- Vision Loss in Older Persons
- Acute Vision Loss – Eye Disorders – Merck Manuals Professional Edition
- Vision impairment and blindness
- Strategies to address vision impairment
- WHO response
- Prevalence and Causes of Unilateral Vision Impairment and Unilateral Blindness in Australia: The National Eye Health Survey
- Transient Vision Loss (TVL) and Amaurosis Fugax: Overview, Pathophysiology, Etiology
Vision Loss in Older Persons
1. Rosenberg EA, Sperazza LC. The visually impaired patient. Am Fam Physician. 2008;77(10):1431–1436….
2. Congdon N, O'Colmain B, Klaver CC, et al., for the Eye Diseases Prevalence Research Group. Causes and prevalence of visual impairment among adults the United States. Arch Ophthalmol. 2004;122(4):477–485.
3. Rowe S, MacLean CH, Shekelle PG. Preventing visual loss from chronic eye disease in primary care. JAMA. 2004;291(12):1487–1495.
4. Campbell AJ, Robertson MC, LaGrow SJ, et al. Randomised controlled trial of prevention of falls in people > or = 75 with severe visual impairment: the VIP trial. BMJ. 2005;331(7520):817.
5. Menon GJ. Complex visual hallucinations in the visually impaired: a structured history taking approach. Arch Ophthalmol. 2005;123(3):349–355.
6. Brézin AP, Lafuma A, Fagnani F, Mesbah M, Berdeaux G. Blindness, low vision, and other handicaps as risk factors attached to institutional residence. Br J Ophthalmol. 2004;88(10):1330–1337.
7. Elliot DB, Trukolo-Ilic M, Strong JG, Pace R, Plotkin A, Bevers P. Demographic characteristics of the vision-disabled elderly. Invest Ophthalmol Vis Sci. 1997;38(12):2566–2575.
8. Field TS, Mazor KM, Briesacher B, Debellis KR, Gurwitz JH. Adverse drug events resulting from patient errors in older adults. J Am Geriatr Soc. 2007;55(2):271–276.
9. Javitt JC, Zhou Z, Willke RJ. Association between vision loss and higher medical care costs in Medicare beneficiaries costs are greater for those with progressive vision loss. Ophthalmology. 2007;114(2):238–245.
10. American Academy of Family Physicians. Recommendations for clinical preventive servicesRevision 6.9, January 2009. https://www.aafp.org/online/etc/medialib/aafp_org/documents/clinical/CPS/rcps08-2005.Par.0001.File.tmp/BOD-CPS-Approved-changes.pdf. Accessed April 22, 2009.
11. American Academy of Ophthalmology. Preferred practice pattern: comprehensive adult medical eye evaluation.http://one.aao.org/CE/PracticeGuidelines/PPP.aspx. Accessed April 22, 2009.
12. Canadian Task Force on the Periodic Health Examination. Periodic health examination, 1995 update: 3. Screening for visual problems among elderly patients CMAJ. 1995;152(8):1211–1222http://www.ctfphc.org/. Accessed April 22, 2009.
13. Institute for Clinical Systems Improvement (ICSI). Preventive services for adults. http://www.icsi.org/preventive_services_for_adults/preventive_services_for_adults_4.html. Accessed April 22, 2009.
14. US Preventive Services Task Force. Screening for visual impairment. Rockville, Md: :Agency for Healthcare Research and Quality 1996http://www.ahrq.gov/clinic/uspstf/uspsvisi.htm. Accessed April 22, 2009.
15. Kniestedt C, Stamper RL. Visual acuity and its measurement. Ophthalmol Clin North Am. 2003;16(2):155–170.
16. US Preventive Services Task Force. Screening for glaucoma: recommendation statement. Rockville, Md: Agency for Healthcare Research and Quality March 2005. http://www.guidelines.gov/summary/summary.aspx?ss=15&doc_id=6194&nbr=003990&string=glaucoma. Accessed April 22, 2009.
17. American Academy of Ophthalmology. Preferred practice patterns: diabetic retinopathy. http://one.aao.org/CE/PracticeGuidelines/PPP.aspx. Accessed April 22, 2009.
18. Kempen JH, Mitchell P, Lee KE, et al., for the Eye Diseases Prevalence Research Group. The prevalence of refractive errors among adults in the United States, Western Europe, and Australia [published correction appears in Arch Ophthalmol. 2005;123(10):1314]. Arch Ophthalmol. 2004;122(4):495–505.
19. National Eye Institute. Amsler grid. ftp://ftp.nei.nih.gov/charts/grid2300.tif. Accessed April 22, 2009.
20. Santaella RM, Fraunfelder FW. Ocular adverse events associated with systemic medications: recognition and management. Drugs. 2007;67(1):75–93.
21. Fraunfelder FW. Visual side effects associated with erectile dysfunction agents. Am J Ophthalmol. 2005;140(4):723–724.
22. Pokhrel PK, Loftus SA. Ocular emergencies [published correction appears in Am Fam Physician. 2008;77(7):920]. Am Fam Physician. 2007;76(6):829–836.
23. Fontal MR, Kerrison JB, Garcia R, Oria V. Ischemic optic neuropathy. Semin Neurol. 2007;27(3):221–232.
24. Warrington KJ, Matteson EL. Management guidelines and outcome measures in giant cell arteritis (GCA). Clin Exp Rheumatol. 2007;25(6 suppl 47):137–141.
