retinal vein occlusion
Introduction
Introduction to retinal vein occlusion Retinal vein occlusion (retinalveinocclusion) is a common fundus vascular disease. Retinal vein occlusion is characterized by: retinal blood stasis, retinal hemorrhage and edema, which can be divided into central retinal vein occlusion and retinal vein branch obstruction, with electron microscopy, laser and The development of techniques such as fundus photography has further understanding and improvement of the etiology, classification, complications, prognosis and treatment of this disease. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: neovascular glaucoma cystoid edema
Cause
Causes of retinal vein occlusion
Vascular wall lesions (40%):
Retinal arteriosclerosis plays an important role in the pathogenesis of retinal vein occlusion. 80% to 95% of patients have arteriosclerosis at the same time. The most common site of obstruction is at the sieve plate area and the arteriovenous intersection. In these two parts, the center of the retina The arteries and veins are close together. There is an outer membrane in the adjacent vessel wall, which is covered by the same connective tissue membrane. When the arteriosclerosis is hardened by the hardened outer membrane, the vein is narrowed, and the endothelial cells of the wall are stimulated. Hyperplasia, the lumen becomes narrower, the blood flow becomes slower, and even stagnates, causing thrombosis of platelets, red blood cells, and fibrinogen to form a thrombus, which is more likely to occur when there is hypertension, diabetes, or blood disease. On the other hand, the toxins produced by the inflammation or inflammation of the retinal vein itself can also thicken the venous wall, damage the intima, proliferate the endothelial cells, change the surface charge, and cause platelet aggregation, formation of blood cell components of the fibrinogen network. Thrombosis, venous inflammation can come from viral infections, tuberculosis, syphilis, sepsis, endocarditis, pneumonia, meningitis, sinusitis, and other systemic immune or vascular diseases. Trauma can cause these changes directly in the venous wall. .
Increased blood viscosity (30%):
In recent years, changes in blood components, especially changes in viscoelasticity, have been associated with the pathogenesis of retinal vein occlusion. Under normal conditions, the surface of red blood cells has a negative charge, so they are mutually repelled and can be suspended in the blood. When hyperlipidemia occurs, When hyperproteinemia, or fibrinogen is elevated, these lipids and fibrinogen can wrap on the surface of red blood cells to lose the negative charge on the surface, so they tend to aggregate and form clumps and adhere to the blood vessel wall, and at the same time due to fibrinogen Increased content or increased content of lipoprotein and globulin can increase plasma viscosity and whole blood viscosity, make blood thicker, increase blood flow resistance, and more likely to form thrombus. Patients with retinal vein occlusion have hyperlipidemia accounted for 61%~ 82%, it has also been reported that the patient's blood viscosity, fibrinogen, plasma viscosity increased, Trope found that patients with capillary non-perfused areas and (or) neovascularization increased blood viscosity, in addition, blood coagulation system and Unbalanced fibrinolytic system, platelet aggregation and release response are enhanced for any reason, -coagulin and platelet factor IV content High can cause enhanced platelet aggregation, thrombosis are easily induced vein occlusion.
Thrombosis (20%):
Increased intraocular pressure has a certain significance in the pathogenesis of this disease. The disease combined with primary open angle glaucoma accounted for 10% to 20%, and even reported up to 50%, due to increased intraocular pressure, first affect the sieve plate The central retinal artery is perfused, and the venous pressure affects the venous return, resulting in stasis of blood flow and thrombosis. Increased intraocular pressure can stimulate the central vein of the sieve plate to proliferate the endometrial cells, narrow the lumen, and cause hemodynamic changes. The formation of thrombosis, other lesions, such as cardiac function compensation, bradycardia, severe heart rate, sudden drop in blood pressure or increased blood viscosity, can cause hemodynamic changes, slowing blood flow, especially in the sieve The resistance between the plate and the arteriovenous junction is greater, the blood flow is slower or even stagnant, promoting thrombosis and inducing venous obstruction.
Prevention
Retinal vein occlusion prevention
1, usually pay attention to protect the eyes, to avoid eye diseases and injuries.
2, pay attention to the mix of nutrition, maintain emotional stability, do not eat irritating food, etc., prevent high blood pressure, coronary heart disease, etc., to prevent these diseases secondary to retinal vein occlusion.
