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Volume 1, Issue 2 2013 A Learning Resource for Optometrists from the School of Optometry & Vision Science, University of Waterloo, and the School of Optometry, University of Montreal The New Normal in Managing Dry Eye Disease B Y S ARAH M AC I VER , OD, FAAO, M ICHELLE S TEENBAKKERS -W OOLLEY, OD, FAAO, AND C. L ISA P ROKOPICH , OD, MS C Although the symptoms associated with the group of ocular conditions known as “dry eye disease” – or dry eye syndrome (DES) – are common, they continue to be the most challenging to manage. Perceptions surrounding DES include the beliefs that few therapeutic tools significantly impact the disease and that overall DES management, as a chronic disease, is inadequate. Identifying and treating DES patients will not only reduce the number of patients suffering a decreased quality of life due to its debilitating symptoms, it will also enable optometrists to optimize their therapeutic management skills. This issue of Optometry Rounds reviews the recent changes in classification, evaluation, and diagnosis of DES. It also outlines the new tools in the management of DES that enable optometrists to treat this chronic disease more effectively. Marlee M. Spafford, OD, PhD, FAAO Professor and Interim Director Thomas F. Freddo, OD, PhD, FAAO Professor and Co-Editor, Optometry Rounds Contributing Faculty Authors: Sarah MacIver, OD, FAAO Clinical Lecturer C. Lisa Prokopich, OD, MSc Clinical Lecturer Michelle Steenbakkers-Woolley, OD, FAAO Clinical Lecturer Why Treat Dry Eye Syndrome (DES)? Based on demographics alone, up to 35% of the population is affected by DES.1 Its significance for patients and impact on quality of life (QOL) are immutable, as is its relationship with other chronic systemic diseases (eg, Sjögren syndrome). Because optometrists have an array of therapeutic options (ie, refractive care, topical and oral agents, lacrimal occlusive therapy) to manage all aspects of DES, along with the insight to engage other healthcare practitioners, they are best placed to address this disease. In most provinces, optometrists still face therapeutic law limitations with some aspects of contemporary DES management; however, most of these can be overcome with appropriate interprofessional collaboration and communication. To effectively manage DES patients, it is important to understand the recent changes in our understanding of its pathophysiology. These changes have affected the clinical categories of DES and, hence, the management approach is now targeted at treating its underlying causes. The Lacrimal Functional Unit (LFU) and a New Definition of DES The LFU is composed of the main and accessory lacrimal glands, the ocular surface (conjunctiva, cornea, and meibomian gland orifices), and the interconnecting innervations consisting of sensory input from the trigeminal nerve and stimulation of the accessory and main lacrimal glands by efferent secretomotor neurons.2,3 The purpose of the LFU is to regulate the major components of the tear film to preserve the integrity of the ocular surface. Goblet cells and conjunctival epithelial cells contribute to the LFU, providing protection to the ocular surface due to their mucin-secreting abilities and production and release of antibacterial agents and immunoglobulins. Damage to any component of the LFU can disrupt the reflex pathway and destabilize the tear film, leading to disease of the ocular surface.1,3 In 1995, the National Eye Institute established a global definition for DES and identified damage to the ocular surface as the main contributor to its symptoms of discomfort. This view was held for over a decade until it became evident that additional key underlying factors – hyperosmolarity and inflammation – contribute to the signs and symptoms of DES and needed to be added to the definition.4 École d’Optométrie School Administration: Christian Casanova, PhD Director and Professor Neurophysiology and Imaging Danielle de Guise, OD, MSc Associate Director of Cycle 1 Studies Binocular Vision and Orthoptics Jocelyn Faubert, PhD, FAAO Associate Director of Research and Advanced Studies Professor, Psychophysiology and Visual Perception Jacques Gresset, OD, PhD, FAAO Secretary and Professor Epidemiology and Low Vision Editorial Committee: Jean-François Bouchard, BPharm, PhD Associate Professor, Neuropharmacology Pierre Forcier, OD, MSc Associate Professor, Ocular Health Langis Michaud, OD, MSc, FAAO (Dipl.) Associate Professor, Contact Lenses Co-Editor, Optometry Rounds Judith Renaud, OD, MSc Assistant Professor, Low Vision Redefining dry eye In 2007, the Dry Eye WorkShop (DEWS) redefined DES as 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. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.”2 This definition specifically excluded the aqueous deficient dry eye (ADDE) and evaporative dry eye (EDE) distinctions, although these are retained in the pathogenic classification of DES.2 While the ability to identify these 2 components is helpful in management Available online at www.optometryrounds.ca University of Waterloo School of Optometry & Vision Science 200 University Avenue West, Waterloo, ON N2L 3G1 Université de Montréal École d’Optométrie 3744 Jean-Brillant, Montreal, QC H3T 1P1 The editorial content of Optometry Rounds is determined solely by the School of Optometry & Vision Science, University of Waterloo, and the School of Optometry, University of Montreal. decisions, the clinical crux is that they are frequently seen concomitantly and, therefore, it is difficult to distinguish the relative contribution of each. Indeed, one may induce the other, due to the initiation of the inflammatory cascade. associated with dry eye disease(s).2,12,13 While increasing age and female gender are 2 of the most significant risk factors for developing DES, the full list of predisposing risk factors is extensive (Table 1).2,14-23 The game changer: inflammation Diagnosing DES During a Routine Eye Examination The pathophysiology of DES is complex and multifactorial. A variety of factors may initiate the dry eye cycle by targeting one of the structures in the LFU. Lacrimal dysfunction may occur from Sjögren syndrome or other systemic conditions affecting the lacrimal glands (eg, sarcoidosis), thus leading to ADDE. It may also be caused by meibomian gland dysfunction (MGD), inadequate blink, or other causes of EDE. The common findings in all of these etiologies are tear film instability and hyperosmolarity.2,5-7 In ADDE, there is an overall decrease in tear clearance that leads to hyperosmolarity.8,9 In EDE, hyperosmolarity is triggered by local drying and exposure of the ocular surface.2,5 Recent evidence has identified an intrinsic inflammatory marker – the human leukocyte antigen (HLA)-DR – in DES patients with and without Sjögren syndrome.9-11 Following activation of the inflammatory cascade, apoptosis is initiated in the ocular surface epithelial cells, including the goblet cells. Goblet cell loss and corresponding reduction in the gel mucin, MUC5Ac, has been identified as a feature in every form of DES.5,7,13 Apoptosis of the surface epithelial cells leads to further tear film instability. This, in turn, leads to an increase in hyperosmolarity, progression of the inflammatory cascade, and further destruction of the ocular surface.1 This “core mechanism” of DES is illustrated in Figure 1. Ideally, DES management should focus at arresting this vicious cycle, allowing a reduction in inflammation and healing of the ocular surface.5 Ideally, all patients should be assessed for risk of DES at their annual eye examination as per the chronic disease model.1 While several tests are available to aid in the diagnosis, none is considered accurate and repeatable enough to be a stand-alone or gold standard. Furthermore, there are no uniform criteria for the diagnosis of the spectrum of dry eye diseases.13 Regardless, tests continue to have important clinical value in determining the presence and severity of DES (Table 2). This sequence of tests adds a minimal amount of time to the total eye examination (Figure 2), but may provide invaluable information in identifying which patients are in need of therapeutic intervention. Many dry eye questionnaires are available to help screen patients with dry eye symptoms. Such questionnaires are invaluable in identifying, diagnosing, and monitoring a patient’s symptoms, and optometrists should choose one with which they are comfortable. Once a patient is identified as having DES, diagnostic tests should be included in the routine eye examination. When there are symptoms, the initial dry eye diagnosis is made at the slit lamp, with assessment of the lid margins, tear film quality, tear meniscus height, and quality of the meibomian gland excretions in white light.13 Once dry eye symptoms or signs are identified, a minimum number of diagnostic tests should be added to the annual routine eye check-up. Phenol red thread testing of tear volume is cost-effective and takes only 15-30 seconds per eye. This is an easy and effective way to identify patients with ADDE, either as Who is at Risk for DES? Many factors play a part in the development of DES. The demographic of the postmenopausal woman is frequently Figure 1: The “core mechanism” of dry eye syndrome (DES) Table 1: Risk factors for DES • Environmental conditions14 – Low-humidity environment including air conditioning, air travel, wind velocity, or other artificial environments • Contact lens wear15-17 • Physiological disposition2,18-20 – Low blink rate, often associated with extended computer use, reading, or television viewing – Larger palpebral aperture – Proptosis Tear film instability Goblet cell and surface epithelial destruction Increased osmolarity