Ocular Ischemic Syndrome

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Practice Essentials

Ocular ischemic syndrome (OIS) is a rare eye disease caused by chronic hypoperfusion of the common or internal carotid artery.

Background

Ocular ischemic syndrome encompasses the ocular signs and symptoms that result from chronic vascular insufficiency. Common anterior segment findings include advanced cataract, anterior-chamber cell and flare, 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. Most patients with ocular ischemic syndrome present with gradual vision loss or pain.[1, 2, 3, 4, 5, 6, 7]

Pathophysiology

The most common etiology of ocular ischemic syndrome is severe unilateral or bilateral atherosclerotic disease of the internal carotid artery or marked stenosis at the bifurcation of the common carotid artery. It is postulated that the decreased vascular perfusion results in tissue hypoxia and increased ocular ischemia, leading to neovascularization.[3, 8, 9] Ocular ischemic syndrome is more likely to develop in patients with poor collateral circulation between the two internal carotid arteries or between the internal and external carotid arteries. Patients with adequate collateral circulation may not develop ocular ischemic syndrome even if the internal carotid artery is totally occluded.[10]

Patients with ocular ischemic syndrome may show decreased blood flow in the retrobulbar vessels. They may also have reversal of blood flow in the ophthalmic artery because blood is shunted away from the ophthalmic artery and into the lower-resistance intracranial blood vessels.[10]

Epidemiology

Frequency

The incidence of ocular ischemic syndrome is estimated to be 7.5 cases per 1 million population per year but is likely underdiagnosed.[11] Among individuals with carotid occlusive disease, approximately 4%have ocular ischemic syndrome.[12] Ocular ischemic syndrome is bilateral in around 20% of cases.

Comorbidities

Patients with ocular ischemic syndrome have a significantly higher rate of vascular disease than the general population; 73% have hypertension, 56% have diabetes, 48% have a history of ischemic heart disease, 27% have had a prior stroke, and 19% have peripheral vascular disease.[13]

Sex

Males are affected more frequently than females, by a ratio of approximately 2:1, because of a higher rate of cardiovascular disease in men.[14]

Age

Ocular ischemic syndrome mainly affects elderly patients, with a mean age of 65 years. Ocular ischemic syndrome is uncommon in patients younger than 50 years.[10]

Prognosis

Patients with ocular ischemic syndrome have an overall poor visual prognosis. However, patients with better visual acuity at presentation are more likely to retain good final vision. The presence of iris neovascularization is associated with significantly lower vision, with 97% of cases resulting in a final visual acuity of count fingers or worse.[15, 13, 16]

Patient Education

Smoking cessation, a diet low in fat and sugar, and regular exercise can decrease the rate of vascular disease and potentially lower the likelihood of developing ocular ischemic syndrome.

History

Decreased Vision

Decreased vision is the most common symptom associated with ocular ischemic syndrome, occurring in 91% of patients. In one study, most patients (67%) noted gradual vision loss over weeks to months, while 12% had decreased vision over days, and another 12% noted decreased vision over seconds to minutes. A history of transient vision loss is present in 10%-15% of patients with ocular ischemic syndrome (OIS).[1]

Patients with ocular ischemic syndrome 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.[1, 17]

Visual fields are variable and may show no defect, central scotoma, nasal defect, cecocentral defects, or presence of only a central or temporal island.[6]

Pain

About 40% of patients with ocular ischemic syndrome have eye pain. Pain secondary to ischemia is characteristically described as a dull ache over the brow, which begins gradually over a period of hours to days. Lying supine may decrease pain since blood flow is increased. Pain can also result from elevated intraocular pressure in the presence of neovascular glaucoma.

Physical

Ophthalmic Examination

Anterior segment

Corneal abnormalities: Descemet folds and corneal edema may be present secondary to ocular hypotony, increased intraocular pressure, or endothelial dysfunction due to ischemia.[1, 3]

Iris neovascularization: Iris neovascularization is encountered in 67-87% of affected eyes and can be caused by retinal ischemia, choroidal ischemia, or both.

