A Continuing Education Review for Optometrists from the New England College of Optometry
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Who Has Glaucoma? Definitions and Diagnosis Steven L. Mansberger, MD, MPH With many questions still remaining in the field of glaucoma— who has it, who will progress, when to intervene—clear definitions lay the groundwork for effectively navigating the many clinical challenges. Like cancer, glaucoma is not a single disease; rather, the term refers to a group of degenerative disorders of the optic nerve characterized by a particular constellation of structural and functional changes; key among them are excavation and enlargement of the optic cup, loss of the nerve fiber TARGET AUDIENCE This educational activity is intended for optometrists. LEARNING OBJECTIVES Upon completion of this activity, participants will be able to: 1. Define glaucoma and common subtypes. 2. Discuss the role of IOP in glaucoma diagnosis. 3. Delineate the relationship between aqueous humor dynamics, IOP, and glaucoma. 4. Identify individual IOP reduction needs in glaucoma patients. EDITORIAL COMMITTEE Baharak Asefzadeh, OD, MS, FAAO, is an adjunct assistant professor of optometry at the New England College of Optometry and director of the VA Boston Optometric Research Fellowship. Tony Cavallerano, OD, FAAO, is an adjunct professor of optometry at the New England College of Optometry, where he is also the director of professional relations and the executive director of clinical training and patient care. Mark T. Dunbar, OD, FAAO, is the director of optometric services and optometry residency supervisor at Bascom Palmer Eye Institute, University of Miami Miller School of Medicine. Key Issues in Glaucoma Management: A Review for Optometrists is sponsored by the New England College of Optometry and supported by an unrestricted educational grant from Bausch + Lomb, Inc. This publication is administered by an independent editorial committee. © 2015 Candeo Clinical/Science Communications, LLC. All rights reserved. Neither the New England College of Optometry nor Candeo Clinical/Science Communications, LLC, assumes any responsibility for injury or damage to persons or property arising from the use of information or ideas contained in this publication. COURSE DIRECTOR Tony Cavallerano, OD, FAAO New England College of Optometry Boston, MA, USA
layer rim, and corresponding visual field deficit.1 A concise medical definition or standard dictionary definition of glaucoma typically includes mention of intraocular pressure (IOP).2 This is understandable in light of the strong clinical association between glaucoma and IOP and the fact that, at present, IOP represents the sole therapeutic target of medical antiglaucoma therapy.1
Glaucoma and IOP
That said, elevated IOP (one description of which is IOP greater than the 97.5 percentile for a specific population) is no longer necessary for a definition of glaucoma, nor is it required for the diagnosis, since it is not universally present among glaucoma patients.1 (“Elevated IOP” can also be defined as IOP over 21 mm Hg or as the IOP at which the optic nerve sustains damage.) In fact, depending on the population studied, between 30% and 80% of eyes with glaucomatous optic nerve damage have “normal” IOPs (ie, IOPs of 21 mm Hg or less).3 The converse is also true: elevated IOP may be present, and quite often is present, without evidence of glaucomatous optic nerve damage. It is also true that some degree of ocular hypertension may be present without evidence of optic nerve damage or vi-
FIGURE 1 Gonioscopy showing angle closure.
sual symptoms. Glaucoma risk estimation and when to treat at-risk patients is the subject of significant debate and ongoing research.
