Chp14 retina

7/30/2019 Chp14 retina

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Diseases of Retina

The 4th Affilitated Hospital of China Medical University

Eye Hospital of China Medical University



Introduction

Eyeball structure and retina



Macula lutea

• Located 3mm temporally to the optic papilla,right on the visual axis.

• A concave central retinal depression is called

Fovea Centralis

macula lutea contains only cones; 1 cone synapes to

1 bipolar cell,which synapes to 1 ganglion

cell,leading to the most sensitive vision.

In periferal retina ,600 rods connect to 1 ganglion.



Histology of retina

Internal limiting membrane

Nerve fiber layer

Ganglion cell layer

Inner plexiform layer

Inner nuclear layer

Outer plexiform layer

Outer nulear layer

External limiting membrane

photoreceptor

RPE

Bruch’s membrane



Neuroconduction of retina 3 neurons:

Photoreceptor

Bipolar

Ganglion cell

Supporting tissue:Müller cell

rod（scotopic vision）

cone（photopic vision）

Connecting cell between

photoreceptor and ganglion

Conduct to brain



Vasculature of retina

inner layer→ central retinal vascular system

outer layer→ choroid（ciliary vascular system）

macula lutea→ choriocapillaries



Retina barrier

• Inner barrier（blood–retina barrier）

dense connection of retinal capillary endothelium

• Outer barrier（choroid-retina barrier）

zonula occludens between the RPE

RPE- Bruch’s membrane- choriocapillaries complex



Symptoms

• Visual impairment

• Metamorphopsia

• Flickering

• Macropsia

• Micropsia

Related to lesion

site

Vitreous

traction to the

retina

Retina edema→

fewer cones stimulated

→micropsia



Signs

• Intracellular edema

• Extracellular edema

• Cystoid macular edema

Retinal artery occlusion:ischemia leads to edema

of bipolar cell,ganglion and RNFL

Capillary endothelium injury，and then

exudation

Henle’s fibers are radically located;This pooling forms a flower-petal pattern.



Intracellular edema Extracellular edema



Exudates

Hard exudate

Cotton-wool spot

Leakage of capillary →absorb →

deposition of lipid in outer plexiform layer

Since be called“soft exudation”

Precapillary arteriole occlusion→

axoplasmic transport blocked→organelles stack



Cotton-wool spot Hard exudate (Hypertensive retinopathy)



Heamarrhage

Deep hemorrhage

Superficial hemorrhage

Preretinal hemorrhage

Vitreous hemorrhage

Between outer plexiform layer

and inner nuclear layer .Small

round ,dark red

Located in nerve fiber layer

line、

strip、

flame-like，

bright red

Crescent-shaped hematocele

with transverse section

Profuse preretinal

hemorrhage into the vitreous

or hemorrhage of retinal

neospastic vasculature



Preretinal hemorrhage Subretianal hemorrhage



Deep hemorrhage Superficial hemorrhage



Neovascularization

• neovessels,NV

A large area of retinal ischemia→

formation of vascular endothelial growth factor→

neovascularization

• neovessels membrane,NVM

Arise from small veins of optic disc and retina; grow along retinalsurface and into the vitreous



Retinal neovascularization

Neovacularizaton of optic disc





A-V cross sign

Vessel white sheath

Microaneurysm

Microaneurysm

A-v cross sign

Vessel white sheath



Changes of RPE

atrophy

alteration

Death or proliferation

Pigment loss

Pigment disorder

Osteocyte-like pigment deposition





Classification of retinal diseases

• Vascular diseases

• Macular diseases

• Retinal detachment

• Retinal degeneration

• Retinal tumor

• Ocular manifestation of general diseases





Central retinal artery occlusion，CRAO

Common causes：

atherosclerotic thrombosis of cribiform plate systemicdiseases,hemicrania, trauma, blood coagulation disorder,inflammation, infectious disease or connective tissuedisease

Occasionally seen in：

retrobulbar injection、retinal detachment or orbitaloperation

Etiology







FFA of CRAO

21s after injection of

fluorescein ,a complete

absence in filling central

retinal artery, exceptsegment of inferior

temperal branch and

macular branch



Treatment

• Target: to reestablish retinal circulation &function

• Timing: the earlier the better

• Drugs: vasodilator( tropical or systemic)+

reduce IOP











CRVO

Nonischemic

CRVO

ischemic





Treatment

– Chinese medicine

– Anitplatelet or antithrombotic drugs: unknown

therapeutic effects

– Systemic examination to find out causes

– Corticosteroid if vasculitis exist

– Grid pattern photocoagulation of macula、PRP

– Laser induced retina-choroid vascular anastomosis



Vasculitis

• Idiopathic retinal vasculitis

Eales disease(Retinalperiphlebitis)

Both A. and V. are involved

Causes is unclear，patient tuberculin reaction (+)

Seen in 20-40 years old men

Bilateral peripheral small vessels occlusion，

recurrent vitreous hemorrhage，retinalneovascularization











Clinical manifestation

– Visual disturbance、strabismus、“leucoria”

– Fundus：

extensive yellow-white lipid exudation withfaring cholesterol crystal；capillary and veindilate，microaneurysm；capillary nonfusion； Secondary glaucoma, exudative RD, uvitis,complicated cataract

– Rare neovascularization







Treatment

– Photocoagulation or cryocoagulation ofcapillary dilation



Macular diseases

• Central serous chorioretinopathy

• Age-related macular degeneration

• Central exudative chorioretinopathy



– Often seen in 20-45 years old men

– Self-limitted

– Related to stress reaction

Central serous chorioretinopathy



• Etiology：unknown

– Anxiety,allergy,infection, insufficient

reflux of choroid vein,thermal regulationdysfunction




• Metamorphopsia，

• blurred vision,

• micropsia



• OCT

• serous detachment

of the sensory retinain the macular area

• Subretinal yellow

deposit in themacular area











• Nonexudate:Drusen

RPE atrophy

Degeneration of photoreceptorChoroid capillary atrophy













• Clinical manifestation:

– Flashes of light, floaters, a curtain or shadowmoving over the field of vision, peripheraland/or central visual loss.

– Normal IOP, then low IOP

– Elevation of the retina and a flap tear or breakin the retina







Retinitis Pigmentosa

• Chronic ,progressive,inherited disease

• Cone cell、rod cell and RPE distrophy

• Inheritance pattern: AD, AR,X-link

• Onset age: childhood,

• Bilateral eyes involved




• Constriction of visual field

• Fundus :

optic disc “wax”color, "bone spicule" pigment deposition

• Nyctalopia is the first symptom

• FFA:

window defect, blocked fluorescein in pigment deposition at

early stage, hypofluorescence and the fluorescein of choroidis seen at late stage





Treatment

• Genetic counselling

• Avoiding sunlight and UV

• Vasodilator, Vitamins

• Suppliment of taurine

• Low vision aids

• Grid laser coagulation is used with caution for CME









Staging

• intraocular stage

• glaucomatous stage

• extraocular stage

• metastasis stage





RB Coats disease



Treatment

– Small tumor localized in central retina can beeffectively treated with photocoagulation

– Small tumor localized in periferal retina can be

treated with cryotherapy

– Moderate localized tumor:Plaque radiationtherapy

– Big tumor: Enucleation

– Extraocular stage: enucleation+ chemotherapy

+ radiation (bad prognosis)– Metastasis : no specific treatment





RB

After plate radiation therapy



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Chp14 retina