Neovascular glaucoma: This is elevated intraocular pressure in the presence of angle neovascularization. Neovascular glaucoma is seen in about one third of patients with ocular ischemic syndrome. Lower arterial perfusion to the ciliary body may induce hypotony or normal intraocular pressure despite significant anterior chamber angle neovascularization due to decreased production of aqueous fluid.

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 and flare is more prominent than cell.

Cataract: Advanced degrees of lens opacities may be seen in patients with ocular ischemic syndrome. Asymmetric cataract may help support the diagnosis of ocular ischemic syndrome.

Posterior segment

Retinal vessels: Retinal arteries are typically narrow in eyes with ocular ischemic syndrome. The veins are usually irregularly dilated but not tortuous, which can help differentiate ocular ischemic syndrome from central retinal vein occlusion (CRVO).[1, 3, 18]

Retinal hemorrhages: Midperipheral dot-and-blot retinal hemorrhages are observed in 24-80% of eyes with ocular ischemic syndrome. Microaneurysms can also be seen.

Cotton-wool spots: These are seen in approximately 5% of eyes with ocular ischemic syndrome and are typically located in the posterior pole.

Neovascularization: Neovascularization of the optic nerve is seen in 13-35% of eyes with ocular ischemic syndrome. 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 ocular ischemic syndrome.

Optic disc: Optic disc pallor, cupping, or edema is also noted in patients with ocular ischemic syndrome.

Causes

The most common cause of ocular ischemic syndrome is atherosclerosis of the carotid artery. In most cases, stenosis must be 90% or greater to cause ocular ischemic syndrome.

Other causes include the following:

Complications

Potential complications include the following:

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.[19, 20]

Referral to a primary care physician or cardiologist is recommended to evaluate vascular risk factors. Cholesterol levels and hemoglobin A1c may be evaluated.

Imaging Studies

Ocular Imaging Studies

Fluorescein angiography

The most sensitive angiographic sign of ocular ischemic syndrome is prolonged retinal arteriovenous time, present in more than 95% of cases; however, this is not specific for ocular ischemic syndrome. Prolonged arm-to-choroid and arm-to-retina time, staining of the retinal vessels (arteries more than veins), leakage from retinal vessels, and retinal capillary nonperfusion may also be seen.[1, 14]

Indocyanine green (ICG) angiography

ICG angiography helps visualize choroidal abnormalities. Arm-to-choroid may be increased, patchy choroidal filling or choroidal filling defects may be seen, or there may be slow filling of the watershed zone (areas between zones supplied by two different vessels).[14]

Ocular coherence tomography (OCT)

In one study, average choroidal thickness was reduced in patients with ocular ischemic syndrome; however, the retinal macular thickness did not differ between patients with ocular ischemic syndrome and age-matched controls.[21] OCT can be also be used to identify macular edema.

Optical coherence tomography angiography (OCT-A)

OCT-A has shown increased foveal avascular zone (FAZ) and decreased retinal vessel density in a case of ocular ischemic syndrome that improved after carotid artery stenting.[22]

Carotid Imaging Studies

Carotid duplex ultrasonography

This is the most commonly used test to diagnose carotid disease. It is a noninvasive method that shows both anatomical imaging of the vessel and flow velocity information.[23, 24, 25]

Magnetic resonance angiography (MRA) and computed tomographic angiography (CTA)

MRA and CTA are second-line noninvasive methods for the evaluation of arterial vessels. These studies can provide accurate anatomical details about intracranial vessels and are often helpful if carotid ultrasonography is not diagnostic or to aid surgical planning.