Primary vs Secondary Glaucomas
Optic nerve damage associated with glaucoma can be thought of as the common endpoint of a variety of pathophysiologic processes. Glaucoma categorization starts with the designation of primary or secondary. Primary glaucoma describes patients with optic nerve damage and visual field loss with no discernable cause; primary open-angle glaucoma (POAG) is a principal subtype of glaucoma in which the angle between the iris and cornea is open. Among the non-POAG categories of glaucoma, elevated IOP is consistently present at least some times in the course of the disease. Primary angle-closure glaucoma is a subtype of glaucoma in which the cause of irridocorneal angle narrowing is unknown (Figure 1).1 Secondary glaucoma may
More INSIDE: Aqueous Humor Dynamics: What IOP Means for the Clinician by John J. McSoley, OD
Key Issues in Glaucoma Supported by an unrestricted educational grant fromManagement Bausch + Lomb, Inc.1
result from a long list of underlying causes, and may affect individuals of any age, from newborns to the elderly. Like primary forms, secondary openangle glaucoma is associated with an open angle; and secondary angle-closure glaucoma with iridotrabecular contact. Any process that impedes drainage of aqueous fluid via the trabecular meshwork—including preceding ocular trauma, diabetes, pigmentary dispersion syndrome, pseudoexfoliation, and dozens of other causes—can cause secondary glaucoma.1
Risk Factors
Multiple studies have attempted to identify risk factors for the development of primary glaucoma. Subanalyses of two large multicenter, prospective, randomized trials—the Ocular Hypertension Treatment Study (OHTS) and the European Glaucoma Prevention Study (EGPS)—looked specifically at patient characteristics and disease parameters associated with conversion from ocular hypertension to glaucoma.4,5 Pooled analysis of untreated patients with ocular hyperten-
Key Issues in Glaucoma Management — Issue 1 STATEMENT OF NEED Glaucoma, a group of ocular diseases characterized by progressive damage to the optic nerve, is the second leading cause of blindness worldwide. It affects a significant and growing portion of the US population.1,2 As primary eyecare providers, medical optometrists are well positioned to identify patients at risk and to diagnose, monitor, and treat glaucoma. However, given that the expanded scope of practice incorporating glaucoma treatment is relatively new, many optometrists lack confidence in their ability to treat this potentially blinding disease. In order to instill confidence and help optometrists make sound clinical judgments about the care of glaucoma patients, Key Issues in Glaucoma Management will help optometrists better understand the various aspects and nuances of the disease, including our current understanding of the role of intraocular pressure (IOP) in glaucomatous optic nerve damage. Course content will also include current rationale on glaucoma diagnosis and evidence-based strategies for reducing IOP. Each installment of Key Issues in Glaucoma Management will look at an important topic in glaucoma diagnosis or therapy. Each issue will build from a basic level to instill understanding and confidence in medical optometrists. Key Issues in Glaucoma Management aims to support optometrists’ clinical reasoning and decision-making abilities and help them turn medical management of glaucoma into a vital segment of their practices. REFERENCES 1. Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on visual impairment in the year 2002. Bull World Health Organ. 2004 November;82(11):844-51. 2. Eye Diseases Prevalence Research Group. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004;122:532-8. OFF-LABEL USE STATEMENT This work may discuss off-label uses of medications. GENERAL INFORMATION This CE activity is sponsored by the New England College of Optometry and is supported by an unrestricted educational grant from Bausch + Lomb, Inc. Directions: Circle the best answer to each question in the exam (questions 1–10) and in the evaluation (questions 11–16). The New England College of Optometry designates this activity for a maximum of 1 hour of COPE-approved continuing education credit. There is no fee to participate in this activity. In order to receive CE credit, participants should read the report and then take the posttest. A score of 70% is required to qualify for CE credit. Estimated time to complete the activity is 60 minutes. On completion, tear out or photocopy the answer sheet and send it to: New England College of Optometry ATTN: Ms. Margery Warren 424 Beacon Street Boston, MA 02115 DATE OF ORIGINAL RELEASE October 2015. Approved for a period of 24 months.
2 Key Issues in Glaucoma management
ACCREDITATION STATEMENT This activity has been planned and implemented through the joint sponsorship of the New England College of Optometry and Candeo Clinical/Science Communications, LLC. The New England College of Optometry is accredited by The Council on Optometric Practitioner Education® (COPE® ), created by the Association of Regulatory Boards of Optometry (ARBO) to accredit continuing education on behalf of optometric licensing boards. CREDIT DESIGNATION STATEMENT The New England College of Optometry designates this activity for a maximum of 1 hour of COPE-approved continuing education credit. Clinicians should only claim credit commensurate with the extent of their participation in the activity. EDITORIAL COMMMITTEE DISCLOSURE STATEMENTS Baharak Asefzadeh, OD, MS, FAAO, is an adjunct assistant professor of optometry at the New England College of Optometry and director of the VA Boston Optometric Research Fellowship. She has no financial disclosures related to this activity. Tony Cavallerano, OD, FAAO, is an adjunct professor of optometry at the New England College of Optometry, where he is also the Director of Professional Relations and the Executive Director of Clinical Training and Patient Care. He has no financial disclosures related to this activity. Mark T. Dunbar, OD, FAAO, is the director of optometric services and optometry residency supervisor at Bascom Palmer Eye Institute, University of Miami Miller School of Medicine. He states that in the last 12 months, he has been a consultant for Allergan and has participated in advisory boards for Carl Zeiss, Regeneron Pharmaceuticals, Inc., Bio-Tissue, ArcticDx, and B&L Nutrition. AUTHOR DISCLOSURE STATEMENTS Steven L. Mansberger, MD, MPH, is vice-chair and director of glaucoma services and fellowship program at Legacy Devers Eye Institute in Portland, OR. Dr. Mansberger has received grant/ research support from the National Eye Institute, Allergan, and Envisia. He has also been a consultant for New World Medical, Allergan, Envisia, Santen Pharmaceutical Co., ForSight Vision5, and Welch Allyn. John J. McSoley, OD, is associate director of optometric services and member of the glaucoma service at Bascom Palmer Eye Institute in Miami, FL. He has no financial disclosures related to this activity. DISCLAIMER Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and professional development. The information presented in this activity is not meant to serve as a guideline for patient care. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications or dangers in use, applicable manufacturers’ product information, and comparison with recommendations of other authorities. COMMERCIAL SUPPORTERS This activity is supported by an unrestricted educational grant from Bausch + Lomb, Inc.
