central retinal vein occlusion
Introduction
Introduction to central retinal vein occlusion The obstruction of the central retinal vein (obstruction of the central retinal vein) is much more common than the central retinal artery occlusion. The visual function damage is not as sharp as the arterial occlusion, but it is also quite serious. Some cases may be completely blind due to secondary angiogenic glaucoma. It is a common fundus disease, which is a common symptom of various etiologies. Most patients cannot recover their vision, especially in ischemic patients, and the prognosis is poor. Since the 1970s, photocoagulation for this disease can reduce bleeding, edema, and reduce complications. The cause of this disease, the elderly and young adults are very different, the former is mostly secondary to retinal arteriosclerosis, the latter is mostly inflammation of the vein itself, retinal arteriosclerosis is common in chronic progressive hypertension or arteries Sclerotherapy; venous inflammation can be caused by perivenous inflammation (Eales disease), uveal inflammation, Behcet syndrome, sarcoidosis, Coats disease, septic embolism, etc., but it is not uncommon for patients to find a clear cause. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: cystoid macular edema
Cause
Cause of central retinal vein occlusion
The cause of this disease, the elderly and young adults are very different, the former is mostly secondary to retinal arteriosclerosis, the latter is mostly inflammation of the vein itself, retinal arteriosclerosis is common in chronic progressive hypertension or arteries Sclerotherapy; venous inflammation can be caused by perivenous inflammation (Eales disease), uveal inflammation, Behcet syndrome, sarcoidosis, Coats disease, septic embolism, etc., but it is not uncommon for patients to find a clear cause.
The pathogenesis of this disease is complex and is not fully understood. Most authors believe that the vascular wall damage is caused by various factors such as insufficient arterial blood supply, venous wall damage, blood and tear rheology changes and hemodynamic changes. May be the main one.
Insufficient arterial blood supply (30%):
Hhayreh (1965, 1971) pointed out that the occurrence of central venous occlusion of the retina is predicated on insufficient blood supply to the arteries. In the laboratory, if only a certain vein is blocked, it is not enough to cause typical changes seen in the clinic, only the arteries. The blood supply can also be formed after the disorder, although the theory of Hayreh is also supported by some clinicians, but so far, the direct evidence of venous obstruction caused by insufficient arterial blood supply is still insufficient. For example, the disease is in the fundus fluorescent blood vessels. No arterial occlusion can be seen on the angiogram. The retinal blood circulation is in a relatively closed clsed vascular circuit (Gass, 1968). Arterial blood flow is reduced during venous obstruction, possibly only venous return. A reflection, not the cause of venous obstruction.
Venous wall damage (25%):
There are two reasons for the damage of the venous wall. One is the atherosclerosis of the adjacent artery. The second is the inflammation of the vein itself. The second production can lead to thickening of the wall, narrowing of the lumen, and hardening can also make the intima and inner Under-membrane cell proliferation, inflammation can make the intimal swelling, cell proliferation and intimal swelling more serious the degree of stenosis, except in severe cases due to intimal contact with the intimal contact directly, but also due to the endometrial surface Rough, altered charge, induces platelet deposition, agglomeration and thrombosis, resulting in incomplete or complete occlusion of the venous lumen. It is well known that the central venous total occlusion of the retina is usually caused by the vein passing through the sieve plate. The branch obstruction is better than the movement and the intersection of the veins. It may be planted here. The arteries and veins are surrounded by a common connective tissue sheath (Scherer, 1923). ) It is not easy to stretch once the venous lumen has been narrowed for the reasons described above.
Blood viscosity change (15%):
Hemorheology and hemodynamic changes Most patients with this disease have changes in blood composition, changes in blood viscosity and increased platelet aggregation, making blood more difficult through venous stenosis and thrombosis more likely.
