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: firstname.lastname@example.org.
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.
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).
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.
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).
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.
Table 2: Strategies to Improve Glaucoma Assessment and Management
- American Academy of Ophthalmology, Glaucoma Panel. (2005). Primary open-angle glaucoma. Preferred Practice Pattern. Retrieved from http://one.aao.org/asset.axd?id=2e86ca2e-9db0-43c9-b605-c004a82b6ea5
- American Academy of Ophthalmology, Hoskins Center for Quality Eye Care. (2010). Comprehensive adult medical eye evaluation. Preferred Practice Pattern. Retrieved from http://one.aao.org/asset.axd?id=5c547997-077b-4952-b155-1a1c232b280d
- Burgoyne, C.F., Downs, J.C., Bellezza, A.J. & Hart, R.T. (2004). Three-dimensional reconstruction of normal and early glaucoma monkey optic nerve head connective tissues. Investigative Ophthalmology and Visual Science, 45, 4388–4399. doi:10.1167/iovs.04-0022 [CrossRef]
- Burr, J., Azuara-Blanco, A. & Avenell, A. (2005). Medical versus surgical interventions for open angle glaucoma (Article No. CD004399). Cochrane Database of Systematic Reviews, Issue 2.
- Buys, Y.M., Alasbali, T., Jin, Y.P., Smith, M., Gouws, P., Geffen, N. & Trope, G.E.,… (2010). Effect of sleeping in a head-up position on intraocular pressure in patients with glaucoma. Ophthalmology, 117, 1348–1351. doi:10.1016/j.ophtha.2009.11.015 [CrossRef]
- Coleman, A.L. (1999). Glaucoma. Lancet, 354, 1803–1810. doi:10.1016/S0140-6736(99)04240-3 [CrossRef]
- Distelhorst, J.S. & Hughes, G.M. (2003). Open-angle glaucoma. American Family Physician, 67, 1937–1944.
- Friedman, D.S., Hahn, S.R., Gelb, L., Tan, J., Shah, S.N., Kim, E.E. & Quigley, H.A.,… (2008). Doctor-patient communication, health-related beliefs, and adherence in glaucoma results from the Glaucoma Adherence and Persistency Study. Ophthalmology, 115, 1320–1327, e1321–e1323. doi:10.1016/j.ophtha.2007.11.023 [CrossRef]
- Gaasterland, D., Tanishima, T. & Kuwabara, T. (1978). Axoplasmic flow during chronic experimental glaucoma. 1. Light and electron microscopic studies of the monkey optic nervehead during development of glaucomatous cupping. Investigative Ophthalmology and Visual Science, 17, 838–846.
- Glynn, R.J., Seddon, J.M., Krug, J.H. Jr.. , Sahagian, C.R., Chiavelli, M.E. & Campion, E.W. (1991). Falls in elderly patients with glaucoma. Archives of Ophthalmology, 109, 205–210.
- Grzybowski, A. (2008). [Present knowledge on the effects of smoking tobacco on the eye diseases]. Przeglad Lekarski, 65, 724–727.
- Jayawant, S.S., Bhosle, M.J., Anderson, R.T. & Balkrishnan, R. (2007). Depressive symptomatology, medication persistence, and associated healthcare costs in older adults with glaucoma. Journal of Glaucoma, 16, 513–520. doi:10.1097/IJG.0b013e31804a5ec6 [CrossRef]
- Kahn, H.A. & Milton, R.C. (1980). Revised Framingham Eye Study prevalence of glaucoma and diabetic retinopathy. American Journal of Epidemiology, 111, 769–776.
- Kass, M.A., Heuer, D.K., Higginbotham, E.J., Johnson, C.A., Keltner, J.L., Miller, J.P. & Gordon, M.O.,… (2002). The Ocular Hypertension Treatment Study: A randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Archives of Ophthalmology, 120, 701–713.
- Kharod, B.V., Johnson, P.B., Nesti, H.A. & Rhee, D.J. (2006). Effect of written instructions on accuracy of self-reporting medication regimen in glaucoma patients. Journal of Glaucoma, 15, 244–247. doi:10.1097/01.ijg.0000212213.18018.8f [CrossRef]
- Kim, E. & Varma, R. (2010). Glaucoma in Latinos/Hispanics. Current Opinion in Ophthalmology, 21, 100–105. doi:10.1097/ICU.0b013e3283360b1e [CrossRef]
- Kuzin, A.A., Varma, R., Reddy, H.S., Torres, M. & Azen, S.P. (2010). Ocular biometry and open-angle glaucoma: The Los Angeles Latino Eye Study. Ophthalmology, 117, 1713–1719. doi:10.1016/j.ophtha.2010.01.035 [CrossRef]
- Kwon, Y.H., Fingert, J.H., Kuehn, M.H. & Alward, W.L. (2009). Primary open-angle glaucoma. New England Journal of Medicine, 360, 1113–1124. doi:10.1056/NEJMra0804630 [CrossRef]
- Lee, B.L., Gutierrez, P., Gordon, M., Wilson, M.R., Cioffi, G.A., Ritch, R. & Mangione, C.M.,… (1998). The Glaucoma Symptom Scale. A brief index of glaucoma-specific symptoms. Archives of Ophthalmology, 116, 861–866.
