eMedicine Specialties > Ophthalmology > Hematologic & Cardiovascular Disorders

Ocular Ischemic Syndrome

Igal Leibovitch, MD, Oculoplastic and Orbital Devision, Department of Ophthalmology, Tel-Aviv Medical Center, Tel-Aviv, Israel
Diego Calonje, MD, Consulting Staff, Department of Ophthalmology, Private Practice; Sherif M El-Harazi, MD, MPH, Consulting Staff, Department of Ophthalmology, Sherif El-Harazi, MD

Updated: May 13, 2009

Introduction

Background

Ocular ischemic syndrome (OIS) encompasses the ocular signs and symptoms that result from chronic vascular insufficiency. Common anterior segment findings include advanced cataract, anterior segment inflammation, and iris neovascularization. Posterior segment signs include narrowed retinal arteries, dilated but nontortuous retinal veins, midperipheral dot-and-blot retinal hemorrhages, cotton-wool spots, and optic nerve/retinal neovascularization. The presenting symptoms include ocular pain and abrupt or gradual visual loss.^{1,2,3,4,5,6,7}

Pathophysiology

The most common etiology of OIS is severe unilateral or bilateral atherosclerotic disease of the internal carotid artery or marked stenosis at the bifurcation of the common carotid artery. OIS may also be caused by giant cell arteritis. It is postulated that the decreased vascular perfusion results in tissue hypoxia and increased ocular ischemia, leading to neovascularization.^3,8,9

Frequency

United States

The true incidence of OIS is unknown. It is estimated that approximately 5% of patients with marked carotid artery stenosis present with OIS. By extrapolating data from previous studies, and by applying it to the population of the United States, approximately 1800 new cases (7.5 cases per 1 million population) are encountered per year.

Mortality/Morbidity

The 5-year mortality rate in patients with OIS is about 40%. The leading cause of death is cardiac disease, followed by stroke and cancer. Predisposing risk factors for atherosclerosis (eg, hypertension, diabetes mellitus) have a higher prevalence in patients with OIS than in age-matched populations.

Sex

Males are affected more frequently than females, by a ratio of approximately 2:1.

Age

OIS mainly affects elderly patients. The age range is 50-80 years, with a mean age range of 65-68 years. OIS is uncommon in patients younger than 50 years.

Clinical

History

Symptoms can include amaurosis fugax, gradual or sudden visual loss, and pain. The diagnosis of OIS should always be suspected in elderly patients with asymmetric anterior uveitis, hypotony, neovascularization cataract, and retinopathy.^1,10

• Loss of vision
  • Loss of visual acuity is the most frequently encountered symptom, present in 70-90% of patients at the time of presentation. Only a minority of patients (<10%) have no visual complaints.
  • Patients with OIS can present with variable degrees of visual loss. Up to two thirds of patients can present with visual acuities of 20/60 or worse. One third of patients will have visual acuities of counting fingers or worse. Although, in most cases, visual loss occurs gradually over a period of weeks to months, in some cases, it can also occur abruptly.
• Pain: About 40% of patients with OIS will present with symptoms of pain. The pain is characteristically described as a dull ache over the brow, which begins gradually over a period of hours to days.
• Amaurosis fugax: Amaurosis fugax is a transient episode of complete or partial monocular blindness, lasting for a period of less than 10 minutes. A history of amaurosis fugax is elicited in 9-15% of patients with OIS.

