Plaque in the eye usually refers to tiny cholesterol fragments that lodge in the small blood vessels of the retina. These deposits, called Hollenhorst plaques, break off from larger fatty buildups in the carotid arteries or aorta and travel through the bloodstream until they get stuck in the much narrower retinal vessels. Less commonly, “plaque in the eye” can mean calcium deposits on the cornea, a condition called band keratopathy with entirely different causes.
How Cholesterol Plaques Reach the Retina
The retina gets its blood supply from the ophthalmic artery, which branches directly off the internal carotid artery in the neck. When fatty deposits (atherosclerosis) build up along the walls of the carotid artery or aorta, small pieces can break free. Blood flow carries these microscopic cholesterol fragments upward through the carotid, into the ophthalmic artery, and finally into the tiny vessels feeding the retina. Once a fragment reaches a vessel too small to pass through, it lodges there and becomes visible during an eye exam as a shiny, yellowish speck.
This means retinal plaques are not really an eye problem. They are a sign of cardiovascular disease happening elsewhere in the body. The same process that narrows heart arteries and causes strokes is sending debris into the eye. Your retina essentially acts as a window into your vascular health, because it’s one of the few places where a doctor can directly observe blood vessels without surgery.
Risk Factors That Drive Plaque Formation
Because retinal plaques originate from atherosclerosis, anything that promotes fatty buildup in your arteries raises the risk. The major contributors include high cholesterol, high blood pressure, smoking, diabetes, and older age. People with significant narrowing of the carotid arteries are at the highest risk, since those vessels sit directly upstream from the eye’s blood supply.
Retinal plaques are more common than most people realize. They often produce no symptoms at all and are discovered incidentally during a routine dilated eye exam. When an eye doctor spots one, it typically triggers a workup of your cardiovascular system, particularly an ultrasound of the carotid arteries, to check for dangerous narrowing.
Symptoms Plaques Can Cause
Many retinal plaques sit quietly without blocking blood flow. But when a fragment is large enough to temporarily or fully obstruct a retinal artery, it causes a dramatic symptom called amaurosis fugax: sudden, painless vision loss in one eye. People typically describe it as a curtain or shade dropping down over their visual field. The episode usually lasts between 2 and 30 minutes before vision returns to normal.
The vision loss can affect the entire field of one eye or just a portion of it. Some people experience repeated brief episodes before a longer blockage occurs. If a retinal artery stays blocked, it can cause a retinal artery occlusion, which is essentially a stroke of the eye and can result in permanent vision loss in the affected area.
The Link to Stroke
Finding a cholesterol plaque in the retina is a red flag for stroke risk. In the Beaver Dam Eye Study, people with retinal emboli had roughly 2.6 times the risk of dying from stroke-related causes compared to those without them, even after accounting for age, sex, and other cardiovascular risk factors. This elevated risk makes sense: if pieces of plaque are reaching the eye, they can just as easily travel to the brain.
This is why an incidental finding of retinal plaque during an eye exam often leads to referrals for vascular imaging and a thorough cardiovascular evaluation. The plaque itself in the retina may not threaten your vision, but it signals that the arteries feeding your brain may be in trouble.
Calcium Deposits on the Cornea
A different type of eye plaque involves calcium, not cholesterol, and it affects the cornea rather than the retina. Band keratopathy occurs when calcium salts accumulate in the outermost structural layer of the cornea, forming a whitish, band-shaped opacity across the center of the eye. Unlike retinal cholesterol plaques, this one is visible to the naked eye and directly impairs vision by clouding the cornea.
The two most common triggers are chronic eye inflammation and high blood calcium levels (hypercalcemia). Systemic conditions that raise calcium or phosphorus in the blood can all lead to band keratopathy, including hyperparathyroidism, chronic kidney failure, sarcoidosis, and certain cancers like multiple myeloma. Long-term exposure to certain chemical irritants, including specific eye drop preservatives, can also contribute. In cases tied to chronic inflammation, the calcium deposits sometimes appear and resolve as the underlying inflammation waxes and wanes.
Plaques vs. Drusen
People sometimes confuse retinal plaques with drusen, the yellowish deposits under the retina associated with age-related macular degeneration. These are fundamentally different. Cholesterol plaques sit inside blood vessels, are caused by cardiovascular disease, and are made of cholesterol fragments that traveled from elsewhere. Drusen form beneath the retina itself, between the light-sensing cells and the blood vessel layer underneath. They accumulate as a natural byproduct of cellular waste that the retina can’t clear efficiently.
Age-related drusen are typically small, dome-shaped deposits averaging about 20 micrometers across. They don’t contain the dystrophic calcification sometimes found in atypical drusen linked to other eye conditions. The distinction matters because the treatment and monitoring are completely different: drusen call for macular degeneration screening, while retinal plaques call for cardiovascular evaluation.
How Retinal Plaques Are Detected
A standard dilated eye exam is often enough to spot Hollenhorst plaques. They appear as bright, reflective yellow-orange crystals sitting at the branch points of retinal arteries. For more detailed assessment, fluorescein angiography has been the gold standard since the 1960s. This involves injecting a fluorescent dye into a vein and photographing the retinal blood vessels as the dye passes through, revealing blockages or slow flow.
Newer imaging techniques, particularly optical coherence tomography angiography (OCTA), can map retinal blood flow without any dye injection. OCTA has increasingly replaced fluorescein angiography for evaluating retinal vascular diseases and can identify areas of reduced blood flow downstream from a plaque.
Once retinal plaques are confirmed, the next step is usually a carotid ultrasound to measure how much narrowing exists in the neck arteries. The goal is to determine whether the plaque source poses an imminent stroke risk and whether intervention on the carotid artery might be needed.
Managing the Underlying Cause
Treatment for retinal cholesterol plaques focuses on the cardiovascular disease driving them, not the plaques themselves. Lowering cholesterol, controlling blood pressure, managing blood sugar, and quitting smoking all slow atherosclerotic progression and reduce the chance of future emboli reaching the eye or brain. For people with significant carotid artery narrowing, procedures to open or bypass the blockage may be recommended to prevent stroke.
For band keratopathy, treatment targets the calcium deposits directly. A procedure called chelation uses a chemical solution applied to the cornea to dissolve the calcium, or a laser can be used to remove the deposits. Treating the underlying cause of high calcium levels is equally important to prevent recurrence.