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CENTRAL RETINAL ARTERY OCCLUSION (CRAO) |
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- Epidemiology -
- Men > Women
- Bilateral in 1 – 2 %
- May have other retinal vascular disease
- History-
- Occurs over period of seconds
- May have prior history of amaurosis fugax
- Painless
- Sudden loss of vision

Etiology
- Systemic Hypertension 66%
- Diabetes mellitus 25%
- Cardiac valve disease 25%
- Carotid atherosclerosis 45%

Ophthalmic Features
- Vision CF to Light Perception (90%)
- Rarely No Light Perception
- Afferent pupillary defect
- Cherry Red Spot- Opacification of ganglion cells around fovea, takes hours to develop and fades in 4-6 weeks. May be “brown” in blacks.
- Both arteries & veins gets thinned.
- May develop rubeosis & glaucoma within 1 month
- Occurs in up to 15-20%
- Retinal neovascularization occurs but rarely
- Ipsilateral carotid obstruction

Investigations
- Fundus Fluorescein Angiography (FFA)
- Electro Retinogram (ERG)
- Visual fields
FFA
- Delayed A-V transit time
- Staining of optic nerve or point of embolus
- Rare retinal vessel staining
- Normal choroidal pattern
- Complete lack of filling, rare in only 2%

ERG
- B-wave origin is inner retina, thus CRAO gives, B wave reduction.
- A-wave is normal, since photoreceptors perfused
- Compare with flat ERG seen in ophthalmic artery occlusion

Visual fields
- Often have a preserved temporal island
- Spared islands corresponding to cilioretinal sparring

Treatment
- Digital massage to dislodge embolus
- A/C Paracentesis
- IV acetazolamide
- Gas Inhalation: Carbogen, Oxygen
- Retrobulbar vasodilators
- Inject Fibrinolytic in supraorbital artery
- Emergent TPPV with/without PFCL
- YAG laser embolysis
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