Vous êtes sur la page 1sur 8

Today News Reference Education Log In Register

Sudden Visual Loss Clinical Presentation

Author: Gino A Farina, MD, FACEP, FAAEM; Chief Editor: Hampton Roy Sr, MD more... Updated: Mar 29, 2013

For any patient with sudden visual loss, the following information should be obtained: Age Duration of visual loss or changes Whether one eye or both eyes affected History of trauma Prior episodes/ophthalmologic history Symptoms - Photophobia, headache, pain It is important to ask about comorbid conditions such as hypertension, hypercholesterolemia, collagen vascular disease, hematological disorders, cancer, or drug use.

Inspect the extraocular area and assess visual acuity, light or movement perception, visual fields, extraocular movements, and pupil reactivity (including the presence or absence of a relative afferent pupillary defect). Initial examination of the external appearance of the eye is part of a good systematic approach. The appearance of the eye is key. A non-injected eye may be painful owing to optic neuritis, cluster headaches, sinusitis, or dental pain. Normal findings on this examination eliminate extraocular causes of visual loss. Red and painful eyes should be examined with a slit lamp, both with and without fluorescein staining. Corneal and conjunctival findings such as inflammation, edema, or defect are associated with etiologies such as abrasions, keratopathy, ulcers, and infection, which should become apparent with this examination. Intraocular pressure should be measured in patients who have red, painful eyes with normal findings on corneal staining. Elevated pressure points to a diagnosis of acute glaucoma. The anterior chamber should be evaluated for hyphema, cells, and floaters. See the image below.

Hyphema - Blood in anterior chamber resulting from trauma.

In injected, painful eyes with normal fluorescein examination and pressure, the presence of inflammatory cells in the anterior chamber suggests iritis or endophthalmitis, especially with any recent history of ocular surgery. Visual field testing with hand movement is used to assess if central or peripheral field vision deficiency is present.

Careful fundus examination is part of a complete ophthalmic assessment. On funduscopy, a detached retina appears gray and detached. To differentiate physiologic from hysterical visual loss, the examiner can double the distance between the patient and the tangent screen (i.e., visual screen test). In physiologic visual loss, this results in doubling of the size of the central visual field, whereas in hysterical visual loss, the visual field remains the same. An optokinetic drum can help identify blindness of hysterical origin. If nystagmus occurs, the patient is seeing the stripes. Moving a mirror (placed close to the patient's face) will cause the eyes to move if vision is present. Funduscopy and visual field testing can be challenging and, when negative, cannot completely rule out retinal detachment, as the retina is only partially visualized with these methods. If available, ultrasound is a useful adjunct to the physical examination of the eye and can be used to detect retinal detachment, vitreous hemorrhage, vitreous detachment, ocular tumors, intraocular foreign bodies, globe rupture, retrobulbar hematoma, and increased intracranial pressure.[2] Retinal detachment is evident by a taut, linear opacity seen in the vitreous chamber that moves in conjunction with eye movement. Vitreous detachment appears as an opaque line separated from the retina that floats in the vitreous humor. Vitreous hemorrhage appears as curved strands connecting with the retina as the eye moves. Severe vitreous hemorrhage causes complete opacification of the vitreous chamber. The examination should also include complete cardiac and neurologic evaluation, including murmurs and carotid bruits.

Multiple conditions are associated with transient visual loss. They can be classified according to origin or pathogenesis, but for the purpose of this article, they are outlined by source. Wray has classified TMVL into 3 different groups based mostly on pathogenesis; they include the following:[3] Type 1 is characterized by loss of all or a portion of vision in one eye, lasting seconds to minutes, with full recovery. It is usually secondary to an embolic phenomenon. The attacks have been related to an ICA origin associated with ulceration but not critical narrowing. Type 2 includes visual loss due to hemodynamically significant, occlusive, low-flow lesions in the ICAs or ophthalmic arteries. Symptoms are more frequent, less rapid in onset, and longer in duration than type 1 attacks, with gradual vision recovery. Type 3 is thought to be due to vasoconstriction or vasospasm.

The pathophysiology of some types of visual loss can be explained by atherosclerotic cerebrovascular disease. The visual disturbances are usually described as dark or gray, or obscuration by a "descending shade." Visual loss lasts for minutes (10-15 min) and painlessly returns to normal afterwards.