Inflammation Apoptosis (includes IL-1α, IL-1β TNF-α, MMP-9) Adapted from the 2007 International Dry Eye WorkShop (DEWS) report2 IL = interleukin; TNF = tumour necrosis factor; MMP = matrix metalloproteinase 2 • Systemic conditions2,19-22 – Any systemic condition that results in a hormonal imbalance, autoimmune conditions, or destruction of lacrimal or meibomian gland; eg, sarcoidosis – Thyroid disease – Diabetes mellitus – Autoimmune conditions; eg, rheumatoid arthritis, systemic lupus erythematosus, and fibromyalgia • Systemic medications2 – Antihistamines, systemic beta-blockers, antispasmodics, diuretics, and antidepressants • Topical medications16-19,23 – Benzalkonium chloride Table 2: Common clinical tests used to diagnosis and monitor DES Test ADDE/EDE 24 Symptom questionnaires eg, McMonnies, DEQ, OSDI,26 CDEQ27 Tear quantity 25 Clinical value “Normal” measurement ADDE / EDE Symptoms graded at visit can be compared to baseline during management Differs for each test Phenol red thread test28-30 ADDE Index of tear volume Schirmer test without anesthesia12,19 ADDE Index of tear secretion helpful for Sjögren diagnosis Tear meniscus height (estimate height with adjustable vertical slit-lamp beam)14 ADDE Aqueous secretion Ocular surface damage31,32 Sodium fluorescein (SF) dye (with Wratten barrier filter #12), lissamine green (LG), rose bengal (RB) ADDE/EDE SF stains/pools in intercellular spaces LG, RB stain cells with membrane damage Grade according to density/location Pattern: diffuse with coalescent patches (Figure 4) MGD Lid margin evaluation (clinical features)33-35 EDE Posterior displacement of gland orifices, lid notching, MG atrophy, telangiectasia Grade according to severity: mild, moderate, severe MG expression20,33,35 EDE Number of expressible glands, quality of secretion See Figures 5 and 6 Tear film quality Slit-lamp biomicroscopy (including specular reflection)14 ADDE/EDE Look for debris, saponification (Figure 3), oil Grade according to findings Tear film osmolarity Commercially available system ADDE/EDE Proposed “gold standard” for diagnosis Tear film stability Tear break up time (fluorescein dye instillation)18 EDE Fast and accurate test good sensitivity (83%) and specificity (85%) ≤12 mm in 15 seconds ≤5 mm in 5 minutes ≤0.25 mm clinically estimated as normal, excessive, or shallow ≤316 mOsm/L <10 seconds ADDE = aqueous deficient dry eye; EDE = evaporative dry eye; DEQ = Dry Eye Questionnaire; OSDI = Ocular Surface Disease Index; CDEQ = Canadian Dry Eye Questionnaire; MGD = meibomian gland dysfunction an isolated entity or as a comorbidity with MGD.28-30 The typical clinical appearance of MGD – “the pink eyeliner sign” (Figure 3) – consists of hyperemic and telangiectatic lid margins, along with early notching, posterior displacement of the meibomian gland orifices, and thick, toothpaste-like glandular expression. The next steps include assessment of tear instability and ocular surface damage to both the cornea and conjunctiva using fluorescein dye and a yellow (Wratten #12) barrier filter. Ideally, damage to the conjunctival surface is evaluated with rose bengal or lissamine green staining; however, conjunctival staining can be graded using fluorescein alone and is a reasonable starting point.13,31,32 The pattern of the staining is telling in Figure 2: Sequence and timing of an initial dry eye assessment (4-5 minutes) Questionnaire Slit-lamp of lids and ocular surface (1.5 min) Phenol red thread (15s per eye, repeated once) (1 min) Tear Break-up Time (30 sec) terms of DES severity and type. Corneal staining is often central in ADDE, inferior along the lid margin in EDE, and becomes coalescent in density as inflammation progresses.13,32 Tear film osmolarity was identified by the DEWS13 as the most important potential test for diagnosing DES. There is considerable value in assessing a parameter that is directly involved in the mechanism of dry eye. MG expression. According to both the DEWS13 and the International Workshop on MGD,33 MGD is the leading cause Figure 3: MGD. Note the “pink eyeliner sign” from hyperemic and telangiectatic lid margins, early notching, posterior displacement of the gland orifices, and thick, toothpaste-like glandular expression. Meibomian gland expression (1-2 min) 3 of DES worldwide. This development has altered the diagnostic paradigm for DES to focus on assessing the ease and quality of meibomian expression in every dry eye patient.34-36 All glands should be expressed with digital pressure for 10–15 seconds in the nasal, central, and temporal section of the lower lid. An assessment should be made of the quality of the expressed oil. There appears to be more clinical utility in assessing the expressibility of the nasal and central glands since damage to the nasal glands causes more MGD symptoms. Figure 5 illustrates the expression of glands in a symptomatic patient with nonobvious MGD. Figure 6 illustrates tear film saponification noted following MG expression. To help manually express the glands, patients may use hot compresses (see below) or MG expressors. These latter tools have been shown to be effective in expressing chronically impacted glands.32 Figure 4: Coalesced superficial punctate keratitis from a patient with Sjögren syndrome. The coalescent pattern is a characteristic sign indicating severe inflammation is present on the ocular surface. Management: Conventional Versus Contemporary Evaluation and management of the patient diagnosed with DES should begin with assessing the severity (Table 3). 