The true pathogenesis of retinal artery obstruction is often difficult to determine. The main causative factors are changes in the vessel wall and thrombosis, vasospasm, various emboli and vascular compression. Most cases are associated with triggers such as migraine, abnormal blood viscosity, blood disorders and trauma. Arterial wall changes and thrombosis: Atherosclerosis, hypertension and other cardiovascular system diseases and systemic or local inflammatory vascular diseases such as temporal arteritis, thrombotic vasculitis, periarteritis nodosa, Behat disease, Eales disease, uveitis, etc.) can involve the central retinal artery, causing intimal hyperplasia or edema in this artery, narrowing the lumen and roughing the inner wall. When the gap is still one-third of the original lumen, there may be no clinical manifestation, but under the action of certain factors such as thrombosis, vasospasm, insufficient perfusion pressure or elevated intraocular pressure, the gap may suddenly close and develop. Arterial spasm: Arterial spasm caused by acute hypertension, renal hypertension, and arterial spasm caused by chronic progressive hypertension based on extensive sclerosis of small arteries throughout the body can involve the central retinal artery and cause transient obstruction of its trunk or branches. Embolism: This disease is rarely caused by emboli in the blood circulation. In cases where obstruction by emboli occurs, the emboli often originate from the heart valves and from redundant organisms detached from the inner wall of nearby large arteries. For example, the redundant organisms on the aortic valve and mitral valve in bacterial endocarditis, the plaque of atherosclerosis of large arteries and the thrombus in the aneurysm. Pathological examination of the emboli revealed the presence of calcium, cholesterol, neutral fat, and platelets. In addition, emboli containing air, fat, tumor fragments, pus clots, parasites and worm eggs have been reported in the literature. Before entering the optic nerve and the globe, the central retinal artery is a good site for embolism because of the narrowing of the scleral sieve plate at the level of the optic nerve sclerotomy. Vascular compression: The central retinal artery travels through several right-angle turns in the orbit and optic nerve, and its diameter becomes smaller when it passes through the scleral plate. These anatomical factors cause any increase in intraorbital pressure or intraocular pressure to cause vascular compression or stimulated spasm and obstruction. For example, increased intraocular pressure in patients with glaucoma, buried vitreous warts in the optic disc, scleral ring ligation, or orbital surgical trauma, or excessive electrocoagulation for hemostasis, postbulbar tumor compression, or traumatic postbulbar hemorrhage. All of them can lead to orbital pressure or increased intraocular pressure resulting in arterial obstruction. Therefore, central retinal artery obstruction is often multifactorial, i.e., it is a combination of vascular pathology and embolism or other causative factors.