eMedicine Specialties > Ophthalmology > Retina

Central Retinal Artery Occlusion

Robert H Graham, MD, Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona
Shehab A Ebrahim, MD, Assistant Professor, Department of Ophthalmology, Tulane University; Vitreoretinal Surgeon, The Retina Institute, LLC

Updated: Feb 12, 2009

Introduction

Background

In 1859, Van Graefe first described central retinal artery occlusion (CRAO) as an embolic event to the central retinal artery in a patient with endocarditis. In 1868, Mauthner suggested that spasmodic contractions could lead to retinal artery occlusion. There is a multitude of causes of CRAO, but patients typically present with sudden, severe, and painless loss of vision.

Pathophysiology

Visual loss from CRAO occurs from the loss of blood supply to the inner layer of the retina. The ophthalmic artery is the first branch of the internal carotid artery and enters the orbit underneath the optic nerve through the optic canal. The central retinal artery is the first intraorbital branch of the ophthalmic artery, which enters the optic nerve 8-15 mm behind the globe to supply the retina. Short posterior ciliary arteries branch distally from the ophthalmic artery and supply the choroid. Anatomical variants include cilioretinal branches from the short posterior ciliary artery, which gives additional supply to the macula from the choroidal circulation. A cilioretinal artery occurs in approximately 14% of the population.

Acutely, obstruction of the central retinal artery results in inner layer edema and pyknosis of the ganglion cell nuclei. Ischemic necrosis results, and the retina becomes opacified and yellow-white in appearance. The opacity is most dense in the posterior pole as a result of the increased thickness of the nerve fiber layer and ganglion cells in this region. Furthermore, the foveola assumes a cherry-red spot because of a combination of 2 factors: (1) the intact retinal pigment epithelium and choroid underlying the fovea, and (2) the foveolar retina is nourished by the choriocapillaris. The late stage shows a homogenous scar replacing the inner layer of the retina.

Approximately 14% of the general population has cilioretinal arteries and 25% of eyes with acute CRAO have cilioretinal artery. The cilioretinal artery supplies part or all of papillomacular bundle. In 10% of eyes, the cilioretinal artery supplies some or all of the foveola. In such an eye, the visual acuity generally returns to 20/50 or better in 80% of eyes over a 2-week period.

The opacification takes as little as 15 minutes to several hours before becoming evident and resolves in 4-6 weeks. The resulting anatomy reflects a catastrophic insult to the inner retinal layers with attenuated retinal arterioles and optic nerve pallor. Pigmentary changes are typically absent since the retinal pigment epithelium remains unaffected. Boxcar appearance of the blood column can be seen in both arteries and veins. Hayreh has shown that irreversible cell injury occurs after 90-100 minutes of total CRAO in the primate model.¹ Controversy exists regarding the optimal window of treatment in humans, but the conservative approach involves treatment up to 24 hours.

Frequency

United States

CRAO is found in 1 per 10,000 outpatient visits. Of these patients, 1-2% present with bilateral involvement.

Mortality/Morbidity

Patients with visualized retinal artery emboli, whether or not obstruction is present, have a 56% mortality rate over 9 years, compared to 27% for an age-matched population without retinal artery emboli. Life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-matched population without CRAO.

Sex

Men are affected slightly more frequently than women.

Age

The mean age of presentation is in the early 60s, although a few cases have been reported in patients younger than 30 years. The etiology of occlusion changes depending on the age of presentation.

Clinical

History

• The most common presenting complaint is an acute, persistent, painless loss of vision in the range of counting fingers to light perception in 90% of patients. Consider ophthalmic artery occlusion if visual acuity is worse.
• Some patients may reveal a history of amaurosis fugax involving transient loss of vision lasting seconds to minutes but which may last up to 2 hours. The vision usually returns to baseline after an episode of amaurosis fugax.
• Ask about symptoms of temporal arteritis in the older population. Patients complain of sudden, painless, nonprogressive vision loss in one eye. History of headaches, jaw claudication, scalp tenderness, proximal muscle and joint aches, anorexia, weight loss, or fever may be elicited.
• Ask about any medical problems that could predispose to embolus formation (eg, atrial fibrillation, endocarditis, coagulopathies, atherosclerotic disease, hypercoagulable state).
• Prolonged direct pressure to the globe during drug-induced stupor or improper positioning during surgery may lead to CRAO.
• Ask about drug history.

