Addressing the Multifactorial Nature of Dry Eye Disease in Clinical Practice

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Interview has been edited for readability.

AJMC®: What percentage of your practice is dedicated to treating dry eye disease (DED), and has this changed over time?

Devries: Approximately 90% of my practice is dedicated to treating DED and other ocular surface conditions. This high percentage is driven by my involvement in a large medical-surgical group that prioritizes presurgical treatment to optimize patient outcomes. Over time, the treatment landscape for DED has evolved significantly, largely due to the industry’s growing focus on addressing the unmet needs of patients with DED. This has led to advancements in diagnostic testing and the introduction of new FDA-approved treatments, including both pharmaceuticals and procedures. These developments are crucial for managing the chronic, progressive nature of DED and helping to mitigate both current inflammation and the damage caused by the disease.

AJMC: As an optometrist, you are often the first point of contact for patients with DED. How do you determine when to refer a patient to an ophthalmologist?

Devries: As a medical optometrist, I often manage advanced DED. But from a primary care perspective, referral decisions are typically based on the provider’s scope of practice, available resources, and clinical comfort level.

Optometry’s scope has expanded considerably, and many optometrists are well equipped to manage a wide range of DED cases. Those with the appropriate training and resources should feel empowered to treat these patients within their practice. However, when a provider lacks access to certain diagnostics or therapeutics—or doesn’t feel confident managing more advanced or refractory cases—that’s the appropriate time to refer to a specialist, whether a medical optometrist or an ophthalmologist.

The decision to refer varies by practitioner and practice model. Some optometrists focus primarily on vision correction, while others offer full-scope medical eye care, including presurgical and disease management. Ultimately, the key is recognizing when a case exceeds the capacity of the practice and ensuring timely referral to prevent progression and optimize outcomes.

AJMC: What role does inflammation play for your patients with DED?

Devries: Inflammation is a central factor in DED, but it is not the initial cause. The disease often begins with evaporative loss, which can lead to inflammation and, in some cases, aqueous deficiencies. When assessing these patients, I measure inflammation using a point-of-care test for MMP-9 (matrix metalloproteinase-9), which helps confirm the presence of inflammation. Other clinical signs—such as rapid tear breakup time, red eyes, and unhealthy eyelid margins—further indicate inflammation.

Most current treatments focus on addressing inflammation, but newer therapies are emerging that target underlying factors such as reducing evaporative loss before they are measurable. If evaporation exceeds the tear supply, inflammation can be triggered over time. Since 2020, a tremendous increase in screen time during the pandemic contributed to reduced blink rate, further exacerbating evaporation and eventually driving inflammation in a growing number of patients.

AJMC: What is the distribution of aqueous-deficient dry eye (ADDE), evaporative dry eye, and mixed etiology DED among your patient population? How do you determine the underlying cause?

Devries: When I evaluate a patient I want to make the determination: What is the most predominant underlying etiology? Is it aqueous deficiency? Is it evaporative loss? Is it inflammation? And what I’ve found through my many years of practice is that patients are on a continuum of how they advance, and different patients will advance at different times [with different presentations]. I really believe that most patients will have various components of both aqueous evaporative loss and inflammation. It just depends on where they [are on the DED continuum]. And to this point, I bring up that the most consummate patient with ADDE would be [one who] has Sjogren syndrome, where they have dry eye, dry mouth, and an autoimmune condition. That’s aqueous deficient, because they have Sjogren syndrome. But those patients also have tremendous evaporative loss, because the meibomian glands that produce the oil to help slow down the evaporation are always affected in [patients with advanced Sjogren syndrome]. So, I really believe that the patients are on a continuum, and what I try to do is [determine the particular therapeutic medication or procedure that will have the most rapid effect on symptoms and signs. However,] it doesn’t mean that I will just go exclusively with that treatment. I may have to consider other modalities that [address] evaporative loss and involve taking care of some of the damage that has been done and the underlying cause.

What we find quite often—and this is newer research—is that there is a tremendous component of inadequate lid seal causing evaporation during the night [that can lead to structural changes], leading to increased inflammation. One of the first questions I’ll ask that patient is, ‘How do your eyes feel first thing in the morning?’ If [the answer is] anything other than ‘that’s the best time of the day for me’ or ‘my eyes feel fine,’ then we have to consider the fact that there is an inadequate lid seal, that the lids are not closely in apposition [while sleeping]. The category is inadequate lid seal, which [may include the more advanced form called] nocturnal lagophthalmos, [as well as] lid lag as a result of a postsurgical blepharoplasty [or an aging change in which the eyelid tissue loses] elasticity and no longer seals. The majority seems to have an inherited trait, as many of these patients report that they were told that their eyes didn’t completely close as a child. We are finding that up to 75% of the patients with DED who are recalcitrant to drugs have that component of inadequate lid seal.

