Retina pdf - D. Wajida

Retina

Gross Anatomy

It is the innermost layer of the eyeball.

*It is starts at ora serrata & ends at optic disc.

*It is very thin & transparent showing the red color

of choroid.

*It is sensitive only to light (translates photons to

electrical impulses that reach the visual cortex and

transformed into a visual sensation).

*Anatomically: the retina is divided into:

1-Central Retina :(Macula Lutea =5.5mm) the center

of the macula is an avascular depression called

"fovea centralis" (1.5mm)

Function: (Mainly cones).

1- Responsible for visual acuity, Color & day vision.

2-Peripheral Retina: ends at the ora serrata.

Function: (Mainly rods) responsible for night vision

and peripheral field

Microscopic anatomy

The retina is composed of 10 layers:

(1) Pigment epithelium (RPE):

* It is the outermost layer (in contact with Bruch's

membrane of choroid).

*It is made of one layer of pigmented cubical cells

(2) Photo-receptors (rode & cones): [Body

]

The light sensitive layer (contains visual pigments).

(3) Outer limiting membrane: It is made of the outer ends

of Muller's fibers.

(4) Outer Nuclear layer: It's made of nuclei of rods & cones.

(5) Outer Plexiform layer [ Hanel layer in the macula

arranged radially]:

(Synapses between photoreceptors & bipolar cells axons &

processes of the horizontal cells).

(6) Inner Nuclear layer:

It is made up bipolar cells & cells of Muller's fibers +

Amacrine & horizontal cells.

(7) Inner pelxiform layer: the synapses between bipolar

cells, Ganglion cells & Possesses of amacrine cells.

(8) Ganglion cell layer.

(9) Nerve fiber layer: It is made up of the axons of ganglion

cells which form the optic n.

(10) Inner limiting membrane:

It's made of the inner ends of Muller's fibers & in contact

with the vitreous

FUNCTION OF THE RPE:

(1) Nutrients & metabolites from & into the choroid.

(2) Essential for Rhodopsin (Vit. A) & Iodopsin

formation.

(3) Absorption of scattered light "prefect optical

image".

(4) Phagocytosis of tissue damage.

(5) Adhesiveness of the underlying sensory retina

(prevents RD).

PHOTORECEPTOR

Rods:

1-Thin (easily affected in some diseases).

2-Contain Rhodopsin.

3-Responsible for night vision. (Scotopic vision).

4-Maximum concentration in perifoveal region 160 000 /

mm2.

5-Total number 120 million.

Cones:

1-Thick.

2-Contains Iodopsin.

3-Responsible for day & colour vision. (photopic vision).

4-Maximum concentration in the Center (faveola 147000 /

mm2).

5-Total number 6.5 milions

Blood supply

(1) Arteries:

*Inner 5 layers: from central retinal artery (from the

ophthalmic artery).

*Outer 5 layers: avascular (nutrition by diffusion the

choroids capillaries.

The Fundus Oculi

Includes:

1- The retina. 2-The optic Disc (the visible part

of the optic nerve).

3-The choroids. 4-The vitreous

Diseases of Retina

Central Retinal Artery Occlusion (CRAO)

Etiology:

1-Thrombosis: In: arteriosclerosis (in old, DM &

hypertension).

2-Embolism:

a-Detached thrombus: as in Myocardial infraction, aortic

aneurysms or sub-acute B. Endocarditis, Atheromatous

plaques from large BVs like carotid or arch of aorta

b- Air Embolism.

c-Fat Embolism: as in –Crush injury -Acute hemorrhagic

pancreatitis.

3-Spasm: as in -Hypertensive Encephalopathy in young

age

-Quinine poisoning.

-Raynaud's disease, burger disease &

Migraine.

4-Arteritis: as in: -Giant cell arteritis (GCA)

-Poly arteritis nodosa.

5-Very high IOP

Signs:

(1) vision: HMNo p.L.

(2) Pupil: *Semi dilated.

*Afferent pupillary defect:

-Direct reaction  absent.

-Consensual  preserved.

(3) Fundus:

(i)Early (within minutes):

*Arteries: attenuated (thread-like).

*Veins: little attenuation & stagnant blood column may

be segmented

*Retina: -White (cloudy)

-Center (fovea)  shows cherry red spot.

(ii) Late (several weeks later):

*Arteries: refill so retina becomes transparent again (but

it's atrophic):

Due to -Relief spasm.