In addition to the above reasons, venous obstruction, especially total venous obstruction, has a certain relationship with high intraocular pressure. According to statistics, this disease is combined with primary open angle glaucoma patients by 10% to 20%, the reason is 1 open angle Most patients with glaucoma have increased blood viscosity; 2 pathological depression of scleral sieve plate may affect central arterial perfusion and venous return in the sieve plate area, other factors such as cardiac compensatory insufficiency, bradycardia, sudden drop in blood pressure, etc., resulting in slow blood flow. Can accelerate the formation of the blockage.
A series of ocular signs of central retinal vein occlusion are secondary to retinal blood circulation disorder after obstruction. For example, retinal hemorrhage is caused by venous return disorder, blood vessel wall fragility and blood flow stagnation cause localized fibrinolysis. Caused by; venous anger and distorted, blood column dark purple caused by blood reflux obstruction; cotton velvet leukoplakia caused by ischemia of the inner capillary bed; yellow-white hard exudation caused by lipids in the blood, In addition, retinal edema turbidity, neovascularization, vascular short circuit, collateral circulation, capillary fusiform expansion, macular septal edema and iris and thick neovascularization (iris red), etc., are all related to this.
Prevention
Central retinal vein occlusion prevention
1. Avoid excessive visual fatigue. Use your eyes to feel tired and pay attention to the correct eye position, distance, light source and so on. Use an eye for about an hour, let your eyes relax, such as closing your eyes, walking, looking at the sky or in the distance, so that your eyes can rest. Try not to read and work in a dimly lit environment for a long time.
2, adhere to regular eye massage. You can do eye exercises for eye acupressure, such as massage Qingming, Hengzhu, scorpion bone, sun, medical wind and other acupuncture points. Through massage, it can accelerate blood circulation in the eye, increase the immune factor in the aqueous humor, and improve the immunity of the eyeball itself.
Complication
Central retinal vein occlusion Complications cystoid edema
There are many complications, which can be divided into two categories, one is the macular complication and sequelae, including cystoid macular edema-macular membrane formation, and the second category is cardiovascular and its complications.
Symptom
Symptoms of central retinal vein occlusion common symptoms retinal hemorrhage changes the retinal edema of the eye
There are many classification methods in the literature: 1 According to the cause of obstruction, it can be divided into two types: sclerosing and inflammatory; 2 according to the obstruction, it can be divided into three main types, branch and half side; 3 can be divided into complete and not according to the degree of obstruction. Complete two; 4 according to the presence or absence of arterial insufficiency can be divided into non-ischemic (stagnation) and ischemic (hemorrhagic) (Hayreh), but this classification, some scholars disagree, think The so-called non-ischemic and ischemic obstruction is incomplete and complete obstruction.
1, visual impairment
Depending on whether the degree of obstruction affects the macular area, the macular spot is affected, and the central vision suddenly drops or falls within a few days, and small vision and variable vision appear. In severe cases, only the pre-expo index or manual, when the vein is blocked, still When a certain visual acuity is maintained, the peripheral visual field is often shadowed or has an irregular centripetality corresponding to the obstructed area; the central visual field often has a central or central dark spot due to damage to the macula and its vicinity.
2, see the bottom of the eye
When the total dry obstruction, the fundus changes due to the disease course sooner or later, the degree of obstruction is different, the optic disc edema is turbid, the boundary disappears, the whole retinal edema is turbid, covered with linear, flaming, foxtail-like nerve fiber layers. Bleeding, sometimes seeing deep or irregular hemorrhage, irregular retinal vein distorted, partially covered by tissue edema and hemorrhage, and different segments, retinal artery appears to be narrow due to reflex contraction, in addition, special In the posterior pole, cotton leukoplakia, macular plaques or cystic edema are seen. The superficial and deep layers of retinal hemorrhage are capillaries. The venules or larger veins are not resistant to high pressure and rupture. Due to the local hyperactivity of fibrinolytic function, pre-retinal hemorrhage can be seen when the amount is large, and even the inner limiting membrane enters the vitreous to form vitreous hemorrhage, which makes the fundus opaque.