Retinal arteriolar emboli are the most important and common ophthalmoscopic abnormality arising from the carotid artery, aorta, cardiac valves, or the heart itself. Particles consist mostly of platelets or fibrin, calcified emboli, or cholesterol crystals. Cholesterol crystals are observed most frequently. These are called Hollenhorst plaques and are found at the bifurcation of the retinal arterioles. They arise from atherosclerotic plaques in the ICA in the carotid siphon or the aorta, and are usually bright, refractile, and small (10-20 m in diameter). They infrequently impede flow or occlude vessels, and they tend to disappear rapidly and rarely damage the vessel wall. They are difficult to see, but placing pressure on the eye may cause the crystals to move and become visible through the ophthalmoscope. Platelet-fibrin emboli are gray-white in color and commonly extend to the small retinal arteries. In contrast to the Hollenhorst plaques, they tend to occlude vessels and obstruct blood flow. Finally, calcified emboli arise most commonly from calcified heart valves. They are white and usually remain in one position, blocking blood flow. Calcific emboli typically reside directly on the optic disc and remain in that location serving as a reminder of calcific aortic valve disease in that patient. Stenotic vascular disease This includes carotid or vertebral artery atherosclerotic disease, fibromuscular dysplasia, arteritis, and dissection.

Cardiac disease Cardiac causes include atrial myxomas, endocarditis, or a dyskinetic wall segment. They predispose patients to the formation of platelet-containing emboli. Dissection usually involves the pharyngeal ICA and can be precipitated by trauma or can begin spontaneously. Pain in the neck, jaw, face, or head, ipsilateral Horner syndrome, ipsilateral spells of TMVL, and transient hemispheric attacks are frequent features.

Ocular Ischemic Syndromes

Persistent eye ischemia can be classified into central retinal artery occlusion (CRAO), branch retinal artery occlusion (BRAO), or ischemia of the optic nerve, which is caused by involvement of the posterior choroidal blood supply of the nerve (anterior ischemic optic neuropathy [AION]). Origin of CRA from the ophthalmic artery is variable. The vessel has several segments on its way to the retina. To reach the fundus, the CRA penetrates the lamina cribrosa. At this point, it narrows; the tissue around the vessel acts as a mechanical barrier to dilatation. This area is not visible by ophthalmoscope and is most often the site of embolic or inflammatory diseases (e.g., giant cell arteritis). The narrowest area of the CRA is where the artery enters through the dural sheath of the optic nerve,[4] also making this region susceptible to emboli. The major symptom of CRAO is sudden, painless blindness with persistent visual loss. Perception of hand movement or light can be preserved in parts of the visual field. Diagnosis is confirmed by ophthalmoscopy, which reveals partial or complete arrest of retinal circulation. Cardinal signs include attenuated retinal arteries and veins (very early only), and a cloudy whitening of the retina (i.e., edema) with the consequent cherry-red spot in the macula in a patient who has lost vision in one eye. Shortly after occlusion, segmentation of the blood column with slow streaming of veins is seen without recovery of vision. If the occlusion lasts more than 1 hour, the retina becomes irreversibly infarcted. In BRAO, visual defect and retinal ischemia are more focal and have an altitudinal, lateral, or scotomatous quality. The incidence of carotid artery and valvular disease is not very different than in CRAO, but temporal arteritis is less often the cause. In AION, the patient usually develops painless visual loss in the eye, which is noted on awakening in the morning without worsening thereafter. The degree of loss is variable but most often incomplete. Ophthalmoscopy shows edema of the optic disc and splinter hemorrhages at the disc margins. When the ischemia is posterior to the disc, the disc may look normal, but this is quite uncommon and may point toward arteritis as the cause. Subsequent involvement of the other eye is common. Other ocular ischemic syndromes involve the retinal vein. Retinal vein occlusions are retinal vascular disorders that are classified clinically as branch retinal vein occlusion (BRVO), hemispheric vein occlusion, and central retinal vein occlusion (CRVO). See the image below.

Central retinal vein occlusion - Diffuse retinal hemorrhages extending to periphery of fundus, "blood and thunder" appearance.

