Retinal Vein Occlusion

Retinal vein occlusion is an eye disease that develops when blood flow through the retinal veins is obstructed by clot formation or structural changes in the vessel wall. The retina is the thin nerve layer lining the back wall of the eyeball that generates visual signals; it needs an uninterrupted blood supply to function properly. While the retinal arteries deliver oxygen and nutrients to the retina, the veins carry used blood away. When one of these veins becomes blocked, blood accumulates behind the blockage, blood and fluid leak through the vessel walls into retinal tissue, and retinal edema and hemorrhage develop. Retinal vein occlusion is the most common retinal vascular disease after diabetic retinopathy and presents with a sudden, painless decrease in vision in one eye.

There are two main types of retinal vein occlusion: central retinal vein occlusion and branch retinal vein occlusion. In the central type, the retina's main vein is blocked; in the branch type, one branch of the main vessel is blocked. The type of disease directly determines the extent of the affected retinal area and therefore the severity of vision loss. In both types, the main cause of vision loss is fluid accumulation in the macular region (macular edema). If untreated, retinal vein occlusion may progress to permanent vision loss, abnormal new blood vessel formation (neovascularization) and bleeding inside the eye. Early diagnosis and timely treatment are crucial for preserving visual function and preventing complications.

Central retinal vein occlusion (CRVO) is blockage of the main vein that collects all venous blood from the retina at the level of the optic nerve head. Because this vessel is the retina's only drainage route, the entire retina is affected when it becomes blocked. Fundus examination reveals widespread flame-shaped hemorrhages in all four quadrants, retinal edema, venous dilation and tortuosity, and soft exudates (cotton-wool spots). CRVO is clinically divided into two subgroups: the non-ischemic (perfused) type and the ischemic type. Non-ischemic CRVO is more common, retinal blood supply is partly preserved and vision loss is usually milder. Ischemic CRVO is characterized by extensive areas of capillary closure in the retina, has a significantly poorer visual prognosis and carries a high risk of progressing to serious complications such as neovascularization.

Distinguishing ischemic from non-ischemic types is critical for treatment planning and assessment of prognosis. Detecting capillary non-perfusion of more than 10 disc diameters in the retina on fundus fluorescein angiography (FFA) indicates a high risk of iris and angle neovascularization, which increases intraocular pressure (neovascular glaucoma). Patients diagnosed with CRVO therefore require regular monitoring and close follow-up for ischemic conversion. Because some non-ischemic CRVO cases may convert to the ischemic type over time, follow-up must not be relaxed even in cases that appear favorable at initial diagnosis. CRVO can occur at any age but most commonly affects one eye in people over 50.

Branch retinal vein occlusion (BRVO) is a retinal vascular disease caused by blockage of one branch of the retina's main vein and is approximately three to four times more common than CRVO. The blockage most often occurs where a retinal artery and vein cross; at these crossing points, the artery and vein share a common adventitial sheath, and an artery thickened by aging or atherosclerosis compresses the adjacent vein, slowing blood flow and predisposing to clot formation. The superotemporal branch is most frequently affected, and patients usually present with blurring or darkening in part of their visual field. Fundus examination shows flame-shaped hemorrhages, retinal edema and dilated venous segments in the sector corresponding to the blocked vein's drainage area.

The degree of vision loss in BRVO is directly related to the blocked branch's proximity to the macular region. When a branch draining the macular region is blocked, macular edema develops and central vision is significantly affected. If a branch away from the macula is blocked, the patient may not notice significant vision loss, and the occlusion may be discovered incidentally during a routine examination. The overall prognosis of BRVO is better than that of CRVO; partial spontaneous improvement occurs over time in a substantial proportion of patients. However, delayed treatment in cases with chronic macular edema, associated retinal ischemia or neovascularization may lead to permanent vision loss. Every patient diagnosed with BRVO therefore needs regular follow-up and timely assessment of whether treatment is indicated.

Hypertension is the most important systemic risk factor for retinal vein occlusion. Chronically elevated blood pressure causes thickening and hardening of retinal artery walls; at crossing points, the thickened artery mechanically compresses the adjacent vein, slowing venous flow and facilitating clot formation. Diabetes increases the risk of venous occlusion by damaging the retinal vascular endothelium and increasing blood viscosity. Hyperlipidemia and atherosclerosis are other important factors that disrupt vessel wall structure. Glaucoma (high intraocular pressure) acts as an independent risk factor, particularly for CRVO, by mechanically obstructing venous flow at the level of the lamina cribrosa.

Older age is the strongest demographic risk factor for retinal vein occlusion; the prevalence rises significantly after the age of 40 and peaks between 60 and 70. However, vein occlusion can also occur in younger patients; in these cases, oral contraceptive use and thrombophilic conditions such as hyperhomocysteinemia, antiphospholipid syndrome, factor V Leiden mutation and protein C or protein S deficiency should be investigated. Smoking increases risk by impairing vascular endothelial function and increasing the tendency for blood to clot. Obesity, a sedentary lifestyle and obstructive sleep apnea syndrome are other factors associated with retinal venous occlusion. Correctly identifying the underlying cause directly affects both treatment planning and assessment of the risk of occlusion in the other eye.