Physical

• Determine the degree of vision loss (eg, no light perception, hand movement, counting fingers).
• Ocular examination includes the following:
  • Check for afferent pupillary defect.
  • Perform an optic nerve examination to look for signs of temporal arteritis. Critical signs include afferent pupillary defect and pale/swollen optic nerve with splinter hemorrhages.
  • Cherry-red spot and a ground-glass retina may take hours to develop.
  • The funduscopic findings typically resolve within days to weeks of the acute event, sometimes leaving a pale optic disc as the only physical finding.
  • Emboli can be seen in about 20% of patients with CRAO.
  • Boxcar segmentation can be seen in both arteries and veins. This is a sign of severe obstruction.
  • Perform a cardiovascular examination for murmurs or carotid bruits.
  • Perform a systemic examination for temporal tenderness, jaw claudication, muscle weakness, and fever to evaluate for temporal arteritis.

Causes

Causes of CRAO vary depending on the age of the patient. A detailed analysis of comorbid disease is necessary to elucidate the cause of the acute visual loss.

• Systemic hypertension seen in two thirds of patients
• Diabetes mellitus
• Cardiac valvular disease seen in one fourth of patients
• Cardiac anomalies, such as patent foramen ovale
• Embolism
  • This is most commonly cholesterol but can be calcific, bacterial, or talc from intravenous drug abuse.
  • This is associated with poorer visual acuity and higher morbidity and mortality.
  • Emboli from the heart are the most common cause of CRAO in patients younger than 40 years.
  • Amaurosis fugax preceding persistent loss of vision suggests branch retinal artery occlusion (BRAO) or temporal arteritis and may represent emboli causing temporary occlusion of the retinal artery.
  • Coagulopathies from sickle cell anemia or antiphospholipid antibodies are more common etiologies for CRAO in patients younger than 30 years.
• Atherosclerotic changes
  • Carotid atherosclerosis is seen in 45% of cases of CRAO, with 60% or greater stenosis in 20% of cases.
  • Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years.
• Giant cell arteritis
  • Giant cell arteritis should be considered in patients older than 65 years, but do not ignore in younger patients.
  • Giant cell arteritis may produce CRAO or ischemic optic neuropathy.
  • Giant cell arteritis needs to be treated to preserve vision in the fellow eye.
• Hypercoagulable state
• Collagen vascular disease
• Oral contraceptives
• Polycythemia
• Polyarteritis nodosa
• Rare causes
• Consider in younger patients
• Behçet disease
• Syphilis
• Sickle cell disease
• Migraine
• Increased intraocular pressure from glaucoma or prolonged direct pressure to the globe in unconscious patients
• Hydrostatic arterial occlusion

Differential Diagnoses

Retinopathy, Purtscher

Other Problems to Be Considered

Inadvertent intraocular injection of gentamicin
Arteritic ischemic optic neuropathy
Other causes of cherry-red spot
Tay-Sach disease or other storage disease

Workup

Laboratory Studies

• Laboratory studies are helpful in determining the etiology of central retinal artery occlusion (CRAO).
  • CBC count to evaluate anemia, polycythemia, and platelet disorders
  • Erythrocyte sedimentation rate (ESR) 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 to evaluate for bacterial endocarditis and septic emboli