-Canalization of the thrombus (by thrombokinase)

*Retina: the cherry red spot disappears (after 2-3 weeks).

*Investigations Cardiologist 

1-Cardio-vascular examination.

2-Echo-cardiogram.

3-Colour Doppler on the carotid

*Treatment: Emergency treatment

*Usually useless (if not immediate, after 30-90 min 

irreversible damage to retina).

*Aim is to induce vasodilation:

relief the spasm.

If embolus: dislodge the embolus to a smaller peripheral

branch.

By: * General:

1-In halation or sublingual nitroglycerin.

2-Inhalation of carbogen (5% O2 + 95% Co2).

*Local:

1-Peracentesis (leading to hypotony.)

2-Ocular massage to lower the IOP.

3-Retrobulbar vasodilators (Acetyl choline –Priscol ).

Central Retinal Vein Occlusion (Thrombosis)CRVO

Etiology

1-Inside the vein: due to increased blood viscosity as in:

-Blood diseases: polycythemia, leukaemia.

-Dehydration & contraceptive pills.

2-In the vein wall:

-Phlebitis: as in typhoid, influenza (young),

autoimmune(Bechet disease ).

-Rough intima: as in atherosclerosis (old), DM &

hypertension.

3-Outside the vein: due to pressure on vein by:

-Orbital tumor.

-Increased IOP.

-Sclerosed artery.

-Orbital cellulitis.

picture:

Clinical

Symptoms: Rapid painless diminution of vision (6/60 

HM) due to hemorrhge , oedema & ischaemia

of the inner 5 layer .

Signs:

*Pupil: -Dilated & sluggish direct reaction (due to retinal

oedema and hge).

-Afferent pupillary defect in ischemic type

*Fundus: shows stormy sunset appearance.

1-Veins: engorged & tortuous.

2-Opto-ciliary shunt:

3-Retina: Show extensive Hemorrhage. (dots, blots & flame

shaped) edema, cotton wool exudates +micro

aneurysms.

4-Macula: shows edema & hemorrhage

5-Disc: Hyperemic, edematous.

*Fluorescein angiography (FA):

-Leakage of FI. Into the retina.

-Areas of retinal ischemia in ischemic type.

*Classification:

(I) Ischemic. (2) Non-Ischemic

Treatment:

(1) Medical:

*Treatment of the cause: control hypertension & DM.

* Helps blood absorption: alpha-chymotrypsin IM.

* Vit. C: increase integrity of capillaries.

* Prevents platelets stickiness: Aspirin in small doses (75

mg)

*Anticoagulant: may cause Hemorrhage (not used).

(2) Laser Photo-coagulation (argon) PRP:

-Indication: in Ischemic cases (after the hemorrhage.

Resolves).

-Aim:

*To destroy the peripheral hypoxic areas (  anoxic) no

vasogenic material release.

*Regression of the neo-vessels.

*Improvement of circulation of the central area.

(3) Intravitreal:

1- Steroids (Triamcinolone acetonide):

-In case of macular edema.

-Steroids  regression of new BVs

2-Avastin: (anti VEGF)

(4) Treatment of Neovascular glaucoma:

* Seeing eye:

- Medical: Timolol +Diamox +Steroid locally.

- Laser treatment (PRP) : to avoid regrowth of new BVs.

-External fistulizing + Implant.

-If failed do cyclocryotherapy.

*Non-seeing (Blind Painful eye):

-Retrobulbar injection of alcohol.

-Cyclocryotherapy .

-Enucleation

Hypertensive retinopathy

Systemic hypertension is diagnosed on several consecutive

measurement of 140 / 90 or more.

*Pathogenesis:

-Chronic mild hypertension leads to Arteriosclerotic

change.

-Chronic hypertension leads to damage of vessel wall with

breakdown of blood retinal barrier & vascular leakage.

picture:

Clinical

*Symptoms:

-May be asymptomatic.

-Blurred vision.

-Episodes of temporary visual loss.

*Fundus picture:

-Arteriolar narrowing:

1-Generalized & Focal.

2-Severe hypertension may lead to obstruction of pre-

capillary arterioles & development of cotton wool

spots.

-Vascular leakage:

1- Flame-shaped hemorrhage.

2-Retinal edema.

