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Primary Open-Angle Glaucoma

  • Author: Jerald A Bell, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
 
Updated: Feb 20, 2014
 

Practice Essentials

Primary open-angle glaucoma is described distinctly as a multifactorial optic neuropathy that is chronic and progressive, with a characteristic acquired loss of optic nerve fibers. Such loss develops in the presence of open anterior chamber angles, characteristic visual field abnormalities, and intraocular pressure that is too high for the continued health of the eye. It manifests by cupping and atrophy of the optic disc (see the image below), in the absence of other known causes of glaucomatous disease.[1, 2]

Advanced glaucomatous damage with increased cuppin Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields, MD.

Essential update: Visual field test may miss early central macular damage in glaucoma

In some patients with glaucoma, the addition of a 10-2 visual field (VF) test to the standard 24-2 VF test or modification of the 24-2 VF equipment to assess more test points may help to detect early central macular damage.[3, 4] In a prospective observational study of 100 eyes from 74 patients with glaucomatous optic neuropathy and a 24-2 VF test with mean deviation better than −6 dB, Traynis et al found that the 24-2 VF test failed to detect early glaucomatous damage in the central macula in 13 of 83 hemifields (15.7%) subsequently shown to be abnormal on 10-2 VF testing. Thus, the 10-2 VF test revealed abnormalities in 22.7% of the 22 eyes that appeared normal with 24-2 VF testing.[4] Among the abnormal hemifields on 10-2 VF testing, 68% were classified as arcuatelike, 8% as widespread, and 25% as other.[3, 4]

Signs and symptoms

Because of the silent nature of glaucoma, patients usually don’t present with any symptoms or visual complaints until late in the disease course, particularly with primary open-angle glaucoma. However, narrow/closed-angle glaucoma and secondary glaucomas can cause rapid closure of the trabecular meshwork, with an equally rapid rise in intraocular pressure, which is usually symptomatic, particularly when intraocular pressure is 35 mm Hg or more.

Significant attention should be given to the following in the patient’s clinical history:

  • Past ocular history
  • Previous ocular surgery, including photocoagulation or refractive procedures
  • Ocular/head trauma
  • Past medical history
  • Current medications
  • Risk factors for glaucomatous optic neuropathy

See Clinical Presentation for more detail.

Diagnosis

Screening the general population for primary open-angle glaucoma is most effective if targeted toward those at high risk, such as African Americans and elderly individuals, especially if the screening consists of intraocular pressure measurements combined with assessment of optic nerve status.

Examination of patients with suspected primary open-angle glaucoma includes the following:

  • Slit lamp examination of the anterior segment
  • Fundoscopy
  • Tonometry
  • Gonioscopy
  • Pachymetry

Lab Tests

Laboratory tests that may be used to rule other causes for optic neuropathy in patients suspected of having normal-tension glaucoma include the following:

  • CBC count
  • Erythrocyte sedimentation rate
  • Serology for syphilis (micro-hemagglutination- Treponema pallidum [MHA-TP], not Venereal Disease Research Laboratory [VDRL] test)
  • Rarely, serum protein electrophoresis: For individuals with potential autoimmune etiology for some glaucomatous optic neuropathies

Imaging studies

The following imaging studies may be used to evaluate patients with suspected primary open-angle glaucoma:

  • Fundus photography
  • Retinal nerve fiber layer imaging on high-contrast black and white film using red-free techniques
  • Confocal scanning laser ophthalmoscopy
  • Scanning laser polarimetry
  • Optical coherence tomography
  • Neuroimaging, if suggested by the patient’s pattern of visual field loss

Investigational imaging modalities in the evaluation and management of patients with primary open-angle glaucoma include the following:

  • Fluorescein angiography
  • Ocular blood flow analysis via laser Doppler flowmetry
  • Color vision measurements
  • Contrast sensitivity testing
  • Electrophysiologic tests
  • Ultrasound biomicroscopy

See Workup for more detail.

