Central retinal artery occlusion usually presents as painless monocular vision loss.
Central retinal artery occlusion (CRAO) is an ophthalmic emergency because irreversible ischemic damage to the retina can occur in as little as 90 minutes.
The central retinal artery and its branches perfuse the inner retina.
Commonly caused by embolism of the retinal artery.
Patients may present with sudden, painless decreased vision in one eye over a matter of seconds, with an afferent pupillary defect.
Central retinal artery occlusion incidence estimated 1-2 per hundred thousand people per year.
It is considered an ocular stroke and the risk of ischemic stroke with large vessel involvement is particularly increased in the first one to four weeks after a diagnosis of a CRAO.
Emboli can travel to the most distal branches of the retinal artery with partial loss of the visual field.
It may be partial vision loss if one of the smaller distal branches are affected.
Sources of retinal emboli include cholesterol plaque associated with atherosclerosis, platelet fibrin emboli associated with cardioembolism or disorders of arterial hypercoagulability, and calcific plaque associated with cardiac valvular disease.
Ophthalmologic emergency.
Visual acuity in affected eye can occur with 80% of patients having a final visual acuity of 20/400 or worse.
Any delay in treatment can result in permanent visual loss.
Immediate treatment improves chances of retaining vision but only 21-35% of individuals maintain adequate vision.
Harbinger of other systemic processes.
Associated with an increased risk of stroke.
Symptomatic stroke, TIA or amarorosis fugax, is common around the time of a central retinal arterial occlusion and requires urgent embolic work up.
Patients may have experienced intermittent transient, painless vision loss.
The retina is supplied with blood flow from the ophthalmic artery which is the first intracranial branch of the internal carotid artery.
The central retinal artery supplies the retina.
The ciliary arteries supply the choroid and the anterior globe.
Fundoscopic exam reveals a pale retina and a red macula.
May be due to embolism, atherosclerosis changes, inflammation, angiospasm or hydrostatic occlusion.
Complete occlusion is rare.
Central retinal artery affected 57% of cases, the branch retinal artery 38% of cases and the cilioretinal artery in 5% of obstructions.
Occlusion of the central retinal artery is characterized by diffuse retinal whitening with a macular cherry red spot.
Branch retinal artery occlusion affects the region of the retina and causes the inner layers of the retina which are normally transparent to become edematous and semiopaque obscuring the pigment epithelium and causing a whitening visible on funduscopic examination.
Risk factors for CRAO include cigarette smoking, hypertension, high body mass index, high serum lipid levels, diabetes, cardiac disease, hypercoagulable conditions such as antiphospholipid antibody syndrome and autoimmune conditions.
Clinically blanched, non perfused retina, and a cherry red spot due to bright red appearance of the fovea on fundoscopic examination may be apparent.
Fundoscopy usually show signs of acute ischemia, including retinal pallor a cherry, red spot, segmented blood flow, and attenuated, retinal arteries, although the fundus may appear normal.
In the acute phase optical coherence tomography usually shows inner retinal, hyperreflexivity and thickening.
Central retinal artery occlusion is typically caused by embolism from a carotid plaque or a cardiac thrombus, but can result from any type of ischemic event.
A boxcar pattern can be seen in the retinal arteries and veins due to segmented blood flow.
No proven therapy exists for retinal artery occlusion.
Digital massage to dislodge the clot to a distal branch and reduce ischemia, anterior chamber paracentesis, and carbogen inhalation have been suggested, all with poor visual outcomes.
Therapy with full dose aspirin and evaluation with carotid imaging and neurological workup, MRI of the brain, echocardiography, Holter monitoring should be performed.
Giant cell arthritis should be ruled out.
Patients should have diet alterations, smoking cessation, and initiation of statin therapy in the case of dyslipidemia.
Intravenous tenecteplase administered within 4.5 hours after onset of central retinal artery occlusion does not result in significantly greater vision recovery at 30 days than oral aspirin, but is associated with the significant serious safety concerns: unlike the management of acute ischemic stroke findings do not suggest the routine use of thrombolytic therapy to treat central retinal artery occlusion.