First discussed in 2002, eye care researchers now have approximately 2 decades of data on lid wiper epitheliopathy (LWE), a condition linked to dry eye disease (DED) that is characterized by lid margin staining. And while it’s clear that LWE is a complex issue likely related to microtrauma from excessive friction between the eyelid margin (lid wiper) and the surface of the eye or contact lens (CL) wear, questions remain as to how physicians can prevent it from happening—and how can they best treat it, once it occurs.

Researchers report an association between LWE and CL wear. In fact, LWE’s reported prevalence in symptomatic CL wearers is 67% to 85%, according to a study by Christopher W. Lievens, OD, MS, FNAP, FAAO, chief of Internal Clinics at The Eye Center and professor at the Southern College of Optometry in Memphis, TN, and colleagues. For asymptomatic CL wearers, that number was lower: 13% to 32%. Those numbers, however, are likely not representing the complete picture of how many people have it, Dr Lievens says, because he only recently established a diagnosis methodology that should help streamline case recognition and, thus, possibly increase cases. He and his colleagues’ recent study, “Natural course of lid wiper epitheliopathy (LWE) in symptomatic contact lens wearers,” published in Contact Lens and Anterior Eye, included that methodology.

It looked at the time course of LWE in 21 symptomatic CL wearers after 1 day (6–10 hours) of daily disposable CL use, the following day post-CL removal, and a week after stopping CL wear. Before CL wear (Visit 1, V1), LWE staining was assessed with semi-automated analysis after 2 drops of 1% lissamine green (10 μL) were instilled to the superior bulbar conjunctiva. They repeated LWE measurements after 6–10 hour of continuous CL wear (Visit 2, V2), post-CL removal the following day (Visit 3, V3), and following 1-week CL discontinuation (Visit 4, V4). Ocular symptoms were measured using the SPEED-8 questionnaire and a set of 0 to 100 visual analogue scales (VAS).


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Dr Lievens and colleagues found that LWE had no significant changes after 6 to 10 hours of continuous CL wear (P =.536), post-CL removal the following day (P =.677), or after 1-week of CL discontinuation (P =.478). They did find significant improvement in symptomatology between V1 and V2 (SPEED-8, P <.01) and improvements in the 0 to 100 VAS scores between V2 and V4 for average daily dryness (P <.01), end-of-day dryness (P <.01), and frequency of end-of-day dryness (P <.05). 

Dr Lievens spoke with Optometry Advisor about his work on this topic, including this study, and his years of research into LWE. 

1. What’s the mechanism of how LWE develops?


In essence, what we’re talking about is the science of tribology. Tribology is known as the science of friction, lubrication, and the determination of what occurs when 2 surfaces slide against one another. Tribology could be a key factor in dissecting the issues that surround and confound dry eye in patients as well as CL discomfort and intolerance. Specifically, it is this issue that is likely the causative underlying factor that leads to LWE. The human eye blinks repeatedly, every waking day, at high velocity. When 2 surfaces (such as the eyelid and ocular surface) are in contact and then rub against one another, some form of friction is the result. When friction is low, the surfaces are considered to be lubricious. At a microscopic or macroscopic level, when this friction causes any removal of either surface material or any deformation of either surface because of the mechanical action, the result is termed “wear.”  

The ocular structures of the eyelids and surface epithelial cells are soft structures, and their microscopic interactions are not akin to sliding hard materials against one another. Instead, the ocular surface interaction is facilitated by the presence of hydrophilic polymer brushes. In patients with CL intolerance and dry eye, there could be insufficient brush-to-brush lubrication and/or altered tear film components and viscosities.  

Intuitively, the ocular surface should have a very low coefficient of friction and be at least as lubricious as other parts of human anatomy that exhibit a great deal of movement (i.e., nonarthrodial joints). The first measurements of human corneal tissue in multiple test solutions quantified the coefficient of friction for the cornea and confirmed its low levels (range: 0.006–0.015). Many factors contribute to normal ocular anatomy to prevent wear and insult. Ocular surface health is maintained by tear film stability, normal surface qualities and components, load and force of the eyelid in apposition to the globe, and eye lid anatomy and dynamics. When these anatomies function normally and in concert, there is an assurance of lubricity and ocular surface health. When this is not the case, lubricity is dysfunctional, and friction, wear, and microtrauma can result.

So whenever the anatomies are in disarray, and whenever the tear film is in disarray, we have potential problems with the tear film, then problems with lubricity, problems with ocular health, and LWE can occur. There are lots of reasons why this condition could be present which suggests that it is present at pretty high prevalence. Just like the reasons why patients can have dry eye or CL intolerance is multifactorial, LWE likely is as well. 