Complication
Retinal vein occlusion complications Complications, neovascular glaucoma, macular cystic edema
Complications and sequelae of retinal vein occlusion are more common. In general, they can be summarized into two categories: Category 1 is the macular complication and sequelae, including cystoid macular edema, macular anterior membrane formation, and macular scar formation. The second category is neovascularization and its complications, including neovascular glaucoma, vitreous hemorrhage, proliferation, mechanized membrane formation, retinal formation and retinal detachment, and macular cystic edema and rejuvenation in the above complications. Blood vessels are the most common.
Macular cystic edema
It is the most common complication of retinal vein occlusion, and it is also one of the main reasons for the decreased vision of this disease. The incidence of total dryness is slightly higher than that of branch obstruction. The incidence of total obstructive cystic edema is 40% to 66%. 30% to 62%, the incidence of cystoid macular edema varies according to the severity of the disease, the severity of the disease occurs earlier, can occur 1 month after venous obstruction, and some appear in the months after the onset, check Glasses are difficult to identify in mild cases. Severe cases are difficult to distinguish due to diffuse edema of the macula. However, optical coherence tomography can be used to confirm the diagnosis. After 1 to several months, diffuse edema in the macular area subsides, and the macular is dark red. Obviously, the macular area has a clear dark red bubble-like bulge, and the vesicles of the division are petal-like or radial. The contact lens is used to detect the retinal thickening in the macular area, and the central concave bulge forms several large vesicles. Honeycomb-like vesicles are still visible around the vesicles. If there is blood in the vesicles, a half-moon-shaped liquid plane is formed. The posterior wall of the vesicles may have pigmentation, and the cystic edema is limited to the central area. The obstruction occupies the upper or lower half of the macula, and the total dry obstruction is severe. The cystic edema can be extended to the lateral edge of the optic disc and the upper and lower vascular arch. The late stage of the fluorescent angiography is typical petal-like or honeycomb-like leakage, and the cystic edema subsides. Very slow, ranging from a few months to a year, individual can not be absorbed for 2 years, the degree of cystic edema is different and the prognosis of vision is also inconsistent. Most of the temporary edema can return to more than 0.5, long-term edema In 14% of patients, the visual acuity can reach or exceed 0.5. After several years, the macular vesicles flatten and appear dark red petal-like pattern, or have pigment and fiber proliferation, or form cystic scars, which seriously affect central vision.
2. Neovascular and neovascular glaucoma
Neovascularization is one of the most common complications of retinal vein occlusion, which often leads to repeated bleeding of the vitreous and severely impaired vision. The earliest time of neovascularization is 3 months after onset, and the incidence increases with the course of the disease. New blood vessels occur in On the retina and optic disc, the total number of neovascularization caused by total dry obstruction is generally less than that of the branch obstruction. This is because neovascularization has occurred in the retina after the total dry ischemic obstruction has not produced more retinal neovascularization. The upper total obstruction was 7.7%, the branch obstruction was 24.1%, the hemi-lateral obstruction was 41.9%, the neovascularization was located in the optic disc, the total dryness was 5.1%, the branch was 11.5%, and the half was 29%. New blood vessels often occurred in The edge of the non-perfused area, or the retina on the optic disc or the optic disc near the ischemic area, the shape of which is initially spore-like, gradually growing into a wire mesh, a wreath or a sea fan: the fluorescent angiography has a large amount of fluorescence There is a close relationship between the neovascularization and the size of the retina without perfusion. If there is no perfusion area above 5~7PD, new blood vessels can be produced, and there is no perfusion area. The larger the infection, the greater the possibility of new blood vessels, the incidence of the authors reported a large difference, generally about 20%, reported total dry obstruction occurred in glaucoma 33.3%, half-sided obstruction was 3.2%, branching Neovascular glaucoma rarely occurs in occlusion. Neovascular glaucoma usually occurs in the total dry obstructive ischemic eye. It usually occurs in the second to third months after obstruction. It is also known as Baiguang Glaucoma. It is characterized by New blood vessels appear in the iris, gradually expanding to the anterior chamber angle, new blood vessels grow into the trabecular meshwork to block the angle of the anterior chamber, leading to adhesions around the iris, headache, eye swelling and other symptoms, conjunctival vasodilatation and congestion, corneal edema, iris pupillary margin Pigment epithelial eversion, pupil dilation, early when the cornea has not edema, fluorescein angiography can show complete occlusion of the capillaries from the peripheral to the posterior pole, even large arteries and veins are completely occluded, only the optic disc and its vicinity Fluorescence of blood vessels and neovascularization, once this complication occurs, the prognosis is extremely poor, drugs and surgery are difficult to work, and most patients have complete loss of vision.