Imaging Studies

• Imaging studies are helpful in determining the etiology of CRAO.
• Carotid ultrasound imaging to evaluate atherosclerotic disease. This appears to be more sensitive than carotid Doppler, which only determines the flow.
• Magnetic resonance angiogram may be more accurate in detecting obstruction.
• Fluorescein angiogram
  • Delay in arteriovenous transit time (<11 seconds is in the reference range)
  • Delay in retinal arterial filling
  • Normal choroidal filling (begins 1-2 seconds before retinal filling and completely filled within 5 seconds of dye appearance in healthy eyes). A delay of 5 seconds or greater is seen in 10% of patients. Consider ophthalmic artery occlusion or carotid artery obstruction if there is a significant delay in choroidal filling.
  • Arterial narrowing with normal fluorescein transit after recanalization

Other Tests

• ECG to evaluate for possible atrial fibrillation (A 24-h Holter monitor may be necessary if arrhythmia is suspected but not detected on ECG testing.)
• Electroretinogram shows a diminished b-wave corresponding to Muller and/or bipolar cell ischemia.
• Echocardiogram (not necessarily an emergency department test)
  • To evaluate valvular disease, wall motion abnormalities, and mural thrombi
  • To evaluate vegetations that may cause septic emboli

Procedures

• The mainstay of therapy is procedure and pharmacologic therapy (see Medical Care and Medication). 
• Ocular massage
  • Apply direct pressure for 5-15 seconds, then release. Repeat several times.
  • A fundus contact lens or digital massage may be used.
  • Ocular massage can dislodge the embolus to a point further down the arterial circulation and improve retinal perfusion.
• Anterior chamber paracentesis
  • Administer local anesthesia. Use a 30-gauge needle on a tuberculin syringe.
  • Enter the eye at the limbus with bevel up.
  • Ensure that the needle does not damage the lens.
  • Withdraw fluid until the anterior chamber shallows slightly (0.1-0.2 cc).
  • Administer a postprocedure topical antibiotic.
  • A decrease in intraocular pressure is believed to allow greater perfusion, pushing emboli further down the vascular tree.
• Intra-arterial fibrinolysis
  • This procedure is controversial.
  • Limited evidence of improved visual acuity with urokinase is available. A few cases of intra-arterial tissue plasminogen activator (tPA) administration have been observed to be successful.
  • Systemic complications include transient ischemic attack (TIA), stroke, and hematoma.

Treatment

Medical Care

• Immediate lowering of intraocular pressure includes acetazolamide 500 mg IV or 500 mg PO once.
• Topical medications are used to lower intraocular pressure.
• Further treatments
  • Carbogen therapy (5% CO₂, 95% O₂): CO₂ dilates retinal arterioles, and O₂ increases oxygen delivery to ischemic tissues. Perform for 10 minutes every 2 hours for 48 hours.
  • Hyperbaric oxygen therapy (HBOT) may be beneficial if begun within 2-12 hours of symptom onset. Institute treatment with other interventions first, as transport to a chamber may usurp precious time.

Consultations

• Hyperbaric medicine
  • Early treatment (<2 h from onset of symptoms) with HBOT may be associated with increased visual recovery, but HBOT can be considered if the duration of visual loss is less than 12 hours.
  • Inhalation of 100% oxygen at 2 atmospheric absolute provides an arterial pO₂ of 1000-1200 mm Hg, resulting in a 3-fold increase in oxygen diffusion distance through ischemic retinal tissues. Some studies show a 40% improvement of 2 or more levels of visual acuity.

Medication

Carbonic anhydrase inhibitors

Carbonic anhydrase is an enzyme found in many tissues of the body, including the eye. The reversible reaction it catalyzes involves the hydration of carbon dioxide and the dehydration of carbonic acid.

Acetazolamide (Diamox)

Reduces rate of aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP. Used most frequently as single diuretic agent in acute management of CRAO. Other diuretics may be added if sufficient decrease in IOP is not attained.

