• Oct 2010
    AAO PPP Glaucoma Panel, Hoskins Center for Quality Eye Care
    Glaucoma
    Compendium Type: I

    Introduction

    The Preferred Practice Pattern® (PPP) guidelines have been written on the basis of three principles.

    • Each Preferred Practice Pattern should be clinically relevant and specific enough to provide useful information to practitioners.
    • Each recommendation that is made should be given an explicit rating that shows its importance to the care process.
    • Each recommendation should also be given an explicit rating that shows the strength of evidence that supports the recommendation and reflects the best evidence available.


    In the process of revising this document, a literature search of the Cochrane Library and PubMed was conducted on December 3, 2008 and April 28, 2009 on the subject of primary open-angle glaucoma (POAG) suspect for the years 2004 to the date of the search. In addition, the evidence synthesis1 prepared by the British National Collaborating Centre for Acute Care for the National Institute for Health and Clinical Excellence clinical guideline on Glaucoma: diagnosis and management of chronic open-angle glaucoma and ocular hypertension clinical guideline was reviewed.2 Details of the literature search are available in the Literature Search Details section. The results were reviewed by the Glaucoma Panel and used to prepare the recommendations, which they rated in two ways. The panel first rated each recommendation according to its importance to the care process. This "importance to the care process" rating represents care that the panel thought would improve the quality of the patient's care in a meaningful way. The ratings of importance are divided into three levels.

    • Level A, defined as most important
    • Level B, defined as moderately important
    • Level C, defined as relevant but not critical


    The panel also rated each recommendation on the strength of evidence in the available literature to support the recommendation made. The "ratings of strength of evidence" also are divided into three levels.

    • Level I includes evidence obtained from at least one properly conducted, well-designed randomized controlled trial. It could include meta-analyses of randomized controlled trials.
    • Level II includes evidence obtained from the following:
      • Well-designed controlled trials without randomization
      • Well-designed cohort or case-control analytic studies, preferably from more than one center
      • Multiple-time series with or without the intervention
    • Level III includes evidence obtained from one of the following:
      • Descriptive studies
      • Case reports
      • Reports of expert committees/organizations (e.g., PPP panel consensus with external peer review)


    Evidence is that which supports the value of the recommendation as it relates to the quality of care. The committee believes that it is important to make available the strength of the evidence underlying the recommendation. In this way, readers can appreciate the degree of importance the committee attached to each recommendation and they can understand what type of evidence supports the recommendation.

    The ratings of importance and the ratings of strength of evidence are given in bracketed superscripts after each recommendation. For instance, "[A:II]" indicates a recommendation with high importance to clinical care [A], supported by sufficiently rigorous published evidence, though not by a randomized controlled trial [II].

    The sections entitled "Orientation" and "Background" do not include recommendations; rather they are designed to educate and provide summary background information and rationale for the recommendations that are presented in the Care Process section. A summary of the major recommendations for care is included in Appendix 2. Appendix 3 has an algorithm for the management of POAG suspect. Appendix 4 contains the ICD-9 classifications for the disease entities that the PPP covers.

    ORIENTATION

    DISEASE DEFINITION

    A glaucoma suspect is an individual with clinical findings and/or a constellation of risk factors that indicate an increased likelihood of developing POAG.

    The clinical findings that define a glaucoma suspect patient are characterized by one of the following in at least one eye in an individual with open anterior chamber angles by gonioscopy:

    • Appearance of the optic disc or retinal nerve fiber layer that is suspicious for glaucomatous damage
      • Enlarged cup-disc ratio
      • Asymmetric cup-disc ratio
      • Notching or narrowing of the neuroretinal rim
      • Disc hemorrhage
      • Nerve fiber layer defect
    • A visual field suspicious for glaucomatous damage in the absence of clinical signs of other optic neuropathies
      • Arcuate bundle defect
      • Nasal step
      • Paracentral scotoma
      • Altitudinal defect
      • Larger mean pattern standard deviation
    • Consistently elevated intraocular pressure (IOP) associated with normal appearance of the optic disc and retinal nerve fiber layer and with normal visual field test results

    This definition excludes known secondary causes for open-angle glaucoma, such as pseudoexfoliation (exfoliation syndrome), pigment dispersion, and traumatic angle recession.

    PATIENT POPULATION

    The patient population includes adults with open anterior chamber angles by gonioscopy with one or more of the clinical findings or risk factors listed in the Disease Definition section.

    ACTIVITY

    The identification and management of patients with POAG suspect.

    PURPOSE
    To detect and manage patients at risk for developing glaucoma, prevent damage to the optic nerve, and preserve patients' quality of life.

    GOALS

    • Document the status of optic nerve structure, by clinical evaluation and imaging, and function, by visual field testing, on presentation
    • Identify patients at high risk of developing POAG
    • Consider treatment of high-risk individuals to prevent or delay the development of POAG
    • Minimize the side effects of treatment and the impact of treatment on the patient's vision, general health, and quality of life
    • Educate and involve patients and appropriate family members/caregivers in the management of their condition

    BACKGROUND

    EPIDEMIOLOGY AND RISK FACTORS

    Although glaucoma is not defined by IOP, and estimates of glaucoma suspects based on suspicious optic nerve or visual field findings are lacking, there are data on ocular hypertension in the United States. The prevalence of ocular hypertension in non-Hispanic Whites who are 40 and older and live in the United States is 4.5% (ranging from 2.7% in persons 43 to 49 years old to 7.7% in those 75 to 79 years old).3 In Latinos 40 and older, the overall prevalence is 3.5% (ranging from 1.7% in persons 40 to 49 years old to 7.4% in those 80 and older).4 There are no published population-based estimates for the prevalence of ocular hypertension in African Americans and Asian Americans. However, it is estimated that 3 to 6 million persons in the United States have ocular hypertension.5 Furthermore, there are no estimates for the number of individuals who are considered to be glaucoma suspects based on the appearance of their optic nerve or visual field. The number of individuals with eye findings that raise a suspicion of glaucoma, usually elevated IOP or asymmetric optic disc morphology, far exceeds the number of people with glaucoma. (It is estimated that over 2.2 million persons in the United States have open-angle glaucoma.)6

    A majority of people with ocular hypertension may be undiagnosed. Seventy-five percent of Latinos with IOP greater than 21 mmHg were previously undiagnosed in the Los Angeles Latino Eye Study.4 The public health importance of early detection and management of these patients lies in the fact that individuals with ocular hypertension are at increased risk of developing glaucomatous optic neuropathy. The Ocular Hypertension Treatment Study (OHTS) demonstrated the rate of untreated participants developing glaucomatous optic neuropathy to be 9.5% in 5 years7,8 and 22% at 13 years, or approximately 2% per year.9 Glaucoma of all types is one of the most common causes of legal blindness in the United States.6,10

    The overall likelihood of developing glaucomatous optic neuropathy increases with the number and relative strength of risk factors, which include the following:

    • Higher IOP7,8,11-20
    • Older age7,8,13,14,21-23
    • Family history of glaucoma14,24
    • Lower ocular perfusion pressure24
    • Lower systolic and diastolic blood pressure24
    • Thinner central cornea7,8
    • Disc hemorrhage25-29
    • Larger cup-to-disc ratio7,8
    • Larger mean pattern standard deviation on threshold visual field testing20,30

    While disc hemorrhage, increased cup-disc ratio and larger mean pattern standard deviation are considered to be risk factors for the development of POAG, it can also be argued that these signs represent early optic nerve damage and unsuspected glaucoma.

    Some studies have shown an association between type 2 diabetes mellitus and a higher prevalence31-35 and incidence36 of open-angle glaucoma; however, other studies17,37,38 have not found such a relationship. The preponderance of the evidence suggests that type 2 diabetes mellitus is associated with a higher prevalence of open-angle glaucoma.35

    Other risk factors that have been associated with open-angle glaucoma include migraine headache, peripheral vasospasm, concurrent cardiovascular disease, systemic hypertension, and myopia.8,39-43However, the association between these risk factors and the development of glaucomatous optic nerve damage has not been demonstrated consistently.8,22,44-50

    DETECTION

    Patients suspected of having POAG can be identified during a comprehensive adult medical eye evaluation.51 While an assessment of IOP can identify individuals who are ocular hypertensive, an assessment of the optic nerve and the visual field is required to identify those patients who have glaucoma with a normal IOP.

    In 2005, the National Committee for Quality Assurance introduced a new quality measure for health plans that offer Medicare Advantage coverage in recognition of the importance of identifying patients with glaucoma and the difficulties of screening. The measure is based on a comprehensive eye examination in the previous 2 years for older adults. The intent of the quality measures is to allow purchasers and consumers to compare the performance of managed health plans reliably.

    CARE PROCESS

    PATIENT OUTCOME CRITERIA

    • Preservation of visual function
    • Maintenance of quality of life

    DIAGNOSIS

    The comprehensive initial glaucoma suspect evaluation (history and physical examination) includes all components of the comprehensive adult medical eye evaluation51 in addition to and with special attention to those factors that specifically bear upon the diagnosis, course, and treatment of POAG. The evaluation may require more than one visit. For instance, an individual might be suspected of having POAG on one visit but may return for further evaluation to confirm the diagnosis, including additional IOP measurements, gonioscopy, central corneal thickness determination, visual field assessment, and optic nerve head and retinal nerve fiber layer evaluation and documentation.

    Evaluation of Visual Function
    Self-reported functional status or difficulty with vision can be assessed either by patient complaints or by specific questionnaires including the National Eye Institute - Visual Function Questionnaire-25.52-56 [A:III]

    Ophthalmic Evaluation
    In completing the elements in the comprehensive adult medical eye evaluation,51 the ophthalmic evaluation specifically focuses on the following elements:

    • History[A:III]
    • Visual acuity measurement[A:III]
    • Pupil examination[B:II]
    • Anterior segment examination[A:III]
    • Intraocular pressure measurement[A:I]
    • Gonioscopy[A:III]
    • Optic nerve head and retinal nerve fiber layer examination[A:III]
    • Fundus examination[A:III]

    History

    • Ocular,[A:III] family,15,57,58 [A:II] and systemic history (e.g., asthma, migraine headache, vasospasm).[A:III] The severity and outcome of glaucoma in family members, including a history of visual loss from glaucoma, should be obtained during initial evaluation.57,58 [B:III]
    • Review of pertinent records,[A:III] with particular reference to the IOP and the status of the optic nerve and visual field[A:III]
    • Ocular and systemic medications (e.g., corticosteroids) and known local or systemic intolerance to ocular or systemic medications[A:III]
    • Ocular surgery[A:III]

    It is important to note that a history of LASIK or photorefractive keratectomy has been associated with a falsely low IOP measurement due to thinning of the cornea.59,60 Cataract surgery may have lowered the IOP when compared with the presurgical baseline.61

    Visual acuity measurement
    Visual acuity with current correction (the power of the present correction recorded) at distance and, when appropriate, at near should be measured.[A:III] Refraction may be indicated to obtain the best-corrected visual acuity.