Neovascular glaucoma is the most serious complication of this disease, and the incidence rate of the authors is relatively large. The data reported since 1974 is 4% to 29%, generally around 20%. It is reported that glaucoma occurs in total dry obstruction. 33.3%, partial obstruction is 3.2%, branch obstruction does not occur neovascular glaucoma; neovascular glaucoma usually occurs in the total dry obstructive ischemic eye, usually 2 to 3 months after the onset, so In the past, it was also called 100-day glaucoma. It was also reported to be caused by 2 weeks or years. It is characterized by the first appearance of new blood vessels in the iris, which gradually spread to the anterior chamber, and the new blood vessels grow into the trabecular meshwork, blocking the angle of the anterior chamber. The anterior adhesion of the iris, the angle of the anterior chamber, the increase of intraocular pressure and the symptoms of headache and eye swelling, conjunctival vasodilatation and hyperemia, corneal edema, iris pigmentation epithelial eversion, pupil dilation, early when the cornea has not edema, fluorescence Contrast can show complete occlusion of the capillaries from the peripheral to the posterior pole of the retina, even large arteries and veins are completely occluded, only the optic disc and its nearby macrovessels and neovascularization Filling, once this complication occurs, the prognosis is extremely poor, both drugs and surgery are difficult to work, and most patients have complete loss of vision.
Symptom
Retinal vein occlusion symptoms Common symptoms Spotted hemorrhagic macular cystic edema Vision defect Retinal hemorrhage Retinal edema Fundus changes in the fundus point or flaming hemorrhage retinal detachment
The main symptoms are central vision loss, or a partial visual field defect, but the incidence is far less acute and severe than arterial occlusion. Generally, part of the visual acuity can be retained. About 3 to 4 months after central venous obstruction, about 5 to 20% of patients can Iris neovascularization occurs and secondary to neovascular glaucoma.
1. Central retinal vein occlusion
Divided into 2 types:
(1) Light type: also known as nonischemic, hyperpermeable or partial obstruction, mild or total asymptomatic symptoms, depending on the degree of macular damage, normal or mild vision Decreased, normal or slight visual field, fundus examination: early: normal optic disc or mildly blurred border, edema, normal or mild edema in the macular area, hemorrhage, normal arterial diameter, varicose veins dilated, 4 along the retina There are small or moderate flaming and punctiform bleeding in the vein, no or occasional cotton-like plaques, mild edema in the retina, normal or slightly prolonged retinal circulation time of the fluorescein angiography, mild fluorescein leakage in the venous wall, capillaries Mild dilatation and a small amount of microangioma formation, normal or mild fluorescein leakage of the macula; late: retinal hemorrhage gradually absorbed after 3 to 6 months, and finally disappeared completely, the macular area returned to normal or mild pigmentation disorder In a small number of patients, the macula is dark red cystic edema, fluorescent angiography is petal-like fluorescein leakage, and finally a cystic scar is formed, which can cause vision loss. The optic disc has ciliary retinal vascular collateral formation, the shape is lobular or wreath-like, venous stasis dilatation is reduced or fully recovered, but there is a white sheath accompanied, no or occasional small non-perfusion area, no neovascularization, visual recovery or normal Mild decline, some patients with mild central retinal vein occlusion can worsen the disease and become a severe ischemic venous obstruction.
(2) Heavy: Also known as ischemic, hemorrhagic or complete obstruction.