Management

Current medical therapy for primary open-angle glaucoma is limited toward lowering intraocular pressure. A rational approach to choosing antiglaucoma medications should minimize the number of medications and the probability of significant adverse effects.

If one medication is not adequate in reaching the target pressure, a second medication should be chosen that has a different mechanism of action, so that the 2 drug therapies will have an additive effect.

Pharmacotherapy

Medications used in the management of primary open-angle glaucoma include the following:

  • Beta-adrenergic blockers (eg, levobunolol 0.25%, 0.5%; timolol maleate/hemihydrate; carteolol ophthalmic; betaxolol ophthalmic; metipranolol hydrochloride; levobetaxolol)
  • Adrenergic agonists (eg, brimonidine; apraclonidine 0.5%, 1%)
  • Less-selective sympathomimetics (eg, dipivefrin, epinephrine, memantine)
  • Carbonic anhydrase inhibitors (eg, dorzolamide, brinzolamide, acetazolamide, methazolamide)
  • Beta-blocker/carbonic anhydrase inhibitor combination (eg, dorzolamide HCl/timolol maleate)
  • Prostaglandin analogs (eg, latanoprost 0.005%, bimatoprost, travoprost ophthalmic solution, unoprostone, tafluprost)
  • Miotic agents (eg, pilocarpine ophthalmic)
  • Hyperosmotic agents (eg, isosorbide dinitrate, mannitol, glycerin)
  • Beta-blocker/alpha agonist combination (eg, brimonidine/timolol)

Surgery

Surgery is indicated in primary open-angle glaucoma when glaucomatous optic neuropathy worsens (or is expected to worsen) at any given level of intraocular pressure and the patient is on maximum tolerated medical therapy.

The following are surgical options that may be used for primary open-angle glaucoma:

  • Argon laser trabeculoplasty
  • Selective laser trabeculoplasty
  • Trabeculectomy
  • Drainage implant (ie, seton/tube/shunt) surgery
  • Ciliary body ablation

Newer techniques that hold potential as surgical options in primary open-angle glaucoma include the following:

  • Deep sclerectomy/viscocanalostomy/with or without collagen implant
  • 360-degree suture canaloplasty

See Treatment and Medication for more detail.

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Background

The definition of glaucoma has changed drastically since its introduction around the time of Hippocrates (approximately 400 BC). The word glaucoma came from the ancient Greek word glaucosis, meaning clouded or blue-green hue, most likely describing a patient having corneal edema or rapid evolution of a cataract precipitated by chronic elevated pressure. Over the years, extensive refinement of the concept of glaucoma has continued, accelerating, especially in the last 100 years, to the present date.

Glaucoma is currently defined as a disturbance of the structural or functional integrity of the optic nerve that causes characteristic atrophic changes in the optic nerve, which may also lead to specific visual field defects over time. This disturbance usually can be arrested or diminished by adequate lowering of intraocular pressure (IOP). Nevertheless, some controversy still exists as to whether IOP should be included in the definition, as some subsets of patients can exhibit the characteristic optic nerve damage and visual field defects while having an IOP within the normal range. The generic term glaucoma should only be used in reference to the entire group of glaucomatous disorders as a whole, because multiple subsets of glaucomatous disease exist. A more precise term should be used to describe the glaucoma, if the specific diagnosis is known.

Primary open-angle glaucoma (POAG) is described distinctly as a multifactorial optic neuropathy that is chronic and progressive with a characteristic acquired loss of optic nerve fibers. Such loss develops in the presence of open anterior chamber angles, characteristic visual field abnormalities, and IOP that is too high for the continued health of the eye. It manifests by cupping and atrophy of the optic disc (shown in the image below), in the absence of other known causes of glaucomatous disease.[1, 2]

Advanced glaucomatous damage with increased cuppin Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields, MD.

