Branch Retinal Artery Occlusion Clinical Presentation

  • Author: Janice C Law, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 16, 2010
 

History

  • Patients with branch retinal artery occlusion (BRAO) typically present with acute, unilateral, painless, partial visual loss. Visual field defects may be central or sectoral. Patients may also 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).
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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 branch retinal artery obstruction.
  • 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. Because 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.[3] 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.
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Causes

  • In elderly patients, embolic disease is the most common etiology of a branch retinal artery obstruction. 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.[4] 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), associations have been noted 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 branch retinal artery obstruction 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 -Syndrome involving recurrent episodes of multiple branch retinal artery obstructions in otherwise healthy individuals, association with Susac syndrome (microangiopathy of brain, retina, and cochlea) in some of patients
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Contributor Information and Disclosures
Author

Janice C Law, MD  Clinical Instructor, Vanderbilt 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 Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Retina Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

Specialty Editor Board

V Al Pakalnis, MD, PhD  Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD 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.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

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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Color fundus photo of right eye with inferior branch retinal artery occlusion from a platelet-fibrin embolus. Retinal whitening surrounding the occluded artery is noted.
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 branch retinal artery occlusion. Delayed filling of the artery (arrow heads) by the fluorescein is noted.
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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