Physical

• Cardiovascular examination
  • Arm pulses
  • Cardiac auscultation
  • Carotid auscultation
• Ophthalmic examination
  • Anterior segment^1,3
    • Corneal abnormalities: Descemet folds and corneal edema may be present secondary to ocular hypotony or increased intraocular pressure.
    • Iris neovascularization: Iris neovascularization is encountered in 67-87% of affected eyes.
    • Neovascular glaucoma: This is elevated intraocular pressure in the presence of angle neovascularization. Neovascular glaucoma is seen in about one third of patients with OIS. Lower arterial perfusion to the ciliary body may induce hypotony or normal intraocular pressure despite significant anterior chamber angle neovascularization.
    • Anterior chamber inflammation: Uveitis, characterized by the presence of cells and flare in the anterior chamber, was estimated to occur in up to 20% of eyes. In most cases, the inflammatory reaction is only mild.
    • Cataract: Advanced degrees of lens opacities may be seen in patients with OIS.
  • Posterior segment^1,3,11
    • Retinal vessels: Retinal arteries are typically narrow in eyes with OIS. The veins are usually irregularly dilated but not tortuous.
    • Retinal hemorrhages: Midperipheral dot-and-blot retinal hemorrhages are observed in 24-80% of eyes with OIS. Microaneurysms can also be seen.
    • Cotton-wool spots: These are seen in approximately 5% of eyes with OIS and are typically located in the posterior pole.
    • Neovascularization: Neovascularization of the optic nerve is seen in 13-35% of eyes with OIS. Retinal neovascularization is less common, and occurs in 3-8% of cases. Neovascularization of the optic nerve can be mild, or it can progress into extensive fibrous proliferation, causing secondary vitreous hemorrhage and tractional retinal detachment.
    • Cherry-red spot: The cherry-red spot appears as a result of ischemia involving the inner layers of the retina, as typically seen in cases of central retinal artery occlusion. It is noted in 12% of eyes with OIS.
    • Optic disc: Optic disc pallor, cupping, or edema is also noted in patients with OIS.
  • Orbit: Ocular ischemia can be part of a rare orbital compartment syndrome that occurs after prolonged spinal surgery in the prone position and was first described by Hollenhorst more than 50 years ago.^12,13 These patients can present with significant proptosis, ophthalmoplegia, eyelid swelling, and ocular ischemia. The exact mechanism is not known, but it is hypothesized that the tamponade action from pressure of the ocular content causes partial or complete collapse of the orbital arterial and venous channels. When the external pressure is released, the ischemic vessels dilate and fluid transudates into the tissue spaces, causing orbital edema.

Causes

• High-grade carotid stenosis: Stenosis of the carotid artery results in concomitant chronic ophthalmic artery insufficiency. Abnormalities of both anterior and posterior segments of the globe are a result of reduced oxygen delivery to the eye.
• Vascular occlusive disease includes occlusive disease of the aortic arch, ophthalmic artery, central retinal artery, and ciliary arteries.

Differential Diagnoses

Central Retinal Vein Occlusion
Giant Cell Arteritis
Retinopathy, Diabetic, Background
Retinopathy, Diabetic, Proliferative

Other Problems to Be Considered

Aortic arch disease

Workup

Laboratory Studies

• Although there are no specific blood tests that are required in the workup of ocular ischemic syndrome (OIS), it is essential to evaluate the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels in patients with suspected giant cell arteritis.^14,15

Imaging Studies

• Fluorescein angiography: Intravenous fluorescein angiographic studies showed the following features in eyes with OIS: prolonged arm-to-choroid and arm-to-retina circulation times, delayed or patchy choroidal filling, increased retinal arteriovenous transit time, staining of the retinal vessels, and retinal capillary nonperfusion.¹
• Color Doppler imaging: This noninvasive imaging quantitates hemodynamic characteristics of the retrobulbar circulation in OIS. It shows reduced peak systolic velocity and increased vascular resistance in ocular end arteries, such as the central retinal and posterior ciliary arteries. It may also show reversal ophthalmic artery blood flow.^16,17,18
• Magnetic resonance angiography (MRA): MRA is a noninvasive technology for the evaluation of arterial vessels. This test can provide accurate anatomical details about intracranial vessels. This imaging modality is still not available in many medical centers, and it is expensive.
• Carotid angiography: Carotid angiography is an essential study for assessing the risk of stroke and for deciding the appropriate treatment of extracranial carotid artery stenosis.¹

Other Tests

• Electroretinography: Electroretinography in OIS shows a reduction or absence of both a-waves and b-waves. The a-wave corresponds to photoreceptor function, and the b-wave is associated with the function of the inner retinal layers.
• Ophthalmodynamometry: If the diagnosis of central retinal vein occlusion cannot be excluded, then consider ophthalmodynamometry. In carotid disease, the ophthalmic artery pressure is low, but it is normal to increased in central retinal vein occlusion.

