Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis

INTRODUCTION — Glaucoma is a group of eye diseases traditionally characterized by elevated intraocular pressure (IOP). However, glaucoma is more accurately defined as an optic neuropathy than a disease of high pressure. In open-angle glaucoma, optic nerve damage results in a progressive loss of retinal ganglion cell axons, which is manifested initially as visual field loss and, ultimately, irreversible blindness if left untreated [1].

This topic will discuss the epidemiology, clinical presentation, and diagnosis of open-angle glaucoma in adults. Glaucoma in children, angle-closure glaucoma, and treatment and prevention of open-angle glaucoma are discussed elsewhere. (See "Overview of glaucoma in infants and children" and "Angle-closure glaucoma" and "Open-angle glaucoma: Treatment".)

CLASSIFICATION — There are different types of glaucoma, generally categorized by the anterior chamber (iridocorneal) angle (figure 1) and the underlying etiology, if known:

●Open-angle glaucoma is an optic neuropathy characterized by progressive peripheral visual field loss followed by central field loss in a typical pattern. It is usually but not always in the presence of elevated intraocular pressure (IOP). Increased aqueous production and/or decreased outflow are possible mechanisms for elevated intraocular pressure (figure 2). The optic nerve or "disc" takes on a hollowed-out appearance on ophthalmoscopic examination, which is described as "cupping." Cupping is associated with the loss of ganglion cell axons.

●Angle-closure glaucoma is characterized by narrowing or closure of the anterior chamber angle. The normal anterior chamber angle provides drainage for the aqueous humor (the fluid that fills the eyeball). When this drainage pathway is narrowed or closed, inadequate drainage leads to elevated IOP and damage to the optic nerve (figure 3). Acute angle-closure glaucoma occurs in eyes with a certain anatomical predisposition. It presents as a painful red eye and must be treated within 24 hours to prevent permanent blindness. (See "Angle-closure glaucoma".)

●Developmental glaucoma occurs in infants and children and is discussed elsewhere. (See "Overview of glaucoma in infants and children" and "Primary infantile glaucoma".)

●Both open-angle and angle-closure glaucoma can be divided into primary and secondary forms. Secondary glaucoma has many subtypes with elevated IOP resulting from uveitis, trauma, glucocorticoid therapy, vasoproliferative retinopathy, or ocular syndromes such as pigment dispersion or pseudoexfoliation (the deposition of white fluffy material within the anterior segment of the eye).

●Glaucoma can also be categorized based on timing (ie, acute, subacute, and chronic).

●Mixed mechanism glaucoma refers to glaucoma with several etiologies (eg, open-angle glaucoma complicated by superimposed angle-closure, or open-angle glaucoma with superimposed uveitis).

EPIDEMIOLOGY — After cataracts, glaucoma is the second leading cause of blindness in the world [2]. It is a leading cause of irreversible blindness and the leading cause of blindness among Black Americans [3,4]. Open-angle glaucoma is the most common type of glaucoma among White and Black populations, whereas angle-closure glaucoma is more common among Asian populations [2,3]. Worldwide in 2015, there were an estimated 57.5 million people with open-angle glaucoma, and this number is projected to increase to 65.5 million by 2020 [5]. It is estimated that there are 2.8 million people with open-angle glaucoma in the United States in 2010 [6] and that the number will increase to 3.4 million in 2020 [7].

Patients with open-angle glaucoma report decreased quality-of-life and difficulties with daily functioning, including driving [8,9]. Patients with glaucoma are also more likely to report falls and motor vehicle collisions [10]. However, one meta-analysis found no association between open-angle glaucoma and all-cause mortality [11].

Risk factors — The major risk factors for developing open-angle glaucoma include age, Black race, family history, and elevated intraocular pressure (IOP) [12-14]. These and other risk factors are discussed below:

●Age – The incidence of open-angle glaucoma increases with age, particularly in patients of White and Black persons [15-17]. The prevalence of open-angle glaucoma is <1 percent in individuals under 55 years of age, approaches 2 percent at age 65, and reaches approximately 4 percent at age 80 [7]. The rate of blindness from open-angle glaucoma also increases with age [4].