25. Mohadmed Q, Gillies MC, Wong TY. Management of diabetic retinopathy: a systematic review. JAMA. 2007;298(8):902–916.
26. Gragoudes ES, Adamis AP, Cunningham ET Jr, Feinsod M, Guyer DR. for the VEGF Inhibition Study in Ocular Neovascularization Clinical Trial Group. Pegaptanib for neovascular age-related macular degeneration N Engl J Med. 2004;351(27):2805–2816.
27. Chang TS, Bressler NM, Fine JT, Dolan CM, Ward J, Klesert TR, for the MARINA Study Group. Improved vision-related function after ranibizumab treatment of age-related macular degeneration: results of a randomized clinical trial. Arch Ophthalmol. 2007;125(11):1460–1469.
28. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701–713.
29. Zimmerman TJ, Kooner KS, Kandarakis AS, Ziegler LP. Improving the therapeutic index of topically applied ocular drugs. Arch Ophthalmol. 1984;102(4):551–553.
30. Drug Facts and Comparisons 2008. 62nd ed.St Louis, Mo: :Lippincott Williams & Wilkins; 2007:1725–1745.
31. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10 year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008;359(15):1577–1589.
32. Lassmann-Vague V. Hypoglycaemia in elderly diabetic patients. Diabetes Metab. 2005;(31 spec no. 2):5S53–5S57.
33. Matthews DR, Stratton IM, Aldington SJ, Holman RR, Kohner EM, for the UK Prospective Diabetes Study Group. Risks of progression of retinopathy and vision loss related to tight blood pressure control in type 2 diabetes mellitus: UKPDS 69. Arch Ophthalmol. 2004;122(11):1631–1640.
34. Holman RR, Paul SK, Bethel MA, Neil HA, Matthews DR. Long term follow-up after tight blood pressure control in type 2 diabetes. N Engl J Med. 2008;359(15):1565–1576.
35. Kohner EM. Microvascular disease: what does the UKPDS tell us about diabetic retinopathy? Diabet Med. 2008;25(suppl 2):20–24.
36. The Eye Disease Case Control Study Group. Risk factors for central retinal vein occlusion. Arch Ophthalmol. 1996;114(5):545–554.
37. Solomon O, Huna-Baron B, Kurtz S, et al. Analysis of prothrombotic and vascular risk factors in patients with nonartertic anterior ischemic optic neuropathy. Ophthalmology. 1999;106(4):739–742.
38. Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL III, for the Age Related Eye Disease Study Group. Risk factors for the incidence of advanced age-related macular degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report No. 19. Ophthalmology. 2005;112(4):533–539.
39. Weintraub JM, Willet WC, Rosner B, Colditz GA, Seddon JM, Hankinson SE. Smoking cessation and risk of cataract extraction among US men and women. Am J Epidemiol. 2002;155(1):72–79.
40. Stratton IM, Kohner EM, Aldington SJ, et al. UKPDS 50: risk factors for the incidence and progression of retinopathy in type II diabetes over 6 years from diagnosis. Diabetologia. 2001;44(2):156–163.
41. Cruickshanks KJ, Klein BE, Klein R. Ultraviolet light exposure and lens opacities: the Beaver Dam Eye Study. Am J Public Health. 1992;82(12):1658–1662.
42. Evans JR, Henshaw K. Antioxidant vitamin and mineral supplements for preventing age-related macular degeneration. Cochrane Database Syst Rev. 2008;(1):CD000253.
43. Age-Related Eye Disease Study Research Group. A randomized, placebo controlled clinical trial of high dose supplementation with vitamins C and E, beta carotene and zinc for age-related macular degeneration and vision loss [published correction appears in Arch Ophthalmol. 2008;126(9):1251]. Arch Ophthalmol. 2001;119(10):1417–1436.
44. Lonn E, Bosch J, Yusuf S, et al., for the HOPE and HOPE-TOO Trial Investigators. Effects of long term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. JAMA. 2005;293(11):1338–1347.
45. Goodman GE, Thornquist MD, Balmes J, et al. The Beta-Carotene and Retinol Efficacy Trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping beta-carotene and retinol supplements. J Natl Cancer Inst. 2004;96(23):1743–1750.
46. Johnson AR, Munoz A, Gottleib JL, Jarrard DF. High dose zinc increases hospitalizations due to genitourinary complications. J Urol. 2007;177(2):639–643.
47. Fernandez MM, Afshari NA. Nutrition and the prevention of cataracts. Curr Opin Ophthalmol. 2008;19(1):66–70.
Acute Vision Loss – Eye Disorders – Merck Manuals Professional Edition
Acute loss of vision has 3 general causes:
- Opacification of normally transparent structures through which light rays pass to reach the retina (eg, cornea, vitreous)
- Abnormalities affecting the optic nerve or visual pathways
History of present illness should describe loss of vision in terms of onset, duration, progression, and location (whether it is monocular or binocular and whether it involves the entire visual field or a specific part and which part).
Important associated visual symptoms include floaters, flashing lights, halos around lights, distorted color vision, and jagged or mosaic patterns (scintillating scotomata).
The patient should be asked about eye pain and whether it is constant or occurs only with eye movement.
Review of systems should seek extraocular symptoms of possible causes, including jaw or tongue claudication, temporal headache, proximal muscle pain, and stiffness (giant cell arteritis); and headaches (ocular migraine).
Family history should note any family history of migraine headaches.
Vital signs, including temperature, are measured.
