o Cotton wool spots.
 Investigation:- FA
 TTT:- Argon laser photocoagulation.

Retinal artery occlusion

Def:- obstraction of central retinal artery (CRA) or branching .
Causes :- MCQ
1- Thrombosis : arteriosclerosis ( old age , DM, HTN , hyperlipidemia ).
2- Embolism : from the heart , ascending aorta , carotid artery .
3- Arthritis : -
a. Systemic lupus erythematosis ( SLE )
b. Poly arteritis nodosa .
c. Giant cell arteritis .
4- Spasm of CRA as in :-
a. Migraine .
b. Hypertensive encephalopathy .
c. Quinine poisoning .
5- Very high IOP during RD surgery .

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 N.B : Retinal artery occlusion less common than vein occlusion
- Retinal artery occlusion more common in left eye why ??

Central retinal artery occlusion

(CRAO)
- It is ocular emergency resulting in sudden painless loss of vision in
few minutes or recurrent attack of amaurosis fugax
 C/P:
- Symptoms : sudden painless loss of vision ( unilateral ) . MCQ
N.B: some time in 20% of normal person centeral vision 6/6
(tubular vision ) is preserved why ??
- Signs :
o Normal ant.segment .
o Pupil:- afferent pupilary defect : -direct is abscent
-indirect is preserved .
o No PL except in patient with cilioretinal artery .
o Fundus :-
 Narrow artery & retinal odema .
 Retinal white ( cloudy ) .
 Central retina ( fovea ) cherry red spot. MCQ
 End stage optic nerve atrophy .
N.B: cherry red spot : appear after 2-3 hrs from CRAO .
- Milky white fundus due to necrosis in gangalion cell layer & NFL.
- Fovea : contains no gangalion cells takes nuteration from the
choroid  remain red colour ( showing choroid )
- Resolve within 4-6 wks .
- D/D of cherry red spot :- SLID & MCQ
o CRAO ( unilateral ) .
o Commotion retina ( berlins edema ).
o Amaurotic family .( Tay- sacks diseases)
o Quinine poising ( bilateral )
 Complication : death from CNS strok
Branche retinal artery occlusion ( BRAO) MCQ
- The most common cause by embolism .
- Decrease in vision if macula involved .

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 - White area in infarction & failed defect .
Cilio-retinal artery occlusion
- Present in 20% of population arises from pos.cilliary a (supply
macula only ) .
- Acute decrease of vision ( sever loss )
- White central retina except fovea .
 Investigation of RAO:-
1- Perimetry BRAO
2- FA.

 TREATMEANT OF RAO: ( emergency case )

- Immediately should lie flat
- Medical TTT :
o Vasodilator to relive spasm :
 retrobulbar priscol ( sympatolytic ).
 Inhalation of CO2 5% + O2 95%.
 Inhalation or sublingual nitroglycerine
o I.V. Acetazolamed 500 mg ( diamox)  lower IOP.
o I.V. mannitol 20%- lower IOP
o I.V. streptokinase.( fibrinolytic)
NB:- paracentasis  leading to hypotony  V.D.
Ocular massage  lower IOP.
- Bad prognosis.
Color blindness ( OSCE)
 Def:-is inability to see the red , green & blue color ( absence 3 cones).
- Absence of color – sensitive pigment in the cones cells of the retina .
 Causes :
1- Congenital ( more common ) Common in male .
2- Acquired :- Optic nerve damage :- papilledema , papilitis .
Macular disease .
Drugs :- chloroquine , digoxin .
 Types :-
1- Achromatic vision :- complet loss of color vision ( absence 3 cones )
2- Monochromatic vision :- absence 2 cones ( most common red & green)

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 3- Dichromatic vision : absence 1 cone .
 Investigation :- ( macular function test )
1- Ishihara test . SLID & MCQ
2- Coloured matching test :- colored beads & wool ( child ).
3- Coloured glass discs : in mature cataract .
 Treatment : no TTT .

Retinal degeneration
Retinitis pigmentosa(MCQ& SLID)
 Def:-it is heredo- familial , bilateral , prograsisve pigmentry retinal
degeneration
 Causes:- Unknown - may be :-
1- Phototoxicity.
2- Hereditary:- +VE family history.
o AD Common  good prognosis
o AR less common.
o X-Linked least common  bad prognosis
 Pathology:-
- Degeneration of photoreceptor start  Rodes . MCQ
- It is start at equatorial due to less blood supply peripherally 
least centrally  leading complete loss of vision ( blindness) at
middle age ( 40yrs).
 Clinical picture:-
Symptoms:-(start before 10 yrs) MCQ
o Night blindness ( nyctalopia) the earliest symptom.
( defective dark adaptation).
o Visual field loss
o Finaly  blindness ( degeneration rods & cones ) .
Signs:-
- Fundus examination:- MCQ
o Pigmentation at periphery ( Bone corpuscle ) black spots .
o Attenuated BVs .
o Optic nerve atrophy ( waxy & yellow disc ).
- Field chang : MCQ
o Ring ( annular) scotoma .
o Tubular vision .

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 Investigation :-MCQ
1- Perimetery .
2- ERG & EOG  change .

NB:
o common association with ocular disease :-
1- OAG , myopia , keratoconus .
2- Post.subcapsular cataract .
3- Post.vetrial detachment .
o Associated with laurance moon biedel syndrome :
1- Obesity .(moon face ).
2- Mental retardation .
3- Hypogonadism .
4- Polydactyly.
5- Night blindness .

 Treatment : no TTT .
- Vit A tablet .
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The end of retina

Good luck
DR. HANAN DARIF 2016

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