●Race – Race is an important risk factor for development and progression of open-angle glaucoma [18]. The estimated prevalence of open-angle glaucoma is approximately three times higher in Black compared with White persons [7]. The age-adjusted rate of blindness from glaucoma among Black persons was 6.6 times that among White persons, with blindness beginning 10 years earlier in Black persons [4]. The incidence of open-angle glaucoma in Hispanic persons is higher than in non-Hispanic White persons, though lower than in Afro Caribbean individuals [19]. Non-Hispanic White females comprise the largest group with open-angle glaucoma in the United States in 2011, but it is anticipated that this will shift to Hispanic males over the next several decades [20].

●Family history – Family history is a significant risk factor for open-angle glaucoma in several population studies [21-24]. The Baltimore Eye Survey found that the relative risk of open-angle glaucoma increased 3.7- and 2.2-fold for individuals with an affected sibling or parent, respectively [21]. Several early-onset glaucoma syndromes are inherited as Mendelian dominant or recessive traits; open-angle glaucoma, however, has a complex inheritance pattern, with the likelihood that multiple genes interact with environmental factors [22]. A report of genetic variants in Japanese primary open-angle glaucoma patients found that non-IOP-related risk (optic nerve vulnerability) was associated with family history of glaucoma, and that IOP-related risk (IOP elevation) was associated with age at the diagnosis [25].

●Diabetes – Observational studies also suggest an association between diabetes and primary open-angle glaucoma. A 2014 systematic review and meta-analysis of 47 observational studies found that the risk for primary open-angle glaucoma was increased for patients with diabetes compared with those without (RR 1.48, 95% CI 1.29-1.71) [26]. The risk increased 5 percent each year after the diagnosis of diabetes.

●Hypertension – Observational studies suggest an association between hypertension and primary open-angle glaucoma. A 2014 systematic review and meta-analysis of 60 observational studies found that the risk for primary open-angle glaucoma was increased in patients with hypertension compared with those without (relative risk [RR] 1.16, 95% CI 1.05-1.28); nearly all studies noted an association between hypertension and increased intraocular pressure [27].

●Elevated intraocular pressure – There is a large body of literature illustrating the association between elevated IOP and both development and progression of open-angle glaucoma [24,28-32].

As an example, the Early Manifest Glaucoma Trial followed 255 patients with a diagnosis of open-angle glaucoma over a mean of eight years; mean IOP was a significant risk factor for progression of glaucoma (hazard ratio [HR] 1.11, 95% CI 1.06-1.17), even when IOP was within the "normal" range of 8 to 22 mmHg [33].

However, nearly 40 percent of patients with otherwise characteristic open-angle glaucoma will not have an elevated IOP [14]. These patients constitute a subgroup commonly referred to as low-tension or normal-tension glaucoma. While a small proportion of open-angle glaucoma in the United States may be classified as normal tension, the majority of patients with open-angle glaucoma in Asia have normal tension glaucoma [34]. By contrast, many patients with elevated pressures never develop the optic nerve and field changes characteristic of glaucoma [28,29]. Thus, although high pressure is clearly associated with open-angle glaucoma, it is neither necessary nor sufficient for the diagnosis and is therefore termed a "risk factor" for the condition.

●Other factors – Other possible risk factors for developing open-angle glaucoma include myopia, pseudoexfoliation, low diastolic perfusion pressure, cardiovascular disease, a history of prior vitreoretinal surgery, hypothyroidism, and high coffee consumption [35-42].

Although risk factors for the development of open-angle glaucoma have been well documented, risk factors for progression of open-angle glaucoma are less certain [43-45]. Results conflict whether fluctuation in IOP is predictive of glaucoma progression [31,32]. Even in patients with documented findings of glaucoma on comprehensive eye examination (eg, visual field deficits, optic disc changes), it is unclear which patients go on to develop loss of visual acuity and blindness [46].