BRVO involves one of the branch retinal veins. Most involve the superior or inferior temporal arcades and occur at an arteriovenous crossing where the vein is compressed by a sclerotic artery. The superior or inferior temporal arcades cause macular vein occlusion with profound visual deficit. Hemispheric vein occlusion involves the venous drainage of either the superior or inferior retina. BRVO affects males and females equally, occurring most frequently in adults aged 60-70 years. Regardless of the primary pathogenic processes, it is clear that disease of the arterial wall and the presence of common adventitia between the artery and the vein at arteriovenous crossings play a role in the pathogenesis. The common symptoms of BRVO are blurring and distortion of vision. During the acute stage, multiple superficial and deep

retinal hemorrhages are seen in a pie configuration in the distribution of the affected vein. The veins in the occluded segment usually are dilated and tortuous. Fluorescein angiography is helpful to delineate the hemodynamic changes that occur in the retinal vasculature. Angiography usually shows slow venous return without complete occlusion of the vein. Approximately 50% of patients recover good visual acuity, although 2 complications may lead to reduced visual acuitymacular edema, which develops in more than 50% of patients, and retinal neovascularization. Management of both involves photocoagulation to ablate the ischemic peripheral retina. CRVO involves occlusion of the main central vein, which usually occurs at the level of the lamina cribrosa. This occlusion interferes with the drainage of the whole retina. Consequent macular edema may develop, with reduction in visual acuity.[5] The mechanism is unknown, but the most important local factor is chronic open-angle glaucoma, which is present in over 20% of patients. CRVO is primarily a disease of the elderly persons, but well-documented cases in younger persons have been reported. Risk factors for CRVO include hypertension, chronic open angle glaucoma, and diabetes mellitus.[6] CRVO has 2 types: nonischemic and ischemic. These types are characterized by the severity of the retinal vein ischemia, although both have very similar ophthalmological findings.[7] Nonischemic is the more common form and occurs when blood flow and oxygen delivery are restored following vein blockage.[5] Visual complaints vary from mild to moderate blurring of vision, which may be transient. Visual fields are usually normal except for occasional central scotomas. Ophthalmoscopic features of nonischemic CRVO include moderate dilatation and tortuosity of all retinal veins with multiple punctate hemorrhages in the peripheral retina and few scattered retinal hemorrhages in the posterior pole. Most hemorrhagic activity resolves over several months. Some patients may be left with some permanent visual loss from the nonresolving cystoid macular edema, macular cystic degeneration, macular retinal pigment epithelial changes, and preretinal fibrosis. Ischemic CRVO occurs in older individuals who have a higher incidence of systemic vascular disease, preexisting glaucoma, and ocular hypertension. These patients have sudden, painless vision loss. Vision usually is decreased markedly, but the majority of patients will be able to count fingers or see hand movement. Peripheral visual fields are almost always normal with a dense central or centrocecal scotoma. One definition includes the presence of an afferent pupillary defect in the affected eye, which has been found to be both sensitive and specific.[5] In nonarteritic ischemic optic neuropathy (NAION), the patient develops painless visual loss in the eye, decreased central visual acuity, peripheral visual field loss, or both. The etiology of NAION is unknown, but pallid swelling of the optic disc is observed. Patients are at risk during the next 5 years to develop involvement of the other eye; risks for fellow eye involvement include poor baseline acuity and diabetes mellitus, but interestingly not age, sex, smoking, or aspirin use. Spontaneous improvement of vision may occur.[8] The ophthalmoscopic features of ischemic CRVO include marked tortuosity and dilatation of all the retinal branch veins, diffuse retinal hemorrhages extending from the optic disc to the periphery of the fundus, and multiple cottonwool patches. The prognosis is poor; central vision seldom recovers, owing to ischemic maculopathy or cystic macular degeneration, macular holes and cysts, macular epithelial fibrosis, ocular neovascularization, or secondary glaucoma.[5] Although none of the following methods has proven efficacious, laser photocoagulation (panretinal), thrombolysis with t-PA, and surgical interventions have been used to attempt to restore or improve visual acuity.[6] In the last few years, treatment with antivascular endothelial growth factor (VEGF) has shown promise.[9]