Just like any other major organ system, the eyes can compensate for years, and they appear to be fine. It’s when they stop compensating that those patients become much more symptomatic, and DED starts to affect their overall quality of vision and quality of life.

AJMC: How do you address inadequate lid seal?

Devries: Addressing inadequate lid seal in DED remains a challenge, as effective therapeutic options have been limited. Over the years, practitioners have relied on ointments, goggles with moisture, and various adhesive strips. However, ointments can be messy, and goggles may increase intraocular pressure or distort the cornea. Tapes often cause irritation or lash loss. Recently, eyelid strips have been commercialized; they are latex free, hypo­allergenic, and porous, and they help hold the lids together at night. While these strips are effective, patients must apply them correctly, and I often recommend starting with 1 eye at a time to avoid overwhelming the patient by sealing both eyes.

By addressing the lid seal issue, we can considerably improve corneal health, allowing standard treatments like immunosuppressive drugs or low-dose steroids to be more effective. It’s important to educate patients on this challenge and emphasize the role of their active involvement in using the treatment. Identifying and managing the inadequate lid seal up front leads to better overall treatment outcomes.

AJMC: How do you approach treatment selection for patients with primarily evaporative versus aqueous disease? And how does this approach impact treatment adherence and clinical outcomes?

Devries: There are a lot of decisions that need to be made when you first see a patient with DED. A patient with predominantly evaporative disease can be managed with a medication that creates a monolayer over the cornea and helps retard some of that evaporative loss. If you evaluate the oil glands (called meibomian glands) by pressing on them, you can immediately determine if they are obstructed or failing to produce high-quality oil that should suppress excessive evaporation. Depending on how much damage is done to the meibomian glands, you may need to consider a procedure to express them. One of the first treatments that will give patients comfort and help them get through their workday is a prescribed semifluorinated alkane, which will put a thin monolayer over the tear film, provide comfort, and ultimately stabilize the patient’s vision by slowing evaporative loss.

If you still see damage on the cornea, you may need to treat the inflammation with an added immunosuppressive agent to treat both the evaporation and the resulting ocular surface inflammation.

AJMC: Can you describe how DED management strategies have changed in alignment with our evolving understanding of its pathophysiology?

Devries: The [Tear Film and Ocular Surface Society’s] Dry Eye Workshop study that came out in 2007 did not even mention evaporative loss, didn’t mention the damage to the meibomian glands. Ten years later, in 2017, there was a big emphasis on it. And now we see the more current and contemporary algorithms have to deal with the lids. Pressing on the lids, seeing if they have elasticity, pushing on the lids, seeing what the oil looks like. [The lids have really come to the forefront.]

The dynamics of the algorithms are changing. The emphasis really has shifted to the causative agents, [which] certainly could be the lids and the changing of those meibomian glands and what type of forces…are actually causing those meibomian glands to change and reduce the amount of oil that we get in our tears with every blink.

AJMC: How do you integrate nonpharmacologic treatments (eg, warm compresses, lid hygiene, environmental modifications) with prescription therapies when you’re treating patients with DED?

Devries: In my practice, nonpharmacologic therapies play an important complementary role alongside prescription treatments for DED. These include nutritional supplements, particularly the combination of omega-3/-6 fatty acids, that can help reduce inflammation and enhance tear production through natural anti-inflammatory pathways. I also recommend warm compresses for their palliative effect; while they won’t unblock obstructed meibomian glands, they can improve function in partially active glands and provide symptomatic relief.

Lid hygiene, over-the-counter artificial tears, and environmental modifications are routinely integrated into care plans. However, it’s critical to assess what patients are already using, as many self-medicate with multiple over-the-counter drops—often with preservatives—which can further irritate the ocular surface when used frequently. Educating patients on proper product selection is key.

Moisture goggles and ointments are additional tools, although they come with challenges such as discomfort, maintenance, or blurred vision. I tailor these interventions based on the severity of disease and individual patient needs. In mild to moderate cases, nonprescription therapies may be sufficient. However, for advanced DED or when structural damage is present, prescription treatments are necessary. Ultimately, a personalized, stepwise approach combining pharmacologic and nonpharmacologic strategies yields the best outcomes.

AJMC: How often do patients need to switch treatments, and what drives these treatment changes (eg, inadequate response, adverse effects)?

Devries: Treatment changes in DED are often driven by a combination of factors, with access and cost being major barriers. Even when the correct therapy is identified, insurance limitations and high out-of-pocket costs frequently prevent patients from initiating or continuing treatment.

When access is not an issue, changes are typically prompted by inadequate therapeutic response. However, before adjusting therapy, it’s essential to assess patient compliance. Nonadherence can often be mistaken for treatment failure, so confirming that the patient is using the medication as prescribed is a critical first step.

