Frontline Ocular Surface Disease Care
Gaining a better understanding of new and advanced technology to diagnose, treat and manage dry eye disease.
By Derek N. Cunningham, OD, FAAO; Kelly Nichols, OD, MPH, PhD, FAAO; Paul Karpecki, OD, FAAO; and Doug Devries, OD, FAAO
Release Date:March 15, 2017
Expiration Date:March 15, 2018
Goal Statement:On completion of this educational activity, participants should have a strong understanding of the need for a thorough exam of the ocular surface and adnexa, know the steps to proper evaluation of the ocular surface for more definitive diagnoses, and be aware of new research on the role that inflammation plays in DED and new ocular surface disease treatments.
Faculty/Editorial Board:Derek N. Cunningham, OD, FAAO; Kelly Nichols, OD, MPH, PhD, FAAO; Paul Karpecki, OD, FAAO; and Doug Devries, OD, FAAO
Credit Statement:This course is COPE approved for 2 hours of CE credit. COPE ID is 52586-AS. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure.
Joint-Sponsorship Statement:This continuing education course is joint sponsored by the University of Alabama School of Optometry.
Disclosure Statement:Dr. Cunningham is a consultant for Alcon, Allergan, Bausch + Lomb, TearLab and Abbot Medical Optics, and serves on the speaker’s bureau for Alcon, Allergan, Bausch + Lomb and Bio-Tissue.
Dr. Nichols is a consultant for Bruder Healthcare Company, InSite Vision, Parion Pharmaceuticals, SARcode Bioscience, Shire Pharmaceuticals, Sun Pharmaceuticals, Kala Pharmaceutical, Eleven Biotherapeutics, Science Based Health, Allergan, Santen Pharmaceutical.
Dr. Karpecki is a consultant for AcuFocus, Alcon, Abbott Medical Optics, Akorn, Allergan, Arctic Dx, Bausch + Lomb, Bio-Tissue, Bruder Healthcare, Beaver-Visitec, Eyes4Lives, OcuSoft, Freedom Meditech, Focus Labs, Eyemaginations, J&J, iCare USA, Konan Medical, Regeneron, Enchroma, Essilor, Eye Solutions, SightRisk, Reichert, Cambium Medical Technologies, Shire Pharmaceuticals, Science Based Health, Smart Vision Labs, TearScience, Topcon, TLC Vision, Vision Care Inc., Vmax and Visiometrics; a research grant principal investigator for Eleven BioTherapeutics, Fera Pharmaceuticals, Shire Pharmaceuticals; has received honoraria for the speaker’s bureaus of Glaukos and Oculus; is director/clinical advisor for Optometric Medical Solutions; and is on the board of directors for TearLab.
Dr. Devries is on the advisory board for Allergan, Odyssey Medical Technologies, Bausch + Lomb, TearLab and Essilor; he is on the speaker’s bureau for Allergan, Odyssey Medical Technologies and OcuSoft.
Supported by: An unrestricted educational grant from Shire.
The more we study dry eye, the clearer it becomes that it’s unwise to make assumptions about risk, severity, signs, symptoms or any other aspect of ocular surface disease based on what we thought we knew about dry eye only a few short years ago. Research including the Beaver Dam Offspring Study (BOSS) startled clinicians when it revealed that age and sex are not always the most accurate predictors of dry eye risk.1 Though we’ve long clung to the notion that dry eye is largely an age-related disease, the BOSS study found that healthy adults between the ages of 21 and 34 have about the same incidence of dry eye as their parents. Furthermore, this age group also showed similar dry eye prevalence between men and women. This data should inspire all practitioners to cast a broader net and look more critically for disease without stereotyping based on age and sex.
BOSS also provided a baseline for estimating the level of dry eye disease (DED) in the general population of US adults. Among 3,257 participants, ages 21 to 84 years, the overall prevalence of DED symptoms was 14.5%—which equates to about 30 million people nationwide.
Admittedly, dry eye has long been a source of frustration for clinicians. But we are much better equipped now than we were just a few years back. By looking closely for dry eye in all patients, especially younger ones, we can prevent a lot of suffering—not to mention disease progression. We would never suggest waiting to see field loss before treating a glaucoma patient, so why ignore structural changes and wait for functional loss before addressing dry eye? By addressing the chronic and progressive nature of dry eye, we may be able to keep patients in contact lenses longer, improve cataract or refractive surgical outcomes, and keep dry eye at bay.
