NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Fleming C, Whitlock E, Beil T, et al. Primary Care Screening for Ocular Hypertension and Primary Open-Angle Glaucoma [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2005 Mar. (Evidence Syntheses, No. 34.)

Cover of Primary Care Screening for Ocular Hypertension and Primary Open-Angle Glaucoma

Primary Care Screening for Ocular Hypertension and Primary Open-Angle Glaucoma [Internet].

Show details


Glaucoma is a progressive optic neuropathy that results in structural changes in the optic nerve head and visual field defects that may lead to severe visual impairment or blindness. Glaucoma may arise secondary to other causes such as trauma, steroid therapy, or inflammatory processes such as uveitis. Most cases of glaucoma, however, have no identifiable etiology and are termed primary glaucoma. Glaucoma is also classified as either open-angle glaucoma, in which the angle between the cornea and the pupil is normal, or closed-angle glaucoma, in which this angle is narrowed.

Primary open-angle glaucoma (POAG) is the most prevalent type in the U.S. population. Based on estimates for the year 2000, 2.5 million people in the U.S. have POAG, of whom 130,000 will be blind as a result of the disease.1 Half of those with POAG may not be aware they have the disease.2, 3 The pathogenesis of optic nerve damage in POAG is not well understood, but is likely multifactorial.4 The primary risk factor for development of POAG is an increase of intraocular pressure (IOP) above 21 mm Hg, which is considered to be the upper limit of normal for IOP. In population studies, increasing IOP is associated with an increased prevalence of POAG.3, 5, 6 Increased IOP was once considered a defining feature of POAG. However, a significant proportion (25–50%) of individuals with primary glaucomatous optic disc changes and visual field deficits have normal IOP measurements, a condition known as normal-tension glaucoma (NTG). As a result, increased IOP is no longer considered to be part of the definition of POAG.4

Race is also an important risk factor for POAG. There is a four-fold increase in the prevalence of POAG in persons of African descent. In a population survey conducted in East Baltimore, the prevalence of POAG was 4.2% in blacks vs. 1.1% in whites.7 Since the distribution of IOP is similar between blacks and whites,5 other pathogenic factors must account for this difference.

The incidence and prevalence of POAG also increase with age. The prevalence of POAG in whites is less than 1.0% for those younger than 70, and 2–3% for those older than70. In blacks, the prevalence increases progressively from approximately 1% in those aged 40–49 to 11% in those older than 80.7 Family history is also an important risk factor, indicating that glaucoma is partly attributable to genetic factors. For example, there is an approximately four-fold increase in risk of POAG in siblings of patients with glaucoma.8 Additional risk factors may include decreased central cornea thickness; low diastolic perfusion pressures (diastolic blood pressure — intraocular pressure); diabetes; and severe myopia.9

There have been no long-term, prospective studies of untreated patients with POAG. As a result, the natural history of POAG is not well understood. Based on estimates derived from a case-series of patients with newly diagnosed POAG, the time of progression to blindness varies from 3 years in patients with IOP measurements > 30 mm Hg to 14 years in patients with IOP measurements in the range of 21–25 mm Hg.10 A model based on cross-sectional data in a population with POAG predicts that the average 40-year-old person presenting with initial visual field deficits would not progress to blindness until the age of 80.11 The average 60year-old person presenting with initial visual field deficits would not progress to blindness in either eye during his or her expected lifetime. Overall progression of visual field deficits develops in a linear fashion over time,11 although progression is faster with higher levels of IOP.10 Although glaucoma is a frequent cause of blindness,1 estimated rates of progression do not appear sufficient to lead to complete blindness during the lifetime of the majority of those affected.11

Since IOP is the only modifiable risk factor in POAG, the cornerstone of glaucoma therapy is IOP reduction. Treatment options include topical medications, systemic medications, laser surgery, and incisional surgery, alone or in combination. In recent years, several large randomized clinical trials have examined the benefits of various treatment strategies for both increased IOP without glaucoma (ocular hypertension), and glaucoma, with and without increased IOP.1214 To update prior USPSTF recommendations, we critically reviewed these recent studies for quality and strength of evidence to support treatment and screening for POAG.

PubReader format: click here to try


  • PubReader
  • Print View
  • Cite this Page

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...