    Pupil examination
    The pupils are examined for reactivity and an afferent pupillary defect.62-64 [B:II]

    Anterior segment examination
    A slit-lamp biomicroscopic examination of the anterior segment can provide evidence of physical findings associated with narrow angles, such as shallow peripheral anterior chamber depth and crowded anterior chamber angle anatomy,65,66 corneal pathology, or a secondary mechanism for elevated IOP such as pseudoexfoliation (exfoliation syndrome), pigment dispersion with iris transillumination defects, iris and angle neovascularization, or inflammation.[A:III]

    Intraocular pressure measurement
    Results from OHTS demonstrate that lowering an elevated IOP reduces the risk of progression of glaucomatous visual field and optic nerve damage.7 [A:I] It is important to determine the full extent of IOP fluctuation over time to determine who is most at risk of developing glaucoma and, therefore, whom to treat to prevent future glaucoma. Intraocular pressure is measured in each eye, preferably by Goldmann applanation tonometry, before gonioscopy or dilation of the pupil.67 [A:III] Recording time of day of IOP measurements may be helpful to assess diurnal variation. Unrecognized IOP fluctuations may be associated with an increased risk of developing glaucomatous damage.68-77 Therefore, additional IOP measurements may be indicated, either at different hours of the day on the same day or on different days.

    Gonioscopy
    The diagnosis of POAG requires careful evaluation of the anterior chamber angle to exclude angle closure or secondary causes of IOP elevation, such as angle recession, pigment dispersion, peripheral anterior synechiae, angle neovascularization, and inflammatory precipitates.78 [A:III] (See www.gonioscopy.org and Selected Reference Texts section for discussion of the techniques of gonioscopy.)

    Optic nerve head and retinal nerve fiber layer examination
    There is evidence that glaucomatous changes detected with optic disc and retinal nerve fiber layer examination may precede defects detected by standard automated perimetry.79-85 In OHTS, optic nerve damage alone without visual field loss occurred in 69 eyes and accounted for 55% of the study endpoints reached.7

    Examination of the optic nerve head and retinal nerve fiber layer provides valuable structural information about glaucomatous optic nerve damage.86 Visible structural alterations of the optic nerve head or retinal nerve fiber layer and development of peripapillary choroidal atrophy frequently occur before visual field defects can be detected.81,87-94 Careful study of the optic disc neural rim for small hemorrhages is important, because these hemorrhages can precede visual field loss and further optic nerve damage.25-29,95,96 In the OHTS, the incidence of POAG in eyes with disc hemorrhage was 13.6% compared with 5.2% in eyes without disc hemorrhage over 8 years.29

    The preferred technique for optic nerve head and retinal nerve fiber layer evaluation involves magnified stereoscopic visualization (as with the slit-lamp biomicroscope), preferably through a dilated pupil.[A:III] In some cases, direct ophthalmoscopy complements magnified stereoscopic visualization, providing additional information of optic nerve detail due to the greater magnification of the direct ophthalmoscope. Red-free illumination of the posterior pole may aid in evaluating the retinal nerve fiber layer.97

    Fundus examination
    Examination of the fundus, through a dilated pupil whenever feasible, includes a search for other abnormalities that may account for optic nerve changes and/or visual field defects (e.g., optic nerve pallor, disc drusen, optic nerve pits, disc edema due to central nervous system disease, macular degeneration, retinal vascular occlusion, and other retinal disease).[A:III]   

    Supplemental Ophthalmic Testing
    Supplemental ophthalmic testing includes the following components:

    • Central corneal thickness measurement[A:II]
    • Visual field evaluation[A:III]
    • Optic nerve head and retinal nerve fiber layer analysis[A:II]

    Central corneal thickness measurement
    Measurement of central corneal thickness (CCT) aids the interpretation of IOP readings and helps to stratify patient risk for optic nerve damage.7,8,98-100 [A:II] Applanation tonometry on thicker than average corneas may overestimate IOP measurement, while thinner than average corneas may yield an underestimate of the true IOP.101 Several studies have sought to quantify the relationship between measured IOP level and CCT, but there is no generally accepted correction formula. There is a controversy over whether CCT is a risk factor due to the potential for IOP under- or overestimations102-104 or whether CCT is a risk factor itself, unrelated to IOP. There is level II evidence from OHTS that CCT is an independent risk factor for the development of POAG.8

    Visual field evaluation
    Automated static threshold perimetry is the preferred technique for evaluating the visual field.105 [A:III] The frequency doubling technology (FDT) method with the central 20-degree test program (C-20) and short-wavelength automated perimetry (SWAP) with the central 24-degree test program (24-2) are two of several alternative testing methods to screen for a defect before conducting more definitive threshold testing.105 Visual field testing based on SWAP106 and FDT107 may detect defects or progression of defects earlier than conventional white-on-white perimetry.108,109 Careful manual combined kinetic and static threshold testing (e.g., Goldmann visual fields) is an acceptable alternative when patients cannot perform automated perimetry reliably or if it is not available.[A:III] Repeat, confirmatory visual field examinations may be required for test results that are unreliable or show a new glaucomatous defect before changing management.110,111 [A:III] In the OHTS, 86% of visual field defects were not confirmed upon subsequent testing.110 It is best to use a consistent examination strategy for visual field testing.

    Optic nerve head and retinal nerve fiber layer analysis
    The appearance of the optic nerve should be documented.83,109 [A:II] Color stereophotography is an accepted method for documenting optic nerve head appearance. In glaucoma suspect patients, longitudinal stereophotographs identified over half the cases of new onset glaucoma in OHTS7; this finding has been confirmed in another study.112 Computer-based image analysis of the optic nerve head and retinal nerve fiber layer is an alternative for documentation of the optic nerve and can identify patients at greater risk of progression to glaucoma.83,113 As improvements in these instruments continue, the capacity for them to help the clinician diagnose glaucoma and identify progressive nerve damage may become more reliable.84,85,114 Stereoscopic disc photographs and computerized images of the nerve are distinctly different methods for optic nerve documentation and analysis.115 Each is complementary with regard to the information they provide the clinician who must manage the patient. In the absence of these technologies, a nonstereoscopic photograph or a drawing of the optic nerve head should be recorded, but these are less desirable alternatives to stereophotography or computer-based imaging.116  [A:III]

    There are three types of computer-based imaging devices currently available for glaucoma: confocal scanning laser ophthalmoscopy, optical coherence tomography, and scanning laser polarimetry. In a systematic review, the versions of these devices that were studied were similar in their ability to distinguish glaucoma patients from controls.83,117 Taken together, computer-based imaging devices for glaucoma provide useful, quantitative information for the clinician when analyzed in conjunction with other relevant clinical parameters.

    MANAGEMENT

    Goals
    The goals of managing patients with POAG suspect are to achieve the following:

    • Intraocular pressure controlled in the target range
    • Stable optic nerve/retinal nerve fiber layer status
    • Stable visual fields

    Intraocular pressure is the only modifiable parameter in glaucoma and glaucoma suspect patients. The decision to begin treatment to lower IOP in the glaucoma suspect patient is complex and based on the ophthalmologist's analysis of the examination results, risk assessment, and evaluation of the patient and the patient's preferences. The number and severity of risk factors present, the prognosis, management plan, and likelihood that therapy, once started, can be long-term, should be discussed with the patient and, when feasible, with the patient's family. Risk assessment based on OHTS and the European Glaucoma Prevention Study may be helpful in managing the patient with glaucoma suspect.30

    The decision to begin treatment for a glaucoma suspect patient is particularly important, since therapy exposes patients to the risks, side effects, and expense of long-term treatment. For some patients, the risk of developing POAG is sufficiently high to justify starting treatment.7,8,118 For example, in the OHTS, untreated patients with a baseline IOP of 26 mmHg or above and a CCT of 555 μm or below had a 36% chance of developing optic nerve damage during long-term follow-up compared with a 2% risk for patients with a baseline IOP of less than 24 and a CCT greater than 588 μm (see Figure 1).6 Whether or not a patient is treated, long-term monitoring for the development of glaucoma is essential.[A:III]

    FIGURE 1. The percentage of participants in the observation group who developed primary open-angle glaucoma grouped by baseline intraocular pressure and by central thickness measurements (PDF 143k)

    The patient who is a glaucoma suspect has a chronic, asymptomatic condition that, when treated, may require frequent use of one or more medications that may cause side effects and have a substantial financial impact. When treatment is appropriate, an effective medication regimen requires attention to its effect on IOP, side effects, and the degree to which efficacy is reduced by nonadherence to therapy. The ophthalmologist should consider these issues in choosing a regimen of maximal effectiveness and tolerance to achieve the desired therapeutic response for each patient.[A:III] The diagnosis, number and severity of risk factors, prognosis and management plan, and likelihood of long-term therapy should be discussed with the patient.[A:III]

    Deciding When to Treat a Patient with Glaucoma Suspect
    The decision to treat a glaucoma suspect patient may arise in various settings.

    • Any patient who shows evidence of optic nerve deterioration based on optic nerve head   appearance, retinal nerve fiber layer loss, or visual field changes consistent with glaucomatous damage has developed POAG and should be treated as described in the Primary Open-Angle Glaucoma PPP.119 [A:III] Development of subtle abnormalities in the optic disc and retinal nerve fiber layer are best detected by comparing periodic fundus imaging with disc and retinal nerve fiber layer photography and computerized imaging of the optic nerve and nerve fiber layer.81,120
    • A new visual field defect that is consistent with a pattern of glaucomatous visual field defect, confirmed on retesting of visual fields, may indicate that the patient has developed POAG.110,121
    • A patient who demonstrates very high IOP in which optic nerve damage is likely to occur may require treatment.
    • In some cases, initiating treatment to lower the risk of glaucomatous damage may be appropriate if the patient has risk factors for glaucoma, such as optic nerve appearance, that is very suspicious for glaucomatous damage, a strong family history of glaucoma, borderline visual field test findings, African American heritage, high myopia, or pseudoexfoliation (exfoliation syndrome).

