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Central Retinal Artery Occlusion

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Title: Central Retinal Artery Occlusion

Author: Justine Cheng, 4th Year Medical Student, University of Iowa School of Medicine


Central Retinal Artery Occlusion (CRAO) is an obstruction of the blood supply to the retina and has been crudely termed a “stroke of the eye.”  It is typically from an embolic source and frequently causes significant vision loss.  Treatment is controversial and typically underwhelming but the work-up has important clinical significance given the increased risk for additional future vascular events such as a CRAO to the other eye or a cerebral vascular accident (CVA).  If an isolated, distal arteriole is obstructed than it is categorized as a branch retinal artery occlusion rather than a CRAO.


The central retinal artery, which is a branch of the ophthalmic artery (OA), serves as the blood supply for the inner retina. The outer retina is supplied by the choriocapillaris of the choroid. Acute occlusion of the central retinal artery deprives nutrients and oxygen to the inner retina, which if prolonged causes irreversible ischemic damage. The exact timing of this irreversible ischemic damage is up for debate, but animal studies have shown that by four hours there is permanent nerve fiber damage. A subset of the population have a cilioretinal artery that supplies the retina between the fovea and optic nerve separate from the central retinal artery (Image A).  If patients have a cilioretinal artery, central vision occasionally may be spared.

Image A


Patients typically present with sudden, dramatic, painless vision loss in one eye—count fingers or worse.  The patient should have a relative afferent pupillary defect (RAPD) in the affected eye. There may be incomplete visual field defects which can be detected on confrontational visual field testing. There is generally a diffuse retinal whitening with a cherry-red spot in the macula (Image B and C), retinal arterial attenuation (Image B) and optic disc edema.  These findings are not always present immediately but develop within hours of the event.  Occasionally the emboli can be observed in the retinal arterioles as a small, yellow and refractile body indicating a cholesterol embolus, or Hollenhorst plaque (see photo). If the embolus is small and pale, it may indicate a fibrin platelet embolus.

Image B

Image C

Further Testing

Although CRAO can be diagnosed clinically, fluorescein angiography can provide additional insight. It shows delayed filling of retinal arteries and delayed arteriovenous transit time, and can differentiate a CRAO from a BRAO, characterizing the extent of ischemic damage.  Ocular Coherence Tomography (OCT) will show edema and thickening of the inner retina in the short term and atrophy of the outer retina in the long term.

If the patient is over 60, ask about giant cell arteritis symptoms such as jaw claudication, scalp tenderness, proximal muscle weakness and have a low threshold to order inflammatory markers (ESR/CRP).  If elevated start high dose steroids and schedule a superficial temporal artery biopsy to diagnose giant cell arteritis.  When a CRAO occurs as a result of this vasculitic disease it is termed an “arteritic,” accounting for only 4.5% of all CRAO cases (Varma et al, 2013).  All other causes are termed “non-arteritic.”

For non-arteritic etiologies, the most common cause of CRAO is emboli from carotid arteries, of which 74% of these emboli are cholesterol, 10.5% are calcific, and the rest are fibrin (Varma et al, 2013). When the offending emboli is a cholesterol plaque and is visible on exam this is termed a Hollenhorst plaque.  Ask about the patient’s atherosclerotic risk factors such as diabetes, hypertension, peripheral vascular disease and coronary artery disease and carefully look for a Hollenhorst plaque.  Consider ordering a carotid ultrasound duplex to look for treatable carotid stenosis.  Alert the primary care physician to readdress their vascular risk factors, including an echocardiogram and electrocardiogram.  If the patient is young and has a paucity of vascular risk factors, consider a coagulopathy such as factor V Leiden and order a corresponding laboratory work-up.


Treatment of CRAO is controversial and often unsuccessful.  Nonetheless, like treating stroke, time is vision and any attempt to improve the dramatic vision loss is worthwhile to the patient. Treatment modalities can be categorized into dislodging the emboli, improving oxygenation, and increasing retinal perfusion pressure by lowering intraocular pressure. Some of the modalities to accomplish these things include ocular massage, inhalation of carbogen, hyperbaric oxygen, performing an anterior chamber tap or giving oral acetazolamide to lower IOP.  Thrombolysis has also been suggested but due to adverse events and mixed results it is not generally recommended.

Prognosis and Complications

Prognosis depends on duration of occlusion and the presence of cilioretinal artery, but typically is poor. One study showed that when occlusion was transient, 87% of non-arteritic CRAO improved (Hayreh, 2007). 67% of those with cilioretinal artery also saw improvement (Hayreh, 2007). Most of the visual acuity improvement happened within the first week. Up to 20% of individuals may develop neovascularization of iris, which in turn can cause glaucoma (Hayreh, 2005).


Varma DD, Cugati S, Lee AW, Chen CS. A review of central retinal artery occlusion: clinical presentation and management. Eye (Lond). 2013 Jun; 27(6): 688–697.

Hayreh SS, Zimmerman MB. Fundus changes in central retinal artery occlusion. Retina. 2007 Mar;27(3):276-89.

Hayreh SS, Zimmerman MB. Central retinal artery occlusion: visual outcome. Am J Ophthalmol. 2005 Sep;140(3):376-91.

Graff-Radford J, Boes CJ, Brown RD. History of Hollenhorst Plaques. Stroke. 2015;46:e82-e84.

Bakri SJ, LUqman A, Pathik B, Chandrasekaran K. Is Carotid Ultrasound Necessary in the Clinical Evaluation of the Asymptomatic Hollenhorst Plaque? Trans Am Ophthalmol Soc. 2013 Sep; 111: 17–23.

Identifier: Moran_CORE_23930