5 things you need to know about TFOS DEWS II

July 26, 2017

With great anticipation, the updated report of the TFOS Dry Eye WorkShop (DEWS II) was released last week. The first DEWS report was released in 2007.

With great anticipation, the updated report of the TFOS Dry Eye WorkShop (DEWS II) was released last week. The first DEWS report was released in 2007.

Get your copy of TFOS DEWS II

Here are five things you need to know about TFOS DEWS II.1

1. There is a revised definition of dry eye disease (DED).

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.”

Key points to note in this definition are the addition of the phrase “loss of homeostasis” and neurosensory abnormalities, which contribute to the common mismatch between signs and symptoms.

Related: New TFOS DEWS II report redefines dry eye

2. Meibomian gland dysfunction (MGD) and Sjögren and non-Sjögren lacrimal disease remain leading causes of evaporative and aqueous-deficient DED; however, many hybrid forms of DED exist.

The core mechanism of DED is tear hyperosmolarity-the hallmark of the disease. Hyperosmolarity damages the ocular surface both directly and by initiating inflammation. These sequelae lead to a cycle of events termed the “vicious circle.” The vicious circle explains how ocular surface damage is initiated and self-perpetuated in DED.

Tear hyperosmolarity, with inflammatory mediators, may induce DED symptoms and cause damage to epithelial cells, surface microvilli, barrier function, the glycocalyx, and goblet cells. Epithelial cell damage, lipid layer and blinking abnormalities, defective glycocalyx, loss of gel mucin, and reduction in tear volume may result in loss of lubrication between the globe and eyelids, resulting in increased friction and dry eye symptoms.

 

3. The role of increased friction in DED and its subsequent sequelae deserves further investigation. Inflammation of the ocular surface can cause inhibition of lacrimal secretion and loss of epithelial barrier function at the ocular surface.

Related: Constructing the TFOS DEWS II report no easy task

4. Considering neuropathic pain in DED, TFOS DEWS II reports that it has been found that cold thermoreceptors continuously discharge nerve impulses at the normal ocular surface temperature, responding to warming or cooling and to osmolarity increases.

This likely contributes to reflex control of basal tear production and blinking. Studies to date suggest potential merit in exploring treatment strategies involving cold receptors to manage DED symptoms.

Restoration of tear film homeostasis is the ultimate goal in DED management. This involves breaking the vicious circle of the disease. Determining whether the major cause(s) of an individual’s DED pertains predominantly to aqueous tear deficiency or to evaporation-or both-is critical in helping select the most appropriate management strategy.

TFOS DEWS II researchers created a clinical algorithm for DED, which you can find in the downloadable report.

 

5. Still in need of discovery in DED, novel approaches and better-validated instrumentation and techniques are crucial to more critically assess DED and to link underlying causes in an individual to the most suitable therapies to manage his DED.

Although staged management and treatment recommendations in DED have been suggested, the heterogeneity of the DED patient population mandates that practitioners manage and treat patients based on individual profiles, characteristics, and responses.

Finally, DEWSII noted that the economic impact of DED primarily results from indirect costs related to decreased work productivity.

Related: Understanding the role of inflammation in dry eye

Dry eye experts weigh in

We asked other dry eye thought leaders their first reactions to the TFOS DEWS II report.

Milton M. Hom, OD, FAAO, FACAAI(Sc)

Optometry Times Editorial Advisory Board Member

In the old days, we read textbooks. In the digital age, books have been replaced by open-access consensus panels. Both are essentially reviews of the current and past knowledge on a particular subject.

The most recent one for dry eyes is groundbreaking TFOS DEWS II. It follows on the footsteps of other great consensus dry eye panels, most notably the original TFOS DEWS report.

What have I learned? Dry eye is the new multi disease: multi-factorial, multi-colored, multi-cultural, multi-flavored.

Now I know that both signs and symptoms are needed to officially diagnose dry eye. How about signs without symptoms? Not dry eye. Symptoms without signs? Not dry eye, either.

According to TFOS DEWS II, we have two new buckets for dry eye: predisposition to dry eye and pre-clinical state. Signs without symptoms is predisposition to dry eye, and symptoms without signs is pre-clinical state. Try explaining that to a patient.

I’m absolutely certain TFOS DEWS II will be the new standard to follow. Hats off to TFOS for a great accomplishment.