    Whatever the scenario, a discussion must occur between the physician and patient to outline the risks and benefits of treatment versus nontreatment.

    Target Intraocular Pressure
    Patients who have evidence of POAG should be treated as in the Primary Open-Angle Glaucoma PPP. When deciding to treat a glaucoma suspect patient, the goal of treatment is to maintain the IOP in a range at which a patient is likely to remain stable.7,122,123 The estimated upper limit of this range is considered the "target pressure." In glaucoma suspect patients for whom treatment has been chosen, target pressure can vary among patients, and in the same patient it may need adjustment during the clinical course. In any patient, target pressure is an estimate and a means toward the ultimate goal of protecting the patient's vision. It is reasonable to begin by choosing a target pressure 20% lower than the mean of several baseline IOP measurements.7 [A:I] Current IOP and its relationship to target IOP should be evaluated at each visit and individualized for each patient.[A:III]

    In a patient who is a glaucoma suspect, a definite deterioration in optic nerve structure or visual field (i.e., conversion to glaucoma patient) suggests that the target pressure should be lower96,124 [A:I] and the patient should be managed as described in the Primary Open-Angle Glaucoma PPP.119 [A:III]

    Therapeutic Choices
    Unless contraindicated, medical therapy usually is the first intervention to lower IOP. There are many drugs available for initial therapy, and medication choice may be influenced by potential cost, side effects, and dosing schedules (see Table 1 for an overview of options available). Patient adherence to therapy is enhanced by using eye drops with the fewest side effects as infrequently as necessary to achieve the target IOP. If target IOP is not achieved by one medication, then additional separate medications, combination therapies, or switching of treatments may be considered to reach the target IOP.

    TABLE 1. Glaucoma Medications (PDF 107k)

    Prostaglandin analogs and beta-adrenergic antagonists are the most frequently used initial eye drops for lowering IOP.125,126 Prostaglandin analogs are the most effective drugs at lowering IOP and can be considered as initial medical therapy unless other considerations such as contraindications, cost, side effects, intolerance, or patient refusal preclude this.127,128 [A:I] Other agents in addition to prostaglandin analogs and beta-adrenergic antagonists include alpha2 adrenergic agonists, topical and oral carbonic anhydrase inhibitors, and parasympathomimetics.129,130 But, because prostaglandins are very safe when used once daily and they have a high IOP-lowering effect, they are usually chosen as the first therapy for a patient with glaucoma suspect.

    To determine the effectiveness of the chosen therapy, it may be useful to begin by treating only one eye and then comparing the relative change of the IOP in the two eyes at follow-up visits.131 However, because the two eyes of an individual may not respond equally to the same medication, and because of the possibility of asymmetric spontaneous fluctuations and the potential for contralateral effect of monocular topical medications,132 it is acceptable to compare the effect in one eye relative to multiple baseline measurements in the same eye.133

    If a drug fails to reduce IOP sufficiently, then either switching to an alternative medication as monotherapy or adding additional medication is appropriate until the desired IOP level is attained.109 [A:III] Since some studies have shown that adding a second medication decreased adherence to glaucoma treatment,134,135 fixed combination therapy, while not recommended for initial treatment, may improve patient adherence.

    The patient and the ophthalmologist together decide on a practical and feasible regimen to follow in terms of dosing, cost, and adherence in the context of the patient's age and preferences.109 The ophthalmologist should assess the patient for local ocular and systemic side effects and toxicity, including interactions with other medications and potential life-threatening adverse reactions.136 [A:III] To reduce systemic absorption after medication instillation, patients can be educated about eyelid closure or nasolacrimal occlusion (see Related Academy Materials section for patient education brochures).137

    Adequate treatment to lower IOP requires a high level of adherence to therapy. Frequently, this is not achieved; studies indicate relatively poor adherence to therapy.138-141 Even with instruction, free medication, once-daily administration, use of a dosing aid, and electronic monitoring of adherence, nearly 45% of patients with glaucoma in one study took fewer than 75% of their prescribed doses.141 Repeated instruction and counseling in proper techniques for using medication as well as a clearly written medication regimen and follow-up telephone calls may improve adherence to therapy.141-143 At each examination, medication dosage and frequency of use should be recorded.[A:III] Reviewing the time of day when medication was taken may be useful. Adherence to the therapeutic regimen and recommendations for therapeutic alternatives or diagnostic procedures should be discussed.[A:III] Cost may be a factor in adherence, especially when multiple medications are used.143,144 Patient education and informed participation in treatment decisions may improve adherence143 and overall effectiveness of management.

    Laser trabeculoplasty may also benefit high-risk glaucoma suspect patients. If incisional surgery is to be considered, the patient can be managed as described in the Primary Open-Angle Glaucoma PPP.119

    FOLLOW-UP EVALUATION

    The purpose of follow-up examination is to evaluate IOP level, visual field status, optic disc appearance, and retinal nerve fiber layer status to determine if damage has occurred. The interaction between patient and disease is unique for every patient, and management for each patient must always be individualized.[A:III]

    History
    The following interval history should be elicited during all follow-up visits for POAG suspect patients:

    • Interval ocular history[A:III]
    • Interval systemic medical and medication history[B:III]
    • Side effects of ocular medications if the patient is being treated[A:III]
    • Frequency and time of last IOP-lowering medications and review of medication use if the patient is being treated[B:III]

    Ophthalmic Examination
    The following components of the ophthalmic examination should be performed during all follow-up visits for POAG suspect patients:

    • Visual acuity measurement[A:III]
    • Slit-lamp biomicroscopy[A:III]
    • Intraocular pressure measurement[A:I]

    The frequency of periodic optic nerve head evaluation and documentation116,145-147 and visual field evaluation148-150 is based on risk assessment. Patients with thinner corneas,7,8 higher IOPs,7,8,11-20 disc hemorrhage,25-29,151 larger cup-to-disc, larger mean PSD, or family history of glaucoma may warrant closer follow-up than patients with lower IOPs, normal corneal thickness, and no disc hemorrhages. Gonioscopy is indicated when there is a suspicion of an angle-closure component, anterior chamber shallowing, anterior chamber angle abnormalities, or if there is an unexplained change in IOP.[A:III] Gonioscopy should be performed periodically (i.e., 1 to 5 years).[A:III]

    Adjustment of Therapy
    The indications for adjusting therapy are as follows:[A:III]

    • Target IOP is not achieved and the benefits of a change in therapy outweigh the risks for the patient
    • Intraocular pressure is consistently below target, or visual field and optic discs remain stable for years. In this situation, a carefully monitored attempt to reduce the medical regimen is appropriate.
    • Patient is intolerant of the prescribed medical regimen
    • Patient does not adhere to the prescribed medical regimen because of cost or compliance issues
    • Contraindications to individual medicines develop

    PROVIDER AND SETTING

    The performance of certain diagnostic procedures (e.g., tonometry, pachymetry, perimetry, fundus imaging and photography) may be delegated to appropriately trained and supervised personnel. However, the interpretations of results and the medical and surgical management of disease require the medical training, clinical judgment, and the experience of an ophthalmologist.

    COUNSELING/REFERRAL

    It is important to educate and engage patients in the management of their condition. This may be especially true for patients with open-angle glaucoma suspect, since some authors have shown that follow-up is poor in patients with this diagnosis.152,153 One reason for this was patients' perception that their disease was "not serious enough."152 Patients should be educated about their condition and its potential to lead to the blinding disease glaucoma, the rationale and goals of intervention, the status of their condition, and the relative benefits and risks of alternative interventions so that they can participate meaningfully in developing an appropriate plan of action.[A:III] Patients should be encouraged to alert their ophthalmologists to physical or emotional changes that occur when taking glaucoma medications, if prescribed.[A:III] Glaucoma suspect diagnosis and treatments frequently affect patients' quality of life, including employment issues (e.g., fear of loss of job and insurance from diminished ability to read and drive), social issues (e.g., fear of negative impact on relationships and sexuality), and loss of independence and activities that require good visual acuity (e.g., sports and other hobbies). The ophthalmologist should be sensitive to these problems and provide support and encouragement.[A:III]

    APPENDICES

    APPENDIX 1. QUALITY OF OPHTHALMIC CARE CORE CRITERIA

     Providing quality care
    is the physician's foremost ethical obligation, and is
    the basis of public trust in physicians.
    AMA Board of Trustees, 1986

    Quality ophthalmic care is provided in a manner and with the skill that is consistent with the best interests of the patient. The discussion that follows characterizes the core elements of such care.

    The ophthalmologist is first and foremost a physician. As such, the ophthalmologist demonstrates compassion and concern for the individual, and utilizes the science and art of medicine to help alleviate patient fear and suffering. The ophthalmologist strives to develop and maintain clinical skills at the highest feasible level, consistent with the needs of patients, through training and continuing education. The ophthalmologist evaluates those skills and medical knowledge in relation to the needs of the patient and responds accordingly. The ophthalmologist also ensures that needy patients receive necessary care directly or through referral to appropriate persons and facilities that will provide such care, and he or she supports activities that promote health and prevent disease and disability.

    The ophthalmologist recognizes that disease places patients in a disadvantaged, dependent state. The ophthalmologist respects the dignity and integrity of his or her patients, and does not exploit their vulnerability.

    Quality ophthalmic care has the following optimal attributes, among others.