13,14,37-39 The goals of treatment should be geared towards ensuring that the patient’s symptoms are improved and that there is no risk of vision loss.14,40 Optometric physicians should be aware that the various guidelines are recommendations and that each patient presents with a unique set of symptoms, signs, and circumstances. There is no cookbook approach to management; therefore, attention should be paid to both determining the etiology of the dry eye and targeting the underlying causes of the disease, inflammation and tear hyperosmolarity. First-line Management The typical first line of treatment is lubricating agents – eye drops and gels, often misnamed “artificial tears” – and general lid hygiene to improve the health of the lids and meibomian glands.14 Lubrication and lid hygiene should be considered as minimum baseline therapy for all DES patients. Table 3: Dry eye severity: a clinical reference guide Severity level 1 2 3 Mild and/or episodic, occurring under environmental stress Moderate episodic or chronic, stress or no stress Severe, frequent or constant Occurs without stress Severe and disabling or constant Visual symptoms None or episodic, mild fatigue Annoying and/or activity-limiting episodic Annoying, chronic, and/or constant, limiting activity Annoying, chronic and/or constant limiting activity Conjunctival injection None to mild None to mild +/– +/++ Conjunctival staining None to mild Variable Moderate to marked Marked Corneal staining (severity/location) None to mild Variable Marked central or peripheral (MGD) Severe punctate erosions Corneal/ tear film signs None to mild Mild debris, decreased meniscus Filamentary keratitis, mucus clumping, increased tear debris Filamentary keratitis, mucus clumping, increased tear debris, ulceration MGD Minimally altered expressibility and secretion quality (meibum: cloudy) Mildly altered expressibility and secretion quality (meibum: cloudy with particles) Moderately altered expressibility and secretion quality (meibum: inspissated, toothpaste like) Tear break up time Variable ≤10 seconds Schirmer score (mm/5 min) Variable ≤10 mm ≤5 seconds Severely altered expressibility and secretion quality May include: Trichiasis, keratinization, symblepharon Phenol red thread test Variable ≤15 mm ≤10 mm ≤5 mm Adapted from Behrens A et al,39 and International Workshop on Meibomian Gland Dysfunction.33 4 4 Discomfort, severity and frequency Immediate ≤2 mm ≤5 mm Figure 5: Expression of meibomian glands in a symptomatic patient with non-obvious MGD. Note the thick, toothpastelike meibum secretion. Lid hygiene Lid hygiene includes hot compresses, massage, and lid scrubs. A warm (40°C) towel compress applied for 5 minutes was shown to increase the tear film lipid layer thickness by up to 80%.41 Combining compresses with firm massage of the eyelids can be an effective means of meibum expression; however, compresses may heat only the anterior portion of the glands and may not reach pathologically compacted glands posteriorly. Lubricating agents Lubricating agents attempt to mimic natural tear composition by containing lipids, aqueous, and mucin components. 10 Various formulations have been found to reduce symptoms and provide objective benefits such as increasing lipid layer thickness and tear volume; 42-47 however, these agents rarely result in the elimination of symptoms. 14,40 According to the DEWS,14 the ideal lubricant would contain potassium, bicarbonate, and other electrolytes, be free of preservatives, have a neutral to slightly alkalinic pH, and contain a polymeric system to prolong retention time. The International Workshop on MGD 35 stated that lubricants with higher viscosities are associated with improved results in the management of DES than lower-viscosity preparations, and that lipid supplements have been shown in clinical studies to improve symptoms and signs of MGD, possibly further to improvement in tear film stability. W-3 fatty acid supplementation W-3 fatty acid supplementation should also be initiated at the onset of DES, especially if MGD is present, because of its impact on the lipid layer.10 W-3 and W-6 fatty acids mediate inflammation in DES.48-50 The importance of W-3 use in dry eye disease and MGD is 3-fold: restoration of the lipid