1 Early: Most patients have blurred vision, visual acuity is significantly reduced, severe visual acuity reduced to manual, combined with arterial obstruction can be reduced to only light perception, there may be dense central dark spot visual field defect or peripheral narrowing, fundus examination It can be seen that the optic disc is highly edematous and hyperemia, the boundary is blurred and can be covered by hemorrhage. The macular area may have obvious edema and hemorrhage. It may be diffuse edema or cystic edema. The cystoid edema of the macula is vesicular, arranged in a petal shape or in a hive. In the same way, there may be bleeding in the sac, forming a semilunar or semi-circular liquid level, the arterial diameter is normal or thin, the vein is highly dilated and distort like a sausage, or in a retina that is undulating in the edema, due to hypoxia The venous blood column is dark red. In severe cases, the blood flow is stagnant, and the red blood cells accumulate in the blood vessels, showing granular blood flow. The severe retinal edema is especially obvious in the posterior part. A large number of punctate punctiform hemorrhages are distributed along the veins. Throughout the fundus, the bleeding from the superficial capillary layer is flaming, and the bleeding from the deep vascular layer is punctate or plaque-like, and the severe surrounding is formed by the optic disc. Petal-like hemorrhage, even into the inner limiting membrane caused by scapular retinal hemorrhage, the heavier ones pierced the inner limiting membrane into vitreous hemorrhage, the retina often has cotton-like plaques, which increase with the severity of the disease, this cotton-like plaque is Because acute anterior capillaries occlusion inhibits the axoplasmic transport of the nerve fiber layer, the b-wave of the electroretinogram is reduced or extinguished, the dark adaptation function is reduced, the retinal circulation time of the fluorescein angiography is prolonged, and the occasional arm-retinal circulation time is prolonged. The optic disc vasodilation, fluorescein leakage exceeds the disc boundary, because the large piece of bleeding masks the capillary bed to form a non-fluorescent area, from the gap can be seen a large amount of fluorescein leakage in the venous wall, the capillaries are highly distorted and expanded A large number of microangioma, the macula is a bit or diffuse fluorescein leakage, if there is cystic edema, it forms petal-like or cellular fluorescein leakage.
2 late: generally enters the late stage after 6 to 12 months of onset, the optic disc edema subsides, the color returns to normal or fades, and the ciliary retinal collateral vessels often form on the surface or the edge, which is annular or spiral, relatively coarse. Or neovascularization, in the form of a filament or a flower ring, relatively narrow, some can protrude into the vitreous, floating in the fundus, macular edema subsided, pigmentation disorder, or petal-like dark red spots, suggesting that there have been yellow spots in the past Cystic edema, severe retinal gliosis, fibroblast aggregation to form a secondary retinal membrane, or pigmented scar formation, severe visual impairment, arterial diameter mostly thin and white sheath, and some Complete occlusion is silver-like, irregular vein diameter, and some narrow with white sheath, especially those caused by inflammation, retinal hemorrhage and cotton-like plaque absorption, or left with hard exudation, slow absorption, generally Complete absorption in 1 year or several years, capillary occlusion, even small arteries and venules are occluded, forming large unperfused areas, and some optic discs and retinas have neovascularization, which can lead Caused by vitreous hemorrhage, fiber proliferation, traction retinal detachment, and some may develop neovascular glaucoma. Fluorescence angiography shows that the optic disc has large collateral or neovascularization, the latter has a large amount of fluorescein leakage, and the macular can be normal or residual. Point-like leakage or petal-like leakage, or in the form of punctate or flaky fluorescence, the diameter of the arterial tube becomes thinner, the venous wall is substantially leak-free or has limited leakage, and the capillary occlusion forms a large unperfused area. Starting from the peripheral part of the retina, it is an island shape. It can be connected into a sheet shape later, and it can be carried out to the equator or even around the optic disc. There are often arteriovenous short circuits near the perfusion area, microangioma and/or neovascularization. The early intraocular pressure of this disease is normal, and the late stage can be increased sharply if combined with neovascular glaucoma.
2. Hemi-central retinal vein occlusion (hemi-central retinal vein occlusion) During the development of retinal blood vessels, the vitreous artery enters the optic cup through the embryonic fissure. When the embryo is 3 months, two veins appear on both sides of the artery into the optic nerve. Humans meet each other in the optic nerve behind the optic disc to form the central retinal vein, usually one of them disappears after birth, leaving one trunk, but some people can be left behind to form two vein trunks, half-sided obstruction is A trunk forms a blockage at the sieve plate or in the optic nerve. This type of obstruction is relatively rare in the clinic. The incidence rate is 6% to 13%. Usually, 1/2 of the retina is involved, and even 1/3 or 2/3 of the retina is involved. Its clinical manifestations, duration and prognosis are similar to central retinal vein occlusion. Newer vascular glaucoma can also be produced if there is a large unperfused area.
