The Tear Film and Ocular Surface Society (TFOS) Dry Eye Workshop (DEWS) II report presents the state-of-the art in knowledge about dry eye disease (DED) and a wealth of information for both clinicians and researchers.
J. Daniel Nelson MD, served as chairman of TFOS DEWS II, and discussed aspects of the report—published as the July 2017 issue of The Ocular Surface. He called attention to a new scheme for patient classification.
“I encourage clinicians to look at the new classification scheme that I think is immensely helpful for identifying patients who should be managed with our classic treatments for DED and those in whom the classic treatments will not work,” said Dr. Nelson, external eye and corneal disease specialist, HealthPartners Eye Care, St. Paul, MN.
The first comprehensive report on DED was issued by the National Eye Institute/Industry Workshop on Clinical Trials in Dry Eye in 1995. The first TFOS DEWS published its report in 2007.
The 2007 TFOS DEWS definition of dry eye read, “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. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.”
The TFOS DEWS II definition states, “Dry eye is 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 hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.”
While the TFOS DEWS definition hinted that tear film instability, increased osmolarity, and inflammation accompanied DED, the TFOS DEWS II definition reflects subsequent research establishing those factors as key elements in DED pathogenesis. The TFOS DEWS II definition newly cites neurosensory abnormalities as having a causal role, he added.
The TFOS DEWS II Pathophysiology Report explains how tear film instability, hyperosmolarity, and inflammation give rise to and sustain DED. The report reiterates the Vicious Circle model for DED pathogenesis. In this model, tear film hyperosmolarity acts as the trigger for a cascade of events that leads to ocular surface damage and inflammation that exacerbate each other and maintain the pathogenic pathway.