If the diagnosis of a transient ischemic attack is under consideration, a complete neurologic examination is done. The temples are palpated for pulses, tenderness, or nodularity over the course of the temporal artery. However, most of the examination focuses on the eye.
Eye examination includes the following:
- Visual acuity is measured.
- Peripheral visual fields are assessed by confrontation.
- Central visual fields are assessed by Amsler grid.
- Direct and consensual pupillary light reflexes are examined using the swinging flashlight test.
- Ocular motility is assessed.
- Color vision is tested with color plates.
- The eyelids, sclera, and conjunctiva are examined using a slit lamp if possible.
- The cornea is examined with fluorescein staining.
- The anterior chamber is examined for cells and flare in patients who have eye pain or conjunctival injection.
- The lens is checked for cataracts using a direct ophthalmoscope, slit lamp, or both.
- Intraocular pressure is measured.
- Ophthalmoscopy is done, preferably after dilating the pupil with a drop of a sympathomimetic (eg, 2.5% phenylephrine), cycloplegic (eg, 1% cyclopentolate or 1% tropicamide), or both; dilation is nearly full after about 20 minutes. The entire fundus, including the retina, macula, fovea, vessels, and optic disk and its margins, is examined.
- If pupillary light responses are normal and functional loss of vision is suspected (rarely), optokinetic nystagmus is checked. If an optokinetic drum is unavailable, a mirror can be held near the patient’s eye and slowly moved. If the patient can see, the eyes usually track movement of the mirror (considered to be the presence of optokinetic nystagmus).
Acute loss of vision is itself a red flag; most causes are serious.
- Difficulty seeing the red reflex during ophthalmoscopy suggests opacification of transparent structures (eg, caused by corneal ulcer, vitreous hemorrhage, or severe endophthalmitis).
- Retinal abnormalities that are severe enough to cause acute loss of vision are detectable during ophthalmoscopy, particularly if the pupils are dilated. Retinal detachment may show retinal folds; retinal vein occlusion may show marked retinal hemorrhages; and retinal artery occlusion may show pale retina with a cherry-red fovea.
- An afferent pupillary defect (absence of a direct pupillary light response but a normal consensual response) with an otherwise normal examination (except sometimes an abnormal optic disk) suggests an abnormality of the optic nerve or retina (ie, anterior to the chiasm).
In addition, the following facts may help:
- Monocular symptoms suggest a lesion anterior to the optic chiasm.
- Bilateral, symmetric (homonymous) visual field defects suggest a lesion posterior to the chiasm.
- Constant eye pain suggests a corneal lesion (ulcer or abrasion), anterior chamber inflammation, or increased intraocular pressure, whereas eye pain with movement suggests optic neuritis.
- Temporal headaches suggest giant cell arteritis or migraine.
Erythrocyte sedimentation rate (ESR), C-reactive protein, and platelet count are done for all patients with symptoms (eg, temporal headaches, jaw claudication, proximal myalgias, stiffness) or signs (eg, temporal artery tenderness or induration, pale retina, papilledema) suggesting optic nerve or retinal ischemia to exclude giant cell arteritis.
- Ultrasonography is done to view the retina if the retina is not clearly visible with pupillary dilation and indirect ophthalmoscopy done by an ophthalmologist.
- Gadolinium-enhanced MRI is done for patients who have eye pain with movement or afferent pupillary defect, particularly with optic nerve swelling on ophthalmoscopy, to diagnose multiple sclerosis.
|phenylephrine||No US brand name|
Vision impairment and blindness
The International Classification of Diseases 11 (2018) classifies vision impairment into two groups, distance and near presenting vision impairment.
Distance vision impairment:
- Mild – presenting visual acuity worse than 6/12
- Moderate – presenting visual acuity worse than 6/18
- Severe – presenting visual acuity worse than 6/60
- Blindness – presenting visual acuity worse than 3/60
Near vision impairment:
- Presenting near visual acuity worse than N6 or M.08 with existing correction..
A person’s experience of vision impairment varies depending upon many different factors. This includes for example, the availability of prevention and treatment interventions, access to vision rehabilitation (including assistive products such as glasses or white canes), and whether the person experiences problems with inaccessible buildings, transport and information.
Globally, it is estimated that at least 2.2 billion people have a vision impairment or blindness, of whom at least 1 billion have a vision impairment that could have been prevented or has yet to be addressed.
This 1 billion people includes those with moderate or severe distance vision impairment or blindness due to unaddressed refractive error (123.7 million), cataract (65.2 million), glaucoma (6.9 million), corneal opacities (4.2 million), diabetic retinopathy (3 million), and trachoma (2 million), as well as near vision impairment caused by unaddressed presbyopia (826 million) (1).
In terms of regional differences, the prevalence of distance vision impairment in low- and middle-income regions is estimated to be four times higher than in high-income regions (1).
With regards to near vision, rates of unaddressed near vision impairment are estimated to be greater than 80% in western, eastern and central sub-Saharan Africa, while comparative rates in high-income regions of North America, Australasia, Western Europe, and of Asia-Pacific are reported to be lower than 10% (2).
Population growth and ageing will increase the risk that more people acquire vision impairment.
Globally, the leading causes of vision impairment are:
- uncorrected refractive errors
- age-related macular degeneration
- diabetic retinopathy
- corneal opacity
There is some variation in the causes across countries. For example, the proportion of vision impairment attributable to cataract is higher in low- and middle-income countries than high-income countries. In high income countries, diseases such as diabetic retinopathy, glaucoma and age-related macular degeneration are more common.