The Evolution of a Dry Eye Definition
Our intense study of dry eye is relatively new. The first definition of dry eye emerged in 1995, when the NEI/Industry Workshop defined it as a disorder of the tear film due to tear deficiency or excessive evaporation, which causes damage to the interpalpebral ocular surface and is associated with symptoms of ocular discomfort.2 This definition recognized two primary etiologies (aqueous deficiency and excessive evaporation), a sign (ocular surface damage, primarily detectable by staining), and a symptom (discomfort) but was otherwise silent with respect to causes, effects or corollaries of the condition.2,3
A second definition emerged 12 years later with the DEWS Report, which stated that dry eye is a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance and tear film instability with potential damage to the ocular surface.4 What’s more, the new definition stated that dry eye is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.
In the last 10 years, as we approach the release of DEWS II, so much more has been discovered, and our understanding of diagnostics and new therapeutic approaches is significantly more evolved. Instead of sending patients on their way with nothing more than a boatload of artificial tears, optometrists now recognize that more can be done. We are proactively treating dry eye and are making real headway in understanding how the disease works.
The Pathophysiology of Dry Eye
We can’t say with certainty whether dry eye is caused by inflammation, or if inflammation is the result of dry eye. But, either way you look at it, inflammation is part of the dry eye process, and is a hallmark of all ocular irritation.
The other important piece of the inflammation puzzle is the concept that there are two types of inflammation—acute and chronic—with different types of inflammatory markers, cells and mediators that occur in each of these
(see Figure 1).
Figure 1. Acute vs. Chronic Inflammation
|Onset||Fast: minutes or hours||Slow: days|
|Cellular Infiltrate||Mainly neutrophils||Monocytes/macrophages and lympohcytes|
|Tissue injury, fibrosis||Usually mild and self-limited||Often severe and progressive|
|Local and systemic signs||Prominent||Less prominent; may be subtle|
Acute inflammation happens very quickly and often appears very pronounced. Chronic inflammation can be born out of an acute event of any severity when it occurs over time. Such is the case with dry eye.
Inflammatory cells are in our blood supply, normally circulating around the body. When they are activated and called to the scene of irritation, they roll down the blood vessels, sticking to the edges. It is through inflammatory mediators that they then move into the tissue itself, resulting in inflammation.
An important point to remember is that, with dry eye in particular, inflammation follows a chronic, well-established pathway. As such, inflammation begets more inflammation. In terms of treatment, patients must be educated about the need for persistent therapy so that the eye is not only quieted, but ultimately is returned to homeostasis.
Tear Film Complexity
The next piece of the dry eye puzzle is the human tear. Tears are exceedingly complex. We’ve never been able to duplicate them in an artificial product. In fact, there are more than 500 unique proteins in human tears.
In addition to water, healthy tears contain a complex mixture of proteins, mucins and electrolytes (see Figure 2). Lysozyme and lactoferrin are the most abundant proteins in tears and also have antimicrobial functions. Immunoglobulins, such as IgA, IgG and IgM, also have protective functions designed to protect the ocular surface.
Cells are constantly sloughed off and lost from the most superficial layer of ocular epithelia. However, growth factors enable replacement. These very small proteins regulate the process for replacement of epithelial cells and are necessary for wound healing. Many growth factors are present in tears, including EGF (epidermal growth factor).
Maintaining a healthy tear film is a delicate balancing act. The outer lipid layer protects against evaporation. Tear lipids are secreted by the meibomian glands with orifices at the lid margins. The aqueous component in tears is thought to form a gel with soluble mucins that decreases in density toward the lipid layer. It includes a complex mixture of proteins, mucins and electrolytes. Mucins are also a crucial component and are critical for the viscosity of the tear film, stabilizing it against the shear force exerted by each blink cycle.
Figure 2. Healthy Tears
Tear electrolyte concentrations are also important, as this affects osmolarity, which is important for many aspects of epithelial and nerve cell function.
Ocular Surface Disease Triggers
When you consider the many triggers that can affect tears, digital device use is the one environmental factor that stands out most. This rapid shift in lifestyle is exceedingly pervasive and is one of the most plausible explanations we have for the high prevalence of dry eye in younger populations that we saw in the Beaver Dam Offspring Study. Also, looking ahead, we should not underestimate the potential effects of light-emitting devices on a generation of kids that use them for several hours per day—often in school—from ages two and up.