Note that the definition of POAG is not synonymous or solely defined by the presence of elevated IOP, but that increased IOP is a risk factor associated with the development of the disease, and is not the disease itself. Patients could develop optic neuropathy of glaucoma in the absence of documented elevated IOP. This condition has been termed normal-tension or low-tension glaucoma.

People who maintain elevated pressures in the absence of nerve damage or visual field loss exist. They are considered at risk for glaucoma and have been termed glaucoma suspects or ocular hypertensives (see Ocular Hypertension). POAG is a major worldwide health concern, because of its usually silent, progressive nature, and because it is one of the leading preventable causes of blindness in the world. With appropriate screening and treatment, glaucoma usually can be identified and its progress arrested before significant effects on vision occur.

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Pathophysiology

The exact cause of glaucomatous optic neuropathy is not known, although many risk factors have been identified, to include the following: elevated IOP, family history, race, age older than 40 years, and myopia.

Elevated IOP is the most studied of these risk factors because it is the main clinically treatable risk factor for glaucoma. Multiple theories exist concerning how IOP can be one of the factors that initiates glaucomatous damage in a patient. Two of the major theories include the following: (1) onset of vascular dysfunction causing ischemia to the optic nerve, and (2) mechanical dysfunction via cribriform plate compression of the axons.

In addition to vascular compromise and mechanically impaired axoplasmic flow, contemporary hypotheses of possible pathogenic mechanisms that underlie glaucomatous optic neuropathy include excitotoxic damage from excessive retinal glutamate, deprivation of neuronal growth factors, peroxynitrite toxicity from increased nitric oxide synthase activity, immune-mediated nerve damage, and oxidative stress. The exact role that IOP plays in combination with these other factors and their significance to the initiation and progression of subsequent glaucomatous neuronal damage and cell death over time is still under debate; the precise mechanism is still a hot topic of discussion.

However, IOP is the only clinical risk factor that has been able to be successfully manipulated to date. Categorizing and managing patients based on their IOP and when IOP should be treated to prevent optic nerve damage became the forefront issue of glaucoma management for most of the last half of the 20th century.

Several studies over the years have shown that as IOP rises above 21 mm Hg, the percentage of patients developing visual field loss increases rapidly, most notably at pressures higher than 26-30 mm Hg. A patient with an IOP of 28 mm Hg is about 15 times more likely to develop field loss than a patient with a pressure of 22 mm Hg. Therefore, a patient population of those with elevated IOP should not be thought of as homogeneous. Furthermore, before initiating treatment of a patient based on a specific IOP measurement, the following factors should be considered regarding that IOP level obtained:

  • Variability of tonometry measurements per examiner (usually found to be about 10%, or 1-2 mm Hg)
  • Effect corneal thickness has on accuracy of IOP measurements (see Other Tests)
  • Diurnal variation of IOP (often highest in the early morning hours, but maximum IOP can be at any time of day in some patients)
  • In addition, remember that while normal eyes have a diurnal variation of approximately 3-4 mm Hg, glaucomatous eyes have even higher variation (>10 mm Hg). Note: Multiple readings should be taken over time and should be considered with correlative evidence of visual field and optic nerve examination before any diagnosis or therapy is rendered.

A study by Costa et al supports the need to more accurately assess the relationship of 24-hour IOP to 24-hour diastolic perfusion pressure in patients with glaucoma. Future methodology that performs noninvasive, real-time IOP measurements throughout the 24 hours of the day may enable a more complete understanding of the roles that IOP and blood pressure have to the etiology of glaucomatous damage and progression of the disease.[5]

Other points of importance when considering a diagnosis of POAG are described below.

Disc cupping and nerve fiber layer losses of up to 40% have been shown to occur before actual visual field loss has been detected. Therefore, visual field examination cannot be the sole tool used to determine when a patient has begun to sustain undeniable glaucomatous damage, and it should not be used in isolation as the benchmark for treatment.

