• 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