sion enrolled in the two studies and followed for 5 years (N=1341) revealed that poorer outcomes were predicted by: older age, higher IOP, decreased central corneal thickness, increased vertical cup-to-disc ratio, and greater visual field index pattern standard deviation (PSD).6 In addition, low perfusion pressure was also identified to be a risk factor in the Barbados Eye Study. Family history is also considered a significant risk factor for the development of POAG. Although some controversy exists, there seems to be a propensity to glaucoma among certain ethnic groups. In the US, individuals of African and Hispanic descent are at highest risk for POAG.7 Asian individuals have high rates of glaucoma, and represent 87% of patients with primary angle-closure glaucoma worldwide.8 Other proposed risk factors for POAG include diabetes mellitus, high blood pressure, and myopia.
Glaucoma Suspects
A patient or eye considered “glaucoma suspect” has some features suggestive of glaucoma but does not meet the full diagnostic criteria.1 Such patients generally present in one of four ways: 1) elevated IOP and normal appearing optic nerve; 2) large cupto-disc ratio and normal optic nerve fiber layer; 3) abnormal visual field but normal optic nerve and disc; or 4) unusual appearing optic nerve with normal visual field and IOP. This begs the question: does the eye that is suspicious for glaucoma indicate a pre-glaucomatous state? And, if so, can early intervention prevent the development of glaucoma? These are some of the questions that OHTS and EGPS were designed to evaluate; however, while helpful, they have not put the issue entirely to rest. In the OHTS, development of glaucoma was reduced by 60% with the use of topical hypotensive medication. Patients with ocular hypertension (baseline IOP 24 to 32 mm Hg) treated with IOPlowering medication developed POAG at a rate of 4.4% over 5 years compared to a rate of 9.5% among untreated patients in the control group.7 EGPS,
a similarly designed trial, did not show statistically significant prevention of POAG with treatment.9 Unfortunately, we lack data regarding early intervention outcomes for the other groups suspicious for glaucoma, and it remains unclear whether treatment is warranted for those groups.
sHould Glaucoma susPects Be treated?
It is important to remember that most patients with identifiable risk factors do not develop glaucoma. This has been shown in prospective studies. As noted, in the OHTS 90% of untreated glaucoma suspect patients with IOP between 24 and 32 mm Hg remained glaucoma-free over the 5 years of follow-up.4 It might seem prudent, then, to limit preventive medical therapy and spare patients the burden of lifelong medication whenever possible. But the stakes are too high to simply leave it at that. For those who do develop glaucoma, the burden of therapy—inconvenience, side effects, cost—likely pales in comparison to the vision-saving benefits they might derive. Clearly, the ability to predict who is at risk for glaucoma and thus who would benefit from intervention holds enormous value. To that end, based on data from large studies, tools for calculating individual risk have been developed to assist clinicians in recommending or not recommending pre-glaucoma therapy. It is generally recommended that individuals identified as having high risk should be considered for treatment, whereas individuals at low risk should be observed without treatment.
rIsk calculators
Like other medical predictive models—such as those used to predict risk for heart disease or osteoporosis— glaucoma risk calculators attempt to enhance objectivity in clinical management by distilling multiple variables down to an actionable metric. A glaucoma risk calculator based upon findings from OHTS uses patient age, baseline IOP, central corneal thickness, PSD, vertical cup-to-disc ratio, and the
presence of diabetes to generate an idea of patients’ 5-year risk.6 The algorithm developed at our institution is available online at: https://www.deverseye. org/grc/. Other calculators can be found at http://ohts.wustl.edu/ risk/calculator.html and http://oil. wilmer.jhu.edu/risk/. A separate risk calculator for the progression of visual field loss among patients being treated for glaucoma has also been developed and validated.
