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Branch Retinal Artery Occlusion

Janice C Law, MD, Staff Physician, Department of Ophthalmology, Wayne State University, Kresge Eye Institute
Gary W Abrams, MD, Professor and Chairman, Department of Ophthalmology, Wayne State University School of Medicine; Director, Kresge Eye Institute; Rubin W Kim, MD, Staff Physician, Department of Ophthalmology, Kresge Eye Institute; Dean Eliott, MD, Associate Professor, Department of Ophthalmology, Division of Vitreoretinal Surgery, Kresge Eye Institute, Wayne State University; Enrique Garcia-Valenzuela, MD, PhD, Clinical Assistant Professor, Department of Ophthalmology, University of Illinois Eye and Ear Infirmary; Consulting Staff, Vitreo-Retinal Surgery, Midwest Retina Consultants, SC, Parkside Center

Updated: Jun 29, 2007

Introduction

Background

The central retinal artery, a branch of the ophthalmic artery, enters the eye through the optic disc and divides into multiple branches to perfuse the inner layers of the retina. A branch retinal artery occlusion (BRAO) occurs when one of these branches of the arterial supply to the retina becomes occluded.

Pathophysiology

Most commonly, a BRAO occurs secondary to an embolus. Emboli typically originate within vessels upstream where they dislodge and travel within the circulatory system to ultimately become lodged downstream in a vessel with a smaller lumen. The most common include cholesterol emboli from aorto-carotid atheromatous plaques, platelet-fibrin emboli from thrombotic disease, and calcific emboli from cardiac valvular disease. Various other endogenous emboli as well as exogenous emboli and nonembolic causes have been reported.

Ischemia of the inner layers of the retina leads to intracellular edema as a result of cellular injury and necrosis. This intracellular edema has the ophthalmoscopic appearance of grayish whitening of the superficial retina. Primate studies have shown that complete occlusion of arterial supply to the retina results in reversible ischemic injury up to 97 minutes. This may help explain why patients may give a history of transient loss of vision prior to an episode of BRAO. Possibly, these episodes are secondary to emboli transiently becoming lodged, causing temporary occlusions and then reperfusing the retina as the emboli are released. 

BRAO is most likely to occur at the bifurcation of an artery since bifurcation sites are associated with a narrowed lumen. In 90% of cases, BRAO involve the temporal retinal vessels. Whether the temporal retinal vessels are affected more often or whether the nasal retinal vessels are undetected more often is uncertain.

Patients with BRAO have a higher risk for morbidity and mortality secondary to cardiovascular and cerebrovascular disease. A thorough medical workup is indicated for all patients with BRAO, and an etiology can be identified in as many as 90% of patients.

Frequency

United States

Of acute retinal artery obstructions, 58% are central retinal artery occlusions (CRAO), 38% are BRAO, and 5% are cilioretinal artery occlusions.

Mortality/Morbidity

  • Multiple studies have shown increased mortality in patients with retinal arterial emboli. Increased mortality secondary to fatal stroke has been shown in studies, but the most common cause of death in this population is cardiovascular disease.
  • One study reported a 10-fold increase in the annual rate of stroke in patients with retinal emboli compared to controls after a follow-up period of 3.4 years. Another study found a 3-fold higher risk of 8-year mortality from stroke in patients with documented retinal emboli at baseline compared to patients without emboli. A case series reported that 15% of patients with retinal emboli died within 1 year, while a mortality rate of 54% was shown within 7 years.
  • The incidence of neovascularization in all retinal artery obstructions is less than 5%. In BRAO, the incidence is even more rare. Neovascularization, when it does occur, is more likely in persons with diabetes. Clinical cases have been reported in which neovascular glaucoma developed after BRAO.

Race

One study compared retinal artery occlusions in African American and white patients and found that both groups have the same risk factors for retinal arterial occlusive disease. This study also suggested that white patients were more likely to have identifiable carotid disease than African Americans.

