Medscape is available in 5 Language Editions – Choose your Edition here.


Sudden Visual Loss Treatment & Management

  • Author: Gino A Farina, MD, FACEP, FAAEM; Chief Editor: Edsel Ing, MD, FRCSC  more...
Updated: May 18, 2016

Medical Care

Medical care for patients with sudden visual loss includes the following:

Aspirin is believed to be beneficial in patients with no hemodynamically significant disease of the carotid artery (ie, greater than 1 mm residual lumen) or in those who are poor surgical candidates.

In general, aspirin together with modification of risk factors (eg, decreasing serum cholesterol level, controlling systemic hypertension) reduces the likelihood of myocardial infarction. It is also very effective in reducing the risk of stroke.

Aspirin was once believed to be most effective in high doses, but recent evidence has shown that similar benefits can be achieved with low-dose aspirin at 81 mg a day.

Advise patients with frequent or severe headaches to stop smoking. Women who smoke and take birth control pills are at increased risk for stroke.

Clopidogrel (Plavix) has been shown to be effective in reducing the risk of stroke and in a study comparing its efficacy to aspirin, was shown to be only minimally better. It can be used easily in patients who are aspirin intolerant. Whether the combination of clopidogrel plus aspirin is better than either medication alone is currently unknown.

Aggrenox (aspirin plus dipyridamole) has been shown to be effective in reducing stroke risk. In a comparison with either agent alone, it was found to be significantly more effective.

The recent results of the PROFESS trial showed that aspirin plus dipyridamole and clopidogrel were equivalent in efficacy. Either medication is an acceptable starting medication for the patient at risk for future stroke.

Inferior retinal detachment is treated with the patient sitting up. Superior detachment is treated with the patient lying prone, so to avoid worsening of the detachment by gravity.

Current guidelines for optic neuritis are based on one randomized control trial (Optic Neuritis Treatment Trial) and suggest either high-dose intravenous methylprednisolone or no treatment. In a review article reporting on 750 participants across 6 randomized trials looking at low-dose, high-dose, oral, and intravenous steroids for optic neuritis, there was no evidence of benefit in terms of recovery of visual acuity, visual field, or contrast sensitivity with either oral or intravenous corticosteroids compared with placebo at 6 months.[11] There was, however, indication that treating with steroids hastened the rate of return of vision to normal compared with placebo. When choosing this treatment, oral steroids must be preceded by intravenous steroids, as oral steroids alone resulted in fewer patients achieving normal visual acuity compared with controls and may in fact be associated with increased recurrence rates.

In cases of acute CRAO, conservative therapy may include the following:[12]

  • Ocular massage
  • Topical glaucoma medications
  • Acetazolamide
  • Mannitol
  • Glycerol
  • Calcium channel blockers
  • Prostaglandin E1
  • Lidocaine hydrochloride
  • Acetylcholine
  • Pentoxifylline
  • Hemodilution
  • Methylprednisolone
  • Hyperbaric oxygen
  • Heparin IV
  • Paracentesis
  • Carbogen inhalation

None of these strategies has been proven more effective than any other. A randomized study by Schumacher et al (EAGLE study) compared these conservative treatments with a more invasive method called local intra-arterial fibrinolysis.[13]

For patients with nonischemic CRVO, there has been much investigation in the last several years into effective treatments to both correct vision and prevent progression to ischemic CRVO. Some treatments to help with the aftermath of the disease include panretinal laser photocoagulation, lowering intraocular pressure, treating underlying medical conditions,[7] laser-induced chorioretinal venous anastomosis (L-CRA),[14] intravitreal anti-VEGF, and intravitreal triamcinolone treatments. The latter 2 methods are proposed to decrease subsequent macular edema from CRVO, whereas L-CRA is intended to directly treat the venous occlusion.

Limited studies have evaluated the efficacy of triamcinolone injections, and it has been found to have only a temporary effect with risk of significant adverse effects.[14]

While anti-VEGF injections have come to the forefront in CRVO and BRVO therapy, further studies are required to target treatment groups that would benefit most from these therapies, as well as to determine specific dosing regimens and window for treatment initiation.

A small, retrospective, single-center study by Ferrara et al demonstrated improved visual acuity and decreased macular edema in patients with CRVO of less than 3 months who were given bevacizumab. In this study, 5 patients (6 eyes) who received intravitreal bevacizumab were tested for visual acuity and retinal appearance before and after treatment.[15] However, small sample size and the nonrandomized nature of the study and other studies evaluating this method limits its use as standard therapy at this time.

