Glaucoma, Suspect, Adult 

  • Author: Robert H Graham, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Sep 13, 2010
 

Background

Glaucoma suspect describes a person with one or more risk factors that may lead to glaucoma, but this individual does not have definite glaucomatous optic nerve damage or visual field defect. A great overlap can exist between findings in patients with early glaucoma and those who are glaucoma suspect without the disease.[1, 2, 3] Five to 10 million Americans with ocular hypertension have elevated intraocular pressure (IOP) above 21 mm Hg without evidence of damage. Many of these patients are being treated, but the indications for treatment are not clear-cut. Many others are glaucoma suspect based on the suspicious appearance of the optic nerve head or other risk factors.

With an earlier accurate diagnosis and timely therapy, the goal for this century should be to prevent glaucoma-related blindness. For example, during Glaucoma 2001, a public service project of the foundation of the American Academy of Ophthalmology, individuals with sufficient risk factors that make them susceptible to glaucomatous visual loss were identified and evaluated. The goal of identifying and treating patients who are glaucoma suspect is to preserve visual function by monitoring them for the earliest signs of glaucomatous damage. In individuals who are at a high risk of developing glaucomatous damage, preventive measures, including lowering IOP, may be indicated.

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Pathophysiology

The mechanisms that cause glaucoma are not fully understood. In most clinical cases, a painless elevation of IOP occurs, which can lead to progressive optic nerve damage and visual field loss.[4] The mechanical theory of resistance to outflow (at the juxtacanicular meshwork) is one postulated mechanism for glaucoma. Disturbances of trabecular meshwork (TM) collagen, TM endothelial cell dysfunction, basement membrane thickening, glycosaminoglycan deposits, narrowing intertrabecular spaces, and/or collapse of the Schlemm canal may occur. Experimental and clinical studies show that sustained elevation of IOP can cause optic nerve damage similar to primary open-angle glaucoma (POAG), thus providing support for the role of IOP.

Vascular risk factors and the role of optic nerve perfusion may be of importance.[5] The blood supply to the optic nerve, the axonal or ganglion cell metabolism, and the lamina cribrosa extracellular matrix may play a role. This is especially important in a subgroup of individuals with low-tension glaucoma who have progressive disease despite IOP of less than 21 mm Hg.

Susceptibility of the optic nerve to damage varies from individual to individual.[6, 7] Along with other risk factors, it also depends on the level of IOP. Certain historical and demographic factors, including age, race, family history, and past ocular history, have been shown to have a high association for the disease. Congenital variations, especially in the appearance of the optic nerve or a onetime vascular insult, may be the underlying etiology for a patient's findings and subsequent diagnosis of glaucoma suspect. The key is whether any progression occurs.

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Epidemiology

Frequency

United States

Elevated IOP (ocular hypertension) is estimated to affect 5-10 million Americans, placing them at risk for developing glaucomatous damage. Each year, about 1% of individuals with ocular hypertension develop glaucomatous damage. Similarly, many patients with other risk factors, such as suspicious optic nerve appearance, nerve fiber layer defects, and family history of glaucoma without definite glaucomatous damage, are observed.[8, 9] More than 7 million office visits occur per year to monitor patients with glaucoma or to observe those who are glaucoma suspect.

International

More than 100 million people have elevated IOP. More than 3 million people worldwide are blind secondary to POAG; about 2.4 million people develop POAG each year.

Mortality/Morbidity

Glaucoma is the second most common cause of legal blindness (described as visual acuity [VA] of 20/200 or poorer and visual field of less than 20° in width of its diameter) in the United States, and it is the leading cause of blindness in African Americans. Between 80,000-116,000 persons are legally blind secondary to glaucoma. Each year, an additional 5,500 people are estimated to become legally blind. At least 2.25 million people older than 40 years have glaucoma, but only one half are aware of it and are being treated. As an example, in the United States in 1977, $400 million was spent on direct health costs related to glaucoma; $1.3 billion was lost because of decreased productivity.

Race

  • African Americans have a significantly increased risk for developing POAG. The prevalence of POAG is 3-6 times higher in African Americans than in whites. Glaucoma usually occurs earlier in African Americans than in whites. African Americans not only are 4-8 times more likely to become blind but also go blind 8 times faster.[10]
  • Asians, Canadians, Alaskans, Greenland Inuit Indians, and certain South American Indians are at an increased risk for narrow-angle glaucoma.

Sex

  • No sexual predilection exists for POAG.
  • Women are at a greater risk for angle-closure glaucoma than men.

Age

  • Increasing age is a definite risk factor.
  • The risk of POAG increases with advancing age.
  • The prevalence of POAG is 3-10 times higher among individuals older than 80 years (than people in their 40s).
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Contributor Information and Disclosures
Author

Robert H Graham, MD  Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona

Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Arizona Ophthalmological Society

Disclosure: WebMD/eMedicine Salary Employment

Specialty Editor Board

Bradford Shingleton, MD  Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Martin B Wax, MD  Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience

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.

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