Among children, the causes of vision impairment vary considerably across countries. For example, in low-income countries congenital cataract is a leading cause, whereas in high income countries it is more ly to be retinopathy of prematurity.
Strategies to address vision impairment
Effective interventions are available for health promotion, prevention, treatment and rehabilitation to address the entire range of needs associated with eye conditions and vision impairment across the life course.
Some are among the most feasible and cost-effective to implement. For example, uncorrected refractive error can be corrected with glasses while cataract surgery can restore vision.
Vision rehabilitation is also effective in improving functioning for people with an irreversible vision impairment.
WHO’s work is guided by the publication Universal eye health: a global action plan 2014-2019, which was agreed to by a resolution at the World Health Assembly in 2013.
- Universal eye health: a global action plan 2014-2019
Over the last few years, WHO has developed and implemented several tools to support countries to assess the provision of eye care services:
- Eye care services assessment tool
- Tool for assessment of diabetes and diabetic retinopathy
- Tool for assessment of rehabilitation services and systems
WHO also developed and launched the World report on vision. The report offers recommendations, including a number focused on ensuring comprehensive and integrated eye care in countries.
It is expected that by shaping the global agenda on vision, the report will assist Member States and their partners in their efforts to reduce the burden of eye conditions and vision impairment and achieve the Sustainable Development Goals (SDGs), particularly SDG target 3.8 on universal health coverage.
1) Bourne RRA, Flaxman SR, Braithwaite T, Cicinelli MV, Das A, Jonas JB, et al.; Vision Loss Expert Group. Magnitude, temporal trends, and projections of the global prevalence of blindness and distance and near vision impairment: a systematic review and meta-analysis. Lancet Glob Health. 2017 Sep;5(9):e888–97.
2) Fricke, TR, Tahhan N, Resnikoff S, Papas E, Burnett A, Suit MH, Naduvilath T, Naidoo K, Global Prevalence of Presbyopia and Vision Impairment from Uncorrected Presbyopia: Systematic Review, Meta-analysis, and Modelling, Ophthalmology. 2018 May 9
Prevalence and Causes of Unilateral Vision Impairment and Unilateral Blindness in Australia: The National Eye Health Survey
1. Wang JJ, Mitchell P, Simpson JM, Cumming RG, Smith W. Visual impairment, age-related cataract, and mortality. Arch Ophthalmol. 2001;119(8):1186-1190. [PubMed] [Google Scholar]
2. Taylor HR, McCarty CA, Nanjan MB. Vision impairment predicts five-year mortality. Trans Am Ophthalmol Soc. 2000;98:91-96. [PMC free article] [PubMed] [Google Scholar]
3. Fielder AR, Moseley MJ. Does stereopsis matter in humans?Eye (Lond). 1996;10(Pt 2):233-238. [PubMed] [Google Scholar]
4. Keeney AH.The dilemma of the monocular driver. Am J Ophthalmol. 1981;91:801-803. [Google Scholar]
5. Vu HT, Keeffe JE, McCarty CA, Taylor HR. Impact of unilateral and bilateral vision loss on quality of life. Br J Ophthalmol. 2005;89(3):360-363. [PMC free article] [PubMed] [Google Scholar]
6. Wilson MR, Mansour M, Ross-Degnan D, et al. . Prevalence and causes of low vision and blindness in the Extreme North province of Cameroon, West Africa. Ophthalmic Epidemiol. 1996;3(1):23-33. [PubMed] [Google Scholar]
7. Ramke J, Palagyi A, Naduvilath T, du Toit R, Brian G. Prevalence and causes of blindness and low vision in Timor-Leste. Br J Ophthalmol. 2007;91(9):1117-1121. [PMC free article] [PubMed] [Google Scholar]
8. Fotouhi A, Hashemi H, Mohammad K, Jalali KH; Tehran Eye Study . The prevalence and causes of visual impairment in Tehran: the Tehran Eye Study. Br J Ophthalmol. 2004;88(6):740-745. [PMC free article] [PubMed] [Google Scholar]
9. Vijaya L, George R, Arvind H, et al. . Prevalence and causes of blindness in the rural population of the Chennai Glaucoma Study. Br J Ophthalmol. 2006;90(4):407-410. [PMC free article] [PubMed] [Google Scholar]
10. Stevens GA, White RA, Flaxman SR, et al. ; Vision Loss Expert Group . Global prevalence of vision impairment and blindness: magnitude and temporal trends, 1990-2010. Ophthalmology. 2013;120(12):2377-2384. [PubMed] [Google Scholar]
11. Bourne RR, Stevens GA, White RA, et al. ; Vision Loss Expert Group . Causes of vision loss worldwide, 1990-2010: a systematic analysis. Lancet Glob Health. 2013;1(6):e339-e349. [PubMed] [Google Scholar]
12. Pascolini D, Mariotti SP. Global estimates of visual impairment: 2010. Br J Ophthalmol. 2012;96(5):614-618. [PubMed] [Google Scholar]
13. Schémann JF, Inocencio F, de Lourdes Monteiro M, Andrade J, Auzemery A, Guelfi Y. Blindness and low vision in Cape Verde Islands: results of a national eye survey. Ophthalmic Epidemiol. 2006;13(4):219-226. [PubMed] [Google Scholar]
