Journal of Gerontological Nursing

Clinical Concepts 

Primary Open-Angle Glaucoma: Clinical Update

Jasmine W. Yumori, OD, FAAO; Mary P. Cadogan, DrPH, RN, GNP-BC

Abstract

Glaucoma is an optic neuropathy that is usually associated with an elevated intraocular pressure. Primary open-angle glaucoma (POAG) is the most common type of glaucoma and is progressive and bilateral but typically asymmetric in patients. Studies have shown that reducing intraocular pressure reduces the risk of vision loss. In the United States, medical intervention by means of prescription eye drops is the initial line of treatment. Nurses play an important role in educating individuals, particularly older adults, about the importance of routine eye care to earlier diagnose, treat, and adequately manage eye diseases such as POAG.

Abstract

Glaucoma is an optic neuropathy that is usually associated with an elevated intraocular pressure. Primary open-angle glaucoma (POAG) is the most common type of glaucoma and is progressive and bilateral but typically asymmetric in patients. Studies have shown that reducing intraocular pressure reduces the risk of vision loss. In the United States, medical intervention by means of prescription eye drops is the initial line of treatment. Nurses play an important role in educating individuals, particularly older adults, about the importance of routine eye care to earlier diagnose, treat, and adequately manage eye diseases such as POAG.

Dr. Yumori is Assistant Professor, Western University of Health Sciences, College of Optometry, Pomona, and Dr. Cadogan is Professor, Adjunct Series, University of California, Los Angeles, School of Nursing, Los Angeles, California.

The authors disclose that they have no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support. The authors express their gratitude to Drs. Elizabeth Hoppe and Raymond Maeda for reading/commenting on the manuscript and to Ms. Ruth Harris for assistance in confirming copyright permissions.

Address correspondence to Jasmine W. Yumori, OD, FAAO, Assistant Professor, Western University of Health Sciences, College of Optometry, 309 E. 2nd Street, Pomona, CA 91766; e-mail: jyumori@westernu.edu.

Posted Online: March 02, 2011
An Example of Normal Vision (top) and Vision in Advanced Stages of Primary Open-Angle Glaucoma (bottom), in Which Patients May Start to Report Problems with Missing Areas in Their Side Vision.

An Example of Normal Vision (top) and Vision in Advanced Stages of Primary Open-Angle Glaucoma (bottom), in Which Patients May Start to Report Problems with Missing Areas in Their Side Vision.

Glaucoma is not one disease but refers to a group of diseases that cause damage to the optic nerve, which connects the retina to the brain. If glaucoma is left untreated, it can lead to vision loss and blindness. Glaucoma has been reported to affect 2.5 million Americans and is the leading cause of visual impairment among African American and Hispanic individuals (Rodriguez et al., 2002; Sommer et al., 1991). Among all Americans, glaucoma is the second-leading cause of irreversible vision loss.

A common method of classifying subtypes of glaucoma is based on the appearance of the iridocorneal angle, which is the angle formed by the iris and the cornea (Kwon, Fingert, Kuehn, & Alward, 2009). The iridocorneal angle has been identified as the primary drainage route for the aqueous humor. Glaucoma is commonly classified as either “open angle” or “closed angle” and divided into primary and secondary types. Primary open-angle glaucoma (POAG) accounts for up to 90% of cases of glaucoma in the United States (Distelhorst & Hughes, 2003) and will be the focus of this clinical review. The American Academy of Ophthalmology’s (AAO) Preferred Practice Pattern (AAO Glaucoma Panel, 2005) describes POAG as a chronic, generally bilateral, and often asymmetric disease characterized in at least one eye by all of the following: evidence of optic nerve damage; characteristic visual field abnormalities; adult onset; open, normal-appearing anterior chamber angles; and absence of other (secondary) causes of OAG.

Etiology and Pathophysiology

Historically, POAG was characterized as a disease of elevated intraocular pressure (IOP), but accumulating evidence points to a much more complex process. While the etiology of POAG is constantly undergoing further investigation, strong evidence suggests glaucoma is caused by damage to the retinal ganglion cell axons within the lamina cribrosa of the optic nerve head (Burgoyne, Downs, Bellezza, & Hart, 2004; Gaasterland, Tanishima, & Kuwabara, 1978), leading to gradual vision loss. Two main theories have emerged to explain the mechanism of ganglion cell dysfunction: mechanical and vasogenic. According to the mechanical theory, elevated IOP causes deformation of the lamina cribrosa structure, which leads to blockage of axon transport and subsequent axon damage (Quigley, 1999). According to the vasogenic theory, vascular insufficiency at the optic nerve head results in hypoxia and decreased nutrition to optic nerve axons ultimately with ganglion cell death (Osborne, Melena, Chidlow, & Wood, 2001).

