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J. Daniel Nelson, MD, chair of The Tear Film and Ocular Surface Society Dry Eye Workshop II, highlights a new scheme for patient classification.
By Cheryl Guttman Krader; Reviewed by J. Daniel Nelson, MD
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.
TFOS DEWS II retains the division of DED into aqueous deficient and evaporative subtypes and underscores that each can lead to the other so that they frequently co-exist. However, TFOS DEWS II also introduces a new classification scheme that ultimately allows the identification of patients with DED who are likely to respond to available treatments.
The classification scheme first considers whether a patient presents with symptoms.
“The fact that patients can have symptoms of dry eye without clinically apparent abnormalities of the ocular surface has been known for some time and increasingly appreciated in the past few years,” Dr. Nelson said. “The members of TFOS DEWS II thought this was a key issue.”
In the classification scheme, patients with symptomatic and asymptomatic presentations are further broken down based on the presence or absence of signs of ocular surface disease (OSD). Asymptomatic patients with no signs are considered normal and require no treatment. Asymptomatic patients with signs of OSD may either be in a prodromal stage and predisposed to develop dry eye or might have a neurotrophic condition such that they do not experience sensations from existing ocular surface damage.
The classification scheme shows that symptomatic patients with no signs of DED could either be in a preclinical state or have a neuropathic condition rather than dry eye. Pain management is the appropriate intervention for the latter patients.
One of the challenges clinicians have faced has been in the care of patients who complain bitterly of symptoms that are associated with DED but who have no signs of OSD. TFOS DEWS II recognizes that the symptoms in these patients probably have a neurogenic etiology, and they need to be treated differently, he said.
Symptomatic patients with signs of OSD may have classic DED or some other OSD that has overlapping clinical features, such as allergy or infection. Triaging questions should enable the differential diagnosis in these cases.
Patients who are determined to have DED are then subtyped according to whether they have an aqueous deficient, evaporative, or mixed condition and managed according to the categorization.
The TFOS DEWS II Management and Therapy Subcommittee report presents a severity-related management algorithm comprised of four steps. The recommendations represent evidence-based consensus opinion-the report notes that there is a relative lack of Level 1 evidence to support therapeutic recommendations.
“It is also unfortunate that the treatments for DED have not changed drastically since TFOS DEWS,” he said. “There is, however, greater understanding of the pathophysiology of DED and a greater interest, from clinicians, researchers, and patients alike, that has stimulated further research and the development of novel therapies and better ways to diagnose DED.”
The inclusion of an Iatrogenic Dry Eye Subcommittee report is new in DEWS II. By emphasizing the roles played by patients and clinicians in causing DED, it also has implications for management.
“Common iatrogenic causes of DED include cosmetics, contact lens wear and use of topical and systemic medications,” Dr. Nelson said.
J. Daniel Nelson, MD
Dr. Nelson is a consultant to Santen and TearSolutions and has a personal financial interest in TearSolutions.