Although we do not yet have any reliable data to indicate how many hours per day an individual can use a digital device without suffering any lasting effects, it is definitely worth our consideration. What’s more, practically speaking, we are already witnessing the fallout. For example, we are beginning to see some patients in their 20s with the meibomian glands of a 70-year-old. Reduced blink rates have dramatically affected these important glands.
Systemic disease is another common ocular surface disease trigger. We commonly think of autoimmune disease as a primary offender in the systemic category, but epidemic disease such as diabetes is equally deserving of our attention. Studies have shown that 50% of patients with diabetes have dry eye.5 Confocal microscopy consistently shows that the very first structure that’s damaged in diabetes is the cornea.6-9
Medications are another ocular surface disease trigger. Several systemic medications have drying side effects, most notably antihistamines, hormone replacement therapy, anticholinergics and some sleep aids.
In some cases, food and drink, particularly consumption of alcoholic beverages, can bring on ocular drying. Long-term exposure to dry air, as is found in some locations, can give rise to dry eye, while the windy nature of air-conditioning and forced heat is one of the worst agitators of the condition.
Pollutants, most notably smoke or exhaust, can cause ocular drying as well. Three other prevalent causes of dry eye are refractive surgery, cataract surgery and long-term contact lens wear.
In short, the risk factors keep mounting, leading to eventual ocular surface breakdown and tear film instability.
How the Cycle of Inflammation Drove Innovation
When a trigger causes the eye to get stressed, the stressed tissue will express an intracellular adhesion molecule. This intracellular adhesion molecule will then be capable of binding with a T-cell. It is this binding activity that has attracted the interest of researchers when developing new dry eye therapies.
For instance, it was recently discovered that T-cells bind to an adhesion molecule by way of lymphocyte function-associated antigen-1 (LFA-1). LFA-1 is an integrin receptor found on the surface of T-cells and ICAM-1 is its binding partner (see Figure 3).10,11
The new drug lifitegrast blocks the binding of the adhesion molecule ICAM-1 to the T-cell surface.12 This, in turn, inhibits T-cell recruitment, activation and cytokine release associated with dry eye.
Our understanding of T-cell behavior grew out of our experience with cyclosporine, which likewise inhibits T-cell activation; however, it does so by allowing apoptosis and blocking the intracellular signal transduction cascade.13 This earlier research taught us that activated T-cells produce inflammatory cytokines that result in the recruitment of more T-cells and more cytokine production.14,15
Our goal as optometrists is to intervene sooner, before this chronic, progressive ocular surface disease spirals further out of control.
Diagnostic MilestonesIn the absence of timely diagnosis, dry eye disease will get worse and be more difficult to manage. For this reason, it is our growing responsibility as optometrists to actively look for dry eye in all patients, whether or not they have symptoms or are forthcoming about them. Admittedly, this is not an easy task. Research shows that fewer than 60% of dry eye patients are symptomatic.16 As such, looking at symptoms alone will likely result in missing a significant percentage of dry eye disease patients, particularly those with early or mild disease.
Fortunately, new diagnostic technology combined with a better understanding of conventional diagnostic methods can aid us in making diagnoses much sooner. Managing a successful dry eye practice 20 years ago would be challenging, if not impossible. Our primary tools at that time were Schirmer strips and artificial tears. It’s astounding how far our knowledge, tools and capabilities have evolved in a span of only two decades. Even the seemingly simple things, like surveys and lissamine green, have made treatment more effective because they help us identify dry eye so much earlier, which makes it easier to treat, which in turn helps slow the progression of this chronic disease.