Carotid angiography

Carotid angiography is an invasive procedure with a 1.2% risk of cerebral infarction. It is typically used only if ultrasonography, MRA, or CTA shows inconclusive or contradictory results.[1, 10]

Other Tests

Electroretinography

Electroretinography (ERG) can help distinguish ocular ischemic syndrome from central retinal vein occlusion (CRVO) or central retinal artery occlusion (CRAO). In ocular ischemic syndrome, both the inner and outer retina are ischemic. Therefore, ERG in ocular ischemic syndrome shows a reduction in both a-waves (which correspond to photoreceptors) and b-waves (which correspond to bipolar and Muller cells). Eyes with CRVO or CRAO typically have an electronegative ERG result because the inner retina is ischemic but the outer retina is unaffected.[10]

Ophthalmodynamometry and Ocular Plethysmography

Both of these tests can indirectly measure carotid disease by evaluating ophthalmic artery pressure and ocular pulsations. These methods have been replaced by carotid imaging studies.

Medical Care

Ocular Treatments for Ocular Ischemic Syndrome

Topical steroids, such as prednisolone, and cycloplegics are used to treat anterior-segment inflammation and pain.

Panretinal photocoagulation (PRP) is used to treat neovascularization of the iris, optic nerve, or retina. PRP was reported to cause regression of neovascularization in about one third of patients with ocular ischemic syndrome. The low rate of regression after PRP is attributed to the fact that choroidal ischemia alone (rather than retinal ischemia) is sufficient to cause neovascularization in some patients with ocular ischemic syndrome. PRP is most beneficial prior to development of neovascular glaucoma, as the visual prognosis is poor once this has developed.[2, 16, 26, 14]

If neovascular glaucoma develops, intraocular pressure-lowering drops are used. Prostaglandin analogues and pilocarpine are generally avoided to prevent worsening of inflammation. Glaucoma surgery may be needed if medical therapy does not control IOP.

If cystoid macular edema is present, intravitreal steroids and or intravitreal anti-VEGF agents can be used; however, multiple injections may be needed, and vision may be significantly limited by ischemia.[27]

Surgical Care

Carotid Endarterectomy

Carotid endarterectomy is recommended for symptomatic stenosis of 50%-99% if the perioperative risk of stroke or death is less than 6%.[28] A small number of publications have reported on the ophthalmic outcome of carotid endarterectomy in patients with ocular ischemic syndrome, and the data presented are inconclusive.[29] Visual acuity is stabilized or improved in about 25% of eyes following endarterectomy. Endarterectomy is likely more beneficial for visual prognosis if performed prior to the development of neovascularization.[30]

Carotid Artery Stenting

Carotid artery stenting, an alternative to endarterectomy, is used in patients who are at high risk for complications after endarterectomy, such as patients with previous neck radiation or radical neck surgery, patients with high carotid stenosis, or patients with congestive heart failure, unstable angina, or recent myocardial infarction.[10]

Extracranial-Intracranial Arterial Bypass Surgery

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 endarterectomy is precluded.

Ocular Surgery

For the treatment of neovascular glaucoma, implantation of glaucoma drainage valves may be needed. In cases with poor visual prognosis, diode cyclophotocoagulation (dCPC) is an option.

Consultations

Consultations may include the following:

Diet

Limited dietary fat, salt, and sugar can help control vascular risk factors such as atherosclerosis, hypertension, and diabetes.

Guidelines Summary

For patients with suspected ocular ischemic syndrome (OIS), carotid Doppler is the first-line test to confirm the diagnosis. Referral to a primary care doctor or cardiologist is recommended, since ocular ischemic syndrome is the first manifestation of carotid disease in 69% of patients, and early identification can prevent heart attack, stroke, or death.[6]

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Prednisolone ophthalmic (Omnipred, Pred Forte, Pred Mild)

Clinical Context:  Prednisolone is used to treat acute inflammation following eye surgery or other insults to the eye. It decreases inflammation and corneal neovascularization, suppresses migration of polymorphonuclear leukocytes, and reverses increased capillary permeability.

Dexamethasone ophthalmic (Maxidex, Ozurdex)

Clinical Context:  Dexamethasone is used for various allergic and inflammatory diseases. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Fluorometholone (Flarex, FML, FML Forte)

Clinical Context:  This agent suppresses the migration of polymorphonuclear leukocytes and reverses capillary permeability.