    • The essence of quality care is a meaningful partnership relationship between patient and physician. The ophthalmologist strives to communicate effectively with his or her patients, listening carefully to their needs and concerns. In turn, the ophthalmologist educates his or her patients about the nature and prognosis of their condition and about proper and appropriate therapeutic modalities. This is to ensure their meaningful participation (appropriate to their unique physical, intellectual and emotional state) in decisions affecting their management and care, to improve their motivation and compliance with the agreed plan of treatment, and to help alleviate their fears and concerns.
    • The ophthalmologist uses his or her best judgment in choosing and timing appropriate diagnostic and therapeutic modalities as well as the frequency of evaluation and follow-up, with due regard to the urgency and nature of the patient's condition and unique needs and desires.
    • The ophthalmologist carries out only those procedures for which he or she is adequately trained, experienced and competent, or, when necessary, is assisted by someone who is, depending on the urgency of the problem and availability and accessibility of alternative providers.
    • Patients are assured access to, and continuity of, needed and appropriate ophthalmic care, which can be described as follows.
      • The ophthalmologist treats patients with due regard to timeliness, appropriateness, and his or her own ability to provide such care.
      • The operating ophthalmologist makes adequate provision for appropriate pre- and postoperative patient care.
      • When the ophthalmologist is unavailable for his or her patient, he or she provides appropriate alternate ophthalmic care, with adequate mechanisms for informing patients of the existence of such care and procedures for obtaining it.
      • The ophthalmologist refers patients to other ophthalmologists and eye care providers based on the timeliness and appropriateness of such referral, the patient's needs, the competence and qualifications of the person to whom the referral is made, and access and availability.
      • The ophthalmologist seeks appropriate consultation with due regard to the nature of the ocular or other medical or surgical problem. Consultants are suggested for their skill, competence, and accessibility. They receive as complete and accurate an accounting of the problem as necessary to provide efficient and effective advice or intervention, and in turn respond in an adequate and timely manner.
      • The ophthalmologist maintains complete and accurate medical records.
      • On appropriate request, the ophthalmologist provides a full and accurate rendering of the patient's records in his or her possession.
      • The ophthalmologist reviews the results of consultations and laboratory tests in a timely and effective manner and takes appropriate actions.
      • The ophthalmologist and those who assist in providing care identify themselves and their profession
      • For patients whose conditions fail to respond to treatment and for whom further treatment is unavailable, the ophthalmologist provides proper professional support, counseling, rehabilitative and social services, and referral as appropriate and accessible.
    • Prior to therapeutic or invasive diagnostic procedures, the ophthalmologist becomes appropriately conversant with the patient's condition by collecting pertinent historical information and performing relevant preoperative examinations. Additionally, he or she enables the patient to reach a fully informed decision by providing an accurate and truthful explanation of the diagnosis; the nature, purpose, risks, benefits, and probability of success of the proposed treatment and of alternative treatment; and the risks and benefits of no treatment.
    • The ophthalmologist adopts new technology (e.g., drugs, devices, surgical techniques) in judicious fashion, appropriate to the cost and potential benefit relative to existing alternatives and to its demonstrated safety and efficacy.
    • The ophthalmologist enhances the quality of care he or she provides by periodically reviewing and assessing his or her personal performance in relation to established standards, and by revising or altering his or her practices and techniques appropriately.
    • The ophthalmologist improves ophthalmic care by communicating to colleagues, through appropriate professional channels, knowledge gained through clinical research and practice. This includes alerting colleagues of instances of unusual or unexpected rates of complications and problems related to new drugs, devices or procedures.
    • The ophthalmologist provides care in suitably staffed and equipped facilities adequate to deal with potential ocular and systemic complications requiring immediate attention.
    • The ophthalmologist also provides ophthalmic care in a manner that is cost effective without unacceptably compromising accepted standards of quality.


    Reviewed by: Council
    Approved by: Board of Trustees
    October 12, 1988

    2nd Printing: January 1991
    3rd Printing: August 2001
    4th Printing: July 2005


    APPENDIX 2. MAJOR RECOMMENDATIONS FOR CARE

    DIAGNOSIS
    The comprehensive initial glaucoma suspect evaluation (history and physical examination) includes all components of the comprehensive adult medical eye evaluation51 in addition to and with special attention to those factors that specifically bear upon the diagnosis, course, and treatment of POAG.

    Evaluation of Visual Function
    Self-reported functional status or difficulty with vision can be assessed either by patient complaints or by specific questionnaires including the National Eye Institute - Visual Function Questionnaire-25.52-56 [A:III]

    Ophthalmic Evaluation

    History

    • Ocular,[A:III] family,15,57,58 [A:II] and systemic history (e.g., asthma, migraine headache, vasospasm).[A:III] The severity and outcome of glaucoma in family members, including history of visual loss from glaucoma, should be obtained during initial evaluation.57,58 [B:III]
    • Review of pertinent records[A:III] with particular reference to the IOP and the status of the optic nerve and visual field[A:III]
    • Ocular and systemic medications (e.g., corticosteroids) and known local or systemic intolerance to ocular or systemic medications[A:III]
    • Ocular surgery[A:III]

    Visual acuity measurement
    Visual acuity with current correction (the power of the present correction recorded) at distance and, when appropriate, at near should be measured.[A:III]

    Pupil examination
    The pupils are examined for reactivity and an afferent pupillary defect.62-64 [B:II]

    Anterior segment examination
    A slit-lamp biomicroscopic examination of the anterior segment can provide evidence of physical findings associated with narrow angles, such as shallow peripheral anterior chamber depth and crowded anterior chamber angle anatomy,65,66 corneal pathology, or a secondary mechanism for elevated IOP such as pseudoexfoliation (exfoliation syndrome), pigment dispersion with iris transillumination defects, iris and angle neovascularization, or inflammation.[A:III]

    Intraocular pressure measurement
    Intraocular pressure is measured in each eye, preferably by Goldmann applanation tonometry, before gonioscopy or dilation of the pupil.67 [A:III]

    Gonioscopy
    The diagnosis of POAG requires careful evaluation of the anterior chamber angle to exclude angle closure or secondary causes of IOP elevation, such as angle recession, pigment dispersion, peripheral anterior synechiae, angle neovascularization, and inflammatory precipitates.78 [A:III]

    Optic nerve head and retinal nerve fiber layer examination
    The preferred technique for optic nerve head and retinal nerve fiber layer evaluation involves magnified stereoscopic visualization (as with the slit-lamp biomicroscope), preferably through a dilated pupil.[A:III]

    Fundus examination
    Examination of the fundus, through a dilated pupil whenever feasible, includes a search for other abnormalities that may account for optic nerve changes and/or visual field defects (e.g., optic nerve pallor, disc drusen, optic nerve pits, disc edema due to central nervous system disease, macular degeneration, retinal vascular occlusion, and other retinal disease).[A:III]   

    Supplemental Ophthalmic Testing

    Central corneal thickness
    Measurement of central corneal thickness (CCT) aids the interpretation of IOP readings and helps to stratify patient risk for optic nerve damage.7,8,98-100 [A:II]

    Visual field evaluation
    Automated static threshold perimetry is the preferred technique for evaluating the visual field.105 [A:III] Careful manual combined kinetic and static threshold testing (e.g., Goldmann visual fields) is an acceptable alternative when patients cannot perform automated perimetry reliably or if it is not available.[A:III] Repeat, confirmatory visual field examinations may be required for test results that are unreliable or show a new glaucomatous defect before changing management.110,111 [A:III]

    Optic nerve head and retinal nerve fiber layer analysis
    The appearance of the optic nerve should be documented.83,109 [A:II] Color stereophotography is an accepted method for documenting optic nerve head appearance. Computer-based image analysis of the optic nerve head and retinal nerve fiber layer is an alternative for documentation of the optic nerve and can identify patients at greater risk of progression to glaucoma.83,113 In the absence of these technologies, a nonstereoscopic photograph or a drawing of the optic nerve head should be recorded, but these are less desirable alternatives to stereophotography or computer-based imaging.116 [A:III]

    Management recommendations are described in the main body of the text.

    FOLLOW-UP EVALUATION

    History
    The following interval history should be elicited during all follow-up visits for POAG suspect patients:

    • Interval ocular history[A:III]
    • Interval systemic medical and medication history[B:III]
    • Side effects of ocular medications if the patient is being treated[A:III]
    • Frequency and time of last IOP-lowering medications and review of medication use if the patient is being treated[B:III]

    Ophthalmic Examination
    The following components of the ophthalmic examination should be performed during all follow-up visits for POAG suspect patients:

    • Visual acuity measurement[A:III]
    • Slit-lamp biomicroscopy[A:III]
    • Intraocular pressure measurement[A:I]

    The frequency of periodic optic nerve head evaluation and documentation116,145-147 and visual field evaluation148-150 is based on risk assessment. Patients with thinner corneas,7,8 higher IOPs,7,8,11-20 disc hemorrhage,25-29,151 larger cup-to-disc, larger mean PSD, or family history of glaucoma may warrant closer follow-up than patients with lower IOPs, normal corneal thickness, and no disc hemorrhages. Gonioscopy is indicated when there is a suspicion of an angle-closure component, anterior chamber shallowing, anterior chamber angle abnormalities, or if there is an unexplained change in IOP.[A:III] Gonioscopy should be performed periodically (i.e., 1 to 5 years).[A:III]

    COUNSELING/REFERRAL
    Patients should be educated about their condition and its potential to lead to the blinding disease glaucoma, the rationale and goals of intervention, the status of their condition, and the relative benefits and risks of alternative interventions so that they can participate meaningfully in developing an appropriate plan of action.[A:III] Patients should be encouraged to alert their ophthalmologists to physical or emotional changes that occur when taking glaucoma medications, if prescribed.[A:III] The ophthalmologist should be sensitive to these problems and provide support and encouragement.[A:III]


    APPENDIX 3. MANAGEMENT ALGORITHM FOR PATIENTS WITH PRIMARY OPEN-ANGLE GLAUCOMA (POAG) SUSPECT

    Management Algorithm for Patients with Primary Open-Angle Glaucoma (POAG) Suspect (PDF 19k)


    APPENDIX 4. INTERNATIONAL STATISTICAL CLASSIFICATION OF DISEASES AND RELATED HEALTH PROBLEMS (ICD-9) CODES

    The POAG Suspect PPP covers the entity of primary open-angle suspect, or borderline glaucoma, (ICD-9 #365.0) and related entities with the following ICD-9 classifications:

    • Preglaucoma, unspecified (365.00)
    • Open angle with borderline findings (e.g., borderline intraocular pressure [IOP] or optic disc appearance suspicious of glaucoma) (365.01)
    • Steroid responders (365.03)
    • Ocular hypertension (365.04) 