14. Newland HS, Harris MF, Walland M, et al. . Epidemiology of blindness and visual impairment in Vanuatu. Bull World Health Organ. 1992;70(3):369-372. [PMC free article] [PubMed] [Google Scholar]
15. Gunnlaugsdottir E, Arnarsson A, Jonasson F. Prevalence and causes of visual impairment and blindness in Icelanders aged 50 years and older: the Reykjavik Eye Study. Acta Ophthalmol. 2008;86(7):778-785. [PubMed] [Google Scholar]
16. Wang JJ, Foran S, Mitchell P. Age-specific prevalence and causes of bilateral and unilateral visual impairment in older Australians: the Blue Mountains Eye Study. Clin Exp Ophthalmol. 2000;28(4):268-273. [PubMed] [Google Scholar]
17. Attebo K, Mitchell P, Smith W. Visual acuity and the causes of visual loss in Australia: the Blue Mountains Eye Study. Ophthalmology. 1996;103(3):357-364. [PubMed] [Google Scholar]
18. Newland HS, Hiller JE, Casson RJ, Obermeder S. Prevalence and causes of blindness in the South Australian population aged 50 and over. Ophthalmic Epidemiol. 1996;3(2):97-107. [PubMed] [Google Scholar]
19. Taylor HR, Xie J, Fox S, Dunn RA, Arnold AL, Keeffe JE. The prevalence and causes of vision loss in indigenous Australians: the National Indigenous Eye Health Survey. Med J Aust. 2010;192(6):312-318. [PubMed] [Google Scholar]
20. Landers J, Henderson T, Craig J. The prevalence and causes of visual impairment in indigenous Australians within central Australia: the Central Australian Ocular Health Study. Br J Ophthalmol. 2010;94(9):1140-1144. [PubMed] [Google Scholar]
21. Creedy J, Taylor PS. Population ageing and social expenditure in Australia. Aust Econ Rev. 1993;(103):56-68. [PubMed] [Google Scholar]
22. Magliano DJ, Peeters A, Vos T, et al. . Projecting the burden of diabetes in Australia—what is the size of the matter?Aust N Z J Public Health. 2009;33(6):540-543. [PubMed] [Google Scholar]
23. Foreman J, Keel S, Dunn R, van Wijngaarden P, Taylor HR, Dirani M. Sampling Methodology And Site Selection In: The Centre for Eye Research Australia; Vision 2020 Australia , eds. The National Eye Health Survey (NEHS): An Australian Population-Based Prevalence Study. Melbourne, Australia: Centre for Eye Research Australia; 2016. [Google Scholar]
24. Australian Institute of Health and Welfare Vision Problems Among Older Australians: Bulletin no. 27: AIHW Catalog no. AUS 60. Canberra, Australia: Australian Institute of Health and Welfare; 2005. [Google Scholar]
25. Australian Bureau of Statistics Australian Statistical Geography Standard. 2014; https://tinyurl.com/y9vv7xl4. Accessed December 11, 2017.
26. Foreman J, Keel S, van Wijngaarden P, Taylor HR, Dirani M. Recruitment and testing protocol in the National Eye Health Survey: a population-based eye study in Australia. Ophthalmic Epidemiol. 2017;24(6):353-363. [PubMed] [Google Scholar]
27. Diabetic Retinopathy Study Report number 6: design, methods, and baseline results; report number 7: a modification of the airlie house classification of diabetic retinopathy: prepared by the Diabetic Retinopathy Study. Invest Ophthalmol Vis Sci. 1981;21(1 Pt 2):1-226. [PubMed] [Google Scholar]
28. Ferris FL III, Wilkinson CP, Bird A, et al. ; Beckman Initiative for Macular Research Classification Committee . Clinical classification of age-related macular degeneration. Ophthalmology. 2013;120(4):844-851. [PubMed] [Google Scholar]
29. Mukesh BN, McCarty CA, Rait JL, Taylor HR. Five-year incidence of open-angle glaucoma: the visual impairment project. Ophthalmology. 2002;109(6):1047-1051. [PubMed] [Google Scholar]
30. Taylor HR, Boudville AI, Anjou MD. The roadmap to close the gap for vision. Med J Aust. 2012;197(11):613-615. [PubMed] [Google Scholar]
31. Keel S, Xie J, Foreman J, van Wijngaarden P, Taylor HR, Dirani M. The prevalence of diabetic retinopathy in australian adults with self-reported diabetes: the National Eye Health Survey. Ophthalmology. 2017;124(7):977-984. [PubMed] [Google Scholar]
32. Foreman J, Xie J, Keel S, Taylor HR, Dirani M. Treatment coverage rates for refractive error in the National Eye Health survey. PLoS One. 2017;12(4):e0175353. [PMC free article] [PubMed] [Google Scholar]
33. Anjou MD, Boudville AI, Taylor HR. Correcting Indigenous Australians’ refractive error and presbyopia. Clin Exp Ophthalmol. 2013;41(4):320-328. [PubMed] [Google Scholar]
34. Turner AW, Mulholland WJ, Taylor HR. Coordination of outreach eye services in remote Australia. Clin Exp Ophthalmol. 2011;39(4):344-349. [PubMed] [Google Scholar]
35. Fricke TR, Holden BA, Wilson DA, et al. . Global cost of correcting vision impairment from uncorrected refractive error. Bull World Health Organ. 2012;90(10):728-738. [PMC free article] [PubMed] [Google Scholar]
36. Lansingh VC, Carter MJ, Martens M. Global cost-effectiveness of cataract surgery. Ophthalmology. 2007;114(9):1670-1678. [PubMed] [Google Scholar]
37. Magliano DJ, Shaw JE, Shortreed SM, et al. . Lifetime risk and projected population prevalence of diabetes. Diabetologia. 2008;51(12):2179-2186. [PubMed] [Google Scholar]
