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Diagnosis and Management of Dry Eye 2011

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Dry eye disease is one of the most common ophthalmic conditions in adults in the United States. A consensus definition and rational classification system (Figures 1 and 2) have recently improved the approach to its diagnosis and management.¹ New tools for evaluation and recommendations for their use and interpretation provide even better approaches to the diagnosis and management of the condition.

Figure 1. DEWS Definition of Dry Eye¹
The 2007 Report of the International Dry Eye Workshop (DEWS) provides a consensus definition of dry eye that informs a comprehensive approach to its diagnosis and evaluation.

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Figure 2. Etiological Classification of Dry Eye¹
Risk factors for dry eye disease are indicated on the left. Dry eye disease may be aqueous-deficient or evaporative in nature, and these categories may be further divided to better characterize the patient’s condition.

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New Approach to Assessment

Conventional diagnosis of dry eye has been based on recognition of symptoms of ocular irritation and evaluation of decreased tear production, predominantly by Schirmer testing and fluorescein or rose bengal staining.² The problem with this approach is that other ocular surface diseases, such as blepharitis and allergy, can produce similar symptoms and ocular-surface staining. A further confounding feature is that symptoms and signs of dry eye do not always correlate with disease severity.³ In addition, evaporative dry eye due predominantly to meibomian gland dysfunction (MGD) is a much more frequently recognized cause of dry eye and occurs in the presence of normal aqueous tear production.⁴

Recent reexaminations of the role of hyperosmolarity of the tear film have implications for diagnosis and management of dry eye.^4,5 Although elevated tear film osmolarity has been recognized since the early 1970s as a hallmark of dry eye disease,^6-8 only recently has rapid and reliable in-office measurement been possible.⁴

DEWS Report

The 2007 Report of the International Dry Eye Workshop (DEWS) provides a consensus definition of dry eye that informs a comprehensive approach to its diagnosis and evaluation (Figure 1).¹ That definition sharpens our appreciation of dry eye symptoms to include not only discomfort, but also fluctuating vision, particularly in situations in which normal blinking is reduced (e.g., reading or computer use).

Patients’ visual complaints can be more disturbing to their quality of life than the discomfort, often described as burning, stinging or feeling something in the eye. Although some patients use the term “itch” to describe the discomfort, further questioning usually reveals a discomfort not provoking the urge to scratch, which is more typical of allergy.

A number of questionnaires help to catalogue and grade symptoms.⁹ The most frequently used instrument is the Ocular Surface Disease Index (OSDI), which determines frequency of symptoms or provocative environmental conditions.¹⁰ An instrument that determines both severity and frequency of symptoms is the Symptom Assessment in Dry Eye (SANDE) questionnaire, which utilizes a visual analog scale.¹¹ For straightforward clinical response, the most revealing questions are “Do you experience discomfort of your eyes particularly when reading, using a computer, or in very dry circumstances?” and “Does your vision blur after you start reading or using a computer, and is the blur improved by blinking?”

Positive response usually indicates dry eye, but confirmation is needed of tear-film instability, another central clinical feature in the definition of dry eye.¹² Instability is usually confirmed after instillation of topical fluorescein with slit lamp observation of dark areas in the tinted tear film, occurring in less than 10 seconds following a full blink (Figure 3).¹²

Figure 3. Rapid Tear Breakup
Tear-film instability can be confirmed by slit-lamp observation of dark areas in the fluorescein-tinted tear film.
Source: Gary N. Foulks, MD, FACS

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Aqueous tear production is most frequently determined by applying a Schirmer strip to the lower eyelid and measuring strip wetting over 5 minutes. Less than 10 mm of wetting is considered indicative of dry eye.¹³ The phenol red-thread test is an alternative that employs a small, impregnated cotton thread applied to the lower lid for 15 seconds. Wetting of 10 mm or less is thought to indicate dry eye.¹²