Sex

Among elderly patients, men are 2.5 times more likely than women to have retinal emboli. This correlates with the higher rate of stroke found in men.

Age

Typically, BRAO presents in the seventh decade of life. BRAO due to embolic causes is rare in patients younger than 30 years. It has been estimated that less than 1 in 50,000 outpatient visits to the ophthalmologist will be a person younger than 30 years with retinal arterial obstruction. These cases are more likely to be nonembolic causes of retinal arterial occlusions.

Clinical

History

  • Patients typically present with acute, unilateral, painless, partial visual loss. Visual field defects may be central or sectoral. Patients also may be asymptomatic.
  • Risk factors include smoking, hypertension, hypercholesterolemia, diabetes, coronary artery disease, or history of stroke or transient ischemic attack (TIA). Seventy-five percent of patients have hypertension or carotid occlusive disease.
  • Patients may give a history of temporary episodes of visual loss (amaurosis fugax) or neurologic loss (TIA).
  • The physician should ask about any medical problems related to increased risk for embolus formation (eg, endocarditis, carotid stenosis, coagulopathies, atrial fibrillation).

Physical

  • Partial visual field deficit may respect the horizontal midline but never the vertical midline.
  • Funduscopic examination shows retinal whitening along the distribution of the affected artery. The site of obstruction is most often at the bifurcation of the arteries where emboli are most likely to become lodged. Affected retina may be edematous.
  • Narrowed branch retinal artery, boxcarring, segmentation of the blood columns, cotton-wool spots, and emboli are other possible findings. Emboli are visible in 62% of eyes with a BRAO.
  • Some of the more common emboli include the following:

    • Cholesterol emboli (also known as Hollenhorst plaques) appear as iridescent, reflective, thin yellow plates. These yellow plates are white rhomboid crystals measuring 10-250 µm in length and less than 3 µm in thickness. They appear yellow on funduscopic examination because of blood showing through their translucent thinness. Digital pressure on the eye can make them turn within the vessel causing them to become more or less visible to the examiner. They usually do not cause occlusion of the artery by themselves because blood can flow around them.However, if they occur in conjunction with platelet-fibrin or if they are large, then they can obstruct arterial blood flow. Since their sources are most likely atheromatous plaques in the aorto-carotid system, even asymptomatic patients need a medical workup.
    • Platelet-fibrin emboli appear as whitish-gray, nonreflective plugs that are mobile. They may appear in "showers" and may pass through without causing an occlusion. They are usually associated with mural thrombus in the carotid artery or cardiac valvular structures.
    • Calcific emboli appear as large, yellowish-white, nonreflective plaques. They more likely are found in the larger arterioles near the optic disc. They are associated with calcified cardiac valves and atheromatous plaques of the carotid artery.
  • One study demonstrated that attempts to categorize emboli into cholesterol, calcific, or other by funduscopic examination had large intraobserver and interobserver variability. The authors recommended that systemic evaluation not be based on qualitative assessment of the type of emboli.
  • Auscultation of the heart and carotid arteries and comparison of ophthalmodynamometry may help identify the source of emboli.

Causes

  • In elderly patients, embolic disease is the most common etiology of a BRAO. In a study of 70 patients with retinal emboli, 40 were found to have cholesterol emboli, 8 platelet-fibrin emboli, 6 calcific emboli, and 1 possible myxomatous embolus. These types of emboli can also be iatrogenically displaced during cardiac angiography, catheterization procedures, or any interventional embolization of any branch of the carotid artery.
  • Types of emboli (endogenous and exogenous) include the following:

    • Cholesterol – Atheromatous plaques from the aorto-carotid system
    • Platelet-fibrin – Carotid or cardiac thrombosis
    • Calcific - Calcified cardiac valves and atheromatous plaques of the carotid artery
    • Leukoemboli - Vasculitis, Purtscher retinopathy, septic endocarditis
    • Fat emboli - Following long bone fractures
    • Amniotic fluid emboli - Complication of pregnancy
    • Tumors - Atrial myxoma, mitral valve papillary fibroelastoma
    • Talc emboli - Long-term intravenous drug abusers
    • Corticosteroid emboli - Complication of intralesional or retrobulbar steroid injection 
    • Air emboli – Following trauma or surgery
    • Synthetic particles – From synthetic materials used in artificial cardiac valves and other vascular procedures; facial dermal filler (Restylane)
       
