Beruflich Dokumente
Kultur Dokumente
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
Neuroconduction of retina
3 neurons:
Photoreceptor Bipolar Ganglion cell
rodscotopic vision conephotopic vision Connecting cell between photoreceptor and ganglion
Conduct to brain
Supporting tissue:
Mller cell
Vasculature of retina
inner layer outer layer
macula lutea
Retina barrier
Inner barrierbloodretina barrier
dense connection of retinal capillary endothelium
Symptoms
Visual impairment
Related to lesion site
Metamorphopsia
Flickering Macropsia Micropsia
Retina edema fewer cones stimulated micropsia Vitreous traction to the retina
Signs
Intracellular edema
Retinal artery occlusion: ischemia leads to edema of bipolar cell,ganglion and RNFL
Extracellular edema
Henles fibers are radically located; This pooling forms a flower-petal pattern.
Intracellular edema
Extracellular edema
Exudates
Hard exudate
Leakage of capillary absorb deposition of lipid in outer plexiform layer
Cotton-wool spot
Since be calledsoft exudation Precapillary arteriole occlusion axoplasmic transport blockedorganelles stack
Cotton-wool spot
Heamarrhage
Deep hemorrhage
Between outer plexiform layer and inner nuclear layer .Small round ,dark red
Superficial hemorrhage
Preretinal hemorrhage
Vitreous hemorrhage
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 retinal surface and into the vitreous
Retinal neovascularization
Microaneurysm
Changes of RPE
Pigment loss Pigment disorder Osteocyte-like pigment deposition Death or proliferation
atrophy
alteration
Choroidal neovascularization
Inflammation , metabolic deposit of RPE or Bruchs membrane break
CNV reach RPE or subsensory layer
Diabetic retinopathy
Vasculitis
Coats disease
Common causes
atherosclerotic thrombosis of cribiform plate systemic diseases,hemicrania, trauma, blood coagulation disorder, inflammation, infectious disease or connective tissue disease
Occasionally seen in
retrobulbar injectionretinal detachment or orbital operation
Clinical manifestation
Symptoms
Sudden painless vision lose of one eye
Signs
CRAO
21s after injection of fluorescein ,a complete absence in filling central retinal artery, except segment of inferior temperal branch and macular branch FFA of CRAO
Treatment
Target: to reestablish retinal circulation & function
Timing: the earlier the better Drugs: vasodilator( tropical or systemic)+ reduce IOP
1massage 2anterior chamber paracentesis 3diamox 500mg st250mg bid NaHCO3 500mg bidtid
3.Oxgen inhalation:
mixture of 95% oxygen &5% carbon dioxide
Prognosis
Ischemic type
More common Extensive retinal hemorrhage and tortuous veinMultiple cotton-wool spots Severe VA decrease Widespread capillary nonperfusion 60% cases present iridal neovascularization.
CRVO Nonischemic
CRVO ischemic
BRVO
BRVO FFA
Treatment
Chinese medicine Anitplatelet or antithrombotic drugs: unknown therapeutic effects
Vasculitis
Idiopathic retinal vasculitis
Eales disease(Retinalperiphlebitis)
Both A. and V. are involved Causes is unclearpatient tuberculin reaction (+) Seen in 20-40 years old men Bilateral peripheral small vessels occlusion recurrent vitreous hemorrhageretinal neovascularization
Ealesdisease: Grey exudate, vessel white shealth and pigment scar is seen near the temperal periferal vein.
Clinical manifestation:
early stage:
no symptoms floaters visual defect
mild hemorrhage:
moderate hemorrhage:
severe hemorrhage:
retinal detachment.
Chinese medicine Nutrition reinforcement: vitamin Remove causes Corticosteroid laser photocoagulation Surgery: vitrectomy
Coats disease
Or retinal telangiectasiaexternal exudative retinopathy Often seen in boyunilateral Youngsters and adults may also suffer No heredityno relation with systemic angiopathy Etiology: unknown
Malformation and telangiectasia of capillary in external plexiform layer Permeability alteration and vessel rupture Exudation
Clinical manifestation
Visual disturbancestrabismusleucoria
Fundus extensive yellow-white lipid exudation with faring cholesterol crystalcapillary and vein dilatemicroaneurysmcapillary nonfusion Secondary glaucoma, exudative RD, uvitis, complicated cataract
Rare neovascularization
Differential diagnosis
RB ROP
FEVR
Treatment
Photocoagulation or cryocoagulation of capillary dilation
Macular diseases
Often seen in 20-45 years old men Self-limitted Related to stress reaction
Etiologyunknown
Anxiety,allergy,infection, insufficient reflux of choroid vein,thermal regulation dysfunction
Clinical manifestation
Metamorphopsia blurred vision, micropsia
OCT serous detachment of the sensory retina in the macular area Subretinal yellow deposit in the macular area
Treatment
80% -90%undergo spontaneous recovery Corticosteroid is forbidden
from macula
Mechanism:
Decreased phagocytosis of RPE leading to dusen.
Clinical presentation
Visual acuity: decreased VA, metamorphopsia, micropsia Visual field: central scotoma Fundus: Dry:
Wet:
drusen, RPE change gray-yellow CNV under retina of posterior pole associated with dark red subretinal hemorrhagewhich covers CNV sometimes
Nonexudate:
Drusen RPE atrophy Degeneration of photoreceptor Choroid capillary atrophy
Exudate:
Dursen Damage of Bruchs membrane CNV Disciform scar formation under macula, bleeding and leakage of CNV
Exudative AMD
Treatment
Anti-oxidation drug CNVM located greater than 200 microns from the center of the foveal avascular zone (FAZ) Photodynamic therapy PDT TTT Surgically remove CNV Macular translocation
Retinal detachment
Retinal detachment denotes
separation of the sensory retina from the underlying RPE
Basis
Incentives
Clinical manifestation:
Flashes of light, floaters, a curtain or shadow moving over the field of vision, peripheral and/or central visual loss. Normal IOP, then low IOP Elevation of the retina and a flap tear or break in the retina
Treatment
Close the tearsby photocoagulation condensationelectric coagulation Scleral buckling Vitrectomy
Retinitis Pigmentosa
Chronic ,progressive,inherited disease
Cone cellrod cell and RPE distrophy Inheritance pattern: AD, AR,X-link
Clinical manifestation
Constriction of visual field Fundus :
optic disc waxcolor, "bone spicule" pigment deposition
Treatment
Genetic counselling Avoiding sunlight and UV Vasodilator, Vitamins Suppliment of taurine Low vision aids Grid laser coagulation is used with caution for CME
Retinal tumor
Retinoblastoma
The most common primary intraocular malignant tumor in children,of which 90%younger than 3 yrs Heritable (AD)or sporadic
Etiology
parents are affected or gene carriers ,or germ cell mutation
Staging
intraocular stage glaucomatous stage extraocular stage metastasis stage
Differential diagnosis
RB
Onset age Eyes involved Microcirculation abnormality 90%<3 yrs 30%both none
Coats disease
>6-8 yrs 95%single Diffuse microanuerysm
Cholesterol cystal
Calcification B-us
none
+
Subretinal ,obvious
-
RB
Coats disease
Treatment
Small tumor localized in central retina can be effectively treated with photocoagulation Small tumor localized in periferal retina can be treated with cryotherapy Moderate localized tumor:Plaque radiation therapy Big tumor: Enucleation Extraocular stage: enucleation+ chemotherapy + radiation (bad prognosis) Metastasis : no specific treatment
RB