PATHOGENESIS — The pathogenesis of primary open-angle glaucoma is not clear. Optic nerve axon loss may be related to ganglion cell susceptibility, microcirculatory deficiency at the optic nerve head, or extracellular matrix factors [12,47]. These factors may play a combined role: circulatory or extracellular matrix factors could account for both high pressures and axon loss; variation in axon susceptibility might explain why the disease state does not correlate well with elevated IOP [48]. It is not clear if elevated intraocular pressure (IOP) is caused by factors related to aqueous production, aqueous outflow, or anatomic or physiologic features of the trabecular meshwork and other outflow structures. Systemic factors may also play a role, as there is some evidence that cardiac autonomic dysfunction, as measured by heart rate variability, may correlate with the presence of normal pressure glaucoma [49].

Mutations in the myocilin gene (MYOC) have been identified in about 4 percent of adults with open-angle glaucoma and in more than 10 percent of cases of juvenile open-angle glaucoma, a rare autosomal dominant condition with glaucoma onset between 3 and 40 years of age [12]. MYOC mutations alter the myocilin protein. Myocilin-associated glaucoma is characterized by elevated IOP, with IOP >40 mmHg in some patients with juvenile open-angle glaucoma. Myocilin is produced in the ciliary body and trabecular meshwork, but its precise role in regulating IOP is unknown.

CLINICAL PRESENTATION AND COURSE — Individuals with open-angle glaucoma rarely experience symptoms. Thus, open-angle glaucoma is generally detected incidentally during comprehensive ophthalmic examination. This is in contrast to angle-closure glaucoma in which patients present with symptoms and signs including loss of visual acuity, pain, conjunctival erythema, and corneal edema. (See "Angle-closure glaucoma", section on 'Clinical presentation'.)

High elevations of intraocular pressure (IOP), up to 40 mmHg in patients with open-angle glaucoma, generally cause no pain, redness, or visual symptoms. There is no loss of visual acuity as long as central vision is preserved. Central visual field loss is a late manifestation of open-angle glaucoma, usually preceded by ganglion cell loss and optic nerve damage. Some patients are unaware of field loss even when it has progressed to central "tunnel vision" of 10 to 20 degrees. Visual field loss cannot be recovered once it has occurred.

The mean progression rate from a full field of vision to blindness takes approximately 25 years in untreated patients [50]. However, it is important to note that the median progression rate is much slower (approximately 70 years), since only a small minority of patients progress rapidly to blindness. Nonetheless, in a Swedish study of 592 glaucoma patients who had died between 2006 and 2010, 250 (42 percent) had at least one eye with blindness (as defined by the World Health Organization criteria) and 16.4 percent were bilaterally blind at their last eye visit; the median age for developing bilateral blindness was 86 years [51].

SCREENING

Controversy regarding screening — There is controversy regarding which (if any) populations should be screened for open-angle glaucoma, what screening tests should be performed, and with what frequency. Elevated intraocular pressure (IOP), also known as ocular hypertension, was previously thought to be a marker of primary open-angle glaucoma, but many persons with glaucoma do not have elevated IOP, and not all persons with elevated IOP will develop glaucoma [52]. Since the prevalence of elevated IOP in the general population is approximately 4 percent among individuals age ≥40 years [53], and an estimated 12 patients would be needed to treat to prevent one case of glaucoma, 300 individuals would need to be screened to prevent one case of glaucoma within five years of treatment. However, primary open-angle glaucoma is a heterogeneous disease and does not progress in all patients, or may progress at a rate that would not interfere with vision or quality of life in a person's lifetime. (See 'Management of isolated ocular hypertension' below.)

Our approach — There is insufficient evidence to recommend for or against population screening for glaucoma. However, given the risk of blindness with untreated glaucoma, the effectiveness of treatment, and that early open-angle glaucoma is asymptomatic, we suggest that in populations with sufficient resources, individuals over age 40 undergo periodic comprehensive eye evaluations by an ophthalmologist to evaluate for glaucoma. Earlier evaluation may be appropriate for individuals with significant risk factors for glaucoma.