  • In younger patients, other more obscure and diverse etiologies are more likely. In patients younger than 30 years with retinal arterial obstruction (RAO), there are associations with migraines, coagulation abnormalities, trauma, increased intraocular pressure, optic nerve drusen, oral contraceptives, and other entities, which merit a more comprehensive review. Atheromatous disease is a rare cause of RAO in this age group, and routine carotid angiography for embolic cause is not recommended. Visual prognosis is similar to older patients.
  •  Nonembolic causes of BRAO include the following:

    • Thrombosis - Atherosclerosis, chemotherapeutic agents, bone marrow transplants
    • Inflammatory conditions – Syphilis, toxoplasma, retinochoroiditis, Behçet disease, Lyme disease, pseudotumor cerebri, Bartonella infection, HIV infection, posterior scleritis, varicella-zoster infection, multifocal retinitis with optic nerve edema, West Nile virus infection
    • Vasospasm – Migraines, cocaine abuse, sildenafil citrate use
    • Coagulopathies - Sickle cell disease, Hodgkin disease, pregnancy, anemia, platelet and clotting factor abnormalities, protein C, protein S, antithrombin III, factor V Leiden deficiencies, oral contraceptives, homocystinuria, antiphospholipid syndrome, chelation therapy
    • Autothrombosis- From a ruptured arteriolar macroaneurysm
    • Compression - Preretinal arterial loops, vitrectomy surgery, trauma
    • Idiopathic - A syndrome of recurrent episodes of multiple BRAOs in otherwise healthy individuals has been described. An association with Susac syndrome (microangiopathy of brain, retina, and cochlea) has been seen in some of these patients.

Differential Diagnoses

Central Retinal Artery Occlusion

Other Problems to Be Considered

Cilioretinal artery occlusion
Retinitis
Inflammatory disease of the choroid and retinal pigment epithelium
Choroidal ischemia
Retinal contusion
Neoplasia
Opaque subretinal precipitates
Myelinated nerve fiber layer

Workup

Laboratory Studies

  • Laboratory tests to consider in light of the clinical picture include the following:

    • In patients older than 50 years, consider ordering an immediateerythrocyte sedimentation rate (ESR) to help rule out giant cell arteritis.
    • In patients younger than 50 years or in patients with the appropriate risk factors, consider the following tests to evaluate for coagulopathies: antitreponemal antibody, antiphospholipid antibody,  antinuclear antibody, rheumatoid factor, serum protein electrophoresis, hemoglobin electrophoresis, prothrombin time/activated partial thromboplastin time (PT/aPTT), fibrinogen, protein C and S, antithrombin III, and factor V Leiden.
    • CBC to evaluate anemia, polycythemia, and platelet disorders
    • Fasting blood sugar, glycosylated hemoglobin, cholesterol, triglycerides, and lipid panel to evaluate for atherosclerotic disease
    • Blood cultures to evaluate for bacterial endocarditis and septic emboli

 

Imaging Studies

  • Fluorescein angiography shows delayed filling of the affected artery and hypofluorescence in the surrounding area. Vessels distal to the site of obstruction may show retrograde filling from surrounding perfused capillaries. Late staining of the vessel walls may be seen. After resolution of the obstruction, flow may return to normal. However, narrowing or sclerosis of the affected artery can occur. Artery-to-artery collaterals may form in the retina and are highly suggestive of an old BRAO.
  • Optical coherence tomography (OCT) has been used to demonstrate structural damage of the retinal layers after retinal artery occlusion.