Branch obstruction, the most common branch of the iliac crest, followed by the branch of the underarm, and the collateral branch again. When the branch is blocked, the various fundus changes (bleeding, edema, exudation, diameter expansion, path distortion, etc.) are limited to the branch. Drainage area, but the upper or lower branch of the iliac crest can also affect the macula.
Most of the primary branches of the central retinal vein have formed a total venous trunk before entering the scleral sieve plate, but some of the congenital abnormalities are combined into the total trunk after a certain distance behind the sieve plate, so there is a presence in the posterior optic nerve of the ball. Two or more venous branches, hence the name dry, when one of them is blocked, it is called hemi-central vein obstruction.
The extent of lesions caused by hemi-lateral obstruction is greater than that of branch obstruction, accounting for 1/2 to 2/3 of the entire fundus, and the optic disc appears to have regional edema opacity consistent with the obstruction site.
Total dry, branch and hemi-vein occlusion can have different fundus changes due to the degree of obstruction. Incomplete obstruction, fundus volume, bleeding area, retinal edema opacity is less than complete obstruction and light, no or even See the cotton velvet plaque, the incidence of cystic edema of the macula is also much lower, after the venous obstruction of the venous circulation is gradually established, the blood circulation has a tendency to slowly recover spontaneously, about the aging, retinal edema, bleeding gradually disappears, venous diameter Restore the original width or uneven width, visible parallel white sheath or tubular white sheath, secondary sclerosis with the artery accompanying the obstruction vein, often seen microangioma, venous obstruction, edema and opacity, when the bleeding edema subsided, In addition to often residual pigmentation, sometimes due to atrophy of the inner retinal layer, there is a granular or mottled appearance, sometimes due to fibroblast proliferation, the formation of the optic disc or the formation of the anterior membrane of the retina, behind the retinal blood vessels, gray or slightly Yellow-white-like spots, which are formed by the sinking of the fingers, and are formed in a star-shaped shape. The margin of the plaque is semi-annular, usually occurs about 2 months after the onset of the occlusion. It is present at the same time as retinal hemorrhage and leeches, but it can remain for a long time after hemorrhage and edema disappear, even after several years. To.
Retinal hemorrhage, absorption of edema depends on the establishment of collateral circulation. The collateral circulation is derived from retinal telangiectasia. It is the shortest path connecting the obstructed blood vessel to the nearby open blood vessel, or the obstruction branch itself forms a channel between the obstructed segments. The flood discharge channel when the dam gate is closed, this collateral circulation starts at the beginning of the disease, but it is not easy to be found because it is covered by hemorrhage and edema. It can only be seen after hemorrhage and edema or disappearance, and it is twisted or spirally twisted. Dry obstruction, partial obstruction, or obstruction of branches near the optic disc, collateral circulation is common at the optic disc surface or at its edges.
The formation of the collateral circulation is effective and has a direct effect on the visual function. Especially when the macular is involved, if there is an early open collateral between the central fossa and the venous obstruction, the prognosis is better, even if it is due to the side. Hemorrhage and edema occur when the load is too heavy, but when hemorrhage, the edema can still recover useful vision. Conversely, if the retina has irreversible damage before the formation of the collateral, it will not help the vision.
In the case of complete obstruction, the inner capillary capillaries (including the pre-capillary micro-arteries, capillaries, and the posterior venules of the capillaries) are blocked by a large area of ischemic area, which is under the ophthalmoscope. See the foundation of the formation of cotton leukoplakia. At the end of the disease, the cotton velvet leukoplakia subsided, and there were reticulated or coiled neovascularization around the ischemic area. The neovascularization and collateral circulation were difficult to discriminate under the ophthalmoscope.
In the case of total dry or partial partial obstruction, iris neovascularization (iris redness) may occur in some cases. When the neovascularization extends to the anterior chamber angle and enters the trabecular meshwork to block the angle of the anterior chamber, it causes neovascular glaucoma.
