Enlarged blood vessels behind the eye are most commonly caused by diabetes, high blood pressure, or age-related macular degeneration. Less frequently, blocked veins, increased pressure inside the skull, or abnormal connections between arteries and veins can also be responsible. In nearly every case, the underlying problem is either too much pressure inside the vessels, too little oxygen reaching the retina, or both.
An eye doctor can often spot these changes during a routine exam, sometimes before you notice any symptoms at all. Understanding what drives the enlargement helps explain why early detection matters so much for preserving your vision.
How Blood Vessels in the Eye Become Enlarged
The retina, the light-sensitive tissue lining the back of your eye, is one of the most metabolically active tissues in the body. It depends on a dense network of tiny blood vessels for oxygen and nutrients. When something disrupts normal blood flow, the vessels respond in predictable ways: they dilate to carry more blood, twist into serpentine paths from longitudinal stretching, or sprout entirely new (and fragile) branches in a desperate attempt to restore oxygen supply.
Vessel dilation results from radial stretching of the vessel wall. When the stretch is longitudinal, the vessel takes on a winding, corkscrew appearance that doctors call tortuosity. Three broad categories of disease produce these changes: conditions that increase blood flow or blood pressure, conditions that trigger new vessel growth, and conditions that cause venous congestion by blocking blood from draining out of the eye.
Diabetes and New Vessel Growth
Diabetic retinopathy is one of the most common reasons for abnormal blood vessels behind the eye. Chronically high blood sugar damages the small vessels of the retina over years, eventually starving patches of tissue of oxygen. When retinal tissue becomes oxygen-deprived, cells produce a signaling protein called vascular endothelial growth factor (VEGF). This protein triggers the growth of new blood vessels, a process called neovascularization.
The problem is that these new vessels are structurally weak. They can grow across the surface of the retina, along the optic disc, and even onto the iris. Because their walls are fragile, they leak fluid, blood, and fatty deposits into the surrounding tissue. When leaking occurs in the macula (the central area responsible for sharp, detailed vision), it causes swelling known as macular edema, which blurs or distorts your central vision. Other warning signs include sudden vision loss in one eye, dark spots or floaters, seeing rings around lights, and flashing lights.
The progression from early, mild vessel damage to full-blown proliferative disease can take years, which is why annual dilated eye exams are so important for anyone with diabetes.
High Blood Pressure
Sustained high blood pressure forces retinal arteries to narrow and thicken as a defense mechanism against the elevated pressure. Over time, the vessel walls weaken, and the veins downstream become congested and dilated. Doctors have graded these changes since 1939 using the Keith-Wagener-Barker classification, a four-stage system that links the severity of retinal vessel changes to overall cardiovascular risk. In the mildest stages, the differences are subtle enough that even clinicians have difficulty distinguishing them. By the more advanced stages, the vessels show obvious narrowing, crossing changes where arteries press on veins, and visible swelling of the optic disc.
What makes hypertensive retinopathy especially important is that the retina is the only place in the body where doctors can directly observe blood vessels without surgery. Changes seen there reflect what is happening to small vessels throughout your body, including in the brain, kidneys, and heart.
Wet Age-Related Macular Degeneration
About 10% of people with age-related macular degeneration develop the “wet” form, where new blood vessels grow from the layer beneath the retina (the choroid) and push through a thin barrier called Bruch’s membrane. These vessels can grow underneath or on top of the retinal pigment layer, and like the fragile vessels in diabetic eye disease, they leak blood and fluid that damages the macula.
Doctors now classify these abnormal vessels into three types based on where they originate. Type 1 stays beneath the retinal pigment layer. Type 2 breaks through into the space just under the retina itself. Type 3 starts within the retina’s own deep capillary network and grows outward. All three types are driven largely by VEGF accumulation, particularly a specific form called VEGF-165. The result is the same: distorted or lost central vision, often noticed first as straight lines appearing wavy.
Retinal Vein Occlusion
When a vein draining blood out of the retina becomes blocked, pressure builds behind the obstruction. The backed-up blood engorges the upstream vessels, making them visibly dilated and tortuous. This can happen in the central retinal vein (affecting the entire retina) or in a single branch (affecting one quadrant).
