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Your faithful dry eye doc tackles DEWS II
The report contains several useful concepts upon which the more practical suggestions are built.
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First, a public service announcement: Do not read the Tear Film and Ocular Surface Society Dry Eye Workshop II report.
Seriously, do not do it. Only a very select few should be asked or required to do so. I believe the list begins and ends with the 150 contributors, anyone who is being paid to do so (conflict of interest disclosure: Ocular Surgery News just doubled my per column fee!*) and naughty ophthalmology residents who are in time out. Seriously, there is simply no reason to wade through all 400+ pages of this behemoth (and I thought the CEDARS/ASPENS opus by Milner and colleagues was thick at 48 pages). Instead, you should do what I did and read the excellent executive summary, also published by TFOS.
Or just read my column.
An incredible amount of time and energy was obviously put into the revised and updated definition of dry eye disease (DED). It is actually poetic, each word parsed and lovingly sorted into what is almost a complete statement of everything there is to know in the diagnosis and treatment of 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.” You could make a case that they should have simply published this, dropped the mic and walked off stage.
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Read about FAQs related to tear osmolarity. Link here.
Unwilling to leave us with a Zen koan rather than a latter-day Gutenberg Dry Eye Bible, the 150 scholars forged on, so I guess I will, too. Before doing so, however, it should be stated that the majority of the concepts and guidelines contained in DEWS II are already standard fare in DED clinics all over the world. This should not be taken as a significant knock on their efforts; any comprehensive tome in any area of medical care should be expected to lag behind the cutting edge.
Looking from 30,000 feet, there are several useful concepts upon which the more practical suggestions are built. DED is partitioned into the now familiar aqueous deficient and evaporative varieties. DEWS II talks about these two entities as occurring along a continuum, almost as if the surface of the eye is afflicted by some degree of each along a sliding scale. In reality, each is probably better visualized individually as a column that rises and falls, elevating or depressing the “Hill of Sorrow.” Still, the emphasis on the critical role being played by evaporative disease and the imperative to treat it are strengths of the new document.
Inflammation takes its proper position as the underlying pathophysiologic cause of all the bad things associated with DED. It remains unclear whether there is any single cause of the inflammation, but the need to reduce inflammation when present is clearly stated throughout the summary. Having said that, it is curious that there is no mention of directly measuring inflammatory markers such as MMP-9, let alone some of the less well-known (for the moment) markers such as Ila-1.
DEWS II has strong positions on the objective findings that characterize DED. A rapid tear breakup time, osmolarity that is either elevated or shows intereye asymmetry, and ocular surface staining with either fluorescein or lissamine green in typical patterns are all diagnostic of DED. I find it intriguing that the authors declare rather firmly in the executive summary that rapid tear breakup time is the cause of elevated tear osmolarity, and it is the abnormal osmolarity that causes the inflammation responsible for tear dysfunction. While speculative, I do think that this is a more elegant way to explain how it is that inflammation in meibomian glands begets inflammation on the surface of the eye; an angel cries every time I tell a patient that eyelid inflammation “spills over” onto the eye.
Perhaps the hottest spot in all of DED is the ciliary ganglion, sometimes labeled the “trigeminal ganglion,” and this is the one area in which DEWS II is breaking ground. So-called neurogenic pain occurs when pain fibers are firing in what appears to be the absence of a clear pathologic stimulus. Anyone who takes care of DED patients has people sitting at the slit lamp who look completely normal. Every single test you run comes up negative, and for the life of you, it is impossible to find a single punctate spot that stains.
Even with (gulp) rose bengal.
Underlying the pain felt by these poor folks is dryness-induced nerve damage on the ocular surface. This is probably both caused by inflammation as well as being an inflammation trigger in its own right. Remember my introduction to neurostimulation column in which I copped to forgetting most of the trigeminal pathways innervating the “tear functional unit?” Here is where I admit to never knowing that a cornea has “cold terminal” nerve endings. Neurogenic pain appears to originate in abnormal activity in these cold terminals, resulting in repetitive aberrant activity along the course of the trigeminal nerve. Sadly, treatment probably consists of a referral to a pain specialist.
What, then, of treatment of DED? Are there any pearls to be found in DEWS II when it comes to treating our DED patients? As with most encyclopedic examinations of a disease state in all of medicine, DEWS II largely confirms what those of us who treat DED patients have been doing for at least 5 years: target the type of DED that appears to be the dominant type at the moment first, usually by attacking inflammation. Once again, the authors of this opus turn a rather elegant phrase here when they assert that the treatment goal is to “restore homeostasis.” Lovely English, that. There must be at least one Williams College grad among those 150 contributors.
At the end of a very long day, DEWS II does a fine job assembling the current state of knowledge about DED. The authors have not missed anything of consequence, and in their section on neurogenic pain associated with DED, they introduce a new and difficult-to-understand type of DED. Again, if you are like me, you could admire the poetry of the definition of DED, skip the 400+ pages of the unabridged version, and just read the most excellent executive summary.
And get on with the work of “restoring homeostasis.”
*My starting salary before my big raise was $0.
- For more information:
- Darrell E. White, MD, can be reached at SkyVision Centers, 2237 Crocker Road, Suite 100, Westlake, OH 44145; email: dwhite@healio.com.
Disclosure: White reports he is a consultant to Allergan, Shire, Sun, Kala, Ocular Science, Rendia, TearLab, Eyevance and Omeros; is a speaker for Shire, Allergan, Omeros and Sun; and has an ownership interest in Ocular Science and Eyevance.
Editor's note: This article has been updated at Dr. White's request to remove the word "erroneously."