We advise a comprehensive eye examination rather than individual tests such as fundus examination or measurement of IOP alone as these will likely fail to detect many cases of glaucoma, which is defined as an optic neuropathy rather than a disease of high pressure alone [54-56]. The decision of whether to perform visual field testing is made by the ophthalmologist based on the patient’s risk factors. (See 'Risk factors' above.)

Our approach is adapted from the American Academy of Ophthalmology (AAO) recommendations for comprehensive eye examinations [57]:

●For adult patients without risk factors for eye disease, a comprehensive eye exam should be performed every 5 to 10 years in patients <40, every two to four years in patients 40 to 54 years, every one to three years in patients 55 to 64 years, and one to two years in patients ≥65 years.

●For patients with risk factors for glaucoma (eg, Black or Hispanic persons, or those with a family history of vision loss from glaucoma), a comprehensive eye examination should be performed by an ophthalmologist every one to two years in patients <40 and ≥55 years, and every one to three years in patients age 40 to 54 years.

Recommendations of others — The US Preventive Services Task Force (USPSTF) found insufficient evidence to recommend for or against screening adults for glaucoma [52]. They cited the fact that there are no tools available to reliably identify persons who may be at increased risk for glaucoma or for whom screening may be beneficial. Further, although they found adequate evidence that treatment of glaucoma reduces intermediate outcomes such as IOP, visual field loss, and optic nerve changes, the evidence was insufficient to conclude that these changes would lead to improvements in visual impairment, vision-related function, and quality of life. They noted that harms associated with treatment for increased IOP and early open-angle glaucoma include local eye irritation and an increased risk for cataracts.

Cost-effectiveness — In the absence of randomized trials assessing screening strategies, several studies have attempted to determine the cost-effectiveness of glaucoma screening, with some using Markov modelling [58-61]. One study in the United Kingdom found that neither IOP measurement alone nor comprehensive eye examination were cost-effective in subjects age ≥40 years but that screening in older or other higher risk populations might be cost-effective [60]. Another study in Finland found that screening with combined fundus examination, visual field testing, and IOP measurement in persons age 50 to 89 was cost-effective for preventing visual disability (EUR €32,603 per one year of avoided visual disability) and quality-adjusted life years (QALY; €9023 per one QALY gained by screening) [61]. There is a great deal of uncertainty in the assumptions of these models, particularly with regard to which is the optimal screening protocol, the harms and benefits associated with early detection, and the thresholds for different treatments in relation to cost (determining follow-up, adherence, and additional testing) [58,60,61].

DIAGNOSIS

Diagnostic criteria — Glaucoma is diagnosed in patients with characteristic nerve damage on fundus examination (picture 1A-B) and visual field testing, typically in the presence of elevated intraocular pressure (IOP). Some authorities consider either characteristic optic nerve change OR visual field defects as sufficient criteria for diagnosis of open-angle glaucoma [62,63].

The American Academy of Ophthalmology (AAO) Preferred Practice Pattern defines primary open-angle glaucoma as a chronic, generally bilateral, and often asymmetrical disease, which is characterized (in at least one eye) by all of the following [14]:

●Evidence of optic nerve damage from either or both of the following:

•Optic disc or retinal nerve fiber layer structural abnormalities (eg, thinning, cupping, or notching of the disc rim, progressive change, nerve fiber layer defects)

•Reliable and reproducible visual field abnormalities (eg, arcuate defect, nasal step paracentral scotoma, generalized depression) in the absence of other causes or explanations for a field defect.

●Adult onset.

●Open, normal appearing anterior chamber angles.

●Absence of known (eg, secondary) causes of open-angle glaucoma.

Who should be referred for comprehensive eye examination? — Patients with abnormal cupping on funduscopic examination or risk factors (eg, age >40) should be referred to an ophthalmologist or optometrist for a comprehensive eye examination. Any patient with high IOP detected during community-based screening or spectacle/contact lens evaluation should also be referred for a comprehensive eye examination. The best available data support examination by an ophthalmologist as the most accurate way to detect glaucoma [64]. (See 'Risk factors' above.)

