Glaucoma, Suspect, Adult
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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.
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. Even sleeping position may play a role; Sedgewick et al have shown that lateral and prone sleeping positions result in a significant IOP elevation in patients with pigment dispersion. [8]
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.
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. [9, 10] 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.
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.
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. [11]
Incidence of OAG in Latinos is higher than in non-Hispanic whites, but lower than in Afro-Caribbeans. [12]
Asians, Canadians, Alaskans, Greenland Inuit Indians, and certain South American Indians are at an increased risk for narrow-angle glaucoma.
No sexual predilection exists for POAG.
Women are at a greater risk for angle-closure glaucoma than men.
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).
Most patients who are glaucoma suspect do not develop glaucomatous optic nerve damage and/or visual field loss. Overall, about 1% of individuals with ocular hypertension develop glaucoma per year. The risk is higher for patients with additional risk factors.
Glaucoma causes silent damage; follow-up care is essential to exclude any progressive change over time that may warrant treatment.
Left untreated, patients with optic nerve damage may progress, resulting in progressive loss of side vision and eventually total optic nerve atrophy and irreversible blindness.
Patients should be educated regarding their risk factors, prognosis, and the importance of follow-up care. Glaucoma can cause silent damage with eventual vision loss.
For excellent patient education resources, visit eMedicineHealth’s Eye and Vision Center. Also, see eMedicineHealth’s patient education articles Adult Glaucoma Suspect, Glaucoma FAQs, Normal-Tension Glaucoma, and Ocular Hypertension.
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Robert H Graham, MD Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona
Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, Arizona Ophthalmological Society, American Medical Association
Disclosure: Partner received salary from Medscape/WebMD for employment.
Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society
Disclosure: Nothing to disclose.
Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience
Disclosure: Nothing to disclose.
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, Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
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, American Academy of Ophthalmology
Disclosure: Nothing to disclose.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor, U Fusun Cardakli, MD, to the development and writing of this article.
Glaucoma, Suspect, Adult
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