The retina is a thin layer of light-sensing nerve tissue lining the back of the eye, converting light into electrical signals sent to the brain. Branch Retinal Vein Occlusion (BRVO) is a common vascular disorder that disrupts the necessary drainage of blood from this sensory tissue. The condition occurs when one of the smaller veins within the retina becomes blocked, impeding blood flow and threatening sight. Because BRVO can lead to permanent vision damage, it requires immediate attention from an eye care professional.
Defining Branch Retinal Vein Occlusion
Branch Retinal Vein Occlusion is characterized by a physical blockage, or thrombus, forming in one of the retinal veins that branch off the main central retinal vein. This typically happens at an arteriovenous crossing point, where a stiffer retinal artery passes over and compresses a softer retinal vein. When the vein is occluded, blood flow backs up, leading to a surge in pressure.
This pressure causes the vessel walls to leak, resulting in intraretinal hemorrhage (bleeding) and fluid leakage into the surrounding tissue. The accumulation of fluid, known as edema, is particularly damaging if it occurs in the macula, the central area responsible for sharp, detailed vision. This condition, called macular edema, is the most common cause of vision loss following a BRVO.
The cessation of proper blood flow can lead to oxygen deprivation, known as retinal ischemia. BRVO affects only the portion of the retina drained by the blocked branch. A Central Retinal Vein Occlusion (CRVO), however, involves the single, main retinal vein, impacting the entire retina and causing more extensive damage. BRVO occurs approximately three times as often as CRVO.
Identifying the Underlying Causes
The physical blockage defining BRVO is closely linked to systemic health issues that compromise the integrity of the body’s blood vessels. High blood pressure (hypertension) is the most significant risk factor. Chronic high pressure causes the walls of the retinal arteries to harden and thicken, a process called arteriosclerosis.
This hardening increases the compressive force exerted by the artery onto the underlying vein at the arteriovenous crossing, promoting clot formation. Other conditions that damage the microvasculature, such as diabetes and high cholesterol (hyperlipidemia), also contribute to this risk by causing endothelial dysfunction and inflammation. Glaucoma, characterized by elevated pressure within the eye, is another factor that may increase susceptibility to vein occlusion.
These systemic diseases predispose the delicate blood vessels in the eye to injury. Addressing these underlying medical conditions is important for managing the risk of a BRVO occurring in the other eye or preventing other vascular complications.
Recognising Symptoms and Confirming Diagnosis
The most common symptom of Branch Retinal Vein Occlusion is the sudden and painless onset of blurred or partial vision loss in one eye. Patients may describe a shadow or a dark area in their field of view, corresponding to the area drained by the blocked vein. The severity of vision reduction depends on whether the leakage and swelling extend into the macula.
If the blockage is in the periphery, the BRVO may be asymptomatic, discovered only during a routine eye examination. Diagnosis is confirmed by an eye care professional using a dilated eye examination to view the retina and observe characteristic signs, such as sectoral hemorrhages and dilated, tortuous veins.
Specialized imaging techniques assess the damage and guide treatment decisions. Optical Coherence Tomography (OCT) creates cross-sectional images of the retina, allowing the clinician to measure the extent of macular edema. Fluorescein Angiography (FA) involves injecting a dye into the bloodstream to visualize circulation, helping identify areas of leakage, capillary non-perfusion, and retinal ischemia.
Therapeutic Approaches to Restore Vision
The primary goal of treatment following a BRVO is to reduce macular edema and prevent the growth of abnormal new blood vessels (neovascularization). First-line treatment involves anti-Vascular Endothelial Growth Factor (anti-VEGF) agents, such as ranibizumab (Lucentis), aflibercept (Eylea), and bevacizumab (Avastin). These medications are delivered via intravitreal injection and work by blocking VEGF, a protein that promotes blood vessel leakage and swelling.
The anti-VEGF injections often require a loading phase of monthly doses, followed by a variable maintenance schedule over many months, as the drug’s effect is temporary. Corticosteroid injections or implants, such as the dexamethasone implant (Ozurdex), offer an alternative approach to reduce inflammation and swelling within the macula. These steroid treatments provide a sustained release of medication over several months, useful for patients who may not respond adequately to anti-VEGF therapy or who have had cataract surgery.
If chronic macular edema persists despite injections, or if ischemia leads to neovascularization, focused laser treatment may be used. Grid laser photocoagulation seals leaky vessels in cases of non-ischemic macular edema, reducing fluid accumulation. Sectoral laser treatment destroys oxygen-deprived tissue in extensive areas of non-perfusion that risk vitreous hemorrhage from new vessel growth. Managing underlying conditions like hypertension and diabetes remains important for preventing future episodes.