Elevated IOP is frequently found in individuals with POAG. The range of distribution for IOP cut-off points used to indicate elevated IOP vary within the literature, ranging from 18 to 26 mmHg with a mode of 22 mmHg (Tavares, Medeiros, & Weinreb, 2006); the IOP associated with POAG is typically defined as more than 22 mmHg. However, some patients may develop glaucoma without elevated IOP; this is termed normotensive glaucoma. Others may have elevated IOP without glaucomatous optic nerve damage; this is termed ocular hypertension (Coleman, 1999). Because IOP remains the leading and only modifiable risk factor for glaucoma, it is important to understand the role of IOP leading to optic nerve damage.

IOP is determined by the balance between production and outflow of aqueous humor in the eye (Marquis & Whitson, 2005). The Figure shows the mechanism of aqueous humor production and drainage. Aqueous humor is produced by the ciliary body in the posterior chamber, the area behind the iris and in front of the lens. Aqueous humor circulates from the posterior chamber through the pupil into the anterior chamber and exits the eye primarily through the trabecular meshwork and canal of Schlemm where it enters the venous system (Marquis & Whitson, 2005). Some aqueous humor also leaves the eye through the secondary uveoscleral drainage pathway (Kwon et al., 2009). While short-term variations are associated with factors such as diurnal variation and posture, treatment for glaucoma is focused on decreasing production or increasing outflow of aqueous humor to decrease IOP and thus minimize damage to the optic nerve.

The Mechanism of Aqueous Humor Production and Drainage. Diagram, Available in the Public Domain, Courtesy of the National Eye Institute, National Institutes of Health.

Figure. The Mechanism of Aqueous Humor Production and Drainage. Diagram, Available in the Public Domain, Courtesy of the National Eye Institute, National Institutes of Health.

Generalized Risk Factors

Generalized risk factors for POAG include a positive patient history of systemic hypertension (Memarzadeh, Ying-Lai, Azen, & Varma, 2008; Yanagi et al., 2010), elevated body mass index (BMI) (Memarzadeh et al., 2008; Shiose & Kawase, 1986), diabetes (Yanagi et al., 2010), and smoking (Grzybowski, 2008; Zanon-Moreno, Garcia-Medina, Zanon-Viguer, Moreno-Nadal, & Pinazo-Duran, 2009).

While many of these variables may be correlated, studies such as the Los Angeles Latino Eye Study have shown that these are independently associated with elevated IOP (Memarzadeh et al., 2008). Based on these risk factors, altered ocular blood flow and oxidative stress are suspected to be a major factor in the development and progression of POAG. Increased age (Miyazaki, Segawa, & Urakawa, 1987); male gender (Kahn & Milton, 1980); African American, Hispanic, and/or Native American heritages (Kuzin, Varma, Reddy, Torres, & Azen, 2010); and a family history of glaucoma (Wang et al., 2010) have also been shown to be possible risk factors for POAG. A slow increase in IOP has been shown with age; it is suspected that as one ages, there may be a decreased outflow of aqueous humor (Miyazaki et al., 1987). This may also be seen due to concomitant increases in blood pressure and BMI associated with age (Kim & Varma, 2010).

Clinical Evaluation

Because POAG is slowly progressive, patients are typically asymptomatic until later stages of the disease (Lee et al., 1998). Furthermore, visual field loss is not commonly appreciated because individual visual fields of each eye overlap when both eyes are open. In advanced stages of the disease, patients may start to report problems with missing areas in their side vision. Vision loss from glaucoma is irreversible. Routine comprehensive dilated eye examinations by an optometrist or ophthalmologist are necessary to allow for early diagnosis and prompt treatment of POAG and other eye diseases to optimally preserve vision. Recommendations for comprehensive eye evaluations can be found in the online document Comprehensive Adult Medical Eye Evaluation (AAO, Hoskins Center for Quality Eye Care, 2010). During a comprehensive eye examination, eye health and visual function are carefully evaluated. While visual acuity may be affected in patients with more advanced glaucoma, the diagnosis of POAG mainly focuses on evaluation of optic nerve head appearance, IOP readings, pachymetry or corneal thickness measurements, visual field performance, and anterior chamber angle appearance.