38. Foreman J, Xie J, Keel S, et al. . The prevalence and causes of vision loss in indigenous and non-indigenous Australians: the National Eye Health Survey. Ophthalmology. 2017;124(12):1743-1752. [PubMed] [Google Scholar]
39. Tapp RJ, Anjou MD, Boudville AI, Taylor HR. The roadmap to close the gap for vision—diabetes-related eye care in the indigenous Australian population. Diabet Med. 2013;30(9):1145-1146. [PubMed] [Google Scholar]
40. Taylor HR.A game changer for eye care for diabetes. Med J Aust. 2017;206(1):8-9. [PubMed] [Google Scholar]
41. Laitinen A, Koskinen S, Härkänen T, Reunanen A, Laatikainen L, Aromaa A. A nationwide population-based survey on visual acuity, near vision, and self-reported visual function in the adult population in Finland. Ophthalmology. 2005;112(12):2227-2237. [PubMed] [Google Scholar]
42. Ngondi J, Ole-Sempele F, Onsarigo A, et al. . Prevalence and causes of blindness and low vision in southern Sudan. PLoS Med. 2006;3(12):e477. [PMC free article] [PubMed] [Google Scholar]
43. Kyari F, Gudlavalleti MV, Sivsubramaniam S, et al. ; Nigeria National Blindness and Visual Impairment Study Group . Prevalence of blindness and visual impairment in Nigeria: the National Blindness and Visual Impairment Study. Invest Ophthalmol Vis Sci. 2009;50(5):2033-2039. [PubMed] [Google Scholar]
44. Chia EM, Mitchell P, Rochtchina E, Foran S, Wang JJ. Unilateral visual impairment and health related quality of life: the Blue Mountains Eye Study. Br J Ophthalmol. 2003;87(4):392-395. [PMC free article] [PubMed] [Google Scholar]
45. Mohamed Q, Gillies MC, Wong TY. Management of diabetic retinopathy: a systematic review. JAMA. 2007;298(8):902-916. [PubMed] [Google Scholar]
46. Chua BE, Mitchell P, Cumming RG. Effects of cataract type and location on visual function: the Blue Mountains Eye Study. Eye (Lond). 2004;18(8):765-772. [PubMed] [Google Scholar]
47. Foreman J, Keel S, Xie J, et al.
; Centre for Eye Research Australia and Vision 2020 Australia The National Eye Health Survey 2016: full report of the first national survey to determine the prevalence and major causes of vision impairment and blindness in Australia. http://www.vision2020australia.org.au/uploads/resource/250/National-Eye-Health-Survey_Full-Report_FINAL.pdf. Accessed December 7, 2017.
48. Buch H, Vinding T, La Cour M, Nielsen NV. The prevalence and causes of bilateral and unilateral blindness in an elderly urban Danish population: the Copenhagen City Eye Study. Acta Ophthalmol Scand. 2001;79(5):441-449. [PubMed] [Google Scholar]
Transient Vision Loss (TVL) and Amaurosis Fugax: Overview, Pathophysiology, Etiology
The etiology of transient vision loss includes the following:
- Local ocular conditions (including intraocular masses)
- Ingestion of a large meal
- Entopic phenomena
- Elevated intracranial pressure (ICP)
- Minor head injury (occipital trauma)
- Familial factors
- Ocular treatments (intravitreal injections, trabeculectomy)
Gaze-evoked amaurosis (compression) is transient vision loss occurring when looking in a particular direction.
Transient vision loss may be related to local ocular conditions, such as ocular surface disorders (eg, dry eyes), intraocular foreign bodies or masses, central or branch retinal vein occlusion, central or branch retinal artery occlusion, arteritic anterior ischemic optic neuropathy, intermittent angle closure glaucoma, hyphema, and optic neuritis.
Transient vision loss is also recognized in association with optic disc drusen and colobomas. [4, 5] The mechanism for transient vision loss in these conditions is not fully understood but may be related to local hypoperfusion of the optic nerve or retina.
Transient vision loss has been reported to occur after ingestion of a large meal.  In this case, visual loss results from hypoperfusion of the eye, as blood is shunted to the mesenteric system. Postprandial visual loss is most common in individuals whose ocular perfusion is already compromised (eg, carotid disease, giant cell arteritis). 
Transient vision loss during exercise may result from increased heat exposure, causing decreased nerve conduction through demyelinated nerves (as in multiple sclerosis), also known as the Uhthoff phenomenon. Exercise can also cause pigment release (eg, pigment dispersion syndrome) or lenticular (dislocation/subluxation) abnormalities, causing transient vision loss.
Entopic phenomena are images produced by the eye’s own structures. These images may occur in the normal eye or may reflect abnormalities of ocular structures. Examples of entopic phenomena include the following:
- Floaters: These may be due to posterior vitreous detachment, vitreous hemorrhage, or the normal vitreous.
- Phosphenes: These are luminous sensations that may be induced by mechanical distortion of the retina resulting from eye rubbing or saccadic eye movements. 
- After-images: These are persistent images that remain after an object in the visual field is removed; this is a normal sensation that depends on the intensity and duration of the stimulus.