treatInG Glaucoma
For patients with a clear diagnosis of glaucoma, treatment is almost always indicated, assuming that the patient is otherwise capable of maintaining an acceptable quality of life. Aggressiveness of the treatment relates to a number of factors, including stage of glaucoma, age and health status of the patient, and the health and visual acuity of the fellow eye. For example, a young patient with early glaucoma would almost always be treated aggressively since s/he will most likely have to live with glaucoma for a long time. A glaucoma patient with a shorter life expectancy, eg, a patient in his/ her late 80s with mild glaucoma and significant heart disease, after a thorough discussion, might elect to be periodically monitored for progression without treatment. And, as a further example, a patient with very advanced glaucoma in one eye and good vision in their other eye might only elect to receive palliative treatment in the affected eye to keep it comfortable rather than aggressive IOP-lowering drugs.
dIaGnostIc ProGress
In many of its forms, glaucoma is a sly, often silent disease—by the time patients notice visual change, up to 90% of the optic nerve may be affected. Because glaucoma is progressive and irreversible, timely diagnosis is paramount to controlling it and preventing vision loss. Late diagnosis increases risk for vision loss and raises the overall costs of the disease.10 New means for detecting glaucoma help to prevent late diagnosis and its consequences. In the past, clinicians
core concePts ● Glaucoma is an optic nerve disease characterized by structural and functional changes including: increased cupping, optic nerve fiber layer degeneration, and visual field loss. ● The relationship between glaucoma and IOP is complex: glaucoma is common among patients with normal IOP; and a majority of patients with elevated IOP will not develop glaucoma— but patients with elevated IOP are at higher risk of glaucoma than patients with normal IOP. ● Primary glaucoma is glaucoma with no known cause. ● Risk factors for POAG include elevated IOP, decreased corneal thickness, high cup-to-disc ratio, visual field PSD, and older age. ● Family history is probably a significant risk factor for glaucoma. ● Other possible risk factors include African, Hispanic, Asian ethnicity; high blood pressure; myopia. ● Risk calculators can aid in predicting conversion from ocular hypertension to glaucoma. ● Risk calculators also exist for predicting progression among patients undergoing treatment for glaucoma. ● Glaucoma remains underrecognized and undertreated. ● State-of-the-art diagnostic equipment and vigilance for the disease are important for early detection.
could only examine the optic nerve with a handheld ophthalmoscope and test the visual fields manually. Currently, laser-based devices allow for glaucomatous optic disc detection without dilation of the pupils. At my practice, we evaluate the optic nerve with ophthalmoscopy at every visit, and we perform stereoscopic disc photography at the initial visit or Key Issues In Glaucoma manaGement 3
when the optic disc has a hemorrhage or we suspect a change. Finally, we use objective structural testing (ocular coherence tomography and Heidelberg Retinal Topography) at least yearly to assess the optic disc and nerve fiber layer for progression. In addition to structural assessment, we use standard automated achromatic visual field testing to assess for visual field loss. Primary care physicians should advise patients to have regular ophthalmic examinations, including testing for glaucoma, every 2 years for individuals over 40 years old and yearly for those over 60. Patients with glaucoma should be reminded to inform family members so that they can be vigilant for the disease and receive appropriate screening.
Conclusion
Glaucoma is a group of diseases that share a common pathophysiologic endpoint: optic nerve degeneration.
4 Key Issues in Glaucoma Management
Early identification and prevention are key to managing glaucoma. Increased physician awareness and more aggressive screening and monitoring with state-of-the-art equipment can be expected to improve outcomes. Overall, the objective is to treat high-risk suspects, monitor low-risk suspects and treat those with glaucoma. Steven L. Mansberger, MD, MPH is vice-chair and director of glaucoma services and fellowship program at Legacy Devers Eye Institute in Portland, OR. Dr. Mansberger has received grant/research support from the National Eye Institute, Allergan, and Envisia. He has also been a consultant for New World Medical, Allergan, Envisia, Santen Pharmaceutical Co., ForSight Vision5, and Welch Allyn. This manuscript was prepared with the assistance of medical writer Noelle Lake, MD. REFERENCES 1. Casson RJ, Chidlow G, Wood JPM, et al. Definition of glaucoma: clinical and experimental concepts. Clin Experimental Ophthalmol. 2012;40:341-9.
