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Retinal artery occlusion
Last reviewed: 05.07.2025

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Causes of retinal artery occlusion
- Atherosclerotic thrombosis at the level of the lamina cribrosa remains the most common cause of central retinal artery occlusion (about 80% of cases).
- Carotid embolism originates from the bifurcation area of the common carotid artery. This is the most vulnerable part for atheromatous lesions and stenosis. Retinal embolism from carotid artery can be of the following types:
- cholesterol emboli (Hollenhorst plaques) - intermittent collections of small, bright gold and yellow-orange crystals that are usually located in the area of arteriolar bifurcations. They rarely cause significant obstruction of retinal arterioles and often remain asymptomatic;
- Fibrinous emboli are grayish, elongated particles, usually multiple, occasionally filling the entire lumen. They can cause transient ischemic attacks followed by amaurosis fugax and, less commonly, complete obstruction. Amaurosis fugax is characterized by
painless, transient, unilateral loss of vision, described as a "curtain in front of the eye," most often in a downward direction, less commonly vice versa. The loss of vision, which may be complete, usually lasts a few minutes. Recovery is also fairly rapid, but sometimes gradual. The frequency of attacks varies: from several times a day to once every few months. Attacks may be associated with ipsilateral cerebral TIA with manifestations on the contralateral side; - Calcified emboli may originate from atheromatous plaques in the ascending aorta or carotid arteries, or from calcified heart valves. They are usually single, white, dull, and often located near the optic disc. When located on the disc itself, they blend in with it and may not be noticed on examination. Calcified emboli are more dangerous than the previous two, as they can cause permanent occlusion of the central retinal arteries or one of its main branches.
- Cardiac embolism accounts for about 20% of retinal arteriolar occlusions and is associated with an increased risk of cerebrovascular disease. As the first branch of the internal carotid artery, the ophthalmic artery is easily penetrated by embolic material from the heart and carotid arteries. Emboli originating from the heart and its valves can be of 4 types:
- calcified from the aortic and mitral valves;
- vegetations (proliferation) of heart valves in bacterial endocarditis;
- thrombi from the left ventricle of the heart that arise after myocardial infarction (mural thrombi), mitral stenosis with atrial fibrillation or mitral valve prolapse;
- myxomatous material originating from atrial myxoma.
- Periarteritis associated with dermatomyositis, systemic lupus erythematosus, polyarteritis nodosa, Wegener's graius and Behcet's disease can sometimes cause occlusion of branches of the central retinal arteries, including several.
- Thrombophilias such as hyperhomocysteinemia, antiphospholipid syndrome, and inherited defects in natural anticoagulants may occasionally accompany central retinal artery obstruction in the young.
- Retinal migraine can very rarely be the cause of central retinal artery occlusion in young people. However, the diagnosis can only be made after excluding other, more common causes.
Branch retinal artery occlusion
Occlusion of the branches of the central retinal arteries is most often caused by embolism, less often by periarteritis.
Occlusion of the branches of the central retinal arteries manifests itself as a sudden and significant impairment of either half of the visual field or the corresponding sector. The deterioration of vision varies.
Fundus of the eye
- Retinal pallor in the area of ischemia due to edema.
- Narrowing of the arteries and veins with slowing and intermittent blood flow.
- Presence of one or more emboli.
Foveal angiography reveals delayed arterial filling and blurred background fluorescence due to retinal edema within the involved sector.
The prognosis is poor, although the obstruction resolves within a few hours. Visual field defects and thinning of the affected artery persist. However, sometimes after recanalization of the occluded artery, ophthalmoscopic signs may be barely noticeable or disappear altogether.
Central retinal artery occlusion
Central retinal artery occlusion is most often a consequence of atherosclerosis, but can also be caused by calcific embolism.
Central retinal artery occlusion is characterized by sudden, significant loss of vision. Visual impairment is significant except in cases where part of the papillomacular bundle is supplied by the cilioretinal artery and central vision is preserved. Afferent pupillary defect is severe or total (amaurotic pupil),
Fundus of the eye
- Thinning of the arteries and veins with slowing and intermittent blood flow.
- Significant retinal pallor.
- Around the thinned foveola there is an orange reflex from the intact choroid in contrast to the surrounding pale retina, which highlights the characteristic "cherry pit" symptom.
- In eyes with cilioretinal blood supply to the macular region, the color of the retina does not change.
Foveal angiography reveals delayed arterial filling and decreased background choroidal fluorescence due to retinal edema. However, filling of a patent cilioretinal artery is possible in the early phase.
The prognosis is unfavorable and is caused by retinal infarction. After a few weeks, the retinal pallor and the "cherry pit" symptom disappear, but the arterial thinning remains. The inner layers of the retina atrophy, gradual atrophy of the optic nerve occurs, leading to the final loss of residual vision. In some cases, rubeosis iridis may develop, requiring panretinal laser coagulation; in 2% of cases, neovascularization appears in the disc area.
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Cilioretinal artery occlusion
The cilioretinal artery is found in 20% of people, it originates from the posterior ciliary arteries and supplies the retina mainly in the area of the macula and papillomacular bundle.
Classification
- isolated often occurs in young people with concomitant systemic vasculitis;
- in combination with central retinal artery occlusion has a similar prognosis to non-ischemic central retinal vein occlusion;
- in combination with anterior ischemic neuropathy, it is more common in patients with giant cell arteritis and has an extremely unfavorable prognosis.
Occlusion of the cilioretinal artery is characterized by a sudden, significant loss of central vision.
- Fundus of the eye. Retinal pallor is localized according to the area of arterial perfusion.
- Foveal angiography reveals a corresponding filling defect.
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Treatment of acute retinal artery occlusion
Treatment of acute retinal artery occlusion must be prompt, as it causes irreversible vision loss despite restoration of retinal blood flow before retinal infarction develops. The visual prognosis is thought to be worse for occlusions caused by calcified emboli than by cholesterol or platelet emboli. Theoretically, if the latter two emboli disintegrate over time, vision loss can be avoided.
In this regard, various mechanical and pharmacological methods have been proposed, and a consistent, vigorous and systematic approach within 48 hours after acute retinal artery occlusion gives patients a good chance of restoring vision.
Urgent Care
- Massage the eyeball using a three-mirror contact lens for 10 seconds to restore pulsation in the central retinal artery, then a break for 5 seconds with a weakening of the blood flow (in case of occlusion of a branch of the central retinal artery). The goal is mechanical slowing and then rapid change of arterial blood flow.
- Sublingual isosorbide dinitrate 10 mg (vasodilator and resistance-lowering agent).
- Intraocular pressure reduction is achieved by administering acetazolamide 500 mg intravenously followed by intravenous administration of 20% mannitol (1 g/kg) or oral administration of 50% glycerol (1 g/kg).
Follow-up treatment
If emergency methods are unsuccessful and blood flow is not restored within 20 minutes, the following additional treatment is carried out.
- Anterior chamber paracentesis.
- Streptokinase intravenously 750,000 IU to destroy fibrinous emboli in combination with methylprednisolone 500 mg also intravenously to reduce the risk of developing allergies and bleeding in response to the administration of streptokinase.
- Retrobulbar injection of tolazoline 50 mg to reduce retrobulbar blood flow resistance.
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