 

 

Leslie O’Dell, OD, FAAO

Optometry Times Editorial Advisory Board Member

Dry eye symptoms remain one of the tops reasons patients seek eye care. Dry eye is a challenging disease to diagnose and treat due the complexity, variability, and chronicity of the disease.

TFOS DEWS II provides the clinician with a step-wise approach to diagnosis and treatment based on thousands of studies reviewed over the two-to-three year time period in which is document was created.

The diagnosis section lays the groundwork with which to base our exams, including triaging the patient to differentiate dry eye disease from other ocular surface conditions. It then goes on to guide the clinician on the best methods for uncovering both the signs and the symptoms of dry eye.

Utilizing a validated questionnaire with the Dry Eye Questionnaire 5 (DEQ-5) or Ocular Surface Disease Index (OSDI) is recommended and an easy addition to the exam. T

FOS DEWS II then states that non-invasive tear break-up time (NIBUT), tear film osmolarity, or ocular surface staining patterns of the corneal and conjunctiva should be used for the clinical signs of DED with easily defined results. Additional testing is required from here to better classify the subtype of disease (aqueous vs. evaporative) as well as the stage of disease to determine the patient's best treatment to optimize outcomes.

Proper diagnosis is critical to improve treatment outcomes. The sequence of testing used is important as well as discussed in TFOS DEWSII, with non-invasive testing to be performed first, followed by more invasive testing.

What I am going to change after reading TFOS DEWS II? My intake survey and utilization of NIBUT.

Related: How to use tear osmolarity to help treat dry eye disease

 

 

Bill Townsend, OD, FAAO

Optometry Times Editorial Advisory Board Member

The release of TFOS DEWS II report is a welcome event for those of us who have interest in and manage dry eye disease. The broad spectrum of contributors from many diverse professions and geographic locations speaks to the universality of dry eye disease. It reminds us that dry eye disease is indeed a global concern. TFOS DEWS II reflects some of advancements that have been made in our understanding of DED since the release of TFOS DEWS I in 2007.

Many of the factors underlying DED as reported in TFOS DEWS I are also found in TFOS DEWS II. These include:

• Ocular symptoms

• Inflammation

• Hyper-osmolarity

• Damage to the ocular surface

TFOS DEWS II contains important additions: loss of homeostasis and neurosensory abnormalities. The concept of failure to maintain homeostasis is widely accepted as an underlying factor in many systemic disease states, notably diabetes, hypertension, and thyroid disease. The model of the “lacrimal functional unit” has helped us to understand how loss of homeostasis underlies virtually all forms of DED.

Interestingly, “visual disturbances,” which was part of TFOS DEWS I, was not included in TFOS DEWS II. This concept is inherent in the “lacrimal functional unit” model. Visual disturbances such as blurring are common findings in dry eye and likely fall within the general category of “neurosensory abnormalities.” I mention this only to emphasize that when patients report blurring, DED is often the underlying cause and should be address in the differential. 

The TFOS DEWS II report is available for download at no cost, and I encourage my colleagues to read it. It sheds important light and offers new evidence about on one of the conditions that ODs commonly encounter. Kudos to this distinguished group for their work leading to this publication. I especially congratulate the numerous ODs who participated in this project, and special thanks for their efforts on behalf of eye care and our profession.

Related: Understanding the link between MGD and OSD

 

 

Scott Schachter, OD

Optometry Times Editorial Advisory Board Member

TFOS DEWS II report is here. It will take some time to get through and absorb, but I have a few initial thoughts.

I am happy to see in TFOS DEWS II:

• The recognition that dry eye is “loss of homeostasis” can help guide our strategies in treating our patients. Many extrinsic and intrinsic factors can disrupt the tear film. We hope to return homeostasis to the lacrimal function unit

• Acknowledgment of the neuro sensory component, our “pain without stain” patients, can lead to future research and perhaps better treatment options for these patients who are frustrated and frustrating at the same time

• Recommendations that we investigate the seemingly increased prevalence of dry eye disease among youth and look into device use as a potential cause

• Clarify that evaporative dry eye (EDE) and aqueous-deficient dry eye (ADDE) are not mutually exclusive. This clarification will encourage practitioners to treat dry eye disease more completely and may lead to better outcomes

Related: Dry eye checklist may help ODs treat patients more efficiently

Reference

1. TFOS International Dry Eye WorkShop (DEWS II). Ocular Surf. 2017 Jul;15(6):269-650.