Retinal vein occlusion

Arteriolosclerosis is an important factor contributing to the development of occlusion of the branches of the central vein of the retina. Retinal arterioles and their corresponding veins have a common adventitial membrane ", so the thickening of the arterioles causes compression of the vein, if the arteriol is anterior to the vein. This leads to secondary changes, including loss of venous endothelial cells, thrombus formation and occlusion. Similarly, the central vein and the retinal artery have a common adventitial membrane behind the lattice plate, so atherosclerotic changes in the artery can cause vein compression and provoke occlusion of the central vein of the retina. In this regard, it is believed that the defeat of both arteries and veins leads to venous retinal occlusions. In turn, venous occlusion leads to an increase in pressure in the veins and capillaries with a decrease in blood flow. This contributes to the development of retinal hypoxia, from which blood is diverted through a vein that has been obstructed. Subsequently, damage to the endothelial cells of capillaries and extravasation of blood components occurs, the pressure on the tissue increases, causing an even slower circulation and hypoxia. So the vicious circle is established.

Classification of retinal vein occlusion

1. Occlusion of the branches of the central vein of the retina.
2. Occlusion of the central vein of the retina.
   • Non-ischemic.
   • Ischemic.
   • Papilloflebitis.
3. Hemiretinal venous occlusion.

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What causes retinal vein occlusion?

Below are the states of importance, which are associated with a high risk of venous occlusion of the retina.

1. Elderly age is the most important factor; more than 50% of cases suffer patients older than 65 years.
2. Systemic diseases, including arterial hypertension, hyperlipidemia, diabetes, smoking and obesity.
3. Increased intraocular pressure (eg, primary open-angle glaucoma, ocular hypertension) increases the risk of occlusion of the central vein of the retina.
4. Inflammatory diseases, such as sarcoidosis and Behcet's disease, may be accompanied by an occlusal periflexitis of the retina.
5. Elevated blood viscosity associated with polycythemia or abnormal plasma proteins (eg, myeloma, ml Waldenstrom microglobuloma).
6. Acquired thrombophilia, including hyperhomocysteinemia and aitiphospholipid syndrome. An elevated plasma homocysteine level is a risk factor for myocardial infarction, strokes and carotid artery disease, as well as the occlusion of the central vein of the retina, especially the ischemic type. Hyperhomocysteinemia in most cases is fairly quickly reversible with the conversion of folic acid.
7. Congenital thrombophilia can be accompanied by venous occlusion in young patients. This increases the level of clotting factors VII and XI, the deficit of anticoagulants, such as antithrombin III, protein C and S, as well as resistance to activated protein C (factor V Leiden).

Factors that reduce the risk of venous occlusion are increased physical activity and moderate alcohol consumption.

Occlusion of branches of the central vein of the retina

Classification

1. Occlusion of the main branches of the central vein of the retina is divided into the following types:
   • Occlusion of the temporal branch of the first order near the optic nerve disk.
   • Occlusion of the temporal branch of the first order far from the optic disc, but with the coverage of branches feeding the macula.
2. Occlusion of small para- macular branches with coverage of only branches feeding the macula.
3. Occlusion of peripheral branches that do not cover the macular circulation.

Clinical Features

The manifestations of the occlusion of the branches of the central vein of the retina depend on the volume of the macular outflow system that has undergone occlusion. With the involvement of the macula, sudden deterioration of vision occurs, metamorphopsia or relative scotoma of the visual fields appear. Occlusion of peripheral branches may be asymptomatic.

Visual acuity varies and depends on the volume of the pathological process of the macular area.

Ocular fundus

• The widening and sinuosity of the veins is more peripheral than the occlusion site.
• Hemorrhages in the form of "tongues of flame" and point hemorrhages, retinal edema and cotton-like foci located in the sector of the affected branch, respectively.

Foveal angiography in the early phases reveals the hypofluorescence caused by the blocking of the background fluorescence of the choroid due to hemorrhage of the retina. In the late phases, hyperfluorescence is determined by sweating.

Flow. Manifestations in the acute period can last 6-12 months to complete resolution and can be expressed as follows:

• The veins are sclerosed and surrounded by a different number of residual hemorrhages, more peripheral than the obstruction.
• Venous collaterals, characterized by a mild tortuosity of the vessels, develop locally along the horizontal seam between the lower and upper vascular arcades or near the optic nerve disc.
• Microaneurysms and solid exudates can be combined with the deposition of cholesterol inclusions.
• In the macular area, sometimes changes in retinal pigment epithelium or epiretinal gliosis are detected.