2. Glaucoma definition. Available at: http://www. merriam-webster.com/dictionary/glaucoma. Accessed on April 22, 2015. 3. Anderson DR. Normal tension glaucoma. Ind J Ophthalmol. 2011;59(Suppl 1):S97-101. 4. 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. 5. Miglior S, Pfeiffer N, Torri V, et al. for the 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. 6. Medeiros FA, Weinreb RN. Predictive models to estimate the risk of glaucoma development and progression. Prog Brain Res. 2008;173:15-24. 7. Kass MA, Gordon MO, Gao F, et al. for the Ocular Hypertension Treatment Study. Delaying treatment of ocular hypertension. Arch Ophthalmol. 2010;128:276-87. 8. Cook C, Foster P. Epidemiology of glaucoma: what’s new? Can J Ophthalmol. 2012;47:223-6. 9. Miglior S, Zeyen T, Pfeiffer N, et al. for the European Glaucoma Prevention Study (EGPS) Group. Results of the European Glaucoma Prevention Study. Ophthalmology. 2005;112:366-75. 10. Traverso CE, Walt JG, Kelly SP, et al. Direct costs of glaucoma and severity of the disease: a multinational long term study of resource utilisation in Europe. Br J Ophthalmol. 2005 Oct;89(10):1245-9.
Aqueous Humor Dynamics: What IOP Means for the Clinician JOHn J. McSOLEy, OD Intraocular pressure is a causative risk factor for glaucoma and, at present, the only target of available glaucoma treatments. Although elevated IOP is no longer recognized as necessary for a diagnosis of glaucoma, it is a key element in the evaluation and management of the disease. Normal intraocular pressure (IOP) is essential to maintaining the structural integrity and visual function of the eye: it ensures inflation of the globe and maintains the eye’s optical components in position. Underlying normal IOP is a delicate balance between aqueous humor inflow and resistance to its outflow. Altered aqueous dynamics, predominantly due to outflow impairment, is the cause of IOP elevation in glaucoma. An understanding of normal aqueous humor dynamics is a cornerstone of understanding both the pathogenesis and treatment of glaucoma.
aQueous dynamIcs and IoP
Precursor to aqueous humor passes from the microvasculature of the ciliary body stroma, through the pigmented and nonpigmented epithelia of the ciliary processes, and then as aqueous humor into the posterior chamber. Aqueous humor forms at a typical rate of approximately 2 to 2.5 microliters per minute. Secretion of aqueous humor is a complicated physiological process that is influenced by many factors, including ionic and osmotic forces, enzymatic reactions, activation of various receptors, circadian rhythm, age, neuropeptides, and hormones. Additional information on this complicated process is available.1-5 After secretion from the ciliary
body into the posterior chamber, aqueous humor circulates through the pupillary space to fill the anterior chamber. From there, aqueous humor exits the eye via one of two routes in the anterior chamber angle: the conventional outflow pathway via the trabecular meshwork (which accounts for the bulk of aqueous drainage), or the uveoscleral pathway. In the trabecular pathway, aqueous humor drains through the trabecular meshwork into Schlemm’s canal and then out through collector channels to the blood vessels and lymphatics (Figure 1). In the uveoscleral pathway, aqueous humor exits the eye via the supraciliary and suprachoroidal spaces.
WHat Is normal?
It is important to remember that the IOP range we call “normal” (IOPs in the 10 to 21 mm Hg range) are derived from measurement of pressures in normal populations, which typically have mean IOPs close to 16 mm Hg (with 2 standard deviations extending about 5 mm Hg).6 In reality, IOP is dynamic, differing considerably from individual to individual and, for any given individual, rising and falling in a diurnal cycle. A normal individual’s IOP may vary by as much as 4 mm Hg or more over the course of the day as aqueous humor production and outflow fluctuate.7 In glaucoma patients, the diurnal IOP variation may be even greater, likely a reflection of the pathophysiologic mechanisms modulating aqueous humor dynamics and possible effects of treatment. The variability of IOP is an important consideration when checking patients’ pressure. Multiple measurements, ideally taken at different times of day, may be necessary for detection of elevated IOP in potential glaucoma patients. Wide ranges of IOP variability may be associated with the clinical course of glaucoma or the result of
core concePts ● IOP is maintained by the balance between aqueous inflow and resistance to outflow. ● IOP is the primary risk factor for the onset and progression of glaucoma. ● Increased resistance to aqueous drainage due to abnormalities of the trabecular outflow pathway is responsible for IOP elevation in open-angle glaucoma. ● Factors other than elevated IOP, such as a patient’s genetic susceptibility, contribute to glaucomatous damage. It is erroneous to assume that pressures within the normal range do not cause harm. ● IOP is particularly variable in glaucoma patients. In evaluating glaucoma, it is important to take multiple measurements at different times of day. ● Current glaucoma medications lower IOP by reducing aqueous formation or increasing aqueous outflow. ● Choice of medical treatment should be based on safety, efficacy, and patients’ ability to comply with/tolerate the regimen.
missed medication. It is prudent to avoid treatment decisions based on a single isolated pressure reading.
