EyeCon 2026: Jade Coats, OD, FAAO, on dry eye disease comorbidities

Dry eye disease (DED) rarely presents in isolation, and comorbid conditions such as neurotrophic keratitis, Demodex blepharitis and cosmetic-related meibomian gland dysfunction (MGD) can drive persistent ocular surface symptoms when they go unrecognized. At EyeCon 2026, a virtual meeting held September 26 that brought optometrists and ophthalmologists together for a day of collaborative education, Jade Coats, OD, FAAO, of Exclusive Eye in Fayetteville, Arkansas, copresented "Why the dry? DED cases from minor to major" with Janelle Davison, OD, and Adam Ramsey, OD.

Following the session, the Eye Care Network asked Coats about the ocular surface conditions that often hide behind a dry eye diagnosis. In the following Q&A, Coats discusses the clinical clues that should raise suspicion for neurotrophic keratitis, the patient history questions that uncover cosmetic contributions to MGD, a layered approach to managing coexisting DED and Demodex blepharitis and how to recognize and break the cycle of mucus fishing syndrome.

Note: transcript edited lightly for clarity and length.

Neurotrophic keratitis can present subtly, especially in its earliest stages, and its risk factors range from prior LASIK to chronic CPAP use. What should prompt a clinician to look more closely for this condition, and why is catching it early so important?

Jade Coats, OD, FAAO: One of the biggest things that should prompt a clinician to look more closely is a mismatch between the patient's symptoms and what you see clinically. If the ocular surface looks significantly compromised but the patient reports surprisingly few symptoms, I want to think about reduced corneal sensitivity and the possibility of neurotrophic keratitis. A history of corneal surgery, herpetic disease, diabetes, chronic topical medication use, or anything that can affect corneal innervation should raise that suspicion. I also pay attention to patients with chronic CPAP use, particularly when there is evidence of exposure or an unhealthy ocular surface. Checking corneal sensitivity can be a simple but important part of that evaluation. Catching neurotrophic keratitis early matters because the loss of corneal sensation can allow epithelial damage to progress without the normal warning signal of pain. What starts as a subtle epithelial defect can progress to persistent epithelial breakdown, ulceration, stromal melting, and potentially vision-threatening complications. Recognizing the condition early gives us an opportunity to protect the ocular surface and intervene before that cycle becomes much more difficult to reverse.

Cosmetic habits, like tattooed eyeliner or makeup applied along the lid margin, can quietly contribute to MGD. What questions do you ask patients to uncover this connection, and how does it change your treatment plan once you find it?

Coats: I have found that sometimes the most revealing question is simply, “how do you remove your makeup?” Patients may not realize that their makeup routine can be contributing to their ocular surface symptoms. I also ask what products they use around the eyes, whether they apply eyeliner directly along the lid margin or waterline, how long they have been using those products, whether they sleep in makeup, and whether they have had permanent or semi-permanent eyeliner applied. I want to understand not only what they are putting on their eyelids, but also how aggressively they are removing it. If I identify a cosmetic contribution to MGD, I explain the connection rather than simply telling the patient to stop wearing makeup. We may modify where products are applied, discuss gentler removal techniques, emphasize lid hygiene, and address the underlying MGD with appropriate therapy. It becomes a conversation about changing the habits that are contributing to the problem while simultaneously treating the ocular surface.

A large share of patients with dry eye disease also have demodex blepharitis, and the two conditions often go untreated together. What does a layered approach to managing both look like in your practice, and why is addressing the comorbidity, not just the dry eye, important for outcomes?

Coats: I approach these patients by thinking about the ocular surface as a system rather than treating “dry eye” as a single diagnosis. First, I want to identify and address the underlying contributors, including demodex when the clinical findings support it. I look closely at the lid margins and lashes for findings such as collarettes, along with MGD, inflammation, tear-film instability, and ocular surface staining. If demodex is present, I address the infestation while also treating the associated lid and ocular surface inflammation. At the same time, I manage the dry eye component, which may include improving meibomian gland function, addressing inflammation, supporting the tear film, and making appropriate environmental or behavioral modifications. The important point is that treating only the dry eye may provide incomplete or temporary relief if an underlying lid-margin disease continues to drive inflammation. Identifying and treating the comorbidity can help break that cycle and gives the ocular surface a better opportunity to stabilize over time.

Mucus fishing syndrome is described as a self-perpetuating cycle where the behavior causing irritation isn't always recognized by the patient. What clinical clues help you distinguish it from other causes of chronic redness or irritation, and how do you approach breaking that cycle with patients?

Coats: One clue is the combination of chronic redness and irritation with a history of repeatedly removing or “fishing” for mucus from the eye. I may see conjunctival injection, mucus strands, localized irritation, or even areas of mechanical conjunctival trauma that don't quite fit the severity of the patient's other findings. Sometimes the patient describes constantly wiping, pulling, or removing something from the eye because it feels like there is always mucus present. The important part is recognizing that the mucus can actually be perpetuating the irritation: the patient sees mucus, removes it, traumatizes the conjunctiva, creates more inflammation and mucus, and then feels compelled to remove it again. I try to approach this without judgment because patients generally aren't intentionally causing harm—they are responding to an uncomfortable sensation. I explain the cycle in simple terms and make the patient part of the solution: the goal is to reduce the underlying irritation and, importantly, stop mechanically manipulating the conjunctiva. Depending on the underlying cause, that may mean treating coexisting dry eye, allergy, blepharitis, or another source of inflammation while giving the patient alternative strategies for managing the sensation. Breaking the behavioral cycle is just as important as treating the ocular surface disease that started it.