Central retinal vein occlusion is a violation of retinal venous blood flow caused by thrombosis of the CRV or its branches. Central retinal vein occlusion is accompanied by a sharp deterioration in the vision of the affected eye, which is sometimes preceded by periodic blurring of vision, distortion of the visibility of objects, dull pain in the depth of the eye socket. The diagnostic algorithm includes visometry, perimetry, tonometry, biomicroscopy, ophthalmoscopy, PHAGE, electrophysiological studies, retinal tomography. Treatment requires systemic administration of thrombolytics, vasodilators, antiplatelet agents; local and general antihypertensive therapy; if necessary, surgical assistance.
Occlusion of the central artery and retinal vein in ophthalmology is attributed to the number of vascular catastrophes, due to the rapidity of their development and the severity of the consequences for visual function. Central retinal vein occlusion develops in 214 people per 100,000 population, mainly over the age of 65. In most cases (67.2%), the patency of the CRV branches is impaired, most often (82.4%) – the upper temporal branch of the central retinal vein. Bilateral central retinal vein occlusion occurs in 10% of cases, usually in patients with systemic diseases (atherosclerosis, hypertension, diabetes mellitus, etc.).
The clinical classification of occlusive CRV lesions takes into account the stage and localization of the process. It distinguishes:
- Prethrombosis of the central retinal vein and its branches (inferior, superior, inferior, superior).
- Thrombosis (incomplete and complete) of CRV and its branches with or without edema of the macular zone.
- Postthrombotic retinopathy.
According to the severity of retinal vein thrombosis , they differentiate:
1. Central retinal vein occlusion:
- ischemic (complete) with nonperfused retinal area of 10 diameters OND;
- non-ischemic (incomplete).
2. Occlusion of branches of the central retinal vein:
- the main branch of the CRV with a retinal lesion area of 5 diameters OND;
- branches of the second order with a retinal lesion area of 2-5 diameters OND;
- branches of the third order with a retinal lesion area of less than 2 diameters OND.
3. Hemicentral retinal occlusion (ischemic and non-ischemic).
The leading pathogenetic link of venous occlusion is thrombosis of the central retinal vein or its branches. The mechanism of thrombosis is caused by compression of the venous vessel by the central retinal artery (usually in the area of the arteriovenous junction or at the level of the lattice plate of the sclera). This is accompanied by a turbulent blood flow and damage to the endothelium, provoking the formation of a venous thrombus. This process is often accompanied by arterial spasm, which causes a violation of retinal perfusion.
As a result of venous stagnation, there is a sharp increase in hydrostatic pressure in the capillaries and venules of the retina, which leads to the exudation of plasma and cellular elements of blood into the circulatory space. In turn, edema further aggravates capillary compression, venous congestion and retinal hypoxia.
The causes predisposing to occlusion of the central retinal artery may be local and systemic processes. Among the local factors, the main role belongs to ocular hypertension and primary open-angle glaucoma. Compression of the vessels by the orbit tumor, the presence of edema and drusus OND, thyroid ophthalmopathy, etc. also matters. Increases the likelihood of venous occlusion of retinal periphlebitis, which often develops against the background of sarcoidosis and Behcet’s disease.
Systemic diseases associated with an increased risk of central retinal vein occlusion include hyperlipidemia, obesity, arterial hypertension, diabetes mellitus, congenital and acquired thrombophilia, increased blood viscosity, etc.
It should be noted that in 50% of cases, central retinal vein occlusion develops against the background of existing arterial hypertension or ophthalmic hypertension.
Disease is accompanied by a sharp painless decrease in vision more often than one eye. Unlike occlusion of the central retinal artery, with venous thrombosis, the drop in visual acuity does not occur so rapidly: usually this process develops within a few hours or days (less often – weeks). The degree of visual impairment with non-ischemic occlusion varies from moderate to severe; with ischemic central retinal vein occlusion, vision drops to low vision or zero.
Sometimes this is preceded by episodes of periodic blurring of vision, distorted vision of objects, the appearance of a dark spot in front of the eyes. In some cases, there are dull pains in the cavity of the eye socket.
