June 13, 2011 | POSTED BY | Articles, Clinical Optometry

By: Dan Strybos – SALUS Optometry School 2012

As optometric students, we face the unique challenge of taking information presented in a classroom setting and recognizing it in a clinical setting. Students often struggle to translate classroom knowledge to clinical success. This series will present “can’t miss” clinical scenarios and the proper diagnosis and treatment in each situation.


As optometrists, we have a unique view of systemic health via the small blood vessels visible during fundus examination. Changes observed in these vessels are also occurring in the rest of the body. Therefore, careful evaluation of retinal vasculature is extremely important, and it is important to remember that anything that happens to the retinal vasculature has the potential to happen elsewhere in the body, including those vessels supplying the heart, lungs, and brain.

The retina has two main sources of arterial blood, both stemming from the ophthalmic artery (a branch of the internal carotid): the central retinal artery and the choroidal blood vessels (choriocapillaris). The central retinal artery enters the eye with the optic nerve and then splits into the large, visible branches we can see during ophthalmoscopy. It has 4 main branches, commonly referred to as arcades, and is responsible for about 20-30% of retinal blood flow. The choroid is responsible for the remaining 70-80% of retinal blood flow. Remember that the choroidal circulation supplies the outer retina (think photoreceptors) and macula, while the CRA supplies the inner retinal layers. When an embolus or thrombus blocks all or part of this blood supply, the retina stops functioning normally and irreversible damage often occurs.



In the clinic, these patients will present with sudden, painless loss of all vision in one eye. Funduscopic evaluation will reveal retinal ischemia. What does this look like? In the case of a CRAO, the entire retina (often including the optic nerve) will appear pale except the macula, which will look bright red. The pallor is due to the swelling of ischemic ganglion cells. Since these ganglion cells are not present in the macula, the underlying choroidal circulation (which is not disrupted) shows through as a bright “cherry red” spot. The responsible embolic culprit is rarely seen in CRAOs, because the obstruction usually occurs before the artery enters the eye. Occasionally, you may see a CRAO that seems to only affect half of the eye. This is likely due to an emboli located in the CRA just after it has split into two portions, just before the lamina cribrosa. This is generally termed a “Hemi CRAO.” A small percentage of the population (around 20%) has a branch of the ciliary circulation called a cilioretinal artery, which exits the optic nerve and supplies the macula and peripapillary retina. These patients will maintain central vision in the case of a CRAO, but will still lose all other vision.


A BRAO appears slightly differently than a CRAO, but with the same general idea. The obstruction of a branch of the central retinal artery results in focal ischemia of the wedge-shaped area supplied by that particular branch. This characteristic wedge of pale, ischemic retina should be what you’re looking for when a patient presents with sudden, partial vision loss. The emboli that cause BRAOs are generally either related to cholesterol, appearing as a yellow, fluffy spot in the artery (Hollenhorst plaque) or are related to the heart valves, which sometimes throw off calcific plaques that appear as a white spot in the artery. Recognizing either the causative plaque and/or the resulting wedge of ischemic retina is the key! Remember, the patient’s vision loss will correspond with this area of ischemia!


Retinal artery occlusions are frustrating events for optometrists because they lack an easy cure. Studies have shown that irreversible changes occur after only 100 minutes of retinal ischemia. What should you do when you look into a pale fundus with a cherry red macula? You have a few options, but they all have the goal of moving the obstruction further “downstream” and therefore limiting the resulting ischemia.

• Digital massage of the eye (Mashing it with your fingers for a few seconds and then releasing) may mechanically move the obstruction

• Have the patient breathe in and out of a paper bag or inhale carbon dioxide (leads to dilation of arterial vessels)

• Promptly use “clot busters” like aspirin, clopidogrel (Plavix), or warfarin (Coumadin)

• Rapidly decrease the IOP using ocular hypotensive agents such as acetazolamide (Diamox), iopidine, and timolol, or via anterior chamber paracentesis (draining the aqueous out of the anterior chamber)

Even though research has shown irreparable damage occurs relatively quickly, these measures should be taken on any patient with recent onset retinal artery occlusion. These measures do not always work, but in these situations, you do what you can, as quickly as possible!

Occlusions of retinal blood supply are linked to serious systemic health concerns. When you have a patient in your chair with a retinal artery occlusion, remember that while their vision is important to you, you are ultimately worried about their life! Associated systemic disorders (and likely causes) include:

• Carotid Artery Disease (including Carotid Dissection)

• Heart Disease

• Hypertension

• High Cholesterol

• Diabetes

• Giant Cell/Temporal Arteritis (Symptoms you should ask about include: headache, jaw or shoulder pain (claudication), fever, scalp tenderness, and weight loss)

• Endocarditis

• Intravenous Drug Use

Because these are such serious systemic diseases, prompt referral to either the primary care physician or the emergency room should also be part of your plan. You may also recommend certain laboratory studies be ordered to determine the underlying pathology.

These should include:

• Complete Blood Count (CBC) with differential and platelets (to evaluate anemia, polycythemia, and platelet disorders)

• EKG (to look for arrhythmias)

• Erythrocyte sedimentation rate (ESR) and C-Reactive Protein (CRP) evaluation (for giant cell arteritis)

• Fibrinogen, antiphospholipid antibodies, prothrombin time/activated partial thromboplastin time (PT/aPTT), and serum protein electrophoresis (to evaluate for coagulopathies)

• Fasting blood sugar, cholesterol, triglycerides, and lipid panel (to evaluate for atherosclerotic disease)

• Blood cultures (for bacterial endocarditis)

• Evaluation of the carotid artery

——-Carotid artery auscultation (listening to the blood flow through the artery)

——-Carotid doppler (evaluation of blood flow through the artery)

Lastly, these patients should be monitored for the development of neovascular glaucoma (NVG), secondary to ocular ischemia. While NVG is most commonly observed after Central Retinal VEIN Occlusions (a topic upcoming!), it also occasionally occurs after retinal artery occlusions and should be monitored. It is important to remember that the vision lost during a retinal artery occlusion may not fully recover, and your patient should be advised of this.

Recognizing and properly treating retinal artery occlusions is a rare, but extremely important part of practicing optometry. These are situations where a routine eye exam may save a patient’s life.

Sources: Check out these great sources to expand your knowledge on this topic.


-The Massachusetts Eye and Ear Infirmary Manual of Ophthalmology

-The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease

A big thank you to the following websites for their excellent pictures, thank you for being there for all us future O.D’s
-Image credits to RedAtlas.org, Ted Montgomery O.D., and The University of Michigan Kellogg Eye Center