3-Hard exudates. (if in the macula  macula star)

4-Papilloedema & exudative RD in case of

malignant(accelerated) hypertension.

-Arteriosclerosis: in chronic hyper tension for many years.

*Grades of hypertensive Retinopathy:

Grade 1: Generalized arteriolar narrowing.

Grade 2: Generalized and focal arteriolar narrowing.

Grade 3: As grade 2+Retinal flame hemorrhge + retinal

exudates + Cotton wool spots + all sclerotic change.

Grade 4: Severe grade 3 + papilledema + macular start

+ Exudative RD.

*Treatment: -Control hypertension.

-Weight control.

-Exercise. –Sodium control

Retinopathy of prematurity

*Pathogenesis:

ROP is a proliferative retinopathy affects pre-term infants

<30 weeks or low birth weight < 1500 gm who exposed to

high O2 concentration leads to damage of incompletely

vascularized retina = temporal periphery  produce VEGF.

month of

reach the nasal periphery at the 8

BVSc

(Retinal

gestation & reach the temporal periphery one month after

delivery)

*Zones:

Zone 1,2&3.

*Staging:

-Stage 1: Demarcation line separate vascular from

avascular retina.

-Stage 2: Elevated ridge.

-Stage 3: Ridge+Extra retinal fibrovascular proliferation

extend from the ridge into the vitreous  retinal

& vitreous hemorrhage.

-Stage 4: Subtotal RD.

-Stage 5: Total RD.

*Extent: number of clock hour involved.

-Treatment: *Stage 1,2  no treatment

*Stage 3 laser photocoagulation or

cyclocryotherapy for the avascular retina

if Threshold disease present.

*Stage 4,5 vitrectomy for tractional RD

Diabetic retinopathy (DR)

*Definition: It's a micro- angiopathy affecting the retinal

retinal arterioles, capillaries & venules.

Always bilateral but asymmetrical.

*Etiology: Unknown (DM more than

10yrs, so DR is related to duration of DM not related to

severity of DM, so DR is commom in insulin

dependent = Juvenile DM).

cause of blindness in Egypt.

is the 3

*Risk factors: -Young age & long duration.

-Poor control of DM.

-Coexisting hypertension.

-High blood lipid level.

-Pergnancy

Pathogenesis:

*Micro-vascular leakage:

1-Due to: loss of pericytes due to sorbital 

disturbance of blood – retinal barrier.

*Micro-vascular occlusion:

A) Due to:

1- Thickening of basement memberane: Due to glycogen

deposition  decrease diffusion  retinal

ischemia.

2-Aggregation & stickiness of platelets 

microthrombus.

3-Endothelial cell damage & proliferation. (by

diabetic metabolites).

4-RBCs changes

-Glycosylated Hemoglobin  decrease O2 transport.

-Lack of deformability (elasticity) of RBCs.

5-ILM thickening  decrease diffusion of O2

from vitreous to retina.

Resulting in

Retinal ischemia which release chemical

(vasogenic) factor which stimulate new vessels

formation.  PROLIFERATIVE.

*Clinical picture:

Symptoms -Asymptomatic.

-Gradual diminution of vision.

-Floaters. –Acute loss of

vision

1- Non – proliferative (simple or Background) DR:

*Retinal Hemorrhage: dot hemorrhage (Deep, rounded

hemorrhage), due to affection of deep plexus.

*Retinal exudate: Deep (hard) exudates arranged in

clumps or rings called circinate + retinal edema.

*Retinal vessels: Micro-aneurysms.

1- Pre-proliferative DR:

*Retinal Hemorrhage.: Dots &blots.

More than 2 quadrants.

*Retinal exudates: soft (cotton wool spots) and hard

exudate & edema.

3-Proliferative DR:

*Retinal exudates: Cotton wool.

*Retinal vessels: neo-vessels (NV) at:

1-The Disc (or within one DD around the disc)

NVD.

2-The Retina  NVE

*Pre-retinal & Vitreous hemorrhage: Bleeding from the neo-

vessels (may be sub-hyaloid=pre-retinal) which may

organize  vitreous fibrosis & epi-retinal membranes

*Tractional retinal detachment: Due to pull by the

vitreous fibrosis & contraction of the epi-retinal

membranes.

4-Advanced Diabetic Eye

(Complication of DR)

*Opaque membranes.

*Tractional RD (Retinitis proliferans).