layer, decreased inflammation and apoptosis, and increased tear secretion.48,51 W-3 fatty acids, including eicosapentaenoic acid (EPA), docosahexaenoic acid, and a-linolenic acid, mediate anti-inflammatory factors, while W-6 fatty acids (ie, g-linolenic acid and arachidonic acid) produce proinflammatory factors.51 Therefore, maintaining a balance between Figure 6: Saponification in the tear film that is secreted following meibomian gland expression. the 2 fatty acids is essential to achieve an optimal overall inflammatory state. W-3 dietary supplementation is recommended since it is often lacking in the diet, while W-6 supplementation is less important.51 Core Management In addition to solely targeting dry eye symptoms, the optometrist should also introduce appropriate core management strategies that target the underlying causes of DES. Specific core management strategies are listed in Table 4. The International Workshop on MGD identified a group of patients that are distinct from the severity scale; this group was designated as having MGD “plus” disease since they have MGD in conjunction with another type of ocular surface disease, including anterior blepharitis.40 This group of patients typically requires more aggressive management from the onset. A decade ago, the steroid class of medications was being prescribed with trepidation in DES, especially in eyes with a compromised cornea. The notion of delayed epithelial wound healing along with other adverse effects associated with topical steroids superseded the potential of these agents, as well as other medications in the anti-inflammatory category. To some extent, these old adages remain, although the plethora of research on the inflammatory nature of DES and associated ocular surface disease supports the incorporation of these medications earlier and more aggressively in the management protocol.10,52-56 It is known that DES, regardless of its etiology, proceeds in a vicious cycle and unless treatment targets part of the cycle, it will progress. Hyperosmolarity, and therefore inflammation, has been identified as the main cause of all forms of DES and it ensures the perpetuation of this cycle, regardless of the cause. A topical anti-inflammatory medication targets the production of inflammatory cytokines, thus preventing further damage to goblet cells and further tear film instability.5 Topical corticosteroids, topical cyclosporine A, and/or oral tetracycline should be considered early in management protocols and part of core management. Topical corticosteroids Topical corticosteroids have been shown to be effective in the treatment of DES. Their mechanism of action involves 5 Table 4: Common treatments for dry eye syndrome14 Minimum baseline therapy (to be initiated on all patients regardless of severity) Hot compresses Lid scrubs and massage Lubricating agents (“artificial tears”) Drops, ointment, gel Preservative and preservative-free Lipid-containing formulations W-3 fatty acid supplementation Core management strategies (To be used in conjunction with above baseline therapy) Antiinflammatory Osmolarity reduction Anti-Inflammatory Therapy Topical corticosteroids Initiate soft /lower-potency steroid (eg, loteprednol etabonatea 0.5% ophthalmic suspension < fluorometholone 0.1% ophthalmic suspension < prednisolone phosphate 1.0% ophthalmic solution) Topical corticosteroids Cyclosporin A 0.05% ophthalmic emulsion Oral tetracyclines • 1 gt qd for 2–4 weeks, and assess efficacy • If good response, 1 gt bid for 2–4 weeks Topical cyclosporine A Lacrimal occlusion Autologous serum Secretagogues Initiate cyclosporine A 0.005% ophthalmic emulsion • 1 gt bid indefinitely Protective Moisture chamber lenses Scleral contact lenses • Can be initiated concomitantly with a corticosteroid; taper the corticosteroid dose and discontinue over 2–4 weeks Anti-infective Topical antibiotics for anterior blepharitis Oral tetracyclinesb inhibition of cytokine production, decreased synthesis of matrix metalloproteinases (MMPs) and arachidonic acid derivatives, and induced lymphocyte apoptosis. 53,57,58 The long-term use of topical corticosteroids for DES is controversial because of the potential risk of posterior subcapsular cataract development, a rise in intraocular pressure, and development of glaucoma and delayed wound healing; 40,58 however, studies showed promising results for the use of these agents in dry eye that support their short-term use.59,60 Less potent topical steroids are being evaluated for their utility in dry eye management. Topical fluorometholone acetate and the soft topical steroid loteprednol etabonate (0.5%) have been shown to be efficacious with a reduction in the incidence of elevated intraocular pressure.58,61 Topical corticosteroids can be used as first-line treatment, before the occurrence of damage, or secondary to inadequate treatment with lubricating agents and/or