Hematological causes of visual loss, such as hypercoagulable states, antiphospholipid syndrome, and anemia, may affect vision through the formation of clots or platelet-containing emboli. Local orbital or ocular disease Angle-closure glaucoma: Often, onset of this disease results in painful vision loss and red eye. In open-angle glaucoma, the aqueous humor has access to the trabecular meshwork, whereas in angle-closure glaucoma, this access is blocked by the peripheral iris. The iris may close the angle in one of 3 ways: (1) pupillary block, in which the iris is bowed forward by aqueous humor, which is unable to get through the pupil because it is adherent to the lens (posterior synechiae); (2) obstruction of the trabecular meshwork directly without pupillary block as a result of posterior pressure from the ciliary body, vitreous, or lens or because of anterior rotation and swelling of the ciliary body; and (3) peripheral anterior synechiae, which are adhesions formed between the peripheral iris and the angle structures.

The diagnosis is not difficult when the presentation is typical; a painful, red eye with increased intraocular pressure that is accompanied by diaphoresis, nausea, and vomiting. Atypical presentations include chronic angle closure or an acute closure without pain. The presence of a midposition, fixed pupil in an eye with reduced vision can suggest unrecognized angle-closure glaucoma. All presentations can be confirmed by tonometry or gonioscopy. Treatment consists of topical miotics and beta-blockers, systemic carbonic anhydrase inhibitors, hyperosmotic agents, and perhaps analgesics and antiemetics. Ophthalmologic consult is warranted; when pupillary block is suspected, iridectomy or iridotomy remains the primary surgical management.[10] Papilledema/neoplasm: Intracranial hypertension causes persisting visual loss by mechanically compressing or physiologically destroying the optic nerve. The visual consequences of postpapilledema optic atrophy start with peripheral visual field constriction, typically most prominent in the inferior nasal or upper nasal quadrant, followed by loss of central visual field with decline in central acuity and dyschromatopsia. A relative afferent pupillary defect can be found in most instances in which visual field or acuity loss is asymmetric between eyes. Visual field defects can include central/paracentral and arcuate scotomas, or nasal steps. Ophthalmoscopy will show a swollen, pale, or normal retina. Patients with papilledema may have unilateral or bilateral transient vision loss and this may be aggravated by standing up or bending over. Intraocular foreign bodies: These are small particles that have penetrated the cornea or sclera. This commonly occurs in the workplace; the signs can be subtle, causing only mild erythema and local discomfort. Visual acuity often is decreased markedly, but normal visual acuity is possible and does not rule out an intraocular foreign body. Smaller objects may produce few, if any, signs or symptoms and may be difficult to discover without a high index of suspicion. With large objects, disruption of the anterior segment, a visible penetration site, hyphema, or cataract may be obvious. Ruptured globe: This results from full-thickness traumatic disruption of the sclera or cornea as a result of blunt or penetrating trauma to the eye. Open globe should be suspected in any patient who has a history of trauma to the eye, especially with a laceration or puncture wound that extends through the eyelid, followed by pain and decreased visual acuity. On examination, visual acuity often is decreased. Flattening of the anterior chamber or hyphema may be present. Note alteration of the pupil size, shape, or location and conjunctival edema or hemorrhage. Extrusion of ocular contents may be seen, and the eye may have a deflated appearance. Leakage of aqueous humor from the anterior chamber may become apparent during examination with fluorescein staining (i.e., Seidel test). Intraocular pressure frequently is decreased, although it should not be measured if an open globe is suspected. Other eye disorders that can cause sudden painless vision loss include a detached retina. A patient with a detached retina presents with the sensation of painless vision loss in one eye, described in the classic presentation as a wall slowly developing over the visual field. The patient may also complain of flashing lights (like an ambulance car light gleaming) or "spider webs" in the peripheral field.