*Rubeosis Iridis that may lead to neo-vascular

glaucoma

5-Diabetic Maculopathy

A) Focal edema: from microaneurysm.

B) Diffuse edema (CME): FA  flower petals.

Due to accumulations of the dye within the

microcystic spaces in the radially arranged Henle layer of the

macula.

C)Ischemic maculopathy: due to macular BVs.

*Investigation: *FA (Fluorescein angiography).

-CSME: focal or diffuse or ischemic.

-To detect leaking micro-aneurysms and

ischemia.

-To differentiate IRMA from new BVs

Treatment:

1-Medical treatment: (background)

* Control DM & hypertension.

*Prevent platelet stickiness  Aspirin (in small

doses)

*increase Oxygenation of the retina: give Duxil.

-Follow up of Adiabatic patient is very important.

3-Argon Laser treatment:

*Indications:

-In pre.and proliferative DR & robeiosis iridis  do PRP.

-In diabetic macular edema do

-Focal treatment (in focal edema).

-Grid treatment (in diffuse edema).

*Aim: as CRVO.

4-Intravitreal Triamcinolone acetonide injection:

5-Vitrectomy+laser endophotocoagulation :

*Indications:

1-Persistent vitreous hemorrhage for 1 month.

2-Viterous traction threaten the

maculaprevent & treat tractional RD.

3-Presistent macular edema.

6-Neovascular glaucoma: as in CRVO

Retinal detachment (RD)

Definition:

It's a condition in which the retina is separated into 2

layers:

1-Retinal pigment epith. (R.P.E).

2-Sensory retina (as there is an embryological

potential space between these 2 layers)

(A) Primary (Simple Rhegmatogenous)

*Def.: It's due to formation of a retinal tear, which allow

liquefied vitreous to enter between the retinal layers causing

retinal separation.

*Risk Factors: of Rhegmatogenous RD:

(a) Chorio-retinal degeneration as in high myopia.

(b) Blunt trauma.

(d) Family history of RD or history of RD in the

fellow eye.

(e) PVD.

(f) Chorio-retinal:  toxins  necrosis & tear.

 Liquefaction of vitreous.

 Vitreo-retinal adhesions.

Shape of retinal tears:

(1) Horse-shoe tear (the most common).

(2) Retinal hole.

(3) Arrow head tear

(4) Operculated tear: the flap is completely torn

away from the retina.

(5) Irregular or linear.

(6) Giant tear: 90 degree or more of globe

circumference (more than 3o'clock)

(B) 2ry Retinal detachment

Def.: It's pushing or pulling of the retina by intraocular

disease with no retinal tear.

1-Tractional RD:

* In which retina is pulled by vitreous fibrosis as in:

-Cyclitic membrane, organized vitreous hemorrhage.

-Proliferative diabetic retinopathy (PDR).

-Retinopathy of prematurity (ROP).

-Penetrating post. Segment trauma: with

vitreous loss & vitreous hemorrhage.

-Exudative RD:

In which the retina is pushed by fluid derived from

the choroid which gain access to the subretinal space

through damaged RPE, as in:

-Choroiditis as in "Harada disease".

-Posterior scleritis.

-Neoplasm (malignant melanoma of choroid or

secondaries).

-Coat's disease.

-Sub-retinal neovascularization & Hemorrhage as in

ARMD.

-Systemic causes: toxemia of pregnancy,

malignant hypertension

Treatment of secondary RD:

Is the treatment of the cause

1-Tractional: Vitrectomy.

2-Exudative:

-Inflammatory (choroiditis & post. Scleritis) 

give cortisone

-Malignant  Enucleation.

*Clinical picture: of rhegmatogenous RD

*Symptoms: May be asymptomatic for long time

1- Early: The retina still has some nutrition.

- Flashes of light (photopsia): Due to mechanical

irritation of rods & cones by vitreous traction.

-Floaters: (Musca volitans): Due to Vitreous

Degeneration  opacities, minute hemorrhage from the

tear into the vitreous & P.E. migration.

-Metamorphopsia, micropsia, macropsia.

-Late: Death of photoreceptors (Choroid)

-Field defect (black curtain):

-Failure of vision (HM or PL vision) :(Painless & rapid)

Due to foveal involvement (foveal detachment

)

*Proliferative Vitreo-retinopathy (PVR): due to

proliferation of membranes:

- On the inner retinal surface (epi-retinal

membrane).

