DEWS II: Redefining Dry Eye

Follow the links below to read the other articles from our coverage of TFOS DEWS II:

What Does “Dry Eye” Mean Today?

New Insights on How Dry Eye Happens

Modernize Your Methods of Dry Eye Care

PDF & Digital Versions

Having chaired the Tear Film and Ocular Surface Society (TFOS) Dry Eye Workshop (DEWS) II steering committee over the last 2.5 years, I witnessed firsthand the magnitude of the task we chose to undertake: to modernize the eye care community’s concepts and clinical practices surrounding this widespread yet poorly understood condition. The Workshop, comprised of 150 experts spanning 23 countries, reviewed thousands of published articles on dry eye disease (DED) to produce TFOS DEWS II, recently published in Ocular Surface. Coming a decade after the original TFOS DEWS report of 2007 and reflecting a body of scientific literature that had nearly doubled in that time alone, this new work—encompassing reports from 10 of the 12 TFOS subcommittees—updates the definition, classification and diagnostic methodology of dry eye disease; explores its causes, mechanisms and global impact; and offers an evidence-based consensus opinion on approaches to treatment.

The DEWS II definition of dry eye will move both research and clinical practice forward. It emphasizes that dry eye is indeed a disease—still a somewhat novel concept, even today—with multiple etiologies, but with the common aspect of a loss of tear film homeostasis due to tear film instability, hyperosmolarity, ocular surface inflammation and damage, or a combination of all three. Symptoms become the key element in the classification of dry eye. 

The DEWS II classification is a significant step forward in our understanding of dry eye. It presents a patient-based approach that begins with the presence or absence of symptoms, and then is further divided into strata based on the presenting symptoms’ correspondence (or lack thereof) with clinical signs, yielding four branches: the absence of symptoms with and without signs, and the presence of symptoms also with and without signs. Asymptomatic individuals without signs obviously do not have dry eye, while asymptomatic patients with signs may be at risk of developing symptoms following ocular procedures (e.g., refractive surgery) or other therapeutic interventions (e.g, systemic medications). Individuals with symptoms and signs are further separated into those with dry eye and those with other ocular surface diseases (e.g., allergy, ocular cicatricial pemphigoid). Individuals with symptoms and no signs may have neuropathic pain or a pre-clinical dry eye.

The Tear Film subcommittee report emphasizes that the tear film should be thought of in terms of a complex two-phase model with the lipid layer overlying a mucoaqueous phase, and that the entire tear film is involved in limiting evaporation.

The remaining subcommittee reports highlight several important areas, including the roles of sex, gender and hormones; epidemiology, with a notably global perspective; and pathophysiology of DED. The Pathophysiology report—the longest of the 10—emphasizes that the etiology is not linear, as in more conventional pathologies where an instigating event triggers a sequential cascade of processes that result in clinical manifestations, but rather a vicious, self-perpetuating circle. Tear hyperosmolarity is shown to be the hallmark of DED, functioning as both a catalyst and consequence of various steps along the circular process. There are many entrances into that circle that can result in DED signs and symptoms.

The Diagnostic Methodology report stresses the importance of using triaging questions to separate dry eye from other ocular surface diseases and then using tear break-up time (preferably noninvasive), osmolarity and ocular surface staining to identify a loss of tear film homeostasis.

TFOS DEWS II argues that management of dry eye should be aimed at restoring tear film homeostasis. Although the Management and Therapy report presents staged management and treatment recommendations, the heterogeneity of DED requires that clinicians manage and treat patients based on individual profiles, characteristics and responses.

The Iatrogenic report emphasizes that the clinician, as well as the patient, may be responsible for causing DED; with greater recognition of this, individual responsibility then becomes a factor in the overall approach toward hastening resolution. 

Finally, the Clinical Trial Design report provides guidelines on how to go about designing future studies that will have a better likelihood of getting therapeutic drugs and devices approved for clinical use in the decade ahead.

A key driver of our work was the goal of grounding the final TFOS DEWS II report in evidence-based medicine as a means of enabling broad adoption, free of influence or ambiguity. It is the fervent wish of all involved that this effort may translate into better clinical protocols that bring our patients sustained, long-term relief.