Increased ICP is a well-known cause of transient vision loss (ie, transient visual obscurations lasting seconds at a time).
Increased pressure in the CSF can transfer through the optic sheath and cause compression on the optic nerve.
The increased intracranial pressure can also cause retinal dysfunction through choroidal compression folds, choroidal neovascularization, and, in severe cases, serous retinal elevation around the nerve head. 
Posttraumatic transient cortical blindness is thought to result from vasospasm and transient ischemia leading to cerebral dysfunction. [9, 10, 11] In these cases, vision returns to normal within minutes to hours, with no permanent neurologic sequelae.
Occasionally, transient vision loss is familial. Multiple episodes of transient vision loss have been described in children with elicited repetitive stereotyped daily blindness of unknown etiology. This rare condition is associated with childhood epilepsy, hemiplegic migraine, and other epileptic disorders through genetic links such as missense mutations in SCN1A. [12, 13]
Migraine with aura is a common cause of transient visual disturbance at any age. Migraine is probably the most common organic cause of organic transient visual loss in children.
 In a study of 83 patients younger than 45 years with episodic visual loss, migraine was the most ly cause in the majority of cases.  In children, 3.
5-5% suffer from recurrent migraine headaches; however, only 18% of those have migraine with aura, and only 5% have aura without headache.
Migrainous visual disturbances are also common in the elderly. Visual aura occurs in 1-2% of elderly patients, and in 58%, aura is not associated with a headache. 
Migraine auras are typically bright and shimmering with a dynamic quality, whereas ischemia tends to produce dark and static defects.
These differences notwithstanding, it may be difficult to distinguish between migraine with aura and amaurosis fugax.
The International Headache Society (IHS) defines a migraine aura as a recurrent disorder that develops over 5-29 minutes and lasts for less than 1 hour. 
Migraine with visual aura is thought to be due to dysfunction of the striate cortex arising from a reduction in cerebral blood flow from the terminal branches of the basilar artery.
Visual symptoms include photopsia, teichopsia (fortification spectra), scotoma, hemianopia, and diplopia and are usually homonymous.
 There may also be other associated neurologic symptoms, such as paresthesia, weakness of limbs, speech disturbance, and vertigo.
Unilateral symptoms are rare but may occur in retinal or ocular migraine. Retinal migraine is presumed to result from retinal vasospasm causing isolated hypoperfusion of the retina or the optic nerve.
[17, 18] This condition is defined as a fully reversible monocular visual disturbance associated with migraine headache and a normal neuro-ophthalmic examination between attacks.
Retinal migraine is not as common as was once thought; one literature review found only 5 cases meeting the IHS criteria for diagnosis. 
Intravitreal injection of ocriplasmin, used to treat symptomatic vitreomacular adhesion, has been reported to cause transient vision loss due to presumed direct retinal side effects but with unknown molecular mechanism.
 Vision loss has also been reported after surgical procedures involving the eye, such as a trabeculectomy. One study showed that more than 50% of patients experienced transient vision loss after trabeculectomy.
There is no test to disprove a patient report of transient vision loss. In addition, eye examination findings may be normal in patients with transient vision loss of both organic and nonorganic etiologies.
Patients with medically unexplained symptoms are frequent attenders. In primary care, 1 of every 5 new consultations involves a patient with symptoms for which no organic cause is found.
 Despite the frequency of unexplained symptoms, there has been little research in this area.
Studies in adults suggest that childhood experiences, including illness in family members and previous medical consultations, are contributing factors to unexplained symptoms in later life. A series by Taich et al found that 26.
7% of patients with medically unexplained visual loss had a previous diagnosis of depression, anxiety, or attention deficit hyperactivity disorder, and 31% had significant stress at school or at home.
 Many patients have been seen by other specialties with unexplained symptoms.
If no medical explanation is found for visual loss in a child, parents may be anxious and keen for further investigations. A supportive approach is required, and the need for investigations must be balanced against the risks of exacerbating fears of disease.  It is important to establish a good rapport with the parents and the child with transient vision loss.
- What Is Glaucoma?
- What Glaucoma Looks
Glaucoma is a condition that damages your eye's optic nerve. It gets worse over time. It's often linked to a buildup of pressure inside your eye. Glaucoma tends to run in families. You usually don’t get it until later in life.
The increased pressure in your eye, called intraocular pressure, can damage your optic nerve, which sends images to your brain. If the damage worsens, glaucoma can cause permanent vision loss or even total blindness within a few years.
Most people with glaucoma have no early symptoms or pain. Visit your eye doctor regularly so they can diagnose and treat glaucoma before you have long-term vision loss.
If you lose vision, it can’t be brought back. But lowering eye pressure can help you keep the sight you have. Most people with glaucoma who follow their treatment plan and have regular eye exams are able to keep their vision.
The fluid inside your eye, called aqueous humor, usually flows your eye through a mesh- channel. If this channel gets blocked, the liquid builds up. Sometimes, experts don’t know what causes this blockage. But it can be inherited, meaning it’s passed from parents to children.
Less-common causes of glaucoma include a blunt or chemical injury to your eye, severe eye infection, blocked blood vessels inside your eye, and inflammatory conditions. It’s rare, but eye surgery to correct another condition can sometimes bring it on. It usually affects both eyes, but it may be worse in one than the other.
It mostly affects adults over 40, but young adults, children, and even infants can have it. African Americans tend to get it more often, when they're younger, and with more vision loss.
