What Is the Retinal Vein?

Retinal vein occlusion is a more common fundus vascular disease. Retinal vein occlusion is characterized by retinal blood stasis, tortuous dilation of the veins, retinal hemorrhage and edema. Can be divided into central retinal vein occlusion and retinal vein branch occlusion.

Basic Information

Visiting department

Ophthalmology

Common causes

Retinal inflammation, retinal hypoperfusion, hypertension, arteriosclerosis, high blood viscosity and hemodynamic abnormalities, etc.

Common symptoms

Loss of central vision or lack of visual field

Causes of retinal vein occlusion

The etiology of retinal vein occlusion is more complex and is multifactorial. It is closely related to retinal inflammation, retinal hypoperfusion, hypertension, arteriosclerosis, high blood viscosity and hemodynamic abnormalities. Trauma, oral contraceptives, or excessive fatigue are all possible causes. In short, retinal vein occlusion is often caused by multiple factors, including both vascular abnormalities and changes in blood composition or hemodynamic abnormalities.

Clinical manifestations of retinal vein occlusion

The main symptom is decreased central vision, or a part of the visual field defect, but the incidence is far less acute and severe than arterial occlusion. Generally, partial vision can still be retained. 3 to 4 months after central vein occlusion, 5% to 20% of patients can Iris neovascularization and secondary neovascular glaucoma occur.

Central retinal vein occlusion

Divided into 2 types:

(1) Light type is also called non-ischemic, high-permeability or partial obstruction. Symptoms are mild or asymptomatic. Depending on the degree of macular damage, vision may be normal or mildly diminished, and the visual field may be normal or slightly altered. Early stage: The optic disc is normal or the border is slightly blurred and edema. The macular area is normal or has mild edema and bleeding. The arterial diameter is normal, the veins are tortuous and dilated, there are a small or moderate amount of flaming and spotting bleeding along the 4 veins of the retina, there are no or occasional cotton floc spots, and the retina has mild edema. The retinal circulation time of fluorescent angiography is normal or slightly prolonged, mild fluorescein leakage in the venous wall, slight dilation of capillaries and formation of a small number of microhemangiomas. The macula is normal or there is a slight spotted fluorescein leak. Late stage: After 3 to 6 months, retinal hemorrhage is gradually absorbed and finally disappears completely. The macular area returned to normal or there was mild pigmentation disorder; a few patients had dark red cystic edema, and fluorescein angiography showed petal-shaped fluorescein leakage, and finally formed cystic scars, which could cause vision loss. In some patients, the optic disc has collateral formation of ciliary retinal blood vessels, with morphology such as petals or wreaths. The venous stasis is dilated or completely recovered, but it is accompanied by a white sheath. There were no or occasional areas of no perfusion, no neovascularization, and vision returned to normal or slightly diminished. Some patients with mild central retinal vein occlusion may worsen their condition and turn into severe ischemic venous occlusion.

(2) Heavy is also called ischemic, hemorrhagic or complete obstruction. Early stage: Most patients have blurred vision and markedly decreased vision. In severe cases, the visual acuity is reduced to only hand index or manual, and in patients with arterial occlusion, it may be reduced to only light perception. May have visual field defects with dense central dark spots or peripheral narrowing. Fundus examination showed a high degree of edema and congestion of the optic disc, blurred borders and concealment by bleeding. Late stage: It usually enters the advanced stage 6 to 12 months after the onset. The disc edema subsides, the color returns to normal or fades, and the ciliary retina collateral vessels are often formed on the surface or edge of the ciliary retina. There may be new blood vessels, which are coiled or flower-shaped, and are relatively narrow. Some can protrude into the vitreous body and float in the fundus. Macular edema subsides, pigmented disorder, or petal-shaped dark red spots, suggesting that there has been macular cystic edema in the past. In severe cases, retinal glial hyperplasia, fibroblasts accumulate, form secondary preretinal membranes, or scars doped with pigments, severely impaired vision.

