A Review of Central Retinal Artery Occlusion

Clinical Presentation and Management

D D Varma; S Cugati; A W Lee; C S Chen


Eye. 2013;27(6):688-697. 

In This Article

Abstract and Introduction


Central retinal artery occlusion (CRAO) is an ophthalmic emergency and the ocular analogue of cerebral stroke. Best evidence reflects that over three-quarters of patients suffer profound acute visual loss with a visual acuity of 20/400 or worse. This results in a reduced functional capacity and quality of life. There is also an increased risk of subsequent cerebral stroke and ischaemic heart disease. There are no current guideline-endorsed therapies, although the use of tissue plasminogen activator (tPA) has been investigated in two randomized controlled trials. This review will describe the pathophysiology, epidemiology, and clinical features of CRAO, and discuss current and future treatments, including the use of tPA in further clinical trials.


Central retinal artery occlusion (CRAO) was first described by von Graefes in 1859.[1] It is analogous to an acute stroke of the eye and is an ophthalmic emergency. The incidence is estimated to be 1 in 100 000 people and accounts for 1 in 10 000 ophthalmological outpatient visits.[2] A prospective study of 260 eyes with CRAO showed that people suffer profound monocular visual loss, with 80% of patients having a visual acuity (VA) of 20/400 or worse.[3] This reduction in vision increases the fall risk and thus results in increased dependency, and in worst-case scenarios leads to institutional care.[4] CRAO signifies end-organ ischaemia and often the underlying atherosclerotic disease. It is the same underlying atherosclerotic risk factors that in turn place an individual at risk of future cerebral stroke and ischaemic heart disease.

Although analogous to a cerebral stroke, there is currently no guideline-endorsed evidence for treatment. Current options for therapy include the so-called 'standard' therapies, such as sublingual isosorbide dinitrate, systemic pentoxifylline or inhalation of a carbogen, hyperbaric oxygen, ocular massage, globe compression, intravenous acetazolamide and mannitol, anterior chamber paracentesis, and methylprednisolone. None of these therapies has been shown to be better than placebo.[5] There has been recent interest in the use of tissue plasminogen activator (tPA) with two recent randomized controlled trials on the treatment of acute CRAO.[6,7]

The aim of this review article is to provide a comprehensive overview of the epidemiology, risk factors, and clinical presentation of CRAO, but more importantly to review the evidence for treatment.