Eyes On 2026—In the Hot Seat 2: A Live Q&A with Cecelia Koetting

I think it's always a good thing to have a refresher on these things. There are three primary tear types (potentially four if we consider the possibility of a separate, distinct tear while we sleep at night): the basal tear, the reflex tear, and the emotional tear. While all of these tears do actually have the same components—having aqueous, mucin, oil, and meibum layers comprised of approximately 1500 different components, such as mediators and nerve growth factors, that are all held in a delicate balance—these different tear types do differ in their exact makeup and balance.^1-5 This is true for the basal tear, as the lacrimal functional unit (LFU) is essentially a liquefied tear, with additional components required for corneal functioning.

Activating basal tear production requires activation of the LFU feedback mechanism, which is comprised of:

Alongside these are the goblet cells, cornea, and LFU neural network. The neural network—particularly the cranial nerve V (the trigeminal nerve), whose branches run to both the tip of the nose and the cornea—is a key component in the actual activation of the LFU. Knowing this gives us a reference point for the medications we now have that activate or utilize this neural network, and thus the LFU.

Options such as BriteSite eye drops and Tyrvaya and oxymetazoline nasal sprays increase the tear volume through LFU activation—a similar approach is taken by Tryptyr, which activates the TRMP8 receptors on the ocular surface, which in turn leads to activation of the LFU. Although Tyrvaya causes some sneezing, the tears produced aren’t reactionary, and the increase in volume is sustained throughout the day. Beyond this, there are neurostimulation devices which stimulate the nasal nerve branches—this can be done either extranasally (iTEAR 100) or intranasally (TrueTear).⁶

But where can all this knowledge be applied? Often, we’re faced with a multifactorial issue, so we're very unlikely to reach for just one treatment. If you have a patient with a low tear volume and low tear meniscus height, your first thought might be to use immunomodulators to help decrease long-term inflammation. But this still leaves the question of how to increase the tear volume. That’s where this knowledge—and these options—fit in.

I love the idea of dysfunctional lens syndrome because it enables patients to understand that they’re on a journey. As doctors, we know that patients don’t all of a sudden lose their near vision as soon as they turn 40, and then suddenly have cataracts—instead, it's all part of the same process. But patients might not have this awareness. I think we need to start talking about lens dysfunction as a journey so that they’re not surprised. That’s really what the idea of dysfunctional lens syndrome offers. Stage one typically occurs between 42 and 50 years of age. At this point, the lens starts to stiffen, and patients will lose some focusing power and some near vision. Next, as they move to stage two (50+ years of age), we, as practitioners, start to see physical changes in the lens, including a change in color towards greater opacity and yellowing. Patients also start to experience loss of accommodation, light scatter formation, degrading vision, and decreased contrast and night vision. Finally, when they reach stage three (65+ years of age), everything has reached the point where we’re observing markers (poor visual quality, yellowing of the nucleus of the lens affecting colors, and opacity with degraded vision) that would lead us to make the call to remove a patient’s cataracts.

I like this framework as a discussion piece for our patients, alongside the idea of being able to physically observe the lens as it continually changes. Technically, we start to develop cataracts as soon as we're born—and lenticular yellowing can be seen as early as 25, becoming really evident at 47, and further progressing from there. Like I mentioned, it’s a journey.

When we talk about presbyopia, dysfunctional lens syndrome is part of that. The lens stiffens, and we lose accommodation. In terms of the new options, I don’t think there’s a one-size-fits-all solution. It’s just like multifocal contact lenses: there’s no one option that will work for every patient—even when it comes to each individual doctor, we may feel more comfortable with the fit guide for one lens versus another. That's really how I feel about these new dropoptions: VUITY, Qlosi, and VIZZ, alongside the two more that are likely coming down the pipeline. I think the discussion should be more about what works for each specific patient, but we aren't going to know that until we get more experience.

But also, don't be afraid of these options. They’re not going to cannibalize our contact lenses and glasses. I, for example, am the forty-something-year-old who would walk in and ask for all three modalities because I’d want the options that would allow me to live my life the way that I’d like to—partaking in all the activities I’d like. Regarding optimal pupil size, there are a couple of different studies that have looked at this. As far as getting that depth of focus, which is what these drops are doing, it's estimated that a pupil size between 2–3 mm is the optimum reduction.⁷

If you've got a patient who's already at 2 mm these drops might not work—that really goes back to how we pick these patients. Because there are multiple things that can shrink a patient’s pupils, such as medications and age. However, the opposite is also true. We shouldn’t say that just because a patient is 80 or because they’re post-cataract surgery, that these options automatically won’t work or that they won’t notice a benefit from them. Each case is different, and we have to treat them as such. But that’s the exciting part about medicine.

Dr. Koetting’s full responses to these and additional questions can be found in the VOD of the live Q&A session.