The etiology of central retinal vein obstruction differs greatly between the elderly and the young adults, with the majority of the former secondary to retinal arteriosclerosis and the latter mostly to inflammation of the vein itself. Retinal arteriosclerosis is commonly caused by chronic progressive hypertension or arteriosclerosis; venous inflammation can be caused by perivenous inflammation (Eales disease), uveitis, Behcet syndrome, nodular disease, Coats disease, septic emboli, etc., but it is not uncommon to find no clear clinical cause. The pathogenesis of this disease is complex and is not fully understood. Most authors believe that it is caused by a combination of factors including inadequate arterial blood supply, venous wall damage, altered blood tear rheology, and altered hemodynamics. Among them, venous wall damage may be the main one. 1.Inadequate arterial blood supply Hhayreh (1965,1971) pointed out that the occurrence of central retinal vein obstruction by arterial experiments is predicated on inadequate arterial blood supply. In the laboratory, if only one vein is blocked, it is not enough to cause the typical changes seen clinically, but only after the arterial supply is also impaired. Although this theory of Hayreh is supported by some clinical practitioners, direct evidence of venous obstruction due to inadequate arterial supply is still insufficient. For example, the disease does not show any arterial obstruction on fundus fluoroscopic angiography. The retinal blood circulation is in a relatively closed vascular circuit (clsedvascularcircuit) (Gass, 1968), and the reduction of arterial blood flow during venous obstruction may simply be a reflection of the obstruction of venous blood return, rather than the cause of venous obstruction. 2, venous wall damage Two causes, one is by its neighboring atherosclerosis of the wave; the second is the inflammation of the vein itself. Both of them can lead to thickening of the wall and narrowing of the lumen. Sclerosis can also proliferate endothelial and subendothelial cells, and inflammation can cause endothelial swelling. Cell proliferation and endothelial swelling increase the degree of luminal narrowing, and in addition to severe occlusion due to direct endothelial to endothelial contact, the endothelial surface may become rough and the charge may change, inducing platelet deposition and coagulation to form thrombi, leading to incomplete or complete obstruction of the venous lumen. It is well known that central retinal vein trunk obstruction occurs at the point where the vein crosses the sieve plate, and branch obstruction occurs at the intersection of the arteries and veins. It is possible that because of this location, the arterioles are surrounded by a common connective tissue sheath (Scherer, 1923), which is not easily stretched once the venous lumen has been narrowed for these reasons. 3, blood rheology and hemodynamic changes Most patients with this disease have blood composition changes, blood viscosity changes and increased platelet coagulation, making it more difficult for blood to pass through the venous stenosis and easier for thrombosis to occur. In addition to these causes, venous obstruction, especially of the common venous trunk, is associated with high intraocular pressure. According to statistics, this disease is combined with primary open-angle glaucoma in 10%-20% of patients. The reasons for this are: (1) most patients with open-angle glaucoma have increased blood viscosity; (2) pathological depression of the scleral sieve plate, which may affect central arterial perfusion and venous return in the sieve plate area. Others, such as cardiac compensatory insufficiency, bradycardia, and sudden decrease in blood pressure that leads to slow blood flow, may accelerate the formation of obstruction. The series of ocular signs that appear in central retinal vein obstruction are secondary to the disturbance of retinal blood circulation after the obstruction. For example, retinal hemorrhage is caused by local hyperfunction of fibrinolysis due to impaired venous blood return, vessel wall fragility, and stagnant blood flow; venous tortuosity and dark purple color of blood columns are caused by obstruction of blood return; cotton-wool white spots are caused by ischemia of the inner capillary bed; and yellow-white hard exudate is caused by deposition of lipid substances in the blood. In addition, the retinal edema clouding, neovascularization, vascular short circuit, collateral circulation, capillary shuttle expansion, macular septum-like edema and iris and the emergence of dense neovascularization (iris redness), etc., are all related to this.