Dosing

Adult

250-500 mg IV; repeat in 2-4 h prn; not to exceed 1 g/d

Pediatric

10-15 mg/kg/d PO divided q6-8h
5-10 mg/kg/dose IV/IM q6h

Interactions

Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Contraindications

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients

Dorzolamide (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Dosing

Adult

1 gtt tid in affected eye(s)

Pediatric

Not established

Interactions

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CA inhibitors

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)

Hyperosmotic diuretics

Lower IOP by creating an osmotic gradient between the ocular fluids and plasma (not for long-term use).

Mannitol (Osmitrol)

Reduces elevated IOP when the pressure cannot be lowered by other means. Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. It should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 min. It should produce a urine flow of at least 1 mL/h over 1-3 h.

Dosing

Adult

1.5-2 g/kg IV as a 20% solution (7.5-10 mL/kg) or as a 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

Initial dose: 0.5-1 g/kg IV
Maintenance dose: 0.25–0.5 g/kg IV q4-6h

Interactions

None reported

Contraindications

Documented hypersensitivity; anuria; severe pulmonary congestion; severe dehydration; active intracranial bleeding; progressive renal damage; progressive heart failure

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Glycerin

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h.

Dosing

Adult

1-2 g/kg PO; repeat q5h prn
Alternatively, 1 mL/kg PO as a 50% solution in juice

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; frank or impending acute pulmonary edema; anuria; severe dehydration; severe cardiac decompensation

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer orally, never parenterally; for oral use only; avoid in acute urinary retention in preoperative period; continued use may result in weight gain; caution in hypervolemia, diabetes, severely dehydrated individuals, confused mental states, congestive heart disease, and cardiac, renal, or hepatic disease

Sympathomimetics

Lower IOP mainly by increasing outflow and reducing the production of aqueous humor. The combination of a miotic and a sympathomimetic has additive effects in lowering IOP. Each may be added in rotation after a 5-minute interval, until target IOP is reached.

Apraclonidine (Iopidine)

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Dosing

Adult

Solution (0.5%): 1-2 gtt in affected eye(s) tid; since apraclonidine 0.5% will be used with other ocular glaucoma therapies, use an approximate 5-min interval between instillation of each medication to prevent washout of previous dose; do not inject into the eye
Solution (1%): 1 gtt in affected eye 1 h before initiating anterior segment laser surgery; second gtt into the same eye immediately upon completion of surgery

Pediatric

Not established

Interactions

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs

Contraindications

Documented hypersensitivity; patients on MAOIs or have taken them in the past 14 d

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in coronary insufficiency, chronic renal failure, recent myocardial infarction, cerebrovascular disease, Raynaud disease, thromboangiitis obliterans, and depressed patients

Dipivefrin (AKPro, Propine)

Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic side effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.

Dosing

Adult

1 gtt into eye(s) q12h

Pediatric

Not established

Interactions

Increased or synergistic effects when used concurrently with agents that lower IOP

Contraindications

Documented hypersensitivity; narrow angles; dilation of pupil may predispose patient to attack of angle-closure glaucoma

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Macular edema occurs in up to 30% of aphakic patients treated with epinephrine; discontinuation of treatment generally results in reversal of maculopathy; caution in vascular hypertension

Beta-adrenergic blocking agents

Lower IOP by decreasing the rate of aqueous humor production and possibly outflow. They may be more effective than either pilocarpine or epinephrine alone and have the advantage of not affecting pupil size or accommodation.

Timolol (Timoptic)

May reduce elevated and normal IOP, with or without glaucoma by reducing the production of aqueous humor or by outflow.

Dosing

Adult

1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory levels, change the dosage to 1 gtt in affected eye(s) qd; if clinical response is not adequate, change dosage to 1 gtt of 0.5% solution in affected eye(s) bid; if IOP is still not at a satisfactory level, consider concomitant therapy

Pediatric

Administer as in adults

Interactions

Coadministration of ophthalmic timolol may cause bradycardia and asystole when used in combination with systemic beta-blockers; rechallenge studies have confirmed these effects; use topical beta-blockers with caution if the patient is already on systemic beta-blockers

Contraindications

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May contain sulfites, which may cause allergic-type reactions in susceptible patients

Corticosteroids

Used in arterial occlusion only when temporal arteritis (GCA) is the suspected or confirmed etiology.