3. Branch retinal vein occlusion Branch branch vein occlusion is most commonly affected by iliac crest, accounting for 90% to 93%, of which the upper sacral occlusion is the most common, accounting for 62% to 72%, nasal collateral branch There is very little occlusion, the incidence rate is 1.5% to 3.0%, and the macular small branch obstruction is better than the main branch obstruction because the small area of the macular branch is small and the capillary layer is thick, and the possibility of producing a non-perfusion area is small, even if The area of production is also small, so the possibility of causing late complications of new blood vessels is small. In contrast, trunk obstruction has more complications.
(1) Early stage: The condition of vision loss is different according to the compression point located in the trunk or small branch. The blockage is located in the trunk and the macular branch. The visual acuity is reduced to some extent. The branch without the macula is blocked. The visual acuity is not affected. The changes corresponding to the damaged area of the retina, the fundus examination, the retinal artery often becomes thin and hardened, and the obstruction point is at the intersection of the arteries and veins. The vein is often located under the artery, and the compression tube diameter of the hardened artery becomes thin and pen-like. Even the venous blood flow is not visible. If the vein is located above the artery, it will travel on the surface of the artery as a bridge, the diameter of the tube will be narrow or irregular, and sometimes there will be white fibrous tissue hyperplasia such as spun yarn or film. The arteries and veins are wrapped in the film, but the diameter of the venous pressure tube becomes thinner and even unrecognizable. The distal end of the occlusion point is distorted and dilated like a sausage, and the fan-shaped retinal shallow layer and deep layer of hemorrhage appear along the vein. Pre-retinal hemorrhage or vitreous hemorrhage, retinal edema thickening, visible cotton-like plaques, such as macular edema invading the macula, and Hemorrhage masking, can also produce cystoid edema of the macula, normal retina in the optic disc and other places, fluorescent angiography can see the delayed filling of the affected vein, the vein at the obstruction point is pen-like or completely broken, no fluorescent blood flow, late angiography The venous vein can present a strong fluorescent spot, indicating that the vascular endothelial cells are damaged, the distal vein of the obstruction point is dilated, the fluorescein leaks in the wall, the capillary vasoconstriction forms a microangioma, accompanied by leakage, and the retinal hemorrhage can cover up the fluorescence. The macular arch ring can be partially broken, and a little fluorescein leakage. If there is cystoid macular edema, incomplete petal-like strong fluorescence is formed.
(2) Late stage: usually after 6 months of onset of bleeding, the edema gradually subsides, the edema subsides, the erythematous or irregular shape of the optic disc macular area appears or the annular exudation of the macula tendon side, this exudation absorption Slower, macular edema subsides, leaving pigmentation disorder or cystic degeneration scar, accompanied by arterial secondary sclerosis, narrowing of the tube diameter with white sheath, occasionally small artery occlusion is silvery, the affected vein diameter is restored or Unevenness in thickness, complete recovery of blood flow in the obstruction, partial recovery, or complete occlusion in the form of silver filaments, white sheath in the wall of the vein, occlusion of small veins, formation of lateral branches near the obstruction point and horizontal seam of the retina, Large capillaries can occur in the optic disc and retinal neovascularization. After 1 year or several years, vitreous hemorrhage can occur suddenly. Fluorescence angiography shows that the affected vein is filled with normal or delayed fluorescence, and the wall is generally free of leakage or occasional Limit leakage, venous thinning or no fluorescein in the obstruction, collateral vessels often form in the vicinity and horizontal seams, and there are two collateral formation pathways, namely obstructive branches and adjacent unobstructed veins. The lateral branch, or the obstructed vein itself, forms a lateral branch in the obstructed and non-obstructed segments. The severe trunk obstruction may have a large unperfused area extending from the peripheral portion to the equatorial portion or even the posterior pole. This case is often There are new blood vessels at the edge of the optic disc and/or non-perfusion area, which are in the form of a filament, a wreath or a sea fan. In the late stage, there is a large amount of fluorescein leakage, and there is often an arteriovenous short circuit near the non-perfusion area.
According to the typical fundus changes, the diagnosis can be determined by combining the results of FFA examination and clinical manifestations.
