Glaucoma is a group of eye diseases characterized by optic nerve damage that is usually associated with elevated intraocular pressure. It can cause permanent visual field loss and irreversible blindness without proper treatment.[1] Glaucoma is the second-leading cause of blindness worldwide after cataract, but, unlike with cataract, blindness caused by glaucoma is irreversible.

The two main categories of glaucoma are open-angle glaucoma and angle-closure glaucoma. Additionally, there are both primary and secondary causes of glaucoma. Open-angle glaucoma is the most common form in the United States. Globally, it is the most common cause of irreversible blindness.[2]

The most common form of this disease, primary open-angle glaucoma (POAG), is the focus of this chapter. This condition is an initially asymptomatic, progressive process that can irreversibly damage peripheral visual fields and, ultimately, central vision. A basic ophthalmologic exam can diagnose glaucoma if elevated intraocular pressure or optic disc “cupping” is present, but identification of unaffected or at-risk eyes is not as simple. High-risk findings on ophthalmologic examination include: increased cup-disc ratio (CDR), CDR asymmetry, disc hemorrhage, or elevated intraocular pressure.[3]

Angle-closure glaucoma generally occurs in an anatomically predisposed eye. As intraocular pressure mounts, the eye often becomes red and painful, but sometimes nausea is the principal symptom. Relief of the elevated pressure must occur emergently to avoid severe visual loss or blindness. There are many causes of secondary glaucoma, such as cataract, inflammation, and derangement of the eye anatomy due to blunt trauma, neovascularization in diabetic retinopathy, pigment dispersion syndrome, pseudoexfoliation, and central retinal vein occlusion.

Risk Factors

Age. There is < 1% prevalence in persons under age 65, approximately 1% at 70 years, and 3% at 75 years.[2]

Elevated intraocular pressure. However, high intraocular pressure is not necessary nor pathognomonic for glaucoma.

Race. Prevalence is 4-5 times greater among African-Americans, compared with whites, and reaches 11% in African-Americans aged 80 and over. The age-adjusted rate of blindness due to glaucoma is 6 times higher in African-Americans, with blindness onset averaging 10 years earlier, compared with whites.[4] ,[5]

Family history. There is a relative risk of 3.7 in siblings of the affected person and 2.2 in those with affected parents.[6]

Additional risk factors include systemic, inhaled, or intravitreal c orticosteroid use, high blood pressure (a risk factor for elevated intraocular pressure),[7] ,[8] ,[9] cardiovascular disease, type 2 diabetes,[7],[10] low occular perfusion pressure, and m yopia.[11]


POAG is generally asymptomatic, and major visual field loss can occur prior to any visual symptoms. This condition is often an incidental finding during routine ophthalmologic examinations.

Fundus examination is required for diagnosis, along with visual field testing (confrontational visual field testing is not sufficiently accurate to diagnose glaucoma) and measurement of intraocular pressure. Most persons with POAG will have an untreated intraocular pressure above 21 mmHg at some point in the disease,[12] compared with a normal intraocular pressure of about 15.3 for women and 15.5 for men.[13] Not all patients with elevated intraocular pressures will go on to develop glaucoma.

The American Academy of Ophthalmology describes POAG as chronic, generally bilateral, often asymmetrical, and with all of the following in one or both eyes:[14]

  • Optic disc or retinal nerve fiber layer damage (including thinning or notching in the optic disc rim, defects in the nerve fiber, or progressive change), or characteristic visual field abnormalities without other explanation.
  • Adult onset.
  • Patent anterior chamber angles.
  • No factors known to cause secondary open-angle glaucoma.


Lowering intraocular pressure is the only known effective treatment for glaucoma. Elevated intraocular pressure can be relieved by decreasing the amount of aqueous humor produced or increasing the drainage from the posterior chamber of the eye. The goal of treatment is to preserve vision and prevent progression of vision loss.[15] ,[16]

The target for intraocular pressure is individualized. Pressure must be lowered until no further damage occurs.[14] Because the disease is generally asymptomatic until severe damage has occurred, many patients do not use their medicines or follow up as recommended. Compliance should be monitored closely. Vision loss tends to be progressive as long as intraocular pressure remains elevated above goal.

Methods of lowering intraocular pressure include eye drops, systemic medications, laser treatment, and surgery.

Topical Medication

Prostaglandins, non-selective alpha-adrenergic agonists, and parasympathomimetic agents increase aqueous outflow. Prostaglandin analogues are typically the first-line agents. They are generally effective, well tolerated, and can be given on a once daily dosing schedule.

Beta-blockers, carbonic anhydrase inhibitors, and selective alpha-adrenergic agonists decrease aqueous production. Beta-blockers had previously been first-line drugs.[17] They are generally effective and well tolerated unless contraindicated for pulmonary or cardiovascular reasons. Topical carbonic anhydrase inhibitors are preferred over systemic preparations because of multiple adverse side effects with systemic use. Adrenergic agonists (i.e., brimonidine) have potential (although uncommon) adverse ocular and systemic side effects.