Disease Management

The standard method of treating POAG is by stabilizing fluctuations in and consistently lowering IOP while minimizing adverse effects of therapy to optimize patients’ health and quality of life. Medical intervention by means of prescription eye drops is the first line of treatment (Vetrugno et al., 2008). The main categories of medications used to treat POAG are prostaglandin analogs, ophthalmic beta blockers, ophthalmic adrenergic agonists, ophthalmic or oral carbonic anhydrase inhibitors, and ophthalmic cholinergic agonists. Information on these classes of medications is summarized in Table 1. Laser and incisional surgical procedures have also been shown to be effective in reducing IOP and decreasing the glaucomatous progression (Parrish, Feuer, Schiffman, Lichter, & Musch, 2009). Although studies have shown no statistically significant difference in the change of visual field defects between medical and surgical intervention (Lichter et al., 2001) and that both methods delay and/or decrease progression of vision loss (Kass et al., 2002; Leske et al., 2007), medical intervention is typically the first line of treatment since surgery is associated with more eye discomfort, an increased risk of cataract, and a slight reduction in distance vision at 5 years (Burr, Azuara-Blanco, & Avenell, 2005). Short-term variations in IOPs are also seen diurnally and with postural changes; a maximum IOP value is usually detected in the morning and the lowest value in the early afternoon (Saccà et al., 1998). A recent study also determined that sleeping with the head erect at 30 degrees lowers IOP compared with a supine position (Buys et al., 2010).

Glaucoma Medication Classes

Table 1: Glaucoma Medication Classes

Strategies to Optimize Chronic Care

Patients are examined following initiation of therapy to evaluate efficacy. Once IOP readings have been adequately reduced, reevaluation is typically in 3- to 6-month intervals, with dilated examinations completed annually. Adjustments in therapy may be implemented if IOP readings are not at target, if there is progressive optic nerve damage, or if there is difficulty with the prescribed medical regimen (either based on contraindications, intolerance, or non-optimal adherence).

Because POAG is a chronic condition, optimal and ongoing management is essential for preservation of vision. Like other chronic illnesses with few or no symptoms, it may be challenging for those with glaucoma to continue treatment and follow up at the recommended intervals. Two measures are used most frequently to understand patterns of medication use among individuals with glaucoma. Adherence is a measure of the degree to which an individual follows the prescribed treatment regimen during a defined time period, and persistence is a measure of the time to discontinuation of the prescribed medications (Schwartz & Quigley, 2008). The Glaucoma Adherence and Persistency Study, the largest study to date among glaucoma patients, used administrative data from 13,956 patients receiving an initial glaucoma medication who were followed for at least 1 year after receiving the initial prescription (Friedman et al., 2008). Of those with data available for evaluation at the end of the year, 59% were using their medication but only 10% had used their medication continuously. Other studies have examined the reasons for low adherence and persistence among those being treated for glaucoma. For example, Tsai, McClure, Ramos, Schlundt, and Pichert (2003) described multiple factors associated with low adherence. These include cost of medication, complexity of regimen, side effects, knowledge/skill, memory, motivation/health beliefs regarding benefit and efficacy, comorbidities and need for multiple other medications, dissatisfaction with provider, inadequate communication by provider about need for continued treatment, living alone, major life events, travel, competing activities, and change in routine. Other factors found to be associated with lower adherence and persistence are lower health literacy (Kharod, Johnson, Nesti, & Rhee, 2006), depression (Jayawant, Bhosle, Anderson, & Balkrishnan, 2007), dependence on others for administering eye drops (Sleath et al., 2006), and hospitalization (Yousuf & Jones, 2010).

Quality of Life

Receiving a diagnosis of POAG may influence patients’ quality of life (QOL). Results of recent studies have found that disabilities related to POAG extend beyond clinically measurable vision deficits. Findings from the Barbados Eye Studies document lower perceived functional status and well-being among those diagnosed with POAG compared with those without the diagnosis (Wu, Hennis, Nemesure, & Leske, 2008). In particular, participants with POAG reported lower QOL for distance activities (e.g., driving), social functioning, and mental health. One study reported lower scores for Mexican Americans with POAG in all QOL subscales except general health and noted that most declines were in subscales associated with driving (Mangione et al., 2001). Others describe that POAG patients report of a loss of confidence in themselves, especially when outside the home (Coleman, 1999). Coleman (1999) noted that this lack of confidence may be associated with the loss of peripheral vision, depth perception, and contrast sensitivity that occur with POAG. These POAG-associated visual impairments may increase risk for falls and motor vehicle accidents (Glynn et al., 1991; Owsley, McGwin, & Ball, 1998).

