Central Retinal Artery Occlusion (CRAO)

• Central Retinal Artery Occlusion (CRAO) is an ophthalmic emergency resulting in sudden, painless vision loss.
• CRAO results from acute ischemia of the retinal artery due to an obstruction.
• Vision recovery prognosis is generally poor and permanent.
• Symptoms of CRAO depend on the vessel occluded, degree and location of the occlusion, and presence/absence of a cilioretinal artery.
• Only 15-30% of people have a cilioretinal artery, which can preserve central vision by supplying the macula area.

Three Stages of CRAO

• Incomplete: Reduced visual acuity, mild retinal edema, delayed blood flow, and a cherry-red spot.
• Subtotal: Substantial blood flow impairment, "cattle track" sign, and severely decreased visual acuity.
• Total: No blood flow and no light perception.

Types of Emboli

• Cholesterol: Most common, yellow or copper-colored, spherical or rectangular, originating from atherosclerotic lesions of the carotid arteries.
• Platelet-fibrin: Mobile, dull grayish-white, caused by carotid and intracardiac thromboses.
• Calcified: White, solid, oval-shaped, generally originate from calcified aortic stenosis or mitral/aortic valve diseases.

Four Types of CRAO

• Non-arteritic permanent: Most common, accounting for more than 2/3 of cases, ability to count fingers or worse, fewer than 25% have any improvement, cherry red-spot, grayish retinal edema, retinal artery narrowing.

• Non-arteritic with cilioretinal artery sparing: Occurs in approximately 14% of patients, cilioretinal arteries may supply the area and result in improved central vision, approximately 67% will have improvement and 20% will achieve 20/40 or better at 7 days.

• Arteritic: Rarest type, only occurring in 4-5% of cases, worst prognosis, generally caused by giant cell arteritis and idiopathic vasculitis, requires a superficial temporal artery biopsy for diagnosis, but it can be confirmed by an elevated CRP; increased SED rate, and the presence of fever, systemic headache, otalgia, and chewing pain, treated with high-dose steroids.

• Non-arteritic transient: Accounts for approximately 16% of CRAO, best prognosis, more than 80% have visual improvement and almost 40% achieve 20/40 vision or better within 7 days, caused by a rapid decrease in perfusion or increase in intraocular pressure, migration of emboli or vasospasm, almost ¼ of patients that have this type of CRAO will experience a stroke on the same side affected within 5 years.

• Choroidal circulation normally supplies approximately 60% of the retina's oxygen needs.

• Under hyperoxic conditions, the choroidal circulation can supply 100% of the retina's oxygen needs.

Key Factors for Treating CRAO with Supplemental Oxygen

• Treatment must be initiated before the retinal tissue is irreparably damaged.
• The degree of occlusion.
• The level of occlusion; if it is at the ophthalmic artery, the patient will not likely respond to HBOT.
• Adequate partial pressure of O2 must be maintained to keep the retina viable until circulation can be restored.

Initial Assessment and Treatment

• Sudden, painless loss of vision should be considered an emergency.
• Initial assessment includes visual acuity; if less than 20/200 without improvement with pinhole, a fundoscopic exam with dilation should occur.
• If CRAO is confirmed, oxygen should be administered immediately at the highest possible FiO2.
• If vision improves significantly within 15 minutes, admit the patient to the hospital on normobaric oxygen for 15 min every hour, alternating with breathing room air for 45 minutes.
• Visual acuity should be checked at the end of each air-breathing period and continued until fluorescein angiogram shows patency, the patient’s vision remains stable on room air for two hours, or a maximum of 96 hours after initiation of oxygen therapy.
• If no response within the first 15 minutes, refer to HBOT.

Stroke Protocol and Workup

• Implement a stroke protocol with combined management from ophthalmology and neurology.
• Workup to screen for conditions that predispose to CRAO includes: CBC, Erythrocyte sedimentation rate (ESR) and C-reactive protein, Coagulation panel, lipid panel, EKG, carotid ultrasound, MRI, fluorescein angiography, and echocardiography.
• More than ¾ of CRAO patients had previously undiagnosed vascular risk factors; and 32% had acute or subacute incidental brain infarcts.
• HBO should not be delayed to accomplish any of these diagnostic measures.
• If suspect arteritic CRAO, IV steroids should be initiated immediately, and HBO should still occur.