Although damage to the ocular surface is not a mandatory feature of the definition of dry eye, it is a frequent clinical feature in more severe cases. Fluorescein staining of the cornea and conjunctiva can be seen by observing the ocular surface through a blue exciting filter on the slit lamp, but the appreciation can be enhanced using a yellow barrier filter before the objective lens of the microscope.¹² The optimal time for viewing staining is between 2.5 and 3 minutes following instillation of the fluorescein. Further evaluation of ocular surface damage can be obtained using topical lissamine green or rose bengal solution through the slit lamp using low illumination between 1 and 4 minutes following instillation of the dye. Lissamine green is better tolerated and less phototoxic to the surface cells than rose bengal.^12-14 The classic interpalpebral band of staining need not be present, and the more likely pattern seen in early disease occurs in a punctate pattern in the inferonasal quadrant of the cornea.¹⁵

Unfortunately, these diagnostic signs are not fully reliable, particularly in milder forms of dry eye, and they do not correlate well with the severity of symptoms of dry eye.^5,16 Fortunately, the codicil statement of the consensus definition identifies two features of dry eye that may provide more sensitive objective measures to diagnose and grade severity of dry eye disease: increased osmolarity of the tear film and inflammation of the ocular surface.¹ Two recent studies indicate that hyperosmolarity of the tear film is the most reliable objective measure of dry eye across all degrees of severity, when compared with OSDI evaluation of symptoms, Schirmer tear testing, tear-film breakup time, or ocular surface staining.^4,5

Management

Recommended management of dry eye as detailed in both the 2007 DEWS Report and the 2011 Report of the International Committee on Meibomian Gland Dysfunction (MGD) is guided by disease severity with sequential adjustment determined by patient response to therapy.^17,18 Patients must be educated about their condition and the goals of specific treatments, particularly with MGD-associated evaporative dry eye since lid massage depends on patient compliance.

An algorithm for management is depicted in Figure 4. Once the diagnosis of dry eye is established and the character of the condition is determined, stepwise treatment can be pursued. Patients should be instructed in both the type of their dry eye disease (aqueous deficient or evaporative or combined mechanism) and the importance of completing the recommended treatments, particularly lid massage following application of warm compresses for MGD-related dry eye. They should also be advised of the fact that prolonged reading or computer use aggravates dry eye and that air travel also increases symptoms and the need for supplemental lubrication.

Figure 4. Algorithm For Management of Dry Eye

Once the character of the dry eye condition is established, stepwise treatment can be pursued.
Source: Gary N. Foulks, MD, FACS

Click here for a larger view of this image.

A mainstay of dry eye management continues to be the use of topical lubricants or tear-stabilizing drops. Among the numerous formulations, including those with polymers of varying concentration and viscosity, are enhanced formulations that can be targeted to the specific tear disturbance most responsible for the problem.¹⁹

For the high-osmolarity, aqueous-deficient form of dry eye, hypotonic formulations or osmoprotective supplements can be used 4 or more times per day. For tear-unstable, lipid-deficient dry eye, supplements containing lipid or lipid emulsions can be more effective. Surface protective lubricants or lubricants containing hyaluronate can be recommended. Hydroxypropyl cellulose dissolvable inserts (Lacrisert) provide relief that is long lasting and usually well tolerated if inserted in the inferior cul-de-sac daily at bedtime. Oral omega-3 essential fatty acid nutritional supplements can improve both aqueous-deficient and evaporative dry eye symptoms, particularly in patients with a diet low in omega-3.^20,21

If symptoms and signs of disease are uncontrolled, progression to anti-inflammatory therapy should be considered using topical cyclosporine or a combination of cyclosporine and topical steroid with a rapid taper of the steroid over the ensuing 2 weeks. Response is usually seen within 2 months, although optimal anti-inflammatory effect may require 6 months of therapy with cyclosporine.

Recent data suggest that reduction of tear hyperosmolarity as measured by the TearLab osmometer is a good prognostic marker of response although improvement of symptoms may lag behind reduction in osmolarity by 1 or 2 weeks (personal communication from Michael Lemp, MD, May 2011). If symptoms occur while the patient is on topical cyclosporine therapy, pulse use of topical steroids may control the flare-up of disease. Although side effects of increased intraocular pressure and possible cataract formation limit the amount of steroid that can be used, the potential arrival to the market of mapracorat, a new selective glucocorticoid receptor agonist (SEGRA) promises greater flexibility in anti-inflammatory therapy of dry eye without the risk of elevated intraocular pressure.

