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ANATOMY AND VASCULAR

DISORDERS OF RETINA-1
Manasa Srinivas
4817
CONTENTS
• EMBRYOLOGY
• ANATOMY
• HISTOLOGY
• VASCULAR DISORDERS- Retinal and Venous
Occlusion
EMBRYOLOGY

•Neuroectoderm
of diencephalon
part of
proscencephalon
•Proximal hyaloid
vessels –
CRA&CRV
ANATOMY
• Neural innermost tunic
• Transparent
• Extent
• Thickness
• Parts- peripheral retina
and posterior pole
• Optic disc and macula
• Examination
OPTIC DISC
• Nasal
• Dimensions
• Layers
• Optic nerve head
• Physiologic cup
• Physiologic blind spot
MACULA
• Temporal to
OD
• Extent
• Fovea- most
sensitive
• Foveal reflex
RETINAL LAYERS
• Retinal pigment
epithelium
• IPM & Subretinal space
• Neurosensory layer
• Rods-120 million-
rhodopsin- scotopic
vision
• Cones- 6.5 million-
cyanopsin, iodopsin,
porhyropsin- photopic
vision
• Types of ganglion cells
• Bipolar cells- Ganglion
cells- nerve of lateral
geniculate
BLOOD SUPPLY
• Outer1/3rd - Choroidal
• Inner 2/3rd - CRA
• End arteries
• Veins follow arteries
• Negative venous pulse
• Central retinal vein-cavernous sinus directly or via
superior ophthalmic vein
• Macula- sup and inf temporal , cilioretinal [20%]
RETINAL ARTERY OCCLUSIONS
ETIOLOGY
1. Emboli from carotid artery/cardiac origin- MC
• Cholesterol emboli (Hollenhorst plaque) –refractile, orange,
atheroma of carotid
• Calcium emboli- white, cardiac valves
• Platelet fibrin emboli- dull white, atheroma of carotid, TIA of retina
2. Atherosclerosis
3. Retinal arteritis(giant cell arteritis) and periareteritis
4. Angiospasm -amaurosis.
5. Raised intraocular pressure
6. Thrombophilic - young individuals
7. Rare causes -retinal migraine, sickling , hypercoagulation disorders.
TYPES
CRAO(60%)
BRAO (35%)- at bifurcation,
permanent sectoral VF defect
Cilioretinal artery (5%)
Symptoms- Signs :
A. CRAO- level of lamina cribrosa.
M>F Visual acuity - reduced (<3/60 in
90% ) cases, PL lost.
Unilateral RAPD and direct pupil reflex lost

Amaurosis fugax FFA- delay in arterial filing and


Sudden painless loss of vision masking of choroidal
vasculature due to retinal
edema
MANAGEMENT
1. Acute episodes- 90–100 minutes/ 240 minutes
a.Immediate lowering of IOP- improve perfusion and dislodge emboli
IV mannitol
Intermittent ocular massage
Paracentesis of AC
Intravenous acetazolamide 500 mg
b.Vasodilators and carbogen-angiospasm.
c.Fibrinolytic therapy.
d.Intravenous steroids- giant cell arteritis.
e.Laser photodisruption- dislodge the embolus/ PPV
2. Work-up for associated systemic conditions- risk of secondary
ischemic events
RETINAL VEIN OCCLUSIONS
ETIOLOGY
1.Pressure on the vein by atherosclerotic retinal artery where
the two share a common adventitia
2. Hypertension and diabetes mellitus - RF
3. Hyperviscosity of blood- OCP, polycythemia, dyslipidemia
4. Periphlebitis retinae - central or peripheral.
5. Raised intraocular pressure- POAG
6. Local causes- are orbital cellulitis, orbital tumors, facial
erysipelas and cavernous sinus thrombosis.
TYPES
1.CRVO- non-ischaemic 75% (venous stasis retinopathy)/
ischaemic (haemorrhagic retinopathy).
2.BRVO
Non-ischaemic CRVO Ischaemic CRVO –acute occlusion

Visual loss- mild to moderate Marked sudden visual loss

No RAPD. RAPD

Resolves with normal vision or 15%-30% Reduced Amplitude of b-wave of


cases to ischemic CRVO electroretinogram.

Non ischemic ischemic


Venous congestion & tortuosity mild massive
Hemorrhages Few, flame shaped, Splashed tomato
periphery>posterior
Papilledema Mild Hyperemic, marked edema,
cottonwool spots
Macula edema Mild or absent Severe, hemorrhages
Late stage Sheathing around veins, Marked
cilioretinal collaterals, sheathing,collaterals, chronic
chronic CME, CME , pigmentary changes,
hemorrhages absorbed
2.BRVO- Hemispheric/ Quadrantic /Small branch occlusion-macular or
peripheral branch
Vision- affected if macula involved.
Retinal edema and haemorrhage , ME, complications are rare.
COMPLICATIONS
90 days glaucoma- NVG
Viterous hemorrhage.
Differential diagnosis
1.Ocular ischaemic syndrome – no tortuosity of veins and mid
peripheral retinal haemorrhages
2.Diabetic retinopathy -bilateral

Investigations
I. Ocular-
• Visual acuity- at every followup
• IOP, Gonioscopy - NVA
• Undilated slit-lamp - NVI
• Fundus examination, perimetry
• FFA-CNP > 10 disc area- ischaemic CRVO.
• OCT, ERG
B. Systemic-
TREATMENT
I. Treatment of systemic associations.
II. Observation and monitoring – Non ischemic CRVO
III. Ocular therapy- Ischemic CRVO or progressive vision loss
1. Medical therapy- Repeated Intravitreal anti-VEGFs and
triamcinolone.
2. Laser therapy –Grid laser in persistent CME of BRVO and not
in CRVO .Panretinal photocoagulation- in CRVO & NVE in BRVO
using frequency doubling YAG laser or argon green laser.
3. Surgical therapy- Pars plana vitrectomy :
• Persistent vitreous haemorrhage
• Tractional retinal detachment
• Epiretinal membrane
• Intractable NVG with GDD