    SUGGESTED REFERENCE TEXTS

    • Allingham RR, Damji KF, Freedman S, Moroi SE, Shafranov G, Shields MB, eds. Shields' Textbook of Glaucoma. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.
    • Alward WLM. www.gonioscopy.org. Accessed September 16, 2010.
    • Alward WLM, Longmuir RA. Color Atlas of Gonioscopy. 2nded. San Francisco, CA: American Academy of Ophthalmology; 2008.
    • Anderson DR, Patella VM. Automated Static Perimetry. 2nd ed. St. Louis, MO: CV Mosby Co.; 1999.
    • Epstein DL, Allingham RR, Shuman JS, eds. Chandler and Grant's Glaucoma. 4th ed. Baltimore, MD: Lippincott Williams and Wilkins; 1997.
    • Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St. Louis, MO: CV Mosby
      Co.; 1996.
    • Stamper RL, Lieberman MF, Drake MV. Becker-Shaffer's Diagnosis and Therapy of the Glaucomas. 8th ed. Philadelphia, PA: Mosby Elsevier; 2009.
    • Tasman W, Jaeger EA, eds. Duane's Ophthalmology. 15th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
    • Weinreb RN, Greve EL, eds. Glaucoma Diagnosis: Structure and Function. World Glaucoma Association Consensus Series - 1. The Netherlands: Kugler Publications; 2004.
    • Weinreb RN, Crowston JG, eds. Glaucoma Surgery: Open Angle Glaucoma. World Glaucoma Association Consensus Series - 2. The Netherlands: Kugler Publications; 2005.
    • Weinreb RN, Brandt JD, Garway-Heath D, Medeiros FA, eds. Intraocular Pressure. World Glaucoma Association Consensus Series - 4. The Netherlands: Kugler Publications; 2007.
    • Weinreb RN, Healy PR, Topouzis F, eds. Glaucoma Screening. World Glaucoma Association  Consensus Series - 5. The Netherlands: Kugler Publications; 2008.

    RELATED ACADEMY MATERIALS

    Basic and Clinical Science Course
         Glaucoma (Section 10, 2010-2011)

    Focal Points
         Current Trends and Challenges in Glaucoma Care (2008)
         Evidence-Based Medicine in Glaucoma: Clinical Trials update (2008)             

    Information Statement
         AAO and American Glaucoma Society Information Statement on Availability of Glaucoma Eye
         Drop Medications (2009) (Free download available at:
         http://one.aao.org/CE/PracticeGuidelines/ClinicalStatements.aspx)

    Ophthalmic Technology Assessments
         
    Aqueous Shunts in Glaucoma (2008)
         Corneal Thickness Measurement in the Management of Primary Open-Angle Glaucoma (2007)
         Optic Nerve Head and Retinal Nerve Fiber Layer Analysis (2007)

    Patient Education
         Digital-Eyes Ophthalmic Animations for Patients, 2nd Edition, Subscription (2009) (All
         presentations are offered in English and Spanish)
         Eyedrops brochure (2010)
         Glaucoma booklet (2010)
         Glaucoma brochure (2010) (Spanish: Entendiendo el Glaucoma [2010])

    Preferred Practice Patterns
         
    Comprehensive Adult Medical Eye Evaluation (2010)
         Primary Angle Closure (2010)
         Primary Open-Angle Glaucoma (2010)
         Vision Rehabilitation for Adults (2007)

    ProVision
         
    Glaucoma (Series 4, 2007)


    To order any of these materials, please call the Academy's Customer Service number, 866.561.8558 (U.S. only) or 415.561.8540 or visit www.aao.org/store.

    REFERENCES

    Recommendations of Care Ratings

    Care Process Ratings:

    • Level A: Most important to the care process
    • Level B: Moderately important to the care process
    • Level C: Relevant but not critical to the care process

    Strength of Evidence Ratings:

    • Level I: Randomized controlled trial or meta-analyses
    • Level II: Controlled trials, cohort, or case-control studies
    • Level III: Descriptive studies or case reports 
    1. National Collaborating Centre for Acute Care. Glaucoma: diagnosis and management of chronic open angle glaucoma and ocular hypertension. Appendices A-G. Available at: www.nice.org.uk/nicemedia/live/12145/43888/43888.pdf. Accessed April 2, 2010.
    2. National Collaborating Centre for Acute Care. Glaucoma: diagnosis and management of chronic open angle glaucoma and ocular hypertension. Methods, evidence & guidance. Available at: www.nice.org.uk/nicemedia/live/12145/43887/43887.pdf. Accessed April 2, 2010.
    3. Klein BE, Klein R, Linton KL. Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci 1992;33:2224-8.
    4. Varma R, Ying-Lai M, Francis BA, et al, Los Angeles Latino Eye Study Group. Prevalence of open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino Eye Study. Ophthalmology 2004;111:1439-48.
    5. Eye drops delay onset of glaucoma in people at higher risk [news release]. Bethesda, MD: National Institutes of Health; June 13, 2002. Available at: www.nih.gov/news/pr/jun2002/nei-13.htm. Accessed September 20, 2010.
    6. Friedman DS, Wolfs RC, O'Colmain BJ, et al. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol 2004;122:532-8.
    7. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:701-13; discussion 829-30.
    8. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:714-20; discussion 829-30.
    9. Kass MA, Gordon MO, Gao F, et al, Ocular Hypertension Treatment Study Group. Delaying treatment of ocular hypertension: the Ocular Hypertension Treatment Study. Arch Ophthalmol 2010;128:276-87.
    10. Sommer A, Tielsch JM, Katz J, et al. Racial differences in the cause-specific prevalence of blindness in east Baltimore. N Engl J Med 1991;325:1412-7.
    11. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey. Arch Ophthalmol 1991;109:1090-5.
    12. Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia. The Blue Mountains Eye Study. Ophthalmology 1996;103:1661-9.
    13. Leske MC, Connell AM, Wu SY, et al. Incidence of open-angle glaucoma: the Barbados Eye Studies. The Barbados Eye Studies Group. Arch Ophthalmol 2001;119:89-95.
    14. Le A, Mukesh BN, McCarty CA, Taylor HR. Risk factors associated with the incidence of open-angle glaucoma: the visual impairment project. Invest Ophthalmol Vis Sci 2003;44:3783-9.
    15. Dielemans I, Vingerling JR, Wolfs RC, et al. The prevalence of primary open-angle glaucoma in a population-based study in The Netherlands. The Rotterdam Study. Ophthalmology 1994;101:1851-5.
    16. Leske MC, Connell AM, Schachat AP, Hyman L. The Barbados Eye Study. Prevalence of open angle glaucoma. Arch Ophthalmol 1994;112:821-9.
    17. Quigley HA, West SK, Rodriguez J, et al. The prevalence of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol 2001;119:1819-26.
    18. Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye Study monograph: An ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration, and visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol 1980;24:335-610.
    19. Klein BE, Klein R, Sponsel WE, et al. Prevalence of glaucoma. The Beaver Dam Eye Study. Ophthalmology 1992;99:1499-504.
    20. Miglior S, Pfeiffer N, Torri V, et al, European Glaucoma Prevention Study (EGPS) Group. Predictive factors for open-angle glaucoma among patients with ocular hypertension in the European Glaucoma Prevention Study. Ophthalmology 2007;114:3-9.
    21. Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open-angle glaucoma. The Baltimore Eye Survey. JAMA 1991;266:369-74.
    22. Armaly MF, Krueger DE, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study. I. Summary report of the risk factors for glaucomatous visual-field defects. Arch Ophthalmol 1980;98:2163-71.
    23. Mason RP, Kosoko O, Wilson MR, et al. National survey of the prevalence and risk factors of glaucoma in St. Lucia, West Indies. Part I. Prevalence findings. Ophthalmology 1989;96:1363-8.
    24. Leske MC, Wu SY, Hennis A, et al, BESs Study Group. Risk factors for incident open-angle glaucoma: the Barbados Eye Studies. Ophthalmology 2008;115:85-93.
    25. Drance SM, Fairclough M, Butler DM, Kottler MS. The importance of disc hemorrhage in the prognosis of chronic open angle glaucoma. Arch Ophthalmol 1977;95:226-8.
    26. Diehl DL, Quigley HA, Miller NR, et al. Prevalence and significance of optic disc hemorrhage in a longitudinal study of glaucoma. Arch Ophthalmol 1990;108:545-50.
    27. Airaksinen PJ, Mustonen E, Alanko HI. Optic disc haemorrhages precede retinal nerve fibre layer defects in ocular hypertension. Acta Ophthalmol (Copenh) 1981;59:627-41.
    28. Siegner SW, Netland PA. Optic disc hemorrhages and progression of glaucoma. Ophthalmology 1996;103:1014-24.
    29. Budenz DL, Anderson DR, Feuer WJ, et al. Detection and prognostic significance of optic disc hemorrhages during the Ocular Hypertension Treatment Study. Ophthalmology 2006;113:2137-43.
    30. Gordon MO, Torri V, Miglior S, et al, Ocular Hypertension Treatment Study Group, European Glaucoma Prevention Study Group. Validated prediction model for the development of primary open-angle glaucoma in individuals with ocular hypertension. Ophthalmology 2007;114:10-9.
    31. Chopra V, Varma R, Francis BA, et al, Los Angeles Latino Eye Study Group. Type 2 diabetes mellitus and the risk of open-angle glaucoma: the Los Angeles Latino Eye Study. Ophthalmology 2008;115:227-32.
    32. Mitchell P, Smith W, Chey T, Healey PR. Open-angle glaucoma and diabetes: the Blue Mountains Eye Study, Australia. Ophthalmology 1997;104:712-8.
    33. Klein BE, Klein R, Jensen SC. Open-angle glaucoma and older-onset diabetes. The Beaver Dam Eye Study. Ophthalmology 1994;101:1173-7.
    34. Dielemans I, de Jong PT, Stolk R, et al. Primary open-angle glaucoma, intraocular pressure, and diabetes mellitus in the general elderly population. The Rotterdam Study. Ophthalmology 1996;103:1271-5.
    35. Bonovas S, Peponis V, Filioussi K. Diabetes mellitus as a risk factor for primary open-angle glaucoma: a meta-analysis. Diabet Med 2004;21:609-14.
    36. Pasquale LR, Kang JH, Manson JE, et al. Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women. Ophthalmology 2006;113:1081-6.
    37. Tielsch JM, Katz J, Quigley HA, et al. Diabetes, intraocular pressure, and primary open-angle glaucoma in the Baltimore Eye Survey. Ophthalmology 1995;102:48-53.
    38. de Voogd S, Ikram MK, Wolfs RC, et al. Is diabetes mellitus a risk factor for open-angle glaucoma? The Rotterdam Study. Ophthalmology 2006;113:1827-31.
    39. Wang J, Mitchell P, Smith W. Is there an association between migraine headache and open-angle glaucoma? Findings from the Blue Mountains Eye Study. Ophthalmology 1997;104:1714-19.
    40. Broadway DC, Drance SM. Glaucoma and vasospasm. Br J Ophthalmol 1998;82:862-70.
    41. Cursiefen C, Wisse M, Cursiefen S, et al. Migraine and tension headache in high-pressure and normal-pressure glaucoma. Am J Ophthalmol 2000;129:102-4.
    42. Memarzadeh F, Ying-Lai M, Chung J, et al, Los Angeles Latino Eye Study Group. Blood pressure, perfusion pressure, and open-angle glaucoma: the Los Angeles Latino Eye Study. Invest Ophthalmol Vis Sci 2010;51:2872-7.
    43. Kuzin AA, Varma R, Reddy HS, et al. Ocular biometry and open-angle glaucoma: The Los Angeles Latino Eye Study. Ophthalmology 2010;117:1713-19.
    44. Leske MC, Connell AM, Wu SY, et al. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol 1995;113:918-24.
    45. Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology 1999;106:2010-5.
    46. Leske MC, Wu SY, Nemesure B, Hennis A. Incident open-angle glaucoma and blood pressure. Arch Ophthalmol 2002;120:954-9.
    47. Jonas JB, Martus P, Budde WM. Anisometropia and degree of optic nerve damage in chronic open-angle glaucoma. Am J Ophthalmol 2002;134:547-51.
    48. Mitchell P, Lee AJ, Rochtchina E, Wang JJ. Open-angle glaucoma and systemic hypertension: the Blue Mountains Eye Study. J Glaucoma 2004;13:319-26.
    49. Bonomi L, Marchini G, Marraffa M, et al. Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study. Ophthalmology 2000;107:1287-93.
    50. Dielemans I, Vingerling JR, Algra D, et al. Primary open-angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly population. The Rotterdam Study. Ophthalmology 1995;102:54-60.
    51. American Academy of Ophthalmology Preferred Practice Patterns Committee. Preferred Practice Pattern® Guidelines. Comprehensive Adult Medical Eye Evaluation. San Francisco, CA: American Academy of Ophthalmology; 2010. Available at: www.aao.org/ppp.
    52. Gutierrez P, Wilson MR, Johnson C, et al. Influence of glaucomatous visual field loss on health-related quality of life. Arch Ophthalmol 1997;115:777-84.
    53. Lee BL, Gutierrez P, Gordon M, et al. The Glaucoma Symptom Scale. A brief index of glaucoma-specific symptoms. Arch Ophthalmol 1998;116:861-6.
    54. Parrish RK II, Gedde SJ, Scott IU, et al. Visual function and quality of life among patients with glaucoma. Arch Ophthalmol 1997;115:1447-55.
    55. Sherwood MB, Garcia-Siekavizza A, Meltzer MI, et al. Glaucoma's impact on quality of life and its relation to clinical indicators. A pilot study. Ophthalmology 1998;105:561-6.
    56. Wilson MR, Coleman AL, Yu F, et al. Functional status and well-being in patients with glaucoma as measured by the Medical Outcomes Study Short Form-36 questionnaire. Ophthalmology 1998;105:2112-6.
    57. Tielsch JM, Katz J, Sommer A, et al. Family history and risk of primary open angle glaucoma. The Baltimore Eye Survey. Arch Ophthalmol 1994;112:69-73.
    58. Wolfs RC, Klaver CC, Ramrattan RS, et al. Genetic risk of primary open-angle glaucoma. Population-based familial aggregation study. Arch Ophthalmol 1998;116:1640-5.
    59. Bashford KP, Shafranov G, Tauber S, Shields MB. Considerations of glaucoma in patients undergoing corneal refractive surgery. Surv Ophthalmol 2005;50:245-51.
    60. Sanchez-Naves J, Furfaro L, Piro O, Balle S. Impact and permanence of LASIK-induced structural changes in the cornea on pneumotonometric measurements: contributions of flap cutting and stromal ablation. J Glaucoma 2008;17:611-8.
    61. Friedman DS, Jampel HD, Lubomski LH, et al. Surgical strategies for coexisting glaucoma and cataract: an evidence-based update. Ophthalmology 2002;109:1902-13.
    62. Kohn AN, Moss AP, Podos SM. Relative afferent pupillary defects in glaucoma without characteristic field loss. Arch Ophthalmol 1979;97:294-6.
    63. Brown RH, Zilis JD, Lynch MG, Sanborn GE. The afferent pupillary defect in asymmetric glaucoma. Arch Ophthalmol 1987;105:1540-3.
    64. Kerrison JB, Buchanan K, Rosenberg ML, et al. Quantification of optic nerve axon loss associated with a relative afferent pupillary defect in the monkey. Arch Ophthalmol 2001;119:1333-41.
    65. Foster PJ, Devereux JG, Alsbirk PH, et al. Detection of gonioscopically occludable angles and primary angle closure glaucoma by estimation of limbal chamber depth in Asians: modified grading scheme. Br J Ophthalmol 2000;84:186-92.
    66. Van Herick W, Shaffer RN, Schwartz A. Estimation of width of angle of anterior chamber. Incidence and significance of the narrow angle. Am J Ophthalmol 1969;68:626-9.
    67. Whitacre MM, Stein R. Sources of error with use of Goldmann-type tonometers. Surv Ophthalmol 1993;38:1-30.
    68. Barkana Y, Anis S, Liebmann J, et al. Clinical utility of intraocular pressure monitoring outside of normal office hours in patients with glaucoma. Arch Ophthalmol 2006;124:793-7.
    69. Bhorade AM, Gordon MO, Wilson B, et al. Variability of intraocular pressure measurements in observation participants in the ocular hypertension treatment study. Ophthalmology 2009;116:717-24.
    70. Choi J, Jeong J, Cho HS, Kook MS. Effect of nocturnal blood pressure reduction on circadian fluctuation of mean ocular perfusion pressure: a risk factor for normal tension glaucoma. Invest Ophthalmol Vis Sci 2006;47:831-6.
    71. Collaer N, Zeyen T, Caprioli J. Sequential office pressure measurements in the management of glaucoma. J Glaucoma 2005;14:196-200.
    72. Dinn RB, Zimmerman MB, Shuba LM, et al. Concordance of diurnal intraocular pressure between fellow eyes in primary open-angle glaucoma. Ophthalmology 2007;114:915-20.
    73. Jonas JB, Budde W, Stroux A, et al. Single intraocular pressure measurements and diurnal intraocular pressure profiles. Am J Ophthalmol 2005;139:1136-7.
    74. Liu JH, Sit AJ, Weinreb RN. Variation of 24-hour intraocular pressure in healthy individuals: right eye versus left eye. Ophthalmology 2005;112:1670-5.
    75. Sit AJ, Liu JH, Weinreb RN. Asymmetry of right versus left intraocular pressures over 24 hours in glaucoma patients. Ophthalmology 2006;113:425-30.
    76. Tajunisah I, Reddy SC, Fathilah J. Diurnal variation of intraocular pressure in suspected glaucoma patients and their outcome. Graefes Arch Clin Exp Ophthalmol 2007;245:1851-7.
    77. Hara T, Tsuru T. Increase of peak intraocular pressure during sleep in reproduced diurnal changes by posture. Arch Ophthalmol 2006;124:165-8.