But despite the outstanding technology that we now have at our disposal, it’s important to recognize that you should never look at only one marker or test. Depending on your practice setting and resources, the tools you use may vary, but just as you would never rely solely on tonometry to monitor a glaucoma patient, one dry eye test—whether that’s staining or osmolarity—should never be relied upon exclusively. Though it may be considered more expensive in the short term, adding additional tests can save you and your patients a lot of time, money and suffering in the long run. Here are some tips on the more popular diagnostic options that we now have to choose from:
• Symptom assessment. Many clinicians agree that symptom assessment ought to be one of the first and most important measures worth considering in any dry eye evaluation. Whether this is a written survey or a verbal exchange, if a patient indicates that something is wrong, pay attention. Of course, many patients are not forthcoming and will tell you everything is fine. Don’t make the mistake of taking this at face value. When you ask probing questions, you’ll often discover that there are many times when patients don’t feel fine—like after several hours on the computer, on airplanes or when it’s windy outside. These are signs of dry eye, and they will not improve on their own. Remember, dry eye is progressive, so the sooner you know, the better. Surveys have come a very long way and have an important place in dry eye diagnosis. For example, the Ocular Surface Disease Index (OSDI) has excellent reliability and validity, as well as good sensitivity and specificity.17 Although OSDI has some limitations, it effectively discriminates between normal, mild to moderate, and severe cases.2,17 The Standard Patient Evaluation of Eye Dryness (SPEED) and the five-question Dry Eye Questionnaire (DEQ-5) are also commonly used to give objective value to subjective complaints.18 Other surveys such as Impact of Dry Eye on Everyday Life (IDEEL), National Eye Institute’s Visual Function Questionnaire (NEI VFQ-25) and Short Form-36 (SF-36) provide information about the patient’s quality of life, which is an important measure in any chronic disease.
Dry Eye on the Rise?• Dry eye is not found only in older patients, but it is an age-related disease. Consider: More than 100 million adults in the US over the age of 50 have been diagnosed, with another 10 million expected by the year 2020.41,42
• The US dry eye population is estimated to be more than 10 times that of other common conditions such as glaucoma.43
• Twenty-nine million Americans (9.3%) have diabetes and half of them have dry eye.44,45 Diabetes rates have been steadily rising for the last 40 years, and there is no indication that this rate is going to decline any time soon.44,46
• Digital device use is creeping into almost every part of our lives and has the potential to be a huge driver of dry eye disease in coming years. A recent study by the Vision Council found that, on average, roughly 88% of adults spend more than two hours per day using a digital device, while approximately one in 10 people spend at least three-fourths of their waking hours on a digital device.47
• Schirmer’s and phenol red thread. Tear volume testing is a staple in dry eye diagnosis. Although it has drawbacks, few practitioners would feel comfortable diagnosing a case of Sjögren’s without it. Schirmer’s is the gold-standard tear volume test in research circles, but it requires anesthesia and takes about five minutes. The alternative, phenol red thread, can be performed without anesthesia and takes only takes 15 seconds.
• Fluorescein staining. This test is useful for assessing the location and possible cause of dry eye. For example, if you see inferior staining, the patient may have incomplete blink, lagophthalmos or closure, whereas patchy, central staining is a good indicator of Sjögren’s syndrome. However, keep in mind that, while fluorescein helps with management, it is not valuable as a screening test because it only picks up moderate to advanced disease. It will not detect early dry eye. In essence, waiting for dry eye to appear with fluorescein staining is like waiting for visual field loss before you treat a patient for glaucoma. Another word of caution when using fluorescein: You have to wait a minimum of two to five minutes, depending on the amount instilled, to let the fluorescein clear the eye so you don’t get quenching. The cornea will look clear right after you put fluorescein in. If you don’t wait, you won’t see what’s underneath the surface of the tears; all you’ll see is the surface fluorescein reacting and sending the light back to you.
• Lissamine green and rose bengal. These vital dyes can help you pick up moderate and some mild cases of dry eye. Indeed, 1% lissamine green stains dead or devitalized cells and is useful in evaluating conjunctival damage, conjunctivochalsis and the line of Marx along the lid margin.19 Rose bengal can provide valuable information too, but many patients say it stings.
• Corneal topography. Although it’s not often thought of as a test for diagnosing dry eye, if you’re considering referring a patient for cataract surgery, this is an important test to perform and is often a first indicator of dry eye disease in surgical settings. Research shows that topography can detect subtle irregularities on the ocular surface and, as such, is an excellent tool for the detection of dry eye.20 The appearance of inferior steepening due to epithelial dehydration is a telltale sign that sometimes looks a bit like keratoconus.21 Other topographical findings of dry eye disease include irregularly shaped placido discs and differences in average keratometry readings between eyes.20,21
• Osmolarity testing. Osmolarity testing indicates whether or not the patient has a higher “salt” content than normal: As the volume of aqueous declines, the solute concentration in tears increases. Hyperosmolar status, whether through decreased tear production or an increased evaporative state, indicates reduced aqueous levels.22 Some clinicians use osmolarity testing as a screening tool, while others use it to track the disease over time. In either case the test delivers valuable information that you can use to guide treatment. A recent study found that cataract patients who had osmolarity scores within normal limits were within a half diopter of intent, whereas 17% of those with hyperosmolarity would have missed their IOL calculation by more than a diopter.23
• MMP-9 Testing. MMP-9 is a proteolytic enzyme produced by stressed epithelial cells, and it has been shown to increase in dry eye patients.24 This test provides qualitative and quantitative information that can aid the diagnosis of dry eye insofar as it indicates inflammation. A positive reading means that the sample contains more than 40ng/ml, which indicates inflammation. However, the inflammation can be due to a number of causes other than dry eye. That being said, MMP-9 has been correlated with dry eye and is a good indicator that further investigation is warranted.25
• Non-invasive Keratograph break-up time (NIKBUT). NIKBUT uses placido disc ring-based corneal topography to measure initial and average breakup. It does not require the instillation of dye, yet it can help determine tear film quality and it can measure the amount of tears at the lower tear meniscus. Interferometry can also allow you to see particle spread.