Summary and Implications for Nurses

POAG is an important condition among older adults for several reasons. It is a common cause of irreversible vision loss among all older adults but particularly among African American and Hispanic older adults. Because it is asymptomatic, significant optic nerve damage and visual loss can occur unless early diagnosis and intervention occur. Once thought of as only a disease related to increased IOP, ongoing research points to a much more complex disorder. Newer technologies allow earlier and more accurate diagnosis of POAG, but reduction of IOP remains the only target for clinical intervention. Longer-acting topical medications have improved treatment options, but adherence and persistence with treatment remains a challenge for both patients and clinicians. Nurses have an important role in recognizing individuals at risk, stressing the importance of regular comprehensive eye evaluations, identifying barriers to treatment, responding to psychosocial impacts of POAG, and providing appropriate referrals and resources for individuals with visual limitations. Table 2 provides specific recommendations for improving care of POAG among older adults.

Strategies to Improve Glaucoma Assessment and Management

Table 2: Strategies to Improve Glaucoma Assessment and Management

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Glaucoma Medication Classes

Drug ClassMechanism of ActionCommon MedicationsCommon Dosing ScheduleaPossible Side EffectsCap Color
Prostaglandin analogsEnhances uveoscleral outflowLatanoprost (Xalatan®), bimatoprost (Lumigan®), travoprost (Travatan®)1 drop before bedtimeIncreased lash pigmentation, hypertrichosis, increased iris and periocular skin pigmentationTeal
Ophthalmic beta blockersDecreases aqueous formationTimolol (Timoptic®), betaxolol (Betoptic®), levobunolol (Betagan®), carteolol (Ocupress®), metipranolol (Optipranolol®)1 drop two times per dayBradycardia, bronchospasm, hypotension, depression, decreased libidoBlue or yellow
Ophthalmic adrenergic agonistsDecreases aqueous formation, may enhance uveoscleral outflowBrimonidine (Alphagan P®), apraclonidine (Iopidine®)1 drop three times per dayDry mouth, dry nose, tachyphylaxis, lethargy, headache, allergic reactionsPurple
Ophthalmic or oral carbonic anhydrase inhibitorsDecreases aqueous formationDorzolamide (Trusopt®), brinzolamide (Azopt®), oral acetazolamide (Diamox®)1 drop three times per dayLethargy, depression, aplastic anemia; contraindicated in patients allergic to sulfaOrange
Ophthalmic cholinergic agonistsIncreases trabecular outflow, may enhance uveoscleral outflowPilocarpine (Isopto Carpine®, Pilocar®, and others), carbachol (Isopto Carbachol®), echothiophate (Phospholine Iodide®)1 drop three times per dayHeadache, miosis, sweating, salivation, bradycardiaGreen

Strategies to Improve Glaucoma Assessment and Management

Nurses’ RoleStrategies to Improve Care
Be familiar with current clinical practice guidelines for diagnosis of glaucoma and recommended intervals for comprehensive eye examinationsAsk about last comprehensive eye examination:

Were the eyes dilated?

Was eye pressure measured?

Has the next appointment been scheduled?

Identify and educate patients about risk factors for glaucoma (i.e., age, race/ethnicity, family history, diabetes, obesity, smoking)

Encourage reduction of modifiable risk factors through smoking cessation, education, and adherence to dietary and exercise guidelines.

Relate nonmodifiable risk factors to increased need for comprehensive eye care and frequency of examination.

Review each patient’s medical history for a diagnosis of glaucoma and note (a) duration of diagnosis, (b) treatment prescribed, and (c) adherence to treatment

Evaluate for the presence of any symptoms or visual limitations

Screen for possible medication side effects

Evaluate self-management ability of individuals with known glaucoma and provide education and referrals as needed

Assess ability to instill eye drops

Identify any barriers to treatment adherence

Encourage sleeping with head propped at 30° angle

Evaluate impact of glaucoma on quality of life

Ensure ability to read medication labels and medical forms

Encourage use of large print and extra-bright lighting if needed

Refer for rehabilitation of visual impairments.

Authors

Dr. Yumori is Assistant Professor, Western University of Health Sciences, College of Optometry, Pomona, and Dr. Cadogan is Professor, Adjunct Series, University of California, Los Angeles, School of Nursing, Los Angeles, California.

The authors disclose that they have no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support. The authors express their gratitude to Drs. Elizabeth Hoppe and Raymond Maeda for reading/commenting on the manuscript and to Ms. Ruth Harris for assistance in confirming copyright permissions.

Address correspondence to Jasmine W. Yumori, OD, FAAO, Assistant Professor, Western University of Health Sciences, College of Optometry, 309 E. 2nd Street, Pomona, CA 91766; e-mail: .jyumori@westernu.edu

10.3928/00989134-20110210-01

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