Examine
Retinal vein occlusion examination
Fluorescence angiography of central venous obstruction is:
1 A large amount of bleeding in the retina, so that the choroid and retinal fluorescence are blocked.
2 There was no perfusion area and no capillary perfusion area.
3 deep edema of the macula.
4 The vein wall is stained or slightly leaked.
5 neovascularization and fluorescein leakage.
6 Radial capillaries compensatory expansion around the optic disc.
Electroretinogram: normal at the onset of the disease. If the blockage cannot be eliminated, the b wave in the ERG gradually decreases to form a negative wave pattern. If the amplitude is smaller, the prognosis is poor.
Blood rheology examination can understand plasma viscosity and whole blood viscosity, and can determine the content of -coagulin and platelet factor IV.
FFA fluorescein findings are also different due to obstruction (total dry, half, branch), degree of obstruction (completeness, incompleteness), and the course of the disease.
Total dry obstruction at the beginning of the course of the disease, early in the angiography due to a large number of hemorrhagic lesions in the retina, so that the choroid and retinal fluorescence are blocked, in the unobstructed, visible slow filling movements, veins (the transition time of the arterio-venous is prolonged, often exceeds 20s); in the late stage of angiography, the venous wall and its adjacent tissues are stained with diffuse strong fluorescence. When fluorescein reaches the capillaries around the macula, if there is no bleeding covering it, there will be obvious fluorescein leakage and gradually enter. And stay in the tiny cystic space, in the late stage of the disease, due to the retinal capillary bed ischemia, there is no perfusion area, no residual capillary around the perfusion area is tumor-like expansion, collateral circulation and new life of various abnormal pathways The blood vessels can appear in any part of the fundus, but the most common in the optic disc surface, the new blood vessels on the optic disc surface can sometimes enter the vitreous body. If the rupture can lead to vitreous hemorrhage, the neovascularization can be differentiated from the collateral circulation due to obvious leakage.
The total dryness is not completely blocked at the beginning of the disease course. In the early stage of FFA, due to the small amount of bleeding, the fluorescence shielding is small, the transition time of the arteriovenous vein is not obvious, the venous wall leakage and the subsequent appearance of the wall and its surrounding tissue staining, It is also lighter than complete obstruction. If the lesion involves the macula and there is no effective collateral circulation, a petal-like strong fluorescent area (cystic edema) appears due to capillary leakage around the fovea, and the capillary loop around the fovea is destroyed. Leakage, no perfusion area and neovascularization are generally absent in the late course of the disease.
The extent of the half-side obstruction and branch-blocking FFA is limited to the drainage area or the drainage area of the branch. In addition, in some cases of branch obstruction, the tube diameter of the branch can be seen at the initial stage of the disease, and the upper end of the branch is limited. Strong fluorescence.
Diagnosis
Diagnosis and differentiation of retinal vein occlusion
diagnosis:
Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.
Differential diagnosis:
According to the characteristics of the fundus of retinal vein occlusion, such as hypertensive venous dilatation and venous hemorrhage and fluorescein angiography, the diagnosis is not difficult, but must be differentiated from the following fundus diseases:
1. Venous stasis retinopathy: due to occlusion or stenosis of the internal carotid artery, the central retinal artery perfusion is reduced, resulting in a decrease in central venous pressure, venous dilatation, markedly slower blood flow, and a small amount of bleeding visible in the fundus. There are small hemangioma and neovascularization, and it is not difficult to distinguish from retinal vein occlusion. The latter has increased venous pressure, the vein is highly distorted and dilated, and the retinal hemorrhage is more and the symptoms are heavier.
2. Diabetic retinopathy: generally bilateral, retinal vein dilatation, but not too severe, and retinal venous pressure is not increased, bleeding is scattered, not as much as venous obstruction, often have hard exudation, elevated blood sugar, systemic symptoms Can be identified, but diabetic patients are also prone to retinal vein occlusion, diabetics are prone to retinal vein occlusion, should be taken seriously.
3. Hypertensive retinopathy: the lesion is often bilaterally symmetrical, retinal hemorrhage is superficially sparse, mostly located in the posterior pole, although the vein is dilated but not distorted and dark, common cotton-like plaques and macular smear-like exudation, and retinal veins Obstructive patients often have high blood pressure, mostly monocular onset, high varicose veins, and more retinal hemorrhage.