If lid margin disease does not respond to lid massage following warm compress, daily topical azithromycin for a month or more often controls the MGD and associated inflammation.²² Systemic doxycycline (20 to 100 mg daily) is also effective in controlling MGD but may take 2 or more months of treatment for full effect.

Once inflammation is controlled, persistent signs and symptoms may warrant placement of punctal plugs. A variety of plugs is available. Ancillary treatment using a humidifier or protective eyewear to reduce tear evaporation can also be helpful.

Aqueous-deficient dry eye can also be treated with oral secretagogues: pilocarpine and cevimeline. Although the secretagogues are approved for dry mouth, they do stimulate tear production, albeit with side effects of sweating and occasional gastrointestinal upset. These agents are most often helpful in Sjögren’s syndrome–associated dry eye. When all else fails, severe cases may require the use of scleral contact lenses or autologous serum eyedrops.^23,24 As a last resort, lid surgery to reduce the exposure of the ocular surface can be done as either lid adhesion or tarsorrhaphy.

References

1. Lemp M, Baudouin C, Baum J, et al. The Definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). The Ocular Surface. 2007;5(2):75-92.
2. Smith J, Nichols KK, Baldwin EK. Current patterns in the use of diagnostic tests in dry eye evaluation. Cornea. 2008 Jul;27(6):656-662.
3. Nichols KK. Patient-reported symptoms in dry dye disease. Ocul Surf. 2006;4:137-145.
4. Lemp MA, Bron AJ, Baudouin C, et al. Tear osmolarity in the diagnosis and management of dry eye disease. Am J Ophthalmol. 2011;151:792-798 e1.
5. Sullivan BD, Whitmer D, Nichols KK, et al. An objective approach to dry eye severity. Invest Ophthalmol Vis Sci. 2010;51:6125-6130.
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12. Bron AJ, Smith JA, Calonge M. 2007 Report of the International Dry Eye Workshop (DEWS): Methodologies to Diagnose and Monitor Dry Eye Disease. Ocul Surf. 2007;5:108-152.
13. Manning F, Wehrly S, Foulks GN. Patient tolerance and ocular surface staining characteristics of lissamine green and rose bengal. Ophthalmology. 1995;102:1953-1957.
14. Bron AJ, Evans VE, Smith JA. Grading of corneal and conjunctival staining in the context of other dry eye tests. Cornea. 2003 Oct;22(7):640-650.
15. Foulks GN. What we have learned from clinical trials in dry eye therapy. In: The Ocular Surface: A Practical Guide to Clinical Management, ed Asbell PA and Lemp MA. Thiemes Medical Publishers, New York. 2006.
16. Nichols KK, Nichols JJ, Mitchell GL. The lack of association between signs and symptoms in patients with dry eye disease. Cornea. 2004 Nov;23(8):762-770
17. Pflugfelder SC. Management and Therapy of Dry Eye Disease. Report of the Management and Therapy Subcommittee of the International Dry Eye WorkShop. Ocul Surf. 2007;5:163-178
18. Geerling G, Tauber J, Baudouin C, et al. The international workshop on meibomian gland dysfunction: report of the subcommittee on management and treatment of meibomian gland dysfunction. Invest Ophthalmol Vis Sci. 2011 Mar 30;52(4):2050-2064.
19. Murube J, Paterson A, Murube E. Classification of artificial tears. I: Composition and properties. Adv Exp Med Biol. 1998;438:693-704.
20. Macsai M: The role of omega-3 dietary supplementation in blepharitis and meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106:336-356.
21. Rosenberg ES, Asbell PA. Essential fatty acids in the treatment of dry eye. Ocul Surf. 2010 Jan;8(1):18-28.
22. Foulks GN, Borchman D, Yappert MC. Topical azithromycin therapy of Meibomian gland dysfunction: clinical response and lipid changes. Cornea. 2010;29:781-788.
23. Stason WB, Razavi M, Jacobs DS, et al. Clinical Benefits of the Boston Ocular Surface Prosthesis. Am J Ophthalmol. 2010;149:54-61.
24. Kojima T, Ishida R, Dogru M, et al. The effect of autologousserum eyedrops in the treatment of severe dry eye disease: aprospective randomized case-control study. Am J Ophthalmol. 2005;139:242–246.