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5 things you need to know about TFOS DEWS II
July 26th, 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.
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.
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.
. 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.
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