Forecast

The forecast is quite favorable. Within 6 months approximately in 50% of patients there is a development of collaterals with restoration of sight up to 6/12 and above. Improvement of visual functions depends on the extent of venous outflow (which is related to the place and size of the occluded vein) and the severity of the macular area ischemia. There are two main sight-threatening states.

Chronic macular edema is the main cause of prolonged vision loss after occlusion of the branches of the central vein of the retina. In some patients with visual acuity from 6/12 and below, an improvement after laser coagulation is possible, which is more effective in swelling than with ischemia.

Neovascularization. Development of neovascularization in the region of the disk occurs in about 10% of cases, and away from the disk - in 20-30%. Its probability increases with the severity of the process and the extent of the lesion. Neovascularization outside the optic nerve disc usually develops on the border with the triangular sector of the ischemic retina where there is no outflow due to occlusion of the vein. Neovascularization can develop at any time within 3 years, but more often it appears in the first 6-12 months. This is a serious complication, which can cause recurrent bleeding in the vitreous and preretinal hemorrhages, and sometimes - traction retina detachment.

Observation

Patients need Foveal angiography in the range of 6-12 weeks, for which there is a sufficient resorption of retinal hemorrhages. Further tactics depend on visual acuity and angiographic findings.

• The PHAG reveals a good perfusion of the macula, visual acuity is improved - treatment is not required.
• Foveal angiography reveals edema of the macula in combination with good perfusion, visual acuity remains at the level of 6/12 and lower, after 3 months a decision is made about laser coagulation. But before treatment, it is important to carefully consider the FAG to determine the zones of sweating. No less is the detection of collaterals that do not pass fluorescein and should not be coagulated.
• The FAG reveals the absence of macular perfusion, visual acuity is low - laser coagulation is ineffective to improve vision. However, if Foveal angiography lacks perfusion of the site to 5 or more DD, it is necessary to examine the patient every 4 months for 12-24 months because of possible neovascularization.

Laser treatment

1. Edema of the macula. Conduct lattice laser coagulation (the size of each coagulum and the distance between them - 50-100 microns), which causes a mild reaction in the field of sweating, revealed na Foveal angiography. Coagulants can not be applied beyond the avascular zone of the fovea and peripheral to the main vascular arcades. It is necessary to be careful and avoid coagulation of the zones with intra-retinal hemorrhages. Re-examination - after 2-3 months. If the macular edema persists, it is possible to perform repeated laser coagulation, despite the fact that the result is often disappointing.
2. Neovascularization. Diffuse laser coagulation (the size of each coagulum and the distance between them - 200-500 microns) is performed to achieve a moderate response with full coverage of the pathological sector, identified in advance in color photography and PLG. Repeated inspection - after 4-6 weeks. If neovascularization persists, repeated treatment usually gives a positive effect.

Non-ischemic occlusion of the central vein of the retina

Clinical Features

The non-ischemic occlusion of the central vein of the retina is manifested by a sudden one-sided decrease in visual acuity. Deterioration of vision - from moderate to severe. The afferent pupillary defect is absent or flaccid (in contrast to ischemic occlusion).

Ocular fundus

• Crimp of varying degrees and expansion of all branches of the central vein of the retina.
• Point or in the form of "flame tongues" of retinal hemorrhage in all four quadrants, most abundantly - on the periphery.
• Sometimes there are vata-like foci.
• Often there is a slight or moderate swelling of the optic nerve and macula disc.

Arteriography reveals a delay in venous outflow, a good perfusion of the retinal capillaries and later sweating.

Non-ischemic occlusion of the central vein of the retina occurs most often and is about 75% of the cases.

Flow. Most acute manifestations disappear after 6-12 months. The residual phenomena include collateral disk of the optic nerve, epiretinal gliosis and redistribution of the pigment in the macula. Transition to ischemic occlusion of the central vein of the retina in 10% of cases is possible within 4 months, in 34% of cases - within 3 years.

Forecast

In those cases when the process does not go into ischemic form, the prognosis is quite favorable with complete or partial restoration of vision in about 50% of patients. The main cause of poor vision recovery is chronic cystic macular edema, which leads to secondary changes in retinal pigment epithelium. To a certain extent, the prognosis depends on the initial visual acuity, namely:

• If in the beginning the visual acuity was 6/18 or higher, then most likely it will not change.
• If the visual acuity was within 6 / 24-6 / 60, the clinical course is different, and the vision subsequently can both improve, and not change or even worsen.
• If visual acuity at the beginning was 6/60, improvement is unlikely.