• Meibography. Meibomian glands plug, swell, become serpiginous, truncate and, ultimately, atrophy.26 Therefore, the appearance of a capped gland doesn’t tell you much. Without looking inside the glands, you can’t really know how many are lost or viable. Meibomian gland imaging has helped significantly in this regard. It not only provides us with information that helps guide treatment, it also helps us communicate the impact of disease to our patients.
Lifitegrast ApprovalIn July 2016, the FDA approved the first in a new class of drugs known as lymphocyte function-associated antigen-1 (LFA-1) antagonists. Commercially known as Xiidra (lifitegrast ophthalmic solution 5%, Shire Pharmaceuticals), the new drug is indicated for the treatment of signs and symptoms of DED. Specifically, this small molecule integrin antagonist blocks the binding of ICAM-1 to LFA-1 on the T-cell surface, inhibiting T-cell recruitment and activation associated with DED inflammation.32,48,49 This preservative-free drop comes in individual vials and is dosed BID.
Lifitegrast went though four separate multicenter, prospective, placebo-controlled, randomized, double-masked FDA clinical trials involving more than 2,000 subjects ranging in age from 19 to 97, with a predominance of female patients, at about 75%.50 Both the active drug and placebo were administered BID for 84 days, and safety and efficacy were determined between the groups.12,35-37,51,52
The study results revealed that the groups using lifitegrast had a statistically significant clinical improvement in signs (inferior corneal staining) and symptoms (eye dryness) compared with placebo. In the OPUS-3 study on symptoms of eye dryness, which involved 355 patients on lifitegrast and 356 on placebo, lifitegrast had a highly statistically significant improvement compared with placebo at day 84 (p=0.0007), day 42 (p<0.0001) and at 14 days after initiating therapy (p<0.0001).12,35-37,51,52
The most common (>5%) ocular finding associated with lifitegrast was burning, and the most common (>5%) nonocular finding was dysgeusia, or a change in taste sensation. Most adverse events were reported as being mild to moderate in severity, and transient.12,35-37,51,52
• Lipid layer thickness (LLT) assessment. An insufficient lipid layer is believed to be the most likely cause of fluctuating vision and is a hallmark of dry eye.4 Automated assessments of the lipid layer let you know when a patient’s dry eye is driven by a deficient lipid layer, which can help guide treatment. For example, if a patient has a deficient lipid layer, treatment should include therapies that encourage meibomian gland expression as well as a lipid-containing artificial tear.
• Blink analysis. You might be surprised at how many of your patients’ dry eye problems are related to their blink patterns. New technology can evaluate routine blink characteristics, including blink rate and partial or incomplete closure. You can use this information and video footage to help educate patients about how blinking contributes to their condition. The information can be used to help encourage treatment compliance and/or blinking exercises.
• Microscopy. These non-contact devices offer objective data about cell loss in the endothelial cell layer, which is often set in motion by dry eye. Specular microscopes are particularly helpful when monitoring patients over time and to measure improvement with certain therapies. The images can also be valuable for patient education purposes and for encouraging compliance.
Four-Pronged Treatment Plan
Dry eye treatment varies based on the presentation and on what your diagnostic tests uncover. However, our approach to treatment ought to take the lids, glands and ocular surface into consideration. One very effective way to do this and to ensure that all potential offenders are addressed is to initiate a four-pronged treatment plan. By systematically considering the need for treatment in all four areas, you can get your patient on the right path sooner and prevent this chronic disease from getting worse. The four areas that ought to be evaluated and addressed in a patient with dry eye are obstruction, inflammation, biofilm and the tear film.