Systemic Therapy

Gingko biloba has improved visual field test results in patients with normal-tension glaucoma[18] but requires cautious use because of its anticoagulant effect.

Other systemic medications, such as carbonic anhydrase inhibitors, are associated with many adverse side effects and are second-line agents.

Laser Therapy

Trabeculoplasty ( laser application to tissues for aqueous absorption in the angle between the cornea and iris) is acceptable as first line-therapy.[19] Laser therapy lowers intraocular pressure by increasing the drainage of aqueous humor.

Laser therapy or cryotherapy can also be used to destroy the ciliary body, which produces the aqueous humor.


Surgery creates an alternative pathway for aqueous flow, but there is no clear advantage to early surgery over medical therapy.[20] ,[21] Surgery is generally reserved for patients with severe disease, refractory to other treatments. Complications associated with surgery include vision loss, infection, and cataract formation.[22]

Nutritional Considerations

Metabolic syndrome, obesity, blood pressure abnormalities, and diabetes are risk factors for POAG.[23] A diet that helps maintain normal blood pressure and blood glucose concentrations may help reduce the risk for this disease, although no controlled trials have investigated this possibility ( see Hypertension and Diabetes chapters).

Nitrate-rich leafy greens. A large prospective study showed that a greater intake of nitrates from green leafy vegetables was associated with 20% to 30% lower risk of POAG.[24] Dietary nitrates increase Nitric Oxide (NO) production via the ‘nitrate‐ nitrite‐ NO’ pathway.[25] Nitric oxide has emerged as a POAG therapeutic target, as it may help to regulate intraocular pressure. The endogenous NO pathway may be compromised in POAG and dietary nitrates from leafy greens offer an alternative pathway to increase NO production.[24]

Antioxidant-rich fruits and vegetables. A study with 584 African-American women found that those who consumed 3 or more servings of fruit or fruit juice per day were 79% less likely to have glaucoma than those who consumed less than one serving. Fruits and vegetables high in vitamins A and C and carotenoids were especially protective.[26]

The Rotterdam Study, including 3500 participants aged 55 years and older, showed that those with a higher retinol intake had half the risk of POAG compared to those with the lowest intakes.[27] The benefits come from food sources; supplemental antioxidant vitamins do not appear to be beneficial.[28] More evidence is needed before specific recommendations can be made.

Studies have noted an association between obesity and both intraocular pressure and ocular hypertension.[29] ,[30] The links between obesity and intraocular pressure have been thought to be the result of excessive intraorbital adipose tissue, increased blood viscosity and episcleral venous pressure, and impairment of aqueous outflow.[29] Evidence does not yet indicate that losing excess weight reduces the risk for glaucoma, although significant decreases in intraocular pressure have been reported in humans during weight loss (0.4 kg- 1.5 kg)[31] and reduced waist circumference[32] associated with fasting.


See Basic Diet Orders Chapter.

Ophthalmology consultation.

What to Tell the Family

It is essential for the patient to have regular ophthalmologic examinations, since affected individuals cannot assess treatment efficacy on their own. Significant optic nerve damage can occur prior to any symptoms. Failure to use glaucoma medications as prescribed can result in severe visual damage. Family members should also be screened for glaucoma by an ophthalmologist or optometrist.