3, fluorescent angiography
Fluorescence angiography also showed different manifestations due to obstruction (total dry, hemi-lateral, 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 is concealed, in the uncovered area, the filling of slow arteriovenous, late angiography, venous wall and its adjacent tissue Dyeing and diffuse strong fluorescence, when the fluorescence reaches the capillaries around the macula, if there is no hemorrhage, there will be obvious fluorescence leakage, and gradually enter, stay in the cystic space, late in the disease, due to the inner layer of the retina The capillary bed is inoculated with no perfusion area, and the remaining capillaries around the perfusion area are tumor-like dilatation. The collateral circulation and new blood vessels of various abnormal pathways can occur in any part of the fundus, but it is most common in the optic disc surface. New blood vessels on the surface of the optic disc can sometimes enter the vitreous body, and the neovascularization can be discriminated from the collateral circulation due to obvious fluorescence leakage.
In the early photos of fluorescein angiography in the early stage of total incomplete obstruction, the amount of bleeding was reduced, the area of fluorescence masking was correspondingly reduced, and the filling time of the venous and venous fluorescence was prolonged (especially in the arteries), and the venous wall leaked and subsequently appeared. The staining of the wall and the surrounding tissue are also lighter than the complete obstruction. The lesion involves the macula, and there is no effective collateral circulation. The capillary around the central fossa leaks and a petal-like strong fluorescence area (cystic edema) appears. The capillary arch ring around the central fossa is destroyed and leaks. In the late stage of the disease, no perfusion area and neovascularization are generally absent.
Semi-obstruction and branch obstruction fluorescein angiography, also because of the complete or incomplete obstruction, and the same performance in the early and late stages of total obstruction, but the scope is limited to the subdivision or the drainage area of the branch, in addition Some branches are obstructed. In the initial stage of the disease, the narrowing of the diameter at the obstruction point of the branch and the presence of localized strong fluorescence near the upper end can be seen.
Examine
Examination of central retinal vein occlusion
Eye examination
(1) Comprehensive eye examination.
(2) fundus fluorescein angiography.
(3) If CRVO can not be diagnosed, retinal arterial pressure measurement can help distinguish between CRVO and carotid artery disease.
2. Whole body examination
(1) Medical history: whether there is medical disease, medical treatment and history of eye disease.
(2) Blood pressure measurement.
(3) Blood test.
3. Laboratory inspection
Blood rheology examination can understand plasma viscosity and whole blood viscosity, and can determine the content of -coagulin and platelet factor IV.
4. Other auxiliary inspections
FFA fluorescein findings are also different due to obstruction (total dry, hemi-lateral, branch), degree of obstruction (complete incompleteness), and the course of the disease.
Diagnosis
Diagnosis and differentiation of central retinal vein occlusion
diagnosis
According to the typical fundus changes, the diagnosis can be determined by combining the results of FFA examination and clinical manifestations.
Differential diagnosis
1. Ocular Ischemic Syndrome: Ocular ischemic syndrome is a series of clinical syndromes of the brain and eyes caused by insufficient blood supply to the brain and eyes caused by chronic severe carotid artery occlusion or stenosis. Caused by chronic, severe carotid artery occlusion or obstruction of the ophthalmary artery.
2. Diabetic retinopathy: Diabetic retinopathy (DR) is the most important manifestation of diabetic microangiopathy. It is a fundus lesion with specific changes and is one of the serious syndromes of diabetes.
3. Radioactive retinopathy: The clinical variation of radioactive retinopathy is large, but the incidence is dose-related. The early clinical features of mild radioactive retinopathy can be seen in the small posterior nucleus of the eye, scattered small capillary occlusion lesions, irregular expansion of the capillaries around the lesion, severe radioactive retinopathy often occurs in remote radiotherapy without good When the eye is protected, there are extensive capillary atresia and retinal vascular abnormalities in the fundus, which can cause macular edema, exudation, and decreased vision.