With hemiretinal thrombosis or occlusion of the branches of the central retinal vein, in addition to a decrease in central vision, the corresponding half or sector of the visual field suffers.
The diagnosis is made by an ophthalmologist taking into account the data of anamnesis, physical and instrumental examination, advisory opinions of a cardiologist, endocrinologist, rheumatologist, hematologist.
Methods of objective diagnosis are: visual acuity testing, perimetry, tonometry, biomicroscopy, ophthalmoscopy, retinal vascular angiography, electrophysiological studies.
In the prethrombosis stage, as well as with occlusion of the second and third order CRV branches, visual acuity decreases slightly or does not change at all. With non-ischemic central retinal vein occlusion and its branches, visometry reveals visual acuity above 0.1. Ischemic thrombosis of CRV and temporal veins is accompanied by a decrease in visual acuity below 0.1. Examination of the visual fields reveals central or paracentral scotomas in the corresponding retinal quadrants, concentric narrowing of the visual fields.
Tonometry makes it possible to detect ophthalmohypertension; with the help of daily tonometry, IOP is evaluated in dynamics. The changes detected by biomicroscopy can be different: neovascularization of the iris; relative afferent pupillary defect; the presence of a suspension of blood elements, exudate, floating blood clots in the vitreous, etc.
Typical signs are detected by ophthalmoscopy. Edema of the OND and macula, hemorrhages in the form of “flames”, tortuosity and moderate expansion of veins, their uneven caliber and microaneurysms, cotton-like foci are characteristic. The ophthalmoscopic picture in lesions of various branches of CRV has its own characteristics.
Fluorescent angiography of vessels reflects delayed retinal contrast, uneven contrast of veins, elongation of the phase of venous perfusion, granularity of blood flow. According to the results of angiograms, the duration of thrombosis, localization and degree of central retinal vein occlusion, the development of neovascularization, the state of the macula and OND are judged.
Electroretinography, reflecting the degree of retinal ischemia, allows you to track the dynamics and make a forecast regarding visual function.
Of the laboratory methods for central retinal vein occlusion, a significant role is played by the study of blood sugar, coagulograms, determination of cholesterol and lipoproteins, coagulation factors.
Differential diagnosis is performed with secondary retinopathy (hypertensive, atherosclerotic, diabetic, etc.).
In the acute stage, the treatment of central retinal vein occlusion is carried out in an ophthalmological hospital; in the future – on an outpatient basis, under the supervision of an optometrist. At the first stage, with the help of intensive therapy, venous blood flow is restored, hemorrhages are resorbed, edema is reduced, and retinal trophism is improved.
With retinal vein thrombosis, subconjunctival, parabulbar, and sometimes intravitreal injections of thrombolytic drugs (tissue plasminogen activator, prourokinase, urokinase) are prescribed. Local (instillation of drops) and general hypotensive and antioxidant therapy are carried out. Administration of antiplatelet agents (aspirin), endothelioprotectors (sulodexide), diuretics (diacarb, furosemide); administration of vasodilators (pentoxifylline, vinpocetine) is indicated. With central retinal vein occlusion, it is possible to inject thrombolytics and vasodilators through a catheter directly into the CRV branch.
The use of surgical tactics is indicated for macular edema and neovascularization. For this purpose, laser coagulation of the retina (panretinal, sectoral, preventive, etc.) is used, which allows to close ischemic zones and destroy neovascular complexes. With non-absorbable hemorrhages in the vitreous body, a vitrectomy is performed.
Prognosis and prevention
In non-ischemic thrombosis of CRV, the prognosis is favorable in most cases; there is a gradual improvement and restoration of vision. Ischemic central retinal vein occlusion is usually complicated by postthrombotic neovascular glaucoma, recurrent vitreous hemorrhages, traction retinal detachment, persistent drop in visual acuity.
Patients who have undergone central retinal vein occlusion, within six months, follow-up by an ophthalmologist with periodic control examination (ophthalmoscopy, biomicroscopy, gonioscopy, IOP control) is indicated. It is necessary to exclude factors contributing to venous thrombosis, to treat concomitant pathology with specialists of the appropriate profile.