Hysteria/malingering The patient with hysterical blindness or loss of vision will, despite alleged loss of vision, still be capable of maneuvering in a room. The pupillary reactions are normal. The loss of vision is a subconscious conversion symptom. A purely functional loss of vision can be assumed when the visual field is markedly constricted, orientation when walking is intact, and pupillary reactions to light are normal. The transition between a hysterical or malingering patient and one with an aggravated loss of vision is fluid. If the patient indicates a unilateral loss of vision, the examination should be conducted in such way that the patient does not know which eye is being tested or the actual size of the optotypes, and a relative afferent pupillary defect should be present. Drugs, such as quinidine, sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) Sudden monocular visual loss due to nonarteric anterior ischemic optic neuropathy (NAION) has been reported in a small number of patients taking the above medications for erectile dysfunction. The US Food and Drug Administration (FDA) has advised health care professionals of the potential risk of sudden visual loss that may be attributed to the use of phosphodiesterase-5 (PDE-5) inhibitors. The visual loss is typically altitudinal and the visual acuity loss is typically mild; severe vision loss with PDE-5 inhibitors should suggest a different etiology. As of May 2005, the FDA has received a total of 43 postmarketing reports of ischemic optic neuropathy in patients using these drugs. Vascular risk factors for NAION overlap with those of erectile dysfunction such as age older than 50 years and a history of heart disease, high blood pressure, high cholesterol, or smoking; hence, the causal role of PDE-5 inhibitors remains unclear.

Patients should be advised to discontinue the use of these medications and seek immediate medical attention if they experience a sudden decrease or loss of vision in one or both eyes. For more information, please visit US Food and Drug Administration Center for Drug Evaluation and Research. Idiopathic Migraine or scintillating scotoma: This may occur on a persistent basis or may recur after an absence of decades. The physiologic and anatomic bases have not been explained fully but are thought to involve vasospasm. Shimmering scotomas with or without perception of color or movement are reported commonly, usually as a binocular symptom but occasionally monocular. Most commonly, these last less than 30 minutes.

Contributor Information and Disclosures

Author Gino A Farina, MD, FACEP, FAAEM Associate Professor of Emergency Medicine, Hofstra North Shore LIJ School of Medicine and Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Coauthor(s) Ellen M Menocal, MD Resident Physician, Department of Emergency Medicine, Long Island Jewish Medical Center Disclosure: Nothing to disclose. Nicholas Lorenzo, MD, CPE Chairman and CEO, Neurology Specialists and Consultants; Senior Vice President, Founding Executive Director, Continuing Medical Education, Gannett Education (Division Gannett Healthcare Group) Nicholas Lorenzo, MD, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives Disclosure: Nothing to disclose. Lien Hong Lam, MD Resident Physician, Department of Emergency Medicine, North Shore Long Island Jewish Hospital Lien Hong Lam, MD, is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Specialty Editor Board Kilbourn Gordon III, MD, FACEP Urgent Care Physician Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment J James Rowsey, MD Former Director of Corneal Services, St Luke's Cataract and Laser Institute J James Rowsey, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, American Medical Association, Association for Research in Vision and Ophthalmology, Florida Medical Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical Association

Disclosure: Nothing to disclose. 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. Additional Contributors The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Angel Feliciano, MD, to the development and writing of this article.

1. Hedges TR. The terminology of transient visual loss due to vascular insufficiency. Stroke. Sep-Oct 1984;15(5):907-8. [Medline]. 2. Shinar Z, Chan L, Orlinsky M. Use of ocular ultrasound for the evaluation of retinal detachment. J Emerg Med. Jan 2011;40(1):53-7. [Medline]. 3. Wray SH. Visual aspects of extracranial internal carotid artery disease. In: Bernstein EF, ed. Amaurosis Fugax. New York: Springer-Verlag; 1988:72-80. 4. Hayreh SS. Intra-arterial thrombolysis for central retinal artery occlusion. Br J Ophthalmol. May 2008;92(5):585-7. [Medline]. 5. Braithwaite T, Nanji AA, Greenberg PB. Anti-vascular endothelial growth factor for macular edema secondary to central retinal vein occlusion. Cochrane Database Syst Rev. Oct 6 2010;CD007325. [Medline]. 6. Berker N, Batman C. Surgical treatment of central retinal vein occlusion. Acta Ophthalmol. May 2008;86(3):245-52. [Medline]. 7. Morley MG, Heier JS. Venous obstructive diseases of the retina. In: Yanoff M, Duker Js. Ophthalmology. 3rd. place unknown: Mosby; Dec 2008:10/6.17. [Full Text]. 8. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up study. Am J Ophthalmol. Sep 2002;134(3):317-28. [Medline]. 9. Varma R, Bressler NM, Suer I, et al. Improved vision-related function after ranibizumab for macular edema after retinal vein occlusion: results from the BRAVO and CRUISE trials. Ophthalmology. Oct 2012;119(10):2108-18. [Medline]. 10. Ng WS, Ang GS, Azuara-Blanco A. Laser peripheral iridoplasty for angle-closure. Cochrane Database Syst Rev. Feb 15 2012;2:CD006746. [Medline]. 11. Gal RL, Vedula SS, Beck R. Corticosteroids for treating optic neuritis. Cochrane Database Syst Rev. Apr 18 2012;4:CD001430. [Medline]. 12. Biousse V, Calvetti O, Bruce BB, Newman NJ. Thrombolysis for central retinal artery occlusion. J Neuroophthalmol. Sep 2007;27(3):215-30. [Medline]. 13. Schumacher M, Schmidt D, Jurklies B, et al. Central retinal artery occlusion: local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology. Jul 2010;117(7):136775.e1. [Medline]. 14. McAllister IL, Gillies ME, Smithies LA, et al. The Central Retinal Vein Bypass Study: a trial of laserinduced chorioretinal venous anastomosis for central retinal vein occlusion. Ophthalmology. May 2010;117(5):954-65. [Medline].