2. Hemilateral retinal vein occlusion

During the development of retinal blood vessels, the vitreous artery enters the optic cup through the embryonic fissure. Three months after the embryo, two veins appear on both sides of the artery to enter the optic nerve. Normal people converge with each other within the optic nerve behind the optic disc to form the central retinal vein. Usually one of them disappears after birth, leaving one trunk. However, some people may leave behind and form two vein trunks. Hemilateral obstruction is the obstruction of one of the trunks at the sieve plate or in the optic nerve. This type of obstruction is relatively rare in clinical practice, with an incidence of 6% to 13%. Usually 1/2 retina is involved. Occasionally 1/3 or 2/3 retinal involvement is seen. Its clinical manifestations, course and prognosis are similar to those of central retinal vein occlusion. Neovascular glaucoma can also occur if there is a large unperfused area.

3. Retinal branch vein occlusion

Temporal branches are most commonly involved in branch venous occlusion, accounting for 90% to 93%. Among them, superior temporal branch occlusion is the most common, accounting for 62% to 72%. Nasal collateral occlusion is rare, and the incidence is 1.5% to 3.0%. . Small macula obstruction has a better prognosis than main branch obstruction, because the small macula branch drainage area is small and the capillary layer is thick there, it is less likely to produce a non-perfusion zone, even if the area is small, it will cause late complications neovascularization The possibility is small. In contrast, trunk obstruction has more complications.

(1) The condition of early vision loss varies depending on whether the compression point is located in the main or small branch of the vein. Those with obstructions located on the trunk and the macula branch have different degrees of vision loss. Branches that do not supply the macula are obstructed, vision is not affected, and the visual field changes corresponding to the damaged area of the retina. Fundus examination of the retinal arteries often thins and changes in sclerosis.

(2) Late bleeding usually absorbs gradually after about 6 months of onset, edema subsides, stellate or irregular point-like hard exudation appears in the macular area of the optic disc, or ring-shaped exudation at the temporal side of the macula. slow. Macular edema subsides, leaving pigmented disorders or cystic degeneration scars. Accompanied arteries produce secondary sclerosis, narrowed tube diameter accompanied by white sheath.

Retinal vein occlusion

Laboratory inspection

Hemorheological examination can understand plasma viscosity and whole blood viscosity, can be used to determine -coagulation protein and platelet factor IV content.

2. Other auxiliary inspections

Fundus fluorescein angiography (FFA) findings also vary depending on the obstruction site (trunk, hemi, branch), the degree of obstruction (completeness, incompleteness), and the duration of the disease.

Diagnosis of retinal vein occlusion

The diagnosis can be determined based on typical fundus changes, combined with FFA results and clinical manifestations.

Retinal vein occlusion complications

The first category is macular complications and sequelae, including macular cystoid edema, macular anterior membrane formation, and macular scar formation. The second category is neovascularization and its complications, including neovascular glaucoma, vitreous hemorrhage, retinal proliferation, mechanized membrane formation, pulling the retina to form a hole, and retinal detachment. Among the above complications, macular cystoid edema and neovascularization are the most common.

Retinal Vein Occlusion Treatment

Treatment principle

(1) Obstruction of the central retinal vein requires close observation of iris neovascularization. Once found, total retinal photocoagulation must be performed immediately.

(2) A large unperfused area of the retinal branch vein occlusion appears in the retina, which can be treated by photocoagulation of the unperfused area of the retina.

(3) Severe macular edema can be treated by photocoagulation of the macula grille or injection of drugs into the vitreous cavity.
2. Drug treatment

The treatment of this disease is difficult, and some therapies are controversial. In theory, thrombosis is treated with anticoagulants, but the effect is not ideal. Many anticoagulants used in the past are no longer used. So far there is no special effective treatment. Generally, it can treat and prevent thrombosis according to the cause, such as lowering blood pressure and intraocular pressure, reducing blood viscosity, reducing thrombosis and tissue edema, and promoting bleeding absorption.

