This episode, Drs. Abbott and Pucker begin an occasional series called “Industry Insights,” welcoming guest Natalie Nguyen, OD, Senior Director of Medical Affairs at Harrow, to discuss what it’s like for optometrists to transition from clinical practice into the pharmaceutical industry.

Dr. Nguyen, a Memphis native who completed her optometry degree at Southern College of Optometry, made the leap in 2022. She first learned about industry careers around 2017 through a pharmaceutical representative who introduced her to the Medical Science Liaison (MSL) role, a career path she hadn't known existed, as it was never discussed during her optometry training. She explains that her motivation to transition wasn’t burnout, as might be expected, but rather a growing curiosity about the science and strategy behind patient care—a desire to influence outcomes on a larger scale than one-on-one clinical encounters allow.

A significant portion of the conversation focuses on demystifying the MSL role. Dr. Nguyen characterizes the MSL role as a scientific bridge between a pharmaceutical company and the medical community—a non-promotional position involving peer-to-peer scientific discussions with clinicians that supports medical education. An important responsibility is bringing field insights back to the company internally. The role demands significant travel (50% to 80%), a high degree of autonomy and a broad skill set that goes well beyond scientific knowledge, she explains, including relationship-building, emotional intelligence, adaptability and self-discipline.

Dr. Nguyen talks candidly about the challenges of breaking into industry, sharing that she was rejected by three or four companies before landing her position at Harrow through a LinkedIn posting. She emphasizes that the field is increasingly competitive, and that a clinical background alone is no longer sufficient—candidates must find ways to differentiate themselves. Once hired at Harrow, she faced the additional challenge of being the company's first-ever medical affairs employee, essentially building the function from the ground up without formal onboarding or mentorship.

Her career advanced rapidly from MSL to Field Medical Director to her current role as Senior Director of Medical Affairs, where she oversees scientific strategy, cross-functional alignment, and long-term planning within the medical affairs function.

For optometrists considering a similar path, Dr. Nguyen’s key advice includes: do thorough research on the role and company, build genuine relationships through networking, find mentors early, embrace discomfort and never burn bridges in what is a surprisingly small professional community. She closes by saying that, given everything she knows now, she would make the same career leap without hesitation.

Kaleb Abbott and Andrew Pucker are joined by Jeff Banas, an OD from Wisconsin specializing in glaucoma and dry eye, to discuss neurotrophic keratitis (NK).

The trio begin by trying to clarify what, specifically, NK is and how it develops. While classically associated with herpetic infections (HSV/HZV), the panel emphasizes that other significant causes include diabetes, ocular or neuro surgery, chronic glaucoma medication use, and severe ocular surface disease. All can damage the trigeminal nerve, leading to loss of tearing and other functions that help sustain corneal health, resulting in formation of corneal epitheliopathy or even a persistent corneal epithelial defect. Left untreated, this has the potential to progress to stromal ulceration or even perforation.

A hallmark warning sign is “stain without pain”—significant corneal staining with little or no patient discomfort. This occurs because damaged nerves fail to transmit appropriate pain signals, which Dr. Abbott likens to having a non-functioning smoke detector during a fire. Dr. Banas also points to delayed healing after corneal epithelial debridement as one warning sign of incipient NK, and also describes the clinical value of the Mackie classification of NK:

• Stage 1: Punctate keratitis, tear film instability, reduced corneal sensitivity
• Stage 2: Persistent epithelial defect
• Stage 3: Stromal involvement, corneal thinning, neurotrophic ulcer

The three ODs stress that Stage 1 is the most common, but is frequently overlooked, and that heightened awareness of early NK is critical. They emphasize the need to test corneal sensitivity with a cotton wisp or, if available, a Cochet-Bonnet esthesiometer, the gold standard in research settings (cutoff of ≤ 4.0cm indicates NK). The panel encourages all clinicians to incorporate corneal sensitivity testing, especially for dry eye patients who are unresponsive to standard treatments.