    • One study showed diffuse thickening of the neurosensory retina where the artery occlusion occurred. Increased reflectivity was noted in the inner retinal layers with decreased reflectivity of the photoreceptors and retinal pigment epithelium, which supported the pathophysiology of increasing intracellular fluid of the inner retinal layer.
    • Another study used OCT to demonstrate the long-term structural result after arterial occlusion. One year after diagnosis of BRAO, the authors found segmental inner retinal layer and peripapillary retinal nerve fiber layer thickness to be reduced. They correlated visual field deficits with OCT thickness and found that a worse functional outcome was associated with a more extensive thinning of the macula and retinal nerve fiber layer.
  • An electroretinogram (ERG) is of limited usefulness. Findings may be normal. In the case of a large BRAO, it may show loss of oscillatory potential and transient depression of the B wave.

Other Tests

  • Serial Humphrey visual field testing will reveal any field deficits and can be used to monitor the stability or improvement of these deficits.
  • Other tests to help evaluate possible sources of emboli include the following:

    • Elderly patients and patients with high-risk characteristics for cardioembolic disease warrant medical workup involving either 2-dimensional or transesophageal echocardiography. High-risk characteristics include a history of rheumatic heart disease, mitral valve prolapse, prosthetic valve placement, history of subacute bacterial endocarditis, recent heart attack, IV drug abuse, any type of valvular heart disease (congenital or acquired), detectable heart murmurs, and ECG changes (eg, atrial fibrillation, changes indicating myocardial damage).
    • Carotid ultrasound studies and magnetic resonance angiogram and/or angiography are crucial tests to evaluate for atherosclerosis. Considering the higher incidence of fatal stroke in the elderly population, atherosclerotic disease should be evaluated if there is no other obvious etiology.
    • ECG/Holter monitor to evaluate for atrial fibrillation

Procedures

  • Since prognosis for BRAO is very good, no interventions usually are taken. In the event of involvement of the perifoveolar capillaries, treatment as for CRAO may be attempted (see Central Retinal Artery Occlusion).
  • Intra-arterial thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) via a guiding catheter inserted into the femoral artery, placed into the internal carotid artery, and advanced into the ophthalmic artery has been used for CRAO with varying success. This has also been applied to some patients with BRAO with limited benefit compared to conventional forms of therapy or observation.
  • Another procedure that has been attempted for both BRAO and CRAO is translumenal Nd:YAG laser embolysis or TYE. This method relies on the Nd:YAG laser to shatter the embolus, clear the arteriole lumen, and improve perfusion without harming the vessel wall. Potential risks include retina tears, vitreous and retinal hemorrhages, choroidal neovascularization, and epiretinal membrane formation. One study found visual improvement to occur immediately after the embolysis.

 

Histologic Findings

BRAO causes ischemia to the inner layers of the retina, which causes inner and intracellular edema and a coagulative necrosis. Eventually, there is loss of the inner retinal layers, which include the nerve fiber layer to the inner nuclear layer. Since the glial cells also have been destroyed, usually there is no gliosis. Histologic evidence of emboli or other etiology may be present.

Treatment

Medical Care

Considering the increased rate of mortality, patients with BRAO should receive a full medical workup with special attention to the cerebrovascular and cardiovascular system. Depending on the findings, carotid endarterectomy or anticoagulation may be indicated. Lab workup for coagulopathies should also be performed if no embolic source is found.

Consultations

Refer to an internist for complete systemic workup.

Medication

To prevent the dreaded complication of stroke, most patients are placed on some form of antiplatelet therapy, such as aspirin, clopidogrel (Plavix), dipyridamole (Aggrenox), and ticlopidine (Ticlid).

Warfarin (Coumadin) is a blood thinner that prevents the blood from clotting. This medication is often used in patients with atrial fibrillation to decrease their risk of stroke.

Follow-up

Further Outpatient Care

  • Patients should initially be evaluated every 3-6 months to monitor progression. Ocular neovascularization after BRAO is rare. If neovascularization occurs, panretinal photocoagulation should be performed.