In cases where POAG is associated with increased IOP, the cause for the elevated IOP generally is accepted to be decreased facility of aqueous outflow through the trabecular meshwork. Occurrence of this increase in resistance to flow has been suggested by multiple theories, to include the following:

  • An obstruction of the trabecular meshwork by accumulated material
  • A loss of trabecular endothelial cells
  • A reduction in trabecular pore density and size in the inner wall endothelium of the Schlemm canal
  • A loss of giant vacuoles in the inner wall endothelium of the Schlemm canal
  • A loss of normal phagocytic activity
  • Disturbance of neurologic feedback mechanisms

Other processes thought to play a role in resistance to outflow include altered corticosteroid metabolism, dysfunctional adrenergic control, abnormal immunologic processes, and oxidative damage to the meshwork.

Numerous other undetermined factors are considered to be at work in the pathogenesis of glaucoma. Basic and clinical science research continues to play a role in the search for such factors that contribute to the development and prognosis of the patient with POAG.

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Epidemiology

Frequency

United States

Multiple population studies (eg, Framingham, Beaver Dam, Baltimore, Rotterdam, Barbados, Egna-Neumarkt) have been performed to estimate the prevalence of eye disease, including that of POAG and those individuals with ocular hypertension (OHT) who are at risk for POAG.

Estimates of the prevalence of glaucoma in studies involving only the United States suggest the following: glaucoma is a leading cause of irreversible blindness, second only to macular degeneration; only one half of the people who have glaucoma may be aware that they have the disease; and more than 2.25 million Americans aged 40 years and older have POAG.

More than 1.6 million have significant visual impairment, with 84,000-116,000 bilaterally blind in the United States alone. These statistics emphasize the need to identify and closely monitor those at risk of glaucomatous damage.

In a white population at risk for glaucoma, visual field loss can be expected to develop in about 3% of subjects over 10 years of follow up without treatment. Risk increases with age and IOP.[6]

In the United States, 3-6 million people, including 4-10% of the population older than 40 years, are currently without detectable signs of glaucomatous damage using present-day clinical testing, but they are at risk due to IOP of 21 mm Hg or higher. Roughly 0.5-1% per year of those individuals with elevated IOP will develop glaucoma over a period of 5-10 years. The risk may be declining to less than 1% per year, now that ophthalmoscopic and perimetric techniques for detecting glaucomatous damage have improved significantly.

Diagram showing the relative proportion of people Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally shaded lines) and/or damage from glaucoma (vertically shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are also those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). Courtesy of M. Bruce Shields, MD.OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines
Diagram of intraocular pressure distribution, with Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, field loss among individuals with pressures in the upper teens can occur. Also, note that the average pressure among those with glaucomas is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.

International

Glaucoma is the second leading cause of blindness in the world (surpassed only by cataracts, a reversible condition). More than 3 million people are bilaterally blind from POAG worldwide, and more than 2 million people will develop POAG each year.

Mortality/Morbidity

Over a 5-year period, several studies have shown the incidence of new onset of glaucomatous damage in previously unaffected patients to be about 2.6-3% for IOPs 21-25 mm Hg, 12-26% incidence for IOPs 26-30 mm Hg, and approximately 42% for those higher than 30 mm Hg.

The Ocular Hypertension Treatment Study (OHTS) found that the overall risk for patients with IOPs ranging from 24-31 mm Hg but with no clinical signs of glaucoma have an average risk of 10% of developing glaucoma over 5 years, with that risk being cut in half if patients are preemptively started on IOP-lowering therapy. Significant subsets of higher and lower risk exist when pachymetry (central corneal thickness [CCT]) is taken into account (see the image below).

Ocular hypertension study (OHTS). Percentage of pa Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).

Some patients' first sign of morbidity from elevated IOP can be presentation with sudden loss of vision due to a central retinal vein occlusion (CRVO), the second most common risk factor for CRVO behind systemic hypertension.