- Leske, M.C., Heijl, A., Hyman, L., Bengtsson, B., Dong, L. & Yang, Z. (2007). Predictors of long-term progression in the early manifest glaucoma trial. Ophthalmology, 114, 1965–1972. doi:10.1016/j.ophtha.2007.03.016 [CrossRef]
- Lichter, P.R., Musch, D.C., Gillespie, B.W., Guire, K.E., Janz, N.K., Wren, P.A. & Mills, R.P. (2001). Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology, 108, 1943–1953. doi:10.1016/S0161-6420(01)00873-9 [CrossRef]
- Mangione, C.M., Lee, P.P., Gutierrez, P.R., Spritzer, K., Berry, S. & Hays, R.D. (2001). Development of the 25-item National Eye Institute Visual Function Questionnaire. Archives of Ophthalmology, 119, 1050–1058.
- Marquis, R.E. & Whitson, J.T. (2005). Management of glaucoma: Focus on pharmacological therapy. Drugs and Aging, 22, 1–21. doi:10.2165/00002512-200522010-00001 [CrossRef]
- Memarzadeh, F., Ying-Lai, M., Azen, S.P. & Varma, R. (2008). Associations with intraocular pressure in Latinos: The Los Angeles Latino Eye Study. American Journal of Ophthalmology, 146, 69–76. doi:10.1016/j.ajo.2008.03.015 [CrossRef]
- Miyazaki, M., Segawa, K. & Urakawa, Y. (1987). Age-related changes in the trabecular meshwork of the normal human eye. Japanese Journal of Ophthalmology, 31, 558–569.
- Osborne, N.N., Melena, J., Chidlow, G. & Wood, J.P. (2001). A hypothesis to explain ganglion cell death caused by vascular insults at the optic nerve head: Possible implication for the treatment of glaucoma. British Journal of Ophthalmology, 85, 1252–1259. doi:10.1136/bjo.85.10.1252 [CrossRef]
- Owsley, C., McGwin, G. Jr.. & Ball, K. (1998). Vision impairment, eye disease, and injurious motor vehicle crashes in the elderly. Ophthalmic Epidemiology, 5, 101–113. doi:10.1076/opep.220.127.116.114 [CrossRef]
- Parrish, R.K. 2nd. , Feuer, W.J., Schiffman, J.C., Lichter, P.R. & Musch, D.C. (2009). Five-year follow-up optic disc findings of the Collaborative Initial Glaucoma Treatment Study. American Journal of Ophthalmology, 147, 717.e1–724.e1.
- Quigley, H.A. (1999). Neuronal death in glaucoma. Progress in Retinal and Eye Research, 18, 39–57. doi:10.1016/S1350-9462(98)00014-7 [CrossRef]
- Rodriguez, J., Sanchez, R., Munoz, B., West, S.K., Broman, A., Snyder, R.W. & Quigley, H.,… (2002). Causes of blindness and visual impairment in a population-based sample of U.S. Hispanics. Ophthalmology, 109, 737–743. doi:10.1016/S0161-6420(01)01008-9 [CrossRef]
- Saccà, S.C., Rolando, M., Marletta, A., Macrí, A., Cerqueti, P. & Ciurlo, G. (1998). Fluctuations of intraocular pressure during the day in open-angle glaucoma, normal-tension glaucoma and normal subjects. Ophthalmologica, 212, 115–119. doi:10.1159/000027290 [CrossRef]
- Schwartz, G.F. & Quigley, H.A. (2008). Adherence and persistence with glaucoma therapy. Survey of Ophthalmology, 53(Suppl. 1), S57–S68. doi:10.1016/j.survophthal.2008.08.002 [CrossRef]
- Shiose, Y. & Kawase, Y. (1986). A new approach to stratified normal intraocular pressure in a general population. American Journal of Ophthalmology, 101, 714–721.