IoP: relatIon to Glaucoma
IOP has been historically linked to glaucoma, and values exceeding the statistically normal range were viewed as leading to glaucoma. Today, glaucoma is defined by the characteristic structural changes in the optic nerve and corresponding impairment of visual function. IOP is not included as a defining feature of glaucoma. Patients Key Issues In Glaucoma manaGement 5
whose IOP exceeds the normal range but have no glaucomatous damage are considered ocular hypertensives. Glaucomatous damage can be identified in patients whose IOP remains within the normal range. The development of glaucoma is related to an individual’s susceptibility to various risk factors, including IOP. Indeed, many patients with open-angle glaucoma have IOPs within the statistically normal range (< 22 mm Hg at a single measurement).8-13 Although no longer included in the definition of glaucoma, IOP is a key component of glaucoma clinical management. First, IOP is a causative risk factor for the development and progression of glaucomatous damage.14-16 As the level of IOP increases, the prevalence of open-angle glaucoma increases.8,17 On the other hand, IOP reduction in known glaucoma patients decreases the risk of visual field loss.15-17 Most importantly, IOP remains the only glaucoma risk factor that can be effectively modified, even though many other potential factors—such as a patient’s genetic susceptibility to optic nerve injury, compromise of blood flow, alterations of the lamina cribrosa, and other potential contributors, some of which may not yet be identified—may also contribute to glaucomatous damage. In most cases, a target IOP provides a short term benchmark to evaluate treatment efficacy, and IOP measurement allows us to monitor response to treatment in an easy and straightforward manner. That said, the ultimate and most important measure of success is preservation of the patient’s vision.
Glaucoma Evaluation
When a patient is identified as having ocular hypertension, further assessment is warranted. Typically, this involves measurement of central corneal thickness, gonioscopy, visual field testing, and examination of the optic nerve head, usually with the help of photography and imaging devices that allow additional qualitative and quantitative measures of the struc6 Key Issues in Glaucoma Management
later. Once a baseline and track record ture of the optic nerve and the retinal have been established, and it is clear nerve fiber layer. These tests serve as that the patient is not progressing, it diagnostic aids, help in staging, and is then reasonable to lengthen followprovide baseline information for future up intervals. At the same time, it is follow-up comparison. In cases where important to educate the patient about the patient shows no signs of glaucomatous damage, the most important step is to determine the risk of progression to glaucoma. Risk assessment includes how elevated the baseline pressure is and the presence or absence of other factors that add to the risk of glaucoma (eg, age, family history, etc.) Visualizing the anterior chamber angle, Figure 1 The trabecular meshwork conventional outflow pathway. Aqueous humor is produced by the ciliary body and it where the traflows (dashed line shown with arrowheads) from the posterior becular meshchamber through the pupil into the anterior chamber. From there work is located, it flows out through the trabecular meshwork into the Schlemm’s is an important canal and is subsequently absorbed into the episcleral veins via the collector channels. (From Goel M, Picciani RG, Lee aspect of t he RK, et al. Aqueous Humor Dynamics: A Review. Open Ophthalmol J. clinical exami2010;4:52-9.) nation for glaucoma. The cause why the tests are necessary and why of impaired aqueous outflow leading ongoing follow-up will be necessary, to IOP elevation varies by the subtype probably for life. of glaucoma, and gonioscopy is an es sential diagnostic tool for determining whether the angle is open or closed and Managing IOP for identification of other pathologies Current glaucoma therapies are that may cause pressure elevation. The aimed almost exclusively at lowering findings can not only provide helpful IOP, which can be done by reducing diagnostic clues but also have imporaqueous humor production or enhanctant treatment implications. ing aqueous outflow. Beta blockers, Based on the risk for progression, topical carbonic anhydrase inhibitors, the patient should be monitored over and the alpha agonists all lower IOP time for any structural or functional by reducing aqueous formation; while impairment. If there is no evidence for prostaglandin analogs, the most widely glaucomatous damage and the pressure used class of glaucoma management is moderate, it may be prudent to just agents, work by increasing aqueous follow up with that patient in 3 or 4 outflow. When a second medication is months. If at the next exam there are added from a different class, the effects no changes in IOP or in the condition may be additive. of the optic nerve, a more detailed A critical aspect of glaucoma manexamination, including visual field agement is selecting the most appropritesting, can be scheduled for 6 months ate IOP-lowering agent. In selecting an
