Diabetic retinopathy (DR)
It's a micro- angiopathy affecting the 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).
Risk factors
: -Young age & long duration.
-Poor control of DM.
-Coexisting hypertension.
-High blood lipid level.
-Pregnancy.
Pathogenesis:
Micro-vascular leakage :
Due to: loss of pericytes due to sorbitol disturbance of blood
retinal barrier
Micro-vascular occlusion: caused by:
1- Thickening of basement membrane.
2-Aggregation & stickiness of platelets.
3-Endothelial cell damage & proliferation
4-RBCs changes
Resulting in :
Retinal ischemia which release chemical (vasogenic factor which
stimulate new vessels formation) proliferative.
Clinical picture:
1- Non – proliferative (simple or Background) DR
Retinal Hemorrhage : dot Hemorrhage (Deep, rounded)
Retinal exudate : Deep hard exudates arranged in clumps or rings
called circinate + retinal edema.
Micro-aneurysms .
2- Pre-proliferative DR:
Retinal Hemorrhage: Dots &blot 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):
1-At the Disc NVD (neovessels at disc).
2-At the Retina NVE (neovessels at elsewhere).
Pre-retinal & Vitreous hemorrhage: Bleeding from the neo vessels
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
Tractional RD ( Retinitis proliferans ).
Rubeosis Iridis that may lead to neo-vascular glaucoma.
5-Diabetic Maculopathy
Either :
a)Focal edema : from microaneurysm .
b) Diffuse edema (Cystoid Macular Edema): Fluorescence Angiograghy
flower petals.
c)Ischemic maculopathy
Treatment:
1-Medical Treatment :
Preproliferative (background)
- Control DM & hypertension .
- Prevent platelet stickiness Aspirin ( in small doses ).
-Argon Laser Treatment:
2
Indications :
-In pre.and proliferative DR & robeiosis iridis do PRP(panretinal
photocoagulation) .
-In diabetic macular edema do
-Focal laser (in focal edema) .
-Grid laser (in diffuse edema).
3-Intravitreal Triamcinolone acetonide injection.
4. Intravitreal AntiVEGEF injection eg. Avastine or Lucentis
5-Vitrectomy+laser endophotocoagulaton :
Indications :
1-Persistent vitreous hemorrhage for 1 month.
2.Tractional RD.
3-Presistent macular edema.
6-Neovascular glaucoma : as in CRVO.
Retinal detachment (RD)
It's a condition in which the retina is separated into 2 layers:
1-Retinal pigment epithelium. (RPE).
2-Sensory retina (as there is an embryological potential space
between these 2 layers
1. Rhegmatogenous RD
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.
(c) Aphakia.
(d) Family history of RD or history of RD in the fellow eye.
Shape of retinal tears:
(1)Horse-shoe tear (the most common).
(2)Retinal hole.
(3)Arrow head tear.
(7) Giant tear
Clinical picture:
Early:
- 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.
-Metamorphopsia , micropsia , macropsia .
Late:
-Field defect ( black curtain).
-Failure of vision (HM or PL vision ):(Painless & rapid) Due to
foveal involvement ( foveal detachment ).
Longstanding (Old)RD :Shows
-Retinal thinning due to atrophy.
Treatment:
Prophylaxis:
Retinal tear sealing.
-Indications:
a) If patient is:
-Myopic.
-Aphakic.
-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:
Especially if the media is clear.
*Cryotherapy: (trans-scleral) especially if the media is Hazy or
peripheral tear).
Curative:
I-Sealing of the break:
By -Cryotherapy . –Laser
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
*Intra-vitreal injection of air or expandable gases like sulpher
hexalflouride
III: pars plane Vitrectomy+Intra-vitreal injection of silicon oil
2-Tractional RD
In which retina is pulled by vitreous fibrosis, as in:
-Cyclitic membrane , organized vitreous hemorrhage.
-Proliferative diabetic retinopathy (PDR).
-Retinopthy of prematurity (ROP).
-Penetrating post. Segment trauma: with vitreous loss &
vitreous hemorrhage.
3-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 (M.M. of choroid or secondary's).
-Coat's disease.
-Systemic causes: toxaemia of pregnancy, malignant hypertension
.
TREATMENT:
1-Tractional: Vitrectomy.
2-Exudative: Inflammatory ( choroiditis & post. Scleritis)
give cortisone.
-Malignant Enucleation.
Degeneration of the Retina
(I) Retinitis Pigmentosa
It is heredo-familial,bilateral, progressive, pigmentry retinal
degeneration of unknown etiology.
Etiology:
Unknown , may be:
1-Abiotrophy: ischemia & Vit A decrease.
2-Photoxicity .
3-Hereditary: mode of inheritance may be,
-Autosomal dominant.
-Autosomal recessive.
-X-linked.(so common in boys).
Clinical pictures :
Symptoms :
-Night blindness(defective dark adaptation) due to affection of rods.
-Progressive visual filed contraction.
-Finally, Complete loss of vision.
Signs:
1-Fundus Picture:
-Retina: Spider (Bone corpuscle) like pigmented spots at 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 pigmentry degeneration
Investigations:
-ERG: is markedly diminished especially Scotopic ERG, it's affected
early while photopic REG is affected later)
-EOG : subnormal.
Treatment:
1-Vitamin A. 2-Vasodilators .
3-Placental extract.
4. Low vision aid.
5. Genetic counseling.
AGE REALTED MACULAR DEGENERATION (ARMD)
It's a macular disease leads to severe affection of the central vision in old
age above 50 yrs. Macular degeneration is
diagnosed as either dry (non- neovascular) or wet (neovascular) which is
refers to growth of new blood vessels in cental part of retina called
macula
Dry macular degeneration (non-neovascular)- Dry AMD is an early
stage of the disease and may result from the aging and thinning of
macular tissues, depositing of pigment in the macula.
Dry macular degeneration is diagnosed when yellowish spots known as
drusen, a small, yellow or white deposit in the eye.
Wet macular degeneration (neovascular)- with wet macular
degeneration, new blood vessels grow beneath the retina and leak
blood and fluid.
Clinical pictures:
(1)Age related maculopathy = drusen:
Small, discrete, yellow white, slighty elevated bilateral symmetrical
spots.
(2)AMD with 2 main types:
1-Dry(atrophic) type:
-There is slowly progressive geographic atrophy of photoreceptors,
RPE & chorio capillaries.
-Clinical pictures: gradual impairment of vision.
-Fluorescence Angiography 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 adefect in the Bruchs membrane
.(appears as gray-green lesion ) leakage.
Clinical pictures: 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 subfoveal CNV.
3) Intravitreal injection of Avastin (Anti VEGF)&
Triamcinolone actinoide .