In a phase II, double-masked, multicenter, randomized sham-controlled trial of pegaptanib sodium for nonischemic CRVO of less than 6 months duration, by Wroblewski et al, 98 patients were randomized to receive either 0.3 mg, 1 g, or sham injections of an anti-VEGF drug, pegaptanib.[16] Subjects who received the 1-mg injection were most benefited in terms of visual acuity compared with the sham group, whose visual acuity declined. Both treatment groups had a significantly lower risk for loss of visual acuity (6-9% of subjects) compared with 31% of controls. Further, there was greater reduction in central retinal thickness compared with controls.

Later analysis reported possible risk of bias due to incomplete outcome data and found that it was not possible to exclude selective reporting.[5] The small sample size resulted in insufficient power to investigate outcome differences between the treatment doses, and the lack of protracted observation allows only for speculation of short term treatment with pegaptanib.

Intravitreal anti-VEGF injection with ranibizumab (approved by the FDA for treatment neovascular age-related macular degeneration in 2006) has shown promise in the short-term treatment of nonischemic CRVO–related macular edema, with recently published follow-up study data and FDA approval of ranibizumab for retinal vein occlusion. In the CRUISE trial, a phase III randomized, double-masked, multicenter, injection-controlled trial by Campochiaro et al, 392 patients with macular edema after CRVO were randomized to receive monthly 0.3-mg, 0.5-mg, or sham intravitreal injections of ranibizumab over 6 months. Those patients who received ranibizumab injections were shown to have significantly improved visual acuity (46.3-47.7%) compared with study controls (16.9%), as well as decreased central foveal thickening.[17]

In a similar prospective, randomized, sham injection–controlled, double-masked, multicenter clinical trial, BRAVO, by Campochiaro et al, intravitreal ranibizumab was also found to improve visual acuity (55.2-61.1%) in patients with BRVO compared with controls (28.8%), in addition to decreased central foveal thickness.[18] Follow up data from both trials, BRAVO and CRUISE, for the subsequent 6 months showed that patients with both conditions continued to improve with repeated injections with no increase in adverse events.[19, 20]

The HORIZON trial, by Heier et al, which included a cohort of patients who completed the BRAVO and CRUISE trials, found no new adverse safety events after an additional year of treatment with ranibizumab.[21] It did, however, find that during the second year of treatment, the clinical improvement of patients with BRVO was persistent, whereas CRVO patients tended to have a decline in vision, perhaps related to a decreased frequency of injections or the differing degrees in retinal damage.[9]

Although the HORIZON study was terminated early secondary to FDA approval of ranibizumab for RVO, several limitations of the aforementioned studies exist and questions remain regarding the utility of ranibizumab for RVO. Follow-up data at the 6-month time point eliminated the control group of sham-injection patients and provided rescue laser treatment for all patients,[22] neither the BRAVO nor CRUISE trials had enough power to investigate differences between the 2 treatment doses,[5] ischemic CRVO was excluded in these trials, and optimal timing of initial treatment has not yet been determined, which is also limited by the small amount of data regarding the disease progression and prognosis of untreated CRVO-related macular edema.


Surgical Care

Carotid artery stenosis increases the risk of hemispheric stroke. This risk is greater after hemispheric ischemic symptoms than after retinal ischemic symptoms. Amaurosis fugax with a carotid stenosis of 70% or greater definitely increases a person's risk of stroke, but with less risk than if the ischemic symptoms were cerebral.

Carotid endarterectomy subsequent to episodes of transient cerebral or retinal ischemia is known to reduce the risk of cerebral infarction. This effect is seen after cerebral ischemia with stenosis greater than 50%. It is seen after retinal ischemia only if stenosis is 70% or greater. Therefore, endarterectomy is advocated in the retinal patient only if the stenosis is 70% or greater while advocated for hemispheric events with stenosis of 50% or greater. Recommendations for this procedure must be individualized. It should be considered for patients with TMB or amaurosis fugax only if the surgical complication rate is less than 2%. For patients with cerebral transient ischemic attacks (TIAs), a complication rate of 3% or less is acceptable.

Local arterial fibrinolysis for the treatment of central retinal artery occlusion (CRAO)

A nonrandomized, single center, interventional study by Aldrich et al. demonstrated improved visual acuity in patients who received local intra-arterial aliquots of tissue plasminogen activator (tPA). In this small study, 21 patients received 3 mg aliquots of intra-arterial tPA and 76% of these patients had improved visual acuity compared with 33% of the patients in the standard therapy group. The authors cautioned that because of the nonrandomized nature of this and previous studies, local arterial fibrinolysis cannot be recommended as standard therapy in daily clinical practice pending the publication of randomized clinical trials.[23]

In a more recent study, results from the first interim analysis of the first randomized clinical trial comparing efficacy of conservative treatment to local arterial fibrinolysis (the European Assessment Group for Lysis in the Eye [EAGLE] study) found no difference in efficacy between the treatment groups.[13] In addition, despite having similar visual improvements in both groups, local intra-arterial fibrinolysis (57%) and conservative treatment (60%), results showed higher occurrences of adverse events in the local intra-arterial fibrinolysis group; thus, the study was discontinued.[13]