15. Ferrara DC, Koizumi H, Spaide RF. Early bevacizumab treatment of central retinal vein occlusion. Am J Ophthalmol. Dec 2007;144(6):864-71. [Medline]. 16. Wroblewski JJ, Wells JA 3rd, Adamis AP, et al. Pegaptanib sodium for macular edema secondary to central retinal vein occlusion. Arch Ophthalmol. Apr 2009;127(4):374-80. [Medline]. 17. D.M. Brown, P.A. Campochiaro, et al. Ranibizumab for macular edema following central retinal vein occlusion: six-month primary end point results of a phase III study. Ophthalmology. 2010;117:1124-1133. [Medline]. 18. Campochiaro PA, Heier JS, Feiner L, Gray S, Saroj N, Rundle AC, et al. Ranibizumab for macular edema following branch retinal vein occlusion: six-month primary end point results of a phase III study. Ophthalmology. 2010;117(6):1102-12. [Medline]. 19. Campochiaro PA, Brown DM, Awh CC, et al. Sustained benefits from ranibizumab for macular edema following central retinal vein occlusion: twelve-month outcomes of a phase III study. Ophthalmology. Oct 2011;118(10):2041-9. [Medline]. 20. Brown DM, Campochiaro PA, Bhisitkul RB, Ho AC, Gray S, Saroj N, et al. Sustained benefits from ranibizumab for macular edema following branch retinal vein occlusion: 12-month outcomes of a phase III study. Ophthalmology. 2011;117(6):1594-602. [Medline]. 21. Heier JS, Campochiaro PA, Yau L, Li Z, Saroj N, Rubio RG, et al. Ranibizumab for macular edema due to retinal vein occlusions: long-term follow-up in the HORIZON trial. Ophthalmology. 2012;119(4):802-9. [Medline]. 22. Mitry D, Bunce C, Charteris D. Anti-vascular endothelial growth factor for macular oedema secondary to branch retinal vein occlusion. Cochrane Database Syst Rev. Jan 31 2013;1:CD009510. [Medline]. 23. Aldrich EM, Lee AW, Chen CS, et al. Local intra-arterial fibrinolysis administered in aliquots for the treatment of central retinal artery occlusion: the Johns Hopkins Hospital experience. Stroke. Jun 2008;39(6):1746-50. [Medline]. 24. Rootman DB, Gill HS, Margolin EA. Intravitreal bevacizumab for the treatment of nonarteritic anterior ischemic optic neuropathy: a prospective trial. Eye (Lond). Feb 1 2013;[Medline]. 25. Dickersin K, Manheimer E, Li T. Surgery for nonarteritic anterior ischemic optic neuropathy. Cochrane Database Syst Rev. Jan 18 2012;1:CD001538. [Medline]. 26. Carter JE. Chronic ocular ischemia and carotid vascular disease. In: Bernestein EF, ed. Amaurosis Fugax. New York: Springer-Verlag; 1988:118-134. 27. FDA. US Food and Drug Administration Center for Drug Evaluation and Research [Web site]. Available at http://www.fda.gov/cder/. Accessed November 2008. 28. Fisher CM. Observations of the fundus oculi in transient monocular blindness. Neurology. May 1959;9(5):333-47. [Medline]. Medscape Reference 2011 WebMD, LLC