Tactics

1. Observation is necessary for 3 years to prevent the transition to an ischemic form.
2. Laser treatment using high power is aimed at creating anastomoses between the retinal and choroidal veins, thereby creating parallel branches in the area of obstruction of the venous outflow. In some cases, this method gives a good result, but it is associated with a potential risk of complications such as fibrosis proliferation in the laser, venous or choroidal hemorrhage. Chronic macular edema will not be amenable to laser treatment.

Ischemic occlusion of the central vein of the retina

Clinical Features

Ischemic occlusion of the central vein of the retina is manifested by a one-sided, sudden and sharp deterioration of vision. Deterioration of vision is almost irreversible. The afferent pupillary defect is pronounced.

Ocular fundus

• The expressed crimp and stagnation of all branches of the central vein of the retina.
• Extensive patchy and in the form of "flame tongues" of hemorrhage with encompassing the periphery and posterior pole.
• Waterskin foci, which can be many.
• Macular edema and hemorrhage.
• Pronounced edema of the optic disc and hyperemia.

Foveal angiography reveals central retinal hemorrhages and extensive areas of absence of capillary perfusion.

Flow. Manifestations of an acute period take place within 9-12 months. The residual changes include collateral disk of the optic nerve, epiretinal macular gliosis and redistribution of the pigment. Less common may develop subretinal fibrosis, similar to that in exudative form associated with age of macular degeneration.

The prognosis is extremely unfavorable in connection with ischemia of the macula. Rubyosis of the iris develops approximately in 50% of cases, usually in the period from 2 to 4 months (100-day glaucoma). If you do not perform panretinal laser coagulation, then there is a high risk of developing neovascular glaucoma

Tactics

Observation is carried out monthly for half a year to prevent neovascularization of the anterior segment. Although neovascularization of the CPC does not yet indicate the presence of neovascular glaucoma, it is the best clinical marker

In this regard, if there is a risk of developing neovascular glaucoma, a detailed gonioscopy is necessary, since examination with only a slit lamp is considered inadequate.

Treatment. In case of neovascularization of the anterior chamber or iris angle, panretinal laser coagulation is immediately performed. Prophylactic laser coagulation is suitable for cases when regular observation is impossible. However, sometimes retinal hemorrhages dissolve insufficiently by the time of laser coagulation.

Papilloflebitis

Papilloflebitis (vasculitis of the optic disc) is considered a rare condition, usually found in completely healthy individuals under the age of 50 years. It is believed that the basis of the disorder is edema of the optic nerve disk with secondary occlusion of the veins, in contrast to venous thrombosis at the level of the trellis plate in the elderly.

It is manifested by a relative deterioration of vision, which is more often noted when lifting from a prone position. Deterioration of vision - from mild to moderate. Afferent pupillary defect is absent.

Ocular fundus:

• The edema of the optic nerve disk, often in combination with vata-like foci, is dominant.
• Expansion and tortuosity of veins, hemorrhages, expressed in varying degrees and usually confined to the parapapillary zone and the posterior pole.
• The blind spot is enlarged.

Foveal angiography reveals a delay in venous filling, hyperfluorescence due to sweating, and good capillary perfusion.

The prognosis is excellent regardless of the treatment. In 80% of cases, vision is restored to 6/12 and above. The rest noted a significant irreversible reduction in vision as a result of macular edema.

Hemiretinal occlusion of veins

Gemiretinal occlusion of the veins compared with the occlusion of the central vein of the retina and its branches is less common. It covers the upper or lower branches of the central vein of the retina.

Classification of hemiretinal occlusion of veins

• occlusion of the hemisphere of the main branches of the central vein of the retina near the optic disc or at a distance;
• hemicentral occlusion is observed less often, it covers one of the two trunks of the central vein of the retina, and it is found on the anterior surface of the optic nerve disc as congenital.

Hemiretinal occlusion of the veins is manifested by a sudden disruption of the upper or lower half of the visual field, depending on the area of the lesion. Deterioration of vision is different.

Ocular fundus. The picture is similar to the occlusion of the branch of the central vein of the retina with the involvement of the upper and lower hemispheres.

Foveal angiography reveals multiple hemorrhages, hyperfluorescence due to sweating and various violations of the perfusion of the retinal capillaries.

The prognosis is determined by the degree of expression of macular ischemia and edema.

Treatment depends on the severity of retinal ischemia. Significant retinal ischemia is associated with the risk of developing neovascular glaucoma, so managing patients is the same as with ischemic occlusion of the central vein of the retina.