Procedures

• Invasive carotid artery evaluation

Histologic Findings

Histopathologic studies have shown loss of endothelial cells and pericytes in the peripheral retinal vessels of eyes with OIS. The posterior pole has a normal 1:1 ratio between endothelial cells and pericytes. As the mid periphery is approached, a greater loss of pericytes occurs than endothelial cells. The loss of cells predisposes to leakage from vessels.

Treatment

Medical Care

• Ocular treatments^2,19,20
  • Panretinal photocoagulation to treat neovascularization of the iris, optic nerve, or retina. It was reported to cause regression of neovascularization in about one third of patients with ocular ischemic syndrome (OIS).
  • Topical medication to lower intraocular pressure
  • Cyclodiathermy and cyclocryotherapy to lower intraocular pressure
  • Intravitreal steroids - Possible adjunct therapy in cases of recurrent cystoid macular edema in OIS²¹
  • Ocular filtering procedures and implantation of glaucoma drainage valves to treat neovascular glaucoma
• Systemic treatments
  • Antiplatelet therapy
  • Thrombolytic therapy: Potential benefits of thrombolytic therapy include fast dissolution of physiologically compromising pulmonary emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.
  • Steroids (when giant cell arteritis is suspected)

Surgical Care

• Carotid endarterectomy²²
  • A small number of publications have reported on the ophthalmic outcome of carotid endarterectomy in patients with OIS, and the data presented are not conclusive.
  • Carotid endarterectomy has been shown to benefit symptomatic patients with a nondisabling stroke, amaurosis fugax, and a hemispheric transient ischemic attack whose carotid stenosis is 70-99%.
  • The North American Symptomatic Carotid Endarterectomy Trial Collaborators found a 2-year stroke rate of 9% in such patients who underwent endarterectomy versus a 26% rate in those treated with antiplatelet therapy alone. Stabilization or improvement of visual acuity occurs in about 25% of eyes following endarterectomy.²³
• Superficial temporal artery to middle cerebral artery anastomoses - Bypass procedures, such as superficial temporal artery to middle cerebral artery anastomoses (STA-MCA), have been tried in patients with 100% carotid obstruction in whom a thrombus has propagated distally and an endarterectomy is precluded.

Consultations

• Cardiology
• Cardiovascular surgery
• Neurology

Diet

A strict, low-fat diet is recommended. A low-salt and low-sugar diet is recommended for patients with hypertension and diabetes.

Medication

Medications include antiplatelet therapy and anticoagulant therapy.

Antiplatelets

Inhibit platelet function by blocking cyclooxygenase and subsequent aggregation.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.
Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Dosing

Adult

325 mg PO qd

Pediatric

Not established

Interactions

May decrease hyponatremic and hypotensive effects of ACE inhibitors due to direct effect on renin-angiotensin conversion pathway; concurrent use of aspirin and acetazolamide can lead to high serum concentrations of acetazolamide (and toxicity) due to competition at renal tubules for secretion; effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses greater than 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; because of association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use during third trimester of pregnancy should be avoided; may cause severe urticaria, angioedema, or bronchospasm; may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

Ticlopidine (Ticlid)

Platelet aggregation inhibitor. Causes a time and dose-dependent inhibition of both platelet aggregation and release of platelet granule constituents. After oral ingestion, interferes with platelet membrane function by inhibiting ADP-induced platelet-fibrinogen binding and subsequent platelet-platelet interactions. Tablets for oral administration are sold as white, oval, film-coated tablets.

Dosing

Adult

250 mg PO bid

Pediatric

Not established

Interactions

Potentiates effect of aspirin or other NSAIDs on platelet aggregation; antacids decrease levels of ticlopidine; cimetidine increases ticlopidine serum levels; ticlopidine decreases digoxin plasma levels; concomitant administration of ticlopidine resulted in a significant increase in theophylline elimination half-time

Contraindications

Documented hypersensitivity; hematopoietic disorders, such as neutropenia and thrombocytopenia; hemostatic disorder or active pathological bleeding; severe liver impairment

Precautions

Pregnancy

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

Precautions

Recommended to help reduce risk of having stroke, for patients who have had a stroke or early warning symptoms while on aspirin; not for use in those who can take aspirin to prevent stroke because ticlopidine can cause life-threatening blood problems; neutropenia occurs in about 2.4% of people on ticlopidine

Clopidogrel (Plavix)

Inhibitor of platelet aggregation. Selectively inhibits binding of ADP to platelet receptor, thereby inhibiting platelet aggregation.