Turning to treatment, the group distinguishes between supportive therapies (artificial tears, punctal occlusion, immunomodulators, warm compresses) and regenerative therapies (amniotic membranes, autologous serum drops, Oxervate) and gives pearls for effective use of each in appropriate circumstances. Prophylactic antibiotics are recommended for Stage 2 and 3 due to infection risk, but not typically for Stage 1, they note.

Drs. Abbott, Pucker and Banas leave listeners with this key advice:

1. Test corneal sensitivity. It’s simple, quick and doesn’t disrupt clinic flow.
2. Think beyond HSV—Consider neurotrophic keratitis in any patient with corneal epitheliopathy and relevant risk factors.
3. Don’t dismiss asymmetric staining. It may signal an underlying neurotrophic component.
4. Treat early and aggressively to prevent progression to more severe stages.

The discussion reinforces that NK is likely far more common than currently diagnosed, and earlier identification can significantly improve patient outcomes.

Relevant Articles:

Neurotrophic Keratitis: Hiding in Plain Sight

Hurt Feelings

Nerve Growth Factor Treatment May Initiate Corneal Recovery in Neurotrophic Keratitis

Corneal Complications of Diabetes: What ODs Need to Know

Mucins play an integral role in ocular surface health. They are the secret ingredient that gives the aqueous its viscosity and moisturizing properties. They entrap pathogens in the tear film to protect the eye. And they provide the glycocalyx anchor that keeps the tear film residing on the ocular surface. In this episode, Anna Tichenor, OD, PhD, of Indiana University explains all this and more in the no-nonsense terms you’d expect from a Midwesterner.

There are two types of mucin: free-floating and membrane-bound. The former are secreted by conjunctival goblet cells into the tear film, where they scavenge for bacteria and pollen while also providing the hydration properties of the tears. Membrane mucins, by contrast, arise from corneal and conjunctival epithelial cells and produce the glycocalyx, “kind of a shag carpet” on the ocular surface. Dr. Tichenor explains. Functionally, this creates a hydrophilic base that adheres the tear film to the eye.

The discussion then delve into clinical manifestations of these mucin properties, beginning with lissamine staining and what it signifies—dead or devitalized corneal epithelial cells that also have patches of missing glycocalyx.“Those areas are not going to be wetting very well,” Dr. Tichenor explains, “and would be very prone to infection.”

The team also offers advice on how to identify the Line of Marx at the mucocutaneous junction on lissamine green staining and what it might signify, as well as the role of mucins in lid wiper epitheliopathy.

Although fluorescein patterns are most often interpreted in the context of lipid layer integrity, Dr. Tichenor offers a nice clinical pearl on what they may say about the state of the glycocalyx, too: watch for the fluorescein spreading pattern across the cornea. If you see dark patches form almost immediately after a blink, “I would interpret that as areas where the glycocalyx is not functioning as well as it could.”

Membrane mucins are an effective early warning system. Inflammation is widely recognized as the key driver of dry eye, and research points to mucin as a potential regulator of inflammatory cytokines, Dr. Tichenor explains. Furthermore, overproduction of mucus happens in response to an antigen on the ocular surface—a threat that needs to be eliminated. This might be a clue to mucin deficiency in, for instance, Sjögren’s Syndrome.

This episode emphasizes that mucins contribute to dry eye cases in important ways that shouldn't be overlooked in favor of lipid-based mechanisms and interventions. Other mucin-mediated conditions include ocular cicatricial pemphigoid, mucus fishing syndrome, filamentary keratitis and Stevens-Johnsons Syndrome.

Despite the paucity of mucin-specific treatments available in the US. Dr. Tichenor explains that some artificial tears have “mucomimetic” properties, especially those containing hyaluronic acid. The potential of topical vitamin A is also touched on, as well as two drugs available internationally: diquafosol and rebamipide.

“Have mucins on your mind” as you assess dry eye and other ocular surface conditions, is Dr. Tichenor’s takeaway for the episode.

Relevant articles:

A Sticky Subject

As Smooth As Silk

Dry Eye Drop Boosts Ocular Mucins

Regional Conjunctival Differences in Glycocalyx Mucin Expression in Dry Eye and Normal Subjects