- On the outer retinal surface (sub-retinal

membrane)

* Treatment:

*Prophylaxis:

Retinal tear  sealing.

-Indications:

a) Patient:

-Myopic.

-Aphakic (vitreous herniation  tear).

-R.D. in the others eye.

b) Break:

-Large.

-Superior  spread rapidly by gravity

-Technique of sealing:

Most breaks are adequately treated by:

*Argon laser: (trans-pupillary):

Especially if the media is clear & the tear is

central.

*Cryotherapy: (trans-scleral) especially if the

media is Hazy and peripheral tear).

*Curative:

a) The pt. is atropinized and examined:

-To determine extent of RD

) The patient rest in bed (to avoid shaking movement)

with tear in the most dependent part.

c)Technique:

I-Sealing of the break:

By -Cryotherapy. –Laser

Which will induce sterile chorio-retinitis  that

heals by chorio-retinal scar  adhesion between retina &

choroid that prevents leakage of fluid under the retina 

prevent spread.

II: Approximation of the retina & choroid (reposition

of the retina):

*Evacuate the Subretinal fluid (SRF)

*Scleral buckling:

Pushing the sclera by:

-Silicone implant: it is sutured on the sclera over the tear

(to do invagination  implant).

*Intra-vitreal injection of air or expandable gases.

*Complication of silicon oil:

-Inverted hypopyon in AC.

-Cataractogenic.

-Close the angle  secondary glaucoma.

-Uveitis.

III: pars plane Vitrectomy+intra-vitreal injection

of silicon oil (to relief retina from vitreo-retinal

traction) and Endo laser.

Degeneration of the Retina

(I) Retinitis Pigmentosa

*Definition: It is heredo-familial, bilateral,

progressive , pigmentry retinal degeneration of

unknown etiology .

*Etiology:

Unknown, may be:

1-Abiotrophy: ischemia & decrease Vit A

2-Photoxicity.

3-Hereditary: mode of inheritance may be,

-Autosomal dominant.

-Autosomal recessive.

-X-linked. (so common in boys)

Clinical picture:

*Symptoms:

-Night blindness (defective dark adaptation): due to

affection of rods.

-Progressive visual filed contraction.

-Finally, Complete loss of vision.

*Signs

-Fundus Picture:

-Retina: Spider (Bone corpuscle) like pigmented

spots as equator, then spread ant. & post.

-Vessels: Markedly attenuated.

-Disc: Consecutive optic atrophy (Waxy or pale

disc).

2-Field changes:

-Early: ring(annular)scotoma: due to equatorial

pigmentary degeneration.

3-Investigations

-ERG: is markedly diminished especially Scotopic

ERG, it's affected early (photopic REG is affected

later)

-EOG: subnormal

Treatment:

*Useless: 1-Vitamin A. 2-Vasodilators.

3-Placental extract.

*Low vision aid.

*Genetic counseling

(III)AGE REALTED MACULAR DEGENERATION

(ARMD).

*Definition: It's a macular disease leads to severe

affection of the central vision in old age above 50 yrs.

*Laterality: bilateral.

*C/P:

(1) Age related maculopathy = drusen:

Small, discrete, yellow white, slightly elevated

bilateral symmetrical spots.

-Pathogenesis: failure to clear the debris discharged

into this region  accumulation of the debris

between the RPE & the Burch's membrane 

thickening of Burch's membrane.

& also lead to RPE atrophy  window defect.

(2) AMD with 2 main types:

1-Dry(atrophic) type:

-There is slowly progressive geographic atrophy

of photoreceptors, RPE & choriocapillaries.

-C/P: gradual impairment of vision.

-FA  Window defect.

-Treatment: No effective treatment (stop

smoking +treat hypertension) low vision aid may be

helpful.

2-Wet type: due to abnormal neovascularization

from the choroids (CNV) under retina grow

through a defect in the Bruch's membrane. (appears

as gray-green lesion ) leakage.

*C/P: sudden impairment of vision.

*Treatment:

1) Argon laser photocoagulation: for well-defined

extrafoveal CNV.

The aim it to destroy the CNV without damage to

the fovea.

2)PTD (Photodynamic therapy): for sub foveal CNV.

3) Intravitreal injection of Avastin (Anti VEGF) &

Triamcinolone actinoid.