    78. Tasman W, Jaeger EA, eds. Duane's Ophthalmology, 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2009.
    79. Chauhan BC, McCormick TA, Nicolela MT, LeBlanc RP. Optic disc and visual field changes in a prospective longitudinal study of patients with glaucoma: comparison of scanning laser tomography with conventional perimetry and optic disc photography. Arch Ophthalmol 2001;119:1492-9.
    80. Mohammadi K, Bowd C, Weinreb RN, et al. Retinal nerve fiber layer thickness measurements with scanning laser polarimetry predict glaucomatous visual field loss. Am J Ophthalmol 2004;138:592-601.
    81. Sommer A, Katz J, Quigley HA, et al. Clinically detectable nerve fiber atrophy precedes the onset of glaucomatous field loss. Arch Ophthalmol 1991;109:77-83.
    82. Quigley HA, Addicks EM, Green WR. Optic nerve damage in human glaucoma. III. Quantitative correlation of nerve fiber loss and visual field defect in glaucoma, ischemic neuropathy, papilledema, and toxic neuropathy. Arch Ophthalmol 1982;100:135-46.
    83. Lin SC, Singh K, Jampel HD, et al. Optic nerve head and retinal nerve fiber layer analysis: a report by the American Academy of Ophthalmology. Ophthalmology 2007;114:1937-49.
    84. Baraibar B, Sanchez-Cano A, Pablo LE, Honrubia FM. Preperimetric glaucoma assessment with scanning laser polarimetry (GDx VCC): analysis of retinal nerve fiber layer by sectors. J Glaucoma 2007;16:659-64.
    85. Lalezary M, Medeiros FA, Weinreb RN, et al. Baseline optical coherence tomography predicts the development of glaucomatous change in glaucoma suspects. Am J Ophthalmol 2006;142:576-82.
    86. Quigley HA, Enger C, Katz J, et al. Risk factors for the development of glaucomatous visual field loss in ocular hypertension. Arch Ophthalmol 1994;112:644-9.
    87. Jonas JB, Martus P, Horn FK, et al. Predictive factors of the optic nerve head for development or progression of glaucomatous visual field loss. Invest Ophthalmol Vis Sci 2004;45:2613-8.
    88. Uchida H, Ugurlu S, Caprioli J. Increasing peripapillary atrophy is associated with progressive glaucoma. Ophthalmology 1998;105:1541-5.
    89. Zeyen TG, Caprioli J. Progression of disc and field damage in early glaucoma. Arch Ophthalmol 1993;111:62-5.
    90. Sommer A, Pollack I, Maumenee AE. Optic disc parameters and onset of glaucomatous field loss. I. Methods and progressive changes in disc morphology. Arch Ophthalmol 1979;97:1444-8.
    91. Pederson JE, Anderson DR. The mode of progressive disc cupping in ocular hypertension and glaucoma. Arch Ophthalmol 1980;98:490-5.
    92. Hart WM Jr, Yablonski M, Kass MA, Becker B. Multivariate analysis of the risk of glaucomatous visual field loss. Arch Ophthalmol 1979;97:1455-8.
    93. Yablonski ME, Zimmerman TJ, Kass MA, Becker B. Prognostic significance of optic disk cupping in ocular hypertensive patients. Am J Ophthalmol 1980;89:585-92.
    94. Odberg T, Riise D. Early diagnosis of glaucoma. The value of successive stereophotography of the optic disc. Acta Ophthalmol (Copenh) 1985;63:257-63.
    95. Drance S, Anderson DR, Schulzer M. Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol 2001;131:699-708.
    96. Leske MC, Heijl A, Hussein M, et al, Early Manifest Glaucoma Trial Group. Factors for glaucoma progression and the effect of treatment: the Early Manifest Glaucoma Trial. Arch Ophthalmol 2003;121:48-56.
    97. Quigley HA, Sommer A. How to use nerve fiber layer examination in the management of glaucoma. Trans Am Ophthalmol Soc 1987;85:254-72.
    98. Medeiros FA, Sample PA, Zangwill LM, et al. Corneal thickness as a risk factor for visual field loss in patients with preperimetric glaucomatous optic neuropathy. Am J Ophthalmol 2003;136:805-13.
    99. Agudelo LM, Molina CA, Alvarez DL. Changes in intraocular pressure after laser in situ keratomileusis for myopia, hyperopia, and astigmatism. J Refract Surg 2002;18:472-4.
    100. Dueker DK, Singh K, Lin SC, et al. Corneal thickness measurement in the management of primary open-angle glaucoma: a report by the American Academy of Ophthalmology. Ophthalmology 2007;114:1779-87.
    101. Hahn S, Azen S, Ying-Lai M, Varma R, Los Angeles Latino Eye Study Group. Central corneal thickness in Latinos. Invest Ophthalmol Vis Sci 2003;44:1508-12.
    102. Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh) 1975;53:34-43.
    103. Ehlers N, Hansen FK. Central corneal thickness in low-tension glaucoma. Acta Ophthalmol (Copenh) 1974;52:740-6.
    104. Manni G, Oddone F, Parisi V, et al. Intraocular pressure and central corneal thickness. Prog Brain Res 2008;173:25-30.
    105. Delgado MF, Nguyen NT, Cox TA, et al. Automated perimetry: a report by the American Academy of Ophthalmology. Ophthalmology 2002;109:2362-74.
    106. Demirel S, Johnson CA. Incidence and prevalence of short wavelength automated perimetry deficits in ocular hypertensive patients. Am J Ophthalmol 2001;131:709-15.
    107. Medeiros FA, Sample PA, Weinreb RN. Frequency doubling technology perimetry abnormalities as predictors of glaucomatous visual field loss. Am J Ophthalmol 2004;137:863-71.
    108. Landers JA, Goldberg I, Graham SL. Detection of early visual field loss in glaucoma using frequency-doubling perimetry and short-wavelength automated perimetry. Arch Ophthalmol 2003;121:1705-10.
    109. Singh K, Lee BL, Wilson MR. A panel assessment of glaucoma management: modification of existing RAND-like methodology for consensus in ophthalmology. Part II: results and interpretation. Am J Ophthalmol 2008;145:575-81.
    110. Keltner JL, Johnson CA, Quigg JM, et al, Ocular Hypertension Treatment Study Group. Confirmation of visual field abnormalities in the Ocular Hypertension Treatment Study. Arch Ophthalmol 2000;118:1187-94.
    111. Lee AC, Sample PA, Blumenthal EZ, et al. Infrequent confirmation of visual field progression. Ophthalmology 2002;109:1059-65.
    112. Medeiros FA, Alencar LM, Zangwill LM, et al. Prediction of functional loss in glaucoma from progressive optic disc damage. Arch Ophthalmol 2009;127:1250-6.
    113. Zangwill LM, Weinreb RN, Beiser JA, et al. Baseline topographic optic disc measurements are associated with the development of primary open-angle glaucoma: the Confocal Scanning Laser Ophthalmoscopy Ancillary Study to the Ocular Hypertension Treatment Study. Arch Ophthalmol 2005;123:1188-97.
    114. Alencar LM, Bowd C, Weinreb RN, et al. Comparison of HRT-3 glaucoma probability score and subjective stereophotograph assessment for prediction of progression in glaucoma. Invest Ophthalmol Vis Sci 2008;49:1898-906.
    115. Vizzeri G, Weinreb RN, Martinez de la Casa JM, et al. Clinicians agreement in establishing glaucomatous progression using the Heidelberg retina tomograph. Ophthalmology 2009;116:14-24.
    116. Shaffer RN, Ridgway WL, Brown R, Kramer SG. The use of diagrams to record changes in glaucomatous disks. Am J Ophthalmol 1975;80:460-4.
    117. Medeiros FA, Zangwill LM, Bowd C, Weinreb RN. Comparison of the GDx VCC scanning laser polarimeter, HRT II confocal scanning laser ophthalmoscope, and stratus OCT optical coherence tomograph for the detection of glaucoma. Arch Ophthalmol 2004;122:827-37.
    118. Palmberg P. Answers from the ocular hypertension treatment study. Arch Ophthalmol 2002;120:829-30.
    119. American Academy of Ophthalmology Glaucoma Panel. Preferred Practice Pattern® Guidelines. Primary Open-Angle Glaucoma. San Francisco, CA: American Academy of Ophthalmology; 2010. Available at: www.aao.org/ppp.
    120. Johnson CA, Sample PA, Zangwill LM, et al. Structure and function evaluation (SAFE): II. Comparison of optic disk and visual field characteristics. Am J Ophthalmol 2003;135:148-54.
    121. Kim J, Dally LG, Ederer F, et al. The Advanced Glaucoma Intervention Study (AGIS): 14. Distinguishing progression of glaucoma from visual field fluctuations. Ophthalmology 2004;111:2109-16.
    122. Anderson DR. Glaucoma: the damage caused by pressure. XLVI Edward Jackson memorial lecture. Am J Ophthalmol 1989;108:485-95.
    123. Jampel HD. Target pressure in glaucoma therapy. J Glaucoma 1997;6:133-8.
    124. Heijl A, Leske MC, Bengtsson B, et al, Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol 2002;120:1268-79.
    125. Whitson JT. Glaucoma: a review of adjunctive therapy and new management strategies. Expert Opin Pharmacother 2007;8:3237-49.
    126. McKinnon SJ, Goldberg LD, Peeples P, et al. Current management of glaucoma and the need for complete therapy. Am J Manag Care 2008;14:S20-7.
    127. Stewart WC, Konstas AG, Nelson LA, Kruft B. Meta-analysis of 24-hour intraocular pressure studies evaluating the efficacy of glaucoma medicines. Ophthalmology 2008;115:1117-22.
    128. Bhosle MJ, Reardon G, Camacho FT, et al. Medication adherence and health care costs with the introduction of latanoprost therapy for glaucoma in a Medicare managed care population. Am J Geriatr Pharmacother 2007;5:100-11.
    129. van der Valk R, Webers CA, Schouten JS, et al. Intraocular pressure-lowering effects of all commonly used glaucoma drugs: a meta-analysis of randomized clinical trials. Ophthalmology 2005;112:1177-85.
    130. Cheng JW, Cai JP, Wei RL. Meta-analysis of medical intervention for normal tension glaucoma. Ophthalmology 2009;116:1243-9.
    131. Shuba LM, Doan AP, Maley MK, et al. Diurnal fluctuation and concordance of intraocular pressure in glaucoma suspects and normal tension glaucoma patients. J Glaucoma 2007;16:307-12.
    132. Piltz J, Gross R, Shin DH, et al. Contralateral effect of topical beta-adrenergic antagonists in initial one-eyed trials in the ocular hypertension treatment study. Am J Ophthalmol 2000;130:441-53.
    133. Realini T, Fechtner RD, Atreides SP, Gollance S. The uniocular drug trial and second-eye response to glaucoma medications. Ophthalmology 2004;111:421-6.
    134. Robin AL, Covert D. Does adjunctive glaucoma therapy affect adherence to the initial primary therapy? Ophthalmology 2005;112:863-8.
    135. Robin AL, Novack GD, Covert DW, et al. Adherence in glaucoma: objective measurements of once-daily and adjunctive medication use. Am J Ophthalmol 2007;144:533-40.
    136. Fung AT, Reid SE, Jones MP, et al. Meta-analysis of randomised controlled trials comparing latanoprost with brimonidine in the treatment of open-angle glaucoma, ocular hypertension or normal-tension glaucoma. Br J Ophthalmol 2007;91:62-8.
    137. Zimmerman TJ, Kooner KS, Kandarakis AS, Ziegler LP. Improving the therapeutic index of topically applied ocular drugs. Arch Ophthalmol 1984;102:551-3.
    138. Nordstrom BL, Friedman DS, Mozaffari E, et al. Persistence and adherence with topical glaucoma therapy. Am J Ophthalmol 2005;140:598-606.
    139. Friedman DS, Quigley HA, Gelb L, et al. Using pharmacy claims data to study adherence to glaucoma medications: methodology and findings of the Glaucoma Adherence and Persistency Study (GAPS). Invest Ophthalmol Vis Sci 2007;48:5052-7.
    140. Schwartz GF, Reardon G, Mozaffari E. Persistency with latanoprost or timolol in primary open-angle glaucoma suspects. Am J Ophthalmol 2004;137:S13-6.
    141. Okeke CO, Quigley HA, Jampel HD, et al. Adherence with topical glaucoma medication monitored electronically the Travatan Dosing Aid study. Ophthalmology 2009;116:191-9.
    142. Haynes R, McDonald H, Garg A, Montague P. Interventions for helping patients to follow prescriptions for medications. Cochrane Database of Syst Rev 2002, Issue 2. Art. No.: CD000011. DOI: 10.1002/14651858.CD000011.
    143. Osterberg L, Blaschke T. Adherence to medication. N Engl J Med 2005;353:487-97.
    144. Kymes SM, Kass MA, Anderson DR, et al. Management of ocular hypertension: a cost-effectiveness approach from the Ocular Hypertension Treatment Study. Am J Ophthalmol 2006;141:997-1008.
    145. Caprioli J, Prum B, Zeyen T. Comparison of methods to evaluate the optic nerve head and nerve fiber layer for glaucomatous change. Am J Ophthalmol 1996;121:659-67.
    146. Lichter PR. Variability of expert observers in evaluating the optic disc. Trans Am Ophthalmol Soc 1976;74:532-72.
    147. Airaksinen PJ, Tuulonen A, Alanko HI. Rate and pattern of neuroretinal rim area decrease in ocular hypertension and glaucoma. Arch Ophthalmol 1992;110:206-10.
    148. Smith SD, Katz J, Quigley HA. Analysis of progressive change in automated visual fields in glaucoma. Invest Ophthalmol Vis Sci 1996;37:1419-28.
    149. Katz J, Tielsch JM, Quigley HA, Sommer A. Automated perimetry detects visual field loss before manual Goldmann perimetry. Ophthalmology 1995;102:21-6.
    150. Heijl A, Asman P. A clinical study of perimetric probability maps. Arch Ophthalmol 1989;107:199-203.
    151. Keltner JL, Johnson CA, Anderson DR, et al. The association between glaucomatous visual fields and optic nerve head features in the Ocular Hypertension Treatment Study. Ophthalmology 2006;113:1603-12.
    152. Kosoko O, Quigley HA, Vitale S, et al. Risk factors for noncompliance with glaucoma follow-up visits in a residents' eye clinic. Ophthalmology 1998;105:2105-11.
    153. Ngan R, Lam DL, Mudumbai RC, Chen PP. Risk factors for noncompliance with follow-up among normal-tension glaucoma suspects. Am J Ophthalmol 2007;144:310-1.