Prednisone (Deltasone, Orasone, Meticorten)

Useful in the treatment of inflammatory and allergic reactions. May decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear lymphocyte activity.

Dosing

Adult

5-60 mg PO qd or divided bid/qid; not to exceed 80 mg/d; taper over 2 wk as symptoms resolve
Once giant cell arteritis is suspected, administer methylprednisolone, 250 mg IV q6h for 12 doses; then, switch to prednisone, 80-100 mg PO qd; adjust dose clinically

Pediatric

4-5 mg/m²/d PO
Alternative: 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hypertension; known to cause cataract formation with long-term use; in prolonged use, withdraw treatment by gradually decreasing frequency of applications to avoid adrenal insufficiency

Follow-up

Further Inpatient Care

• Inpatient care is indicated only if comorbid disease is present.

Further Outpatient Care

• A follow-up ophthalmic examination should be performed 1-4 weeks after the event to check for neovascularization of the disc or iris.
  • Neovascularization of the iris occurs in 20% of patients at an average of 4-5 weeks after the event. The range is 1-15 weeks. Panretinal photocoagulation is effective in causing regression of iris neovascularization in 65% of patients.
  • Neovascularization of the disc occurs in 2-3% of patients. Panretinal photocoagulation is effective for optic disc neovascularization.
• A complete systemic workup should be performed by a primary care provider.
• If hyperbaric oxygen therapy (HBOT) is to be used, several treatments may be necessary.

Inpatient & Outpatient Medications

• In/out patient medications are indicated only if comorbid disease is present.

Transfer

• Transfer to a hyperbaric facility is necessary if HBOT is to be administered.

Deterrence/Prevention

• Patients should control their blood pressure, lower their cholesterol, avoid intravenous drugs, and take their medication.

Complications

• Further emboli to the brain resulting in a cerebrovascular accident
• Further emboli to the same or contralateral eye, resulting in further visual loss
• Progression of temporal arteritis, resulting in loss of vision to the contralateral eye

Prognosis

• Most patients continue to experience severe vision loss in the counting fingers to hand motion range.
• As many as 10% of patients retain central vision because of the presence of a cilioretinal artery. In this case, visual acuity improves to 20/50 or better in 80% of cases over a 2-week period.
• The presence of a retinal embolus is associated with a 56% mortality rate over 9 years compared to 27% in patients without arterial emboli.
• Life expectancy of patients with central retinal artery occlusion (CRAO) is 5.5 years compared to 15.4 years for an age-matched population without CRAO.

Patient Education

• Patients must understand that the prognosis for visual recovery is poor and that the visual changes are usually a result of a systemic process that needs treatment.

Miscellaneous

Medicolegal Pitfalls

• Failure to perform a workup of the systemic cause of CRAO, leading to a progression of disease or recurrence of symptoms

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Keywords

central retinal artery occlusion, central retina artery occlusion, CRAO, ophthalmic artery occlusion, central retinal artery, retinal artery occlusion, RAO, branch retinal artery occlusion, BRAO, embolism of the retinal artery, retinal artery emboli, ocular stroke, retina, visual loss, vision loss, loss of vision, blindness

Contributor Information and Disclosures

Author

Robert H Graham, MD, Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona
Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Arizona Ophthalmological Society
Disclosure: WebMD/eMedicine Salary Employment

Coauthor(s)

Shehab A Ebrahim, MD, Assistant Professor, Department of Ophthalmology, Tulane University; Vitreoretinal Surgeon, The Retina Institute, LLC
Shehab A Ebrahim, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Retina Specialists, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

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.

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, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest 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.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors, Enoch Huang, MD, MPH, and DooHo Brian Kim, BA, to the development and writing of this article.

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