Diagnostic tests

Fundus examination — The primary care clinician should be attentive to the presence of cupping seen in the fundus. Cupping describes a hollowed-out appearance of the optic nerve or "disc" on fundus examination. A cup whose diameter is greater than 50 percent of the vertical disc diameter is suspicious for glaucoma.

Although cupping has the highest sensitivity and specificity of any other finding on eye examination, there is no single cutoff criteria that yields sufficiently high sensitivity and specificity to make cupping a useful diagnostic test [65]. One study found that ophthalmologists, using direct ophthalmoscopy, detected less than one-half of cases of glaucoma [54]. Combining cupping with other criteria increased diagnostic yield.

Other findings on fundus examination indicative of glaucoma include thinning or notching of the disc rim, progressive change of the size or shape of the cup, and asymmetry of the cup-to-disc ratio between the eyes [65,66].

Visual field testing — Open-angle glaucoma ideally should be diagnosed before there is significant visual field loss. However, confrontational field testing, using the examiner's fingers, is not useful in the detection of glaucoma. Automated perimetry is an important diagnostic tool that is much more reliable at detecting visual field loss in glaucoma compared with confrontational field testing (figure 4) [67].

There are several types of automated perimetry technologies, including standard threshold automated perimetry, frequency-doubling technology perimetry, and short-wavelength automated perimetry [55]. Automated perimetry has become the standard of care for optometric and ophthalmic practice in the detection and monitoring of glaucoma, although there is a role for careful manual perimetry in some cases, particularly in patients with advanced field loss or dementia. Reliable field testing requires comprehension and cooperation on the part of the patient. Dementia and other mental or physical problems may preclude testing in certain individuals, forcing the clinician to rely upon other variables in diagnostic and therapeutic decision-making.

Visual field testing can be time consuming and of variable specificity and sensitivity, depending on user characteristics and the type of test being used. Newer technologies to measure visual fields with greater reliability are in development. (See 'Newer technologies' below.)

Intraocular pressure — Elevated IOP alone does not establish the diagnosis of open-angle glaucoma [14,68]. One-third to one-half of individuals with glaucoma field defects have intraocular pressures ≤21 mmHg when first detected (normal IOP 8 to 21 mmHg) [69]. In addition, over 90 percent of adults with pressures >21 mmHg have no optic nerve damage. However, patients with elevated IOP should be referred to an ophthalmologist given their higher risk of open-angle glaucoma. (See 'Risk factors' above and 'Management of isolated ocular hypertension' below.)

A prospective population study of risk factors associated with glaucomatous field loss found that, during a period of five years, 99 percent of eyes with an initial pressure <20 mmHg continued to be free of glaucomatous field defects, compared with 93 percent of eyes with an initial pressure ≥20 mmHg [70]. The sensitivity for the diagnosis of open-angle glaucoma by IOP measurement was 47.1 percent and the specificity over 90 percent at an IOP cutoff point of >21 mmHg [56]. The presence of either increased IOP (>21 mmHg) or increased vertical cup/disc ratio (≥0.5) increased the sensitivity to 61 percent but decreased the specificity to 84 percent. There was no cutoff value for IOP that had reasonable sensitivity and specificity as a screening tool for the diagnosis of open-angle glaucoma.

Ophthalmologists and optometrists can measure IOP by applanation tonometry, pneumotonometry, or air-puff tonometry. Applanation tonometry is a method that determines the IOP from the force required to flatten (applanate) a constant area of the cornea (picture 2). Applanation tonometry is most accurate and less subject to artifact. All tonometry methods require specialized equipment and skill and thus fall out of the realm of the primary care clinician. Due to the effects of central corneal thickness on the mechanics of applanation tonometry, falsely higher measurements occur in patients with thicker corneas and falsely lower measurements occur in those with thinner corneas [71]. This can be partially corrected with pachymetry. (See 'Pachymetry' below.)