Dosing

Adult

75 mg PO qd

Pediatric

Not established

Interactions

Concomitant administration of aspirin and clopidogrel not established; concomitant use with heparin should be undertaken with caution; concomitant administration with NSAIDs associated with increased occult GI blood loss; safety of coadministration with warfarin not established

Contraindications

Documented hypersensitivity; active pathological bleeding such as peptic ulcer or intracranial hemorrhage

Precautions

Pregnancy

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

Precautions

Use during pregnancy only if clearly needed; in breastfeeding, decision should be made whether to discontinue breastfeeding or discontinue drug, taking into account importance of drug to breastfeeding women

Anticoagulant therapy

Prevent recurrent or ongoing thromboembolic occlusion of vertebrobasilar circulation.

Warfarin (Coumadin)

Acts by inhibiting synthesis of vitamin K-dependent clotting factors. Believed to interfere with clotting factor synthesis by inhibiting regeneration of vitamin K-1 epoxide. Degree of depression is dependent upon dose administered.

Dosing

Adult

5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR

Pediatric

Not established

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Anticoagulation is contraindicated in any localized or general physical condition or personal circumstance in which the hazard of hemorrhage might be greater than the potential clinical benefits of anticoagulation, such as pregnancy; hemorrhagic tendencies or blood dyscrasias; recent or completed surgery of central nervous system, eye, or traumatic surgery resulting in large open surfaces; bleeding tendencies associated with active ulceration; threatened abortion; unsupervised patients with senility; spinal puncture

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Perform periodic determination of PT/INR or other suitable coagulation test; numerous factors, alone or in combination, including travel, changes in diet, environment, physical state, and medication may influence response of patient to anticoagulants; generally a good practice to monitor patient's response with additional PT/INR determinations in period immediately after discharge from hospital

Heparin

Inhibits reactions that lead to clotting of blood and formation of fibrin clots in vitro and in vivo. Acts at multiple sites in normal coagulation system. Prevents formation of stable fibrin clot by inhibiting activation of fibrin-stabilizing factor. Dosage adequate when activated partial thromboplastin time (aPTT) is 1.5-2 times normal or when whole-blood clotting time is elevated approximately 2.5-3 times control value.

Dosing

Adult

Initial dose: 40-70 U/kg IV
Maintenance infusion: 18 U/kg/h IV
Alternatively, 50 U/kg/h IV initially, followed by continuous infusion of 15-25 U/kg/h and increase dose by 5 U/kg/h q4h prn using PTT results

Pediatric

Not established

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

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 on heparin may develop new thrombus formation in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin, the so-called white-dot syndrome; increased resistance to heparin frequently is encountered in fever, thrombosis, thrombophlebitis, infections with thrombosing tendencies, myocardial infarction, cancer, and postsurgical patients
Increased risk in older women: A higher incidence of bleeding has been reported in women >60 y

Follow-up

Further Outpatient Care

• Monitor recovery from surgery.

Inpatient & Outpatient Medications

• Anticoagulant therapy
• Antiplatelet therapy

Complications

• Sudden death
• Stroke
• Blindness

Prognosis

• Patients with ocular ischemic syndrome (OIS) have a poor visual prognosis.^24,25,19
• The presence of iris neovascularization is an indicator of poor visual prognosis.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize signs and symptoms of OIS

References

1. Brown GC, Magargal LE. The ocular ischemic syndrome. Clinical, fluorescein angiographic and carotid angiographic features. Int Ophthalmol. Feb 1988;11(4):239-51. [Medline].

2. Brown GC. Ocular ischemic syndrome. In: Retina. 2nd ed. Mosby;1994: 1515-27.

3. Kahn M, Green WR, Knox DL, et al. Ocular features of carotid occlusive disease. Retina. Winter 1986;6(4):239-52. [Medline].

4. Kearns TP, Hollenhurst RW. Venous-stasis retinopathy of occlusive disease of the carotid artery. Proc Staff Meet Mayo Clin. Jul 17 1963;38:304-12. [Medline].

5. Eugene JR, Abdallah M, Miglietta M, et al. Carotid occlusive disease: primary care of patients with or without symptoms. Geriatrics. May 1999;54(5):24-6, 29-30, 33 passim. [Medline].

6. Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology. May 1997;104(5):859-64. [Medline].

7. Chen CS, Miller NR. Ocular ischemic syndrome: review of clinical presentations, etiology, investigation, and management. Compr Ophthalmol Update. Jan-Feb 2007;8(1):17-28. [Medline].

8. Smith VH. Pressure changes in the ophthalmic artery after carotid occlusion (an experimental study in the rabbit). Br J Ophthalmol. 1961;45:1-26.

9. Takaki Y, Nagata M, Shinoda K, et al. Severe acute ocular ischemia associated with spontaneous internal carotid artery dissection. Int Ophthalmol. Dec 2008;28(6):447-9. [Medline].

10. Kubicka-Trzaska A, Romanowska-Dixon B. Non-malignant uveitis masquerade syndromes. Klin Oczna. 2008;110(4-6):203-6. [Medline].

11. Ho TY, Lin PK, Huang CH. White-centered retinal hemorrhage in ocular ischemic syndrome resolved after carotid artery stenting. J Chin Med Assoc. May 2008;71(5):270-2. [Medline].

12. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness occurring during anaesthesia for neuro- surgical operations. Arch Ophthalmol. 1954;52:819-30.

13. Leibovitch I, Casson R, Laforest C, et al. Ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Ophthalmology. Jan 2006;113(1):105-8. [Medline].

14. Casson RJ, Fleming FK, Shaikh A, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis. Arch Ophthalmol. Feb 2001;119(2):306-7. [Medline].

15. Hwang JM, Girkin CA, Perry JD, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis progressing despite corticosteroid treatment. Am J Ophthalmol. Jan 1999;127(1):102-4. [Medline].

16. Bosley TM. The role of carotid noninvasive tests in stroke prevention. Semin Neurol. Jun 1986;6(2):194-203. [Medline].

17. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischemic syndrome. Ophthalmology. Sep 1992;99(9):1453-62. [Medline].

18. Lee HM, Fu ER. Orbital colour Doppler imaging in chronic ocular ischaemic syndrome. Aust N Z J Ophthalmol. 1997;25:157-63. [Medline].

19. Sivalingam A, Brown GC, Magargal LE. The ocular ischemic syndrome. III. Visual prognosis and the effect of treatment. Int Ophthalmol. Jan 1991;15(1):15-20. [Medline].

20. Amselem L, Montero J, Diaz-Llopis M, et al. Intravitreal bevacizumab (Avastin) injection in ocular ischemic syndrome. Am J Ophthalmol. Jul 2007;144(1):122-4. [Medline].

21. Klais CM, Spaide RF. Intravitreal triamcinolone acetonide injection in ocular ischemic syndrome. Retina. 2004;24:459-61. [Medline].

22. Wolintz RJ. Carotid endarterectomy for ophthalmic manifestations: Is it ever indicated?. J Neuroophthalmol. 2005;25:299-302. [Medline].

23. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. Aug 15 1991;325(7):445-53. [Medline].

24. Ros MA, Magargal LE, Hedges TR Jr, et al. Ocular ischemic syndrome: long-term ocular complications. Ann Ophthalmol. Jul 1987;19(7):270-2. [Medline].

25. Sivalingam A, Brown GC, Magargal LE, et al. The ocular ischemic syndrome. II. Mortality and systemic morbidity. Int Ophthalmol. May 1989;13(3):187-91. [Medline].

Keywords

ocular ischemic syndrome, OIS, venous stasis retinopathy, ischemic ocular inflammation, ischemic oculopathy, carotid occlusive disease

Contributor Information and Disclosures

Author

Igal Leibovitch, MD, Oculoplastic and Orbital Devision, Department of Ophthalmology, Tel-Aviv Medical Center, Tel-Aviv, Israel
Igal Leibovitch, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Diego Calonje, MD, Consulting Staff, Department of Ophthalmology, Private Practice
Disclosure: Nothing to disclose.

Sherif M El-Harazi, MD, MPH, Consulting Staff, Department of Ophthalmology, Sherif El-Harazi, MD
Sherif M El-Harazi, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, and International Society of Refractive Surgery
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: eMedicine Salary Employment

Managing Editor

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

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 assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

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