Triamcinolone intravitreal (Triesence, Trivaris Intravitreal)

Clinical Context:  Triamcinolone is used to treat inflammatory reactions that are responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. May be used intravitreally to treat cystoid macular edema.

Class Summary

Ophthalmic steroids are used to treat pain and anterior segment inflammation.

Atropine ophthalmic (IsoptoAtropine)

Clinical Context:  Atropine acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia.

Cyclopentolate (Cyclogyl)

Clinical Context:  Cyclopentolate is the anticholinergic drug of choice in the treatment of cornea abrasions. It prevents the muscle of ciliary body and sphincter muscle of the iris from responding to cholinergic stimulation, causing mydriasis and cycloplegia.

Class Summary

Cycloplegic drops are used to decrease pain and to stabilize the blood-aqueous barrier.

Dorzolamide (Trusopt)

Clinical Context:  Dorzolamide is a reversible carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably, it slows bicarbonate ion formation, producing a subsequent reduction in sodium and fluid transport. Systemic absorption can affect carbonic anhydrase in the kidney, reducing hydrogen ion secretion at the renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water. Dorzolamide is less stinging on instillation secondary to buffered pH.

Brinzolamide (Azopt)

Clinical Context:  Brinzolamide catalyzes a reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. It may be used concomitantly with other topical ophthalmic drug products to lower IOP. If more than 1 topical ophthalmic drug is being used, administer them at least 10 minutes apart.

Brimonidine (Alphagan P)

Clinical Context:  Brimonidine is a relatively selective alpha2 adrenergic-receptor agonist that decreases IOP by dual mechanisms, reducing aqueous humor production and increasing uveoscleral outflow. Brimonidine has minimal effect on cardiovascular and pulmonary parameters. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine. IOP lowering of up to 27% has been reported.

Alphagan-P contains the preservative Purite and has been shown to be much better tolerated than its counterpart, Alphagan.

Apraclonidine (Iopidine)

Clinical Context:  Apraclonidine is a potent alpha adrenergic agent that is selective for alpha2 receptors, with minimal cross-reactivity with alpha1 receptors. It suppresses aqueous production and reduces elevated, as well as normal, IOP, whether accompanied by glaucoma or not. Apraclonidine does not have significant local anesthetic activity. It has minimal cardiovascular effects.

Latanoprost (Xalatan)

Clinical Context:  Latanoprost may decrease IOP by increasing the outflow of aqueous humor. Patients should be informed about possible cosmetic effects to the eye/eyelashes, especially if uniocular therapy is to be initiated.

Bimatoprost (Latisse, Lumigan)

Clinical Context:  This agent is a prostamide analogue with ocular hypotensive activity. It mimics the IOP-lowering activity of prostamides via the prostamide pathway. Bimatoprost ophthalmic solution is used to reduce IOP in open-angle glaucoma and ocular hypertension.

Travoprost ophthalmic (Travatan Z)

Clinical Context:  This agent is a prostaglandin F2-alpha analogue. It is a selective FP prostanoid receptor agonist that is believed to reduce IOP by increasing uveoscleral outflow. Travoprost ophthalmic solution is used to treat open-angle glaucoma and ocular hypertension.

Unoprostone ophthalmic (Rescula)

Clinical Context:  This agent is a prostaglandin F2-alpha analogue. It is a selective FP prostanoid receptor agonist that is believed to reduce IOP by increasing uveoscleral outflow. Unoprostone ophthalmic solution is used to treat open-angle glaucoma and ocular hypertension.

Tafluprost (Zioptan)

Clinical Context:  Tafluprost is a topical, preservative-free, ophthalmic prostaglandin analogue that is indicated for elevated IOP associated with open-angle glaucoma or ocular hypertension. The exact mechanism by which it reduces IOP is unknown, but it is thought to increase uveoscleral outflow.