agent (or agents), the best strategy is the one that is safest, most effective, and creates the least burden—including economic burden—to the patient. This explains how prostaglandin analogs became the most popular first-line therapy for glaucoma: they provide very effective IOP lowering, are generally well tolerated, and are taken only once each day. Contrast that with an older agent like pilocarpine, which although effective, requires frequent dosing and has multiple side effects. Today pilocarpine is rarely used to treat glaucoma. For patients who cannot tolerate prostaglandins, the next option is typically a beta blocker. Topical beta blockers are well tolerated by most patients, but there are some caveats. Topical beta blockers can greatly aggravate some ailments, such as asthma and certain cardiovascular conditions, and should be avoided in patients with a history of those disorders. Additionally, a topical beta blocker to reduce IOP may be less effective than expected when administered to a patient who is already on a systemic beta blocker. The bottom line is that no single medication is ideal in all circumstances. It is necessary to individualize each patient’s treatment regimen, and the therapeutic choice comes down to the patient’s response and ability to tolerate the treatment.
Treatment Goals
The goal in treating glaucoma is to halt or slow disease progression and, to the degree possible, preserve the current level of vision. How much IOP lowering is required depends on several factors: the severity of disease, the rate of progression, and the baseline IOP. The extent of damage at diagnosis and the rapidity of progression are good indicators of a patient’s susceptibility to IOP-caused damage and, thus, indicate how low the target IOP should be
set. In general, a patient with minimal damage over an extended period of time would be at less risk for further vision loss than someone who has extensive damage or one whose damage has evolved quickly. An initial treatment goal of 25% to 30% reduction in IOP makes a reasonable target for initial therapy in patients with mild damage. Prevention of progression in patients with more advanced damage usually requires a more aggressive target—eg, up to 50% of their baseline IOP or to the low–normal range of IOP. Even when patients reach their short-term goals for IOP reduction, they still require ongoing, careful follow-up. The term “maximally tolerated medical therapy” well encapsulates the notion that IOP-lowering therapies should be effective, safe, and well tolerated. This may vary from patient to patient or may change for an individual patient during the follow-up period. Laser trabeculoplasty may be a good option at any point during the course of follow-up care. If despite having optimized medical and laser therapy, there is progression (or a high likelihood of progression) more aggressive measures should be sought. We are fortunate to practice at a time when there are several good surgical options available to our patients. Referral to surgeons skilled in these methods has an important role in visual preservation. John J. McSoley, OD, is associate director of optometric services and member of the glaucoma service at Bascom Palmer Eye Institute in Miami, FL. He has no financial disclosures related to this activity. Medical writer Ying Guo, MBBS, PhD, assisted in the preparation of this manuscript. REFERENCES 1. Brubaker RF. Flow of aqueous humor in humans [The Friedenwald Lecture]. Invest Ophthalmol Vis
Sci. 1991;32(13):3145-66. 2. Brubaker RF, Nagataki S, Townsend DJ, et al. The effect of age on aqueous humor formation in man. Ophthalmology. 1981;88(3):283-8. 3. Do CW, Civan MM. Basis of chloride transport in ciliary epithelium. J Membr Biol. 2004;200(1):1-13. 4. Freddo TF. Ocular Anatomy and Physiology Related to Aqueous Production. In: Fingeret M, Lewis TL, Primary Care of the Glaucomas. 2nd Edition. New York, McGraw-Hill;2001:17-41. 5. Gabelt BT, Kaufman PL, Aqueous Humor Hydrodynamics In: Kaufman PL, Alm A. Adler’s Physiology of the Eye. 10th Edition. St. Louis, Mosby;2003:237-89. 6. Colton T, Ederer F. The distribution of intraocular pressures in the general population. Surv Ophthalmol. 1980;25(3):123-9. 7. David R, Zangwill L, Briscoe D, et al. Diurnal intraocular pressure variations: an analysis of 690 diurnal curves. Br J Ophthalmol. 1992;76:280-3. 8. Sommer AE, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. Arch Ophthalmol. 1991;109(8):1090-5. 9. Leske MC, Heijl A, Hyman L et al. Early manifest glaucoma trial: design and baseline data. Ophthalmology. 1999:106:2144-53. 10. Quigley HA, West S, Rodriguez J, et al. Prevalence of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol. 2001;119:1819-26. 11. Varma R, Ying-Lai M, Francis BA, et al. Prevalence of open angle glaucoma and ocular hypertension in Latinos: The Los Angeles Latino eye study. Ophthalmology. 2004;111:1439-48. 12. Le A, Mukesh BN, McCarty CA, et al. Risk factors associated with the incidence of open-angle glaucoma: the visual impairment project. Invest Ophthalmol Vis Sci. 2003;44:3783-9. 13. Leske MC,Wu S-Y, Hennis A, et al. Risk factors for open-angle glaucoma: the Barbados eye studies. Ophthalmology 2008;115:85-93. 14. 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(6):714-20; discussion 829-30. 15. 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(10):1268-79. 16. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130(4):429-40. 17. Francis B, Varma R, Chopra V, et al, Los Angeles Latino Eye Study Group. Intraocular pressure, central corneal thickness, and prevalence of openangle glaucoma: the Los Angeles Latino Eye Study. Am J Ophthalmol. 2008;146(5):741-6.
