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  CENTRAL RETINAL ARTERY OCCLUSION (CRAO)  
 

 

  • 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