2. Do we know how many people have LWE — and what is the diagnostic methodology you created that helps determine that?

My early work was to come up with a consistent methodology to uncover LWE, because up until now, there wasn’t one. That’s been a major challenge when trying to interpret all of the published research. Because there was not a consistent way to identify it. So [the amount of people with LWE is] difficult to pinpoint, but hopefully, with many of us now on the same page with how to identify it, we can come up with these numbers in short order.

As for diagnostic methodology, a lot of things that we do when examining the anterior of the eye call for the use of vital dyes. Sodium fluorescein, for example, is a really common dye to use, and it can be used to identify the lid wiper as well. The problem with sodium fluorescein, though, is it stains lots of things. And when we’re looking at, let’s say, the upper lid wiper, we need to evert the lids, or flip it inside out once dye has been instilled, and sodium fluorescein pools in many locations. So if I’m a clinician and I put in sodium fluorescein and evert the lid, my visual attention as a clinician is actually not going to go to the lid wiper, it’s going to the lid tarsus, the inside of the lid fold since there’s so much more visually interesting things there. That’s probably why this whole condition has gone unmentioned for decades [before 2002], because visually, it’s not where our eyes are directed. 

Though you can use sodium fluorescein, we’re recommending using lissamine green. This is not a system by which we instill a single drop and then immediately examine the eye. Instead, this approach is to put in a drop, wait 3 minutes, and then take a look. When the patient has LWE, that tissue stains green [in those 3 minutes], and the remainder of the lid doesn’t. When you evert the lid, after the drops of dye, your eyes go right to the area of interest and nowhere else. That’s a really optimal situation when taking care of a patient on a busy patient day; you want your eyes immediately to go to the area of question and not to be confounded by other areas of interest.

3. Looking at your recent study, “Natural course of lid wiper epitheliopathy (LWE) in symptomatic contact lens wearers,” temporarily stopping the use of CL did not lead to resolution of clinical signs of LWE — are there any potential therapeutic management options for patients dealing with LWE right now?

Categorically, the treatment for dry eye falls into several categories. They include: Tear supplements and lubricants, tear retention agents, tear stimulants, biological tear substitutes, anti-inflammatory therapy, essential fatty acids, treatment of meibomian gland dysfunction, and environmental strategies. Because of the lack of full understanding of LWE, some of the aforementioned therapies have been proposed and studied already. Not all of them would be likely to have direct impact and depending on whether or not CL are in use, the strategies would differ. Additional strategies might include the use of contemporary artificial tears, corticosteroids, punctal plugs, meibomian gland treatment, CL refitting, longer CL discontinuation, and ways to improve blinking.

Treatment strategies for LWE would be in the exact same buckets that we’re trying to use for dry eye CL intolerance. Ultimately, it’s not just that LWE is this quandary — dry eye and CL intolerance haven’t been solved yet either. It’s just all in this mix of conditions, in which there’s lots of reasons for them. What I tell people when I talk about conditions like dry eyes, ocular surface disease, CL intolerance is, these conditions are all multifactorial and LWE could be as well. Whenever you have a multifactorial disease state, typically, there’s no silver bullet, there’s no single thing that solves the problem for every patient. What that means is that there are several different strategies to employ. Beyond hypothesis, it’s very difficult today to know which treatment strategies are going to be the most impactful. We’re at the infancy of trying to gain a better understanding of this finding, and really what it means for patients with CL-related issues and ocular surface disease.

4. Can ODs get patients back to being comfortable in contact lenses after LWE?

Hypothetically, the relief from an intervention that can relieve or reduce friction comes with all the plausible treatment strategies that we just discussed. Anything that we can do to improve lubricity and relieve friction has the potential to remedy the trauma on this anatomy and deliver the patients less symptoms and more comfortable CL wear. 

5. Is there any way to prevent LWE from becoming a recurring problem?

Once the LWE is effectively treated, it is unknown when it might recur. I would propose that if a small or pilot study identified 1 or more “treatments” for LWE that got it to resolve, it would be of great interest (at least to me), when the LWE would be reinitiated if nothing else were to change (and the treatment stopped). Today, this is still an unknown and is a definite opportunity for future work. Once we figure out how to get it to resolve, then the next unknown is, when it might reoccur. Maybe LWE resolution requires a longer discontinuation from contacts, a quality artificial tear, or a refit into a better, more lubricious lens. Once we are able to note improvement, it would be interesting to allow the patient or research subject to return to what they were doing prior to study, and then watch them closely and see how long does it take for the LWE to reoccur. Does it return in 24 hours, does it take a week, does it take a month, does it take minutes for the friction trauma to come back? Today, this is just absolutely an unknown, and definitely an opportunity for future work for me. 

Reference

Lievens CW, Norgett Y, Briggs N, Allen PM, Vianya-Estopa M. Natural course of lid wiper epitheliopathy (LWE) in symptomatic contact lens wearers. Cont Lens Anterior Eye. Published online October 26, 2021. doi:10.1016/j.clae.2021.101529