Dr Ben Wild
Overview |
Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells then to the brain. To help keep these photoreceptors healthy, there are 2 sources of blood flow. One is behind the eye located in the choroid and the other is inside the eye either resting on or inside the retina. Both of these sources represent very strong blood vessels that help create the blood-retinal barrier.
A frontal view of a healthy retina.
A retinal artery occlusion occurs when one of the arteries that extends into the eye is blocked. This usually occurs due to health conditions that cause arteries to thicken (atherosclerosis). If this thickening occurs outside of the eye, a piece of debris (cholesterol plaque) can break off and clog a retinal artery (embolism). If it occurs in a retinal blood vessel, a cholesterol plaque can clog that vessel (thrombosis). When an artery is blocked, blood flow stops and the retina may become completely oxygen deprived (anoxic) and turns white. Unlike with a vein occlusion, fluid does not start to leak into the retina.
If the blockage occurs inside the optic nerve, it is termed a central retinal artery occlusion (CRAO) and if the blockage occurs in an artery on the retina, it is termed a branch retinal artery occlusion (BRAO). CRAOs cause complete vision loss whereas BRAOs cause a blind spot corresponding to where the blockage lies.
A frontal view of a retina with a CRAO (top) showing a white retina and red macula, and a BRAO (bottom) showing a yellow embolism/thrombosis and retinal whitening around the occlusion.
Signs and Symptoms |
Signs
CRAO | Pupil non-reactive to light, no light perception vision, cherry red spot in retina (retina is white except the macula that is red), rare retinal bleed, in 20% of cases a visible embolism or thrombosis, whitening of blood vessels after a few days, optic nerve death after a few days, rare small blood vessel growth. |
BRAO | Pupil mildly reactive to light, large blind spot in vision, thin retinal arteries, white retina around the occlusion, visible embolism/thrombosis. |
Symptoms
CRAO | Sudden painless severe vision loss to no light perception. |
BRAO | Sudden painless vision loss, blind spot in area corresponding to where the BRAO occurred. |
Causes and Risk Factors |
Causes
Blocked retinal artery.
Risk Factors
Giant cell arteritis, systemic lupus erythematosus, granulomatosis with polyangiitis, vasopasms (migraines), low blood pressure, hyperhomocysteinemia, sickle cell disease, antiphospholipid antibody syndrome, high blood pressure, high cholesterol, diabetes, more.
Prevention and Treatment |
Prevention
Avoid all cardiovascular risk factors (high blood pressure, diabetes, etc.), avoid smoking.
Treatments
· Monitor the eye while doing an urgent (within 24 hours) full stroke work up including assessing pulse, blood pressure, blood viscosity, complete blood count, random glucose, cholesterol, testing for giant cell arteritis. Other testing may include carotid artery imaging, electrocardiogram, chest x-ray, and more.
· CRAO:
o Panretinal photocoagulation laser.
o Anti-VEGF eye injections.
o Review monthly.
· BRAO
o Lie face up to increase perfusion pressure.
o Eye massage.
o Glaucoma drops to lower eye pressure.
o Increased oxygen.
o Laser embolism with YAG.
o Discontinue smoking.
o Antiplatelet therapy.
Prognosis |
Prognosis depends on the severity of the blockage for both CRAOs and BRAOs. For CRAOs, most patients do not regain vision. Some patients have a cilioretinal artery (artery entering the eye from a different source). These patients may regain some central vision. For BRAOs, vision does not usually improve after the occlusive event. Some BRAOs can lead to severe vision loss while others only small blind spots. Vision loss is dependent on where the occlusion occurred. CRAOs and BRAOs do not typically get worse but vision usually does not improve over time.
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