Only 13% of patients are fully satisfied with their current DED treatment, highlighting the need to dig deeper into the reasons behind suboptimal outcomes. These may include unaddressed underlying causes, environmental stressors, or lack of patient education—particularly around screen time, blinking habits, and the chronic nature of the disease.

AJMC: What is the role of in-office education, particularly for patients being treated with prescription medications with different mechanisms of action?

Devries: I [believe] in the treatment of DED that education is paramount. A patient has to understand why they’re taking something, why they’re doing treatments, [and] what our goals are. Sometimes, when we deal with eye drugs such as antibiotics…a patient gets a bacterial infection, we put an antibiotic on, and it’s done, it’s cured, it’s over. DED doesn’t work that way.

You [need to] educate the patient that this has been a chronic and progressive condition that has now gotten to the level that has affected their lifestyle and affected their vision. And so, I think that that’s really important—to outline the goals of what you’re trying to do and always tell the patient that this isn’t the last thing we could do. There are other treatments, there are other step progressions. And I always tell the patient, ‘My ultimate goal is to have you on the least treatment possible.’

AJMC: What has been your experience with step-therapy policies requiring use of tear-stimulating drugs in patients who may not have ADDE?

Devries: In managing DED, step-therapy policies [can] often create barriers to optimal care, particularly when mandating the use of tear-stimulating treatments in patients who might not have aqueous deficiency. In practice, we are constantly balancing clinical need with access, and insurance constraints [can]frequently delay or limit the ability to initiate the most appropriate therapy.

Coverage does not always equate to access; even when a therapy is technically covered, high out-of-pocket costs can make it unattainable. As a result, we spend a considerable amount of time navigating formularies and trying various lower-tier treatments, often taking weeks to identify an affordable and effective option.

This is especially problematic when step-therapy protocols require the use of tear secretagogues for patients whose primary issue is evaporative loss or inadequate lid seal—cases for which those medications offer limited to no benefit. These policies ignore the heterogeneity of DED and can delay more appropriate interventions, such as addressing meibomian gland dysfunction or mechanical eyelid issues.

Ultimately, step-therapy requirements that are not aligned with the underlying pathophysiology of DED [can] compromise patient outcomes, increase administrative burden, and prolong patient discomfort. A more individualized, evidence-based approach is essential to improve access to timely and effective care.

AJMC: What evidence gaps should be addressed to support better individualized treatment?

Devries: Significant evidence gaps remain in the individualized treatment of DED, particularly in our ability to identify early disease and intervene proactively. Eye care providers tend to be reactive—waiting for overt symptoms or structural damage before initiating treatment. This reactive model limits long-term success.

One critical area of unmet need is the evaluation and monitoring of corneal nerve health. Corneal nerves play a central role in ocular surface homeostasis—they influence epithelial regeneration, blink dynamics, and tear production. The cornea is the most innervated tissue in the body, yet we have few standardized tools to assess nerve integrity in clinical practice.

Emerging technologies now allow for quantifiable and reproducible measurement of corneal nerve status, opening the door for earlier detection of dysfunction—whether from surgery, contact lens wear, or disease progression. These insights could guide timely initiation of therapies targeting nerve regeneration or neurostimulation; these include nasally administered sprays that activate the trigeminal nerve to stimulate natural tear production.

We can take cues from fields like dentistry, which transitioned from reactive management to preventive care through early identification of biofilm-related pathology. In contrast, eye care still largely intervenes only after significant functional loss (eg, discontinuation of contact lenses, cataract development, or elevated intraocular pressure) occurs.

To support more individualized and effective treatment, we need research that validates early biomarkers of disease, particularly those involving the corneal nerves. This includes studying the impact of therapies like regenerative growth factors, amniotic tissue, or autologous serum tears in subclinical or early-stage disease. That’s the big gap that we have in eye care. Right now, everything is reactive. Especially with ocular surface disease or DED, we wait until it’s broken before we try to fix it.

Because there are so many unmet needs within the dry eye space, you see [a great deal of research within the] industry. [The numbers speak for themselves with] 140 million patients in the United States [experiencing] either intermittent or constant dry eye symptoms. Of those, about 38 [million] to 40 million would be classified as DED. And the number of people who are actually under a therapeutic treatment are about 1.5 million. [The] gap between 1.5 [million] and 38 million [is huge and drives innovation].

And I think that we can’t underestimate how [DED affects someone’s] life. It’s estimated that there’s about $4 [billion] to $5 billion spent on dry eye treatment. [That is a large number, but about] $50 billion is lost in productivity within the United States. Until somebody is affected by DED, they really don’t know the impact. [It can affect] driving [and the ability] to perform daily activities.