Key Issues in Glaucoma Management 7
Examination Answer sheet — Key Issues in Glaucoma Management — Issue 1 This CE activity is sponsored by the New England College of Optometry and is supported by an unrestricted educational grant from Bausch + Lomb, Inc. Directions: Circle the best answer to each question in the exam (questions 1–10) and in the evaluation (questions 11–16). The New England College of Optometry designates this activity for a maximum of 1 hour of COPE-approved continuing education credit. There is no fee to participate in this activity. In order to receive CE credit, participants should read the report and then take the posttest. A score of 70% is required to qualify for CE credit. Estimated time to complete the activity is 60 minutes.
1. Which of the following is true of glaucoma risk calculators? A. Their difficulty makes them of value only to glaucoma specialists B. None is currently available for clinical use C. They help apply results from large studies to individual patients D. They are meaningful to research study participants only 2. Which of the following classes of glaucoma agents reduces IOP by increasing aqueous outflow? A. Beta blockers B. Carbonic anhydrase inhibitors C. Alpha agonists D. Prostaglandin analogs 3. Which of the following is NOT a risk factor for the development of glaucoma? A. Ocular trauma B. Family history of glaucoma C. Thick central corneal pachymetry D. Large vertical cup-todisc ratio
4. How much pressure reduction is typically recommended when initiating therapy in glaucoma patients with mild damage? A. 5% or more B. 10% or more C. 25% or more D. 65% or more 5. Early detection of glaucoma is important because: A. Glaucoma is reversible with treatment B. Newly available neuroprotective agents can halt disease progression C. Both A and B are true D. None of the above is true 6. Primary open angle glaucoma: A. Is glaucoma with no known cause B. Remains asymptomatic at every stage C. Does not affect Asians D. Is caused by angle closure
7. Which of the following is true about the relationship between IOP and glaucoma? A. A single measurement can give a true and complete picture of a patient’s IOP status B. Glaucomatous damage can occur in patients whose pressure is consistently found in the normal range C. The prevalence of open-angle glaucoma decreases as IOP increases D. IOP lowering is one of many therapeutic options for glaucoma 8. Which of the following is NOT integral to the definition of glaucoma? A. Enlarged optic cup B. Increased IOP C. Loss of the retinal nerve fiber layer D. Visual field deficit 9. Which of the following can influence aqueous humor production? A. Age B. Circadian rhythm C. Hormones D. All of the above
10. Which of the following changes in aqueous flow is primarily responsible for increasing IOP in open-angle glaucoma? A. Excessive aqueous production B. Increased outflow through the trabecular meshwork C. Decreased uveoscleral outflow D. Both A and C are correct
Examination Answer sheet — Key Issues in Glaucoma Management — Issue 1 This CE activity is sponsored by the New England College of Optometry and is supported by an unrestricted educational grant from Bausch + Lomb, Inc. Directions: Circle the best answer to each question in the exam (questions 1–10) and in the evaluation (questions 11–16). In order to receive CE credit, participants should read the report and then take the posttest. A score of 70% is required to qualify for CE credit. On completion, tear out or photocopy the answer sheet and send it to: New England College of Optometry, ATTN: Ms. Margery Warren, 424 Beacon Street Boston, MA 02115 CE exam expires September 30, 2017.
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8 Key Issues in Glaucoma management
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