See References for additional resources.

Race

Prevalence of POAG is 3-4 times higher in blacks than in Caucasians; in addition, blacks are up to 6 times more susceptible to optic disc nerve damage than Caucasians. A higher prevalence of larger cup-to-disc ratios exists in the normal black population as compared with white controls.

Glaucoma is the most common cause of blindness among people of African descent. They are more likely to develop glaucoma early in life, and they tend to have a more aggressive form of the disease.

  • The Barbados Eye Study over 4 years showed a 5 times higher incidence of developing glaucoma in a group of black ocular hypertensives as compared with a predominantly white population.
  • Some population studies have found the mean IOP in blacks to be higher than Caucasian controls. Other studies (eg, Baltimore) found no difference. Consequently, further study needs to be conducted to clarify this issue.
  • Furthermore, the OHTS has suggested that black patients overall may have a thinner average central corneal thickness, thereby leading to underdiagnosis of elevated pressure, and consequently, exposure to higher risk of developing glaucoma. Therefore, pachymetry measurement is particularly important in establishing a baseline for African-American patients who are glaucoma suspects.

Sex

Reports on sex predilection also differ. Although some age-controlled studies have reported significantly higher mean IOP values in women than in men, others have failed to find such a difference, while others have even shown males to have a higher prevalence of glaucoma.

Age

Age older than 40 years is a risk factor for the development of POAG, with up to 15% of people affected by the seventh decade of life.

  • Consequently, glaucoma is found to be more prevalent in the aging population, even after compensating for the fact that mean IOP slowly rises with increasing age.
  • However, the disease itself is not limited to only middle-aged and elderly individuals.
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Contributor Information and Disclosures
Author

Jerald A Bell, MD Staff Physician, Department of Ophthalmology, Billings Clinic

Jerald A Bell, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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.

Chief Editor

Inci Irak Dersu, MD, MPH Associate Professor of Clinical Ophthalmology, State University of New York Downstate College of Medicine; Attending Physician, SUNY Downstate Medical Center, Kings County Hospital, and VA Harbor Health Care System

Inci Irak Dersu, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Additional Contributors

Neil T Choplin, MD Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences

Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society, California Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors, Robert J Noecker, MD, and Emily Patterson, MD, to the development and writing of this article.

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Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields, MD.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, field loss among individuals with pressures in the upper teens can occur. Also, note that the average pressure among those with glaucomas is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.
Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally shaded lines) and/or damage from glaucoma (vertically shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are also those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). Courtesy of M. Bruce Shields, MD.OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines
Humphrey visual field, right eye, showing patient with advanced glaucomatous field loss. Notice both the arcuate extension from the blind spot (Bjerrum scotoma) and the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields, MD.
Illustration of progressive optic nerve damage. Notice the deepening (saucerization) along the neural rim, along with notching and increased excavation/sloping of the optic nerve and circumlinear vessel inferiorly. Courtesy of M. Bruce Shields, MD.
Example of progressive visual field loss over time (from top to bottom) in a patient with glaucoma. Notice the early appearance of an inferior nasal step and arcuate loss, with progressive enlargement and increasing density of the scotomata over time. Courtesy of M. Bruce Shields, MD.
Optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly (similar to Image 5). Courtesy of M. Bruce Shields, MD.
Glaucomatous optic nerve damage, with sloping and nerve fiber layer rim hemorrhage at the 7-o'clock position. Hemorrhage is indicative of progressive damage, usually due to inadequate pressure control. Further notching and pallor corresponding to the area of hemorrhage usually is seen several weeks after resorption of the blood. Courtesy of M. Bruce Shields, MD.
Correction values according to corneal thickness.
Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).
Intraocular pressure measurements. Adapted from Reichert Ophthalmic Instruments, Ocular Response Analyzer, How does it work Web page.
 
 
 
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