varicose retinal veins
Introduction
Introduction The retinal veins are stunned and reddish, and are often buried in edema or hemorrhagic plaques. If they are intermittent, they look like sausages. The artery is narrow and there is no pulsation when the eye is pressed. In the early stage, the retina can still show edema, and then the grayish white cotton blisters appear to be oozing. If mixed with the bleeding spots, a complex form of fundus changes can be formed. The late optic disc is in a state of secondary atrophy, and the veins and veins become thinner. Hemorrhage and exudate can be absorbed, leaving irregular pigmentation, and sometimes new blood vessels appear around the optic disc and affected veins.
Cause
Cause
The etiology of the vein is complex and is closely related to hypertension, arteriosclerosis, high blood viscosity and hemodynamic abnormalities.
Changes in the wall: Retinal arteriosclerosis accounts for a large proportion of the incidence of central retinal vein occlusion. The most common site of obstruction is at the intersection of the sieve plate and the arteriovenous vein. The retinal arteries are in close proximity at these two sites. The adjacent vessel wall has only one outer membrane and is covered by the same connective tissue membrane. When arteriosclerosis is limited by the hardened outer membrane, the vein is compressed, the lumen is narrowed, and the blood flow becomes slow, causing thrombosis of platelets, red blood cells, and fibrous proteins. In addition, the toxins produced by inflammation or inflammation of the retina itself can also thicken the venous wall, damage the intima, cause platelet aggregation, fiber protein, and changes in blood cell components to form a thrombus.
Changes in blood rheology: changes in blood composition, especially changes in viscoelasticity, are associated with the onset of retinal vein occlusion.
Changes in blood flow: Increased intraocular pressure has an effect on the essential pathogenesis. Because when the intraocular pressure rises, it first affects the central retinal artery perfusion in the sieve plate area and affects the venous return. The blood flow stagnates and forms a blood clot. Sudden decrease in blood pressure or increased blood viscosity caused by other lesions can also cause hemodynamic changes, slowing blood flow and promoting thrombosis.
Examine
an examination
Related inspection
Ultrasound examination of the eyeball and eyelid and CT examination of the temporal region
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.
Diagnosis
Differential diagnosis
According to the fundus features of retinal vein occlusion, such as hypertensive venous dilatation and venous hemorrhage and fluorescein angiography, diagnosis is not difficult. However, it must be identified with 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, a dilated vein, and a marked slowing of blood flow. A small amount of bleeding can be seen in the fundus, and small hemangiomas and neovascularization can be seen. It is not difficult to distinguish from retinal vein occlusion, the latter has increased venous pressure, the vein is highly distorted and dilated, the retinal hemorrhage is more, and the symptoms are heavier.
2. Diabetic retinopathy is generally bilateral, retinal vein dilatation is distorted, but not too serious, and retinal venous pressure is not increased, bleeding is scattered, not as much as venous obstruction, often with hard exudation, elevated blood sugar, systemic symptoms can be Identification, but diabetic patients are also prone to retinal vein occlusion. Diabetic patients are prone to retinal vein occlusion and should be taken seriously.
3. Hypertensive retinopathy lesions are often bilaterally symmetrical, retinal hemorrhage is superficially sparse, mostly located in the posterior pole, although the vein is dilated but not distorted. Common cotton-like spots and yellow spots are oozing. Patients with retinal vein occlusion often have high blood pressure, mostly monocular onset, hypertensive venous dilatation, and more retinal hemorrhage. 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.
