BLOG: Skin oil is bad for your eyes: A new theory to explain evaporative DED
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Key takeaways:
- A study set out to determine the effects of skin oil on tear function.
- Skin oil may infiltrate and contaminate tears by breaching an ineffective or absent meibomian oil border wall.
It’s a conundrum. Your patient has classic evaporative dry eye disease.
They have burning and tearing, fluctuating vision, and all of their symptoms get worse as the day goes on. The tear breakup time is 4 or 3 or 2, and they have inferior corneal staining. You check their tear osmolarity, and even that stacks up: It’s low in both eyes. Meibography shows profound gland obstruction. All that’s left is the tear oil measurement. Surely it will be less than 60. How can it be anything but?
Riddle me this: It’s more than 100.
Enter Tom Millar, PhD, from Australia, researcher in dry eye disease (DED) and inventor of TearView. Never heard of TearView? Until last spring, neither had I. We can be forgiven because when I was introduced to the technology by Tom, there were only 10 or so devices in the world, only one of which is in the U.S. (Doug Borchman at the University of Louisville). The prevailing theory to explain our patient above is that oil from the skin surrounding the eye somehow makes its way into the tear film, explaining the bountiful volume of oil in the otherwise ineffective tears of our patient. Tom and his co-authors set out to determine the effects of skin oil on tear function and to try to figure out why some people get skin oil in their tears while others do not.
Three subjects were studied (the authors), none of whom had a diagnosis of DED. Skin substances obtained by swabbing (SSS) were compared with acetic acid (to mimic pH of skin oil), normal meibum and castor oil. All four substances were applied to the ocular surface, the tear lake, the posterior edge of the lid and the base of the eyelashes. TearView and slit lamp analyses of fluorescein patterns were then carried out for all substances. Acetic acid had no effect on the tear film via any application. None of the study substances applied to the base of the lashes were detected in tears. All three of the remaining substances could be detected in the tears via the three other routes of application.
Meibum quickly diffused in the tear film in all cases. Castor oil could be seen as discrete “lenses” that spread across the tear film and otherwise had no effect. SSS placed directly on the ocular surface caused a darkening in both fluorescein and TearView images, localized staining, and severe discomfort in all three subjects. SSS applied to the tear lake caused an inferior darkening that gradually spread upward through the tear film and was mildly irritating. Of particular interest, SSS applied to the posterior lid margin stimulated the excretion of meibum while creating an otherwise similar effect to SSS applied to the tear lake.
Millar and his co-authors hypothesize that normal meibum on the lid margin forms a barrier that prevents skin oils from entering the tear film. Either the absence of meibum or the presence of abnormal meibum allows the ingress of skin oils. These non-resident lipids then produce the double insult of reducing the effectiveness of the tears (increased evaporation), while also directly causing pain.
Is this how evaporative DED works? Skin oil infiltrates and contaminates the tears by breaching an ineffective or absent meibomian oil border wall? Is low meibum concentration in the tear film the culprit, or is the presence of skin oils a necessary component? I’m pretty sure the answer is some version of “yes,” and I’m pretty sure that Dr. Millar and his co-investigators and worldwide teammates like Dr. Borchman would say it’s not yet clear. Makes you wonder about conjunctivochalasis a bit differently; is it air or skin oil or both?
Tip o’ the cap to all involved.
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