Deterrence/Prevention

  • Controlling blood pressure, cholesterol, and diabetes can greatly reduce the risk of atherosclerotic disease.
  • Smoking cessation can also lower the risk of stroke.

Complications

  • Stroke is a devastating complication of emboli in the arterial circulation. Few studies report the prospective association between retinal emboli and risk of stroke and stroke mortality. One study reported a 10-fold increase in the annual rate of stroke in patients with retinal emboli compared to controls after a follow-up period of 3.4 years. Another study found a 3-fold higher risk of 8-year mortality from stroke in patients with documented retinal emboli at baseline compared to patients without emboli. A case series reported that 15% of patients with retinal emboli died within 1 year, while a mortality rate of 54% was shown within 7 years.

Prognosis

  • Recovery from BRAO is usually very good without treatment; 80-90% of patients improve to a visual acuity of 20/40 or better. However, some degree of visual field deficit usually persists.

Patient Education

  • Patients should know that this disorder may serve as a warning of more serious systemic diseases, such as cardiovascular disease or stroke.
  • For excellent patient education resources, visit eMedicine's Eye and Vision Center and Cholesterol Center. Also, see eMedicine's patient education articles Anatomy of the Eye, High Cholesterol, and Cholesterol FAQs.

Miscellaneous

Medicolegal Pitfalls

  • Failure to perform workup for a systemic cause of BRAO, leading to further morbidity, including stroke and death.

Multimedia

Color fundus photo of right eye with inferior bra...

Media file 1: Color fundus photo of right eye with inferior branch retinal artery occlusion from a platelet-fibrin embolus. There is retinal whitening surrounding the occluded artery.

Red-free photograph (before injection of fluoresc...

Media file 2: Red-free photograph (before injection of fluorescein) of right eye with inferior branch retinal artery occlusion. The red-free photograph greatly accentuates the retinal whitening surrounding the occluded artery.

Fluorescein angiogram of right eye with inferior ...

Media file 3: Fluorescein angiogram of right eye with inferior branch retinal artery occlusion. There is delayed filling of the artery (arrow heads) by the fluorescein.

Optical coherence tomography (OCT) of right eye w...

Media file 4: Optical coherence tomography (OCT) of right eye with inferior branch retinal artery occlusion. Cross-section goes through inferior retina to superior retina, capturing the abnormally thickened retina associated with intracellular edema.

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Keywords

branch retinal artery obstruction, BRAO, arterial occlusive disease, central retinal artery

Contributor Information and Disclosures

Author

Janice C Law, MD, Staff Physician, Department of Ophthalmology, Wayne State University, Kresge Eye Institute
Janice C Law, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, Michigan Society of Eye Physicians & Surgeons, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Gary W Abrams, MD, Professor and Chairman, Department of Ophthalmology, Wayne State University School of Medicine; Director, Kresge Eye Institute
Gary W Abrams, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Club Jules Gonin, International Society for Ophthalmic Ultrasound, Macula Society, Pan-American Association of Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.

Rubin W Kim, MD, Staff Physician, Department of Ophthalmology, Kresge Eye Institute
Rubin W Kim, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Dean Eliott, MD, Associate Professor, Department of Ophthalmology, Division of Vitreoretinal Surgery, Kresge Eye Institute, Wayne State University
Dean Eliott, MD is a member of the following medical societies: American Academy of Ophthalmology and American Medical Association
Disclosure: Nothing to disclose.

Enrique Garcia-Valenzuela, MD, PhD, Clinical Assistant Professor, Department of Ophthalmology, University of Illinois Eye and Ear Infirmary; Consulting Staff, Vitreo-Retinal Surgery, Midwest Retina Consultants, SC, Parkside Center
Enrique Garcia-Valenzuela, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, Association for Research in Vision and Ophthalmology, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Vytautas A Pakainis, MD, Chief of Ophthalmology, Dorn Veterans Administration Medical Center, Professor of Ophthalmology, Ophthalmology, University of South Carolina School of Medicine
Vytautas A Pakainis, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

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