You’re more ly to get it if you:
- Are of African American, Irish, Russian, Japanese, Hispanic, Inuit, or Scandinavian descent
- Are over 40
- Have a family history of glaucoma
- Have poor vision
- Have diabetes
- Take certain steroid medications such as prednisone
- Have had an injury to your eye or eyes
- Have corneas that are thinner than usual
- Have high blood pressure, heart disease, diabetes, or sickle cell anemia
- Have high eye pressure
- Are nearsighted or farsighted
There are two main kinds:
Open-angle glaucoma. This is the most common type. Your doctor may also call it wide-angle glaucoma. The drain structure in your eye (called the trabecular meshwork) looks fine, but fluid doesn’t flow out it should.
Angle-closure glaucoma. This is more common in Asia. You may also hear it called acute or chronic angle-closure or narrow-angle glaucoma.
Your eye doesn’t drain it should because the drain space between your iris and cornea becomes too narrow. This can cause a sudden buildup of pressure in your eye.
It’s also linked to farsightedness and cataracts, a clouding of the lens inside your eye.
Less common types of glaucoma include:
Secondary glaucoma. This is when another condition, cataracts or diabetes, causes added pressure in your eye.
Normal-tension glaucoma. This is when you have blind spots in your vision or your optic nerve is damaged even though your eye pressure is within the average range. Some experts say it’s a form of open-angle glaucoma.
Pigmentary glaucoma. With this form, tiny bits of pigment from your iris, the colored part of your eye, get into the fluid inside your eye and clog the drainage canals.
Most people with open-angle glaucoma don’t have symptoms. If symptoms do develop, it’s usually late in the disease. That’s why glaucoma is often called the “sneak thief of vision.” The main sign is usually a loss of side, or peripheral, vision.
Symptoms of angle-closure glaucoma usually come on faster and are more obvious. Damage can happen quickly. If you have any of these symptoms, get medical care right away:
- Seeing halos around lights
- Vision loss
- Redness in your eye
- Eye that looks hazy (particularly in infants)
- Upset stomach or vomiting
- Eye pain
Glaucoma tests are painless and don’t take long. Your eye doctor will test your vision. They’ll use drops to widen (dilate) your pupils and examine your eyes.
They’ll check your optic nerve for signs of glaucoma. They may take photographs so they can spot changes at your next visit. They’ll do a test called tonometry to check your eye pressure. They may also do a visual field test to see if you've lost peripheral vision.
Your doctor may use prescription eye drops, oral medications, laser surgery, or microsurgery to lower pressure in your eye.
Eye drops. These either lower the creation of fluid in your eye or increase its flow out, lowering eye pressure. Side effects include allergies, redness, stinging, blurred vision, and irritated eyes. Some glaucoma drugs may affect your heart and lungs. Be sure to tell your doctor about any other medications you’re taking or are allergic to.
Oral medication. Your doctor might also prescribe medication for you to take by mouth, such as a beta-blocker or a carbonic anhydrase inhibitor. These drugs can improve drainage or slow the creation of fluid in your eye.
Laser surgery. This procedure can slightly raise the flow of fluid from your eye if you have open-angle glaucoma. It can stop fluid blockage if you have angle-closure glaucoma. Procedures include:
- Trabeculoplasty. This opens the drainage area.
- Iridotomy. This makes a tiny hole in your iris to let fluid flow more freely.
- Cyclophotocoagulation. This treats areas of the middle layer of your eye to lower fluid production.
Microsurgery. In a procedure called a trabeculectomy, your doctor creates a new channel to drain the fluid and ease eye pressure. This form of surgery may need to be done more than once. Your doctor might implant a tube to help drain fluid. This surgery can cause temporary or permanent vision loss, as well as bleeding or infection.
Open-angle glaucoma is most often treated with combinations of eye drops, laser trabeculoplasty, and microsurgery. Doctors tend to start with medications, but early laser surgery or microsurgery could work better for some people.
Infant or congenital glaucoma — meaning you are born with it — is usually treated with surgery because the cause is a problem with your drainage system.
You can’t prevent glaucoma. But if you find it early, you can lower your risk of eye damage. These steps may help protect your vision:
- Have regular eye exams. The sooner your doctor spots the signs of glaucoma, the sooner you can start treatment. If you’re over age 40 and have a family history of the disease, get a complete eye exam from an eye doctor every 1 to 2 years. If you have health problems diabetes or are at risk of other eye diseases, you may need to go more often.
- Learn your family history. Ask your relatives whether any of them have been diagnosed with glaucoma.
- Follow your doctor’s instructions. If they find that you have high eye pressure, they might give you eye drops to prevent glaucoma.
- Exercise. Moderate activity walking or jogging at least three times a week might help lower eye pressure.
- Protect your eyes. Use protective eyewear when playing sports or working on home improvement projects.
Glaucoma Research Foundation.
National Institutes of Health.
Glaucoma Research Foundation: “Other Types of Glaucoma,” “Questions & Answers: Normal-Tension Glaucoma,” “Symptoms of Angle-Closure Glaucoma,” “Medication Guide,” “What Can I Do To Prevent Glaucoma?”
American Academy of Ophthalmology: “What Are the Symptoms of Glaucoma?” “Who Is at Risk for Glaucoma?”
Mayo Clinic: “Glaucoma.”
CDC: “Don’t Let Glaucoma Steal Your Sight!”
© 2019 WebMD, LLC. All rights reserved. Symptoms