(1) Fibrinolytic preparations dissolve fibrin, reduce or remove thrombosis. Including urokinase, streptokinase, defibrase, and tissue plasminogen activator (t-PA). Fibrinogen and thrombinogen time should be checked before treatment, and it should not be used if it is lower than normal. Urokinase: Turn plasminogen into plasmin. Plasmin has a strong hydrolyzing effect on fibrin, and may have the effect of dissolving thrombus. Intravenous infusion: It should be prepared fresh, 5 to 7 times as a course of treatment. Post-ball injection: once a day or every other day, 5 times a course. Ion penetration: 1 time / day, 10 days is a course of treatment. Streptokinase: Combined with plasminogen in the blood to become a complex activation factor, and make its activation into plasmin, solubilize fibrin to achieve the effect of dissolving thrombus. Intramuscular promethazine and intravenous dexamethasone or hydrocortisone were administered half an hour before streptokinase administration to reduce side effects. Defibrinase: Also known as defibrinase, it is an enzyme preparation isolated from the venom of the Agkistrodon acutus snake venom, which significantly reduces fibrinogen and produces a significant anticoagulant effect. tissue plasminogen activator (t-PA): plasmin produced by vascular endothelial cells in vivo. After genetic engineering technology is produced into artificial recombinant t-PA, it can activate plasminogen into plasmin in the body to dissolve the thrombus. Systemic application of t-PA is more likely to cause severe bleeding, so some people at home and abroad now use t-PA as a retinal vein micropuncture to treat this disease.

(2) Aspirin and dipyridamole are commonly used as antiplatelet aggregation agents . Aspirin can inhibit collagen-induced platelet aggregation and release ADP, and has a longer-lasting inhibitory effect on platelet aggregation. Dipyridamole inhibits platelet release response and reduces platelet aggregation.

(3) The principle of hemodilution therapy is to reduce hematocrit, reduce blood viscosity, and improve microcirculation. It is most suitable for patients with increased blood viscosity. The method is to draw 500ml blood and add 75ml sodium citrate to anticoagulate, centrifuge at high speed to separate blood cells from plasma, and instill 250ml of low molecular dextran intravenously during the waiting process. The separated plasma is then returned to the patient. Repeat this therapy 3 to 6 times within 10 days until the hematocrit decreases to 30% to 35%. This therapy is not suitable for severe anemia. Effective rate is 42% to 88%.

(4) Corticosteroids can reduce edema and improve circulation in young patients, especially those caused by inflammation and patients with macular cystic edema. Some people do not approve the application of corticosteroids, and believe that venous occlusion is blocked blood flow, increased venous pressure, increased vascular permeability, and corticosteroids are ineffective.

(5) Other drug treatments such as activating blood circulation and removing blood stasis can expand blood vessels, inhibit platelet aggregation, reduce capillary permeability, and improve microcirculation. For example, Xueshuantong, Danshen injection and other intravenous drips, the effective rate for treating this disease is 69. %about. In addition, antihypertensive drugs or ocular hypotensive drugs can be given according to the cause. Symptomatic treatments such as intramuscular injection of iodine preparations or iontophoresis to promote bleeding absorption. Comprehensive Chinese and Western Medicine Treatment. Vitamin C, rutin, and vasodilators can be taken orally. At the same time, she was given traditional Chinese medicine treatment, mainly in the early stage of clearing heat and cooling blood, and promoting blood circulation and removing blood stasis.

3. Laser treatment

The mechanism is: reduce capillary leakage and form a barrier to prevent liquid from penetrating into the macula; close the non-perfusion zone to prevent the formation of new blood vessels; close the new blood vessels to reduce and prevent vitreous blood. Laser blocking of the main trunk can only prevent new blood vessels and reduce macular cystic edema. It has little effect on improving vision, but it has better effect on branch blocking.

Laser choroid-retinal vein anastomosis: In 1992, McAllister et al. First performed an experimental laser choroid-retinal vein anastomosis using argon laser and applied it to clinical treatment of non-ischemic retinal vein occlusion. In 1998, the combination of YAG treatment increased the success rate from 33% to 54%. Since then, many authors at home and abroad have applied this method for treatment and achieved certain results.

4. Retinal arteriovenous sheath incision

Can be applied to branch retinal vein occlusion. The arteriovenous sheath is cut at the intersection of the compressed vein and artery to reduce venous compression. Restore blood flow. About 80% of patients have stable or improved vision after surgery.