Schiotz tonometry is a handheld device that is relatively inexpensive but requires frequent use for reliable results. Generalists who practice in populations that do not have access to optometric or ophthalmic care can learn Schiotz tonometry and use it in conjunction with the optic disc examination in deciding whom to treat or refer. In developed countries, it is less common for primary care providers to measure IOP.

There is some evidence that wearing a tight necktie may temporarily increase IOP [72]. The clinical implications of these findings require further study. Regardless, it is prudent to ask patients to loosen collars and ties prior to measuring IOP.

Pressure parameters for referral — There are no standard criteria for referral to an ophthalmologist for patients with elevated pressures. Primary open-angle glaucoma rarely presents with IOP >30 mmHg, which is more common among patients with angle-closure glaucoma or secondary (rather than primary) open-angle glaucoma. (See "Angle-closure glaucoma" and "The red eye: Evaluation and management".)

The following represent indications for ophthalmologic referral based on clinical practice experience:

●IOP >40 mmHg – Emergency referral

●IOP 30 to 40 mmHg – Urgent referral (within 24 hours) if no symptoms suggesting acute glaucoma

●IOP 25 to 29 mmHg – Evaluation within one week

●IOP 23 to 24 mmHg – Repeat measurement to confirm and/or referral for comprehensive eye examination

These indications are not absolute and should be interpreted in the context of patient history and examination findings. As an example, a patient with an IOP of 28 and advanced open-angle glaucoma including field loss and cupping may represent an emergency because of risk of imminent field loss, while a patient with a healthy nerve could withstand an IOP at that level for weeks with little risk of further nerve damage.

Pachymetry — Pachymetry is the measurement of corneal thickness; it can be performed by ultrasound or other methods. Patients with thin corneas are at higher risk for the development of open-angle glaucoma [73,74]. Ophthalmologists may perform pachymetry in patients with suspected or diagnosed open-angle glaucoma to further evaluate their risk for development or progression of open-angle glaucoma [75]. Additionally, corneal thickness affects the results of applanation tonometry, and pachymetry may adjust for this effect. (See 'Intraocular pressure' above.)

Newer technologies — Several newer technologies have been developed to evaluate the optic disc, retinal nerve fiber layer, and visual field. These may aid in the early detection of glaucoma, as well as other eye diseases.

●Optical coherence tomography – Optical coherence tomography (OCT), Heidelberg retinal tomography (HRT), and scanning laser polarimetry are noninvasive imaging techniques that analyze light reflected off the fundus [76,77]. The need for pupil dilation varies with the particular device and the part of the fundus being studied. These tests are well-tolerated by patients. The devices generate a digital image and quantification of specific features of optic nerve head anatomy.

One study comparing OCT, HRT, and scanning laser polarimetry with conventional qualitative assessment of stereoscopic photographs of the optic disc showed that the three newer technologies performed as well as, but not better than, stereoscopic photographs [78]. Accuracy of results from stereoscopic images is, however, dependent on the experience and skill of the interpreter, whereas the newer technologies provide more quantitative data that is less user-dependent. A study from Finland found that screening capabilities of newer technologies including OCT, scanning laser polarimetry (GDx), and HRT were similar, with only moderate accuracy, and concluded that screening with these parameters alone is not reliable [79].

Additionally, in highly myopic but otherwise healthy eyes where there may be visual field defects and the optic nerve may have an abnormal appearance, OCT may provide the clinician an additional tool to help distinguish these findings from true glaucomatous changes [80].

●Visual field testing with brain computer interface – A portable brain-computer interface (wearable, wireless, dry electroencephalogram and electrooculogram systems) that assesses electrical brain responses to visual field stimulation has shown promise as an alternative and potentially more reliable means of diagnosing glaucoma compared with standard visual field testing [81].