hot compresses. Most patients with DES of severity ≥2 report immediate symptom relief.51 Topical cyclosporine A Cyclosporine A 0.05% ophthalmic emulsion was approved by Health Canada in 2010 for the treatment of moderate to moderately severe (DEWS level 2-3) ADDE.62 Oral cyclosporine A was initially used as systemic immunosuppressive therapy following organ transplantation; however, it showed an increase in tear lacrimation.23 Topical ophthalmological application results in no measureable levels of cyclosporine in the bloodstream, and thus is considered to be a local anti-inflammatory agent with local immunomodulatory, but not immunosuppressant, activity.62 Cyclosporine A is most effective in individuals with suppressed tear production associated with inflammation. It decreases inflammatory markers and therefore inflammation on the ocular surface. Compliance with cyclosporine A is not always optimal, which can also reduce its effectiveness. In general, a compliant patient will experience improvement in approximately 6–8 6 PRACTICE PEARLS Initiate oral tetracycline derivative (eg, doxycycline or minocycline) • 20–40 mg daily for ~3 monthsc a Loteprednol etabonate is indicated by Health Canada for use postcataract surgery; Not indicated by Health Canada for the treatment of ocular inflammation; c The optimal duration of therapy with doxycycline or minocycline has not been established40 b weeks, and there may be a delay between clinical evidence of benefit and patient reporting of improvement. Compliance can be improved with patient education and application of a topical corticosteroid. Oral tetracyclines Inflammation in MGD is generated due to excessive lipase activation and changes in lipid composition that lead to a destabilized tear film.5,33 Macrolide antibiotics contain antiinfective, distinct immunomodulatory, and anti-inflammatory properties. 10,33,40 Tetracyclines are not indicated by Health Canada for the reduction of ocular inflammation, but their use for this condition is supported by several guidelines, particularly for ocular rosacea.14,27,40 Reduction of inflammation may be achieved at a lower dose than that routinely prescribed for antimicrobial use. The exact mechanism behind the antiinflammatory component is unknown, but clinical studies support their role in decreasing both lipases and MMP-8.40,63,64 The tetracycline derivatives doxycycline and minocycline are more lipophilic than tetracyclines and, therefore, have better potential to penetrate into the ocular tissues at lower concentrations, including the lids, meibomian glands, and the tears.40,65,66 Doxycycline and minocycline can be effective as anti-inflammatories at 20–40 mg daily, as opposed to their typical antibiotic dose of 50–100 mg once or twice daily. Duration of therapy is usually 3 months; however, an optimal time course has not been proven.40 Common adverse effects of the oral medication include sun sensitivity and gastrointestinal upset if taken on an empty stomach. Unlike oral tetracyclines, oral doxycycline can be taken with food and milk.67 Oral tetracyclines interact with a number of different medications so it is important to be alert for any potential drug-drug interactions with the patient’s list of medications. Other Therapies Secretagogues The muscarinic agonist pilocarpine has been found to be effective in increasing tear and saliva production in individuals with Sjögren syndrome.68 However, this agent is associated with systemic cholinergic adverse effects, such as excessive perspiration (40%), chill (20%), nausea (13%), hypersalivation (13%), and intestinal cramping (7%). Moisture-retaining eyewear Eyewear such as moisture chamber lenses and hydrophilic bandage or scleral contact lenses improve ocular hydration; the latter also act as a barrier between the eye and lid. The primary complication associated with bandage contact lenses is infection. Conclusion Although DES is a chronic and, at times, recalcitrant disease, its management can be rewarding for both patients and practitioners. Earlier and more accurate identification of patients with, or at risk of, DES will minimize reductions in their QOL. Minimum baseline therapy entails lid hygiene, eye lubrication, and W-3 fatty acid supplementation. More severe cases of DES often require additional interventions. As hyperosmolarity and inflammation are at the core of dry eye, core management strategies that target these conditions should be considered concomitantly with conventional treatments. While management strategies are always dependent on the individual patient’s symptoms, signs, circumstances, and adherence to therapy, practitioners are encouraged to consider anti-inflammatory options early in the treatment regimen. Dr. MacIver is a Clinical Lecturer at the University of Waterloo, School of Optometry and Vision Science. 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