Betaxolol ophthalmic (Betoptic, Betoptic S)

Clinical Context:  This agent selectively blocks beta1 adrenergic receptors, with little or no effect on beta2 receptors. It lowers IOP by reducing the production of aqueous humor. The drug may have less effect on the pulmonary system. Its IOP-lowering effect is slightly less than that of nonselective beta blockers. It may increase optic nerve perfusion and confer neuroprotection.

Carteolol ophthalmic

Clinical Context:  Carteolol has an intrinsic sympathomimetic activity (partial agonist activity), with possibly less adverse effect on cardiac and lipid profiles.

Timolol ophthalmic (Betimol, Istalol, Timoptic)

Clinical Context:  Timolol may reduce elevated and normal IOP, with or without glaucoma, by reducing the production of aqueous humor.

Levobunolol (Betagan)

Clinical Context:  Levobunolol is a nonselective beta adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increasing the outflow of aqueous humor.

Class Summary

Glaucoma eyedrops such as beta-blockers, alpha-2 agonists, prostaglandin analogs, and carbonic anhydrase inhibitors are frequently used to control intraocular pressure.

Pegaptanib (Macugen)

Clinical Context:  This agent suppresses neovascularization and slows vision loss, resulting from macular degeneration, by binding to extracellular VEGF and selectively inhibiting VEGF from binding to its receptor.

Aflibercept intravitreal (Eylea)

Clinical Context:  Used in the treatment of macular edema. This agent inhibits the activation of endothelial cell receptors, thereby suppressing neovascularization, which can slow vision loss due to macular degeneration.

Class Summary

Anti-VEGF injections can be used to treat cystoid macular edema or to promote (temporary) regression of neovascularization.

Author

Tahira M Scholle, MD, Assistant Professor of Ophthalmology, Division of Vitreoretinal Diseases and Surgery, Baylor College of Medicine; Staff Ophthalmologist, Ben Taub Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steve Charles, MD, Founder and CEO of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Andrew G Lee, MD, Chair, Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital; Clinical Professor, Associate Program Director, Department of Ophthalmology and Visual Sciences, University of Texas Medical Branch School of Medicine; Clinical Professor, Department of Surgery, Division of Head and Neck Surgery, University of Texas MD Anderson Cancer Center; Professor of Ophthalmology, Neurology, and Neurological Surgery, Weill Medical College of Cornell University; Clinical Associate Professor, University of Buffalo, State University of New York School of Medicine

Disclosure: Received ownership interest from Credential Protection for other.

Additional Contributors

Diego Calonje, MD, Consulting Staff, Department of Ophthalmology, Private Practice

Disclosure: Nothing to disclose.

Igal Leibovitch, MD, Consulting Staff, Oculoplastic and Orbital Division, Department of Ophthalmology, Tel-Aviv Medical Center, Israel

Disclosure: Nothing to disclose.