The most characteristic symptom of retinal vein occlusion is a sudden, painless decrease in vision in one eye. Patients often report noticing marked blurring in one eye on waking in the morning; in some cases, vision gradually deteriorates over a few hours or days. Because the whole retina is affected in CRVO, vision loss tends to be more extensive and severe. In BRVO, vision loss may remain limited to the region corresponding to the retinal area served by the blocked branch; the patient may perceive a dark area, shadow or blurring in a particular part of the visual field.

In patients who develop macular edema, symptoms such as images appearing wavy or distorted (metamorphopsia), straight lines appearing curved and difficulty reading become prominent. Some patients may see floaters or black spots; this may be associated with retinal bleeding leaking into the vitreous cavity. Retinal vein occlusion is generally painless; however, if neovascular glaucoma develops because of ischemic CRVO, symptoms such as eye pain, redness, headache and nausea may occur. Every patient experiencing a sudden change in vision in one eye should consult an ophthalmologist without delay; early assessment plays a critical role in identifying the type of occlusion and starting treatment promptly.

Retinal vein occlusion is primarily diagnosed through a comprehensive eye examination. Measurement of visual acuity, assessment of intraocular pressure and a dilated fundus examination form the basis of the initial evaluation. Fundus examination assesses retinal hemorrhages, venous dilation and tortuosity, retinal edema, cotton-wool spots and possible signs of neovascularization. Whether the occlusion is CRVO or BRVO is determined by the distribution of hemorrhages: widespread hemorrhage in all four quadrants suggests CRVO, whereas hemorrhage confined to a particular sector suggests BRVO.

Optical coherence tomography (OCT) is indispensable for both diagnosis and monitoring the response to treatment, providing high-resolution images of the presence and amount of fluid accumulation in the macular region (macular edema) and the structural integrity of the retinal layers. Fundus fluorescein angiography (FFA) is used to assess retinal vessel structure, capillary perfusion, the extent of ischemic areas and the presence of neovascularization; it is particularly decisive in distinguishing ischemic from non-ischemic types. OCT angiography (OCTA) is a noninvasive method that images retinal vessel structure and perfusion without requiring dye injection. To investigate underlying systemic causes, blood pressure measurement and laboratory tests such as fasting blood glucose, HbA1c, lipid profile, complete blood count, erythrocyte sedimentation rate and thrombophilia screening in younger patients are requested.

Because there is no proven treatment to reopen the blocked vessel in retinal vein occlusion, the main goals of treatment are to control macular edema, halt vision loss or restore vision, and prevent complications such as neovascularization. Intravitreal anti-VEGF injections are currently the most effective and most commonly used treatment for macular edema. Anti-VEGF agents such as ranibizumab, aflibercept and bevacizumab are injected into the eye with a fine needle to reduce vascular permeability, allow accumulated retinal fluid to resolve and improve visual acuity. Anti-VEGF treatment initially consists of monthly injections; treatment intervals are then individualized according to OCT findings and visual response. Most patients require long-term treatment and follow-up.

Intravitreal steroid implants (such as a dexamethasone implant) are an alternative treatment option for cases that respond inadequately to anti-VEGF treatment or have chronic macular edema. Steroid implants provide a longer duration of action but require close monitoring because of side effects such as increased intraocular pressure and cataract development. In cases with marked retinal ischemia and neovascularization, panretinal laser photocoagulation aims to cause regression of abnormal new vessels and reduce the risk of bleeding inside the eye. Focal or grid laser treatment may also be an option for chronic macular edema due to BRVO. Effective control of underlying systemic diseases (hypertension, diabetes and hyperlipidemia) is an integral part of treatment; ocular treatments alone may not be sufficiently effective without adequate regulation of blood pressure and blood glucose.

Retinal vein occlusion is a retinal vascular disease that can cause permanent vision loss and serious complications without early intervention. In Samsun, vein occlusion is managed effectively through comprehensive eye examinations, accurate diagnosis and individualized treatment planning. Correctly identifying the type of occlusion and the degree of retinal ischemia is the most critical step directly affecting treatment success and long-term visual outcomes.

Retinal vein occlusion is not contagious and does not spread directly from one eye to the other. However, underlying systemic risk factors such as hypertension, diabetes or clotting disorders affect both eyes. The other eye is therefore also at risk of developing a vein occlusion, and effective control of systemic diseases is important in reducing that risk.

Anesthetic drops are applied to the eye's surface before the injection, so there is no significant pain during the procedure; a slight stinging or pressure sensation may occur. The number of sessions varies according to the patient's response to treatment and the course of macular edema. Injections are initially given monthly, after which treatment intervals are individualized according to OCT follow-up findings. Treatment may last a few months in some patients and several years in others.

The visual outcome varies according to the type of occlusion, the degree of ischemia, the duration of macular edema and how early treatment is started. A substantial proportion of BRVO cases achieve a good improvement in vision with treatment. The prognosis is more limited in ischemic CRVO. Early diagnosis and regular treatment can stop the progression of vision loss and preserve existing vision.