The blockage is usually caused by a blood clot forming where a hardened artery crosses over and compresses a vein. Risk factors overlap heavily with cardiovascular disease: high blood pressure, high cholesterol, diabetes, and smoking. Vision loss can range from mild blurriness to severe, depending on which vein is blocked and how completely. In many cases, the resulting oxygen deprivation also triggers VEGF release and secondary new vessel growth, compounding the problem.
Increased Pressure Inside the Skull
Elevated intracranial pressure, from causes ranging from brain tumors to a condition called idiopathic intracranial hypertension, transmits force along the optic nerve and into the back of the eye. This produces papilledema, a swelling of the optic disc that progressively obscures and engorges the retinal vessels.
Doctors grade papilledema on a five-point scale developed by ophthalmologist Lars Friesen. In Grade 1, only the nasal border of the disc appears blurred. By Grade 3, the swollen disc margins obscure one or more major retinal vessel segments. Grade 4 involves total obscuration of a segment of the central retinal artery or vein. At Grade 5, all disc vessels are completely hidden by the swelling. Headaches, transient visual blackouts lasting a few seconds, and a whooshing sound in the ears are common accompanying symptoms.
Carotid-Cavernous Fistula
A carotid-cavernous fistula is an abnormal connection between the carotid artery and the cavernous sinus, a collection of veins behind the eye. When high-pressure arterial blood is shunted directly into these veins, it causes venous hypertension throughout the orbit. The veins behind and around the eye become engorged and pressurized with blood that is, in effect, “arterialized.”
This condition is rare but distinctive. Between 72% and 98% of patients develop proptosis (the eye bulging forward), 55% to 100% have chemosis (swelling of the clear membrane covering the white of the eye), and 71% to 80% can hear a pulsing or whooshing noise (bruit) in the affected eye. Most cases result from trauma or occur spontaneously in older adults with atherosclerosis.
How Enlarged Vessels Are Detected
A standard dilated eye exam allows your doctor to see the retinal vessels directly through the pupil. For more detailed assessment, optical coherence tomography angiography (OCTA) creates a three-dimensional map of blood flow through every layer of the retina without requiring dye injections. OCTA measures vessel density (the fraction of retinal area occupied by visible vessels), vessel tortuosity, branching point density, and vessel diameter. These metrics can detect dropout of blood vessels in diseases like diabetic retinopathy and retinal vein occlusion, and they can identify microaneurysms and regions where blood flow has stopped entirely.
Fluorescein angiography, where a yellow dye is injected into a vein in your arm and photographed as it flows through the retinal vessels, remains useful for pinpointing active leaks and classifying the type of new vessel growth in wet macular degeneration.
How Abnormal Vessels Are Treated
For conditions driven by VEGF, the primary treatment is injections of anti-VEGF medication directly into the eye. Three agents are widely used: aflibercept, ranibizumab, and bevacizumab. Large clinical trials have shown that monthly bevacizumab injections produce visual gains comparable to monthly ranibizumab, though ranibizumab may reduce retinal swelling slightly more. After an initial loading phase of monthly injections (typically three), many patients transition to a treat-and-extend schedule where the interval between injections is gradually lengthened based on how the eye responds.
Laser photocoagulation is still used in some cases, particularly to seal off leaking vessels in diabetic retinopathy or to reduce oxygen demand in areas of the retina that have lost their blood supply. For retinal vein occlusions, treatment focuses on managing the downstream complications (swelling, new vessel growth) while addressing the underlying cardiovascular risk factors. Carotid-cavernous fistulas often require an interventional radiology procedure to close the abnormal connection from inside the blood vessel.
Controlling the root cause matters as much as treating the eye itself. Tighter blood sugar control slows diabetic retinopathy progression. Bringing blood pressure into a healthy range can halt or partially reverse hypertensive vessel changes. In every case, the enlarged vessels you see on an eye exam are a signal about what is happening elsewhere in your body, not just in your eye.