May 21, 2019


By Alan L Wagner MD, FACS, FICS


Stop, Drop, and Roll. Apply direct pressure to a wound. Thirty chest compressions before two rescue breaths. Sixty minutes “door to needle” within 240 minutes of symptoms with an ischemic stroke.

Here’s another rule everyone should know: 97 minutes until irrevocable loss of vision with a Central Retinal Artery Occlusion (CRAO). Blindness at six hours!

The retina, highly specialized brain tissue, is one of the most metabolically active parts of our body. Most think of changes in vision as non-emergent, or something that goes along with age.

Yet we recently received a “semi-urgent” referral of a 72-year-old female with an acute loss of vision for three hours in her non-dominant left eye. A painless change, without systemic complaints. She carried the diagnosis of a possible retinal detachment. Could we please see her later in the afternoon, or tomorrow?

We had her come in directly. She had a CRAO. An evolving ischemic stroke of the eye! Our emergent intervention restored blood flow, and she got her sight back. Few are as fortunate.

A CRAO usually presents as painless, acute and with profound loss of vision (visual acuity of barely counting fingers to no light perception). The U.S. incidence of a CRAO is 1.9/100,000.

The cause of the CRAO is usually a thromboembolus. It lodges where the central retinal artery, a division of the internal carotid artery, enters the optic nerve adjacent to the globe. Only if the thrombus/embolus can be dislodged, or lysed, will vision recover. Retinal recovery depends upon age and pre-existing conditions.CRAOs may be associated with: carotid artery disease, atherosclerosis, valvular heart disease, myxoma, atrial fibrillation, hypertension, smoking, IV drug abuse, oral contraceptives, sickle cell disease, homocystinuria and pregnancy. Most patients are in their 60s, with men at greater risk than women. Arteritic causes are rare (<5%).  

A macular cilioretinal artery is present in 15 to 30 percent of the general population. It spares the central 5º– 10° of the visual field, maintaining its flow during a CRAO. These fortunate patients experience an acute loss of their peripheral vision. If a CRAO develops in the non-dominant eye possessing a cilioretinal artery, a constrained “tunnel vision” is discovered when the dominant eye is covered.

 If a CRAO is suspected, immediate referral to an eye surgeon is crucial, because time equals sight!

There is no definitive treatment for a CRAO. Removing fluid from the eye, vasodilators, and lytic therapy are options. Reducing intraocular pressure abruptly allows the systemic blood pressure to better push the embolus “downstream”, sparing more retina. Similarly, drops or systemic mannitol can be employed. Thrombolytic therapy and vasodilators have had mixed results. Carotid ultrasound, echocardiogram and Holter monitor are standards of care for primary testing, identifying the most likely origin of the thromboembolus.  A CRAO, or branch retinal artery occlusion, BRAO, can be associated with increased mortality.  The American Academy of Ophthalmology recommends emergent referral to the emergency room, and the Neurology service, following initial treatment for CRAO/BRAO. The highest window for risk of a stroke is within seven days of presentation of a CRAO/BRAO. That risk remains elevated for the first 30 days.Close follow-up by both the surgeon and medical team is of paramount importance to optimize the patient’s success and survival, and to avoid complications.  

Remain suspicious of, and sensitive to, reported vision loss.

Alan L. Wagner, MD, FACS founded the Wagner Macula & Retina Center in 1987. A Board-certified ophthalmologist specializing in vitreoretinal surgery, Dr. Wagner received his medical degree from Vanderbilt University School of Medicine. He completed his residency in Ophthalmology at EVMS, and furthered his training as the Dyson Fellow in vitreoretinal disease and surgery at Weill Cornell University Medical Center.