- Sleath, B., Robin, A.L., Covert, D., Byrd, J.E., Tudor, G. & Svarstad, B. (2006). Patient-reported behavior and problems in using glaucoma medications. Ophthalmology, 113, 431–436. doi:10.1016/j.ophtha.2005.10.034 [CrossRef]
- Sommer, A., Tielsch, J.M., Katz, J., Quigley, H.A., Gottsch, J.D., Javitt, J.C. & Erzine, S.,… (1991). Racial differences in the cause-specific prevalence of blindness in east Baltimore. New England Journal of Medicine, 325, 1412–1417. doi:10.1056/NEJM199111143252004 [CrossRef]
- Tavares, I.M., Medeiros, F.A. & Weinreb, R.N. (2006). Inconsistency of the published definition of ocular hypertension. Journal of Glaucoma, 15, 529–533. doi:10.1097/01.ijg.0000212279.03595.70 [CrossRef]
- Tsai, J.C., McClure, C.A., Ramos, S.E., Schlundt, D.G. & Pichert, J.W. (2003). Compliance barriers in glaucoma: A systematic classification. Journal of Glaucoma, 12, 393–398. doi:10.1097/00061198-200310000-00001 [CrossRef]
- Vetrugno, M., Cantatore, F., Ruggeri, G., Ferreri, P., Montepara, A., Quinto, A. & Sborgia, C. (2008). Primary open angle glaucoma: An overview on medical therapy. Progress in Brain Research, 173, 181–193.
- Wang, X., Harmon, J., Zabrieskie, N., Chen, Y., Grob, S., Williams, B. & Zhang, K.,… (2010). Using the Utah Population Database to assess familial risk of primary open angle glaucoma. Vision Research, 50, 2391–2395. doi:10.1016/j.visres.2010.09.018 [CrossRef]
- Wu, S.Y., Hennis, A., Nemesure, B. & Leske, M.C. (2008). Impact of glaucoma, lens opacities, and cataract surgery on visual functioning and related quality of life: The Barbados Eye Studies. Investigative Ophthalmology and Visual Science, 49, 1333–1338. doi:10.1167/iovs.07-1252 [CrossRef]
- Yanagi, M., Kawasaki, R., Wang, J.J., Wong, T.Y., Crowston, J. & Kiuchi, Y. (2010). Vascular risk factors in glaucoma: A review. Clinical and Experimental Ophthalmology. Advance online publication. doi: doi:10.1111/j.1442-9071.2010.02455.x [CrossRef]
- Yousuf, S.J. & Jones, L.S. (2010). Adherence to topical glaucoma medication during hospitalization. Journal of Glaucoma. Advance online publication. doi: doi:10.1097/IJG.0b013e3181f4661b [CrossRef]
- Zanon-Moreno, V., Garcia-Medina, J.J., Zanon-Viguer, V., Moreno-Nadal, M.A. & Pinazo-Duran, M.D. (2009). Smoking, an additional risk factor in elder women with primary open-angle glaucoma. Molecular Vision, 15, 2953–2959.
Glaucoma Medication Classes
|Drug Class||Mechanism of Action||Common Medications||Common Dosing Schedulea||Possible Side Effects||Cap Color|
|Prostaglandin analogs||Enhances uveoscleral outflow||Latanoprost (Xalatan®), bimatoprost (Lumigan®), travoprost (Travatan®)||1 drop before bedtime||Increased lash pigmentation, hypertrichosis, increased iris and periocular skin pigmentation||Teal|
|Ophthalmic beta blockers||Decreases aqueous formation||Timolol (Timoptic®), betaxolol (Betoptic®), levobunolol (Betagan®), carteolol (Ocupress®), metipranolol (Optipranolol®)||1 drop two times per day||Bradycardia, bronchospasm, hypotension, depression, decreased libido||Blue or yellow|
|Ophthalmic adrenergic agonists||Decreases aqueous formation, may enhance uveoscleral outflow||Brimonidine (Alphagan P®), apraclonidine (Iopidine®)||1 drop three times per day||Dry mouth, dry nose, tachyphylaxis, lethargy, headache, allergic reactions||Purple|
|Ophthalmic or oral carbonic anhydrase inhibitors||Decreases aqueous formation||Dorzolamide (Trusopt®), brinzolamide (Azopt®), oral acetazolamide (Diamox®)||1 drop three times per day||Lethargy, depression, aplastic anemia; contraindicated in patients allergic to sulfa||Orange|
|Ophthalmic cholinergic agonists||Increases trabecular outflow, may enhance uveoscleral outflow||Pilocarpine (Isopto Carpine®, Pilocar®, and others), carbachol (Isopto Carbachol®), echothiophate (Phospholine Iodide®)||1 drop three times per day||Headache, miosis, sweating, salivation, bradycardia||Green|
Strategies to Improve Glaucoma Assessment and Management
|Nurses’ Role||Strategies to Improve Care|
|Be familiar with current clinical practice guidelines for diagnosis of glaucoma and recommended intervals for comprehensive eye examinations||Ask 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.