Nonarteritic-Ischemic Optic Neuropathy

No good surgical option or therapeutic treatment for nonarteritic ischemic optic neuropathy has yet been elucidated.[24] In a study by Dickersin et al, an optic nerve decompression surgery involving cutting 2 or more slits within the tissue around the optic nerve with the intention to allow CSF to escape and reduce pressure around the nerve was stopped early for futility.[25] Surgical patients experienced both intraoperative and postoperative adverse events, including CRAO during surgery and light perception vision at 6 months. There was also immediate loss of light perception following surgery and loss of vision that persisted to the 12-month visit.

Central Retinal Vein Occlusion

Surgical options for CRVO include radial optic neurotomy, chorioretinal venous anastomosis, vitrectomy, and retinal vein injection with tPA. None of these surgical treatments has been proven to be more effective than nonsurgical methods for improving vision loss and are still experimental at this time.[6]



Ophthalmic consultation is prudent in any case of sudden visual loss that cannot be easily and confidently explained and managed by emergency department physicians.

Cardiac and neurologic consultation is recommended. A complete cardiac and neurologic examination, including murmurs and carotid bruits, should be performed.

Contributor Information and Disclosures

Gino A Farina, MD, FACEP, FAAEM Professor of Emergency Medicine, Hofstra North Shore-LIJ School of Medicine at Hofstra University; 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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

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, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Ellen M Menocal, MD Resident Physician, Department of Emergency Medicine, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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, Sigma Xi, Southern Medical Association, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Chief Editor

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Physicians and Surgeons of Canada, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, Canadian Society of Oculoplastic Surgery, European Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical Association, Ontario Medical Association, Statistical Society of Canada, Chinese Canadian Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

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, Wilderness Medical Society

Disclosure: Nothing to disclose.


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. 1984 Sep-Oct. 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. 2011 Jan. 40(1):53-7. [Medline].

  3. Wray SH. Visual aspects of extracranial internal carotid artery disease. 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. 2008 May. 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. 2010 Oct 6. CD007325. [Medline].

  6. Berker N, Batman C. Surgical treatment of central retinal vein occlusion. Acta Ophthalmol. 2008 May. 86(3):245-52. [Medline].

  7. Morley MG, Heier JS. Venous obstructive diseases of the retina. 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. 2002 Sep. 134(3):317-28. [Medline].

  9. Varma R, Bressler NM, Suñer I, et al. Improved vision-related function after ranibizumab for macular edema after retinal vein occlusion: results from the BRAVO and CRUISE trials. Ophthalmology. 2012 Oct. 119(10):2108-18. [Medline].

  10. Ng WS, Ang GS, Azuara-Blanco A. Laser peripheral iridoplasty for angle-closure. Cochrane Database Syst Rev. 2012 Feb 15. 2:CD006746. [Medline].

  11. Gal RL, Vedula SS, Beck R. Corticosteroids for treating optic neuritis. Cochrane Database Syst Rev. 2012 Apr 18. 4:CD001430. [Medline].

  12. Biousse V, Calvetti O, Bruce BB, Newman NJ. Thrombolysis for central retinal artery occlusion. J Neuroophthalmol. 2007 Sep. 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. 2010 Jul. 117(7):1367-75.e1. [Medline].

  14. McAllister IL, Gillies ME, Smithies LA, et al. The Central Retinal Vein Bypass Study: a trial of laser-induced chorioretinal venous anastomosis for central retinal vein occlusion. Ophthalmology. 2010 May. 117(5):954-65. [Medline].

  15. Ferrara DC, Koizumi H, Spaide RF. Early bevacizumab treatment of central retinal vein occlusion. Am J Ophthalmol. 2007 Dec. 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. 2009 Apr. 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. 2011 Oct. 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. 2013 Jan 31. 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. 2008 Jun. 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). 2013 Feb 1. [Medline].

  25. Dickersin K, Manheimer E, Li T. Surgery for nonarteritic anterior ischemic optic neuropathy. Cochrane Database Syst Rev. 2012 Jan 18. 1:CD001538. [Medline].

  26. Carter JE. Chronic ocular ischemia and carotid vascular disease. 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 Accessed: November 2008.

  28. Fisher CM. Observations of the fundus oculi in transient monocular blindness. Neurology. 1959 May. 9(5):333-47. [Medline].

Hyphema - Blood in anterior chamber resulting from trauma.
Central retinal vein occlusion - Diffuse retinal hemorrhages extending to periphery of fundus, "blood and thunder" appearance.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.