    PPP COMMITTEE/PANEL MEMBERS AND DISCLOSURES

    Prepared by the American Academy of Ophthalmology Glaucoma Panel

    Glaucoma Panel Members
    Bruce E. Prum, Jr., MD, Chair
    David S. Friedman, MD, MPH, PhD, American Glaucoma Society Representative
    Steven J. Gedde, MD
    Leon W. Herndon, MD
    Young H. Kwon, MD, PhD
    Michele C. Lim, MD
    Lisa F. Rosenberg, MD
    Rohit Varma, MD, MPH, Methodologist

    Preferred Practice Patterns Committee Members
    Christopher J. Rapuano, MD, Chair
    David F. Chang, MD
    Emily Y. Chew, MD
    Robert S. Feder, MD
    Stephen D. McLeod, MD
    Bruce E. Prum, Jr., MD
    R. Michael Siatkowski, MD
    David C. Musch, PhD, MPH, Methodologist

    Academy Staff
    Flora C. Lum, MD
    Nancy Collins, RN, MPH
    Doris Mizuiri
    Medical Editor: Susan Garratt
    Design: Socorro Soberano
    Reviewed by: Council
    Approved by: Board of Trustees
                        September 11, 2010

    The panel and committee members have disclosed the following financial relationships occurring from January 2009 to September 2010:

    David F. Chang, MD: Advanced Medical Optics - Consultant/Advisor; Alcon Laboratories, Inc. - Consultant/Advisor; Allergan, Inc. - Lecture fees; Calhoun Vision, Inc. - Consultant/Advisor, Equity owner; Eyemaginations, Inc. - Consultant/Advisor, Patent/Royalty; Ista Pharmaceuticals - Consultant/Advisor, Grant support; LensAR - Consultant/Advisor; Hoya - Consultant/Advisor; Peak Surgical - Consultant/Advisor; Revital Vision - Equity owner; SLACK, Inc. - Patent/Royalty; Transcend Medical - Consultant/Advisor; Visiogen, Inc. - Consultant/Advisor, Equity owner

    Emily Y. Chew, MD: No financial relationships to disclose.

    Robert S. Feder, MD: No financial relationships to disclose.

    David S. Friedman, MD, MPH, PhD: Alcon Laboratories, Inc. - Grant support; NiCox - Consultant/Advisor; Novartis Pharmaceuticals Corp. - Consultant/Advisor; ORBIS International - Consultant/Advisor; Pfizer, Inc. - Consultant/Advisor, Lecture fees, Grant support; Promedior - Consultant/Advisor; Zeiss Meditec - Grant support

    Steven J. Gedde, MD: Lumenis, Inc. - Lecture fees

    Leon W. Herndon, MD: Alcon Laboratories, Inc. - Consultant/Advisor, Lecture fees; Allergan, Inc. - Lecture fees; iScience - Lecture fees; Ista Pharmaceuticals - Consultant/Advisor, Lecture fees; Merck & Co., Inc. - Lecture fees; Optonol, Ltd. - Lecture fees; Pfizer, Inc. - Lecture fees; Reichert, Inc. - Lecture fees

    Young H. Kwon, MD, PhD: Allergan, Inc. - Consultant/Advisor; Free Educational Publications, Inc. - Equity owner; Pfizer, Inc. - Consultant/Advisor

    Michele C. Lim, MD: No financial relationships to disclose.

    Stephen D. McLeod, MD: Abbott Medical Optics - Consultant/Advisor, Equity owner; Visiogen, Inc. - Consultant/Advisor, Equity owner

    David C. Musch, PhD, MPH: Glaukos Corp. - Consultant/Advisor; MacuSight, Inc. - Consultant/Advisor; National Eye Institute - Grant support; NeoVista, Inc. - Consultant/Advisor; Neurotech USA, Inc. - Consultant/Advisor; OPKO Health, Inc. - Consultant/Advisor; Oraya Therapeutics, Inc. - Consultant/Advisor; Pfizer Ophthalmics - Grant support; Washington University - Grant support

    Bruce E. Prum, Jr., MD: Alcon Laboratories, Inc. - Grant support; Allergan, Inc. - Consultant/Advisor

    Christopher J. Rapuano, MD: Alcon Laboratories, Inc. - Lecture fees; Allergan, Inc. - Consultant/Advisor, Lecture fees; Bausch & Lomb - Lecture fees; Inspire - Lecture fees; EyeGate Pharma - Consultant/Advisor; Inspire - Lecture fees; Rapid Pathogen Screening - Equity owner; Vistakon Johnson & Johnson Visioncare, Inc. - Lecture fees

    Lisa F. Rosenberg, MD: No financial relationships to disclose.

    R. Michael Siatkowski, MD: National Eye Institute - Grant support

    Rohit Varma, MD, MPH: Alcon Laboratories, Inc. - Consultant/Advisor, Lecture fees; Allergan, Inc. - Consultant/Advisor, Grant support; Aquesys - Consultant/Advisor, Equity owner, Grant support; Bausch & Lomb Surgical - Consultant/Advisor; Genentech, Inc. - Consultant/Advisor, Grant support; Merck & Co., Inc. - Consultant/Advisor; National Eye Institute - Grant support; Optovue - Grant support; Pfizer, Inc. - Consultant/Advisor, Lecture fees, Grant support; Replenish, Inc. - Consultant/Advisor, Equity owner, Grant support

    Copyright © 2010
    American Academy of Ophthalmology
    All rights reserved

    This document should be cited as:
    American Academy of Ophthalmology Glaucoma Panel. Preferred Practice Pattern®Guidelines. Primary Open-Angle Glaucoma Suspect. San Francisco, CA: American Academy of Ophthalmology; 2010. Available at: www.aao.org/ppp.

    ABOUT PREFERRED PRACTICE PATTERNS

    As a service to its members and the public, the American Academy of Ophthalmology has developed a series of guidelines called Preferred Practice Patterns that identify characteristics and components of quality eye care. (See Appendix 1.)

    The Preferred Practice Pattern® guidelines are based on the best available scientific data as interpreted by panels of knowledgeable health professionals. In some instances, such as when results of carefully conducted clinical trials are available, the data are particularly persuasive and provide clear guidance. In other instances, the panels have to rely on their collective judgment and evaluation of available evidence.

    Preferred Practice Pattern guidelines provide the pattern of practice, not the care of a particular individual. While they should generally meet the needs of most patients, they cannot possibly best meet the needs of all patients. Adherence to these PPPs will not ensure a successful outcome in every situation. These practice patterns should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed at obtaining the best results. It may be necessary to approach different patients' needs in different ways. The physician must make the ultimate judgment about the propriety of the care of a particular patient in light of all of the circumstances presented by that patient. The American Academy of Ophthalmology is available to assist members in resolving ethical dilemmas that arise in the course of ophthalmic practice.

    Preferred Practice Patternguidelines are not medical standards to be adhered to in all individual situations. The Academy specifically disclaims any and all liability for injury or other damages of any kind, from negligence or otherwise, for any and all claims that may arise out of the use of any recommendations or other information contained herein.

    References to certain drugs, instruments, and other products are made for illustrative purposes only and are not intended to constitute an endorsement of such. Such material may include information on applications that are not considered community standard, that reflect indications not included in approved U.S. Food and Drug Administration (FDA) labeling, or that are approved for use only in restricted research settings. The FDA has stated that it is the responsibility of the physician to determine the FDA status of each drug or device he or she wishes to use, and to use them with appropriate patient consent in compliance with applicable law.  

    Innovation in medicine is essential to assure the future health of the American public, and the Academy encourages the development of new diagnostic and therapeutic methods that will improve eye care. It is essential to recognize that true medical excellence is achieved only when the patients' needs are the foremost consideration.

    All PPPs are reviewed by their parent panel annually or earlier if developments warrant and updated accordingly. To ensure that all PPPs are current, each is valid for 5 years from the "approved by" date unless superseded by a revision. Preferred Practice Pattern guidelines are developed by the Academy's H. Dunbar Hoskins Jr., M.D. Center for Quality Eye Care without any external financial support. Authors and reviewers of PPPs are volunteers and do not receive any financial compensation for their contributions to the documents. The PPPs are externally reviewed by experts and stakeholders before publication.