  1. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363(9422):1711-20.  [PMID:15158634]
  2. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014;311(18):1901-11.  [PMID:24825645]
  3. Hollands H, Johnson D, Hollands S, et al. Do findings on routine examination identify patients at risk for primary open-angle glaucoma? The rational clinical examination systematic review. JAMA. 2013;309(19):2035-42.  [PMID:23677315]
  4. Sommer A, Tielsch JM, Katz J, et al. Racial differences in the cause-specific prevalence of blindness in east Baltimore. N Engl J Med. 1991;325(20):1412-7.  [PMID:1922252]
  5. Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open-angle glaucoma. The Baltimore Eye Survey. JAMA. 1991;266(3):369-74.  [PMID:2056646]
  6. Tielsch JM, Katz J, Sommer A, et al. Family history and risk of primary open angle glaucoma. The Baltimore Eye Survey. Arch Ophthalmol. 1994;112(1):69-73.  [PMID:8285897]
  7. Hennis A, Wu SY, Nemesure B, et al. Hypertension, diabetes, and longitudinal changes in intraocular pressure. Ophthalmology. 2003;110(5):908-14.  [PMID:12750088]
  8. Nemesure B, Wu SY, Hennis A, et al. Factors related to the 4-year risk of high intraocular pressure: the Barbados Eye Studies. Arch Ophthalmol. 2003;121(6):856-62.  [PMID:12796259]
  9. Zhao D, Cho J, Kim MH, et al. The association of blood pressure and primary open-angle glaucoma: a meta-analysis. Am J Ophthalmol. 2014;158(3):615-27.e9.  [PMID:24879946]
  10. Distelhorst JS, Hughes GM. Open-angle glaucoma. Am Fam Physician. 2003;67(9):1937-44.  [PMID:12751655]
  11. Girkin CA, McGwin G, McNeal SF, et al. Hypothyroidism and the development of open-angle glaucoma in a male population. Ophthalmology. 2004;111(9):1649-52.  [PMID:15350317]
  12. Primary Open-Angle Glaucoma PPP – 2015. American Academy of Ophthalmology website. Available at: . Published November 2015. Accessed March 22, 2016.
  13. Klein BE, Klein R, Linton KL. Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci. 1992;33(7):2224-8.  [PMID:1607232]
  14. Prum B, Rosenberg L, Gedde S, et al. Primary Open-Angle Glaucoma Preferred Practice Pattern® guidelines. Ophthalmology . 2016;123:P41-P111.
  15. Heijl A, Leske MC, Bengtsson B, et al. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002;120(10):1268-79.  [PMID:12365904]
  16. Higginbotham EJ, Gordon MO, Beiser JA, et al. The Ocular Hypertension Treatment Study: topical medication delays or prevents primary open-angle glaucoma in African American individuals. Arch Ophthalmol. 2004;122(6):813-20.  [PMID:15197055]
  17. van der Valk R, Webers CA, Lumley T, et al. A network meta-analysis combined direct and indirect comparisons between glaucoma drugs to rank effectiveness in lowering intraocular pressure. J Clin Epidemiol. 2009;62(12):1279-83.  [PMID:19716679]
  18. Quaranta L, Bettelli S, Uva MG, et al. Effect of Ginkgo biloba extract on preexisting visual field damage in normal tension glaucoma. Ophthalmology. 2003;110(2):359-62; discussion 362-4.  [PMID:12578781]
  19. Samples JR, Singh K, Lin SC, et al. Laser trabeculoplasty for open-angle glaucoma: a report by the american academy of ophthalmology. Ophthalmology. 2011;118(11):2296-302.  [PMID:21849211]
  20. Lichter PR, Musch DC, Gillespie BW, et al. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology. 2001;108(11):1943-53.  [PMID:11713061]
  21. Janz NK, Wren PA, Lichter PR, et al. The Collaborative Initial Glaucoma Treatment Study: interim quality of life findings after initial medical or surgical treatment of glaucoma. Ophthalmology. 2001;108(11):1954-65.  [PMID:11713062]
  22. Gedde SJ, Schiffman JC, Feuer WJ, et al. Treatment outcomes in the Tube Versus Trabeculectomy (TVT) study after five years of follow-up. Am J Ophthalmol. 2012;153(5):789-803.e2.  [PMID:22245458]
  23. Davis BM, Crawley L, Pahlitzsch M, et al. Glaucoma: the retina and beyond. Acta Neuropathol. 2016;132(6):807-826.  [PMID:27544758]
  24. Kang JH, Willett WC, Rosner BA, et al. Association of Dietary Nitrate Intake With Primary Open-Angle Glaucoma: A Prospective Analysis From the Nurses' Health Study and Health Professionals Follow-up Study. JAMA Ophthalmol. 2016;134(3):294-303.  [PMID:26767881]
  25. Lidder S, Webb AJ. Vascular effects of dietary nitrate (as found in green leafy vegetables and beetroot) via the nitrate-nitrite-nitric oxide pathway. Br J Clin Pharmacol. 2013;75(3):677-96.  [PMID:22882425]
  26. Giaconi JA, Yu F, Stone KL, et al. The association of consumption of fruits/vegetables with decreased risk of glaucoma among older African-American women in the study of osteoporotic fractures. Am J Ophthalmol. 2012;154(4):635-44.  [PMID:22818906]
  27. Ramdas WD, Wolfs RC, Kiefte-de Jong JC, et al. Nutrient intake and risk of open-angle glaucoma: the Rotterdam Study. Eur J Epidemiol. 2012;27(5):385-93.  [PMID:22461101]
  28. Bussel II, Aref AA. Dietary factors and the risk of glaucoma: a review. Ther Adv Chronic Dis. 2014;5(4):188-94.  [PMID:24982753]
  29. Cheung N, Wong TY. Obesity and eye diseases. Surv Ophthalmol. 2007;52(2):180-95.  [PMID:17355856]
  30. Wang S, Xu L, Jonas JB, et al. Major eye diseases and risk factors associated with systemic hypertension in an adult Chinese population: the Beijing Eye Study. Ophthalmology. 2009;116(12):2373-80.  [PMID:19815279]
  31. Dadeya S, Kamlesh , Shibal F, et al. Effect of religious fasting on intra-ocular pressure. Eye (Lond). 2002;16(4):463-5.  [PMID:12101455]
  32. Hassan MB, Isawumi MA. Effects of fasting on intraocular pressure in a black population. Middle East Afr J Ophthalmol. 2014;21(4):328-31.  [PMID:25371639]