MANAGEMENT OF ISOLATED OCULAR HYPERTENSION

●Diagnosis – Ocular hypertension is defined as abnormally high intraocular pressure (IOP) with no evidence of glaucoma, that is, no field loss or abnormality of the optic nerve. It is asymptomatic. After a finding of an elevated IOP measurement, it is good practice to measure intraocular pressure on a second occasion within a few weeks because of the possibility of measurement artifact related to method or technician. This can be done at the time of field testing and fundus examination for exclusion of open-angle glaucoma.

●Rationale for treatment – Among patients who are found to have ocular hypertension, treatment to lower IOP may delay or prevent the onset of open-angle glaucoma [73,82-84]. A meta-analysis of 10 trials demonstrated that medical treatment for ocular hypertension reduced the risk of visual field defects due to glaucoma compared with placebo or no treatment (odds ratio [OR] 0.62, 95% CI 0.47-0.81) [84].

●When to reduce IOP – Although there is no clear consensus regarding a threshold IOP for initiation of treatment, in our experience, most clinicians would initiate treatment in a patient with two instances of IOP >25 mmHg, although some would do so for two instances of IOP >22 mmHg.

Other findings, such as the presence of a disc hemorrhage, may lower IOP treatment thresholds due to greater risk of visual field deterioration [85].

●Treatment – Treatment is typically with topical prostaglandins, beta blockers, or laser therapy [86]. (See "Open-angle glaucoma: Treatment", section on 'Pharmacologic therapies' and "Open-angle glaucoma: Treatment", section on 'Laser therapy'.)

●Follow-up – Similar to patients with glaucoma, patients with ocular hypertension are followed with IOP measurements, field testing, and evaluation of the optic nerves, although it may be at longer intervals than patients with glaucoma.

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●Basics topics (see "Patient education: Age-related vision loss (The Basics)" and "Patient education: Open-angle glaucoma (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Classification – Open-angle glaucoma is an optic neuropathy characterized by progressive peripheral visual field loss followed by central field loss in a typical pattern. It is usually but not always in the presence of elevated intraocular pressure (IOP). Increased aqueous production and/or decreased outflow are possible mechanisms for elevation of intraocular pressure (figure 2). (See 'Classification' above.)

●Epidemiology – Open-angle glaucoma is a leading cause of irreversible blindness in the world. The major risk factors for developing open-angle glaucoma include age, Black race, family history, and elevated IOP. (See 'Epidemiology' above.)

●Clinical presentation – Individuals with open-angle glaucoma rarely experience symptoms. Some patients are unaware of field loss even when it has progressed to central "tunnel vision." Thus, open-angle glaucoma is generally detected incidentally on comprehensive ophthalmic examination. (See 'Clinical presentation and course' above.)

●Screening – We suggest that all individuals over age 40 be screened for glaucoma by referral for comprehensive eye examination to an ophthalmologist or an optometrist skilled in the assessment of the optic nerve and knowledgeable about glaucoma (Grade 2B). Screening with individual tests (eg, fundus examination or measurement or intraocular pressure alone) is insufficient to evaluate for the presence of glaucoma. Earlier screening may be appropriate for individuals with significant risk factors for glaucoma. (See 'Screening' above.)

●Referral for comprehensive eye examination – Patients with abnormal cupping on fundus examination should be referred for a comprehensive eye examination. (See 'Who should be referred for comprehensive eye examination?' above.)

●Diagnosis – Glaucoma is diagnosed in patients with characteristic nerve damage on fundus examination and on visual field testing (picture 1A-B), typically in the presence of elevated IOP. Some authorities consider either characteristic optic nerve change OR visual field defects as sufficient criteria for diagnosis of open-angle glaucoma. Patients with elevated IOP but normal optic nerves and visual fields may be diagnosed as having ocular hypertension.(See 'Diagnosis' above and 'Management of isolated ocular hypertension' above.)

●Management of isolated ocular hypertension – Among patients with ocular hypertension, treatment to lower IOP may delay or prevent the onset of open-angle glaucoma. (See 'Management of isolated ocular hypertension' above.)