• Obstruction. For the obstruction, options include lid margin debridement and scaling, warm hydrating or moist-heat compresses, manual expression and thermal pulsation. The trick to warm compresses is to use a system that can deliver moist heat consistently for several minutes. Another option that’s been proven effective for obstruction is LipiFlow thermal pulsation.27-29
• Bacterial biofilm. To clear up the biofilm in patients who have blepharitis, lid scrubs and mechanical treatments like BlephEx can be helpful. Depending on severity, antibiotics may also be indicated.
• Inflammation. For inflammation associated with MGD, lifitegrast, cyclosporine or omega-3 fatty acids may be suitable. Steroids, azithromycin and oral doxycycline are sometimes helpful too.
• Tear film instability. The key to effective tear supplementation lies in choosing a product that’s appropriate for each patient’s unique presentation. A patient with high osmolarity will benefit from a different tear than a patient who is lipid or aqueous deficient with low osmolarity. For example, MGD patients tend to respond well to a lipid-based, osmolarity-lowering tear product.
In some cases, even after you have initiated treatment in the four areas listed above, additional strategies may need to be employed. For example, punctal plugs can benefit many patients, provided they are producing healthy tears. And, for more severe cases, treatments such as autologous serum and amniotic membrane may be beneficial.
Tips on Targeting Inflammation
As our understanding of inflammation has evolved, so, too, has our ability to address it clinically. Twenty years ago, treating dry eye was frustrating. Most of the time, we used short-term steroids, lubricated the eyes and put plugs in. That was all we had at our disposal. Then, when cyclosporine was introduced, we began to realize that arresting inflammation is at the heart of successful dry eye treatment. More recently, lifitegrast is showing us new ways to inhibit T-cell recruitment and activation associated with dry eye disease inflammation.30-32
It is clear that we can’t rely on tears for treatment. In fact, research has shown that when artificial tears alone were used for one year, patients experienced a 40% increase in T-cells, which is equivalent to no treatment at all.33
Inflammation is present in both aqueous-deficient and evaporative dry eye, and now that there are two pharmaceuticals—cyclosporine and lifitegrast—many clinicians are taking a close look at which therapy to use on individual patients and whether it is ever worthwhile to switch medications.
The efficacy and safety of the newer drug, lifitegrast, has been evaluated in four randomized controlled trials involving more than 2,000 patients.34-37 And, as we all know from research and clinical experience, cyclosporine likewise has proven to be very safe and effective. With this in mind, it is obvious that, if your patient is already using cyclosporine successfully, there is no reason to change or add medications. But for new cases and for patients who have not responded favorably to cyclosporine, the question becomes when should you consider using steroid induction therapy? If you consider onset of improvement, the need may be reduced in patients who are treated with lifitegrast.
One of the benefits of lifitegrast is that the data show that patients experience improvement in two weeks.38 This period of time should not be too long for most patients to stick it out, even in the absence of a temporary steroid. But whatever treatment you choose, setting appropriate expectations is essential. Make sure your patient understands that dry eye is a chronic condition that they are going to have their whole life. One way to convey this is by emphasizing the “-itis.” Use terms like blepharitis, keratitis and meibomitis. This will help you draw a parallel between dry eye and other diseases that patients are more familiar with, such as arthritis. Patients understand that, even with appropriate treatment, arthritis can flare up at times. The same happens with dry eye.
When patients don’t comprehend the chronic, progressive nature of dry eye, they are less likely to adhere to therapy. We’ve all had patients stop taking cyclosporine because they thought they were healed. In fact, these patients often feel great 30 to 60 days after stopping cyclosporine. However, 90 days down the road, the patient is miserable again and can’t make the connection that it has anything to do with the fact that he stopped using the drops. It’s a difficult narrative to make a patient understand, but it’s a very important one, particularly when you are prescribing cyclosporine.
Make sure your dry eye patients understand that this is a marathon, not a sprint. We can do our best to control it—and we can now do so quite effectively—but we’re not yet able to permanently cure dry eye.
We Can Do More
Dry eye disease is a chronic, progressive disease that affects millions of people, yet in the United States alone, less than one million are receiving medical treatment.1,39,40 While there is no cure for dry eye, improved diagnosis and treatment advances can not only provide symptomatic relief, they can also prevent escalation. As such, we would be doing our patients a great disservice if we failed to help shut down the inflammatory cascade and instead clung to old models and followed outdated algorithms.
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