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64 Surgeons see OSD treatment as integral to practice success G reater than 25% of cata- ract patients present with asymptomatic dry eye preoperatively, and 1 in 5 cataract patients present for their preoperative consultation symptomatic of OSD that re- quires intervention beyond artificial tears, according to the ASCRS Clinical Survey on ocular surface disease (OSD). Respondents say more than half— 53%—of their dry eye patients have a mix of meibomian gland dysfunction (MGD) and aqueous deficient dry eye disease (ADDE). Thermal lid expression and lid hygiene are the most common treatments for MGD; artificial tears and lubricants followed by oral omega-3 supplements are the most common treatments for moderate dry eye (Figure 1). A related survey found that queried cataract and refractive surgeons think it is very important to understand the etiology of their patient's OSD, whether it be MGD, ADDE, or both MGD and ADDE, and most are either very confident or somewhat confident in their ability to appropriately match treatments to the etiology and se- verity of OSD. Approximately 65% strongly agree that anterior segment imaging such by Marjan Farid, MD as topography and meibography can help guide therapy and patient education about OSD, and a notable 82% agree that treating OSD can benefit their surgical practice. When asked what they consider to be the greatest barrier to more consistently evaluating the tear film, lids, and mei- bomian glands in preoperative patients, the leading cause was not having access to advanced tear film or other diagnostic testing in their office, and the second most frequent factor was limited time during the preoperative work-up period. This supplement presents advice from leaders in our field on the diagnosis and management of dry eye. Editors' note: Dr. Donnenfeld practices with Ophthalmic Consultants of Long Island, is professor of ophthalmology, New York University, and is a trustee, Dartmouth Medical School. He has financial interests with AcuFocus, Allergan, Alcon, AqueSys, Avedro, Bausch + Lomb, Beaver-Visitec, CRST, Elenza, Foresight, Glaukos, Icon Biosciences, Johnson & Johnson Vision, Kala, Katena, LacriPen, LensGen, Mati Pharmaceuticals, MDback- line, Merck, Mimetogen, Mynosys, NovaBay, Novaliq, OcuHub, Ocular Therapeutics, Odyssey, Omega Ophthalmics, Omeros, Oyster Point, Pogotec, PRN, RPS, Shire, Strathspey Crown, Sun, TearLab, TLC Laser Centers, TrueVision, Versant Ventures, Visionary Ventures, and Zeiss. He can be contacted at ericdonnenfeld@gmail.com. Identifying the underlying causes of ocular surface disease for more accurate diagnosis and treatment Supplement to EyeWorld October 2018 digital.eyeworld.org e news magazine of the American Society of Cataract & Refractive Surgery by Eric Donnenfeld, MD The role of tear film instability, inflammation, hyperosmolarity, and neurosensory abnormalities in OSD D ry eye disease (DED) is defined by the Tear Film & Ocular Surface Society (TFOS) DEWS II Report as "a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperos- molarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles." This follow-up re- port represents insights from 150 research- ers based on knowledge accrued since the original DEWS findings were promulgated a decade ago. DEWS II stresses the pivotal role of hyperosmolarity in ocular surface disease (OSD) and suggests that the earlier the diagnosis and management of OSD, the better the outcome. The goal of treatment is to break the cycle of inflammation and restore tear homeostasis. Mechanisms and management The central mechanism of DED is an evap- orative water loss that leads to hyperosmo- lar tissue damage and loss of homeostasis. Direct or indirect insult to the ocular surface via inflammation can cause loss of epithelial and goblet cells, and this results in decreased surface wettability with rapid tear breakup time, which initiates tear film instability and amplified hyperosmolarity. DED can be initiated by a variety of causes including Sjögren's syndrome, rheumatoid arthritis, lupus, decreased an- drogen levels in postmenopausal women, MGD resulting in a poor lipid layer of the tear film, allergy medications, and contact lens wear. LASIK and other ocular surgeries that cut corneal nerves can exacerbate pre-existing subclinical dry eye disease as well. 1 All of these are capable of triggering a cascade of pro-inflammatory cytokines resulting in hyperosmolarity; thus the goal of OSD treatment is restoration of the tear film homeostasis. 2 Visual fluctuations due to increased tear breakup time (TBUT) and the resulting hyperosmolarity are one of the most common, and often overlooked, symp- toms of DED. Other factors that influence hyperosmolarity include the lipid layer thickness, palpebral aperture width, blink interval, tear film stability, environmental conditions, and body hydration. When a hyperosmolar tear film is not treated and homeostasis is not reached, epithelial cells recruit inflammatory cells to the ocular surface, exacerbating inflam- mation and causing reduced expression of glycocalyx mucins. This leads to ocular surface staining and rapid TBUT, as well as apoptosis of surface epithelial cells and loss of goblet cells. The DEWS II difference DED has traditionally been divided into primary aqueous deficient dry eye or evaporative dry eye. DEWS II indicates that these are not mutually exclusive. In fact, up to 85% of DED patients who have aqueous deficiency have some degree of meibomian gland dysfunction (MGD) as well. continued on page 65 64 Primary therapies and treatments for managing moderate dry eye disease 100% 80% 60% 40% 20% 0% AT/ lubricants Oral omega-3 Cyclosporine Lifitegrast Punctal occlusion 94% 63% 53% 58% 54% Figure 1. Respondents use various treatment options to treat dry eye disease.

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