Sherif M El-Harazi, MD, MPH, Private Practice in Ophthalmology

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

References

  1. Brown GC, Magargal LE. The ocular ischemic syndrome. Clinical, fluorescein angiographic and carotid angiographic features. Int Ophthalmol. 1988 Feb. 11(4):239-51. [View Abstract]
  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. 1986 Winter. 6(4):239-52. [View Abstract]
  4. Kearns TP, Hollenhurst RW. Venous-stasis retinopathy of occlusive disease of the carotid artery. Proc Staff Meet Mayo Clin. 1963 Jul 17. 38:304-12. [View Abstract]
  5. Eugene JR, Abdallah M, Miglietta M, et al. Carotid occlusive disease: primary care of patients with or without symptoms. Geriatrics. 1999 May. 54(5):24-6, 29-30, 33 passim. [View Abstract]
  6. Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology. 1997 May. 104(5):859-64. [View Abstract]
  7. Chen CS, Miller NR. Ocular ischemic syndrome: review of clinical presentations, etiology, investigation, and management. Compr Ophthalmol Update. 2007 Jan-Feb. 8(1):17-28. [View Abstract]
  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. 2008 Dec. 28(6):447-9. [View Abstract]
  10. Mendrinos E, Machinis TG, Pournaras CJ. Ocular ischemic syndrome. Surv Ophthalmol. 2010 Jan-Feb. 55 (1):2-34. [View Abstract]
  11. Sturrock GD, Mueller HR. Chronic ocular ischaemia. Br J Ophthalmol. 1984 Oct. 68 (10):716-23. [View Abstract]
  12. KEARNS TP, HOLLENHORST RW. VENOUS-STASIS RETINOPATHY OF OCCLUSIVE DISEASE OF THE CAROTID ARTERY. Proc Staff Meet Mayo Clin. 1963 Jul 17. 38:304-12. [View Abstract]
  13. Sivalingam A, Brown GC, Magargal LE, et al. The ocular ischemic syndrome. II. Mortality and systemic morbidity. Int Ophthalmol. 1989 May. 13(3):187-91. [View Abstract]
  14. Terelak-Borys B, Skonieczna K, Grabska-Liberek I. Ocular ischemic syndrome - a systematic review. Med Sci Monit. 2012 Aug. 18 (8):RA138-144. [View Abstract]
  15. Ros MA, Magargal LE, Hedges TR Jr, et al. Ocular ischemic syndrome: long-term ocular complications. Ann Ophthalmol. 1987 Jul. 19(7):270-2. [View Abstract]
  16. Sivalingam A, Brown GC, Magargal LE. The ocular ischemic syndrome. III. Visual prognosis and the effect of treatment. Int Ophthalmol. 1991 Jan. 15(1):15-20. [View Abstract]
  17. Kubicka-Trzaska A, Romanowska-Dixon B. Non-malignant uveitis masquerade syndromes. Klin Oczna. 2008. 110(4-6):203-6. [View Abstract]
  18. Ho TY, Lin PK, Huang CH. White-centered retinal hemorrhage in ocular ischemic syndrome resolved after carotid artery stenting. J Chin Med Assoc. 2008 May. 71(5):270-2. [View Abstract]
  19. Casson RJ, Fleming FK, Shaikh A, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis. Arch Ophthalmol. 2001 Feb. 119(2):306-7. [View Abstract]
  20. Hwang JM, Girkin CA, Perry JD, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis progressing despite corticosteroid treatment. Am J Ophthalmol. 1999 Jan. 127(1):102-4. [View Abstract]
  21. Wang H, Wang Y, Li H. Multimodality Imaging Assessment of Ocular Ischemic Syndrome. J Ophthalmol. 2017. 2017:4169135. [View Abstract]
  22. Saito K, Akiyama H, Mukai R. Alteration Of Optical Coherence Tomography Angiography In a Patient with Ocular Ischemic Syndrome. Retin Cases Brief Rep. 2019 Feb 4. [View Abstract]
  23. Bosley TM. The role of carotid noninvasive tests in stroke prevention. Semin Neurol. 1986 Jun. 6(2):194-203. [View Abstract]
  24. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischemic syndrome. Ophthalmology. 1992 Sep. 99(9):1453-62. [View Abstract]
  25. Lee HM, Fu ER. Orbital colour Doppler imaging in chronic ocular ischaemic syndrome. Aust N Z J Ophthalmol. 1997. 25:157-63. [View Abstract]
  26. Amselem L, Montero J, Diaz-Llopis M, et al. Intravitreal bevacizumab (Avastin) injection in ocular ischemic syndrome. Am J Ophthalmol. 2007 Jul. 144(1):122-4. [View Abstract]
  27. Klais CM, Spaide RF. Intravitreal triamcinolone acetonide injection in ocular ischemic syndrome. Retina. 2004. 24:459-61. [View Abstract]
  28. Goldstein LB, Adams R, Alberts MJ, Appel LJ, Brass LM, Bushnell CD, et al. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2006 Jun 20. 113 (24):e873-923. [View Abstract]
  29. Wolintz RJ. Carotid endarterectomy for ophthalmic manifestations: Is it ever indicated?. J Neuroophthalmol. 2005. 25:299-302. [View Abstract]
  30. 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. 1991 Aug 15. 325(7):445-53. [View Abstract]